AACN Essentials of Critical Care Nursing 3rd Edition by Suzanne Burns [Dr.soc]

Also from McGraw-Hill Medical:

978-0-07-182279-4

Available everywhere medical books are sold

AACN Essentials of Critical Care Nursing Third Edition

Suzanne M. Burns, MSN, RRT, ACNP, CCRN, FAAN, FCCM, FAANP Professor Emeritus, School of Nursing University of Virginia Consultant, Critical and Progressive Care and Clinical Nursing Research Charlottesville, Virginia

New York Chicago San Francisco Athens London Madrid Mexico City Milan New Delhi Singapore Sydney Toronto

Copyright © 2014, 2010, 2006 by McGraw-Hill Education. All rights reserved. Except as permitted under the United States Copyright Act of 1976, no part of this publication may be reproduced or distributed in any form or by any means, or stored in a database or retrieval system, without the prior written permission of the publisher. ISBN: 978-0-07-182553-5 MHID: 0-07-182553-3 The material in this eBook also appears in the print version of this title: ISBN: 978-0-07-182279-4, MHID: 0-07-182279-8. eBook conversion by codeMantra Version 1.0 All trademarks are trademarks of their respective owners. Rather than put a trademark symbol after every occurrence of a trademarked name, we use names in an editorial fashion only, and to the benefit of the trademark owner, with no intention of infringement of the trademark. Where such designations appear in this book, they have been printed with initial caps. McGraw-Hill Education eBooks are available at special quantity discounts to use as premiums and sales promotions or for use in corporate training programs. To contact a representative, please visit the Contact Us page at www.mhprofessional.com. NOTICE Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required. The authors and the publisher of this work have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards accepted at the time of publication. However, in view of the possibility of human error or changes in medical sciences, neither the authors nor the publisher nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work. Readers are encouraged to confirm the information contained herein with other sources. For example and in particular, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs. TERMS OF USE This is a copyrighted work and McGraw-Hill Education and its licensors reserve all rights in and to the work. Use of this work is subject to these terms. Except as permitted under the Copyright Act of 1976 and the right to store and retrieve one copy of the work, you may not decompile, disassemble, reverse engineer, reproduce, modify, create derivative works based upon, transmit, distribute, disseminate, sell, publish or sublicense the work or any part of it without McGraw-Hill Education’s prior consent. You may use the work for your own noncommercial and personal use; any other use of the work is strictly prohibited. Your right to use the work may be terminated if you fail to comply with these terms. THE WORK IS PROVIDED “AS IS.” McGRAW-HILL EDUCATION AND ITS LICENSORS MAKE NO GUARANTEES OR WARRANTIES AS TO THE ACCURACY, ADEQUACY OR COMPLETENESS OF OR RESULTS TO BE OBTAINED FROM USING THE WORK, INCLUDING ANY INFORMATION THAT CAN BE ACCESSED THROUGH THE WORK VIA HYPERLINK OR OTHERWISE, AND EXPRESSLY DISCLAIM ANY WARRANTY, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO IMPLIED WARRANTIES OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. McGraw-Hill Education and its licensors do not warrant or guarantee that the functions contained in the work will meet your requirements or that its operation will be uninterrupted or error free. Neither McGraw-Hill Education nor its licensors shall be liable to you or anyone else for any inaccuracy, error or omission, regardless of cause, in the work or for any damages resulting therefrom. McGraw-Hill Education has no responsibility for the content of any information accessed through the work. Under no circumstances shall McGraw-Hill Education and/or its licensors be liable for any indirect, incidental, special, punitive, consequential or similar damages that result from the use of or inability to use the work, even if any of them has been advised of the possibility of such damages. This limitation of liability shall apply to any claim or cause whatsoever whether such claim or cause arises in contract, tort or otherwise.

To my critical care nursing colleagues around the world, whose wonderful work and efforts ensure the safe passage of patients through the critical care environment. Special thanks to Marianne Chulay RN, PhD, FAAN, my dear friend and colleague, for her many contributions and mentoring during the development of the first two editions of the Essentials of Critical Care Nursing and the Essentials of Progressive Care Nursing books. Her inspiration, drive, and thoughtful approach to the books continue to be an inspiration to me and the authors with whom she worked.

This page intentionally left blank

Contents

Contributors..........................................................................................................................................................................................................................................................xvii Reviewers............................................................................................................................................................................................................................................................. xix Preface................................................................................................................................................................................................................................................................. xxi Section I. The Essentials........................................................................................................................................................................................... 1

1. Assessment of Critically Ill Patients and Their Families.................................................................................................................. 3 Mary Fran Tracy 2. Planning Care for Critically Ill Patients and Their Families........................................................................................................... 19 Mary Fran Tracy 3. Interpretation and Management of Basic Cardiac Rhythms.......................................................................................................... 35 Carol Jacobson 4. Hemodynamic Monitoring................................................................................................................................................................. 69 Leanna R. Miller 5. Airway and Ventilatory Management.............................................................................................................................................. 119 Robert E. St. John and Maureen A. Seckel 6. Pain, Sedation, and Neuromuscular Blockade Management....................................................................................................... 159 Yvonne D’Arcy and Suzanne M. Burns 7. Pharmacology..................................................................................................................................................................................... 183 Earnest Alexander 8. Ethical and Legal Considerations..................................................................................................................................................... 215 Sarah Delgado Section II. Pathologic Conditions............................................................................................................................................................................ 231

9. Cardiovascular System....................................................................................................................................................................... 233 Barbara Leeper 10. Respiratory System............................................................................................................................................................................. 263 Maureen A. Seckel 11. Multisystem Problems....................................................................................................................................................................... 293 Ruth M. Kleinpell 12. Neurologic System.............................................................................................................................................................................. 311 Dea Mahanes

Contents

13. Hematologic and Immune Systems................................................................................................................................................. 337 Diane K. Dressler 14. Gastrointestinal System....................................................................................................................................................................... 351 Deborah A. Andris, Elizabeth Krzywda, Carol Rees Parrish, and Joe Krenitsky 15. Renal System....................................................................................................................................................................................... 383 Carol Hinkle 16. Endocrine System............................................................................................................................................................................... 399 Christine Kessler 17. Trauma................................................................................................................................................................................................. 415 Allen C. Wolfe and Benjamin W. Hughes Section III. Advanced Concepts in Caring for the Critically Ill Patient................................................................................................................................. 431

18. Advanced ECG Concepts.................................................................................................................................................................. 433 Carol Jacobson 19. Advanced Cardiovascular Concepts................................................................................................................................................ 475 Barbara Leeper 20. Advanced Respiratory Concepts: Modes of Ventilation.................................................................................................................. 507 Suzanne M. Burns 21. Advanced Neurologic Concepts....................................................................................................................................................... 517 Dea Mahanes Section IV. Key Reference Information..................................................................................................................................................................... 541

22. Normal Values Table.......................................................................................................................................................................... 543 Suzanne M. Burns 23. Pharmacology Tables......................................................................................................................................................................... 545 Earnest Alexander 24. Advanced Cardiac Life Support Algorithms................................................................................................................................... 559 Suzanne M. Burns 25. Hemodynamic Troubleshooting Guide........................................................................................................................................... 563 Leanna R. Miller 26. Cardiac Rhythms, ECG Characteristics, and Treatment Guide................................................................................................... 571 Carol Jacobson Index ............................................................................................................................................................................................................... 581

Contents in Detail

Contributors.............................................................................................................................................................................................................................................................xvii Reviewers..................................................................................................................................................................................................................................................................xix Preface................................................................................................................................................................................................................ xxi Section I. The Essentials........................................................................................................................................................................................... 1

1. Assessment of Critically Ill Patients and Their Families.................................................................................................................. 3 Mary Fran Tracy Assessment Framework 3 Prearrival Assessment 4 / Admission Quick Check 4 / Comprehensive Initial Assessment 4 / Ongoing Assessment 4 / Patient Safety Considerations in Admission Assessments 4

Prearrival Assessment: Before The Action Begins 5 Admission Quick Check Assessment: The First Few Minutes 6

Airway and Breathing 6 / Circulation and Cerebral Perfusion 7 / Chief Complaint 7 / Drugs and Diagnostic Tests 7 / Equipment 8

Comprehensive Initial Assessment 8

Past Medical History 9 / Social History 9 / Physical Assessment by Body System 9 / Psychosocial Assessment 14

Ongoing Assessment 16 Selected Bibliography 16

Critical Care Assessment 16 / Evidence-Based Practice 16

2. Planning Care for Critically Ill Patients and Their Families........................................................................................................... 19 Mary Fran Tracy Multidisciplinary Plan of Care 19 Planning Care Through Staffing Considerations 20 Patient Safety Considerations in Planning Care 20 Prevention of Common Complications 21 Physiologic Instability 21 / Deep Venous Thrombosis 22 / Hospital-Acquired Infections 22 / Skin Breakdown 23 / Sleep Pattern Disturbance 24 / Psychosocial Impact 24

Patient and Family Education 26

Assessment of Learning Readiness 26 / Strategies to Address Patient and Family Education 26 / Principles for Educational Outcome Monitoring 27

Family-Focused Care 27 Transporting The Critically Ill Patient 28

Assessment of Risk for Complications 29 / Level of Care Required During Transport 30 / Preparation 30 / Transport 31 / Interfacility Transfers 32

Transitioning to the Next Stage of Care 33 Supporting Patients and Families During the Dying Process 33 Selected Bibliography 33

vii

viii

Contents in Detail

Patient and Family Needs 33 / Infection Control 33 / Patient and Family Education 34 / Psychological Problems 34 / Sleep Deprivation 34 / Transport of Critically Ill Patients 34 / Evidence-Based Practice 34

3. Interpretation and Management of Basic Cardiac Rhythms.......................................................................................................... 35 Carol Jacobson Basic Electrophysiology 35 ECG Waveforms, Complexes, and Intervals 36 P Wave 36 / QRS Complex 37 / T Wave 37 / U Wave 37 / PR Interval 37 / ST Segment 37 / QT Interval 37

Basic Electrocardiography 37 Cardiac Monitoring 37 Determination of the Heart Rate 40 Determination of Cardiac Rhythm 40 Common Arrhythmias 41 Rhythms Originating in the Sinus Node 41

Normal Sinus Rhythm 41 / Sinus Bradycardia 41 / Sinus Tachycardia 42 / Sinus Arrhythmia 42 / Sinus Arrest 42

Arrhythmias Originating in the Atria 43

Premature Atrial Complexes 43 / Wandering Atrial Pacemaker 44 / Atrial Tachycardia 44 / Atrial Flutter 45 / Atrial Fibrillation 47 / Supraventricular Tachycardia (SVT) 51

Arrhythmias Originating in the Atrioventricular Junction 52

Premature Junctional Complexes 52 / Junctional Rhythm, Accelerated Junctional Rhythm, and Junctional Tachycardia 53

Arrhythmias Originating in the Ventricles 53

Premature Ventricular Complexes 53 / Ventricular Rhythm and Accelerated Ventricular Rhythm 54 / Ventricular Tachycardia 55 / Ventricular Fibrillation 56 / Ventricular Asystole 56

Atrioventricular Blocks 57

First-Degree Atrioventricular Block 57 / Second-Degree Atrioventricular Block 57 / High-Grade Atrioventricular Block 58 / Third-Degree Atrioventricular Block (Complete Block) 59

Temporary Pacing 60

Indications 60 / Transvenous Pacing 61 / Epicardial Pacing 62 / Components of a Pacing System 62 / Basics of Pacemaker Operation 62 / Initiating Transvenous Ventricular Pacing 64 / Initiating Epicardial Pacing 64 / External (Transcutaneous) Pacemakers 64

Defibrillation and Cardioversion 64

Defibrillation 64 / Automatic External Defibrillators 65 / Cardioversion 65

Selected Bibliography 66

Evidence-Based Practice 67

4. Hemodynamic Monitoring................................................................................................................................................................. 69 Leanna R. Miller Hemodynamic Parameters 69 Cardiac Output 69 / Components of Cardiac Output/Cardiac Index 71 / Stroke Volume and Stroke Volume Index 72 / Ejection Fraction 72 / Factors Affecting Stroke Volume/Stroke Volume Index 72

Basic Components of Hemodynamic Monitoring Systems 76

Pulmonary Artery Catheter 76 / Arterial Catheter 77 / Pressure Tubing 77 / Pressure Transducer 78 / Pressure Amplifier 78 / Pressure Bag and Flush Device 78 / Alarms 78

Obtaining Accurate Hemodynamic Values 79

Zeroing the Transducer 79 / Leveling the Transducer to the Catheter Tip 79 / Calibration of the Transducer/Amplifier System 80 / Ensuring Accurate Waveform Transmission 81

Insertion and Removal of Catheters 81

Pulmonary Artery Catheters 81 / Arterial Catheters 85

Obtaining and Interpreting Hemodynamic Waveforms 85

Patient Positioning 88 / Interpretation 88 / Artifacts in Hemodynamic Waveforms: Respiratory Influence 95 / Cardiac Output 96

Continuous Mixed and Central Venous Oxygen Monitoring 101

Continuous Mixed and Central Venous Oxygen Monitoring 101 / Selected Examples of Clinical Applications 103

Contents in Detail

Right Ventricular Ejection Fraction Catheters 103 Monitoring Principles 103 / Troubleshooting 104

Minimally Invasive Hemodynamic Monitoring 104

Thoracic Bioimpedance 104 / Esophageal Doppler Cardiac Output 104 / Carbon Dioxide Rebreathing 105 / Gastric Tonometry 105 / Sublingual Capnometry 105 / Pulse Contour Measurement 106

Application of Hemodynamic Parameters 107

Low Cardiac Output States 107 / High Cardiac Output States 111

Selected Bibliography 114

Hemodynamic Monitoring 114 / Minimally Invasive Hemodynamic Monitoring 115 / Therapeutics 116 / Evidence-Based Practice Guidelines 118

5. Airway and Ventilatory Management.............................................................................................................................................. 119 Robert E. St. John and Maureen A. Seckel Diagnostic Tests, Monitoring Systems and Respiratory Assessment Techniques 119 Arterial Blood Gas Monitoring 119 / Venous Blood Gas Monitoring 124 / Pulse Oximetry 124 / Assessing Pulmonary Function 126

Airway Management 127

Oropharyngeal Airway 127 / Nasopharyngeal Airway 128 / Artificial Airways 128 / Endotracheal Suctioning 131

Oxygen Therapy 133

Complications 133 / Oxygen Delivery 133

Basic Ventilatory Management 136

Indications 136 / General Principles 137 / Modes 140 / Complications of Mechanical Ventilation 142 / Weaning from Short-Term Mechanical Ventilation 144 / Weaning From Long-Term Mechanical Ventilation 146 / Respiratory Fatigue, Rest, and Conditioning 148 / Wean Trial Protocols 148 / Other Protocols for Use 148 / Critical Pathways 149 / Systematic Institutional Initiatives for the Management of the LTMV Patient Population 149 / Troubleshooting Ventilators 149 / Communication 150 / Principles of Management 153

Selected Bibliography 155

General Critical Care 155 / Ventilator Management 156 / Weaning From Mechanical Ventilation 156 / Communication 156 / Evidence-Based Resources 156

6. Pain, Sedation, and Neuromuscular Blockade Management....................................................................................................... 159 Yvonne D’Arcy and Suzanne M. Burns Physiologic Mechanisms of Pain 159 Peripheral Mechanisms 159 / Spinal Cord Integration 160 / Central Processing 161

Responses to Pain 161 Pain Assessment 162 A Multimodal Approach to Pain Management 162 Nonsteroidal Anti-Inflammatory Drugs 164 Side Effects 164

Opioids 164

Side Effects 164 / Intravenous Opioids 166 / Patient-Controlled Analgesia 166 / Switching From IV to Oral Opioid Analgesia 166

Epidural Analgesia 167

Epidural Opioids 167 / Epidural Local Anesthetics 169

Cutaneous Stimulation 169 Distraction 170 Imagery 171 Relaxation Techniques 171

Deep Breathing and Progressive Relaxation 171 / Presence 171

Special Considerations for Pain Management in the Elderly 171 Assessment 171 / Interventions 172

Sedation 172

Reasons for Sedation 172 / Drugs for Sedation 173 / Drugs for Delirium 174 / Goals of Sedation, Monitoring, and Management 174

Neuromuscular Blockade 175

Neuromuscular Blocking Agents 175 / Monitoring and Management 178

Contents in Detail

Selected Bibliography 179

Pain Management 179 / Sedation and Neuromuscular Blockade 180 / Evidence-Based Practice Guidelines 181

7. Pharmacology..................................................................................................................................................................................... 183 Earnest Alexander Medication Safety 183 Medication Administration Methods 184 Intravenous 184 / Intramuscular or Subcutaneous 184 / Oral 184 / Sublingual 185 / Intranasal 185 / Transdermal 185

Central Nervous System Pharmacology 185

Sedatives 185 / Analgesics 189 / Neuromuscular Blocking Agents 190 / Anticonvulsants 192

Cardiovascular System Pharmacology 196

Miscellaneous Agents 196 / Parenteral Vasodilators 196 / Antiarrhythmics 199 / Vasopressor Agents 201 / Inotropic Agents 202

Antibiotic Pharmacology 202

Aminoglycosides 203 / Vancomycin 203

Pulmonary Pharmacology 204

Theophylline 204 / Albuterol 205 / Levalbuterol 205

Gastrointestinal Pharmacology 205

Stress Ulcer Prophylaxis 205 / Acute Peptic Ulcer Bleeding 206 / Variceal Hemorrhage 206

Renal Pharmacology 206 Diuretics 206

Hematologic Pharmacology 208

Anticoagulants 208 / Factor Xa Inhibitors 209 / Direct Thrombin Inhibitors 210 / Glycoprotein IIb/ IIIa Inhibitor 210 / Thrombolytic Agents 210

Immunosuppressive Agents 211

Cyclosporine 211 / Tacrolimus (FK506) 212 / Sirolimus (Rapamycin) 212

Special Dosing Considerations 213

Continuous Renal Replacement Therapy 213 / Drug Disposition in the Elderly 213 / Therapeutic Drug Monitoring 213

Selected Bibliography 214

General 214 / Evidence-Based Practice Guidelines 214

8. Ethical and Legal Considerations..................................................................................................................................................... 215 Sarah Delgado The Foundation for Ethical Decision Making 215 Professional Codes and Standards 215 / Position Statements and Guidelines 216 / Institutional Policies 217 / Legal Standards 217 / Principles of Ethics 217 / The Ethic of Care 220 / Paternalism 220 / Patient Advocacy 221

The Process of Ethical Analysis 222

Assessment 222 / Plan 222 / Implementation 222 / Evaluation 222

Contemporary Ethical Issues 222

Informed Consent 222 / Determining Capacity 223 / Advance Directives 223 / End-of-Life Issues 224 / Resuscitation Decisions 227

Building an Ethical Environment 227

Values Clarification 227 / Provide Information and Clarify Issues 227 / Recognize Moral Distress 228 / Engage in Collaborative Decision Making 228

Selected Bibliography 228

Professional Codes, Standards, and Position Statements 229 / Evidence-Based Guidelines 229 / Online References of Interest: Related to Legal and Ethical Considerations 229

Section II. Pathologic Conditions............................................................................................................................................................................ 231

9. Cardiovascular System....................................................................................................................................................................... 233 Barbara Leeper Special Assessment Techniques, Diagnostic Tests, and Monitoring Systems 233 Assessment of Chest Pain 233 / Coronary Angiography 233 / Percutaneous Coronary Interventions 234 / Other Percutaneous Coronary Interventions 235

Contents in Detail

Pathologic Conditions 237

Acute Ischemic Heart Disease 237 / Heart Failure 247 / Shock 254 / Hypertension 258

Selected Bibliography 261

General Cardiovascular 261 / Coronary Revascularization 261 / Acute Ischemic Heart Disease 261 / Heart Failure 261 / Shock 262 / Hypertension 262 / Evidence-Based Practice Guidelines 262

10. Respiratory System............................................................................................................................................................................. 263 Maureen A. Seckel Special Assessment Techniques, Diagnostic Tests, and Monitoring Systems 263 Chest X-Rays 263 / Computed Tomography and Magnetic Resonance Imaging 268 / Pulmonary Angiograms, CTPA, and V/Q Scans 268 / Chest Tubes 269

Thoracic Surgery and Procedures 270

Principles of Management for Thoracic Surgery and Procedures 270

Pathologic Conditions 270

Acute Respiratory Failure 270 / Acute Respiratory Distress Syndrome (ARDS) 275 / Acute Respiratory Failure in the Patient with Chronic Obstructive Pulmonary Disease 277 / Acute Respiratory Failure in the Patient with Asthma (also called acute severe asthma) 280 / Principles of Management for Asthma Exacerbations 282 / Principles of Management for Acute Severe Asthma 282 / Pulmonary Hypertension 282 / Pneumonia 284 / Pulmonary Embolism 287

Selected Bibliography 290

Critical Care Management of Respiratory Problems 290 / Chest X-Ray Interpretation 290 / Miscellaneous 290 / Evidence-Based Practice Guidelines 290

11. Multisystem Problems....................................................................................................................................................................... 293 Ruth M. Kleinpell Pathologic Conditions 293 Sepsis and Multiple Organ Dysfunction Syndrome 293

Overdoses 300

Etiology, Risk Factors, and Pathophysiology 300

Complex Wounds and Pressure Ulcers 305 Pressure Ulcer Stages 305

Healthcare-Acquired Infections 306 Selected Infectious Diseases 307

Selected Bibliography 308

SIRS, Sepsis, and MODS 308 / Overdose 309 / Complex Wounds and Pressure Ulcers 309 / Healthcare-Acquired Infections 309 / Selected Infectious Diseases 310

12. Neurologic System.............................................................................................................................................................................. 311 Dea Mahanes Special Assessment Techniques, Diagnostic Tests, and Monitoring Systems 311 Level of Consciousness 311 / Glasgow Coma Scale 312 / Full Outline of UnResponsiveness (FOUR) Score 313 / Mental Status 313 / Motor Assessment 315 / Sensation 316 / Cranial Nerve Assessment and Assessment of Brain Stem Function 316/ Vital Sign Alterations in Neurologic Dysfunction 318 / Death by Neurologic Criteria 319

Diagnostic Testing 319

Lumbar Puncture 319 / Computed Tomography 320 / Magnetic Resonance Imaging 320 / Cerebral (Catheter) Angiography 321 / Transcranial Doppler Ultrasound 321 / Electroencephalography 322 / Electromyography/Nerve Conduction Studies 322

Intracranial Pressure: Concepts and Monitoring 322

Cerebral Blood Flow 322 / Causes of Increased Intracranial Pressure 323 / Clinical Presentation 323 / Invasive Monitoring of ICP 324 / Principles of Management of Increased ICP 325

Acute Ischemic Stroke 327

Etiology, Risk Factors, and Pathophysiology 327 / Clinical Presentation 328 / Diagnostic Tests 329 / Principles of Management of Acute Ischemic Stroke 329

Hemorrhagic Stroke 331

Etiology, Risk Factors, and Pathophysiology 331 / Clinical Presentation 331 / Diagnostic Tests 332 / Principles of Management of Intracerebral Hemorrhage 332

Seizures 332

Etiology, Risk Factors, and Pathophysiology 332 / Clinical Presentation 332 / Diagnostic Testing 333 / Principles of Management of Seizures 333

xii

Contents in Detail

Infections of the Central Nervous System 334

Meningitis 334 / Encephalitis 334 / Intracranial Abscess 334

Neuromuscular Diseases 334

Myasthenia Gravis 335 / Guillain-Barré Syndrome 335

Selected Bibliography 335

Assessment and Diagnostic Testing 335 / Intracranial Pressure 336 / Acute Ischemic Stroke and Hemorrhagic Stroke 336 / Seizures 336 / Infections of the Central Nervous System 336 / Neuromuscular Diseases 336 / Evidence-Based Practice 336

13. Hematologic and Immune Systems................................................................................................................................................. 337 Diane K. Dressler Special Assessment Techniques, Diagnostic Tests, and Monitoring Systems 337 Complete Blood Count 337 / Red Blood Cell Count 337 / Hemoglobin 338 / Hematocrit 338 / Red Blood Cell Indices 338 / Total White Blood Cell Count 338 / White Blood Cell Differential 339 / Platelet Count 339 / Coagulation Studies 339 / Additional Tests and Procedures 340

Pathologic Conditions 340

Anemia 340 / Immunocompromise 342 / Coagulopathies 344

Selected Bibliography 348

Anemia 348 / Immunocompromised Patient 349 / Coagulopathy 349

14. Gastrointestinal System....................................................................................................................................................................... 351 Deborah A. Andris, Elizabeth Krzywda, Carol Rees Parrish, and Joe Krenitsky Pathologic Conditions 351 Acute Upper Gastrointestinal Bleeding 351 / Liver Failure 359 / Acute Pancreatitis 364 / Intestinal Ischemia 366 / Bowel Obstruction 367 / Bariatric (Weight Loss) Surgery 369 / Surgical Procedure 369

Nutritional Support for Critically Ill Patients 371

Nutritional Requirements 371 / Nutritional Case: Special Populations 371 / Gastric Residual Volume 372 / Aspiration 373 / Bowel Sounds 375 / Nausea and Vomiting 375 / Osmolality or Hypertonicity of Formula 375 / Diarrhea 376 / Flow Rates and Hours of Infusion 377 / Formula Selection 377

Selected Bibliography 377

Upper GI Bleeding 377 / Liver Failure 378 / Acute Pancreatitis 378 / Intestinal Ischemia/Bowel Obstruction 378 / Nutrition 379 / Bariatric (Gastric Bypass) Surgery 380

15. Renal System....................................................................................................................................................................................... 383 Carol Hinkle Special Assessment Techniques, Diagnostic Tests, and Monitoring Systems 383 Pathologic Conditions 383 Acute Renal Failure 383 / Life-Threatening Electrolyte Imbalances 388

Renal Replacement Therapy 393

Access 393 / Dialyzer/Hemofilters/Dialysate 394 / Procedures 394 / Indications for and Efficacy of Renal Replacement Therapy Modes 395 / General Renal Replacement Therapy Interventions 397

Selected Bibliography 397

General Renal and Electrolytes 397 / Renal Failure 398 / Renal Replacement Therapy 398 / Web Resources 398

16. Endocrine System............................................................................................................................................................................... 399 Christine Kessler Special Assessment Techniques, Diagnostic Tests, and Monitoring Systems 399 Blood Glucose Monitoring 399

Pathologic Conditions 401

Hyperglycemic States 401 / Hyperglycemic Emergencies 402 / Acute Hypoglycemia 408 / Syndrome of Inappropriate Antidiuretic Hormone Secretion 409 / Diabetes Insipidus 411

Selected Bibliography 413

Blood Glucose Monitoring 413 / Hyperglycemia, DKA, and HHS 413 / SIADH and Diabetes Insipidus 413

Contents in Detail

xiii

17. Trauma................................................................................................................................................................................................. 415 Allen C. Wolfe and Benjamin W. Hughes Specialized Assessment Techniques, Diagnostic Tests, and Monitoring Systems 415 Primary and Secondary Trauma Survey Assessment 415 / Diagnostic Studies 417 / Mechanism of Injury 418 / Physiologic Consequences of Trauma 421

Common Injuries in the Trauma Patient 421

Thoracic Trauma 421 / Abdominal Trauma 423 / Musculoskeletal Trauma 425

Complications of Traumatic Injury in Severe Multisystem Trauma 427

Acute Respiratory Distress Syndrome 428 / Infection/Sepsis 428 / Systemic Inflammatory Response Syndrome 428

Psychological Consequences of Trauma 429 Selected Bibliography 430

General Trauma 430 / Selected Web sites 430 / Evidence-Based Practice 430

Section III. Advanced Concepts in Caring for the Critically Ill Patient................................................................................................................................. 431

18. Advanced ECG Concepts.................................................................................................................................................................. 433 Carol Jacobson The 12-lead Electrocardiogram 433 Axis Determination 437 / Bundle Branch Block 438 / Acute Coronary Syndrome 442 / Preexcitation Syndromes 448

Advanced Arrhythmia Interpretation 452

Supraventricular Tachycardias 452 / Polymorphic Ventricular Tachycardias 456 / Differentiating Wide QRS Beats and Rhythms 458

St-Segment Monitoring 461

Measuring the ST Segment 461 / Choosing the Best Leads for ST-Segment Monitoring 461

Cardiac Pacemakers 463

Evaluating Pacemaker Function 465 / VVI Pacemaker Evaluation 465 / DDD Pacemaker Evaluation 468

Selected Bibliography 472

Evidence-Based Practice 473

19. Advanced Cardiovascular Concepts................................................................................................................................................ 475 Barbara Leeper Pathologic Conditions 475 Cardiomyopathy 475 / Valvular Heart Disease 480 / Pericarditis 486 / Aortic Aneurysm 488 / Cardiac Transplantation 492 / Intra-Aortic Balloon Pump Therapy 497 / Ventricular Assist Devices 500

Selected Bibliography 503

General Cardiovascular 503 / Cardiomyopathy 503 / Heart Transplantation 504 / Valvular Disorders 504 / Pericarditis 504 / Thoraco-Abdominal Aneurysms 504 / Intra-aortic Balloon Pump Therapy 504 / Ventricular Assist Devices 504 / Evidence-Based Practice/Guidelines 505

20. Advanced Respiratory Concepts: Modes of Ventilation.................................................................................................................. 507 Suzanne M. Burns Advanced Modes of Mechanical Ventilation 507 New Concepts: Mechanical Ventilation 507 / Volume Versus Pressure Ventilation 508 / Advanced Modes: What Do We Know? 514

Selected Bibliography 515

Mechanical Ventilation: Modes 515 / Selected Vendor Web Pages 516 / Evidence-Based Practice 516 / Additional Readings 516

21. Advanced Neurologic Concepts....................................................................................................................................................... 517 Dea Mahanes Subarachnoid Hemorrhage 517 Etiology, Risk Factors, and Pathophysiology 517 / Clinical Presentation 517 / Diagnostic Tests 518 / Principles of Management of Aneurysmal-Subarachnoid Hemorrhage 519

xiv

Contents in Detail

Traumatic Brain Injury 522

Etiology, Risk Factors, and Pathophysiology 522 / Clinical Presentation 525 / Diagnostic Tests 525 / Principles of Management of Traumatic Brain Injury 526

Traumatic Spinal Cord Injury 528

Etiology, Risk Factors, and Pathophysiology 528 / Clinical Presentation 528 / Diagnostic Tests 530 / Principles of Management of Acute Spinal Cord Injury 530 / Future Spinal Cord Injury Treatment 536

Brain Tumors 536

Etiology, Risk Factors, and Pathophysiology 536 / Clinical Presentation 536 / Diagnostic Tests 537 / Principles of Management of Intracranial Tumors 537

Advanced Technology: Brain Tissue Oxygen Monitoring 538 Selected Bibliography 539

Subarachnoid Hemorrhage 539 / Traumatic Brain Injury 539 / Spinal Cord Injury 539 / Brain Tumors 539 / Advanced Technology: Brain Tissue Oxygen Monitoring 539 / Evidence-Based Guidelines 539

Section IV. Key Reference Information..................................................................................................................................................................... 541

Acknowledgments

Special thanks to those who made contributions to the previous editions of both the Essentials of Critical Care Nursing and the Essentials of Progressive Care Nursing. To Cathie Guzzetta RN, PhD, FAAN and Barbara Dossey RN, MS, FAAN for their early work in creating the Handbook of Critical Care Nursing which preceded the Essentials of Critical Care Nursing and the Essentials of Progressive Care Nursing books. To Marianne Chulay RN, PhD, FAAN, my dear friend and colleague, for her many contributions and mentoring during the development of the first two editions of the Essentials of Critical Care Nursing and the Essentials of Progressive Care Nursing books. Her inspiration, drive, and thoughtful approach to the books continue to be an inspiration to me and the authors with whom she worked. Thank you to the many authors for their past contributions: Tom Ahrens, RNS, DNS, CCNS, FAAN (Chapter 4 and key reference materials) Suzanne M. Burns, RN, MSN, RRT ACNP, CCRN, FAAN, FCCM, FAANP (Chapters 5, 11) Deb Byram, RN, MS (Chapter 1) Karen Carlson, RN, MN (Chapter 15)

Joan Michiko Ching, RN, MN, CPHQ (Chapter 6) Marianne Chulay, RN, PhD, FAAN (Chapter 10, and the key reference materials) Maria Connolly, RN, DNSc (Chapters 5, 10) Dorrie Fontaine, RN, DNSc, FAAN (Chapter 17) Bradi Granger, RN, PhD (Chapter 9) Anne Marie Gregoire, RN, MSN, CRNP (Chapter 19) Joanne Krumberger, RN, MSN, CHE, FAAN (Chapters 14, 16) Sally Miller, RN, PhD, APN, FAANP (Chapter 14) Carol A. Rauen, RN, MS, CCNS, CCRN, PCCN (Chapter 17) Juanita Reigle, RN, MSN, ACNP (Chapter 8) Anita Sherer, RN, MSN (Chapter 2) Sue Simmons-Alling, RN, MSN (Chapter 2) Jamie Sinks, RN, MS (Chapter 17) Greg Susla, Pharm D, FCCM (Chapter 7 and key reference materials) Debbie Tribett, RN, MS, CS, LNP (Chapter 13) Debra Lynn-McHale Wiegand, RN, PhD, CS (Chapter 19) Lorie Wild, RN, PhD (Chapter 6) Susan Woods, PhD, RN (Chapters 3, 18) Marlene Yates, RN, MSN (Chapter 2)

This page intentionally left blank

Contributors

Earnest Alexander, PharmD, FCCM Assistant Director, Clinical Pharmacy Services Program Directlor, PGY2 Critical Care Residency Department of Pharmacy Services Tampa General Hospital Tampa, Florida Chapter 7: Pharmacology Chapter 23: Pharmacology Tables Deborah A. Andris, MSN, APNP Nurse Practitioner Division of Colorectal Surgery Medical College of Wisconsin Milwaukee, Wisconsin Chapter 14: Gastrointestinal System Yvonne D’Arcy, MS, CRNP, CNS Pain Management and Palliative Care Nurse Practitioner Suburban Hospital-Johns Hopkins Medicine Bethesda, Maryland Chapter 6: Pain, Sedation, and Neuromuscular Blockade Management Suzanne M. Burns, RN, MSN, RRT, ACNP, CCRN, FAAN, FCCM, FAANP Professor Emeritus, School of Nursing University of Virginia Consultant, Critical and Progressive Care and Clinical Nursing Research Charlottesville, Virginia Chapter 6: Pain, Sedation, and Neuromuscular Blockade Management Chapter 20: Advanced Respiratory Concepts: Modes of Ventilation Chapter 22: Normal Values Table Chapter 24: Advanced Cardiac Life Support Algorithms Sarah Delgado, RN, MSN, ACNP Chronic Care Nurse Practitioner PIH Health Physicians Whittier, California Chapter 8: Ethical and Legal Considerations

Diane K. Dressler, MSN, RN, CCRN Clinical Assistant Professor Marquette University College of Nursing Milwaukee, Wisconsin Chapter 13: Hematologic and Immune Systems Carol Hinkle, MSN, RN-BC Brookwoood Medical Center Birmingham, Alabama Chapter 15: Renal System Benjamin W. Hughes, RN, MSN, MS, CCRN Director Trauma Institute and Cardiopulmonary Services University of Louisville Hospital Louisville, Kentucky Chapter 17: Trauma Carol Jacobson, RN, MN Director, Quality Education Services and Partner Cardiovascular Nursing Education Associates Clinical Faculty University of Washington School of Nursing Seattle, Washington Chapter 3: Interpretation and Management of Basic Cardiac Rhythms Chapter 18: Advanced ECG Concepts Chapter 24: Cardiac Rhythms, ECG Characteristics, and Treatment Guide Chapter 26: Cardiac Rhythms, ECG Characteristics, and Treatment Guide Christine Kessler, MN, CNS, ANP, BC-ADM Nurse Practitioner, Diabetes Institute Department of Endocrinology and Metabolic Medicine Walter Reed Army Medical Center Washington, DC Chapter 16: Endocrine System

xvii

xviii

Contributors

Ruth M. Kleinpell, PhD, RN-CS, FAAN, FCCM, FAANP, ACNP, CCRN Director, Center for Clinical Research and Scholarship Rush University Medical Center Professor, Rush University College of Nursing Nurse Practitioner, Our Lady of the Resurrection Medical Center Chicago, Illinois Chapter 11: Multisystem Problems Joe Krenitsky, MS, RD Nutrition Support Specialist Digestive Health Center of Excellence Department of Nutrition Services University of Virginia Health System Charlottesvillle, Virginia Chapter 14: Gastrointestinal System Elizabeth Krzywda, MSN, APNP Nurse Practitioner Pancreaticobiliary Surgery Program Medical College of Wisconsin Milwaukee, Wisconsin Chapter 14: Gastrointestinal System Barbara Leeper, MN, RN-BC, CNS-MS, CCRN, FAHA Clinical Nurse Specialist Cardiovascular Services Baylor University Medical Center Dallas, Texas Chapter 9: Cardiovascular System Chapter 19: Advanced Cardiovascular Concepts Dea Mahanes, RN, MSN, CCRN, CNRN, CCNS Advanced Practice Nurse 3 Clinical Nurse Specialist Nerancy Neuro ICU University of Virginia Health System Charlottesville, Virginia Chapter 12: Neurologic System Chapter 21: Advanced Neurologic Concepts Leanna R. Miller, RN, MN, CCRN-CMC, PCCN-CSC, CEN, CNRN, CMSRN, NP Instructor Western Kentucky University Bowling Green, Kentucky Chapter 4: Hemodynamic Monitoring Chapter 25: Hemodynamic Troubleshooting Guide

Carol Rees Parrish, MS, RD Nutrition Support Specialist Digestive Health Center of Excellence Department of Nutrition Services University of Virginia Health System Charlottesvillle, Virginia Chapter 14: Gastrointestinal System Robert E. St. John, MSN, RN, RRT Covidien Care Area Manager—US Patient Monitoring Respiratory and Monitoring Solutions Boulder, Colorado Chapter 5: Airway and Ventilatory Management Maureen A. Seckel, APN, ACNS, BC, CCNS, CCRN Clinical Nurse Specialist Medical Pulmonary Critical Care Christiana Care Health System Newark, Delaware Chapter 5: Airway and Ventilatory Management Chapter 10: Respiratory System Mary Fran Tracy, PhD, RN, CCNS, FAAN Critical Care Clinical Nurse Specialist University of Minnesota Medical Center, Fairview Minneapolis, Minnesota Chapter 1: Assessment of Critically Ill Patients and Their Families Chapter 2: Planning Care for Critically Ill Patients and Their Families Allen C. Wolfe, Jr., MSN, RN, CFRN, CCRN, CMTE Clinical Education Director/Clinical Specialist Air Methods Corporation Community Based Services Denver, Colorado Chapter 17: Trauma

Reviewers

John M. Allen, PharmD, BCPS Assistant Professor Department of Pharmacotherapeutic and Clinical Research University of South Florida College of Pharmacy Tampa, Florida Richard B. Arbour, MSN, RN, CCRN, CNRN, CCNS, FAAN Liver Transplant Coordinator Thiomas Jefferson University Hospital Advanced Practice Nurse/Educator/Researcher Philadelphia, Pennsylvania Cheri S. Blevins, MSN RN CCRN CCNS APN-2 Clinical Nurse Specialist Medical ICU University of Virginia Health System Charlottesville, Virginia Shawn Cosper, MSN, RN Education Consultant-Critical Care Education Department Brookwood Medical Center Birmingham, Alabama Sarah JaneWhite Craig, MSN, RN, CCNS, CCRN, CSC Clinical Nurse Specialist Postoperative Thoracic-Cardiovascular SurgeryService Universityof VirginiaHealth System Charlottesville, Virginia Tina Cronin, APRN, CCNS, CCRN, CNRN Senior Director Clinical Programs and Outcomes Piedmont Medical Center Rock Hill, South Carolina Linda DeStefano, CNS, NP, FCCM Clinical Nurse Specialist, Critical Care Services Saddleback Memorial Medical Center Laguna Hills, California

Beth Epstein, PhD, RN Associate Professor University of Virginia School of Nursing Faculty Affiliate University of Virginia Center for Biomedical Ethics and Humanities University of Virginia Charlottesville, Virginia John J. Gallagher, MSN, RN, CCNS, CCRN, RRT Trauma Program Manager Division of Traumatology, Surgical Critical Care and Emergency Surgery Hospital of the University of Pennsylvania Philadelphia, Pennsylvania Tonja Hartjes, DNP, ACNP/FNP-BC, CCRN-CSC Associate Clinical Professor University of Florida, College of Nursing Adult Gerontology and Acute Care ARNP Program & Cardiothoracic Surgery ARNP Shands UF Gainesville, Florida Barbara S. Jacobs, MSN, RN-BC, CCRN, CENP Senior Director/Chief Nurse Officer Suburban Hospital Bethesda, Maryland Katherine Johnson, MS, CNRN, CCRN, CNS-BC Neuroscience Clinical Nurse Specialist The Queens Medical Center Honolulu, Hawaii Victoria A. Kark, RN, MSN, CCRN, CCNS, CSC Clinical Nurse Specialist SICU/MICU Walter Reed National Military Medical Center Bethesda, Maryland

xix

Reviewers

Deborah Klein, MSN, RN, ACNS-BC, CCRN, CHFN, FAHA Clinical Nurse SpecialistCoronary ICU,Heart Failure ICU, and Cardiac Short Stay/PACU Cleveland Clinic Cleveland, Ohio

Michelle A. Weber, RN, MSN, ACNP-BC Nurse Practitioner Division of General Surgery Medical College of Wisconsin Milwaukee, Wisconsin

Julie Painter, RN, MSN, OCN Community Health Network Oncology Clinical Nurse Specialist Indianapolis, Indiana

Brian Widmar, PhD, RN, ACNP-BC, CCRN-CSC-CMC Assistant Professor of Nursing Vanderbilt University School of Nursing Nashville, Tennessee

Carol A Rauen, RN, MS, CCNS, CCRN, PCCN, CEN Independent Clinical Nurse Specialist and Education Consultant Kill Devil Hills, North Carolina

Susan L. Woods, PhD, RN, FAAN Professor Emerita Department of Biobehavioral Nursing and Health Systems School of Nursing University of Washington Seattle, Washington

Christine Schulman, MS, RN, CNS, CCRN Critical Care CNS Legacy Health Portland, Oregon Michelle VanDemark, MSN, RN, ANP-BC, CNRN, CCSN Neurocritical Care Nurse Practitioner Sanford Medical Center Sioux Falls, South Dakota

Amanda Zomp, PharmD, BCPS Critical Care Clinical Pharmacist University of Virginia Medical Center Charlottesville, Virginia

Preface

Critical care nursing is a complex, challenging area of nursing practice where clinical expertise is developed over time by integrating critical care knowledge, clinical skills, and caring practices. This textbook succinctly presents essential information about how best to safely and competently care for critically ill patients and their families. As it has since the first edition, the American Association of Critical-Care Nurses reaffirms this book’s value to the AACN community and especially to clinicians at the point of care. The title continues to carry AACN’s name, as it has since the first edition. AACN Essentials of Critical Care Nursing provides essential information on the care of adult critically ill patients and families. The book recognizes the learner’s need to assimilate foundational knowledge before attempting to master more complex critical care nursing concepts. Written by nationally acknowledged clinical experts in critical care nursing, this book sets a new standard for critical care nursing education. AACN Essentials of Critical Care Nursing represents a departure from the way in which most critical care books are written because it: • Succinctly presents essential information for the safe and competent care of critically ill adult patients and their families, building on the clinician’s significant medical-surgical nursing knowledge base, avoiding repetition of previously acquired information; • Stages the introduction of advanced concepts in critical care nursing after essential concepts have been mastered; • Provides clinicians with clinically-relevant tools and guides to use as they care for critically ill patients and families. AACN Essentials of Critical Care Nursing is divided into four parts: • Part I: The Essentials presents core information that clinicians must understand to provide safe, competent nursing care to all critically ill patients, regardless of their underlying medical diagnoses. This part includes

content on essential concepts of assessment, diagnosis, planning, and interventions common to critically ill patients and their families; interpretation and management of cardiac rhythms; hemodynamic monitoring; airway and ventilatory management; pain, sedation and neuromuscular blockade management; pharmacology; and ethical and legal considerations. Chapters in Part I present content in enough depth to ensure that essential information is available for the critical care clinician to develop competence, while sequencing pathological conditions in part II and advanced content in a later part of the book (Part III). • Part II: Pathologic Conditions covers pathologic conditions and management strategies commonly encountered in critical care units, closely paralleling the blueprint for the CCRN certification examination. Chapters in this part are organized by body systems and selected critical care conditions, such as cardiovascular, respiratory, multisystem, neurologic, hematologic and immune, gastrointestinal, renal, endocrine, and trauma. • Part III: Advanced Concepts in Caring for the Critically Ill Patient presents advanced critical care concepts or pathologic conditions that are more complex and represent expert level information. Specific advanced chapter content includes ECG concepts, cardiovascular concepts, respiratory concepts (ie, modes of ventilation), and neurologic concepts. • Part IV: Key Reference Information contains reference information that clinicians will find helpful in the clinical area (normal laboratory and diagnostic values; algorithms for advanced cardiac life support; troubleshooting guides for hemodynamic monitoring; and summary tables of critical care drugs and cardiac rhythms). Content is presented primarily in table format for quick reference. Each chapter in Part I, II, and III, begins with “Knowledge Competencies” that can be used to guide informal or formal teaching and to gauge the learner’s progress. In addition, xxi

xxii

Preface

each of the chapters provide “Essential Content Case” studies that focus on key information presented in the chapters in order to assist clinicians in understanding the chapter content and how to best assess and manage conditions and problems encountered in critical care. The case studies are also designed to enhance the learners understanding of the magnitude of the pathologic problems/conditions and their impact on patients and families. Questions and answers are provided for each case so the learner may test his/her knowledge of the essential content.

It is my belief that there is no greater way to protect our patients than to ensure that an educated clinician cares for them. Safe passage in critical care is ensured by competent, skilled, knowledgeable, and caring clinicians. I sincerely believe that this textbook will help you make it so! Suzi Burns

The Essentials

This page intentionally left blank

Assessment Of Critically Ill Patients and Their Families Mary Fran Tracy

KNOWLEDGE COMPETENCIES 1. Discuss the importance of a consistent and systematic approach to assessment of critically ill patients and their families. 2. Identify the assessment priorities for different stages of a critical illness: • Prearrival assessment • Admission quick check

The assessment of critically ill patients and their families is an essential competency for critical care practitioners. Information obtained from an assessment identifies the immediate and future needs of the patient and family so a plan of care can be initiated to address or resolve these needs. Traditional approaches to patient assessment include a complete evaluation of the patient’s history and a comprehensive physical examination of all body systems. This approach, although ideal, rarely is possible in critical care as clinicians struggle with life-threatening problems during admission and must balance the need to gather data while simultaneously prioritizing and providing care. Traditional approaches and techniques for assessment must be modified in critical care to balance the need for information, while considering the critical nature of the patient and family’s situation. This chapter outlines an assessment approach that recognizes the emergent and dynamic nature of a critical illness. This approach emphasizes the collection of assessment data in a phased, or staged, manner consistent with patient care priorities. The components of the assessment can be used as a generic template for assessing most critically ill patients and families. The assessment can then be individualized by adding more specific assessment requirements depending on the

• Comprehensive admission assessment • Ongoing assessment 3. Describe how the assessment is altered based on the patient’s clinical status.

specific patient diagnosis. These specific components of the assessment are identified in subsequent chapters. Crucial to developing competence in assessing critically ill patients and their families is a consistent and systematic approach to assessments. Without this approach, it would be easy to miss subtle signs or details that may identify an actual or potential problem and also indicate a patient’s changing status. Assessments should focus first on the patient, then on the technology. The patient needs to be the focal point of the critical care practitioner’s attention, with technology augmenting the information obtained from the direct assessment. There are two standard approaches to assessing patients: the head-to-toe approach and the body systems approach. Most critical care nurses use a combination, a systems approach applied in a “top-to-bottom” manner. The admission and ongoing assessment sections of this chapter are presented with this combined approach in mind.

ASSESSMENT FRAMEWORK Assessing the critically ill patient and family begins from the moment the nurse is made aware of the pending admission of the patient and continues until transitioning to the next 3

CHAPTER 1. Assessment Of Critically Ill Patients and Their Families

phase of care. The assessment process can be viewed as four distinct stages: (1) prearrival, (2) admission quick check (“just the basics”), (3) comprehensive initial, and (4) ongoing assessment.

Prearrival Assessment A prearrival assessment begins the moment the information is received about the upcoming admission of the patient. This notification comes from the initial healthcare team contact. The contact may be paramedics in the field reporting to the emergency department (ED), a transfer from another facility, or a transfer from other areas within the hospital such as the emergency room (ER), operating room (OR), or medical/ surgical nursing unit. The prearrival assessment paints the initial picture of the patient and allows the critical care nurse to begin anticipating the patient’s physiologic and psychological needs. This prearrival assessment also allows the critical care nurse to determine the appropriate resources that are needed to care for the patient. The information received in the prearrival phase is crucial because it allows the critical care nurse to adequately prepare the environment to meet the specialized needs of the patient and family.

Admission Quick Check An admission quick check assessment is obtained immediately upon arrival and is based on assessing the parameters represented by the ABCDE acronym (Table 1-1). The admission quick check assessment is a quick overview of the adequacy of ventilation and perfusion to ensure early intervention for any life-threatening situations. Energy is also focused on exploring the chief complaint and obtaining essential diagnostic tests to supplement physical assessment findings. The admission quick check is a high-level view of the patient but is essential because it validates that basic cardiac and respiratory function is sufficient.

Comprehensive Initial Assessment A comprehensive initial assessment is performed as soon as possible, with the timing dictated by the degree of physiologic stability and emergent treatment needs of the patient. If the patient is being admitted directly to the intensive care unit (ICU) from outside the hospital, the comprehensive assessment is an in-depth assessment of the past medical and social history and a complete physical examination of each body system. If the patient is being transferred to the ICU TABLE 1-1. ABCDE ACRONYM Airway Breathing Circulation, Cerebral perfusion, and Chief complaint Drugs and Diagnostic tests Equipment

from another area in the hospital, the comprehensive assessment includes a review of the admission assessment data and comparison to the current state of the patient. The comprehensive assessment is vital to successful outcomes because it provides the nurse invaluable insight into proactive interventions that may be needed.

Ongoing Assessment After the baseline comprehensive initial assessment is completed, ongoing assessments, an abbreviated version of the comprehensive initial assessment, are performed at varying intervals. The assessment parameters outlined in this section are usually completed for all patients, in addition to other ongoing assessment requirements related to the patient’s specific condition, treatments, and response to therapy.

Patient Safety Considerations in Admission Assessments Admission of an acutely ill patient can be a chaotic and fast-paced event with multiple disciplines involved in many activities. It is at this time, however, that healthcare providers must be particularly cognizant of accurate assessments and data gathering to ensure the patient is cared for safely with appropriate interventions. Obtaining inaccurate information on admission can lead to ongoing errors that may not be easily rectified or discovered and lead to poor patient outcomes. Obtaining information from an acutely ill patient may be difficult, if possible at all. If the patient is unable to supply information, other sources must be utilized such as family members, electronic health records (EHRs), past medical records, transport records, or information from the patient’s belongings. Of particular importance at admission is obtaining accurate patient identification, as well as past medical history including any known allergies. Current medication regimens are extremely helpful if feasible, as they can provide clues to the patient’s medical condition and perhaps contributing factors to the current condition. With the increasing use of EHRs, opportunities are improving for timely access to past and current medical histories of patients. Critical care providers may have access to both inpatient and outpatient records within the same healthcare system, assisting them in quickly identifying the patient’s most recent medication regimen and laboratory and diagnostic results. In addition, many healthcare systems within the same geographic locations are working together to make access available to intersystem medical records of patients being treated at multiple healthcare institutions. This is particularly beneficial in the intensive care setting where patients may be unable to articulate imperative medical information, including advance directives, allergies, and next of kin. Careful physical assessment on admission to the critical care unit is pivotal for providing prevention and/or early treatment for complications associated with critical illness. Of particular importance is the assessment of risk for pressure

PREARRIVAL ASSESSMENT: BEFORE THE ACTION BEGINS 5

ulcer formation, alteration in mental status, and/or falls. Risks associated with accurate patient identification never lessen, particularly as these relate to interventions such as performing invasive procedures, medication administration, blood administration, and obtaining laboratory tests. Nurses need to be cognizant of safety issues as treatment begins as well. For example, accurate programming of pumps infusing high-risk medications is essential. It is imperative that nurses use all safety equipment available to them such as preprogrammed drug libraries in infusion pumps and bar-coding technology. Healthcare providers must also ensure the safety of invasive procedures that may be performed emergently.

PREARRIVAL ASSESSMENT: BEFORE THE ACTION BEGINS A prearrival assessment begins when information is received about the pending arrival of the patient. The prearrival report, although abbreviated, provides key information about the chief complaint, diagnosis, or reason for admission, pertinent history details, and physiologic stability of the patient (Table 1-2). It also contains the gender and age of the patient and information on the presence of invasive tubes and lines, medications being administered, other ongoing treatments, TABLE 1-2. SUMMARY OF PREARRIVAL AND ADMISSION QUICK CHECK ASSESSMENTS Prearrival Assessment • Abbreviated report on patient (age, gender, chief complaint, diagnosis, pertinent history, physiologic status, invasive devices, equipment, and status of laboratory/diagnostic tests) • Allergies • Complete room setup, including verification of proper equipment functioning Admission Quick Check Assessment • General appearance (consciousness) • Airway: Patency Position of artificial airway (if present) • Breathing: Quantity and quality of respirations (rate, depth, pattern, symmetry, effort, use of accessory muscles) Breath sounds Presence of spontaneous breathing • Circulation and Cerebral Perfusion: ECG (rate, rhythm, and presence of ectopy) Blood pressure Peripheral pulses and capillary refill Skin, color, temperature, moisture Presence of bleeding Level of consciousness, responsiveness • Chief Complaint: Primary body system Associated symptoms • Drugs and Diagnostic Tests: Drugs prior to admission (prescribed, over-the-counter, illicit) Current medications Review diagnostic test results • Equipment: Patency of vascular and drainage systems Appropriate functioning and labeling of all equipment connected to patient

and pending or completed laboratory or diagnostic tests. It is also important to consider the potential isolation requirements for the patient (eg, neutropenic precautions or special respiratory isolation). Being prepared for isolation needs prevents potentially serious exposures to the patient or the healthcare providers. This information assists the clinician in anticipating the patient’s physiologic and emotional needs prior to admission and in ensuring that the bedside environment is set up to provide all monitoring, supply, and equipment needs prior to the patient’s arrival. Many critical care units have a standard room setup, guided by the major diagnosis-related groups of patients each unit receives. The standard monitoring and equipment list for each unit varies; however, there are certain common requirements (Table 1-3). The standard room setup is modified for each admission to accommodate patient-specific needs (eg, additional equipment, intravenous [IV] fluids, medications). Proper functioning of all bedside equipment should be verified prior to the patient’s arrival. It is also important to prepare the medical record, which usually consists of a manual flow sheet or computerized data entry system to record vital signs, intake and output, medication administration, patient care activities, and patient assessment. The prearrival report may suggest pending procedures, necessitating the organization of appropriate supplies at the bedside. Having the room prepared and all equipment available facilitates a rapid, smooth, and safe admission of the patient. If the ICU is partnering in an tele-ICU (e-ICU) model, inform the tele-ICU hub of the pending admission so they can also prepare to begin surveillance of the critically ill patient upon arrival. Consider and plan for the fact that family members often arrive with the patient or even prior to the patient’s arrival in the ICU. Designate a healthcare worker who will connect with family members on their arrival by answering questions, giving them a brief orientation to the unit, showing them to a place where they can comfortably wait, providing them specific information as to when they will be able to see their loved one, and offering support resources.

TABLE 1-3. EQUIPMENT FOR STANDARD ROOM SETUP

• Bedside ECG and invasive pressure monitor with appropriate cables • ECG electrodes • Blood pressure cuff • Pulse oximetry • Suction gauges and canister setup • Suction catheters • Bag-valve-mask device • Oxygen flowmeter, appropriate tubing, and appropriate oxygen delivery device

• IV poles and infusion pumps • Bedside supply cart that contains such things as alcohol swabs, nonsterile gloves, syringes, chux, and dressing supplies

• Admission kit that usually contains bath basin and general hygiene supplies

• Admission and critical care paper and/or electronic documentation forms

CHAPTER 1. Assessment Of Critically Ill Patients and Their Families

ADMISSION QUICK CHECK ASSESSMENT: THE FIRST FEW MINUTES From the moment the patient arrives in the ICU setting, his or her general appearance is immediately observed and assessment of ABCDEs is quickly performed (see Table 1-1). On arrival, verify any urgent changes in patient condition or equipment in use since the prearrival report. The seriousness of the problem(s) is determined so that life-threatening emergent needs can be addressed first. The patient is connected to the appropriate monitoring and support equipment, critical medications are administered, and essential laboratory and diagnostic tests are ordered. Simultaneous with the ABCDE assessment, the nurse must validate that the patient is appropriately identified through a hospital wristband, personal identification, or family identification. In addition, the patient’s allergy status is determined, including the type of reaction that occurs and what, if any, treatment is used to alleviate the allergic response. There may be other healthcare professionals present to receive the patient and assist with admission tasks. The critical care nurse, however, is the leader of the receiving team. While assuming the primary responsibility for assessing the ABCDEs, the patient’s nurse directs the team in completing delegated tasks, such as changing over to the ICU equipment or attaching monitoring cables. Without a leader of the receiving team, care can be fragmented and vital assessment clues overlooked. The critical care nurse rapidly assesses the ABCDEs in the sequence outlined in this section. If any aspect of this

Essential Content Case

Prearrival Assessment The charge nurse notifies Sue that she will be receiving a 26-year-old man from the ER who was involved in a serious car accident. The ED nurse caring for the patient has called to give Sue a report following the hospital’s standardized report format. The patient was an unrestrained driver in a lowspeed head-on collision and has sustained a closed-head injury and chest trauma with collapsed left lung. The patient was intubated and placed on a mechanical ventilator. IV access had been obtained, and a left chest tube had been inserted. The ED nurse provides the latest trend of the patient’s vital signs and neurologic assessments and how he has responded to the administered pain medication. After a computed tomographic (CT) scan of the head, chest, and abdomen is obtained, the patient will be transferred to the ICU. Sue questions the ED nurse regarding whether the patient has been agitated, had a Foley catheter and nasogastric tube placed, and whether family had been notified of the accident. Sue goes to check the patient’s room prior to admission and begins to do a mental check of what will be needed. “The patient is intubated so I’ll connect the AMBU bag to the oxygen source, check for suction

catheters, and make sure the suction systems are working. The pulse oximetry and the ventilator are ready to go. I have an extra suction gauge to connect to the chest tube system. I’ll also turn on the ECG monitor and have the ECG electrodes ready to apply. An arterial line kit is at the bedside, and the flush system and transducer are also ready to be connected. The IV infusion devices are set up. This patient has an altered LOC, which means frequent neuro checks and potential insertion of an ICP catheter for monitoring. I have my pen light handy, but I better check to see if we have all the equipment to insert the ICP catheter in case the physician wants to perform the procedure here after the CT scan. The computer in the room is on and ready for me to begin documentation. I think I’m ready.” Case Question 1: What basic information will Sue want to know from the prearrival communication with the ED nurse? Case Question 2: What patient issues are likely to need immediate assessment and/or intervention on arrival to the ICU in order to ensure the appropriate equipment is set up in the room? Case Question 3: What information should be included in the more formal handoff between the ED nurse and Sue after the patient is settled in the ICU? Answers 1. Patient name/age; type and timing of accident; extent of accident injuries; pertinent medical history, allergies, vital signs, and significant assessment information; placement of tubes and lines; medications being administered; significant laboratory results; anticipated plan on admission; presence of family; and any other special instructions. 2. Vital signs, neurologic status, and information such as whether the ventilator is adequately addressing the patient’s ventilation needs, medications are appropriately infusing, and whether the patient is agitated or experiencing extensive pain. 3. Using an SBAR (situation-background-assessmentrecommendation) format, the ED nurse can give more detailed information about the injuries from the car accident; the patient’s complete medical history as known; reiteration of known allergies; a system by system assessment review; diagnostic test results; confirmation of all invasive lines and equipment settings; the anticipated plan for ongoing assessments and interventions; and any pertinent family information. Sue should also have an opportunity to ask any clarifying questions she might have.

preliminary assessment deviates from normal, interventions are immediately initiated to address the problem before continuing with the admission quick check assessment. Additionally, regardless of whether the patient appears to be conscious or not, it is important to talk to him or her throughout this admission process regarding what is occurring with each interaction and intervention.

Airway and Breathing Patency of the patient’s airway is verified by having the patient speak, watching the patient’s chest rise and fall, or

both. If the airway is compromised, verify that the head has been positioned properly to prevent the tongue from occluding the airway. Inspect the upper airway for the presence of blood, vomitus, and foreign objects before inserting an oral airway if one is needed. If the patient already has an artificial airway, such as a cricothyrotomy, endotracheal (ET) tube, or tracheostomy, ensure that the airway is secured properly. Note the position of the ET tube and size marking on the ET tube that is closest to the teeth, lips, or nares to assist future comparisons for proper placement. Suctioning of the upper airway, either through the oral cavity or artificial airway, may be required to ensure that the airway is free from secretions. Note the amount, color, and consistency of secretions removed. Note the rate, depth, pattern, and symmetry of breathing; the effort it is taking to breathe; the use of accessory muscles; and, if mechanically ventilated, whether breathing is in synchrony with the ventilator. Observe for nonverbal signs of respiratory distress such as restlessness, anxiety, or change in mental status. Auscultate the chest for presence of bilateral breath sounds, quality of breath sounds, and bilateral chest expansion. Optimally, both anterior and posterior breath sounds are auscultated, but during this admission quick check assessment, time generally dictates that just the anterior chest is assessed. If noninvasive oxygen saturation monitoring is available, observe and quickly analyze the values. If the patient is receiving assistive breaths from a bag-valve-mask or mechanical ventilator, note the presence of spontaneous breaths and evaluate whether ventilation requires excessive pressure and whether the patient’s breathing appears comfortable and synchronized with the ventilator. If chest tubes are present, note whether they are pleural or mediastinal chest tubes. Ensure that they are connected to suction, if appropriate, and are not clamped or kinked. In addition, assess whether they are functioning properly (eg, air leak, fluid fluctuation with respiration) and review the amount and character of the drainage.

Circulation and Cerebral Perfusion Assess circulation by quickly palpating a pulse and viewing the electrocardiogram (ECG) monitor for the heart rate, rhythm, and presence of ectopy. Obtain blood pressure and temperature. Assess peripheral perfusion by evaluating the color, temperature, and moisture of the skin along with capillary refill. Based on the prearrival report and reason for admission, there may be a need to inspect the body for any signs of blood loss and determine if active bleeding is occurring. Evaluating cerebral perfusion in the admission quick check assessment is focused on determining the functional integrity of the brain as a whole, which is done by rapidly evaluating the gross level of consciousness (LOC). Evaluate whether the patient is alert and aware of his or her surroundings, whether it takes a verbal or painful stimulus to obtain

ADMISSION QUICK CHECK ASSESSMENT: THE FIRST FEW MINUTES 7

a response, or whether the patient is unresponsive. Observing the response of the patient during movement from the stretcher to the ICU bed can supply additional information about the LOC. Note whether the patient’s eyes are open and watching the events around him or her. For example, does the patient follow simple commands such as “Place your hands on your chest” or “Slide your hips over”? If the patient is unable to talk because of trauma or the presence of an artificial airway, note whether his or her head nods appropriately to questions.

Chief Complaint Optimally, the description of the chief complaint is obtained from the patient, but this may not be realistic. The patient may be unable to respond or may not speak English. Data may need to be gathered from family, friends, bystanders, and prehospital personnel. If the patient or family cannot speak English, an approved hospital translator should be contacted to help with the interview and subsequent evaluations and communication. It is not recommended that family or friends are used to translate for a non-English speaking patient in order to protect the patient’s privacy, to avoid the likelihood that family will not understand appropriate medical terminology for translation, and to eliminate wellintentioned but potential bias in translating back and forth for the patient. In the absence of a history source, practitioners must depend exclusively on the physical findings (eg, presence of medication patches, permanent pacemaker, or old surgery scars), knowledge of pathophysiology, and access to prior paper, electronic medical records (EMRs), or transport records to identify the potential causes of the admission. Assessment of the chief complaint focuses on determining the body systems involved and the extent of associated symptoms. Additional questions explore the time of onset, precipitating factors, and severity. Although the admission quick check phase is focused on obtaining a quick overview of the key life-sustaining systems, a more in-depth assessment of a particular system may need to be done at this time. For example, in the prearrival case study scenario presented, completion of the ABCDEs is followed quickly by more extensive assessment of both the nervous and respiratory systems.

Drugs and Diagnostic Tests Information about drugs and diagnostic tests is integrated into the priority of the admission quick check. If IV access is not already present, it should be immediately obtained and intake and output records started. If IV medications are presently being infused, check the drug(s) and verify the correct infusion of the desired dosage and rate. Obtain critical diagnostic tests. Augment basic screening tests (Table 1-4) by additional tests appropriate to the underlying diagnosis and chief complaint. Review any available laboratory or diagnostic data for abnormalities or indications of potential problems requiring immediate intervention.

CHAPTER 1. Assessment Of Critically Ill Patients and Their Families

TABLE 1-4. COMMON DIAGNOSTIC TESTS OBTAINED DURING ADMISSION QUICK CHECK ASSESSMENT Serum electrolytes Glucose Complete blood count with platelets Coagulation studies Arterial blood gases Chest x-ray ECG

The abnormal laboratory and diagnostic data for specific pathologic conditions will be covered in subsequent chapters.

Equipment Quickly evaluate all vascular and drainage tubes for location and patency, and connect them to appropriate monitoring or suction devices. Note the amount, color, consistency, and odor of drainage secretions. Verify the appropriate functioning of all equipment attached to the patient and label as required. While connecting the monitoring and care equipment, it is imperative that the nurse continue to assess the patient’s respiratory and cardiovascular status until it is clear that all equipment is functioning appropriately and can be relied on to transmit accurate patient data. The admission quick check assessment is accomplished in a matter of a few minutes. After completion of the ABCDEs assessment, the comprehensive initial assessment begins. If at any phase during the admission quick check a component of the ABCDEs has not been stabilized and controlled, energy is focused first on resolving the abnormality before proceeding to the comprehensive admission assessment. After the admission quick check assessment is complete, and if the patient requires no urgent intervention, there may now be time for a more thorough report from the healthcare providers transferring the patient to the ICU. It is important to note that handoffs with transitions of care are possible intervals when safety gaps may occur. Omission of pertinent information or miscommunication at this critical juncture can result in patient care errors. Use of a standardized handoff format, such as the SBAR format, can minimize the potential for miscommunication. Use the handoff as an opportunity to confirm observations such as dosage of infusing medications, abnormalities found on the quick check assessment, independent double check and confirmation of equipment settings, and any potential inconsistencies noted between your assessment and the prearrival report. It is easier to clarify questions while the transporters are still present if possible. This may also be an opportunity for introductory interactions with family members or friends, if present. Introduce yourself, offer reassurance, and confirm the intention to give the patient the best care possible (Table 1-5). If feasible, allow them to briefly see the patient. If this is not feasible, give them an approximate time frame when they can expect to

TABLE 1-5. EVIDENCE-BASED PRACTICE: FAMILY NEEDS ASSESSMENT Quick Assessment • Offer realistic hope • Give honest answers and information • Give reassurance Comprehensive Assessment • Use open-ended communication and assess their communication style • Assess family members’ level of anxiety • Assess perceptions of the situation (knowledge, comprehension, expectations of staff, expected outcome) • Assess family roles and dynamics (cultural and religious practices, values, spokesperson) • Assess coping mechanisms and resources (what do they use, social network and support)

receive an update from you on the patient’s condition. Have another member of the healthcare team escort them to the appropriate waiting area.

COMPREHENSIVE INITIAL ASSESSMENT Comprehensive initial assessments determine the physiologic and psychosocial baseline so that future changes can be compared to determine whether the status is improving or deteriorating. The comprehensive initial assessment also defines the patient’s pre-event health status, determining problems or limitations that may impact patient status during this admission as well as potential issues for future transitioning of care. The content presented in this section is a template to screen for abnormalities or determine the extent of injury to the patient. Any abnormal findings or changes from baseline warrant a more in-depth evaluation of the pertinent system. The comprehensive initial assessment includes review of the patient’s medical and brief social history, and physical examination of each body system. The comprehensive admission assessment of the critically ill patient is similar to admission assessments for noncritically ill patients. This section describes only those aspects of the assessment that are unique to critically ill patients or require more extensive information than is obtained from a non–critical care patient. The entire assessment process is summarized in Tables 1-6 and 1-7. Changing demographics of critical care units indicate that an increasing proportion of patients are elderly, requiring assessments to incorporate the effects of aging. Although assessment of the aging adult does not differ significantly from that of younger adults, understanding how aging alters the physiologic and psychological status of the patient is important. Key physiologic changes pertinent to the critically ill elderly adult are summarized in Table 1-8. Additional emphasis must also be placed on the past medical history because the aging adult frequently has multiple coexisting illnesses and is taking several prescriptive and overthe-counter medications. Social history includes addressing issues related to home environment, support systems, and self-care abilities. The interpretation of clinical findings in the elderly must also take into consideration the fact that the

COMPREHENSIVE INITIAL ASSESSMENT 9

TABLE 1-6. SUMMARY OF COMPREHENSIVE ADMISSION ASSESSMENT REQUIREMENTS Past Medical History • Medical conditions, surgical procedures • Psychiatric/emotional problems • Hospitalizations • Medications (prescription, over-the-counter, illicit drugs) and time of last medication dose • Allergies • Review of body systems (see Table 1-7) Social History • Age, gender • Ethnic origin • Height, weight • Highest educational level completed • Occupation • Marital status • Primary family members/significant others/decision makers • Religious affiliation • Advance Directive and Durable Power of Attorney for Health Care • Substance use (alcohol, drugs, caffeine, tobacco) • Domestic abuse or vulnerable adult screen Psychosocial Assessment • General communication • Coping styles • Anxiety and stress • Expectations of critical care unit • Current stresses • Family needs Spirituality • Faith/spiritual preference • Healing practices Physical Assessment • Nervous system • Cardiovascular system • Respiratory system • Renal system • Gastrointestinal system • Endocrine, hematologic, and immune systems • Integumentary system

coexistence of several disease processes and the diminished reserves of most body systems often result in more rapid physiologic deterioration than in younger adults.

Past Medical History Besides the primary event that brought the patient to the hospital, it is important to determine prior medical and surgical conditions, hospitalization, medications, and symptoms (see Table 1-7). In reviewing medication use, ensure assessment of over-the-counter medication use as well as any herbal or alternative supplements. For every positive symptom response, additional questions should be asked to explore the characteristics of that symptom (Table 1-9).

Social History Inquire about the use and abuse of caffeine, alcohol, tobacco, and other substances. Because the use of these agents can

have major implications for the critically ill patient, questions are aimed at determining the frequency, amount, and duration of use. Honest information regarding alcohol and substance abuse, however, may not be always forthcoming. Alcohol use is common in all age groups. Phrasing questions about alcohol use by acknowledging this fact may be helpful in obtaining an accurate answer (eg, “How much alcohol do you drink?” vs “Do you drink alcohol and how much?”). Family or friends might provide additional information that might assist in assessing these parameters. The information revealed during the social history can often be verified during the physical assessment through the presence of signs such as needle track marks, nicotine stains on teeth and fingers, or the smell of alcohol on the breath. Patients should also be asked about physical and emotional safety in their home environment in order to uncover potential domestic or elder abuse. It is best if patients can be assessed for vulnerability when they are alone to prevent placing them in a position of answering in front of family members or friends who may be abusive. Ask questions such as “Is anyone hurting you?” or “Do you feel safe at home?” in a nonthreatening manner. Any suspicion of abuse or vulnerability should result in a consultation with a social worker to determine additional assessments.

Physical Assessment by Body System The physical assessment section is presented in the sequence in which the combined system, head-to-toe approach is followed. Although content is presented as separate components, generally the history questions are integrated into the physical assessment. The physical assessment section uses the techniques of inspection, auscultation, and palpation. Although percussion is a common technique in physical examinations, it is infrequently used in critically ill patients. Pain assessment is generally linked to each body system rather than considered as a separate system category. For example, if the patient has chest pain, assessment and documentation of that pain is incorporated into the cardiovascular assessment. Rather than have general pain assessment questions repeated under each system assessment, they are presented here. Pain and discomfort are clues that alert both the patient and the critical care nurse that something is wrong and needs prompt attention. Pain assessment includes differentiating acute from chronic pain, determining related physiologic symptoms, and investigating the patient’s perceptions and emotional reactions to the pain. Explore the qualities and characteristics of the pain by using the questions listed in Table 1-9. Pain is a very subjective assessment and critical care practitioners sometimes struggle with applying their own values when attempting to evaluate the patient’s pain. To resolve this dilemma, use the patient’s own words and descriptions of the pain whenever possible and use a patientpreferred pain scale (see Chapter 6, Pain, Sedation, and Neuromuscular Blockade Management) to objectively and

CHAPTER 1. Assessment Of Critically Ill Patients and Their Families

TABLE 1-7. SUGGESTED QUESTIONS FOR REVIEW OF PAST HISTORY CATEGORIZED BY BODY SYSTEM Body System Nervous

History Questions

• Have you ever had a seizure? • Have you ever fainted, blacked out, or had delirium tremens (DTs)?

• Do you ever have numbness, tingling, or weakness in any part of your body? • Do you have any difficulty with your hearing, vision, or speech? • Has your daily activity level changed due to your present condition? • Do you require any assistive devices such as canes? Cardiovascular

• Have you experienced any heart problems or disease such as heart attacks or strokes? • Do you have any problems with extreme fatigue? • Do you have an irregular heart rhythm? • Do you have high blood pressure? • Do you have a pacemaker or an implanted defibrillator?

Respiratory

• Do you ever experience shortness of breath? • Do you have any pain associated with breathing? • Do you have a persistent cough? Is it productive? • Have you had any exposure to environmental agents that might affect the lungs? • Do you have sleep apnea?

Renal

• Have you had any change in frequency of urination? • Do you have any burning, pain, discharge, or difficulty when you urinate? • Have you had blood in your urine?

Gastrointestinal

• Has there been any recent weight loss or gain? • Have you had any change in appetite? • Do you have any problems with nausea or vomiting? • How often do you have a bowel movement and has there been a change in the normal pattern? Do you have blood in your stools? • Do you have dentures? • Do you have any food allergies?

Integumentary

• Do you have any problems with your skin?

Endocrine

• Have you had a change in your energy level?

Hematologic

• Do you have any problems with bleeding?

Immunologic

• Do you have problems with chronic infections? • Have you recently been exposed to a contagious illness?

Psychosocial

• Do you have any physical conditions which make communication difficult (hearing loss, visual disturbances, language barriers, etc)? • How do you best learn? Do you need information repeated several times and/or require information in advance of teaching sessions? • What are the ways you cope with stress, crises, or pain? • Who are the important people in your “family” or network? Who do you want to make decisions with you, or for you? • Have you had any previous experiences with critical illness? • Have you ever been abused? • Have you ever experienced trouble with anxiety, irritability, being confused, mood swings, or suicidal thoughts or attempts? • What are the cultural practices, religious influences, and values that are important to you or your family? • What are family perceptions and expectations of the critical care staff and the setting? • What is your faith or spiritual preference? • What practices help you heal or deal with stress? • Would you like to see a chaplain, priest, or other spiritual guide?

Spiritual

consistently evaluate pain levels. If the patient is nonverbal, there are several validated tools that can be used to assess pain beyond physiologic signs such as the critical care pain observation tool (CPOT) or the behavioral pain scale (BPS). Nervous System

The nervous system is the “master computer” of all systems and is divided into the central and peripheral nervous systems. With the exception of the peripheral nervous system’s cranial nerves, almost all attention in the critically ill patient

is focused on evaluating the central nervous system (CNS). The physiologic and psychological impact of critical illness, in addition to pharmacologic interventions, frequently alters CNS functioning. The single most important indicator of cerebral functioning is the LOC. The LOC is assessed in the critically ill patient using the Glasgow Coma Scale (see Chapter 12, Neurologic System). Assess pupils for size, shape, symmetry, and reactivity to direct light. When interpreting the implication of altered pupil size, remember that certain medications such as

COMPREHENSIVE INITIAL ASSESSMENT 11

TABLE 1-8. PHYSIOLOGIC EFFECTS OF AGING Body System Nervous

Cardiovascular Respiratory Renal Gastrointestinal Endocrine, hematologic, and immunologic Integumentary Miscellaneous Psychosocial

Effects Diminished hearing and vision, short-term memory loss, altered motor coordination, decreased muscle tone and strength, slower response to verbal and motor stimuli, decreased ability to synthesize new information, increased sensitivity to altered temperature states, increased sensitivity to sedation (confusion or agitation), decreased alertness levels Increased effects of atherosclerosis of vessels and heart valves, decreased stroke volume with resulting decreased cardiac output, decreased myocardial compliance, increased workload of heart, diminished peripheral pulses Decreased compliance and elasticity, decreased vital capacity, increased residual volume, less effective cough, decreased response to hypercapnia Decreased glomerular filtration rate, increased risk of fluid and electrolyte imbalances Increased presence of dentition problems, decreased intestinal mobility, decreased hepatic metabolism, increased risk of altered nutritional states Increased incidence of diabetes, thyroid disorders, and anemia; decreased antibody response and cellular immunity Decreased skin turgor, increased capillary fragility and bruising, decreased elasticity Altered pharmacokinetics and pharmacodynamics, decreased range of motion of joints and extremities Difficulty falling asleep and fragmented sleep patterns, increased incidence of depression and anxiety, cognitive impairment disorders, difficulty with change

atropine, morphine, or illicit drugs may affect pupil size. Baseline pupil assessment is important even in patients without a neurologic diagnosis because some individuals have unequal or unreactive pupils normally. If pupils are not checked as a baseline, a later check of pupils during an acute event could inappropriately attribute pupil abnormalities to a pathophysiologic event. LOC and pupil assessments are followed by motor function assessment of the upper and lower extremities for symmetry and quality of strength. Traditional motor strength exercises include having the patient squeeze the nurse’s hands and plantar flexing and dorsiflexing of the patient’s feet. If the patient cannot follow commands, an estimate of strength and quality of movements can be inferred by observing activities such as pulling against restraints or thrashing around. If the patient has no voluntary movement or is unresponsive, check the gag and Babinski reflexes. TABLE 1-9. IDENTIFICATION OF SYMPTOM CHARACTERISTICS Characteristic Onset Location Frequency Quality Intensity

Sample Questions How and under what circumstances did it begin? Was the onset sudden or gradual? Did it progress? Where is it? Does it stay in the same place or does it radiate or move around? How often does it occur? Is it dull, sharp, burning, throbbing, etc? Rank pain on a scale (numeric, word description, FACES, FLACC)

Quantity Setting Associated findings

How long does it last? What are you doing when it happens? Are there other signs and symptoms that occur when this happens?

Aggravating and alleviating factors

What things make it worse? What things make it better?

If head trauma is involved or suspected, check for signs of fluid leakage around the nose or ears, differentiating between cerebral spinal fluid and blood (see Chapter 12, Neurologic System). Complete cranial nerve assessment is rarely warranted, with specific cranial nerve evaluation based on the injury or diagnosis. For example, extraocular movements are routinely assessed in patients with facial trauma. Sensory testing is a baseline standard for spinal cord injuries, extremity trauma, and epidural analgesia. Now is a good time to assess mental status if the patient is responsive. Assess orientation to person, place, and time. Ask the patient to state their understanding of what is happening. As you ask the questions, observe for eye contact, pressured or muted speech, and rate of speech. Rate of speech is usually consistent with the patient’s psychomotor status. Underlying cognitive impairments such as dementia and developmental delays are typically exacerbated during critical illness due to physiologic changes, medications, and environmental changes. It may be necessary to ascertain baseline level of functioning from the family. Laboratory data pertinent to the nervous system include serum and urine electrolytes and osmolarity and urinary specific gravity. Drug toxicology and alcohol levels may be evaluated to rule out potential sources of altered LOC. If the patient has an intracranial pressure (ICP) monitoring device in place, note the type of device (eg, ventriculostomy, epidural, subdural) and analyze the baseline pressure and waveform. Check all diagnostic values and monitoring system data to determine whether immediate intervention is warranted. Cardiovascular System

The cardiovascular system assessment is directed at evaluating central and peripheral perfusion. Revalidate your admission quick check assessment of the blood pressure, heart rate,

CHAPTER 1. Assessment Of Critically Ill Patients and Their Families

TABLE 1-10. EDEMA RATING SCALE Following the application and removal of firm digital pressure against the tissue, the edema is evaluated for one of the following responses: • 0 No depression in tissue • +1 Small depression in tissue, disappearing in 75, hypertension, HF, LVEF < 35%, diabetes). (level A) 4. INR should be determined at least weekly during initiation of therapy with a vitamin K antagonist and monthly when anticoagulation is stable. (level A) 5. Dabigatran is useful as an alternative to warfarin for the prevention of stroke and systemic thromboembolism in patients with paroxysmal to permanent AF and risk factors for stroke or systemic embolization who do not have a prosthetic heart valve or hemodynamically significant valve disease, severe renal failure (CrCl 48 hours duration, or when the duration is unknown, anticoagulation (INR 2.0 to 3.0) is recommended for at least 3 weeks prior to and 4 weeks after cardioversion (electrical or pharmacological). (level B) 9. For patients with AF of more than 48 hours duration requiring immediate cardioversion, heparin should be administered concurrently (unless contraindicated) by an initial IV bolus followed by a continuous infusion in a dose adjusted to prolong the aPTT to 1.5 to 2 times the reference control value. Oral anticoagulation (INR 2.0 to 3.0) should be given for at least 4 weeks after cardioversion. Limited data support SQ administration of LMWH in this indication. (level C) 10. For patients with AF of less than 48 hours duration and hemodynamic instability (angina, MI, shock, or pulmonary edema), cardioversion should be performed immediately without delay for prior anticoagulation. (level C) Cardioversion of Atrial Fibrillation 1. Administration of flecainide, dofetilide, propafenone, or ibutilide is recommended for pharmacological cardioversion. (level A) 2. Immediate electrical (direct-current) cardioversion is recommended for patients with AF involving preexcitation when very rapid tachycardia or hemodynamic instability occurs. (level B) 3. When a rapid ventricular response does not respond promptly to pharmacological measures in patients with MI, symptomatic hypotension, angina, or HF, immediate R-wave synchronized cardioversion is recommended. (level C) 4. Electrical cardioversion is recommended in patients without hemodynamic instability when symptoms of AF are unacceptable to the patient. In case of early relapse of AF after cardioversion, repeated electrical cardioversion attempts may be made following administration of antiarrhythmic medication. (level C) 5. Electrical cardioversion is recommended for patients with acute MI and severe hemodynamic compromise, intractable ischemia, or inadequate rate control with drugs. (level C) Maintenance of Sinus Rhythm 1. An oral beta-blocker to prevent postoperative AF is recommended for patients undergoing cardiac surgery (unless contraindicated). (level A) 2. Before initiating antiarrhythmic drug therapy, treatment of precipitating or reversible causes of AF is recommended. (level C) There are no class I recommendations for pharmacologic maintenance of sinus rhythm. See the guidelines for recommendations for maintenance of sinus rhythm. Level of Evidence Definitions Level A: Data derived from multiple randomized clinical trials or meta-analyses. Level B: Data derived from a single randomized trial or nonrandomized studies. Level C: Only consensus opinion of experts, case studies, or standard-of-care. Source: Data from Fuster V, Ryden LE, Cannom DS, et al. 2011 ACCF/AHA/HRS focused updates incorporated into the ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2011;123:e269–e367. Wann LS, Curtis AB, Ellenbogen KA, et al. 2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (update on dabigatran): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2011; 123:1144–1150. Abbreviations used in this table: AF: atrial fibrillation; aPTT: activated partial thromboplastin time; CCB: calcium channel blocker; HF: heart failure; INR: international normalized ratio; LMWH: low molecular weight heparin; LV: left ventricular; MI: myocardial infarction; TIA: transient ischemic attack.

CHAPTER 3. Interpretation and Management of Basic Cardiac Rhythms

risk patients or those with contraindications. Dabigatran, rivaroxaban, and apixaban are three new oral drugs recently approved by the FDA for stroke prevention in patients with nonvalvular AF. Table 3-5 contains class I recommendations for thromboembolism prevention in patients with AF or atrial flutter.

Nonpharmacological Management of Atrial Fibrillation

Radiofrequency (RF) catheter ablation and surgical management of AF include AV node ablation, pulmonary vein ablation, surgical or ablation Maze procedures, and occlusion or surgical removal of the left atrial appendage. These procedures are briefly described here.

Essential Content Case

Atrial Arrhythmia and Cardioversion You are caring for a patient who was admitted for an elective cardioversion. She was seen in her physician’s office this morning for complaints of SOB and palpitations that had started around 7 am. She has a history of hypertension and diabetes but no previous cardiac history. In the office, her ECG showed atrial fibrillation with a ventricular response between 120 and 130 beats/minute. Previous ECGs had all shown normal sinus rhythm, and since her symptoms were new and time of onset was just a few hours ago, her physician elected to treat her with cardioversion. Her BP is 136/74 and she is breathing comfortably at this time. You place her on the bedside cardiac monitor in lead V1. Case Question 1. What are the diagnostic features of AF that you expect to see on the monitor? Figure 3-22A shows her rhythm strip:

Case Question 2. Is her admitting diagnosis of AF correct? Case Question 3. What other treatments besides electrical cardioversion would be appropriate for managing this rhythm? You gather the equipment and supplies needed for the cardioversion. The cardiologist arrives and an anesthesiologist is present to sedate the patient. The cardiologist asks you to deliver a 100 joule shock after the patient is asleep. Case Question 4. What safety considerations are necessary before delivering the cardioversion shock? The shock is delivered and Figure 3-22B shows the postshock rhythm. Case Question 5. What is the rhythm?

A II

Figure 3-22.

Answers 1. Atrial fibrillation is characterized by the presence of “fibrillation” waves instead of organized P waves, and an irregularly irregular ventricular response. 2. Yes. This is a typical example of AF. 3. The first goal of treatment for AF is ventricular rate control. AV nodal blocking agents such as a beta-blocker or calcium channel blocker (ie, verapamil or diltiazem) are used for rate control. Antiarrhythmics such as flecainide, dofetilide, propafenone, ibutilide or amiodarone can be used for pharmacological conversion of atrial fibrillation to sinus rhythm. Patients with persistent AF are on chronic therapy with a rate control drug and oral anticoagulation.

4. Every member of the team participating in the procedure should be involved in assuring patient safety. The patient should be monitored with non-invasive BP monitoring and pulse oximetry. Airway management supplies, emergency drugs, and sedation reversal agent should be present at the bedside. The patient should be adequately sedated prior to shock delivery. The defibrillator must be synchronized on the QRS complex to avoid delivering the shock on the T wave, which could cause ventricular fibrillation. Prior to shock delivery, the operator should assure that no one is touching the patient or the bed. 5. This is normal sinus rhythm, indicating a successful cardioversion.

ARRHYTHMIAS ORIGINATING IN THE ATRIA 51

Radiofrequency AV node ablation is the most common nonpharmacologic method of rate control in AF and is usually done only when drug therapy for rate control is ineffective or not tolerated. RF energy is directed at the AV node to heat the tissue and destroy its ability to conduct impulses to the ventricle. This procedure results in complete AV block and requires a ventricular pacemaker implant to maintain an adequate ventricular rate. AV node ablation does not stop atrial fibrillation; therefore, patients must be chronically anticoagulated to prevent stroke. Radiofrequency ablation of AF trigger sites in the pulmonary veins or atria is the mainstay of ablation therapy for AF. The most common site of AF triggers is the first 2-4 cm inside the pulmonary veins leading into the left atrium, although triggers can be present in multiple sites within both atria. The most successful procedures are segmental ostial pulmonary vein isolation (PVI) and circumferential PVI. In segmental ostial PVI, specific sites of electrical conduction in the ostia of the pulmonary veins are ablated. In circumferential PVI, continuous ablation lesions encircle the ostia of all four pulmonary veins, usually in two pairs (ie, one circle of lesions around the left pulmonary veins and another circle around the right pulmonary veins). These ablation lesions completely isolate the pulmonary veins from the atrial myocardium and prevent conduction from trigger sites in to the atria. The Cox-Maze III procedure involves creation of multiple incisions within both atria using the “cut and sew” technique during cardiac surgery. The incisions create scars in the atria that direct the impulse from the sinus node to the AV node through both atria in an orderly fashion and prevent reentry of impulses that could lead to AF. Similar scars can be created using bipolar RF ablation clamps (CoxMaze IV procedure), which still requires cardiac surgery and cardiopulmonary bypass. Catheter-based RF ablation procedures create the lesions from the endocardial approach and are done percutaneously in the electrophysiology laboratory rather than requiring surgery. Left atrial appendage (LAA) amputation is done along with surgical Cox-Maze procedures as well as with mitral valve procedures to reduce the likelihood of thromboembolism, since most clots develop in the LAA during AF. Left atrial appendage occlusion devices can be inserted via the right femoral vein and into the LAA through a trans-septal approach and expanded within the LAA to seal it from the rest of the atrium, thus trapping clots and preventing them from embolizing.

Supraventricular Tachycardia (SVT) A supraventricular tachycardia by definition is any rhythm at a rate faster than 100 beats/min that originates above the ventricle or utilizes the atria or AV junction as part of the circuit that maintains the tachycardia. Technically, this can include sinus tachycardia, AT, atrial flutter, atrial fibrillation, and junctional tachycardia. However, the term SVT is meant

to be used to describe a regular, narrow QRS tachycardia in which the exact mechanism cannot be determined from the surface ECG. If P waves or atrial activity such a fibrillation or flutter waves can be clearly seen, then the mechanism can usually be identified. Occasionally in AT the P waves are hidden in preceding T waves and in that case use of the term SVT is appropriate. The two most common arrhythmias for which the term SVT is appropriate are AV nodal reentry tachycardia (AVNRT) and circus movement tachycardia (CMT) that occurs when an accessory pathway is present, such as in WPW. Another term used to describe CMT is AV reentry tachycardia (AVRT) but CMT is used here to prevent confusion between these two common arrhythmias. The mechanisms of these SVTs are described in detail in Chapter 18, Advanced Arrhythmia Interpretation. ECG characteristics of both SVTs are very similar and described here. ECG Characteristics

• Rate: 140-250 beats/minute. • Rhythm: Regular. • P waves: Usually not visible. In AVNRT, the P wave is hidden in the QRS or barely peeking out at the end of the QRS. In CMT, the P wave is usually present in the ST segment, but is often not visible. • PR interval: Not measurable, since P waves are usually not visible. • QRS complex: Usually normal. • Conduction: In AVNRT, the impulse travels in a small circuit that includes the AV node as one limb of the circuit and a slower conducting pathway just outside the AV node as the second limb of the circuit. The impulse depolarizes the atria in a retrograde direction at the same time as it depolarizes the ventricles through the normal His-Purkinje system, resulting in a regular narrow QRS tachycardia. In CMT, the impulse follows a reentry circuit that includes the atria, AV node, ventricles, and accessory pathway. The most common type of CMT is called orthodromic CMT, in which the impulse travels from atria to ventricles through the normal AV node and His-Purkinje system, then back to the atria from the ventricles through the accessory pathway. This results in a regular, narrow QRS tachycardia because the ventricles are depolarized via the normal conduction system. If the circuit reverses direction and the ventricles depolarize through conduction down the accessory pathway, this is called antidromic CMT, and the resulting tachycardia has a wide QRS complex. • Example of SVT: See Figure 3-23 A, B.

Treatment

These SVTs are usually well tolerated and often paroxysmal in nature. If the ventricular rate is very rapid and sustained, symptoms such as palpitations, dizziness, or syncope can occur.

CHAPTER 3. Interpretation and Management of Basic Cardiac Rhythms

V2 A V1 B

Figure 3-23. (A) SVT at a rate of 190 beats/min found to be AVNRT at electrophysiology study. (B) SVT at a rate of 214 found to be CMT at electrophysiology study.

Vagal maneuvers such as carotid sinus massage, Valsalva’s maneuver, gagging or coughing, drinking ice water, or putting the face in ice water may be effective in terminating the tachycardia. Adenosine (6 mg given rapidly IV, may repeat with 12 mg if necessary) is the most effective drug to terminate the tachycardia. Drugs that slow AV conduction, like calcium channel blockers (diltiazem, verapamil) or beta-blockers, can terminate tachycardia and can be used long term to prevent recurrences. Synchronized cardioversion can be used if drugs are contraindicated or fail to terminate tachycardia. Radiofrequency ablation offers a cure for AVNRT and CMT. See Table 3-4 for class I recommendations for management of supraventricular tachycardias.

impulse reaches the ventricles. In this case the PR interval is very short, usually 0.10 second or less. • If the junctional impulse reaches both the atria and the ventricles at the same time, only a QRS is seen on the ECG because the ventricles are much larger than the atria and only ventricular depolarization will be seen, even though the atria are also depolarizing. • If the junctional impulse reaches the ventricles before it reaches the atria, the QRS precedes the P wave on the ECG. Again, the P wave is usually inverted because of retrograde atrial depolarization, and the RP interval (distance from the beginning of the QRS to the beginning of the following P wave) is short.

ARRHYTHMIAS ORIGINATING IN THE ATRIOVENTRICULAR JUNCTION

Premature Junctional Complexes

Cells surrounding the AV node in the AV junction are capable of initiating impulses and controlling the heart rhythm (Figure 3-24). Junctional beats and junctional rhythms can appear in any of three ways on the ECG depending on the location of the junctional pacemaker and the speed of conduction of the impulse into the atria and ventricles:

Premature junctional complexes (PJCs) are due to an irritable focus in the AV junction. Irritability can be because of coronary heart disease or MI disrupting blood flow to the AV junction, nicotine, caffeine, emotions, or drugs such as digitalis.

Figure 3-24. Arrhythmias originating in the AV junction.

• When a junctional focus fires, the wave of depolarization spreads backward (retrograde) into the atria as well as forward (antegrade) into the ventricles. If the impulse arrives in the atria before it arrives in the ventricles, the ECG shows a P wave (usually inverted because the atria are depolarizing from bottom to top) followed immediately by a QRS complex as the

ECG Characteristics

• Rate: 60 to 100 beats/min or whatever the rate of the basic rhythm. • Rhythm: Regular except for occurrence of premature beats. • P waves: May occur before, during, or after the QRS complex of the premature beat and are usually inverted. • PR interval: Short, usually 0.10 second or less when P waves precede the QRS. • QRS complex: Usually normal but may be aberrant if the PJC occurs very early and conducts into the ventricles during the refractory period of a bundle branch. • Conduction: Retrograde through the atria; usually normal through the ventricles. • Example of a PJC: Figure 3-25.

Figure 3-25. Premature junctional complexes.

ARRHYTHMIAS ORIGINATING IN THE VENTRICLES 53

Treatment

Treatment is not necessary for PJCs.

Junctional Rhythm, Accelerated Junctional Rhythm, and Junctional Tachycardia Junctional rhythms can occur if the sinus node rate falls below the rate of the AV junctional pacemakers or when atrial conduction through the AV junction has been disrupted. Junctional rhythms commonly occur from digitalis toxicity or following inferior MI owing to disruption of blood supply to the sinus node and the AV junction. These rhythms are classified according to their rate. Junctional rhythm usually occurs at a rate of 40 to 60 beats/min, accelerated junctional rhythm occurs at a rate of 60 to 100 beats/min, and junctional tachycardia occurs at a rate of 100 to 250 beats/min.

ARRHYTHMIAS ORIGINATING IN THE VENTRICLES Ventricular arrhythmias originate in the ventricular muscle or Purkinje system and are considered to be more dangerous than other arrhythmias because of their potential to initiate VT and severely decrease cardiac output (Figure 3-27). However, as with any arrhythmia, ventricular rate is a key determinant of how well a patient can tolerate a ventricular rhythm. Ventricular rhythms can range in severity from mild, well-tolerated rhythms to pulseless rhythms leading to sudden cardiac death.

ECG Characteristics

• Rate: Junctional rhythm, 40 to 60 beats/min; accelerated junctional rhythm, 60 to 100 beats/min; junctional tachycardia, 100 to 250 beats/min. • Rhythm: Regular. • P waves: May precede or follow QRS. • PR interval: Short, 0.10 second or less. • QRS complex: Usually normal. • Conduction: Retrograde through the atria; normal through the ventricles. • Example of junctional rhythm and accelerated junctional rhythm: Figure 3-26A, B.

Figure 3-26. (A) Junctional rhythm. (B) Accelerated junctional rhythm.

Treatment

Treatment of junctional rhythm rarely is required unless the rate is too slow or too fast to maintain adequate cardiac output. If the rate is slow, atropine is given to increase the sinus rate and override the junctional focus or to increase the rate of firing of the junctional pacemaker. If the rate is fast, drugs such as verapamil, propranolol, or beta-blockers may be effective in slowing the rate or terminating the arrhythmia. Because digitalis toxicity is a common cause of junctional rhythms, the drug should be held.

Figure 3-27. Arrhythmias originating in the ventricles.

Premature Ventricular Complexes Premature ventricular complexes (PVCs) are caused by premature depolarization of cells in the ventricular myocardium or Purkinje system or to reentry in the ventricles. PVCs can be caused by hypoxia, myocardial ischemia, hypokalemia, acidosis, exercise, increased levels of circulating catecholamines, digitalis toxicity, caffeine, and alcohol, among other causes. PVCs increase with aging and are more common in people with coronary disease, valve disease, hypertension, cardiomyopathy, and other forms of heart disease. PVCs are not dangerous in people with normal hearts but are associated with higher mortality rates in patients with structural heart disease or acute MI, especially if left ventricular function is reduced. PVCs are considered potentially malignant when they occur more frequently than 10 per hour or are repetitive (occur in pairs, triplets, or more than three in a row) in patients with coronary disease, previous MI, cardiomyopathy, and reduced ejection fraction. ECG Characteristics

• Rate: 60 to 100 beats/min or the rate of the basic rhythm. • Rhythm: Irregular because of the early beats. • P waves: Not related to the PVCs. Sinus rhythm is usually not interrupted by the premature beats, so sinus P waves can often be seen occurring regularly throughout the rhythm. P waves may occasionally

CHAPTER 3. Interpretation and Management of Basic Cardiac Rhythms

follow PVCs due to retrograde conduction from the ventricle backward through the atria. These P waves are inverted. • PR interval: Not present before most PVCs. If a P wave happens, by coincidence, to precede a PVC, the PR interval is short. • QRS complex: Wide and bizarre; greater than 0.10 second in duration. These may vary in morphology (size, shape) if they originate from more than one focus in the ventricles (multifocal PVCs). • Conduction: Impulses originating in the ventricles conduct through the ventricles from muscle cell to muscle cell rather than through Purkinje fibers, resulting in wide QRS complexes. Some PVCs may conduct retrograde into the atria, resulting in inverted P waves following the PVC. When the sinus rhythm is undisturbed by PVCs, the atria depolarize normally. • Example of PVCs: Figure 3-28A, B.

Ventricular Rhythm and Accelerated Ventricular Rhythm Ventricular rhythm occurs when an ectopic focus in the ventricle fires at a rate less than 50 beats/min. This rhythm occurs as an escape rhythm when the sinus node and junctional tissue fail to fire or fail to conduct their impulses to the ventricle. Accelerated ventricular rhythm occurs when an ectopic focus in the ventricles fires at a rate of 50 to 100 beats/min. The causes of this accelerated ventricular rhythm are similar to those of VT, but accelerated ventricular rhythm commonly occurs in the presence of inferior MI when the rate of the sinus node slows below the rate of the latent ventricular pacemaker. Accelerated ventricular rhythm is a common arrhythmia after thrombolytic therapy, when reperfusion of the damaged myocardium occurs. ECG Characteristics

• Rate: Less than 50 beats/min for ventricular rhythm and 50 to 100 beats/min for accelerated ventricular rhythm. • Rhythm: Usually regular. • P waves: May be seen but at a slower rate than the ventricular focus, with dissociation from the QRS complex. • PR interval: Not measured. • QRS complex: Wide and bizarre. • Conduction: If sinus rhythm is the basic rhythm, atrial conduction is normal. Impulses originating in the ventricles conduct via muscle cell-to-cell conduction, resulting in the wide QRS complex. • Example of escape ventricular rhythm and accelerated ventricular rhythm: Figure 3-29 A, B.

Figure 3-28. Premature ventricular complexes.

Treatment

The significance of PVCs depends on the clinical setting in which they occur. Many people have chronic PVCs that do not need to be treated, and most of these people are asymptomatic. There is no evidence that suppression of PVCs reduces mortality, especially in patients with no structural heart disease. If PVCs cause bothersome palpitations, patients are told to avoid caffeine, tobacco, other stimulants, and try stress reduction techniques. Low-dose beta-blockers may reduce PVC frequency and the perception of palpitations and can be used for symptom relief. In the setting of an acute MI or myocardial ischemia, PVCs may be precursors of more dangerous ventricular arrhythmias, especially when they occur near the apex of the T wave (R on T PVCs). Unless PVCs result in hemodynamic instability or symptomatic VT, most providers elect not to treat them. If PVCs are to be treated, IV lidocaine or amiodarone are the drugs usually used. Procainamide can also be used IV for acute control. Beta-blockers are often effective in suppressing repetitive PVCs and have become the drugs of choice for treating post-MI PVCs that are symptomatic. Several antiarrhythmic drugs are effective in reducing the frequency of PVCs but are not recommended due to the risk of proarrhythmia and their association with sudden cardiac death in patients with structural heart disease.

Figure 3-29. (A) Escape ventricular rhythm. (B) Accelerated ventricular rhythm.

Treatment

The treatment of accelerated ventricular rhythm depends on its cause and how well it is tolerated by the patient. This arrhythmia alone is usually not harmful because the ventricular rate is within normal limits and usually adequate to maintain cardiac output. Suppressive therapy is rarely used because abolishing the ventricular rhythm may leave an even less desirable heart rate. If the patient is symptomatic because of the loss of atrial kick, atropine can be used to increase the rate of the sinus node and overdrive the ventricular rhythm.

ARRHYTHMIAS ORIGINATING IN THE VENTRICLES 55

If the ventricular rhythm is an escape rhythm, then treatment is directed toward increasing the rate of the escape rhythm or pacing the heart temporarily. Usually, accelerated ventricular rhythm is transient and benign and does not require treatment.

Ventricular Tachycardia Ventricular tachycardia (VT) is a rapid ventricular rhythm at a rate greater than 100 beats/min. VT can be classified according to: (1) duration, nonsustained (lasts less than 30 seconds), sustained (lasts longer than 30 seconds), or incessant (VT present most of the time); and (2) morphology (ECG appearance of QRS complexes), monomorphic (QRS complexes have the same shape during tachycardia), polymorphic (QRS complexes vary randomly in shape), or bidirectional (alternating upright and negative QRS complexes during tachycardia). Polymorphic VT that occurs in the presence of a long QT interval is called torsades de pointes (meaning “twisting of the points”). The most common cause of VT is coronary artery disease, including acute ischemia, acute MI, and prior MI. Other causes include cardiomyopathy, valvular heart disease, congenital heart disease, arrhythmogenic right ventricular dysplasia, cardiac tumors, cardiac surgery, and the proarrhythmic effects of many drugs. See Chapter 18 for more information on ventricular tachycardias and the differential diagnosis of wide QRS tachycardias. ECG Characteristics

• Rate: Ventricular rate is faster than 100 beats/min. • Rhythm: Monomorphic VT is usually regular, polymorphic VT can be irregular. • P waves: Dissociated from QRS complexes. If sinus rhythm is the underlying basic rhythm, they are regular. P waves may be seen but are not related to QRS complexes. P waves are often buried within QRS complexes. • PR interval: Not measurable because of dissociation of P waves from QRS complexes. • QRS complex: Usually 0.12 second or more in duration. • Conduction: Impulse originates in one ventricle and spreads via muscle cell-to-cell conduction through both ventricles. There may be retrograde conduction through the atria, but more often the sinus node continues to fire regularly and depolarize the atria normally. • Example of VT: Figure 3-30.

Immediate treatment of VT depends on how well the rhythm is tolerated by the patient. The two main determinants of patient tolerance of any tachycardia are ventricular rate and underlying left ventricular function. VT can be an emergency if cardiac output is severely decreased because of a very rapid rate or poor left ventricular function. Hemodynamically unstable VT is treated with synchronized cardioversion. If VT is pulseless then immediate defibrillation is required. VT that is hemodynamically stable can be treated with drug therapy. Amiodarone is often the drug of choice but lidocaine or procainamide can also be used. Drugs used to treat VT on a long-term basis include amiodarone, sotalol, and beta-blockers. Some VTs can be treated with radiofrequency catheter ablation to abolish the ectopic focus. The implantable cardioverter defibrillator is frequently used for recurrent VT in patients with reduced ejection fractions or drug refractory VT. See Table 3-6 for class I recommendations for management of ventricular arrhythmias. TABLE 3-6. GUIDELINES FOR MANAGEMENT OF VENTRICULAR ARRHYTHMIAS (Class I Recommendations Only) Sustained Monomorphic Ventricular Tachycardia 1. Wide QRS tachycardia should be presumed to be VT if the diagnosis is unclear (level C). 2. Electrical cardioversion with sedation is recommended with hemodynamically unstable sustained monomorphic VT (level C). Contraindicated: Calcium channel blockers (verapamil, diltiazem) should not be used to terminate wide QRS tachycardia of unknown origin, especially with history of myocardial dysfunction. Polymorphic Ventricular Tachycardia 1. Electrical cardioversion with sedation is recommended for sustained PVT with hemodynamic compromise (level B). 2. IV beta-blockers are useful if ischemia is suspected or cannot be excluded (level B). 3. IV amiodarone is useful for recurrent PVT in the absence of QT prolongation (congenital or acquired) (level C). 4. Urgent angiography and revascularization should be considered with PVT when myocardial ischemia cannot be excluded (level C). Torsades de Pointes 1. Withdrawal of any offending drugs and correction of electrolyte abnormalities are recommended for TdP (level A). 2. Acute and long-term pacing is recommended for TdP due to heart block and symptomatic bradycardia (level A). Incessant Ventricular Tachycardia 1. Revascularization and beta blockade followed by IV antiarrhythmic drugs such as procainamide or amiodarone are recommended for recurrent or incessant PVT (level B). Level of Evidence Definitions Level A: Data derived from multiple randomized clinical trials or meta-analyses. Level B: Data derived from a single randomized trial or nonrandomized studies. Level C: Only consensus opinion of experts, case studies, or standard of care.

