American Red Cross

Focused Updates and Guidelines

2020 Version

Advanced Life Support

Participant’s Manual
Advanced Life Support | Participant’s Manual
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Advanced Life Support
Participant’s Manual
This Participant’s Manual is part of the American Red Cross Advanced Life Support program. The emergency care
procedures outlined in the program materials reflect the standard of knowledge and accepted emergency practices
in the United States at the time this manual was published. It is the reader’s responsibility to stay informed of
changes in emergency care procedures.

PLEASE READ THE FOLLOWING TERMS AND CONDITIONS (the “Terms and Conditions”) BEFORE
AGREEING TO ACCESS, USE OR DOWNLOAD THE FOLLOWING AMERICAN NATIONAL RED CROSS
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TERMS AND CONDITIONS AND THE AMERICAN NATIONAL RED CROSS TERMS OF USE (AVAILABLE AT
redcross.org/terms-of-use). YOU AGREE THAT THE INCLUDED COURSE MATERIALS ARE PROVIDED “AS IS”
AND WITHOUT WARRANTIES OF ANY KIND, AND THAT ANY ACCESS TO OR USE OF THESE COURSE
MATERIALS IS AT YOUR OWN RISK.

The following materials (including downloadable electronic materials, as applicable) including all content, graphics,
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■ The Recipient is prohibited from removing these Terms and Conditions in otherwise-permitted copies, and is
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Copyright © 2019, 2021 by The American National Red Cross. ALL RIGHTS RESERVED.

Revised in 2021 to reflect updated 2020 science guidelines. To review a summary of the key 2020 focused updates
and guidelines for ALS, go to the Red Cross Learning Center.

The Red Cross emblem, and the American Red Cross name and logos are trademarks of The American National Red
Cross and protected by various national statutes.

Printed in the United States of America

ISBN: 978-1-7367447-0-3
Science and Technical Content
The scientific content and evidence within the Amercan Red Cross Advanced Life Support program is consistent
with the American Red Cross Focused Updates and Guidelines 2020 and the most current science and treatment
recommendations from:
■ The International Liaison Committee on Resuscitation (ILCOR)
■ The International Federation of Red Cross and Red Crescent Societies
■ The Policy Statements, Evidence Reviews and Guidelines of:
c American Academy of Pediatrics (AAP)
c American College of Emergency Physicians (ACEP)
c American College of Obstetrics and Gynecology (ACOG)
c American College of Surgeons (ACS)
c Committee on Tactical Combat Casualty Care (CoTCCC)
c Obstetric Life Support™ (OBLS™ )
c Society of Critical Care Medicine (SCCM) and the American College of Critical Care Medicine (ACCM)
c Surviving Sepsis Campaign (SSC)

Guidance for this course was provided by the Red Cross Scientific Advisory Council, a panel of 60+ nationally
and internationally recognized experts from a variety of medical, nursing, EMS, advanced practice, allied health,
scientific, educational and academic disciplines. Members of the Scientific Advisory Council have a broad range of
professional specialties including resuscitation, emergency medicine, critical care, obstetrics, pediatrics, anesthesia,
cardiology, surgery, trauma, toxicology, pharmacology, education, sports medicine, occupational health, public
health and emergency preparedness. This gives the Scientific Advisory Council the important advantage of broad,
multidisciplinary expertise in evaluating existing and new assessment methodologies, technologies, therapies and
procedures—and the educational methods to teach them. More information on the science of the course content can
be found at the following websites:
■ ilcor.org
■ redcross.org/science

Dedication
This program is dedicated to the nurses, physicians, prehospital professionals, therapists, technicians, law
enforcement, fire/rescue, advanced practice professionals, lifeguards, first responders, lay responders and all other
professionals and individuals who are prepared and willing to take action when an emergency strikes or when a
person is in need of care. These updates and guidelines are also dedicated to the employees and volunteers of the
American Red Cross who contribute their time and talent to supporting and teaching lifesaving skills worldwide.

Acknowledgments
Many individuals shared in the development of the American Red Cross Advanced Life Support program in various
technical, editorial, creative and supportive ways. Their commitment to excellence made this manual possible.

Acknowledgments | iii
American Red Cross Scientific Advisory Council
We would like to extend our gratitude to the American Red Cross Scientific Advisory Council for their guidance and
review of this program:

David Markenson, MD, MBA, FCCM, FAAP, E. M. “Nici” Singletary, MD, FACEP
FACEP, FACHE Scientific Advisory Council Co-Chair
Scientific Advisory Council Co-Chair Professor, Department of Emergency Medicine
Chief Medical Officer, American Red Cross University of Virginia

Aquatics Subcouncil

Peter G. Wernicki, MD, FAAOS Bridget L. McKinney, PhD(h), MS, BS

Aquatics Subcouncil Chair District Supervisor, Miami Dade PSS
Orthopedic Surgeon, Pro Sports PSWAP-Mentoring and Swim Organization, Inc.
Vero Beach, Florida
Linda Quan, MD
Assistant Clinical Professor of Orthopedic Surgery
Bellevue, Washington
Florida State University College of Medicine
Kevin M. Ryan, MD
William Dominic Ramos, MS, PhD
Assistant Professor of Emergency Medicine
Aquatics Subcouncil Vice Chair
Boston University School of Medicine
Indiana University
Associate Medical Director, Boston EMS
Bloomington, Indiana
Boston, Massachusetts
Angela K. Beale-Tawfeeq, PhD
Andrew Schmidt, DO, MPH
Chair Associate Professor
Assistant Professor
Department of STEAM Education
Department of Emergency Medicine
College of Education, Rowan University
University of Florida College of Medicine—Jacksonville
Glassboro, New Jersey
Jacksonville, Florida
Jodi Jensen, PhD
Leslie K. White, BRec
Assistant Professor and Director of Aquatics
Supervisor—Citizen Services (Access 311)
Hampton University
Department of Community Services
Hampton, Virginia
City of St. John’s
Stephen J. Langendorfer, PhD Newfoundland and Labrador, Canada
Bowling Green, Ohio

