Ebook Civetta, taylor, & kirby’s manual of critical care: Phần 1

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Civetta, Taylor, & Kirby’s

MANUAL OF
CRITICAL CARE
Andrea Gabrielli, MD, FCCM

Mihae Yu, MD, FACS

Professor of Anesthesiology and Surgery
Division of Critical Care Medicine
Section Head, NeuroCritical Care
University of Florida College of Medicine
Medical Director, Cardiopulmonary Service
and Hyperbaric Medicine
Shands Hospital at the University of Florida
Gainesville, Florida

Professor of Surgery
University of Hawaii John A. Burns School of Medicine
Vice Chair of Education
University of Hawaii Surgical Residency Program
Program Director of Surgical Critical Care Fellowship
Program
Director of Surgical Intensive Care
The Queen’s Medical Center
Honolulu, Hawaii

A. Joseph Layon, MD, FACP
Director, Critical Care Medicine
Geisinger Health System
Danville, PA

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Acquisitions Editor: Brian Brown
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Printed in China
Library of Congress Cataloging-in-Publication Data
Gabrielli, Andrea.
Civetta, Taylor, and Kirby’s manual of critical care / Andrea Gabrielli, A. Joseph Layon,
Mihae Yu. – 1st ed.
p. ; cm.
Manual of critical care
Includes bibliographical references and index.
ISBN 978-0-7817-6915-0 (alk. paper)

I. Layon, A. Joseph. II. Yu, Mihae. III. Civetta, Joseph M. IV. Title.
V. Title: Manual of critical care.
[DNLM: 1. Critical Care–Handbooks. 2. Intensive Care Units–Handbooks. WX 39]
616.02 8–dc23
2011035304
Care has been taken to confirm the accuracy of the information presented and to describe generally
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omissions or for any consequences from application of the information in this book and make no
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The authors, editors, and publisher have exerted every effort to ensure that drug selection and
dosage set forth in this text are in accordance with current recommendations and practice at the time
of publication. However, in view of ongoing research, changes in government regulations, and the
constant flow of information relating to drug therapy and drug reactions, the reader is urged to
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Some drugs and medical devices presented in the publication have Food and Drug
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D E D I C AT I O N
To the memory of my father and mother, Pietro and Giuliana:
They would have been proud to see the results of my efforts
—Andrea Gabrielli
To my best friend and partner Susana E. Picado—who makes me better.
To those who, in service to our people, struggle for justice and peace;
Giuliana and Pietro were two.
—A. Joseph Layon
To my dad, General Jae Hung Yu, and the Seventh Division for their sacrifices and
changing history for the better.
To my Mom, the late Esang Yoon who was the wind beneath our wings.
To the late Dr. Thomas J. Whelan Jr. who continues to mentor me in the practice of
Surgery and Code of conduct.

To Joe and Judy Civetta who sparked my continuing love for Critical Care and being the
guiding light for all Peepsters.
And to my late daughter Pearl (and CD) who has the Master Key to All. . .
—Mihae Yu

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■ CONTRIBUTING AUTHORS

The authors would like to gratefully acknowledge the efforts of the contributors of the original chapters in Civetta, Taylor, and
Kirby’s Critical Care, Fourth Edition.

Steven G. Achinger, MD

Maher A. Baz, MD

Gareth Adams, MD

Elizabeth Cordes Behringer, MD

Olufemi Akindipe, MD

Giuseppe Bello, MD

Serge Alfandari, MD, MSc

Rinaldo Bellomo, MBBS, MD, FRACP, FJFICM

Adrian Alvarez, MD

Howard Belzberg, MD, FCCM

Marcelo Amato, MD

Ira M. Bernstein, MD

Giuditta Angelini

Rebecca J. Beyth, MD

Djillali Annane, MD, PhD

Indermeet S. Bhullar, MD

Massimo Antonelli, MD

Luca M. Bigatello, MD

Juan Carlos Ayus, MD, FACP, FASN

Thomas P. Bleck, MD, FCCM

Keri A. Baacke, MD

Ernest F.J. Block, MD, MBA

Sean M. Bagshaw, MD, MSc, FRCPC

Eric L. Bloomfield, MD

Philip S. Barie, MD, MBS, FCCM, FACS

Karen L. Booth, MD

Claudia L. Barthold, MD

Karen Bordson, DO

Robert H. Bartlett, MD

Adrien Bougle, MD

Miho K. Bautista, MD

Philip Boysen, MD
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Contributing Authors