Treatment

Figure 3-30. Monomorphic ventricular tachycardia.

Source: Data from Zipes DP, Camm JA, Borggrefe M., et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: executive summary: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients with Atrial Fibrillation). Circulation. 2006;114:10881132. Abbreviations: PVT, polymorphic ventricular tachycardia; TdP, torsades de pointes; VT, ventricular tachycardia.

CHAPTER 3. Interpretation and Management of Basic Cardiac Rhythms

Ventricular Fibrillation Ventricular fibrillation (VF) is rapid, ineffective quivering of the ventricles and is fatal without immediate treatment (Figure 3-31). Electrical activity originates in the ventricles and spreads in a chaotic, irregular pattern throughout both ventricles. There is no cardiac output or palpable pulse with VF.

cardioverter defibrillator has become the standard of care for survivors of VF that occurs in the absence of acute ischemia.

Ventricular Asystole Ventricular asystole is the absence of any ventricular rhythm: no QRS complex, no pulse, and no cardiac output (Figure 3-33). Ventricular asystole is always fatal unless the cause can be identified and treated immediately. If atrial activity is still present the term ventricular standstill is used.

Figure 3-31. Ventricular fibrillation.

ECG Characteristics

• Rate: Rapid, uncoordinated, ineffective. • Rhythm: Chaotic, irregular. • P waves: None seen. • PR interval: None. • QRS complex: No formed QRS complexes seen; rapid, irregular undulations without any specific pattern. • Conduction: Multiple ectopic foci firing simultaneously in ventricles and depolarizing them irregularly and without any organized pattern. Ventricles are not contracting. • Example of ventricular fibrillation: Figure 3-32.

Figure 3-33. Ventricular asystole.

ECG Characteristics

• Rate: None. • Rhythm: None. • P waves: May be present if the sinus node is functioning. • PR interval: None. • QRS complex: None. • Conduction: Atrial conduction may be normal if the sinus node is functioning. There is no conduction into the ventricles. • Example of ventricular asystole: Figure 3-34.

Figure 3-32. Ventricular fibrillation.

Treatment

Ventricular fibrillation requires immediate defibrillation. Synchronized cardioversion is not possible because there are no formed QRS complexes on which to synchronize the shock. Cardiopulmonary resuscitation (CPR) must be performed until a defibrillator is available, and then defibrillation at 200 J (biphasic defibrillation) or 360 J (monophasic defibrillation) is recommended followed by CPR and drug therapy. Antiarrhythmic agents such as lidocaine, amiodarone, or magnesium are commonly used in an effort to convert VF. Once the rhythm has converted, maintenance therapy with IV antiarrhythmic agents is continued. Betablockers and amiodarone appear to be the most effective agents for long-term drug therapy options. The implantable

Figure 3-34. Ventricular asystole.

Treatment

Cardiopulmonary resuscitation must be initiated immediately if the patient is to survive. IV epinephrine and vasopressin are the only drugs currently recommended for treating asystole. The cause of asystole should be determined and treated as rapidly as possible to improve the chance of survival. Asystole has a very poor prognosis despite the best resuscitation efforts because it usually represents extensive myocardial ischemia or severe underlying metabolic

ATRIOVENTRICULAR BLOCKS 57

problems. Pacing and atropine are no longer recommended for treatment for asystole.

ATRIOVENTRICULAR BLOCKS The term atrioventricular block is used to describe arrhythmias in which there is delayed or failed conduction of supraventricular impulses into the ventricles. AV blocks have been classified according to location of the block and severity of the conduction abnormality.

First-Degree Atrioventricular Block First-degree AV block is defined as prolonged AV conduction time of supraventricular impulses into the ventricles (Figure 3-35). This delay usually occurs in the AV node, and all impulses conduct to the ventricles, but with delayed conduction times. First-degree AV block can be due to coronary heart disease, rheumatic heart disease, or administration of digitalis, beta-blockers, or calcium channel blockers. Firstdegree AV block can be normal in people with slow heart rates or high vagal tone.

Treatment

Treatment of first-degree AV block is usually not required, but the rhythm should be observed for progression to more severe block.

Second-Degree Atrioventricular Block Second-degree AV block occurs when one atrial impulse at a time fails to be conducted to the ventricles. Second-degree AV block can be divided into two distinct categories: type I block, occurring in the AV node, and type II block, occurring below the AV node in the bundle of His or bundle-branch system (Figure 3-37).

Figure 3-37. Type I second-degree AV block.

Type I Second-Degree Atrioventricular Block

Figure 3-35. First-degree AV block.

ECG Characteristics

• Rate: Can occur at any sinus rate, usually 60 to 100 beats/min. • Rhythm: Regular. • P waves: Normal; precede every QRS complex. • PR interval: Prolonged above 0.20 second. • QRS complex: Usually normal. • Conduction: Normal through the atria, delayed through the AV node, and normal through the ventricles. • Example of first-degree AV block: Figure 3-36.

Figure 3-36. First-degree AV block.

Type I second-degree AV block, often referred to as Wenckebach block, is a progressive increase in conduction times of consecutive atrial impulses into the ventricles until one impulse fails to conduct, or is “dropped.” The PR intervals gradually lengthen until one P wave fails to conduct and is not followed by a QRS complex, resulting in a pause, after which the cycle repeats itself. This type of block is commonly associated with inferior MI, coronary heart disease, aortic valve disease, mitral valve prolapse, atrial septal defects, and administration of digitalis, beta-blockers, or calcium channel blockers. ECG Characteristics

• Rate: Can occur at any sinus or atrial rate. • Rhythm: Irregular. Overall appearance of the rhythm demonstrates “group beating.” • P waves: Normal. Some P waves are not conducted to the ventricles, but only one at a time fails to conduct to the ventricle. • PR interval: Gradually lengthens on consecutive beats. The PR interval preceding the pause is longer than that following the pause (unless 2:1 conduction is present). • QRS complex: Usually normal unless there is associated bundle branch block.

CHAPTER 3. Interpretation and Management of Basic Cardiac Rhythms

• Conduction: Normal through the atria; progressively delayed through the AV node until an impulse fails to conduct. Ventricular conduction is normal. Conduction ratios can vary, with ratios as low as 2:1 (every other P wave is blocked) up to high ratios such as 15:14 (every 15th P wave is blocked). • Example of second-degree AV block type I: Figure 3-38.

Figure 3-38. Second-degree AV block, type I.

Treatment

Treatment of type I second-degree AV block depends on the conduction ratio, the resulting ventricular rate, and the patient’s tolerance for the rhythm. If ventricular rates are slow enough to decrease cardiac output, the treatment is atropine to increase the sinus rate and speed conduction through the AV node. At higher conduction ratios where the ventricular rate is within a normal range, no treatment is necessary. If the block is due to digitalis, calcium channel blockers, or beta-blockers, those drugs are held. This type of block is usually temporary and benign, and seldom requires pacing, although temporary pacing may be needed when the ventricular rate is slow. Type II Second-Degree Atrioventricular Block

Type II second-degree AV block is sudden failure of conduction of an atrial impulse to the ventricles without progressive increases in conduction time of consecutive P waves (Figure 3-39). Type II block occurs below the AV node and is usually associated with bundle branch block; therefore, the

dropped beats are usually a manifestation of bilateral bundle branch block. This form of block appears on the ECG much the same as type I block except that there is no progressive increase in PR intervals before the blocked beats and the QRS is almost always wide. Type II block is less common than type I block, but is a more serious form of block. It occurs in rheumatic heart disease, coronary heart disease, primary disease of the conduction system, and in the presence of acute anterior MI. Type II block is more dangerous than type I because of a higher incidence of associated symptoms and progression to complete AV block. ECG Characteristics

• Rate: Can occur at any basic rate. • Rhythm: Irregular due to blocked beats. • P waves: Usually regular and precede each QRS. Periodically a P wave is not followed by a QRS complex. • PR interval: Constant before conducted beats. The PR interval preceding the pause is the same as that following the pause. • QRS complex: Usually wide because of associated bundle branch block. • Conduction: Normal through the atria and through the AV node but intermittently blocked in the bundle branch system and fails to reach the ventricles. Conduction through the ventricles is abnormally slow due to associated bundle branch block. Conduction ratios can vary from 2:1 to only occasional blocked beats. • Example of second-degree AV block type II: Figure 3-40. Treatment

Treatment usually includes pacemaker therapy because this type of block is often permanent and progresses to complete block. External pacing can be used for treatment of symptomatic type II block until transvenous pacing can be initiated. Atropine is not recommended because it may result in further slowing of ventricular rate by increasing the number of impulses conducting through the AV node and bombarding the diseased bundles with more impulses than they can handle, resulting in further conduction failure.

High-Grade Atrioventricular Block

Figure 3-39. Type II second-degree AV block.

High-grade (or advanced) AV block is present when two or more consecutive atrial impulses are blocked when the atrial rate is reasonable (less than 135 beats/min) and conduction fails because of the block itself and not because of interference from an escape pacemaker. High-grade AV block may be type I, occurring in the AV node, or type II, occurring below the AV node. The importance of high-grade block depends

Figure 3-40. Second-degree AV block, type II.

ATRIOVENTRICULAR BLOCKS 59

on the conduction ratio and the resulting ventricular rate. Because ventricular rates tend to be slow, this arrhythmia is frequently symptomatic and requires treatment. ECG Characteristics

• Rate: Atrial rate less than 135 beats/min. • Rhythm: Regular or irregular, depending on conduction pattern. • P waves: Normal. Present before every conducted QRS, but several P waves may not be followed by QRS complexes. • PR interval: Constant before conducted beats. May be normal or prolonged. • QRS complex: Usually normal in type I block and wide in type II block. • Conduction: Normal through the atria. Two or more consecutive atrial impulses fail to conduct to the ventricles. Ventricular conduction is normal in type I block and abnormally slow in type II block. • Example of high-grade AV block: Figure 3-41.

Figure 3-41. High-grade AV block.

Treatment

Treatment of high-grade block is necessary if the patient is symptomatic. Atropine can be given and is generally more effective in type I block. An external pacemaker may be required until transvenous pacing can be initiated, and permanent pacing is often necessary in type II high-grade block.

Third-Degree Atrioventricular Block (Complete Block) Third-degree AV block is complete failure of conduction of all atrial impulses to the ventricles (Figure 3-42). In thirddegree AV block, there is complete AV dissociation; the atria are usually under the control of the sinus node, although complete block can occur with any atrial arrhythmia; and either a junctional or ventricular pacemaker controls the ventricles. The ventricular rate is usually less than 45 beats/ min; a faster rate could indicate an accelerated junctional or ventricular rhythm that interferes with conduction from the atria into the ventricles by causing physiologic refractoriness in the conduction system, thus causing a physiologic failure of conduction that must be differentiated from the abnormal conduction system function of complete AV block. Causes of complete AV block include coronary heart disease, MI, Lev disease, Lenègre disease, cardiac surgery, congenital heart disease, and drugs that slow AV conduction such as digitalis, beta-blockers, and calcium channel blockers.

B Figure 3-42. Third-degree AV block (complete block). (A) Third-degree AV block with junctional escape pacemaker. (B) Third-degree AV block with ventricular escape pacemaker. (Gilmore SB, Woods SL. Electrocardiography and vectorcardiography. In: Woods SL, Froelicher ES, Motzer SU, eds. Cardiac Nursing. 3rd ed. Philadelphia, PA: JB Lippincott; 1995:291.)

ECG Characteristics

• Rate: Atrial rate is usually normal. Ventricular rate is less than 45 beats/min. • Rhythm: Regular. • P waves: Normal but dissociated from QRS complexes. • PR interval: No consistent PR intervals because there is no relationship between P waves and QRS complexes. • QRS complex: Normal if ventricles are controlled by a junctional pacemaker. Wide if controlled by a ventricular pacemaker. • Conduction: Normal through the atria. All impulses are blocked at the AV node or in the bundle branches, so there is no conduction to the ventricles. Conduction through the ventricles is normal if a junctional escape rhythm occurs, and abnormally slow if a ventricular escape rhythm occurs. • Examples of third-degree AV block: Figure 3-44A,B. Treatment

Third-degree AV block can occur without significant symptoms if it occurs gradually and the heart has time to compensate

CHAPTER 3. Interpretation and Management of Basic Cardiac Rhythms

Essential Content Case

Heart Block and Epicardial Pacemaker You are caring for a patient who had an aortic valve replacement yesterday. He has been extubated, he has a mediastinal chest tube, and two ventricular epicardial pacing leads are in place and coiled under a dressing. He is in sinus rhythm at a rate in the 80s, BP is 146/80, RR is 16 and he is breathing comfortably. The monitor alarm sounds and when you enter the room he is pale and complaining of dizziness but no chest pain. This is what you now see on the monitor:

Case Question 1. What is his rhythm? He is dizzy and his BP is 92/60.

Figure 3-43A

Figure 3-43 B

Case Question 2. What can you do to treat this arrhythmia? Case Question 3. Describe how to initiate epicardial ventricular pacing. You connect the pacing leads to a temporary pulse generator and set the rate at 70 beats/min. This is the rhythm:

II A V1

Figure 3-43.

Case Question 4. What is this rhythm? Case Question 5. Evaluate pacemaker function in terms of ventricular capture and ventricular sensing. Answers 1. This rhythm is third degree AV block with a ventricular pacemaker at a rate of about 40 beats/minute. 2. Third degree AV block is best treated with pacing. Atropine may speed up the rate of the sinus rhythm but it doesn’t improve conduction in complete heart block. Since this patient has ventricular epicardial pacing leads in place, the best treatment is to initiate temporary ventricular pacing.

3. To initiate ventricular epicardial pacing with two ventricular leads present, connect one epicardial lead to the negative terminal of the temporary pacemaker pulse generator and connect the other lead to the positive terminal of the pacemaker. Set the desired rate, output, and sensitivity and turn the pacemaker on. 4. Ventricular paced rhythm at a rate of 70 beats/min. Sinus P waves are present and two of them are conducted to the ventricles. 5. Capture is good: every ventricular pacing spike is followed by a wide QRS complex. Sensing is also good: the two conducted beats are sensed and the pacemaker inhibits its output appropriately.

for the slow ventricular rate. If it occurs suddenly in the presence of acute MI, its significance depends on the resulting ventricular rate and the patient’s tolerance. Treatment of complete heart block with symptoms of decreased cardiac output includes external pacing until transvenous pacing can be initiated. Atropine can be given but is not usually effective in restoring conduction.

TEMPORARY PACING B

Figure 3-44. (A) Third-degree AV block with a junctional escape pacemaker at a

rate of about 36 beats/min. (B) Third-degree AV block with a ventricular escape pacemaker at a rate of about 40 beats/min.

Indications If the heart fails to generate or conduct impulses to the ventricle, the myocardium can be electrically stimulated using

TEMPORARY PACING 61

a cardiac pacemaker. A cardiac pacemaker has two components: a pulse generator and a pacing electrode or lead. Temporary cardiac pacing is indicated in any situation in which bradycardia results in symptoms of decreased cerebral perfusion or hemodynamic compromise and does not respond to drug therapy. Signs and symptoms of hemodynamic instability are hypotension, change in mental status, angina, or pulmonary edema. Temporary pacing is also used to terminate some rapid reentrant tachycardias by briefly pacing the heart at a faster rate than the existing rate. When pacing is stopped, the sinus node may resume control of the rhythm if the tachycardia has been terminated. This type of pacing is termed overdrive pacing to distinguish it from pacing for bradycardic conditions.

Temporary cardiac pacing is accomplished by transvenous, epicardial, or external pacing methods. If continued cardiac pacing is required, insertion of permanent pacemakers is done electively. The following section presents an overview of temporary ventricular pacing principles. A more detailed explanation of pacemaker functions is covered in Chapter 18, Advanced ECG Concepts.

Transvenous Pacing Transvenous pacing is usually done by percutaneous puncture of the internal jugular, subclavian, antecubital, or femoral vein and advancing a pacing lead into the apex of the right ventricle so that the tip of the pacing lead contacts the wall of the ventricle (Figure 3-45A). The transvenous pacing lead

Pacing cable Transvenous pacing wire

Single chamber pulse generator

Figure 3-45. Temporary single chamber ventricular pacing. (A) Transvenous pacing with pacing lead in apex of right ventricle. (B) Bipolar epicardial pacing with two epicardial wires on ventricle. (C) Unipolar epicardial pacing with one wire on ventricle and one ground wire in mediastinum.

CHAPTER 3. Interpretation and Management of Basic Cardiac Rhythms

is attached to an external pulse generator that is kept either on the patient or at the bedside. Transvenous pacing is usually necessary only for a few days until the rhythm returns to normal or a permanent pacemaker is inserted.

as the negative pole of the pacing circuit. In a bipolar lead, the end of the lead is a metal tip that contacts myocardium and serves as the negative pole, and the positive pole is an exposed metal ring located a few millimeters proximal to the distal tip.

Epicardial Pacing Epicardial pacing is done through electrodes placed on the atria or ventricles during cardiac surgery. The pacing electrode end of the lead is looped through or loosely sutured to the epicardial surface of the atria or ventricles and the other end is pulled through the chest wall, sutured to the skin, and attached to an external pulse generator (Figure 3-45B,C). A ground wire is often placed subcutaneously in the chest wall and pulled through with the other leads. The number and placement of leads varies with the surgeon.

Components of a Pacing System The basic components of a cardiac pacing system are the pulse generator and the pacing lead. The pulse generator contains the power source (battery) and all of the electronic circuitry that controls pacemaker function. A temporary pulse generator is a box that is kept at the bedside and is usually powered by a regular 9-V battery. It has controls on the front that allow the operator to set pacing rate, strength of the pacing stimulus (output), and sensitivity settings (Figure 3-46). The pacing lead is an insulated wire used to transmit the electrical current from the pulse generator to the myocardium. A unipolar lead contains a single wire and a bipolar lead contains two wires that are insulated from each other. In a unipolar lead, the electrode is an exposed metal tip at the end of the lead that contacts the myocardium and serves

Basics of Pacemaker Operation Electrical current flows in a closed-loop circuit between two pieces of metal (poles). For current to flow, there must be conductive material (ie, a lead, muscle, or conductive solution) between the two poles. In the heart, the pacing lead, cardiac muscle, and body tissues serve as conducting material for the flow of electrical current in the pacing system. The pacing circuit consists of the pacemaker pulse generator (the power source), the conducting lead (pacing lead), and the myocardium. The electrical stimulus travels from the pulse generator through the pacing lead to the myocardium, through the myocardium, and back to the pulse generator, thus completing the circuit. Temporary transvenous pacing is done using a bipolar pacing lead with its tip in the apex of the RV (see Figure 3-45A). Epicardial pacing can be done with either bipolar or unipolar leads. The term bipolar means that both of the poles in the pacing system are in or on the heart (see Figure 3-45B). In a bipolar system, the pulse generator initiates the electrical impulse and delivers it out the negative terminal of the pacemaker to the pacing lead. The impulse travels down the lead to the distal electrode (negative pole or cathode) that is in contact with myocardium. As the impulse reaches the tip, it travels through the myocardium and returns to the positive pole (or anode) of the system, completing the circuit. In a transvenous bipolar system, the positive pole is the proximal ring located a few millimeters proximal to the distal tip. The circuit over which the electrical impulse travels in a bipolar system is small because the two poles are located close together on the lead. This results in a small pacing spike on the ECG as the pacing stimulus travels between the two poles. If the stimulus is strong enough to depolarize the myocardium, the pacing spike is immediately followed by a P wave if the lead is in the atrium, or a wide QRS complex if the lead is in the ventricle. A unipolar system has only one of the two poles in or on the heart (see Figure 3-45C). In a temporary unipolar epicardial pacing system, a ground lead placed in the subcutaneous tissue in the mediastinum serves as the second pole. Unipolar pacemakers work the same way as bipolar systems, but the circuit over which the impulse travels is larger because of the greater distance between the two poles. This results in a large pacing spike on the ECG as the impulse travels between the two poles. Capture and Sensing

Figure 3-46. Temporary pacemaker pulse generator. (Medtronic, Inc., Minneapolis, MN.)

The two main functions of a pacing system are capture and sensing. Capture means that a pacing stimulus results in depolarization of the chamber being paced (Figure 3-47A).

TEMPORARY PACING 63

Figure 3-47. (A) Ventricular pacing with 100% capture. Arrows show pacing spikes, each one followed by a wide QRS complex indicating ventricular capture. (B) Rhythm strip of a ventricular pacemaker in the demand mode. There is appropriate sensing of intrinsic QRS complexes and appropriate pacing with ventricular capture when the intrinsic QRS complexes fall below the preset rate of the pacemaker. The seventh beat is fusion between the intrinsic QRS and the paced beat, a normal phenomenon in ventricular pacing.

Capture is determined by the strength of the stimulus, which is measured in milliamperes (mA), the amount of time the stimulus is applied to the heart (pulse width), and by contact of the pacing electrode with the myocardium. Capture cannot occur unless the distal tip of the pacing lead is in contact with healthy myocardium that is capable of responding to the stimulus. Pacing in infarcted tissue usually prevents capture. Similarly, if the catheter is floating in the cavity of the ventricle and not in direct contact with myocardium, capture will not occur. In temporary pacing, the output dial on the face of the pulse generator controls stimulus strength, and can be set and changed easily by the operator. Temporary pulse generators usually are capable of delivering a stimulus of 0.1 to 20 mA. Sensing means that the pacemaker is able to detect the presence of intrinsic cardiac activity (Figure 3-47B). The sensing circuit controls how sensitive the pacemaker is to intrinsic cardiac depolarizations. Intrinsic activity is measured in millivolts (mV), and the higher the number, the larger the intrinsic signal; for example, a 10-mV QRS complex is larger than a 2-mV QRS. When pacemaker sensitivity needs to be increased to make the pacemaker “see” smaller signals, the sensitivity number must be decreased; for example, a sensitivity of 2 mV is more sensitive than one of 5 mV. A fence analogy may help to explain sensitivity. Think of sensitivity as a fence standing between the pacemaker and what it wants to see, the ventricle; for example, if there is a 10-ft-high fence (or a 10-mV sensitivity) between the two, the pacemaker may not see what the ventricle is doing. To make the pacemaker able to see, the fence needs to be lowered. Lowering the fence to 2 ft would probably enable the pacemaker to see the ventricle. Changing the sensitivity from 10 to 2 mV is like lowering the fence—the pacemaker becomes more sensitive and is able to “see” intrinsic activity more easily. Thus, to increase the sensitivity of a pacemaker, the millivolt number (fence) must be decreased.

Asynchronous (Fixed-Rate) Pacing Mode

A pacemaker programmed to an asynchronous mode paces at the programmed rate regardless of intrinsic cardiac activity. This can result in competition between the pacemaker and the heart’s own electrical activity. Asynchronous pacing in the ventricle is unsafe because of the potential for pacing stimuli to fall in the vulnerable period of repolarization and cause VF. Demand Mode

The term demand means that the pacemaker paces only when the heart fails to depolarize on its own, that is, the pacemaker fires only “on demand.” In demand mode, the pacemaker’s sensing circuit is capable of sensing intrinsic cardiac activity and inhibiting pacer output when intrinsic activity is present. Sensing takes place between the two poles of the pacemaker. A bipolar system senses over a small area because the poles are close together, and this can result in “undersensing” of intrinsic signals. A unipolar system senses over a large area because the poles are far apart, and this can result in “oversensing.” A unipolar system is more likely to sense myopotentials caused by muscle movement and inappropriately inhibit pacemaker output, potentially resulting in periods of asystole if the patient has no underlying cardiac rhythm. The demand mode should always be used for ventricular pacing to avoid the possibility of VF. A paced ventricular beat begins with a pacing spike, which indicates that an electrical stimulus was released by the pacemaker (Figure 3-48). If the pacing stimulus is strong enough to depolarize the ventricle, the spike is followed by a wide QRS complex and a T wave that is oriented in the opposite direction of the QRS complex. Figure 3-47A illustrates ventricular pacing with 100% capture. Figure 3-47B is the ECG of a ventricular pacemaker that is functioning correctly in the demand mode. The pacemaker generates an impulse when it senses that the heart rate has

CHAPTER 3. Interpretation and Management of Basic Cardiac Rhythms

To initiate unipolar ventricular pacing (one lead on the ventricle; see Figure 3-45C):

Figure 3-48. Temporary pacing lead in RV apex.

1. Connect the negative terminal of the pulse generator to the ventricular lead. 2. Connect the positive terminal of the pulse generator to the ground lead. 3. Set the rate at 70 to 80 beats/min or as ordered by physician. 4. Set the output at 5 mA, then determine stimulation threshold and set two to three times higher. 5. Set the sensitivity at 2 mV and adjust according to sensitivity threshold. See Chapter 18, Advanced ECG Concepts, for information on how to obtain capture and sensing thresholds.

External (Transcutaneous) Pacemakers decreased below the set pacing rate. Therefore, the pacemaker senses the intrinsic cardiac rhythm of the patient and only generates an impulse when the rate falls below the preset pacing rate. Refer Chapter 18, Advanced ECG Concepts, for more detailed information on single and dual chamber pacing.

Initiating Transvenous Ventricular Pacing Temporary transvenous pacing leads are bipolar and have two tails, one marked “positive” or “proximal” and the other marked “negative” or “distal,” that are connected to the pulse generator. To initiate ventricular pacing using a transvenous lead (see Figure 3-45A): 1. Connect the negative terminal of the pulse generator to the distal end of the pacing lead. 2. Connect the positive terminal of the pulse generator to the proximal end of the pacing lead. 3. Set the rate at 70 to 80 beats/min or as ordered by physician. 4. Set the output at 5 mA, then determine stimulation threshold and set two to three times higher. 5. Set the sensitivity at 2 mV and adjust according to sensitivity threshold.

The emergent nature of many bradycardic rhythms requires immediate temporary pacing. Because transvenous catheter placement is difficult to accomplish quickly, external pacing is the preferred method for rapid, easy initiation of cardiac pacing in emergent situations until a transvenous pacemaker can be inserted. External pacing is done through largesurface adhesive electrodes attached to the anterior and posterior chest wall and connected to an external pacing unit (Figure 3-49). The pacing current passes through skin and chest wall structures to reach the heart; therefore, large energies are required to achieve capture. Sedation and analgesia are usually needed to minimize the discomfort felt by the patient during pacing. Transcutaneous pacing spikes are usually very large, often distorting the QRS complex. The presence of a pulse with every pacing spike confirms ventricular capture.

Front

Back

Initiating Epicardial Pacing To initiate bipolar ventricular pacing (two leads on the ventricle; see Figure 3-45B): 1. Connect the negative terminal of the pulse generator to one of the ventricular leads. 2. Connect the positive terminal of the pulse generator to the other ventricular lead. 3. Set the rate at 70 to 80 beats/min or as ordered. 4. Set the output at 5 mA, then determine stimulation threshold and set two to three times higher. 5. Set the sensitivity at 2 mV and adjust according to sensitivity threshold.

Figure 3-49. External pacemaker with pacing electrode pads on anterior and posterior chest and back.

DEFIBRILLATION AND CARDIOVERSION Defibrillation Defibrillation is the therapeutic delivery of electrical energy to the myocardium to terminate life-threatening ventricular arrhythmias (VF and pulseless VT). The defibrillating shock

DEFIBRILLATION AND CARDIOVERSION 65

Figure 3-50. Paddle or adhesive pad placement for external defibrillation via (A) anterolateral position and (B) anteroposterior position.

depolarizes all cells in the heart simultaneously, stopping all electrical activity and allowing the sinus node to resume its function as the normal pacemaker of the heart. Early defibrillation is the only treatment for VF or pulseless VT and should not be delayed for any reason when a defibrillator is available. If a defibrillator is not immediately available, CPR should be started until a defibrillator arrives. Defibrillation is done externally using two paddles or adhesive pads applied to the skin in the anterolateral position (Figure 3-50A). One paddle or pad is placed under the right clavicle to the right of the sternum and the other paddle or pad is placed to the left of the cardiac apex. If paddles are used, place conductive gel pads on the patient’s skin, then place paddles on the gel pads using 25 lb of pressure to decrease transthoracic impedance and protect the skin from burns. Avoid placing paddles over medication patches or over pacemaker or implantable cardioverter defibrillator (ICD) pulse generators. Advanced Cardiac Life Support (ACLS) guidelines recommend an initial energy of 360 J with a monophasic defibrillator and the manufacturer’s recommended energy level for biphasic defibrillators. If the manufacturer’s suggested energy level is not known, a 200-J shock is recommended. Make sure no one is touching the patient, the bed, or anything attached to the patient when the shock is delivered; call “all clear” and visually verify before delivering the shock. Depress the discharge button to release the energy. If using paddles, depress both discharge buttons (one on each paddle) simultaneously. The shock is delivered immediately when buttons are pushed (Figure 3-50A). Immediately resume CPR for 2 minutes before rhythm and pulse check (this may be modified in a monitored situation where ECG and hemodynamic monitoring is available).

Automatic External Defibrillators An automatic external defibrillator (AED) is a device that incorporates a rhythm-analysis system and a shock advisory

system for use by trained laypeople or medical personnel in treating victims of sudden cardiac death. The American Heart Association recommends that AEDs should be available in selected areas where large gatherings of people occur and where immediate access to emergency care may be limited, such as on airplanes, in airports, sports stadiums, health and fitness facilities, and so on. It is well known that early defibrillation is the key to survival in patients experiencing VF or pulseless VT. Any delay in the delivery of the first shock, including delays related to waiting for the arrival of trained medical personnel and equipment, can decrease the chance of survival. The availability of an AED in public areas can prevent unnecessary delays in treatment and improve survival in victims of sudden cardiac death. Operation of an AED is quite simple and can be performed by laypeople. Instructions for use are printed on the machines and voice commands also guide the operator in using the AED. Adhesive pads are placed in the standard defibrillation position on the chest (see Figure 3-50A), the machine is turned on, and the rhythm analysis system analyzes the patient’s rhythm. If the rhythm analysis system detects a shockable rhythm, such as VF or rapid VT, a voice advises the operator to shock the patient. Delivery of the shock is a simple maneuver that only involves pushing a button. The operator is advised to “stand clear” prior to delivering the shock. After a shock is delivered, the system prompts the operator to resume CPR. After 2 minutes of CPR it prompts the operator to stop CPR while it reanalyzes the rhythm.

Cardioversion Cardioversion is the delivery of electrical energy that is synchronized to the QRS complex so that the energy is delivered during ventricular depolarization in order to avoid the T wave and the vulnerable period of ventricular repolarization. The delivery of electrical energy near the T wave can lead to

CHAPTER 3. Interpretation and Management of Basic Cardiac Rhythms

Figure 3-51. (A) Defibrillation of VF to sinus rhythm. (B) Cardioversion of atrial fibrillation to sinus rhythm. Note the synchronization mark on the QRS.

ventricular fibrillation. Synchronized cardioversion is used to terminate both supraventricular and ventricular tachycardias and is usually an elective procedure, although it should be performed urgently if the patient is hemodynamically unstable. Cardioversion can be performed via anterolateral electrode placement (see Figure 3-50A) or via anteroposterior (AP) electrode placement (see Figure 3-50B). Anteroposterior placement is preferred because less energy is required and the success rate is higher when energy travels through the short axis of the chest. Either paddles or hands-free adhesive pads can be used. Sedation is required for cardioversion since the patient is usually awake and alert and able to feel the pain caused by the procedure. Sedation can be accomplished with drugs like midazolam (Versed), methohexital (Brevital Sodium), propofol, or others at the discretion of the physician; or an anesthesiologist may be used to administer deep sedation. Because sedation is used, an emergency cart, emergency drugs (lidocaine, epinephrine, amiodarone, atropine), sedation-reversal agent, O2-delivery equipment, and suction equipment should be immediately available; and an O2 saturation monitor and noninvasive blood pressure (BP) monitoring should be done continuously during the procedure and until the patient is completely awake and recovered. Initial energy level for cardioversion is typically 50 to 100 J and varies with different arrhythmias. If the first shock is unsuccessful, energy level is increased for subsequent shocks. The machine must be synchronized to the QRS complex for cardioversion. Most machines put a bright dot or similar marker on the QRS complex when in the “synch” mode (Figure 3-51B). The machine will not discharge its energy until it sees the synch marker. Make sure to visually verify that the synch marker is actually on the QRS complex and not on a tall T wave. When delivering energy during cardioversion, push and hold the discharge button until

the energy is delivered; the synchronized machine will not discharge until it sees a QRS complex. When the energy is released, the machine automatically returns to the asynchronous mode, so if subsequent shocks are needed the machine must be resynchronized.

SELECTED BIBLIOGRAPHY Brenyo, AJ, Aktas, MK. Non-pharmacologic management of atrial fibrillation. Am J Cardiol. 2011;108:317-325. Calkins, H. Supraventricular tachycardia: atrioventricular nodal reentry and Wolff-Parkinson-White syndrome. In Fuster V, Walsh RA, Harrington RA. eds. Hurst’s The Heart. 13th ed. New York: McGraw Hill. 2011: 987-1005. Jacobson, C. Arrhythmias and conduction disturbances. In Woods SL, Froelicher ES, Motzer SU, Bridges EJ. eds. Cardiac Nursing. 6th ed. Philadelphia: Lippincott Williams & Wilkins. 2010: 333-387. Jacobson, C. Gerity, D. Pacemakers and implantable difibrillators. In Woods SL, Froelicher ES, Motzer SU, Bridges EJ. eds. Cardiac Nursing. 6th ed. Philadelphia: Lippincott Williams & Wilkins. 2010: 655-704. Jacobson C, Marzlin K, Webner C. Cardiovascular Nursing Practice: A Comprehensive Resource Manual and Study Guide for Clinical Nurses. Burien, WA: Cardiovascular Nursing Education Associates. 2007. Kenny, T. The Nuts and Bolts of Cardiac Pacing. Malden, MA: Blackwell Futura. 2005. Kerber, RE. Indications and techniques of electrical defibrillation and cardioversion. In Fuster V, Walsh RA, Harrington RA. eds. Hurst’s The Heart. 13th ed. New York: McGraw Hill. 2011: 1088-1093. Link, MS, Atkins, DL, Passman, RS, et al. Electrical therapies: automated external defibrillators, defibrillation, cardioversion, and pacing: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010:122(suppl 3), Part 6, S706–S719.

Olgin, J, Zipes, DP. Specific arrhythmias: diagnosis and treatment. In Bonow RO, Mann DL, Zipes DP, Libby P. eds. Braunwald’s Heart Disease—A Textbook of Cardiovascular Medicine. 9th ed. Philadelphia: Elsevier. 2011: 771-824. Prystowsky, EN, Padanilam, BJ, Waldo, AL. Atrial fibrillation, atrial flutter, and atrial tachycardia. In Fuster V, Walsh RA, Harrington RA. eds. Hurst’s The Heart. 13th ed. New York: McGraw Hill. 2011: 963-986. Pugazhendhi, V, Ellenbogen, KA. Bradyarrhythmias and pacemakers. In Fuster V, Walsh RA, Harrington RA. eds. Hurst’s The Heart. 13th ed. New York: McGraw Hill. 2011: 1025-1057. Rho, RW, Page, RL. Ventricular arrhythmias. In Fuster V, Walsh RA, Harrington RA. eds. Hurst’s The Heart. 13th ed. New York: McGraw Hill. 2011: 1006-1024.

Evidence-Based Practice Advanced Cardiovascular Life Support Provider Manual. Dallas, TX: American Heart Association. 2011. Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al. ACC/ AHA/ESC Guidelines for the Management of Patients with Supraventricular Arrhythmias - Executive Summary. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias). Circulation. 2003:108;1871-1909. Bourgault, A. (2008). AACN Practice Alert: Dysrhythmia Monitoring. Aliso Viejo, CA: American Association of Critical Care Nurses. http://www.aacn.org Drew, BJ, Califf, RM, Funk, M, et al. Practice standards for electrocardiographic monitoring in hospital settings. Circulation. 2004:110;2721-2746.

SELECTED BIBLIOGRAPHY 67

Furie, KL, Goldstein, LB, Albers, GW, et al. Oral antithrombotic agents for the prevention of stroke in nonvalvular atrial fibrillation: a science advisory for healthcare professionals from the American Heart Association/American Stroke Association. Stroke, 2012:43;3442-3453. Fuster, V, Ryden, LE, Cannom, DS, et al. 2011 ACCF/AHA/HRS focused updates incorporated into the ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: a report of the American College of Cardiology Foundation/ American Heart Association Task Force on Practice Guidelines. Circulation, 2011:123;e269–e367. Jacobson C. Bedside cardiac monitoring. In Burns S, ed. AACN Protocols for Practice: Noninvasive Monitoring. 2nd ed. Boston: Jones and Bartlett; 2006. Wann, LS, Curtis, AB, January, CT, et al. 2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (updating the 2006 guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2011(a):123; 104-123. Wann, LS, Curtis, AB, January, CT, et al. 2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (update on dabigatran): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2011(b):123;1144-1150. Zipes, D, Camm, A, Borggrefe, M, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines Circulation, 2006:114;e385-e484.

This page intentionally left blank

Hemodynamic Monitoring Leanna R. Miller

KNOWLEDGE COMPETENCIES 1. Identify the characteristics of normal and abnormal waveform pressures for the following hemodynamic monitoring parameters: • Central venous pressure • Pulmonary artery pressure • Arterial blood pressure • Cardiac output 2. Describe the basic elements of hemodynamic pressure-monitoring equipment and methods used to ensure accurate pressure measurements. 3. Discuss the indications, contraindications, and general management principles for the following common hemodynamic monitoring parameters: • Central venous pressure • Pulmonary artery pressure

The term hemodynamics refers to the interrelationship of blood pressure (BP), blood flow, vascular volumes, heart rate, ventricular function, and the physical properties of the blood. Monitoring the hemodynamic status of the critically ill patient is an integral part of critical care nursing. It is essential that critical care nurses have a working knowledge of how to obtain accurate data, analyze waveforms, and interpret and integrate the data. Clinical examination findings may be late indicators of hemodynamic compromise. Although noninvasive assessment techniques such as physical examination, history taking, and laboratory analysis are helpful and necessary, they do not provide the specific physiologic data available with hemodynamic monitoring. Parameters such as cardiac output (CO) and intracardiac pressures can be directly measured and monitored with special indwelling catheters. The

• Right ventricular pressure • Mixed venous oxygenation • Arterial blood pressure • Cardiac output 4. Describe the use of Svo2/Scvo2 monitoring in the critically ill patient. 5. Compare and contrast the clinical implications and management approaches to abnormal hemodynamic values. 6. Explain the basic elements of minimally invasive hemodynamic monitoring techniques.

information provided by the catheters can provide accurate and timely information to clinicians so that appropriate interventions are ensured.

HEMODYNAMIC PARAMETERS Cardiac Output Cardiac output (CO) is the amount of blood pumped by the ventricles each minute. It is the product of the heart rate (HR) and the stroke volume (SV) (the amount of blood ejected by the ventricle with each contraction; Figure 4-1). CO = HR × SV The normal value is 4.0 to 8.0 L/min (Table 4-1). It is important to note that these values are relative to size. 69

CHAPTER 4. Hemodynamic Monitoring

Cardiac output

Heart rate

Stroke volume

Preload Diastolic filling

Afterload

Contractility

Ventricular pressure

Fiber stretch

Figure 4-1. Factors affecting CO. (Reprinted from: Price S,

Ventricular size

Wilson L. Pathophysiology: Clinical Concepts of Disease Processes. Philadelphia, PA: Mosby; 1992:390, with permission from Elsevier.)

Wall thickness

Values within the normal range for a person 5-ft tall weighing 100 lb, may be totally inadequate for a 6-ft, 200-lb individual. Cardiac index (CI) is the CO that has been adjusted to individual body size. It is determined by dividing the CO by the individual’s body surface area (BSA), which

may be obtained from the DuBois body surface area chart or by pressing the CI button on the cardiac monitor. The normal value is 2.5 to 4.3 L/min/m2 (Table 4-1). CI = CO/BSA

TABLE 4-1. NORMAL HEMODYNAMIC AND BLOOD FLOW PARAMETERS Parameter Cardiac output Cardiac index Mean arterial pressure Right atrial pressure Pulmonary artery wedge pressure Pulmonary artery diastolic Pulmonary vascular resistance Pulmonary vascular resistance index Pulmonary artery mean Systemic vascular resistance Systemic vascular resistance index Right ventricular stroke work index Left ventricular stroke work index Oxygen delivery Oxygen delivery index Oxygen consumption Oxygen consumption index Stroke volume Stroke volume index Right ventricular end-diastolic volume Right ventricular end-diastolic volume index Right ventricular end-systolic volume Right ventricular end-systolic volume index Right ventricular ejection fraction Mixed venous saturation Oxygen extraction ratio Oxygen extraction index

Abbreviation CO CI MAP RAP PAOP PAD PVR PVRI PAM SVR SVRI RVSWI LVSWI DO2 DO2I VO2 VO2I SV SVI RVEDV RVEDVI RVESV RVESVI RVEF Svo2 O2ER O2EI

Formula Stroke volume (SV) × heart rate (HR) CO/BSA ÷ 1000 2(DBP) + SBP ÷ 3 cm H2O = mm Hg × 1.34

PAM – PAOP × 80 ÷ CO PAM – PAOP × 80 ÷ CI MAP – RAP × 80 ÷ CO MAP – RAP × 80 ÷ CI (PAM – RAP) SVI × 0.0138 (MAP – PAOP) SVI × 0.0138 CaO2 × CO × 10 CaO2 × CI × 10 C(a – v)O2 × CO × 10 C(a – v)O2 × CI × 10 CO/HR × 1000 CI/HR × 1000 SV/EF EDV/BSA EDV – SV ESV/BSA SV/EDV (Cao2 – Cvo2)/Cao2 × 100 Sao2 – Svo2/Sao2 × 100

Normal Range 4-8 L/min 2.5-4.3 L/min/m2 70-105 mm Hg 2-8 mm Hg 8-12 mm Hg 10-15 mm Hg 100-250 dynes-sec/cm–5 255-285 dynes-sec/cm–5/m2 15-20 mm Hg 800-1200 dynes-sec/cm–5 1970-2390 dynes-sec/cm–5/m2 7-12 g-m/M2 35-85 g-m/M2 900-1100 mL/min 360-600 mL/min/m2 200-250 mL/min 108-165 mL/min/m2 50-100 mL/beat 35-60 mL/beat/m2 100-160 mL 600-100 mL/m2 50-100 mL 30-60 mL/m2 40%-60% 60%-75% 22%-30% 22%-30%

HEMODYNAMIC PARAMETERS 71

Cardiac output measurements are used to assess the patient’s perfusion status, response to therapy, and as a rapid means to evaluate the patient’s hemodynamic status. As mentioned, CO is composed of heart rate and SV, or the amount of blood ejected with each contraction of the ventricle. Normal SV range is 50-100 mL/beat (see Table 4-1). SV depends on preload, afterload, and contractility. Therefore, CO is determined by: 1. Heart rate (and rhythm) 2. Preload 3. Afterload 4. Contractility Low Cardiac Output/Cardiac Index

Because the SV of the left ventricle is a component used in the determination of CO, any condition or disease process which impairs the pumping (ejection) or filling of the ventricle may contribute to a decreased CO. Alterations that lead to diminished CO can be divided into two general categories: inadequate ventricular filling and inadequate ventricular emptying. Inadequate Ventricular Filling

Factors that lead to inadequate ventricular filling include arrhythmias, hypovolemia, cardiac tamponade, mitral or tricuspid stenosis, diastolic dysfunction, constrictive pericarditis, and restrictive cardiomyopathy. Each of these abnormalities leads to a decrease in preload (the amount of volume in the ventricle at end diastole), which results in a decrease in CO. Inadequate Ventricular Ejection

Factors that lead to inadequate ventricular emptying include mitral/tricuspid insufficiency, myocardial infarction, increased afterload (hypertension, aortic/pulmonic stenosis), myocardial diseases (myocarditis, cardiomyopathies), metabolic disorders (hypoglycemia, hypoxia, severe acidosis), and use of negative inotropic drugs (beta-blockers, calcium channel blockers). High Cardiac Output/Index

In theory, in the normal, healthy individual, any factor that increases heart rate and contractility and decreases afterload can contribute to an increase in CO. Hyperdynamic states, such as seen in sepsis, anemia, pregnancy, and hyperthyroid crisis, may cause CO values to be increased. Increased heart rate is a major component in hyperdynamic states; however, in sepsis a profound decrease in afterload also contributes to an increased CO.

Components of Cardiac Output/Cardiac Index Heart Rate and Rhythm Rate

Normal heart rate is 60 to 100 beats/min. In a normal, healthy individual, an increase in heart rate can lead to an increase in CO. In a person with cardiac dysfunction, increases in heart rate can lead to a decreased CO and often

myocardial ischemia. The increase in heart rate decreases the ventricular filling time, by reducing preload, which decreases SV and leads to decreased CO. A lower heart rate does not necessarily result in a decrease in CO. Decreased heart rates with normal COs are often found in athletes. Their training and conditioning strengthens the myocardium such that each cardiac contraction produces an increased SV. In individuals with left ventricular (LV) dysfunction, a slow heart rate can produce a decrease in CO. This is caused by decreased contractility, as well as fewer cardiac contractions each minute. Because CO is a product of SV times heart rate, any change in SV normally produces a change in the heart rate. If the SV is elevated, the heart rate may decrease (eg, as seen in adaptation to exercise). If the SV falls, the heart rate normally increases. Subsequently, evaluating the cause of the tachycardia becomes an essential component of hemodynamic assessment. Bradycardias and tachycardias are potentially dangerous because they may result in a decrease in CO if adequate stroke volume is not maintained. Sudden-onset bradycardia is almost always reflective of a falling CO. The cause of tachycardia, on the other hand, must be determined because it may not reflect a low output state but rather a normal physiologic response (eg, tachycardia secondary to fever). Heart rate varies between individuals and is related to many factors. Some are described below. Decreased Heart Rate

•• Parasympathetic stimulation (vagus nerve stimulation) is a common occurrence in the critical care setting. It can occur with Valsalva maneuvers such as excessive bearing down during a bowel movement, vomiting, coughing, and suctioning. •• Conduction abnormalities, especially second- and third-degree blocks, are often seen in patients with cardiovascular diseases. Many drugs used in the critical care setting may lead to a decreased heart rate, including digitalis, beta-blockers, calcium channel blockers, and phenylephrine (Neosynephrine). •• Athletes often have resting heart rates below 60 beats/ min without compromising CO. •• The actual heart rate is not as important as the systemic effect of the heart rate. If the patient’s heart rate leads to diminished perfusion (decreased level of consciousness, decreased urinary output, hypotension, prolonged capillary refill, new-onset chest pain, etc), treatment is initiated to increase the heart rate. Increased Heart Rate

•• Stress, anxiety, pain, and conditions resulting in compensatory release of endogenous catecholamines such as hypovolemia, fever, anemia, and hypotension may all produce tachycardia. •• Drugs with a direct positive chronotropic effect include epinephrine and dopamine.

CHAPTER 4. Hemodynamic Monitoring

Tachycardia is very common in critically ill patients. When evaluating a rapid heart rate, each of the main sources for the tachycardia are evaluated; for example, if a patient has a heart rate of 120 beats/min, the clinician rules out such factors as fever, pain, and anxiety before assuming that the tachycardia is due to a reduced SV. Once these are ruled out, an investigation of the cause of a low SV is accomplished. The two most common reasons for a low SV are hypovolemia and LV dysfunction. Both causes of low SV can produce an increased heart rate if no abnormality exists in regulation of the heart rate (such as autonomic nervous system dysfunction or use of drugs that interfere with the sympathetic or parasympathetic nervous system such as beta-blockers). An increased heart rate can compensate for a decrease in SV, although this compensation is limited. The faster the heart rate, the less time exists for ventricular filling. As an increased heart rate reduces diastolic filling time, the potential exists to eventually reduce the SV. There is no specific heart rate where diastolic filling is reduced so severely that SV decreases. However, as the heart rate increases, it is important to remember that SV may be negatively affected. Increased heart rate also has the potential to increase myocardial oxygen demand (MVO2). The higher the heart rate, the more likely it is that the heart consumes more oxygen. Some patients are more sensitive to elevated MVO2 than others; for example, a young person may tolerate a sinus tachycardia as high as 160 for several days, whereas a patient with coronary artery disease may decompensate and develop pulmonary edema with a heart rate in the 130s. Keeping heart rates as low as possible, particularly in patients with altered myocardial blood flow, is one way of protecting myocardial function.

decreased stroke volume/stroke volume index (SV/SVI) is inadequate blood volume (preload), impaired ventricular contractility (strength), increased systemic vascular resistance (SVR; afterload), and cardiac valve dysfunction. High SV/SVI occurs when the vascular resistance is low (sepsis, use of vasodilators, neurogenic shock, and anaphylaxis).

Ejection Fraction The ejection fraction (EF) is defined as how much blood is pumped with each contraction in relation to the volume of available blood; for example, assume the left ventricular enddiastolic volume (LVEDV is the amount of blood left in the heart just before contraction) is 100 mL. If the SV is 80 mL the EF is 80%; 80 mL of the possible 100 mL in the ventricle were ejected. Right ventricular volumes are roughly equal to those of the left ventricle (RVEF) (see Table 4-1). A normal EF is usually over 60%. The EF may change before the SV in certain conditions, such as LV failure and sepsis; for example, the left ventricle may dilate in response to LV dysfunction from coronary artery disease, and LVEDV increases. Although the increase in LVEDV may prevent a drop in SV, EF may not be preserved. Thus, EF and LVEDV are early indicators of ventricular dysfunction and are ideal monitoring parameters. Unfortunately, EF and LVEDV are not routinely available. SV and SVI, then, are the best available measures to assess left and right ventricular dysfunction. The SV is very important because it typically falls with hypovolemia or when the left ventricle is too weak to eject blood (LV dysfunction).

Factors Affecting Stroke Volume/Stroke Volume Index

Rhythm

Many of us have observed the deleterious effects produced by a supraventricular tachycardia, or a change from normal sinus rhythm to atrial fibrillation or flutter. Loss of “atrial kick” may contribute to decreased CO. Normally, atrial contraction contributes 20% to 40% of the ventricular filling volume. With tachycardia, that atrial contribution to SV may diminish significantly. Although those with normal cardiac function are unlikely to experience compromise, it is more likely in those with impaired cardiac function.

Stroke Volume and Stroke Volume Index Stroke volume is the amount of blood ejected from each ventricle with each heartbeat. The right and left ventricle eject nearly the same amount, which is normally from 50 to 100 mL per heartbeat (see Table 4-1). SV = CO/HR × 1000 Stroke volume indexed to the patient’s BSA is SVI. Indexing helps to compare values regardless of the patient’s size. This is calculated by most monitors. Normal SVI is 35-60 mL/beat/m 2 (see Table 4-1). Common causes of

Preload

Preload is the volume of blood that exerts a force or pressure (stretch) on the ventricles during diastole. It may also be described as the filling pressure of the ventricles at the end of diastole or the amount of blood that fills the ventricles during diastole. According to the Frank-Starling law of the heart, the force of contraction is related to myocardial fiber stretch prior to contraction. As the fibers are stretched, the contractile force increases up to a certain point. Beyond this point, the contractile force decreases and is referred to as ventricular failure (Figure 4-2). With increased preload there is an increase in the volume of blood delivered to the ventricle, the myocardium is stretched, and a more forceful ventricular contraction is produced. This forceful ventricular contraction yields an increase in SV, and therefore, CO. Too much preload causes the ventricular contraction to be less effective. A commonly referred to analogy uses the properties of a rubber band. The more a rubber band is stretched, the greater “snap” is produced when released. The rubber band may be stretched further and further, until it reaches a point where it loses its tautness and fails to recoil.

HEMODYNAMIC PARAMETERS 73

vasodilators, neurogenic shock, severe sepsis), and profound diaphoresis. Venous dilatation also results in diminished preload. Etiologies that increase venous pooling and result in decreased venous return to the heart include hyperthermia, septic shock, anaphylactic shock, and drug administration (nitroglycerin, nitroprusside) (Table 4-2). Factors leading to increased preload include excessive administration of crystalloids or blood products and the presence of renal failure (oliguric phase and/or anuria). Venous constriction results in the shunting of peripheral blood to the central organs (heart and brain). The increased venous return results in an increased preload. This may occur in hypothermia, some forms of shock (hypovolemic, cardiogenic, and obstructive) and with administration of drugs that stimulate the alpha receptors (epinephrine, dopamine at doses greater than 10 mcg/kg/min, norepinephrine) (see Table 4-2).

Stroke volume, mL/beat

160

120

Cardiac reserve

Cardiac failure

100 200 300 End-diastolic volume, mL

400

Figure 4-2. Ventricular function curve. As the end-diastolic volume increases, so does the force of ventricular contraction. The SV becomes greater up to a critical point after which SV decreases (cardiac failure). (From Langley LF. Review of Physiology. 3rd ed. New York, NY: McGraw-Hill; 1971.)

Clinical Indicators of Preload

The right ventricle pumps blood into the pulmonary circulation and the left ventricle ejects blood into the systemic circulation. Both circulatory systems are affected by preload, afterload, and contractility. These are discussed below and, when appropriate, the clinical indicators are differentiated by right or left heart.

Determinants of Preload

Preload is determined primarily by the amount of venous return to the heart. Venous constriction, venous dilation, and alterations in the total blood volume all affect preload. Preload decreases with volume change. This can occur in hemorrhage (traumatic, surgical, gastrointestinal [GI], postpartum), diuresis (excessive use of diuretics, diabetic ketoacidosis, diabetes insipidus), vomiting and diarrhea, third spacing (ascites, severe sepsis, heart failure [HF]), redistribution of blood flow (use of

Right Ventricular preload

Normal right ventricular (RV) preload is 2 to 8 mm Hg or 2 to 10 cm H2O (see Table 4-1) (CVP = central venous pressure; RAP = right atrial pressure). Right atrial pressures are

TABLE 4-2. HEMODYNAMIC EFFECTS OF CARDIOVASCULAR AGENTS Drug Norepinephrine (Levophed) Phenylephrine (Neosynephrine)

PAOP

SVR

MAP

CVP

PVR

↑ (slight)

↑

↔, ↑

↑

↔,↓

↑

↔,↓

↑

Epinephrine (Asthmahaler)

↑

Dobutamine (Dobutrex)

↑

↓

↑

↔, ↑ (slight)

↓

Dopamine (Intropin)

↑

< 5 mcg/kg/min

↑

↑↑

↑ (slight)

↑↑

(with ↑ CO)

> 5 mcg/kg/min Digoxin (Lanoxin)

↑

↔

Isoproterenol (Isuprel)

↑

↓

↔, ↓ (related to ↑ SVR)

↑

Levosimendan (Simdox)

Vasopressin Milrinone (Primacor)

↑ ↔

↑

↑↑

↑

↔

↓

↔

↓

↑

↓

↑

↔, ↓

↑

↔, ↓ (related to ↑ SVR)

↑

↔, ↓

↑

↓

↔ (↓ in preloadsensitive patient)

↔ (↑ in preloadsensitive patient)

↓

Nitroglycerine (Tridil)

↔

↓

↔

↓

↔

20-40 mcg/min

↑

↓

↑

↓

50-250 mcg/min(max dose) Nitroprusside (Nipride)

↑

↓

↑

↓

CHAPTER 4. Hemodynamic Monitoring

measured to assess right ventricular function, intravascular volume status, and the response to fluid and drug administration. CVP/RAP pressures increase because of intravascular volume overload, cardiac tamponade (effusion, blood, etc), restrictive cardiomyopathies, and RV failure. There are three etiologies of RV failure: 1. Intrinsic disease such as RV infarct or cardiomyo pathies; 2. Secondary to factors that increase pulmonary vascular resistance (PVR) such as pulmonary arterial hypertension, pulmonary embolism, hypoxemia, chronic obstructive pulmonary disease (COPD), acute respiratory distress syndrome (ARDS), sepsis; and 3. Severe LV dysfunction as seen in mitral stenosis/ insufficiency or LV failure. In contrast, the only clinically significant reason for a decreased CVP/RAP is hypovolemia. CVP/RAP is a late indicator of alterations in LV function therefore limiting its value in clinical decision making. Left Ventricular Preload

Normal LV preload is 8 to 12 mm Hg (PAOP = pulmonary artery occlusion pressure; PCWP = pulmonary capillary wedge pressure; PAWP = pulmonary artery wedge pressure; LAP = left atrial pressure). The most commonly used term is PAOP (see Table 4-1). With the insertion of 1.25 to 1.50 mL of air into the balloon port of the pulmonary artery (PA) catheter, the balloon becomes lodged in a portion of the PA that is smaller than the balloon. This occludes blood flow distal to the catheter tip. The pressure in the left atrium is sensed by the catheter tip. When the mitral valve is open during ventricular diastole, the pressure that is sensed is that of the left ventricle, the left ventricular end-diastolic pressure (LVEDP) or LV preload (Figure 4-3). PAOP increases because of conditions such as intravascular volume overload, cardiac tamponade (blood, effusion,

Afterload

Afterload is the resistance to ventricular emptying during systole. It is the pressure or resistance, that the ventricles must overcome to open the aortic and pulmonic valves and to pump blood into the systemic and pulmonary vasculature.

etc), impaired ventricular relaxation (diastolic dysfunction, restrictive cardiomyopathy and constrictive pericarditis), and LV dysfunction. Common etiologies of LV dysfunction include mitral stenosis/insufficiency, aortic stenosis/ insufficiency, and diminished LV compliance (ischemia, fibrosis, hypertrophy). The only clinically significant reason for a decreased PAOP is hypovolemia. There are some conditions in which PAOP and LVEDP do not correlate. LV failure with PAOP greater than 15 to 20 mm Hg and conditions with diminished LV compliance result in a PAOP less than the true LVEDP. Patients on positive end-expiratory pressure (PEEP, continuous positive airway pressure), zone 1 or 2 catheter tip placement (Figure 4-4), tachycardia (> 130 beats/min), mitral stenosis/insufficiency, COPD, or pulmonary venoocclusive disease have a measured PAOP that is greater than the true LVEDP. These factors must be considered prior to therapeutic management. The pulmonary artery diastolic (PAD) is normally 1 to 4 mm Hg higher than the PAOP due to resistance of blood flow into the pulmonary vessels; however, when the catheter is “wedged,” there is no flow or resistance to flow and the number reflects PAOP. When the patient has an increased PVR, the PAD and PAOP no longer correlate and cannot be used interchangeably. Conditions that cause increased PVR are hypoxemia, acidemia, massive pulmonary embolism, and pulmonary vascular disease. If the PAD and PAOP closely correlate, the PAD can be used to trend the LVEDP. This allows prolonged balloon life, and reduces the chance for pulmonary ischemia, PA damage, and rupture.

LV RV

Pulmonary capillaries

Figure 4-3. Schematic representation of the PA in the wedge position. From its position in small occluded segment of the pulmonary circulation, the PA catheter in the wedged position allows the electronic monitoring equipment to “look through” a nonactive segment of the pulmonary circulation to the hemodynamically active pulmonary veins and left atrium. (From Darovic GO. Hemodynamic Monitoring: Invasive and Noninvasive Clinical Application. Philadelphia, PA: WB Saunders; 2002:207, with permission from Elsevier.)

HEMODYNAMIC PARAMETERS 75

I PaPv II PaPv III

Pa>PA 90% of cases if brachial or femoral artery is used. Replace transducer. “Fast-flush” through system. Tighten all connections. Tighten all connections.

Remove catheter.

Remove catheter. Prescribe antibiotic.

Adapted from: Daily E, Schroeder J. Techniques in Bedside Hemodynamic Monitoring. 5th ed. St Louis, MO: CV Mosby; 1994:165-166, with permission from Elsevier.

120 80 40 0

Figure 4-18. Graphic tracing of an arterial waveform preceded by calibration scale markings (0/40/80/120 mm Hg). Note how the scale markers line up with the heavy line of the tracing paper. Each 1-mm line represents 4 mm Hg in this scale.

return. High CVP values reflect overhydration, increased venous return, or right-sided cardiac failure. If the CVP and SV are low, hypovolemia is assumed. If the CVP is high and the SV is low, RV dysfunction is likely. Central venous pressure is obtained from the proximal port of the PA catheter or the tip of central venous catheter. Measurement of CVP is done simultaneously with the ECG. Using the ECG allows the identification of the point where the CVP best correlates with the RVEDP. The CVP is read by one of two techniques. The first technique is to take the mean (average) of the A wave of the CVP waveform (Figure 4-20). Although three waves normally exist on atrial waveforms (A, C, and V waves), the mean of the A wave most closely approximates ventricular enddiastolic pressure. The A wave of the CVP waveform starts

CHAPTER 4. Hemodynamic Monitoring

Figure 4-19. Referencing and zeroing the hemodynamic monitoring system in a patient in the lateral position. (A) For the right lateral position, the reference point

is at the intersection of the fourth ICS and the midsternum. (B) For the left lateral position, the reference point is the intersection of the fourth ICS and the left parasternal border. (From Keckeisen M, Chulay M, Gawlinski A, eds. Pulmonary artery pressure monitoring. In: Hemodynamic Monitoring Series. Aliso Viejo, CA: AACN; 1998:12.)

just after the P wave on the ECG is observed and represents atrial contraction. By taking the reading at the highest point of the A wave, adding it to the reading at the lowest point of that A wave, and dividing by 2, the average or mean CVP reading is obtained (generally a line is drawn through the middle of the A waves to derive a number). A second method, the Z-point technique, also can be used to estimate ventricular end-diastolic pressures (Figure 4-21). The Z-point is taken just before the closure of the tricuspid valve. This point is located on a CVP tracing in the mid to late

QRS complex area. The Z-point technique is especially useful when an A wave does not exist, for example, in atrial fibrillation when atrial contraction is absent. By isolating the A wave or using the Z-point technique, atrial pressures can reasonably estimate ventricular enddiastolic pressure. It is helpful to read these values off a multichannel strip recorder and not the digital display on the bedside monitor. Monitor values tend to be accurate in simple waveforms but become less reliable when the waveforms are complex (see Table 4-4).

40 30

20 10

0 A wave starting in PR interval

V wave in TP interval

V wave A wave 24 + 15 Mean CVP = , or 19.5 or 20 mm Hg 2

Figure 4-20. Reading a CVP waveform by averaging the A wave. (From: Ahrens TS, Taylor L. Hemodynamic Waveform Analysis. Philadelphia, PA: WB Saunders; 1992:31.)

OBTAINING AND INTERPRETING HEMODYNAMIC WAVEFORMS 91

ECG

S Z point

A wave

C wave

V wave

Atrial wave

X 1 descent

X 2 descent

Y descent

Figure 4-21. Use of the Z-point to read a CVP waveform. (From: Ahrens TS. Hemodynamic Waveform Analysis. Philadelphia, PA: WB Saunders; 1992:24.)

Central Venous Pressure: Abnormal Venous Waveforms

Two types of abnormal CVP waveforms are common. Large A waves (also called cannon A waves) occur when the atrium contracts against a closed tricuspid value (Figure 4-22). This occurs most commonly with arrhythmias like PVCs or third-degree

heart block. Giant V waves are common in conditions such as tricuspid insufficiency or ventricular failure. Using the Z-point for CVP readings prevents incorrect interpretations associated with the use of large A or V waves.

40 30 20 10 0 Large A waves follow each PVC

Figure 4-22. Giant A waves with loss of atrioventricular synchrony. (From Ahrens TS. Hemodynamic Waveform Analysis. Philadelphia, PA: WB Saunders; 1992:54.)

CHAPTER 4. Hemodynamic Monitoring

Pulmonary Artery Wedge Pressure (Occlusion Pressure)

Although the CVP is useful in assessing RV function, the assessment of LV function is generally more important. In LV dysfunction (eg, with myocardial infarction or cardiomyopathies), a threat to tissue oxygenation and survival may exist due to low CO. The PAOP is used to assess LV function and provide appropriate therapy. Interpreting the PAOP is very similar to interpreting a CVP waveform with the obvious exception that the PAOP assesses LVEDP, not RVEDP. The LVEDP is used to assess LV function and systemic fluid status. A normal PAOP is 8 to 12 mm Hg. Low values reflect hypovolemia, with high values indicating hypervolemia and/or LV failure. Mitral valve abnormalities also cause elevations in PAOP. When PAOP and SV are normal normovolemia and acceptable LV function is assumed. If the PAOP and SV are low hypovolemia is likely. When PAOP is high (usually greater than 18 mm Hg) but SV is low, LV dysfunction is assumed. A PAOP waveform is obtained from the distal port of the PA catheter when the balloon on the catheter is inflated. Inflation of the balloon is performed for only a few seconds (8-15 seconds) to avoid a disruption in pulmonary blood flow. When inflating the balloon, inflate only to the volume necessary to obtain the PAOP waveform (1.25-1.50 mL). Record how much air it takes to inflate the balloon. If it takes less air to obtain a PAOP value than at a previous inflation, the catheter may have migrated further into the pulmonary artery. If it takes more air to obtain a PAOP, the catheter may have moved back. If no resistance is felt when the balloon is inflated and no PAOP tracing occurs, notify the physician of a possible balloon rupture. When deflating the balloon, allow air to leave the balloon passively. Actively aspirating the air out of the balloon damages the balloon and is not necessary for complete emptying. The characteristics and interpretation of PAOP and CVP waveforms are similar. The difference between interpreting a CVP and a PAOP waveform mainly centers on the delay in waveform correlation with the ECG (Figure 4-23). This delay

o PAW o RA

Figure 4-23. PAOP and RA waveforms illustrating the difference in timing of waveform components relative to the ECG. (From Daily EK. Hemodynamic waveform analysis. J Cardiovasc Nurs. 2001;15[2]:6-22.)

occurs because the tip of the PA catheter is further away from the left atrium. On a PAOP waveform, the A wave begins near the end of the QRS complex. Averaging the A wave’s highest and lowest values, as previously described for CVP readings, is one method for obtaining the PAOP. If the Z-point is to be used for a PAOP reading, this point is found at the end or immediately after (about 0.08 s) the QRS complex (Figure 4-24). Assessment of LV function is commonly performed with the PAOP. The use of the PAOP to estimate LVEDP is based on the assumption that a measurement from an obstructed pulmonary capillary reflects an uninterrupted flow of blood to the left atrium because no valves exist in the PA system. A second assumption is that when the mitral valve is open, left atrial pressures reflect LVEDP. As long as these assumptions are accurate, the use of the PAOP to estimate LVEDP is acceptable. Pulmonary Artery Wedge Pressure: Abnormal Waveforms

Similar abnormal PAOP waveforms occur as with CVP measurements. Large A waves are observed when the left atrium contracts against a closed mitral valve. Large V waves are observed during mitral valve insufficiency and left heart failure (see Figures 4-22 and 4-24). Arterial and Ventricular Waveforms

An arterial waveform, such as seen in systemic and PA tracings, has three common characteristics: rapid upstroke; dicrotic notch; and progressive diastolic runoff (Figure 4-25). Diastole is read near the end of the QRS complex with systole read before the peak of the T wave. The mean arterial pressure can be calculated (see Table 4-1) or obtained from the digital display on the bedside monitor. A ventricular waveform also has three common characteristics: rapid upstroke, rapid drop in pressure, and terminal diastolic rise (Figure 4-26). Systole and diastole are read in the same manner as for an arterial waveform. LV waveforms are not available in the clinical area but can be obtained during cardiac catheterization. Normally, RV waveforms are only observed during insertion of the PA catheter or if an extra lumen is present on the catheter which exists into the RV (see Table 4-7). If an RV waveform is present during monitoring, it is important to verify the location of the catheter. The catheter may have migrated out of the PA and into the RV. A catheter that is floating free in the ventricle tends to cause ventricular ectopy (PVC) if the catheter comes into contact with the ventricular wall. In addition, assessment of PA pressures is not possible. If the RAP/CVP is high (> 6 mm Hg), particularly if the SV is low, some ventricular dysfunction is suspected. If the RAP/CVP is low (< 2 mm Hg) and the SV is low, hypovolemia is suspected. Hypovolemia is also possible if the PAOP is low (< 8 mm Hg) and the SV is reduced. If the PAOP is high (> 18 mm Hg) and SV is reduced, LV dysfunction may be present. PA Waveforms

Pulmonary artery pressures are obtained from a flowdirected PA catheter (see Figure 4-5). The PA pressure is

OBTAINING AND INTERPRETING HEMODYNAMIC WAVEFORMS 93

End QRS valve V wave

V wave 30 20

15 15

10 0

Figure 4-24. Use of the Z-point to read a wedge waveform (PAOP, 15 mm Hg). (From: Ahrens TS, Taylor L. Hemodynamic Waveform Analysis. Philadelphia, PA: WB Saunders; 1992:320.)

typically low in comparison to the systemic pressure. The PA pressure is determined by the RV CO and the PVR. PA blood pressure is generally in the region of 20 to 30 mm Hg systolic and 10 to 15 mm Hg diastolic (Figure 4-27). PA pressure reading is measured from the distal port of the PA catheter. The low-pressure pulmonary system is critical to adequate gas exchange in the lungs. If the pressure in the pulmonary vasculature elevates, the capillary hydrostatic pressure exceeds capillary osmotic pressure and forces fluid out of the vessels. If the pulmonary lymphatic drainage capability is exceeded,

Systole

Diastole

interstitial and alveolar flooding occur, with resulting interference in oxygen and carbon dioxide exchange. Normally, the PA pressure is high enough to ensure blood flow through the lungs to the left atrium. Subsequently, BP in the pulmonary arteries only needs to be high enough to overcome the resistance in the left atrium. The mean PA pressure must always be higher than left atrial pressure or blood flow through the lungs is not possible. As a practical guideline, the PAD pressure is higher than the mean left atrial pressure (the mean left atrial pressure is generally estimated

Dicrotic notch

Progressive diastolic run-off

Figure 4-25. Characteristics of an arterial waveform. (From: Ahrens TS, Prentice D. Critical Care: Certification Preparation and Review. 3rd ed. Stamford, CT: Appleton & Lange; 1993:82.)

CHAPTER 4. Hemodynamic Monitoring

Rapid upstroke

40 30

24 Systole

20 10

10 Diastole

10 End-diastolic rise RV pressure ≅

24 mm Hg 10

Figure 4-26. Characteristics of a ventricular waveform. (From: Ahrens TS, Taylor L. Hemodynamic Waveform Analysis. Philadelphia, PA: WB Saunders; 1992:96.)

by PAOP). If the PAD value is less than the left atrial or wedge pressure, either a very low pulmonary blood flow state exists or the waveforms have been misinterpreted. Measurement of PA pressures can be helpful in diagnosing many clinical conditions. Elevated PA pressures occur in pulmonary hypertension, chronic pulmonary disease, mitral

valve disease, LV failure, hypoxia, and pulmonary emboli. Below-normal PA pressures occur primarily in conditions that produce hypovolemia. If blood volumes are reduced, less resistance to ventricular ejection occurs, resulting in a drop in arterial pressures. In this situation, the PAD pressure is also close to the left atrial pressure.

ECG

PAP 60 40 20

1 2

4 3

Figure 4-27. PA waveform and components. 1, PA systole; 2, dichrotic notch; 3, PA end diastole; 4, anacrotic notch of PA valve opening. (From: Boggs R, WooldridgeKing M. AACN Procedure Manual for Critical Care, 3rd ed. Philadelphia, PA: WB Saunders; 1993:316.)

OBTAINING AND INTERPRETING HEMODYNAMIC WAVEFORMS 95

Systemic Arterial Pressures

Direct measurement of systemic arterial pressures is obtained from the tip of an arterial catheter and leveled to the phlebostatic axis (see Figure 4-11), with pressure waveforms interpreted as described. Normal pressures are generally in the region of 100 to 120 mm Hg systolic, 60 to 80 mm Hg diastolic, and 70 to 105 mm Hg mean (see Table 4-1). Systemic arterial pressures are not interpreted without other clinical information. In general, however, hypotension is assumed if the mean arterial pressure drops below 60 mm Hg. Hypertension is assumed if the systolic blood pressure (SBP) is greater than 140 to 160 mm Hg or the diastolic pressure exceeds 90 mm Hg. The arterial pressure is one of the most commonly used parameters for assessing the adequacy of blood flow to the tissues. Blood pressure is determined by two factors: CO and SVR. Blood pressure does not reflect early clinical changes in hemodynamics because of the interaction with CO and SVR. In addition, the CO consists of heart rate and SV. These two interact to maintain a normal CO. Subsequently, if the SV begins to fall due to loss of volume (hypovolemia) or dysfunction (LV failure), the heart rate increases to offset the decrease in SV. The net effect is to maintain the CO at near normal levels. If the CO does not change, then there is no change in the blood pressure.

A key point for the nurse to consider is that because of these compensatory mechanisms, BP may not signal early clinical changes in hemodynamic status. If a patient begins to bleed postoperatively, the blood pressure generally does not reflect this change until compensation is no longer possible. In addition, hypotension is sometimes difficult to evaluate. It is possible that true hypotension exists only when tissue hypoxia is present and end organs are affected. Although tradition dictates that we identify hypotension using predefined levels of BP, other measures such as mixed venous saturation of hemoglobin (Svo2) and lactate levels may be better indicators. Svo2 monitoring is described later in the Section Continuous Mixed and Central Venous Oxygen Monitoring (Svo2/Scvo2). Although studies identify the role of hypertension in circulatory damage, the specific level of hypertension that results in the damage is unclear. Therefore, any SBP over 140 is considered potentially injurious to the vasculature.

Artifacts in Hemodynamic Waveforms: Respiratory Influence Respiration can physiologically change hemodynamic p ressures. Spontaneous breathing augments venous return and slightly increases resistance to left ventricle filling. Mechanical ventilation does the opposite, potentially reducing venous return and reducing the resistance on the heart. The effect of respiration on waveforms is noted in Figures 4-28 and 4-29.

120 80 40 0 End expiration

During mechanical ventilation

Figure 4-28. Effect of respiration on arterial pressures. (From: Ahrens TS. Hemodynamic Waveform Analysis. Philadelphia, PA: WB Saunders; 1992:161.)

CHAPTER 4. Hemodynamic Monitoring

Exhalation Inspiration

Inspiration

Exhalation

Spontaneous ventilation

Exhalation

Inspiration

Inspiration Exhalation

Mechanical ventilation

Figure 4-29. A PA waveform demonstrating respiratory effects. During spontaneous ventilation, hemodynamic pressures fall during inspiration and rise during exhalation. With mechanical ventilation, pressures rise during inspiration and fall during exhalation. The circled waveforms identify end expiration in each ventilatory mode. (From: Daily EK. Hemodynamic waveform analysis. J Cardiovasc Nurs. 2001;15[2]:6-22.)

A spontaneous breath or a triggered ventilator breath produces a drop in the waveform because of the decrease in pleural pressure (Figure 4-30). A ventilator breath produces an upward distortion of the baseline, due to an increase in pleural and intrathoracic pressure (Figures 4-31 and 4-32). The key to reading the waveform correctly is to isolate the point where

pleural pressure is closest to atmospheric pressure. This point is usually at end expiration, just prior to inspiration (Figure 4-33).

Cardiac Output Perhaps the most important information obtained from the PA catheter is the measurement of blood flow parameters such

30 20

10 5

0 End expiration Spontaneous breath

Spontaneous breath

A wave Mean CVP = 16 + 5 , or 10.5 or 11 mm Hg 2

Figure 4-30. Effect of a spontaneous breath on a CVP waveform. (From: Ahrens TS. Hemodynamic Waveform Analysis. Philadelphia, PA: WB Saunders; 1992:165.)

OBTAINING AND INTERPRETING HEMODYNAMIC WAVEFORMS 97

60 40 20 10 0

20 0

Figure 4-31. Right atrial waveform, from a PA catheter with simultaneously recorded ECG from a head-injured patient with neurogenic pulmonary edema. The patient is being maintained on controlled mechanical ventilation with 30 cm H2O PEEP. Peak inspiratory pressure is 100 cm H2O. The open arrows indicate the positive-pressure (ventilator) breaths and the solid arrows indicate end expiration. It is at this point that the RAP is recorded. Note that the end-expiratory pressure measurement is approximately 20 mm Hg. This grossly elevated value should not be considered to be a “true” indication of intravascular volume or RV function. Rather, the pressure measurement is spuriously elevated as a result of the excessively high intrathoracic pressure surrounding the heart and blood vessels. (Darovic GO. Hemodynamic Monitoring, Invasive and Noninvasive Clinical Application. 3rd ed. Philadelphia, PA: WB Saunders; 1995.)

40 30 20 10 0

Expiration PA pressure = 31 –– mm Hg 21

Mechanical ventilator breath

Figure 4-32. Effect of a mechanical ventilator breath on PA waveform. (From: Ahrens TS. Hemodynamic Waveform Recognition. Philadelphia, PA: WB Saunders; 1993:92.)

CHAPTER 4. Hemodynamic Monitoring

40 30 20 10 0

Inspiratory artifact

Inspiratory artifact End-expiratory points for reading values Mean PCWP = 20 mm Hg

Figure 4-33. Reading end expiration before a spontaneous breath. (From: Ahrens TS, Taylor L. Hemodynamic Waveform Analysis. Philadelphia, PA: WB Saunders; 1992:170.)

as CO and SV. Understanding these parameters is critical to assessing the adequacy of cardiac function. Flow parameters like CO and SV are the first parameters assessed when monitoring hemodynamic data. Descriptions of the parameters are found at the beginning of this chapter. If flow parameters are adequate, tissue oxygenation is generally maintained. If flow parameters are abnormal, the clinician must suspect a threat to tissue oxygenation and consider interventions aimed at improving cardiac function. Keep in mind that blood flow can fluctuate with many conditions. If hypovolemia is present (eg, from GI bleeding or postoperative complications), blood flow drops. If LV failure is present (eg, from myocardial infarction or HF), blood flow drops. The bedside nurse detects these changes and intervenes appropriately. Although noninvasive CO and other bioimpedance devices may be helpful in assessing blood flow, the gold standard continues to be the hemodynamic monitoring with a PA catheter. Although changes in blood flow may at times be obvious (the patient loses pulses, changes level of consciousness, decreases urine output), the measures are nonspecific and are often late signs of compromise. The most important

component of tissue oxygenation is blood flow. Hemodynamic monitoring is an accurate and important means of assessing the adequacy of tissue oxygen delivery. Measurement of Cardiac Output

Cardiac output measurements using a PA catheter are obtained by one of two methods: the intermittent thermodilution technique or the continuous technique. Both types of measures rely on measuring changes in blood temperatures. The most commonly used technique is the intermittent thermodilution technique (Figure 4-34). The technique is based on injecting a known volume of fluid at a given temperature into the blood. As the blood temperature changes to near the injectate temperature, a sensor near the distal tip of the PA catheter measures this change. CO is then computed based on the temperature change and the time it takes the injected volume to pass the thermistor. The calculation of CI is automatically done by most CO computers if body surface information is available (see Table 4-1). The temperature change during injection can be graphically displayed on the CO computer or bedside monitor as a CO curve (Figure 4-35A). If the CO is low, the curve is small and the tail of the curve is long

OBTAINING AND INTERPRETING HEMODYNAMIC WAVEFORMS 99

Nonvented IV spike Snap clamp Injectate delivery tubing

Mounting tab

Co-Set ice bucket

Balloon

Tubing coil

10-cc syringe

Thermal tubing Inline tubing connector place inside cooling container

Proximal injectate hub User supplied 3-way stopcock and continuous flush device To IV/pressure monitoring

Inside partition Temperature probe

Catheter connector

Remote switch

Flow-through housing

Check valve

Cooling coil Co-Set cooling container mounting bracket

Distal lumen hub

Proximal injectate Distal lumen port

Thermistor

Thermistor connector

Model 131-7F Swan-Ganz thermodilution catheter

Lid

Injectate probe connector Balloon inflation valve

Cardiac output computer

Reusable flow-through injectate temperature probe

Sterile injectate solution (user supplied)

Nonvented IV spike Model 131-7F Swan-Ganz thermodilution catheter

Snap clamp

Thermistor connector

Thermistor Distal lumen

Balloon

Co-Set injectate delivery tubing

Check valve

Temperature probe

Proximal injectate port

10-cc syringe Flow-through housing Proximal injectate hub User supplied 3-way stopcock and continuous flush device To IV/pressure monitoring

Remote switch

Injectate probe connector

Catheter connector

Cardiac output computer

Balloon inflation valve Reusable flow-through injectate temperature probe assembly

Figure 4-34. Co-Set closed thermodilution CO setup. (A) Iced injectable setup. (B) Room-temperature injectable setup. (From: Edwards Lifesciences, Irvine, CA.)

100

CHAPTER 4. Hemodynamic Monitoring

Figure 4-35. (A) Normal CO curve. (B) Low CO curve. (C) High CO curve.

reflecting the slow change in temperature past the thermistor (Figure 4-35B). If the CO is high, the curve is high and the tail of the curve is short reflecting the rapid change in temperature sensed by the thermistor (Figure 4-35C). Key Concepts in Measuring Cardiac Output

To correctly measure the CO, the nurse needs to program the bedside CO computer with the following information: •• Type of PA catheter. Different companies may have different catheter configurations. This requires a slightly different computation by the computer. The manufacturer provides the correct computation constant to be programmed into the CO computer. •• Volume of injectate. Normally, 5 or 10 mL of D5W or NS is used. •• Temperature of the injectate. Either cold (also called iced) or room-temperature injectate can be used. When using cold injectable, the injectate solution must be

placed in a container of ice water (see Figure 4-34A, B). Room-temperature injectate has an advantage—in that it avoids the cumbersome cooling system necessary with iced injectate. Whichever technique is used, the system should be a closed system to prevent increased risk of IV nosocomial infections. •• Computation constant. The manufacturer of the CO system provides the correct computation constant to use based on the specific solution volume and temperature used for CO measurements. This information is programmed into the CO computer before performing CO measurements. Failure to provide the correct computation constant will result in inaccurate hemodynamic values. Factors Affecting Accuracy

For thermodilution CO to be accurate, several factors should be present. These factors include a functioning tricuspid value, no ventricular septal defect, and a stable cardiac

CONTINUOUS MIXED AND CENTRAL VENOUS OXYGEN MONITORING 101

TABLE 4-10. TISSUE OXYGENATION PARAMETERS Svo2 Lactate pH Pyruvate HCO3

60%-75% 1-2 mEq/L 7.35-7.45 0.1-0.2 mEq/L 22-26 mEq/L

rhythm. The presence of cardiac valve or rhythm abnormalities causes the thermodilution CO measurement to be inaccurate. Chapter 25, Hemodynamic Monitoring Troubleshooting Guide, identifies common problems associated with measurement of CO. Interpreting Cardiac Output and Cardiac Index

The CI is a critical parameter to monitor because blood flow is the key to adequate oxygen delivery. If a threat to blood flow occurs, tissue oxygenation is immediately placed at risk. If adequate blood flow is present, as measured with the CO or CI, generally one can assume the patient does not have a major disturbance in oxygenation. There is no one CI that requires intervention. However, CI less than 2.5 L/min/m 2 is considered circulatory compromise and further assessment is warranted. If the CI drops to less than 2.2 L/min/m2, the investigation becomes urgent. However, some patients tolerate low CI without clinical problems. Tracking trends in CI values is generally more useful than monitoring single data points because temporary changes in values may not be clinically significant. In any event, with drops in CI circulatory compromise and tissue hypoxia may ensue. Using both CI and tissue oxygenation parameters, such as Svo2, increases the accuracy in identifying a clinically dangerous event (Table 4-10).

CONTINUOUS MIXED AND CENTRAL VENOUS OXYGEN MONITORING Continuous Mixed and Central Venous Oxygen Monitoring Monitoring Principles

The PA catheter allows clinicians many monitoring capabilities that help to guide therapeutic interventions in the critically ill. One such option is the continuous monitoring of mixed venous oxygenation. Svo2 catheters are different from other PA catheters—in that they have two special fiber-optic bundles within the catheter that determine the oxygen saturation of hemoglobin by measuring the wavelength (color) of reflected light. Light is transmitted down one bundle and is reflected off the oxygen-saturated hemoglobin, returning up the other bundle. This information is quantified by the bedside computer and numerically displayed as the percentage of saturation of the mixed venous blood. A newer strategy is measurement of central venous oxygen saturation (ScvO2). This requires the placement of a central venous catheter which can be easily placed and is less risky than a PA catheter. Theoretically, it measures the degree of oxygen extraction from the brain and upper body

Essential Content Case

Svo2 A 35-year-old woman with pancreatitis and ARDS experiences a progressively worsening oxygenation status. The care team decides to replace her PA catheter with a Svo2 catheter to better monitor and manage her. Once the Svo2 catheter is in place and calibrated, it is noted that her Svo2 is only 55%. A quick assessment of oxygen supply variables yields the following: Hct CO PAOP Sao2

22% 6 L/min 18 mm Hg 91% on an Fio2 of 0.6, PEEP of 15 cm H2O

Given the high level of ventilatory support already in place, the team felt that augmentation of oxygen-carrying capacity with transfusions of packed red blood cells (PRBC) would provide the greatest boost to oxygenation. Following the infusion of 2 U of PRBC, the Svo2 increased to 70%. Over the course of the next few days, ventilatory support was gradually decreased by monitoring the effect of ventilatory changes on Svo2 in conjunction with other supplyside variables. On day 6, she became increasingly agitated and her Svo2 decreased to 60%. She was febrile and her sputum was noted to be purulent appearing. Sputum cultures were obtained and other reasons for the agitation were also considered. A STAT chest radiograph was obtained to rule out pneumothorax (it was ruled out), and an arterial blood gas was obtained. AGB revealed a PaCO2 of 45 mm Hg, and a Pao2 of 55 mm Hg. Her ventilator settings were IMV of 12/min (spontaneous rate was 10 above the ventilation), Fio2 of 0.45, PEEP of 5 cm H2O, Hct of 29%, and CO of 6 L/min. The team recognized that both supply and demand needed to be addressed to optimize her oxygenation. Thus, ventilatory settings were increased as follows: Fio2 PEEP IMV

0.60 10 cm H2O 20/min

Case Question 1. What parameters contribute to changes in the Svo2? Case Question 2. Would the patient benefit from fluid resuscitation? If so, what? Answers 1. Svo2 parameters are CO, Hgb, Sao2, and consumption. Normal value is 60% to 75%. Alarms should be set @ 60%, so the patient’s monitoring is alarming. It is now important to determine whether the decreased Svo2 is due to a decreased delivery or an increased consumption. The CO is normal; the Sao2 is adequate; the Hgb is marginal. More information is needed about her regarding work of breathing, signs and symptoms of infection, etc. 2. The patient’s PAOP is already elevated so care must be given when considering fluid administration. Given the high level of ventilatory support already in place, the

CHAPTER 4. Hemodynamic Monitoring

and trends well with Svo2. The goal for Scvo2 is greater than 70%. The Scvo2 is usually less than the Svo2 except in shock states. This occurs because of redistribution of blood flow in classic shock states. Continuous Svo2/Scvo2 monitoring is used as a diagnostic and therapeutic management tool. It provides early warning of alterations in hemodynamic status and a continuous monitor of the relationship between oxygen delivery and consumption. Many therapeutic strategies are added and adjusted in response to the changes in the Svo2. If a BP is considered low (mean arterial pressure 10 L/min). In this hypermetabolic, hyperdynamic output state, blood moves very quickly past the tissues and extraction is less than optimal. Svo2 levels are frequently above normal (> 80%), indicating that extraction of oxygen at the tissue level is low. Despite the availability of oxygen, tissue hypoxia exists and is confirmed with lactic acid measurements (although this is a late sign of tissue hypoxia). Svo2 and Blood Loss

In acute blood loss, hemoglobin is decreased and the body extracts more from the available hemoglobin. Svo2 levels decrease and are an early indication of acute blood loss. Transfusions (providing they are adequate in number and rate) result in an increase in Svo2. To enhance oxygen delivery and decrease consumption the components of supply and demand are considered. Oxygen supply may be increased by improving CO (fluids followed by inotropes), increasing saturation (Fio2 level, PEEP, etc), and by increasing hemoglobin (transfusion of red cells). Examples of how demand may be lowered include decreasing activity, controlling patient-ventilator dyssynchrony, preventing agitation and thrashing, and avoiding shivering. The Svo2 catheter may be used to rapidly calculate and assess oxygen supply and consumption (Table 4-11) and direct therapies. Troubleshooting the Svo2 Catheter

The instructions for calibration of the Svo2 catheter must be followed if readings are to be accurate. It is also important that

measurements be compared periodically with co-oximeter measurements of Svo2 drawn slowly from the distal port of the PA. The Svo2 monitor can be recalibrated if saturations vary. This is referred to as an in vivo calibration. It is also important that the catheters be free floating in the PA and not have fibrin or clots attached to the end, which might affect the fiber-optic measurement of saturation. A guide for this is called light intensity and refers to the amount of transmitted light required to obtain a suitable reflected signal back to the monitor. Guidelines for the levels of light intensity help the clinician to assess the accuracy of the Svo2 readings. The size and position of the light intensity signal (called signal quality index, or SQI, on many monitors) help the nurse to detect such complications as a catheter in wedge position or clot formation. Svo2 catheters can be helpful in the assessment of oxygenation in the critically ill patient. An additional benefit may be a reduction in the need for frequent CO measurements, arterial blood gas parameters, and hemoglobin levels. However, as with any tool, the successful application of SvO2 monitoring depends on user familiarity and a comprehensive knowledge of essential concepts.

RIGHT VENTRICULAR EJECTION FRACTION CATHETERS Monitoring Principles The amount of blood in the ventricle at end diastole that is ejected during systole is the EF. It is a key indicator of the contractile force of the heart. A catheter has been designed with a rapid-responding thermistor that detects temperature changes between contractions to identify the EF. The catheter consists of two intracardiac electrodes that sense R-wave activity and a fast-response thermistor that senses changes in PA temperature. A known amount of injectate at a known temperature is injected into the right atrium. The injectate mixes with blood and is propelled by the RV into the PA. The thermistor, located in the PA, senses changes in temperature resulting from the bolus of injectate. EF is dependent on a beat-to-beat change in temperature. To determine the right ventricular ejection fraction (RVEF), the thermistor senses changes of temperature and correlates the change in temperature with an R wave, allowing the computer to calculate EF or percent of blood ejected with each beat. Once EF is obtained, the computer determines the SV and calculates

104

CHAPTER 4. Hemodynamic Monitoring

TABLE 4-12. FACTORS THAT ALTER RIGHT VENTRICULAR PARAMETERS Parameter

Increase

RV end-diastolic Volume volume Increased RV afterload Decreased RV contractility Decreased HR RV end-systolic Volume volume Increased RV afterload Decreased RV contractility RV ejection Volume fraction Decreased RV afterload Increased RV contractility

Decrease Diuretics Decreased RV afterload Increased RV contractility Increased HR Diuretics Decreased RV afterload Increased RV contractility Diuretics Increased RV afterload Decreased RV contractility

noting the volume required to produce a “wedge” waveform ensures the catheter is properly positioned and free floating to maximize accuracy. Any condition that causes wide fluctuations in temperature can cause inaccuracies in the values. Large changes in venous return, administration of large volumes of fluid, and rapid changes in core temperature lead to variations in the values. Heart rates above 150 beats/min alter the patient’s RR interval and lead to unreliable measurements.

MINIMALLY INVASIVE HEMODYNAMIC MONITORING Thoracic Bioimpedance

end-diastolic volume (EDV = SV/EF). The SVI divided by the EF provides the ventricular end-diastolic volume index, which is a better indicator of volume status (preload) than PAOP or RAP. The RV volumes and RVEF can be used to determine the optimal preload of the right ventricle. The end- diastolic volume (EDV) represents the amount of volume in the ventricle at the end of diastole or the amount of volume available for the ventricle to eject. The preload value of the RV normally is 100 to 160 mL (see Table 4-1). The end-systolic volume is the volume of blood remaining in the ventricle after systole or the residual amount of blood that remains in the ventricle after contraction and normally is 50 to 100 mL (see Table 4-1). As the RV afterload acutely increases or contractility decreases, the ventricles are unable to pump as effectively and this value increases (Table 4-12).

The resistance of current flow (impedance) across the chest is inversely related to the thoracic fluid. Using a current that flows from outer electrode (transmit current) to inner sensor (Figure 4-37), the SV can be determined. Changes in impedance occur with changes in blood flow and velocity through the ascending aorta. The impedance changes reflect aortic flow, which is directly related to ventricular function (contractility). Variables that change the bioimpedance and alter the relationship between impedance and SV are changes in hematocrit, lung water, lead contact, shivering, mechanical ventilation, and rhythm changes. Thoracic bioimpedance is a useful method for trend analysis but is not accurate enough for diagnostic interpretation. Its major application has been outside the critical care setting (HF clinics, emergency department, pacemaker clinics). Management of acutely ill patients in the outpatient setting may be the most important contribution of this technology.

Troubleshooting

Esophageal Doppler Cardiac Output

The catheter must be positioned properly to interpret volume and blood flow. Assessing the RA and PA waveforms and

The esophageal Doppler uses sound to measure the aortic blood flow velocity. The red blood cells moving toward

Injecting (strip) 5 cm apart

Sensing (dot) ECG

ECG

Sensing (dot) Injecting (strip)

5 cm apart ECG LL

Figure 4-37. Electrode placement for thoracic electrical bioimpedance. (From: Von Reuden K, Turner MA, Lynn CA. A new approach to hemodynamic monitoring. RN. 1999;62[8]:53-58.)

MINIMALLY INVASIVE HEMODYNAMIC MONITORING 105

altered CO2 production that alters the exhaled CO2 and leads to less accurate interpretation of CO.

Gastric Tonometry

Figure 4-38. Esophageal Doppler monitor oral probe placement. (Reproduced with kind permission from Deltex Medical, Chichester, UK.)

the Doppler appear red. A waveform is used to interpret “capture” of the blood flow velocity. Doppler CO provides immediate measures of blood flow velocity unlike delayed measurements achieved with the PA catheter. A transducer probe is lubricated and inserted into the esophagus to a depth of 35 to 40 cm if placed orally, or 40 to 45 cm if placed nasally. It is positioned to measure blood flow velocity in the descending thoracic aorta at about the level of T5/T6 (Figure 4-38). Reassessment of probe placement (monitoring the waveform) is crucial to accurate measurement. A beam is directed at the red blood cells flowing into the descending aorta and their movement is depicted as a waveform of blood velocity versus flow time. From this information, CO and SV are determined as well as information of preload, afterload, and contractility. Contraindications for the use of transesophageal Doppler monitoring include coarctation of the aorta, esophageal pathology, coagulopathies, and patients with intra-aortic balloon pumps. Sedation may be required for monitoring, but some awake patients will tolerate a softer probe placed nasally.

When stressed, the body shunts perfusion toward vital organs (brain and heart) at the expense of less vital areas (splanchnic circulation). Mucosal tonometry is an indirect monitor of regional blood flow and metabolic balance. A special nasogastric tube is placed (Figure 4-39). CO2 diffuses from the mucosa into the lumen of the stomach and across the silicone balloon of the tonometer. The balloon is permeable to CO2 and the gas diffuses from the gastric mucosa into the saline solution within the gastric balloon. This should closely reflect the Pco2 of the gastric mucosa. Gastric tonometry (pHi) is then used as a marker of perfusion abnormality and the adequacy of resuscitation. Gastric enteral feedings usually cause gastric hypersecretion and lower the pHi, which leads to inaccurate values. This conflicts with the trend to early enteral feedings for improved patient outcomes. Placement of a postpyloric tube and close monitoring of residual can eliminate this limitation. Accurate measurement is totally dependent on complete blockade of gastric secretion of acid requiring drug administration.

Sublingual Capnometry Esophageal tissue and proximal gastric intestinal mucosa (sublingual) (PSLCO2) respond similarly to decreased blood flow as does the gastric mucosa. Increase in PSLco2 directly correlates with a decrease in sublingual blood flow. It is a noninvasive method of identifying regional abnormalities in blood flow.

Gastric tonometry

Carbon Dioxide Rebreathing A modified Fick equation is used to predict CO: CO = Vco2/Cvco2 − Caco2. Mixed venous CO2 is estimated through a rebreathing technique using a special device. This monitoring technique is relatively new in the United States and has several limitations when used to assess the critically ill. End-tidal CO2 (Petco2) is used to replace arterial CO2 values. Exhaled air is obtained from a rebreathing circuit attached to the ventilator. The CO can be measured by noting the change in exhaled CO2 during normal breathing and rebreathing. One of the major limitations to CO2 rebreathing is that it does not measure the intracardiac pressures. Patients must be on controlled mechanical ventilation (no spontaneous ventilations). Other variables that alter the accuracy of this method are rapidly fluctuating CO, . . changes in dead space, and arrhythmias. Patients with V/Q matching diseases have

Tonometer balloon

Mucosa Muscularis Blood supply

Figure 4-39. Gastric tonometry. (From: Boswell SA, Scalea TM. Sublingual capnometry. AACN Clin Issues. 2003;14[2]:180 [Illustration by Mark Wieber]).

106

CHAPTER 4. Hemodynamic Monitoring

Sublingual capnometry

Figure 4-40. Sublingual capnometry. The CapnoProbe Sublingual System. (From: Boswell S, Scalea T. Sublingual capnometry. AACN Clin Issues. 2003;14[2]:181. Reprinted with permissions of Nellcor Puritan Bennett, Inc., Pleasanton, CA [A] and Mark Wieber [B].)

It consists of a disposable Pco2 sensor, a fiberoptic cable that connects to a blood gas analyzer and a blood gas monitoring instrument (Figure 4-40). The optical fiber is coated with a silicone membrane with a CO2-sensitive dye that is permeable to CO2. The CO2 passes through the membrane and comes into contact with the dye. A signal is transmitted and converted to a numeric CO2 value displayed on the handheld blood gas analyzer. The PSLco2 measurements are obtained by placing the disposable sensor under the tongue with the sensor facing the sublingual mucosa. Within 5 minutes, a PSLco2 measurement is recorded. The technology has been used to diagnose and quantify the severity of circulatory shock, with a predictive value of 100%. It has also been used to validate the endpoints of resuscitation. A PSLco2 lower than 45 mm Hg accurately predicts hemodynamic stability. The only significant limitation with the method is noncontinuous data collection.

pressure, mean arterial pressure, heart rate, stroke volume, stroke volume variation, pulse pressure variation and systemic vascular resistance. It also includes pulse oximetry and noninvasive hemoglobin. The hemodynamic parameters will allow for the calculation of oxygen delivery. The technology has been validated for measuring arterial pressure and has been found especially useful in cardiology clinics during tilt-test to detect orthostatic hypotension. It has also been used successfully in the perioperative management of patients. However, studies are needed to test the reliability of the measurement of cardiac index in critically ill patients. The sensor should only be

Pulse Contour Measurement Pulse contour measurement of hemodynamic parameters can be achieved invasively with an arterial line (PiCCO, LiDCO, FloTrac) and noninvasively with a finger pneumatic cuff (Nexfin). Various formulas are used to compute CCO values from the BP waveform. The device provides a continuous beat-by-beat finger BP measure through the volume-clamp method. It then transforms the finger BP curve into a brachial arterial BP waveform and calculates CCO from the brachial pressure pulse contour (Figure 4-41). Hemodynamic parameters that can be measured with the noninvasive system are CO/index, systolic/diastolic blood

Figure 4-41. Nexfin monitor. (Courtesy of: Edwards Lifesciences.)

APPLICATION OF HEMODYNAMIC PARAMETERS 107

continuously used on a finger for an 8-hour period then moved to another finger.

APPLICATION OF HEMODYNAMIC PARAMETERS Low Cardiac Output States Hemodynamic disturbances present as either a high or low blood flow state. Initially, compensatory mechanisms may present to keep blood flow normal, but eventually the output becomes either too high or too low. The most common situation is the development of a low CO state. Low CO states fall into two categories: hypovolemia or LV dysfunction. Although many conditions can cause either hypovolemia or LV dysfunction, all produce a low CO state.

Essential Content Case

Hypovolemia A 67-year-old woman is admitted to the critical care unit with the diagnosis of hypotension of unknown origin. She presently is unresponsive but is breathing spontaneously and is not intubated. Breath sounds are clear, urine output is 15 mL in 8 hours, and her skin is cool. A PA catheter is inserted to aid in the interpretation of the situation. The following data are available: BP

86/54 mm Hg

16 mL/m2

30 breaths/min

PAOP

6 mm Hg

118/min 37.3°C

1.9 L/min/m

CVP Svo2

24/10

3 mm Hg

50%

Case Question 1. Which hemodynamic parameters are abnormal? Case Question 2. What is the significance of the abnormal findings? Case Question 3. What is the priority treatment for this patient? Answers 1. BP, SI, PAOP, CVP, CI, and Svo2 are all low. HR is elevated (compensatory response to decrease in BP and CI). 2. Note the low blood flow (CI and SI below normal) and low intracardiac pressures (PAOP). This combination of low flows and intracardiac pressures is consistent with hypovolemia. In addition, the Svo2 is low, indicating that a threat to tissue oxygenation is likely. The exact cause of the hypovolemia cannot be discerned from the hemodynamics. Further investigation to isolate the exact problem, such as GI bleeding, dehydration, or other forms of blood loss, is necessary to diagnose the underlying cause of the hypovolemia. 3. The priority treatment is to administer fluids. Start with crystalloid (preferably NS). Get a H/H to determine if there is blood loss. If the patient has Hgb less than 7.0 g/dL a transfusion should also be considered.

Before the CO falls, however, the SV decreases. Therefore, the SV or SI is an earlier warning sign of impending lowflow states. As such, it should be examined before the CO or index. When SV can no longer be compensated (by heart rate), the total blood flow (CO) decreases. From a tissue oxygenation perspective, the drop in SV does not harm oxygen delivery as long as the total blood flow (CO) is maintained. Parameters such as Svo2 remain normal as long as total blood flow is unchanged. Because SV decreases in both hypovolemia and LV dysfunction, without necessarily changing CO or Svo2 levels, it is important to assess SVI first when examining hemodynamic parameters. Identifying the cause of the low-flow state (eg, hypovolemia or LV dysfunction) is based on a combination of clinical and hemodynamic information; for example, the patient’s physical assessment and history might reveal the presence of a pathologic clinical condition such as LV failure. From a hemodynamic monitoring perspective, the use of intracardiac pressures (PAOP, CVP) is the most common method of differentiating the cause of the low blood flow state. Management of low CO states begins by treating problems of either LV dysfunction or hypovolemia. Left Ventricular Dysfunction

Low CO states that are caused by LV dysfunction are managed with a variety of therapies to decrease LV work and improve performance: improvement of contractility, preload reduction, and afterload reduction. Generally, pharmacologic therapies are used to treat the dysfunctional left ventricle. However, a few physical interventions are available, such as allowing the patient to sit up, attempting to reduce anxiety, as well as mechanical supports, such as intra-aortic balloon pumping and ventricular assist devices (see Chapter 19, Advanced Cardiovascular Concepts). Improvement of LV function, however, relies heavily on pharmacologic support (see Table 4-2). Improvement of Contractility

If a patient presents with symptoms of LV dysfunction, relief is obtained by improving LV function. Inotropic therapy commonly is employed during an acute episode of LV dysfunction. Inotropic therapy increases the strength of the cardiac contraction, thereby increasing EF, SV, CO, and tissue oxygenation. Three common inotropic drugs are used in critical care to improve ventricular contractility: dobutamine (Dobutrex), dopamine (Intropin), and milrinone (Primacor) (Table 4-13). Although other agents are used occasionally, by far the most common drug used in acute treatment is dobutamine. Dobutamine acts as a sympathetic stimulant, increasing the stimulation of beta cells of the sympathetic nervous system. This stimulation produces a positive inotropic (contractile) response, as well as a positive chronotropic (heart rate) response. Dobutamine also has a slight vasodilator effect due to B2 stimulation, causing a slight reduction in preload and afterload. Based on these effects, dobutamine is an ideal first choice to pharmacologically increase the CO and SV.

108

CHAPTER 4. Hemodynamic Monitoring

TABLE 4-13. COMMON INOTROPIC THERAPIES IN TREATING ABNORMAL HEMODYNAMICS Drug Dobutamine (Dobutrex) Dopamine (Intropin) Milrinone (Primacor) Digoxin (Lanoxin) (normally not used in acute LV failure)

Dosage

Onset of Action

Route

1-20 mcg/kg/min

1-2 minutes

2-10 mcg/kg/min

1-2 minutes

Loading 0.75 mg/kg, then 5-10 mcg/kg/min 0.5 mg at first; then 0.25 every 6 hours until desired effect, then 0.125-0.25 mg/day

< 5 minutes

1-2 hours

If dobutamine is not effective, milrinone may be used because its action is different from dobutamine. Dobutamine may not be effective in cases where sympathetic stimulation has already achieved its maximal impact. Milrinone is a phosphodiesterase inhibitor, increasing the availability of intracellular calcium. Although milrinone is associated with coagulopathic side effects (decreases platelet count), it is a logical alternative to dobutamine or dopamine. Dopamine also can be used to improve the contractile state of the heart. Because dopamine also stimulates alpha cells of the sympathetic nervous system, afterload also increases, a situation that is not always desired in low CO states. The net effect is an improvement in BP and possibly CO and SV, but the cost in terms of myocardial oxygen consumption is higher than with the other two inotropes. As such, dopamine is not a first-line drug to treat acute LV dysfunction unless hypotension is present. The potential negative effect of inotropic therapy is the increase in myocardial oxygen consumption that accompanies the increased contractile state. Unfortunately, it is not easy to measure myocardial oxygenation. Because of this potential problem, many clinicians prefer to use agents that either reduce preload or afterload, neither of which increases myocardial oxygen consumption.