Education Subcouncil

Jeffrey L. Pellegrino, PhD, MPH, EMT-B/FF, EMS-I Rita V. Burke, PhD, MPH
Education Subcouncil Chair Department of Preventive Medicine
Assistant Professor of Emergency Management and University of Southern California
Homeland Security Los Angeles, California
University of Akron
Brian Miller, MS, MSEd, MEd, CHES
Akron, Ohio
Program Director, Health Sciences
Nicholas Asselin, DO, MS Murphy Deming College of Health Sciences
Education Subcouncil Vice Chair Chair, Institutional Review Board
Department of Emergency Medicine Mary Baldwin University
Division of EMS Fishersville, Virginia
Alpert Medical School of Brown University
LifePACT Critical Care Transport
Providence, Rhode Island

iv | American Red Cross | Advanced Life Support

Gamze Ozogul, PhD Thomas E. Sather, Ed.D, MS, MSS, CAsP, CDR,
Instructional Systems and Technology Department MSC, USN
School of Education, Indiana University Branch Chief, Training Operations
Bloomington, Indiana Defense Health Agency Life Support Training Manager
Assistant Professor, Uniformed Services University of the
Health Sciences
Education and Training, Military Medical Treatment
Facility Operations Division
J-7 Education and Training Directorate
Defense Health Agency (DHA)
Falls Church, Virginia

First Aid Subcouncil

Nathan P. Charlton, MD Craig Goolsby, MD, MEd, FACEP

First Aid Subcouncil Chair Professor and Vice Chair, Department of Military and
Associate Professor Emergency Medicine
Department of Emergency Medicine Science Director, National Center for Disaster Medicine
University of Virginia Health System and Public Health
Charlottesville, Virginia Uniformed Services University
Bethesda, Maryland
S. Robert Seitz, MEd, RN, NRP
First Aid Subcouncil Vice Chair Elizabeth Kennedy Hewett, MD
Center of Emergency Medicine Assistant Professor of Pediatrics
University of Pittsburgh University of Pittsburgh School of Medicine
Pittsburgh, Pennsylvania Faculty Physician
UPMC Children’s Hospital of Pittsburgh
David C. Berry, PhD, MHA, AT, ATC, ATRIC, CKTP Pittsburgh, Pennsylvania
Professor/Professional Athletic Training Program
Director Morgan Hillier, MD, BSc, BKin, FRCPC, MSc
Department of Kinesiology Staff Emergency Physician
College of Health and Human Services Sunnybrook Health Sciences Centre Toronto
Saginaw Valley State University Medical Director
University Center, Michigan Toronto Fire Services
Toronto, Ontario, Canada
Adelita G. Cantu, PhD, RN
Associate Professor, UT Health San Antonio School of Angela Holian, PharmD, BCPS
Nursing Clinical Pharmacy Specialist, Emergency Medicine,
San Antonio, Texas Department of Pharmacy
UVA Health System
Jestin Carlson, MD, MS, FACEP Charlottesville, Virginia
St. Vincent Hospital
Erie, Pennsylvania Deanna Colburn Hostler, DPT, PhD, CCS
Clinical Assistant Professor
Sarita A. Chung, MD, FAAP Department of Rehabilitation Sciences
Department of Medicine University at Buffalo
Division of Emergency Medicine Buffalo, New York
Children’s Hospital
Boston, Massachusetts Robin M. Ikeda, MD, MPH, RADM, USPHS
Associate Director for Policy and Strategy
Theodore John Gaensbauer, MD, FAPA, FAACAP Office of the Director
Clinical Professor, Department of Psychiatry Centers for Disease Control and Prevention
University of Colorado Health Sciences Center Atlanta, Georgia
Denver, Colorado

Acknowledgments | v
Amy Kule, MD, FACEP Aaron M. Orkin, MD, MSc, MPH, PhD(c),
Loyola University Medical Center CCFP(EM), FRCPC
Maywood, Illinois Assistant Professor
Department of Family and Community Medicine
Matthew J. Levy, DO, MSc, FACEP, FAEMS, NRP University of Toronto
Johns Hopkins University School of Medicine Emergency Physician
Department of Emergency Medicine St. Joseph’s Health Centre and Humber River Hospital
Baltimore, Maryland Toronto, Ontario, Canada
Howard County Government
Department of Fire and Rescue Services Amita Sudhir, MD
Columbia, Maryland Associate Professor
University of Virginia
Edward J. McManus, MD Department of Emergency Medicine
I.D. Care, Inc./I.D. Associates, P.A.
Hillsborough, New Jersey Jeffrey S. Upperman, MD
Professor of Surgery and Surgeon-in-Chief
Nathaniel McQuay, Jr, MD Vanderbilt Children’s Hospital
Chief, Acute Care Surgery Nashville, Tennessee
University Hospitals Cleveland Medical Center
Cleveland, Ohio