James E. Calvin, Jr., MD

Clifford S. Deutschman, MS, MD, FCCM

William G. Cance, MD

Karen E. Doucette, MD, MSc

Lawrence J. Caruso, MD

Quan-Yang Duh, MD

Juan C. Cendan, MD

Stephanie H. Dunlap, DO

Cherylee W.J. Chang, MD, FACP

Herbert L. DuPont, MD

Marianne E. Cinat, MD, FACS

Soumitra R. Eachempati, MD, FACS

Cornelius J. Clancy, MD

Rodney K. Edwards, MD, MS

Michael Coburn, MD

Elamin M. Elamin, MD, MSc, FACP, FCCP

Giorgio Conti, MD

Timothy C. Fabian, MD, FACS

Jamie B. Conti, MD, FACC, FHRS

Samir M. Fakhry, MD, FACS

Timothy J. Coons, RRT, MBA

Kevin J. Farrell, MD

Mark S. Cooper, BM, BCh, PhD

Robert J. Feezor, MD

C. Clay Cothren, MD, FACS

Niall D. Ferguson, MD, FRCPC, MSc

Douglas B. Coursin, MD

Sebastian Fernandez-Bussy, MD

Claudia Crimi, MD

Joseph Ferreira, BS, CPTC, CTOP II

Kristina Crothers, MD

Henry E. Fessler, MD

Gohar H. Dar, MD

Jay A. Fishman, MD

Rabih O. Darouiche, MD

Timothy C. Flynn, MD

Elizabeth Lee Daugherty, MD, MPH

Michael A. Frölich, MD, MS

David A. Decker, MD

Brian Fuehrlein, PhD

Leonardo De Luca, MD

Andrea Gabrielli, MD, FCCM

Demetrias Demetriades, MD, PhD, FACS

Robert Peter Gale, MD

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Contributing Authors

George D. Garcia, MD

Charles W. Hoopes, MD

Achille Gaspardone, MD, Mphil

Ramona O. Hopkins, PhD

Dany E. Ghannum, MD

David B. Hoyt, MD, FACS

Lewis R. Goldfrank, MD

Laurence Huang, MD

Shankar P. Gopinath, MD

Thomas S. Huber, MD, PhD

Dietrich Gravenstein, MD

Ahamed H. Idris, MD

J.S. Gravenstein, MD

Steven R. Insler, DO

David M. Greer, MD, MA

Felicia A. Ivascu, MD

Jeffrey S. Groeger, MD

James C. Jackson, PsyD

Jonathan Haft, MD

Sridivya Jaini, MD, MS

Stephen B. Hanauer, MD

Michael A. Jantz, MD, FCCP

Ikram U. Haque, MD

Edgar Jimenez, MD, FCCM

Cathleen Harris, MD

Aaron Joffe, MD

Kevin W. Hatton, MD

Raja Kandaswamy, MD

George Hatzakis, MSc, PhD

Scott R. Karlan, MD

Steven O. Heard, MD

Paraskevi A. Katsaounou, MD

Alan W. Hemming, MD, MSc

Robin D. Kim, MD

Dean R. Hess, PhD, RRT

Craig S. Kitchens, MD

Zoltan G. Hevesi, MD

Charles T. Klodell, MD

Thomas L. Higgins, MD, MBA

Marin H. Kollef, MD

Brian L. Hoh, MD

Meghavi S. Kosboth, DO

M. Barbara Honnebier, MD, PhD

Andreas H. Kramer, MD, FRCPC

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Contributing Authors

Anand Kumar, MD

Jerome H. Modell, MD

Aseem Kumar, PhD

Ernest E. Moore, MD

Franco Laghi, MD

Frederick A. Moore, MD, FACS

A. Joseph Layon, MD, FACP

Sharon E. Moran, MD

Marc Leone, MD, PhD

Jan S. Moreb, MD

Olivier Y. Leroy, MD

Alison Morris, MD, MS

David M. Levi, MD

Thomas C. Mort, MD

Lawrence Lottenberg, MD, FACS

David W. Mozingo, MD, FACS

Harrinarine Madhosingh, MD

Susanne Muehlschlegel, MD

Michael E. Mahla, MD

Deane Murfin, MBBCh, DA(SA), FCA(SA)

Patrick T. Mailoux, DO

Michael J. Murray, MD, PhD

Daniel R. Margulies, MD, FACS

Neil A. Mushlin, DO

Paul E. Marik, MD, FCCm, FCCP

Ece A. Mutlu, MD, MBA

Claude Martin, MD

Gökhan M. Mutlu, MD

Larry C. Martin, MD

Bhiken I. Naik, MBBCh(Wits), DA(SA)

Mali Mathru, MD

Minh-Hong Nguyen, MD

S. Anjani D. Mattai, MD

Minh-Ly Nguyen, MD

Kristin L. Mekeel, MD

Jennifer A. Oakes, MD

Richard J. Melker, MD, PhD

Nimisha K. Parekh, MD, MPH

Scott T. Micek, PharmD

Robert I. Parker, MD

William M. Miles, MD

David A. Paulus, MD

Taro Mizutani, MD, PhD

V. Ram Peddi, MD

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Contributing Authors

Kevin Y. Pei, MD

Sherry J. Saxonhouse, MD

Carl W. Peters, MD

Thomas M. Scalea, MD

Frederic M. Pieracci, MD, MPH

Denise Schain, MD

Michael R. Pinsky, MD, CM, Drhc, FCCP, FCCM

Carten M. Schmalfuss, MD

F. Elizabeth Poalillo, RN, MSN, ARNP, CCRN

Eran Segal, MD

Andrew Pollak, MD

Allen M. Seiden, MD, FACS

David T. Porembka, DO, FCCM

Steven A. Seifert, MD, FACMT, FACEP

Raymond O. Powrie, MD, FRCP, FACP

Hani Seoudi, MD

Issam I. Raad, MD

Christoph N. Seubert, MD, PhD

Amin Rahemtulla, PhD, FRCP

David Shade, BA, JD

S. Sujanthy Rajaram, MD

Stephen D. Shafran, MD, FRCPC

H. David Reines, MD

Jack D. Shannon, MD

Zaccaria Ricci, MD

Marc J. Shapiro, MD, MS, FACS, FCCM

Winston T. Richards, MD

Takeru Shimizu, MD, PhD

Claudia S. Robertson, MD

William C. Shoemaker, MD

Steven A. Robicsek, MD, PhD

Marc A. Simon, MD, MS, FACC

Claudio Ronco, MD

Jennifer A. Sipos, MD

Amy F. Rosenberg, PharmD

Lee P. Skrupky, PharmD, BCPS

Stephen J. Roth, MD, MPH

Robert N. Sladen, MBChB, MRCP(UK),
FRCP(C), FCCM

Daniel T. Ruan, MD
Matthew S. Slater, MD
Steven Sandoval, MD
Danny Sleeman, MD, FACS, FRCS