Essential Content Case

Left Ventricular Dysfunction A 76-year-old man is admitted to the critical unit with the diagnosis of acute inferior wall myocardial infarction and a history of COPD. During the shift he begins to complain of shortness of breath. He has crackles one-third the way up his posterior lobes along with expiratory wheezing. He has an S3 (gallop) and a II/VI systolic murmur. The following hemodynamic information was obtained on admission: BP P CI CO S

100/58 mm Hg 112/min 2.1 L/min/m2 4.6 L/min 19

PA PAOP CVP Svo2

38/23 21 mm Hg 13 mm Hg 49%

Case Question 1. Which hemodynamic parameters are abnormal? Case Question 2. What is the significance of these findings? Case Question 3. What are the treatment priorities for this patient? Answers 1. PA pressures, PAOP, CVP elevated; SI, CI, and Svo2 decreased. 2. This patient presents with low blood flow (CI and SI) and high intracardiac pressures (PAOP, CVP). The combination of low blood flow and high filling pressures suggests LV and RV dysfunction. The low Svo2 level suggests a serious disturbance in tissue oxygenation. 3. Interventions to support CI are required. Monitor heart rate and stroke volume. Reduce preload, assess afterload and contractility. The CI is not profoundly low so further investigation into the reason for the extremely low Svo2 must be found. Further investigation to isolate the exact problem, such as HF, myocardial infarction, or cardiomyopathy, is necessary.

Preload Reduction

Reduction of preload is thought to be beneficial in the patient with LV dysfunction by decreasing the distention of overstretched myocardial muscle fibers. Many therapies have been designed for preload reduction, although they generally fall into one of two groups: drugs that reduce blood volume (diuretics) and those that promote vasodilation (nitrates, calcium channel blockers, and beta-blockers) (Table 4-14). The most common approach to reduce preload is diuretic therapy. Diuretics are preferred because they eliminate excess fluid. As the left ventricle begins to fail, blood flow is decreased to the kidneys. This reduced blood flow is interpreted by the kidneys as insufficient blood volume. The kidneys then increase the reabsorption of water, producing an increase in

TABLE 4-14. COMMON PRELOAD REDUCERS FOR ABNORMAL HEMODYNAMICS Drug

Dosage

Onset of Action

Route

Diuretic Agents Furosemide (Lasix)

20 mg or higher

< 5 minutes

IV/PO

Bumetanide (Bumex)

0.5-10 mg/day

< 5 minutes

IV/PO

Ethacrynic Acid (Edecrin)

50-100 mg/day

< 5 minutes 500-2000 mg/day 1-2 hours 2.5-20 mg/day 1 hour 12.5-200 g/day < 5 minutes

IV/PO

1-2 mcg/kg/min 5-400 mcg

IV IV

Chlorothiazide (Diuril) Metolazone (Zaroxolyn) Mannitol (Osmitrol) Vasodilating Agents Dopamine (Intropin) Nitroglycerine (Tridil, Nitrostat IV)

5 minutes 1-2 minutes

IV/PO PO IV

APPLICATION OF HEMODYNAMIC PARAMETERS 109

Essential Content Case

Inotropic Therapy A 71-year-old man is admitted to the ICU with hypotension of unknown origin. He presently has a fiberoptic PA catheter in place to determine the origin of the hypotension. He is unresponsive with a Glasgow coma scale of 4. His vital signs and PA catheter reveal the following information: BP P CO CI SI PA PAOP CVP Svo2

102/68 mm Hg 101/min 3.9 L/min 2.3 L/min/m2 23 42/22 18 mm Hg 12 mm Hg 51%

Case Question 1. Which hemodynamic parameters are abnormal? Case Question 2. What are the treatment priorities for this patient? Answers 1. CI, SI, and Svo2 are low. HR, PA pressures, PAOP, and CVP are elevated. 2. Dobutamine is added to the patient’s management regime. One hour after the dobutamine, a repeat set of hemodynamics reveals the following: BP P CO CI SI PA PAOP CVP Svo2

104/66 mm Hg 106/min 4.4 L/min 2.6 L/min/m2 25 40/20 14 mm Hg 13 mm Hg 57%

Based on the slight improvement in SI, CI, and Svo2, as well as the decrease in PAOP, there has been a mild improvement in the hemodynamic parameters. Further titration of dobutamine should be considered because Svo 2 is not within normal limits. Milrinone is another possible drug that could improve this patient’s presentation. Remember the importance of following trends. Results are usually not immediate, so close monitoring of trends will allow improved outcomes.

intravascular volume. This increase contributes to venous engorgement and dependent edema in HF. The most common diuretics used to reduce preload are the loop diuretics. Loop diuretics work by blocking the reabsorption of sodium and water in the loop of Henle. The

subsequent loss of sodium and water allows for a reduction in vascular volume. The reduction in vascular volume theoretically reduces the amount of blood returning to the heart and reduces the tension on myocardial muscle. The reduced tension allows the heart to return to a more normal contractile state. Other preload reducers, such as nitroglycerine, act by promoting vasodilation. The result of vasodilation is to reduce the amount of blood returning to the heart. The net effect is to reduce preload and improve the LV contractile state. In clinical practice, it is common to use either form of preload reduction or both. Preload reducers such as nitroglycerine have the added benefit of improving myocardial blood flow. However, they do not contribute to diuresis. Afterload Reduction

The cornerstone of long-term LV dysfunction management is the use of drugs to reduce afterload (resistance to ejection of blood). Short-term reduction of afterload, such as one sees in the acutely ill patient with LV dysfunction, is important, but is used only after ensuring the presence of an adequate SV. When afterload reduction should be used in acute care is not universally agreed upon. However, it may be beneficial to lower BP or SVR to decrease afterload because doing so reduces LV work, improves LV contractility, and reduces myocardial oxygen consumption. In an acutely ill patient with LV dysfunction, afterload reduction is employed when the patient is hypertensive or has a high SVR. Generally, afterload reducers are used initially only if the BP or high SVR is considered to be the cause of the LV dysfunction. Otherwise, afterload reducers are added after inotropic therapy and preload reduction. In acute management of an increased afterload, the most common afterload reducer is nitroprusside (Nipride) (Table 4-15). This arterial dilating agent works very fast (within 2 minutes) and has only a short-acting half-life (about 2 minutes). The disadvantage of nitroprusside is that it breaks down into thiocyanate, a precursor to cyanide. Toxic levels of thiocyanate can accumulate within 2 days of administration. The antidote for thiocyanate poisoning is sodium thiosulfate. Other rapid afterload-reducing agents are available, including newer calcium channel- and beta-blocking agents. Keep in mind that these agents might act as negative inotropes and actually weaken the heart. Their use in acute management of LV dysfunction is controversial, although their long-term use in managing HF is well established. Other common agents to reduce afterload are the angiotensin-converting enzyme inhibitors. Generally, these drugs are used for the chronic management of afterload in an oral form, although some IV forms are available (enalapril). See Chapter 7, Pharmacology, for additional information on drug therapy.

110

CHAPTER 4. Hemodynamic Monitoring

Hypovolemia

Essential Content Case

Preload Reduction A 77-year-old woman is in the unit following an episode of angina that precipitated an episode of HF. She has a PA catheter in place, which reveals her initial set of information. Also, she has a second set of hemodynamics that indicates her status following the initiation of nitroglycerine. Based on these data, was the nitroglycerine effective in improving her hemodynamics?

BP P CI SI PA PAOP CVP Svo2

Initial Values 114/76 mm Hg 106/min 2.4 L/min/m2 23 40/23 22 mm Hg 12 mm Hg 56%

Post-nitroglycerine Values 112/72 mm Hg 92/min 2.6 L/min/m2 28 35/20 17 mm Hg 9 mm Hg 65%

Case Question 1. Based on these data, was the nitroglycerin effective in improving her hemodynamics? Case Question 2. Is the patient stabilized? Answers 1. Based on the increase in SI and Svo2, as well as a decrease in PAOP, this therapy appears to have been effective. Even though the CO did not change markedly, the increase was enough to improve tissue oxygenation. This example illustrates the need to evaluate more than one parameter (such as PAOP, Svo2, etc). 2. No. The patient is stabilized when the Svo 2 is 70%. Consider titrating up the nitroglycerin and re-evaluating the hemodynamic values.

If the underlying cause of the low CO state is hypovolemia, two key approaches are used: preload augmentation and identification of the optimal type of preload agent. Identifying when to treat a patient who is potentially hypovolemic is greatly enhanced with hemodynamic monitoring. It is critical to use the guidelines outlined to avoid common errors in interpretation of hemodynamic monitoring data; for example, in the patient who is hypovolemic, the SV or SVI changes when vascular volume has been significantly altered. This change in SV is frequently accompanied by reduced cardiac pressures (eg, PAOP, CVP). However, the key parameter to monitor is SV. Keep in mind that cardiac pressures do not necessarily reflect changes in volume, due to ventricular compliance. To avoid errors in interpreting hypovolemia, always examine if a low SV is present before examining the cardiac pressures. Perhaps one of the most controversial areas in the treatment of hypovolemia is the choice of the agent to use in improving vascular volume. There are three major categories of agents to be considered: blood, crystalloids, and colloids. Blood solutions such as packed cells or whole blood are in somewhat of a special category. They are not restricted to the patient who has a low SV, unlike the other categories. Blood is used when hemoglobin levels are less than 7 g/dL, regardless of any other clinical sign. This approach is necessary due to the potential decrease in oxygen-carrying capacity. Crystalloids are solutions such as normal saline and lactated Ringer solution. They obtain their benefit primarily through the sodium in the solution. Sodium levels in crystalloid solutions are generally near blood levels (approximately 140 mEq). Colloids are solutions such as blood products (albumin) or synthetic solutions (hetastarch, a glucose polymer). Their fluid-retaining effect is because of the large molecules (protein or glucose polymers) in the solution.

TABLE 4-15. COMMON AFTERLOAD REDUCING AGENTS Drug Smooth Muscle Relaxants and Alpha Inhibitors Nitroprusside (Nipride) Nitroglycerine (Tridil, Nitrostat IV) Diazoxide (Hyperstat IV) Hydralazine (Apresoline) Methyldopa (Aldomet) Trimethaphan (Arfonad) Phentolamine (Regitine) Angiotension-Converting Enzyme Inhibitors Captopril (Capoten) Enalapril/Enalaprilat (Vasotec/Vasotec IV) Lisinopril (Zestril)

Dose

Onset of Action

Route

0.5-10 mcg/kg/min 5-400 mcg 50-150 mg 10-40 mg 250 mg-1 g 3-6 mg/min 0.1-2 mg/min

1-2 minutes 1-2 minutes 1-2 minutes 10-20 minutes 2 hours 1-2 minutes < 1 minute

IV IV IV IV/IM IV IV IV

25-400 mg/day in 2-3 doses 2.5-4.0 mg/day 10-40 mg/day

15-30 minutes 15 minutes 1 hour

PO PO/IV PO

APPLICATION OF HEMODYNAMIC PARAMETERS 111

There are several advantages of crystalloid solutions. They are inexpensive and do not produce immunologic responses. The key clinical advantage is that they expand into all fluid compartments (vascular, interstitial, and intracellular) because most of the solution does not remain in just the vascular bed; for example, if 1000 mL of normal saline is given, less than 200 mL is believed to stay in the vascular bed. The rest diffuses into the other fluid compartments. This makes crystalloids ideal for treating patients who have chronic hypovolemia or dehydration. This advantage is also a limitation in some cases. If a rapid vascular expansion is

Essential Content Case

Hypovolemia A 62-year-old man is in the critical care unit with the diagnosis of ruptured diverticula. He presently is unresponsive and is being prepared for surgery. Breath sounds are clear, urine output is 20 mL in 9 hours, and his skin is cool and dry. A PA catheter is inserted to aid in the interpretation of the situation. The following data are available: BP P RR T CI SI PA PAOP CVP Svo2

82/58 mm Hg 111/min 33/min 38.4°C 1.7 L/min/m2 15 23/11 7 mm Hg 2 mm Hg 53%

Case Question 1. Which hemodynamic parameters are abnormal? Case Question 2. What is the treatment priority for this patient? Answers 1. BP, CI, SI, PAOP, CVP, and Svo2 are all low. HR and temperature are elevated. 2. The most important parameters to treat are the low SI, CI, and Svo2. A threat to tissue oxygenation clearly exists based on these parameters. Immediate supportive therapy includes a fluid bolus of normal saline or lactated Ringer solution. Infusing LR could contribute to an elevated lactate level. Lactate levels are important to monitor if the patient is in shock. Blood products (whole blood, albumin) or other colloids (hetastarch or pentastarch) could also be considered until the patient is taken to surgery. The other key problem with this patient is probable sepsis. Cultures and administration of antibiotics should be considered as a priority, followed by fluid administration. If the BP is still marginal after the CVP reaches 10 mm Hg, consider administration of vasopressors.

required, it takes large volumes of crystalloids because most of the solution is not staying in the vascular system. Colloids have one key advantage over crystalloids in that they rapidly expand the vascular volume. Virtually all the colloid solution infused remains in the vascular bed, at least initially. This allows for a much more rapid treatment of hypovolemia, frequently necessary in conditions such as trauma and postoperative bleeding. One disadvantage to colloids is their expense. Controversy does exist, however, about whether colloids are any more effective than crystalloids. Concerns have been raised that colloids may potentially cause harm in conditions with capillary leak syndromes (eg, sepsis and ARDS). In these conditions, the leakage of fluid through damaged capillaries is exacerbated if large proteins (or glucose polymers) leak through the capillaries because they pull large amounts of fluid along with them. Although crystalloids appear to be generally as effective as colloids, the best agent is still controversial. Each has its own benefits and limitations. Regardless of which is to be used, its effect should be measured on how well it improves tissue oxygenation, SV, SVI, and intracardiac pressures.

High Cardiac Output States Cardiac Output values can be elevated as well as lowered. In healthy people, COs elevate secondary to increased oxygen demand (eg, exercise) or psychological stimulation (fear, anxiety). In clinical practice, three reasons exist for an increased CO: response to a systemic inflammation (eg, sepsis, systemic inflammatory response syndrome), hepatic disease, or neurogenic-mediated vasodilation (Table 4-16). The most common reason for the CO to elevate is systemic inflammation. Inflammation, which is common in conditions such as sepsis, causes SVR to decrease. This decrease in resistance produces a compensatory increase in CO. The increase in CO might be minimal or marked. The key point to remember is that the CO elevation is a sign of a problem rather than the problem. If the problem is treated, the CO will return to normal. When a patient has high COs in sepsis, it does not mean the heart is functioning normally. Because of the release of myocardial depressant factors, the EF normally is depressed in sepsis. The method by which the SV is maintained is through an increase in EDV. This increase in EDV allows SV to be maintained even though the EF is reduced. If the hemodynamic problem appears to be a low SVR, initial treatment centers on increasing afterload (SVR), augmenting preload, and administration of inotropic therapy. None of these therapies for managing low SVR states is curative, and the underlying cause of the low SVR (such as infection) must be corrected. The following section only addresses the management of low SVR states, because preload and inotropic therapies have been discussed.

112

CHAPTER 4. Hemodynamic Monitoring

TABLE 4-16. HEMODYNAMIC PROFILES IN SHOCK Septic Shock Parameters

Hypovolemic Shock

Cardiogenic Shock

Neurogenic Shock

Anaphylactic Shock

Early

Late

Obstructive Shock

RAP

↓

↑

↓

↑

PAOP

↓

↑

↓

↑

CO/CI

↓

N↓

↓

N↑

↓

PAP

N↓↑

↑

N↓

N↓↑

N↓

↑

SVR

↑

↓

↑

Abbreviation: N, normal.

Essential Content Case

Low SVR A 65-year-old man is in the critical care unit after developing hypotension on the floor. He had femoral-popliteal bypass surgery 4 days earlier and was doing well until yesterday. He began to complain of generalized malaise with the following vital signs: BP P

102/58 mm Hg 110/min

RR T

27 breaths/min 38.1°C

His wound site is reddened but has no drainage. This m orning, he was less oriented and was hypotensive (BP 88/54, P 114/min), prompting the transfer to the intensive care unit. He does not complain of any discomfort or shortness of breath. His lung sounds are clear and he has a pulse oximeter value of 99%. A flow-directed PA catheter is inserted to assist in the assessment of the cause of hypotension. The following data are available from the PA catheter: CO CI PA PAOP

10.5 L/min 6.0 L/min/m2 22/11 8 mm Hg

SVR PVR CVP Svo2

475 51 2 mm Hg 84%

Case Question 1. Which hemodynamic parameters are abnormal? Case Question 2. What is the treatment required for this patient? Answers 1. CI, HR, and Svo2 are elevated. BP, SVR, PAOP, and CVP are decreased. 2. Based on this information, the patient is septic and progressing into septic shock as evidenced by low SRV (< 500) and increased CI. In addition, the vasodilation is also producing low cardiac pressures. The most likely immediate therapies are fluid therapies (normal saline or lactated Ringer solution) and perhaps vasopressors (norepinephrine, phenylephrine, or vasopressin). Obviously, none of these therapies is curative and a more definitive therapy (such as appropriate antibiotics and identification of source of septic trigger) needs to be applied. Cultures and antibiotic administration are the most important early strategies for this patient.

Increasing the afterload/SVR is usually accomplished by administering an alpha-stimulating drug. Three common agents used for this purpose are: norepinephrine (Levophed), dopamine (Intropin), and phenylephrine (Neosynephrine). Norepinephrine and dopamine have a combination of alpha and beta stimulation, producing both vasoconstriction and increased cardiac stimulation (inotropic and chronotropic responses). This makes the heart beat both stronger and faster. These two agents have a greater likelihood of increasing BP and SVR due to this combined cardiac and vascular effect. Phenylephrine is only an alpha stimulant, which has some advantages. Because it only causes alpha stimulation, there is less direct effect on the heart. Although the SVR and BP might not be increased as quickly with phenylephrine, it does avoid some of the direct increase of myocardial oxygen consumption that is seen with norepinephrine and dopamine. Clinically, any of these agents may be used to increase the SVR. Because they are strong alpha stimulants, their use should be considered with a degree of caution. Direct alpha stimulants can cause severe vasoconstriction. These agents are so strong that if they infiltrate into normal tissue, the resulting vasoconstriction might cause local tissue death. As a precaution, these drugs are only given in large, central veins. From an assessment perspective, if these drugs are effective, the SVR should increase as well as the BP. However, it is critical to remember that when these drugs are used, tissue oxygenation as well as SVR and BP must be assessed. If the SVR or BP increases, parameters such as Svo2 also increase. SVR and BP do not always directly correlate with blood flow, which makes the addition of tissue oxygenation parameters (like Svo2) an essential part of assessing the effect of vasopressors like norepinephrine, dopamine, and phenylephrine. Fluid administration with crystalloids (or colloids) is common because the low SVR produces a pseudohypovolemia from vasodilation. Fluid is administered to the same end points as in the case of the patient with hypovolemia (Figure 4-42). Inotropic therapy can be given to try to increase CO and oxygen delivery. Administration of inotropic therapy might seem unusual in a patient with a high CO. However, some investigators believe that oxygen delivery needs to be increased to supranormal levels to help improve patient outcome. Supranormal oxygen delivery can be achieved by such methods as

APPLICATION OF HEMODYNAMIC PARAMETERS 113

Sepsis-induced hypoperfusion (Clinical picture of sepsis plus one or both of the following criteria) (1) Hypotension after initial fluid bolus or (2) Lactate ≥ 4 mmol/L with any BP With hypotension defined as: SBP ≤ 90 mm Hg or MAP ≤ 65 mm Hg

Supplemental O2 ± ETI with mechanical ventilation (if necessary)

Continue crystalloid resuscitation 250-1000 mL boluses Critical care consultation (if not already consulted)

Crystalloid

CVP 90%) are given for long periods of time and nitrogen is washed out of the lungs. The nitrogen in inspired gas is approximately 79% of the total atmospheric gases. The large partial pressure of nitrogen in the alveoli helps maintain open alveoli because it is not absorbed. Removal of nitrogen by inspiring 90% to 100% O2 results in alveolar closure because oxygen readily diffuses into the pulmonary capillary. Oxygen Toxicity

OXYGEN THERAPY Oxygen is used for any number of clinical problems (Table 5-6). The overall goals for oxygen use include increasing alveolar O2 tension (Pao2) to treat hypoxemia, decreasing the work of breathing, and maximizing myocardial and tissue oxygen supply.

Complications As with any drug, oxygen should be used cautiously. The hazards of oxygen misuse can be as dangerous as the lack of appropriate use. Alveolar hypoventilation, absorption atelectasis, and oxygen toxicity can be life threatening. Alveolar Hypoventilation

Alveolar hypoventilation is underventilation of alveoli, and is a side effect of great concern in patients with chronic obstructive pulmonary disease (COPD) with carbon dioxide retention. As the patient with COPD adjusts to chronically high levels of Paco2, the chemoreceptors in the medulla of TABLE 5-6. COMMON INDICATIONS FOR OXYGEN THERAPY

• Decreased cardiac performance • Increased metabolic need for O2 (fever, burns) • Acute changes in level of consciousness (restlessness, confusion) • Acute shortness of breath • Decreased O2 saturation • Pao2 < 60 mm Hg or Sao2 < 90% • Normal Pao2 or Sao2 with signs and symptoms of significant hypoxia • Myocardial infarction • Carbon monoxide (CO) poisoning • Methemoglobinemia (a form of hemoglobin where ferrous iron is oxidized to ferric form, causing a high affinity for O2 with decreased O2 release at tissue level) • Acute anemia • Cardiopulmonary arrest • Reduced cardiac output • Consider in the presence of hypotension, tachycardia, cyanosis, chest pain, dyspnea, and acute neurologic dysfunction • During stressful procedures and situations, especially in high-risk patients (eg, endotracheal suctioning, bronchoscopy, thoracentesis, PA catheterization, travel at high altitudes)

The toxic effects of oxygen are targeted primarily to the pulmonary and central nervous systems (CNS). CNS toxicity usually occurs with hyperbaric oxygen treatment. Signs and symptoms include nausea, anxiety, numbness, visual disturbances, muscular twitching, and grand mal seizures. The physiologic mechanism is not understood fully but is felt to be related to subtle neural and biochemical changes that alter the electric activity of the CNS. Pulmonary oxygen toxicity is due to prolonged exposure to high Fio2 levels that may lead to ARDS or bronchopulmonary dysplasia. Two phases of lung injury result. The first phase occurs after 1 to 4 days of exposure to higher O2 levels and is manifested by decreased tracheal mucosal blood flow and tracheobronchitis. Vital capacity decreases due to poor lung expansion and progressive atelectasis persists. The alveolar capillary membrane becomes progressively impaired, decreasing gas exchange. The second phase occurs after 12 days of high exposure. The alveolar septa thickens and an ARDS picture develops, with associated high mortality. Caring for the patient who requires high levels of oxygen requires astute monitoring by the critical care nurse. Monitor those patients at risk for absorption atelectasis and oxygen toxicity. Signs and symptoms include nonproductive cough, substernal chest pain, general malaise, fatigue, nausea, and vomiting. An oxygen concentration of 100% (Fio2 = 1.0) is regarded as safe for short periods of time (< 24 hours). Oxygen concentrations greater than 50% for more than 24 to 48 hours may damage the lungs and worsen respiratory problems. Oxygen delivery levels are decreased as soon as Pao2 levels return to clinically acceptable levels (> 60 mm Hg or higher).

Oxygen Delivery Noninvasive Devices

Face masks and nasal cannulas are standard oxygen delivery devices for the spontaneously breathing patient (Figure 5-14). Oxygen can be delivered with a high- or low-flow device, with the concentration of O2 delivered ranging from 21% to approximately 100% (Table 5-7). An example of a high-flow

134

CHAPTER 5. Airway and Ventilatory Management

Nasal prongs

Malleable metal piece conforms to shape of nose Exhalation ports Mask strap B

O2 tubing C Exhalation valve closes

Exhalation valve opens

Mask strap

Valve opens Reservoir bag deflates slightly

Valve closes

O2 line

Reservoir bag expands fully

Inhalation

Exhalation

Figure 5-14. Noninvasive and invasive methods for O2 delivery. (A) Nasal prongs. (B) Nasal catheter. (C) Face mask. (D) Non-rebreathing mask. (From: Kersten L. Comprehensive Respiratory Nursing. Philadelphia, PA: WB Saunders; 1989:608,609.)

OXYGEN THERAPY 135

TABLE 5-7. APPROXIMATE OXYGEN DELIVERY WITH COMMON NONINVASIVE AND INVASIVE OXYGEN DEVICESa Device

% O2

Nasal Prongs/Cannula • 2 L/min • 4 L/min • 5 L/min Face Mask • 5 L/min • 10 L/min Nonbreathing Mask 10 L/min Partial Rebreathing Mask 6-10 L/min Venturi Mask • 24% • 28% • 35% Manual Resuscitation Bag (MRB) • Disposable MRB

28 36 40 30 50 60-80 40-70 24 28 35 Dependent on model

Actual delivery dependent on minute ventilation rates except for Venturi mask.

device is the Venturi mask system that can deliver precise concentrations of oxygen (Figure 5-15). The usual Fio2 values delivered with this type of mask are 24%, 28%, 31%, 35%, 40%, and 50%. Often, Venturi masks are useful in patients with COPD and hypercapnia because the clinician can titrate the Pao2 to minimize carbon dioxide retention. An example of a low-flow system is the nasal cannula or prongs. Nasal prongs flow rate ranges are limited to 6 L/min. Flow rates less than 4 L/min need not be humidified. The main advantage of nasal prongs is that the patient can drink, eat, and speak during oxygen administration. Their disadvantage is that the exact Fio2 delivered is unknown,

because it is influenced by the patient’s peak inspiratory flow demand and breathing pattern. As a general guide, 1 L/min of O2 flow is an approximate equivalent to Fio2 of 24%, and each additional liter of oxygen flow increases the Fio2 by approximately 4%. Simple oxygen face masks can provide an Fio 2 of 34%-50% depending on fit, at flowrates from 5 to 10 L/min. Flowrates should be maintained at 5 L/min or more in order to avoid rebreathing exhaled CO2 that can be retained in the mask. Limitations of using a simple face mask include difficulty in delivering accurate delivery of low concentrations of oxygen and long-term use can lead to skin irritation and potential pressure breakdown. Non-rebreathing masks can achieve high oxygen concentrations of between 60%–80% with a minimum flow rate of 10 L/min. A one-way valve placed between the mask and reservoir bag with a nonrebreathing system prevents exhaled gases from entering the bag, thus maximizing the delivered Fio2. A variation of the non-rebreathing mask without the one-way valves is called a partial rebreathing mask. Oxygen should always be supplied to maintain the reservoir bag at least one-third to one-half full on inspiration. At a flow of 6 to 10 L/min, the system can provide 40% to 70% oxygen. High-flow delivery devices such as aerosol masks or face tents, tracheostomy collars, and t-tube adapters can be used with supplemental oxygen systems. A continuous aerosol generator or large-volume reservoir humidifier can humidify the gas flow. Some aerosol generators cannot provide adequate flows at high oxygen concentrations. Because conventional low-flow nasal cannulae and o xygen masks are constrained by flow, humidity, and accuracy of delivered inspired oxygen, the recent introduction of high flow nasal oxygen devices capable of delivering well-humidified blended

B Manual resuscitation bag (MRB)

Exhaled gas

Exhalation port

Mask strap

Air entrainment port Narrowed orifice

Flex tube (6 in long)

Entrained room air

Inhaled mixture of 100% O2 and room air

100% O2

A Venturi device. Removable adapter (jet diluter)

To humidifier Humidification hood

C T-piece in this figure.

Figure 5-15. Venturi device. (From: Kersten L. Comprehensive Respiratory Nursing. Philadelphia, PA: WB Saunders; 1989:611, 629.)

136

CHAPTER 5. Airway and Ventilatory Management

oxygen (using vapor) across a wide range of oxygen concentrations has been found to be useful in those patients who require a greater degree of support than what is possible by using traditional low-flow oxygen devices. These devices provide oxygen at very high flow rates. Invasive Devices Manual Resuscitation Bags

Manual resuscitation bags provide 40% to 100% O2 at adult VT and respiratory rates to an ET tube or tracheostomy tube. Mechanical Ventilators

The most common method for delivering oxygen invasively is with a mechanical ventilator. Oxygen can be accurately delivered from 21% to 100% O2. Mechanical ventilation is discussed below in more detail. Transtracheal Oxygen Therapy

Transtracheal oxygen therapy is a method of administering continuous oxygen to patients with chronic hypoxemia. The therapy requires the percutaneous placement of a small plastic catheter into the trachea. The catheter is inserted directly into the trachea above the suprasternal notch under local anesthesia in an outpatient setting. This device allows for low O2 flow rates (< 1-2 L/min) to treat chronic hypoxemia. Advantages of this method for chronic O2 delivery include improved mobility and patient aesthetics because the tubing and catheter, unlike the nasal cannula or face mask, can often be hidden from view, avoidance of nasal and ear irritation from nasal cannulas, decreased O2 requirements, and correction of refractory hypoxemia.

Typically, these patients are managed in the outpatient setting, but occasionally they may be in critical care. It is important to maintain the catheter unless specifically ordered to discontinue its use. The stoma formation process takes several weeks and if the catheter is removed, the stoma is likely to close. The catheter is cleaned daily to prevent the formation of mucous plugs. Refer to the manufacturer’s guidelines for further recommendations on care of the catheter while the patient is hospitalized. T-Piece

Oxygen can also be provided directly to an ET or tracheostomy tube with a T-piece, or blow by, in spontaneously breathing patients who do not require ventilatory support. The T-piece is connected directly to the ET tube or tracheostomy tube 15 mm adapter providing 21% to 80% O2.

BASIC VENTILATORY MANAGEMENT Indications Mechanical ventilation is indicated when noninvasive management modalities fail to adequately support oxygenation and/or ventilation. The decision to initiate mechanical ventilation is based on the ability of the patient to support their oxygenation and/or ventilation needs. The inability of the patient to maintain clinically acceptable CO2 levels and acidbase status is referred to as respiratory failure and is a common indicator for mechanical ventilation. Refractory hypoxemia, which is the inability to establish and maintain acceptable oxygenation levels despite the administration of oxygenenriched breathing environments, is also a common reason for mechanical ventilation. Table 5-8 presents a variety of

TABLE 5-8. INDICATIONS FOR MECHANICAL VENTILATION Basic Physiologic Impairment Apnea Inadequate alveolar ventilation (acute ventilatory failure) Hypoxemia (acute oxygenation failure) Impending ventilator failure Inadequate lung expansion

Inadequate respiratory muscle strength Excessive work of breathing

Unstable ventilator drive

Best Available Indicators Neuromuscular and/or cardiovascular collapse. Paco2 mm Hg elevated above normal Arterial pH (acidosis) without compensation Alveolar-to-arterial PO2 gradient breathing 100% O2 Pao2/Fio2 ratio, mm Hg Serial decrement of arterial blood gas values Symptoms of increased work of breathing Tidal volume, ml/kg Vital capacity, ml/kg Respiratory rate, breaths/min (adult) Maximum inspiratory pressure, cm H2O Maximum voluntary ventilation, L/min Vital capacity, ml/kg Minute ventilation necessary to maintain normal Paco2, L/min Dead space ratio, percentage Respiratory rate, breaths/min (adult) Breathing pattern; clinical setting

Approximate Normal Range 35-45

Values Indicating Need for Ventilatory Support

7.35-7.45 50-70 mm Hg > 300

Acute increase from normal or patient’s baseline < 7.25-7.30 > 350 mm Hg < 300

5-7 65-75 10-20 −80 to –100 120-180 65-75 5-6 25-40 10-20

35 ≥ −20 < 2 × resting ventilator support < 10-12 > 10 > 60 < 10 or > 35

Abnormal breathing pattern or asynchronous pattern

From: Luce J, Pierson D, eds. Critical Care Medicine. Philadephia, PA: WB Saunders; 1988:219 and Wiegand DL, ed. AACN Procedure Manual for Critical Care. 6th ed. Philadephia, PA: Saunders; 2011.

BASIC VENTILATORY MANAGEMENT 137

physiologic indicators for initiating mechanical ventilation. By monitoring these indicators, it is possible to differentiate stable or improving values from continuing decompensation. The need for mechanical ventilation may then be anticipated to avoid emergent use of ventilatory support. Depending on the underlying cause of the respiratory failure, different indicators may be assessed to determine the need for mechanical ventilation. Many of the causes of respiratory failure, however, are due to inadequate alveolar ventilation and/or hypoxemia, with abnormal ABG values and physical assessment as the primary indicators for ventilatory support.

General Principles Mechanical ventilators are designed to partially or completely support ventilation. Two different categories of ventilators are available to provide ventilatory support. Negative-pressure ventilators decrease intrathoracic pressure by applying negative pressure to the chest wall, typically with a shell placed around the chest (Figure 5-16A). The decrease in intrathoracic pressure causes atmospheric gas to be drawn into the lungs. Positive-pressure ventilators deliver pressurized gases into the lung during inspiration (Figure 5-16B). Positive-pressure ventilators can dramatically increase intrathoracic pressures during inspiration, potentially decreasing venous return and CO. Negative-pressure ventilators are rarely used to manage acute respiratory problems in critical care. These devices are typically used for long-term noninvasive ventilatory support when respiratory muscle strength is inadequate to support unassisted, spontaneous breathing. Since the emergence of other, noninvasive modes of positive pressure (eg, BiPAP),

and negative pressure ventilators are infrequently selected (refer to Chapter 20, Advanced Respiratory Concepts: Modes of Ventilation). This chapter focuses only on the use of positive-pressure ventilators for ventilatory support. Patient-Ventilator System

Positive-pressure ventilatory support can be accomplished invasively or noninvasively. Invasive mechanical ventilation is still widely used in most hospitals for supporting ventilation, although noninvasive technologies, which do not require the use of an artificial airway, are becoming more popular. To provide invasive positive-pressure ventilation, intubation of the trachea is required via an ET or tracheostomy tube. The ventilator is then connected to the artificial airway with a tubing circuit to maintain a closed delivery system (Figure 5-17). During the inspiratory cycle, gas from the ventilator is directed through a heated humidifier or a heat and moisture exchanger (HME) prior to entering the lungs through the ET tube or tracheostomy tube. Contraindications to HME use are listed in Table 5-9. At the completion of inspiration, gas is passively exhaled through the expiratory side of the tubing circuit. Ventilator Tubing Circuit

The humidifier located on the inspiratory side of the circuit is necessary to overcome two primary problems. First, the presence of an artificial airway allows gas entering the lungs to bypass the normal upper airway humidification process. Second, the higher flows and larger volumes typically administered during mechanical ventilation require additional humidification to avoid excessive intrapulmonary membrane drying.

Chest wall suction applied with resulting negative intrathoracic pressure –10 cm H2O

Early inspiration

+2 cm H2O

+5 cm H2O

Late inspiration

Expiration

Positive pressure ventilator

+40 cm H2O

Inspiration

+2 cm H2O Expiration

Figure 5-16. Principles of mechanical ventilation as provided by (A) negative-pressure and (B) positive-pressure ventilators.

138

CHAPTER 5. Airway and Ventilatory Management

Y-junction Medication nebulizer Humidifier

Nebulizer gas source

Figure 5-17. Typical setup of a ventilator, closed system tubing circuit, and humidifier connected to an ET tube.

Pressure within the ventilator tubing circuit is continuously monitored to alert clinicians to excessively high or low airway pressures. Airway pressure is dynamically displayed on the front of the ventilator control panel. Traditionally, ventilator circuits have incorporated special water collection cups in the tubing to prevent the condensation from humidified gas from obstructing the tubing. Recently, however, it has become common to use ventilator circuits containing heated wires that run through the inspiratory and expiratory limbs of the circuit. These wires maintain the temperature of the gas at or close to body temperature, significantly reducing the condensation and rainout of humidity in the gas, eliminating the need for in-line water traps. Certain medications, such as bronchodilators or steroids, can also be administered via metered dose inhaler (MDI) or nebulized into the lungs through a low volume Table 5-9. Contraindications to Use of Heated Moisture Exchanger (HME)

• Frank bloody or thick, copious secretions • Patients with large bronchopleural fistulas • Uncuffed or malfunctioning ET tube cuffs • During lung protective strategies such as patients with ARDS • Patients with body temperature < 32° Celsius Data from American Association for Respiratory Care. AARC clinical practice guideline: humidification during invasive and noninvasive mechanical ventilation: 2012. Resp Care. 2012;57:782-788.

aerosol-generating device located in the inspiratory side of the circuit. The ventilator tubing circuit is maintained as a closed circuit as much as possible to avoid interrupting ventilation and oxygenation to the patient, as well as to decrease the potential for ventilator-associated pneumonias (VAP). Avoiding frequent or routine changes of the ventilator circuit also decreases the risk of VAP (see Chapter 10, Respiratory System). Ventilator Control Panel

The user interface or control panel of the ventilator usually incorporates three basic sections or areas: 1. Control settings for the type and amount of ventilation and oxygen delivery; 2. Alarm settings to specify desired high and low limits for key ventilatory measurements; and 3. Visual displays of monitored parameters (Figure 5-18). The number and configuration of these controls and displays vary from ventilator model to model, but their function and principles remain essentially the same. Control Settings

The control settings area of the user interface allows the clinician to set the mode of ventilation, volume, pressure, respiratory rate, Fio2, PEEP level, inspiratory trigger sensitivity

BASIC VENTILATORY MANAGEMENT 139

–10

50 80

–10

20 10

Alarms, which continuously monitor ventilator function, are essential to ensure safe and effective mechanical ventilation. Both high and low alarms are typically set to identify when critical parameters vary from the desired levels. Common alarms include exhaled VT, exhaled minute volume, Fio 2 delivery, respiratory rate, and airway pressures (Table 5-10).

Expiration

Alarm Settings

Inspiration

or effort, and a variety of other breath delivery options (eg, inspiratory flow rate, inspiratory waveform pattern).

20 10

40 30

Figure 5-18. Ventilator display control panel. (With permission, Covidien.)

–10

Inspiration

–10

Expiration

Figure 5-19. Typical airway pressure gauge changes during a (A) ventilatorassisted breath and a (B) spontaneous breath (cm H2O).

Visual Displays

Airway pressures, respiratory rate, exhaled volumes, and the inspiratory to expiratory (I:E) ratio are among the most common visually displayed breath-to-breath values on the ventilator. Airway pressures are monitored during inspiration and exhalation and are often displayed as peak pressure, mean pressure, and end-expiratory pressure. A breath delivered by the ventilator produces higher airway pressures than an unassisted, spontaneous breath by the patient (Figure 5-19).

TABLE 5-10. TRADITIONAL VENTILATOR ALARMS Disconnect Alarms (Low-Pressure or Low-Volume Alarms) • It is essential that when disconnection occurs, the clinician be immediately notified. Generally, this alarm is a continuous one and is triggered when a preselected inspiratory pressure level or minute ventilation is not sensed. With circuit leaks, this same alarm may be activated even though the patient may still be receiving a portion of the preset breath. Physical assessment, digital displays, and manometers are helpful in troubleshooting the cause of the alarms. Pressure Alarms • High-pressure alarms are set with volume modes of ventilation to ensure notification of pressures exceeding the selected threshold. These alarms are usually set 10-15 cm H2O above the usual peak inspiratory pressure (PIP). Some causes for alarm activation (generally an intermittent alarm) include secretions, condensate in the tubing, biting on the endotracheal tubing, increased resistance (ie, bronchospasm), decreased compliance (eg, pulmonary edema, pneumothorax), and tubing compression. • Low-pressure alarms are used to sense disconnection, circuit leaks, and changing compliance and resistance. They are generally set 5-10 cm H2O below the usual PIP or 1-2 cm H2O below the PEEP level or both. • Minute ventilation alarms may be used to sense disconnection or changes in breathing pattern (rate and volume). Generally, low-minute ventilation and highminute ventilation alarms are set (usually 5-10 L/min above and below usual minute ventilation). When stand-alone pressure support ventilation (PSV) is in use, this alarm may be the only audible alarm available on some ventilators. • Fio2 alarms. Most new ventilators provide Fio2 above and below the selected Fio2. Alarms are set 5% above and below the selected Fio2. • Alarm silence or pause. Because it is essential that alarms stay activated at all times, ventilator manufacturers have built-in silence or pause options so that clinicians can temporarily silence alarms for short periods (ie, 20 seconds). The ventilators “reset” the alarms automatically. Alarms provide important protection for ventilated patients. However, inappropriate threshold settings decrease usefulness. When threshold gradients are set too narrowly, alarms occur needlessly and frequently. Conversely, alarms that are set too loosely (wide gradients) do not allow for accurate and timely assessments. Originally written and taken from: Burns SM. Mechanical Ventilation and Weaning. In: Kinney MR, et al, eds. AACN Clinical Reference for Critical Care Nursing, 4th ed. St Louis, MO: Mosby; 1998.

140

CHAPTER 5. Airway and Ventilatory Management

The presence of PEEP is identified by a positive value at the end of expiration rather than 0 cm H2O. Careful observation of the airway pressures provides the clinician with a great deal of information about the patient’s respiratory effort, coordination with the ventilator, and changes in lung compliance. The display of the patient’s exhaled V T reflects the amount of gas that is returned to the ventilator via the expiratory tubing with each respiratory cycle. Exhaled volumes are measured and displayed with each breath. The patient’s total exhaled minute volume is also often displayed. Exhaled Vts for ventilator-assisted mandatory breaths should be similar (± 10%) to the desired VT setting selected on the control panel. The VT of spontaneous breaths, or partially ventilatorsupported breaths, however, may be different from the VT control setting.

Modes

Tidal volume (L/min)

Airway pressure (cm H2O)

The mode of ventilation refers to one of several different methods that a ventilator uses to support ventilation. Modes are often classified as invasive (via an ET tube or tracheostomy tube) or noninvasive (via a face or nasal interface). These modes generate different levels of airway pressures, volumes, and patterns of respiration and, therefore, different

levels of support. The greater the level of ventilator support, the less muscle work performed by the patient. This “work of breathing” varies considerably with each of the modes of ventilation (see Chapter 20, Advanced Respiratory Concepts: Modes of Ventilation). The different modes of ventilation used to support ventilation depend on the underlying respiratory problem and clinical preferences. A brief description of the basic modes of mechanical ventilation follows. Applications of modes of ventilation and more complex modes are discussed in Chapter 20, Advanced Respiratory Concepts: Modes of Ventilation. Control Ventilation

The control mode of ventilation ensures that patients receive a predetermined number and volume of breaths each minute. No deviations from the respiratory rate or VT settings are delivered with this mode of ventilation. Generally the patient is heavily sedated and/or paralyzed with neuromuscular blocking agents to achieve the goal (see Chapter 6, Pain, Sedation, and Neuromuscular Blockade Management). The airway pressures, VT delivery, and pattern of breathing typically observed with control ventilation are shown in Figure 5-20A. All the inspiratory waveforms appear in a regular pattern and appear

0 –10

1000

500

Tidal volume (L/min)

Airway pressure (cm H2O)

0 B

0 C

0 –10

1000

500

0 E

0 F

Figure 5-20. Airway pressures, tidal volumes (VT), and patterns of breathing for different modes of mechanical ventilation. (A) Controlled ventilation. (B) Assist-

control ventilation. (C) SIMV. (D) Spontaneous breathing. (E) Pressure support. (F) PEEP with SIMV. (G) CPAP. (From: Dossey B, Guzzetta C, Kenner C. Critical Care Nursing: Body-Mind-Spirit. Philadelphia, PA: JB Lippincott; 1992:225.)

BASIC VENTILATORY MANAGEMENT 141

the same in configuration. The lack of waveform deflections prior to inspiration indicates the breath was initiated by the ventilator and not by the patient. Assist-Control Ventilation

The assist-control mode of ventilation ensures that a predetermined number and volume of breaths is delivered by the ventilator each minute should the patient not initiate respirations at that rate or above. If the patient attempts to initiate breaths at a rate greater than the set minimum value, the ventilator delivers the spontaneously initiated breaths at the prescribed V T; the patient may determine the total rate (Figure 5-20B). Work of breathing with this mode is variable (see Chapter 20, Advanced Respiratory Concepts: Modes of Ventilation). Assist-control ventilation is often used when the patient is initially intubated (because minute ventilation requirements can be determined by the patient), for short-term ventilatory support such as postanesthesia, and as a support mode when high levels of ventilatory support are required. Excessive ventilation can occur with this mode in situations where the patient’s spontaneous respiratory rate increases for nonrespiratory reasons (eg, pain, CNS dysfunction). The increased minute volume may result in potentially dangerous respiratory alkalosis. Changing to a different mode of ventilation or employing sedation may be necessary in these situations. Synchronized Intermittent Mandatory Ventilation

The synchronized intermittent mandatory ventilation (SIMV) mode of ventilation ensures (or mandates) that a predetermined number of breaths at a selected V T are delivered each minute. Any additional breaths initiated by the patient are allowed but, in contrast to the assist-control mode, these breaths are not delivered by the ventilator. The patient is allowed to spontaneously breathe at the depth and rate desired until it is time for the next ventilator-assisted, or mandatory, breath. Mandatory breaths are synchronized with the patient’s inspiratory effort, if present, to optimize patient-ventilator synchrony. The spontaneous breaths taken during SIMV are at the same Fio2 as the mandatory breaths (Figure 5-20C). Originally designated as a ventilator mode for the gradual weaning of patients from mechanical ventilation, the use of a high-rate setting of SIMV can provide total ventilatory support. Reduction of the number of mandatory breaths allows the patient to slowly resume greater and greater responsibility for spontaneous breathing. SIMV can be used for similar indications as the assist-control mode, as well as for weaning the patient from mechanical ventilatory support. The work of breathing with this mode of ventilation depends on the VT and rate of the spontaneous breaths. When the mandatory, intermittent breaths provide the majority of minute volume, the work of breathing by the patient may be less than when spontaneous breathing constitutes a larger proportion of the patient’s total minute volume.

Although strong clinician and institutional biases exist regarding whether to use SIMV or other modes for ventilatory support, little data exist to clarify which mode of ventilation is best. Close observation of the physiologic and psychological response to the ventilatory mode is required, and consideration is given to trials on alternative modes if warranted. Spontaneous Breathing

Many ventilators have a mode that allows the patient to breathe spontaneously without ventilator support (Figure 5-20D). This is similar to placing the patient on a T-piece or blow-by oxygen setup, except it does have the benefit of providing continuous monitoring of exhaled volumes, airway pressures, and other parameters along with maintaining a closed circuit. All the work of breathing is performed by the patient during spontaneous breathing. Use of the ventilator rather than the T-piece during spontaneous breathing actually may slightly increase the work of breathing. This occurs because of the additional inspiratory muscle work that is required to trigger flow delivery for each spontaneous breath. The amount of additional work required varies with different ventilator models. In some situations, removing the patient from the ventilator for weaning may result in a decrease in the work of breathing. This mode of ventilation is often identified as CPAP, flow-by, or spontaneous (SPONT) on the ventilator. Continuous positive airway pressure (CPAP) is a spontaneous breathing setting with the addition of PEEP during the breathing cycle (see below). If no PEEP has been applied, the CPAP setting is similar to spontaneous breathing. Some ventilators have an additional adjunct that compensates for the resistance secondary to endotracheal tube diameter. It is called automatic tube compensation (ATC). ATC can be used with ventilatory support or alone with spontaneous breathing. Pressure Support

Pressure support (PS) is a spontaneous breath type, available in SIMV and SPONT modes, which maintains a set positive pressure during the spontaneous inspiration (Figure 5-20E). The volume of a gas delivered by the ventilator during each inspiration varies depending on the level of pressure support and the demand of the patient. The higher the pressure support level, the higher the amount of gas delivered with each breath. Higher levels of pressure support can augment the spontaneous VT and decrease the work of breathing associated with spontaneous breathing. At low levels of support, it is primarily used to overcome the airway resistance caused by breathing through the artificial airway and the breathing circuit. The airway pressure achieved during a pressure support breath is the result of the pressure support setting plus the set PEEP level. PEEP/CPAP

Positive end-expiratory pressure is used in conjunction with any of the ventilator modes to help stabilize alveolar lung

142

CHAPTER 5. Airway and Ventilatory Management

v olume and improve oxygenation (Figure 5-20F, G). The application of positive pressure to the airways during expiration may keep alveoli open and prevent early closure during exhalation. Lung compliance and ventilation-perfusion matching are often improved by prevention of early alveolar closure. If alveolar “recruitment” is not needed and excessive PEEP/CPAP is applied, it may result in adverse hemodynamic or respiratory compromise. Positive end-expiratory pressure/CPAP is indicated for hypoxemia, which is secondary to diffuse lung injury (eg, ARDS, interstitial pneumonitis). PEEP/CPAP levels of 5 cm Hg or less are often used to provide “physiologic PEEP.” The presence of the artificial airway allows intrathoracic pressure to fall to zero, which is below the usual level of intrathoracic pressure at end expiration (2 or 3 cm H2O). Use of PEEP may increase the risk of barotrauma due to higher mean and peak airway pressures during ventilation, especially when peak pressures are greater than 40 cm H2O. Venous return and CO may also be affected by these high pressures. If CO decreases with PEEP/CPAP initiation and oxygenation is improved, a fluid bolus may correct hypovolemia. Other complications from PEEP/CPAP are increases in intracranial pressure, decreased renal perfusion, hepatic congestion, and worsening of intracardiac shunts. Bilevel Positive Airway Pressure

Bilevel positive airway pressure (ie, BiPAP) is a noninvasive mode of ventilation that combines two levels of positive pressure (PSV and PEEP) by means of a full face mask, nasal mask (most common), or nasal pillows. The ventilator is designed to compensate for leaks in the setup, and a snug fit is needed often requiring head or sometimes chin straps. This form of therapy can be very labor intensive, requiring frequent assessment of patient tolerance. Full face mask ventilation is cautiously used because the potential for aspiration is high. If full face mask ventilation is chosen, the patient should be able to remove the mask quickly if nausea occurs or vomiting is imminent. Obtunded patients and those with excessive secretions are not good choices for BiPAP ventilation. A number of options are available with BiPAP and include a spontaneous mode where the patient initiates all the pressure, supported breaths; a spontaneous-timed option, similar to PSV with a backup rate (some vendors call this A/C); and a control mode. The control mode requires the selection of a control rate and inspiratory time. Bilevel positive airway pressure is used successfully in a wide variety of progressive care patients such as those with sleep apnea, some patients with chronic hypoventilation syndromes and also to prevent intubation and reintubation following extubation. Use of BiPAP in patients with COPD and heart failure has been associated with decreased mortality and need for intubation. These patients are often difficult to wean from conventional ventilation given their underlying disease processes. Study results also demonstrate that outcomes in immunocompromised patients may also be better with noninvasive ventilation.

Complications of Mechanical Ventilation Significant complications can arise from the use of mechanical ventilation and can be categorized as those associated with the patient’s response to mechanical ventilation or those arising from ventilator malfunctions. Although the approach to minimizing or treating the complications of mechanical ventilation relate to the underlying cause, it is critical that frequent assessment of the patient, ventilator equipment, and the patient’s response to ventilatory management be accomplished. Many clinicians participate in activities to assess the patient and ventilator, but the ultimate responsibility for ensuring continuous ventilatory support of the patient falls to the critical care team, including the nurse and respiratory therapist. Newer team members include the use of Tele-ICU staff when integrated into the critical care environment. Critically evaluating clinical indicators such as pH, Paco2, Pao2, Spo2, heart rate, BP, and so on, in conjunction with patient status and ventilatory parameters, is essential to decrease complications associated with this highly complex technology. Patient Response Hemodynamic Compromise

Normal intrathoracic pressure changes during spontaneous breathing are negative throughout the ventilatory cycle. Intrapleural pressure varies from about + 5 cm H2O during exhalation to – 8 cm H2O during inhalation. This decrease in intrapleural pressure during inhalation facilitates lung inflation and venous return. Thoracic pressure fluctuations during positive-pressure ventilation are opposite to those that occur during spontaneous breathing. The mean intrathoracic pressure is usually positive and increases during inhalation and decreases during exhalation. The use of positive pressure ventilation increases peak airway pressures during inspiration which in turn, increases mean airway pressures. It is this increase in mean airway pressure which may impede venous return to the right atrium, thus decreasing CO. In some patients, this decrease in CO can be clinically significant, leading to increased heart rate and decreased blood pressure and perfusion to vital organs. Whenever mechanical ventilation is instituted, or when ventilator changes are made, it is important to assess the patient’s cardiovascular response. Approaches to managing hemodynamic compromise include increasing the preload of the heart (eg, fluid administration), decreasing the airway pressures exerted during mechanical ventilation by ensuring appropriate airway management techniques (suctioning, positioning, etc), and by judiciously applying ventilator adjuncts can increase ventilating pressures. Ventilation strategies employing different modes and breath types may be helpful in managing airway pressures and are discussed in Chapter 20, Advanced Respiratory Concepts: Modes of Ventilation. Barotrauma and Volutrauma

Barotrauma describes damage to the pulmonary system due to alveolar rupture from excessive airway pressures or

BASIC VENTILATORY MANAGEMENT 143

overdistention of alveoli. Alveolar gas enters the interstitial pulmonary structures causing pneumothorax, pneumomediastinum, pneumoperitoneum, or subcutaneous emphysema. The potential for pneumothorax and cardiovascular collapse requires prompt management of pneumothorax and should be considered whenever airway pressure increases acutely, breath sounds are diminished unilaterally, or blood pressure falls abruptly. Patients with obstructive airway diseases (eg, asthma, bronchospasm), unevenly distributed lung disease (eg, lobar pneumonia), or hyperinflated lungs (eg, emphysema) are at high risk for barotrauma. Techniques to decrease the incidence of barotrauma include the use of small Vts, cautious use of PEEP, and the avoidance of high airway pressures and development of auto-PEEP in high-risk patients. Volutrauma describes alveolar damage that results from high pressures resulting from large-volume ventilation in patients with ARDS. A common technique to reduce this risk is the use of smaller Vts (4-6 ml/kg of ideal body weight) and sometimes this is described as the “low stretch” protocol. Different from barotrauma, this damage results in alveolar fractures and flooding (non-ARDS, ARDS; see Chapter 20, Advanced Respiratory Concepts: Modes of Ventilation). Auto-PEEP occurs when a delivered breath is incompletely exhaled before the onset of the next inspiration. This gas trapping increases overall lung volumes, inadvertently raising the end-expiratory pressure in the alveoli. The presence of auto-PEEP increases the risk for complications from PEEP. Ventilator patients with COPD (eg, asthma, emphysema) or high respiratory rates are at increased risk for the development of auto-PEEP. Auto-PEEP, also termed intrinsic PEEP, is difficult to diagnose because it cannot be observed on the airway pressure display at end expiration. The technique for assessment for auto-PEEP varies with different ventilatory models and modes, but typically involves measuring the airway pressure close to the artificial airway during occlusion of the expiratory ventilator circuit during end expiration. This method requires that the patient be completely passive and not trigger a breath; it is not possible to measure auto-PEEP in actively breathing patients. Another technique of monitoring auto-PEEP in actively breathing patients is the use of the flow-time curve displayed by the ventilator. If flow does not return to baseline at the end of exhalation before the next breath starts, the patient has auto-PEEP. Auto-PEEP can be minimized by: •• Maximizing the length of time for expiration (eg, increasing inspiratory flow rates) •• Decreasing obstructions to expiratory flow (eg, using larger diameter ET tubes, eliminating bronchospasm and secretions) •• Avoiding overventilation Ventilator-Associated Pneumonia

Ventilator-association pneumonia (VAP) is a hospital-acquired complication, and is associated with increased patient morbidity and mortality. Prevention is aimed at avoiding colonization

Figure 5-21. Cuffed endotracheal tube with dedicated lumen for continuous aspiration of subglottic secretions accumulated immediately above cuff. The dedicated lumen connector is attached to wall suction. (With permission, Covidien.)

and subsequent aspiration of bacteria into the lower airway. Elevation of the head of the bed and avoiding excessive gastric distention are thought to help minimize the occurrence of aspiration. A specially designed ET (Figure 5-21) incorporates a dedicated suction lumen over the ET cuff, which permits continuous low suction pressure (–20 mmHg) or intermittent suctioning of subglottic secretions pooled above the cuff. Removal of the accumulated secretions may be particularly helpful before cuff deflation or manipulation. Studies have demonstrated that the application of continuous aspiration of subglottic secretions with ET tubes may only prevent or delay the onset of VAP. Although subglottic suctioning is now available in tracheostomy tubes, there are currently no recommendations for the use of subglottic suctioning in these tubes. In addition, recent research suggests that oral care protocols including chlorhexidine gluconate 0.12% mouth rinse and tooth brushing to remove plaque, may be important adjuncts to VAP prevention. See Chapter 10, Respiratory System: Preventing Hospital Acquired Pneumonia. Positive Fluid Balance and Hyponatremia

Hyponatremia is a common occurrence following the institution of mechanical ventilation and develops from several factors, including applied PEEP, humidification of inspired gases, hypotonic fluid administration and diuretics, and increased levels of circulating antidiuretic hormone. Upper Gastrointestinal Hemorrhage

Upper gastrointestinal (GI) bleeding may develop secondary to ulceration or gastritis. The prevention of stress ulcer bleeding requires ensuring hemodynamic stability and the administration of proton-pump inhibitors, H 2 receptor antagonists, antacids, or cytoprotective agents as appropriate

144

CHAPTER 5. Airway and Ventilatory Management

(see Chapter 7, Pharmacology and Chapter 14, Gastrointestinal System for discussions of GI prophylaxis). Ventilator Malfunction

Problems related to the proper functioning of mechanical ventilators, although rare, may have devastating consequences for patients. Many of the alarm systems on ventilators are designed to alert clinicians to improperly functioning ventilatory systems. These alarm systems must be activated at all times if ventilator malfunction problems are to be quickly identified and corrected, and untoward patient events avoided (Table 5-10). Many of the “problems” identified with ventilatory equipment are actually related to inappropriate setup or use of the devices. Ventilator circuits that are not properly connected, alarm systems that are set improperly, or inadequate ventilator settings for a particular clinical condition are examples of some of these operator-related occurrences. There are occasions, however, when ventilator systems do not operate properly. Examples of ventilator malfunctions include valve mechanisms sticking and obstructing gas flow, inadequate or excessive gas delivery, electronic circuit failures in microprocessing-based ventilators, failures with complete shutdown, and power failures or surges in the institution. The most important approach to ventilator malfunction is to maintain a high level of vigilance to determine if ventilators are performing properly. Ensuring that alarm systems are set appropriately at all times, providing frequent routine assessment of ventilator functioning, and the use of experienced support personnel to maintain the ventilator systems are some of the most crucial activities necessary to avoid patient problems. In addition, whenever ventilator malfunction is suspected, the patient should be immediately removed from the device and temporary ventilation and oxygenation provided with an MRB or another ventilator until the question of proper functioning is resolved. Any sudden change in the patient’s respiratory or cardiovascular status alerts the clinician to consider potential ventilator malfunction as a cause.

Weaning from Short-Term Mechanical Ventilation The process of transitioning the ventilator-dependent patient to unassisted spontaneous breathing is weaning from mechanical ventilation. This is a period of time where the level of ventilator support for oxygenation and ventilation is decreased, either gradually or abruptly, while monitoring the patient’s response to the resumption of spontaneous breathing. A standardized approach along with weaning readiness criteria has been shown to reduce ventilator days and improve outcomes. Weaning, or “liberation,” is considered to be complete, or successful, when the patient has been extubated successfully without the need for reintubation within 48 hours. The majority of patients intubated and ventilated for short periods of time (< 72 hours) are successfully weaned with the first spontaneous breathing trial (SBT). Additionally, there is a subset of patients with long-term tracheostomy tubes, who may require short-term ventilation, who are able to wean

quickly once the clinical issue requiring mechanical ventilation is resolved. Approximately 30% of patients, however, require extended time periods to successfully complete the weaning process, with some being unable to breathe without partial or complete mechanical ventilation. Weaning proceeds when the underlying pulmonary disorder that led to mechanical ventilation has sufficiently resolved, and the patient is alert and able to protect the airway. Unnecessary delays in weaning from mechanical ventilation increase the likelihood of complications such as ventilator-induced lung injury, pneumonia, discomfort, and increases in hospitalization costs. Thus, aggressive and timely weaning trials such as SBTs are encouraged. Steps in the Weaning Process Assessment of Readiness

Readiness to wean from short-term mechanical ventilation (STMV) may be assessed with a wide variety of criteria. However, in most institutions, assessment of readiness to wean includes just three or four criteria for most short-term ventilator patients. Along with assessing the patient’s clinical stability, some examples are: •• ABGs within normal limits on minimal to moderate amounts of ventilatory support (Fio2 ≤ 0.50, minute ventilation ≤ 10 L/min, PEEP ≤ 5 cm H2O) •• Negative inspiratory pressure that is more negative than –20 cm H2O •• Spontaneous VT ≥ 5 mL/kg •• Vital capacity ≥ 10 mL/kg •• Respiratory rate < 30 breaths/min •• Spontaneous rapid-shallow breathing index < 105 breaths/min/liter Following selection of the method for weaning (see the discussion below), the actual weaning trial can begin. It is important to prepare both the patient and the critical care environment properly to maximize the chances for weaning success (Table 5-11). Interventions include appropriate explanations of the process to the patient, positioning and medication to improve ventilatory efforts, and the avoidance of unnecessary activities during the weaning trial. Throughout the weaning time, TABLE 5-11. STRATEGIES TO FACILITATE WEANING • Explain the weaning process to the patient/family and maintain open communication throughout weaning. • Position to maximize ventilatory effort (sitting upright in bed or chair). • Administer analgesics to relieve pain and sedatives to control anxiety, if appropriate. • Remain with the patient during the weaning trial and/or provide a highly vigilant presence. • Frequently assess the patient’s response to the weaning trial. • Avoid unnecessary physical exertion, painful procedures, and/or transports during the weaning trials. • Maximize the physical environment to be conducive to weaning (eg, temperature, noise, distractions).

BASIC VENTILATORY MANAGEMENT 145

continuous monitoring for signs and symptoms of respiratory distress or fatigue is essential. Many of these indicators are subtle, but careful monitoring of baseline levels before weaning progresses and throughout the trial provides objective indicators of the need to return the patient to previous levels of ventilator support. The need to temporarily stop the weaning trial is not viewed as, or termed, a failure. Instead it simply suggests that more time needs to be provided to ensure success. A full evaluation of the multiple reasons for inability to wean is necessary, however. Weaning Trials

Generally, weaning trials for patients ventilated short term are accomplished with SBT on T-piece or on the ventilator using CPAP or a low level of pressure support. Readiness for weaning is assessed daily using a “safety screen” which includes such factors as hemodynamic stability, oxygenation status and improvement in the condition that necessitated the use of mechanical ventilation. Once the patient is assessed as “ready” the spontaneous breathing trial is initiated for a duration of at least 30 minutes but no more than 120 minutes. The trial is stopped should the patient show signs of distress and/ or deterioration. Extubation follows a successful trial. A decision to extubate is made with the conclusion of a successful trial. The need for reintubation is associated with increased mortality. Thus, premature attempts at extubation are to be avoided. Some suggest that noninvasive positive-pressure ventilation via face or nasal mask may be useful for patients with respiratory failure following extubation. However, research has demonstrated that this therapy does not prevent the need for reintubation or reduce mortality in these cases. Methods

A variety of methods are available for weaning patients from mechanical ventilation. To date, research on these techniques has not clearly identified any one method as optimal for weaning from STMV. Most institutions, however, use one or two approaches routinely. A number of recently published randomized controlled trials demonstrated that the outcomes of patients managed under protocols driven by nonphysician clinicians were better than those managed with standard physician-directed care. Most experts on weaning believe that, with short-term ventilator-dependent patients, the actual method used to wean the patient is less important to weaning success than using a consistently applied protocol strategy. •• T-piece, blow by, or trach collar: The T-piece method of weaning involves removing the patient from the mechanical ventilator and attaching an oxygen source to the artificial airway with a “T” piece for a SBT. A trach collar also provides oxygen but attaches by elastic strap around the neck instead of directly to the artificial airway. No ventilatory support occurs with this device, with the patient completely breathing spontaneously the entire time this device is

connected. The advantage of this method of weaning is that the resistance to breathing is low, because no special valves need to be opened to initiate gas flow. Rapid assessment of the patient’s ability to spontaneously breathe is another purported advantage. Limitations of this SBT are that it may cause ventilatory muscle overload and fatigue. When this occurs, it usually appears early in the SBT, so the patient must be closely monitored during the initial few minutes. A PEEP valve can be added to the T-piece; however, similar to trach collar weaning, there are no alarm or backup systems to support the patient should ventilation be inadequate. It is critical to recognize that this technique relies on the clinician to monitor for signs and symptoms of respiratory difficulty and fatigue. Frequently, the Fio2 is increased by at least 10% over the Fio2 setting on the ventilator to prevent hypoxemia resulting from the lower VT of spontaneous breaths. Patients who fail a SBT should receive a stable, nonfatiguing, comfortable form of ventilatory support for rest following the trial. •• CPAP: The use of the ventilator to allow spontaneous breathing periods without mandated breaths, similar to the T-piece, can be done with the CPAP mode. With this approach, ventilator alarm systems can be used to monitor spontaneous breathing rates and volumes, and a small amount of continuous pressure (5 cm H2O) can be applied if needed. The disadvantage of this approach is that the work of breathing resulting from the need to open the demand valve to receive gas flow for the breath is higher than with the T-piece. For most patients, this slight additional work of breathing is not likely to be a critical factor to their weaning success or failure unless the trial is unduly long. If needed, a low level of pressure support (eg, 5-7 cm H2O) may also be added to offset this workload (CPAP + PS). •• Pressure support: Another method for weaning from ventilation is the use of low level PS ventilation. With this method, patients can spontaneously breathe on the ventilator with a small amount of ventilator “support” to augment their spontaneous breaths. This technique overcomes some of the resistance to breathing associated with ET tubes and demand valves. The main disadvantage with this approach is that clinicians may underestimate the degree of support of spontaneous breathing provided with this method and prematurely stop the weaning process. •• SIMV: One of the most popular methods of weaning patients in the past, this modality has recently been shown to prolong the duration of mechanical ventilation in comparison to weaning with SBT or pressure support. By progressively decreasing the number of mandated breaths delivered by the ventilator, the patient performs more and more of the work of breathing by increasing spontaneous breathing.

146

CHAPTER 5. Airway and Ventilatory Management

Advantages to the SIMV mode are the presence of built-in alarms to alert clinicians when ventilation problems occur and, in some modes, the guarantee of a minimum amount of minute ventilation. The disadvantage of SIMV is that each spontaneous breath requires some additional work of breathing to open a valve, which allows gas flow to the patient for the spontaneous breath. SIMV is used either alone or in conjunction with pressure support (SIMV + PS).

Weaning From Long-Term Mechanical Ventilation In contrast to patients who require short-term (< 3 days) ventilation, those that require long-term mechanical ventilation (defined as > 3 days), may take weeks or even months to liberate from the ventilator. In these long-term mechanically ventilated (LTMV) patients, the weaning process varies and consists of four stages. The first stage is marked by instability and high ventilatory support requirements. During the second stage, called the prewean stage, many physiologic factors continue to require attention, and the patient’s overall status may fluctuate. Ventilatory requirements are less and adjustments are made to maintain oxygenation and acid-base status as well as provide ventilatory muscle conditioning. The third, or weaning stage, is evident when the patient is stable, and rapid progress with weaning trials is possible. Finally, the last stage is called the outcome stage, which consists of extubation, partial or full ventilatory support. Long-term mechanical ventilation is associated with high morbidity and mortality rates, and institutions lose money on patients’ ventilated long term because reimbursement rarely covers the associated costs. As a result, clinicians, scientists, and institutions are interested in testing methods of care delivery that improve the clinical and financial outcomes of the patients. Research in the area of weaning offers guidance to clinicians working with these patients. The following discussions of weaning patients from LTMV address wean assessment, wean planning, and weaning modes and methods, including comprehensive institutional approaches. Wean Assessment

Traditionally, the decision about when to begin the weaning process is determined once the condition that necessitates mechanical ventilation is improved or resolved. During this prewean stage, other factors that contribute to wean ability are considered prior to attempting weaning trials. In the past, “traditional” weaning predictors were used in an attempt to determine the optimal timing for extubation. More recently, investigators combined pulmonary elements to improve predictive ability in LTMV patients. An example is the index of rapid shallow breathing, also known as the frequency (fx)/ tidal volume (V T) index, which integrates rate and tidal volume. Unfortunately, predictors have not predicted wean ability. This is in part because they focus exclusively on pulmonary specific components to the exclusion of other important nonpulmonary factors (Table 5-12). Although the

TABLE 5-12. PULMONARY SPECIFIC WEAN CRITERIA THRESHOLDS Traditional Weaning Criteria • Negative inspiratory pressure (NIP) ≤ –20 cm H2O • Positive expiratory pressure (PEP) ≥ + 30 cm H2O • Spontaneous tidal volume (SVT) ≥ 5 mL/kg • Vital capacity (VC) ≥ 15 mL/kg • Fraction of inspired oxygen (Fio2) ≤ 50% • Minute ventilation (MV) ≤ 10 L/min Integrated Weaning Criteria • Index of rapid shallow breathing or frequency tidal volume ratio (fx/VT) ≤ 105

standard weaning criteria are not predictive, the components are helpful for assessing the patient’s overall condition and readiness for weaning. As noted, assessment of weaning potential starts with an evaluation of the underlying reason for mechanical ventilation (sepsis, pneumonia, trauma, etc). Resolution of the underlying cause is necessary before gains in the weaning process can be expected. However, it is important to remember that resolution alone is frequently not sufficient to ensure successful weaning. Patients who require prolonged mechanical ventilation, sometimes referred to as the “chronically, critically ill,” often suffer from a myriad of conditions that impede weaning. Even with resolution of the disease or condition that necessitated mechanical ventilation, the patient’s overall status is often below baseline (weak, malnourished, etc). Therefore, a systematic, comprehensive approach to weaning assessment is important. One example of a tool that encourages such an approach is the Burns’ Wean Assessment Program (BWAP) (Table 5-13). The BWAP score is used to track the progress of the patient and keep care planning on target. Factors important to weaning are listed in the BWAP bedside checklist. Wean Planning

Once impediments to weaning are identified, plans that focus on improving the impediments are made in collaboration with a multidisciplinary team. A collaborative approach to assessment and planning greatly enhances positive outcomes in the LTMV patient. However, for care planning to be successful, it must also be systematic. The wean process is dynamic and regular reassessment and adjustment of plans are necessary. Tools like the BWAP can be used to systematically assess and track weaning progress. Other methods that have demonstrated efficacy in assuring consistency in care management and good outcomes for the patients include care delivery models using clinical pathways, protocols for weaning, and institution-wide approaches to managing and monitoring the patients. Weaning Trials, Modes, and Methods

A wide variety of weaning modes and methods are available for weaning the patient ventilated short term as described earlier. To date, no data support the superiority of any one mode for weaning those requiring LTMV, however methods using

BASIC VENTILATORY MANAGEMENT 147

TABLE 5-13. BURNS’ WEAN ASSESSMENT PROGRAM (BWAP)a I. General Assessment Yes No Not Assessed _____ _____ ________ _____ _____ ________

_____ _____ ________ _____ _____ ________ _____ _____ ________

_____ _____ ________

_____ _____ ________ _____ _____ ________ _____ _____ ________ _____ _____ ________ _____ _____ ________

Essential Content Case

Long-Term Weaning 1. Hemodynamically stable (pulse rate, cardiac output)? 2. Free from factors that increase or decrease metabolic rate (seizures, temperature, sepsis, bacteremia, hypo/hyperthyroid)? 3. Hematocrit > 25% (or baseline)? 4. Systemically hydrated (weight at or near baseline, balanced intake and output)? 5. Nourished (albumin > 2.5, parenteral/enteral feedings maximized)? *If albumin is low and anasarca or third spacing is present, score for hydration should be “no.” 6. Electrolytes within normal limits (including Ca++, Mg+, PO4)? *Correct Ca++ for albumin level. 7. Pain controlled (subjective determination)? 8. Adequate sleep/rest (subjective determination)? 9. Appropriate level of anxiety and nervousness (subjective determination)? 10. Absence of bowel problems (diarrhea, constipation, ileus)? 11. Improved general body strength/endurance (ie, out of bed in chair, progressive activity program)? 12. Chest x-ray improving?

_____ _____ ________ II. Respiratory Assessment Yes No Not Assessed Gas Flow and Work of Breathing _____ _____ 13. Eupneic respiratory rate and pattern (spontaneous RR < 25, without dyspnea, absence of accessory muscle use)? *This is assessed off the ventilator while measuring #20-23. _____ _____ 14. Absence of adventitious breath sounds (rhonchi, rales, wheezing)? _____ _____ 15. Secretions thin and minimal? _____ _____ 16. Absence of neuromuscular disease/deformity? _____ _____ 17. Absence of abdominal distention/obesity/ ascites? _____ _____ 18. Oral ETT > #7.5 or trach > #6.5? Airway Clearance _____ _____ ________ 19. Cough and swallow reflexes adequate? Strength _____ _____ ________ 20. NIP < 20 (negative inspiratory pressure)? _____ _____ ________ 21. PEP > 30 (positive expiratory pressure)? Endurance _____ _____ ________ 22. STV > 5 mL/kg (spontaneous tidal volume)? _____ _____ ________ 23. VC > 10-15 mL/kg (vital capacity)? ABGs _____ _____ ________ 24. pH 7.30-7.45? _____ _____ ________ 25. Paco2, 40 mm Hg (or baseline) with mV < 10 L/min? *This is evaluated while on ventilator. _____ _____ ________ 26. Pao2 > 60 on Fio2 < 40%?

a The BWAP score is obtained by dividing the total number of BWAP factors scored as “yes” by 26. ©Burns 1990.

A 75-year-old man with COPD and oxygen dependence was admitted to the ED in respiratory distress. He was intubated and placed on the ventilator secondary to profound hypercarbia and acidosis and then transferred to the MICU for management of respiratory failure and right upper lobe pneumonia. On day 2, he met criteria for his daily awakening trial but was unable to meet criteria for a spontaneous breathing trial. Weaning assessment parameters included: NIF: VC: RR: HR:

–10 cm H2O 770 ml 37 bpm 118 bpm

His sedation was at a minimal level, his delirium score was negative, and on day 3 he began ambulation with a walker while receiving ventilatory support with physical therapy, and was able to take several steps with minimal assistance. Due to anticipation of need for long-term weaning, the patient and family agreed to a tracheostomy tube. He received a tracheostomy tube on day 5 and was transferred on day 6 to the respiratory progressive care unit for further management and weaning. Additional major impediments to weaning as assessed by the unit team included factors such as: • Poor nutritional status (albumin 1.8 g/dL) • Anxiety • Debilitation • Persistent upper lobe infiltrate • Copious secretions • Minute ventilation: 15 L/min with a PaCO2 of 50 mm Hg Case Question 1. What weaning modality could be used in this patient for long-term weaning and why? Case Question 2. What components of the ABCDE protocol were used for this patient? Answers 1. As the research has not demonstrated any mode or method to be superior for a patient weaning with a tracheostomy, progressively longer spontaneous breathing trials may be used effectively. The modes can vary and include t-piece, trach collar, or low levels of PSV with intermittent rest periods on the ventilator (with support settings such as AC or a higher level of PSV). When the patient is able to sustain spontaneous breathing for a full 12 hours during the day, the nighttime ventilator support (at the “rest” level) may then be reduced, or if clinically appropriate, curtailed. The next steps would be to work on removal of the tracheostomy tube following downsizing and or use of a talking trach to determine tolerance. This stepwise approach allows the patient to gradually transition to liberation from the ventilator. 2. The patient received daily spontaneous awakening and assessment for readiness to wean (ABC). His delirium was addressed by using a modified sleep protocol and by using the family to reorient the patient as well as encouraging the use of personal items when possible (D). Early exercise was implemented in the ICU and continued after transfer and integrated into his daily routine (E).

148

CHAPTER 5. Airway and Ventilatory Management

protocols and other systematic, multidisciplinary approaches do appear to make a difference and are to be encouraged. These methods are described following a discussion of respiratory muscle fatigue, rest, and conditioning because the concepts are integrated into the section on protocols.

Respiratory Fatigue, Rest, and Conditioning Respiratory muscle fatigue is common in ventilated weaning patients and occurs when the respiratory workload is excessive. When the workload exceeds metabolic stores, fatigue and hypercarbic respiratory failure ensue. Examples of those at risk include patients who are hypermetabolic, weak, or malnourished. Signs of encroaching fatigue include dyspnea, tachypnea, chest-abdominal asynchrony, and elevated Paco2 (a late sign). These signs and symptoms indicate a need for increased ventilatory support. Once fatigued, the muscles require 12 to 24 hours of rest to recover, and careful application of selected modes of ventilation is required. For the respiratory muscles to recover from fatigue, the inspiratory workload must be decreased. In the case of volume ventilation (eg, assist-control, intermittent mandatory ventilation), this means complete cessation of spontaneous effort, but in the case of pressure ventilation, a high level of PSV may accomplish the necessary “unloading.” Generally, this means increasing the PSV level to attain a spontaneous respiratory rate of 20 breaths per minute or less and the absence of accessory muscle activity. However, in patients with obstructive diseases (eg, asthma and COPD), this higher level of support may result in further hyperinflation and adverse clinical outcomes. If the technique is used in these patients, it should be done cautiously. Respiratory muscle conditioning employs concepts borrowed from exercise physiology. To condition muscles and attain an optimal training effect from exercise, the concepts of endurance and strength conditioning may be considered. With strength training, a large force is moved a short distance. The muscles are worked to fatigue (short duration intervals) and rested for long periods of time. Spontaneous breathing trials on T-piece or continuous positive airway pressure (CPAP) both mimic this type of training because they employ high pressure and low-volume work. Endurance conditioning, which requires that the workload be increased gradually, is easily accomplished with PSV because the level of support can be decreased over time. This kind of endurance training employs low pressure and high-volume work. Central to the application of both conditioning methods is the provision of adequate respiratory muscle rest between trials. Prolonging trials once the patient is fatigued serves no useful purpose and may be extremely detrimental physiologically and psychologically.

Wean Trial Protocols Study results suggest that no mode of ventilation is superior for weaning, however, the method of weaning, specifically the use of protocols, decreases variations in care and

improves outcomes. Protocols direct caregivers by clearly delineating the protocol components. The protocol components consist of weaning readiness criteria (wean screens), weaning trial method and duration (ie, CPAP, T-piece, or PSV), and definitions of intolerance and respiratory muscle rest. SBTs (described earlier), primarily using CPAP or T-piece, are commonly used for the trials. The duration of such trials is generally between 30 minutes and 2 hours, although in those patients with tracheotomy tubes, the duration may be much longer. While CPAP or T-piece is often used for trials, in most cases the choice between PSV (an endurance mode) and T-piece or CPAP (strengthening modes) is somewhat arbitrary if the protocol is appropriately aggressive, and easily understood and applied by the caregivers. There are some conditions that require more selective decision making. One example is that of patients with heart failure. In these patients, the sudden transition from ventilator support to the use of T-piece or CPAP for an SBT may result in an increased venous return that may overwhelm the heart’s ability to compensate. Until appropriate preload and after-load reduction is addressed in these patients, PSV may be a gentler method of weaning. Another example is that of patients with profound myopathies or extremely debilitated states that may benefit from more gradual increases in work such as provided by PSV. Some new pressure modes such as Proportional Assist Ventilation and Adaptive Support Ventilation, may potentially decrease the patient’s workload during weaning. For more on this see Chapter 20: Advanced Respiratory Concepts: Modes of Ventilation. A popular and common sense approach to wean trial progression is to attempt weaning trials during the daytime, allowing the patient to rest at night until the protocol threshold for extubation is reached. In the case of the patient with a tracheostomy, progressively longer episodes of spontaneous breathing, usually on tracheostomy collar or T-piece, are accomplished until tolerated for a specified amount of time. Then, decisions about discontinuation of ventilation and tracheostomy downsizing or decannulation may be made. Wean plans need to be communicated clearly to all members of the health-care team, and especially the patient, so that the plan is sufficiently aggressive but safe and effective. It is important that the philosophy of weaning is accepted by the health-care team so that care planning is consistent and effective. Table 5-14 describes some general mechanical ventilation weaning philosophy concepts.

Other Protocols for Use Patients who require LTMV often are affected by a variety of clinical conditions that prolong ventilator duration and other clinical outcomes such as length of stay and death. Research has demonstrated that outcomes of critically ill patients are improved with protocol-directed management. Randomized controlled trials (RCT) have demonstrated that decreased sedation infusion use and methods to withdraw sedation daily using a “sedation interruption” improve outcomes such as

BASIC VENTILATORY MANAGEMENT 149

TABLE 5-14. GENERAL WEANING GUIDELINES FOR LTMV PATIENTS Active Weaning Should Occur • When patient is stable and reason for mechanical ventilation is resolved or improving. • When the “wean screen protocol criteria” are attained. A temporary hold and even an increase in support may be necessary when setbacks occur. • During the daytime, not at night (to allow respiratory muscle rest). Considerations for Temporary Hold • With acute changes in condition • During procedures that require that the patient be flat or in the Trendelenburg position (ie, during line insertion) • During “road trips” (increased ventilatory support will protect the patient while off the unit) • If suctioning is excessive (every half hour) • When febrile, bacteremic, septic, or with Clostridium difficile disease. Rest and Sleep Rest is important for psychological and physiologic reasons. Complete rest in the mechanically ventilated patient is defined as that level of ventilatory support that offsets the work of breathing and decreases fatigue (refer to detailed description in text). Decisions about when rest is important include the following: • When an acute event has occurred (ie, hypercarbic respiratory failure, pulmonary embolus, pulmonary edema). • A reasonable approach for the chronic or nonacute patient is to work on active weaning trials during the day with rest at night until most of the daytime wean is accomplished (≥ 10 hours). Then, nighttime wean trials can be accomplished fairly rapidly. At night, the patient is allowed to sleep—if work of breathing is high, sleep is not possible. Ventilator rate should be high enough to allow for relaxation and optimal resting. If night sleeping aids are used, administer them early in the night to enhance sleep and ventilatory synchronization and so that the drugs can be metabolized before the daytime trials begin.

ventilator duration and LOS. In addition, studies linked sedation use (specifically benzodiazapines) to delirium and subsequent cognitive dysfunction, further stimulating a decrease in sedation use in the ventilated patient population. Further emphasizing the importance of decreasing sedation use in these patients, a multicenter RCT combined a sedation interruption with a “wake-up and breathe” trial (ie, SBT). In this study patients assigned to the intervention (sedation interruption and wake-up) had significantly more days of spontaneous breathing, earlier discharge from ICU and hospital, and better 1-year survival than those in the control group. The “ABCDE” bundle incorporates sedation awakening trials (Figure 5-22) along with other best evidence based practice for ICU management (Table 5-15). Bundles are a structured method of improving patient care processes and when collectively performed, have resulted in improved patient outcomes. The importance of factors such as sedation, delirium, and early mobility to weaning outcomes is essential to understand if the goal of attaining positive outcomes is to be attained. Protocols that assure that these important elements of care are routinely addressed decrease practice variation and improve outcomes.

Critical Pathways Critical pathways are used to assure that evidence-based care is provided and that variation in care delivery is

reduced. The pathways may be very directive in selected categories of patients, such as in patients with hip replacements, where progression can be anticipated by hours or days; however, such specificity is not possible in the ventilated patient. Instead, pathways for the LTMV patient combine elements of care by specific time intervals (ie, begin deep vein thrombosis prophylaxis by day 1) with those that are designated by the stage of illness (ie, patient up to the chair during the prewean stage). In addition to providing an evidence-based blueprint for a wide variety of care elements, the pathways encourage multidisciplinary input and collaboration. In general, they are incorporated into systematic institutional approaches to care of the LTMV patient population.

Systematic Institutional Initiatives for the Management of the LTMV Patient Population Given the importance of systematic assessment and care planning, it is not surprising that many institutions have taken a very comprehensive approach to the care for the LTMV patient. Solutions to reduce variation and promote standardization of care are implemented to ensure that best practices are adhered to and good outcomes result. In one study, an algorithmic approach to weaning in three adult ICUs used nurses to manage the process. In another study, advanced practice nurses called “Outcomes Managers” managed and monitored long-term ventilated patients using a multidisciplinary clinical pathway and protocols for the management of sedation and weaning trials. The two studies demonstrated that statistically significant positive differences in most variables of interest, such as ventilator duration, ICU and hospital lengths of stay (LOS), mortality rate, and cost savings, were attainable with the approaches. The healthcare environment is often chaotic. Short lengths of stay and decreased staffing levels affect the continuity of care and contribute to gaps in practice and care planning. Given the complexity of the care of the ventilated patient, it is clear that approaches to care that decrease variation may improve patient outcomes and are to be encouraged.

Troubleshooting Ventilators The complexity of ventilators and the dynamic state of the patient’s clinical condition, as well as the patient’s response to ventilation, create a variety of common problems that may occur during mechanical ventilation. It is crucial that critical care clinicians be expert in the prevention, identification, and management of ventilator-associated problems in critically ill patients. During mechanical ventilation, sudden changes in the clinical condition of the patient, particularly respiratory distress, and the occurrence of ventilator alarms or abnormal functioning of the ventilator, require immediate assessment and intervention. A systematic approach to each of these situations prevents or minimizes untoward ventilator events (Figure 5-23).

150

CHAPTER 5. Airway and Ventilatory Management

Daily Assessment of Safety Screen to Remove Sedation • Is sedation for active seizures? • Is sedation for alcohol withdrawal? • Is a paralytic agent used? • Is the patient agitated by validated assessment score? • Has there been myocardial ischemia in previous 24 hours? • Is intracranial pressure (ICP) elevated?

READY

NOT READY

Perform SAT • Increased agitation measured by validated assessment score? • Pulse oximetry < 88% for 5 minutes or longer? • Respirations > 35/min for 5 minutes or longer? • New cardiac arrhythmias? • Two or more of the following? • Heart rate increase ≥ 20 bpm • Heart rate < 55 bpm • Use of accessory muscles • Abdominal paradoxical breathing • Diaphoresis • Dyspnea NOT READY

Resume sedation

READY Coordinate SBT with respiratory therapist

Figure 5-22. Spontaneous Awakening Trial—SAT (Data from Balas MC, et al. Critical care nurses’ role in implementing the “ABCDE Bundle” into practice. Crit Care Nurse. 2012;32:35-47.)

The first step is to determine the presence of respiratory distress or hemodynamic instability. If either is present, the patient is removed from the mechanical ventilator and manually ventilated with an MRB and 100% O2 for a few minutes. During manual ventilation, a quick assessment of the respiratory and cardiovascular system is made, noting changes from previous status. Clinical improvement rapidly following removal from the ventilator suggests a ventilator problem. Manual ventilation is continued while another clinician corrects the ventilator problem (eg, tubing leaks or disconnections, inaccurate gas delivery) or replaces the ventilator. Continuation of respiratory distress after removal from the ventilator and during manual ventilation suggests a patient-related cause.

Communication Mechanically ventilated patients are unable to speak and communicate verbally due to the presence of a cuffed ET or tracheostomy tube. The inability to speak is frustrating for the patient, nurse, and members of the healthcare team. Impaired communication results in patients experiencing anxiety and fear, symptoms that can have a deleterious effect on their physical and emotional conditions. Patients interviewed after extubation reveal how isolated and alone they felt because of their inability to speak. Methods to Enhance Communication

A variety of methods for augmenting communication are available and can be classified into two categories: nonvocal

BASIC VENTILATORY MANAGEMENT 151

Table 5-15. ABCDE Bundle and Components Requires a coordinated effort between the heath care team ABC— Awakening and Breathing Coordination 1. Spontaneous Awakening Trial ° Daily assessment of safety screen to turn off sedation ° Daily awakening, sedation vacation, or daily interruption of sedation trial 2. Spontaneous Breathing Trial ° Daily assessment of safety screen ° Daily spontaneous breathing trial D—Delirium Assessment and Management 3. Routine Assessment of Delirium ° Confusion Assessment Method for the ICU (CAM-ICU) ° Intensive Care Delirium Screening Checklist (ICDSC) 4. Stop ° Evaluate risk factors for delirium 5. Think ° Modify risk factors T—Toxic situations • CHF, shock, dehydration • Medications • New organ failure H—Hypoxemia I—Infection/sepsis N—Nonpharmacologic interventions • Hearing aids, glasses, reorientation, sleep protocols, music, noise control, ambulation, family K+ – electrolye problems 6. Medicate if needed E—Early Exercise and Progressive Mobility 7. Early Mobility Protocol ° Daily assessment of mobility readiness ° Mobility program ■

PROBLEMS: • Signs/symptoms of respiratory distress • Sudden change in clinical condition • Ventilator alarm • Abnormal ventilator function

Is the patient in respiratory distress? or hemodynamic instability? NO

Check ventilator to determine if problem exists.

YES

• Remove patient from ventilator and ventilate manually with 100% O2. • Perform rapid exam, with CP emphasis.

■ ■ ■

■

Data from American Association for Critical Care. AACN PEARL: Implementing the ABCDE Bundle at the Bedside. http://www.aacn.org/dm/practice/aacnpearl.aspx?menu=practice. Accessed March 10, 2013. OR Data from Balas MC, et al. Critical care nurses’ role in implementing the “ABCDE Bundle” into practice. Crit Care Nurse. 2012;32:35-47.

treatments (gestures, lip reading, mouthing words, paper and pen, alphabet/numeric boards, flashcards, etc) and vocal treatments (talking tracheostomy tubes and speaking valves for tracheostomy tubes only). The best way for the patient to communicate, who has an artificial airway or who is being mechanically ventilated, is still unknown. Nonvocal Treatments

Individual patient needs vary and it is recommended that the nurse use a variety of nonvocal treatments (eg, gestures, alphabet board, and paper and pen). Success with communication interventions varies with the diagnosis, age, type of injury or disease, type of respiratory assist devices, and psychosocial factors. Writing Typically the easiest, most common method of communication readily available is the paper and pen. The absence of proper eyeglasses, an injured or immobilized dominant writing hand, or lack of strength can make writing difficult for mechanically ventilated patients. Some patients prefer to use a Magic Slate (Western Publishing Co., Racine, WI)

Does the condition resolve?

YES

Check ventilator to determine if problem exists.

• Verify O2 delivery appropriate. • Suction to remove secretions and verify airway patency. • Auscultate chest. • Check vasoactive drips.

Figure 5-23. Algorithm for management of ventilator alarms and/or development of acute respiratory distress.

or a Magna Doodle (Tyco Industries, Mount Laurel, NJ). These pressure-sensitive, inexpensive toy screens can be purchased at any department store; with them messages can be easily erased, maintaining the privacy of a written message. Although costly computer keyboards or touch pads may facilitate writing in patients who are comfortable with “high-tech” solutions. Gesturing Another nonvocal method of communication that can be very effective is the deliberate use of gestures. Gestures are best suited for the short-term ventilated patient who is alert and can move at least one hand, even if only minimally. Generally, well-understood gestures are emblematic, have a low level of symbolism, and are easily interpreted by most people.

152

CHAPTER 5. Airway and Ventilatory Management

Alphabet Board/Picture Board For patients who do not speak English, a picture board is sometimes useful along with well-understood gestures. Picture boards have images of common patient needs (eg, bedpan, glass of water, medications, family, doctor, nurse) that the patient can point to. Picture boards, although commercially available, can be made easily and laminated to more uniquely meet the needs of a specific critical care population. Another approach is the use of flash cards that can be purchased or made. Language flash cards contain common words or phrases in English or foreign languages. Vocalization Techniques

If patients with tracheostomy tubes in place have intact organs of speech, they may benefit from vocal treatment strategies like pneumatic and electrical devices, fenestrated tracheostomy tubes, talking tracheostomy tubes, and tracheostomy speaking valves. Several conditions preclude use of vocalization devices, such as neurologic conditions that impair vocalization (eg, Guillain-Barré syndrome), severe upper airway obstruction (eg, head/neck trauma), or vocal cord adduction (eg, presence of an ET tube). A number of vocal treatments for tracheostomized patients exist. Generally, they require that the cuff be completely deflated to allow for air to be breathed in and out through the mouth and nose as well as around the sides of the tracheostomy. On exhalation the gases pass through the vocal cords allowing for speech. Some use o ne-way speaking valves (eg, Passy-Muir valve, shown in Figure 5-24) to allow for air to be inhaled through the valve but to close during exhalation to direct air up past the vocal cords. A fenestrated tracheostomy tube (Figure 5-25) also allows passage of air through the vocal cords. A cap or speaking valve may be used in conjunction with the fenestrated tube to ensure that all exhaled air moves through the vocal cords for vocalization. There have been reported incidences of granuloma tissue development at the site adjacent to the fenestration, which resolves after removal of the tube. In addition, fenestrated ports often become clogged with secretions, again preventing voicing. It is imperative that if

the tracheostomy tube is capped, that the cuff of the tracheostomy be completely deflated. Another vocal treatment is the talking tracheostomy tube, which is designed to provide a means of verbal communication for the ventilator-dependent patient. Patients who were otherwise considered to be “unweanable” have been reported to take a renewed interest in the weaning process and some successfully wean upon hearing their own voice. Currently there are two talking tracheostomy tubes available, which maintain a closed system with cuff inflation but differ in how they function. 1. The Portex tracheostomy operates by gas flowing (4-6 L/min) through an airflow line, which has a fenestration just above the tracheostomy tube cuff (Figure 5-26). The air flows through the glottis, thus supporting vocalization if the patient is able to form words with their mouth. However, an outside air source must be provided, which is usually not humidified and the trachea can become dry and irritated. The line for this air source requires diligent cleaning and flushing of the air port to prevent it from becoming clogged. The patient or staff must be able to manually divert air through the tube via a thumb port control. 2. The Blom tracheostomy tube system (Figure 5-27) uses a 2-valve system in a specialized speech inner cannula that redirects air and does not require use of an air source. During inhalation the flap valve opens and the bubble valve seals the fenestration, preventing air leak to the upper airway. On exhalation, the flap valve closes and the bubble valve collapses to unblock the fenestration to allow air to the vocal cords. An additional component is the exhaled volume reservoir, which is attached to the circuit and return volume to minimize false, low expiratory minute volume alarms. Teaching Communication Methods

The critical care environment presents many teaching and learning challenges. Patients and families are under a

Figure 5-24. Passy-Muir Speaking Valves. (Image courtesy of Passy-Muir, Inc., Irvine, CA.)

BASIC VENTILATORY MANAGEMENT 153

Occlude thumb port to talk

A Gas flow

Figure 5-26. Tracheostomy tube with side port to facilitate speech. (With permission, Smith Medical, Keen, NH.)

Principles of Management The majority of interventions related to mechanical ventilation focus on maximizing oxygenation and ventilation, and preventing complications associated with artificial airways and the sequelae of assisting the patient’s ventilation and oxygenation with an invasive mechanical device. Maximizing Oxygenation and Ventilation Ensure Synchrony of Respiratory Patterns

Figure 5-25. (A) Fenestrated tracheostomy tube. (B) Opening above the cuff site allowing gas, flow past the vocal cords during inspiration and expiration. (With permission, Covidien.)

considerable amount of stress, so the nurse must be a very creative teacher and offer communication techniques that are simple, effective, and easy to learn. The desire to communicate with loved ones, however, often makes the family very willing to learn. Frequently, it is the family who makes up large-lettered communication boards, or purchases a Magic Slate or brings in a laptop or touch pad computer for the patient to use. Suggesting that families do this is usually very well received, because loved ones want so desperately to help in some way. Emphasize with patients and their families that being unable to speak is usually temporary, just while the breathing tube is in place.

•• Provide frequent explanations of the purpose of the ventilator. •• Monitor the patient’s response to ventilator therapy and for signs that the patient is dyssynchronous with the ventilator respiratory pattern. The use of graphic displays, common on many ventilator systems, is often a helpful aid to patient assessment. •• Consider ventilator setting changes to maximize synchrony (eg, changes in flow rates, respiratory rates, sensitivities, and/or modes). •• Administer sedative agents as required to prevent asynchrony with the ventilator. Avoid the use of neuromuscular blocking agents unless absolutely necessary.

Maintain a Patent Airway

•• Suction only when clinically indicated according to patient assessment (see Table 5-5). •• Decrease secretion viscosity by maintaining adequate hydration and humidification of all inhaled gases. Rarely, the administration of mucolytic agents may be necessary. •• Monitor for signs and symptoms of bronchospasm and administer bronchodilator therapy as appropriate (see Chapter 9, Cardiovascular System). •• Prevent obstruction of oral ET tubes by using an oral bite block if necessary.

154

CHAPTER 5. Airway and Ventilatory Management

INHALATION

EXHALATION

No air escapes past the cuff allowing all the air to fill the lungs

Exhaled air flow is available for phonation

Fenestration Air to larynx Inflated cuff

Bubble valve—expanded

Bubble valve—collapsed

Flap valve—closed

Flap valve—open Air

Figure 5-27. Tracheostomy tube with inner cannula for speaking (Blom Tracheostomy Tube System). (Courtesy of: Pulmodyne, Indianapolis, IN [http://www. dolema.com/uploads/6869E_Blom_Brochure.pdf])

Monitor Oxygenation and Ventilation Status Frequently

•• ABG analysis as appropriate (eg, after some ventilator changes, with respiratory distress or cardiovascular instability, or with significant changes in clinical condition). •• Continuous noninvasive monitoring of Spo2. Validate noninvasive measures with periodic ABG analysis (see Table 5-4). •• Observe for signs and symptoms of decreases in Pao2, increases in Paco2, and respiratory distress. Development of respiratory distress requires immediate intervention (see Figure 5-24). •• Reposition frequently to improve ventilation- perfusion relationships and prevent atelectasis. •• Aggressively manage pain, particularly chest and upper abdominal pain, to increase mobility, deep breathing, and coughing (see Chapter 6, Pain, Sedation, and Neuromuscular Blockade Management).

Physiotherapy and Monitoring

•• Administer chest physiotherapy for selected clinical conditions (eg, large mucus production, lobar atelectasis). •• Monitor oxygenation status closely during chest physiotherapy for signs and symptoms of arterial desaturation.

Maintain Oxygenation and Ventilatory Support at All Times

•• Ensure proper operation of the mechanical ventilator by activation of appropriately set alarms and frequent assessment of device function (usually, check every 1 to 2 hours). •• During even brief periods of removal from mechanical ventilation, maintain ventilation and oxygenation with MRB. During intrahospital transport, verify adequacy of ventilatory support equipment, particularly the

maintenance of PEEP (when > 10 cm H2O is required) as well as ensuring adequate portable oxygen supply tank pressure. When possible, a portable mechanical ventilator should be used instead of a MRB. •• Emergency sources of portable oxygen should be readily available in the event of loss of wall oxygen capabilities. Weaning from Mechanical Ventilation

•• Systematically assess wean potential and address factors impeding weaning. •• Use a weaning protocol with a “wean screen.” Assure that the patient, family, and key caregivers are aware of weaning trials. •• Stop weaning trial if signs of intolerance emerge. •• Use a systematic evidence-based multidisciplinary approach to weaning.

Preventing Complications

1. Maintain ET tube or tracheostomy cuff pressures less than 25 mm Hg (30 cm H2O). 2. Maintain artificial airway position by securing with a properly fitting holder device or selected tapes. Frequently verify proper ET position by noting ET marking at lip or nares placed after intubation. 3. Ensure tape or devices used to secure the artificial airway are properly applied and are not causing pressure areas or skin breakdown. Periodic repositioning of ET tubes may be required to prevent skin integrity problems. 4. Use a bite block with oral ET tubes if necessary to prevent accidental biting of the tube. 5. Provide frequent mouth care and assess for development of pressure areas from ET tubes. Move the ET from one side of the mouth to the other daily or more frequently if necessary.

SELECTED BIBLIOGRAPHY 155

6. Assess for signs and symptoms of sinusitis with nasal ET tube use (eg, pain in sinus area with pressure, purulent drainage from nares, fever, increased white blood cell count). Maximizing Communication

1. Assess communication abilities and establish at least a method for nonverbal communication (see the discussion of communication previously). Assist family members in using that approach with the patient. 2. Anticipate patient needs and concerns in the planning of care. 3. Ensure that call lights, bells, or other methods for notifying unit personnel of patient needs are in place at all times.

Reducing Anxiety and Providing Psychosocial Support

1. Maintain a calm, supportive environment to avoid unnecessary escalation of anxiety. Provide brief explanations of activities and procedures. The vigilance and presence of healthcare providers during anxiety periods is crucial to avoid panic by patients and visiting family members. 2. Teach the patient relaxation techniques to control anxiety. 3. If needed, administer doses of anxiolytics that do not depress respiration (see Chapter 6, Pain, Sedation, and Neuromuscular Blockade; and Chapter 9, Cardiovascular System). 4. Encourage the family to stay with the patient as much as desired and to participate in caregiver activities as appropriate. Presence of a family member provides comfort to the patient and assists the family member to better cope with the critical illness. 5. Promote sleep at night by decreasing light, noise, and unnecessary interruptions.

SELECTED BIBLIOGRAPHY General Critical Care Ahrens T, Sona C. Capnography application in acute and progressive care. AACN Clin Issues. 2003;14:123-132. American Society of Anesthesiologists Task Force on Sedation and Analgesia by Non-Anesthesiologists. Practice guidelines for sedation and analgesia by non-anesthesiologists. Anesthesiology. 2002;96:1004-1017. Balas MC, Rice M, Chaperon C, et al. Management of delirium in critically ill adults. Crit Care Nurs. 2012;32:15-25. Balas MC, Vasilevskis EE, Burke WJ, et al. Critical care nurses’ role in implementing the “ABCDE Bundle” into practice. Crit Care Nurs. 2012;32:35-47. Berry E, Zecca H. Daily interruptions of sedation: a clinical approach to improve outcomes in clinically ill patients. Crit Care Nurs. 2012;32:43-51. Branson RD, Mannheimer PD. Forehead oximetry in critically ill patients: the case of a new monitoring site. Respir Care Clin N Am. 2004;10(3):359-367.

Chang L, Wang KK, Chao F. Influence of physical restraint on unplanned extubation of adult intensive care patients: a casecontrol study. Am J Crit Care. 2008;17:408-415. Cuccio L, Cerullo E, Paradis H, et al. An evidence-based oral care protocol to decrease ventilator-associated pneumonia. Dimens Crit Care Nurs. 2012;31:301-308. Dolovich MB, Ahrens RC, Hess DR, et al. Device selection and outcomes of aerosol therapy: evidence-based guidelines. Chest. 2006;127:335-371. Ely EW, Shintani A, Truman B. Delirium as a predictor of mortality in mechanically ventilated patients in the intensive care unit. JAMA. 2004;291:1753-1762. Girard TD, Jackson JC, Pandharipande PP, et al. Delirium as a predictor of long-term cognitive impairment in survivors of critical illness. Crit Care Med. 2010;38:1513-1520. Halm M, Amrola R. Effect of oral care on bacterial colonization and ventilator-associated pneumonia. Am J Crit Care. 2009;18: 275-278. Hellstom A, Fagerstom C, Willman A. Promoting sleep by nursing interventions in health care settings: a systematic review. Worldviews Evid Based Nurs. 2011;8:128-142. Jarachovic M, Mason M, Kerber K, McNett M. The role of standardized protocols in unplanned extubations in a medical intensive care unit. Am J Crit Care. 2011;20:304-311. Jongerden IP, Rovers MM, Grypdonck MH, Bonten MJ. Open and closed endotracheal suction systems in mechanically ventilated intensive care patients: a meta-analysis. Crit Care Med. 2007;35:260-270. Kazmarek, RM, Stoller JK, Heur AJ. Egan’s Fundamentals of Respiratory Care. 10th ed. St. Louis, MO: Mosby; 2013. Kjonegaard R, Fields W, King ML. Current practice in airway management: a descriptive evaluation. Am J Crit Care. 2009;doi: 10.4037/ajcc2009803. MacLeod DB, Cortinez LI, Keifer JC, et al. The desaturation response time of finger pulse oximeters during mild hypothermia. Anaesthesia. 2005;60(1):65-71. Matthews EE. Sleep disturbances and fatigue in critically ill patients. AACN Adv Crit Care. 2011;22:204-224. Munro CL, Grap MJ, Jones DJ, et al. Chlorhexidine, toothbrushing, and preventing ventilator-associated pneumonia in critically ill adults. Am J Crit Care. 2009;18:428-437. Neumar RW, Otto CW, Link MS, et al. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18 suppl 3): S729-767. Seckel MA. Ask the experts: does the use of a closed suction system help to prevent ventilator-associated pneumonia? Crit Care Nurse. 2008;28(1):65-66. Seckel MA. Ask the experts: normal saline and mucous plugging. Crit Care Nurs. 2012;32:66-68. Seckel MA, Schulenburg K. Ask the experts: eating while receiving mechanical ventilation. Crit Care Nurs. 2011;31:95-97. Stauffer JL. Complications of endotracheal intubation and tracheotomy. Respir Care. 1999;44(7):828-844. St John RE, Malen JF. Airway management. Crit Care Nurs Clin N Am. 2004;16:413-430. Stonecypher K. Ventilator-associated pneumonia: the importance of oral care in intubated adults. Crit Care Nurs Q. 2010;33: 339-347.

156

CHAPTER 5. Airway and Ventilatory Management

Unoki T, Serita A, Grap MJ. Automatic tube compensation during weaning from mechanical ventilation: evidence and clinical implications. Crit Care Nurs. 2008;28:34-42. Valdez-Lowe C, Ghareeb SA, Artinian NT. Pulse oximetry in adults. AJN. 2009;109(6):52-59.

Ventilator Management Aloe K, Ryan M. Creation of an intermediate respiratory care unit to decrease intensive care utilization. JONA. 2009;39:494-498. Burns SM. Mechanical ventilation and weaning. In: Carlson KK, ed. AACN Advanced Critical Care Nursing. St Louis, Missouri: Saunders-Elsevier; 2009. Burns SM. Pressure modes of mechanical ventilation: the good, the bad, and the ugly. AACN Adv Crit Care. 2008;19:399-411. Esteban A, Frutos-Vivar F, Ferguson ND, et al. Noninvasive positivepressure ventilation for respiratory failure after extubation. N Engl J Med. 2004;350:2452-2460. Kane C, York NL. Understanding the alphabet soup of mechanical ventilation. Dimens Crit Care Nurse. 2012;31:217-222. MacIntyre NR, Branson RD. Mechanical Ventilation. Philadelphia, PA: Saunders; 2009. Pierce LN. Management of the Mechanically Ventilated Patient. Philadelphia, PA: Saunders-Elsevier; 2007. Restrepo RD, Walsh BK. Humidification during invasive and noninvasive mechanical ventilation: 2012. Resp Care. 2012;57: 782-788. St. John R. End-tidal CO2 monitoring. In Burns SM, ed. AACN’s Protocols for Practice: Non-Invasive Monitoring Series. Sudbury, MA: Jones and Bartlett; 2006. Tobin MJ. Principles and Practice of Mechanical Ventilation. New York, NY: McGraw-Hill Medical Publishing Division; 2006. Unroe M, Kahn JM, Carson SS, et al. One-year trajectories of care and resource utilization for recipients of prolonged mechanical ventilation: a cohort study. Ann Intern Med. 2010;153: 167-175. Walkey AJ, Wiener RS. Use of noninvasive ventilation in patient with acute respiratory failure, 2000-2009. Annals ATS. 2013;10: 10-17. White AC. Long-term mechanical ventilation: management strategies. Resp Care. 2012;57:889-897.