Preparedness and Health Subcouncil

Dr. Steven J. Jensen, DPPD Lauren M. Sauer, MS

Preparedness and Health Subcouncil Chair Assistant Professor of Emergency Medicine
Advisor, Emergency Management Department of Emergency Medicine
Lecturer Johns Hopkins Medical Institutions
California State University at Long Beach Baltimore, Maryland
Long Beach, California
Samir K. Sinha, MD, DPhil, FRCPC, AGSF
James A. Judge II, BPA, CEM, FPEM EMT-P Mount Sinai Hospital
Preparedness and Health Subcouncil Vice Chair Toronto, Ontario, Canada
Emergency Management Director
Jacqueline Snelling, MS
Volusia County Department of Public Protection
Arlington, Virginia
Daytona Beach, Florida

Resuscitation Subcouncil

Joseph W. Rossano, MD Michael G. Millin, MD, MPH, FACEP, FAEMS

Resuscitation Subcouncil Chair Resuscitation Subcouncil Vice Chair
Chief, Division of Cardiology Department of Emergency Medicine
Co-Executive Director of the Cardiac Center Johns Hopkins University School of Medicine
Jennifer Terker Endowed Chair in Pediatric Cardiology Baltimore, Maryland
Associate Professor of Pediatrics at the Children’s Medical Director
Hospital of Philadelphia and the Perelman School of Maryland and Mid-Atlantic Wilderness Rescue Squad/
Medicine at the University of Pennsylvania Austere Medical Professionals
Philadelphia, Pennsylvania
Bruce J. Barnhart, MSN, RN, CEP
Senior Program Manager
Arizona Emergency Medicine Research Center
The University of Arizona College of Medicine-Phoenix
Phoenix, Arizona

vi | American Red Cross | Advanced Life Support

Lynn Boyle, MSN, RN, CCRN Bryan F. McNally, MD, MPH
Nurse Manager-PICU Professor, Emergency Medicine
The Children’s Hospital of Philadelphia Department of Emergency Medicine
Philadelphia, Pennsylvania Emory University School of Medicine
Atlanta, Georgia
Richard N. Bradley, MD
147th Medical Group
Houston, Texas Ira Nemeth, MD
Medical Director
Meredith Gibbons, MSN, CPNP Ben Taub Emergency Department
Pediatric Nurse Practitioner Senior Faculty, Baylor College of Medicine
Columbia University Medical Center Houston, Texas
New York, New York
Joshua M. Tobin, MD
Wendell E. Jones, MD, MBA, CPE, FACP Adjunct Clinical Associate Professor
Chief Medical Officer Stanford University Medical Center
Veteran’s Integrated Service, Network 17 Stanford, California
Arlington, Texas
Bryan M. White, Lt Col, USAF, MC MD, FACC,
Andrew MacPherson, MD, CCFP-EM, FCFP FASE, RPVI
Clinical Professor Las Vegas, Nevada
Dept. of Emergency Medicine
University of British Columbia Lynn White, MS, FAEMS
Royal Jubilee Hospital National Director of Clinical Practice, Global Medical
Victoria, British Columbia, Canada Response

Table of Contents | vii

Content Direction
The development of this program would not have been possible without the leadership, valuable insights and
dedication of the subject matter experts, who generously shared their time to ensure the highest quality program:

David Markenson, MD, MBA, FCCM, FAAP, FACEP, FACHE

Scientific Advisory Council Co-Chair
Chief Medical Officer, American Red Cross

Program Development
Special thanks to the program development team for their expertise and mix of patience and persistence to bring this
program through to completion: Danielle DiPalma, Anna Kyle, Sarah Kyle, Maureen Pancza, Anna Pruett, Maureen
Schultz, Melanie Sosnin, Cindy Tryniszewski, Ryan Wallace, Laurie Willshire, Ernst & Young, Iperdesign, Iyuno, Out of
the Blue Productions, Sealworks, and Surround Mix Group.

Clinical Editors and Supporting Organizations

Thank you to the Defense Health Agency for their ongoing review and feedback, which has helped us improve the
clarity and quality of this program.

Thank you to the following clinical editors and supporting organizations for assisting the Red Cross with the
development of the previous edition.
■ Jonathan L. Epstein, MEMS, NRP
■ Jannah N. Amiel, MS, BSN, RN
■ Bob Page, M.Ed., NRP, CCP, NCEE
■ ETHOS Health Communications
■ Fairfax County Fire and Rescue Department
■ Chester County Intermediate Unit Practical Nursing Program (CCIU PNP) Learning Lab—The Technical College
High School Brandywine Campus
■ Independence Blue Cross Medical Simulation Center at Drexel University College of Medicine
■ Jefferson Stratford Hospital
■ St. Christopher’s Hospital for Children

viii | American Red Cross | Advanced Life Support

 Table of Contents
Drug Therapy����������������������������������������������������������������������������� 40
Chapter 1
Skill Sheet: Inserting an Oropharyngeal Airway����������44
Advanced Life Support
Course Introduction 1 Skill Sheet: Inserting a Nasopharyngeal Airway���������46

Course Purpose������������������������������������������������������������������� 2 Skill Sheet: Using a Bag-Valve-Mask (BVM)