Stephanie A. Savage, MD
Wendy I. Sligl, MD

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Contributing Authors

Arthur S. Slutsky, MD

Kimi R. Ueda, PharmD

Eric S. Sobel, MD, PhD

Kürsat Uzun, MD

Howard K. Song, MD, PhD

Johannes H. van Oostrom, PhD

Edward D. Staples, MD

Thomas C. Vary, PhD

John K. Stene, MD, PhD

Theordoros Vassilakopoulos, MD

Deborah Stern, MD, MPH

George C. Velmahos, MD, PhD, MSEd

Andrew Stolbach, MD

J. Matthias Walz, MD

R. Todd Stravitz, MD, FACP, FACG

Hsiu-Po Wang, MD

Kathirvel Subramaniam, MD

Michael F. Waters, MD, PhD

Murat Sungur, MD

Carl P. Weiner, MD, MBA, FACOG

David E.R. Sutherland, MD, PhD

Eelco F.M. Wijdicks, MD

Maria Suurna, MD

Robert D. Winfield, MD

Sankar Swaminathan, MD

Charles C.J. Wo, BS

Danny M. Takanashi, Jr., MD, FACS

Linda L. Wong, MD

Christopher D. Tan, PharmD, BCPS

Gregory W. Woo, MD

Jamie Taylor, MD

Kenneth E. Wood, DO

Lisa Thannikary, MD

Jean-Pierre Yared, MD

S. Rob Todd, MD, FACS

Mihae Yu, MD, FACS

Krista L. Turner, MD

Arno L. Zaritsky, MD

Andreas G. Tzakis, MD, PhD

Janice L. Zimmerman, MD

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■ P R E FA C E

In the Preface to the Fourth Edition of the textbook, we quote
Nikos Kazantzakis’ Report to Greco. Did our attempt succeed?
Early reports suggest yes.
However much we have succeeded, the foundation for this
was laid by Doctors Civetta, Taylor and Kirby—our teachers
and mentors. We truly stand on the shoulders of giants.
We hope you—our readers—will provide us feedback on the
quality of this handbook, as you have the textbook. Our desire
with the Manual was to distill the full textbook into a short,
pithy and readable contribution. We are pretty sure the “short”
part did not work too well; let us know if we have, however,
created something useful for you.
As we noted in the Preface to the textbook, the mistakes of
omission or commission found herein are ours and ours alone.

We three editors share a friendship, have given each other
guidance and moral support, and will share any failures and
successes of our travail.
A. Joseph Layon
()
Danville, Pennsylvania
Andrea Gabrielli
()
Gainesville, Florida
Mihae Yu

()
Honolulu, Hawaii

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■ ACKNOWLEDGMENTS

We thank our colleagues at Lippincott—Nicole Dernoski, Tom Gibbons, and Brian Brown–for
their assistance. Indu Jawwad from Aptara did superb work.
Our families are part of this handbook, to them, we bow in thanks and respect.
Andrea Gabrielli
A. Joseph Layon
Mihae Yu