Weaning From Mechanical Ventilation Blackwood B, Alderdice F, Burns K, et al. Use of weaning protocols for reducing duration of mechanical ventilation in critically ill adults’ patients: Cochrane systematic review and meta-analysis. BMJ. 2011;342c7237.doi:1-.1136/bmj.b7237. Boles JM, Blon J, Connors A, et al. Task force: weaning from mechanical ventilation. Eur Respir J. 2007;29:1033-1056. BouAki I, Bou-Khalil P, Kanazi G. Weaning from mechanical ventilation. Curr Opin Anesthesiol. 2012;25:42-47. Brochard L, Thille AW. What is the proper approach to liberating the weak from mechanical ventilation? Crit Care Med. 2009;37:S410-S415. Burns SM. Adherence to sedation withdrawal protocols and guidelines in ventilated patients. Clin Nurs Spec. 2012;26:22-8. doi: 10.1097/NUR.0b013e31823bfae8. Burns SM. Weaning from mechanical ventilation: where were we then, and where are we now? Crit Care Nurs Clin N Am. 2012;24:457-458.

Burns SM, Fisher C, Tribble SS, et al. The relationship of 26 clinical factors to weaning outcome. Am J Crit Care. 2012;21:52-58. Epstein SK. Weaning from ventilatory support. Curr Opin Crit Care. 2009;15:36-43. Eskandar N, Apostolakos MJ. Weaning from mechanical ventilation. Crit Care Clin. 2007;23:263-274. Girard TD, Kress JP, Fuchs BD, et al. Efficacy and safety of a paired sedation and ventilator weaning protocol for mechanically ventilated patients in intensive care (Awakening and Breathing Controlled trial): a randomised controlled trial. Lancet. 2008;371:126-134. Haas CF, Loik PS. Ventilator discontinuation protocols. Resp Care. 2012;57:1649-1662. Kollef, MH, Shapiro SD, Silver P, et al. A randomized, controlled trial of protocol-directed versus physician-directed weaning from mechanical ventilation. Crit Care Med. 1997;25(4):557-574. MacIntyre NR. Discontinuing mechanical ventilator support. Chest. 2007;132:1049-1056. MacIntyre NR. Evidence-based assessments in the ventilator discontinuation process. Resp Care. 2012;57:1611-618. McConville JF, Kress JP. Current concepts: weaning patients from the ventilator. NEJM. 2012;367:2233-2239. Mendes-Tellez PA, Needham DM. Early physical rehabilitation in the ICU and ventilator liberation. Resp Care. 2012;57:1663-1669. Olff C, Clark-Wadkins C. Tele-ICU partners enhanced evidencebased practice: ventilator weaning initiative. AACN Adv Crit Care. 2012;23:312-322. Penuelas O, Frutos-Vivar F, Fernandez C, et al. Characteristics and outcomes of ventilated patients according to time to liberation from mechanical ventilation. Am J Respir Crit Care Med. 2011;184:430-437. Tobin MJ, Guenther SM, Perez W, et al. Konno-Mead analysis of ribcage-abdominal motion during successful and unsuccessful trials of weaning from mechanical ventilation. Am Rev Respir Dis. 1987;135:1320-1328. White V, Currey J, Botti M. Multidisciplinary team developed and implemented protocols to assist mechanical ventilation weaning: a systematic review of literature. Worldviews Evid Based Nurs. 2011;8:51-59.

Communication Batty S. Communication, swallowing and feeding in the intensive care unit patient. Nurs Crit Care. 2009;14:175-179. Baumgartner CA, Bewyer E, Bruner D. Management of communication and swallowing in intensive care. AACN Adv Crit Care. 2008;19:433-443. Happ MB. Communicating with mechanically ventilated patients: state of the science. AACN Clin Issues. 2001;12:247-258. Windhorst C, Harth R, Wagoner C. Patients requiring tracheostomy and mechanical ventilation: a model for interdisciplinary decision-making. AHSA Leader. 2009;14:10-13.

Evidence-Based Resources A Collective Task Force Facilitated by the American College of Chest Physicians, the American Association for Respiratory Care, and the American College of Medicine. Evidence-based guidelines for weaning and discontinuing ventilator support. Resp Care. 2002;47:69-90. American Association of Respiratory Care. AARC clinical practice guideline: capnography/capnometry during mechanical ventilation: 2011. Resp Care. 2011;56:503-509.

American Association for Respiratory Care. AARC clinical practice guideline: care of the ventilator circuit and it relation to ventilatorassociated pneumonia. Resp Care. 2003;48:869-879. American Association of Respiratory Care. AARC clinical practice guideline: endotracheal suctioning of mechanically ventilated patients with artificial airways: 2010. Resp Care. 2010;55:758-764. American Association for Respiratory Care. AARC clinical practice guideline: removal of the endotracheal tube-2007 revision and update. Resp Care. 2007:52;81-93. American Association of Critical Care Nurses (AACN). Practice Alert: Delirium Assessment and Management. Alisio Viejo, CA: AACN;2011. www.aacn.org. Accessed March 1, 2013. American Association of Critical Care Nurses (AACN). Practice Alert: Ventilator Associated Pneumonia. Alisio Veijo, CA; AACN: 2008. www.aacn.org. Accessed January 10, 2010. American Association of Critical Care Nurses (AACN). Practice Alert: Oral Care in the Critically Ill. Alisio Veijo, CA: AACN;2010. www.aacn.org Accessed March 1, 2013. http://classic.aacn.org/ AACN/practiceAlert.nsf/vwdoc/pa2. Accessed January 10, 2010. American Association of Critical Care Nurses (AACN). Practice Alert: Prevention of aspiration. Alisio Viejo, CA: AACN; 2011. www.aacn.org. Assessed March 1, 2013. American Thoracic Society and the Infectious Diseases Society of America. Guidelines for the management of adults with hospitalacquired, ventilator-associated, and healthcare-associated pneumonia. Am J Respir Crit Care Med. 2005;171:388-416. Barden, C, Davis T, Seckel M, et al. C. AACN Tele-ICU Nursing Practice Guidelines. 2013. Available at http://www.aacn.org/wd/ practice/docs/tele-icu-guidelines.pdf. Barr J, Fraser Gl, Puntillo K, et al. Clinical practice guidelines for the management of pain, agitation, and delirium in adult patients in the intensive care unit. Crit Care Med. 2013;41:263-306.

SELECTED BIBLIOGRAPHY 157

Burns SM. Practice protocol: weaning from mechanical ventilation. In: Care of the Mechanically Ventilated Patient. 2nd ed. Sudbury, MA: Jones and Bartlett; 2007. Burns SM, ed. AACN Protocols for Practice Series. Centers for Disease Control and Prevention. Guidelines for preventing health-care-associated pneumonia, 2003: recommendations of CDC and the Health Care Infection Control Practices Advisory Committee. MMWR. 2004;53(No. RR-3):1-35. Grap MJ. Pulse oximetry. In: Burns SM, ed. AACN’s Protocols for Practice: Noninvasive Monitoring Series. Sudbury, MA: Jones and Bartlett; 2006. MacIntyre, NR, Cook DJ, Ely EW, Jr., et al. Evidence-based guidelines for weaning and discontinuing ventilatory support: a collective task force facilitated by the American College of Chest Physicians; the American Association for Respiratory Care; and the American College of Critical Care Medicine. Chest. 2001;120(6 suppl):375S-395S. Muscedere J, Dodek P, Keenan S, et al. Comprehensive evidencebased clinical practice guidelines for ventilator-associated pneumonia: prevention. J Crit Care. 2008;23:126-137. Pierce LN. Invasive and noninvasive modes and methods of mechanical ventilation. In: Burns SM, ed. AACN’s Protocols for Practice: Care of the Mechanically Ventilated Patient Series. Sudbury, MA: Jones and Bartlett; 2006. St John RE. End-tidal carbon dioxide monitoring. In: Burns SM, ed. AACN’s Protocols for Practice: Noninvasive Monitoring Series. Sudbury, MA: Jones and Bartlett; 2006. St John RE, Seckel MA. Airway management. In: Burns SM, ed. AACN’s Protocols for Practice: Care of the Mechanically Ventilated Patient Series. Sudbury, MA: Jones and Bartlett; 2006. Wiegand DL, ed. AACN Procedure Manual for Critical Care. 6th ed. Philadephia, PA: Saunders; 2011.

This page intentionally left blank

Pain, Sedation, and Neuromuscular Blockade Management Yvonne D’Arcy and Suzanne M. Burns

KNOWLEDGE COMPETENCIES 1. Describe the elements of pain assessment in critically ill patients. 2. Identify how to use a behavioral pain scale to assess pain in patients who cannot self-report it. 3. Compare and contrast pain-relieving modalities for the critically ill: • Nonsteroidal anti-inflammatory drugs • Opioids, including patient-controlled analgesia • Epidural analgesia with opioids and/or local anesthetics (LAs) • Elastomeric pumps with LA • Nonpharmacologic modalities: distraction, cutaneous stimulation, imagery, and relaxation techniques

Pain management is central to the care of the critically ill or injured patient. Unfortunately critically ill patients may not be able to self-report their pain management needs to their healthcare team. Patients identify physical care that promotes pain relief and comfort as an important element of their hospitalization and recovery, especially while in the critical care environment. Providing optimum pain relief for critically ill patients not only enhances their psychoemotional well-being, but can also help avert additional physiologic injury for a patient who is already compromised. This chapter explores a multimodal approach to pain management in critically ill patients based on the physiologic mechanisms of pain transmission and human responses to pain. Patients identify physical care that promotes pain relief and comfort as an important element of their hospitalization and recovery, especially while in the critical care environment. Providing optimum pain relief for

4. Identify the important elements of pain control for a patient who is an addict. 5. Describe special considerations for pain management in vulnerable populations such as the elderly. 6. Identify the need for sedation, common sedative drugs, and how to monitor and manage the patient requiring sedation and potential related complications such as delirium. 7. Discuss different neuromuscular blocking agents used in critically ill ventilated patients, clinical indications and monitoring.

critically ill patients not only enhances their psychoemotional w ell-being, but also can help avert additional physiologic injury. Using a m ultimodal approach, specific pharmacologic and nonpharmacologic pain management techniques are described, including the integral relationships among relaxation, sedation, and pain relief. Strategies also are presented that promote comfort and are easy to incorporate into a plan of care for critically ill patients. Finally, special considerations are delineated for vulnerable populations within the critical care setting.

PHYSIOLOGIC MECHANISMS OF PAIN Peripheral Mechanisms The pain response is elicited with tissue injuries, whether actual or potential. Undifferentiated free nerve endings, or nociceptors, are the major receptors signaling tissue injury (Figure 6-1). 159

160

CHAPTER 6. Pain, Sedation, and Neuromuscular Blockade Management

Limbic forebrain • Feeling and reaction to pain

Nociceptors are polymodal and can be stimulated by thermal, mechanical, and chemical stimuli. Nociception refers to the transmission of impulses by sensory nerves, which signal tissue injury. At the site of injury, the release of a variety of neurochemical substances potentiates the activation of peripheral nociceptors. Many of these substances are also mediators of the inflammatory response and they can facilitate or inhibit the pain impulse. These substances include histamine, kinins, prostaglandins, serotonin, and leukotrienes (Figure 6-2). The nociceptive impulse travels to the spinal cord via specialized, afferent sensory fibers. Small, myelinated A-delta (δ) fibers conduct nociceptive signals rapidly to the spinal cord. The A-delta fibers transmit sensations that are generally localized and sharp in quality. In addition to A-delta fibers, smaller, unmyelinated C fibers also transmit nociceptive signals to the spinal cord. Because C fibers are unmyelinated, their conduction speed is much slower than their A-delta counterparts. The sensory quality of signals carried by C fibers tends to be dull and unlocalized (Figure 6-3).

Cerebrocortex • Perception of pain

Thalamus Axons project to other areas of brain Endorphin release

Brain stem PAIN TRANSMISSION

PSIN INHIBITION Descending pathway

Ascending pathway • STT • SRT

Dorsal horn • Opening and closing the pain gate Release of substance P

Spinal cord

Peripheral transmission

Noxious stimulus (may be chemical, thermal, or mechanical)

Nociceptors

Peripheral activity • Vasodilation • Edema • Hyperalgesia • Release of chemicals

Spinal Cord Integration Sensory afferent fibers enter the spinal cord via the dorsal nerve, synapsing with cell bodies of spinal cord interneurons

Figure 6-1. Physiologic pathway of pain transmission. (From: Wild LR, Evans L. Pain. In: Copstead L, ed. Perspectives on Pathophysiology. Philadelphia, PA: WB Saunders; 1995:934.)

Mast cell or neutrophil Substance P

Bradykinin Tissue injury

Histamine NGF

Stimulus

Representative receptor

NGF Bradykinin Seratonin ATP H+ Lipids Heat Pressure

TrkA BK2 5-HT3 P2X3 ASIC3NR1 PGE2/CB1NR1 VR1NRL-1 DEG/ENaC

DRG cell body

5-HT Prostaglandin ATP H+

CGRP Substance P

Blood vessel

Spinal cord

Figure 6-2. Peripheral nociceptors and the inflammatory response at the site of injury. (From: Julius D, Basbaum AI. Molecular mechanisms of nociception. Nature. 2001;413:203-210.)

RESPONSES TO PAIN 161

Aα, β

Primary afferent axons Thermal threshold Myelinated Large diameter Proprioception, light touch

None

Voltage

Aα and Aδ fibers

Aδ Aδ fibers Lightly myelinated Medium diameter Nociception (mechanical, thermal, chemical)

C fiber Unmyelinated Small diameter Innocuous temperature, itch Nociception (mechanical, thermal, chemical)

C Time

– 53°C type I First pain

– 43°C type II

Second pain

– 43°C

Figure 6-3. Different nociceptors detect different types of pain. (A) Peripheral nerves include small-diameter (Aδ) and medium- to large-diameter (Aα, β) myelinated afferent fibers, as well as small-diameter unmyelinated afferent fibers (C). (B) The fact that conduction velocity is directly related to fiber diameter is highlighted in the compound action potential recording from a peripheral nerve. Most nociceptors are either Aδ or C fibers, and their different conduction velocities (6-25 and ~1.0 m/s, respectively) account for the first (fast) and second (slow) pain responses to injury.

in the dorsal horn (see Figure 6-1). Most of the A-delta and C fibers synapse in laminae I through V, in an area referred to as the substantia gelatinosa. Numerous neurotransmitters (eg, substance P, glutamate, and calcitonin gene-related peptide) and other receptor systems (eg, opiate, alpha-adrenergic, and serotonergic receptors) modulate the processing of nociceptive inputs in the spinal cord.

Central Processing Following spinal cord integration, nociceptive impulses travel to the brain via specialized, ascending somatosensory pathways (see Figure 6-1). The spinothalamic tract conducts nociceptive signals directly from the spinal cord to the thalamus. The spinoreticulothalamic tract projects signals to the reticular formation and the mesencephalon in the midbrain, as well as to the thalamus. From the thalamus, axons project to somatosensory areas of the cerebrocortex and limbic forebrain. The unique physiologic, cognitive, and emotional responses to pain are determined and modulated by the specific areas to which the somatosensory pathways project. The stimulus to the cerebrocortex can also activate the patient’s previous memories of the experience of pain; for example, the thalamus regulates the neurochemical response to pain, and the cortical and limbic projections are responsible for the perception of pain and aversive response to pain, respectively. Similarly, the reticular activating system regulates the heightened state of awareness that accompanies pain.

The modulation of pain by activities in these specific areas of the brain is the basis of many of the analgesic modalities available to treat pain.

RESPONSES TO PAIN Human responses to pain can be both physical and emotional. The physiologic responses to pain are the result of hypothalamic activation of the sympathetic nervous system associated with the stress response. Sympathetic activation leads to: •• Blood shifts from superficial vessels to striated muscle, the heart, the lungs, and the nervous system •• Dilation of the bronchioles to increase oxygenation •• Increased cardiac contractility •• Inhibition of gastric secretions and contraction •• Increases in circulating blood glucose for energy

TABLE 6-1. TYPES OF PAIN Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage (APS, 2008). There are three main types of pain that can occur alone or in combination: • Acute pain from which the patient expects to recover • Chronic pain that lasts beyond the normal healing period • Neuropathic pain, a special type of chronic pain that is the result of nerve damage

162

CHAPTER 6. Pain, Sedation, and Neuromuscular Blockade Management

Signs and symptoms of sympathetic activation which frequently accompany nociception and pain: •• Increased heart rate •• Increased blood pressure •• Increased respiratory rate •• Pupil dilation •• Pallor and perspiration •• Nausea and vomiting Although patients experiencing acute pain often exhibit signs and symptoms as noted above, it is critical to note that the absence or presence of any or all of these signs and symptoms does not negate or confirm the presence of pain. In fact, some patients, especially those who are critically ill and with little or no compensatory reserves, may exhibit a shock-like clinical picture in the presence of pain. Patients who are accustomed to underlying chronic pain may have a decreased physiologic response to it while the actual intensity of the pain remains high (Table 6-1). Critically ill patients also express pain both verbally and nonverbally. The expressions can take many forms, some of which are subtle cues that could easily be overlooked (Table 6-2). Any signs that may indicate pain warrant further exploration and assessment. Although physiologic and behavioral expressions of acute pain have been described, each person’s response to pain is unique. Also, it is important to remember that patients who are receiving neuromuscular blocking agents (eg, mivacurium, vecuronium, atracurium, or cisatricurium) may be unable to exhibit even subtle signs of discomfort because of the therapeutic paralysis. Neuromuscular blocking agents do not affect sensory nerves and have no analgesic qualities. Consequently, patients who are receiving blockade will require a continuous infusion of opioids to ensure pain relief.

PAIN ASSESSMENT Pain assessment is a core element of ongoing surveillance of the critically ill patient. Self-report of pain intensity and distress should be used whenever possible, especially for patients who can talk or communicate effectively. In those who cannot communicate, such self-reporting is not possible and specific tools designed for pain assessment in non-verbal patients should be used. Unfortunately, it has been found that TABLE 6-2. EXAMPLES OF PAIN EXPRESSION IN CRITICALLY ILL PATIENTS Verbal Cues Moaning Crying Screaming Silence

Facial Cues Grimacing Wincing Eye signals

Body Movements Splinting Rubbing Rocking Rhythmic movement of extremity Shaking or tapping bed rails Grabbing the nurse’s arm

up to a third of critical care nurses do not use pain assessment tools on their patients who are unable to communicate. Regular documentation of pain assessment not only helps monitor the efficacy of analgesic modalities, but also helps ensure communication among caregivers regarding patients’ pain. A variety of tools to assess pain intensity are available. There are three commonly used scales. The numeric rating scale (NRS) uses numbers between 0 and 10 to describe pain intensity; the anchors are “no pain to worst pain imaginable.” Some patients find it easier to use adjectives to describe their pain. The verbal descriptive scale (VDS) offers patients a standardized list of adjectives to describe their pain intensity. The descriptors are “none,” “mild,” “moderate,” and “severe.” With the visual analogue scale (VAS), a tool developed primarily for research, patients indicate their pain intensity by drawing a vertical line, bisecting a horizontal baseline. The baseline is anchored at either end by the terms “no pain” and “worst pain imaginable.” A numeric conversion is done by measuring the line from the left anchor to the patient’s mark, in millimeters. Any of these scales can be used with patients who are intubated or unable to speak for other medical reasons; for example, patients can be asked to use their fingers to indicate a number between 0 and 10; similarly, patients can be asked to indicate by nodding their head or pointing to the appropriate adjective or number as they either hear or read the list of choices. With the VAS, the line can be printed on a sheet of paper or marker board and the patients asked to mark the line to indicate their level of pain. While the VAS has been used in some critical care patients, it may be difficult to use in many as it requires dexterity that may be inhibited by invasive lines, bandages, etc. Unfortunately, some critically ill patients are unable to indicate their pain intensity either verbally or nonverbally. In these situations, nurses must often use other clues to assess their patient’s pain. Using a behavioral pain scale provides a guide for identifying and assessing pain in non-verbal patients (Table 6-3). In addition, by monitoring physiologic parameters, nurses may also anticipate and recognize clinical situations where pain is likely to occur and use their knowledge of physiology and pathophysiology and experience with other patients with similar problems. By combining their knowledge and experience with well-developed interviewing and observational skills, critical care nurses can assess patients’ pain effectively and intervene appropriately.

A MULTIMODAL APPROACH TO PAIN MANAGEMENT Today there are numerous approaches and modalities available to treat acute pain. Whereas pharmacologic techniques traditionally have been the mainstay of analgesia, other complementary or nonpharmacologic methods are growing in their acceptance and use in clinical practice. Most modalities used in the treatment of acute pain can be used effectively in the critically ill. Evidenced-based practice guidelines to maximize analgesia in critically ill patients are summarized in Table 6-4.

A MULTIMODAL APPROACH TO PAIN MANAGEMENT 163

Table 6-3. DMC PAIN ASSESSMENT BEHAVIOR SCALE (NON VERBAL) FOR PATIENTS UNABLE TO PROVIDE A SELF-REPORT OF PAIN FACE

0 Face muscles relaxed.

RESTLESSNESS

0 Quite, relaxed appearance, normal movement. 0 Normal muscle tone, relaxed.

MUSCLE TONE*

VOCALIZATION**

0 No abnormal sounds.

CONSOLABILITY

0 Content, relaxed.

1 Facial muscle tension, frown, grimace. 1 Occasional restless movement shifting position. 1 Increased tone, flexion of fingers and toes. 1 Occasional moans, cries, whimpers or grunts. 1 Reassured by touch or talk. Distractible.

2 Frequent to constant frown, clenched jaw. 2 Frequent restless movement may include extremities or head. 2 Rigid tone.

Face Score:

2 Frequent or continuous moans, cries, whimpers or grunts. 2 Difficult to comfort by touch or talk.

Vocalization Score:

Restlessness Score:

Muscle Tone Score:

Consolability Score:

Behavioral Pain Assessment Scale Total (0–10) *Assess muscle tone in patients with spinal cord lesion or injury at a level above the lesion or injury. Assess patients with hemiplegia on the unaffected side. ** This item cannot be measured in patients with artificial airways. How to Use the Pain Assessment Behavioral Scale: 1. Observe behaviors and mark appropriate number for each category. 2. Total the numbers in the pain assessment behavioral score column. 3. Zero = no evidence of pain. Mild pain = 1-3. Moderate pain = 4-6. Severe uncontrolled pain is > 6. Considerations: 4. Use the standard pain scale whenever possible to obtain the patient’s self-report of pain. Self-report is the best indicator of the presence and intensity of pain. 5. Use this scale for patients who are unable to provide a self-report of pain. 6. In addition, a “proxy pain evaluation” from family, friends, or clinicians close to the patient may be helpful to evaluate pain based on previous knowledge of patient response. 7. When in doubt, provide an analgesic. “If there is reason to suspect pain, an analgesic trial can be diagnostic as well as therapeutic.” Used with permission by the Detroit Medical Center via Margaret L. Campbell, PhD, RN.

TABLE 6-4. EVIDENCED-BASED PRACTICE: PAIN MANAGEMENT

• Pain should be routinely monitored. • Use the behavioral pain scale (BPS) or critical-care pain observation tool (CPOT) for patients who cannot self-report pain.

• Do not use vital signs alone for pain assessment in ICU patients. • Use preemptive analgesia prior to procedures. • Consider IV opioids as the first line to treat non-neuropathic pain. • Non-opioids and co-analgesics such as gabapentin or carbamazepine be considered for use with opioids.

• Epidural analgesia is recommended for rib fractures and postoperative analgesia for abdominal aortic aneurysm. Data from: Barr, Fraser, Puntillo et al, SCCM 2013.

Peripheral Nociceptive Input

Transmission

Prostaglandin inhibitors (NSAIDs)

Regional or epidural local anesthetics Vibration Massage Heat Cold TENS Acupuncture Acupressure

One of the central goals of pain management is to combine therapies or modalities that target as many of the processes involved in nociception and pain transmission as possible. Analgesic modalities, both pharmacologic and nonpharmacologic, exert their effects by altering nociception at specific structures within the peripheral or central nervous system (CNS; ie, the peripheral nociceptors, the spinal cord, or the brain) or by altering the transmission of nociceptive impulses between these structures (Figure 6-4). By understanding where analgesic modalities work, nurses can more effectively select a combination of modalities working at different sites to best treat the source or type of pain patients experience and, subsequently, help patients achieve optimal analgesia.

Spinal Cord Integration

Epidural opioids systemic opioids (minor)

Transmission

Dorsal column stimulation (used for chronic pain management)

Figure 6-4. A multimodal approach to pain management.

Central Processing

Distraction Imagery Anxiolysis Biofeedback Endorphins Systemic opioids

164

CHAPTER 6. Pain, Sedation, and Neuromuscular Blockade Management

To assist nurses to select and maximize analgesic modalities, for each of the analgesic modalities presented here, there is a brief description of where and how the selected modality works, clinical situations where it can be used most effectively, and strategies for titrating the modality. Finally, because few modalities exert a singular effect, a summary of secondary or side effects commonly associated with them, and strategies to minimize their occurrence are also addressed.

NONSTEROIDAL ANTI-INFLAMMATORY DRUGS Nonsteroidal anti-inflammatory drugs (NSAIDs) target the peripheral nociceptors. The NSAIDs exert their effect by modifying or reducing the amount of prostaglandin produced at the site of injury by inhibiting the formation of the enzyme cyclooxygenase, which is also responsible for the breakdown of arachidonic acid. As prostaglandin inhibitors, the NSAIDs have been shown to have opioid-sparing effects and are very effective in managing pain associated with inflammation, trauma to peripheral tissues (eg, soft tissue injuries), bone pain (eg, fractures, metastatic disease), and pain associated with indwelling tubes and drains (eg, chest tubes). One of the NSAIDs commonly used in the critical care setting is ketorolac tromethamine (Toradol). Ketorolac is currently the only parenteral NSAID preparation available in the United States and can be administered safely via the intravenous (IV) route. Intramuscular administration is not recommended due to the potential for irregular and unpredictable absorption. Recommended dosing for ketorolac is a 30-mg loading dose followed by 15 mg every 6 hours. Like all NSAIDs, ketorolac has a ceiling effect where administration of higher doses offers no additional therapeutic benefit yet significantly increases the risk of toxicity. Another non-opioid alternative to ketorolac is acetaminophen IV (Orfirmev), for patients who can tolerate the drug and do not have liver disease or other potential contraindications. The Society of Critical Care Medicine (SCCM) recommends the use of adjuvant analgesics such as NSAIDs to reduce opioid analgesic use and reduce opioid related side effects.

Side Effects The side effects associated with the use of NSAIDs relate to the function of prostaglandins in physiologic processes in addition to nociception; for example, gastrointestinal (GI) irritation and bleeding may result from NSAID use because prostaglandins are necessary for maintaining the mucous lining of the stomach. Similarly, the enzyme cyclooxygenase is needed for the eventual production of thromboxane, a key substance involved in platelet function. As a result, when NSAIDs are used chronically or in high doses, platelet aggregation may be altered, leading to bleeding problems. NSAID use can also lead to renal toxicity. Cross-sensitivities

with other NSAIDs have also been documented (eg, ibuprofen, naproxen, indomethacin, piroxicam, aspirin). For these reasons, ketorolac and other NSAIDs should be avoided for patients who have a history of gastric ulceration, renal insufficiency, and coagulopathies or a documented sensitivity to aspirin or other NSAIDs. In addition, NSAID use is not recommended in patients with heart disease, recent heart bypass surgery, or patients with a history of ischemic attacks or strokes. An alternative to intravenous ketorolac for patients who are not good candidates for NSAIDs is intravenous acetaminophen, as noted above. The severity of all NSAID-related side effects increases with high doses or prolonged use. For this reason, ketorolac and other such drugs are designed for short-term use only.

OPIOIDS The principal modality of pain management in the critical care setting continues to be opioids. The SCCM guidelines recommend that opioids be considered as first line treatment for non-neuropathic pain. Traditionally referred to as narcotics, opioids produce their analgesic effects primarily by binding with specialized opiate receptors throughout the CNS and thereby altering the perception of pain. Opiate receptors are located in the brain, spinal cord, and GI tract. Although opioids work primarily within the CNS, they also have been shown to have some local or peripheral effects as well. There are at least 45 variations in opiate receptors that account for the varied responses in individual patients. Opioids are well tolerated by most critically ill patients and can be administered by many routes including IV, oral, buccal, nasal, rectal, transdermal, and intraspinal. Morphine sulfate is still the most widely used opioid and serves as the gold standard against which others are compared. Other opioids commonly used in the care of the critically ill include hydromorphone (Dilaudid) and fentanyl (Sublimaze). Opioid polymorphisms may cause opioids to affect patients differently, thus careful use and assessment of the drugs are necessary to determine optimal dosing.

Side Effects Patients’ responses to opioids, both analgesic responses and side effects, are highly individualized. Just as all the opioid agents have similar pain-relieving potential, all opioids currently available share similar side effect profiles. When side effects do occur, it is important to remember that they are primarily the result of opioid pharmacology and patient response, as opposed to the route of administration. Nausea and Vomiting

Nausea and vomiting are distressing side effects often related to opioids that, unfortunately, many patients experience. Generally, nausea and vomiting result from stimulation of the chemoreceptor trigger zone (CTZ) in the brain and/or from slowed GI peristalsis. Nausea and vomiting often can

OPIOIDS 165

be managed effectively with antiemetic medications. Metoclopramide (Reglan), a procainamide derivative, works both centrally at the CTZ and at the GI level to increase gastric motility. However, there are significant risks with metoclopramide use, such as the potential for seizures and tardive dyskinesia. These conditions occur more commonly in the elderly and with prolonged use of the drug. The vestibular system also sends input to the CTZ. For this reason, opioid-related nausea frequently is exacerbated by movement. If patients complain of movement-related nausea, the application of a transdermal scopolamine patch can help prevent and treat opioid-induced nausea. The use of transdermal scopolamine is best avoided in patients older than 60 years because the drug has been reported to increase the incidence and severity of confusion in older patients. The phenothiazines (ie, prochlorperazine [Compazine], 2.5-10 mg IV) treat nausea through the effects at the CTZ. The serotonin antagonist ondansetron (Zofran) is also effective for treatment of opioid-related nausea. The doses required for postoperative or opioid-related nausea are significantly smaller doses (4 mg IV) than those used with emetogenic chemotherapy. Pruritus

Pruritus is another opioid-related side effect commonly reported by patients. The actual mechanisms producing opioid-related pruritus are unknown. Although antihistamines can provide symptomatic relief for some patients, the role of histamine in opioid-related pruritus is unclear. One of the drawbacks of using antihistamine agents, such as diphenhydramine (Benadryl), is the sedation associated with their use. In addition, the use of diphenhydramine has been shown to have a 70% increase in cognitive deterioration in geriatric patients. Similar to other opioid side effects, the incidence and severity of pruritus is dose related and tends to diminish with ongoing use. Another option to treat opioid-induced pruritis is nalbuphine (Nubain), dosed at small doses of 2.5 to 5.0 mg IV every 6 hours as needed. Constipation

Constipation, another common side effect, results from opioid binding at opiate receptors in the GI tract and decreased peristalsis. The incidence of constipation may be low in some critically ill patients, but it is important to remember that it is likely to be a problem for many patients after the critical phase of their illness or injury. The best treatment for constipation is prevention by ensuring adequate hydration, as well as by administering stimulant laxatives and stool softeners, as needed. For patients with opioid induced constipation, the use of methylnaltrexone (Relistor) can be given as a subcutaneous injection for palliative care patients with advanced illness. Urinary Retention

Urinary retention can result from increased smooth muscle tone caused by opioids, especially in the detrussor muscle of

the bladder. Opioids have no effect on urine production and neither cause nor worsen oliguria. Urinary retention was not seen frequently in critically ill patients because of indwelling urinary catheters used to measure bladder drainage. However, with the decreased use of indwelling urinary catheters in all hospitalized patients this problem may be seen more often in patients in critical care units. Respiratory Depression

The use of opioid medications can result in respiratory depression through its effects on the respiratory centers in the brain stem. Both respiratory rate and the depth of breathing can decrease as a result of opioids, usually in a dose-dependent fashion. Patients at increased risk for respiratory depression include the elderly, those with preexisting cardiopulmonary diseases, patients receiving other respiratory depressive medications such as benzodiazipines, and those who receive large doses. Frequently, the earliest sign of respiratory depression is an increased level of sedation, making this an important component of patient assessment. Other signs and symptoms of respiratory depression include decreased depth of breathing, often combined with slowed respiratory rate, constriction of pupils, hypoxemia, and hypercarbia. Clinically significant respiratory depression resulting from opiate use is usually treated with IV naloxone (Narcan). Naloxone is an opioid antagonist; it binds with opiate receptors, temporarily displacing the opioid and suspending its pharmacologic effects. As with other medications, naloxone should be administered in very small doses and titrated to the desired level of alertness since the abrupt, complete withdrawal of all opiate effect can cause an acute, severe, and frightening pain response for a patient (Table 6-5). It should be emphasized that the half-life of naloxone is short—approximately 30 to 45 minutes. Careful assessment of the patient should continue and because of its short half-life, additional doses of naloxone may be needed. It may also be given as an infusion for profound levels of sedation. Naloxone should be used with caution in patients with underlying cardiovascular disease. The acute onset of hypertension, pulmonary hypertension, and pulmonary edema with naloxone administration has been reported. Also, naloxone should be avoided in patients who have developed a tolerance to opioids since opioid antagonists can precipitate withdrawal or acute abstinence syndrome.

TABLE 6-5. ADMINISTRATION OF NALOXONE 1. Support ventilation. 2. Dilute 0.4 mg (400 mcg) ampule of naloxone with normal saline to constitute a 10-mL solution. 3. Administer in 1-mL increments, every 2-5 minutes, titrating to desired effect. Onset of action: approximately 2 minutes. 4. Continue to monitor patient; readminister naloxone as needed. Duration of action: approximately 45 minutes. 5. For patients requiring ongoing doses, consider naloxone infusion: administer at 50-250 mcg/h, titrating to desired response.

166

CHAPTER 6. Pain, Sedation, and Neuromuscular Blockade Management

Intravenous Opioids Many critically ill patients are unable to use the oral route, thus the IV route is used most often. One of the advantages of IV opioids is their rapid onset of action, allowing for easy titration. Their rapid onset is beneficial during most invasive procedures in critical care. Loading doses of IV opioids should be administered to achieve an adequate blood level of the drug. Additional doses can then be administered intermittently to maintain analgesic levels. Some critically ill patients can benefit from the addition of a continuous IV opioid infusion; for example, patients who are not able to communicate their pain management needs effectively, including those who are receiving neuromuscular blocking agents, are candidates for continuous opioid infusions. The continuous infusion not only helps achieve the appropriate blood levels, but also can be easily titrated to maintain consistent blood levels. Patients who experience significant fluctuations in analgesia or side effects related to opioid administration may also benefit from the constant blood levels provided by continuous infusions. Whenever possible, the maintenance dose for the infusion should be based on patients’ previous opioid requirements.

Patient-Controlled Analgesia Patient-controlled analgesia (PCA) pumps can also be used effectively in the critical care setting with patients who are alert and able to activate the PCA button. With PCA, patients self-administer small doses of an opioid infusion using a programmable pump. PCA prescriptions typically include a bolus dose of the selected drug, a lockout or delay interval, and either a 1- to 4-hour limit. The bolus dose refers to the amount of the drug the patient receives following pump activation. The initial dose usually ranges between 0.5 and 2.0 mg of morphine, or its equivalent. The lockout or delay interval typically ranges between 5 and 10 minutes, which is enough time for the prescribed drug to circulate and take effect, yet allows the patient to easily titrate the medication over time. The 1- to 4-hour limit serves as an additional safety feature by regulating the amount of medication the patient can receive over this period of time. Assessing whether a critically ill patient is capable of using PCA is critical to the success of this analgesic modality. PCA should not be prescribed for the patient who is unable to reliably self-administer pain medication (eg, a patient with a decreased level of consciousness). A patient, however, who is cognitively intact but unable to activate the PCA button due to lack of manual dexterity or strength may utilize a PCA device that has been ergonomically adapted to suit the patient with impaired motor abilities (eg, a pressure switch pad). Lastly, if PCA is prescribed, patients, family members, and visitors should be educated that the patient is the only person to activate the PCA device. Family members and friends may think they are helping by activating the PCA

device for the patient and not realize this can produce lifethreatening sedation and respiratory depression. Titrating PCA

Patients using PCAs usually find a dose and frequency that balances pain relief with other medication-related side effects such as sedation. It is best to start PCA modality after the patient has received loading doses to achieve adequate blood levels of the prescribed opioid. For patients who continue experiencing pain while using the PCA pump, the first step in titration is to give an additional loading dose and increase the bolus dose, usually by 25% to 50% depending on the pain intensity. If patients continue to have pain in spite of the increased dose, the lockout interval or delay should then be reduced, if possible. Continuous PCA infusions are no longer recommended for the majority of patients as they increase sedation and do not provide additional pain relief. However in patients who have preexisting opioid tolerance, a continuous infusion may maintain their baseline opioid requirements while the patient-controlled bolus doses are available to help manage any new pain they experience. The hourly dose of the continuous infusion should be equianalgesic to and calculated from patients’ preexisting opioid requirements. Regional Analgesia

One additional method of reducing pain for critically ill patients is to combine standard options such as opioids with a regional analgesia. This is commonly done with a block during surgery lasting 6 to 8 hours using local anesthetics (LAs) or a continuous infusion using a small selfcontinued elastomeric pump. These pumps include the drug reservoir for the LA that resembles a filled softball and there is a preset flow control that allows the LA to infuse at the present rate. The pump is attached to a catheter that can be placed as a soaker hose configuration along the surgical incision or along a nerve, such as the femoral nerve, for patients undergoing procedures such a total knee replacement, where a continuous flow can be provided for a period of several days. This method can be very effective for patients who have undergone a total knee replacement. The concentrations of regional analgesics do not cause motor blockade. This technique is especially helpful for thoracotomy patients where pain with respiratory effort may be significantly reduced.

Switching From IV to Oral Opioid Analgesia Most often switching from IV to oral opioids is accomplished when acute pain subsides and the patient is able to tolerate oral or enteral nutrition. Patients who receive analgesics by mouth or via the enteral route can experience comparable pain relief to parenteral analgesia with less risk of infection and at lowered cost. Calculating the equianalgesic dose increases the likelihood that the transition to the oral route will be made without loss of pain control. A creative

EPIDURAL ANALGESIA 167

Essential Content Case

Pain Management Using an Epidural Catheter A 59-year-old man was admitted to the surgical ICU following a thoracotomy with wedge resection of the left lung for small-cell lung cancer. He was extubated on the morning of the first postoperative day. He had two left pleural chest tubes in place with moderate amounts of drainage and a continuing air leak. He was alert, responsive, and able to communicate his needs by writing notes and gesturing. He had a thoracic epidural catheter in place (T7-T8) with a bupivacaine (0.625 mg/mL) and fentanyl (4 mcg/mL) combination infusing at 6 mL/h. He also had an elastomeric infusion device that was providing a localized block at the incision site using LA only. When asked about his pain level, he wrote that it was 5 on a scale of 0 (no pain) to 10 (worst pain imaginable). After he was extubated, his nurse noticed he was reluctant to cough and seemed to have some difficulty taking a deep breath. She also noticed his oxygen saturation was slowly drifting downward from 97% to 95%. His respiratory rate was increasing, as was his heart rate. When she listened to his breath sounds, they were bilateral and equal, but diminished throughout with scattered rhonchi. When she asked him about his pain, he said his pain was still a 5 as long as he did not move or cough. He also indicated that he tried to avoid taking a deep breath because it would make him cough and increase the pain level to an 8 or 10. The nurse knew it would be important for this patient to breathe deeply and cough to clear his lungs, but his pain and discomfort were limiting his ability to perform those maneuvers. He also refused to move from the bed to a chair. The nurse discussed strategies to help minimize the pain associated with this activity. First, she found an extra pillow for him not only to use as a splint to support his incision and chest wall, and to stabilize his chest tubes. Then she called the anesthesiologist to confer about increasing the rate of the bupivacaine/fentanyl infusion to increase the pain relief. She also inquired about adding ketorolac or IV acetaminophen to his analgesic regimen to help with pain associated with the chest tubes. Because the patient also had an elastomeric infusion pump with LA along the surgical incision, she checked to make sure the clamp was open and the medication was infusing. The addition of the pillows for splinting especially helped the patient to take deep breaths. The anesthesiologist prescribed a bolus of 3 mLs of the epidural solution via the pump and increased the continuous rate to 8 mL/h and added ketorolac, 15 mg, IV every 6 hours and a dose of IV acetaminophen. Over the course of the next 2 hours, the patient was able to cough more effectively, with less pain. His oxygen saturation returned to 97% and he was also able to sit in his chair for lunch. Case Question 1. What are the advantages of using epidural analgesia? (A) Local anesthetic blocks the entire surgical area (B) Combining an opioid with LA improves pain relief, decreases opioid needs, and can increase respiratory efforts (C) An epidural provides the patient with a method of continuous pain relief

(D) Patients like epidurals because they provide superior pain relief Case Question 2. What is the value of adding Toradol ketorolac or acetaminophen to the pain regimen? (A) IV medications work very quickly (B) The two medications do not make the patient sedated (C) Adding non-opioid medications can reduce opioid needs and decrease opioid related side effects. (D) Patients have fewer allergies to non-opioid medications Answers 1. B 2. C

way to wean PCA is to substitute oral or enteral opioid (like morphine or oxycodone) for one-half of the total dosage of PCA demand doses. Over the next 24 hours, reducing PCA consumption by increasing the lockout period or reducing the bolus size may help transition the patient and narrow the “analgesic gap” between different routes. To prevent opioid over dosage, controlled-release preparations of morphine and oxycodone, designed to be taken less frequently than their immediate-release counterparts, should not be crushed, halved, or administered into enteral feeding tubes.

EPIDURAL ANALGESIA Over the past decade the use of epidural analgesia has grown rapidly, especially in the critical care setting. The advantages of epidural analgesia include improved pain control with less sedation, lower overall opioid doses, and generally longer duration of pain management. Epidural analgesia has been associated with a lower morbidity and mortality in critically ill patients. Both opioids and LAs, either alone or in combination, commonly are administered via the epidural route. Epidural analgesia may be administered by several methods, including intermittent bolus dosing, continuous infusion or PCA technology. The mechanisms of action and the resultant clinical effects produced by epidurally administered opioids and LAs are distinct. For this reason, these agents not only are discussed separately, but also should be distinguished when used in clinical practice.

Epidural Opioids When opioids are administered epidurally, they diffuse into the cerebrospinal fluid and into the spinal cord (Figure 6-5). There, the opioids bind with opiate receptors in the substantia gelatinosa, preventing the release of the neurotransmitter, substance P, and subsequently alter the transmission of nociceptive impulses from the spinal cord to the brain. Because the opioid is concentrated in the areas of high opiate receptor density where nociceptive impulses are entering the spinal cord, lower doses offer enhanced analgesia, with few supraspinal effects such as drowsiness.

168

CHAPTER 6. Pain, Sedation, and Neuromuscular Blockade Management

Pia mater Spinal cord Subarachnoid space Dura mater L-2

Epidural space

Figure 6-5. Epidural space for catheter placement.

Essential Content Case

The Addicted Patient A 22-year-old woman was admitted to the cardiovascular ICU (CVICU) following a tricuspid valve replacement related to recurrent subacute bacterial endocarditis. She had a self-reported history of heroin use (approximately 2 g/day). She was extubated within the first 24 hours after surgery, but remained in the CVICU for stabilization of fluid balance. During the change-of-shift report, the offgoing nurse commented that “She is a constant whine. She refuses to do anything. All she wants is to go out for a smoke and more drugs. She had 10 mg of IV morphine from the PCA pump.” When the nurse came in to make her initial assessment, the patient said, “I can’t take much more of this pain.” The nurse probed further and asked her to use some numbers to describe her pain. She replied, “It’s at 10!” The nurse noticed that the patient was reluctant to move and refused to cough. Her vital signs were: Heart rate 130 beats/min BP 150/85 mm Hg Temperature 38.5°C (orally) Respiration rate 26 breaths/min, shallow The nurse was concerned that because of this preoperative use of heroin, she might not be receiving adequate doses of morphine. She consulted the clinical nurse specialist for assistance in calculating an equivalent dose of morphine based on the usual heroin use. Using an estimated equivalence of heroin of 1 g = 10 to 15 mg morphine, the nurse calculated that the patient would need approximately 20 to 30 mg of morphine per day to account for her preexisting opioid tolerance. Consequently, analgesic dosing related to her surgery would need to be relative to this baseline requirement. The patient’s nurse approached the surgical team to discuss the potential benefits of using a PCA pump in addition to a continuous infusion of morphine. “By doing this,” the nurse explained, “she will receive her baseline opioid requirements related to her tolerance by the continuous infusion and the patient-controlled boluses could be used

to treat her new surgical pain. The PCA may also offer her some control during a time in her recovery when there are few options to do so.” In addition to starting the PCA with a continuous infusion, the surgical team and the primary nurse also discussed using other nonopioid agents such as NSAIDs to augment her analgesia. The team also discussed adding morphine sulfate Controlled-Release (MS-Contin) to the patient’s regimen once she was more comfortable on the PCA and titrating the oral medication doses up while decreasing the PCA. Once the MS-Contin was titrated to an effective dose, the PCA could be discontinued and short acting oral breakthrough medication used for additional pain relief. The nurse noted she would also need to monitor the patient for any signs or symptoms of withdrawal. In addition to the changes in the medications, the primary nurse worked with the patient to use relaxation techniques. The nurse explained that relaxation techniques could be thought of as “boosters” to her pain medications and were something that she could do to control the pain. They also agreed to try massage in the evening to try to promote sleep and relaxation. Case Question 1. In order to maintain adequate pain control after surgery in a patient who is addicted to heroin or takes regular opioids the nurse will need to: (A) Provide a continuous rate on the PCA (B) Provide a continuous rate on the PCA to account for her presurgical heroin usage and add additional pain medications for the surgical pain (C) Try to limit the patient’s opioid use because she is an addict (D) Substitute a non-opioid medication such as acetaminophen or ketoralac because the patients is an addict Case Question 2. The best way to control postoperative pain is to: (A) Use opioids exclusively (B) Use only medications (C) Encourage the patient to cough and deep breathe (D) Use a multimodal approach with medications and complementary techniques such as relaxation Answers 1. B 2. D

A variety of opioids are commonly used for epidural analgesia including morphine, fentanyl, and hydromorphone. Preservative-free (PF) preparations are used because some preservative agents can have neurotoxic effects. The opioids can be administered either by intermittent bolus or continuous infusion depending on the pharmacokinetic activity of the selected agent; for example, fentanyl is generally administered via continuous infusion due to its high lipid solubility, resulting in a short duration of action. In contrast, the low lipid solubility of PF morphine results in a delayed onset of action (30-60 minutes) and a prolonged duration of action (6-12 hours). Because of the delayed onset of action (ie, 60 minutes), PF morphine is recommended for use as a continuous infusion but not as a patient controlled bolus dose.

CUTANEOUS STIMULATION 169

Side Effects

The side effects associated with epidural opioids are the same as those described for oral opioids. It is important to remember that side effects of opioids are related more closely to the drug administered than by the route of administration; for example, the incidence of nausea and vomiting with epidural morphine is similar to that associated with IV morphine. Although epidural opioids were once feared to be associated with a higher risk of respiratory depression, clinical studies and experience have not confirmed this risk. The incidence of respiratory depression has been reported as being no higher than 0.2%. Risk factors for respiratory depression are similar to those seen with IV opioids: increasing age, high doses, underlying cardiopulmonary dysfunction, obstructive sleep apnea, obesity, and the use of perioperative or supplemental parenteral opioids or other agents causing sedation such as benzodiazipines in addition to epidural opioids.

Epidural Local Anesthetics Epidural opioids can also be combined with dilute concentrations of LAs. When administered in combination, these agents work synergistically, reducing the amount of each agent that is needed to produce analgesia. Whereas epidurally administered opioids work in the dorsal horn of the spinal cord, epidural LAs work primarily at the dorsal nerve root by blocking the conduction of afferent sensory fibers. The extent of the blockade is dose related. Higher LA concentrations block more afferent fibers within a given region, resulting in an increased density of the blockade. Higher infusion rates of LA-containing solutions increase the extent or spread of the blockade because more afferent fibers are blocked over a broader region. Bupivacaine is the LA most commonly used for epidural analgesia and is usually administered in combination with either fentanyl or PF morphine as a continuous infusion. The concentration of bupivacaine used for epidural analgesia usually ranges between 1/16% (0.065 mg/mL) and 1/8% (1.25 mg/mL). These concentrations are significantly lower than those used for surgical anesthesia, which usually range between 1/4% and 1/2% bupivacaine. The type and concentration of opioid used in combination with bupivacaine vary by practitioner and organizational preferences, but usually range between 2 and 5 mcg/mL fentanyl or between 0.02 and 0.04 mg/mL PF morphine. Ropivacaine, a LA alternative to bupivacaine, has a lower profile for causing motor block. For older patients with rib fractures or flail chest, an epidural catheter with LA only may provide positive results with less respiratory compromise and reduced pain.

efferent and autonomic nerve fibers within the same dermatomal regions. Side effects associated with epidural LAs include hypotension—especially postural hypotension from sympathetic blockade—and functional motor deficits from varying degrees of efferent motor fiber blockade. Sensory deficits, including changes in proprioception in the joints of the lower extremities, can accompany epidural LA administration due to the blockade of non-nociceptive sensory afferents. The extent and type of side effects that can be anticipated with epidural LAs depend on three primary factors: the location of the epidural catheter, the concentration of the LA administered, and the volume or rate of infusion; for example, if a patient has an epidural catheter placed within the midthoracic region, one can anticipate signs of sympathetic nervous blockade, such as postural hypotension, because the sympathetic nerve fibers are concentrated in the thoracic region. In contrast, a patient with a lumbar catheter may experience a mild degree of motor weakness in the lower extremities because the motor efferent and nerves exit the spine in the lumbar region. This usually presents clinically as either heaviness in a lower extremity or an inability to “lock” the knee in place when standing. Also, as noted, both the concentration and infusion rate of the LA influence the severity and extent of side effects. The density of the blockade and intensity of observed side effects may be increased with high LA concentrations. With higher infusion volumes, greater spread of the LA can be anticipated which can, in turn, lead to a greater number or extent of side effects. If side effects occur, the dose of the LA often is reduced either by decreasing the concentration of the solution or by decreasing the rate. Titrating Epidural Analgesia

To maximize epidural analgesia, doses may need to be adjusted. With opioids alone, the dose needed to produce effective analgesia is best predicted by the patients’ response as opposed to body size. Older patients typically require lower doses to achieve pain relief than those who are younger. Small bolus doses of fentanyl (50 mcg) can help safely titrate the epidural dose or infusion to treat pain. Similarly, a small bolus dose of fentanyl can also help treat breakthrough pain that may occur with increased patient activity or procedures. For patients receiving combinations of LAs and opioids, a small bolus dose of the prescribed infusate in conjunction with an increased rate can help titrate pain relief. Recall, however, that increasing the rate of the LA infusion increases the spread of the drug to additional dermatomes, whereas increasing the LA concentration increases the depth or intensity of the blockade and subsequent analgesia.

Side Effects

The side effects accompanying LAs are a direct result of the conduction blockade produced by the agents. Unfortunately, the LA agents are relatively nonspecific in their capacity to block nerve conduction. That is, LAs not only block sensory afferent fibers, but also can block the conduction of motor

CUTANEOUS STIMULATION One of the primary nonpharmacologic techniques for pain management used in the critical care setting is cutaneous stimulation. Cutaneous stimulation produces its analgesic effect

170

CHAPTER 6. Pain, Sedation, and Neuromuscular Blockade Management

by the altering conduction of sensory impulses as they move from the periphery to the spinal cord through the stimulation of the largest sensory afferent fibers, known as the A-alpha (α) and A-beta (b) fibers. The sensory information transmitted by these large fibers is conducted more rapidly than that carried by their smaller counterparts (A-delta [δ] and C fibers) (see Figure 6-3). As a result, nociceptive input from the A-delta and C fibers is believed to be “preempted” by the sensory input from the non-noxious cutaneous stimuli. Examples of cutaneous stimulation include the application of heat, cold, vibration, or massage. Transcutaneous electrical nerve stimulation units produce similar effects by electrically stimulating large sensory fibers. Cutaneous stimulation can produce analgesic effects whether used as a complementary modality with other pharmacologic treatments or as an independent treatment modality. Nurses can integrate these modalities easily and safely into analgesic treatment plans for the critically ill, especially for patients who may be unable to tolerate higher opioid doses. To apply or administer cutaneous stimulation, one simply needs to stimulate sensory fibers anywhere between the site of injury and the spinal cord, but within the

sensory dermatome (Figure 6-6). Massage, especially back massage, has additional analgesic benefits; it has been shown to promote relaxation and sleep, both of which can influence patients’ responses to pain.

DISTRACTION Distraction techniques such as music, conversation, television viewing, laughter, and deep breathing for relaxation can be valuable adjuncts to pharmacologic modalities. These techniques produce their analgesic effects by sending intense stimuli through the thalamus, midbrain, and brain stem which can increase the production of modulating substances such as endorphins. Also, because the brain can process only a limited amount of incoming signals at any given time, the input provided by distraction techniques “competes” with nociceptive inputs. This is particularly true for the reticular activating system. When planning for and using distraction techniques, keep in mind that they are most effective when activities are interesting to the patient (eg, their favorite type of music, television program, or video) and when they involve multiple senses such as hearing, vision, touch, and movement.

C3 C2 C4 C 5

T4 T5

T7 T8 T9

T1 T6

C 5

T10

T11 T12

C7 C 8

T3 T4 T5 T6 T7 T8 T9 T10 T11 T12 L1

C 5

T2 T3

C 5

C C7 8

Coccyx

S4 L2

L 5

L4 L 4

L 5

L 4

L 5

S1 L5

Figure 6-6. Sensory dermatomes.

C6 C7 C8

Activities should be consistent with patients’ energy levels and, most of all, be flexible to meet changing demands.

IMAGERY Imagery is another technique that can be used effectively with critically ill patients, particularly during planned procedures. Imagery alters the perception of pain stimuli within the brain, promotes relaxation, and increases the production of endorphins in the brain. Patients can use imagery independently or use guided imagery where either a care provider, family member, or friend helps “guide” the patient in painting an imaginary picture. The more details that can be pictured with the image, the more effective it can be. As with distraction techniques, tapping into multiple sensations is beneficial. Some patients prefer to involve the pain in their picture and imagine it melting or fading away. Other patients may prefer to paint a picture in their mind of a favorite place or activity. Strategies to help guide patients include the use of details to describe the imaginary scene (eg, “smell the fresh scent of the ocean air” or “see the intense red hue of the sun setting beyond the snow-capped mountains”) and the use of relaxing sensory terms such as floating, smooth, dissolving, lighter, or melting. If the patients are able to talk, it can be helpful to have them describe the image they see using appropriate detail, although some patients will prefer not to talk and instead focus on their evolving image. Again, it is important to be flexible in the approach to imagery to maximize its benefits.

SPECIAL CONSIDERATIONS FOR PAIN MANAGEMENT IN THE ELDERLY 171

can work with them to begin progressive relaxation of their muscles. To do this, the nurse can say to the patient as he or she just begins to exhale, “Now begin to relax, from the top of your head to the tips of your toes.” Change the pitch of the voice to be higher for “top of your head,” lower for “tips of your toes,” and be timed such that the final phrase ends as the patient completes exhalation. This procedure capitalizes on the positive aspects of normal body functions, as the body tends to relax naturally during exhalation. This process can and should be practiced during nonstressful periods to augment its efficacy. In fact, teaching and coaching patients to use deep breathing exercises helps equip them with a lifelong skill that can be used any time stressful or painful situations arise.

Presence Probably the single most important aspect of promoting comfort in the critically ill or injured patient is the underlying relationship between the patient, the family, and his or her care providers. Family presence at the patient’s bedside has been shown to decrease anxiety and promote healing. Including the people identified by the patient as their family support (with a broad definition of family) can provide enormous comfort for the patient resulting in relaxation. Presence refers not only to physically “being there,” but also to psychologically “being with” a patient. Although presence has not been well-defined as an intervention protocol, patients regularly describe the importance of the support that their nurses render simply by “being there” and “being with” them.

RELAXATION TECHNIQUES

SPECIAL CONSIDERATIONS FOR PAIN MANAGEMENT IN THE ELDERLY

Because critically ill patients experience numerous stressors, most patients benefit from the inclusion of relaxation or anxiolytic modalities. The use of relaxation techniques can help interrupt the vicious cycle involving pain, anxiety, and muscle tension that often develops when pain goes unrelieved. The physiologic response associated with relaxation includes decreased oxygen consumption, respiratory rate, heart rate, and muscle tension; blood pressure may either normalize or decrease. A wide variety of pharmacologic and nonpharmacologic techniques can be used safely and effectively with critically ill patients to achieve relaxation and/or sedation. Relaxation techniques are simple to use and can be particularly useful in situations involving brief procedures such as turning or minor dressing changes, and following coughing or endotracheal suctioning or other stressful events.

The pain experience of elderly patients has often been shadowed by myths and misperceptions. Some believe that older patients have less pain because their extensive life experiences have equipped them to cope with discomfort more effectively. This may be true for some individuals, to accept this generalization as truth for all elderly patients is short sighted. In fact, the incidence of and morbidity associated with pain is higher in the elderly than in the general population. Many elderly patients continue to experience chronic pain in addition to any acute pain associated with their critical illness or injury. Major sources of underlying pain in the elderly include low back pain, arthritis, headache, chest pain, and neuropathies.

Deep Breathing and Progressive Relaxation Guided deep breathing and progressive relaxation can be incorporated easily into a plan of care for the critically ill patient. Nurses can coach patients with deep breathing exercises by helping them to focus on and guide their breathing patterns. As patients begin to control their breathing, nurses

Assessment Elderly patients often report pain very differently from younger patients due to physiologic, psychological, and cultural changes accompanying age. Some patients may fear loss of control, loss of independence or being labeled as a “bad patient” if they report pain-related concerns. Also, for some patients the presence of pain may be symbolic of impending death, especially in the critical care setting. In such cases, a patient may be reticent to report his or her

172

CHAPTER 6. Pain, Sedation, and Neuromuscular Blockade Management

pain to a care provider or family member as if to deny pain is to deny death. For reasons such as these, it is important for nurses not only to assure patients about the nature of their pain and the importance of reporting any discomfort. Nurses may also use a variety of pain assessment strategies to incorporate behavioral or physiologic indicators of pain. Similar strategies are often needed to assess pain in persons who are cognitively impaired. Preliminary reports from ongoing work among nursing home patients suggest that many patients with moderate to severe cognitive impairment are able to report acute pain reliably at the time they are asked. For these patients, pain recall and integration of pain experience over time may be less reliable.

Interventions Critically ill elderly patients can benefit from any of the analgesic modalities discussed. Older patients can tolerate opioids well if the doses are individualized and the patient is monitored for effect. However, it is important to recognize that medication requirements may be reduced in some elderly patients due to age related renal insufficiency and the potential for decreased renal clearance of the drugs. In addition, they have a reduced muscle-to-body fat ratio which affects the way that opioids bind and activate in the body. Analgesic requirements are highly individualized and doses should be carefully titrated to achieve pain relief.

SEDATION The critical care environment can be uncomfortable and anxiety producing for patients. Once pain is addressed, anxiolysis may be appropriate to enhance comfort, decrease anxiety, reduce awareness of noxious stimuli, and induce sleep. In some cases the use of sedatives may be necessary to ensure tolerance of medical modalities, clinical stability, and to protect patients from inadvertent self-harm. While the treatment of anxiety is an important aspect of the care of patients who are critically ill, continuous use of sedatives as either an infusion or a bolus intravenous dosing method to induce a more depressed sensorium (ie, amnesia) in these patients is discouraged. The use of sedation infusions in mechanically ventilated patients has been associated with negative outcomes such as prolonged mechanical ventilation, increased lengths of stay, and even death. In an attempt to improve these outcomes, studies have focused on how best to minimize infusion use. Daily interruptions of sedation infusions have been associated with improved outcomes and do not appear to incur additional psychological stress. This finding is in direct opposition to the commonly held philosophy that amnesia protects the patient from the psychological stress induced by the critical care environment. Further, there is a strong association between sedation infusion use and delirium. Compounding the issue is the fact that those who develop delirium are then at risk for the development of long-term

cognitive dysfunction (more on delirium in the section below). Because of these studies and others that demonstrate the positive effect of less sedation use in critically ill ventilated patients, recent evidence-based guidelines published by the SCCM focus on the management of pain, agitation, and delirium in adult patients in the ICU. Guideline recommendations for the use of sedation in these ventilated patients are summarized below (additional recommendations on agitation and delirium are delineated in pertinent sections of this chapter). 1. Treatment of pain with analgesics is to be addressed first, as the presence of pain is anxiety producing and treating pain may negate the need for sedatives. 2. Sedatives may be necessary and, in some cases, lifesaving in some patient situations; however, traditional reasons for providing sedatives, especially at high doses and/or by continuous infusion, except when absolutely necessary, is not recommended. 3. Daily sedation interruptions or a light target level of sedation is recommended in mechanically ventilated adult ICU patients. 4. Use nonpharmacologic means of promoting sleep (eg, control light and noise, clustering nursing activities, decreasing stimuli at night). Traditional reasons for providing sedation, sedative agents, assessment methods, and other management strategies follow.

Reasons for Sedation Amnesia

The goal of attaining amnesia is appropriate in the case of procedures, surgery, and other invasive critical care interventions. However, when used to create amnesia in patients for extended lengths of time (> 24 hours), the patients may experience the negative outcomes described previously. Amnesia may not be an appropriate reason for prolonged sedation use, the absolute exception being when neuromuscular blockade (NMB) is required. When paralytics are necessary, it is essential that both comfort (with analgesics) and sedation are ensured. Ventilator Tolerance

Ineffective, dyssynchronous, and excessive respiratory effort results in increased work of breathing and increased oxygen consumption. The reason for the dyssynchronous breathing should be quickly assessed and managed. Efforts are made to improve tolerance by first treating potential pain and adjusting the ventilator to optimize patient-ventilator interaction. Sedative use in the form of infusions or frequent IV bolus dosing in severe cases of patient/ventilator dssynchrony may be necessary and in some cases lifesaving. (See Chapter 5, Airway and Ventilatory Management for more on patient/ventilator dyssynchrony and Chapter 20:

SEDATION 173

Advanced Respiratory Concepts: Modes of Ventilation, for more on specific characteristics of ventilator modes.) Anxiety and Fear

Anxiety and fear are symptoms that can be experienced by critically ill patients who are conscious. However, these symptoms are often difficult to assess in critically ill patients because many cannot adequately communicate their feelings secondary to the underlying condition, the presence of an artificial airway, or a reduced sensorium. When the patient can identify anxiety or fear, the treatment goals are clear. However, in the patient who cannot, the presence of behaviors and signs that are associated with anxiety and/or fear are often used as evidence and are the reason sedatives are provided. Manifestations of severe anxiety and/or fear include nonspecific signs of distress such as agitation, thrashing, diaphoresis, facial grimacing, blood pressure elevation, and increased heart rate. These nonspecific signs may also be indicative of pain or delirium. Thus, an in-depth evaluation of the source of the distress (eg, pain, delirium, etc) is essential if the patient is to be appropriately and adequately treated. Some studies have suggested the use of the GI tract (eg, oral and/or gastric tube) as vehicles for sedatives when needed to decrease anxiety. Because gastric absorption of drugs is different from when they are provided intravenously, the steady state may be more reliably attained with less profound changes in sensorium (ie, peaks and valleys). As noted, in some cases sedatives are essential. However, the use of sedatives by infusion and/or repeated IV bolus for more than 24 hours is discouraged; they should be discontinued as early as possible. Patient Safety and Agitation

Agitation includes any activity that appears unhelpful or potentially harmful to the patient. The patient may be aware of the activity and be able to communicate the reason for the activity; more commonly they are not aware, making it difficult to identify the reason for the agitation. The patient appears distressed and the associated activity includes episodic or continuous nonpurposeful movements in the bed, severe thrashing, attempts to remove tubes, efforts to get out of bed, or other behaviors which may threaten patient or staff safety. Reasons for agitation include pain and anxiety, delirium, preexisting conditions that require pharmacologic interventions (ie, preexisting psychiatric history), withdrawal from certain medications such as benzodiazepines (especially if they have been on them for a long time), and delirium tremens secondary to alcohol withdrawal (see Chapter 11: Multisystem Problems, section on alcohol withdrawal). Patients who experience inadequately controlled agitation face a high risk of morbidity and mortality. Thus, potential reasons for the agitation are explored so that appropriate therapy may be initiated. Sleep Deprivation

Sleep deprivation is common among critically ill patients. Although patients may appear restful, physiologically they

may never experience stages of sleep that ensure a “rested” state (ie, rapid eye movement sleep, stages 2, 3, and 4). These restorative stages of sleep are adversely affected by many factors, including a wide variety of medications. Sleep deprivation is also common among those with pain, discomfort, and anxiety. Additionally, sleep deprivation may be a result of the increased auditory, tactile, and visual stimuli ubiquitous to the critical care environment. The SCCM guidelines recommend the use of non-pharmacologic interventions when possible. In some patients pharmacologic sleep aides may be prescribed. Delirium

Delirium is said to be present in 50% to 80% of critically ill patients. Patients are especially at risk if they are elderly, have preexisting dementia, a history of hypertension, and high severity of illness at admission. Coma is an independent risk factor for the development of delirium. As noted earlier, the risk of long-term cognitive dysfunction is increased in patients who experience delirium. In the past, delirium was commonly associated with agitation. In fact, the agitated presentation of delirium accounts for less than 5% of those who experience the condition. The remainder presents with the hypoactive (calm, quiet) or mixed presentation of the condition. This hypoactive category is underdiagnosed and the associated outcomes are worse than for those with the agitated/active form of delirium. The hallmarks of the condition are disorientation and disorganized thinking. Awareness of the potential for delirium and early recognition are essential for effective management and prevention of undesirable outcomes. The SCCM guidelines recommend that routine assessment of delirium be done with the use of a valid and reliable delirium-monitoring tool such as the Confusion Assessment Method for the ICU (CAM-ICU) or the Intensive Care Delirium Screening Checklist (ICDSC). Sedative infusions (eg, benzodiazepines and others) are to be avoided. The pharmacologic options for treatment of delirium in the critical care setting are discussed later in this chapter under “Drugs for Delirium,” and in Chapter 7, Pharmacology. The Confusion Assessment Method for the ICU is discussed in Chapter 12: Neurologic System, Figure 12-2.

Drugs for Sedation After ensuring that the presence of pain is either ruled out or addressed with the appropriate administration of analgesics, sedatives may be selected based on patient-specific factors such as the level and duration of sedation required. Sedative category summaries follow and comprehensive descriptions of the drugs are found in Chapter 7: Pharmacology. Short-Term Sedatives

These sedatives have a rapid onset of action and a short duration of effect. •• Midazolam is a popular benzodiazepine that fits in this category. It can be administered intermittently in a bolus IV form or as a continuous infusion.

174

CHAPTER 6. Pain, Sedation, and Neuromuscular Blockade Management

Long-term infusions (> 24 hours) of midazolam are discouraged because the drug has an active metabolite that may accumulate in the presence of drugs, renal disease, liver disease, or old age. •• Propofol is an IV general anesthetic designed for use as a continuous infusion. This drug is often preferred for short-term sedation use (< 24 hours) and when a very rapid offset of effect is desired. An example is the patient requiring frequent neurologic assessments. Propofol is lipid based and serves as a source of calories. It should be used cautiously in those with high triglycerides and the drug is contraindicated in those with egg allergies. High doses of propofol should be cautiously used with other lipid formulas. Frequent changes of the containers and tubing are required to prevent potential growth of microorganisms. The current evidence-based guidelines recommend the use of propofol or dexmedetomidine (discussed below) over sedation with benzodiazepines (either midazolam or lorazepam) to improve outcomes in mechanically ventilated patients. •• Dexmedetomidine is an alpha-2 receptor agonist that has been approved only for very short-term use (< 24 hours) in the ICU setting. Two of the reasons the drug may be an attractive choice include the drug’s ability to either eliminate or decrease the need for other analgesic medications such as opioids, and the fact that it does not produce respiratory depression when used as designed (ie, boluses of the drug are not recommended). Further, patients on the drug are rapidly arousable and alert when stimulated. •• Ketamine is an IV general anesthetic that produces analgesia, anesthesia, and amnesia without loss of consciousness. It may be given in an IV bolus form, intranasally, or orally. Although contraindicated in those with elevated intracranial pressure, its bronchodilatory properties make it a good choice in those with asthma. A well-known side effect of ketamine is hallucinations; however, these may be prevented with concurrent use of benzodiazepines. It is rarely a first-line sedative of choice, but is commonly used in patients requiring painful, frequent skin debridement procedures (eg, burn patients). The nurse needs to be aware of hospital policy for use of this medication as some limit it to physician use only. Intermediate-Term Sedatives

These drugs have an intermediate onset of action and duration of effect. However, when given as infusions they may last much longer as they are lipophilic. •• Lorazepam is the most commonly used benzodiazepine in critical care and can be administered orally and IV as an intermittent bolus or continuous infusion. When given orally or in a bolus intermittent

form, the drug effect is intermediate; however, when used as a continuous infusion (> 24 hours), its effect is more long term (and it should be considered as such) because awakening may take hours to days to accomplish. Lorazepam may accumulate in those with decreased metabolic function such as the elderly or those with hepatic dysfunction; however, there is less risk overall because there is minimal active metabolite accumulation with the drug. Long-Acting Sedatives

•• Diazepam, a long acting benzodiazepine, and chlordiazepoxide are rarely used in critical care; however, they may be selected for treatment of severe alcohol withdrawal. They may be given orally or as an IV bolus.

Drugs for Delirium In the past, the most commonly used drug for the prevention and treatment of delirium in critical care units has been haloperidol. The drug has been popular in the past as it sedates without significant respiratory depression and is not associated with potential development of tolerance or dependence. It does, however, have potential adverse side effects that must be closely monitored. Extrapyramidal reactions such as dystonia and the potential for neuroleptic malignant syndrome are possible. Another is the effect of haloperidol on QTc intervals. QTc interval monitoring is essential and required when using the drug. While the drug is still being used to treat delirium in some critical care units, no evidence supports the use of haloperidol as a pharmacologic agent to reduce the duration of delirium. Some limited data does suggest that atypical antipsychotics may be useful; however, the SCCM guidelines do not recommend their use either. Instead, the guidelines suggest that with delirium unrelated to alcohol or benzodiazepine withdrawal, dexmedetomidine (described earlier) be used instead of benzodiazepine infusions to reduce the duration of delirium (see Chapter 7, Pharmacology for more on these classes of drugs).

Goals of Sedation, Monitoring, and Management The goal of sedation administration is important to identify in order to determine the appropriate approach and drug. If the reason is to decrease pain and increase comfort, the selection of an analgesic is indicated. If, however, pain has adequately been treated and the need for sedation is still present, a sedative and level of sedation may be determined; for example, in the patient who is anxious and unable to sleep, the goal is very different than if the patient is unstable, on a ventilator, and suffering from profound hypoxemia. Sedation scales have been developed in an effort to assist with the management of sedation and are helpful tools for the bedside clinician.

NEUROMUSCULAR BLOCKADE 175

Sedation Scales: Goals and Monitoring

Sedation scales allow the health-care team to select a level of sedation for the patient. Descriptors of each level of sedation are provided so that the sedative may be adjusted appropriately. Sedation monitoring is done at least hourly and the level of sedation achieved is recorded. Use of a valid and reliable sedation assessment scale is recommended (Table 6-6), rather than scales that are institutionally developed and lack proper testing. It is important for the interdisciplinary team to determine the level of sedation daily so the infusion rate can be adjusted accordingly; however, addressing sedation level only once a day may not be often enough. A concern related to the use of sedation scales is that they do not promote the aggressive withdrawal of the sedative drugs. This is important because the use of sedative infusions is linked to prolonged ventilator duration and ICU and hospital lengths of stay.

TABLE 6-6. SEDATION ASSESSMENT SCALES WITH VALIDITY AND RELIABILITY IN ADULT PATIENTS Sedation-Agitation Scalea 1 Unarousable (minimal or no response to noxious stimuli, does not communicate or follow commands) 2 Very sedated (arouses to physical stimuli but does not communicate or follow commands; may move spontaneously) 3 Sedated (difficult to arouse, awakens to verbal stimuli or gentle shaking but drifts off again, follows simple commands) 4 Calm and cooperative (calm, awakens easily, follows commands) 5 Agitated (anxious or mildly agitated, attempting to sit up, calms down to verbal instructions) 6 Very agitated (does not calm, despite frequent verbal reminding of limits; requires physical restraints, biting ET tube) 7 Dangerous agitation (pulling at ET tube, trying to remove catheter, climbing over bed rail, striking at staff, thrashing side to side)

Richmond Agitation-Sedation Scaleb – 5 Unresponsive (no response to voice or physical stimulation) – 4 Deep sedation (no response to voice, but any movement to physical stimulation) – 3 Moderate sedation (any movement, but no eye contact to voice) – 2 Light sedation (briefly, < 10 seconds, awakening with eye contact to voice) – 1 Drowsy (not fully alert, but has sustained, > 10 seconds, awakening with eye contact to voice) 0 Alert and calm

1 Restless (anxious or apprehensive but movements not aggressive or vigorous) 2 Agitated (frequent nonpurposeful movement or patientventilator dysynchrony) 3 Very agitated (pulls on or removes tubes or catheters or has aggressive behavior toward staff) 4 Combative (overly combative or violent; immediate danger to staff)

Data compiled from: aRiker et al (1994); bSessler, Gosnet M, Grap MJ (2002).

Sedation Management

Management of sedation is an essential step in attaining positive outcomes for critically ill patients. Patients may require sedatives for the treatment of mild anxiety while in the critical care unit. Treatment of such anxiety is appropriate and rarely results in adverse effects. Generally the sedatives are provided orally. The doses are adjusted to prevent excessive drowsiness or respiratory depression. Appropriately dosed, use of the sedatives does not interfere with clinical progress such as weaning or rehabilitation. (See Figure 6-7: Pocket guide summary for the treatment of pain, agitation and delirium.)

NEUROMUSCULAR BLOCKADE The use of NMB in the critical care unit is generally confined to those severe situations where aggressive management of analgesics and sedatives, in addition to ventilator parameter manipulations, are not enough to ensure patient ventilator synchrony and the patient’s safety. In these cases, the patient’s muscular movements contribute to hemodynamic and pulmonary instability. NMB may also be necessary, as previously noted, when protective lung strategies are employed in very critically ill patients. These strategies are used to manage ventilated patients with severe conditions such as ARDS, life threatening elevations in intracranial pressure, or acute severe asthma (ASA), and are referred to as “protective lung strategies.” The strategies for the patient with ASA include long expiratory times and low tidal volumes in an effort to reduce the potential for auto-PEEP and subsequent barotrauma. In the ARDS patient, low tidal volumes, long inspiratory times, and high PEEP levels may be necessary to prevent volu-trauma. The result of these strategies is often the development of hypercarbia and acidosis (called “permissive hypercarbia”), which are poorly tolerated by the alert patient thus commonly necessitating sedation and NMB (see Chapter 20, Advanced Respiratory Concepts: Modes of Ventilation). In these cases, the use of NMB agents may be lifesaving and are an important part of care. Unfortunately, NMB is associated with prolonged neuropathies and myopathies, especially when used in conjunction with steroids. In addition, the evaluation of neurologic status is difficult and may obviate the use of the agents. Thus, NMB agents should be used sparingly and only in the most severe situations as described.

Neuromuscular Blocking Agents The most common neuromuscular blocking agents used in critical care are the nondepolarizing agents (see Chapter 7, Pharmacology, for a comprehensive discussion of chemical paralytic agents). The agents block the transmission of nerve impulses by blocking cholinergic receptors; muscle paralysis results. The degree of blockade varies depending on the dose and the amount of receptor blockade. Examples of short, intermediate, and long-acting NMB agents follow. More

CHAPTER 6. Pain, Sedation, and Neuromuscular Blockade Management

• Agitation in critically ill patients may result from inadequately treated pain, anxiety, delirium, and/or ventilator dysynchrony. • Detection and treatment of pain, agitation, and delirium should be reassessed often in these patients. • Patients should be awake and able to purposely follow commands in order to participate in their care unless a clinical indication for deeper sedation exists.

PAIN

Statements and Recommendations • Pain assessment should be routinely performed in all lCU patients (1B). • Self report is preferred over the use of behavioral pain scales to assess pain in ICU patients who are able to communicate (B). • The BPS and CPOT are the most valid and reliable behavioral pain scales for use in ICU patients who cannot communicate (B). • Vital signs should not be used alone to assess pain, but they may be used adjunctively for pain assessments (2C). • Preemptively treat chest tube removal with either analgesics and/or non-pharmacologic therapy (1C). • Suggest preemptively treating other types of procedural pain with analgesic and/or non-pharmacologic therapy (2C). • Use opioids as first line therapy for treatment of non-neuropathic pain (1C). • Suggest using non-opioid analgesics in conjunction with opioids to reduce opioid requirements and opioid-related side effects (2C). • Use gabapentin or carbamazepine, in addition to intravenous opioids, for treatment of neuropathic pain (1A). • Use thoracic epidural for postoperative analgesia in abdominal aortic surgery patients (1B). • Suggest thoracic epidural analgesia be used for patients with traumatic rib fractures (2B).

AGITATION

Assess and Treat

• Depth and quality of sedation should be routinely assessed in all lCU patients (1B). • The RASS and SAS are the most valid and reliable scales for assessing quality and depth of sedation in ICU patients (B). • Suggest using objective measures of brain function to adjunctively monitor sedation in patients receiving neuromuscular blocking agents (2B). • Use EEG monitoring either to monitor non-convulsive seizure activity in ICU patients at risk for seizures, or to titrate electrosuppressive medication to achieve burst suppression in lCU patients with elevated intracranial pressure (1A). • Target the lightest possible level of sedation and/or use daily sedative interruption (1B). • Use sedation protocols and checklists to facilitate ICU sedation management (1B). • Suggest using analgesia-first sedation for intubated and mechanically ventilated lCU patients (2B). • Suggest using non-benzodiazepines for sedation (either propofol or dexmedetomidine) rather than benzodiazepines (either midazolam or lorazepam) in mechanically ventilated adult ICU patients (2B).

DELIRIUM

176

• Delirium assessment should be routinely performed in all lCU patients (1B). • The CAM-ICU and ICDSC delirium monitoring tools are the most valid and reliable scales to assess delirium in ICU patients (A). • Mobilize lCU patients early when feasible to reduce the incidence and duration of delirium, and to improve functional outcomes (1B). • Promote sleep in ICU patients by controlling light and noise, clustering patient care activities, and decreasing stimuli at night (1C). • Avoid using rivastigmine to reduce the duration of delirium in ICU patients (1B). • Suggest avoiding the use of antipsychotics in patients who are at risk for torsades de pointes (2B). • Suggest not using benzodiazepines in ICU patients with delirium unrelated to ETOH/benzodiazepine withdrawal (2B).

Figure 6-7. Pocket guide and summary of guideline recommendations for the management of pain, agitation and delirium. (From: Barr, Fraser, Puntillo et al, SCCM 2013.)

NEUROMUSCULAR BLOCKADE 177

Summary of PAD Guidelines

PAIN AND ANALGESIA

1. lCU patients routinely experience pain at rest and with ICU care (B). Pain in cardiac surgery patients, especially women, is poorly treated (B). Procedural pain is common in ICU patients (B). 2. Perform routine pain assessment in all patients (1B). In motor intact patients unable to self report, we suggest using behavioral pain scales rather than vital signs to assess pain (2C). The BPS and CPOT are the most valid and reliable behavioral pain scales (B). Vital signs should only be used as a cue for further pain assessment (2C). 3. For non-neuropathic pain, use intravenous opioids as first line analgesic therapy (1C); use non-opioid analgesics to reduce opioid side effects (1C); and use either gabapentin or carbamazepine in conjunction with intravenous opioids for neuropathic pain (1A). 4. Suggest preemptively treating procedural pain (2C), especially chest tube removal (1C). 5. Use thoracic epidural analgesia for abdominal aortic surgery (1B), and suggest also using for traumatic rib fractures (2B). No evidence guides the use of lumbar epidural analgesia for abdominal aneurysm surgery (0A), or thoracic epidural analgesia for either intrathoracic or nonvascular abdominal surgical procedures (0B). No evidence guides the use of regional vs. systemic analgesia in medical lCU patients (0).

AGITATION AND SEDATION

1. Maintaining lighter levels of sedation in ICU patients is associated with improved clinical outcomes (B); light levels of sedation should be maintained in these patients (1B). 2. The RASS and SAS scales are most valid and reliable instruments for assessing adequacy and depth of sedation (B). 3. Use brain function monitors only as adjuncts to subjective sedation scales in unparalyzed patients (1B), but suggest using brain function monitors to primarily monitor depth of sedation in patients receiving neuromuscular blocking agents (2B). 4. Use EEG monitoring to monitor non-convulsive seizure activity in lCU patients at risk for seizures, and to titrate burst suppression therapy in ICU patients with elevated intracranial pressure (1A). 5. Use daily sedative interruption or titrate sedative medications to maintain light levels of sedation (1B). Suggest using Analgesia-first sedation (2B). Suggest using non-benzodiazepines rather than benzodiazepine infusions for sedation (2B). Use sedation protocols and daily checklists to integrate and to facilitate management of pain, sedation, and delirium in ICU patients (1B). 1. Delirium is associated with increased mortality (A), prolonged ICU and hospital LOS (A), and post-ICU cognitive impairment (B).

DELIRIUM

2. Delirium risk factors include: pre-existing dementia, HTN, history of alcoholism, and a high severity of illness at baseline (B); coma (B); and benzodiazepine use (B). Mechanically ventilated ICU patients at risk for delirium have a lower delirium prevalence when treated with dexmedetomidine rather than with benzodiazepines (B). 3. Routinely monitor ICU patients for delirium (1B). The CAM-ICU and ICDSC are the most valid and reliable instruments for this purpose (A). 4. Pursue early mobilization to reduce the incidence and duration of delirium (1B). 5. Suggest not using either haloperidol or atypical antipsychotics prophylactically to prevent delirium (2C). 6. Promote sleep in adult ICU patients by optimizing patients’ environments, using strategies to control light and noise, to cluster patient care activities, and to decrease stimuli at night in order to protect patients’ sleep cycles (1C). 7. Do not use rivastigmine to reduce the duration of delirium in ICU patients (1C). 8. Suggest withholding antipsychotics in patients with baseline QT prolongation, a history of torsades de pointes, or in those receiving concomitant medications known to prolong the QT interval (2C). 9. When sedation is required in delirious ICU patients, suggest using dexmedetomidine rather than benzodiazepine infusions for sedation in these patients, unless delirium is related to either alcohol or benzodiazepine withdrawal (2B). Figure 6-7. (Continued ) BPS = Behavioral Pain Scale; CPOT = Critical-Care Pain Observation Tool; RASS = Richmond Agitation and Sedation Scale; SAS = Sedation-Agitation Scale; EEG = electroencephalography; CAM-ICU = Confusion Assessment Method for the ICU; ICDSC = ICU Delirium Screening Checklist; ETOH = ethanol; LOS = length of stay; HTN = hypertension.

178

CHAPTER 6. Pain, Sedation, and Neuromuscular Blockade Management

extensive descriptions of the drugs are found in Chapter 7, Pharmacology.

How these aspects of care and others are managed is essential to ensuring good outcomes.

Short-Acting NMB

Peripheral Nerve Stimulation

Mivacurium is rapid acting and has a short duration of action (15 minutes). It may be given as an IV bolus initially but then is provided by infusion. Mivacurium is metabolized by pseudocholinesterase. Intermediate-Acting NMB

These agents may be administered via an IV bolus, at least initially (ie, intubation), but then are provided by infusion because they are rapidly metabolized (20 to 50 minutes). Vecuronium, a steroidal-like agent, is metabolized by the liver and excreted renally. The combination of steroids and vecuronium may contribute to myopathies. Atracurium (and cis-atracurium) are metabolized in the plasma by Hofmann elimination. There is minimal to no histamine release with the drug. Long-Acting NMB

Pancuronium also has a steroidal-like molecular structure. It is generally given by intermittent IV bolus. Although labor intensive (the bolus is often required hourly), the intermittent dosing does allow for frequent reassessment. Pancuronium is vagolytic and can cause tachycardia; it may be contraindicated in patients with cardiovascular disease. Pancuronium is metabolized by the liver and is renally excreted.

Monitoring and Management Monitoring NMB is accomplished with the use of a peripheral nerve stimulator (PNS) or by monitoring airway pressure waveforms. The goal is to provide the least amount of the drug so that recovery is rapid when the drug is discontinued.

Peripheral nerve stimulators are devices that deliver a series of electrical stimuli via electrodes to nerves under the skin (Figure 6-8). The electrical stimuli cause muscular contractions if the neuromuscular junction is functioning properly. Typically, peripheral nerve stimulation is performed on the ulnar nerve at the wrist, with the temple area of the head as another potential site for nerve stimulation. When electrical stimuli are applied to the ulnar nerve, the thumb abducts and the fingers flex if the neuromuscular junction is intact. The stimulator technique most commonly used to assess NMB is the train of four. With this technique, four small electrical stimuli are given every half second. The degree of NMB can be assessed by observing or palpating the number of muscle twitches elicited during the series of four electrical stimuli (see Figure 6-8). When no NMB is present, four twitches of similar intensity, or height, are noted. Following the administration of a nondepolarizing neuromuscular blocking agent, many of the neuromuscular junctions are blocked. This produces minimal response to the four delivered stimuli. As the level of NMB decreases over time, the number of twitches observed increases until four strong, equal twitches are observed, indicating that no NMB is present. The degree of NMB is approximately 90% when one small twitch is palpated, 80% with two small twitches, and about 75% with three small twitches. Typically, in critical care patients, a moderate blockade level of 75% to 80% is usually sufficient to achieve respiratory muscle relaxation and improved gas exchange. The presence of two or three twitches in response to the train-of-four stimulation indicates

Peripheral nerve stimulator 1.5 seconds

Stimulation A

1.5 seconds

Stimulation B

Response

1.5 seconds

Stimulation

Response

Figure 6-8. (A) PNS and graphic display of a train-of-four pattern for: (B) no NMB, (C) moderate block (80%), and (D) complete block.

SELECTED BIBLIOGRAPHY 179

25 20 15 10 5 0

Figure 6-9. Example of spontaneous effort on assist-control volume ventilation. Note negative deflection prior to volume breath indicating inadequate level of NMB. (Courtesy of: Suzanne M. Burns).

a reasonable level of NMB for most critically ill patients. At this level of blockade, stimulation of the nerve does not result in excessive muscular contraction but saturation (100% block) has not occurred. Although the PNS is helpful in the short term, it may be less reliable in patients requiring NMB for days. This is especially true when anasarca is present because the increase in edema decreases stimulus transmission. It is important to remember that the technique is somewhat uncomfortable and frequent assessments using the PNS should be avoided if possible. Airway Pressure Monitoring

Most ventilators today provide respiratory waveform graphic displays. The simplest of the waveforms, airway pressure, may be used to monitor patient-generated respiratory activity (Figure 6-9); for example, regardless of the mode of ventilation, if chemical paralysis is adequate, there is an absence of spontaneous respiratory effort. If a spontaneous effort is noted on the waveform (a negative deflection), the NMB agents are increased. The airway pressure monitoring technique is especially helpful when initiating NMB and to assess withdrawal of the drug. Management

Patients who are paralyzed may still experience pain, anxiety, and fear. To that end, it is essential that patients receiving NMB agents are provided with analgesics and sedatives. With virtually no exceptions, sedation and analgesia should be used in combination for those receiving NMB agents. Amnesia is a desired outcome; no patient should experience a “trapped in body” state. In addition, because patients are unable to move or breathe on their own, the nurse must be extremely vigilant about situations that potentially may affect the patient’s safety (ventilator disconnect, harm from external forces). Physical care interventions are extremely important as well, and include the use of eye lubricants, frequent turning, and the use of prophylactic agents such as heparin to prevent deep vein thrombosis. Because the patient cannot communicate yet may hear, it is important to verbally reassure the patient

and provide frequent explanations about what is happening throughout the course of the day and night. Determining whether NMB agents need to be continued may be very difficult. One practical method is to stop the infusions of NMB agents daily to assess the need for continuation. Then, if signs of intolerance such as rapid oxygen desaturation occur with the intervention, the narcotics and sedatives may be increased first. Tolerance of sedatives and analgesics is common and to be expected; increasing doses of the drugs may be necessary. If intolerance is still noted, the NMB agents may be resumed. Another method, using depth-of-anesthesia monitoring systems such as bispectral index (BIS) monitoring, is increasingly being used in critical care units to monitor the depth of sedation while concomitantly administering neuromuscular blocking agents. The BIS monitor provides a number, which ranges from 0 to 100. A BIS value of 0 equals complete electroencephalogram (EEG) silence while a number near 100 is indicative of a fully awake state. The manufacturer recommends a level between 40 and 60 if general anesthesia is desired. To date it is unclear if this index range is an appropriate target in critical patients requiring sedatives and neuromuscular blocking agents for long periods of time. Regardless of the method used to monitor, it is clear that the goal should be to use neuromuscular blocking agents for as short a time as possible. The decision to use them in the first place should be carefully made.

SELECTED BIBLIOGRAPHY Pain Management American Pain Society. Principles of Analgesic Use in the Treatment of Acute Pain and Cancer Pain. 6th ed. Glenview, IL: American Pain Society; 2008. American Society of Pain Management Nursing. Core Curriculum for Pain Management Nursing. Dubuque IA: Hunt Publishing; 2009. Barr J, Fraser G, Puntillo K, et al. Clinical practice guidelines for the management of pain, agitation, and delirium in adult patients in the intensive care unit. Crit Care Med. 2013;41(1):263-306.

180

CHAPTER 6. Pain, Sedation, and Neuromuscular Blockade Management

Barthelmey O, Limbourg T, Collet J, et al. Impact of non-steroidal anti-inflammatory drugs (NSAIDs) on cardiovascular outcomes in patients with stable atherothrombosis or multiple risk factors. Int J of Cardiol. June 28, 2011. Bavry A, Khaliq A, Gong Y, et al. Harmful effects of NSAIDs among patients with hypertension and coronary artery disease. Am J Med. 2011;124:614-620. Bennett JS, Daugherty A, Herrington D, et al. The use of non-steroidal anti-inflammatory drugs (NSAIDs): a science advisory from the American Heart Association. Circulation. 2005;111(13): 1713-1716. Berry P, Covington E, Dahl J, Katz J, and Miaskowski C. Pain: current understanding of assessment, management, and treatments. Reston VA: National Pharmaceutical Council, Inc., and the Joint Commission on Accreditation of Healthcare Organizations. 2006. Carr DB, Jacox AK, Chapman CR, et al, eds. Acute pain management. In: Research TAfHCpa. Rockville, MD: Department of Health and Human Services, Public Health Service; 1995. D’Arcy Y. A Compact Clinical Guide to Acute Pain Management. New York, NY: Springer Publishing, 2011. Doyle C, Lennox L, Bell D. A systematic review of evidence on the links between patient experiences and clinical safety and effectiveness. January 2013. Available at http://bmjopen.bmj.com/ content/3/1/e001570.full Faucett J. Care of the critically ill patient in pain: the importance of nursing. In: Puntillo KA, ed. Pain in the Critically Ill. Gaithersburg, MD: Aspen; 1991. Fine P and Portenoy R. A Clinical Guide to Opioid Analgesia. New York, NY: Vendome Group LLC. 2007. Gardner DL. Presence. In: Bulechek GM, McCloskey JC, eds. Nursing Interventions: Essential Nursing Treatments. Philadelphia, PA: WB Saunders; 1992:316-324. Gordon DB, Dahl J, Phillips P, et al. The use of “as-needed” range orders for opioid analgesics in the management of acute pain: a consensus statement of the American Society for Pain Management Nursing and the American Pain Society. Pain Manage Nurs. 2004;5:53-58. Julius D, Basbaum AI. Molecular mechanisms of nociception. Nature. 2001;413:203-210. Khatta M. A complementary approach to pain management. Topics in Advanced Practice Nursing e-Journal. 2007. Available at www. medscape.com. Marmo L and D’Arcy Y. A Compact Clinical Guide to Critical Care, ER, and Trauma Pain Management. New York NY: Springer Publishing, 2013. Maxam-Moore VA, Wilkie DJ, Woods SL. Analgesics for cardiac surgery patients in critical care: describing current practice. Am J Crit Care. 1994;3:31-39. Melton S and Liu S. Regional anesthesia techniques in Fishman S, Ballantyne J, and Rathmell J, eds. Bonica’s Management of Pain. 5th ed. Philadelphia, PA: Lippincott Wiliams and Wilkins; 2010:92-106. Morrison RS, Ahronheim JC, Morrison GR, et al. Pain and discomfort associated with common hospital procedures and experiences. J Pain Symptom Manage. 1998;15:91-101. Pasternak GW. Molecular biology of opioid analgesia. J Pain Symp Manage. 2005;29(5S):S2-S9. Pettigrew J. Intensive nursing care: the ministry of presence. Crit Care Nurs Clin North Am. 1990;2(3):503-508.

Puntillo K. Advances in management of acute pain: great strides or tiny footsteps? Capsules comments. Crit Care Nurs. 1995;3:97-100. Puntillo K. Pain experience in intensive care patients. Heart Lung. 1990;19:526-533. Puntillo K, Weiss SJ. Pain: its mediators and associated morbidity in critically ill cardiovascular surgical patients. Nurs Res. 1994;43:31-36. Puntillo KA, Morris AB, Thompson CL, et al. Pain behaviors observed during six common procedures: results from Thunder Project II. Crit Care Med. 2004;32(2):421-427. Puntillo KA, White C, Morris AB, et al. Patients’ perceptions and responses to procedural pain: results from Thunder Project II. Am J Crit Care. 2001;10(4):238-251. Puntillo KA, Wild LR, Morris AB, et al. Practices and predictors of analgesic interventions for adults undergoing painful procedures. Am J Crit Care. 2002;11(5):415-429. Puntillo KA, Wilke DJ. Assessment of pain in the critically ill. In: Puntillo KA, ed. Pain in the Critically Ill. Gaithersburg, MD: Aspen; 1991:45-64. Richman J, Liu S, Courpas C, et al. Does peripheral nerve block provide superior pain control to opioids? A metanalysis. Anesthesia & Analgesia. 2006;102(1):248-257. Rose L, Smith O, Gelinas C, et al. Critical care nurses’ pain assessment and management practices: a survey in Canada. Am J Crit Care. 2012;21(4):151-259. Schulz-Stübner S, Boezaart A, Hata JS. Regional analgesia in the critically ill. Crit Care Med. 2005;33:1400-1407. Stanik-Hutt JA, Soeken KL, Belcher AE, Fontaine DK, Gift AG. Pain experiences of traumatically injured patients in a critical care setting. Am J Crit Care. 2001;10:252-259. Summer G, Puntillo K. Management of surgical and procedural pain in the critical care setting. Crit Care Clin North Am. 2001;13:233-242. Sun X, Weissman C. The use of analgesics and sedatives in critically ill patients: physicians’ orders versus medications administered. Heart Lung. 1994;23:169-176. Thompson C, White C, Wild L, et al. Translating research into practice. Crit Care Nurs Clin North Am. 2001;13:541-546. Tittle M, McMillan SC. Pain and pain-related side effects in an ICU and on a surgical unit: nurses’ management. Am J Crit Care. 1994;3:25-39. Wong DL, Baker CM. Pain in children: comparison of assessment scales. Pediatr Nurs. 1988;14(1):9-17. Wu CL, Cohen SR, Richman JM, et al. Efficacy of postoperative patient-controlled and continuous infusion epidural analgesia versus intravenous patient-controlled analgesia with opioids: a meta-analysis. Anesthesiology. 2005;103:1079-1088.

Sedation and Neuromuscular Blockade Bisp ectral index: http://w w w.covidien.com/rms/pages. aspx?page=OurBrands/BIS. Accessed June 2, 2013. Brook AD, Ahrens TS, Schaff R, et al. Effect of a nursing- implemented sedation protocol on the duration of mechanical ventilation. Crit Care Med. 1999;27:2609-2615. Ely W, Truman B, Shintani A, et al. Monitoring sedation status over time in ICU patients: reliability and validity of the Richmond Agitation-Sedation Scale (RASS). JAMA. 2003;22(289):2983-2991. Frenzel D, Greim C, Sommer C, Bauerle K, Roewer N. Is the bispectral index appropriate for monitoring the sedation level

of mechanically ventilated surgical ICU patients? Intensive Care Med. 2002;28:178-183. Girard TD, Pandharipande PP, Ely EW. Review: delirium in the intensive care unit. Crit Care. 2008;12(suppl 3):1-9. Kress JP, Gehlbach B, Lacy M, et al. The long-term psychological effects of daily sedative interruption on critically ill patients. Am J Respir Crit Care Med. 2003;168:1457-1461. Kress JP, Pohlman A, O’Connor MF, Hall JB. Daily interruption of sedative infusions in critically ill patients undergoing mechanical ventilation. N Engl J Med. 2000;342:1471-1477. Kress JP, Pohlman AS, Hall JB. Sedation and analgesia in the Intensive Care Unit. Am J Respir Crit Care Med. 2002;166:1024-1028. Riker R, Picard J, Fraser G. Prospective evaluation of the SedationAgitation Scale for adult critically ill patients. Crit Care Med. 1999; 27:1325-1329. Riker RR, Shehabi Y, Bokesch PM, Ceraso D, Wisemandle W. Dexmedetomidine vs midazolam for sedation of critically ill patients: a randomized trial. JAMA. 2009;301:489-499. Sessler C, Gosnet M, Grap MJ. The Richmond agitation-sedation scale: validity and reliability in adult intensive care unit patients. Am J Respir Crit Care Med. 2002;166:1338-1344.

Evidence-Based Practice Guidelines American Geriatric Society (AGS). The pharmacological management of persistent pain in older persons. J Am Geriatr Soc. 2009;57:1331-1346.

SELECTED BIBLIOGRAPHY 181

American Psychiatric Association. Practice guideline for the treatment of patients with delirium. Am J Psychiatry. 1999;156:1-20. American Society of Anesthesiologists Taskforce on Acute Pain Management. Practice guidelines for acute pain management in the perioperative setting. Anesthesiology. 2004;100(6): 1573-1581. Barr J, Fraser G, Puntillo K, et al. Clinical practice guidelines for the management of pain, agitation, and delirium in adult patients in the intensive care unit. Crit Care Med. 2013;41(1):263-306. Burns SM. Practice protocol: respiratory waveform monitoring. In: Non-invasive Monitoring. 2nd ed. Boston, MA: Jones and Bartlett Publishers; 2006. Burns SM, ed. AACN Protocols for Practice Series. Herr K, Coyne P, Kry T, et al. Pain assessment in the nonverbal patient: position statement with clinical practice recommendations. Pain Manage Nurs. 2006;7(2):44-52. Medina J, Puntillo K, eds. AACN’s Protocols for Practice: Palliative Care and End-of-Life Issues in Critical Care. Sudbury, MA: Jones and Bartlett Publishers; 2006. Society of Critical Care Medicine, American Society of Health- System Pharmacists. Clinical practice guidelines for sustained neuromuscular blockade in the adult critically ill patient. Crit Care Med. 2002;30(1):142-156. Woods S. Spiritual and complementary therapies to promote healing and reduce stress. In: Molter NC, ed. AACN’s Protocols for Practice: Creating Healing Environments. 2nd ed. Sudbury, MA: Jones and Bartlett Publishers; 2007.

This page intentionally left blank

Pharmacology Earnest Alexander

KNOWLEDGE COMPETENCIES 1. Discuss advantages and disadvantages of various routes for medication delivery in critically ill patients.

Critically ill adult patients often receive multiple medications during their admissions to an intensive care unit. These patients may be at risk for increased adverse effects from their medications because of altered metabolism and elimination that is commonly seen in the critically ill patient. Organ dysfunction or drug interactions may produce increased serum drug or active metabolite concentrations, resulting in enhanced or adverse pharmacologic effects. Therefore, it is important to be familiar with each patient’s medications, including the drug’s metabolic profile, drug interactions, and adverse effect profile. This chapter reviews medications commonly used in intensive care units and discusses mechanisms of action, indications for use, common adverse effects, contraindications, and usual doses. A summary of intravenous (IV) medication information is provided in Chapter 23, Pharmacology Tables.

MEDICATION SAFETY In the care of the critically ill, the medication use process is particularly complex. Each step in the process is fraught with the potential for breakdowns in medication safety (ie, adverse drug events [ADEs], medication errors). Improvement in medication safety requires interdisciplinary focus and attention. The Institute for Safe Medication Practices (ISMP) has highlighted the following key elements which must be optimized in order to maintain patient safety in the medication use process:

2. Identify indications for use, mechanism of action, administration guidelines, side effects, and contraindications for drugs commonly administered in critical illness.

•• Patient information: Having essential patient information at the time of medication prescribing, dispensing, and administration will result in a significant decrease in preventable ADEs. •• Drug information: Providing accurate and usable drug information to all health-care practitioners involved in the medication-use process reduces the amount of preventable ADEs. •• Communication of drug information: Miscommunication between physicians, pharmacists, and nurses is a common cause of medication errors. To minimize medication errors caused by miscommunication, it is important to always verify drug information and eliminate communication barriers. •• Drug labeling, packaging, and nomenclature: Drug names that look alike or sound alike, as well as products that have confusing drug labeling and nondistinct drug packaging significantly contribute to medication errors. The incidence of medication errors is reduced with the use of proper labeling and the use of unit dose systems within hospitals. •• Drug storage, stock, standardization, and distribution: Standardizing drug administration times, drug concentrations, and limiting the dose concentration of drugs available in patient care areas will reduce the risk of medication errors or minimize their consequences should an error occur. 183

184

CHAPTER 7. Pharmacology

•• Drug device acquisition, use, and monitoring: Appropriate safety assessment of drug delivery devices should be made both prior to their purchase and during their use. Also, a system of independent double checks should be used within the institution to prevent device-related errors such as, selecting the wrong drug or drug concentration, setting the rate improperly, or mixing the infusion line up with another. •• Environmental factors: Having a well-designed system offers the best chance of preventing errors; however, sometimes the ICU environment may contribute to medication errors. Environmental factors that can often contribute to medications errors include poor lighting, noise, interruptions, and a significant workload. •• Staff competency and education: Staff education should focus on priority topics, such as new medications being used in the hospital, high-alert medications, medication errors that have occurred both internally and externally, protocols, policies, and procedures related to medication use. Staff education can be an important error-prevention strategy when combined with the other key elements for medication safety. •• Patient education: Patients must receive ongoing education from physicians, pharmacists, and the nursing staff about the brand and generic names of medications they are receiving, their indications, usual and actual doses, expected and possible adverse effects, drug or food interactions, and how to protect themselves from errors. Patients can play a vital role in preventing medication errors when they are encouraged to ask questions and seek answers about their medications before drugs are dispensed at a pharmacy or administered in a hospital. •• Quality processes and risk management: The way to prevent errors is to redesign the systems and processes that lead to errors rather than focus on correcting the individuals who make errors. Effective strategies for reducing errors include making it difficult for staff to make an error and promoting the detection and correction of errors before they reach a patient and cause harm.

MEDICATION ADMINISTRATION METHODS Intravenous Intravenous (IV) administration is the preferred route for medications in critically ill patients because it permits complete and reliable delivery. Depending on the indication and the therapy, medications may be administered by IV push, intermittent infusion, or continuous infusion. Typically, IV push refers to administration of a drug over 3 to 5 minutes; intermittent infusion refers to 15-minute to 2-hour drug administration several times per day, and continuous infusion administration occurs over a prolonged period of time.

Intramuscular or Subcutaneous Intramuscular (IM) or subcutaneous (SC) administration of medications should rarely be used in critically ill patients. This is due to a number of factors including delayed onset of action, unreliable absorption because of decreased peripheral perfusion (particularly in patients who are hypotensive or hypovolemic), or inadequate muscle or decreased SC fat tissue. Furthermore, SC/IM administration may result in incomplete, unpredictable, or erratic drug absorption. If medication is not absorbed from the injection site, a depot of medication can develop. If this occurs, once perfusion is restored, absorption can potentially lead to supratherapeutic or toxic effects. Additionally, patients with thrombocytopenia or who are receiving thrombolytic agents or anticoagulants may develop hematomas and bleeding complications due to SC or IM administration. Finally, administering frequent IM injections may also be inconvenient and painful for patients.