Resuscitator—One Provider��������������������������������������������48
Course Preparation������������������������������������������������������������� 2
Skill Sheet: Using a Bag-Valve-Mask (BVM)
Course Objectives��������������������������������������������������������������� 2
Resuscitator—Two Providers������������������������������������������49
Your Role as an Advanced Life Support Provider�������� 3
Skill Sheet: Placing Electrodes
Course Completion Requirements���������������������������������� 3 for Electrocardiography��������������������������������������������������������� 50

Skill Sheet: Manual Defibrillation������������������������������������53

Chapter 2 Skill Sheet: Synchronized Cardioversion���������������������55

Basic Life Support Review 5 Skill Sheet: Transcutaneous Pacing������������������������������57

Cardiac Chain of Survival�������������������������������������������������� 6 Skill Sheet: Intraosseous Access (Drill)������������������������59

High-Quality CPR���������������������������������������������������������������� 7 Skill Sheet: Intraosseous Access

(Manual Insertion)��������������������������������������������������������������63
Approach to the Patient: Basic Life Support���������������� 9

Approach to the Patient: Obstructed Airway��������������11

Chapter 4
Code Card: Basic Life Support:
Adults and Adolescents ��������������������������������������������������13 Working Well Together in an Emergency 67

Skill Sheet: Rapid Assessment for Adults��������������������15 Rapid Response and Resuscitation Teams�����������������68

Skill Sheet: CPR for Adults���������������������������������������������17 Functioning as a Team������������������������������������������������������69

Skill Sheet: AED Use for Adults�������������������������������������21 Working as a High-Performance Team�������������������������70

Chapter 3 Chapter 5
Tools and Therapies 25 Assessment 75

Airway Management����������������������������������������������������������26 Assess, Recognize and Care������������������������������������������76

Bag-Valve-Mask Ventilation���������������������������������������������31 Systematic Approach to Assessment���������������������������76

Supplemental Oxygen�������������������������������������������������������32 Code Card: Adult Systematic Assessment ����������������81

Cardiac Monitoring������������������������������������������������������������34

Electrocardiography����������������������������������������������������������35

Electrical Therapies�����������������������������������������������������������36

Vascular Access�����������������������������������������������������������������38

Fluid Therapy�����������������������������������������������������������������������39

Table of Contents | ix
Chapter 6 Chapter 9
Respiratory Emergencies 83 Post–Cardiac Arrest Care  125
Respiratory Anatomy and Physiology����������������������������84 Pathophysiologic Consequences of
Cardiac Arrest����������������������������������������������������������������� 126
Pathophysiologic Mechanisms Contributing to
Respiratory Emergencies�������������������������������������������������87 Approach to the Patient������������������������������������������������� 126

Respiratory Distress, Respiratory Failure and Post–Cardiac Arrest Prognostication������������������������ 129

Respiratory Arrest��������������������������������������������������������������88
Code Card: Adult Post–Cardiac Arrest Care���������� 130
Capnography in Respiratory Emergencies������������������89

Patient Assessment�����������������������������������������������������������91 Chapter 10

Approach to the Patient����������������������������������������������������92
Acute Coronary Syndromes 133
Code Card: Adult Suspected or Known Opioid
Classification of Acute Coronary Syndromes���������� 134
Toxicity����������������������������������������������������������������������������������94
Goals for Management�������������������������������������������������� 134

Chapter 7 Pathophysiology of Acute Coronary Syndromes����� 134

STEMI Chain of Survival����������������������������������������������� 135

Arrhythmias 95
Recognizing Acute Coronary Syndromes����������������� 135
Electrical Conduction��������������������������������������������������������96
Patient Assessment�������������������������������������������������������� 137
Recognizing Bradyarrhythmias���������������������������������������98
Approach to the Patient������������������������������������������������� 138
Recognizing Tachyarrhythmias��������������������������������������101
Code Card: Adult Acute Coronary Syndromes������� 141
Patient Assessment���������������������������������������������������������104

Approach to the Patient��������������������������������������������������104

Chapter 11
Code Card: Adult Bradyarrhythmia�����������������������������108
Stroke 143
Code Card: Adult Tachyarrhythmia������������������������������109
Overview of Stroke��������������������������������������������������������� 144

Chapter 8 Acute Stroke Chain of Survival������������������������������������ 144

The 8 Ds of Stroke Care����������������������������������������������� 145

Cardiac Arrest 111
Recognizing Stroke�������������������������������������������������������� 147
Recognizing Cardiac Arrest Rhythms������������������������ 112
Patient Assessment�������������������������������������������������������� 147
Reversible Causes of Cardiac Arrest
(Hs and Ts)����������������������������������������������������������������������� 113 Approach to the Patient������������������������������������������������� 149
Approach to the Patient������������������������������������������������� 117 Code Card: Adult Acute Stroke���������������������������������� 151
Terminating the Resuscitation Effort��������������������������� 119 National Institutes of Health Stroke Scale���������������� 153
Cardiac Arrest in Pregnancy���������������������������������������� 120 Glossary157
Code Card: Adult Cardiac Arrest������������������������������� 122 Bibliography161
Code Card: Cardiac Arrest in Pregnancy����������������� 123 Index175