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■ CONTENTS

Contributing Authors
Preface
Acknowledgments

v
xi
xiii

SECTION I ■ EMERGENCY SITUATIONS
CHAPTER 1

Fundamentals of Cardiopulmonary Resuscitation

1

CHAPTER 2

Airway Management

9

CHAPTER 3

Temporary Cardiac Pacemakers

21

CHAPTER 4

Altered Consciousness and Coma in the Intensive Care Unit

27

CHAPTER 5

Bioterrorism

33

SECTION II ■ CARDIOVASCULAR MONITORING: INVASIVE
AND NONINVASIVE
CHAPTER 6

Invasive Pressure Monitoring: General Principles

48

CHAPTER 7

Hemodynamic Monitoring: Arterial and Pulmonary Artery
Catheters

50

CHAPTER 8

Noninvasive Cardiovascular Monitoring

60

CHAPTER 9

Pulse Oximetry and Photoplethysmography

61

CHAPTER 10

Capnography

63

CHAPTER 11

Echocardiography in the ICU

64

SECTION III ■ TECHNIQUES, PROCEDURES, AND TREATMENT
CHAPTER 12

Clean and Aseptic Techniques at the Bedside

65

CHAPTER 13

Vascular Cannulation

66

CHAPTER 14

Feeding Tube Placement

74

CHAPTER 15

Flexible Bronchoscopy

76

CHAPTER 16

Other Important Intensive Care Procedures

83

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Contents

SECTION IV ■ ESSENTIAL PHYSIOLOGIC CONCERNS
CHAPTER 17

Fluids and Electrolytes

CHAPTER 18

Blood Gas Analysis and Acid-Base Disorders

93
103

SECTION V ■ MODULATING THE RESPONSE TO INJURY
CHAPTER 19

The Host Response to Injury and Critical Illness

114

CHAPTER 20

Multiple Organ Dysfunction Syndrome

117

SECTION VI ■ SHOCK STATES
CHAPTER 21

Shock: General

124

CHAPTER 22

Cardiogenic Shock

125

CHAPTER 23

Sepsis and Septic Shock

129

CHAPTER 24

Hypovolemic and Hemorrhagic Shock

136

CHAPTER 25

Neurogenic Shock

141

CHAPTER 26

Anaphylactic Shock

143

SECTION VII ■ PHARMACOLOGY, NUTRITION, TOXICOLOGY,
AND THE ENVIRONMENT
CHAPTER 27

Sedation and Neuromuscular Blockade

144

CHAPTER 28

Nutritional Issues

151

CHAPTER 29

Practical Aspects of Nutritional Support

154

CHAPTER 30

Toxicology

162

CHAPTER 31

Substance Abuse and Withdrawal: Alcohol, Cocaine,
Opioids, and Other Drugs

185

Envenomation

196

CHAPTER 32

SECTION VIII ■ THE SURGICAL PATIENT: PREOPERATIVE, IMMEDIATE
POSTOPERATIVE EVALUATION AND TRAUMA
CHAPTER 33

Perioperative Pulmonary Function Testing and
Consultation

211

CHAPTER 34

Preoperative Evaluation of the High-Risk Surgical Patient

215

CHAPTER 35

Anesthesia: Physiology and Postanesthesia Problems

227

CHAPTER 36

Initial Management of the Trauma Patient

236

CHAPTER 37

Secondary and Tertiary Triage of the Trauma Patient

239

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Contents

CHAPTER 38

Surgical and Postsurgical Bleeding

246

CHAPTER 39

Abdominal Trauma: Nonoperative Management and
Postoperative Considerations

251

CHAPTER 40

Neurologic Injury: Prevention and Initial Care

255

CHAPTER 41

Orthopedic Trauma

262

CHAPTER 42

Facial Trauma

264

CHAPTER 43

Burn Injury: Thermal and Electrical

268

CHAPTER 44

Temperature-Related Injuries

272

CHAPTER 45

Evaluating the Acute Abdomen

279

CHAPTER 46

The Difficult Postoperative Abdomen

285

CHAPTER 47

Critical Care of Hepatopancreatobiliary Surgery Patients

292

CHAPTER 48

Critical Care of The Thoracic Surgical Patient

300

CHAPTER 49

Postoperative Management of the Adult Cardiovascular
Patient

308

CHAPTER 50

Management of the Pediatric Cardiac Surgical Patient

317

CHAPTER 51

Vascular Surgery in the Intensive Care Unit

329

CHAPTER 52

CNS Vascular Disease

334

CHAPTER 53

Urologic Surgery and Trauma

343

SECTION IX ■ ORGAN TRANSPLANTATION
CHAPTER 54

Critical Care and Transplantation: Overview

351

CHAPTER 55

Heart Transplantation

353

CHAPTER 56

Lung Transplantation

358

CHAPTER 57

Liver Transplantation

363

CHAPTER 58

Pancreatic Transplantation

368

CHAPTER 59

Renal Transplantation

371

CHAPTER 60

Critical Care Aspects of Stem Cell Transplantation

377

SECTION X ■ SPECIAL PATIENT POPULATION
CHAPTER 61

The Obstetric Patient: General

383

CHAPTER 62

Cardiac Disease and Hypertensive Disorders in Pregnancy

389

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Contents

CHAPTER 63

Hemorrhagic and Liver Disorders of Pregnancy

400

CHAPTER 64

Acute Abdomen and Trauma During Pregnancy

404

CHAPTER 65

Fetal Monitoring Concerns

411

CHAPTER 66

The Obese Surgical Patient

416

CHAPTER 67

The Geriatric Patient

426

SECTION XI ■ INFECTIOUS DISEASE
CHAPTER 68

Universal Precautions: Protecting The Practitioner

436

CHAPTER 69

An Approach to the Febrile Intensive Care Unit Patient

444

CHAPTER 70

The Role of Antibiotics in the Management of Serious
Hospital-Acquired Infections

453

CHAPTER 71

Surgical Infections

465

CHAPTER 72

Skin Wounds and Musculoskeletal Infection

482

CHAPTER 73

Neurologic Infections

490

CHAPTER 74

Infections of the Head and Neck

511

CHAPTER 75

Catheter-Related Bloodstream Infections (CRBSI)

520

CHAPTER 76

Respiratory Infections in the ICU

526

CHAPTER 77

Adult Gastrointestinal Infections in the ICU

545

CHAPTER 78

Catheter-Associated Urinary Tract Infections in the ICU:
Implications for Clinical Practice

551

CHAPTER 79

Fungal and Viral Infections

560

CHAPTER 80

Infections in the Immunocompromised Host

582

CHAPTER 81

Human Immunodeficiency Virus in the ICU

592

CHAPTER 82

Unusual Infections

604

SECTION XII ■ CARDIOVASCULAR DISEASE AND DYSFUNCTION
(OTHER CV DISEASE): ACS IN THE ICU
CHAPTER 83

Non-ST Elevation Acute Coronary Syndrome:
Contemporary Management Strategies

615

ST Elevation Myocardial Infarction (STEMI):
Contemporary Management Strategies

624

CHAPTER 85

Evaluation and Management of Heart Failure

638

CHAPTER 86

Cardiac Mechanical Assist Devices

649

CHAPTER 84

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Contents

CHAPTER 87

Valvular Heart Disease

656

CHAPTER 88

Cardiac Dysrhythmias

665

CHAPTER 89

Pericardial Disease

679

CHAPTER 90

Acute Hypertension Management in the ICU

689

SECTION XIII ■ RESPIRATORY DISORDERS
CHAPTER 91

Noninvasive Ventilatory Support Modes

698

CHAPTER 92

Invasive Ventilatory Support Modes

703

CHAPTER 93

High-Frequency Ventilation

712

CHAPTER 94

Extracorporeal Circulation for Respiratory or Cardiac
Failure

714

CHAPTER 95

Weaning from Mechanical Ventilation

716

CHAPTER 96

Acute Lung Injury and Acute Respiratory Distress
Syndrome

722

CHAPTER 97

Drowning

729

CHAPTER 98

Severe Asthma Exacerbation

731

CHAPTER 99

Acute Respiratory Failure in Chronic Obstructive
Pulmonary Disease

741

CHAPTER 100

Pulmonary Embolism (PE)

744

CHAPTER 101

Other Embolic Syndromes (Air, Fat, Amniotic Fluid)

753

SECTION XIV ■ NEUROLOGIC DISEASE AND DYSFUNCTION
CHAPTER 102

Elevated Intracranial Pressure

762

CHAPTER 103

Neurologic Monitoring

769

CHAPTER 104

Behavioral Disturbances in the ICU

783

SECTION XV ■ GASTROINTESTINAL (GI) BLEEDING
CHAPTER 105

Upper Gastrointestinal Bleeding

788

CHAPTER 106

Approach to Lower Gastrointestinal Bleeding

794

CHAPTER 107

Liver Failure: Acute and Chronic

801

CHAPTER 108

Pancreatic Disease

813

CHAPTER 109

Inflammatory Bowel Disease and Toxic Megacolon

819

CHAPTER 110

Mesenteric Ischemia

824

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Contents

SECTION XVI ■ RENAL DISEASE AND DYSFUNCTION
CHAPTER 111

Acute Renal Failure (ARF)