Oral Oral (PO) administration of medication in the critically ill patient can also result in incomplete, unpredictable, or erratic absorption. This may be caused by a number of factors including the presence of an ileus impairing drug absorption, or to diarrhea decreasing gastrointestinal (GI) tract transit time and time for drug absorption. Diarrhea may have a pronounced effect on the absorption of sustainedrelease preparations such as theophylline, procainamide, or calcium channel–blocking agents, resulting in a suboptimal serum drug concentration or clinical response. Several medications such as fluconazole and the fluoroquinolones have been shown to exhibit excellent bioavailability when orally administered to critically ill patients. The availability of an oral suspension for some of these agents makes oral administration a reliable and cost-effective alternative for patients with limited IV access. In patients unable to swallow, tablets are often crushed and capsules opened for administration through nasogastric or orogastric tubes. This practice is time consuming and can result in blockage of the tube, necessitating removal of the clogged tube and insertion of a new tube. If enteral nutrition is being administered through the tube, it often has to be stopped for medication administration, resulting in inadequate nutrition for patients. Also, several medications (eg, phenytoin, carbamazepine, and warfarin) have been shown to compete, or interact, with enteral nutrition solutions. This interaction results in decreased absorption of these agents, or complex formation with the nutrition solution leading to precipitation and clogging of the feeding tube. Liquid medications may circumvent the need to crush tablets or open capsules, but have their own limitations. An example is ciprofloxacin (Cipro) oral solution which is an oil-based preparation that should not be given via feeding tube because of the high probability of clogs. Many liquid dosage forms contain sorbitol as a flavoring agent or as the

CENTRAL NERVOUS SYSTEM PHARMACOLOGY 185

primary delivery vehicle. Sorbitol’s hyperosmolarity is a frequent cause of diarrhea in critically ill patients, especially in patients receiving enteral nutrition. Potassium chloride elixir is extremely hyperosmolar and requires dilution with 120 to 160 mL of water before administration. Administering undiluted potassium chloride elixir can result in osmotic diarrhea. Lastly, sustained-release or enteric-coated preparations are difficult to administer to critically ill patients. When sustained-release products are crushed, the patient absorbs the entire dose immediately as opposed to gradually over a period of 6, 8, 12, or 24 hours. This results in supratherapeutic or potentially toxic effects soon after the administration of the medication, with subtherapeutic effects at the end of the dosing interval. Sustained-release preparations must be converted to equivalent daily doses of immediate-release dosing forms and administered at more frequent dosing intervals. Enteric-coated dosage forms that are crushed may be inactivated by gastric juices or may cause stomach irritation. Enteric-coated tablets are specifically formulated to pass through the stomach intact so that they can enter the small intestine before they begin to dissolve.

Sublingual Because of the high degree of vascularity of the sublingual mucosa, sublingual administration of medication often produces serum concentrations of medication that parallel IV administration, and an onset of action that is often faster than orally administered medications. Traditionally, nitroglycerin has been one of the few medications administered sublingually (SL) to critically ill patients. Several oral and IV medications, however, have been shown to produce therapeutic effects after sublingual administration. Captopril has been shown to reliably and predictably lower blood pressure in patients with hypertensive urgency. Oral lorazepam tablets have been administered SL to treat patients in status epilepticus; preparations of oral triazolam and IV midazolam have been shown to produce sedation after sublingual administration.

Intranasal Intranasal administration is a way to effectively administer sedative and analgesic agents. The high degree of vascularity of the nasal mucosa results in rapid and complete absorption of medication. Agents that have been administered successfully intranasally include meperidine, fentanyl, sufentanil, butorphanol, ketamine, and midazolam.

Transdermal Transdermal administration of medication is of limited value in critically ill patients. Although nitroglycerin ointment is extremely effective as a temporizing measure before IV access is established in the acute management of patients with angina, heart failure (HF), pulmonary edema, or hypertension, nitroglycerin transdermal patches are of limited

benefit. Transdermal patches are limited by their slow onset of activity and their inability for dose titration. Also, patients with decreased peripheral perfusion may not sufficiently absorb transdermally administered medications to produce the desired therapeutic effect. Transdermal preparations of clonidine, nitroglycerin, or fentanyl may be beneficial in patients who have been stabilized on IV or oral doses, but require chronic administration of these agents. Chronic use of nitroglycerin transdermal patches is further complicated by the development of tolerance. However, the development of tolerance can be avoided by removing the patch at bedtime, allowing for an 8- to 10-hour “nitrate-free” period. A eutectic mixture of local anesthetic (EMLA) is a combination of lidocaine and prilocaine. This local anesthetic mixture can be used to anesthetize the skin before insertion of IV catheters or the injection of local anesthetics that may be required to produce deeper levels of topical anesthesia. Although transdermal administration of medications is an infrequent method of drug administration in critically ill patients, its use should not be overlooked as a potential cause of adverse effects in this patient population. Extensive application to burned, abraded, or denuded skin can result in significant systemic absorption of topically applied medications. Excessive use of viscous lidocaine products or mouthwashes containing lidocaine to provide local anesthesia for mucositis or esophagitis also can result in significant systemic absorption of lidocaine. Lidocaine administered topically to the oral mucosa has resulted in serum concentrations capable of producing seizures. The diffuse application of topical glucocorticosteroid preparations also can lead to absorption capable of producing adrenal suppression. This is especially true with the high-potency fluorinated steroid preparations such as betamethasone dipropionate, clobetasol propionate, desoximetasone, or fluocinonide.

CENTRAL NERVOUS SYSTEM PHARMACOLOGY Sedatives Sedatives can be divided into four main categories: benzodiazepines, barbiturates, neuroleptics, and miscellaneous agents. Benzodiazepines are the most commonly used sedatives in critically ill patients. Neuroleptics typically are used in patients who manifest a psychological or behavioral component to their sedative needs, and barbiturates are reserved for patients with head injuries and increased intracranial pressure. Propofol is a short-acting IV general anesthetic that is approved for use as a sedative for mechanically ventilated, critically ill patients. Dosing of sedatives should be guided by frequent assessment of the level of sedation with a valid and reliable sedation assessment scale (see Chapter 6, Pain, Sedation, and Neuromuscular Blockade Management). Benzodiazepines

Benzodiazepines are the most frequently used agents for sedation in critically ill patients. These agents provide sedation,

186

CHAPTER 7. Pharmacology

decrease anxiety, have anticonvulsant properties, possess indirect muscle-relaxant properties, and induce anterograde amnesia. Benzodiazepines bind to gamma-aminobutyric acid (GABA) receptors located in the central nervous system, modulating this inhibitory neurotransmitter. These agents have a wide margin of safety as well as flexibility in their routes of administration. Benzodiazepines are frequently used to provide shortterm sedation and amnesia during imaging procedures, other diagnostic procedures, and invasive procedures such as central venous catheter placement or bronchoscopy. A common long-term indication for using benzodiazepines is sedation and amnesia during mechanical ventilation. Excessive sedation and confusion can occur with initial doses, but these effects diminish as tolerance develops during therapy. Elderly and pediatric patients may exhibit a paradoxical effect manifested as irritability, agitation, hostility, hallucinations, and anxiety. Respiratory depression may be seen in patients receiving concurrent narcotics, as well as in elderly patients and patients with chronic obstructive pulmonary disease (COPD) or obstructive sleep apnea (OSA). Benzodiazepines have also been associated with the development of ICU delirium, which has been linked with worse clinical outcomes. Monitoring Parameters •• Mental status, level of consciousness, respiratory rate, and level of comfort should be monitored in any patient receiving a benzodiazepine. Signs and symptoms of withdrawal reactions should be monitored for patients receiving short-acting agents (ie, midazolam). Midazolam

Midazolam is a short-acting, water-soluble benzodiazepine that may be administered IV, IM, SL, PO, intranasally, or rectally. Clearance of midazolam has been shown to be extremely variable in critically ill patients. The elimination half-life can be increased by as much as 6 to 12 hours in patients with liver disease, shock, or concurrently receiving enzyme inhibiting drugs such as erythromycin or fluconazole and hypoalbuminemia. Midazolam’s two primary metabolites, 1-hydroxymidazolam and 1-hydroxymidazolam glucuronide, have been shown to accumulate in critically ill patients, especially those with renal dysfunction, contributing additional pharmacologic effects. Geriatric patients demonstrate prolonged half-lives secondary to age-related reduction in liver function. Dose •• IV bolus: 0.025 to 0.05 mg/kg •• Continuous infusion: 0.5 to 5 mcg/kg/min Lorazepam

Lorazepam is an intermediate-acting benzodiazepine that offers the advantage of not having its metabolism affected by impaired hepatic function, age, or interacting drugs.

Glucuronidation in the liver is the route of elimination of lorazepam. Because lorazepam is relatively water insoluble, it must be diluted in propylene glycol, and it is propylene glycol that is responsible for the hypotension that may be seen after bolus IV administration. Large volumes of fluid are required to maintain the drug in solution, so that only 20 to 40 mg can be safely dissolved in 250 mL of dextrose-5%-water (D5W). In-line filters are recommended when administering lorazepam by continuous infusion because of the potential for the drug to precipitate. Finally, lorazepam’s long elimination half-life of 10 to 20 hours limits its dosing flexibility by continuous infusion. Patients requiring high-dose infusions may be at risk for developing propylene glycol toxicity, which is manifested as a hyperosmolar state with a metabolic acidosis. Dose •• IV bolus: 0.5 to 2 mg q1-4h •• Continuous infusion: 0.06 to 0.1 mg/kg/h Diazepam

Diazepam is a long-acting benzodiazepine with a faster onset of action than lorazepam or midazolam. Although its duration of action is 1 to 2 hours after a single dose, it displays cumulative effects because its active metabolites contribute to its pharmacologic effect. Desmethyldiazepam has a halflife of approximately 150 to 200 hours, so it accumulates slowly and then is slowly eliminated from the body after diazepam is discontinued. Diazepam metabolism is reduced in patients with hepatic failure and in patients receiving drugs that inhibit hepatic microsomal enzymes. Diazepam may be used for one or two doses as a periprocedure anxiolytic and amnestic, but should not be used for routine sedation of mechanically ventilated patients. Dose •• IV bolus: 2.5 to 10 mg q2-4h •• Continuous infusion: Not recommended Benzodiazepine Antagonist Flumazenil

Flumazenil is a specific benzodiazepine antagonist indicated for the reversal of benzodiazepine-induced moderate sedation, recurrent sedation, and benzodiazepine overdose. It should be used with caution in patients who have received benzodiazepines for an extended period of time to prevent the precipitation of withdrawal reactions. Dose •• Reversal of conscious sedation: 0.2 mg IV over 2 minutes, followed in 45 seconds by 0.2 mg repeated every minute as needed to a maximum dose of 1 mg. Reversal of recurrent sedation is the same as for conscious sedation, except doses may be repeated every 20 minutes as needed. •• Benzodiazepine overdose: 0.2 mg over 30 seconds followed by 0.3 mg over 30 seconds; repeated doses

CENTRAL NERVOUS SYSTEM PHARMACOLOGY 187

of 0.5 mg can be administered over 30 seconds at 1-minute intervals up to a cumulative dose of 3 mg. With a partial response after 3 mg, additional doses up to a total dose of 5 mg may be administered. In all of the above-mentioned scenarios, no more than 1 mg should be administered at any one time, and no more than 3 mg in any 1 hour. •• Continuous infusion: 0.1 to 0.5 mg/h (for the reversal of long-acting benzodiazepines or massive overdoses). Monitoring Parameters •• Level of consciousness and signs and symptoms of withdrawal reactions. Neuroleptics Haloperidol

Haloperidol is a major tranquilizer that has commonly been used for the management of agitated or delirious patients who fail to respond adequately to nonpharmacologic interventions or other sedatives. This agent has the advantage of limited respiratory depression and little potential for the development of tolerance or dependence. Although its exact mechanism of action is unknown, it probably involves dopaminergic receptor blockade in the central nervous system, resulting in central nervous system depression at the subcortical level of the brain. Intravenous haloperidol is the most frequently used neuroleptic for controlling agitation in critically ill patients. Initial doses of 2 to 5 mg may be doubled every 15 to 20 minutes until the patient is adequately sedated. Single IV doses as large as 150 mg have been safely administered to patients, as well as total daily doses of approximately 1000 mg. As soon as the patient’s symptoms are controlled, the total dose required to calm the patient should be divided into four equal doses and administered every 6 hours on a regularly scheduled basis. When the patient’s symptoms are stable, the daily dose should be rapidly tapered to the smallest dose that controls the patient’s symptoms. Continuous IV infusions have also been advocated to allow flexible dosing to control patient’s symptoms. Higher doses and IV administration of haloperidol may prolong the QTc interval in patients, especially those patients receiving haloperidol continuous infusions. Monitoring the QTc interval is mandatory for all patients receiving haloperidol by IV injection or continuous infusion. The major side effect of haloperidol is its extrapyramidal reactions, such as akathisia and dystonia. These reactions usually occur early in therapy and may resolve with dose reduction or discontinuation of the drug. However, in more severe cases, diphenhydramine, 25 to 50 mg IV, or benztropine, 1 to 2 mg IV, may be required to relieve the symptoms. Extrapyramidal reactions appear to be more common after oral haloperidol than after IV haloperidol administration. Neuroleptic malignant syndrome may also be seen with this agent, manifested by hyperthermia, severe extrapyramidal reactions, severe muscle rigidity, altered mental status, and autonomic instability. Treatment involves supportive

care and the administration of dantrolene. Cardiovascular side effects include hypotension. It is important to note that despite the common usage of this agent to treat delirium, there is no published evidence that haloperidol reduces the duration of delirium. The lack of this supporting evidence is leading to reconsideration of the role of haloperidol in this setting compared with other potentially more well-tolerated agents (ie, atypical antipsychotics). Dose •• IV bolus: 1 to 10 mg (titrated up as clinically indicated) •• Continuous infusion: 10 mg/h (not generally recommended) Monitoring Parameters •• Mental status, blood pressure, electrocardiogram (ECG), bedside delirium monitoring, and electrolytes (especially with continuous infusions) Atypical Antipsychotics

Atypical antipsychotic agents such as quetiapine, olanzapine, risperidone, and ziprasidone have been suggested as possible alternatives to haloperidol, due to their similar mechanism of action and more favorable side effect profile, including reduced incidence of extrapyramidal reactions and QT prolongation. The use of atypical antipsychotics to manage ICU delirium has increased during recent years with reported usage as high as 40% in some studies. Despite these increases, additional well-controlled studies are warranted. Monitoring Parameters •• Mental status, level of consciousness, electrocardiogram (ECG), bedside delirium monitoring Quetiapine

Quetiapine is the most well studied of these agents to this point, with a randomized, placebo-controlled trial demonstrating a reduction in duration of delirium. Quetiapine can be administered as scheduled dosing, with additional doses of haloperidol as needed. Dose escalation of the scheduled quetiapine may be required in 50 mg increments in patients still requiring breakthrough management with haloperidol. Sedation is the most commonly associated adverse effect. Dose •• PO or per tube: 50 to 200 mg q12h Monitoring Parameters •• Mental status, level of consciousness, electrocardiogram (ECG), bedside delirium monitoring Barbiturates

Barbiturates are primarily used to reduce intracranial pressure in head injury patients after conservative therapy has failed. Barbiturates decrease cerebral oxygen consumption, decrease cerebral blood flow, and potentially scavenge free oxygen radicals.

188

CHAPTER 7. Pharmacology

The general central nervous system depression associated with the use of barbiturates may cause excessive sedation as well as respiratory depression. Barbiturates produce direct myocardial depression, reducing cardiac output and increasing venous capacitance. Rapid IV administration can result in arrhythmias and hypotension. Pentobarbital

Pentobarbital continuous infusions are commonly used to induce barbiturate coma. The infusion should be titrated to maintain intracranial pressure less than 20 mm Hg and cerebral perfusion pressure greater than 60 mm Hg. The mean arterial pressure should be maintained in a range that provides an adequate cerebral perfusion pressure. Therapeutic serum pentobarbital concentrations are 20 to 50 mg/L. Dose •• IV bolus: 5 to 10 mg/kg infused over 2 hours •• Continuous infusion: 0.5 to 4 mg/kg/h Monitoring Parameters •• Level of consciousness, intracranial pressure, cerebral perfusion pressure, blood pressure, and serum pentobarbital concentration Miscellaneous Agents Propofol

Propofol is an IV general anesthetic that has become popular for sedation of mechanically ventilated patients. Limits on propofol use to fewer than 3 days are advocated because of the rapid development of tolerance. The agent is often used as the primary sedative in daily awakening protocols. The advantages of propofol are its rapid onset and short duration of action compared to the benzodiazepines. Propofol is associated with pain on injection, respiratory depression, and hypotension, especially in critically ill patients who are already hypotensive or hypovolemic. Hypotension can be avoided by limiting bolus doses to 0.25 to 0.5 mg/kg and the initial infusion rate to 5 mcg/kg/min. The fat-emulsion vehicle of propofol has been shown to support the growth of microorganisms. The manufacturer recommends changing the IV tubing of extemporaneously prepared infusions every 6 hours, or every 12 hours if the infusion bottles are used. Propofol is formulated in a fat-emulsion vehicle that provides 1.1 calories/mL and its infusion rate must be accounted for when determining a patient’s nutrition support regimen because the fat-emulsion base can be considered as a calorie source. High infusion rates can be a cause of hypertriglyceridemia. This agent can also cause a rare but serious adverse effect known as propofol infusion syndrome (PRIS). PRIS is associated with the use of propofol for more than 48 hours and at doses greater than 75 mcg/kg/min. Hyperkalemia, tachyarrythmia, bradycardia, rhabdomyolysis, and lactic acidosis combined with hypertriglyceridemia as previously described are common signs of PRIS. The bedside nurse should monitor closely for these signs as discontinuance of therapy may avoid the serious outcomes of PRIS: myocardial

failure, metabolic acidosis, rhabdomyolysis, dysrhythmias, and renal failure. Propofol is available in 50- and 100-mL infusion vials. To decrease waste, 50-mL vials may be used when changing vials in patients who are scheduled for IV line changes, extubation from mechanical ventilation, and low infusion rates. Dose •• IV bolus: 0.25 to 0.50 mg/kg •• Continuous infusion: 5 to 50 mcg/kg/min Monitoring Parameters •• Level of consciousness, blood pressure, lactic acid, creatinine kinase, and serum triglyceride level, especially at high infusion rates Ketamine

Ketamine is an analog of phencyclidine that is commonly used as an IV general anesthetic. It is an agent that produces analgesia, anesthesia, and amnesia without the loss of consciousness. The onset of anesthesia after a single 0.5- to 1.0-mg/kg bolus dose is within 1 to 2 minutes and lasts approximately 5 to 10 minutes. Ketamine causes sympathetic stimulation that normally increases blood pressure and heart rate while maintaining cardiac output. This may be important in patients with hypovolemia. Ketamine is useful in patients who require repeated painful procedures such as wound debridement. The bronchodilatory effects of ketamine may be beneficial in patients experiencing status asthmaticus. However, ketamine may increase intracranial pressure and should be avoided or used with caution in patients with head injuries, space-occupying lesions, or any other conditions that may cause an increase in intracranial pressure. Emergence reactions or hallucinations, commonly seen after ketamine anesthesia, may be prevented with the concurrent use of benzodiazepines. Dose •• IV bolus: 0.1 to 1 mg/kg •• Continuous infusion: 0.05 to 3 mg/kg/hr •• Oral: 10 mg/kg diluted in 1 to 2 oz of juice •• Intranasal: 5 mg/kg Monitoring Parameters •• Levels of sedation and analgesia, heart rate, blood pressure, and mental status Dexmedetomidine

Dexmedetomidine is a relatively selective alpha-2-adrenergic agonist with sedative properties indicated for the short-term (< 24 hours) sedation of intubated and mechanically ventilated patients. Dexmedetomidine is not associated with respiratory depression but has been associated with reductions in heart rate and blood pressure. Some patients may complain of increased awareness while receiving the drug in the intensive care unit. Dexmedetomidine has minimal amnestic properties and most patients require breakthrough doses of sedatives

CENTRAL NERVOUS SYSTEM PHARMACOLOGY 189

and analgesics while receiving the drug. The agent has been evaluated for longer term sedation, up to 28 days in a limited number of patients. In this setting, a reduction of the loading infusion is advised to minimize cardiovascular depression. However, a higher maintenance infusion (up to 1.5 mcg/kg/h) may be required compared to short-term sedation. Dose •• IV bolus: 1 mcg/kg over 10 minutes •• Continuous infusions: 0.2 to 1.5 mcg/kg/h Monitoring Parameters •• Levels of sedation and analgesia, heart rate, and blood pressure

Analgesics Opioids

Opioids, also known as narcotics, produce their effects by reversibly binding to the mu, delta, kappa, and sigma opiate receptors located in the central nervous system. Mu-1 receptors are associated with analgesia, and mu-2 receptors are associated with respiratory depression, bradycardia, euphoria, and dependence. Delta receptors have no selective agonist and modulate mu-receptor activity. Kappa receptors function at the spinal and supraspinal levels and are associated with sedation. Sigma receptors are associated with dysphoria and psychotomimetic effects. Monitoring Parameters •• Level of pain or comfort, blood pressure, renal function, and respiratory rate Morphine

Morphine is a commonly used narcotic analgesic. Morphine is hepatically metabolized to several metabolites, including morphine-6-glucuronide (M6G), which is approximately 5 to 10 times more potent than morphine. M6G is renally eliminated and after repeated doses can accumulate in patients with renal dysfunction, producing enhanced pharmacologic effects. Morphine’s clearance is reduced in critically ill patients due to increased protein binding, decreased hepatic blood flow, or reduced hepatocellular function. Morphine possesses vasodilatory properties and can produce hypotension because of either direct effects on the vasculature or histamine release. Dose •• IV bolus: 2 to 5 mg •• Continuous infusion: 2 to 30 mg/h Patient-Controlled Analgesia (PCA) •• IV bolus: 0.5 to 3.0 mg •• Lockout interval: 5 to 20 minutes Meperidine

Meperidine is a short-acting opioid that has one-seventh the potency of morphine. It is hepatically metabolized to normeperidine, which is renally eliminated, and is also a

neurotoxin. Normeperidine can accumulate in patients with renal dysfunction, resulting in seizures. Meperidine should be avoided in patients taking monoamine oxidase inhibitors because of the potential for development of a hypertensive crisis when these agents are administered concurrently. The role of this agent as an analgesic has been reduced dramatically due to seizure potential. In many institutions, the agent has been limited to serve as an adjunctive therapy to minimize shivering in hypothermic patients. Dose •• IV bolus: 25 to 100 mg Fentanyl

Fentanyl is an analog of meperidine that is 100 times more potent than morphine. After single doses, its duration of action is limited by its rapid distribution into fat tissue. However, after repeated dosing or continuous infusion administration, fat stores become saturated, thereby prolonging its terminal elimination half-life to more than 24 hours. Fentanyl does not have active metabolites, although accumulation can occur in hepatic dysfunction. Unlike morphine, fentanyl does not cause histamine release. Dose •• IV bolus: 25 to 100 mcg q1-2h •• Continuous infusion: 50 to 300 mcg/h •• Transdermal: Patients not previously on opioids: 25 mcg/h •• Opioid-tolerant patients: 25 to 100 mcg/h PCA •• IV bolus: 25 to 100 mcg •• Lockout interval: 5 to 10 minutes Hydromorphone

Hydromorphone is a morphine derivative that is 5 to 7.5 times more potent than morphine with a similar duration of action. Because of the relative potency compared to morphine, caution must be used in dose conversions. Hydromorphone can accumulate and intensify pharmacologic effects in patients with hepatic and renal impairment. The agent primarily has a role in refractory pain management. Dose •• IV bolus: 0.4 to 2 mg •• Continuous infusion: 0.2 to 2 mg/h PCA •• IV bolus: 0.1 to 1 mg •• Lockout interval: 5 to 20 minutes Opioid Antagonist Naloxone

Naloxone is a pure opiate antagonist that displaces opioid agonists from the mu-, delta-, and kappa-receptor–binding sites. Naloxone reverses narcotic-induced respiratory

190

CHAPTER 7. Pharmacology

depression, producing an increase in respiratory rate and minute ventilation, a decrease in arterial Pco2, and normalization of blood pressure if reduced. Narcotic-induced sedation or sleep is also reversed by naloxone. Naloxone reverses analgesia, increases sympathetic nervous system activity, and may result in tachycardia, hypertension, pulmonary edema, and cardiac arrhythmias. Naloxone administration produces withdrawal symptoms in patients who have been taking narcotic analgesics chronically. Diluting and slowly administering naloxone in incremental doses can prevent the precipitation of acute withdrawal reactions as well as prevent the increase in sympathetic stimulation that may accompany the reversal of analgesia. One 0.4-mg ampule should be diluted with 0.9% NaCl (saline) to 10 mL to produce a concentration of 0.04 mg/mL. Sequential doses of 0.04 to 0.08 mg should be administered slowly until the desired response is obtained. Because its duration of action is generally shorter than that of opiates, the effect of opiates may return after the effects of naloxone dissipate, approximately 30 to 120 minutes. Dose •• Opiate depression: Initial dose: 0.1 to 0.2 mg given at 2- to 3-minute intervals until the desired response is obtained. Additional doses may be necessary depending on the response of the patient and the dose and duration of the opiate administered. •• Continuous infusion: 3 to 5 mcg/kg/h •• Known or suspected opiate overdose: Initial dose: 0.4 to 2.0 mg administered at 2- to 3-minute intervals if necessary. If no response is observed after a total of 10 mg has been administered, other causes of the depressive state should be determined. •• Continuous infusion: Loading dose: 0.4 mg, followed by 2.5 to 5 mcg/kg/h and titrated to the patient’s response. Monitoring Parameters •• Signs and symptoms of withdrawal reactions, respiratory rate, blood pressure, mental status, level of consciousness, and pupil size Nonsteroidal Anti-Inflammatory Drugs Ketorolac

Ketorolac is a nonsteroidal anti-inflammatory drug (NSAID) that is indicated for the short-term treatment of moderately severe acute pain that requires analgesia at the opioid level. The drug exhibits anti-inflammatory, analgesic, and antipyretic properties. Its mechanism of action is thought to be due to inhibition of prostaglandin synthesis by inhibiting cyclooxygenase, an enzyme that catalyzes the formation of endoperoxidases from arachidonic acid. NSAIDs are more efficacious in the treatment of prostaglandin-mediated pain. Ketorolac is the only currently available NSAID approved for IM, IV, and oral administration, and it is often used in combination with other analgesics because pain often involves multiple mechanisms. Combination therapy may be more

efficacious than single-drug regimens, and combinations with narcotics can decrease narcotic requirements, minimizing narcotic side effects. Ketorolac is associated with the same adverse effects as orally administered NSAIDs, such as reversible platelet effects, GI bleeding, and reduced renal function. Ketorolac is contraindicated in patients with advanced renal failure and in patients at risk for renal failure because of volume depletion. Therefore, volume depletion should be corrected before administering ketorolac. Because of the potential for significant adverse effects, the maximum combined duration of parenteral and oral use is limited to 5 days. Dose •• Loading dose: < 65 years: 60 mg; > 65 years or < 50 kg: 30 mg •• Maintenance dose: < 65 years: 30 mg q6h; > 65 years or < 50 kg: 15 mg q6h Monitoring Parameters •• Renal function and volume status Acetaminophen

Acetaminophen is an analgesic and antipyretic that is now available in the United States in an IV formulation. This agent has been used extensively in European countries. In the United States, intravenous acetaminophen is indicated for the management of mild to moderate pain, and management of moderate to severe pain with adjunctive opioid analgesics. The preferred route of administration for acetaminophen continues to be oral, but the IV route has proven beneficial in the perioperative setting when oral therapy is not feasible. The IV form of this agent is not cost-effective for antipyretic usage as equally effective options exist (eg, acetaminophen rectal suppositories). Use of intravenous acetaminophen should be restricted to post-surgical patients who are unable to take oral or rectal acetaminophen. Dose •• IV bolus: 1gm IV every 6 hours for 24 to 48 hours postoperative (Maximum of 4 gm in 24 hours) Monitoring parameters •• Liver function test, pain control

Neuromuscular Blocking Agents Neuromuscular blocking agents (NMBA; see Table 23-2) are primarily used to obtain, protect, and maintain a safe secure airway and to assist with mechanical ventilation. These agents have no sedative, amnestic, anesthetic, or analgesic properties. The indications for using NMBA in critically ill patients can be divided into short- and long-term indications. Shortterm indications include endotracheal intubation, stability during patient transport, hemodynamic monitoring, radiologic procedures, dressing changes, and minor surgical procedures. The primary long-term indications are optimizing

CENTRAL NERVOUS SYSTEM PHARMACOLOGY 191

mechanical ventilation, decreasing oxygen consumption, controlling increased intracranial pressure, treating refractory shivering associated with hypothermia, and managing muscle spasms associated with tetanus. NMBAs are categorized as either depolarizing or nondepolarizing agents. Depolarizing Agents Succinylcholine

Succinylcholine is the only depolarizing agent available for clinical use and is the agent of choice for rapid intubation of the trachea. Succinylcholine binds to acetylcholine receptors causing a persistent depolarization of the muscle endplate resulting in paralysis. Succinylcholine may increase serum potassium approximately 0.5 mEq/L after a standard intubating dose of 1 to 2 mg/kg. Critically ill patients with burns, spinal cord injury, and trauma with extensive skeletal muscle damage, upper and lower motor neuron disease, and prolonged bed rest are predisposed to the development of hyperkalemia after a dose of succinylcholine because of the development of nonfunctional extrajunctional acetylcholine receptors. These receptors bind succinylcholine without causing paralysis, but depolarize the muscle cells, releasing potassium and increasing serum potassium concentrations into the supratherapeutic or toxic range. Although hyperkalemia can occur within the first 24 hours after injury, patients are most at risk during the period from 7 days after injury until 9 months later. Therefore, succinylcholine is contraindicated in these patients. As a depolarizing agent, succinylcholine alone or in combination with inhalational anesthetics may trigger malignant hyperthermia. The mechanism appears to be related to increases in intracellular concentration of calcium in normal muscle. Because of the clear association with malignant hyperthermia, the agent should be avoided in patients with a family history of malignant hyperthermia. In situations where succinylcholine is contraindicated, a shortacting or intermediate-acting nondepolarizing agent may be used. Succinylcholine is rapidly hydrolyzed by pseudocholinesterase; however, patients with atypical pseudocholinesterase may experience prolonged blockade. Other conditions associated with prolonged blockade resulting from reduced cholinesterase activity include pregnancy, liver disease, acute infections, carcinomas, uremia, and burns. Dose •• See Table 23-2 Neuromuscular Blocking Agents. Monitoring Parameters •• Renal function, electrolytes (especially potassium), acid-base status, and level of paralysis Nondepolarizing Agents

Nondepolarizing agents are competitive antagonists of acetylcholine at the acetylcholine receptor. Nondepolarizing agents are subdivided according to chemical class either aminosteroid (pancuronium, rocuronium, vecuronium) or

benzylisoquinolinium (atracurium, cis-atracurium). These agents are further classified according to duration of action: intermediate (atracurium, cis-atracurium, rocuronium, vecuronium), and long (pancuronium). Nondepolarizing agents can be used for short- or long-term indications in critically ill patients. Short-term indications include intubation, stability during intrahospital transport, and immobility during procedures. Long-term indications include mechanical ventilation after optimal doses of sedatives and analgesics have not been able to prevent patient/ventilator dysynchrony. Selecting an Agent

Several factors should be considered when selecting the most appropriate agent for a patient. The onset and duration of paralysis should match that required by the procedure. Short procedures (ie, endotracheal intubation) may require a shortacting agent with rapid onset, such as succinylcholine. Bolus doses of intermediate- or long-acting agents may be selected for longer procedures (ie, dressing changes, radiologic scans). Long-term indications such as mechanical ventilation may require intermittent doses of long-acting agents or continuous infusions of intermediate-acting agents. The patient’s underlying pathophysiology also must be considered when selecting a NMBA. Succinylcholine should be avoided in patients at risk for developing hyperkalemia. Pancuronium’s vagolytic effect can increase heart rate and blood pressure and should be used with caution in patients with unstable coronary artery disease. Vecuronium and pancuronium are metabolized to 3-hydroxy metabolites that have 50% of the activity of the parent compounds. These metabolites are renally eliminated and have been shown to accumulate in patients with renal dysfunction producing prolonged periods of paralysis. Monitoring patients and adjusting doses, dosing intervals, or continuous infusion rates with the aid of a peripheral nerve stimulator to maintain one or two twitches of a train-of-four (TOF) stimulation can usually prevent this adverse effect from occurring (see Chapter 6, Pain, Sedation, and Neuromuscular Blockade Management). Atracurium or cis-atracurium should be considered for patients in multisystem organ failure because of their independence on organ function for metabolism and elimination. Neuromuscular blocking agents should be used for management of an adult ICU patient only when all other means to manage the patient have been tried without success. The majority of critically ill patients can be managed effectively with pancuronium. For patients for whom vagolysis is contraindicated (eg, cardiovascular disease), NMBAs other than pancuronium may be used. For patients with significant hepatic or renal disease, cis-atracurium or atracurium is recommended. Patients receiving NMBAs should be assessed both clinically and by TOF monitoring with a goal of adjusting the neuromuscular blocking agent to achieve one to two twitches. Patients receiving NMBA therapy should also be medicated to provide adequate sedation and analgesia.

192

CHAPTER 7. Pharmacology

Side Effects

Although adverse effects are minimal, several can be significant. Atracurium can cause histamine release after rapid IV bolus injection, resulting in hypotension and flushing. Injecting each agent over at least 60 seconds can prevent this adverse effect. Laudanosine, atracurium’s primary metabolite, has been shown to produce seizures in dogs after it achieves high concentrations in the cerebral spinal fluid. However, there are no reports of critically ill patients experiencing adverse central nervous system events from the accumulation of laudanosine. The steroid-based agents, pancuronium and vecuronium are metabolized to 3-hydroxy metabolites that have 50% of the activity of the parent compounds. These metabolites are renally eliminated and have been shown to accumulate in patients with renal dysfunction, producing prolonged periods of paralysis. Monitoring patients and adjusting doses, dosing intervals, or continuous infusion rates with the aid of a peripheral nerve stimulator to maintain one or two twitches of a TOF stimulation can usually prevent this adverse effect from occurring (see Chapter 6, Pain, Sedation, and Neuromuscular Blockade Management). A more serious complication associated with the use of nondepolarizing agents is the development of a prolonged disuse atrophy syndrome. This syndrome has been shown to occur after the extended administration of steroid-based and benzylisoquinolinium agents and cannot be prevented with peripheral nerve stimulation monitoring. Patients receiving steroids may be predisposed to developing this complication; however, this association remains to be conclusively proven. Tolerance or the need to increase doses to maintain a stable level of paralysis is often encountered in patients receiving these agents for an extended duration. Tolerance may be attributed to the proliferation of nonfunctional extrajunctional receptors that bind drug but do not cause paralysis, increased volume of distribution resulting in lower serum concentrations at the neuromuscular junction, and binding to acute phase reactant proteins, decreasing the free, pharmacologically active fraction. An additional consideration for patients requiring NMBAs is the use of prophylactic eye care to prevent corneal abrasions. For patients receiving NMBA and corticosteroids, every effort should be made to discontinue the NMBAs as soon as possible. Dose •• See Table 23-2. Monitoring Parameters •• Level of paralysis (peripheral nerve stimulation), renal function, and liver function

Anticonvulsants Hydantoins Phenytoin

Phenytoin is an anticonvulsant used for the acute control of generalized tonic clonic seizures, following the administration

of benzodiazepines, and for maintenance therapy once the seizure has been controlled. Phenytoin stabilizes neuronal cell membranes and decreases the spread of seizure activity. Phenytoin may inhibit neuronal depolarizations by blocking sodium channels in excitatory pathways and prevent increases in intracellular potassium concentrations and decreases in intracellular calcium concentrations. The bioavailability of oral phenytoin is approximately 90% to 100%. Dissolution is the rate-limiting step in phenytoin absorption with peak serum concentrations occurring 3 to 12 hours after a dose. The rate of absorption is dose dependent, with increasing times to peak concentration with increasing doses. In addition, the dissolution and absorption rate depend on the phenytoin formulation administered. The Dilantin Kapseal brand of phenytoin capsules has the dissolution characteristics of an extended-release preparation, whereas generic phenytoin products possess rapid-release characteristics and are absorbed more quickly. Extendedrelease and rapid-release products are not interchangeable, and only extended-release products may be administered in a single daily dose. Phenytoin is 90% to 95% bound to albumin. In critically ill patients, the pharmacologically free fraction is highly variable and ranges between 10% and 27% of the total serum concentration. The free fraction has been shown to increase by more than 100% from baseline during the first week of illness and is generally associated with a significant reduction in serum albumin concentration. Alterations in albumin binding also may be seen in hypoalbuminemia (< 2.5 g/dL), major trauma, sepsis, burns, malnutrition, and surgery, as well as liver or renal disease, and may result in an increase in a free concentration with potentially toxic effects. Significant alterations in phenytoin metabolism usually do not occur until the serum albumin falls below 2.5 g/dL. Equations used to normalize the phenytoin concentration in patients with hypoalbuminemia are usually unreliable, and direct measurement of the free phenytoin concentration should be used to adjust therapy. Phenytoin is metabolized by the cytochrome P-450 enzyme system to its inactive primar y metabolite 5-(p-hydroxyphenyl)-5-phenylhydantoin, which is glucuronidated and renally eliminated. Phenytoin undergoes dose-dependent metabolism such that proportional increases in the dose may result in greater than proportional increases in the serum concentration. It is difficult to predict the concentration at which a patient’s metabolism will become saturated, so that any changes in dose above 400 to 500 mg/day need to be carefully monitored. Because phenytoin displays nonlinear metabolism, half-life is an inappropriate term to describe phenytoin elimination. Phenytoin metabolism is usually referred to as the time it takes to eliminate 50% (t50) of a given daily dose. In normal patients taking 300 mg/ day, the t50 is about 22 hours. As the dose is increased, the t50 increases, with the time to reach steady-state becoming progressively longer. The time to steady-state may vary from several days to several weeks depending on the dose

CENTRAL NERVOUS SYSTEM PHARMACOLOGY 193

and the patient’s ability to metabolize the drug. Phenytoin metabolism can be affected by drugs that induce or inhibit its metabolic pathway. The effects of enzyme induction can occur within 2 days to 2 weeks after starting an agent. Inhibition usually occurs within 1 to 2 days after a drug is started and its effects usually last until the inhibiting drug is eliminated from the body. Phenytoin clearance is increased in critically ill patients, resulting in serum concentrations less than 10 mg/L. The mechanism for the increase in clearance is unclear, but may be caused by changes in protein binding, induction in phenytoin metabolism, or a stress-related transient increase in hepatic metabolic function. The recommended phenytoin loading dose of 15 to 20 mg/kg produces serum concentrations between 20 and 30 mg/L. Loading doses of 18 to 20 mg/kg are recommended for treating status epilepticus, and loading doses of 15 to 18 mg/kg are recommended for seizure prophylaxis after head injury or neurosurgery. The serum concentration increases approximately 1.4 mg/L for each 1 mg/kg of phenytoin administered. The maintenance dose should be started 8 to 12 hours after the loading dose. The usual adult maintenance dose is 5 to 6 mg/kg/day, although critically ill patients or patients with neurotrauma may require doses of 6.0 to 7.5 mg/kg/day. Intravenous maintenance doses should be administered every 6 to 8 hours to maintain therapeutic serum concentrations. Phenytoin precipitates in dextrose-containing solutions and should only be mixed in 0.9% sodium chloride solutions. To prevent phlebitis, the maximum concentration for peripheral administration is 10 mg/mL; a final concentration of 20 mg/ mL may be used if the dose is being administered through a central venous catheter. Phenytoin solution must be administered through an in-line 1.2- or 5.0-μ filter to prevent the administration of phenytoin crystals into the systemic circulation. Phenytoin doses should not be administered at a rate faster than 50 mg/min because hypotension and arrhythmias may occur because of its propylene glycol diluent. The infusion rate should be decreased by 50% if hypotension or arrhythmias develop. Oral administration is not usually recommended in critically ill patients because of the risk of erratic or incomplete absorption. Phenytoin oral suspension may adhere to the inside walls of oro- or nasogastric tubes, reducing the dose delivered to the patient. If phenytoin is administered through a feeding tube, the tube should be flushed with 30 to 60 mL of 0.9% sodium chloride before and after administering the dose. After the dose is administered, the feeding tube should be clamped for an hour before restarting the feeding solution. Oral absorption may be impaired by concomitant administration with enteral nutrition solutions, reducing its bioavailability and resulting in erratic serum concentrations with seizures occurring as a result of subtherapeutic serum concentrations. Phenytoin oral solution must be shaken prior to use to ensure uniformity in the distribution of the phenytoin particles throughout the suspension. If the suspension is not shaken before obtaining a dose, the phenytoin powder

settles to the bottom of the bottle producing subtherapeutic doses when the bottle is first opened and toxic doses as the bottle is used. Hemodialysis and hemofiltration have no effect on phenytoin clearance. Agents known to inhibit or enhance this enzymatic pathway may affect phenytoin’s clearance. Early adverse effects that may be associated with increasing concentrations are nystagmus (> 20 mg/L), ataxia (> 30 mg/L), and lethargy, confusion, and impaired cognitive function (> 40 mg/L). The normal therapeutic range for the total phenytoin serum concentration is 10 to 20 mg/L with the free fraction therapeutic range of 1 to 2 mg/L. Serum concentration of 20 to 30 mg/L may be required in patients who are having seizures. Phenytoin serum concentrations can be obtained 30 to 60 minutes after the loading dose is infused to assess the adequacy of the dose. Trough concentrations should be monitored 2 to 3 times a week, particularly after the first week of therapy. Measurement of free phenytoin concentrations may be indicated in critically ill patients, patients with serum albumin concentrations less than 2.5 g/dL, renal failure, or receiving drugs known to displace phenytoin from albumin-binding sites. Other monitoring parameters include the patient’s seizure activity and medication profile for agents known to alter phenytoin’s metabolism. Dose •• Loading dose: 15 to 20 mg/kg IV •• Maintenance dose: 5 mg/kg/day IV or PO Monitoring Parameters •• Seizure activity, electroencephalogram (EEG), serum phenytoin concentration (free phenytoin concentration if applicable), albumin, liver function, infusion rate, blood pressure, ECG with IV administration, and IV injection site Fosphenytoin

Fosphenytoin is a phenytoin prodrug with good aqueous solubility that was developed to be a water-soluble alternative to phenytoin. In patients unable to tolerate oral phenytoin, equimolar doses of fosphenytoin have been shown to produce equal or greater plasma phenytoin concentrations. Although phenytoin sodium 50 mg is equal to fosphenytoin sodium 75 mg, phenytoin should be converted to fosphenytoin on a milligram-per-milligram basis (eg, phenytoin 300 mg should be converted to fosphenytoin 300 mg). Fosphenytoin, administered IM or IV, is rapidly and completely converted to phenytoin in vivo, resulting in essentially 100% bioavailability. The conversion half-life to phenytoin is about 33 minutes following IM administration and about 15 minutes after IV infusion. After IM administration, peak plasma fosphenytoin concentrations occur approximately 30 minutes postdose, with peak phenytoin concentrations occurring in about 3 hours. Fosphenytoin’s peak concentration following IV administration occurs at the end of the infusion, with peak phenytoin concentrations occurring in

194

CHAPTER 7. Pharmacology

approximately 40 to 75 minutes. In patients with renal or hepatic dysfunction or hypoalbuminemia, there is enhanced conversion to phenytoin without an increase in clearance. Fosphenytoin is 90% to 95% bound to plasma proteins and is saturable with the percent of bound fosphenytoin decreasing as the fosphenytoin dose increases. The maximum total phenytoin concentration increases with increasing fosphenytoin doses, but the total phenytoin concentration is less affected by increasing fosphenytoin infusion rates. Maximum free phenytoin concentrations are nearly constant at infusion rates up to 50 mg phenytoin equivalents (PE)/min, whereas they increase with faster infusion rates secondary to phenytoin displacement from albumin-binding sites in the presence of high fosphenytoin concentrations. For the treatment of status epilepticus, the recommended loading dose of IV fosphenytoin is 15 to 20 PE/kg, and it should not be administered faster than 150 mg PE/min because of the risk of hypotension. Fosphenytoin 15 to 20 mg PE/kg infused at 100 to 150 mg PE/min yields plasma-free phenytoin concentrations over time that approximate those achieved when an equimolar dose of IV phenytoin is administered at 50 mg/min. In the treatment of status epilepticus, total phenytoin concentrations greater than 10 mg/L and free phenytoin concentrations greater than 1 mg/mL are achieved within 10 to 20 minutes after starting the infusion. In nonemergent situations, loading doses of 10 to 20 PE/kg administered IV or IM is recommended. In nonemergent situations, IV administration of infusion rates of 50 to 100 mg PE/min may be acceptable, but results in slightly lower and delayed maximum free phenytoin concentrations as compared with administration at higher infusion rates. The initial daily maintenance dose is 4 to 6 mg PE/kg/day. Dosing adjustments are not required when IM fosphenytoin is substituted temporarily for oral phenytoin. However, patients switched from once-daily extended-release phenytoin capsules may require twice-daily or more frequent administration of fosphenytoin to maintain similar peak and trough phenytoin concentrations. The incidence of adverse effects tends to increase as both dose and infusion rate are increased. At doses above 15 mg PE/kg and infusion rates higher than 150 mg PE/min, transient pruritus, tinnitus, nystagmus, somnolence, and ataxia occur more frequently than at lower doses or infusion rates. Severe burning, itching, and paresthesias of the groin are commonly associated with infusion rates greater than 150 mg PE/min. Slowing or temporarily stopping the infusion can minimize the frequency and severity of these reactions. Continuous cardiac rate and rhythm, blood pressure, and respiratory function should be monitored throughout the fosphenytoin infusion and for 10 to 20 minutes after the end of the infusion. Following fosphenytoin administration, phenytoin concentrations should not be monitored until the conversion to phenytoin is complete. This occurs within 2 hours after the end of an IV infusion and 5 hours after an IM injection. Prior

to complete conversion, commonly used immunoanalytic techniques such as fluorescence polarization and enzymemediated assays may significantly overestimate plasma phenytoin concentrations because of cross-reactivity with fosphenytoin. Blood samples collected before complete conversion to phenytoin should be collected in tubes containing EDTA as an anticoagulant to minimize the ex vivo conversion of fosphenytoin to phenytoin. Monitoring is similar to phenytoin. In critically ill patients with renal failure receiving fosphenytoin, one or more metabolites of adducts of fosphenytoin accumulate and display significant cross-reactivity with several phenytoin immunoassay methods. Levetiracetam

Levetiracetam is a second-generation antiepileptic drug with increasing usage in the critical care setting. The agent leads to selective prevention of burst firing and seizure activity. Levetiracetam is commonly prescribed for adjunctive treatment of partial onset seizures with or without secondary generalization. Other approved indications include monotherapy treatment of partial onset seizures with or without secondary generalization, and adjunctive treatment of myoclonic seizures associated with juvenile myoclonic epilepsy and primary generalized tonic-clonic (GTC) seizures associated with idiopathic generalized epilepsy. Seizure prophylaxis in post-traumatic brain injury patients is also an established role for levetiracetam. Levetiracetam lacks cytochrome P450 isoenzymeinducing potential and is not associated with clinically significant interactions with other drugs, including other antiepileptic drugs. Sedation is the most common adverse effect noted. Dose •• Maintenance dose: 250 mg to 1000 mg q12 IV or PO Monitoring Parameters •• Seizure activity, electroencephalogram (EEG), sedation Barbiturates Pentobarbital

Pentobarbital is a barbiturate mainly used to control intracranial pressure in patients with head injuries. Pentobarbital may also be used in patients with status epilepticus who are refractory to other anticonvulsants. The central nervous system protective effect of pentobarbital may be attributed to decreased cerebral oxygen consumption allowing a proportionate decrease in cerebral blood flow and potentially scavenging free oxygen radicals. Its anticonvulsant effects are similar to phenobarbital. Pentobarbital produces a dosedependent depression of the central nervous system beginning with sedation and ending with coma and death. At high serum concentrations, pentobarbital suppresses the respiratory drive necessitating mechanical ventilation during therapeutic pentobarbital coma. Pentobarbital has a greater affinity for adipose tissue than phenobarbital. Its lipophilicity causes it to cross the

blood-brain barrier faster than phenobarbital to produce its central nervous system effects. Pentobarbital is hepatically metabolized with an average half-life of 22 hours. In head injured patients, pentobarbital’s clearance is faster with its half-life averaging 15 to 19 hours. Alterations in hepatic microsomal enzymes can be expected to alter its clearance and half-life. The usual loading dose required to induce pentobarbital coma is 5 to 10 mg/kg infused over 2 hours. Each 1 mg/kg increases the serum concentration approximately 1 mg/L. The maintenance infusion is begun at a rate of 1 mg/kg/h and can be adjusted in increments of 0.5 to 1.0 mg/kg/h to a final infusion rate that achieves an appropriate reduction in intracranial pressure. Typical maintenance infusion rates range from 0.5 to 4.0 mg/kg/h producing serum concentrations between 20 and 50 mg/L. The usual dose for control of status epilepticus is an initial loading dose of 5 to 10 mg/kg followed by a maintenance infusion of 0.5 to 1.0 mg/kg/h. Rapid administration of pentobarbital may result in hypotension and arrhythmias secondary to its propylene glycol diluent. If the systolic blood pressure drops 10 to 20 mm Hg, the infusion rate should be reduced by 50%, and if the systolic blood pressure drops more than 20 mm Hg, volume resuscitation and vasopressors may be required for blood pressure support. The IV administration of pentobarbital also may cause respiratory depression, apnea, laryngospasm, or hypotension, particularly if injected too rapidly. The infusion may be discontinued after 72 hours of intracranial pressure control or if there is deterioration in the cardiovascular status of the patient. The infusion should be tapered over 48 to 72 hours by decreasing the infusion rate by 25% every 12 hours. The patient should be monitored during this time for increases in intracranial pressure or the development of seizures. Serum concentrations should be obtained 1 to 2 hours after the loading infusion and then daily. The serum concentration within 24 hours after starting therapy does not reflect steady-state conditions. If the 24-hour concentration has changed from the post-loading dose by 33% to 50% and is less than 20 mg/L or greater than 50 mg/L, the infusion should be increased or decreased by 0.5 to 1.0 mg/kg/h. Serum concentrations should be monitored in conjunction with the patient’s physiologic parameters such as brain stem reflexes, intracranial pressure, systemic blood pressure, EEG, and hemodynamic parameters. Acceptable therapeutic endpoints include a mean arterial pressure of 70 to 80 mm Hg, cerebral perfusion pressure of greater than 60 mm Hg, intracranial pressure of greater than 20 mm Hg, EEG showing a 30- to 60-second burst suppression pattern, and an absence of muscular movement and brainstem reflexes on neurologic examination. However, deeper levels of sedation may not be needed if seizures are controlled, or intracranial pressure is less than 20 mm Hg. Phenobarbital

Phenobarbital may be added for patients who have not responded to IV benzodiazepines and phenytoin. Phenobarbital

CENTRAL NERVOUS SYSTEM PHARMACOLOGY 195

depresses excitatory postsynaptic seizure discharge and increases the convulsive threshold for electrical and chemical stimulation. This effect is due to the inhibiting effects of GABA. Phenobarbital is 90% to 100% bioavailable with peak concentrations occurring in 0.5 to 4 hours after an oral or IM dose. Peak brain concentrations occur approximately 20 to 40 minutes after an administered dose. Phenobarbital is primarily hepatically metabolized by the cytochrome P-450 microsomal enzyme system with approximately 25% of a dose excreted unchanged in the urine. The half-life of phenobarbital is 96 hours with steady-state conditions being achieved in about 2 to 3 weeks. The usual loading dose of phenobarbital is 20 mg/kg and achieves a serum concentration of about 20 mg/L. Each 1 mg/kg dose increment increases the serum concentration by about 1.5 mg/L. The loading dose has the potential to decrease respiratory drive in patients who have received other central nervous system depressants. The maximum IV infusion rate is 50 mg/min or less. Infusion rates above 50 mg/min may cause hypotension because of its propylene glycol diluent. Blood pressure should be monitored during the loading infusion, and the infusion rate should be decreased by 50% if hypotension develops. The maintenance dose should be started within 24 hours after the loading dose. The typical adult maintenance dose of 2 to 4 mg/kg/day produces serum concentrations in the range of 10 to 30 mg/L. Each 1 mg/kg/day increase in the maintenance dose increases the serum concentration about 10 mg/L. Lower doses should be used in elderly patients, patients with renal failure, and patients with liver dysfunction because of their reduced abilities to eliminate the drug. The maintenance dose should be administered as a single daily dose because of its long half-life, with this dose usually given at bedtime because of phenobarbital’s sedative properties. In cases of excessive sedation, the daily dose may be administered as smaller doses 2 to 3 times per day. Tolerance usually develops to sedation with long-term administration. Hemodialysis removes a significant amount of phenobarbital. Posthemodialysis serum concentrations should be monitored and supplemented doses administered after hemodialysis to maintain the serum concentration within the therapeutic range. Phenobarbital serum concentrations can be monitored 30 to 60 minutes after the end of the loading infusion to assess the adequacy of the dose. Maintenance doses should be monitored every 3 to 4 days in patients with changing hemodynamic status, because the patients may have alterations in their ability to eliminate the drug, resulting in increased or decreased serum concentrations. If the serum concentrations are fluctuating, they should be monitored daily to prevent excessive rises in the serum concentrations and toxicity or subtherapeutic serum concentrations and seizures. The serum concentration may be monitored once a week if stable. Trough concentrations are typically monitored, but because of its long half-life, there is minimal peak to trough variation in the serum concentration so that a drug level can

196

CHAPTER 7. Pharmacology

be drawn anytime during the dosing interval. When patients regain consciousness, serum levels may not be needed if the patients are not having seizures. Dose •• Loading dose: 20 mg/kg IV (1 mg/kg increases the serum concentration 1 mg/L) •• Maintenance dose: 3 to 5 mg/kg/day IV or PO Monitoring Parameters •• Seizure activity, EEG, serum phenobarbital concentration, infusion rate, blood pressure, and ECG with IV administration Benzodiazepines

Benzodiazepines are the primary agents in the management of status epilepticus. These agents suppress the spread of seizure activity but do not abolish the abnormal discharge from a seizure focus. Although IV diazepam has the fastest onset of action, lorazepam or midazolam are equally efficacious in controlling seizure activity. They are the agents of choice to temporarily control seizures and to gain time for the loading of phenytoin or phenobarbital. Phenytoin may also be used prophylactically in patients who are at risk for seizures after neurosurgery or following head injuries. Monitoring Parameters •• Seizure activity, EEG, and respiratory rate and quality

CARDIOVASCULAR SYSTEM PHARMACOLOGY Miscellaneous Agents Nesiritide

Nesiritide is a recombinant human b-type natriuretic peptide, which is a cardiac hormone that regulates cardiovascular homeostasis and fluid volume during states of volume and pressure overload. The agent is effective in reducing pulmonary capillary wedge pressure and improving dyspnea symptoms in patients with acutely decompensated HF who have dyspnea at rest or with minimal activity. The most common adverse effects include hypotension, tachycardia, and/ or bradycardia. Dose •• IV bolus: 2 mcg/kg •• Continuous infusion: 0.01 mcg/kg/min Monitoring Parameters •• Blood pressure, heart rate, urine output, and hemodynamic parameters Fenoldopam

Fenoldopam is a benzapine derivative with selective dopamine-1 receptor agonist properties, similar to dopamine. This dopaminergic stimulation results in a decrease in systemic blood pressure with an increase in natriuresis and urine output. The primary use of fenoldopam is in the management of severe hypertension, particularly in patients with renal impairment.

Dose •• Continuous infusion: 0.1 to 1.6 mcg/kg/min Monitoring Parameters •• Blood pressure, urine output, and hemodynamic parameters

Parenteral Vasodilators (see Chapter 23) Nitrates Sodium Nitroprusside

Sodium nitroprusside is a balanced vasodilator affecting the arterial and venous systems. Blood pressure reduction occurs within seconds after an infusion is started, with a duration of action of less than 10 minutes once the infusion is discontinued. Sodium nitroprusside is considered the agent of choice in acute hypertensive conditions such as hypertensive encephalopathy, intracerebral infarction, subarachnoid hemorrhage, carotid endarterectomy, malignant hypertension, microangiopathic anemia, and aortic dissection, and after general surgical procedures, major vascular procedures, or renal transplantation. If sodium nitroprusside is used for longer than 48 hours, there is the risk of thiocyanate toxicity. However, this may only be a concern in patients with renal dysfunction. In this setting, thiocyanate serum concentrations should be monitored to ensure that they remain below 10 mg/dL. Other potential side effects include methemoglobinemia and cyanide toxicity. Nitroprusside should be used with caution in the setting of increased intracranial pressure, such as head trauma or postcraniotomy, where it may cause an increase in cerebral blood flow. Nitroprusside’s effects on intracranial pressure may be attenuated by a lowered Paco2 and raised Pao2. In pregnant women, nitroprusside should be reserved only for refractory hypertension associated with eclampsia, because of the potential risk to the fetus. Dose •• Continuous infusion: 0.5 to 10.0 mcg/kg/min Monitoring Parameters •• Blood pressure, renal function, thiocyanate concentration (prolonged infusions), acid-base status, and hemodynamic parameters Nitroglycerin

Nitroglycerin is a preferential venous dilator affecting the venous system at low doses, but relaxes arterial smooth muscle at higher doses. The onset of blood pressure reduction after starting a nitroglycerin infusion is similar to sodium nitroprusside, approximately 1 to 3 minutes, with a duration of action of less than 10 minutes. Headaches are a common adverse effect that may occur with nitroglycerin therapy and can be treated with acetaminophen. Tachyphylaxis can be seen with the IV infusion, similar to what is seen after the chronic use of topical nitroglycerin preparations. In patients receiving unfractionated heparin in addition to nitroglycerin,

CARDIOVASCULAR SYSTEM PHARMACOLOGY 197

increased doses of unfractionated heparin may be required to maintain a therapeutic partial thromboplastin time (PTT). The mechanism by which nitroglycerin causes unfractionated heparin resistance is unknown. However, the PTT should be closely monitored in patients receiving nitroglycerin and unfractionated heparin concurrently. Nitroglycerin is the preferred agent in the setting of hypertension associated with myocardial ischemia or infarction because its net effect is a reduction in oxygen consumption. Dose •• Continuous infusion: 10 to 300 mcg/min Monitoring Parameters •• Blood pressure, heart rate, signs and symptoms of ischemia, hemodynamic parameters (if applicable), and PTT (in patients receiving unfractionated heparin concurrently) Arterial Vasodilating Agents Hydralazine

Hydralazine reduces peripheral vascular resistance by directly relaxing arterial smooth muscle. Blood pressure reduction occurs within 5 to 20 minutes after an IV dose and lasts approximately 2 to 6 hours. Common adverse effects include headache, nausea, vomiting, palpitations, and tachycardia. Reflex tachycardia may precipitate anginal attacks. Co-administration of a beta receptor antagonist can decrease the incidence of tachycardia. Dose •• 10 to 25 mg IV q2-4h Monitoring Parameters •• Blood pressure and heart rate Diazoxide

Diazoxide is a nondiuretic that reduces peripheral vascular resistance by directly relaxing arterial smooth muscle. Side effects such as hypotension, nausea and vomiting, dizziness, weakness, hyperglycemia, and reflex tachycardia have been associated with the use of the higher than 300-mg dosing regimen. Using lower dose regimens produces similar but less severe side effects. Caution should be used when diazoxide is administered with other antihypertensive agents because excessive hypotension may result. Blood pressure reduction occurs within 1 to 2 minutes and lasts 3 to 12 hours after a dose. Blood pressure should be monitored frequently until stable, and then monitored hourly.

Alpha- and Beta-Adrenergic Blocking Agents Labetalol

Labetalol is a combined alpha- and beta-adrenergic blocking agent with a specificity of beta receptors to alpha receptors of approximately 7:1. Labetalol may be administered parenterally by escalating bolus doses or by continuous infusion. The onset of action after the administration of labetalol is within 5 minutes with a duration of effect from 2 to 12 hours. Because labetalol possesses beta-blocking properties, it may produce bronchospasm in individuals with asthma or reactive airway disease. It also may produce conduction system disturbances or bradycardia in susceptible individuals, and its negative inotropic properties may exacerbate symptoms of HF. Labetalol may be considered as an alternative to sodium nitroprusside in the setting of hypertension associated with head trauma or postcraniotomy, spinal cord syndromes, transverse lesions of the spinal cord, Guillain-Barré syndrome, or autonomic hyperreflexia, as well as hypertension associated with sympathomimetics (eg, cocaine, amphetamines, phencyclidine, nasal decongestants, or certain diet pills) or withdrawal of centrally acting antihypertensive agents (eg, beta-blockers, clonidine, or methyldopa). It also may be used as an alternative to phentolamine in the setting of pheochromocytoma because of its alpha- and beta-blocking properties. Dose •• IV bolus: 20 mg over 2 minutes, then 40 to 80 mg IV q10min to a total of 300 mg •• Continuous infusion: 1 to 4 mg/min and titrate to effect Monitoring Parameters •• Blood pressure, heart rate, ECG, and signs and symptoms of HF or bronchospasm (if applicable) Alpha-Adrenergic Blocking Agents Phentolamine

Phentolamine is an alpha-adrenergic blocking agent that may be administered parenterally by bolus injection or continuous infusion. Onset of action is within 1 to 2 minutes, with a duration of action of 3 to 10 minutes. Potential adverse effects that may occur with phentolamine include tachycardia, GI stimulation, and hypoglycemia. Phentolamine is considered the drug of choice for the treatment of hypertension associated with pheochromocytoma because of its ability to block alpha-adrenergic receptors. Also, it is the primary agent used to treat acute hypertensive episodes in patients receiving monoamine oxidase inhibitors.

Dose •• IV bolus: 50 to 150 mg q5min •• Continuous infusion: 7.5 to 30.0 mg/min

Dose •• IV bolus: 5 to 10 mg q5-15min •• Continuous infusion: 1 to 10 mg/min

Monitoring Parameters •• Blood pressure, heart rate, and serum glucose

Monitoring Parameters •• Blood pressure and heart rate

198

CHAPTER 7. Pharmacology

Beta-Adrenergic Blocking Agents

Beta-adrenergic blocking agents available for IV delivery include propranolol, esmolol, and metoprolol. Propranolol and metoprolol may be administered by bolus injection or continuous infusion. Atenolol typically is administered by bolus injection, and esmolol is administered by continuous infusion. A continuous infusion of esmolol may or may not be preceded by an initial bolus injection. Esmolol has the fastest onset and shortest duration of action, approximately 1 to 3 minutes and 20 to 30 minutes, respectively. Propranolol and metoprolol have similar onset times, but durations of action vary between 1 and 6 hours. The duration of action after a bolus dose of atenolol is approximately 12 hours. All agents may produce bronchospasm in individuals with asthma or reactive airway disease and may produce conduction system disturbances or bradycardia in susceptible individuals. Also, because of their negative inotropic properties, they may exacerbate symptoms of HF. Beta-blocking agents typically are used as adjuncts with other agents in the treatment of acute hypertension. They may be used with sodium nitroprusside in the treatment of acute aortic dissections. They should be administered to patients with hypertension associated with pheochromocytoma only after phentolamine has been given. Also, they are the agents of choice in patients who have been maintained on beta-blocking agents for the chronic management of hypertension but who have abruptly stopped therapy. Beta-blocking agents should be avoided in patients with hypertensive encephalopathy, intracranial infarctions, or subarachnoid hemorrhages because of their central nervous system depressant effects. They also should be avoided in patients with acute pulmonary edema because of their negative inotropic properties. Finally, beta-blocking agents should be avoided in hypertension associated with eclampsia and renal vasculature disorders. Dose •• Esmolol: IV bolus 500 mcg/kg; continuous infusion: 50 to 400 mcg/kg/min •• Metoprolol: IV bolus: 5 mg IV q2min; maintenance 1.25 to 5mg q6-12h × 3 doses •• Propranolol: IV bolus: 0.5 to 1.0 mg q5-15min; continuous infusion: 1 to 4 mg/h Monitoring Parameters •• Blood pressure, heart rate, ECG, and signs and symptoms of HF or bronchospasm (if applicable) Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE) inhibitors competitively inhibit angiotensin-converting enzyme, which is responsible for the conversion of angiotensin I to angiotensin II (a potent vasoconstrictor). In addition, these agents inactivate bradykinin and other vasodilatory prostaglandins,

resulting in an increase in plasma renin concentrations and a reduction in plasma aldosterone concentrations. The net effect is a reduction in blood pressure in hypertensive patients and a reduction in afterload in patients with HF. Angiotensin-converting enzyme inhibitors are indicated in the management of hypertension and HF. Adverse effects associated with ACE inhibitors include rash, taste disturbances, and cough. Initial-dose hypotension may occur in patients who are hypovolemic, hyponatremic, or who have been aggressively diuresed. Hypotension may be avoided or minimized by starting with low doses or withholding diuretics for 24 to 48 hours. Worsening of renal function may occur in patients with bilateral renal artery stenosis. Enalapril

Enalapril is a prodrug that is converted in the liver to its active moiety, enalaprilat, a long-acting ACE inhibitor. Enalapril is available in an oral dosage form, and enalaprilat is available in the IV form. Following an IV dose of enalaprilat, blood pressure lowering occurs within 15 minutes and lasts 4 to 6 hours. Dose •• Enalaprilat: IV bolus: 0.625 to 1.250 mg over 5 minutes q6h; continuous infusion: not recommended •• Enalapril: oral: 2.5 to 40.0 mg qd Monitoring Parameters •• Blood pressure, heart rate, renal function, and electrolytes Angiotensin Receptor Blockers

Angiontensin receptor blockers (ARBs) selectively block the binding of angiotensin II (a powerful vasoconstrictor in vascular smooth muscle) to the receptors in tissues such as vascular smooth muscle and the adrenal gland. This receptor blockade results in vasodilation and decreased secretion of aldosterone, which leads to increased sodium excretion and potassium-sparing effects. ARBs are indicated for both hypertension and HF. ARBs currently available in oral formulations include valsartan, candesartan, irbesartan, azilsartan, eprosartan, losartan, telmisartan, and olmesartan. The most common adverse effects of ARBs are hypotension, dizziness, and headache. Although rare, cough can also be associated with ARBs. This cough can be reversed by discontinuance of therapy. Overall, these agents are relatively well-tolerated and thus commonly used for the chronic management of hypertension. The role in the acute blood pressure lowering is limited due to the lack of a parenteral formulation. Monitoring Parameters •• Blood pressure and heart rate, and electrolytes Calcium Channel–Blocking Agents

Calcium channel–blocking agents may be used as alternative therapy in the treatment of hypertension resulting from hypertensive encephalopathy, myocardial ischemia, malignant hypertension, or eclampsia, or after renal transplantation.

CARDIOVASCULAR SYSTEM PHARMACOLOGY 199

Nicardipine

Nicardipine is an IV calcium channel–blocking agent that is primarily indicated for the treatment of hypertension. Onset is within 5 minutes with duration of approximately 30 minutes. Nicardipine also is available in an oral dosage form so that patients started on IV therapy can convert to oral therapy when indicated. Dose •• Continuous infusion: 5 mg/h, increase every 15 minutes to a maximum of 15 mg/h •• Oral: 20 to 40 mg q8h Monitoring Parameters •• Blood pressure and heart rate Clevidipine

Clevidipine is an IV calcium channel—blocking agent that is also indicated for the treatment of hypertension. An onset of 2 minutes is faster than nicardipine with a shorter duration of 10 minutes. Clevidipine is delivered as an injectable lipid emulsion (20%), similar to intralipids, and is not available in an oral dosage form. Similar to propofol, vials of clevidipine and IV tubing must be changed every 12 hours during therapy because the phospholipids support microbial growth. Dose •• Continuous infusion: 1 to 2 mg/h, increase by doubling dose every 90-second interval initially to achieve blood pressure reduction. As the blood pressure approaches goal, increase dose less aggressively every 5 to 10 minutes. Maximum recommended dose of 16 mg/h. Monitoring Parameters •• Blood pressure and heart rate Central Sympatholytic Agents Clonidine

Clonidine is an oral agent that stimulates alpha-2-adrenergic receptors in the medulla oblongata, causing inhibition of sympathetic vasomotor centers. Although clonidine typically is used as maintenance antihypertensive therapy, it can be used in the setting of hypertensive urgencies or emergencies. Its antihypertensive effects may be seen within 30 minutes and last 8 to 12 hours. Once blood pressure is controlled, oral maintenance clonidine therapy may be started. Centrally acting sympatholytics rarely are indicated as first-line agents except when hypertension may be due to the abrupt withdrawal of one of these agents. Dose •• Hypertensive urgency: 0.2 mg PO initially, then 0.1 mg/h PO (to a maximum of 0.8 mg) •• Transdermal: TTS-1 (0.1 mg/day) to TTS-3 (0.3 mg/ day) topically q1wk Monitoring Parameters •• Blood pressure, heart rate, and mental status

Antiarrhythmics Antiarrhythmic agents are divided into five classes. Dosage information for individual antiarrhythmic agents is listed in Chapter 23 (see Table 23-4). Class I Agents

Class I agents are further divided into three subclasses: Ia (procainamide, quinidine, disopyramide), Ib (lidocaine, mexiletine), and Ic (flecainide, propafenone). All class I agents block sodium channels in the myocardium and inhibit potassium-repolarizing currents to prolong repolarization. Class Ia Agents

Class Ia agents inhibit the fast sodium channel (phase 0 of the action potential), slow conduction at elevated serum drug concentrations, and prolong action potential duration and repolarization. Class Ia agents can cause proarrhythmic complications by prolonging the QT interval or by depressing conduction and promoting reentry. Monitoring Parameters •• ECG (QRS complex, QT interval, arrhythmia frequency) Class Ib Agents

Class Ib agents have little effect on phase 0 depolarization and conduction velocity, but shorten the action potential duration and repolarization. QT prolongation typically does not occur with class Ib agents. Class Ib agents act selectively on diseased or ischemic tissue where they block conduction and interrupt reentry circuits. Monitoring Parameters •• ECG (QT interval, arrhythmia frequency) Class Ic Agents

Class Ic agents inhibit the fast sodium channel and cause a marked depression of phase 0 of the action potential and slow conduction profoundly, but have minimal effects on repolarization. The dramatic effects of these agents on conduction may account for their significant proarrhythmic effects, which limit their use in patients with supraventricular arrhythmias and structural heart disease. Monitoring Parameters •• ECG (PR interval and QRS complex, arrhythmia frequency) Class II Agents

Beta-blocking agents inactivate sodium channels and depress phase 4 depolarization and increase the refractory period of the atrioventricular node. These agents have no effect on repolarization. Beta-blockers competitively antagonize catecholamine binding at beta-adrenergic receptors. Beta-blocking agents can be classified as selective or nonselective agents. Nonselective agents bind to beta-1 receptors

200

CHAPTER 7. Pharmacology

located on myocardial cells and beta-2 receptors located on bronchial and skeletal smooth muscle. Stimulation of beta-1 receptors causes an increase in heart rate and contractility, whereas stimulation of beta-2 receptors results in bronchodilation and vasodilation. Selective beta-blocking agents block beta-1 receptors in the heart at low or moderate doses, but they become less selective with increasing doses. Class II agents are used for the prophylaxis and treatment of both supraventricular arrhythmias and arrhythmias associated with catecholamine excess or stimulation, slowing the ventricular response in atrial fibrillation, lowering blood pressure, decreasing heart rate, and decreasing ischemia. Esmolol is useful especially for the rapid, short-term control of ventricular response in atrial fibrillation or flutter. Nonselective beta-blocking agents should be avoided or used with caution in patients with HF, atrioventricular nodal blockade, asthma, COPD, peripheral vascular disease, Raynaud phenomenon, and diabetes. Beta-1 selective beta-blocking agents should be used with caution in these populations. Monitoring Parameters •• ECG (heart rate, PR interval, arrhythmia frequency)

Monitoring Parameters •• ECG (PR and QT intervals, QRS complex, arrhythmia frequency) Dofetilide

Dofetilide is a class III antiarrhythmic (potassium channel blocker) agent used for rhythm conversion in patients with atrial fibrillation. The agent has been FDA approved with substantial restrictions, as prescribers must undergo drugspecific training before being permitted to prescribe. Initiation of drug therapy is also limited to hospitalized patients with continuous ECG monitoring and dosing based on a prespecified dosing algorithm. Proarrhythmic events and sudden cardiac death are the most substantial adverse events associated with dofetilide administration leading to these restrictions. The dose should be adjusted according to QT prolongation and creatinine clearance. If the QTc is greater than 400 millisecond, dofetilide is contraindicated. Dofetilide is also contraindicated in patients with severe renal impairment. Dose •• Modified based on creatinine clearance and QT or QTc interval. The usual recommended oral dose is 250 mcg bid.

Class III Agents

Class III agents (amiodarone, dofetilide, and sotalol) lengthen the action potential duration and effective refractory period and prolong repolarization. Additionally, amiodarone possesses alpha- and beta-blocking effects and calcium channel–blocking properties and inhibits the fast sodium channel. Sotalol possesses nonselective beta-blocking properties. Although torsades de pointes is relatively rare with amiodarone, precautions should be taken to prevent hypokalemia- or digitalis-toxicity–induced arrhythmias. Sotalol may be associated with proarrhythmic effects in the setting of hypokalemia, bradycardia, high sotalol dose, and QTinterval prolongation, and in patients with preexisting HF. Sotalol is also contraindicated in patients with severe renal impairment. Amiodarone

The antiarrhythmic effect of amiodarone is due to the prolongation of the action potential duration and refractory period, and secondarily through alpha-adrenergic and beta-adrenergic blockade. In patients with recent-onset (< 48 hours) atrial fibrillation or atrial flutter, IV amiodarone has been shown to restore normal sinus rhythm within 8 hours in approximately 60% to 70% of treated patients. Although IV amiodarone has been associated with negative inotropic effects, minimal side effects are associated with its short-term administration. Amiodarone is recommended as an option for the treatment of wide-complex tachycardia; stable, narrow-complex supraventricular tachycardia; stable, monomorphic or polymorphic ventricular tachycardia; atrial fibrillation and flutter; ventricular fibrillation; and pulseless ventricular tachycardia.

Ibutilide

Ibutilide is a class III antiarrhythmic agent indicated for the conversion of recent-onset atrial fibrillation and atrial flutter to normal sinus rhythm. Ibutilide causes the prolongation of the refractory period and action potential duration, with little or no effect on conduction velocity or automaticity. Its electrophysiologic effects are predominantly derived from activation of a slow sodium inward current. Ibutilide can cause slowing of the sinus rate and atrioventricular node conduction, but has no effect on heart rate, PR interval, or QRS interval. The drug is associated with minimal hemodynamic effects with no significant effect on cardiac output, mean pulmonary arterial pressure, or pulmonary capillary wedge pressure. Ibutilide has not been shown to lower blood pressure or worsen HF. Ibutilide has been shown to be more effective than procainamide and sotalol in terminating atrial fibrillation and atrial flutter. In addition, ibutilide has been shown to decrease the amount of joules required to treat resistant atrial fibrillation and atrial flutter during cardioversion. Depending on the duration of atrial fibrillation or flutter, ibutilide has an efficacy rate of 22% to 43% and 37% to 76%, respectively, for terminating these arrhythmias. Ibutilide is only available as an IV dosage form and cannot be used for the long-term maintenance of normal sinus rhythm. Sustained and nonsustained polymorphic ventricular tachycardia is the most significant adverse effect associated with ibutilide. The overall incidence of polymorphic ventricular tachycardia diagnosed as torsades de pointes was 4.3%, including 1.7% of patients in whom the arrhythmia was sustained and required cardioversion. Ibutilide administration should be avoided in patients receiving other agents

CARDIOVASCULAR SYSTEM PHARMACOLOGY 201

that prolong the QTc interval, including class Ia or III antiarrhythmic agents, phenothiazines, antidepressants, and some antihistamines. Before ibutilide administration, patients should be screened carefully to exclude high-risk individuals, such as those with a QTc interval greater than 440 millisecond or bradycardia. Serum potassium and magnesium levels should be measured and corrected before the drug is administered. The ibutilide infusion should be stopped in the event of nonsustained or sustained ventricular tachycardia or marked prolongation in the QTc interval. Patients should be monitored for at least 4 hours after the infusion or until the QTc returns to baseline, with longer monitoring if nonsustained ventricular tachycardia develops. Class IV Agents

Calcium channel–blocking agents inhibit calcium channels within the atrioventricular node and sinoatrial node, prolong conduction through the atrioventricular and sinoatrial nodes, and prolong the functional refractory period of the nodes, as well as depress phase 4 depolarization. Class IV agents are used for the prophylaxis and treatment of supraventricular arrhythmias and to slow the ventricular response in atrial fibrillation, flutter, and multifocal atrial tachycardia. Monitoring Parameters •• ECG (PR interval, arrhythmia frequency) Class V Agents

Adenosine, digoxin, and atropine possess different pharmacologic properties but ultimately affect the sinoatrial node or atrioventricular node. Adenosine

Adenosine depresses sinus node automaticity and atrioventricular nodal conduction. Adenosine is indicated for the acute termination of atrioventricular nodal and reentrant tachycardia, and for supraventricular tachycardias, including Wolff-Parkinson-White syndrome. Atropine

Atropine increases the sinus rate and decreases atrioventricular nodal conduction time and effective refractory period by decreasing vagal tone. The major indications for the use of atropine include symptomatic sinus bradycardia, and type I second-degree atrioventricular block. Digoxin

Digoxin slows the sinoatrial node rate of depolarization and conduction through the atrioventricular node primarily through vagal stimulating effects. Digoxin is indicated for the treatment of supraventricular tachycardia and for controlling ventricular response associated with supraventricular tachycardia. Monitoring Parameters •• ECG (heart rate, PR interval, ST segment, T wave, arrhythmia frequency)

Vasopressor Agents The 2012 Surviving Sepsis Campaign international guidelines for management of severe sepsis and septic shock recommend norepinephrine as the first-choice vasopressor in this setting. It is recommended that vasopressor therapy initially target a mean arterial pressure (MAP) of 65 mm Hg. Norepinephrine is a direct-acting vasoactive agent. It possesses alpha- and beta-adrenergic agonist properties producing mixed vasopressor and inotropic effects. Dopamine is recommended as an alternative vasopressor agent to norepinephrine only in highly selected patients (eg, patients with low risk of tachyarrhythmias and absolute or relative bradycardia). Dopamine is both an indirect-acting and a direct-acting agent. Dopamine works indirectly by causing the release of norepinephrine from nerve terminal storage vesicles as well as directly by stimulating alpha and beta receptors. Dopamine is unique in that it produces different pharmacologic responses based on the dose infused. At doses less than 5 mcg/kg/min, dopamine stimulates dopaminergic receptors in the kidneys. Doses between 5 and 10 mcg/kg/min are typically associated with an increase in inotropy resulting from stimulation of beta receptors in the heart, and doses above 10 mcg/kg/min stimulate peripheral alpha-adrenergic receptors, producing vasoconstriction and an increase in blood pressure. Dopamine and norepinephrine are both effective for increasing blood pressure. Dopamine raises cardiac output more than norepinephrine, but its use is limited by tachyarrhythmias. Norepinephrine may be a more effective vasopressor in some patients, thus the first line designation. Epinephrine is an option for addition to norepinephrine as needed to maintain adequate blood pressure in refractory patients. Epinephrine possesses alpha- and beta-adrenergic effects, increasing heart rate, contractility, and vasoconstriction with higher doses. Epinephrine’s use is reserved for when other vasoconstrictors are inadequate. Adverse effects include tachyarrhythmias; myocardial, mesenteric, renal, and extremity ischemia; and hyperglycemia. Phenylephrine is not recommended in the treatment of septic shock except in the following circumstances: (a) norepinephrine is associated with serious arrhythmias, (b) cardiac output is known to be high and blood pressure persistently low, or (c) as salvage therapy when combined inotrope/vasopressor drugs and low-dose vasopressin have failed to achieve the MAP target. Phenylephrine is a pure alpha-adrenergic agonist. It produces vasoconstriction without a direct effect on the heart, although it may cause a reflex bradycardia. Phenylephrine may be useful when dopamine, dobutamine, norepinephrine, or epinephrine cause tachyarrhythmias and when a vasoconstrictor is required. Vasopressin is an emerging therapeutic agent for the hemodynamic support of septic and vasodilatory shock. Vasopressin is a hormone that mediates vasoconstriction via V1-receptor activation on vascular smooth muscle. During septic shock, vasopressin levels are particularly low. Exogenous vasopressin administration is based on the theory of

202

CHAPTER 7. Pharmacology

hormone replacement. Vasopressin (up to 0.03 unit/min) can be added to norepinephrine with the intent of raising MAP to target or decreasing norepinephrine dosage. Low-dose vasopressin is not recommended as the single initial vasopressor for treatment of sepsis-induced hypotension, and vasopressin doses higher than 0.03-0.04 units/min should be reserved for salvage therapy (failure to achieve an adequate MAP with other vasopressor agents). It is important to note that harmful vasoconstriction of the gut vasculature will occur with dose escalation greater than 0.04 units/min. Dose •• See Table 23-3. Monitoring Parameters •• Blood pressure, heart rate, ECG, urine output, and hemodynamic parameters

Inotropic Agents (see Table 23-3) Catecholamines Dobutamine

Dobutamine produces pronounced beta-adrenergic effects such as increases in inotropy and chronotropy along with vasodilation. Dobutamine is useful especially for the acute management of low cardiac output states. Adverse effects associated with the use of dobutamine include tachyarrhythmias and ischemia. A trial of dobutamine infusion up to 20 mcg/kg/min may be administered or added to vasopressors (if in use) in the presence of: (a) myocardial dysfunction as suggested by elevated cardiac filling pressures and low cardiac output, or (b) ongoing signs of hypoperfusion, despite achieving adequate intravascular volume and adequate MAP. Norepinephrine and dobutamine can be titrated separately to maintain both blood pressure and cardiac output. Dopamine

Dopamine in the range of 5 to 10 mcg/kg/min typically produces an increase in inotropy and chronotropy. Doses above 10 mcg/kg/min typically produce alpha-adrenergic effects. Isoproterenol

Isoproterenol is a potent pure beta-receptor agonist. It has potent inotropic, chronotropic, and vasodilatory properties. Its use typically is reserved for temporizing life-threatening bradycardia. Adverse effects associated with isoproterenol include tachyarrhythmias, myocardial ischemia, and hypotension. Epinephrine

Epinephrine produces pronounced effects on heart rate and contractility and is used when other inotropic agents have not resulted in the desired pharmacologic response. Epinephrine is associated with tachyarrhythmias; myocardial, mesenteric, renal, and extremity ischemia; and hyperglycemia. Dose •• See Table 23-3.

Monitoring Parameters •• Blood pressure, heart rate, ECG, urine output, and hemodynamic parameters Phosphodiesterase Inhibitors Inamrinone and Milrinone

Inamrinone and milrinone produce increases in contractility and heart rate, as well as vasodilation. The mechanism of action of these agents is thought to be due to the inhibition of myocardial cyclic adenosine monophosphate phosphodiesterase (AMP) activity, resulting in increased cellular concentrations of cyclic AMP. These agents are useful in the setting of low-output HF and can be combined with dobutamine to increase cardiac output. Inamrinone is formerly known as amrinone. The product was renamed because of potential to confuse with amiodarone. Inamrinone has been associated with thrombocytopenia and a flulike syndrome. Both inamrinone and milrinone can produce tachyarrhythmias, ischemia, and hypotension. Dose •• Inamrinone: loading dose: 0.75 mg/kg; maintenance dose: 5 to 20 mcg/kg/min •• Milrinone: loading dose: 50 mcg/kg; maintenance dose: 0.375 to 0.75 mcg/kg/min Monitoring Parameters •• Blood pressure, heart rate, ECG, urine output, hemodynamic parameters, and platelet count (especially inamrinone)

ANTIBIOTIC PHARMACOLOGY There are a wide variety of antibiotic agents used in hospitalized patients. Commonly used antibiotic classes include beta lactams or penicillins (eg, penicillin G potassium, ampicillin ± sulbactam, oxacillin, nafcillin, ticarcillin ± clavulanic acid, and piperacillin ± tazobactam ), carbapenems (eg, meropenem, doripenem, and imipenem/cilastatin), monobactams (eg, aztreonam), cephalosporins (eg, cefazolin, cefotetan, cefoxitin, cefotaxime, ceftazidime, ceftriaxone, and cefepime), fluoroquinolones (eg, levofloxacin, moxifloxacin, and ciprofloxacin), macrolides (eg, azithromycin, erythromycin), lincosamides (eg, clindamycin), nitroimidazoles (eg, metronidazole), lipopetides (eg, daptomycin), oxazolidinones (eg, linezolid), glycopeptides (eg, vancomycin, telavancin), and aminoglycosides (eg, amikacin, tobramycin, and gentamicin). Since the development of the first antibiotic (penicillin) in 1944, microorganisms have consistently evolved by developing resistance to these agents. This has led to the need for newer and more innovative classes of antibiotics with different targets and ways to avoid resistance. Selection of the correct agent(s) is a key consideration, along with correct identification of the site of infection, and knowledge of resistance patterns within your institution. In some instances, combinations of different antibiotic classes (eg, aminoglycoside + beta lactam, or fluoroquinolone + beta lactam) may

ANTIBIOTIC PHARMACOLOGY 203

be used as a strategy to address resistance patterns. This is used particularly with gram negative organisms, and may be advocated vs monotherapy for certain indications. Additionally, the antibiotic dose, frequency, and/or length of infusion can also be modified as well. As noted, there are a number of factors related to optimal antibiotic therapy. A complete review of all antibiotic classes is beyond the scope of this text, and the focus of this section is on aminoglycosides and vancomycin due to the commonality of their usage and the link to therapeutic drug monitoring.

Aminoglycosides Gentamicin, tobramycin, and amikacin are the most commonly used aminoglycoside antibiotics in critically ill patients. These agents are typically used with antipseudomonal penicillins or third- or fourth-generation cephalosporins for additional gram-negative bacteria coverage. Occasionally they are added to vancomycin or a penicillin for synergy against staphylococcal, streptococcal, or enterococcal organisms. Aminoglycosides are not metabolized but are cleared from the body through the kidney by glomerular filtration with some proximal tubular reabsorption occurring. The clearance of aminoglycosides parallels glomerular filtration, and a reduction in glomerular filtration results in a reduction in clearance with elevation in serum concentrations. Additional factors accounting for the reduced aminoglycoside clearance in critically ill patients include the level of positive end-expiratory pressure and the use of vasoactive agents to maintain blood pressure and perfusion. Aminoglycosides are removed from the body by hemodialysis, peritoneal dialysis, continuous renal replacement therapy (CRRT), extracorporeal membrane oxygenation, exchange transfusion, and cardiopulmonary bypass. The major limiting factors in the use of aminoglycosides are drug-induced ototoxicity and nephrotoxicity. Ototoxicity results from the loss of sensory hair cells in the cochlea and vestibular labyrinth. Gentamicin is primarily vestibulotoxic, amikacin causes primarily cochlear damage, and tobramycin affects vestibular and cochlear function equally. Symptoms of ototoxicity typically appear within the first 1 to 2 weeks of therapy but may be delayed as long as 10 to 14 days after stopping therapy. Early damage may be reversible, but it may become permanent if the agent is continued. Vestibular toxicity may be manifested by vertigo, ataxia, nystagmus, nausea, and vomiting, but these symptoms may not be apparent in a sedated or paralyzed, critically ill patient. Cochlear damage occurs as subclinical high-frequency hearing loss that is usually irreversible and may progress to deafness even if the drug is discontinued. It is difficult to diagnose hearing loss in the absence of pretherapy audiograms. Risk factors for ototoxicity include advanced age, duration of therapy for more than 10 days, total dose, previous aminoglycoside therapy, and renal impairment. Nephrotoxicity has been estimated to occur in up to 30% of critically ill patients and typically develops 2 to

5 days after starting therapy. An increase in serum creatinine of 0.5 mg/dL above baseline has been arbitrarily defined as significant and as possible evidence of nephrotoxicity. Nephrotoxicity is associated with a reduction in glomerular filtration rate, impaired concentrating ability, increased serum creatinine, and increased urea nitrogen. In most cases, the renal insufficiency is nonoliguric and reversible. The mechanism of nephrotoxicity is possibly related to the inhibition of intracellular phospholipases in lysosomes of tubular cells in the proximal tubule, resulting in rupture or dysfunction of the lysosome, leading to proximal tubular necrosis. Risk factors for the development of aminoglycoside nephrotoxicity include advanced age, prolonged therapy, preexisting renal disease, preexisting liver disease, volume depletion, shock, and concurrent use of other nephrotoxins such as amphotericin B, cyclosporine, or cisplatin. Aminoglycosides are effectively removed during hemodialysis. However, there is a rebound in the serum concentration within the first 2 hours after the completion of hemodialysis as the serum and tissues reach a new equilibrium. Therefore, a serum concentration should be drawn at least 2 hours after a dialysis treatment. Typically a dose of 1 to 2 mg/kg of gentamicin or tobramycin (amikacin 4-8 mg/kg) is sufficient to increase the serum level into the therapeutic range after dialysis. Continuous hemofiltration is also effective at removing aminoglycosides. Up to 35% of a dose can be removed during a 24-hour period of CRRT. Initially, several blood samples may be required to determine the drug’s pharmacokinetic profile for dosing regimen adjustments. If the hemofiltration rate remains constant, aminoglycoside clearance should remain stable, permitting the administration of a stable dosing regimen. In this setting, drug concentration monitoring may only be required 2 to 3 times a week.

Vancomycin Vancomycin is a glycopeptide antibiotic active against gram-positive and certain anaerobic organisms. It exerts its antimicrobial effects by binding with peptidoglycan and inhibiting bacterial cell wall synthesis. In addition, the antibacterial effects of vancomycin also include alteration of bacterial cell wall permeability and selective inhibition of RNA synthesis. Vancomycin is minimally absorbed after oral administration. After single or multiple doses, therapeutic vancomycin concentrations can be found in ascitic, pericardial, peritoneal, pleural, and synovial fluids. Vancomycin penetrates poorly into cerebrospinal fluid (CSF), with CSF penetration being directly proportional to vancomycin dose and degree of meningeal inflammation. Vancomycin is eliminated through the kidneys primarily via glomerular filtration with a limited degree of tubular secretion. Nonrenal elimination occurs through the liver and accounts for about 30% of total clearance. The elimination half-life of vancomycin is 3 to 13 hours in patients with normal renal function and increases

204

CHAPTER 7. Pharmacology

in proportion to decreasing creatinine clearance. In acute renal failure, nonrenal clearance is maintained but eventually declines approaching the nonrenal clearance in chronic renal failure. In critically ill patients with reduced renal function, the increase in half-life may be due to a reduction in clearance as well as an increase in the volume of distribution. Vancomycin is removed minimally during hemodialysis with cuprophane filter membranes, so that dosage supplementation after hemodialysis is not necessary. Vancomycin’s half-life averages 150 hours in patients with chronic renal failure. With the newer high-flux polysulfone hemodialysis filters, vancomycin is removed to a greater degree, resulting in significant reductions in vancomycin serum concentrations. However, there is a significant redistribution period that takes place over the 12-hour period after the high-flux hemodialysis procedure with postdialysis concentrations similar to predialysis concentrations. Therefore, dose supplementation should be based on concentrations obtained at least 12 hours after dialysis. Vancomycin is removed very effectively by CRRT resulting in a reduction in half-life to 24 to 48 hours. Up to 33% of a dose can be eliminated during a 24-hour hemofiltration period. Supplemental doses of vancomycin may need to be administered every 2 to 5 days in patients undergoing CRRT. The most common adverse effect of vancomycin is the “red-man syndrome,” which is a histamine-like reaction associated with rapid vancomycin infusion and characterized by flushing, tingling, pruritus, erythema, and a macular papular rash. It typically begins 15 to 45 minutes after starting the infusion and abates 10 to 60 minutes after stopping the infusion. It may be avoided or minimized by infusing the dose over 2 hours or by pretreating the patient with diphenhydramine, 25 to 50 mg, 15 to 30 minutes before the vancomycin infusion. Other rare, but reported, adverse effects include rash, thrombophlebitis, chills, fever, and neutropenia.

PULMONARY PHARMACOLOGY Theophylline Theophylline is a phosphodiesterase inhibitor which produces bronchodilatation possibly by inhibiting cyclic AMP phosphodiesterase, inhibition of cellular calcium translocation, inhibition of leukotriene production, reduction in the reuptake or metabolism of catecholamines, and blockade of adenosine receptors. The use of theophylline for bronchospastic or lung disease has declined over the past decade. Most clinicians no longer use it as standard therapy for patients admitted to the hospital with bronchospasm; however, occasional patients may benefit from theophylline therapy. Theophylline should be used with caution in critically ill patients for several reasons. First, theophylline is metabolized in the liver and illnesses such as low cardiac output, HF, or hepatic failure may impair the ability of the liver to metabolize theophylline, resulting in increased serum concentrations. Second, antibiotics and anticonvulsants

routinely administered to critically ill patients are known to alter theophylline’s metabolism. In patients without a recent history of theophylline ingestion, the parenteral administration of 6 mg/kg of IV aminophylline (aminophylline = 85% theophylline) produces a serum theophylline concentration of approximately 10 mg/L. In patients with a recent history of theophylline ingestion, a serum theophylline concentration should be obtained before administering a loading dose. Once the serum concentration is known, a partial loading dose may be administered to increase the concentration to the desired level. Each 1.2 mg/kg aminophylline (theophylline 1.0 mg/ kg) increases the theophylline serum concentration approximately 2 mg/L. The loading dose should be administered over 30 to 60 minutes to avoid the development of tachycardia or arrhythmias. The maintenance infusion should be started following the completion of the loading dose and should be adjusted according to the patient’s underlying clinical status (smokers: 0.9 mg/kg/h; nonsmokers: 0.6 mg/kg/h; liver failure or HF: 0.3 mg/kg/h). These infusion rates are designed to achieve a serum concentration of approximately 10 mg/L. In most patients, concentrations above 10 mg/L are rarely indicated and may be associated with adverse effects. When an IV regimen is converted to an oral regimen, the total daily theophylline dose should be calculated and divided into two to four equal doses depending on the theophylline product selected for chronic administration. When switching to a sustained-release product, the IV infusion should be discontinued with administration of the first sustained-release dose to maintain constant serum theophylline concentrations. Overlapping of the oral dose and IV infusion is not recommended because of the increase in serum theophylline concentrations and the potential development of toxicity resulting from the absorption of the sustained-release product. Adverse effects occur more frequently at serum concentration above 20 mg/L and include anorexia, nausea, vomiting, epigastric pain, diarrhea, restlessness, irritability, insomnia, and headache. Serious arrhythmias and convulsions usually occur at serum concentrations above 35 mg/L, but have occurred at lower concentrations and may not be preceded by less serious toxicity. Theophylline concentrations should be determined daily until they are stable. In addition, theophylline concentrations should be obtained daily in unstable patients and in whom interacting drugs are started or stopped. Levels may be measured once or twice weekly if the patient, theophylline level, and drug regimen are stable. Dose •• Loading dose: 6 mg/kg IV or PO (each 1.2 mg/kg aminophylline increases the theophylline serum concentration by 2 mg/L) •• Continuous infusion: smokers: 0.9 mg/kg/h; nonsmokers: 0.6 mg/kg/h; liver failure, HF: 0.3 mg/kg/h

GASTROINTESTINAL PHARMACOLOGY 205

Monitoring Parameters •• Serum theophylline concentration, signs and symptoms of toxicity such as tachycardia, arrhythmias, nausea, vomiting, and seizures

Albuterol Albuterol is a selective beta-2 agonist, used to treat or prevent reversible bronchospasm. Adverse effects tend to be associated with inadvertent beta-1 stimulation leading to cardiovascular events including tachycardia, premature ventricular contractions, and palpitations. Monitoring Parameters •• Heart rate and pulmonary function tests

Levalbuterol Levalbuterol is the active enantiomer of racemic albuterol. Dose ranging studies in stable ambulatory asthmatics and patients with COPD have documented that levalbuterol 0.63 mg and albuterol 2.5 mg produced equivalent increases in the magnitude and duration of FEV1. There are no studies evaluating the efficacy of levalbuterol in hospitalized or critically ill patients. One study assessing the tachycardic effects of these agents in critically ill patients showed a clinically insignificant increase in heart rate following the administration of either agent. Monitoring Parameters •• Heart rate and pulmonary function tests

GASTROINTESTINAL PHARMACOLOGY Stress Ulcer Prophylaxis Stress ulcers are superficial lesions commonly involving the mucosal layer of the stomach that appear after stressful events such as trauma, surgery, burns, sepsis, or organ failure. Risk factors for the development of stress ulcers include coagulopathy, patients requiring mechanical ventilation for more than 48 hours, patients with a history of GI ulceration or bleeding within the past year, sepsis, an ICU stay longer than 1 week, occult bleeding lasting more than 6 days, and the use of high-dose steroids (> 0.250 mg of hydrocortisone or the equivalent). Numerous studies support the use of antacids, H2-receptor antagonists, and sucralfate. There are limited prospective comparative studies supporting the use of proton pump inhibitors (PPI) for preventing stress ulcer formation in critically ill patients. More studies are warranted to highlight the role of PPIs in this setting. Antacids

Antacids once were considered the primary agents for the prevention of stress gastritis. Their main attributes were their effectiveness and low cost. However, this was offset by the need to administer 30- to 120-mL doses every 1 to 2 hours. Large doses of antacids had the potential to produce large

gastric residual volumes, resulting in gastric distention and bloating, as well as increasing the risk for aspiration. Magnesium-containing antacids are associated with diarrhea and can produce hypermagnesemia in patients with renal failure. Aluminum-containing antacids are associated with constipation and hypophosphatemia. Large, frequent doses of antacids prevent the effective delivery of enteral nutrition. Finally, antacids are known to impair the absorption of digoxin, fluoroquinolones, and captopril. Also, alkalinization of the GI tract may predispose patients to nosocomial pneumonias with gram-negative organisms that originate in the GI tract. Dose •• 30 to 120 mL PO, NG q1-4h Monitoring Parameters •• Nasogastric aspirate pH, serum electrolytes, bowel function (diarrhea, constipation, bloating), hemoglobin, hematocrit, and nasogastric aspirate and stool guaiac H2 Antagonists

Ranitidine and famotidine essentially have replaced antacids as therapy for the prevention of stress gastritis. These agents have the benefit of requiring administration only every 6 to 12 hours or may be delivered by continuous infusion. When they are administered by continuous infusion, they may be added to parenteral nutrition solutions, decreasing the need for multiple daily doses. Each agent has been associated with thrombocytopenia and mental status changes. Mental status changes typically occur in elderly patients or in patients with reduced renal function in whom the doses have not been adjusted to account for the reduction in renal function. Also, similar to antacids, alkalinization of the GI tract with H2 antagonists may predispose patients to nosocomial pneumonias with gram-negative organisms that originate in the GI tract. Dose •• Ranitidine: Intermittent IV: 50 mg q8h; continuous infusion: 6.25 mg/h •• Famotidine: Intermittent IV: 20 mg q12h; continuous infusion: not recommended Monitoring Parameters •• Nasogastric aspirate pH, platelet count, hemoglobin, hematocrit, and nasogastric aspirate and stool guaiac Other Agents Sucralfate

Sucralfate is an aluminum disaccharide compound that has been shown to be safe and effective for the prophylaxis of stress gastritis. Sucralfate may work by increasing bicarbonate secretion, mucus secretion, or prostaglandin synthesis to prevent the formation of stress ulcers. Sucralfate has no effect

206

CHAPTER 7. Pharmacology

on gastric pH. It can be administered either as a suspension or as a tablet that can be partially dissolved in 10 to 30 mL of water and administered orally or through a nasogastric tube. Although sucralfate is free from systemic side effects, it has been reported to cause hypophosphatemia, constipation, and the formation of bezoars. Because sucralfate does not increase gastric pH, it lacks the ability to alkalinize the gastric environment and may decrease the development of gram-negative nosocomial pneumonias. Sucralfate has a limited role as an alternative to H2 antagonists in patients with thrombocytopenia or mental status changes. Dose •• 1 g PO, NG q6h Monitoring Parameters •• Hemoglobin, hematocrit, nasogastric aspirate, and stool guaiac

Acute Peptic Ulcer Bleeding Proton Pump Inhibitors

Proton pump inhibitors have demonstrated efficacy in preventing rebleeding and reducing transfusion requirements in several randomized-controlled trials. The rationale for adjunctive acid-suppressant therapy is based on in vitro data demonstrating clot stability and platelet aggregation enhancement at high gastric pHs > 6. High-dose IV PPI therapy in conjunction with therapeutic endoscopy is the most cost-effective approach for the management of hospitalized patients with acute peptic ulcer bleeding. Pantoprazole and esomeprazole are available in oral and injectable forms, while lansoprazole and omeprazole are available in oral forms only. It is advisable to transition to oral/enteral PPI therapy, if possible, after 72 hours of IV therapy. The 72-hour time period for continuous infusions is the longest duration that has been studied. Dose •• Pantoprazole and esomeprazole: IV bolus dosing: 40 to 80 mg IV q12h for 72 hours; continuous infusion: 80 mg IV bolus; then 8 mg/h for 72 hours Monitoring Parameters •• Hemoglobin, hematocrit, and stool guaiac

Variceal Hemorrhage Upper GI bleeding is a common problem encountered in the intensive care unit. Its mortality remains around 10%. Vasoactive drugs to control bleeding play an important role in the immediate treatment of acute upper GI bleeding associated with variceal hemorrhage. Vasopressin

Vasopressin remains a commonly used agent for acute variceal bleeding. Vasopressin is a nonspecific vasoconstrictor

that reduces portal pressure by constricting the splanchnic bed and reducing blood flow into the portal system. Vasopressin is successful in stopping bleeding in about 50% of patients. Many of the adverse effects of vasopressin are caused by its relative nonselective vasoconstrictor effect. Myocardial, mesenteric, and cutaneous ischemia have been reported in association with its use. Drug-related adverse effects have been reported in up to 25% of patients receiving vasopressin. The use of transdermal or IV nitrates with vasopressin reduces the incidence of these adverse effects. Dose •• 0.3 to 0.9 units/min Monitoring Parameters •• Hemoglobin, hematocrit, nasogastric aspirate, stool guaiac, ECG, signs and symptoms of ischemia, blood pressure, and heart rate Octreotide

Octreotide, the longer acting synthetic analog of somatostatin, reduces splanchnic blood flow and has a modest effect on hepatic blood flow and wedged hepatic venous pressure with little systemic circulation effects. Although octreotide produces the same results as vasopressin in the control of bleeding and transfusion requirements, it produces significantly fewer adverse effects. Continuous infusion of octreotide has been shown to be as effective as injection sclerotherapy in control of variceal hemorrhage. Dose •• Initial bolus dose: 100 mcg, followed by 50 mcg/h continuous infusion Monitoring Parameters •• Hemoglobin, hematocrit, nasogastric aspirate, and stool guaiac Propranolol

Propranolol has been shown to reduce portal pressure both acutely and chronically in patients with portal hypertension by reducing splanchnic blood flow. The primary use of propranolol has been in the prevention of variceal bleeding. Propranolol or other beta-blockers should be avoided in patients experiencing acute GI bleeding, because beta-blocking agents may prevent the compensatory tachycardia needed to maintain cardiac output and blood pressure in the setting of hemorrhage. Monitoring Parameters •• Hemoglobin, hematocrit, heart rate, and blood pressure

RENAL PHARMACOLOGY Diuretics Diuretics may be categorized in a number of ways, including site of action, chemical structure, and potency. Although

RENAL PHARMACOLOGY 207

many diuretics are available for oral and IV administration, intravenously administered agents typically are given to critically ill patients because of their guaranteed absorption and more predictable responses. Therefore, the primary agents used in intensive care units are the intravenously administered loop diuretics, thiazide diuretics, and osmotic agents. However, the oral thiazidelike agent, metolazone, is used commonly in combination with loop diuretics to maintain urine output for patients with diuretic resistance. Monitoring Parameters •• Urine output, blood pressure, renal function, electrolytes, weight, fluid balance, and hemodynamic parameters (if applicable) Loop Diuretics

Loop diuretics (furosemide, bumetanide, torsemide) act by inhibiting active transport of chloride and possibly sodium in the thick ascending loop of Henle. Administration of loop diuretics results in enhanced excretion of sodium, chloride, potassium, hydrogen, magnesium, ammonium, and bicarbonate. Maximum electrolyte loss is greater with loop diuretics than with thiazide diuretics. Furosemide, bumetanide, and torsemide have some renal vasodilator properties that reduce renal vascular resistance and increase renal blood flow. Additionally, these three agents decrease peripheral vascular resistance and increase venous capacitance. These effects may account for the decrease in left ventricular filling pressure that occurs before the onset of diuresis in patients with HF. Loop diuretics typically are used for the treatment of edema associated with HF or oliguric renal failure, the management of hypertension complicated by HF or renal failure, in combination with hypotensive agents in the treatment of hypertensive crisis, especially when associated with acute pulmonary edema or renal failure, and in combination with 0.9% sodium chloride to increase calcium excretion in patients with hypercalcemia. Common adverse effects associated with loop diuretic administration include hypotension from excessive reduction in plasma volume, hypokalemia and hypochloremia resulting in metabolic alkalosis, and hypomagnesemia. Reduction in these electrolytes may predispose patients to the development of supraventricular and ventricular ectopy. Tinnitus, with reversible or permanent hearing impairment, may occur with the rapid administration of large IV doses. Typically, IV bolus doses of furosemide should not be administered faster than 40 mg/min. Dose •• Furosemide: IV bolus: 10 to 100 mg q1-6h; continuous infusion: 1 to 15 mg/h •• Bumetanide: IV bolus: 0.5 to 2.5 mg q1-2h; continuous infusion: 0.08 to 0.30 mg/h •• Torsemide: IV bolus: 5 to 20 mg qd

Thiazide Diuretics

Thiazide (IV chlorothiazide) and thiazidelike (PO metolazone) diuretics enhance excretion of sodium, chloride, and water by inhibiting the transport of sodium across the renal tubular epithelium in the cortical diluting segment of the nephron. Thiazides also increase the excretion of potassium and bicarbonate. Thiazide diuretics are used in the management of edema and hypertension as monotherapy or in combination with other agents. They have less potent diuretic and antihypertensive effects than loop diuretics. Intravenously administered chlorothiazide or oral metolazone is often used in combination with loop diuretics in patients with diuretic resistance. By acting at a different site in the nephron, this combination of agents may restore diuretic responsiveness. Thiazide diuretics decrease glomerular filtration rate, and this effect may contribute to their decreased efficacy in patients with reduced renal function (glomerular filtration rate < 20 mL/min). Metolazone, unlike thiazide diuretics, does not substantially decrease glomerular filtration rate or renal plasma flow and often produces a diuretic effect even in patients with glomerular filtration rates less than 20 mL/min. Adverse effects that may occur with the administration of thiazide diuretics include hypovolemia and hypotension, hypochloremia and hypokalemia resulting in a metabolic alkalosis, hypercalcemia, hyperuricemia, and the precipitation of acute gouty attacks. Dose •• Chlorothiazide: 500 to 1000 mg IV q12h •• Metolazone: 2.5 to 20.0 mg PO qd Osmotic Diuretics Mannitol

Mannitol is an osmotic diuretic commonly used in patients with increased intracranial pressure. Mannitol produces a diuretic effect by increasing the osmotic pressure of the glomerular filtrate and preventing the tubular reabsorption of water and solutes. Mannitol increases the excretion of sodium, water, potassium, and chloride, as well as other electrolytes. Mannitol is used to treat acute oliguric renal failure, and reduce intracranial and intraocular pressures. The renal protective effects of mannitol may be due to its ability to prevent nephrotoxins from becoming concentrated in the tubular fluid. However, its ability to prevent or reverse acute renal failure may be because of restoring renal blood flow, glomerular filtration rate, urine flow, and sodium excretion. To be effective in preventing or reversing renal failure, mannitol must be administered before reductions in glomerular filtration rate or renal blood flow have resulted in acute tubular damage. Mannitol is useful in the treatment of cerebral edema, especially when there is evidence of herniation or the development of cord compression. The most severe adverse effect of mannitol is overexpansion of extracellular fluid and circulatory overload, producing acute HF and pulmonary edema. This effect typically

208

CHAPTER 7. Pharmacology

occurs in patients with severely impaired renal function. Therefore, mannitol should not be administered to individuals in whom adequate renal function and urine flow have not been established. Dose •• 0.25 to 0.50 g/kg, then 0.25 to 0.50 g/kg q4h Monitoring Parameters •• Urine output, blood pressure, renal function, electrolytes, weight, fluid balance, hemodynamic parameters (if applicable), serum osmolarity, and intracranial pressure (if applicable)

HEMATOLOGIC PHARMACOLOGY Anticoagulants Unfractionated Heparin

Unfractionated heparin consists of a group of mucopolysaccharides derived from the mast cells of porcine intestinal tissues. It binds with antithrombin III, accelerating the rate at which antithrombin III neutralizes coagulation factors II, VII, IX, X, XI, and XII. Unfractionated heparin is used for prophylaxis and treatment of venous thrombosis and pulmonary embolism, atrial fibrillation with embolization, and treatment of acute disseminated intravascular coagulation. Subcutaneously administered unfractionated heparin is absorbed slowly and completely over the dosing interval. The total amount of unfractionated heparin required to achieve the same degree of anticoagulation over the same time period does not appear to differ whether the unfractionated heparin is administered subcutaneously or intravenously. The apparent volume of distribution of unfractionated heparin is directly proportional to body weight, and it has been suggested that the dose should be based on ideal body weight in obese patients. Others suggest that in obese patients the dose should be normalized to total body weight. The metabolism and elimination of unfractionated heparin involves the process of depolymerization and desulfation. Enzymes reported to be involved in unfractionated heparin metabolism include heparinase and desulfatase, which cleave unfractionated heparin into oligosaccharides. The half-life of unfractionated heparin ranges from 0.4 to 2.5 hours. Patients with underlying thromboembolic disease have been shown to have shorter elimination half-lives, faster clearance, and require larger doses to maintain adequate thrombotic activity. A weight-based nomogram is utilized with a loading dose followed by a continuous infusion. The infusion is titrated based on activated PTT monitoring. The main adverse effects may be attributed to excessive anticoagulation. Bleeding occurs in 3% to 20% of patients receiving short-term, high-dose therapy. Bleeding is increased threefold when the PTT is 2.0 to 2.9 times above control and eightfold when the PTT is more than 3.0 times the control

value. Unfractionated heparin–induced thrombocytopenia may occur in 1% to 5% of patients receiving the drug. The PTT is the test used to monitor and adjust unfractionated heparin doses. Although unfractionated heparin is typically administered as a continuous infusion, it is important that samples are collected as close to steady state as possible. After starting unfractionated heparin therapy or adjusting the dose, PTT values should be drawn at least 6 to 8 hours after the change. Samples drawn too early are misleading and may result in inappropriate dose adjustments. Once the unfractionated heparin dose has been determined, daily monitoring of the PTT for minor adjustments in the unfractionated heparin dose is indicated. Large variations in subsequent coagulation tests should be investigated to ensure that the patient’s condition has not changed or the patient is not developing thrombocytopenia. Platelet counts should be monitored every 2 to 3 days while a patient is receiving unfractionated heparin to assess for unfractionated heparin–induced thrombocytopenia, thrombosis, or hemorrhage. Hemoglobin and hematocrit should be monitored every 2 to 3 days to assess for the presence of bleeding. Additionally sputum, urine, and stool should be examined for the presence of blood. Patients should be examined for signs of bleeding at IV access sites and for the development of hematomas and ecchymosis. In addition, IM injections should be avoided in patients receiving unfractionated heparin and elective invasive procedures should be avoided or rescheduled. Dose •• Individualized dosing: bolus: 80 units/kg followed by a continuous infusion of 18 units/kg/h; infusion rates should be adjusted to maintain a PTT between 1.5 and 2.0 times the control value Monitoring Parameters •• PTT, hemoglobin, hematocrit, and signs of active bleeding Low-Molecular-Weight Heparins

Low-molecular-weight heparins have a role in the treatment of deep venous thrombosis, pulmonary embolism, and acute MI. Low-molecular-weight heparins are less time consuming for nurses and laboratories and more comfortable for patients by allowing them to be discharged earlier from the hospital. The use of a fixed-dose regimen avoids the need for serial monitoring of the PTT and follow-up dose adjustments. Enoxaparin is the most studied low molecularweight heparin. Its dose for the treatment of deep venous thrombosis, pulmonary embolism, and acute MI is 1 mg/kg q12h. Dalteparin is another agent that has been shown to be as effective as unfractionated heparin in the treatment of thromboembolic disease and acute MI. Dalteparin 200 units/kg once daily is the typical dose used for the treatment of thromboembolic disease; 120 units/kg followed by 120 units/kg 12 hours later has been used in patients with acute MI receiving

HEMATOLOGIC PHARMACOLOGY 209

streptokinase. Warfarin can be started with the first dose of enoxaparin or dalteparin. Enoxaparin or dalteparin should be continued until two consecutive therapeutic international normalized ratio (INR) values are achieved, typically in about 5 to 7 days. Both dalteparin and enoxaparin are primarily renally eliminated with the potential for drug accumulation in patients with renal impairment. The approach for managing these patients differs between the two drugs. Because these agents work by inhibiting factor Xa activity, it is possible to monitor their anticoagulation by measuring anti-factor Xa levels. This is a useful monitoring tool, particularly when compared with serum drug levels. Doses of either agent may be adjusted based on anti-factor Xa levels in patients with significant renal impairment (ie, creatinine clearance < 30 mL/min). The dosing adjustment for enoxaparin in patients with creatinine clearances less than 30 mL/min is to extend the dosing interval from 12 hours to 24 hours in both prophylaxis and treatment of thrombosis. No such dosage adjustment guideline has been approved for dalteparin, thus anti-factor Xa levels may be required. Several studies have documented that critically ill patients have significantly lower anti-Xa levels in response to single daily doses when compared to patients on general medical wards. Factor Xa activity may need to be monitored in critically ill patients to adjust doses to ensure adequate anticoagulation to prevent deep venous clots from developing. Dose •• Enoxaparin: 1 mg/kg SC q12h Monitoring parameters •• Hemoglobin, hematocrit, and signs of active bleeding, anti-factor Xa levels Warfarin

Warfarin prevents the conversion of vitamin K back to its active form from the vitamin K epoxide, impairing the formation of vitamin K–dependent clotting factors II, VII, IX, X, protein C, and protein S. Warfarin is indicated in the treatment of venous thrombosis or pulmonary embolism following full-dose parenteral anticoagulant (eg, unfractionated or low-molecular weight heparin) therapy. Warfarin is also used for chronic therapy to reduce the risk of thromboembolic episodes in patients with chronic atrial fibrillation. Warfarin is rapidly and extensively absorbed from the GI tract. Peak plasma concentrations occur between 60 and 90 minutes after an oral dose with bioavailability ranging between 75% and 100%. Albumin is the principal binding protein with 97.5% to 99.9% of warfarin being bound. Warfarin’s metabolism is stereospecific. The R-isomer is oxidized to 6-hydroxywarfarin and further reduced to 9S, 11R-warfarin alcohols. The S-isomer is oxidized to 7-hydroxywarfarin and further reduced to 9S, 11R-warfarin

alcohols. The stereospecific isomer alcohol metabolites have anticoagulant activity in humans. The warfarin alcohols are renally eliminated. The elimination half-lives of the two warfarin isomers differ substantially. The S-isomer halflife is approximately 33 hours and the R-isomer half-life is 45 hours. Warfarin therapy may be started on the first day of unfractionated or low-molecular weight heparin therapy. Traditionally, warfarin 5 mg daily is started for the first 2 to 3 days then adjusted to maintain the desired prothrombin time (PT) or INR. The timing of INR measurements relative to changes in daily dose is important. After the administration of a warfarin dose, the peak depression of coagulation occurs in about 36 hours. It is important to select an appropriate time during a given dosing interval and perform coagulation tests consistently at that time. After the first four to five doses, the fluctuation in the INR over a 24-hour dosing interval is minimal. The time course of stabilization of warfarin plasma concentrations and coagulation response during continued administration of maintenance doses is less clear. A minimum of 10 days appears to be necessary before the doseresponse curve shows interval-to-interval stability. During the first week of therapy two INR measurements should be determined to assess the impact of warfarin accumulation on INR. Several factors should be assessed when evaluating an unexpected response to warfarin. Laboratory results should be verified to exclude inaccurate or spurious results. The medication profile should be reviewed to exclude drugdrug interactions including changes in warfarin product, and the patient should be evaluated for disease-drug interactions, nutritional-drug interactions, and noncompliance. Bleeding is the major complication associated with the use of warfarin, occurring in 6% to 29% of patients receiving the drug. Bleeding complications include ecchymoses, hemoptysis, and epistaxis, as well as fatal or life-threatening hemorrhage. Dose •• 5 mg PO qd × 3 days, then adjusted to maintain the INR between 2 and 3. •• To prevent thromboembolism associated with prosthetic heart valves, the dose should be adjusted to maintain an INR between 2.5 and 3.5. Monitoring Parameters •• INR, hemoglobin, hematocrit, and signs of active bleeding

Factor Xa Inhibitors Rivaroxaban

Rivaroxaban is an oral factor Xa inhibitor, indicated for venous thromboembolism (VTE) prophylaxis post hip or knee replacement or prophylaxis of embolism or cerebrovascular accident (CVA) in patients with nonvalvular atrial fibrillation. Additionally, the agent is also indicated for PE and deep venous thrombosis (DVT) treatment.