x | American Red Cross | Advanced Life Support

 Photography Credits
Figure 3-6 | 30 iStock Signature Collection: miralex

Figure 4-1 | 68 iStock Signature Collection: JohnnyGreig

Table of Contents | xi
 CHAPTER
1

Advanced Life Support

Course Introduction
Introduction
This chapter provides an overview of American Red Cross advanced life support
(ALS) training.
Course Purpose High-quality CPR skills (including high-quality chest
compressions and basic airway management) and
When a patient experiences a life-threatening AED skills are an essential part of ALS (Figure 1-2). In
cardiovascular, cerebrovascular or respiratory addition, strong patient assessment skills; knowledge and
emergency, you need to act swiftly to assess the understanding of the medications used in cardiovascular,
situation and the patient and provide lifesaving care. cerebrovascular and respiratory emergencies; expert
medication administration skills; and an ability to read and
The purpose of the American Red Cross Advanced Life interpret ECG rhythms are valuable before taking this
Support course is to ensure that healthcare providers course.
have the requisite knowledge and skills to assess,
recognize and care for patients who are experiencing
a cardiovascular, cerebrovascular or respiratory Course Objectives
emergency (Figure 1-1). The course emphasizes
providing high-quality patient care by integrating Upon successfully completing the American Red Cross
psychomotor skills, rhythm interpretation, electrical Advanced Life Support course, you will be able to:
interventions and pharmacologic knowledge with ■ Demonstrate high-quality basic life support skills,
critical thinking and problem solving to achieve the best including high-quality chest compressions, effective
possible patient outcomes. ventilations and use of an AED.
■ Apply concepts of effective teamwork when
The American Red Cross Advanced Life Support caring for a patient experiencing a cardiovascular,
course covers the skills required for certification as an cerebrovascular or respiratory emergency.
ALS provider. In addition, the key concepts that support ■ Integrate advanced communication, critical thinking
proficient performance of these skills are reviewed. and problem-solving skills when responding as part
of a team to a cardiovascular, cerebrovascular or
respiratory emergency.
Course Preparation ■ Effectively assess a cardiovascular, cerebrovascular
or respiratory emergency situation using a systematic
The American Red Cross Advanced Life Support course is approach.
designed for professional healthcare providers who directly ■ Quickly recognize the nature of a cardiovascular,
care for patients in a variety of settings and who could be cerebrovascular or respiratory emergency.
called on to care for a critically ill patient. This could include, ■ Provide effective and appropriate advanced
but is not limited to, nurses, nurse practitioners, physicians, life support care to address a cardiovascular,
physician assistants, respiratory therapists, dentists, cerebrovascular or respiratory emergency.
emergency medical services personnel, public safety ■ Provide effective and appropriate care after a
personnel and other professional responders. return of spontaneous circulation (ROSC) during a
resuscitation effort.

Figure 1-1 | The goal of advanced life support training is

to ensure that healthcare providers working in healthcare
settings have the skills to provide care to patients who
are experiencing a cardiovascular, cerebrovascular or Figure 1-2 | High-quality CPR is the foundation of every
respiratory emergency. successful cardiac arrest resuscitation effort.

2 | American Red Cross | Advanced Life Support

Your Role as an Advanced Life an instructor verified that a course participant could
demonstrate competency in all required skills taught
Support Provider in the course. Competency is defined as being able
to demonstrate correct decision-making processes,
ALS refers to the healthcare that providers deliver
sequence care steps properly and demonstrate
to adults who are experiencing a cardiovascular,
proficiency in completing all required skills without any
cerebrovascular or respiratory emergency. The
coaching or assistance.
psychomotor skills needed to perform high-quality
CPR; use an AED, a defibrillator, or both; and relieve There are two ways to complete American Red Cross
an obstructed airway are the foundation of ALS. As an ALS training. You may take a traditional instructor-led
ALS provider, you must also be able to use advanced course, or you may take a blended learning course that
assessment skills to recognize problems and prioritize consists of an online session and an in-person skills
interventions. Finally, you must be able to provide session conducted by a Red Cross–certified instructor.
effective care for cardiovascular, cerebrovascular and
respiratory emergencies based on specific advanced To successfully complete the Advanced Life Support
life support science-based recommendations. ALS Instructor-Led Training course, you must:
integrates the following key concepts to help providers ■ Attend the entire course and participate in all class
achieve optimal patient outcomes (Figure 1-3): lessons.
■ Teamwork: Integration and coordination of all team ■ Actively participate in all course activities, including
members working together toward a common goal assuming various roles during skill practice and
practice scenarios.
■ Communication: A closed-loop process involving
a sender, message and receiver ■ Demonstrate competency in all required skills.
■ Critical thinking: Clear and rational thinking used ■ Demonstrate competency in leading a team
to identify the connection between information and response during the team response testing
actions scenarios.
■ Problem solving: Using readily available resources ■ Successfully pass the final exam with a minimum
to identify solutions to issues that arise while grade of 84 percent.
providing care To successfully complete the Advanced Life Support
Blended Learning course, you must:

Course Completion ■ Complete the online session, which includes:

c Successfully completing each lesson, including
Requirements the post-assessment.
c Successfully passing the online final exam with a
Many agencies, organizations and individuals look to the minimum grade of 84 percent.
Red Cross for formal training that results in certification.
■ Attend and actively participate in the in-person skills
Red Cross certification means that on a particular date session, during which you must:
c Participate in all skill stations.
c Demonstrate competency in all required skills.
c Demonstrate competency in leading a team
response during the team response testing
scenarios.
Upon successful completion of the course and after
the training has been reported, you will receive a
course completion certificate from the American Red
Cross that includes your name, the course name, the
completion date and the certification validity period.
The course completion certificate can be downloaded,
printed or shared, as needed. Each American Red
Cross certification contains a QR code that can be
used by participants, instructors, employers or the
Figure 1-3 | Teamwork, communication, critical thinking
and problem solving are essential for achieving optimal American Red Cross to validate certificate authenticity.
patient outcomes.