831

CHAPTER 112

Renal Replacement Therapies in the Critically Ill Patient

840

SECTION XVII ■ ENDOCRINE DISEASE AND DYSFUNCTION
CHAPTER 113

Endocrinopathy in the Intensive Care Unit

848

CHAPTER 114

Disordered Glucose Metabolism

856

CHAPTER 115

The Adrenal Gland in Critical Illness

863

CHAPTER 116

Pheochromocytoma

867

CHAPTER 117

Thyroid Disease in the Intensive Care Unit

871

SECTION XVIII ■ HEMATOLOGIC AND ONCOLOGIC DISEASE
AND DYSFUNCTION
CHAPTER 118

Coagulation Disorders in the Intensive Care Unit

881

CHAPTER 119

Antithrombotics and Thrombolytic Therapy

895

CHAPTER 120

Transfusion Therapy: When to Use it and How to
Minimize It

909

CHAPTER 121

Hematologic Conditions in the ICU

919

CHAPTER 122

Oncologic Emergencies

933

Appendices: Critical Care Catalog
Index

955
993

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SECTION I

August 27, 2011

■

EMERGENCY SITUATIONS

CHAPTER 1 ■ FUNDAMENTALS OF
CARDIOPULMONARY RESUSCITATION
MAJOR PROBLEMS
sCardiopulmonary resuscitation (CPR) is a series of assessments and interventions performed during a variety of acute
medical and surgical events wherein death is likely without
immediate intervention.
sSudden cardiac arrest (SCA) is a leading cause of adult death
in the United States and Canada.
sCardiac arrest (CA) is defined as “cessation of cardiac
mechanical activity as confirmed by the absence of signs
of circulation.”
❝ In the prehospital arena, CA is most commonly due to
ventricular fibrillation (VF) secondary to ischemic heart
disease.
– Asystole and pulseless electrical activity (PEA) are less
common initial rhythms with SCA, although these
rhythms may represent the initial identified rhythm in
adults who actually experienced an acute VF or ventricular tachycardia (VT) event.
❝ Although VF and VT are considered to be the most common out-of-hospital (OOH) arrest rhythms, only 20%

to 38% of in-hospital arrest patients have VF or VT as
their initial rhythm.
❝ Children and young adults require CPR most commonly for respiratory arrest, airway obstruction, or drug
toxicity.
– VF/VT is identified as the initial rhythm in 5% to 15%
of OOH arrests in children.
❝ Other conditions such as trauma, external or internal
hemorrhage, and drowning may call for resuscitation at
any age.
sImmediate and effective CPR can save lives.
sWith witnessed VF CA, CPR doubles or triples the rate of
survival.
sOnly about 27% of OOH arrest victims receive bystander
CPR.
sThe primary goal of CPR is to generate sufficient oxygen
delivery to the coronary and cerebral circulations to maintain cellular viability while attempting to restore a perfusing
cardiac rhythm by defibrillation, pharmacologic intervention, or both.

IMMEDIATE CONCERNS
sEffective CPR can be performed by following a few basic
rules.

sImmediately assess the environment for danger and move
the patient if necessary. Never assume that an environment
is safe.
sMinimize the time from CA recognition to starting effective
CPR.
sFor every minute without CPR during witnessed VF CA,
survival decreases by 7% to 10%.
sThis is cut in half (3%–4% per minute) when bystander

CPR preceded attempted defibrillation.
sDefibrillate immediately if a defibrillator is rapidly available (less than 3–5 min) in patients with VF.
❝ This is the primary treatment focus within the first few
minutes of SCA due to VF.
– For each minute delay in defibrillation, chances of
eventual hospital discharge decreased by 8% to
10%.
– If the time from arrest to emergency medical service
(EMS) arrival and initiation of CPR is more than
5 minutes, provision of 2 minutes of CPR before defibrillation is associated with improved outcome.
s“Push hard and fast” during chest compressions and minimize the duration of interruptions to reassess the patient’s
rhythm.
sInterrupt chest compressions only briefly, about every
2 minutes, to assess the rhythm, and switch rescuer if feasible.
sWhile CPR is in progress, attempt to identify the cause of
arrest.
sOther resuscitation interventions may be indicated based
on the cause of CA.
sIf no response to standard CPR interventions, think
about delayed recognition and recall the H’s and T’s
(Table 1.1).
sGood teamwork increases the effectiveness of resuscitation
when more than one rescuer is available.
sAttention to postresuscitation care is an important element
of neurologic outcome.
sRestore and support adequate cardiac output and tissue
perfusion.
sMonitor and maintain normal blood glucose concentrations.
sTreat the underlying cause of the arrest.
sMaintain normothermia.

sConsider therapeutic hypothermia to maximize survival
and cerebral recovery.
sIf there is no response to effective CPR, appropriate judgment is needed in determining when to stop resuscitative
efforts.

1

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August 27, 2011

Section I: Emergency Situations

TA B L E 1 . 1
POTENTIAL CORRECTABLE PROBLEMS DURING

CARDIAC ARREST: “6 H’S AND 5 T’S”
Hypovolemia
Hypoxia
Hydrogen ion (acidosis)
Hypo-/hyperkalemia
Hypoglycemia
Hypothermia
Toxins
Tamponade, cardiac
Tension pneumothorax
Thrombosis, coronary or pulmonary
Trauma
Adapted from 2005 American Heart Association Guidelines for
Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.
Circulation. 2005;112[24]SIV-1–IV-211.