210

CHAPTER 7. Pharmacology

Dose •• VTE prophylaxis post-surgery: 10 mg PO qd •• Atrial fibrillation, Nonvalvular-CVA prophylaxis: 20 mg PO qd •• DVT or PE treatment, and secondary prophylaxis: 15 mg PO bid × 21 days followed by 20 mg PO qd Monitoring Parameters •• Hemoglobin, hematocrit, renal function, and signs of active bleeding

Direct Thrombin Inhibitors Dabigatran

Dabigatran is an oral direct thrombin inhibitor, indicated for use for stroke prevention in patients with non-valvular atrial fibrillation. In clinical trials, dabigatran was superior to warfarin in reducing the risk for stroke and systemic embolism with lower minor bleed risk comparatively. Dabigatran also has a developing role as VTE prophylaxis after total knee or hip arthroplasty, as well as the treatment of DVT and PE. It is important to note that dabigatran capsules cannot be opened for feeding tube or oral administration. Dose •• 150 mg PO bid Monitoring Parameters •• Hemoglobin, hematocrit, aPTT, ecarin clotting time (ECT), and signs of active bleeding Bivalirudin

Bivalirudin is an anticoagulant with direct thrombin inhibitor properties. Bivalirudin, when given with aspirin, is indicated for use as an anticoagulant in patients with unstable angina undergoing coronary angioplasty. It has been used as a substitute for unfractionated heparin; potential advantages over unfractionated heparin include activity against clot-bound thrombin, more predictable anticoagulation, and no inhibition by components of the platelet release reaction. One study has suggested the efficacy of SC bivalirudin in preventing deep vein thrombosis in orthopedic surgery patients. The place in therapy of bivalirudin will be determined by further comparisons with heparin, low-molecular-weight unfractionated heparins, and recombinant hirudin. Dose •• Bolus: 1 mg/kg •• Continuous infusion: 2.5 mg/kg/h × 4 hours, if necessary 0.2 mg/kg/h for up to 20 hours Monitoring Parameters •• Activated PTT, activated clotting time (ACT), hemoglobin, hematocrit, and signs of active bleeding

heparin–induced thrombocytopenia and for use in percutaneous coronary interventions (PCIs). It has also shown effectiveness in ischemic stroke and as an adjunct to thrombolysis in patients with acute MI. Further studies are needed to establish effectiveness for other indications. Argatroban is dosed as a continuous infusion that is titrated based on activated PTT, similar to unfractionated heparin. During PCI, the ACT may be used. A notable drug-laboratory value interaction is the increase in PT and INR values that occurs with argatroban therapy, which may complicate the monitoring of warfarin therapy once oral anticoagulation is initiated. Dose •• Percutaneous coronary intervention: Bolus: 350 mcg/ kg; continuous infusion: 25 mcg/kg/min •• Heparin-induced thrombocytopenia with thrombosis: continuous infusion: 2 mcg/kg/min Monitoring Parameters •• Activated PTT, ACT, PT, INR, hemoglobin, hematocrit, and signs of active bleeding

Glycoprotein IIb/IIIa Inhibitor Glycoprotein IIb/IIIa inhibitors are recommended, in addition to aspirin and unfractionated heparin, in patients with acute coronary syndrome awaiting PCI. If the glycoprotein IIb/IIIa inhibitor is started in the catheterization laboratory just before PCI, abciximab is the agent of choice. Dose •• Abciximab: Bolus: 0.25 mg/kg over 10 to 60 minutes; continuous infusion: 0.125 mcg/kg/min for 12 hours (maximum infusion of 10 mcg/kg/min) •• Tirofiban: Bolus infusion: 0.4 mcg/kg/min over 30 minutes; continuous infusion: 0.1 mcg/kg/min for 12 to 24 hours after angioplasty or arthrectomy •• Eptifibatide: Bolus: 180 mcg/kg; continuous infusion: 2 mcg/kg/min until discharge or coronary artery bypass grafting (maximum of 72 hours) Monitoring Parameters •• Platelet count, hemoglobin, hematocrit, and signs of active bleeding

Thrombolytic Agents Thrombolytic agents may be beneficial as reperfusion therapy in ST-Elevation Myocardial Infarction (STEMI). The 2013 American College of Cardiology Foundation/American Heart Association guidelines for the management of STEMI include the following recommendations in order from most supported by published literature (Class I) to least supported (Class III). Class I Recommendations

Argatroban

Argatroban is a selective thrombin inhibitor indicated for the prevention or treatment of thrombosis in unfractionated

•• In the absence of contraindications, fibrinolytic therapy should be given to patients with STEMI and onset

IMMUNOSUPPRESSIVE AGENTS 211

of ischemic symptoms within the previous 12 hours when it is anticipated that primary percutaneous coronary intervention (PCI) cannot be performed within 120 minutes of first medical contact. Class IIa Recommendations

•• In the absence of contraindications and when PCI is not available, fibrinolytic therapy is reasonable for patients with STEMI if there is clinical and/or electrocardiographic evidence of ongoing ischemia within 12 to 24 hours of symptom onset and a large area of myocardium at risk or hemodynamic instability. Class III Recommendations

•• Fibrinolytic therapy should not be administered to patients with ST depression except when a true posterior (inferobasal) MI is suspected or when associated with ST elevation in lead aVR. Absolute contraindications to the use of thrombolytic agents include any active or recent bleeding; suspected aortic dissection; intracranial or intraspinal neoplasm; arteriovenous malformation or aneurysms; neurosurgery or significant closed head injury within the previous 3 months; ischemic stroke within the previous 3 months (except acute ischemic stroke within 3 hours); or facial trauma in the preceding 3 months. Relative contraindications include acute or chronic severe uncontrolled hypertension; ischemic stroke more than 3 months prior; traumatic or prolonged cardiopulmonary resuscitation greater than 10 minutes in duration; major surgery within the previous 3 weeks; internal bleeding within 2 to 4 weeks; noncompressible vascular punctures; prior allergic reaction to thrombolytics; pregnancy; active peptic ulcer; and current anticoagulation (risk increasing with increasing INR). Adverse effects include bleeding from the GI or genitourinary tracts, as well as gingival bleeding and epistaxis. Superficial bleeding may occur from trauma sites such as those for IV access or invasive procedures. Intramuscular injections, and noncompressible arterial punctures, should be avoided during thrombolytic therapy. Monitoring Parameters •• For short-term thrombolytic therapy of MI: ECG, signs and symptoms of ischemia, and signs and symptoms of bleeding at IV injection sites (laboratory monitoring is of little value) •• Continuous infusion therapy: Thrombin time, activated PTT, and fibrinogen, in addition to abovementioned monitoring parameters Alteplase

Alteplase (recombinant tissue-type plasminogen activator) has a high affinity for fibrin-bound plasminogen, allowing activation on the fibrin surface. Most plasmin formed remains bound to the fibrin clot, minimizing systemic effects. The risk of an intracerebral bleed is approximately 0.5%.

Dose •• Acute MI: Accelerated infusion: patients over 67 kg, total dose 100 mg IV (15 mg IV bolus, then 50 mg over 30 minutes, then 35 mg over 60 minutes) •• Acute MI: Accelerated infusion: patients 67 kg or less, (15 mg IV bolus, then 0.75 mg/kg over 30 minutes, then 0.5 mg/kg over 60 minutes); total dose not to exceed 100 mg •• Acute MI: 3-hour infusion: weight 65 kg or more, 60 mg IV in the first hour (6 to 10 mg of which to be given as bolus), then 20 mg over the second hour, and 20 mg over the third hour •• Acute MI: 3-hour infusion: weight less than 65 kg, 1.25 mg/kg IV administered over 3 hours, give 60% in the first hour (10% of which to be given as bolus), give remaining 40% over the next 2 hours •• Pulmonary embolism: 100 mg IV over 2 hours Tenecteplase

Tenecteplase (recombinant TNK-tissue type plasminogen activator) has a longer elimination half-life (20-24 minutes) and is more resistant to inactivation by plasminogen activator inhibitor-1 than alteplase. Tenecteplase appears more fibrin specific than alteplase, which may account for a lower rate of noncerebral bleeding comparatively. However, there have been reports of antibody development to tenecteplase. Tenecteplase and alteplase have similar clinical efficacy for thrombolysis after MI. Dose •• Acute MI: 30 to 50 mg (based on weight) IV over 5 seconds Reteplase

Reteplase is a recombinant plasminogen activator for use in acute MI and pulmonary embolism as a thrombolytic agent. Reteplase has a longer half-life (13-16 minutes) than that of alteplase, allowing for bolus administration. The dosing regimen requires double bolus doses. Dose •• Acute MI and pulmonary embolism: Two 10-units I V bolus doses, infused over 2 minutes via a dedicated line. The second dose is administered 30 minutes after the initiation of the first injection.

IMMUNOSUPPRESSIVE AGENTS Cyclosporine Cyclosporine is used to prevent allograft rejection after solid organ transplantation and graft-vs-host disease in bone marrow transplant patients. Unlike other immunosuppressive agents, cyclosporine does not suppress bone marrow function. Cyclosporine inhibits cytokine synthesis and receptor expression needed for T-lymphocyte activation by interrupting signal transduction. A lack of cytokine disrupts

212

CHAPTER 7. Pharmacology

the activation and proliferation of the helper and cytotoxic T-cells that are essential for rejection. Cyclosporine is poorly absorbed from the GI tract with bioavailability averaging 30%. Its absorption is influenced by the type of organ transplant, time from transplantation, presence of biliary drainage, liver function, intestinal dysfunction, and the use of drugs that alter intestinal function. Cyclosporine is metabolized by cytochrome P-450 isoenzyme 3a to numerous metabolites with more than 90% of the dose excreted into the bile and eliminated in the feces. The kidneys eliminate less than 1% of the dose. There is no evidence that the metabolites have significant immunosuppressive activity compared with cyclosporine and none of the metabolites are known to cause nephrotoxicity. Because of poor oral absorption, the oral dose is 3 times the IV dose. When converting from IV to oral administration, it is important to increase the oral dose by a factor of three to maintain stable cyclosporine concentrations. The oral solution can be administered diluted with chocolate milk or juice and administered through a nasogastric tube. The tube should be flushed before and after cyclosporine is administered to ensure complete drug delivery and optimal absorption. The microemulsion formulation of cyclosporine capsules and solution has increased bioavailability compared to the original formulation of cyclosporine capsules and solution. These formulations are not bioequivalent and cannot be used interchangeably. Converting from cyclosporine capsules and solution for microemulsion to cyclosporine capsules and oral solution using as 1:1 mg/kg/day ratio may result in lower cyclosporine blood concentrations. Conversion between formulations should be made utilizing increased monitoring to avoid toxicity due to high concentrations or possible organ rejection owing to low concentrations. Nephrotoxicity is cyclosporine’s major adverse effect. Three types of nephrotoxicity have been shown to occur. The first is an acute reversible reduction in glomerular filtration; second, tubular toxicity with possible enzymuria and aminoaciduria; and third, irreversible interstitial fibrosis and arteriopathy. The exact mechanism of cyclosporine nephrotoxicity is unclear, but may involve alterations in the various vasoactive substances in the kidney. Other side effects include a dose-dependent increase in bilirubin that occurs within the first 3 months after transplantation. Hyperkalemia can develop secondary to cyclosporine nephrotoxicity. Cyclosporine-induced hypomagnesemia can cause seizures. Neurotoxic effects such as tremors and paresthesias may occur in up to 15% of treated patients. Hypertension occurs frequently and may be because of the nephrotoxic effects or renal vasoconstrictive effects of the drug.

Tacrolimus (FK506) Tacrolimus is a macrolide antibiotic produced by the fermentation broth of Streptomyces tsukubaensis. Although it bears no structural similarity to cyclosporine, its mode of action

parallels cyclosporine. Tacrolimus exhibits similar in vitro effects to cyclosporine, but at concentrations 100 times lower than those of cyclosporine. Tacrolimus is primarily metabolized in the liver by the cytochrome P-450 isoenzyme 3A4 to at least 15 metabolites. There is also some evidence to suggest that tacrolimus may be metabolized in the gut. The 13-O-demethyl-tacrolimus appears to be the major metabolite in patient blood. Less than 1% of a dose is excreted unchanged in the urine of liver transplant patients. Renal clearance accounts for less than 1% of total body clearance. The mean terminal elimination half-life is 12 hours but ranges from 8 to 40 hours. Patients with liver impairment have a longer tacrolimus half-life, reduced clearance, and elevated tacrolimus concentrations. The elevated tacrolimus concentrations are associated with increased nephrotoxicity in these patients. Because tacrolimus is primarily metabolized by the cytochrome P-450 enzyme system, it is anticipated that drugs known to interact with this enzyme system may affect tacrolimus disposition. In most cases, IV therapy can be switched to oral therapy within 2 to 4 days after starting therapy. The oral dose should start 8 to 12 hours after the IV infusion has been stopped. The usual initial oral dose is 150 to 300 mcg/kg/day, administered in two divided doses every 12 hours. Nephrotoxicity is the most common adverse effect associated with the use of tacrolimus. Nephrotoxicity occurs in up to 40% of transplant patients receiving tacrolimus. Other side effects observed during tacrolimus therapy include headache, tremor, insomnia, diarrhea, hypertension, hyperglycemia, and hyperkalemia.

Sirolimus (Rapamycin) Sirolimus is an immunosuppressive agent used to the prophylaxis of organ rejection in patients receiving renal transplants. It typically is used in regimens containing cyclosporine and corticosteroids. Sirolimus inhibits T-lymphocyte activation and proliferation that occurs in response to antigenic and cytokine stimulation. Sirolimus also inhibits antibody production. Sirolimus is administered orally once daily. The initial dose of sirolimus should be administered as soon as possible after transplantation. It is recommended that sirolimus be taken 4 hours after cyclosporine modified oral solution or capsules. Routine therapeutic drug level monitoring is not required in most patients. Sirolimus levels should be monitored in patients with hepatic impairment, during concurrent administration of cytochrome P-450 cyp3a4 inducers and inhibitors, or when cyclosporine dosing is reduced or discontinued. Mean sirolimus whole blood trough concentrations, as measured by immunoassay, are approximately 9 ng/mL for the 2-mg/day dose and 17 ng/mL for the 5-mg/ day dose. Results from other assays may differ from those with an immunoassay. On average, chromatographic methods such as HPLC or mass spectroscopy yield results that are 20% lower than immunoassay whole blood determinations.

SPECIAL DOSING CONSIDERATIONS 213

SPECIAL DOSING CONSIDERATIONS Continuous Renal Replacement Therapy The techniques used to provide renal support to critically ill patients have changed considerably during the last 20 years. Continuous renal replacement therapies such as continuous arteriovenous hemofiltration (CAVH) or continuous venovenous hemofiltration (CVVH), are replacing conventional hemodialysis in critically ill patients. Recommendations for drug dosage adjustments in conventional dialysis cannot be applied to these newer techniques because of their continuous character and lower clearance rates. Clinical studies on the influence of CRRT on drug elimination are limited. Hemofiltration alone typically produces an effective glomerular filtration rate of approximately 20 mL/min, and the addition of dialysis increases the effective glomerular filtration rate to 30 to 40 mL/min. Increasing the dialysis flow rate from 1 to 2 L/h further increases the effective glomerular filtration rate. Several points should be remembered when selecting drug doses in patients receiving CRRT. First, drugs that are less than 80% protein bound, have a volume of distribution less than 1 L/kg, and a renal clearance greater than 35% will be removed during CRRT. Second, medication removal is highest with CVVH with dialysis, next highest with CVVH, and lowest with CAVH. Shorter dosing intervals should be chosen for patients being treated with hemofiltration with dialysis, and longer dosing intervals should be selected for patients on hemofiltration alone, especially CAVH. Third, the following guidelines may be used for dosage adjustments during CRRT in the absence of published recommendations. The manufacturer’s dosage recommendations for creatinine clearances < 20 mL/min may be used in patients receiving hemofiltration alone. In patients receiving hemofiltration with dialysis, the manufacturer’s dosage recommendations for creatinine clearances below 30 to 40 mL/min may be used. Fourth, serum concentration monitoring should be used to adjust the doses of aminoglycoside antibiotics and vancomycin. Finally, drugs such as catecholamines, narcotics, and sedatives are minimally removed during CRRT. The doses of these drug classes should be titrated based on the patient’s clinical response.

Drug Disposition in the Elderly The elderly population is the fastest growing segment of the population in the United States. Older patients consume nearly 3 times as many prescription drugs as younger patients and therefore are at risk for experiencing significantly more drug-drug interactions and ADEs. The most common risk factors that contribute to adverse events include polypharmacy, low body mass, preexisting chronic disease, excessive length of therapy, organ dysfunction, and prior history of drug reaction. Special attention must be paid on the part of health-care professionals when dosing medications in these patients with low body mass and potentially impaired metabolism and clearance of drug secondary to age-related

organ dysfunction (eg, renal or hepatic impairment). Agents that are of particular interest in this population include sedatives, antihypertensives, narrow therapeutic index drugs, and anti-infectives. These agents often require a decrease in dose or the extension of the dosing interval to facilitate drug clearance and minimize the likelihood of toxicity.

Therapeutic Drug Monitoring Therapeutic drug monitoring (TDM) is the process of using drug concentrations, pharmacokinetic principles, and pharmacodynamics to optimize drug therapy (see Table 23-5). The goal of TDM is to maximize the therapeutic effect while avoiding toxicity. Drugs that are toxic at serum concentrations close to those required for therapeutic effect are the drugs most commonly monitored. The indications for TDM include narrow therapeutic range, limited objective monitoring parameters, potential for poor patient response, the need for therapeutic confirmation, unpredictable dose-response relationship, suspected toxicity, serious consequences of toxicity or lack of efficacy, correlation between serum concentration and efficacy or toxicity, identification of drug interactions, determination of individual pharmacokinetic parameters, and changes in patient pathophysiology or disease state. The specific indication for TDM is important, because it affects the timing of the sample. Timing of sample collection depends on the question being asked. The timing of serum drug concentrations is critical for the interpretation of the results. The timing of peak serum drug concentrations depends on the route of administration and the drug product. Peak serum drug concentrations occur soon after an IV bolus dose, whereas they are delayed after IM, SC, or oral doses. Oral medications can be administered as either liquid or rapid- or slow-release dosage forms (eg, theophylline). The absorption and distribution phases must be considered when obtaining a peak serum drug concentration. The peak serum concentration may be much higher and occur earlier after a liquid or rapid-release dosage form compared to a sustained-release dosage form. Trough concentrations usually are obtained just prior to the next dose. Drugs with long half-lives (eg, phenobarbital) or sustained-release dosage forms (eg, theophylline) have minimal variation between their peak and trough concentrations. The timing of the determination of serum concentrations may be less critical in patients taking these dosage forms. Serum drug concentrations may be drawn at any time after achieving a steady state in a patient who is receiving a drug by continuous IV infusion. However, in patients receiving a drug by continuous infusion, the serum specimen should be drawn from a site away from where the drug is infusing. If toxicity is suspected, serum drug concentrations can be obtained at any time during the dosing interval. Appropriate interpretation of serum concentrations is the step that requires an understanding of relevant patient factors, pharmacokinetics of the drug, and dosing regimen. Misinterpretation of serum drug concentrations can result

214

CHAPTER 7. Pharmacology

Essential Content Case

Tips for Calculating IV Medication Infusion Rates Information Required to Calculate IV Infusion Rates to Deliver Specific Medication Doses • Dose to be infused (eg, mg/kg/min, mg/min, mg/h) • Concentration of IV solution (eg, dopamine 400 mg in D5W 250 mL = 1.6 mg/mL; nitroglycerin 50 mg in D5W 250 mL = 200 mcg/mL) • Patient’s weight

Answer: Setting the infusion pump at 234 mL/h will infuse the aminophylline loading dose over 1/2 hour. Maintenance dose: 0.6 mg/kg/h × 70 kg = 42 mg/h 42 mg/h ÷ 2 mg/mL = 21 mL/h Answer: Setting the infusion pump at 21 mL/h will deliver the aminophylline maintenance dose at 42 mg/h, or 0.6 mg/kg/h.

Calculation: 5 mcg/kg/min × 70 kg = 350 mcg/min 350 mcg/min × 60 min/h = 21,000 mcg/h 21,000 mcg/h ÷ 2000 mcg/mL = 10.5 mL/h

in ineffective and, at worst, harmful dosage adjustments. Interpreting serum concentrations includes an assessment of whether the patient’s dose is appropriate, if the patient is at a steady state, the timing of the blood samples, an assessment of whether the time of blood sampling is appropriate for the indication, and an evaluation of the method of delivery to assess the completeness of drug delivery. Serum drug concentrations should be interpreted within the context of the individual patient’s condition. Therapeutic ranges serve as guidelines for each patient. Doses should not be adjusted on the basis of laboratory results alone. Individual dosage ranges should be developed for each patient as various patients may experience therapeutic efficacy, failure, or toxicity within a given therapeutic range.

Answer: Setting the infusion pump at 10.5 mL/h will deliver dobutamine at a dose of 5 mcg/kg/min.

SELECTED BIBLIOGRAPHY

Case Question 1. Calculate the IV infusion rate in milliliters per hour for a 70-kg patient requiring dobutamine 5 mcg/kg/min using a dobutamine admixture of 500 mg in D5W 250 mL. • Dose to be infused: 5 mcg/kg/min • Dobutamine concentration: 500 mg/250 mL = 2 mg/mL or 2000 mcg/mL • Patient weight: 70 kg

Case Question 2. Calculate the IV infusion rate in milliliters per hour for a 70-kg patient requiring nitroglycerin 50 mcg/m in using a nitroglycerin admixture of 50 mg in D5W 250 mL. • Dose to be infused: 50 mcg/min • Nitroglycerin concentration: 50 mg/250 mL = 0.2 mg/ mL or 200 mcg/mL • Patient weight: 70 kg Calculation: 50 mcg/min × 60 min/h = 3000 mcg/h 3000 mcg/h ÷ 200 mcg/mL = 15 mL/h Answer: Setting the infusion pump at 15 mL/h will deliver nitroglycerin at a dose of 50 mcg/min. Case Question 3. Calculate the IV loading dose and infusion rate in milliliters per hour for a 70-kg patient requiring aminophylline 0.6 mg/kg/h using an aminophylline admixture of 1 g in D5W 500 mL. The loading dose should be diluted in D5W 100 mL and infused over 30 minutes. • Desired dose: Loading dose: 6 mg/kg Maintenance infusion: 0.6 mg/kg/h • Aminophylline concentration: Aminophylline vial: 500 mg/20 mL = 25 mg/mL Aminophylline infusion: 1 g/500 mL = 2 mg/mL • Patient weight: 70 kg Calculation: Loading dose: 6 mg/kg × 70 kg = 420 mg 420 mg ÷ 25 mg/mL = 16.8 mL Infusion rate: Aminophylline 16.8 mL + D5W 100 mL = 116.8 mL 116.8 mL ÷ 0.5/h = 233.6 mL/h

General Institute of Safe Medication Practices. www.ismp.org. Accessed February 8, 2013. Martin SJ, Olsen KM, Susla GM. The Injectable Drug Reference. 2nd ed. Des Plaines, IL: Society of Critical Care Medicine; 2006. Sulsa GM, Suffredini AF, McAreavey D, et al. The Handbook of Critical Care Drug Therapy. 3rd ed. Philadelphia, PA: Lippincott William and Wilkins; 2006. Vincent J, Abraham E, Kochanek P, et al. Textbook of Critical Care. 6th ed. Philadelphia, PA: Elsevier; 2011.

Evidence-Based Practice Guidelines Barr J, Fraser GL, Puntillo K, et al. Clinical practice guidelines for the management of pain, agitation, and delirium in adult patients in the intensive care unit. Crit Care Med. 2013;41:263-306. Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. doi: 10.1097/ CCM.0b013e31827e83af. O’Gara PT, Kushner FG, Ascheim DD, et al. American College of Cardiology Foundation/American Heart Association guidelines for management of ST-elevation myocardial infarction. Executive summary. Circulation. 2013;127:529-555. Surviving Sepsis Campaign Management Guidelines Committee. Surviving sepsis campaign guidelines for management of severe sepsis and septic shock. Crit Care Med. 2004;32:858-873. Task Force of the American College of Critical Care Medicine (ACCM) of the Society of Critical Care Medicine (SCCM), American Society of Health-System Pharmacist, American College of Chest Physicians. Clinical practice guidelines for sustained neuromuscular blockage in the adult critically ill patient. Crit Care Med. 2002;30:142-156.

Ethical and Legal Considerations Sarah Delgado

KNOWLEDGE COMPETENCIES 1. Characterize the nurse’s role in recognizing and addressing ethical concerns. 2. Identify ethical principles and describe their application in the healthcare setting.

As new ethical issues in critical care continue to emerge, practitioners must develop skills in ethical decision making. An ethical dilemma occurs when two (or more) ethically acceptable but mutually exclusive courses of action are present. The dilemma is further complicated as either choice can be supported by an ethical principle, yet there are consequences for either choice. Moral distress, another common ethical problem, occurs when a provider believes he or she knows the ethically acceptable action to take but feels unable to do so. Competence in moral decision making evolves throughout one’s professional career. However, there are general moral principles and guidelines that direct ethical reasoning and provide a standard to which professional nurses are held. Beginning clinicians, as well as more experienced nurses, should be familiar with the moral expectations and ethical accountability embedded in the nursing profession. This chapter introduces the elements that serve as a foundation for addressing ethical problems including professional codes and standards, institutional policies, and ethical principles. Advance directives, endof-life issues, and the ethical environment are also discussed.

THE FOUNDATION FOR ETHICAL DECISION MAKING Professional Codes and Standards The purpose of professional codes is to identify the moral requirements of a profession and the relationships in which they engage. The Code for Nurses developed by the American

3. Describe the steps involved in analyzing an ethical problem.

Nurses Association (ANA) articulates the essential values, principles, and obligations that guide nursing actions. The nine provisions of the ANA Code of Ethics identify the ethical obligations of nurses and are applicable across all nursing roles (American Nurses Association, Code of Ethics for Nurses with Interpretive Statements, 2001. http://www. nursingworld.org/MainMenuCategories/EthicsStandards/ CodeofEthicsforNurses). While these provisions do not address specific ethical problems, they do provide a framework for examining issues and understanding the nurse’s role in resolving them. In addition to the ANA Code of Ethics, nurses function in accordance with particular standards of practice. Standards of nursing practice are delineated by professional organizations and statutory bodies that govern the practice of nursing in various jurisdictions. Derived from nursing’s contract with society, professional nursing standards define the criteria for the assessment and evaluation of nursing practice. External bodies, such as state boards of nursing, impose certain regulations for licensure, regulate the practice of nursing, and evaluate and monitor the actions of professional nurses. Many organizations also delineate standards of practice for registered nurses practicing in a defined area of specialty; for example, the American Association of Critical-Care Nurses (AACN) has established standards and expectations of performance for nurses practicing in critical care. 215

216

CHAPTER 8. Ethical and Legal Considerations

Standards of practice outlined by statutory bodies and specialty organizations are not confined to clinical skills and knowledge. Nurses are expected to function within the profession’s code of ethics and are held morally and legally accountable for unethical practice. When allegations of unsafe, illegal, or unethical practice arise, the regulatory body serves to protect the public by investigating and disciplining the culpable professional. Although specialty organizations do not have authority to retract professional licensure, issues of professional misconduct are reviewed and may result in revocation of certification and notification of external parties.

Position Statements and Guidelines In an effort to address specific issues in clinical practice, many professional organizations develop position statements or guidelines. The purpose of position statements is to apply the values, principles, and rules described in the Code for Nurses to particular contemporary ethical issues. Familiarity with the AACN and ANA position statements helps the critical care nurse to clarify and articulate a position consistent with the professional values of nursing. To illustrate the application of position statements, consider a situation in which a nurse is asked to intentionally hasten a patient’s death. The Code for Nurses and ANA position statements on assisted suicide and active euthanasia clarify the nurse’s role when such requests are made. In addition, the ANA position statement on pain management and control of distressing symptoms in dying patients provides guidance for addressing the physical and emotional needs of patients at the end of life. In this case, the nurse and physician should explore the patient’s request for an accelerated death and explain the legal and moral boundaries of his request. The option to withdraw treatment and provide aggressive palliative care should be offered and examined with the patient. Interventions that are continued or newly introduced should be done so with the expressed approval of the patient and the intent of increasing his comfort.

Institutional Policies Because nurses practice within organizations, institutional policies and procedures also guide their practice. Institutional guidelines for assessing decision-making capacity, caring for un-represented patients who lack capacity, or policies for the determination of brain death are intended to guide employees of an organization when they are faced with ethical uncertainty. These policies usually reflect ethical expectations congruent with the professional codes of ethics. However, in some circumstances, organizations may assume a particular position or value and therefore expect the employees to uphold this position; for example, some hospitals endorse particular religious positions and may prohibit professional practices that violate these positions. Ideally, the nurse and institution have complementary values and beliefs about professional responsibilities and obligations.

Institutions often provide internal resources to help clinicians resolve difficult ethical issues. Institutional ethics committees provide consultation on ethical situations and institutional policies outlining the procedures of case review, which should be available to all employees. In the case example “Who Decides,” the critical care nurse should consider what resources, such as the ethics committee, a physician, a Essential Content Case

Working Together Julia is a 28-year-old registered nurse who recently married and moved to a new city. She was pleased to land a job in a neuro-intensive care unit in a large academic medical center. While still on orientation, she was caring for a patient with traumatic brain injury and the family asked her questions about his prognosis. She relayed the information she knew and then called the neurosurgeon on the case. As she began to describe her conversation with the family, the neurosurgeon stated “you are a nurse and it’s not your place to talk to the patient’s family. Stop trying to practice medicine without a license,” and then hung up on her. When she spoke with her preceptor about the phone call, he advised “Oh don’t worry, he’s made every nurse here cry at one time or another. He’s just like that. But he’s a great surgeon and the hospital is really lucky to have him.” As Julia leaves at the end of her shift, she starts to question her “luck” in getting a position on this unit. Case Question. How does Julia’s position as a new nurse in the neuro-ICU affect her response to this situation? Answer As a new member of the ICU staff, Julia has not had the time to demonstrate the leadership and strong clinical skills that would make her an opinion leader among the nurses on the unit. However, being new also has an advantage. While other nurses may have reached a state of accepting the unprofessional, verbally abusive conduct of this surgeon because “it’s always been that way,” Julia’s fresh perspective lends conviction to her belief that the behavior should not be tolerated. In addition, she can observe the interactions of other nurses and begin to identify opinion leaders to support her effort as a change agent. The AACN position statement Zero Tolerance for Abuse addresses Julia’s surprise and disgust that the neurosurgeon’s disrespectful behavior is tolerated and accepted by the nurses on her unit. In addition, the AACN Position Statement on Moral Distress describes how nurses and managers are obligated to recognize and address sources of moral distress, including verbal abuse from colleagues. Julie’s colleagues had experienced verbal abuse and felt the surgeon should be reported to a higher authority but they felt unable to do so because the surgeon is highly regarded for his skill and reputation. Applying these position statements to her current situation, Julia knows that the neurosurgeon’s behavior is abusive and therefore unacceptable. Furthermore, accepting such abuse can generate moral distress and therefore she is compelled to take action. The fifth provision of the ANA Code of Ethics similarly advises nurses of the ethical obligation to care for themselves and supports Julia’s decision to report the neurosurgeon’s behavior to her manager.

THE FOUNDATION FOR ETHICAL DECISION MAKING 217

nurse manager, or an advanced practice nurse might assist her in advocating for this patient. While the ANA code states that nurses are obligated to advocate for patients, finding support is an essential step in that process. Essential Content Case

Who Decides? A 72-year-old grandmother has been in the coronary care unit for 4 weeks following a large anterolateral myocardial infarction. She has suffered from CHF, pulmonary edema, and hypotension, and now has developed ARDS. Her family is very supportive and visits her often. The physicians have communicated with the family, and, because the patient does not have an advance directive, the family has entrusted the physicians with making the “right decisions.” Currently, she requires maximal ventilator support to maintain adequate oxygenation and a balloon pump to maintain her cardiac output. She is also on IV vasopressors and inotropic agents. Attempts to keep her pain free are sometimes thwarted by a drop in her blood pressure when she receives morphine and other sedatives. After several failed attempts to wean the balloon pump and the IV infusions, the nurses are concerned that the technology is being used to prolong the patient’s inevitable death. Furthermore, because the patient does not tolerate high doses of sedatives, she is able to follow simple commands and communicate with gestures such as nodding or shaking her head. Often, she grimaces and reaches to remove tubes which the nurses interpret as an effort to communicate her discomfort with the current treatment modalities. When Rhonda, the patient’s primary nurse on dayshift, asks the physician to discuss the options of a do not resuscitate order or a withdrawal of care with the patient and the family, the physician responds that the patient is “not competent because of her illness and prolonged stay in the CCU.” The physician states that the family told him to make the “right decisions” and that gives him the authority to decide what is best for this patient. Rhonda is uncomfortable continuing to provide care in accordance with the physician’s perspective rather than a clear understanding of the patient’s values and goals regarding continued treatment. Case Question. What steps can be taken to address the discomfort the CCU nurses are experiencing in caring for this patient? Answer As described in AACN’s 4 A’s to Address Moral Distress, a stepwise approach is appropriate to addressing the distress these nurses are experiencing. The first step, to “Ask,” has already been completed in this case; the staff has already questioned whether their feelings about this situation are justified and they are aware that the distress they feel is the result of providing a level of care that may not be consistent with the patient’s wishes. The next step is to “Affirm” their feelings, which may require an interdisciplinary team meeting with all the staff involved in the care of this patient, giving each the chance to voice their feelings and be validated by other members of the group. The third step, “Assess,” requires the nurses to evaluate the severity of their distress and determine their motivation to take action. The final step is to act, which may involve working with the medical team to identify an appropriate course of action,

calling an ethics committee consult, asking the family to take a more active role in making decisions about the patient’s care, or seeking support from the nurse manager or supervisor. Rhonda and her colleagues may feel hesitant to advocate for this patient but also need to remember that inaction will worsen the distress, and may ultimately affect the care of all patients on the unit. Furthermore, health care teams in which all members share their perspectives deliver high quality nursing care. Addressing morally distressing situations such as this empowers nurses to remain involved in difficult patient situations and to recognize that information gained through nursing care is critical to effective and appropriate care.

Legal Standards Public policies and state and federal laws also influence the practice of healthcare professionals. Policies from agencies such as the Centers for Disease Control and Prevention (CDC) or the Department of Health and Human Services (DHHS) generate changes in practice and in the actions of health professionals. In addition, the Centers for Medicare and Medicaid Services (CMS), a major payor for health care, sets standards for hospitals and providers that must be abided to ensure reimbursement for services. State legislation can also influence critical care nursing practice. For instance, states differ in their recognition of unmarried domestic partners and the right of a partner to serve as the medical decision maker when a patient is rendered incompetent by illness or injury. The Affordable Care Act (ACA) passed in 2010 requires hospitals to report quality indicators, such as the rate of hospital-acquired infections (CMS, 2010). This legislation ties these indicators to Medicare reimbursement. The ACA thus creates financial incentives for hospitals to ensure they endeavor to prevent infection as a complication of hospital admission. In this way, the ACA offers a legal manifestation of the ethical principle of non-maleficence, discussed below. The Health Information Portability and Accountability Act (HIPAA) Privacy Rules similarly create a legal mandate to honor the ethical obligation of confidentiality (DHHS). When faced with an ethical problem, professional guidelines, institutional policies, or legal standards can assist, and sometimes resolve, the issue. Thus, it is imperative that nurses be familiar with these resources and how to access them. However, nurses also need to recognize that guidelines and policies and even the law do not always answer the question of what action should be taken. In such situations, the nurse must be prepared to identify the ethical principles involved and follow a step-wise approach to addressing the problem.

Principles of Ethics One of the most influential perspectives in biomedical ethics is that of principle-based ethics. This framework arose in the 1970s through the work of Beauchamp and Childress and continues to be a dominant method of bioethical thinking

218

CHAPTER 8. Ethical and Legal Considerations

today. Inherent in this viewpoint is the belief that some basic moral principles define the essence of ethical obligations in human society. Four basic principles, and derivative imperatives or rules, are considered prima facie binding. In other words, to breach a principle is wrong unless there are prevailing and compelling reasons that outweigh the necessary infringement. The principles and rules are binding, but not absolute. Because many approaches to ethics integrate the rules and principles outlined by the principle-oriented approach, understanding the fundamental concepts of principlebased ethics is helpful to the critical care nurse. The primary principles used are nonmaleficence, beneficence, justice, and respect for persons (or autonomy). The derivative principles or rules include privacy, confidentiality, veracity, and fidelity. The principles are not ordered in a particular hierarchy, but their application and interpretation are based on the specific features of the dilemma and the values of the team members involved. Articulating the principles involved and recognizing the personal values of the providers and family members are essential steps to resolving an ethical problem. Nonmaleficence

The principle of nonmaleficence imposes the duty to do no harm. This injunction suggests that the nurse should not knowingly inflict harm and is responsible if negligent actions result in detrimental consequences. In general, a critical care nurse preserves the principle of nonmaleficence by maintaining competence and practicing within accepted standards of care. When the patient’s safety or well-being is threatened by the actions of others, the nurse is obligated to act. Knowledge of unsafe, illegal, or unethical practice by any healthcare provider obligates the nurse both morally and legally to intervene. The nurse must remove the immediate danger and communicate the infringement to the appropriate sources to prevent further harm. The nurse should turn to institutional policies and state nurse practice acts for guidance on in the appropriate process of reporting. Beneficence

The ethical principle of beneficence affirms an obligation to prevent harm, remove harm, and promote good by actively helping others to advance and realize their interests. Intrinsic to this principle is action. The nurse moves beyond the concept of not inflicting harm (nonmaleficence) by actively promoting the best interests of the patient and family. To optimize the patient’s well-being, nurses must practice with the essential knowledge and skills required of the clinical setting. Nurses are expected to practice according to established standards of practice, to continue professional learning to improve clinical practice, and to refrain from providing care measures in which they are not proficient.

Beyond the provision of safe nursing care, the promotion of the patient’s well-being requires that the patient’s perspective be known and valued. Therefore, the nurse must gain an understanding of the patient’s underlying value structure to ensure that the care provided is consistent with the patient’s wishes. The duty to do good requires that the healthcare team understand the patient’s interpretation of what is “good.” The obligations to do no harm (nonmaleficence) and to promote good or remove harm (beneficence) extend beyond provider incompetence and safe care. In ethically challenging situations, the potential harms associated with each of the available treatment options should be considered before deciding the best action. This can be difficult because sometimes an identified harm is death and in some of these cases, death is not the worst harm. Careful and thorough thinking with regard to harms and benefits to a patient can often clarify not only which actions might be “right” for a patient, but also which actions might be “wrong.” Respect for Persons (Autonomy)

The principle of respect for persons or autonomy affirms the freedom and right of an individual to make decisions and choose actions based on that individual’s personal values and beliefs. In other words, an autonomous choice is an informed decision made without coercion that reflects the individual’s underlying interests and values. To respect a person’s autonomy is to recognize that patients may hold certain views and take particular actions that are incongruent with the values of the healthcare providers. Often this concept is difficult for healthcare providers to accept and endorse, particularly when the patient’s choice conflicts with the caregivers’ view of what is best in this situation. As an advocate, the nurse appreciates this diversity and continues to provide care as long as the patient’s choice is an informed decision and does not infringe on the autonomous actions of others. Patients in the critical care setting frequently have varying degrees of autonomy. The capacity of ill patients to participate in the decision-making process often is compromised and constrained by internal factors such as the effects of pharmacologic agents, the emotional elements associated with a sudden acute illness, and the physiologic factors related to the underlying illness. External factors, such as the hospital environment, also influence the patient’s potential to make autonomous choices. As demonstrated in the case example “Who Decides,” providers may differ in their assessment of patient capacity. Often, institutions have policies outlining a process for determining a patient’s capacity. In the case of “Who Decides,” the nurses involved in the patient’s care may find these policies helpful in guiding their thinking as well as their action. The critical care nurse advocates for the patient by limiting, as much as possible, the factors that constrain the patient’s freedom to make autonomous choices. In this way the nurse supports the principle of respect for personal autonomy and upholds the ethical duty of beneficence.

THE FOUNDATION FOR ETHICAL DECISION MAKING 219

Justice

The principle of justice is defined as fairness, and in health care is often applied to the manner in which goods, burdens, and services are distributed among a population. When resources are limited, justice demands that they be fairly allocated. There are three interpretations of the justice principle that will be described here by the following example. Imagine a population of people who have a set of goods that must be shared fairly among them. (1) Egalitarian justice would demand that the goods be divided into equal portions and every member of the population given the same share. (2) Humanitarian justice would demand that the goods be divided according to the needs of each member, with the neediest members getting larger portions. (3) Libertarian justice would demand the goods be distributed according to the contributions made by each member of the population; those making the greatest contributions get the greater share. Organ transplantation offers a clear example of the justice principle in health care. Organs are a scarce resource and some of those listed for transplant will not survive the wait. Priority for transplant can be based strictly on time spent waiting (an egalitarian approach), or on illness severity (a humanitarian approach), or based on assessment of an individual’s contributions and potential contributions to society (libertarian approach). On a day-to-day basis, nurses make decisions involving the allocation of nursing care—which patient to assess first or how to assign patients on the unit to the staff on the next shift. The complex and competing demands for nursing resources can lead to chaotic and random decisions. The principle of justice argues for a comprehensive, thoughtful approach to address competing claims to resources. Privacy and Confidentiality

Privacy and confidentiality are associated, but distinct, concepts that are derived from the principles of respect for autonomy, beneficence, and nonmaleficence. Privacy refers to the right of an individual to be free from unjustified or unnecessary access by others. In the critical care setting the patient’s privacy often is disregarded. The design of many units includes easy visualization of patients from the nurses’ station, and open access to the patient is presumed by most caregivers. This suggests a breach of individual privacy. Practitioners should be particularly attentive to requesting permission from the patient for any bodily intrusion or physical exposure. The casual infringement of an individual’s privacy erodes the foundation for establishing a trusting and caring practitionerpatient relationship. Confidentiality refers to the protection of information. When the patient shares information with the nurse or a member of the healthcare team, the information should be treated as confidential and discussed only with those directly involved in the patient’s care. Exceptions to confidentiality include quality improvement activities, mandatory disclosures to public health agencies, reporting abuse, or required

disclosure in a judicial setting. Other disclosures of information obtained in a confidential manner should be shared with appropriate persons only when strong and compelling reasons to do so exist. The patient should be informed of the impending disclosure, and ideally the patient should authorize the disclosure. Violations of patient confidentiality occur in many subtle ways. The computerization of medical records and the use of facsimile distribution of personal medical information is common practice in many institutions. Persons unrelated to the patient’s medical care who have access to the computers or facsimile may view confidential information without the individual’s permission. Other ways in which confidentiality is unprotected include casual conversations in hallways or elevators in which patient information is shared within earshot of strangers, the unauthorized release of patient information to friends or the media, and healthcare professionals within the institution taking the liberty to view a coworker’s medical record. Nurses may feel conflicted when a patient discloses confidential information. The profession of nursing strongly values the principle of respect for persons and highly regards the concept of protecting confidential information. Therefore, decisions to break a patient’s confidentiality must be well considered and require balancing competing obligations and claims; for example, a nurse may consider breaking a patient’s confidentiality if there is a clear indication that, without doing so, harm may come to another individual. Clearly, this decision should not be made in isolation, and the nurse should seek advice when confronted with this difficult situation. Fidelity

Fidelity is the obligation to be faithful to commitments and promises and uphold the implicit and explicit commitments to patients, colleagues, and employers. The nurse portrays this concept by maintaining a faithful relationship with the patient, communicating honestly, and meeting the obligations to oneself, the profession of nursing, other healthcare professionals, and the employer. The concept of fidelity is particularly important in critical care. The vulnerability of critically ill patients increases their dependency on the relationship with the nurse, thus making the nurse’s faithfulness to that relationship essential. Nurses demonstrate this faithfulness by fulfilling the commitments of the relationship, which include the provision of competent care and advocacy on the patient’s behalf. In addition, the nurse is obligated to demonstrate fidelity in relationships with colleagues and employers. In this way, the principle of fidelity can be difficult to uphold as institutions may have policies, such as those related to resource utilization, that the nurse finds are in conflict with the patient’s best interests. When confronted with such situations, the nurse is wise to carefully weigh the ethical principles involved, to seek guidance if necessary, and to consider a role as a moral agent of change if appropriate.

220

CHAPTER 8. Ethical and Legal Considerations

Veracity

The rule of veracity simply means that one should tell the truth and not lie or deceive others. Derived from the principle of respect for persons and the concept of fidelity, veracity is fundamental to relationships and society. The nursepatient relationship is based on truthful communication and the expectation that each party will adhere to the rules of veracity. Deception, misrepresentation, or inadequate disclosure of information undermines and erodes the patient’s trust in healthcare providers. Patients expect that information about their condition will be relayed in an open, honest, and sensitive manner. Without truthful communication, patients are unable to assess the options available and make fully informed decisions. However, the complex nature of critical illness does not always manifest as a single truth with clear boundaries. Uncertainty about the course of the illness, the appropriate treatment, or the plan of care is common in critical care and a single “truth” may not exist. As emphasized in patient-centered care, patients or surrogate decision makers must be kept informed of the plan of care and areas of uncertainty should be openly acknowledged. Disclosure of uncertainty enables the patient or surrogate to realistically examine the proposed plan of care and reduces the likelihood that the healthcare team will proceed in a paternalistic manner.

The Ethic of Care The ethic of care is viewed as an alternative to the principled approach in bioethics. Rather than distinguish the ethical dilemma as a conflict of principles, the ethic of care involves the analysis of important relationships in a case, and emphasizes that the correct ethical action is one that preserves the most important relationships (eg, patient-spouse, patient-child). Carol Gilligan (1984) first described the phenomenon of using relationships to identify correct moral actions by observing how children make ethical decisions. Some adhere to rules (eg, “do not steal,” “do not lie”) and others consider how an action will affect others involved (eg, hurt feelings, loss of trust or respect). These ways of thinking carry through to adulthood. Most adults can view a situation through both the rules lens and the relationships lens. The ethic of care begins from an attached, involved, and interdependent position. From this standpoint, morality is viewed as caring about others, developing relationships, and maintaining connections. Moral problems result from disturbances in interpersonal relationships and disruptions in the perceived responsibilities within relationships. The resolution of moral issues emerges as the involved parties examine the contextual features and embrace the relevance of the relationship and the related responsibilities. In contrast, a principle-oriented or justice approach typically originates from a position of detachment and individuality. This approach recognizes the concepts of fairness, rights, and equality as the core of morality. Therefore, dilemmas arise when these elements are compromised. From this

perspective, the approach to moral resolution is a reliance on formal logic, deductive reasoning, and a hierarchy of principles. For nursing, the ethic of care provides a useful approach to moral analysis. Traditionally, nursing is a profession that necessitates attachment, caring, attention to context, and the development of relationships. To maintain this position, nurses develop proficiency in nurturing and sustaining relationships with patients and within families. The importance of relationships is also suggested in the first provision of the ANA Code of Ethics. The ethic of care legitimizes and values the emotional, intuitive, and informal interpretation of moral issues. This perspective expands the sphere of inquiry and promotes the understanding and resolution of moral issues. In addition to the care-based and principle-based approaches, there are other frameworks for examining ethical problems. Examples include the casuistry approach, which applies outcomes of past cases to the current situation and the narrative approach, which examines the contextual features of the ethical problem. A full description of these approaches is beyond the scope of this chapter; however, an awareness of the variety of approaches to ethical problems is essential to collaborative decision making. The nurse, as member of the healthcare team, recognizes that other team members and patients and families may adopt different approaches when faced with the same ethical problem. Active listening and open-ended questions enable the nurse to recognize the approach adopted by another provider or family member and this recognition improves communication and ultimately leads to resolution of the ethical problem.

Paternalism In ethics, paternalism refers to instances in which the principle of beneficence overrides that of autonomy. In such cases healthcare providers select and implement interventions that they believe will lead to the best outcomes without (or even against) consent from the patient. Sometimes these actions are appropriate. An example of paternalism in critical care is the use of wrist restraints to prevent self extubation when a patient with capacity to make his or her own decisions objects. Restraint overrides the patient’s autonomy, but is justified by the benefit of ensuring patient safety. Most times, however, paternalism is not justified—it is generally not acceptable to override an autonomous patient’s decisions without his or her consent. Critical care nurses may find the balance between the patient’s beliefs and the duty to promote good difficult and confusing. In the critical care setting it is often unclear what actions or course of treatment will most benefit the patient physiologically and which plan best reflects the patient’s values. This lack of certainty may result in fragmented discussions with the patient or surrogate and a treatment plan that reflects the values of the healthcare team rather than the patient. The nurse’s moral obligation is to continue to promote the patient’s interests by pursuing an accurate representation

THE FOUNDATION FOR ETHICAL DECISION MAKING 221

Essential Content Case

Examples of Different Ethical Frameworks and How They Affect Provider Conclusions An 8-year-old boy diagnosed 2 years ago with glioblastoma is admitted to the PICU with refractory seizures. He is intubated and placed on high doses of sedatives to prevent further seizures. An MRI done on the second day after admission shows that his tumor has progressed despite treatment. His parents are both involved and supportive but are divorced and schedule their visits to avoid each other. 72 hours after admission to the PICU, the parents are asked to participate in a family conference in accordance with unit policy. The oncologist, the pediatric intensivist, and the PICU nurse are all in attendance with the parents. The oncologist describes the child’s prognosis as poor, and the intensivist explains the measures being taken to support him in his critical state, and explains the options of a DNR order and of withdrawal of life support. Both parents seem to appreciate the severity of illness and the mother requests to take her son home because “that’s where he’d want to be.” The father, who is a respiratory therapist, becomes angry, stating “you don’t get it, do you? He has to be here in the ICU. He’s too sick to move, even though I know you want to take him away from me.” The mother stands up and states “you always want to make it about us, but this is about him!” and exits the conference room. The father then tells the team that he understands that withdrawal of care is the right course of action, but he’s not sure his ex-wife is capable of making that decision, and “whatever happens, I want to be with my son as much as I can.” In a separate conversation with the patient’s mother, she tells the team “we can stop the machines, if I can just take him home.” The three providers—the oncologist, the intensivist, and the nurse—all witness the same situation but they interpret it through different ethical frameworks and arrive at different conclusions as to how to proceed: • The intensivist, noting that the care they are providing is increasingly futile and that both parents do agree with withdrawal of life support, proposes establishing a day and time for terminal extubation to take place, ensuring that both parents are present. He believes this action is supported by several ethical principles: benef icence—his desire to do what is best for his patient, nonmalef icience—to prevent any complications of ICU care, autonomy (parental authority)—honoring the parents’ expressed wish to remove life support, and finally justice—because there are other children who will need this PICU bed. • The oncologist, who has known the family longer than the other two providers, advises waiting for a few days to see if the parents can get on better terms with each other. He has seen them come together periodically throughout the child’s illness and thinks this might happen again. Like the intensivist, he feels that withdrawal of life support is the action supported by the ethical principles of beneficience and nonmaleficience. However, he has no concern about the allocation of PICU beds, and he has seen complicated grief in families in which the patient died while the family was still in conflict about the plan

of care. He feels that the setting in which the child’s death occurs is of importance, if only because the parents are polarized on this issue. • The nurse takes a care-based approach and focuses exclusively on the relationships in the situation. She notes that if the team sets a date, as suggested by the intensivist, the family, particularly the patient’s mother, may resent the healthcare team for “siding with” the father and feels this will affect her grieving process. She notes that the parents have been separated for a long time and feels that waiting a few days is unlikely to bring them to a point of agreement. By asking open-ended questions and actively listening, she learns more about each parent’s relationship with the son, particularly the father’s sense that he did not get to spend enough time with his son during this illness, and the mother’s strong desire to honor the child’s last statement to her: “I just want to go home.” After carefully listening to their separate views, she then proposes a compromise: transfer the child to the oncology floor where he has been cared for throughout the course of this illness. Both parents speak in positive terms about their relationships with the staff there, and their prior knowledge enables the staff to accommodate the parents’ mutual desire to be with their son despite the bitterness between them. This case illustrates how professionals adopting different ethical frameworks can arrive at different conclusions about the right course of action. It also offers an example of ethical creativity, which is required in difficult situations, particularly in ethical dilemmas where two opposing courses of action are justified. What is needed in such situations is often a third option.

of the patient’s beliefs and values, and to raise concerns of conflicting interpretations to appropriate members of the healthcare team.

Patient Advocacy Patient advocacy is an essential role of the nurse, as emphasized in the ANA Code of Ethics. Although there are many models for defining and interpreting the relationship between the nurse and patient and no model can thoroughly describe its complexity and uniqueness, the patient advocacy role offers an essential description of the moral nature of this relationship. In addition, the third provision of the ANA Code of Ethics, “The nurse promotes, advocates for, and strives to protect the health, safety, and rights of the patient,” specifically identifies the nurse’s role as a patient advocate. The term advocacy refers to the use of one’s own skills and knowledge to promote the interests of another. Nurses, through their education and experience, are able to interpret healthcare information and understand the impact of disease and medical interventions in a unique way. A nurse acts as a patient advocate by applying this unique understanding to ensure that the patient’s beliefs and values guide the plan of care. The nurse does not impose personal values or preferences when acting as an advocate, but instead guides the

222

CHAPTER 8. Ethical and Legal Considerations

patient or surrogate decision maker through values clarification, identification of the patient’s best interests, and the process of communicating decisions. Thus, the patient or surrogate is empowered by the nurse to participate in the healthcare plan. Assuming the role of patient advocate is not without risk. Nurses may find that obligations to oneself, the patient, the patient’s family, other members of the healthcare team, or the institution are in conflict and have competing claims on nursing resources. These situations are intensely troubling to nurses and the support of colleagues is essential to resolving these dilemmas. In circumstances of conflict, nurses should clarify the nature and significance of the moral problem, engage in a systematic process of moral decision making, communicate concerns openly, and seek mutually acceptable resolutions. A framework within which to identify and compare options provides the necessary structure to begin the process of moral resolution.

•• Analyze each course of action. In a principle-based approach, identify which principles support the alternative courses of action. In a care-based approach, consider the impact of each course of action on the existing relationships. •• Search for professional organizations’ position statements and institutional guidelines that address this issue. •• Seek input from the resources available to help with ethical problems. In many cases, this is an ethics consult service or an ethics committee. Any hospital that is accredited by the joint commission must have in place a mechanism for dealing with ethical issues.

Implementation •• Choose a plan and act. •• Anticipate objections.

Evaluation THE PROCESS OF ETHICAL ANALYSIS When faced with an ethical problem, the nurse is expected to implement a formal process that promotes resolution. A structured approach to ethical dilemmas provides consistency, eliminates the risks of overlooking relevant contextual features, and invites thoughtful reflection on moral problems. Even so, analysis of ethical dilemmas is not easy. It often requires the assistance of an ethics consult service, the members of which have specific training in handling ethical dilemmas. While there are a variety of ethical decision-making processes, the one described here mirrors the nursing process. The following steps are involved in case analysis.

Assessment •• Identify the problem. Is it an ethical dilemma? Is it moral distress? Clarify the competing ethical claims, the conflicting obligations, and the personal and professional values in contention. Acknowledge the emotional components and communication issues. •• Gather data. Distinguish the morally relevant facts. Identify the medical, nursing, legal, social, and psychological facts. Clarify the patient’s and family’s religious and philosophical beliefs and values. •• Identify the individuals involved in the problem. Clarify who is involved in the problem’s development and who should be involved in the decision-making process. Identify who should make the final decision, and discern what factors may impede that individual’s ability to make the decision.

Plan •• Consider all possible courses of action and avoid restricting choices to the most obvious. •• Identify the risks and benefits likely to arise from each option.

•• Outline the results of the plan. Identify what harm or good occurred as a result of the action. •• Identify the necessary changes in institutional policy or other strategies to avoid similar conflicts in the future. This stepwise process of ethical analysis incorporates ethical principles and rules, relevant medical and nursing facts, and specific contextual features, and reflects a model of shared decision making. This ideology is essential if current and future moral issues are to be addressed and negotiated.

CONTEMPORARY ETHICAL ISSUES Informed Consent As a patient advocate, the critical care nurse recognizes the patient’s or surrogate’s central role in decision making. Patients must make informed decisions based on accurate and appropriate information. By uncovering the patient’s primary values and beliefs, the nurse empowers patients and surrogates to articulate their preferences. Therefore, the nurse does not speak for the patient, but instead maintains an environment in which the patient’s autonomy and right to self-determination are respected and preserved. The doctrine of informed consent encompasses four elements: disclosure, comprehension, voluntariness, and competence. The first two of these elements are related because the patient’s comprehension often depends on how the information is disclosed. Information must be provided in a manner that promotes the patient’s understanding of the current medical status, the proposed interventions (including the nature of the therapy and its purpose, risks, and benefits), and the reasonable alternatives to the proposed treatment. Full disclosure in clear language is supported by the principle of veracity.

CONTEMPORARY ETHICAL ISSUES 223

The overall goal of the treatment, rather than just the procedure, should be discussed with the patient and family and the goals should reflect the desirable and likely outcomes for this individual. The nurse can contribute significantly to the comprehension portion of the consent process by clarifying the patient’s or surrogate’s perception of the situation. Questions such as “What additional information do you need to help you make this decision?” or “What do you understand are the goals of this treatment?” help to highlight the patient’s interests and comprehension of the situation. Decisions must be reached voluntarily, and any threat of coercion, manipulation, duress, or deceit is unethical. Voluntary decisions uphold the principle of respect for persons and support the concept of self-determination. In addition, the patient must be capable of making decisions about medical care. Competence is a legal term and reflects judicial involvement in the determination of a patient’s decision-making capacity. Capacity reflects the ability of an individual to participate in the medical decision-making process. Determining capacity is discussed in the next section. The intent of the informed consent process is based on the principle of autonomy. In theory, the consent process provides an individual with the necessary information to compare options and make a reasoned choice. Unfortunately, the consent process is handled more as an event than a process. The focus is to “get consent” rather than to help the patient gain an understanding of the proposed treatment. The critical care nurse must be sensitive to the timing of such discussions and should attempt to optimize the environment and enhance the patient’s and family’s ability to participate in the decision-making process. Interactions should be uninterrupted, free from distractions, during intervals when the patient is fully awake, and, if desired by the patient, in the presence of loved ones. Nurses have both a moral and a legal duty in the consent process. Incorrect information given with the intent to deceive or mislead the patient or family must be reported according to institutional guidelines and in some states may qualify as professional misconduct to be reported to the profession’s state board. The ANA Code of Ethics for nurses portrays the nurse’s role during the consent process as a patient advocate upholding the patient’s right to self-determination. Therefore, the nurse must respect the competent patient’s choice and support the patient’s decisions even if the decision is contrary to the judgments of the healthcare team.

Determining Capacity Patients are presumed to possess decision-making capacity unless there are clear indications that the individual’s choices are harmful or inconsistent with previously stated wishes. Questioning another’s ability to engage in the decision-making process should be executed with caution. Value-laden judgments of an individual’s capacity, such as restricting involvement based on mental illness or advanced age, should be avoided. Cultural, religious, or ethical differences should

not be misinterpreted as evidence of incapacity. In addition, evaluations of capacity based on the presumed outcome of the decision are equally unjust. Capacity to make decisions is based on the patient’s physical and mental health and the ability to be consistent in addressing issues. Capacity is not based on the ability to concur with healthcare providers or family members. Instead, a functional standard to evaluate capacity is recommended. At many institutions, this functional standard is used to create a policy for establishing decisional capacity. The functional standard of determining capacity focuses on the patient’s abilities as a decision maker rather than on the condition of the patient or the projected outcome of the decision. The three elements necessary for a patient to meet the functional standard are the abilities to comprehend, to communicate, and to form and express a preference. The ability to comprehend implies that the patient understands the information relevant to the decision. A patient must exhibit abilities sufficient to understand only the facts pertinent to the prevailing issue. Therefore, orientation to person, place, and time does not guarantee or preclude the patient’s ability to understand and comprehend the relevant information. Decision-making capacity requires a communication of the decision between the patient and healthcare team. Communication with very ill patients often is compromised by pharmacologic or technological interventions. The critical care nurse should attempt to remove barriers to communication and advance the patient’s opportunity to engage in the decision-making process. The final component essential for evaluating functional capacity is evidence of the patient’s ability to reason about his or her choices. An individual’s choices should reflect the person’s own goals, values, and preferences. To evaluate this aspect, comments such as “Tell me about some of the most difficult healthcare decisions that you had to make in the past,” or “Describe how you reached the decision you did,” are useful. The patient should recount a pattern of reasoning that is consistent with personal goals and that reflects an accurate understanding of the consequences of the decision. When the patient lacks decision-making capacity, and attempts to control factors and return the patient to an autonomous state are unsuccessful, the healthcare team must rely on other sources for direction in approximating the patient’s preferences. Advance directives and surrogate decision makers are two ways in which the patient’s choices can be understood.

Advance Directives The Patient Self Determination Act (PSDA), effective December 1, 1991, is a federal law that requires healthcare institutions receiving Medicare or Medicaid funds to inform patients of their legal rights to make healthcare decisions and execute advance directives. The purpose of the PSDA is to preserve and protect the rights of adult patients to make choices

224

CHAPTER 8. Ethical and Legal Considerations

regarding their medical care. The PSDA also requires institutions to inform individuals of relevant state laws surrounding the preparation and execution of advance directives. Advance directives are statements made by an individual with decision-making capacity that describe the care or treatment he or she wishes to receive when no longer competent. Most states recognize two forms of advance directives, the treatment directive, or “living will,” and the proxy directive. The treatment directive enables the individual to specify in advance his or her treatment choices and which interventions are desired. Usually treatment directives focus on cardiopulmonary resuscitation (CPR), mechanical ventilation, nutrition and hydration, and other life-sustaining technologies. Proxy directives, also called the durable power of attorney for health care, expand the sphere of decision making by identifying an individual to make treatment decisions when the patient is unable to do so. The appointed individual, a relative or close friend, assumes responsibility for healthcare decisions as soon as the patient loses the capacity to participate in the decision-making process. Treatment decisions by the healthcare proxy are based on a knowledge and understanding of the patient’s values and wishes regarding medical care. Most states have statutory provisions that recognize the legal authority of the healthcare proxy, and this individual is given complete authority to accept or refuse any procedure or treatment on behalf of a patient who lacks capacity. Although most adults should complete both, a treatment and proxy directive, the proxy directive has some important advantages over a treatment directive. Many treatment directives are valid only under certain conditions. Terminal illness or an imminent death are common limitations required before the patient’s treatment directive is enacted. Such restrictions are not relevant in proxy directives, and the sole requirement before the proxy assumes responsibility on the individual’s behalf is that the patient lacks decisional capacity. Furthermore, the proxy directive enables the authorized decision maker to consider the contextual and unique features of the specific situation before arriving at a decision. A treatment directive may indicate refusal of mechanical ventilation, but a durable power of attorney speaking for the patient with a reversible acute respiratory process may consent to a trial of noninvasive ventilation. In this way, the benefits and burdens of proposed interventions are considered in partnership with the knowledge and understanding of the patient’s preferences and values. If a patient lacks decision-making capacity and has not previously designated a proxy decision maker in an advance directive, the healthcare team must identify an appropriate surrogate to make decisions on the patient’s behalf. Guidelines for identifying surrogate decision makers vary from state to state. Generally, family members have the patient’s best interests in mind, and many state statutes identify a hierarchy of relatives as appropriate surrogate decision makers. Regardless of whether the decision maker is a designated proxy or family member, the process of making

decisions on behalf of the incapacitated patient is difficult and arduous. If the patient left no written treatment directive, the surrogate decision maker and the designated proxy follow the same guidelines for making decisions. The decisions are made based on either the substituted judgment standard or the best interest standard. Substituted Judgment

When a patient previously has expressed his or her wishes regarding medical care, the surrogate decision maker invokes the standard of substituted judgment. The patient’s goals, beliefs, and values serve to guide the surrogate in constructing and shaping a decision that is congruous with the patient’s expressed wishes. An ideal interpretation of substituted judgment is that the patient, if competent, would arrive at the same decision as the surrogate. This standard originates in the belief that when we know someone well enough, we often are able to determine how he or she would have reacted to a particular situation, and therefore can make decisions on that person’s behalf. Best Interests

The best interest standard is used when the patient’s values, ideals, attitudes, or philosophy are not known; for example, a patient who never gained decision-making capacity and lacked competence throughout his or her life would not have the opportunity to articulate wishes and beliefs about health care. Using the best interest standard, the surrogate decision maker determines the course of treatment based on what would be in the patient’s best interests, considering the needs, risks, and benefits to the affected person. This burden/ benefit analysis includes considering the relief of suffering, restoration of function, likelihood of regaining capacity, and quality of an extended life. Although neither the best interest standard nor the substituted judgment standard is problem free, when possible the decision maker for an incapacitated patient should follow the principles of substituted judgment. Knowledge of the patient’s underlying values should guide the surrogate and will most likely result in a decision reflective of the patient’s interests and well-being. Nurses’ support surrogate decision makers in the same way that they serve as patient advocates by providing consistent, accurate information and asking questions to clarify the patient’s values.

End-of-Life Issues Decisions to Forego Life-Sustaining Treatments

Decisions to forego life-sustaining treatments are made daily in the hospital setting. The prevalence of these decisions does not diminish the difficulty that patients, families, nurses, and physicians face when considering this treatment decision. The model for this decision-making process is a collaborative approach that promotes the patient’s interests and well-being.

CONTEMPORARY ETHICAL ISSUES 225

The patient’s interests are best served when information is shared among the caregivers, patient, and family in an open and honest manner. Through this process, a plan of care that reflects the patient’s goals, values, and interests is developed. Continued collaboration is essential to ensure that the plan promotes the patient’s well-being and reflects the patient’s preferences. However, the patient may determine that the current plan imposes treatments that are more burdensome than beneficial, and may choose to forego new or continued therapies. Grounded in the principle of patient autonomy, patients with capacity have the moral and legal right to forego lifesustaining treatments. The right of a capable patient to refuse treatment, even beneficial treatment, must be upheld if the elements of informed consent are met and innocent or third parties are not injured by the refusal. Ongoing dialogue among the healthcare team, family, and patient is appropriate so that mutually satisfactory realistic goals are adopted. Patients must understand that refusal of treatment will not lead to inadequate care or abandonment by members of the healthcare team. In patients without decisional capacity, the determination to withdraw or withhold treatments is made by the identified surrogate. If the wishes and values of the patient are known, the surrogate makes treatment decisions based on this framework. If, however, the patient’s values or wishes are unknown, or the patient never had capacity to express underlying beliefs, the decision maker must consider and weigh the benefits and burdens imposed by the particular treatments. Any treatment that inflicts undue burdens on the patient without overriding benefits or that provides no benefit may be justifiably withdrawn or withheld. If the benefits outweigh the burdens, the obligation is to provide the treatment to the patient. In cases where the identified surrogate is not acting in the patient’s best interests, healthcare professionals have a moral obligation to negotiate an acceptable resolution to the problem. Critical care nurses should intervene when the best interest of the patient is in question. If extensive attempts to resolve the differences through the use of internal and external resources are unsuccessful in facilitating an acceptable solution, the healthcare professional should seek the appointment of an alternative surrogate. Often, the burden of proof is on the healthcare professional to justify the need for an alternative decision maker. In situations in which the patient’s life is threatened and the refusal of treatment by the surrogate would jeopardize the patient’s safety, the healthcare team must seek an alternative surrogate without prolonged discussion with the identified surrogate. This situation arises when parents who are Jehovah’s Witnesses refuse a life-saving blood transfusion for their child. The healthcare team can rapidly acquire court approval to transfuse the minor. In less emergent situations, attempts to convince the surrogate of the need for treatment and to reach a satisfactory settlement may take more time. In the case “The Patient’s Wishes,” members of the healthcare team interpreted the patient’s actions as a

decision made by a competent individual. They realized that even after aggressive treatment the patient would most likely be dependent on hemodialysis, and therefore his independence and living environment would change. On the other hand, his daughter saw her father’s act as a reflection of his depression from Parkinson disease and the loss of his wife. His daughter believed that additional antidepressant medications and more frequent psychiatric evaluations would renew her father’s desire to live. In this case, both parties believe they are advancing the patient’s best interests. Reflection on the patient’s life, work, actions, religion, and beliefs helps all parties to clarify the patient’s values, and may help in the development of an acceptable resolution. Conflicts regarding the withdrawal of life-sustaining treatments often reflect differences in values and beliefs. Typically, healthcare professionals value life and health. When patients or surrogates choose to forego treatments that have minimal benefit, relinquishing the original goal of restoring health is difficult. This dilemma is particularly apparent in the intensive care setting, where actions and interventions are aggressive, dramatic, and often life saving. Shifting from this model to a paradigm that advocates for a calm and peaceful death requires the critical care nurse and healthcare team to relinquish control and to change the treatment goals to promote comfort and support the grieving process. The intensity required to support the patient and family during the process of withdrawal of treatment must also be valued and appreciated by healthcare professionals in all settings. In some circumstances, surrogate decision makers insist on treatment that members of the healthcare team believe is burdensome and nonbeneficial for the patient. Frequently, the request for futile treatment reflects the surrogate or patient’s desire to be assured that “everything” is being done to eradicate the disease or restore health. Emotional, financial, and social concerns can all motivate individuals to pursue nonbeneficial, and even harmful, treatments. If patients and surrogates are kept fully informed of the goals and the successes and failures throughout the course of treatment, the request for futile therapies is less likely. If, after numerous discussions, the patient or surrogate continues to request futile treatment, eliciting help from an uninvolved party, such as an ethics committee, can facilitate discussions. Healthcare institutions often have policies that delineate the responsibilities of the caregiver and the resources within the institution to resolve these unusual situations. In rare circumstances, judicial involvement is necessary to determine the outcome of the case. Nutrition and Hydration

To many nurses and healthcare consumers, the provision of nutrition and hydration is fundamental to patient care. Therefore, nurses may be distressed when the withdrawal of nutrition and hydration are considered. However, the provision of nutrition and hydration is a medical intervention and thus has both risks and benefits. Medical nutrition

226

CHAPTER 8. Ethical and Legal Considerations

Essential Content Case

The Patient’s Wishes An 86-year-old widower resides in an assisted living facility. He has one adult daughter who lives out of town and regularly visits him twice a month. One morning the care providers at the facility find him unresponsive with shallow respirations and a bradycardic pulse. A note, written by Mr. Johnson, is attached to his body and states that he intentionally took a lethal overdose and that he does not wish to be resuscitated. Empty bottles of levodopa and amitriptyline are found in his room next to a glass partially filled with alcohol. Residents of the facility said that Mr. Johnson had continued to express sadness over the loss of his wife 2 years ago and that progression of the Parkinson disease also was troubling to him. The providers at the geriatric facility call the rescue squad, and he is rapidly transported to the hospital. The patient is hypotensive and unresponsive on admission to the medical intensive care unit. Laboratory tests reflecting his renal and hepatic function are grossly abnormal. Gastric lavage and activated charcoal are initiated to remove the drugs. The patient’s daughter requests that everything be done to save her father. The healthcare team respects the daughter’s wishes as surrogate, but is concerned that this is not what the patient wanted. They believe that the likelihood of a full recovery is remote and he should be allowed a peaceful death. Case Question 1. What factors need to be considered to evaluate Mr. Johnson’s capacity when he wrote the statement indicating he did not desire resuscitation? Case Question 2. What guidance can Mr. Johnson’s nurse offer to his daughter to help her in her role as surrogate decision maker? Answers 1. If Mr. Johnson had untreated or undertreated depression or dementia, than his capacity when he wrote his wish not to be resuscitated is called into question. Contacting his outpatient providers or seeking to review records from outpatient appointments may assist in determining if the patient had capacity and if his statement in his note should dictate a DNR order, and influence the care provided. 2. The patient’s daughter should be encouraged to consider what kind of care her father, in the absence of mental illness or dementia, would desire. While she is grieving, and probably feeling guilty about the drastic action her father has taken, her ethical obligation is to speak on her father’s behalf and not to speak for herself. The nurse can encourage the daughter to recall conversations the two had during her visits in which he may have indicated his preferences regarding resuscitation, life support, and the use of medical hydration and nutrition.

and hydration are administered through intravenous access, nasogastric and duodenal feeding tubes, or via gastrostomy. The image of gently spoon feeding a dying patient is replaced with the reality of meeting the nutritional requirements through invasive and uncomfortable technologies.

Provision of medical nutrition and hydration should occur following a careful burden-benefit analysis. If medical nutrition and hydration support and expedite the patient’s return to an acceptable level of functioning (as defined by the patient or surrogate) then provision of the therapy is beneficial. When uncertainty exists, the presumption should be to provide nutrition and hydration. On the other hand, when continued provision of nutrition and hydration will not effectively restore the patient to a functional status consistent with the patient’s values, the treatment may be discontinued. Pain Management

When faced with a potentially life-limiting disease process, issues regarding the aggressive management of pain and comfort develop. Although palliation or relief of troubling symptoms is a priority in the care of all patients, once the decision to forego life-sustaining measures is made, palliation becomes the main focus of all care. In some circumstances, patients experience distressing symptoms despite the availability of pharmacologic agents to manage the uncomfortable effects of chronic and terminal illness. Whether due to a lack of knowledge, time, or a deliberate unwillingness to prescribe the necessary medication, inadequate symptom management is unethical. Nurses are obligated to ensure that patients receive care and treatments that are consistent with their choices. There are few patients in whom adequate pain management cannot be achieved. The ANA Position Statement on pain management and control of distressing symptoms in dying patients delineates the role of the nurse in the assessment and management of pain. When patients require large doses of medications, such as narcotics, to effectively alleviate their symptoms, providers may be concerned that the side effects of such doses may hasten the patient’s death. The ANA Code of Ethics for Nurses helps clarify this concern for nurses by affirming that nurses “should provide interventions to relieve pain and other symptoms in the dying patient even when those interventions entail risks of hastening death.” The essential element in this situation is the nurse’s intent in providing the medication. Because the intent is to relieve pain and suffering, and not to deliberately hasten death, the action is morally justified. The concept that supports this reasoning is called the principle of double effect. This principle states that if an action has both a good and bad effect, a person is justified in taking that action if the intent was the good effect, the bad effect was a possible but not certain outcome of the action, and there was no additional course of action which could produce the good effect and avoid the bad one. The US Supreme Court cited the principle of double effect in a decision that distinguished palliative care from assisted suicide. A provider who assists in a patient’s death intends to cause that person’s death, which is ethically and legally distinct from a provider who seeks to control symptoms and gives medications that may, inadvertently, hasten death.

BUILDING AN ETHICAL ENVIRONMENT 227

Resuscitation Decisions Critically ill patients are susceptible to sudden and unpredictable changes in cardiopulmonary status. Most hospitalized patients presume that, unless discussed otherwise, resuscitation efforts will be instituted immediately upon cardiopulmonary arrest. In-hospital resuscitation is moderately successful, and delay in efforts significantly reduces the chance of the victim’s survival. The emergent nature, the questionable effectiveness, and the presumed provision of CPR contribute to the ethical dilemmas that surround this intervention. Do not Resuscitate Orders

“Do not resuscitate” (DNR) or “no code” are orders to withhold CPR. Other medical or nursing interventions are not influenced directly by a DNR order. In other words, the decision to forego CPR is not a decision to forego any other medical interventions. The communication surrounding this decision is one of the most important elements in designing a mutually acceptable treatment plan for a particular patient. Appropriate discussions with the patient or surrogate must occur before a resuscitation decision is made. Conversations about resuscitation status and the overall treatment goals should occur with the patient or surrogate, physician, nurse, and other appropriate members of the healthcare team. Open communication and a shared understanding of the treatment plan are essential to understanding and responding to the patient’s interests and preferences. Once a decision is made regarding resuscitation status, the physician must document the discussion and decision in the medical record according to the institution’s policy. When the issue of resuscitation status is not addressed with the patient or surrogate or the decision is not documented or communicated with caregivers, then a code is initiated, risking the provision of unwanted care. Slow Codes or Partial Codes

The failure to define the DNR status and other treatment or nontreatment decisions often reflects the absence of an overall treatment goal. Patients or their surrogates must be involved in decisions surrounding resuscitation. Although some providers believe that decisions to withhold CPR can be made without involving patients or surrogates, such decisions violate the principle of patient autonomy. Just as patient’s consent to other interventions in the plan of care, including decisions to omit particular treatments, the provision or withholding of CPR is based on discussions with the patient and family. In some instances healthcare providers rely on “slow” or “partial” codes in which interventions are administered with less effort and less speed than the emergent situation demands, increasing the likelihood that the resuscitative effort will be unsuccessful. Slow or partial codes are always unethical and often indicate failed communication between the patient and family and the healthcare team. It is the

responsibility of healthcare providers to explain CPR, ensure that the family and patient understand both the risks and benefits and likely outcomes of the procedure, and either provide or withhold the intervention in accordance with the patient and family’s wishes. Most institutions have policies that address the process of writing and implementing a DNR order. In addition, many states have an approved process and format to indicate a desire to forgo life support so that this wish can be conveyed across all healthcare settings. Examples of such forms include the Durable DNR form in Virginia and the Physician Order for Life Sustaining Treatment or POLST form in California. Nurses should be familiar with the forms available in the states they practice, understand institutional policies for recognizing such forms, and encourage patients and families to use these means to convey their wishes. These forms are tools for preventing the provision of undesired care. Family Presence during Resuscitation

The practice of allowing family members to be present during resuscitative efforts and other invasive procedures is a key consideration in the ethical care of critically ill patients. Protocols or procedures for allowing family presence may be available on an individual nursing unit or for all nursing units in a given institution, and can guide nurses in providing this care. Some considerations include having a staff member available to narrate the experience for the family members, and documenting family presence in the patient’s chart. AACN’s 2010 Practice Alert lists the strong evidence in favor of allowing family members to be present during resuscitation and invasive procedures, noting primarily the benefit of this practice for family and patients. Thus, the principles of beneficence support family presence during resuscitation and other invasive procedures. The ethic of care similarly supports this practice as it acknowledges the priority of the patient and family relationships.

BUILDING AN ETHICAL ENVIRONMENT Values Clarification One of the most useful and essential skills offered by nurses is that of assisting the patient and family in values clarification. This process helps families to weigh the burdens and benefits of medical interventions and provides them with a framework of the patient’s preferences and interests. Additionally, families are less encumbered during the bereavement process, when reflecting on the patient’s hospitalization, if they feel the decisions they made for the patient reflect the patient’s values.

Provide Information and Clarify Issues Patients and families rely on nurses to clarify medical information and support the exploration and meaning of different treatment decisions. The trusting relationship that develops is based on the nurse’s abilities to communicate and

228

CHAPTER 8. Ethical and Legal Considerations

understand the patient’s needs. Questions that help to unveil patients’ and families’ perceptions of the situation include: “What information do you need to make this decision?” “What do you understand of your (or your loved one’s) condition?” and “What are your fears about being sick?” The information provided to patients and surrogates must be more than simply disclosing facts. The dialogue must be ongoing, open, honest, and expressed with concern. Because the understanding of new knowledge is often rooted in past learning, the nurse begins by assessing the patient’s or surrogate’s prior experiences with the healthcare system. Patients and families often draw conclusions or create relationships based on incomplete or inaccurate interpretations of information. Nurses play a key role in facilitating communication and translating discrepancies in perceptions.

Recognize Moral Distress Moral distress refers to the suffering that occurs when individuals feel compelled to act in ways they think are unethical. Nurses can feel trapped between institutional constraints, medical directives, patient and family wishes, and personal beliefs, duties, and values. Although all ethical problems are challenging, situations that result in moral distress are particularly troubling because they may have lasting effects on the individual’s professional and personal life. Recognizing situations that contribute to moral distress and developing strategies to preserve moral integrity are essential tools for the critical care nurse. The AACN booklet 4 A’s to Rise above Moral Distress provides an approach to addressing situations that create moral distress and to prevent the harmful consequences that it causes. Increasingly, institutions are recognizing the importance of addressing moral distress in the workplace. Many other strategies are being designed and implemented, such as unit-based conversations in ethics and moral distress consult services.

Engage in Collaborative Decision Making Nursing offers a distinct perspective that is grounded in humanistic and caring values. Nurses recognize, interpret, and react to the patient’s and family’s response to health problems. Factors such as the patient’s ability to adapt to changes in health, cope with a diagnosis, or adjust to a treatment are valuable contributions to a model of shared decision making. Because nursing embraces this viewpoint, nurses must have a consistent presence on the healthcare team. Patients and families expect and need nurses to be actively involved in planning and implementing the plan of care. In a collaborative model, the nurse’s contributions and perspectives are valued, pursued, and acknowledged. The nurse, in exchange, is open to the contributions of other team members, actively listening and encouraging their participation. When nurses are absent from the circle of decision making, moral problem occur and communication falters. Every critical care nurse must remain involved, attached, and committed to the process of shared decision making and collaborative interaction.

SELECTED BIBLIOGRAPHY Ahronheim J, Moreno JC, Zuckerman C. Ethics in Clinical Practice. 2nd ed. Gaithersburg, MD: Aspen; 2000. American Nurses Association Code of Ethics for Nurses: http://www. nursingworld.org/Mobile/Code-of-Ethics Beauchamp TL, Childress JF. Principles of Biomedical Ethics. 6th ed. Oxford, England: Oxford University Press; 2009. Burkhardt MA, Nathaniel AK. Ethics and Issues in Contemporary Nursing. 2nd ed. Independence, KY: Delmar Thomson Learning; 2001. Campbell GM, Delgado S, Heath JE, et al. The 4A’s to Rise Above Moral Distress. Wavra T. ed. Aliso Viejo, CA: AACN; 2004. Campbell ML. Foregoing Life-Sustaining Therapy. Aliso Viejo, CA: AACN; 1998. CMS regulations: http://www.cms.gov/apps/docs/aca-update-implementing-medicare-costs-savings.pdf. Accessed February 27, 2013. Coughennower M. Physician assisted suicide. Gastroenterol Nurs. 2003;26(2):55-59. Davis AJ, Aroskar MA, Liaschenko J, Drought TS. Ethical Dilemmas and Nursing Practice. 4th ed. Stamford, CT: Appleton & Lange; 1997. DHHS Privacy rule: http://www.hhs.gov/ocr/privacy/. Accessed February 27, 2013. Fry ST, Veatch RM. Case Studies in Nursing Ethics. 2nd ed. Boston: Jones & Bartlett Publishers; 2000. Georges J-J, Grypdonck M. Moral problems experienced by nurses when caring for terminally ill people: a literature review. Nurs Ethics. 2002;9:155-178. Gilligan C. Moral orientation and moral development. In: Kittay EF, Meyers DT, eds. Women and Moral Theory. New York: Rowman & Littlefield Publishers, Inc; 1987:19-33. Gordon EJ, Hamric AB. The courage to stand up: the cultural politics of nurses’ access to ethics consultation. J Clin Ethics. 2006;17(3):231-254. Hamric AB, Davis WS, Childress MD. Moral distress in health care providers: what is it and what can we do about it? The Pharos. 2006; Winter:17-23. Hamric, AB, Wocial, LD, Epstein, EG (October, 2011). Transforming moral distress into moral agency. Panel presentation. ASBH annual conference, Minneapolis, MN. Kuczewski MG. Ethics committees at work: the illegal alien who needs surgery. Camb Q Healthc Ethics. 2000;9:128-135. La Puma, J, Orentlicher, D., Moss, RJ. (1991). Advance directives on admission. Clinical implications and analysis of the Patient Self Determination Act of 1990. J Am Med Assoc. 266(3), 402-405. Lo B. Resolving Ethical Dilemmas: A Guide for Clinicians. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2000. Manojlovich M. Power and empowerment in nursing: looking backward to inform the future. Online J Issues Nurs. January 31, 2007: 12(1). Manuscript 1. www.nursingworld.org/MainMenuCategories/ ANAMarketplace/ANAPeriodicals/OJIN/TableofContents/ Volume122007/No1Jan07/LookingBackwardtoInformtheFuture. aspx. Accessed February 27, 2013. Matzo M, Sherman D, Penn B, Ferrell B. The end of life nursing education consortium (ELNEC) experience. Nurse Educ. 2003;28(6):266-270. Meisel, A, Snyder, L, and Quill, T. (2000). Seven legal barriers to end of life care: myths, realities and grains of truth. J Am Med Assoc, 284(19), 2495-2501. Naden D, Eriksson K. Understanding the importance of values and moral attitudes in nursing care in preserving human dignity. Nurs Sci Q. 2004;17(1):86-91.

SELECTED BIBLIOGRAPHY 229

National Consensus Project for Quality Palliative Care. Clinical Practice Guidelines for Quality Palliative Care. Brooklyn, NY: National Consensus Project for Quality Palliative Care; 2004. Oberle K, Hughes D. Doctors’ and nurses’ perceptions of ethical problems in end-of-life decisions. J Adv Nurs. 2001;33(6): 707-715. Rushton CH, Penticuff JH. A framework for analysis of ethical dilemmas in critical care nursing. AACN Adv Crit Care. 2007;19(3):323-329. Westphal, C., Wavra, T. (2005). Acute and critical choices: guide to advance directives. American Association of Critical Care Nurses, online at http://www.aacn.or/wd/Practice/Docs/Acute_ and_Critical_Care_Choices_to Advance_Directives.pdf. Wocial, LD, Hancock, M., Bledsoe, PD, Chamness, AR, Helft PR. (2010) An evaluation of unit-based ethics conversations. JONA’s Healthc Law, Ethics, and Regul. 12(2): 48-54.

American Nurses’ Association. Position Statement on Pain Management and Control of Distressing Symptoms in Dying Patients. Washington, DC: ANA; 2003. American Nurses’ Association. Position Statement on Nursing Care and Do-Not-Resuscitate (DNR) Decisions. Washington, DC: ANA; 2003.

Professional Codes, Standards, and Position Statements

The ANA Center for ethics and human rights. http://www.nursingworld. org/MainMenuCategories/ThePracticeofProfessional-Nursing/ EthicsStandards.aspx. Accessed January 10, 2010. American Association of Critical-Care Nurses: AACN Ethics website: http://w w w.aacn.org/WD/AACNNews/C ontent/2008/ oct-practice.pcms?menu=Practice. Accessed January 10, 2010. NIH site for ethics resources: http://bioethics.od.nih.gov/. Accessed January 10, 2010. The American Journal of Bioethics: http://www.bioethics.net/. Accessed January 10, 2010. The Hastings Center: http://www.thehastingscenter.org/. Accessed January 10, 2010.

AACN Position paper: zero tolerance for violence: http://www.aacn. org/wd/practice/docs/publicpolicy/zero_tolerance_for_abuse. pdf. Accessed February 7th, 2013. AACN Position paper: moral distress: http://www.aacn.org/wd/ practice/docs/moral_distress.pdf. Accessed February 7th, 2013. ACCN Practice alert: family presence during resuscitation and invasive procedures. http://www.aacn.org/wd/practice/docs/ practicealerts/family%20presence%2004-2010%20final.pdf. Accessed February 27, 2013. American Nurses’ Association. Code for Nurses with Interpretive Statements. Washington, DC: ANA; 2001.

Evidence-Based Guidelines Puntillo K, Medina J, Rushton C, et al. End-of-life and palliative care issues in critical care. In: Medina J, Puntillo K, eds. Protocols for Practice: End of Life and Palliative Care Issues in Critical Care. Aliso Viejo, CA: AACN; 2007.

Online References of Interest: Related to Legal and Ethical Considerations

This page intentionally left blank

Pathologic Conditions

This page intentionally left blank

Cardiovascular System Barbara Leeper

KNOWLEDGE COMPETENCIES 1. Identify indications for, complications of, and nursing management of patients undergoing coronary angiography and percutaneous coronary interventions. 2. Describe the etiology, pathophysiology, clinical presentation, patient needs, and principles

SPECIAL ASSESSMENT TECHNIQUES, DIAGNOSTIC TESTS, AND MONITORING SYSTEMS Assessment of Chest Pain Obtaining an accurate assessment of chest pain history is an important aspect of differentiating cardiac chest pain from other sources of pain (eg, musculoskeletal, respiratory, anxiety). Ischemic chest pain, caused by lack of oxygen to the myocardium, must be quickly identified for therapeutic interventions to be effective. The most important descriptors of ischemic pain include precursors of pain onset, quality of the pain, pain radiation, severity of the pain, what relieves the pain, and timing of onset of the current episode of pain that brought the patient to the hospital. Each of these descriptors can be assessed using the “PQRST” nomogram (Table 9-1). This nomogram prompts the clinician to ask a series of questions which help clarify the characteristics of the cardiac pain.

Coronary Angiography Coronary angiography is a common and effective method for visualizing the anatomy and patency of the coronary arteries. This procedure, also known as cardiac catheterization, is used to diagnose atherosclerotic lesions or thrombus in the coronary vessels. Cardiac catheterization is also used for evaluation of valvular heart disease (including stenosis or insufficiency),

of management of patients with ischemic heart disease. 3. Discuss the etiology, pathophysiology, clinical presentation, patient needs, and principles of management of patients in shock, heart failure, and hypertensive crisis.

atrial or ventricular septal defects, congenital anomalies, and myocardial wall motion abnormalities (Table 9-2). Procedure

Prior to cardiac catheterization, the patient should be NPO for at least 6 to 12 hours, in the event that emergency intubation is required during the procedure. NPO may indicate everything except medications, which should be taken with small sips of water the day of the procedure. Typically, if the patient is on insulin or taking hypoglycemics, the doses may need to be adjusted the day of the procedure. Benadryl may be administered prior to beginning the procedure as a precautionary measure against allergic reaction to the dye. Aspirin, clopidogrel, or other platelet inhibitor agents may be administered to prevent catheter-induced platelet aggregation during the procedure. Typically, patients remain awake during the procedure, allowing them to facilitate the catheterization process by controlling respiratory patterns (eg, breath holding during injection of radiopaque dye to improve the quality of the image). An anxiolytic agent, such as lorazapam or diazepam, is frequently administered during the procedure to decrease anxiety or restlessness. An intracoronary catheter is inserted through a “sheath” or vascular introducer placed in a large artery, most commonly the femoral artery (Figure 9-1A). In recent years there 233

234

CHAPTER 9. Cardiovascular System

TABLE 9-1. CHEST PAIN ASSESSMENT Ask the Question P (Provoke)

Q (Quality)

R (Radiation)

S (Severity)

T (Timing)

What provokes the pain or what precipitates the pain? What is the quality of the pain?

Does the pain radiate to locations other than the chest? What is the severity of the pain (on a scale of 1-10)?

Examples Climbing the stairs, walking; or may be unpredictable— comes on at rest Pressure, tightness; may have associated symptoms such as nausea, vomiting, diaphoresis Jaw, neck, scapular area, or left arm

On a scale of 1-10, with 10 being the worst, how bad is your pain? What is the time of onset of When did this episode of pain this episode of pain that that brought you to the caused you to come to the hospital start? hospital? Did this episode wax and wane or was it constant? For how many days, months, or years have you had similar pain?

has been an increase in the use of the radial artery as catheters have been made smaller, allowing easier access to the vessel. If inserted via the femoral artery, the catheter is advanced into the ascending abdominal aorta, across the aortic arch, and into the coronary artery orifice located at the base of the aorta (Figure 9-1B). Ionic dye, visible to the observer or operator under fluoroscopy (x-ray), is then injected into the coronary arterial tree via the catheter. If the cardiac valves, septa, or ventricular wall motion is being evaluated, the catheter is advanced directly into the left ventricle, followed by injection of dye (Figure 9-1C). During a right heart catheterization, the catheter is inserted into the venous system via the inferior vena cava, passed through the right ventricle, and advanced into the pulmonary artery. Interpretation of Results

The coronary vascular tree consists of a left and a right system (Figure 9-2). The left system consists of two main TABLE 9-2. INDICATIONS FOR CARDIAC CATHETERIZATION Right Heart • Measurement of right-sided heart pressures: ° Suspected cardiac tamponade ° Suspected pulmonary hypertension • Evaluation of valvular disease (tricuspid or pulmonic) • Evaluation of atrial or ventricular septal defects • Measurement of AVo2 difference Left Heart • Diagnosis of obstructive coronary artery disease • Identification of lesion location prior to CABG surgery • Measurement of left-sided heart pressures: Suspected left heart failure or cardiomyopathy • Evaluation of valvular disease (mitral or aortic) • Evaluation of atrial or ventricular septal defects

branches, the left anterior descending (LAD) artery and the left circumflex (LCx) artery. The right system has one main branch, the right coronary artery (RCA). Both systems have a number of smaller vessels that branch off these three primary arterial vessels. A clinically significant stenosis is considered to be an obstruction of 75% or greater in a major coronary artery or one of its major branches. If there is significant disease in only one of the major arteries, the patient is said to have single-vessel disease. If two major vessels are affected, the patient has two-vessel disease. If significant disease exists in all three major coronary arteries, the patient has three-vessel disease. Frequently, the microvasculature, or smaller vessels branching off the major coronary artery, may also have blockages. It is common to refer to these multiple lesions as diffuse disease. A cineventriculogram is obtained by radiographic imaging during the injection of dye after advancing the catheter from the aorta, through the aortic valve, and into the left ventricle (see Figure 9-1C). A cineventriculogram provides information on ventricular wall motion, ejection fraction, and the presence and severity of mitral regurgitation and aortic regurgitation. Ejection fraction, the percentage of blood volume ejected from the left ventricle with each contraction, is the gold standard for determining left ventricular function and is helpful in selecting treatment strategies. A left ventricular ejection fraction (LVEF) normal value is 55% to 60%. The LVEF is one of the most important predictors of long-term outcome following acute myocardial infarction (AMI). Patients with ejection fractions less than 20% have nearly 50% 1-year mortality. Another important measurement is the pressure in the left ventricle at the end of diastole. This is called “left ventricular end-diastolic pressure (LVEDP).” It, too, is an important determinant of ventricular function and is considered to be a predictor of morbidity and mortality in patients with heart failure and those undergoing cardiac surgery. The normal LVEDP is 6 to12 mm Hg. Complications

During cardiac catheterization, a number of complications may occur, including arrhythmia; coronary vasospasm; coronary dissection; allergic reaction to the dye; atrial or ventricular perforation from the catheter resulting in pericardial tamponade; embolus to an extremity, a lung, or, rarely, the brain; acute closure of the left main coronary; myocardial infarction (MI); or cardiac arrest. Common management and prevention strategies for catheterization complications are summarized in Table 9-3.

Percutaneous Coronary Interventions Percutaneous coronary interventions (PCIs) include percutaneous transluminal coronary angioplasty (PTCA), insertion of one or more stents, and coronary atherectomy. PTCA, also termed angioplasty or balloon angioplasty, is a cardiac catheterization with the addition of a balloon apparatus on the tip of the catheter for revascularizing the myocardium

SPECIAL ASSESSMENT TECHNIQUES, DIAGNOSTIC TESTS, AND MONITORING SYSTEMS 235

Ascending abdominal aorta Catheter

Guidewire

Femoral artery

Introducer Femoral vein Incision B

Catheter

Figure 9-1. Coronary angiography. (A) Insertion of the coronary catheter into the femoral artery through a percutaneously inserted introducer sheath. (B) Coronary catheter advancement into the aorta and the left coronary artery. (C) Catheter advancement into the left ventricle.

(Figure 9-3). The catheter tip is advanced, generally over a guidewire, into the coronary artery until the balloon is positioned across the atherosclerotic lesion in the vessel. Once properly positioned, the balloon is inflated, resulting in fracture and compression of the atherosclerotic plaque, improving blood flow through the vessel. As a result, the degree of stenosis is reduced. This allows a higher rate and volume of blood flow through the vessel improving perfusion of the tissues, which translates clinically into fewer symptoms of angina and better exercise tolerance.

emergency coronary artery bypass surgery (1%-2% incidence). The most important predictor of complications of MI and abrupt vessel closure is reduced coronary flow through the lesion prior to the procedure. A universal scale, the thrombolysis in myocardial ischemia (TIMI) scale, is used to quantify this rate of coronary flow. The scale rates the coronary blood flow as follows: no perfusion, penetration without perfusion, partial perfusion and complete perfusion.