Chapter 1 | Advanced Life Support Course Introduction | 3

 CHAPTER
2

Basic Life Support Review

Introduction
Expert basic life support (BLS) skills (performing high-quality CPR, using an AED
and relieving an obstructed airway) are essential skills for all healthcare providers
to possess. Mastery of these foundational skills is vital in order to achieve the best
possible outcomes for patients in cardiac or respiratory arrest and for patients who
have an obstructed airway.
Cardiac Chain of Survival restore an effective heart rhythm, increasing the
patient’s chance for survival.
The Cardiac Chain of Survival describes six actions ■ Integrated post–cardiac arrest care to
that, when performed in rapid succession, increase optimize ventilation and oxygenation and
the patient’s likelihood of surviving sudden cardiac treat hypotension immediately after the return
of spontaneous circulation. After return of
arrest. The six links in the Cardiac Chain of Survival vary
spontaneous circulation (ROSC), survival outcomes
slightly, depending on where the cardiac arrest occurs. are improved when providers work to stabilize the
patient, minimize complications, and diagnose and
In-Hospital Cardiac Chain of treat the underlying cause.
Recovery. Continued follow-up during the recovery
Survival ■
process in the form of rehabilitation, therapy and
support from family and healthcare providers
Only one of every five cardiac arrests in the United improves outcomes.
States occurs inside of a hospital. The Adult In-Hospital
Cardiac Chain of Survival (Figure 2-1) includes six links: Out-of-Hospital Cardiac Chain of
■ Surveillance and prevention. Hospitalized Survival
patients often show changes in vital signs and other
clinical parameters in the minutes and hours leading
up to cardiac arrest. Closely monitoring for changes Most sudden cardiac arrests occur outside of the
in the patient’s condition that could be warning hospital. When this is the case, the patient relies on
signs of impending arrest and activating the rapid members of the community, EMS and healthcare
response team as appropriate may allow providers to providers to implement the Cardiac Chain of Survival.
intervene and prevent the arrest from occurring. The Adult Out-of-Hospital Cardiac Chain of Survival
■ Recognition of a cardiac emergency and (Figure 2-2) includes six links:
activation of the emergency response system.
Recognizing cardiac arrest and summoning ■ Recognition of a cardiac emergency and
advanced help in the form of the resuscitation team activation of the emergency response system.
provides the patient with access to necessary Immediate recognition of cardiac arrest and
personnel, equipment and interventions as soon after activation of the EMS system provides the patient
arrest as possible. with access to necessary personnel, equipment and
interventions as soon after arrest as possible.
■ Early high-quality CPR. High-quality CPR, starting
with compressions, should be initiated immediately ■ Early high-quality CPR. High-quality CPR, starting
once cardiac arrest is recognized. with compressions, should be initiated immediately
once cardiac arrest is recognized, ideally by those at
■ Early defibrillation to help restore an effective the scene prior to EMS arrival.
heart rhythm and significantly increase the
patient’s chance for survival. Defibrillation may

Figure 2-1 | The In-Hospital Cardiac Chain of Survival for adults

6 | American Red Cross | Advanced Life Support

 Figure 2-2 | The Out-of-Hospital Cardiac Chain of Survival for adults

■ Early defibrillation to help restore an effective Principles of High-Quality CPR

heart rhythm and significantly increase the
patient’s chance for survival. Use of an AED by
those at the scene prior to EMS arrival may restore an To provide high-quality CPR:
effective heart rhythm, increasing the patient’s chance ■ Position the patient supine on a firm, flat surface and
for survival. expose the patient’s chest, then immediately begin
■ Advanced life support using advanced medical chest compressions.
personnel who can provide the proper tools ■ Provide compressions at the correct rate (100 to
and medication needed to continue the 120 per minute) and at the proper depth (at least 2
lifesaving care. Early advanced life support inches [5 cm] but no more than 2.4 inches [6 cm] for
provided by EMS professionals at the scene and en an adult). When given at the proper rate, it should
route to the hospital provides the patient with access take 15 to 18 seconds to perform 30 compressions.
to emergency medical care delivered by trained ■ Allow the chest to recoil fully after each
professionals. compression. Compression and recoil times should
■ Integrated post–cardiac arrest care to be approximately equal. This allows the heart to fill
optimize ventilation and oxygenation and treat adequately during recoil, maximizing the cardiac
hypotension immediately after the return of output generated with the next compression.
spontaneous circulation. After ROSC, survival ■ Minimize interruptions in chest compressions. When
outcomes are improved when providers work to compressions stop, blood flow to vital organs stops.
stabilize the patient, minimize complications, and In addition, after stopping compressions, some time is
diagnose and treat the underlying cause. required to regain the minimum coronary perfusion
■ Recovery. Continued follow-up during the recovery pressure (CPP) necessary to achieve ROSC (Figure
process in the form of rehabilitation, therapy and 2-3). The CPP is the difference between the pressure
support from family and healthcare providers in the aorta and the pressure in the right atrium during
improves outcomes. diastole and is a reflection of myocardial blood flow.
Maintaining adequate CPP (greater than 20 mmHg)
during CPR has been shown to increase the likelihood
High-Quality CPR of ROSC and survival.
■ Avoid excessive ventilations. Each ventilation should
The point of CPR is to circulate oxygenated blood to vital last about 1 second and deliver just enough volume
organs when the heart and normal breathing have stopped. to make the chest begin to rise.
However, even at its best, CPR provides only a fraction of
Proper compression technique is important. Position
the normal blood flow to the brain and heart. To optimize
the heel of one hand in the center of the chest, on the
patient outcomes and increase the likelihood of ROSC,
lower half of the sternum, with your other hand on top.
providers must strive to provide the highest quality CPR at
Interlace your fingers and lift your fingers off the chest.
all times.
Position yourself so that your shoulders are directly over
your hands, and keep your arms as straight as possible
(Figure 2-4). Compress the chest using a straight up-
and-down motion. Avoid leaning on the patient’s chest.