OUT-OF-HOSPITAL CARDIAC ARREST
sDespite improvement in the scientific basis for resuscitation
practices and extensive efforts at CPR training of lay and
professional rescuers
sOutcome of most adult victims of out-of-hospital cardiac
arrest (OOHCA) remains poor.
sMedian reported survival to hospital discharge is 6.4%.
sAdults who had a witnessed CA were more likely to arrive
to the hospital alive (39% vs. 31%, p = 0.049) and
were more likely to have a good neurologic outcome after
6 months (35% vs. 25%, p = 0.023) as compared with
patients who had a CA in a nonpublic location.
sIn children, epidemiology and physiology of OOHCA are
different.

sRecent systematic review of 41 OOHCA studies, including
trauma, revealed a restoration of spontaneous circulation
(ROSC) of 30%, with survival to admission of 24% but
survival to discharge of 12% and neurologically intact survival of only 4%.
sInitial cardiac rhythms observed in these children were as
follows:
❝ Asystole, 78%
❝ PEA, 12.8%
❝ VF/pulseless VT, 8.1%
❝ Bradycardia with a pulse, 1%

IN-HOSPITAL CARDIAC ARREST
sObjective survival rates over the years have hardly changed.
sCurrent adult in-hospital cardiac arrest (IHCA) has overall
survival of about 18%.
sAnalysis of data from the national CPR registry found
sPrevalence of VF or pulseless VT as the first documented
pulseless rhythm during IHCA was only 23% in adults
and 14% in children.
sPrevalence of asystole as the initial rhythm was 35% in
adults and 40% in children.
sPrevalence of PEA was 32% versus 24% in adults and
children, respectively.
sSurvival rate to hospital discharge after pulseless CA

sHigher in children than adults (27% vs. 18%, respectively)
sOf these survivors, 65% of children and 73% of adults
had good neurologic outcome.
sAfter adjusting for known predictors, such as arrest location and monitoring at time of arrest, outcome was surprisingly worse when the rhythm was VF/VT in children
compared with asystole and PEA.

❝ Further analysis of these data showed that VF/VT
occurred during CPR in children more commonly than
it occurred as the initial rhythm.
❝ Survival to discharge is highest (35%) when VF/VT is
the initial rhythm compared with survival of 11% if this
rhythm develops during resuscitation.

NEUROLOGIC OUTCOME
sDetermined by the following:
sThe cause of arrest (e.g., degree of shock or hypoxemia prior
to arrest)
sThe duration of no flow, adequacy of flow during CPR
sRestoration of adequate flow after ROSC
sSubsequent injury secondary to postarrest management
such as the occurrence of hyperthermia or hypoglycemia
sSurvivors who ultimately have a good outcome
sGenerally awaken within 3 days after CA
sMost patients who remain neurologically unresponsive due
to anoxic–ischemic encephalopathy for more than 7 days
will fail to survive.
sThose who do survive often have poor neurologic recovery.
❝ Neurocognitive impairment ranges from dependency on
others for care to remaining in a minimally conscious or
vegetative state.
sAchieving good functional outcome is the ultimate goal for
successful CPR.
sThe financial implications of caring for patients with disordered consciousness are substantial.
sMost studies reporting outcome data have used crude
methods to describe neurologic outcome, such as the composite scores from the Glasgow Outcome Scale and Cerebral Performance Category.
❝ An important limitation of these scales is the possibility

of wide variation of neurologic function for the same score.
❝ In children, the Pediatric Cerebral Performance Category
and Pediatric Overall Performance Category have been
used.
s11% to 48% of CA patients admitted to the hospital will
be discharged with good neurologic outcome.
❝ Recent data from the National Registry for Cardiopulmonary Resuscitation (NRCPR) show that neurologic
outcome in discharged adult survivors is generally good,
with 73% of patients with Cerebral Performance Category 1.

INITIAL CONSIDERATIONS
sCPR is primarily based on two principles.
sProviding artificial ventilation and oxygenation through an
unobstructed airway
sCardiac output is limited; avoid ventilation in excess of
that required for adequate ventilation/perfusion matching.

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Chapter 1: Fundamentals of Cardiopulmonary Resuscitation

sDelivering chest compressions to maintain threshold blood
flow
sEspecially to the heart and brain, while minimizing interruption of compressions

Basic Life Support
sBasic life support (BLS) is the initial “ABCs” phase of CPR.
sA: airway
sB: breathing
sC: circulation
sEffective BLS can provide almost 30% of normal cardiac output with adequate arterial oxygen content.
sSufficient to protect the brain for minutes until effective
defibrillation or other definitive therapeutic maneuvers are
provided Table 1.2.

Advanced Life Support
sAdvanced life support (ALS) entails the following:
sAdvanced airway management including use of ancillary
equipment to support ventilation and oxygenation

sPrompt recognition and, when appropriate, treatment of
life-threatening arrhythmias using electrical therapy including defibrillation, cardioversion, pacemaker insertion, and
pharmacologic therapy
sInclusion of the use of pharmacologic therapy and advanced
procedures extending into the postarrest setting such as the

use of therapeutic hypothermia

Advanced Airway Management
sTracheal intubation
sEndotracheal intubation (ETI) is indicated if unable to adequately ventilate or oxygenate the arrested or unconscious
patient with bag-mask ventilation or if prolonged ventilation is required and airway protective reflexes are absent in
the patient with a perfusing rhythm
sA properly placed endotracheal tube (ET) is the gold standard method for securing the airway.
sAttempted ETI by less skilled rescuers results in a 6% to
14% incidence of misplaced or displaced ETs.
sConfirmation of correct ET placement
sClinical signs used to confirm correct ET placement
sVisualization of bilateral chest rise

TA B L E 1 . 2
SUMMARY OF BASIC LIFE SUPPORT ABCD MANEUVERS FOR INFANTS, CHILDREN, AND ADULTS FOR LAY
RESCUERS AND HEALTH CARE PROVIDERS (NEWBORN INFORMATION NOT INCLUDED)
Maneuver
Airway

Breathing: Initial
HCPs: Rescue breathing without
chest compressions
HCPs: Rescue breaths for CPR
with advanced airway
Foreign-body airway obstruction
Circulation
HCPs: Pulse check (≤10 s)
Compression landmarks

Adult lay rescuer: ≥ 8 y
HCPs: Adolescent and older
Head tilt–chin lift (HCPs:
Suspected trauma, use
jaw thrust)
Two breaths at 1 sec/breath
10–12 breaths/min
(approximate)
8–10 breaths/min
(approximately)
Abdominal thrusts
Carotid

Child lay rescuers: 1– 8 y
HCPs: 1 y to adolescent

Infant ≤ 1 y of age

Two breaths at 1 sec/breath
12–20 breaths/min (approximate)