Complications

In addition to routine balloon angioplasty, a number of other devices are now commonly used for percutaneous coronary revascularization. Intracoronary stents are small metallic mesh tubes placed across the stenotic area and expanded with an angioplasty balloon (Figure 9-4). Once expanded, the tube is permanently anchored in the vessel wall. Stents are effective in decreasing the rate of abrupt vessel closure seen with

Angioplasty is associated with the same complications found during cardiac catheterization. In addition, complications related to manipulation of the coronary artery itself may also occur. The most common serious complications include a 2% to 10% incidence of complete occlusion of the vessel (“abrupt closure”), AMI (1%-5% incidence), and the need for

Other Percutaneous Coronary Interventions

236

CHAPTER 9. Cardiovascular System

LCx LAD RCA

Narrowed artery Plaque

Figure 9-2. Coronary artery circulation with a coronary vessel narrowed with plaque formation.

TABLE 9-3. CARDIAC CATHETERIZATION: COMMON COMPLICATIONS AND NURSING INTERVENTIONS Complication Local bleeding due to catheter site artery damage (hematoma, hemorrhage, pseudoaneurysm)

Coronary artery dissection

Tamponade because of perforation of the heart or bleeding due to antiplatelet medications Peripheral thromboembolism

Thromboembolism: CVA due to embolus Pulmonary embolism

Arrhythmia Infection

Pulmonary edema due to recumbent position, stress of angiographic contrast, or poor left ventricular function Acute tubular neurosis and renal failure

Vasovagal reaction

Intervention Keep patient flat; head of bed (HOB) < 30°. Discontinue unfractionated heparin infusion if present. Compress the artery just above the incision (pedal pulse should be faint). Monitor for hypotension, tachycardia, or arrhythmia. Embolectomy or vascular repair may be deemed necessary following groin ultrasound. Stent will typically be placed during procedure. Monitor for arrhythmia or tamponade. Administer unfractionated heparin. Typically this will be evident in the catheter laboratory at the time of perforation. Monitor patient for equalization of cardiac pressures. Emergency surgery may be required for repair. Extremity will exhibit pain, pallor, pulselessness, paresthesias, and paralysis; may also be cool to touch. Unfractionated heparin or other anticoagulant should be continued. Thrombolytic therapy may be administered directly to the clot using a tracking catheter. Surgical intervention may be necessary. Monitor for signs and symptoms of neurologic compromise including speech patterns, orientation, vision, equal grips and pedal pushes, and sensation. Provide supplemental O2. Monitor for adequate arterial oxygen saturation and respiratory rate. Continue administration of unfractionated heparin or other anticoagulant IV. Direct thrombolytic therapy may be administered using a tracking catheter; direct extraction of the clot may also be attempted. Ventilation-perfusion scan or pulmonary arteriograms may be done to verify thrombus location. Direct irritation of the ventricular wall by the catheter tip poses the greatest risk; postprocedure risk is extremely low. Monitor the patient in lead V1. Use aseptic technique for all dressing changes. Monitor catheter insertion sites for erythema, inflammation, heat, or exudate. Monitor patient temperature trends. Elevate HOB 30°. Administer diuretics as necessary. Consider use of flexible sheath or brachial access. Hydrate patient well prior to and following procedure with continuous infusion of normal saline (typically 8 hours before and 8 hours after at 100 mL/h). Monitor for elevations in serum creatinine. Administer pain medications prior to sheath removal. Monitor BP and heart rate before and after sheath removal, then every 15 minutes for 4 times after removal.

PATHOLOGIC CONDITIONS 237

mismatch, known as ischemia, is most often caused by thrombus formation at a site of atherosclerotic plaque rupture within a coronary artery. Decreased oxygen supply to myocardial tissue may cause a variety of symptoms such as chest discomfort (angina), shortness of breath, diaphoresis, and nausea. Unstable angina, defined as angina that is of new onset, increasing in frequency, or occurring at rest, and AMI are referred to as Acute Coronary Syndrome (ACS), which form the spectrum of acute ischemic heart disease. Etiology and Pathophysiology

Figure 9-3. Percutaneous transluminal coronary angioplasty (PTCA). (A) PTCA catheter being advanced into the narrowed coronary artery over a guidewire. (B) Catheter position prior to balloon inflation. (C) Balloon inflation. (D) Coronary vessel following catheter removal.

traditional PTCA. Some stents are coated with a drug that is bonded to a material on the stent causing the drug to be released directly on to the arterial wall over several months to years. These drug-coated stents have been shown to significantly reduce the restenosis rate associated with metal stents. Atherectomy catheters and lasers are used infrequently; however, patient outcomes are not significantly better than those achieved with traditional balloon catheters and stent deployment and may result in higher rates of complication, including AMI. Each of these devices may offer advantages over traditional balloon angioplasty catheters in situations involving specific vascular anatomy (eg, ostial lesions) or lesion morphology (eg, high degree of calcified plaque).

PATHOLOGIC CONDITIONS Acute Ischemic Heart Disease Myocardial ischemia (MI) is the lack of adequate blood supply to the heart, resulting in an insufficient supply of oxygen to meet the demands of the heart muscle. This supply-demand

Intracoronary thrombus formation, and the resulting obstruction of coronary blood flow, is the pathophysiologic mechanism of acute ischemic heart disease. Preexisting atherosclerosis and spasm of the smooth muscle wall of the coronary arteries, termed fixed obstructions, may also contribute to reduced flow. In some situations, coronary artery spasm may play a major role, unrelated to underlying atherosclerosis, causing MI. These occurrences are sometimes associated with cocaine abuse in young patients. The formation of a thrombus in coronary arteries is initiated by the fissuring and rupture of atherosclerotic plaque in the vessel wall of the coronary artery (Figure 9-5). A continuous, dynamic process occurs whereby plaque may become unstable during periods of active accumulation of more lipid into the core of the plaque. The plaque then ruptures, dispelling its contents into the lumen of the coronary artery and causing activation of clotting factors at the site of plaque rupture. The rupture of plaque and resultant thrombus formation may eventually occlude the coronary artery. Although most people have some degree of atherosclerotic plaque formation by age 30, the vast majority of these plaques are considered “stable.” They are covered by smooth fibrous caps that allow adequate blood flow through the coronary arteries, and are not prone to development of unstable angina or MI. In young, growing plaques, the fibrous cap may become thin and rupture, resulting in unstable angina, ischemia, or MI. A variety of factors predispose a plaque to fissure and rupture. Characteristics of plaque at increased risk for rupture include: •• Location of the lesion in the vascular tree: Areas of greater turbulence of flow and dynamic activity during the cardiac cycle are at higher risk. •• Size of the lipid pool within the plaque: A large amount of lipid inside the plaque core is more likely to be associated with plaque disruption. •• Infiltration of the plaque with macrophages: Macrophages are thought to weaken the integrity of the fibrous cap of the plaque, making it more susceptible to rupture. Although these characteristics determine the likelihood of plaque rupture, they are not easily identified by clinical assessment, stress testing, or cardiac catheterization. Plaque

238

CHAPTER 9. Cardiovascular System

1 in

Figure 9-4. Intracoronary stent. (A) Size of stent device when fully deployed. (B) Insertion of stent into a narrowed area of a coronary artery on a balloon-inflatable catheter. (C) Inflation of the balloon catheter to expand the stent. (D) Inflation complete with stent fully expanded. (E) Stent following removal of balloon catheter.

A Plaque rupture

Platelets and thrombin

Fissure

Thrombus

Figure 9-5. Atherosclerotic plaque formation. (A) Stable plaque. (B) Plaque with cap disruption. (C) Moderate amount of layered thrombus. (D) Occlusive thrombus.

PATHOLOGIC CONDITIONS 239

Essential Content Case

Unstable Angina A 62-year-old man presents to the emergency department (ED) with complaints of pain in his chest and jaw. The pain, originally occurring only with exertion and resolving with rest, became increasingly persistent over the past 2 to 3 days. On the evening of his arrival, the patient experienced a 15-minute episode of severe pain while watching television. This episode he characterized as a “tight, burning feeling in my chest, and an aching in my jaw” that did not vary with respiratory effort and was accompanied by diaphoresis, nausea, and shortness of breath. On arrival to the ED, his pain and nausea had resolved, pulse oximetry showed oxygen saturation of 98% on room air, and his vital signs were: BP 148/86 mm Hg HR 90 beats/min RR 18 breaths/min T 37.6°C orally On physical examination, heart sounds were normal, without S3, S4, or murmurs. Initial diagnostic tests revealed: • ECG: Normal sinus rhythm with nonspecific ST-T wave changes • Chest x-ray: Normal cardiac silhouette, clear lungs A more detailed assessment of his history revealed increasing dyspnea on exertion and fatigue for the previous 6 months. Despite these symptoms, he had continued his daily 2.5-mile walking routine, sometimes experiencing shortness of breath several times during the walk. The patient reported smoking cigarettes in the past, one pack per day for 20 years, but quit 25 years ago. No ankle swelling, nocturnal dyspnea, or orthopnea were reported, nor was he aware of any family history of cardiac problems, coronary artery disease, diabetes, or hypertension. He was started on aspirin based on his history and the likelihood of underlying coronary artery disease. He was then admitted for observation and evaluation of cardiac enzymes. (See section on cardiac enzymes in section on MI below). Emergency Department 4 hours later

CK Total 169 mcg/L

CK-M B 5 ng/mL

Troponin I 0.4

163 mcg/L

5 ng/mL

0.4

Six hours after presenting to the ED, the patient had recurrent tightness in his chest. An ECG showed T-wave inversion in the anterior leads. Sublingual nitroglycerin 0.4 mg was administered every 5 minutes with complete relief of the pressure following the second tablet. An unfractionated heparin infusion was started. Subsequent cardiac enzymes showed: 8 hours 12 hours

CK Total 159 mcg/L 152 mcg/L

CK-MB 4 ng/mL 4 ng/mL

Troponin I 0.4 0.4

Other laboratory results were normal with the exception of elevated cholesterol and triglycerides on the lipid panel. Following receipt of these results, he was scheduled for an exercise tolerance test. The ECG recorded a heart rate of 118 beats/min after 6 minutes of exercise. Onset of chest tightness during

the last minute of exercise was described as similar to that which brought him to the hospital and correlated with 1.5-mm ST depression in leads V4 to V6. A cardiac catheterization was scheduled. Coronary angiography showed a 75% obstruction of the LAD artery and 90% obstruction of the diagonal branch of the same artery. LVEF was 55%. A coronary angioplasty (PTCA) was performed on both lesions. Case Question 1. While in the ED, an important aspect of his care would be to: (A) Obtain repeat ECGs intermittently every 4 hours (B) Monitor the patient’s ECG continuously with continuous ST-segment monitoring (C) Monitor platelet levels every 6 hours (D) Assess breath sounds every 2 hours Case Question 2. The ST-segment depression and T-wave inversion would be indicative of a: (A) Non-ST-segment elevation MI (B) ST-segment elevation MI (C) Coronary spasm (D) Pericarditis Case Question 3. Following the PTCA, which of the following would be a clear sign of acute closure of one or both target vessels? (A) Increased heart rate of 115 beats/min (B) Hypotension (C) 4mm ST-segment elevation in leads V3–V4 (D) All of the above Answers 1. B; 2. A; 3. C

rupture may be caused by a number of environmental or hormonal factors, known as triggers (Table 9-4). These triggers may precipitate an acute coronary event. Some of the triggers for atherosclerotic plaque rupture can be manipulated or controlled, such as blood pressure (BP), blood glucose level, and stress. In the clinical setting, management of these variables may decrease the risk for AMI, reinfarction, and reocclusion. They should be closely monitored. When these triggers combine to cause plaque rupture, the lipid pool is exposed and a rough surface on the intima of the vessel wall occurs, stimulating the local effects of hormonal and immune factors and initiating thrombus formation. At the same time, the fibrinolytic system is stimulated, creating a dynamic process of simultaneous attempts to form and dissolve the clot. Because of the dynamic nature of the clotting process, the thrombus may be completely or only partially obstructive, or may fluctuate intermittently between the two stages. Regardless of the maturity of the clot, the process of thrombus formation may lead to obstruction of blood flow, diminishing oxygen delivery to distal myocardium and creating a mismatch between the supply of and demand for oxygen.

240

CHAPTER 9. Cardiovascular System

TABLE 9-4. HORMONAL AND ENVIRONMENTAL TRIGGERS OF PLAQUE RUPTURE Acute

Chronic

Hemodynamic Reactivity • Morning increase in BP • Morning increase in heart rate • Physical exertion • Emotional stress • Exposure to cold Hemostatic Reactivity • Increased coronary blood flow velocity • Increased viscosity of blood • Decreased tPA activity • Increased platelet aggregation Vasoreactivity • Increased plasma epinephrine • Increased plasma cortisol

Basal Hemodynamic Forces • Increased resting BP • Increased resting heart rate Basal Hemostatic Variables • Location of the plaque • Size of the lipid pool within the core plaque • Degree of macrophage infiltration of the plaque Chronic Risk Factors • Gender (male > female) • Increasing age • Diabetes mellitus • Hypercholesterolemia • Cigarette smoking

Because the underlying pathology of the ischemiarelated diagnoses is the same (plaque rupture and thrombus formation), ischemic heart disease encompasses the entire spectrum of ischemic coronary events that are referred to as the acute coronary syndrome (ACS). ACS represents a continuum of clinical events that may result from the supply-demand mismatch including unstable angina, non–STsegment elevation MI (NSTEMI), or ST-segment elevation MI (STEMI) (Figure 9-6). Following a decrease in oxygen supply to the myocardium, the cell membranes lose their integrity and fluid moves into the cell. The cell is no longer able to regulate its internal and external environment. The cell dies, releasing cytotoxic substances into the bloodstream. When they die, cardiac myocytes release significant amounts of myoglobin, troponin I and T as well as cardiac-specific creatine kinase (CK-MB) causing elevation in these laboratory values and confirming the MI diagnosis.

Disrupted atherosclerotic plaque

Thrombus formation

Unstable angina

NSTEMI

STEMI

Sudden death

Clinical Presentation

Clinical presentation across the spectrum of ACS is similar, with slight differences depending on the involved vessels (Table 9-5). 1. Pain or discomfort, usually in the chest (see Table 9-1) •• Pressure or tightness in the chest •• Jaw or neck pain •• Left arm ache or pain •• Epigastric discomfort •• Scapular back pain 2. Nausea/vomiting 3. Hemodynamic instability •• Hypotension (systolic BP less than 90 mm Hg or 20 mm Hg below baseline) •• Cardiac index (CI) (< 2.0 L/min/m2) •• Elevated pulmonary artery diastolic (PAD) and/or pulmonary artery occlusion pressure (PAOP) •• Skin cool, clammy, diaphoretic 4. Dyspnea 5. Dysrhythmias/conduction defects •• Left bundle branch block (LBBB) •• Tachycardia/bradycardia •• Frequent premature ventricular contractions •• Ventricular fibrillation 6. Anxiety, sense of impending catastrophe 7. Denial Some patient populations are predictably different in their description of chest discomfort, such as women and diabetics. Women frequently present with symptoms that are more vague, such as feeling tired, short of breath, and a lack of energy. Women may be prone to deny their symptoms for longer periods of time than men, delaying their arrival to the ED and often rendering them ineligible for thrombolytic therapy. In addition, women are typically postmenopausal when signs and symptoms of atherosclerotic disease become apparent. This predominantly older patient population may pose problems of its own such as anxiety, fear of the inability to care for oneself following MI, and other concerns to geriatric patient populations, which must be considered. Diabetics are another patient population with atypical symptoms when experiencing an MI. Diabetics have atypical pain secondary to neuropathies, and early development of atherosclerotic disease. Coronary artery disease in this patient population is diffuse, and poor distal vascular anatomy is common. Lesion morphology in diabetic patients is also more difficult to revascularize, using either percutaneous or surgical methods. Diagnostic Tests Unstable Angina

T-wave inversion

ST depression

ST elevation

Ventricular fibrillation

Figure 9-6. Pathophysiologic steps leading to acute coronary events.

1. 12-Lead electrocardiogram (ECG): Transient changes may occur and resolve; most commonly T-wave inversion or ST-segment depression.

1"5)0-0(*$$0/%*5*0/4

TABLE 95. CLINICAL PRESENTATION OF MYOCARDIAL ISCHEMIA AND INFARCTION Type MI

Arterial Involvement

Muscle Area Supplied

Assessment

Anteroseptal wall

LAD

Anterior LV wall, Anterior LV septum Apex LV #VOEMFPG)JT #VOEMFCSBODIFT

↓ LV function → ↓ CO, ↓#1 ↑ PAD, ↑ PAOP S3 and S, with HF Rales with pulmonary edema

Posterior septal lateral

RCA circumflex branches (right and left)

Posterior surface of LV 4"OPEF "7OPEF Left atrium Lateral wall of LV

Murmurs indicating VSD (septal) PA catheter to assess R to L shunt in VSD Signals/symptoms of LV aneurysm with lateral displaced PMI leading to signs and symptoms of mitral regurgitation

Inferior or “diaphragmatic”

RCA

RV, RA 4"OPEF "7OPEF RA, RV Inferior LV Posterior VI septum 1PTUFSJPS-### Posterior LV

4ZNQUPNBUJDCSBEZDBSEJB ↓#1-0$DIBOHFTEJBQIPSFTJT ↓ CO ↑ PAD ↑ PAOP .VSNVSTBTTPDJBUFEXJUIQBQJMMBSZ muscle dysfunction mid/ holosystolic rates, pulmonary edema, nausea

Right ventricular infarction

RCA

RA, RV, inferior LV SA node AV node Posterior IV septum

Kussmaul sign JVD Hypotension ↑ SVR, ↓ PAOP, ↑ CVP S3 with noncompliant RV Clear breath sounds initially Hepatomegaly; peripheral edema; cool, clammy, pale skin

241

242

CHAPTER 9. Cardiovascular System

ECG Changes

Likely Arrhythmias

Possible Complications

Indicative ST elevation with or without abnormal Q waves in V1-4 Loss of R waves in precordial leads Reciprocal ST depression in II, III, aVF.

RBBB, LBBB AV blocks Atrial fibrillation or flutter Ventricular tachycardia (VT) Tachycardia (septal)

Cardiogenic shock VSD Myocardial rupture Heart blocks may be permanent (LBBB) High mortality associated with this location of MI

Lateral Indicative ST elevation I, aVL, V5-6 Loss of R wave and ↑ ST in I, aVL, V5-6 Posterior Indicative Tall, broad R waves (> 0.04 second) in V1-3 ↑ ST V4R (right-sided 12 lead, V4 position) Posterior Reciprocal ST depression in V1,2, upright T wave in V12

Bradycardia Mobitz I (posterior)

RV involvement Aneurysm development Papillary muscle dysfunction Heart blocks frequently resolve

Indicative ↑ ST segments in II, III, aVF Q waves in II, III, aVF Reciprocal ST depression in I, aVL, V1-4

AV blocks; often progress to CHB which may be transient or permanent; Wenckebach; bradyarrhythmias

Hiccups Nausea/vomiting Papillary muscle dysfunction MR Septal rupture (0.5%-1.0%) RV involvement associated with atrial infarcts especially with atrial arrhythmias

Indicative 1- to 2-mm ST-segment elevation in V4R ST- and T-wave elevation in II, III, aVF Q waves in II, III, aVF ST-elevation decreases in amplitude over V1-6

First-degree AV block Second-degree AV block, type I Incomplete RBBB Transient CHB Atrial fibrillation VT/VF

Hypotension requiring large volumes initially to maintain systemic pressure. Once RV contractility improves fluids will mobilize, possibly requiring diuresis

PATHOLOGIC CONDITIONS 243

Principles of Management of Acute Ischemic Heart Disease

Because most complications of acute ischemic heart disease directly result from reduced coronary flow, a primary objective in patient management is to optimize blood flow to the myocardium. Additional goals are to prevent complications of ischemia and infarction, alleviate chest discomfort/pain, and reduce anxiety.

Multiples of the upper limit of normal

Troponin (large MI) 20 10 CK-MB 5

Troponin (small MI) 99th percentile

2 1 0 0

3 4 5 6 Days after onset of AMI

Optimize Blood Flow to the Myocardium

Figure 9-7. Timing and levels of biomarkers associated with heart injury. (Modified from: Antman EM. Decision making with cardiac troponin tests. N Engl J Med 346:2079, 2002; and Jaffe AS, Babiun L, Apple FS. Biomarkers in acute cardiac disease: The present and the future. J Am Coll Cardiol 48:1, 2006.)

2. Cardiac enzymes (Troponin [I or T], myoglobin, and CK-MB): Normal (Figure 9-7). 3. Cardiac catheterization: Not recommended in the acute setting, except in the case of continued pain/ discomfort without relief from nitroglycerin. Catheterization results may be normal, or with visible atherosclerotic disease, but is not completely occluded. Myocardial Infarction

1. 12-lead ECG: Thirty-five percent of patients with AMI have ST-segment elevation (see Chapter 18, Advanced ECG Concepts). Approximately 65% of those with AMI have no ECG or other diagnostic changes. 2. Creatine kinase (CK and CK-MB). •• Total CK > 150 to 180 mcg/L. •• MB band > 10 ng/mL or > 3% of total. •• Peaks at 12 hours after symptom onset. •• CK-MB isoforms have better sensitivity and specificity for detecting MI within the first 6 hours. 3. Troponin T: > 0.1 to 0.2 ng/mL. •• Begins to increase 3 to 5 hours after symptom onset •• Remains elevated for 14 to 21 days 4. Troponin I: > 0.4 ng/mL. •• Begins to increase 3 hours after onset of MI •• Peaks at 14 to 18 hours •• Remains elevated for 5 to 7 days 5. Myoglobin: Present in serum. 17.4 to 105.7 ng/mL •• Released from myocardium within 2 hours of coronary occlusion •• Peaks in 6 to 7 hours •• Better marker for early detection of MI; better negative indicator if negative 6. Cardiac catheterization: Ventricular wall motion abnormalities (also may be seen by echocardiography); total occlusion of one or more coronary arteries.

Regardless of whether a patient presents with unstable angina or AMI, restoration and maintenance of coronary blood flow is important to improve patient outcomes. Interventions to optimize blood flow to the myocardium include pharmacologic measures, such as antiplatelet or antithrombin agents, and mechanical measures, such as percutaneous coronary revascularization (eg, angioplasty, stent, or other) or coronary artery bypass grafting (CABG). Refer to Table 9-6 for evidenced-based guidelines for AMI. The intervention selected and the optimal timing of the intervention depends on whether the occlusion of the artery is total or partial. This determination must be made as accurately and as quickly as possible, as a totally occluded artery will soon result in tissue necrosis or MI (see Figure 9-8 for algorithm on acute chest pain management). All unstable arteries benefit from the

TABLE 9-6. EVIDENCED-BASED PRACTICE: ACUTE CORONARY SYNDROME— ST-ELEVATION MI AND NON–ST-ELEVATION MI Diagnosis • Diagnosis of AMI is based on two of three findings:a,b 1. History of ischemic-like symptoms 2. Changes on serial ECGs 3. Elevation and fall in level of serum cardiac biomarkers • Of AMI patients, 50% do not present with ST-segment elevation. Other indicators:a,b 1. ST-segment depression may indicate non-ST-elevation MI (NSTEMI). 2. New LBBB. 3. ST-segment depression that resolves with relief of chest pain. 4. T-wave inversion in all chest leads may indicate NSTEMI with a critical stenosis in the proximal LAD. Acute Management • Optimal time for initiation of therapy is within 1 hour of symptom onset. Rarely feasible due to delay in treatment-seeking behavior.a,b • Initial ECG should be obtained within 10 minutes of emergency department arrival.a,b • Oxygen, nitroglycerine, and aspirin should be administered if not contraindicated.a,b • Reperfusion strategy: STEMI only.a,b 1. Fibrinolytic agent should be initiated within 30 minutes of arrival if no contraindication 2. If primary PCI to be done, culprit vessel should be opened within 90 minutes of arrival • Reperfusion strategy for NSTEMI.a,b 1. Fibrinolytics not recommended 2. PCI to be done within 24 hours of arrival • Weight-based heparin or low-molecular-weight heparin.a,b • IV beta-blocker should be given within 12 hours of arrival.a,b • Lipid-lowering agent should be initiated.a,b From: aAntman, Hand, Armstrong et al. (2004); bCasey (2002).

244

CHAPTER 9. Cardiovascular System

Patient arrives at emergency department with chest pain ECG within 10 minutes of arrival ST-segment elevation on ECG > 1 mm in two contiguous leads?

Yes

Begin fibrolytic within 30 minutes if catheterization laboratory not available

If catheterization laboratory available, do primary PCI and open vessel within 90 minutes of arrival

Continue to monitor, obtain cardiac biomarkers, and repeat ECG if chest distress continues

ST-segment depression or T-wave inversion is suggestive of NSTEMI, admit to hospital and plan cardiac catheterization/PCI within 24 hours

Figure 9-8. Algorithm for management of acute chest pain.

following interventions which stabilize the artery and optimize coronary arterial flow. Medical Management

1. Decrease activity of coagulation system with pharmacologic therapy (Figure 9-9): •• Antiplatelet agents: aspirin, GP IIb/IIIa receptor blocking agents (eg, abciximab [Reopro], eptifibatide [Integrilin], and tirofiban [Aggrastat]), thienopyridine agents (eg, clopidogrel [Plavix]) •• Antithrombin agents: indirect (eg, unfractionated heparin, low-molecular-weight heparin), direct (eg, bivalirudin [Angiomax]) 2. Increase ventricular filling time (decrease heart rate): •• Beta-blockers •• Bed rest for 24 hours 3. Decrease preload: •• Nitrates •• Diuretics •• Morphine sulfate 4. Decrease afterload: •• Angiotensin-converting enzyme (ACE) inhibitors •• Hydralazine 5. Decrease myocardial oxygen consumption (MVO2): •• Beta-blockers •• Bed rest for 24 hours Totally occluded arteries require, in addition to the above pharmacologic interventions, further reperfusion therapy, such as fibrinolysis, angioplasty, or CABG, to effectively restore blood flow to the coronary artery. In the event of left main coronary artery stenosis or three-vessel disease,

urgent or emergent CABG is usually considered. In the acute setting, for ST-segment elevation MI (STEMI), fibrinolytic therapy is often the fastest, most universally available method for reperfusion if a catheterization laboratory is not available or operational 24 hours a day. The indications, contraindications, and common complications of fibrinolytic therapy are listed in Tables 9-7 and 9-8. In those settings where the catheterization laboratory is operational 24 hours a day primary PCI is indicated. Studies have indicated that primary PCI may be associated with better outcomes and fewer complications than with the use of fibrinolytic agents. Surgical Management Coronary artery bypass grafting is one method of revascularization generally used in patients with atherosclerosis of three or more coronary vessels or in the case of significant left main coronary artery disease. CABG is performed both electively, as well as emergently, and may be performed either prior to or following an MI. The CABG procedure requires “induction” with general anesthesia, and possible initiation of cardiopulmonary bypass (blood is diverted outside of the body to a pump that mechanically oxygenates the blood before returning it to the arterial circulation) and placement of a graft into the coronary arterial tree (Figure 9-10). Technological advances have resulted in the development of stabilizer devices permitting CABG to be performed without placing the patient on cardiopulmonary bypass. The heart continues to beat while the surgeon places a device over the coronary artery site where the bypass graft is to be anastomosed, which stabilizes the small area allowing for suturing to occur. This is often referred to as beating heart surgery or “off pump” coronary artery bypass (OPCAB). The graft, generally a leg vein,

PATHOLOGIC CONDITIONS 245

Warfarin (inhibits II, X, VII and IX)

Tissue factor VII IX, XI, XII, VIII

Unfractionated heparin + Antithrombin III (thrombin inhibitor)

Hirudin (direct thrombin inhibitor)

Prothrombinase complex (X, V, Ca++, phospholipid) XIII Thrombin (factor II)

Prothrombin

Fibrinogen

Fibrin

Cross-linked fibrin

XIII activated

Abciximab (IIb/IIIa antagonists) Platelet + Aspirin (antiplatelet)

n rinoge

Fib

Plasminogen

Platelet Glycoprotein IIb/IIIa receptor (50,000 receptors per platelet)

Plasmin (lyses clot)

t-PA reteplase tenecteplase (plasminogen activators)

Ticlopidine (platelet inhibitor) Subendothelial surface of blood vessel

Figure 9-9. Coagulation sequence and site of antithrombotic/antiplatelet drug activity.

left internal mammary artery, or radial artery, is inserted past the distal end of the blockage in the coronary artery and, in the case of a leg vein graft and radial artery graft, anastomosed TABLE 9-7. INDICATIONS AND CONTRAINDICATIONS FOR THROMBOLYTIC THERAPY Indications • Chest pain > 20 minutes, but typically < 12 hours • ST elevation ≥ 1 mm in two contiguous leads • LBBB • High-risk patients with chest pain > 12 hours in duration may still be candidates if pain persists Absolute Contraindications • Active internal bleeding • History of intracranial bleeding, cerebral neoplasm, or other intracranial pathology • Stroke or head trauma within 6 months • Known allergy to the drug chosen Relative Contraindications • Major surgery or GI bleeding within 2 months • Traumatic puncture of noncompressible vessel • Pregnancy or 1 month postpartum • Uncontrolled hypertension (systolic > 200 or diastolic > 110) • Trauma within 2 weeks, including CPR with rib fracture

to the aorta. Multiple grafts may be inserted based on the number of blockages present and the availability of viable insertion sites in the patient’s native coronary tree. Indications The indications for CABG and long-term patient outcome following this procedure have been intensively reviewed over the past decade. In general, patients with three-vessel disease, poor LVEF (< 35%), or significant disease in the left main coronary artery have lower long-term morbidity and mortality with surgical revascularization (CABG) compared TABLE 9-8. COMPLICATIONS OF FIBROLYTIC THERAPY Complication Groin bleeding, local (compressible external) Intracerebral bleeding Retroperitoneal bleeding (noncompressible internal) Gastrointestinal bleeding Genitourinary bleeding Other bleeding

Percentage Occurrence 25-45 1.45 1 4-10 1-5 1-5

246

CHAPTER 9. Cardiovascular System

Internal mammary artery (from chest)

Saphenous vein (from leg)

Figure 9-10. Coronary artery bypass grafting (CABG).

to medical therapy or percutaneous interventions such as angioplasty or stent. Diabetics with multivessel disease have also been found to fare better following CABG than following percutaneous interventions including drug-eluting stents. CABG may also be indicated as an emergent “rescue” procedure in patients whose coronary artery severely dissects or fractures during an attempted percutaneous procedure. Contraindications Several populations of patients may be considered poor candidates for coronary bypass, including the very elderly, debilitated patients, patients with severely diseased distal coronary vasculature (eg, some diabetics), and patients with extremely low LVEF (eg, < 5%-15%). Patients with low ejection fractions often have difficulty being weaned from cardiopulmonary bypass following the procedure. Other contraindications are those related to general anesthesia risk, including pulmonary edema, severe chronic obstructive pulmonary disease, or pulmonary hypertension. Postoperative Management The following is a general overview of the early postoperative management of CABG patients.

1. Maintain hemodynamic stability: A variety of cardiac drugs are administered to maintain hemodynamic stability in the first 24 hours postoperatively. The following hemodynamic values may serve as guides for inotropic and vasopressor administration along with intravascular fluid therapy. In general, values greater or lower than the following require intervention: •• Mean arterial pressure: 70 to 80 mm Hg •• CI: 2.0 to 3.5 L/min/m2 •• PAD/PAOP: 10 to 12 mm Hg (used primarily to evaluate need for volume replacement)

•• Central venous pressure (CVP): 5 to 10 mm Hg (used primarily to evaluate need for volume replacement) •• HR: Intrinsic or paced rhythm in range of 80 to 100 beats/min to keep CI ≥ 2.0 •• If radial artery graft used, monitor for arterial spasm. Prophylactic nitroglycerin drip and nitro paste. 2. Maintain ventilation and oxygenation: Ventilation and oxygenation are maximized in the early postoperative period with mechanical ventilation. Within 2 to 12 hours, most patients have recovered from the anesthesia effects and are sufficiently stable to allow weaning from mechanical ventilation and extubation. Individuals with preexisting pulmonary problems may require longer periods of intubation until weaning can be successfully accomplished. Following weaning and extubation, supplemental O 2 therapy usually is required for 1 to 2 days to maintain Pao2 or SaO2 in normal ranges. Postoperative atelectasis and pleural effusions are common occurrences after cardiopulmonary bypass, usually requiring frequent pulmonary interventions (eg, coughing and deep breathing, incentive spirometry, ambulation) to maintain ventilation and oxygenation. 3. Prevention of postoperative complications A. Bleeding from vascular graft anastomosis sites: Frequent monitoring of mediastinal tube drainage, hematocrit, and coagulation status; avoidance of even brief periods of hypertension. B. C ardiac tamponade: Frequent assessment for signs and symptoms of tamponade, which include tachycardia, SOB, anxiety/decreased LOC, paradoxus, sinus tachycardia decreased mediastinal tube drainage, increased CVP, PAD, and PAOP (note: these are often within 2 to 3 mm Hg of each

PATHOLOGIC CONDITIONS 247

other). This is called equalization of pressures or diastolic plateau and is accompanied by muffled heart tones, decreased BP and cardiac output. Also, monitor closely for cardiac tamponade after epicardial wire removal. C. Infection: Antibiotics may be used prophylactically for 48 hours; temperature spike within 24 hours postoperatively is not abnormal (may be related to pulmonary atelectasis). D. Cardiac arrhythmias: ECG and continuous STsegment monitoring, treat unstable rhythms, maintain K+ and Mg+ within normal limits with IV replacement. E. Relief of postoperative pain and anxiety: Analgesic administration is typically required to ensure pain relief, especially to facilitate ambulation, coughing, and deep breathing. F. If median sternotomy is performed, ensure sternal precautions are implemented, eg, avoid hyperextension of chest (arms and shoulders pulled posteriorly). Preventing Complications Associated With Coronary Obstruction

Complications associated with acute ischemic syndromes include recurrent ischemia, infarction or reinfarction, onset of heart failure (HF), and arrhythmias. 1. Prevent recurrent ischemia, infarction, or reinfarction: Continue pharmacologic interventions to inhibit prothrombotic events, including ischemia and infarction (eg, antiplatelet and antithrombin agents). Assess for recurrent angina with frequent chest pain assessment and serial 12-lead ECG and continuous ST-segment ischemia monitoring. (See AACN Practice Alert: Continuous ST-segment Monitoring). 2. Continuously monitor for arrhythmia: Monitor, if possible, for 24 to 72 hours following an ischemic episode. 3. Minimize potential for HF: Minimize myocardial oxygen consumption with the administration of beta-blockers, limit physical activity (bed rest), and avoid increases in metabolic rate (eg, fever). Reduce left ventricular afterload with the administration of ACE inhibitors and hydralazine. Alleviating Pain

Pain relief improves coronary flow by decreasing the level of circulating catecholamines, thereby decreasing BP (afterload) and heart rate (myocardial oxygen consumption). Nitrates typically relieve anginal pain by dilating coronary arteries and increasing blood flow, thereby improving myocardial oxygenation and directly treating the source of the pain. Another pharmacologic intervention commonly used to relieve pain in ischemia is morphine sulfate. Although morphine is a potent narcotic that has been criticized for masking cardiac pain, it is also a potent vasodilator and effectively vasodilates

coronary as well as peripheral arteries, resulting in mild afterload reduction. Severe pain, unable to be relieved with nitrates or a combination of nitrates and morphine, is typically an indication for immediate PCI if available, or transfer to a referring institution for emergency PCI. Reducing Anxiety

The reduction of anxiety in ischemic heart disease is important for a number of reasons. The most important physiologically is the reduction of catecholamine secretion and decrease in sympathetic tone following relaxation in the anxious patient. This effect has been shown to decrease the incidence of arrhythmias and promote vasodilation and afterload reduction. Decreasing anxiety may also increase the patient’s ability to process new information regarding his or her diagnosis, and to better understand instructions for tests or procedures that will be done. Relief of pain typically is most effective in reducing patient anxiety. In the event that pain is not relieved with nitroglycerin, or fibrinolytics in the initial treatment of ischemia, pain relievers such as morphine sulfate or anxiolytics such as midazolam or lorazepam (short- or intermediate-acting benzodiazepines, respectively) are usually effective. A number of interventions may be done at the bedside to promote relaxation, including specific relaxation and imagery techniques, meditation, music therapy, and the use of relaxation tapes. Providing the patient and family with adequate information regarding unfamiliar surroundings, when the physician may be available to speak with them, possible “unknowns” such as tests or procedures, and important expectations such as visitation guidelines helps provide a sense of security and facilitates relaxation by increasing the patient’s level of comfort with the situation. Anxiety can also be decreased by offering the patient opportunities for control in the acute setting. Examples include the timing of simple activities such as visitor presence, bathing, and eating.

Heart Failure Heart Failure (HF) is a broad term referring to the inability of the heart to eject an adequate cardiac output to meet the oxygen and metabolic requirements of the body. A number of underlying disease processes may contribute to this “weak pump” syndrome, with coronary atherosclerosis, valvular heart disease, hypertension, and cardiomyopathy as the most common causes. While the underlying causes are diverse, the pathophysiological process which occurs in response to one of these initiating events is the same. Etiology, Risk Factors, and Pathophysiology

Although HF may result from a number of underlying etiologies, those causing left ventricular systolic dysfunction are the most common contributors. The pathophysiology of

248

CHAPTER 9. Cardiovascular System

Pathophysiology

Phase I

Phase II

Phase III

Initial event

Compensatory phase

Clinical syndromes

Myocardial insult and/or excessive load

• Dyspnea • Pulmonary edema • PND • JVD • Angina • Peripheral edema • Cool, pale skin • Oliguria • Weight gain • Fatigue

Impaired LV function

Afterload Neurohormones

Clinical symptoms

Often no obvious symptoms are seen due to compensatory response.

Severity and timing of onset of clinical symptoms is variable.

Severity of clinical symptoms is variable.

Figure 9-11. Pathophysiology of HF during phases I, II, and III.

HF is a three-stage process, beginning with an initial insult to the myocardium (phase I), followed by a response phase (phase II), and resulting in the clinical syndrome known as HF, characterized by exhaustion of compensatory mechanisms (phase III) (Figure 9-11). Regardless of the precipitating event, the physiologic progression of the syndrome, once initiated, is the same. Phase I

Phase I of HF is characterized by an initiating event (eg, MI, viral infection, chemotherapeutic agents, valvular heart disease, hypertension, idiopathic cardiomyopathy), which causes loss of myocytes. This cell loss or permanent damage to the myocytes can be either localized or diffuse, resulting in compromised ventricular function. To date, over 700 initiating factors, such as acute ischemic damage, viruses, and toxins, have been isolated as contributors to myocardial insult and HF. •• Result of phase I: Decreased stroke volume secondary to an initial insult to the myocardium. Phase II

A number of adaptive mechanisms occur in response to the initial insult in an effort to maintain adequate cardiac output to meet the body’s needs. This phase is sometimes referred to as the compensatory phase (Figures 9-11 and 9-12). These compensatory mechanisms or responses include the FrankStarling response, myocardial remodeling, and the neurohormonal response.

Frank-Starling Response As cardiac output decreases and the sympathetic nervous system is activated, alpha-1 receptors are stimulated, resulting in arteriolar and venous vasoconstriction. This adaptive response initially results in increased venous return to the ventricle, increased ventricular end-diastolic volume, stretching of the ventricular myocytes, and improved stroke volume. Later, as overstretching of the ventricle occurs, this compensatory mechanism is lost, resulting in left ventricular decompensation and myocardial hypertrophy (Figure 9-13). Additionally, there is increased expression of granules in the left ventricle causing an increased release of brain natriuretic peptide (BNP). Increased BNP levels in the serum are used as markers of severity of ventricular failure. myocardial hypertrophy (remodeling) In response to increased vascular volume and decreased myocardial function (loss of the Frank-Starling response), the left ventricle dilates and hypertrophies. This distortion of the normal left ventricular anatomy causes mitral regurgitation and further left ventricular dilatation. Angiotensin II, a by-product of the renin-angiotensin system activation systemically and in the endothelial cells of the blood vessels throughout the body, directly induces myocyte hypertrophy as well. The result of these factors is decreased left ventricular reserve (stretch), increased preload (high residual volume in the ventricle following systole), and further mitral regurgitation.

PATHOLOGIC CONDITIONS 249

Initial insult: impaired LV function LV filling pressure Blood volume

LV dilatation

CO stroke volume

Afterload (LV impedance)

NaCI + H2O retention Reflex arteriolar vasoconstriction Renal perfusion

Systolic vascular resistance

Renin angiotensin II aldosterone vasopressin

Figure 9-12. Compensatory mechanisms of HF.

neurohormonal response In response to decreased stroke volume and decreased renal perfusion, several neurohormonal systems are activated, each of which acts to compensate for the decrease in stroke volume. These include:

1. Adrenergic nervous system: Adrenergic nervous system activity is heightened in the setting of impaired Increased contractility

Stroke volume

Normal Congestive symptoms Decreased contractility

Low-output symptoms

Congestive and low-output symptoms

Left ventricular end-diastolic pressure

Figure 9-13. Frank-Starling curve.

ventricular function as a direct result of baroreceptor stimulation. These baroreceptors mediate the sympathetic nervous system, which in turn stimulates the beta-1 receptors. This results in an increase in heart rate and contractility. 2. Renin-angiotensin-aldosterone system: Decreased renal perfusion stimulates the release of renin, increasing the production of angiotensin I and II and the release of aldosterone. This causes arteriolar vasoconstriction, decreased cardiac output, increased arterial BP and peripheral resistance, increased ventricular filling pressures, sodium and potassium retention (imbalance), increased volume overload, increased left ventricular wall stress, increased ventricular dilation and hypertrophy, and increased sympathetic nervous system arousal. 3. Arginine vasopressin (AVP) system: AVP is a potent vasoconstrictor that is normally inhibited by stretch receptors in the atria during atrial distension. In HF, these receptors are less sensitive, causing a decrease in AVP inhibition. This results in systemic vasoconstriction, further increasing afterload (the pressure the ventricle must work against to eject blood out to the system). Increases in AVP availability also lead to an inability to excrete free water, hypoosmolarity, and, in general, inability to autoregulate further AVP production.

250

CHAPTER 9. Cardiovascular System

4. Atrial natriuretic peptide (ANP): ANP is a counterregulatory hormone that opposes all three of the above systems, resulting in vasodilation and sodium excretion. ANP is produced in response to atrial distension and results in decreased formation of renin, decreased effects of angiotensin II, decreased release of aldosterone and vasopressin, and enhanced renal excretion of sodium and water. In chronic HF, the levels of ANP remain elevated, but are less so than in the acute phase (phase II). The effects of the compensatory mechanisms in phase II lead to an increase in circulating volume and perfusion to vital organs. Eventually, these mechanisms are self-limiting and a vicious cycle of increased afterload and volume overload results. The neurohormonal response is no longer beneficial in the chronic state but, as seen in phase III, becomes detrimental leading to changes in the myocyte DNA, resulting in programmed cell death (apoptosis) and further loss of myocytes. •• Result of phase II: Ventricular hypertrophy, weakened myocytes, increased arteriolar resistance, increased vascular volume, and increased ventricular wall stress occur in an effort to maintain adequate cardiac output. Phase III

When the adaptive mechanisms of phase II fail, the clinical syndrome of HF follows. This third phase of HF is extremely variable in onset and presentation. The clinical expression and course of the disease is determined by the extent of the initial insult and myocyte damage, the severity of hemodynamic burden (volume overload), and the patient’s individual neurohormonal response to these changes. Phase III is characterized by a progressive deterioration of cardiovascular functioning due to the relationship between compromised left ventricular function and excessive cardiac afterload (Figure 9-14). •• Result of phase III: Clinical signs and symptoms of HF are evident, resulting in decreased functional status and activity intolerance for the patient. Clinical Presentation

Regardless of the underlying cause of the weak pump, patients with HF present with clinical signs and symptoms of intravascular and interstitial volume overload, as well as manifestations of inadequate tissue perfusion. Common findings in HF include: •• Dyspnea (especially with exertion, commonly severe in the acute setting) •• Paroxysmal nocturnal dyspnea •• Pulmonary edema (pronounced crackles) •• Jugular venous distention (JVD) •• Chest discomfort or tightness •• Peripheral edema •• Cool, pale, cyanotic skin •• Oliguria

•• Reported weight gain •• Fatigue

Essential Content Case

Heart Failure A 75-year-old man presents to the ED with diaphoresis and severe dyspnea. Initial assessment revealed the following: RR 32 breaths/min BP 110/90 mm Hg HR 110 beats/min, irregular JVD Bilateral 7-mm elevation Lungs Bibasilar crackles throughout the lower lobes Cardiovascular S1, S2 with an S3

A pulse oximeter revealed 83% oxygen saturation. Laboratory work, including an arterial blood gas sample, was done with the following results:

Pao2 60 mm Hg Paco2 28 mm Hg pH 7.51 Sao2 93%

Oxygen was initiated at 4 L/min via nasal cannula. An ECG was done and showed left ventricular hypertrophy and left bundle branch block. His chest x-ray showed an enlarged cardiac silhouette and bilateral infiltrates. A pulmonary artery catheter was placed and the following parameters were found (refer to Chapter 3 for hemodynamic parameters): RA PA PAOP CO CI

10 mm Hg 41/35 mm Hg 32 mm Hg 3.8 L/min 1.9 L/min/m2

A dobutamine drip was started at 2.5 mcg/kg/min, and furosemide 40 mg IV was given. Cardiac catheterization was performed the next morning with the following findings: LAD 95% occlusion RCA 50% occlusion LCx 75% EF 28% Severe asyneresis

Case Question 1. The purpose of starting the dobutamine infusion and administering the furosimide is to: (A) Increase myocardial contractility and reduce ventricular preload (B) Increase myocardial contractility and reduce ventricular afterload (C) Reduce myocardial contractility and increase ventricular preload (D) Increase myocardial contractility and increase ventricular afterload Case Question 2. Following the initiation of dobutamine and administration of furosemide, you would expect which of the following to occur?

PATHOLOGIC CONDITIONS 251

(A) HR 120 beats/min; PA 40/38; PAOP unchanged (B) HR 110 beats/min; PA 32/25 mm Hg; PAOP 24 mm Hg (C) HR 95 beats/min; PA unchanged; RA 14 mm Hg (D) B P 1 0 5 / 8 0 m m H g ; PA 4 9 / 3 8 m m H g ; RA 14 mm Hg Case Question 3. After reviewing the cardiac catheterization results, you would anticipate the patient having one of the following procedures: (A) Implantation of a HeartMate II LVAD as destination therapy (B) Ventricular aneurysmectomy/reconstruction surgery (C) Mitral valve repair (D) Insertion of a dual chamber biventricular pacemaker Answers: 1. A; 2. B; 3. D

More specific physical signs and symptoms may vary in individuals depending on the ventricle which is primarily involved. A summary of clinical findings specific to left and right ventricular failure is presented in Table 9-9. Because subjective assessment of symptoms and their severity may vary from clinician to clinician, classification systems have been developed to standardize symptom severity as well as the evolution and progression of HF. The American College of Cardiology and the American Heart

TABLE 9-9. CLINICAL SIGNS AND SYMPTOMS SPECIFIC TO RIGHT-AND LEFT-SIDED HEART FAILURE Right Heart Failure

Signs and Symptoms of Pulmonary Congestion Pulmonary edema Rales Atrial fibrillation or other atrial arrhythmias secondary to atrial distension Pulsus alternans (every other beat diminished) Dyspnea Cough Hyperventilation Dizziness, syncope, fatigue Cardiac Pressures Increased LV and LA pressure Increased pulmonary artery pressures Heart Sounds S3 and (occasionally) S4 Pansystolic murmur at apex secondary to mitral regurgitation

Association developed a staging system that addresses the evolution and progression of HF. A second system, known as the New York Heart Association Functional (NYHA) Classification System, is used to provide systematic assessment of • Fatigue • Syncope • Dizziness

CO Forward failure

Renal perfusion

Hypotension

Baroreceptors JVD

Backward failure

Renal failure • Exertional and rest dyspnea • Cough • Pulmonary edema

Tricuspid regurgitation

Left Heart Failure

Signs and Symptoms of Hepatic Congestion JVD Liver enlargement and tenderness Positive hepatojugular reflex (pressure on liver increases JVD) Dependent edema Ascites Decreased appetite, nausea, vomiting Cardiac Pressures Increased RV pressure Increased RA pressure Heart Sounds S3 (early sign) S4 (may also present) Wide split S2 Pansystolic murmur at lower left sternal border secondary to stretching of tricuspid ring

Neurohormonal activation • Tachycardia • Peripheral edema • Oliguria

LV dilatation

• LV, LA pressure

More backward failure • Liver engorgement and tenderness • Ascites • Appetite nausea/vomiting

• S3/S4

• Murmur due to MR

Afterload increase

LV function falls further

Backward failure

Venous pooling forward failure worse

Figure 9-14. Clinical features of HF.

252

CHAPTER 9. Cardiovascular System

TABLE 9-10. CLASSIFICATION OF CARDIOVASCULAR DISABILITY AHA/ACC Stages of Heart Failure Stage A: Stage B: Stage C: Stage D:

Patients at high risk for HF due to the presence of conditions strongly associated with the development of HF. Asymptomatic. Patients with structural disease, such as previous MI, but have never shown signs or symptoms of HF. Patients with structural heart disease who have current or prior symptoms of HF. Patients with advanced structural heart disease and marked symptoms at rest in spite of optimal medical therapy and who require specialized interventions. New York Heart Association Functional Classification

Class I

III

Patients with cardiac disease but without resulting limitations of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain. Patients with cardiac disease resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain. Patients with cardiac disease resulting in marked limitation of physical activity. They are comfortable at rest. Less than ordinary physical activity causes fatigue, palpitation, dyspnea, or anginal pain. Patient with cardiac disease resulting in inability to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency or of the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort is increased.

patient status and to benchmark improvement or deterioration from initial evaluation (Table 9-10). A number of conditions, both cardiac and noncardiac, are similar to HF in their clinical presentation and should be ruled out as possible diagnoses in the initial assessment. These conditions include MI, pulmonary disease, arrhythmias, anemia, renal failure, nephrotic syndrome, and thyroid disease. Diagnostic Tests

•• 12-lead ECG: Acute ST-T wave changes, low voltage, left ventricular hypertrophy, atrial fibrillation or other tachyarrhythmias, bradyarrhythmias, Q waves from previous MI, LBBB •• Chest x-ray: Cardiomegaly, cardiothoracic ratio > 0.5 •• Complete blood count: Low red cell count (anemia) •• Urinalysis: Proteinuria, red blood cells, or casts •• Creatinine: Elevated •• Albumin: Decreased •• Serum sodium and potassium: Decreased •• PAP: Elevated •• CI: < 2.0 L/min/m2 •• Echocardiography: Dilated left ventricle, right ventricle, or right atria; hypertrophied left ventricle; AV valve incompetence; diffuse or segmental hypocontractility; atrial thrombus; pericardial effusion; LVEF < 40% •• Radionuclide ventriculography: More precise measure of right ventricular dysfunction and LVEF

Principles of Management for Heart Failure

Acute management of HF has changed dramatically over the past decade, from an emphasis on the micromanagement of hemodynamic parameters, primarily using positive inotropes, to an emphasis on functional capacity and long-term survival with the use of neurohormonal blocking agents. This shift is due to a better understanding of the neurohormonal response and the dependence of the body on these mechanisms for compensation in low output states. Goals of patient management in HF revolve around four general principles: (1) treatment of the underlying cause (eg, ischemia, valvular dysfunction), (2) management of fluid volume overload, (3) improvement of ventricular function, and (4) patient and family education. Limiting the Initial Insult and Treating the Underlying Cause

The most effective, but often the most difficult, management strategy for HF is to limit the damage done by the initial insult. This limitation of myocardial damage and cell loss maximizes the amount of viable ventricular muscle, myocardial contractility, and overall ventricular function. •• Administer fibrinolytic therapy as soon as possible for eligible patients in the setting of AMI or facilitate immediate transfer to the cardiac catheterization laboratory for primary PCI (see the previous section on acute ischemic heart disease). •• Revascularization may be warranted in patients with persistent ischemia as a preventive measure against eventual tissue necrosis. •• Valve replacement or repair or other surgical corrections (ventricular reconstruction surgery) should be undertaken as soon as possible to prevent prolonged overstretching of the ventricular myocardium. Management of Fluid Volume Overload

Decrease preload by the use of diuretic therapy, limitation of dietary sodium, and restriction of free water. •• Diuretics should be initiated according to the severity of the patient’s signs and symptoms. More severe symptoms require intravenous therapy and loop diuretics, and less severe symptoms may be managed adequately on loop diuretics. Thiazide diuretics may be added later if the patient does not respond to the loop diuretics. •• Sodium and fluid restriction should be monitored carefully, with sodium intake not exceeding 2 g/day and free water not exceeding 1500 mL in a 24-hour period. Obtain nutrition consult to reinforce sodium and water restrictions. •• Serum sodium and potassium should be monitored on a regular basis to prevent inadvertent electrolyte imbalances (each day or two in the acute setting, depending on the aggressiveness of therapy). Improvement of Left Ventricular Function

Improvement in left ventricular function is accomplished by decreasing the workload on the heart with preload and afterload

PATHOLOGIC CONDITIONS 253

reduction and by augmenting ventricular contractility. Ventricular function is often measured directly in the acute setting by monitoring CI. As has been demonstrated by a number of large clinical trials, traditional micromanagement of hemodynamic variables, such as CI with inotropic drugs, may be detrimental to long-term patient outcome. Current recommendations do not advocate this as an initial management strategy. •• Decrease preload (see above). •• Decrease afterload by administration of pharmacologic therapy, including ACE inhibitors and vasodilators. ACE inhibitors are recommended in all HF patients with a left ventricular EF < 40% unless otherwise contraindicated. Contraindications to ACE inhibitor therapy include previous intolerance, potassium > 5.5 mEq/L, hypotension with systolic BP less than 90 mm Hg, and serum creatinine greater than 3.0 mg/dL. Cautious initiation of low-dose therapy in patients with contraindications may still be considered. Vasodilators may also be used in conjunction with diuretics and ACE inhibitors if further afterload reduction is necessary. Nitrates are often used concomitantly with ACE inhibitors and diuretics to augment afterload reduction, especially in the case of underlying atherosclerotic disease, the largest single contributor to HF. Angiotensin Receptor Blockers (ARBs) may be used if the patient does not tolerate the side effects of an ACE inhibitor (eg, cough). •• ACE inhibitors and beta-blockers are considered cornerstone therapy for HF in an effort to reverse the remodeling of the left ventricle. Aldosterone antagonists may be used as add-on therapy. Lastly isosorbide dinitrate and hydralazine are used for special populations. Digoxin has been shown to improve symptoms but is no longer considered to be first-line therapy unless paroxysmal atrial fibrillation or atrial flutter is present. Digoxin may be used to control the ventricular rate in this situation. •• Beta-blockers are also used to reduce the incidence of ventricular tachycardia and ventricular fibrillation, the most common cause of death in HF patients. Recommended beta-blockers for the management of HF include carvedilol, metoprolol, and bisoprolol. Caution should be taken when initiating a beta-blocker in a patient with reactive airway disease. •• BNP (nesiritide [Natrecor]) has been another recent addition to the management of decompensated HF. Nesiritide’s effects includes promoting diuresis and vasodilation thereby decreasing ventricular preload and afterload. The agent may also inhibit angiotensin II as well as some of the other neuroendocrine compensatory mechanisms associated with HF. Nesiritide is recommended for acutely decompensated ventricular failure. •• Dual chamber biventricular pacemaker/implantable cardioverter defibrillator (ICD): Approximately 60%

of patients with dilated cardiomyopathy develop LBBB. In the presence of LBBB, the right and left ventricles no longer contract simultaneously but in a series causing the intraventricular septum to shift inappropriately, interfering with the aortic and mitral valve functioning. There have been several studies demonstrating significantly improved outcomes (quality of life, survival rates, etc) with the use of a dual chamber biventricular pacemaker. This technology stimulates both ventricles simultaneously, causing both to contract at the same time resulting in a narrowing of the QRS complex and improved myocardial contractility and cardiac output. Often the pacing technology is combined with an ICD because sudden cardiac death related to ventricular tachycardia (VT)/fibrillation is the most common cause of death in these patients. •• Cardiac assist devices (left ventricular, right ventricular, or both) can provide temporary maintenance or preservation of ventricular function, especially as a bridge to recovery, bridge to cardiac transplantation, or as destination therapy (discharge to home). These devices may be inserted percutaneously via the femoral artery or femoral vein, or surgically using the medial sternotomy or thoracotomy approach (see Chapter 19, Advanced Cardiovascular Concepts). Left ventricular apical cannulation allows ambulation and physical rehabilitation. Technological developments have contributed to the development of small axial flow pumps allowing many to be implanted with the drive line (power source) exiting the skin. Risks related to insertion of these devices include infection, peripheral embolization including stroke, and, for some, long-term weaning difficulties in the event that an organ donor is not available. Presently, the Heart Mate II is approved for destination therapy (ie, a replacement for heart transplant). 1. Intra-aortic balloon pump (IABP): Femoral or brachial artery cannulation with the IABP allows for ventricular support, but restricts the patient to bed rest (femoral primarily) and compromises arterial flow to the cannulated limb. 2. Minimally invasive catheter-based micro-axial flow ventricular assist devices: These are frequently used to reduce ventricular afterload and myocardial work. They may be inserted through the femoral artery across the aortic valve into the left ventricle or introduced via the femoral vein into the right atrium and through an atrial septostomy, and positioned in the left atrium. As with the IABP, the patient is restricted to bed rest. 3. Ventricular reconstruction: Many patients with end-stage HF have a previous history of coronary artery disease and MI, resulting in the development of a ventricular aneurysm on the anterior

254

CHAPTER 9. Cardiovascular System

wall of the left ventricle. A surgical procedure can be performed removing the aneurysm, reducing the size of the ventricle, resulting in increased contractility and cardiac output. Studies have shown that some patients experience improvement in physical functioning and NYHA Functional Class following this procedure. 4. Extracoporeal Membrane Oxygenation (ECMO): In recent years the use of ECMO has become more common for severely decompensated heart failure patients who are in cardiogenic shock. This is used as a bridge to recovery, a bridge to a ventricular assist device (VAD), or a bridge to transplant. The use of this technology is limited to the ICU. Patient Education

Patients who present with HF to the critical care unit have high acuity levels, require more intensive interventions, and have an increased need for emotional support surrounding the serious nature of the hospital admission. Previous admissions for HF make patients more aware of the serious nature of acute episodes. Patient education, which is appropriately addressed in the acute care setting includes the following: 1. Both patient and family may require crisis interventions. The nurse may help by encouraging the verbalization of fears related to role adaptations or changes in family responsibility, lifestyle alterations and limitations, and death and dying. The completion of advanced directives and living wills should be initiated if not previously addressed. 2. Family involvement in the critical care phase should be strongly encouraged, including assistance with activities of daily living such as bathing, and “patterning” of daily activities to allow for frequent periods of rest and spacing of exertional activity. In addition, family involvement in reading or other leisure activity with the patient is often restful and relaxing, and may be useful as a diversional activity. If possible, the family should also be present for reinforcement of patient teaching regarding the medical regimen, the importance of fluid and sodium restriction, and the need for daily weights.

Shock Shock is the inability of the circulatory system to deliver enough blood to meet the oxygen and metabolic requirements of body tissues. This clinical syndrome may result from ineffective pumping of the heart (cardiogenic shock), insufficient volume of circulating blood (hypovolemic shock), or massive vasodilation of the vascular bed causing maldistribution of blood (distributive shock). Although the specific definition of shock and strategies for patient management vary according to the underlying pathophysiology, the principle of ineffective or insufficient oxygen delivery to meet the needs of body tissues remains consistent.

Etiology, Risk Factors, and Pathophysiology

The ineffective delivery of oxygen to the tissues leads to cellular dysfunction, rapidly progressing to organ failure, and finally to total body system failure. The cause of the initial onset of the shock syndrome may be from any number of underlying problems, including heart problems, fluid loss, and trauma. Because the body responds in the same way, differences between cardiogenic, hypovolemic, and distributive shock are obvious to the clinician only after the initial assessment has provided key information about the patient’s acute illness. Given the history, the clinician can classify shock into one of three major pathologic groups and proceed to further determine the patient’s needs with the help of diagnostic testing. Because interventions for patient management are directed at the cause, it is essential for the underlying pathophysiology to be clearly understood. Cardiogenic Shock

In cardiogenic shock, the heart is unable to pump enough blood to meet the oxygen and metabolic needs of the body. Pump failure is caused by a variety of factors, the most common being coronary artery disease. A number of other factors may cause pump failure, however, and are typically categorized as coronary or noncoronary causes (Table 9-11). In all cardiogenic shock cases, the heart ceases to function effectively as a pump, resulting in decreases in stroke volume and cardiac output. This leads to a decrease in blood pressure and tissue perfusion. The inadequate emptying of the ventricle increases left atrial pressure, which then increases pulmonary venous pressure. As a result, pulmonary capillary pressure increases, resulting in pulmonary edema. Hypovolemic Shock

Hypovolemic shock occurs when there is inadequate volume in the vascular space. This volume depletion may be caused by blood loss, either internal or external, or by the vascular fluid volume shifting out of the vascular space into other body fluid spaces (Table 9-12). The loss of vascular volume results in insufficient circulating blood to maintain tissue perfusion. The pathophysiology of hypovolemic shock is related directly to decreased circulating blood volume. When an TABLE 9-11. CAUSES OF CARDIOGENIC SHOCK Coronary Causes • MI with resultant cell death in a significant portion of the ventricle • Rupture of ventricle or papillary muscle secondary to MI • Dysfunctional ischemic—“shock ventricle”—which occurs as a result of myocardial ischemia, not involving cell death, and is therefore transient Noncoronary Causes • Myocardial contusion • Pericardial tamponade • Ventricular rupture • Arrhythmia (PEA—pulseless electrical activity—new name) • Valvular dysfunction resulting in ventricular congestion • Cardiomyopathies • End-stage HF

PATHOLOGIC CONDITIONS 255

TABLE 9-12. CAUSES OF HYPOVOLEMIC SHOCK Sources of External Loss of Body Fluid • Hemorrhage (loss of whole blood) • Gastrointestinal tract (vomiting, diarrhea, ostomies, fistulas, nasogastric suctioning) • Renal (diuretic administration, diabetes, insipidus, Addison disease, hyperglycemic osmotic diuresis) Sources of Internal Loss of Body Fluid • Internal hemorrhage • Movement of body fluid into interstitial spaces (“third spacing,” often the result of bacterial toxin, thermal injury, or allergic reaction)

insufficient amount of blood is circulating, the venous blood returning to the heart is insufficient. As a result, right and left ventricular filling pressures are insufficient, decreasing stroke volume and cardiac output. As in cardiogenic shock, when cardiac output is decreased, BP is low and tissue perfusion is poor.

Essential Content Case

Shock Following AMI A 49-year-old man was found slumped in his living room chair, cool and clammy but still breathing. His wife phoned emergency medical services, which arranged air transportation to the local emergency room. On arrival, his vital signs were as follows: BP 68/44 mm Hg HR 122 beats/min RR 33 breaths/min T 36.1°C, orally Sao2 91%

Oxygen at 60% by face mask had been initiated in flight, as well as intravenous normal saline running wide open, 450 mL having already infused. Dopamine was started at a rate of 5 mcg/kg/min. A stat ECG showed “tombstone” ST elevation in the anterior leads (V2, V3, V4), with reciprocal changes in leads II, III, and a VF. The patient was taken for immediate PTCA. In the laboratory, cardiac catheterization findings were as follows: LAD 99% proximal lesion RCA 70% mid lesion LCx Normal LVEF 13% Wall motion Left ventricular akinesis On return to the ICU, the nurse obtained hemodynamic parameters as follows: PA RA PAOP CO CI

45/25 mm Hg 15 mm Hg 22 mm Hg 4.0 L/min 1.5 L/min/m2

Case Question 1. Given the patient’s history, ECG changes and hemodynamic profile, you know the type of shock this patient is experiencing is: (A) Hypovolemic (B) Distributive

(C) Cardiogenic (D) Neurogenic Case Question 2. Following the interventional procedure the primary goal for this patient is to: (A) Reduce myocardial workload (B) Dilate the pulmonary vascular bed (C) Administer a diuretic (D) Intubate the patient to improve oxygen delivery Case Question 3. You anticipate the next intervention for this patient will be: (A) Initiate a vasodilator to reduce afterload (B) Give volume to improve preload (C) Titrate the dopamine infusion up to 7.5 mcg/Kg/min (D) Insertion of an intra-aortic balloon Answers: 1. C; 2. A; 3. D

Distributive Shock

Distributive shock is characterized by an abnormal placement or distribution of vascular volume, occurring in three situations: (1) sepsis, (2) neurologic damage, and (3) anaphylaxis. In each of these situations, the pumping function of the heart and the total blood volume are normal, but the blood is not appropriately distributed throughout the vascular bed. Massive vasodilation occurs in each of these situations for various reasons, causing the vascular bed to be much larger than normal. In this enlarged vascular bed, the usual volume of circulating blood (approximately 5 L) is no longer sufficient to fill the vascular space, causing a decrease in BP and inadequate tissue perfusion. For this reason distributive shock is also referred to as relative hypovolemic shock. Of the distributive shock syndromes, septic shock is most commonly seen in the critical care setting. In the field or emergency department setting, anaphylaxis and neurogenic shock are also common and typically result from allergic reactions and trauma-related spinal cord injury. Stages of Shock

Regardless of underlying etiology, all three types of shock (cardiogenic, hypovolemic, distributive) activate the sympathetic nervous system, which in turn initiates neural, hormonal, and chemical compensatory mechanisms in an attempt to improve tissue perfusion (Figure 9-15). Cellular changes that occur as a result of these compensatory mechanisms are similar in all types of shock. Progression of these cellular changes follows a predictable, four-stage course. Initial Stage

The initial stage of shock represents the first cellular changes resulting from the decrease in oxygen delivery to the tissue. These changes include decreased aerobic and increased anaerobic metabolism, leading to increases in serum lactic acid. No obvious clinical signs and symptoms are apparent during this stage of shock.

256

CHAPTER 9. Cardiovascular System

Cardiogenic shock

Hypovolemic shock

• Decreased LV function • Myocardial infarction • Cardiomyopathy • Other cardiac diseases

• Decreased intravascular volume • Bleeding • Fluid shifts • Dehydration

Distributive shock

• Vasodilation from • Sepsis • Neurologic damage • Anaphylaxis

Venous return

Stroke volume

Cardiac output

Blood pressure

Tissue perfusion

Figure 9-15. Pathophysiology of shock.

Compensatory Stage

The compensatory stage is composed of a number of physiologic events that represent an attempt to compensate for decreases in cardiac output and restore adequate oxygen and nutrient delivery to the tissues (Figure 9-16). These events can be organized into neural, hormonal, and chemical responses. The neural response involves the baroreceptors in the aortic arch and carotid arteries, detecting changes in the arterial BP, and responding by activating the vasomotor center of the medulla. Hypovolemia and resultant hypotension lead to activation of the sympathetic nervous system. The sympathetic nervous system initiates neural, hormonal, and chemical compensatory mechanisms causing peripheral vasoconstriction and elevation of the BP. Vasoconstriction of the peripheral circulation shunts blood to vital organs (autoregulation), reducing renal blood flow, which activates the hormonal response. Hormonal responses include increased production of catecholamines and adrenocorticotropic hormone (ACTH) and activation of the renin-angiotensin-aldosterone system. As a direct result of decreased renal blood flow, renin is released from the juxtaglomerular cells in the kidney, combining with angiotensinogen from the liver resulting in the

production of angiotensin I. Angiotensin I, circulating in the blood, is converted to angiotensin II in the lungs. As was discussed in more detail in the HF section, this hormonal response results in direct peripheral vasoconstriction, in addition to release of aldosterone from the adrenal cortex and antidiuretic hormone (ADH) from the pituitary gland. Sodium and potassium retention, in conjunction with increased ADH, ACTH, and circulating catecholamines, effectively increases intravascular volume, heart rate, and BP, and decreases urine output. Chemical responses during the compensatory stage are related to the respiratory ventilation-perfusion imbalance, which occurs as a result of sympathetic stimulation, redistribution of blood flow, and decreased pulmonary perfusion. A respiratory alkalosis ensues, adversely affecting the patient’s level of consciousness and causing restlessness and agitation. These compensatory mechanisms are effective for finite periods of time, which may vary depending on the individual and presence of comorbidities. The younger and healthier the patients are prior to the shock episode, the more likely they are to survive a prolonged episode of shock. In the absence of vascular volume replacement, these intrinsic

PATHOLOGIC CONDITIONS 257

Decreased cardiac output

Decreased blood pressure

Pressoreceptors Blood vessels in skin, GI tract, kidneys

Blood vessels in skeletal muscles Sympathetic nervous system activation

Constrict

Dilate

Sweat glands

Coronary arteries

Sweat

Dilate Heart

Heart rate

Lungs

Force of contraction

Rate and depth of breathing

Pupils

Dilate

Sympathetic nervous system activation

Renal blood flow

Anterior pituitary gland

Adrenal medulla

ACTH

Epinephrine and norepinephrine

Renin

Aldosterone

ADH

Sodium and water retention

Cortisol

Liver

Blood glucose

Figure 9-16. Compensatory response to shock. (A) Neural compensation. (B) Hormonal compensation.

vasopressors eventually fail as a compensatory mechanism, and the patient enters the progressive, and finally refractory, stages of shock, usually resulting in death. Progressive Stage

The progressive stage is characterized by end-organ failure due to cellular damage from prolonged compensatory changes. The compensatory changes, which were effective in supporting BP and therefore tissue perfusion, are no longer effective and severe hypoperfusion ensues. Impaired oxygen

delivery to the tissues results in multiple organ dysfunction syndrome (MODS), typically beginning with gastrointestinal and renal failure, followed by respiratory and/or cardiac failure and loss of liver and cerebral function. (See Chapter 11 for more on sepsis and MODS.) Refractory Stage

The refractory stage, as its name implies, is the irreversible stage of shock. At this stage cell death has progressed to such a point as to be irreparable, and death is imminent.

258

CHAPTER 9. Cardiovascular System

Clinical Presentation

Clinical signs and symptoms vary, depending on the underlying cause of shock and the stage of shock in which the patient presents. •• Initial stage: No visible signs and symptoms evident from ongoing cellular changes. •• Compensatory stage •• Consciousness: Restless, agitated, confused •• Blood pressure: Normal or slightly low •• Heart rate: Increased •• Respiratory rate: Increased (> 20 breaths/min) •• Skin: Cool, clammy, may be cyanotic •• Peripheral pulses: Weak and thready •• Urine output: Concentrated and scant (< 30 mL/h) •• Bowel sounds: Hypoactive, possible abdominal distension •• Laboratory results: •• Glucose: Increased •• Sodium: Increased •• Pao2: Decreased •• Paco2: Decreased •• pH: Increased •• Progressive stage •• Consciousness: Unresponsive to verbal stimuli •• Blood pressure: Inadequate (< 90 mm Hg systolic) •• Heart rate: Increased (> 90 beats/min) •• Respiratory rate: Increased, shallow •• Skin: Cold, cyanotic, mottled •• Peripheral pulses: Weak and thready, may be absent •• Urine output: Scant (< 20 mL/h) and concentrated •• Bowel sounds: Absent •• Laboratory results: •• Amylase: Increased •• Lipase: Increased •• SGPT/SGOT: Increased •• Lactate: Increased •• CPK: Increased •• Creatinine: Increased •• Blood urea nitrogen: Increased •• Pao2: Decreased •• Paco2: Increased •• pH: Decreased •• HCO3: Decreased Diagnostic Tests

•• ECG: Tachycardia •• Pulmonary arterial pressure: PAD/PAOP high (> 12 mm Hg), RAP high (> 8 mm Hg) •• Echocardiogram: Ventricular wall motion abnormalities, cardiac tamponade, ventricular rupture •• Hypovolemia •• Pulmonary arterial pressure: PAD/PAOP low (< 8 mm Hg), RAP low (< 5 mm Hg), RVEDVI low •• Ultrasound: Groin or retroperitoneal hemorrhage •• Distributive

•• Septic: WBC ≥ 12,000 or ≤ 4,000, > 10% neutrophils, serum lactate >4 mmol/L, positive blood cultures (in 50% of patients). •• Anaphylactic: Arterial blood gas shows inadequate oxygenation. •• Neurogenic: Computed tomography (CT) scan and magnetic resonance imaging (MRI) shows spinal cord damage. Principles of Management for Shock

Differences in the underlying cause of shock lead to some variation in the principles of management. The basic goals of therapy for all forms of shock, however, include the need to correct the underlying cause of shock, improvement of oxygenation, and restoration of adequate tissue perfusion. Correction of the Underlying Cause of Shock

•• Cardiogenic: Remove coronary obstruction or correct tamponade, if present, and support ventricular contractility to increase cardiac output. •• Hypovolemic: Identify source and stop bleeding if possible; correct fluid shunting or third spacing with electrolyte management. •• Distributive –Anaphylactic: Intubate for oxygenation and treat the underlying allergic reaction using antidote or steroid therapy. –Septic: Implement 3 hour “bundle” including obtaining blood cultures and serum lactate; administer broad spectrum antibiotics and 30mL/Kg crystalloid for hypotension; implement early goal directed therapy protocol; removal of infected tissue or device; refer to AACN Practice Alert: Severe Sepsis for evidenced-based practices for the management of severe sepsis and septic shock. (See Chapter 11 for more on sepsis.) –Neurogenic: Severing of the cord may be irreversible; however, intubation provides respiratory support while the underlying cause is identified.

Improve Oxygenation

•• Assess for patent airway and intubate if necessary. •• Administer oxygen at 100% or as necessary until Pao2 is adequate (> 60 to 70 mm Hg). Restore Adequate Tissue Perfusion

•• Administer fluid volume expanders (normal saline, lactated Ringers solution, or plasmanate) in large rapid boluses. Type and cross-match for blood type and administer blood as necessary for hypovolemic shock. •• Initiate vasoactive drug therapy.

Hypertension Hypertension is typically a chronic disease of BP elevation that is often masked, especially in the early years of onset, by lack of warning signs or symptoms. Hypertensive crisis is

PATHOLOGIC CONDITIONS 259

an acute episode or exacerbation, occurring infrequently in a small percentage of hypertensive patients and characterized by the pivotal effect the particular episode and its treatment may have on the patient’s long-term outcome. In most cases, the numerical or absolute value of the arterial BP is less important than its impact on the individual’s underlying risk of target organ damage, specifically cerebrovascular, coronary, and renal diseases. Etiology, Risk Factors, and Pathophysiology

Although a number of clinical syndromes commonly are associated with hypertension and many underlying etiologies may contribute to the progression of hypertensive disease, the pathophysiology of hypertension is similar regardless of the cause. An acute hypertensive crisis begins with elevation of the systolic or diastolic BP causing a threat, direct or indirect, to an organ or body system. Acute, severe increases in pressure may cause serious, life-threatening cerebrovascular and cardiovascular compromise. Prolonged hypoperfusion of an organ system leads to ischemia, necrosis, and organ system failure. Classification

Because of the increased risk of such events in all hypertensive patients, morbidity and mortality directly related to hypertension is high, and long-term, consistent therapy in all stages of hypertension is necessary. Hypertension can be described in stages as described below or classified according to the value of the blood pressure. Refer to Table 9-13. TABLE 9-13. COMMON DRUGS USED TO MANAGE ACUTE HYPERTENSIVE EPISODES Nitroprusside

• Dilates arterioles and veins. • Administer IV at 0.5 to 10.0 mcg/kg/min (mix in normal saline only; 100 mg in 500 mL). Cover bottle with foil to avoid light exposure. • Titrate up to desired BP, recognizing that the effect will be evident within 1 minute of change in dose.

Nicardipine

• Calcium channel blocker. • Administer 5 mg/h initially, titrate 2.5 mg/h at 5- to 15-minute intervals to a maximum dose of 15 mg/h.

Nitroglycerin

• Dilates veins more than arterioles. • Administer IV at a rate of 5 to 100 mcg/min. Mix 100 mg in 100 mL NS or D5 IV.

Esmolol

• Beta1 selective blocker and at higher doses inhibits B2 receptors in the blood vessels. • Useful for treating hypertension • Administer 0.5 mg/Kg over 1 min loading dose followed by 50 mcg/Kg/min infusion. • Titrate to achieve desired lower BP • Onset of action within minutes • Peak effect in less than 5 minutes

Enalapril

• An ACE inhibitor. • Administer IV at a rate of 5 mg/min.

Labetalol

• Beta-receptor agonist (beta-blocker). • Particularly indicated in patients with suspected MI or angina. • Administer 5 mg bolus over 5 minutes and repeat 3 times. IV drip may then be started.

•• Stage I hypertension: Benign hypertension is characterized by slightly elevated BP (140-160 mm Hg systolic/90 mm Hg diastolic, in adults) for long periods of time, with little if any end-organ damage. Stage I hypertension does not tend to cause acute problems or complications, unless other comorbid conditions, such as atherosclerotic disease, are present. The pressure does not typically exacerbate or precipitate an acute emergent event (generally not > 140-160 mm Hg systolic/90 mm Hg diastolic, in adults). •• Accelerated hypertension: Often used interchangeably with malignant hypertension, the stage known as accelerated hypertension is generally considered a precursor to malignant hypertension, and is characterized by an increase in the patient’s baseline BP. •• Malignant hypertension: Hypertension typically is a chronic disease in which elevation in BP occurs slowly, over a period of several years. Because of its gradual onset, the body adapts to increased pressures in the vascular bed and the patient frequently is asymptomatic for years, eventually able to tolerate pressures of up to 200/120 mm Hg without experiencing significant symptoms or clinical events. This type of presentation often is identified “accidentally,” secondary to hospitalization for another problem. Generally patients with malignant hypertension are at risk for significant end-organ damage because of the severity of high pressure in the vascular bed and inability of the circulatory system to further adapt or compensate in the event of additional stressors. •• Hypertensive crisis: Hypertensive crisis is characterized by a severe elevation in BP, relative to the individual’s baseline BP, which causes risk of end-organ damage and poor long-term outcome due to permanent organ system damage if the immediate episode is not treated quickly and aggressively. •• Special populations: In pregnant women and in children a less severe elevation in BP may result in significant end-organ damage and is therefore considered to be a “hypertensive crisis” at values much lower than would be expected to be problematic in the average adult. The absolute value of the BP varies significantly depending on the situation and the individual involved; for example, preeclampsia, considered to be a hypertensive crisis in pregnancy, may occur at pressures as low as 130/100 to 160/100 mm Hg. Clinical Presentation

Diagnosis of hypertensive crisis is not based on the absolute value of the BP, but rather on the following combined criteria: •• Rapidity of the rise of the BP •• Duration of prior hypertension •• Clinical determination of the immediate threat to vital organ function •• Headache

260

CHAPTER 9. Cardiovascular System

•• Blurred vision •• Nosebleed •• Dizziness or vertigo •• Transient ischemic attack •• Diminished peripheral pulses or bruits •• Carotid or abdominal bruit •• Heart sounds with S3 and/or S4 •• Systolic and/or diastolic murmurs •• Gastrointestinal bleeding •• Pulmonary edema •• Shortness of breath •• Fatigue •• Malaise •• Weakness •• Nausea and vomiting •• Hematuria •• Dysuria •• Funduscopic findings: Arteriovenous thickening, arteriolar narrowing, hemorrhage, papilledema, or exudates Diagnostic Tests

•• Chest x-ray: Myocardial hypertrophy, pulmonary infiltrates •• CT: Arteriolar narrowing and arteriovenous thickening •• Specific tests to target organ damage – Renal angiography – Coronary angiography – Carotid/cerebral angiography •• MRI: Cerebral vascular malperfusion

A number of agents are used in the acute setting for management of hypertensive crisis (Table 9-13). Aggressiveness of pharmacologic intervention should be based on the severity of BP elevation (immediate risk of stroke), the immediate risk of irreversible target organ damage (renal and hepatic function related to drug metabolism and clearance also should be considered), and any confounding conditions or risk factors which are present (eg, the fetus in preeclampsia). In general, acute severe (accelerated malignant/ stages 3 and 4) hypertension should be treated as quickly and aggressively as can be tolerated by the patient in order to prevent the immediate risk of hypertensive encephalopathy, dissecting aortic aneurysm, MI, or intracranial hemorrhage. Maintenance of cerebral perfusion pressure is imperative during treatment, and overly aggressive pharmacologic management poses the threat of cerebrovascular compromise due to a sudden drop in arterial pressure and inability of the autoregulatory mechanism to adjust. Other organ systems dependent on higher pressure for perfusion include the renal and coronary systems. A sudden, severe drop in systemic arterial pressure may result in ischemic episodes or acute renal failure. For nonacute hypertension, dietary alteration and relaxation or biofeedback techniques may be used in addition to pharmacologic measures to reduce the morbidity and mortality of hypertension. Although these measures are most effective when employed long term as part of a cohesive outpatient follow-up program, initiating these strategies in the acute setting may help emphasize their importance. Evaluation and Treatment of Target Organ Disease

Principles of Management for Hypertension

Management of the patient with acute exacerbation of hypertension, or hypertensive crisis, revolves around three primary objectives: reduction of arterial pressure, evaluation and treatment of target organ damage, and preparation and planning for continuous and consistent outpatient follow-up. Reduction of Arterial Pressure

Ascertain correct arterial BP. Verify arterial BP, being sure to assess bilateral measurements with the correct cuff size if using sphygmomanometry, as well as orthostatic pressures if possible (lying and sitting up, if standing is not possible). Each measurement should be 2 minutes apart and both right and left measurements should be documented. If differences between the right and left measurements are greater than 10 mm Hg, the higher reading should be used to gauge therapy. In most acute situations, priority should be given to establishing a stable arterial access site for direct, invasive monitoring of BP. Initiate pharmacologic intervention. For acute high arterial pressure, intravenous pharmacologic intervention is the fastest, most effective means of reducing arterial BP.

Concomitant to initiation of pharmacologic intervention, the assessment and prevention of target organ disease is important to avoid irreversible damage. Target organs typically at risk include the brain, heart, kidneys, and eyes. Strategies to prevent damage to these organ systems during hypertensive crisis include the following: •• Brain: Reduce diastolic pressure by one-third (not to go < 95 mm Hg) using aggressive pharmacologic measures (see Table 9-13). •• Heart: Reduce diastolic and systolic pressure by onethird; administer combination therapy if possible (vasodilator and beta-blocker) or ACE inhibitor for afterload reduction; monitor for ischemic changes on ECG. •• Kidneys: Reduce systolic and diastolic BP using pharmacologic measures; monitor serum creatinine and urine specific gravity as well as proteinuria and hematuria; for patients with severe existing renal impairment, use of ACE inhibitors may exacerbate their renal compromise and is therefore contraindicated in patients with bilateral renal artery stenosis; administer diuretics to maintain serum sodium and adequate diuresis.

SELECTED BIBLIOGRAPHY 261

•• Eyes: Reduce systolic and diastolic BP; observe retina for evidence of hemorrhage, exudate, or papilledema; instruct the patient with blurring of vision regarding his or her environment, especially location of the call bell. Patient Education on Lifestyle Modification and Follow-Up

Following control of hypertension in the acute phase, patient education should be initiated regarding the serious and chronic nature of the disease. Often, the clinician may have an opportunity in the acute stage to make an impact regarding the seriousness of uncontrolled hypertension and it’s potentially debilitating effects. Prior to beginning the educational process, assessment should include: 1. Family history of hypertension, cardiovascular disease, coronary artery disease, stroke, diabetes mellitus, and hyperlipidemia 2. Lifestyle history including weight gain, exercise, and smoking habits 3. Dietary patterns including high sodium, alcohol, and dietary fat intake or low-potassium intake 4. Knowledge of hypertension and impact of previous medical therapy for hypertension (compliance, side effects, results, or efficacy)

Essential Content Case

Thinking Critically You are taking care of a patient, 4 days post anterior MI, who is just transferred into the ICU from an intermediate floor with severe shortness of breath. Your initial assessment reveals the following: HR 128 beats/min BP 110/82 mm Hg RR 36 breaths/min T 37.6°C, orally Pulse Oximetry 88% Lung sounds Coarse, bilateral crackles in lower lobes, poor respiratory effort Heart sounds S1, S2, S3 Skin Flushed, diaphoretic, 2+ pedal edema ECG Sinus tachycardia, with tall R-waves in V5-V6 indicating left ventricular hypertrophy Case Question 1. What is your initial intervention? (A) Obtain an arterial blood gas measurement (B) Initiate a nesiritide infusion (C) Prepare to intubate the patient (D) Call a Code Blue Case Question 2. What is the most likely underlying cause for this patient’s respiratory compromise? (A) Acute decompensated heart failure with pulmonary edema

(B) Abrupt onset of septic shock with adult respiratory distress syndrome (C) Acute anxiety attack (D) Hypovolemic shock Case Question 3. Management of this situation would most likely include what interventions? (1) (2) (3) (4)

Administration of a diuretic to reduce preload Initiation of a dobutamine infusion at 5 mcg/Kg/min Consideration for mechanical support Consideration for intubation and ventilator support

(A) 4 (B) 1 and 2 (C) 3 and 4 (D) All of the above Answers: 1. C; 2. A; 3. D

SELECTED BIBLIOGRAPHY General Cardiovascular Bonow RO, Mann DL, Zipes DP, Lippy P, eds. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 9th ed. Philadelphia, PA: WB Saunders; 2012. Moser DK, Riegel B. Cardiac Nursing: A Companion to Braunwald’s Heart Disease. Canada: Saunders; 2008. Woods SL, Froelicher ESS, Motzer SA, Bridges EJ. Cardiac Nursing. 6th ed. Philadelphia, PA: Lippincott, Williams & Wilkins; 2010.

Coronary Revascularization Hardin S, Kaplow R. Cardiac Surgery Essentials for Critical Care Nursing. Sudbury, MA: Jones & Bartlett Publishing; 2010. South T. Coronary artery bypass surgery. Crit Care Nurs Clin NA. 2011;23(4):573-586. Todd BA. Cardiothoracic Surgical Nursing Secrets. St Louis, MO: Mosby–Year Book, Inc; 2005.

Acute Ischemic Heart Disease Cahoon W, Flattery MP. ACC/AHA Non-ST elevation myocardial infarction guidelines revision: 2007: implications for nursing practice. Prog Cardiovasc Nurs. 2008;23(1):53-56. Naples RM, Harris JW, Ghaemmaghami CA. Critical care aspects in the management of patients with acute coronary syndromes. Emerg Med Clin N Am. 2008;26:685-702. Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. Circ. 2012;126:2020-2035.

Heart Failure Albert NM. Heart failure with preserved systolic function: giving well-deserved attention to the “other” heart failure. Crit Care Nurs Q. 2007;30(4):287-296. Albert NM. Fluid management strategies in heart failure. Crit Care Nurs. 2012;32(2):20-33. Daleiden-Burns A (issue editor). Heart failure. Crit Care Nurs Q. 2007;30(4):285-286.

262

CHAPTER 9. Cardiovascular System

English MA. Advanced concepts in heart failure. Crit Care Nurs Q. 1995;18(1):56-64. Fara-Erny A. Heart failure: challenges and outcomes. J Cardiovasc Nurs. 2000;14(4):v-vii. Litton KA. Demystifying ventricular assist devices. Crit Care Nurs Q. 2011;34(2):200-207.

Shock Bridges EJ, Dukes S. Cardiovascular aspects of septic shock. Crit Care Nurs. 2005;25(2):14-42. Cheng JM, den Ull CA, Hoeks SE, et al. Percutaneous left ventricular assist devices vs intra-aortic balloon pump counterpulsation for treatment of cardiogenic shock: a meta-analysis on controlled trials. Eur Heart J. 2009:30(17):2101-2108. Kelley DM. Hypovolemic shock: an overview. Crit Care Nurs Q. 2005;28(1):2-19. McAtee ME. Cardiogenic shock. Crit Care Nurs Clin NA. 2011;23 (40):607-616. Reynolds HR, Hochman JS. Cardiogenic shock: current concepts and improving outcomes. Circ. 2008;117(5):686-697. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Eng J Med. 2001;345(19):1368-1377. Topalian S, Ginsberg F, Parillo JE. Cardiogenic shock. Crit Care Med. 2008;36(suppl 1):S66-S74.

Hypertension Schulenburg M. Management of hypertensive emergencies: implications for the critical care nurse. Crit Care Nurs Q. 2007;30(2):80-93. Smithburger PL, Kane-Gill SL, Seybert AL. Recent advances in the treatment of hypertensive emergencies. Crit Care Nurs. 2010;30(5). Sodium, blood pressure, and cardiovascular disease: further evidence supporting the American Heart Association sodium reduction recommendations. Circ. 2012;126:2880-2889.

Evidence-Based Practice Guidelines Adams D, Bridges CR, Casey DE, et al. 2012 ACCF/AHA focused update of the Guideline for the Management of Patients with Unstable Angina/non-ST-elevation myocardial infarcton: a report of the American College of Cardiology Foundation/ American Heart Association Task Force on Practice Guidelines. Circ. 2012;126:875-910. American Association of Critical-Care Nurses. AACN Practice Alert: Severe Sepsis. Aliso Viejo, CA: American Association of Critical-Care Nurses; 2006, April. American Association of Critical-Care Nurses. AACN Practice Alert: Noninvasive Blood Pressure Monitoring. Aliso Viejo, CA: American Association of Critical-Care Nurses; 2006, June. American Association of Critical-Care Nurses. AACN Practice Alert: ST-Segment Monitoring. Aliso Viejo, CA: American Association of Critical-Care Nurses; 2008, April.

Chobanian AV, Bakris GL, Black HR, et al. Seventh report of the joint national committee on prevention, detection, evaluation, and treatment of high blood pressure. Hypertension. 42: 1206-1252. Dellinger RP, Carlet JM, Masur H, Gerlach H. The surviving sepsis guidelines for the management of severe sepsis and septic shock: background, recommendations, and discussion from an evidenced-based review. Crit Care Med. 2004;32(suppl 11). Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013:41(2):580-637. Drew BJ, Calif RM, Funk M, et al. Practice standards for electrocardiographic monitoring in hospital settings. Circ. 2004;110:2721-2746. Hillis LD, Smith PK, Anderson JL, et al. 2011 ACCF/AHA Guidelines for coronary artery bypass surgery: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. 2011:124;e652-e735. James PA, Oparil S, Carter BL, et al. 2014 evidenced-based guideline for the management of high blood pressure in adults. Report from the panel members appointed to the Eighth Joint National Committee (JNC8). JAMA. doi:10.1001/jama. 2013.284427, December 18, 2013. Levine GN, Bates ER, Blankenship JC, et al. 20100 ACCF/AHA/ SCAI Guidelines for percutaneous coronary intervention: a report of the American College of Cardiology Foundation/ American Heart Association Task Force on Practice Guidelines and the society for cardiovascular angiography and interventions. Circ. 2011;124:e574-e651. Lindenfeld J, Albert NM, Boehmer JP, et al. Executive summary: HSFA 2010 comprehensive heart failure practice guideline. J Card Fail. 2010;16(6):475-539. Masoudi FA, Bonow RO, Brindis RG, et al. ACC/AHA 2008 statement on performance measurement and reperfusion therapy: a report of the ACC/AHA Task Force on Performance Measures. Circ. 2008;118:2649-2661. National Institute of Health. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. U.S. Department of Health and Human Services. [NIH Publication No. 04-5230]. Bethesda, MD: NIH: August 2004. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA Guidelines for the management of ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. 2013;127:529-555. Peura JL, Colvin-Adams M, Francis GS, et al. Recommendations for the use of mechanical circulatory support: device strategies and patient selection: a scientific statement from the American Heart Association. Circ. 2012;126:2648-2667.

Respiratory System Maureen A. Seckel

KNOWLEDGE COMPETENCIES 1. Identify various radiologic and pulmonary anatomic features relevant to interpretation of chest x-rays. 2. Describe different systems and principles of management for chest tubes. 3. Describe the etiology, pathophysiology, clinical presentation, patient needs, and principles of management of acute respiratory failure (ARF). 4. Compare and contrast the pathophysiology, clinical presentation, patient needs, and management approaches for common diseases leading to ARF:

SPECIAL ASSESSMENT TECHNIQUES, DIAGNOSTIC TESTS, AND MONITORING SYSTEMS Chest X-Rays Chest radiography is an important tool in respiratory assessment, providing visualization of the heart and lungs. Chest x-rays are a complement to bedside assessment. Critical care nurses need to know basic radiographic concepts and how to optimize portable chest x-ray technique, as well as how to systematically view a chest x-ray image. Chest x-rays are obtained as part of routine screening procedures, when respiratory disease is suspected, to evaluate the status of respiratory abnormalities (eg, pneumothorax, pleural effusion, tumors), to confirm proper invasive tube placement (ie, endotracheal, tracheostomy, or chest tubes, and pulmonary artery catheters), or following traumatic chest injury. Basic Concepts

An x-ray is a form of radiant energy, and a radiographic image is made by x-ray machines. Only a few rays are absorbed by

• Acute respiratory distress syndrome (ARDS) • ARF in the chronic obstructive pulmonary disease patient (asthma, emphysema, bronchitis) • COPD exacerbation • Acute asthma • Pulmonary hypertension • Pneumonia • Interstitial lung disease • Pulmonary embolism (PE) • Venous thromboembolism (VTE)

air as beams pass through the atmosphere, whereas all rays are absorbed by metal as the beams attempt to pass through a sheet of metal. When nothing but air lies between the film cassette and the x-ray source, the radiographic image is blackness or radiolucency. If density increases, more beams are absorbed between the film cassette or detectors and the x-ray source, and the radiographic image is whiteness or radiopacity. Many institutions are replacing traditional x-ray film with detectors that convert the x-ray-energy to a digital radiograph. These images can then be stored and distributed in a digital format. As the x-ray beam passes through the patient, the denser tissues absorb more of the beam, and the less dense tissues absorb less of the beam. The lungs are primarily sacs of air or gas, so normal lungs look black on chest films. Conversely, the skeletal thorax appears white, because bone is very dense and absorbs the most x-rays (Table 10-1). The heart and mediastinum appear gray because those structures are made up of mostly water. Breast tissue is made up of mostly fat and it appears whitish-gray. 263

264

CHAPTER 10. Respiratory System

TABLE 10-1. BASIC X-RAY DENSITIES Radiolucent (black) Gas, air (dark or black) • Lungs, trachea, bronchi, alveoli Water (dark or gray) • Heart, muscle, blood, blood vessels, diaphragm, spleen, liver Fat (lighter or whitish-gray) • Breasts, marrow, hilar streaking Radiopaque (white) Metal, bone (lightest or white) • Ribs, scapulae, vertebrae • Bullets, coins, teeth, ECG electrodes

Basic Views of the Chest

The most common method of obtaining a chest x-ray is the posterior-anterior (PA) view. PA chest x-rays are typically done in the radiology department with the machine about 6 ft away from the x-ray film cassette and the patient standing with the anterior chest wall against the x-ray plate and the posterior chest wall toward the x-ray machine. The patient is told to take a deep breath and hold it as the x-ray beam is delivered through the posterior chest wall to the x-ray film cassette. The PA view results in a very accurate, sharp picture of the chest. Critically ill patients are rarely able to tolerate the positioning requirements of a PA chest x-ray or the logistics of transport to the department. Most chest x-rays in critical care are obtained with an anterior-posterior (AP) view with the patient supine in bed, with or without back rest elevation. With portable AP chest films, the film cassette is placed behind the patient and the x-ray beam is delivered through the anterior chest to the x-ray film. The x-ray machine is only 3 ft away from the patient, which results in greater distortion of chest images, making the AP chest x-ray less accurate than the PA method. Of particular concern is that the heart size is enlarged on an AP film. When viewing chest x-rays, it is important to know whether a PA or AP view was used to avoid misinterpretation of heart size as cardiomegaly. Distortions can be minimized by placing the patient in a high Fowler position, or as erect as possible, with the thorax symmetrically placed on the x-ray film cassette. Explain the procedure to the patient and the need to avoid movement. All unnecessary objects lying on the anterior chest (such as ventilator tubing, safety pins, jewelry, ECG wires, nasogastric tubes, etc) are removed or repositioned as possible. If the patient is unconscious, securing the forehead in a neutral position may be necessary, especially in the high Fowler position to avoid mispositioning of the head. All caregivers assisting with the chest x-ray need to protect themselves from radiation exposure by positioning themselves behind the x-ray machine or by using lead aprons covering the neck, chest, and abdomen. Other chest x-ray views include: (1) lateral views to identify normal and abnormal structures behind the heart, along the spine, and at the base of the lung; (2) oblique views

to localize lesions without interference from the bony thorax or to get a better picture of the trachea, carina, heart, and great vessels; (3) lordotic views to better visualize the apical and middle regions of the lungs and to differentiate anterior from posterior lesions; and (4) lateral decubitus (cross-table) views, done with the patient supine or side-lying, to assess for air-fluid levels or free-flowing pleural fluid. Systematic Approach to Chest X-Ray Interpretation

A systematic approach should be used when analyzing a chest x-ray film. It is important to first make sure that the image has been properly labeled (correct name and medical record number) and to identify the right and left sides before viewing the image. If previous images are available, place them next to the new images for comparison. View the chest x-ray from the lateral borders, moving to the medial aspects of the thorax and asking the series of questions found in Table 10-2. Begin the chest x-ray analysis by comparing the right side to the left side using the following sequence (Figures 10-1 and 10-2): (1) soft tissues—neck, shoulders, breasts, and subcutaneous fat; (2) trachea—the column of radiolucency readily visible above the clavicles; (3) bony thorax—note size, shape, and symmetry; (4) intercostal spaces (ICS)—note width and angle; (5) diaphragm—dome-shaped with distinct margins, right dome 1 to 3 cm higher than left dome; (6) pleural surfaces—visceral and parietal pleura appear like a thin hairlike line along the apices and lateral chest; (7) mediastinum— size varies with age, gender, and size; (8) hila—large pulmonary arteries and veins; (9) lung fields—largest area of the chest and most radiolucent; and (10) catheters, tubes, wires, and line. Normal Variants and Common Abnormalities

When the soft tissues are examined, the two sides of the lateral chest should be symmetric. A mastectomy makes one TABLE 10-2. STEPS FOR INTERPRETATION OF A CHEST X-RAY FILM Step 1 Look at the different densities (black, gray, and white), and answer the question, What is air, fluid, tissue, and bone? Step 2 Look at the shape or form of each density, and answer the question, What normal anatomic structure is this? Step 3 Look at both right and left sides, and answer the question, Are the findings the same on both sides or are there differences (both physiologic and pathophysiologic)? Step 4 Look at all the structures (bones, mediastinum, diaphragm, pleural space, and lung tissue), and answer the question, Are there any abnormalities present? Step 5 Look for all tubes, wires, and lines, and answer the question, Are the tubes, wires, and lines in the proper place? Reprinted from: Urden L, Stacy KM, Lough M. Thelan’s Critical Care Nursing: Diagnosis and Management. 5th ed. St Louis, MO: Mosby; 2006:612, with permission from Elsevier.

SPECIAL ASSESSMENT TECHNIQUES, DIAGNOSTIC TESTS, AND MONITORING SYSTEMS 265

Right inominate vein Superior Vena Cava Ascending Aorta

Right Atrium Diaphragm

Left inominate vein Aortic Arch Aortopulmonary Window Left Pulmonary Artery Left Ventricle Descending Aorta Diaphragm

Figure 10-1. Normal chest x-ray with anatomical references. Courtesy of: University of Virginia Health Sciences Center, Department of Radiology (From Spencer B Gay, MD, Juan Olazagasti, MD,Jack W Higginbotham, MD, et al. Introduction to Chest Radiology. University of Virginia Health Sciences Center. http://www.med-ed. virginia.edu/courses/rad/cxr/anatomy4chest.html)

Left Upper Lobe Right Upper Lobe

Lingula Right Middle Lobe

Right Lower Lobe

Left Lower Lobe

Figure 10-2. Normal chest x-ray with anatomical references. Courtesy of: University of Virginia Health Sciences Center, Department of Radiology (From Spencer B Gay, MD, Juan Olazagasti, MD,Jack W Higginbotham, MD, et al. Introduction to Chest Radiology. University of Virginia Health Sciences Center. http://www.med-ed. virginia.edu/courses/rad/cxr/anatomy4chest.html)

lung look more radiolucent than the other due to the absence of fatty tissue. The trachea should be midline, with the carina visible at the level of the aortic knob or second ICS. The most common cause of tracheal deviation is a pneumothorax, which causes a tracheal and mediastinal shift to the area away from the pneumothorax (Table 10-3 and Figures 10-3 and 10-4). Bony thorax inspection reveals general body build. Clavicles should be symmetric and may have an irregular notch or indentation in the inferior medial aspect of the clavicle called a rhomboid fossa, a normal variant. Deformities of the thorax can be detected, such as scoliosis, pectus excavatum (also called funnel chest), or pectus carinatum (also called pigeon chest). Decreases in the density (less white) of the spine, ribs, and other bones may indicate loss of calcium from the bones due to osteoporosis or long-term steroid dependency. Careful examination of the ICSs and rib angles may indicate pathology. Patients with chronic obstructive pulmonary disease (COPD) have widened ICS and the angle of the ribs to the spine increases to 90° instead of the normal 45° angle because of severe hyperinflation (see Figure 10-3). Conversely, narrowed ICS may be visible in cystic fibrosis patients with severe interstitial fibrosis. Rib fractures, if present, are commonly visible along the lateral borders of the rib cage. Elevation of the diaphragm can be a result of abdominal distention, phrenic nerve paralysis, or lung collapse. Depression or flattening of the diaphragm can occur when 11 or 12 ribs show on a chest x-ray as a result of COPD or severe hyperinflation due to asthma. The usual number of ribs visible without a depressed diaphragm are 9 to 10. Normal costophrenic angles can be seen where the tapered edges of the diaphragm and the chest wall meet. Because breast tissue can obscure the angles in women, these angles are more distinct in men. Obliteration or “blunting” of the costophrenic angle may occur with pleural effusion or atelectasis. Identification of a pleural space on a chest x-ray is an abnormal finding (see Figure 10-4). The pleural space is not visible unless air (pneumothorax) or fluid (pleural effusion) enters it. These findings commonly are seen in the ICU population. Two terms often heard regarding the mediastinum are shifting and widening. Mediastinal structures, usually the trachea, bronchi, and heart, can shift with atelectasis, with the shift directed toward the alveolar collapse. Pneumothorax shifts the mediastinum away from the area of involvement. A widening of the mediastinum can indicate several pathologic conditions, such as cardiomegaly, aneurysms, or aortic disruption. Bleeding into the mediastinum, following chest trauma or cardiac surgery, also may cause widening of the mediastinum. Heart size can be estimated easily by measuring the cardiothoracic ratio on a PA film. It is measured with a PA chest x-ray and is measured by comparing the ratio of the maximal horizontal cardiac diameter to the maximal horizontal thoracic diameter. A normal measurement is less than 50%.

266

CHAPTER 10. Respiratory System

TABLE 10-3. CHEST X-RAY FINDINGS Assessed Area Trachea

Usual Adult Findings

Remarks

Midline, translucent, tubelike structure found in the anterior mediastinal cavity Present in upper thorax and are equally distant from sternum Thoracic cavity encasement

Clavicles Ribs Mediastinum

Shadowy-appearing space between the lungs that widens at the hilum Solid-appearing structure with clear edges visible in the left anterior mediastinal cavity; heart should be less than one-half the width of the chest wall on a PA film The lowest tracheal cartilage at which the bronchi bifurcate

Heart

Carina Main-stem bronchus Hilum

Bronchi (other than main stem) Lung fields

Diaphragm

The translucent, tubelike structure visible to approximately 2.5 cm from hilum Small, white, bilateral densities present where the bronchi join the lungs; left hilum should be 2 to 3 cm higher than the right hilum Not usually visible

Deviation from the midline suggests tension, pneumothorax, atelectasis, pleural effusion, mass, or collapsed lung Malalignment or break indicates fracture Widening of intercostal spaces indicates emphysema; malalignment or break indicates fractured sternum or ribs Deviation to either side may indicate pleural effusion, fibrosis, or collapsed lung Shift may indicate atelectasis or tension pneumothorax; if heart is greater than one-half the chest wall width, heart failure or pericardial fluid may be present If the end of the endotracheal tube is seen 3 cm above the carina, it is in the correct position Densities may indicate bronchogenic cyst A shift to either side indicates atelectasis; accentuated shadows may indicate emphysema or pulmonary abscess If visible, may indicate bronchial pneumonia

Usually not completely visible except as fine white areas from hilum; fields should be clear as normal lung tissue is radiolucent; normal “lung markings” should be present to the periphery Rounded structures visible at the bottom of the lung fields; right side is 1 to 2 cm higher than the left; the costophrenic angles should be clear and sharp

If visible, may indicate atelectasis; patchy densities may be signs of resolving pneumonia, silicosis, or fibrosis; nasogastric tubes, pulmonary artery catheters, and chest tubes will appear as shadows and their positions should be noted An elevated diaphragm may indicate pneumonia, pleurisy, acute bronchitis, or atelectasis; a flattened diaphragm suggests COPD; unilateral elevation indicates a pneumothorax or pulmonary infection; the presence of scarring or fluid causes blunting of costophrenic angles; 300 to 500 mL of pleural fluid must be present before blunting is seen

From: Talbot I, Meyers-Marquardt M. Pocket Guide to Critical Assessment. St. Louis, MO: CV Mosby; 1990.

Clavicle heads

Trachea appears deviated to left Bullae

Spinal pedicle

L clavicle appears longer in length than R clavicle

Hyperlucency Slight mediastinal shift Widened intercostal spaces in left thorax

Lung

Hyperinflation 10 cm

Flattened diaphragms

Widened intercostal spaces

Figure 10-3. COPD, flattened diaphragms, hyperinflation, widened intercostals spaces, apical bullae, and chest rotation. (Reprinted from: Siela D. Chest radiograph evaluation and interpretation. AACN Adv Crit Care. 2008;19:444-473.)

Figure 10-4. Left pneumothorax, hyperlucency, and widened intercostals spaces. (Reprinted from: Siela D. Chest radiograph evaluation and interpretation. AACN Adv Crit Care. 2008;19:444-473.)