Chapter 2 | Basic Life Support Review | 7

Minimum CPP for
ROSC (20 mmHg)

0 mmHg

Figure 2-3 | When compressions stop, the coronary perfusion pressure (CPP) drops below 20 mmHg, the minimum level
needed to increase the likelihood of return of spontaneous circulation (ROSC) and survival.

High-performance CPR refers to providing high-quality performance. Data collected about the effectiveness of
CPR as part of a well-organized team response to a CPR allows for continuous improvement, both “in the
cardiac arrest. Coordinated, efficient teamwork helps to moment” and during future resuscitation events. After
minimize interruptions to compressions (Figure 2-5). In every resuscitation event, a debriefing session should be
addition, a team approach to CPR helps to maintain the held, during which the team analyzes their performance
quality of compressions by minimizing provider fatigue. using both qualitative and quantitative data. The purpose
Providers should switch off giving compressions every 2 of this analysis is to make changes as necessary to
minutes—or sooner if the provider giving compressions positively affect the outcome of future resuscitation
is fatigued. Finally, working as a team helps to ensure events.
that high-quality CPR is provided because the team
Methods of evaluating CPR quality include visual
leader is responsible for monitoring the delivery of CPR
observation, the use of feedback devices, calculations
and making adjustments in real time, enabling the team
such as the chest compression fraction (CCF) and
to achieve quality goals.
physiologic data obtained through capnography or
hemodynamic monitoring.
Continuous Quality Improvement
Visual Observation
Healthcare providers and their employers have a Visual observation is an important qualitative measure of
responsibility to ensure that they provide the highest high-quality CPR. Visual observation allows for in-the-
quality CPR throughout every resuscitation event. To moment adjustments to technique based on feedback
achieve this goal, it is necessary to gather data and use from the team leader or another team member. For
that data to inform improvements in individual and team

Figure 2-4 | Providing high-quality CPR relies on using Figure 2-5 | Efficient teamwork contributes to the provision
proper technique. of high-quality CPR.

8 | American Red Cross | Advanced Life Support

example, the team leader may observe that the provider 50

ETCO² mmHg
giving compressions is tiring or that compressions are
40
30
20
not being delivered at the correct rate or depth. These 10
0
observations allow the team leader to redirect the team
as necessary to get back on track. Figure 2-6 | The normal capnography waveform is square
with a flat plateau. In patients with normal perfusion,
Feedback Devices capnography values are between 35 and 45 mmHg.
Feedback devices use technology to gather data about
CPR performance and provide real-time feedback. expected range also suggests that ventilations are
These devices collect objective data, such as the rate at effective.
which compressions and ventilations are being delivered, Normal ETCO2 levels are in the range of 35 to 45 mmHg.
the depth of compressions and the amount of chest In low-perfusion states such as cardiac arrest, the ETCO2
recoil. Many different types of feedback devices are levels are much lower (15 to 20 mmHg when high-
available, ranging from apps on smart watches to self- quality CPR is provided). If ETCO2 levels fall below 10
contained systems, some with attachments to place on mmHg, there could be a problem with the rate or quality
the patient. All feedback devices are designed to act as of compressions. Information obtained by monitoring
“virtual coaches,” guiding providers to adjust technique in capnography values allows the team to make the
order to perform effective, high-quality CPR. In addition, necessary adjustments to achieve higher-quality CPR.
most feedback devices record data that can be analyzed
after the resuscitation event, enabling improvements to Capnography is also an effective tool for determining
be implemented for future resuscitation events. ROSC and for helping the resuscitation team to decide
when to discontinue CPR. A sudden and sustained
Chest Compression Fraction increase in ETCO2 levels is a strong indicator that the
The chest compression fraction (CCF) represents patient has achieved ROSC. Conversely, if ETCO2
the amount of time spent performing compressions and levels remain less than 10 mmHg in an intubated
is another way to gain objective feedback about the patient who has been receiving high-quality CPR for
quality of CPR. It is calculated by dividing the time that at least 20 minutes, the likelihood that the patient will
providers are in contact with the patient’s chest by the achieve ROSC is decreased, and the decision may be
total duration of the resuscitation event, beginning with made to terminate the resuscitation effort. If, however,
the arrival of the resuscitation team and ending with ETCO2 levels remain greater than 15 mmHg, the
the achievement of ROSC or the cessation of CPR. patient has an increased chance to achieve ROSC and
According to expert consensus, a CCF of at least 60% resuscitation efforts should continue.
is needed to promote optimal outcomes, and the goal
should be 80%. Many feedback devices are able to Invasive Hemodynamic Monitoring
calculate the CCF based on the data they collect. When In-hospital cardiac arrest often occurs in settings in
a feedback device is not in use, a team member may be which invasive hemodynamic monitoring is in progress
assigned to record data that can be used to calculate or can be quickly established. In such cases, if the
the CCF, such as the duration of the resuscitation event patient already has an indwelling arterial catheter, the
and the duration of periods when compressions were arterial diastolic pressure can be used to evaluate the
paused. adequacy of chest compressions. ROSC is more likely
when the arterial diastolic pressure is greater than 25
Capnography mmHg.
Capnography is a noninvasive technique that uses
sensors to detect end-tidal carbon dioxide (ETCO2)
levels, which are displayed as waveforms on a Approach to the Patient:
monitor (Figure 2-6). Carbon dioxide delivery to the Basic Life Support
lungs depends on cardiac output. When circulation
is adequate, a predictable amount of carbon dioxide The Basic Life Support: Adults and Adolescents Code
should be exhaled. So, the ETCO2 level is a quantitative Card summarizes the approach to providing basic life
measure of cardiac output—and by extension, the support care for an adult.
effectiveness of compressions. An ETCO2 level in the