Back slaps and chest thrust
Brachial or femoral

Lower half of sternum,
between nipples
Heel of one hand, other
hand on top

Just below nipple line (lower half

of sternum)
Heel of one hand or as for adults

Compression depth

11/2 –2 inches

Approximately one-third to
one-half the depth of the chest

Compression rate
Compression:ventilation ratio

Approximately 100/min
30:2 (one or two rescuers)

Defibrillation AED

Use adult pads
Do not use child pads

Compression method
s Push hard and fast
s Allow complete recoil

3

30:2 (single rescuer)
HCPs: 15:2 (two rescuers)
Use AED after five cycles of CPR

(out of hospital)
Use pediatric system for child 1–8
y if available
HCPs: For sudden collapse (out of
hospital) or in-hospital arrest
use AED as soon as available

Two or three fingers
HCPs (two rescuers):
Two thumb–
encircling hands

No recommendation for
infants <1 y of age

AED, automated external defibrillator; CPR, cardiopulmonary resuscitation.
Note: Maneuvers used by only health care providers are indicated by HCPs. AED, automated external defibrillator; CPR, cardiopulmonary resuscitation.
Adapted from 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation.
2005;112[24]SIV-1–IV-211.

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Section I: Emergency Situations

sBilateral breath sounds over the lateral lung fields
sAbsent breath sounds over the epigastrium
sPresence of water vapor/mist in the tube

sNone of these signs is confirmatory, and an ETCO2 detector
or esophageal detector is indicated to confirm correct tube
placement.
sETCO2 detector device is a disposable colorimetric device
that detects ETCO2 has been investigated as a guide to
correct ET placement.
❝ The device fits on the end of the ET and is normally
purple; exhaled CO2 turns the color to bright yellow,
indicating that the ET is in the trachea.
❝ The positive predictive value of this device for correct
tube placement is close to 100%, but the negative predictive value ranges from 20% to 100% depending on
whether the patient has a perfusing rhythm.
– False-negative results are seen if there is no or very low
pulmonary blood flow, such as during CA or with a
large pulmonary embolus.

– False-positive (i.e., the detector remains yellow) results
are seen when it is contaminated with an acidic drug
(e.g., epinephrine) or gastric contents.
sEsophageal detector device comes in two versions: the bulb
and the syringe esophageal detector devices (EDD).
❝ Bulb EDD consists of a bulb that is compressed and
attached to the ET. When released, if the tube is in the
esophagus, the suction collapses the lumen of the esophagus or pulls the esophageal tissue against the tip of the
tube, and the bulb will not re-expand (positive result for
esophageal placement).
❝ Syringe EDD consists of a syringe attached to the ET; the
rescuer attempts to pull the plunger of the syringe. If the
tube is in the esophagus, it will not be possible to pull
out the plunger (i.e., aspirate air) with the syringe.
– This device has high sensitivity for esophageal placement of ETs in both CA and patients with a
perfusing rhythm but poor specificity for tracheal
placement.

Electrical Therapy
sOne of the mainstays of ALS, especially in adults
sElectrical energy is used to treat life-threatening cardiac dysrhythmias.
sConstitute 16% to 85% of OOH and 14% to 56% of
in-hospital CAs
❝ Recent data suggest that VF and VT are decreasing, with
only 24% of the initial rhythms in more than 36,000
adult arrests being VF- or VT-based in a recent analysis
from the NRCPR.
❝ In hospitalized children with CA, VF is the initial rhythm
in approximately 10% of cases and subsequently occurs
during 15% of the cases.

sDefibrillation
sDefined as delivery of electrical energy resulting in termination of VF for at least 5 seconds after the shock
sThe goal is to quickly depolarize the entire myocardium,
terminating the rhythm and hoping that a sinus rhythm will
start.
sDefibrillator device
sManual defibrillator devices require the rescuer to analyze the rhythm and then manually set and determine the
electrical energy dose.

sAutomatic defibrillator devices analyze the rhythm, determine whether a shock is required, and deliver the shock if
needed automatically.
❝ Two types of automatic defibrillators: internal implantable cardioverter defibrillator and automated external
defibrillator (AED)
sDefibrillators are also characterized by the mode and
waveform of electrical current delivered into monophasic
and biphasic defibrillators.
❝ Animal and human data show that biphasic defibrillators have a higher first-shock success in terminating VF
compared with monophasic devices.
sDefibrillation dose
sOptimal initial energy dose for the first shock \ required
for effective defibrillation remains unknown despite multiple studies.
❝ Reasonable to use selected energies of 150 J to 200 J with
a biphasic truncated exponential waveform or 120 J with
a rectilinear biphasic waveform for the initial shock
❝ For second and subsequent biphasic shocks, the same or
higher energy can be given.
– Most manual defibrillators are set to an initial default
of 200 J of energy.
❝ If only a monophasic defibrillator is available, an energy
dose of 360 J is recommended for all shocks.

sThe optimal dose for effective defibrillation in infants and
children
❝ Not known
❝ Upper limit for safe defibrillation also not known
– Doses more than 4 J/kg (as high as 9 J/kg) have effectively defibrillated children.
– Recommended manual defibrillation (monophasic or
biphasic) doses for children are 2 J/kg for the first
attempt and 4 J/kg for subsequent attempts.
sElectrode position
sEither handheld paddles or self-adhesive pads are used for
shocks.
sElectrodes are applied to the bare chest in the conventional
sternal–apical (anterolateral) position.
❝ The right (sternal) chest pad is placed on the victim’s
right superior–anterior (infraclavicular) chest, and the
apical (left) pad is placed on the victim’s inferior–lateral
left chest, lateral to the left breast.
sElectrode size
sThe largest pad or paddle that can be placed on the chest
while avoiding contact between the pads or paddles should
be used. There should be at least 1 inch between the
pads.
sPaddles that are too small increase the risk of skin burn
injury.
sElectrical cardioversion
sUsed for some life-threatening arrhythmias causing rapid
cardiovascular deterioration
sIncluding VT and supraventricular tachycardias (SVTs)
such as paroxysmal atrial tachycardia, atrial flutter, or
atrial fibrillation with a rapid ventricular response

sThe technique, unlike defibrillation, must be synchronized
with the patient’s electrocardiogram.
sDelivery of the energy during the T wave of the QRS may
result in VF.
sEnergy level
sThe amount of energy recommended for emergency cardioversion varies with the rhythm.