SPECIAL ASSESSMENT TECHNIQUES, DIAGNOSTIC TESTS, AND MONITORING SYSTEMS 267

Figure 10-5. Right lower lobe pneumonia with minor fissure visualized. (Reprinted from: Siela D. Chest radiograph evaluation and interpretation. AACN Adv Crit Care. 2008;19:444-473.)

Greater percents are indicative of cardiac enlargement. This method for determining normal heart size is not accurate using an AP chest x-ray, the most common type taken in the critically ill. The lung fields should be assessed for any areas of increased density (whiteness) or increased radiolucency (blackness), which can indicate an abnormality. Density increases when water, pus, or blood accumulates in the lungs, as in pneumonia (Figure 10-5). Increased radiolucency is caused by increased air in the lungs, as may occur with COPD. A fine line present on the right side of the lung at the sixth rib level (midlung) is a normal finding, representing the horizontal fissure separating the right upper and middle lobes.

Figure 10-6. Carina and right bronchus. (Reprinted from: Siela D. Chest radiograph evaluation and interpretation. AACN Adv Crit Care. 2008;19: 444-473.)

stomach. The stomach can be identified by the radiolucency just under the diaphragm on the left side, which is called the gastric air bubble. Small bore nasoenteric tubes may be positioned with the tip in the stomach or the small bowel depending on whether gastric or small bowel feedings are intended. Pulmonary artery catheters should be viewed running through the right atrium and right ventricle into the pulmonary artery. These can be difficult to identify at first, but be sure and look at both sides of the hila (right and left pulmonary arteries found on either side of the mediastinum).

Invasive Lines

Chest x-rays are frequently obtained in critical care to confirm proper placement of invasive equipment (endotracheal tubes, central venous and pulmonary artery catheters, intraaortic balloons, nasogastric tubes, chest tubes). All invasive tubes have radiopaque lines running the length of the tube that are visible on the x-ray. When in the proper position, the endotracheal tube tips should be 4 to 6 cm above the carina with the patient’s head in neutral position (Figures 10-6 and 10-7). Flexion or extension of the patient’s head causes a 2-cm change in the position of the tip of the endotracheal tube. Look for a thin white line in the trachea and follow it down to the level of the clavicles and measure the space between the end of the tube and the carina. The tip of the endotracheal tube should be at least 3 cm distal to the vocal cords. Identify all white lines and follow their paths. The nasogastric tube should run the length of the esophagus with the tip of the tube beyond the gastroesophageal junction in the

ET tube PAC

Chest tube ET tube tip

PAC

Figure 10-7. Pulmonary artery catheter, endotracheal tube, and left chest tube. (Reprinted from: Siela D. Chest radiograph evaluation and interpretation. AACN Adv Crit Care. 2008;19:444-473.)

268

CHAPTER 10. Respiratory System

Chest tube should be visualized by viewing the radiopaque stripe and location of the tip is dependent on whether the tube is inserted for air or fluid removal. The side holes should be positioned medial to the inner margin of the ribs. Identify all items in the chest, such as temporary or permanent pacing wires, pacing generators, automatic implantable defibrillators, and surgical wires, drains, or clips (see Figure 10-7).

Computed Tomography and Magnetic Resonance Imaging

chest in situations where two-dimensional chest x-rays are insufficient. CT and MRI are particularly advantageous over chest x-rays to evaluate mediastinal and pleural abnormalities, particularly those with fluid collections. Pleural effusions or empyemas, malpositioned or occluded chest tubes, mediastinal hematomas, and mediastinitis are problems for which CT and MRI are more sensitive than chest x-rays. The need for transportation to the radiology department and positioning restrictions within the scanning devices pose certain risks to critically ill patients. Of particular concern is the automatic movement of patients during the procedure into and out of the scanning device. Accidental disconnection of invasive devices can easily occur if additional tubing lengths and potential obstructions are not considered. Decreased visualization of patients during the procedures requires vigilant monitoring of cardiovascular and respiratory parameters and devices, as well as establishing a method for conscious patients to alert nearby clinicians in case of difficulties. The strong magnetic field of MRI units may interfere with ventilator performance and a non-magnetic ventilator is required. Magnetic resonance imaging testing can be a frightening experience for the patient. Anxiety-related reactions, occurring in up to almost one-third of patients, range from mild apprehension to severe anxiety. These reactions can result in cancellation of the test or interference with its results. It is suggested that all patients receive basic information regarding the MRI procedure, including details of the small chamber they will be placed in, the noise and temperature they will experience, and the duration of the procedure. If possible, use of relaxation or music tapes, ear plugs or headsets, and the presence of a family member or friend should be considered. In addition, short-acting anxiolytics should be used for patients who need them.

Computed tomography (CT) and magnetic resonance imaging (MRI) allow for the three-dimensional examination of the

Pulmonary Angiograms, CTPA, and V/Q Scans

Helpful Hints

Chest x-rays should be taken after every attempt to insert central venous catheters to detect the presence of an accidental pneumothorax. A common error is to mistake the area above the clavicles as a pneumothorax, especially on AP views. Two common abnormal x-ray signs frequently discussed are the silhouette sign and the air bronchogram. For any structure to be visible, the density of its edge must contrast with the surrounding density. The loss of contrast is called the silhouette sign. It means that two structures of the same density have come in contact with each other and the borders are lost; for example, the heart is a water density, so if the alveoli near the left heart border fill with fluid, the two densities are the same and there is a loss of contrast and no left heart border. An air bronchogram is air showing through a greater density, such as water (Figure 10-8). The bronchi are not seen on a normal chest x-ray, except for the main-stem bronchi, because they have thin walls, contain air, and are surrounded by air in the alveoli (two structures of the same density). If water surrounds the bronchi, as in pneumonia and pulmonary edema, then the bronchi filled with air are in contrast to the water density and are visible.

Visualization of the trachea and major bronchi

Figure 10-8. Air bronchogram. (From: Yale School of Medicine/Wikimedia Commons.)

Pulmonary angiograms are one of the most sensitive tools for diagnosis of pulmonary emboli. A catheter is advanced into the pulmonary artery and contrast material is injected during rapid filming. Emboli appear as filling defects, or dark circumscribed areas, within the white vascular images of the artery. The invasive nature of this diagnostic test, coupled with potential reactions to the contrast material, restricts its use. As a result, the use of computed tomography of the pulmonary arteries (CTPA) is quickly replacing pulmonary angiograms as the gold standard for detecting PE. Computed tomography of the pulmonary arteries is a less invasive but very specific method of diagnosing a PE. The CTPA only requires a peripheral line through which to inject the contrast material. Similar to the pulmonary angiogram, defects may be readily seen in the pulmonary artery and the study can be done very quickly. This technology is not available in all institutions; however, it is quickly emerging as the diagnostic choice and gold standard for PE detection.

SPECIAL ASSESSMENT TECHNIQUES, DIAGNOSTIC TESTS, AND MONITORING SYSTEMS 269

Some still use ventilation-perfusion (V/Q) scans to diagnose a PE, although they are also being rapidly replaced by the CTPA. A V/Q scan is a nuclear medicine diagnostic tool that requires medical isotopes to be inhaled or injected in order to view the lungs and pulmonary arteries respectively. Generally the perfusion (or blood circulation) part of the test is done first. If there is no defect detected, the scan is read as “low probability.” If the scan detects a defect, then the inhaled (ventilation) portion of the test is done. If no matching defect is seen in the lung, the test is interpreted as “high probability.” But if a “matched defect” is noted (ie, there is a defect in the lung scan that corresponds with that of the perfusion scan), then the interpretation is “indeterminate” or “matched defect.” This may be the result of an atelectasis, pneumonia, or other infiltrate where circulation to that inactive area of the lung is redistributed to other active areas, thus resulting in a “matched defect.” In addition to the cumbersome nature of the V/Q scan, the critically ill patient may require both tests (perfusion and ventilation) rather than just one and the diagnostic yield is often poor.

From patient Vent

A Water-seal

Drainage collection

To wall suction

From patient

Chest Tubes Chest tubes are commonly used in critically ill patients to drain air, blood, or fluid from the pleural spaces (pleural chest tubes) or from the mediastinum (mediastinal tubes). Indications for chest tube insertion are varied (Table 10-4), with no contraindications to chest tube insertion because the need to restore lung function supersedes any potential complications associated with insertion. Pleural tube insertion sites vary based on the type of drainage to be removed (air: second ICS, midclavicular line; fluid: fifth or sixth ICS, midaxillary line). Mediastinal tubes are placed during surgery, exiting from the mediastinum below the xiphoid process. Type of chest tube insertions include tube thoracostomy (traditional rigid tubes) or smaller percutaneously inserted catheters (pigtails). TABLE 10-4. INDICATIONS FOR CHEST TUBE INSERTION Pneumothorax • Open: Both chest wall and pleural spaces are penetrated. • Closed: Pleural space is penetrated with an intact chest wall, allowing air to enter the pleural space from the lungs. • Tension: Air leaks into the pleural space through a tear in the lungs, with no means to escape the space, leading to lung collapse. Hemothorax Hemopneumothorax Thoracostomy Pyothorax or empyema Chylothorax Cholothorax Hydrothorax Pleural effusion Special Applications • Installation of anesthetic or sclerosing agent Adapted from: Lusardi PA, Scott SS, Scott F. Chest Tube Placement (Perform). In Wiegand Dl, ed. AACN Procedure Manual for Critical Care. 6th ed. Philadelphia, PA: Saunders 2011.

B Suction

Drainage Water-seal

Figure 10-9. Two-bottle chest drainage system. (A) Drainage collection bottle

and a water-seal bottle. (B) Water-seal/drainage collection bottle and suction control bottle. (Reprinted from: Luce JM, Tyler ML, Peirson DJ. Intensive Respiratory Care. Philadelphia, PA: WB Saunders; 1984:164, with permission from Elsevier.)

Following insertion, chest tubes are connected to a closed drainage collection system which uses gravity or suction to restore negative pressure in the pleural space and facilitate drainage of fluids or air (Figure 10-9). A Heimlich flutter valve is an alternative to the closed drainage system and consists of a one-way valve that allows air or drainage to collect in a vented drain bag (Figure 10-10). The PleurX catheter also has a one-way valve and connects as needed to a drainage system (Figure 10-11). Patients may be discharged home with either a Heimlich flutter valve or PleurX catheter for long-term use. Connections to the drainage system must be airtight and secure for proper functioning and to prevent inadvertent entry of air into the pleural space (Figure 10-12). Patency of the system is ensured by avoiding kinking of the drainage tubing, periodic inspection of the tubing for visible clot formation, and gentle squeezing of the tubing between the thumb and index finger. Removal of the chest tube occurs when restoration of lung expansion and fluid or air removal has been accomplished and the underlying lung abnormality has been resolved or corrected. An occlusive dressing at the chest

270

CHAPTER 10. Respiratory System

Positioning

• It was once taught that optimal patient ventilation and perfusion matching would be improved and should be prioritized with the “good lung” positioned in the dependent position. While blood flow is improved to the dependent lung, patients require frequent repositioning side-to-side to prevent atelectasis and other complications. • Early ambulation and sitting at the bedside or in a chair improves diaphragmatic excursion, enhancing ventilation and maximum inflation. • Deep breathing and use of incentive spirometry are encouraged regularly. These activities both help promote lung re-expansion of collapsed lung tissue and prevent atelectasis.

Cut off bevel here

PATHOLOGIC CONDITIONS Acute Respiratory Failure

C Tubing in bag D Drainage bag

Figure 10-10. Heimlich chest drain valve with connection to drain bag. (From: BD Medical Systems, Franklin Lakes, NJ.)

tube removal site is typically used to prevent introduction of air into the pleural space until the skin has formed a protective seal. Analgesic administration is appropriate prior to removal; discomfort associated with removal is often as much or even greater than during insertion.

Thoracic Surgery and Procedures Thoracic surgery and procedures are terms inclusive of a number of procedures involving the thoracic cavity and the lungs. See Table 10-5 for definitions and indications.

Principles of Management for Thoracic Surgery and Procedures Management of the patient after lung surgery or post procedure is similar to the patient with trauma to the chest. Refer to the section on thoracic trauma in Chapter 17, Trauma, with the following additions: Pain Control

The thoracotomy incision is one of the most painful surgical incisions and pain control is an important factor in recovery and prevention of respiratory complications. The routine use of epidural catheters, intercostal blocks, intrapleural local anesthetic administration, or PCA narcotics has improved pain management significantly. Relaxation therapy, deep breathing exercises, and guided imagery may also be effective in helping to reduce pain and anxiety.

Each of the case studies below represents a common situation in a critical care unit—respiratory dysfunction. This rapid onset of respiratory impairment, which is severe enough to cause potential or actual morbidity or mortality if untreated, is termed acute respiratory failure (ARF). Although the origin of the respiratory failure may be a medical or surgical problem, the management approaches share similar features. Acute respiratory failure is a change in respiratory gas exchange (CO2 and O2) such that normal cellular function is jeopardized. ARF is defined as a Pao2 less than 60 mm Hg and Paco2 greater than 50 mm Hg with a pH less than or equal to 7.30. Actual Pao2 and Paco2 values that define ARF vary, depending on a variety of factors that influence the patient’s normal (or baseline) arterial blood gas values. Factors such as age, altitude, chronic cardiopulmonary disease, or metabolic disturbances may alter the “normal” blood gas values for an individual, requiring an adjustment to the classic definition of ARF; for example, if Paco2 levels in a 75-year-old man with COPD are normally 56 mm Hg, ARF would not be diagnosed until pH is less than or equal to 7.30. Etiology, Risk Factors, and Pathophysiology

Many abnormalities can lead to ARF (Table 10-6). Regardless of the specific underlying cause, the pathophysiology of ARF can be organized into four main components: impaired ventilation, impaired gas exchange, airway obstruction, and ventilation-perfusion abnormalities. Impaired Ventilation

Conditions that disrupt the muscles of respiration or their neurologic control can impair ventilation and lead to ARF (see Table 10-6). Decreased or absent respiratory muscle movement may be due to fatigue from excessive use, atrophy from disuse, inflammation of nerves, nerve damage (eg, surgical damage to the vagus nerve during cardiac surgery), neurologic depression, progressive disease states such as

PATHOLOGIC CONDITIONS 271

Procedure Pack

Vacuum Bottle with Drainage Line

Blue Wrapping around the following: Gloves Green Vacuum Indicator

White Slide Clamp

Access Tip Cover

Catheter Valve Cap

Blue Emergency Slide Clamp

500 ml Plastic Vacuum Bottle

Access Tip

Gauze Pads

Drainage Line

Foam Catheter Pad

Pinch Clamp

Self-Adhesive Dressing

Alcohol Pads

Figure 10-11. Components of a pleurx drainage kit. (From Elsevier: Baker EM, Melander S. Management of recurrent pleural effusions with a tunneled catheter. Heart Lung. 2010;39:314-318.)

Guillian-Barré or amyotrophic lateral sclerosis (ALS), or following administration of neuromuscular blocking agents. Impaired respiratory muscle movement decreases movement of gas into the lungs, resulting in alveolar hypoventilation. Inadequate alveolar ventilation causes retention of CO2 and hypoxemia. Impaired Gas Exchange

Conditions that damage the alveolar-capillary membrane impair gas exchange. Direct damage to the cells lining the

alveoli may be caused by inhalation of toxic substances (gases or gastric contents), pneumonia, and/or other pulmonary conditions leading to two detrimental alveolar changes. The first is an increase in alveolar permeability, increasing the potential for interstitial fluid to leak into the alveoli and causing noncardiac pulmonary edema (Figure 10-13A). The second alveolar change is a decrease in surfactant production by alveolar type II cells, increasing alveolar surface tension, which leads to alveolar collapse (Figure 10-13B).

272

CHAPTER 10. Respiratory System

Tape strips

Unobstructed view of connection

Parham band

Figure 10-12. Methods for securing connections of chest tube and drainage

system. (A) Tape. (B) Parham bands. (Reprinted from: Kersten LD. Comprehensive Respiratory Nursing: A Decision-Making Approach. Philadelphia, PA: WB Saunders; 1989:783, with permission from Elsevier.)

Another cause of impaired gas exchange occurs when fluid leaks from the intravascular space into the pulmonary interstitial space (Figure 10-13C). The excess fluid increases the distance between the alveolus and the capillary, decreasing the efficiency of the gas exchange process. Interstitial edema also compresses the bronchial airways, which are surrounded by interstitial tissue, causing bronchoconstriction. Capillary leakage may occur when pressures within the cardiovascular system are excessively high (eg, in heart failure) or when pathologic conditions elsewhere in the body release

TABLE 10-6. CAUSES OF ACUTE RESPIRATORY FAILURE IN ADULT Impaired Ventilation • Spinal cord injury (C4 or higher) • Phrenic nerve damage • Neuromuscular blockade • Guillain-Barré syndrome • CNS depression • Drug overdoses (narcotics, sedatives, illicit drugs) • Increased intracranial pressure • Anesthetic agents • Respiratory muscle fatigue Impaired Gas Exchange • Pulmonary edema • ARDS • Aspiration pneumonia Airway Obstruction • Aspiration of foreign body • Thoracic tumors • Asthma • Bronchitis • Pneumonia Ventilation-Perfusion Abnormalities • Pulmonary embolism • Emphysema Alveolus

Fluid

Interstitial space Capillary

TABLE 10-5. THORACIC SURGERY AND PROCEDURES

Leakage of fluid into alveolus Alveolus

Definitions Thoracic Surgery Pneumonectomy Lobectomy Wedge resection Segmental resection Bullectomy Lung volume reduction surgery (LVRS) Open lung biopsy Decortication Video-assisted thoracic surgery (VATS) Procedure Pulmonary stent

Bronchoscopy (rigid or flexible)

Removal of entire lung Resection of one or more lobes of the lung Removal of small wedge-shaped section of lung tissue Removal of bronchovascular segment of the lung lobe Resection of emphysematous bullae Resection of diseased and functionless lung tissue Resection of portion of lung for biopsy through a thoracotomy incision Surgical removal of pleural fibrous tissue and pus from pleural space Endoscopic procedure through small incision Device(s) placed by flexible or rigid bronchoscopes to keep airways open in the central tracheobronchial tree Invasive procedure used to visualize the oropharynx, larynx, vocal cords, and tracheal bronchial tree for diagnosis and treatment

Interstitial space

Capillary B

Atelectasis Alveolus

Interstitial space

Capillary C

Interstitial Edema

Figure 10-13. Pathophysiologic processes in ARF that impair gas exchange. (A) Increased alveolar membrane permeability. (B) Alveolar collapse from decreased surfactant production. (C) Increased capillary membrane permeability and interstitial edema.

PATHOLOGIC CONDITIONS 273

Essential Content Case

Motor Vehicle Accident A 22-year-old man was admitted to the surgical ICU following a motor vehicle accident in which he suffered blunt chest trauma and a concussion. During his second day in the unit, his arterial blood gases began deteriorating (decreases in Pao2, increases in Paco2), and he required increasing amounts of supplemental oxygen to maintain Pao2 levels of greater than 60 mm Hg. He was dyspneic, restless, and somewhat agitated. He verbalized a fear of impending death. Admission RR 24 breaths/min Chest x-ray clear ABGs 40% Fio2 40% Pao2 120 mm Hg Paco2 33 mm Hg pH 7.42 HCO3 24 mEq/L

Day 2 34 breaths/min bilateral diffuse infiltrates by 100% non-rebreather mask 100% non-rebreather mask 58 mm Hg 50 mm Hg 7.35 27 mEq/L

Case Question 1. What signs and symptoms of ARF is this patient exhibiting? Case Question 2. What intervention do you next anticipate based on his arterial blood gases? Answers: 1. Signs and symptoms include dyspnea, restless, agitated, fear of impending death, and hypoxemia despite increasing Fio2 to 100% non-rebreather mask. 2. Intubate and initiate mechanical ventilation to improve hypoxemia along with analgesia and sedation. Patient has known bilateral diffuse infiltrates by chest x-ray. See next section on Acute Respiratory Distress Syndrome.

Essential Content Case

Postanesthesia A woman was directly admitted to the surgical ICU following thoracic surgery for the removal of a malignant tumor of the right upper lobe. She was intubated and being changed over from the transport ventilator to the ICU ventilator by respiratory therapy. A right pleural chest tube was draining minimal amounts of blood, with no evidence of air leaks or obstructions. The patient was unresponsive to verbal and pain stimulation on admission. No spontaneous respirations were noted on the ventilator respiratory waveform screen or by physical assessment. Fifteen minutes after arrival to the unit (SIMV of 10 breaths/min, tidal volume of 10 mL/ kg, PEEP of 5 cm H2O, 0.40 Fio2), ABGs were: 145 mm Hg Pao2 Paco2 41 mm Hg pH 7.38 HCO3 24 mEq/L

Case Question 1. What ventilator changes do you anticipate will be made? Case Question 2. What missing assessment items in report from anesthesia do you need to continue to care for this patient? Answers 1. Patient is oxygenating adequately with Pao2 of 145 mm Hg and Fio2 should be titrated down to maintain a Pao2 goal of 60-70 mm Hg. 2. Since the patient is unresponsive without spontaneous respirations, additional history is obtained from anesthesia regarding anesthetic agents used, analgesia, and sedation use in the operating room, and any use of neuromuscular blocking agents. Assessment for an acute neurological event also needs to be considered.

biochemical substances (eg, serotonin, endotoxin) that increase capillary permeability. Airway Obstruction

Conditions that obstruct airways increase resistance to airflow into the lungs, causing alveolar hypoventilation and decreased gas exchange (Figure 10-14). Airway obstructions can be due to conditions that: (1) block the inner airway lumen (eg, excessive secretions or fluid in the airways, inhaled foreign bodies) (Figure 10-14A), (2) increase airway wall thickness (eg, edema or fibrosis) or decrease airway circumference (eg, bronchoconstriction) as occurs in asthma (Figure 10-14B), or (3) increase peribronchial compression of the airway (eg, enlarged lymph nodes, interstitial edema, tumors) (Figure 10-14C). Ventilation-Perfusion Abnormalities

Conditions disrupting alveolar ventilation or capillary perfusion lead to an imbalance in ventilation and perfusion. This decreases the efficiency of the respiratory gas exchange process (Figure 10-15A). In an effort to keep the ventilation and perfusion ratios balanced, two compensatory changes occur: (1) to avoid wasted alveolar ventilation when capillary perfusion is decreased (eg, with pulmonary embolism [PE]), alveolar collapse occurs to limit ventilation to alveoli with poor or absent capillary perfusion (Figure 10-15B); (2) to avoid capillary perfusion of alveoli that are not adequately ventilated (eg, with atelectasis), arteriole constriction (ie, hypoxic vasoconstriction) occurs and shunts blood away from hypoventilated

Figure 10-14. Mechanism of airway obstruction. (A) Fluid secretions present

within airway. (B) Intraluminal edema narrowing airway diameter. (C) Peribronchial compression of airway.

274

CHAPTER 10. Respiratory System

Air

Alveolus Oxygenated blood O2

CO2

Capillary A Blockage Unoxygenated blood

B Air

• Confusion • Diaphoresis • Anxiety • Hypercarbia (Paco2 >50 mm Hg) • Hypertension • Irritability • Somnolence (late) • Cyanosis (late) • Loss of consciousness (late) • Pallor or cyanosis of skin • Use of accessory muscles of respiration • Abnormal breath sounds (crackles, wheezes) • Manifestations of primary disease (see description of individual diseases below) Diagnostic Tests

• Arterial blood gases—Pao2 less than 60 mm Hg and Paco2 more than 50 mm Hg; with pH less than or equal to 7.30 or Pao2 and Paco2 in abnormal range for that individual • Tests specific to underlying cause (see description of individual diseases below) Principles of Management for Acute Respiratory Failure

Blockage

Figure 10-15. Pathophysiologic processes in ARF from ventilation-perfusion abnormalities. (A) Normal ventilation and perfusion relationship. (B) Decreased ventilation and normal perfusion. (C) Normal ventilation and decreased perfusion.

alveoli to normally ventilated alveoli (Figure 10-15C). As the number of alveolar–capillary units affected by these compensatory changes increases, gas exchange eventually is affected negatively. Each of these pathophysiologic changes results in inadequate CO2 removal, O2 absorption, or both. The severity of ARF can be further increased when anxiety and fear of impending death develop, a common consequence of severe dyspnea and hypoxemia. These symptoms increase oxygen demands and the work of breathing, further compromising O2 availability for crucial organ function and depleting respiratory muscle strength. Clinical Presentation Signs and Symptoms

• Hypoxemia (Pao2 40 breaths/min) • Intercostal retractions • Copious secretions • Panic, fear of impending death • Crackles and/or wheezes Diagnostic Tests

• Chest x-ray shows diffuse, bilateral pulmonary infiltrates without increased cardiac size

• Pao2/Fio2 less than or equal to 300 mm Hg • Static compliance (tidal volume/inspiratory plateau pressure PEEP) less than 40 mL/cm H2O Principles of Management for ARDS

Much of the management of ARDS relies on supportive care and the prevention of complications. To date, interventions to limit the disease progression or reverse the underlying structural defects are not known. Improving Oxygenation and Ventilation

Interventions specific to ARDS to improve oxygenation and ventilation include the following: 1. Administer high Fio2 levels with high-flow system or rebreathing mask. A constant positive airway pressure (CPAP) mask may be tolerated in alert, cooperative patients. Continuous, vigilant monitoring for contraindications of noninvasive CPAP (decreased loss of consciousness, nausea/vomiting, increased dyspnea or panic) is imperative. 2. Intubation and mechanical ventilation if cardiovascular instability is present, severe hypoxemia persists, or if fatigue develops. – Oxygen support at high Fio2 levels with PEEP is usually required to achieve an acceptable Pao 2 (> 50 mm Hg) without hemodynamic compromise. Decreasing Fio2 levels to less than 0.6 once Pao2 of greater than 50 mm Hg is a primary goal. – Decrease work of breathing initially by using ventilator modes and ventilator rates to decrease respiratory effort by the patient. – Prevent “volu-trauma.” Studies have demonstrated that large tidal volumes (which contribute to high plateau pressures) cause damage to the alveoli if used for prolonged periods (48 hours) in patients with ARDS. The use of small tidal volumes (6ml/kg lean body weight) is indicated. These low volumes correlate with normal plateau pressures of 30 cm H2O or less. 3. Sedation and analgesia may be necessary after intubation to maximize gas exchange and minimize oxygen consumption. “Patient/ventilator dyssynchrony” is a common complication of ventilatory support in the severely dyspneic, hypoxemic patient. 4. Short term use of neuromuscular blockade when used early in severe ARDS may improve long-term outcomes. This early and brief use of paralytics is thought to decrease lung and systemic inflammation along with alveolar collapse or over distention. Sedation is required prior to and for the duration of neuromuscular blockade. (See Chapter 6: Pain, Sedation, and Neuromuscular Blockade Management for additional information.) 5. While transfusions may improve oxygen-carrying capacity, evidence has shown that transfusion itself

PATHOLOGIC CONDITIONS 277

is a cause of ARDS and increases the risk of mortality (TRALI-transfusion related acute lung injury). Transfusions should be reserved for hemoglobin below 7 g/dl unless underlying cardiac disease exists. 6. Enteral is the preferred route of nutrition and may help decrease bacterial translocation across the gut along with benefits of gastric prophylaxis for gastrointestinal bleeding (Chapter 14, Gastrointestinal System). 7. Data on prone positioning has suggested that mortality in patients with severe ARDS (Pao2/Fio2 ratio < 100 mm Hg) may be reduced. Ventilation in the prone position recruits atelectatic regions of the lungs without increasing airway pressure. Reducing Anxiety

Same as previously described for ARF management. Achieving Effective Communications

Refer to Chapter 5: Airway and Ventilatory Management for detailed discussion of communication techniques for intubated patients. Maintaining Hemodynamic Stability and Adequate Perfusion

1. Minimize cardiovascular instability by careful hemodynamic monitoring during PEEP therapy; conservative fluid management is recommended. 2. Vasoactive drugs may be required to maintain adequate perfusion. Preventing Complications

In addition to complications listed for ARF: 1. ARDS patients are at higher risk for development of hospital-acquired pneumonias. Follow prevention strategies delineated for hospital-acquired pneumonias described later in the chapter. Prophylactic antibiotics have not been shown to decrease hospital-acquired pneumonia rates in ARDS patients. Meticulous attention to head of bed elevation, hand washing, and removal of invasive devices as soon as possible are key prevention strategies. 2. The incidence of barotrauma, volutrauma, PE, GI bleeding, and electrolyte disorders is particularly high in patients with ARDS.

Acute Respiratory Failure in the Patient with Chronic Obstructive Pulmonary Disease Individuals with COPD are at high risk for the development of ARF due to progressive airflow limitation with chronic inflammatory airway and lung response. Altered host defenses, increased secretion volume and viscosity, impaired secretion clearance and airway changes, and common pathophysiologic changes predispose the patient with COPD to acute exacerbations or episodes of ARF. The etiology, clinical presentation, and management of ARF in the COPD patient

varies somewhat from ARF without chronic underlying pulmonary dysfunction. This section of the chapter highlights differences in ARF management in the patient with underlying COPD. Etiology, Risk Factors, and Pathophysiology

Any systemic or pulmonary illness can precipitate ARF in patients with COPD. In addition to the etiologies of ARF listed in Table 10-5, diseases or situations that decrease ventilatory drive, muscle strength, chest wall elasticity, or gas exchange capacity, or increase airway resistance or metabolic oxygen requirements can easily lead to ARF in patients with COPD (Table 10-8). The most common precipitating events include • Airway infection (pneumonia, bronchitis): Frequent antibiotic administration, hospitalization, and impaired cough and host defenses in COPD increase acute airway infections. Infections are commonly caused by gram-negative enteric bacteria or Legionella, with Haemophilus influenzae and Streptococcus pneumoniae causing acute bronchitis. Moraxella catarrhalis is also a common respiratory organism causing infection in these patients.

TABLE 10-8. PRECIPITATING EVENTS OF ACUTE RESPIRATORY FAILURE IN COPD Decreased Ventilatory Drive • Oversedation • Hypothyroidism • Brain stem lesions Decreased Muscle Strength • Malnutrition • Shock • Myopathies • Hypophosphatemia • Hypomagnesemia • Hypocalcemia Decreased Chest Wall Elasticity • Rib fractures • Pleural effusions • Ileus • Ascites Decreased Lung Capacity for Gas Exchange • Atelectasis • Pulmonary edema • Pneumonia • Pulmonary embolus • Heart failure Increased Airway Resistance • Bronchospasm • Increased secretions • Upper airway obstructions • Airway edema Increased Metabolic Oxygen Requirements • Systemic infection • Hyperthyroidism • Fever

278

CHAPTER 10. Respiratory System

• Pulmonary embolus: The high incidence of right ventricular failure in COPD increases the risk of pulmonary embolus from right ventricular mural thrombi. • Heart failure: In the presence of pulmonary hypertension and right-sided heart failure, treatment of leftsided heart failure is often delayed due to difficulties in early diagnosis. • Nonadherence with medication regime: The complicated treatment regime for management of COPD, which includes frequent administration of both oral and inhaled agents, frequently leads to underuse of medications. The development of ARF in COPD patients places a tremendous burden on the pulmonary system. The chronic disease process leads to impairment of ventilation, poor gas exchange, and airway obstruction. The additional burden of an acute disease process, even a relatively minor one, further impairs ventilation and gas exchange and increases airway obstruction. Compensatory mechanisms can easily be overwhelmed, with lethal consequences. Clinical Presentation

Signs and symptoms are similar to ARF, but usually more pronounced. Diagnostic Tests

• Chest x-ray: Evidence of COPD (flat diaphragms, hyperinflation of air fields), in addition to x-ray findings specific to the cause of the ARF. (See Figure 10-3.) • Arterial blood gases: Paco2 greater than 50 mm Hg and higher than baseline levels during stable, chronic disease periods. Principles of Management for ARF in Patients with COPD

The presence of chronic respiratory dysfunction and an acute respiratory problem leads to some changes in the typical management of ARF. Treating the Underlying Disease State

Treatment is directed at both the acute precipitating event and the chronic airflow obstruction problems associated with COPD. 1. Increase airway diameter with bronchodilators and reduce airway edema with corticosteroids. Betaadrenergic and anticholinergic agents are often used concurrently (Table 10-9). Higher than usual doses may be necessary until the precipitating event is resolved. Systemic corticosteroids are used to decrease airway inflammation and thus bronchospasm. The steroids may also enhance secretion clearance. 2. Treat pulmonary infections with appropriate antibiotics. 3. Improve secretion removal. Strategies to improve secretion removal include adequate hydration,

TABLE 10-9. BRONCHODILATOR CATEGORIES Category Beta-agonists (short-acting) (goal is beta2 specificity) Beta-agonists (long-acting) Anticholinergics Combination beta-agonist (short-acting) and anticholinergic Methylxanthines

Examples Albuterol, beta2-specific (often given as a continuous aerosol treatment) Epinephrine (beta1 and beta2) Salmeterol Ipratropium bromide Glycopyrrolate Albuterol and ipratropium bromide Aminophylline

coughing, heated moist aerosolization, and mobilization. The routine use of chest physiotherapy has not been shown to be supported by the literature and is not recommended. Secretions may be thick and tenacious. Monitor response to these therapies and discontinue them if no additional benefits are observed. Improving Oxygenation and Ventilation

Correction of hypoxemia is done by small increases in Fio2 levels, preferably with a controlled O2 delivery device such as a Venturi mask, biphasic intermittent positive airway pressure (BIPAP), or CPAP. Frequent monitoring of arterial blood gases is essential to ensure adequate arterial oxygenation (Pao2 of 55-60 mm Hg or baseline values during nonacute situations) without significantly increasing Paco2 levels. The administration of oxygen to COPD patients was once felt to eliminate the “hypoxic drive,” putting the patient at risk for hypercarbia, acidosis, and death. This drive is responsible for approximately 10% of the total drive to breathe. Oxygen should never be withheld and is essential to prevent further deleterious effects of hypoxia and potential organ failure. While it is correct that higher than necessary Fio2 levels may increase Paco2, this effect occurs by three physiologic mechanisms: • The Haldane effect: As hemoglobin becomes desaturated with oxygen, the affinity for carbon dioxide increases. The administration of oxygen then displaces carbon dioxide on hemoglobin and increases carbon dioxide levels in the plasma. Patients with COPD are unable to increase minute ventilation or “blow off ” carbon dioxide. This leads to an increase in carbon dioxide, lowering the pH and resulting in a respiratory acidosis. • Hypoxic vasoconstriction: This physiologic adaptive mechanism is a response to a decrease in alveolar oxygen and moves capillary blood flow from a closed or atelectatic alveolus to an open alveolus. In patients with COPD, this adaptive mechanism no longer occurs. As a result, dead space ventilation or decreased perfusion (Figure 10-15C) occurs with resulting increased carbon dioxide levels.

PATHOLOGIC CONDITIONS 279

• Decreased minute ventilation: As a result of increased dead space ventilation with resulting increased carbon dioxide, some COPD patients will decrease their minute ventilation. This decrease will further limit the patient’s inspiratory reserve capacity. Oxygen administration in COPD patients is necessary to prevent hypoxia and organ failure and should never be withheld. Titration and considerations for mechanical ventilation in the COPD patient with CO2 retention (Paco2 > 50 mm Hg) should be guided by the pH and Paco2 (Figure 10-16). Position the patient to maximize ventilatory efforts and relaxation/rest during spontaneous breathing. A high Fowler position and leaning on an overbed table may be a position of comfort prior to intubation and mechanical ventilation. Relaxation techniques and diaphragmatic, pursed lip breathing may be helpful to decrease anxiety and improve

ventilatory patterns. Anxiolytics and other sedatives should be used cautiously to avoid decreasing MV. COPD patients with ARF may benefit from early use of noninvasive mechanical ventilation. The decision to intubate and mechanically ventilate the patient is based primarily on the deterioration of mental status, coupled with knowledge of the patient’s baseline pulmonary function and functional status, and the reversibility of the underlying cause. Weaning from mechanical ventilation is frequently more difficult, and in some cases not possible, in the presence of COPD. Informed discussions with the patient and family regarding intubation options should be undertaken. The presence of an advanced directive and power of attorney designee for healthcare decisions can help guide clinician’s actions when patients are unable to make treatment decisions themselves (see Chapter 8: Ethical and Legal Considerations).

Assess patient, obtain ABG, begin oxygen

Assure PaO2 >60 mm Hg Adjust O2 to SaO2 >90%

Hypercapnia? (PaCO2 >50 mm Hg)

Yes

pH 60 mm Hg)

No change in oxygen setting

Yes

No Maintain O2 SaO2 >90%

Reassess ABG in 1-2 hours

Hypercapnia? (PaCO2 >50 mm Hg) No Maintain O2 SaO2 >90%

Yes

Reassess ABG in 2 hours

pH 60 mm Hg)

Yes

Consider mechanical ventilation, NPPV, or intubation

Yes No change in oxygen setting

Figure 10-16. Algorithm to correct hypoxemia in an acutely ill COPD patient. ABG: arterial blood gas; NPPV: noninvasive positive pressure ventilation; O2: oxygen; Paco2: arterial carbon dioxide tension; Pao2: arterial oxygen tension; Sao2: arterial oxygen saturation. (From: American Thoracic Society and European Respiratory Society. Standards for the diagnosis and management of patients with COPD. 2004;183. http://www.thoracic.org/sections/copd/resources. Accessed December 11, 2009.)

280

CHAPTER 10. Respiratory System

Ventilatory management of COPD patients differs from other ARF conditions in that slow correction of hypercarbia should be done to avoid life-threatening alkalemia. This is because they generally have a higher than normal bicarbonate level secondary to the long-term metabolic compensation of the kidneys. CO2 can be quickly decreased with mechanical ventilation resulting in an even higher alkalemia. The development of auto-PEEP and barotrauma is increased in patients with COPD, necessitating smaller tidal volumes, lower respiratory rates, short inspiratory times, and long expiratory times. Nutritional Support

Typically, patients with COPD have protein-calorie malnutrition, as well as low levels of phosphate, magnesium, and calcium. These chronic nutritional deficits lead to muscle weakness and may interfere with the weaning process. Early enteral feeding of these patients is essential to avoid further deterioration in their nutritional status during acute illness and should be initiated as soon as hemodynamically stable. Enteral feeding is preferred over parenteral nutrition due to decreased risk of infectious complications. COPD patients who are malnourished have greater air trapping, lower diffusing capacity, and less able to mobilize (see Chapter 14: Gastrointestinal System). Preventing and Managing Complications

In addition to the complications associated with ARF, the following complications commonly are observed in COPD patients with ARF: • Arrhythmia: High incidence of both atrial and ventricular arrhythmia in patients with COPD due to hypoxemia, acidosis, heart disease, medications, and electrolyte abnormalities. Cardiac monitoring and correction of the underlying cause is the goal, with pharmacologic treatment of arrhythmia only for lifethreatening situations. • Pulmonary embolus: High incidence. Observe for signs and symptoms and follow the usual treatment and prevention guidelines. • GI distention and ileus: Aerophagia is common in dyspneic patients, increasing the incidence of this complication. • Auto-PEEP and barotraumas (if ventilated): High incidence, especially in the elderly and in individuals with high ventilation needs.

Acute Respiratory Failure in the Patient with Asthma (also called acute severe asthma) Individuals with asthma are at risk for exacerbations that are characterized by a progressive increase in shortness of breath, cough, wheezing, or decrease in expiratory airflow. Acute asthma, status asthmaticus, and asthma attack are also terms that have been used to describe this condition. Asthma differs from COPD in both pathophysiology, and therapeutic

response and the airway restriction is usually reversible with aggressive treatment (Figure 10-17). Etiology, Risk Factors, and Pathophysiology

Asthma exacerbations are first and foremost due to uncontrolled airway inflammation. The pathology results in the severe bronchospasm and increased mucus production present during asthma “attacks,” both of which contribute to the overall airway obstruction. Triggers vary and include infection, inhaled seasonal antigens, foods, exercise, or medications to name just a few. While triggers may stimulate an exacerbation of asthma, they are not causal. Bronchoconstriction results from mediator release from mast cells and include histamine, prostaglandins, and leukotrienes that contract the smooth muscle. Mucus plugging is thought to be due to eosinophil and shed bronchial epithelial cells as well as impaired mucus transport. Additionally, over time some patients may exhibit airway remodeling (thickening that contributes to airflow narrowing and airflow obstruction) especially if their airway inflammation is not controlled. All of these contribute to the severe and often unrelenting nature of the asthma “attack.” Some risk factors for the development of an acute severe asthma episode include frequent need for use of their “rescue” inhalers, recent illness, frequent past emergency room visits or hospitalizations, prior intubations and ICU admissions, noncompliance with medical therapy, and inadequate access to healthcare. Clinical Presentation

Clinical findings are related to severe airflow obstruction and may include the inability to say a whole sentence, shortness of breath, wheezing, pulsus paradoxus, use of accessory muscles of inspiration, diaphoresis, and need to maintain upright position. However, peak flow measurement is one of the best assessment tools for determining the severity of the exacerbation. An absolute peak flow measurement of < 100 L/min in an adult generally indicates severe bronchoconstriction especially in combination with failure to respond to aggressive bronchodilator treatments. These patients are generally admitted to a critical care unit for monitoring and aggressive therapy (see Figure 10-17). Diagnostic Tests

• Arterial blood gases: Initial findings may show pH greater than 7.45, Paco2 less than 35 mm Hg, and mild to moderate hypoxia (respiratory alkalosis). In severe airflow obstruction, findings may progress to pH less than 7.35 and Paco2 greater than 50 mm Hg (metabolic acidosis). • Pulsus paradoxus: A decrease of greater than 10 mm Hg in systolic blood pressure during inspiration. • Pulmonary function tests: FEV1 of less than 20% or peak expiratory flow rate (PEFR) of less than 40% of predicted despite aggressive bronchodilator therapy. • Spo2: Observe for hypoxia. The Spo2 should be greater than 92%.

PATHOLOGIC CONDITIONS 281

Initial Assessment • History, physical examination (auscultation, use of accessory muscles, heart rate, respiratory rate, PEF or FEV1, oxygen saturation, arterial blood gas if patient in extremis) Initial Treatment • Oxygen to achieve O2 saturation ≥ 90% (95% in children) • Inhaled rapid-acting β2-agonist continuously for 1 hour. • Systemic glucocorticosteroids if no immediate response, or if patient recently took oral glucocorticosteroid, or if episode is severe. • Sedation is contraindicated in the treatment of an exacerbation.

Reassess after 1 Hour Physical Examination, PEF, O2 saturation, and other tests as needed

Criteria for Moderate Episode: • PEF 60%-80% predicted/personal best • Physical exam: moderate symptoms, accessory muscle use Treatment: • Oxygen • Inhaled β2-agonist and inhaled anticholinergic every 60 min • Oral glucocorticosteroids • Continue treatment for 1-3 hours, provided there is improvement

Criteria for Severe Episode: • History of risk factors for near fatal asthma • PEF < 60% predicted/personal best • Physical exam: severe symptoms at rest, chest retraction • No improvement after initial treatment Treatment: • Oxygen • Inhaled β2-agonist and inhaled anticholinergic • Systemic glucocorticosteroids • Intravenous magnesium

Reassess after 1-2 Hours

Good Response within 1-2 Hours: • Response sustained 60 min after last treatment • Physical exam normal: No distress • PEF > 70% • O2 saturation > 90% (95% children)

Incomplete Response within 1-2 Hours: • Risk factors for near fatal asthma • Physical exam: mild to moderate signs • PEF < 60% • O2 saturation not improving Admit to Acute Care Setting • Oxygen • Inhaled β2-agonist ± anticholinergic • Systemic glucocorticosteroid • Intravenous magnesium • Monitor PEF, O2 saturation, pulse

Poor Response within 1-2 Hours: • Risk factors for near fatal asthma • Physical exam: symptoms severe, drowsiness, confusion • PEF < 30% • PCO2 > 45 mm Hg • P O2 < 60 mm Hg Admit to Intensive Care • Oxygen • Inhaled β2-agonist + anticholinergic • Intravenous glucocorticosteroids • Consider intravenous β2-agonist • Consider intravenous theophylline • Possible intubation and mechanical ventilation

Reassess at intervals Improved: Criteria for Discharge Home • PEF > 60% predicted/personal best • Sustained on oral/inhaled medication

Poor Response (see above): • Admit to lntensive Care

Home Treatment: • Continue inhaled β2-agonist • Consider, in most cases, oral glucocorticosteroids • Consider adding a combination inhaler Take medicine correctly • Patient education: Review action plan Close medical follow-up

Incomplete response in 6-12 hours (see above) • Consider admission to Intensive Care if no improvement within 6-12 hours Improved (see opposite)

Figure 10-17. Management of asthma exacerbations in acute care setting. From National Heart, Lung, and Blood Institute. Global Initiative for Asthma ([GINA], Global Strategy for Asthma Management and Prevention. 2013. http://www.ginasthma.org/uploads/users/files/GINA_Report_2012Feb13.pdf.)

282

CHAPTER 10. Respiratory System

Principles of Management for Asthma Exacerbations Same as previously described for principles of management in patients with exacerbation of COPD.

Principles of Management for Acute Severe Asthma Treat the Underlying Disease State

Treatment is directed at decreasing airway inflammation, reversal of airflow obstruction, and correction of hypercapnia or hypoxemia if present. 1. Reduce airway inflammation with edema with systemic corticosteroids and provide aggressive bronchodilation. Beta-2 specific bronchodilators (eg, albuterol) are the drug of choice and may be provided continuously by nebulizer through a mouthpiece, mask, or if ventilated, through the ventilator circuit. Concomitant use of anticholinergic bronchodilators is generally provided to enhance rapid reversal of bronchospasm. If bronchospasm is refractory to aggressive pharmacologic management (eg, beta-2 specific drugs and anticholinergics), subcutaneous epinephrine may be used. However, epinephrine should be avoided in adults except in extreme cases as it may precipitate heart attacks, especially in those with pre-existing cardiac disease. The use of magnesium sulfate is not supported in the literature although it is still sometimes used in patients with acute severe asthma. 2. Treat pulmonary infections with appropriate antibiotics. 3. Improve secretion removal. Generally secretions will be easier to mobilize as bronchodilation is enhanced. Until then, strategies are limited. Adequate hydration (generally provided parenterally) is important as the asthma patient is often dehydrated.

improve ventilatory patterns. Anxiolytics and other sedatives should not be given unless the patient is intubated. Studies have demonstrated that doing so increases the potential for death. The decision to intubate and mechanically ventilate the patient may be made urgently in patients who are failing to respond to treatment and are fatiguing. Ventilatory management of asthma patients focuses on restoring acid-base status and oxygenation while decreasing lung hyperinflation (known as dynamic hyperinflation in the spontaneously breathing patient and auto-PEEP in the mechanicallyventilated patient). The development of auto-PEEP is due to the inability of the patient to exhale totally with each breath. Auto-PEEP should be assumed in these patients and when possible monitoring of auto-PEEP and plateau pressure measurements should be done to assess the adequacy of pharmacologic and ventilator interventions. Low tidal volumes, low ventilator rates, short inspiratory times, and long expiratory times may help prevent hyperinflation. If this strategy is employed the patient may require sedatives and sometimes paralytics. Preventing and Managing Complications

Prevention and management are similar to ARF.

Pulmonary Hypertension Pulmonary hypertension is a progressive, life-threatening disorder of the pulmonary circulation characterized by high pulmonary artery pressures (> 25 mm Hg) leading from the right side of the heart to the lungs. This persistent high pulmonary artery pressure ultimately leads to right ventricular failure. Patients with PAH are often on a chronic regimen of therapy that should not be interrupted during hospitalization. Abrupt cessation of therapy can lead to rebound pulmonary hypertension that can be fatal. Etiology, Risk Factors, and Pathophysiology

Improving Oxygenation and Ventilation

Severe hypoxemia should be corrected by providing high Fio2 levels until an adequate oxygen saturation is obtained (90% or greater). Oxygen masks and high flow O 2 systems may be used to deliver oxygen. Mechanical ventilation may be necessary if the patient does not respond to more conservative methods. The use of non-invasive ventilation in an asthmatic is discouraged as it may lead to increased hyperinflation and respiratory failure. Frequent monitoring of arterial blood gases is essential to monitor pH and Paco2. Helium-oxygen (heliox) mixtures may be used to decrease the work of breathing and improve ventilation. Heliox can be administered via mask, or invasive ventilation. Due to high levels of helium in the heliox mixtures, the use of heliox may be limited in patients with high Fio2 requirements. Position the patient to maximize ventilatory efforts and relaxation/rest during spontaneous breathing. Relaxation techniques may be helpful to decrease anxiety and

Pulmonary hypertension may result from a number of etiologies (Table 10-10). The pathophysiology is multifactoral with evidence that endothelial dysfunction leads to remodeling of the pulmonary artery vessel wall causing exaggerated vasoconstriction and impaired vasodilatation. This results in decreased blood flow and return of deoxygenated blood to the lungs. Clinical Presentation

Signs and symptoms include pallor, dyspnea, fatigue, chest pain, and syncope. Cor pulmonale or enlargement of the right ventricle can be a result of pulmonary hypertension and may lead to right ventricular failure. The diagnostic strategy is related to both establishing the diagnosis of pulmonary hypertension and if possible the underlying cause. Diagnostic Tests

• Echocardiogram: Valvular heart disease, left ventricular dysfunction, and intracardiac shunts.

PATHOLOGIC CONDITIONS 283

TABLE 10-10. World Health Organization classification of pulmonary hypertensiona Group

Main classification

Diseases included

Pulmonary arterial hypertension (PAH)

PAH: Idiopathic, familial, associated with corrective tissue disease, associated with congenital heart disease, associated with HIV infection, associated with drugs or toxins

Pulmonary hypertension due to leftsided heart disease

Systolic dysfunction, diastolic dysfunction, valvular disease

Pulmonary hypertension due to lung disease and/or hypoxia

Chronic obstructive pulmonary disease, interstitial lung disease, mixed restrictive and obstructive pattern, sleep disordered breathing, alveolar hypoventilation disorders, chronic exposure to high altitude, developmental abnormalities

Chronic thromboembolic pulmonary hypertension

Chronic thromboembolic disease

Pulmonary hypertension with unclear multifactorial mechanisms

Hematologic disorders: myeloproliferative disorders, splenectomy; systemic disorders: sarcoidosis, pulmonary Langerhans cell histiocytosis: lymphangioleiomyomatosis, neurofibromatosis, vasculitis; metabolic disorders: glycogen storage disease, Gaucher disease, thyroid disorders; others: tumoral obstruction, fibrosing mediastinitis, chronic renal failure on dialysis

Revisions made at the 4th World Symposium on Pulmonary Hypertension held at Dana Point, California, in 2008. (Reproduced with permission from Poms A1, Kingman M: Inhaled treprostinil for the treatment of pulmonary arterial hypertension. Crit Care Nurse. 2011 Dec;31(6):e1-10.)

• Chest x-ray: Enlarged hilar and pulmonary arterial shadows and enlargement of the right ventricle. • 12-lead ECG: Right ventricular strain, right ventricular hypertrophy, and right axis deviation. • CTPA, ventilation-perfusion scan, or pulmonary angiogram: These are done to rule out thromboembolism. • CT chest: Assess for presence or absence of parenchymal lung disease. • 6-minute-walk test: Measurement of distance used to monitor exercise tolerance, response to therapy, and progression of disease. • Right-heart cardiac catheterization: Gold standard for diagnosis with vasodilator (adenosine, nitric oxide, epoprostenol) testing for benefit from long-term therapy with calcium channel blockers. Positive response is a decrease in mean PAP of 10 to 40 mm Hg with an increased or unchanged CO from baseline values. • Serology testing: Antinuclear antibodies. • Pulmonary function testing: Used to rule out any other diseases contributing to shortness of breath. • Sleep study: Done as a screen for sleep apnea, which may also contribute to the pulmonary hypertension.

Principles of Management

Current treatment options can slow the progression of the disease. • Long-term anticoagulation therapy to prevent thrombosis. • Avoidance of beta-blockers, decongestants or other medications that worsen pulmonary hypertension or decrease right heart function. • Symptom limited physical activity. • Oxygen to prevent additional pulmonary vasoconstriction due to low oxygen levels. Maintain Sao2 greater than 90% if possible. • Diuretics to control edema and ascites if right-sided heart failure present. • Calcium channel blockers only if positive response to vasodilator during cardiac catheterization. Newer Medical Treatment Options

Prostacyclin therapy is a potent vasodilator of both the systemic and pulmonary arterial vascular beds and is an inhibitor of platelet aggregation. Patients must be preapproved through their insurance prior to starting these costly medications and be able to self-administer. • Remodulin (treprostinil sodium) is a continuous subcutaneous or intravenous infusion. • Veletri (epoprostenol sodium room temperature stable) is a continuous intravenous infusion. • Ventavis (iloprost sodium) and Tyvaso (treprostinil sodium) are intermittent inhalation treatments using medication specific nebulizers. These medications cannot be administered during invasive mechanical ventilation. Endothelin receptor antagonists block the neurohormone endothelin from binding in the endothelium and vascular smooth muscle. • Tracleer (bosentan) and Letairis (ambrisentan) are oral agents. Phosphodiesterase inhibitors blocks phosphodiesterase type 5 which is responsible for the degradation of cyclic guanosine monophosphate (cGMP). Increased cGMP concentration results in pulmonary vasculature relaxation; vasodilation in the pulmonary bed and the systemic circulation (to a lesser degree) may occur. • Revatio (sildenafil) and Adcirca (tadalafil) are oral agents specific for use in patients with pulmonary hypertension. Surgical options include the following: • Atrial septostomy to create a right-to-left shunt to help decompress a failing right ventricle in select patients who are unresponsive to medical therapies. This also leads to significant hypoxemia in an already compromised patient.

284

CHAPTER 10. Respiratory System

• Pulmonary thromboendarterectomy for those with suspected chronic thromboembolic pulmonary hypertension to improve hemodynamics and functional status. • Lung transplantation is indicated when the pulmonary hypertension has progressed despite optimal medical and surgical therapy.

Pneumonia Respiratory infection is a common cause of ARF. Infections developed before hospitalization (community-acquired), during medical treatment (healthcare-acquired), and those acquired during hospitalization (hospital-acquired and ventilator-associated) can lead to significant morbidity and mortality, and require critical care management. A variety of respiratory infections occur in critically ill patients, including bronchitis and pneumonia. This section focuses on pneumonia, the most common respiratory infection and the most common cause of respiratory failure in critically ill patients. Etiology, Risk Factors, and Pathophysiology

At high risk for the development of pneumonia are the young, the elderly, those with chronic cardiopulmonary disease, and immunocompromised individuals. In addition, immobility, decreased level of consciousness, and mechanical ventilation place hospitalized patients at high risk for development of hospital-acquired pneumonias. These latter pneumonias are most

commonly referred to as ventilator-associated pneumonias or VAP. The major routes of entry of causative organisms for pneumonia are aspiration of oropharyngeal or gastric contents into the lungs, inhalation of aerosols or particles containing the organisms, and hematogenous spread of the organism into the lungs from another site in the body (Figure 10-18). Most hospital-acquired pneumonias are due to aspiration of bacteria colonizing the oropharynx or upper GI tract. Pneumonia develops when the normal bronchomucociliary clearance mechanism or phagocytic cells are overwhelmed by the number or virulence of organisms aspirated or inhaled into the airways. The proliferation of organisms in the pulmonary parenchyma elicits an inflammatory response, with large influxes of phagocytic cells into the alveoli and airways and production of protein-rich exudates. This inflammatory response impairs the distribution of ventilation and decreases lung compliance, resulting in increased work of breathing and the sensation of dyspnea. Hypoxemia results from the shunting of blood through poorly ventilated areas of pulmonary consolidation. The inflammatory response leads to fever and leukocytosis. Pneumonia also can develop through hematogenous spread, when organisms remote from the lungs gain access to the blood, become lodged in the pulmonary vasculature, and proliferate. Pneumonias with a hematogenous origin usually are distributed diffusely in both lung fields, rather than localized to a single lung or lobe.

Ve nti lat or

2 1

Gram positive bacilli

Aspiration • Invasive devices • Oropharyngeal colds • Gastric colonization • Position (supine); immobilized • Decreased level of consciousness

Inhalation • Respiratory treatment equipment • Anesthesia • Contaminated water or medications

Hematogenesis Spread

Host Factors • Extreme ages • Chronic diseases (CP, AIDS) • Immunocompromised state (steroids, AIDS, malignancy, transplantation)

Figure 10-18. Pathogenesis of pneumonia.

PATHOLOGIC CONDITIONS 285

Several factors present in critically ill patients increase the risk for the development of VAP. Aspiration of oropharyngeal and gastric secretions is increased in the presence of tracheostomy tubes, endotracheal tubes, nasogastric tubes, poor GI motility, gastric distention, and immobility, all of which are common situations in critically ill patients. Treatments that neutralize the normally acidic gastric contents, such as antacids, H2 blockers, proton-pump inhibitors, or tube feeding, allow increased growth of gram-negative bacteria in gastric contents. This increases the potential for aspiration of gram-negative bacteria and/or hematogenous spread. The high frequency of gastric and pulmonary intubation further increases the risk for pneumonia. Within 24 hours of admission to a critical care unit, there is colonization of the pharynx with gram-negative bacteria. Approximately 25% of colonized patients develop a clinical infection (tracheobronchitis or pneumonia). Critically ill patients at high risk for hospital-acquired pneumonias are those immunocompromised from malignancy, AIDS, and chronic cardiac or respiratory disease; the elderly; or those with depressed alveolar macrophage function (oxygen, corticosteroids). Although a variety of similar organisms cause community and hospital-acquired pneumonias, their frequency distribution is different (Table 10-11). Of particular concern in hospital-acquired infections is the polymicrobial origin of the pneumonia and the potential for causative organisms to be resistant to antimicrobial therapy. Development of a VAP is a serious complication in critically ill patients. Increased morbidity and mortality, in addition to increases in critical care and hospital lengths of stay and costs, make VAPs one of the most important sources of negative outcomes for critically ill patients.

Clinical Presentation Signs and Symptoms

TABLE 10-11. INFECTIOUS ETIOLOGIC AGENTS IN SEVERE COMMUNITY-ACQUIRED PNEUMONIA REQUIRING INTENSIVE CARE SUPPORT AND HOSPITAL-ACQUIRED PNEUMONIA IN CRITICALLY ILL PATIENTS

Improving Oxygenation and Ventilation

Etiologic Agent (Decreasing Rank) Community-acquired pneumonias

Ventilator-acquired pneumonias

Streptococcus pneumoniae Staphylococcus aureus Legionella species Gram-negative bacilli Haemophilus influenzae Staphylococcus aureus Pseudomonas aeruginosa Klebsiella oxytoca Enterobacter species Acinetobacter baumannii Escherichia coli Serratia spp

Data from: Mandell LA, Wunderink RG, Anzueto A, et al. Infections Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis. 2007;44:(suppl 2):S27-S72. Sievert DM, Ricks P, Edwards JR, et al. Antimicrobial-resistant pathogens associated with healthcare-associated infections: summary of data reported to the National Healthcare Safety Network at the Centers for Disease Control and Prevention. 2009-2010. Infect Control Hosp Epidemiol. 2013;34:1-14.

• Fever • Cough, typically productive • Purulent sputum or hemoptysis • Dyspnea • Pleuritic chest pain • Tachypnea • Abnormal breath sounds (crackles, bronchial breath sounds) Diagnostic Tests

• Gram stain and culture of sputum for causative organisms. May require fiberoptic bronchoscopy with brush specimen or bronchoalveolar lavage specimen retrieval in situations where pneumonia responds poorly to treatment. This may also be necessary early in admission in those patients who are immunocompromised, such as those with HIV/AIDS. The pneumonias in these immune deficient patients are often due to opportunistic organisms that may require very specific antibiotic coverage. • New or progressive infiltrates on chest x-ray. Infiltrates may be either localized or diffuse in nature. • Elevated WBC. • Abnormal arterial blood gases (hypoxemia, hypocapnia). Principles of Management for Pneumonia Treating the Underlying Disease

Appropriate empirical broad spectrum antimicrobial therapy should be initiated based on likely causative organisms until definitive culture results are obtained. Fluids should be administered to correct hypovolemia and hypotension, if present. Hypotension unresponsive to fluid therapy should alert the clinician to the potential for septic shock. Similar to ARF management, with the following additions: • PEEP and CPAP are unlikely to improve oxygenation in the presence of pneumonia, and may exacerbate the ventilation-perfusion abnormalities associated with pneumonia. These techniques should be used with caution in pneumonia. • Voluminous, tenacious respiratory secretions may require endotracheal intubation to assist with clearance. Chest physiotherapy may be helpful to increase secretion clearance, particularly when lobar atelectasis is present. Fiberoptic bronchoscopy may also be required to assist with secretion management. Assessment and Surveillance

Although the signs and symptoms of VAP are known, clinical diagnosis is complicated by lack of specific and sensitive criteria. In 2013, the National Healthcare Safety Network lead by the Centers for Disease Control developed new surveillance criteria for ventilator-associated events which include

286

CHAPTER 10. Respiratory System

ventilator-associated conditions (VAC), infection-related ventilator-associated conditions (IVAC), possible VAP, and probable VAP (Figure 10-19). Preventing Ventilator-Associated Pneumonias

In addition to the high morbidity and mortality associated with pneumonia in critically ill patients, high priority must

be given to strategies to prevent the development of VAPs. The development of a VAP in a critically ill patient increases requirements for ventilatory support (mechanical ventilation, oxygen, duration of treatment). It is estimated that a hospitalacquired pneumonia increases hospitalization 4 to 10 days, and increases costs by $20,000 to $40,000 per episode. Prevention strategies (Table 10-12) include the following:

Patient has a baseline period of stability or improvement on the ventilator, defined by ≥ 2 calendar days of stable or decreasing daily minimum FiO2 or PEEP values. The baseline period is defined as the 2 calendar days immediately preceding the first day of increased daily minimum PEEP or FiO2.

After a period of stability or improvement on the ventilator, the patient has at least one of the following indicators of worsening oxygenation: 1. Minimum daily FiO2 values increase ≥ 0.20 (20 points) over the daily minimum FiO2 in the preceding 2 calendar days (the baseline period), for ≥ 2 calendar days. 2. Minimum daily PEEP values increase ≥ 3 cm H2O over the daily minimum PEEP in the preceding 2 calendar days (the baseline period), for ≥ 2 calendar days.

Ventilator-Associated Condition (VAC)

On or after calendar day 3 of mechanical ventilation and within 2 calendar days before or after the onset of worsening oxygenation, the patient meets both of the following criteria: 1. Temperature > 38°C or < 36°C, OR white blood cell count ≥ 12,000 cells/mm3 or ≤ 4,000 cells/mm3. AND 2. A new antimicrobial agent(s)* is started, and is continued for ≥ 4 calendar days.

Infection-Related Ventilator-Associated Complication (lVAC)

On or after calendar day 3 of mechanical ventilation and within 2 calendar days before or after the onset of worsening oxygenation; ONE of the following criteria is met: 1. Purulent respiratory secretions (from one or more specimen collections) • Defined as secretions from the lungs, bronchi, or trachea that contain > 25 neutrophils and ≤ 10 squamous epithelial cells per low power field [lpf, x 100]. • If the laboratory reports semi-quantitative results, those results must be equivalent to the above quantitative thresholds. 2. Positive culture (qualitative, semi-quantitative or quantitative) of sputum* , endotracheal aspirate*, bronchoalveolar lavage*, lung tissue, or protected specimen brushing* * Excludes the following: • Normal respiratory/oral flora, mixed respiratory/oral flora or equivalent • Candida species or yeast not otherwise specified • Coagulase-negative Staphylococcus species • Enterococcus species

Possible Ventilator-Associated Pneumonia

On or after calendar day 3 of mechanical ventilation and within 2 calendar days before or after the onset of worsening oxygenation; ONE of the following criteria is met: 1. Purulent respiratory secretions (from one or more specimen collections– and defined as for possible VAP) AND one of the following: • Positive culture of endotracheal aspirate*, ≥ 105 CFU/ml or equivalent semi-quantitative result • Positive culture of bronchoalveolar lavage*, ≥ 104 CFU/ml or equivalent semi-quantitative result • Positive culture of lung tissue, ≥ 104 CFU/g or equivalent semi-quantitative result • Positive culture of protected specimen brush*, ≥ 103 CFU/ml or equivalent semi-quantitative result *Same organism exclusions as noted for Possible VAP. 2. One of the following (without requirement for purulent respiratory secretions): • Positive pleural fluid culture (where specimen was obtained during thoracentesis or initial placement of chest tube and NOT from an indwelling chest tube) • Positive lung histopathology • Positive diagnostic test for Legionella spp. • Positive diagnostic test on respiratory secretions for influenza virus, respiratory syncytial virus, adenovirus, parainfluenza virus, rhinovirus, human metapneumovirus, coronavirus

Probable Ventilator-Associated Pneumonia

Figure 10-19. Ventilator-associated events (VAE) surveillance definition algorithm. (From Centers for Disease Control and Prevention [CDC].) NHSN e-News ventilator-associated event (VAE) surveillance for adults special edition. 2012. www.cdc.gov/nhsn/psc_da-vae.html.

PATHOLOGIC CONDITIONS 287

TABLE 10-12. EVIDENCE-BASED PRACTICE GUIDELINES FOR THE PREVENTION OF VENTILATOR-ASSOCIATED PNEUMONIA Preventing Gastric Reflux 1. All mechanically ventilated patients, as well as those at high risk for aspiration (eg, decreased level of consciousness; enteral tube in place), should have the head of the bed elevated at an angle of 30°-45° unless medically contraindicated.a,b,c 2. Routinely verify appropriate placement of the feeding tube.a Airway Management 1. If feasible, use an endotracheal tube with a dorsal lumen above the endotracheal cuff to allow drainage (by continuous or intermittent suctioning) of tracheal secretions that accumulate in the patient’s subglottic area.a,b 2. Unless contraindicated by the patient’s condition, perform orotracheal rather than nasotracheal intubation.a 3. ET cuff management: Before deflating the cuff of an endotracheal tube in preparation for tube removal, or before moving the tube, ensure that secretions are cleared from above the tube cuff.a 4. Use only sterile fluid to remove secretions from the suction catheter if the catheter is to be used for reentry into the patient’s lower respiratory tract.a 5. Perform tracheostomy under aseptic conditions.a 6. Sedation interruption and daily assessment for readiness to wean.c Oral Care 1. Develop and implement a comprehensive oral hygiene program.a,c 2. Use an oral chlorhexidine gluconate (0.12%) rinse.c Cross-Contamination 1. Hand washing: Decontaminate hands with soap and water or a waterless antiseptic agent after contact with mucous membranes, respiratory secretions, or objects contaminated with respiratory secretions, whether or not gloves are worn.a 2. Decontaminate hands with soap and water or a waterless antiseptic agent before and after contact with a patient who has an endotracheal or tracheostomy tube, and before and after contact with any respiratory device that is used on the patient, whether or not gloves are worn.a 3. Wear gloves for handling respiratory secretions or objects contaminated with respiratory secretions of any patient.a 4. When soiling with respiratory secretions is anticipated, wear a gown and change it after soiling and before providing care to another patient.a 5. Room-air humidifiers: Do not use large-volume room-air humidifiers that create aerosols (nebulizers) unless they can be sterilized or subjected to high-level disinfection at least daily and filled only with sterile water.a Mobilization 1. Ambulate as soon as medically indicated in the postoperative period.a Equipment Changes 1. Do not change routinely, on the basis of duration of use, the patient’s ventilator circuit. Change the circuit when it is visibly soiled or mechanically malfunctioning. Periodically drain or discard any condensate that collects in the tubing. Do not allow condensate to drain toward the patient.a,b 2. Between use on different patients, sterilize or subject to high-level disinfection all MRBs.a Compiled from: aCenters for Disease Control and Prevention (2004), bAACN VAP Practice Alert (2008), and cInstitute for Healthcare Improvement (2012).

• Decrease the risk of cross-contamination or colonization via the hands of hospitalized personnel. Hand washing is the most effective strategy. • Decrease the risk of aspiration. Avoid supine positioning and keep the head of the bed elevated to 30° to 45° at all times, unless medically contraindicated. Use an endotracheal tube with a dorsal lumen above the endotracheal cuff to remove drainage with continuous suction. Suction above the endotracheal tube

cuff before removing or repositioning the tube. Assess for, and correct, gastric reflux problems. Ambulate as soon as possible. • Implement a comprehensive oral hygiene program that includes oral suctioning, teethbrushing, and use of oral 0.12% chlorhexidine gluconate. • Maintain a closed system on ventilator/humidifier circuits, and avoid pooling of condensation or secretions in the tubing. Do not routinely change the ventilator circuit, except when visibly soiled or malfunctioning. Use sterile water or saline for use with any respiratory equipment. • Use sterile technique for endotracheal suctioning and suction only when necessary to clear secretions from large airways. • Provide nutritional support to improve host defenses. • Eliminate invasive devices and equipment as soon as possible. Assess weaning readiness daily and limit the use of sedatives (see Chapter 6: Pain, Sedation, and Neuromuscular Blockade Management).

Pulmonary Embolism Etiology, Risk Factors, and Pathophysiology

Pulmonary embolism (PE) is a complication of deep venous thrombosis (DVT), long bone fracture, or air entering the circulatory system. There are many risk factors for PE (Table 10-13), with critically ill patients being especially prone due to the presence of central venous and PA catheters, immobility, use of muscle relaxants, and heart failure. Venous Thromboembolism

Venous thrombi form at the site of vascular injuries or where venous stasis occurs, primarily in the leg or pelvic veins. Thrombi that dislodge travel through the venous circulation until they become wedged in a branch of the pulmonary circulation. Depending on the size of the thrombi, and the location of the occlusion, mild to severe obstruction of blood flow occurs beyond the thrombi. The primary sequela, and major contributor to mortality, of the pulmonary obstruction is circulatory impairment. The physical obstruction of the pulmonary capillary bed increases right ventricular afterload, dilates the right ventricle, and impedes coronary perfusion. This predisposes the right ventricle to ischemia and right ventricular failure (cor pulmonale). A secondary consequence of thromboemboli is a mismatching of ventilation to perfusion in gas exchange units beyond the obstruction (see Figure 10-15C), resulting in arterial hypoxemia. This hypoxemia further compromises oxygen delivery to the ischemic right ventricle. Air Emboli

Air or other nonabsorbable gases entering the venous system also travel to the right heart, pulmonary circulation, arterioles, and capillaries. A variety of surgical and nonsurgical situations predispose patients to the development of air embolization (see Table 10-13). Damage to the pulmonary

288

CHAPTER 10. Respiratory System

TABLE 10-13. RISK FACTORS FOR THE DEVELOPMENT OF PULMONARY EMBOLISM Thromboemboli Obesity Prior history of thromboembolism Advanced age Malignancy Estrogen Immobility Paralysis Heart failure Postpartum Postsurgical Posttrauma Hypercoagulability states Central venous and PA catheters Air Emboli Neurosurgery Liver transplant Harrington rod insertion Open heart surgery Arthroscopy Pacemaker insertion Cardiopulmonary resuscitation Gastroscopy Positive pressure ventilation Scuba diving Intravenous infusion Central venous catheter insertion or removal Fat Emboli Long bone fracture Blunt trauma to liver Pancreatitis Lipid infusions Sickle cell crisis Burns Cardiopulmonary bypass Cyclosporine administration

endothelium occurs from the abnormal air-blood interface, leading to increased capillary permeability and alveolar flooding. Bronchoconstriction also occurs with air embolization. In addition to hypoxemia, Pco2 removal is also impaired. Arterial embolization may occur if air passes to the left heart through a patent foramen ovale, present in approximately 30% of the population. Peripheral embolization to the brain, extremities, and coronary perfusion leads to ischemic manifestations in these organs. Fat Emboli

Fat enters the pulmonary circulation most commonly when released from the bone marrow following long bone fractures (see Table 10-13). Nontraumatic origins of fat embolization also occur and are thought to be due to the agglutination of low-density lipoproteins or liposomes from nutritional fat emulsions. The presence of fat in the pulmonary circulation injures the endothelial lining of the capillary, increasing permeability and alveolar flooding. Clinical Presentation

The diagnosis of PE is based primarily on clinical signs and symptoms. Because many of the signs and symptoms are

nonspecific, PE frequently is difficult to diagnosis. In critically ill patients, diagnosis is especially difficult due to alterations in communication and level of consciousness, and the nonspecific nature of other cardiopulmonary alterations. Signs and Symptoms

• Dyspnea • Pleuritic chest pain • Cough • Rales • Apprehension • Diaphoresis • Evidence of DVT • Hemoptysis • Tachypnea • Fever • Tachycardia • Syncope • Hypoxia • Hypotension Diagnostic Tests

• Chest x-ray: Evaluate for basilar atelectasis, elevation of the diaphragm, and pleural effusion, although most patients have nonspecific findings on chest x-ray; diffuse alveolar filling in air embolism. • Arterial blood gas analysis: Hypoxemia with or without hypercarbia. • ECG: Signs of right ventricular strain (right axis deviation, right bundle branch block) or precordial strain; sinus tachycardia. • See earlier discussion of diagnostics for PE. Principles of Management for Pulmonary Emboli

The key to preventing morbidity and mortality from PE is primarily prevention and secondarily early diagnosis and treatment to prevent reembolization. Objectives include the improvement of oxygenation and ventilation, improvement of cardiovascular function, prevention of reembolization, and prevention of pulmonary embolus. Improving Oxygenation and Ventilation

Oxygen therapy is usually very effective in relieving hypoxemia associated with PE. When cardiopulmonary compromise is severe, mechanical ventilation may be required to achieve optimal oxygenation. Improving Cardiovascular Function

Controversy exists as to the benefit of vasoactive drug administration (such as norepinephrine and/or inotropic agents) to improve myocardial perfusion of the right ventricle. In severe embolic events, where cardiac failure is profound, additional therapy to hasten clot resolution, such as use of thrombolytic agents and/or interventional removal of massive emboli may be warranted.

PATHOLOGIC CONDITIONS 289

Essential Content Case

Mechanical Ventilation You are caring for a patient in ARF with the following interventions: • Mechanical ventilatory support (assist-control rate 10/min tidal volume 600 mL, PEEP 15 cm H2O, Fio2 0.85) • Pao2 63 mm Hg • MAP 68 mm Hg on vasoactive drug support (norepinephrine at 6 mcg/min) • Neuromuscular blockade (vecuronium) • Sedation (lorazepam) Case Question 1. How might the level of PEEP this patient is receiving affect his response to suctioning? Case Question 2. What precautions could you take to avoid or respond to potential complications? Answers 1. When high levels of PEEP (> 10 cm H2O) are disrupted (such as during suctioning without an in-line catheter), functional residual capacity (the volume restored by PEEP) is lost and the alveoli lose their distending volume. A decrease in PaO2 will ensue. 2. Hyper oxygenate the patient and use a PEEP valve on the manual resuscitation bag if not using an in-line suction catheter.

Pum

Figure 10-20. Intermittent pneumatic compression (IPC) device for prevention of DVT and PE.

• Insertion of vena cava filters to prevent emboli from legs, pelvis, and inferior vena cava from migrating to pulmonary circulation if anticoagulation therapy is contraindicated. Filters are placed percutaneously in the inferior vena cava. Preventing Venous Thromboembolism (VTE)

Preventing Reembolization

Several strategies are employed to prevent the likelihood of future embolization and cardiopulmonary compromise: • Limiting activity to prevent dislodgement of additional clots. • Use of anticoagulation therapy with unfractionated heparin to maintain a PTT 1.5 to 2.5 times the control when no contraindication exists.

• An important recommendation for the prevention of VTE is awareness and access to a hospital prevention policy including risk assessment (Table 10-14). • A risk assessment should be done on admission to the unit and discussion daily on rounds should take place. Discussion should also include current VTE prevention intervention, risk for bleeding, and response to treatment. • If ordered, graduated compression stocking or IPCs (Figure 10-20; Table 10-15) should be in use at all times except when being removed for correct fitting or skin assessment.

TABLE 10-14. RISK FACTORS, ASSESSMENT AND THROMBOPROPHYLAXIS FOR VTE Risk Factors for VTE • • • • • • • • •

Surgery Trauma Immobility Cancer Venous compression Previous VTE Age Pregnancy and postpartum Oral contraceptives and hormone replacement therapy • Erythropoiesis-stimulating agents • Acute medical illness • Inflammatory bowel disease • Nephritic syndrome • Myeloproliferative disorders • Paraxysmal nocturnal hemoglobinuria • Obesity • Central venous catheter • Thrombophilia

Risk Assessment Low Risk Minor surgery in mobile patients Medical patient who are fully mobile Moderate Risk Most general, open gynecologic or urologic surgery Patients Medical patient who are immobile Moderate Risk plus Bleeding Risk

High Risk Hip or knee arthroplasty Hip fracture surgery Major trauma Spinal cord injury High Risk plus Bleeding Risk

Suggested Thromboprophylaxis Early and aggressive ambulation

Low-molecular-weight heparin, unfractioned heparin, or fondaparinux Mechanical thromboprophylaxis, consider switch to pharmacologic prophylaxis when bleeding risk decreases

Low-molecular-weight heparin, fondaparinux, oral vitamin K antagonist

Low-molecular-weight heparin, unfractionated heparin, or fondaparinux

Data from: Geerts WH, Bergqvist D, Pineo GF, et al. Prevention of venous thromboembolism: American College of Chest Physicians practice guideline, 8th ed. Chest. 2008;133:381S-453S.

290

CHAPTER 10. Respiratory System

TABLE 10-15. TIPS FOR SAFE AND EFFECTIVE USE OF INTERMITTENT PNEUMATIC COMPRESSION DEVICES • Follow manufacturer recommendations for the correct fit including patient measurement. • Include ongoing assessment for fit as changes in weight and fluid shifts occur. • Monitor that the devices are on the patient and in correct placement. • Implement patient and family teaching regarding VTE and the role of mechanical prophylaxis COPD. • Ensure that devices do not impede ambulation.

• Placement of prophylactic vena cava filters in highrisk patients. • Early fixation of long bone fractures to prevent fat emboli. • Early mobilization. As soon as hemodynamic stability is achieved, and there are no other contraindications to mobilization, activity level should begin increasing to include sitting in a chair several times per day and short periods of ambulation.

SELECTED BIBLIOGRAPHY Critical Care Management of Respiratory Problems Burns S, ed. Protocols for Practice: Care of the Mechanically Ventilated Patient. Aliso Viejo, CA: AACN; 2006. Burns SM. Mechanical ventilation of patients with acute respiratory distress syndrome and patients requiring weaning: the evidence guiding practice. Crit Care Nurse. 2005;25:14-23. Burns SM. Ventilating patient with acute severe asthma: what do we really know? AACN Adv Crit Care. 2006;17:186-193. Carlson KK, ed. Advanced Critical Care Nursing. St Louis, MO: Saunders Elsevier; 2008. Coffin SE, Klompas M, Classen D, et al. Strategies to prevent ventilator-associated pneumonia in acute care hospitals. Infect Control Hosp Epidemiol. 2008;29:S31-S40. Collins PF, Stratton RJ, Elia M. Nutritional support in chronic obstructive pulmonary disease: a systematic review and meta-analysis. Am J Clin Nutr. 2012;95:1385-1395. DR, Sessler C. Severe hypoxemic respiratory failure, part 2; nonventilatory strategies. Chest. 2010;137:1437-1448. Esan A, Hess DR, Raoof S, George L, Sessler C. Severe hypoxemic respiratory failure, part 1: ventilatory strategies. Chest. 2010:137:1203-1216. Flanders S, Gunn S. Pulmonary issues in acute and critical care: pulmonary embolism and ventilator-induced lung injury. Crit Care Nurs Clin N Am. 2011;23:617-634. Geiger-Bronsky M, Wilson DJ, eds. Respiratory Nursing: A Core Curriculum. New York, NY: Springer Publishing Company; 2008. Ginn MB, Cox G, Heath J. Evidence-based approach to an in-patient tobacco cessation protocol. AACN Adv Crit Care. 2008;19:268-278. Halm MA. Relaxation: a self-care healing modality reduces harmful effects of anxiety. Am J Crit Care. 2009;18:169-172. Louie S, Morrissey BM, Kenyon NJ, Albertson TE, Avdalovic M. The critically ill asthmatic; from ICU to discharge. Clinic Rev Allerg Immunol. 2012;43:30-44. Maki MB, Martin SA, Burns S, Philbrick D, Rauen C. Putting evidence into nursing practice: four traditional practices not supported by evidence. Crit Care Nurse. 2013;33:28-42.

Matthay MA, Ware LB, Zimmerman GA. The acute respiratory distress syndrome. J Clin Invest. 2012;122:2731-2740. McLean B. Acute respiratory failure and intensive measure. Crit Care Nurs Clin N Am. 2012;24:361-375. Paprazian L, Forel J, Gacouin A, et al. Neuromuscular blockers in early acute respiratory distress syndrome. NEJM. 2010;363: 1107-1116. Raghavendran K, Napolitano LM. Definition of ALI/ARDS. Crit Care Clin. 2011;27:429-437. Raoff S, Goulet K, Esan A, Hess DR, Sessler C. Severe hypoxemic respiratory failure, part 2; nonventilatory strategies. Chest. 2010;137:1437-1448. Raven CA, Makic MB, Bridges E. Evidence-based practice habits. Transforming research into bedside practice. Crit Care Nurse. 2009;29:46-159. Sud S, Friedrich JO, Taccone P, et al. Prone ventilation reduces mortality in patients with acute respiratory failure and severe hypoxemia: systematic review and meta-analysis. Intensive Care Med. 2010:36:585-599. The ARDS Definition Task Force. Acute respiratory distress syndrome; the Berlin definition. 2012;307:2526-2533. Urden LD, Stacy KM, Lough ME. Thelan’s Critical Care Nursing: Diagnosis and Management. 6th ed. St Louis, MO: Mosby; 2010.

Chest X-Ray Interpretation Connolly MA. Black, white, and shades of gray: common abnormalities in chest radiographs. AACN Clinical Issues. 2001;12(2): 259-269. Eisenhuber E, Schaefer-Prokop CM, Prosch H, Schima W. Bedside chest radiography. Resp Care. 2012;57:427-443. Godoy MC, Leitman BS, deGroot PM, Viahos J, Naidich DP. Chest radiography in the ICU: part 1; evaluation of airway, enteric, and pleural tubes. Am J Roentgenology. 2012;198:563-571. Sanchez F. Fundamentals of chest x-ray interpretation. Crit Care Nurse. 1986;6:41-52. Siela D. Chest radiograph evaluation and interpretation. AACN Adv Crit Care. 2008;19:444-473.

Miscellaneous Lynn-McHale DJ. AACN Procedure Manual for Critical Care. 6th ed. Philadelphia, PA: Elsevier-Saunders; 2011.

Evidence-Based Practice Guidelines AACN Venous Thromboembolism Prevention Practice Alert. Aliso Viejo, CA: AACN; 2010. http://www.aacn.org. Accessed February 18, 2013. AACN VAP Practice Alert. Aliso Viejo, CA: AACN; 2008. http:// www.aacn.org. Accessed February 18, 2013. American College of Chest Physician, Antithrombotic and thrombolytic therapy: American College of Chest Physicians evidence-based clinical practice guidelines 2012 (9th ed) http://journal.publications.chestnet.org/issue.aspx?journalid= 99&issueid=23443. Accessed February 21, 2013. American Thoracic Society and the Infectious Diseases Society of America. Guidelines to the management of patients with hospital-acquired, ventilator-associated, and healthcareassociated pneumonia. Am J Resp Crit Care Med. 2005;171: 388-416.

Barr J, Fraser GL, Puntillo K, et al. Clinical practice guidelines for the management of pain, agitation, and delirium in adult patients in the intensive care unit. Crit Care Med. 2013;41:263-306. Centers for Disease Control and Prevention: Guidelines for prevention of health-care-associated pneumonia, 2003: recommendations of CDC and the Healthcare Infection Control Practices Advisory Committee. MMWR. 2004;53(No. RR-3): 1-35. Filore MC, Jaen CR, Baker TB. Treating tobacco use and dependence: 2008 Update. Quick Reference Guide for Clinicians. Rockville, MD: U.S. Department of Health and Human Services. Public Health Services: April 2009. Gold Executive Committee. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease (Updated 2013). http://www.goldcopd.org/. Accessed February 20, 2013. Mandell LA, Wunderink RG, Anzueto A, et al. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis. 2007;44:(suppl 2):S27-S72. McClave SA, Martindale RG, Vanek VW. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and the American Society for Parenteral and Enteral Nutrition (ASPEN). J Parenter Enteral Nutr. 2009;33:277-316. McLaughlin VV, Archer SL, Badesch DB, et al. ACCF/AHA 2009 expert concensus document on pulmonary hypertension: a report of the American College of Cardiology foundation task force on expert consensus documents and the American Heart Association. Circulation. 2009;119:2250-2294.

SELECTED BIBLIOGRAPHY 291

National Heart, Lung, and Blood Institute. Expert Panel Report 3: Guidelines for the diagnosis and management of asthma, Full Report 2007. http://www.nhlbi.nih.gov/guidelines/asthma/ asthgdln.pdf. Accessed February 21, 2013. National Heart, Lung, and Blood Institute. Global Initiative for Asthma (GINA) Global Strategy for Asthma Management and Prevention. http://www.ginasthma.org/uploads/users/ files/GINA_Report_2012Feb13.pdf. Accessed February 21, 2013. National Heart, Lung, and Blood Institute. Global Initiative for Chronic Obstructive Lung Disease (GOLD) global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. http://www.goldcopd.org/uploads/users/ files/GOLD_Report_2013_Feb20.pdf. Accessed February 21, 2013. Qaseem A, Wilt TJ, Weingberger SE, et al. Diagnosis and management of stable chronic obstructive pulmonary disease: a clinical practice guideline update from the American College of Physicians, American College of Chest Physicians, American Thoracic Society, and European Respiratory Society. Annals Intern Med. 2011;155:179-192. Task Force for Diagnosis and Treatment of Pulmonary Hypertension of European Society of Cardiology (ESC), European Respiratory Society (ERS), International Society of Heart and Lung Transplantation (ISHLT). Guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Respir J. 2009:34: 1219-1263. The ARDS Definition Task Force. Acute respiratory distress syndrome: the Berlin definition. JAMA. 2012;307:2526-2533.

This page intentionally left blank

Multisystem Problems Ruth M. Kleinpell

KNOWLEDGE COMPETENCIES 1. Identify the relationship between the cellular mediators and clinical manifestations of systemic inflammatory response syndrome (SIRS). 2. Describe the etiology, pathophysiology, clinical manifestations, patient needs, and principles of management of SIRS, sepsis, and associated conditions leading to multisystem problems. 3. Compare and contrast the pathophysiology, clinical manifestations, patient needs, and management approaches for multisystem problems

PATHOLOGIC CONDITIONS Sepsis and Multiple Organ Dysfunction Syndrome Critical illness can predispose patients to several complex conditions including sepsis and multiple organ dysfunction syndrome (MODS) (Table 11-1). Sepsis results from an infectious process and represents a systemic response to infection. Sepsis with acute organ dysfunction (severe sepsis) commonly occurs in critically ill patients. Sepsis is a serious global healthcare condition that is associated with high mortality rates despite improvements in the ability to manage infection. Severe sepsis incidence increases annually by 13% with associated mortality rates of 15% to 29%. It is the third most common cause of death in the United States and one of the most common causes of death in the intensive care unit (ICU). Systemic inflammatory response syndrome (SIRS) is a systemic response to a clinical insult, such as an infection or burn (Figure 11-1). In some cases, the syndrome may progress to sepsis and MODS. The stimulus for SIRS can be singular or multifactorial. Examples of situations that can

resulting from SIRS, sepsis, multiple organ dysfunction, and overdoses. 4. Describe the symptoms and pharmacologic management of the patient suffering from alcohol withdrawal syndrome. 5. Describe treatment considerations for complex wounds and pressure ulcers. 6. Identify factors related to the development of healthcare acquired infections.

precipitate SIRS are burns, trauma, transfusions, pancreatitis, or infection. Following the insult, an inflammatory response is initiated as a normal physiologic response. The inflammatory response consists of vasodilatation, increased microvascular permeability, cellular activation and release of mediators, and coagulation (see Figure 11-1). In SIRS, there is an excessive release of these mediators, which may lead to severe tissue damage, with hypoperfusion of organ systems. Systemic inflammatory response syndrome is manifested in a variety of ways: fever, tachycardia, tachypnea, altered level of consciousness, and decreased urine output. These findings may or may not be the result of an infection. If the response progresses unchecked, the result may be the development of sepsis or dysfunction of one or more organ systems, or MODS. The SIRS, sepsis, and MODS may be thought of as progressively severe conditions along a continuum. The key is early identification of the signs and symptoms of SIRS, and prompt development of a treatment plan to avoid further progression. Early intervention is important to ensure good outcomes in these patients. 293

294

CHAPTER 11. Multisystem Problems

TABLE 11-1. INFLAMMATORY RESPONSES: DEFINITIONS Term Bacteremia Hypotension Infection

MODS

Sepsis

Septic shock

Severe sepsis

SIRS

Initiating insult Trauma Burns Infection Pancreatitis Other

Definition The presence of viable bacteria in the blood. A systolic BP of < 90 mm Hg or a reduction of > 40 mm Hg from baseline in the absence of other causes for hypotension. Microbial phenomenon characterized by an inflammatory response to the presence of microorganisms or the invasion of normally sterile host tissue by those organisms. Presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention. The systemic response to infection. This systemic response is manifested by two or more of the following conditions as a result of infection: • Temperature > 38.0°C (100.4°F) • Heart rate > 90 beats/min • Respiratory rate > 20 breaths/min or Paco2, 12,000 cells/mm3, < 4000 cells/mm3, or > 10% immature (band) forms Sepsis with hypotension, despite adequate fluid resuscitation, along with the presence of perfusion abnormalities that may include, but are not limited to, lactic acidosis, oliguria, or an acute alteration in mental status. Patients who are on inotropic or vasopressor agents may not be hypotensive at the time that perfusion abnormalities are measured. Sepsis associated with organ dysfunction, hypoperfusion, or hypotension. Hypoperfusion and perfusion abnormalities may include, but are not limited to, lactic acidosis, oliguria, or an acute alteration in mental status. The systemic inflammatory response to a variety of severe clinical insults. The response is manifested by two or more of the following conditions: • Temperature > 38.0°C (100.4°F) • Heart rate > 90 beats/min • Respiratory rate > 20 breaths/min or Paco2 < 32 mm Hg • WBC > 12,000 cells/mm3, < 4000 cells/mm3, or 10% immature (band) forms

Data from ACCP/SCCM Consensus Committee: Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med. 1992;20:866.

Etiology, Risk Factors, and Pathophysiology Systemic Inflammatory Response Syndrome

Systemic inflammatory response syndrome consists of a series of systemic events that occur in response to an insult to the body. This response is a cellular reaction that initiates a number of mediator-induced responses, and is both inflammatory and immune in nature (Figure 11-2). There are essentially four different types of cells that are activated as part of the response to an insult or stimulus: polymorphonuclear cells (neutrophils), macrophages, platelets, and endothelial cells. These cells are activated to become either directly involved in the reaction (ie, platelet aggregation) or are stimulated to produce and release chemical mediators into the circulation, such as cytokines or plasma enzymes. Once activated, “a checks and balances system” is normally in place to control the inflammatory response. In some situations, however, when the response is large or the injury diffuse, local control of the response is lost, leading to

Coagulation

Inflammation

Vasodilatation Clot formation

Capillary permeability

Leaky capillary syndrome

Widespread microvascular thrombi

Endothelial damage

SIRS Figure 11-1. SIRS results from activation of interactive cascades of inflammation and coagulation.

excessive mediator release with consequent organ damage. The cellular activation response is highly individualized, and subsequent organ compromise is also variable. A general understanding of the various mediators responsible for the SIRS is important. Mediators can be divided into five groups: cytokines, plasma enzyme cascades, lipid mediators, toxic oxygen-derived metabolites, and unclassified mediators such as nitric oxide and proteases. These mediators are stimulated after cellular activation in response to a certain stimulus (eg, infection, trauma, pancreatitis). Cytokines are active chemical substances secreted by cells in response to a stimulus. If secreted by lymphocytes, they are called lymphokines, and if secreted by monocytes or macrophages, they are called monokines. Examples of cytokines include tumor necrosis factor, interleukin, interferon, and colony-stimulating factors such as granulocyte colonystimulating factor. In addition to cytokines, there is also activation of different enzymatic plasma cascades. Examples of these include the complement cascade and the various coagulation cascades. In addition, there are various lipid mediators that are either stimulated or produced as part of a cellular destructive process. These lipid mediators include arachidonic acid metabolites, leukotrienes, prostaglandins, and platelet-activating factor. Oxygen-derived free radicals are another group of mediators that exert a negative effect as part of the SIRS.

PATHOLOGIC CONDITIONS 295

Infection

Immune system response Release of mediators from WBCs and vascular endothelium Increased inflammation

Increased coagulation

Altered tissue perfusion

Decreased fibrinolysis

Endothelial damage

Microthrombi

Capillary leak

Organ system dysfunction

Death

Examples of these include hydrogen peroxide and hydroxyl radical. Nitric oxide and proteases are other mediators that are not grouped into any of the previous categories, but are mediators that enhance the SIRS. In addition to the mediators stimulated as part of the inflammatory and immune responses, mediators related to hormonal stimulation and regulation are also produced. The hormonal response component of the SIRS is characterized by the release of stress hormones (catecholamines, glucagon, cortisol, and growth hormone), suppression of thyroid hormone, and hormonal regulation of fluid and electrolyte balance. Toll-like receptors, or transmembrane proteins that are expressed on various immune cells, such as neutrophils and macrophages, have been implicated in ischemia-reperfusion injury that can further alter perfusion and contribute to inflammation. Sepsis

Sepsis is the manifestation of the SIRS in response to an infectious process (see Table 11-1). The source of infection may be bacterial, viral, fungal, or on rare occasions, rickettsial or protozoal. Risk factors for the development of sepsis are many and include malnutrition, immunosuppression, prolonged antibiotic use, and the presence of invasive devices (Table 11-2). It is important to remember that a large number of infections in critically ill patients are hospital acquired and can lead to sepsis. Many of these hospital-acquired infections can be prevented with simple measures. The role of the critical care nurse is instrumental in preventing hospital-acquired infections. Hand washing remains the single most effective method for preventing nosocomial infections. Research suggests that relatively simple measures such as ensuring

Edema formation

Figure 11-2. Interactive cascade of inflammation and coagulation leading to endothelium damage, diffuse thrombi, and organ system dysfunction. (Reprinted with permission, Kleinpell R. New initiatives focus on prevention and early recognition of sepsis. Nurs Spectrum. 2004;17[12]:24-26.)

TABLE 11-2. RISK FACTORS FOR THE DEVELOPMENT OF SEPSIS Host-Related Factors Malnutrition Immune deficiency disorders Immunosuppression Skin breakdown Fragile skin/mucous membranes Traumatic injuries Burns Pressure sores IV drug abuse EtOH abuse Chronic illness Diabetes mellitus Neoplastic disease Cirrhosis Renal failure Cardiac disease Pulmonary disease Pregnancy associated with prolonged rupture of membranes Immune senescence (elderly) Poor mobility Bedridden status BPH Decreased mucociliary transport mechanisms Decreased cough and clearance function Increased response to influenza vaccine UTI Vaginal colonization with GBS Perineal colonization with Escherichia coli Premature rupture of membranes

Treatment-Related Factors Invasive diagnostic devices Invasive therapeutic devices Surgical procedures Prolonged hospitalization Therapeutic immunosuppression Chemotherapy Radiation therapy Splenectomy Urinary catheters Use of H2 receptor antagonists (leading to gastric bacterial overgrowth and aspiration pneumonia) Aggressive resuscitation Prolonged TPN Extensive antibiotic therapy Pain/stress

Adapted with permission from Klein DM, Witek-Janusek L. Advances in immunotherapy of sepsis. Dimens Crit Care Nurs. 1992;11(2):75-81.

296

CHAPTER 11. Multisystem Problems

head-of-bed elevation and meticulous mouth care may prevent ventilator-associated pneumonia, a common source of sepsis in critically ill patients. Therefore, nursing measures to target sepsis prevention as well as early recognition and treatment are important in reducing the high mortality rates associated with severe sepsis (Table 11-3). Severe Sepsis and Septic Shock

Sepsis can progress to severe sepsis, with organ dysfunction, hypoperfusion, or severe hypotension. Severe sepsis is the term used when sepsis has progressed to cellular dysfunction and organ damage and organ hypoperfusion is evident. Septic shock is sepsis with persistent hypotension despite adequate fluid resuscitation. Both are associated with high mortality rates despite improvements in the ability to manage infection. Hypoperfusion and perfusion abnormalities that occur in severe sepsis may include oliguria, lactic acidosis, hypoxemia, and alteration in mental status (Table 11-4). Severe sepsis is associated with three integrated responses: activation of inflammation, activation of coagulation, and impairment of fibrinolysis. The result is systemic inflammation, widespread coagulopathy, and microvascular thrombosis, conditions that often lead to multiple organ dysfunction. Multiple Organ Dysfunction

Multiple organ dysfunction (MODS) is the worsening progression of the systemic inflammatory response. If SIRS is allowed to persist unchecked, or becomes overwhelming, the patient develops clinical manifestations of organ dysfunction. The mortality rates for MODS vary depending on the underlying cause, with mortality rates ranging from 50% to 100% as the number of involved organs increases. Multiple organ dysfunction can be classified as either primary or secondary. In primary MODS, organ dysfunction is a direct effect of an insult to an organ that has been compromised; for example, aspiration causes lung dysfunction, or acetaminophen overdose causes liver dysfunction. With primary MODS, the onset occurs relatively soon after the insult. In secondary MODS, the organ dysfunction occurs as the result of persistent and prolonged mediator release following an insult such as a thermal burn or pancreatitis. Generally, the time frame for secondary MODS is 7 to 10 days; however, this onset is variable. Clinical Presentation Systemic Inflammatory Response Syndrome

Systemic Inflammatory Response Syndrome is the clinical manifestations of two or more of the following conditions: •• Temperature > 38°C (100.4°F) or < 36°C (96.8°F) •• Heart rate > 90 beats/min •• Respiratory rate > 20 breaths/min or Paco2 12,000 cells/mm3, < 4000 cells/mm3, or > 10% immature neutrophils (band) forms Close monitoring and assessment are essential for the detection of early signs of SIRS.

Essential Content Case

Sepsis A 67-year-old man with a 6-year history of hypertension and a 30-pack per year cigarette history was admitted to the ICU with a diagnosis of cirrhosis secondary to biliary obstruction. He underwent an exploratory laparotomy and cholecystectomy 3 days ago. Postoperatively, he was relatively stable, experiencing an episode of hypotension 12 hours postoperatively, which was corrected by fluid administration. He remains intubated and attempts at weaning have been delayed due to periodic hypoxemia. He currently has an arterial line, central venous pressure (CVP) monitoring, pulmonary artery catheter, T-tube drain, and an indwelling urinary catheter. He is alert and oriented, moving in bed with little assistance. Physical examination reveals that his skin is pale pink and warm to touch, lungs have a few bibasilar crackles, and pedal edema is present bilaterally. His abdomen is nondistended, no active bowel sounds. His 5-inch midline abdominal wound requires dressing changes 3 times daily and is approximated with retention sutures. Current vital signs are: T 38.6°C (101.0°F) core HR 122 beats/min Sinus tachycardia RR 34 breaths/min BP 82/60 mm Hg Current laboratory results are: ABG: pH 7.30, Pao2 62, Paco 2 46, HCO 3 18, Sao 2 94% WBC: 22,000, 65 neutrophils, 50 segs, 12 bands, 40,000 platelets RBC: 4.5, Hct 39, Hgb 13, bili 2.2 mg, LDH 220, Na1 140, K1 3.5, Cl 100, CO2 20, BUN 22, Creat 1.1

Case Question 1. Why might this patient be at risk for developing sepsis? Case Question 2. What clinical signs and symptoms may be evidence of early sepsis? Case Question 3. Is he exhibiting SIRS criteria? Answers 1. Postoperative status, intubated, invasive lines and catheters, abdominal wound requiring dressing changes are risk factors for sepsis in this patient. 2. Elevated temperature, elevated white blood cell count with bandemia, sinus tachycardia, elevated respiratory rate are clinical symptoms of early sepsis. 3. Yes.

Severe Sepsis

The clinical manifestation of severe sepsis is the result of altered perfusion to vital organ systems. Organ system dysfunction develops due to hypoperfusion and microvascular thrombosis. Table 11-4 summarizes the common manifestations of severe sepsis. Signs of organ system dysfunction include cardiovascular alterations (hypotension, tachycardia, arrhythmias), respiratory system alterations (tachypnea, hypoxemia), renal system alterations (oliguria, elevated

PATHOLOGIC CONDITIONS 297

TABLE 11-3. NURSING CARE OF PATIENTS WITH SEVERE SEPSIS Recognition

Early identification of patients at risk for developing sepsis • Elderly • Immunocompromised • Patients with surgical/invasive procedures • Patients with indwelling catheters • Mechanically ventilated patients Monitoring physical assessment parameters Vital signs • Fever/hypothermia • Tachycardia • Tachypnea • Hypotension Hemodynamic parameters • Heart rate/rhythm and presence of ectopy • Hemodynamic monitoring parameter changes (elevated CO and low systemic vascular resistance) Ventilatory parameters • Respiratory rate • Lung sounds • Oxygenation status (pulse oximetry, arterial blood gases, mixed venous oxygen saturation levels) Renal parameters • Hourly urine output monitoring • Note sudden/gradual decreases in urine output • Monitor laboratory parameters of renal function (creatinine, BUN levels, fractional excretion of sodium levels) Coagulation parameters • Monitor coagulation indices (thrombocytopenia, prothrombin time, activated partial thromboplastin time, INR) • Monitor for bruising, bleeding Metabolic parameters • Provide nutritional support • Recognize role of intact gut barrier in preventing translocation of gram-negative bacteria • Maintain nitrogen balance in hypermetabolic state • Provide normalization of hyperglycemia Mental status parameters • Mental status changes (restlessness, confusion) • Changes in GCS Provide comprehensive sepsis treatment • Implement the sepsis bundles • Circulatory support with fluids, inotropes, and vasopressors • Supportive treatment with oxygenation and ventilation • Antibiotic administration • Monitoring and reporting patient response to treatment Promote patient and family comfort care Promote patient comfort/pain relief/sedation • Turning/skin care • Patient and family teaching • Address needs of families of critically ill patients Sepsis prevention Prevention remains the best treatment • Hand washing • Universal precautions • Measures to prevent hospital-acquired infections and iatrogenic complications: – Ventilator-associated pneumonia (see practice guidelines in Chapter 10, Respiratory System) – DVT and GI prophylaxis – Invasive catheter care – Wound care – Urinary catheter care • Astute clinical assessment – Maintain mucosal integrity – Prevent translocation • Formulate a sepsis prevention plan • Educate members of the healthcare team on identification and treatment of sepsis • Screen patients daily for signs of sepsis • Monitor sepsis cases and outcomes • Track changes in sepsis incidence rates and outcomes Adapted from Ely, Kleinpell, and Goyette. Advances in the understanding of clinical manifestations and therapy of severe sepsis: An update of critical care nurses. Am J Crit Care. 2003. 12(2):120-133.

298

CHAPTER 11. Multisystem Problems

TABLE 11-4. SIGNS OF ACUTE ORGAN SYSTEM DYSFUNCTION Cardiovascular

• Tachycardia • Arrhythmias • Hypotension • Elevated central venous and pulmonary artery pressures Respiratory • Tachypnea • Hypoxemia Renal • Oliguria • Anuria • Elevated creatinine Hematologic • Jaundice • Elevated liver enzymes • Decreased albumin • Coagulopathy Gastrointestinal • Ileus (absent bowel sounds) Hepatic • Thrombocytopenia • Coagulopathy • Decreased protein C levels • Increased d-dimer levels Neurologic • Altered consciousness • Confusion • Psychosis Data from Balk R. Pathogenesis and management of multiple organ dysfunction or failure in severe sepsis and septic shock. Crit Care Clin. 2000;16(2):337-352.

creatinine), hematologic system alterations (thrombocytopenia), gastrointestinal alteration (change in bowel sounds, ileus), hepatic alterations (elevated liver enzymes, jaundice, coagulopathies), and neurologic system alterations (confusion, agitation). Early recognition and treatment are extremely important as the prognosis of patients with severe sepsis is related to the number or organs involved and the severity of dysfunction. Multiple Organ Dysfunction

The clinical manifestations of primary and secondary MODS are the same as in SIRS and depend on which organs are affected. In patients with severe sepsis, MODS appears to result from a cascade of inflammatory mediators, endothelial injury, altered perfusion, and microcirculatory failure. Mortality in severe sepsis is directly related to the number of failing organ systems and the severity of dysfunction. MODS is regarded as one of the most common causes of death among patients in the ICU. Diagnostic Tests

•• Complete blood cell count: White blood cell count > 12,000 cells/mm3, or < 4000 cells/mm3, or > 10% immature bands •• Arterial blood gas: Paco2 < 32 mm Hg •• Serum lactate: More than 4 mmol/L (36 mg/dL) •• Chest x-ray: May be normal or show signs of infiltrates •• Culture and sensitivity: Generally is positive from a normally sterile source •• Axial computed tomography scan: May be negative or show abscess collection

Principles of Management of Severe Sepsis

The treatment of a patient with severe sepsis (SIRS + infection + new organ dysfunction) consists of several objectives: treating or eliminating the underlying cause, maximizing oxygen delivery, and use of evidence-based practice guidelines to include early antibiotic administration and ensure that initial resuscitation, organ system support, and targeted interventions are provided. Additional components of the management plan include providing nutrition and psychological support for the patient and family. Treating the Underlying Cause

The management plan begins with recognition and treatment of the source or stimulus of the response. Until this is done, no other therapy may be successfully applied. Examples include the drainage of an abscess or the removal of an infected invasive line, vascular graft, or orthopedic device. Once the source (or presumed source) has been identified, empiric antibiotic therapy is initiated and adjusted when definitive culture results are available. Maximizing Oxygen Delivery

Parallel to the administration of antibiotics are measures to maximize oxygen delivery. The components of oxygen delivery include cardiac output (CO), oxygen saturation (Sao2), hemoglobin (Hgb), and t

AACN Essentials of Critical Care Nursing 3rd Edition by Suzanne Burns [Dr.soc] - PDFCOFFEE.COM (2024)