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5

❝ 100 J is recommended for atrial fibrillation and 50 J for

sHalf-life of 10 to 20 minutes compared to the 3 to 5 minutes

atrial flutter.
❝ Monomorphic VT responds well to cardioversion, and
100 J should be attempted first.
❝ Pulseless VT behaves like VF, and 200 J should be used
initially.
❝ In conscious patients, sedation with intravenous
diazepam, midazolam, or methohexital is indicated, and
the cardioversion is accomplished with the lowest energy
possible (50–200 J).
❝ In children, the recommended initial cardioversion dose
is 0.5 to 1 J/kg.
sExternal cardiac pacing
sExternal (transcutaneous) pacing is not recommended for
patients in asystolic CA, but it should be always considered
in the ICU or other critical care areas of the hospital where
the device and adequate skill are promptly available.
sPacing can be considered in patients with symptomatic
bradycardia when a pulse is present.

observed with epinephrine
sSodium bicarbonate
sMetabolic and respiratory acidosis develops during CA
resulting from anaerobic metabolism, leading to lactic acid
generation and inadequate ventilation along with reduced
blood flow during CPR, which leads to inadequate pulmonary delivery of carbon dioxide for elimination.
sUntreated acidosis suppresses spontaneous cardiac activity, decreases the electrical threshold required for the
onset of VF, decreases ventricular contractile force, and
decreases cardiac responsiveness to catecholamine such as

epinephrine.
sElevated PCO2 tension probably is more detrimental to
myocardial function and catecholamine responsiveness
than metabolic acidosis.
sIf arterial blood gas and pH measurements not available:
sRecommended initial dose of sodium bicarbonate is
1 mEq/kg intravenously.
sHalf of this dose may be repeated at 10-minute intervals.
sIn pediatric patients, the 1 mEq/kg dose should be diluted
1:1 with sterile water to reduce the osmolality.
sAtropine
sUsed in sinus bradycardia when accompanied by hypotension or frequent premature ventricular contractions (PVCs)
secondary to unsuppressed ectopic electrical activity arising
in the area of injured tissue during the prolonged period
after repolarization
sSinus bradycardia after myocardial infarction may predispose the heart to the onset of VF.
sWhen profound bradycardia is present, acceleration of the
heart rate above 60 bpm may improve cardiac output and
reduce the incidence of VF.
sDosage of atropine for severe symptomatic bradycardia is
0.5 to 1.0 mg intravenously repeated every 3 to 5 minutes
until the desired pulse rate is obtained or a maximum of
0.04 mg/kg has been given.
sA larger dose has little therapeutic value, and a smaller
dose may actually slow the heart rate.
sEndotracheal dose is 2 to 2.5 mg.
sLidocaine
sDecreases ectopic electrical myocardial activity by raising
the electrical stimulation threshold of the ventricle during
diastole

sIn ischemic myocardial tissue after infarction, it may suppress re-entrant arrhythmias such as VT or VF.
sThe 2005 guidelines recommend lidocaine only when
amiodarone is not available.
sLidocaine may be used in stable monomorphic VT and
polymorphic VT with normal or prolonged QT interval if
ventricular function is not decreased.
sLoading dose of lidocaine is approximately 1 to 1.5 mg/kg
given as an IV bolus.
sIf needed, repeat 0.5 to 0.75 mg/kg every 5 to 10 minutes,
up to a total of 3 mg/kg.
sFollowed by a continuous infusion of 30 to 50 μg/kg/
minute (1–4 mg/min in a 70-kg patient)
sToxicity may occur in oliguric or anuric patients because
renally excreted lidocaine degradation products also have
pharmacologic effects and toxic potential.
sEarly signs of lidocaine toxicity are due to central nervous system effects and include anxiety, loquacity, tremors,
metallic taste, and tinnitus.

Pharmacologic Therapy
sUsed in CA to increase the rate of ROSC and terminate or
limit the risk of recurrent arrhythmias
sRoute of administration for resuscitation medications
sA central venous line may not be available at the time of the
arrest and immediate placement is not necessary to ensure
survival.
sPeripheral IV access can be used effectively with the advantage of not interrupting CPR.
❝ Rapidly follow the medication bolus with a 10- to 20-mL
fluid bolus to ensure central delivery.
❝ Intraosseous cannulation is an effective alternate for
drug delivery.

❝ Instillation can be made through an ET, if available.
Lipid-soluble medications that can be delivered via ET
are lidocaine, epinephrine, atropine, naloxone, and vasopressin.
❝ Recommended to administer at least 2 to 21/2 times the
IV recommended doses.
sEpinephrine
sThe most commonly used medication during CPR
sPrimary action in CA is to increase the coronary perfusion
pressure through systemic vasoconstriction mediated by its
α-adrenergic effects. The β-adrenergic effects are relatively
unimportant.
sEpinephrine is used primarily during CA due to asystole
and PEA.
sA second-line agent used for shock-refractory VF or pulseless VT
sLittle pharmacologic data supporting the currently recommended dose of 1 mg of epinephrine in adult CA and
0.01 mg/kg in children
sVasopressin
sAn endogenous antidiuretic hormone that, when given at
high doses, causes vasoconstriction by directly stimulating
vascular smooth-muscle V1 receptors.
sImproves coronary perfusion pressure but, unlike epinephrine, offers theoretical advantages of cerebral vasodilation, possibly improving cerebral perfusion.
sLack of β 1 -adrenergic activity potentially avoids unnecessary increases of myocardial oxygen consumption, resulting in postresuscitation arrhythmias.

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