Chapter 2 | Basic Life Support Review | 9

Rapid Assessment
Practice Note
The rapid assessment is used to gather information
Use the A-B-C mnemonic to easily recall and
about the patient and the emergency. First, conduct
perform the steps of the breathing and pulse check.
a quick visual survey: assess for safety, form an initial
Open the airway (A), check for the presence or
impression about the patient’s condition and determine
absence of normal breathing (B) and simultaneously
the need for additional resources. Look for life-
assess for circulation (C) by a pulse check. If
threatening bleeding while gathering an initial impression
necessary, begin CPR immediately, starting with
of the patient. If there is life-threatening bleeding, control
chest compressions.
it with any available resources (including a tourniquet,
hemostatic dressing, or both as appropriate) and, if not
If the patient is unresponsive, is not breathing (or has
already done, activate EMS, the rapid response team
ineffective ventilation) but has a pulse, the patient is in
or the resuscitation team. Next, if the patient appears
respiratory arrest or failure. Provide 1 ventilation every
to be unresponsive, quickly check for responsiveness,
6 seconds. Each ventilation should last about 1 second
breathing and a central pulse (Figure 2-7).
and make the chest begin to rise. Continue giving
■ To check for responsiveness, use a “shout-tap-shout” ventilations until the patient begins to breathe normally
sequence. Shout “Are you OK?” using the patient’s on their own, another trained provider takes over, you are
name if you know it. Tap the patient on the shoulders,
presented with a valid do not resuscitate (DNR) order,
then shout again. If the patient does not respond,
initiate the emergency response by calling for EMS, the pulse becomes absent (in which case you should
the rapid response team or the resuscitation team as begin CPR or use an AED if one is available and ready
appropriate and send someone to get an AED. to use) or the situation becomes unsafe.
■ To check for breathing and a pulse, open the airway
by using the head-tilt/chin-lift technique to tilt the If the patient is unresponsive, is not breathing normally
head to a past-neutral position. Use the modified jaw- (or is only gasping) and has no pulse, the patient is in
thrust maneuver if you suspect a head, neck or spinal cardiac arrest. Begin CPR immediately, starting with
injury. Once the airway is open, simultaneously check compressions, and use an AED as soon as it is available.
for breathing and a carotid pulse for no more than
10 seconds. Look again for life-threatening bleeding If the patient is breathing and has a pulse, perform
while checking for breathing and a pulse. Quickly the primary assessment and provide emergent/initial
scan down the body, looking for blood or other signs interventions. Position the patient as approprate for
and symptoms that might not have been seen during their clinical condition, and perform the secondary
the initial impression. assessment as the patient’s condition allows. Continually
reassess the patient, recognize issues and provide care
as needed.

The Rapid Assessment for Adults Skill Sheet provides

step-by-step guidance for conducting a rapid assessment.

CPR and AED

CPR
In most cases, when caring for an adult in cardiac arrest
(regardless of whether care is being provided by a
single provider or multiple providers), the hand position,
compression rate, compression depth and compression-
to-ventilation ratio of 30:2 remain the same. The exception
to this is when a patient has an advanced airway in
place. At minimum, two providers must be present. One
provider delivers 1 ventilation every 6 seconds. At the
same time, the second provider performs compressions.
Figure 2-7 | When a patient appears to be unresponsive,
Compressions should be delivered continuously (100
check for responsiveness, breathing and a pulse.

10 | American Red Cross | Advanced Life Support

to 120 per minute) with no pauses for ventilations when to 2 ventilations) until the AED prompts that it is
providing CPR to an adult patient with an advanced reanalyzing, the patient shows signs of ROSC or you
airway in place. are instructed by the team leader or more advanced
personnel to stop.
When multiple providers are available, the first provider
performs the rapid assessment and begins providing The AED Use for Adults Skill Sheet provides step-by-
CPR, starting with chest compressions. Meanwhile, step guidance for using an AED.
another provider calls for additional resources and
gets and prepares the AED, if available. The first
provider continues to provide high-quality CPR with 30 Approach to the Patient:
compressions to 2 ventilations until another provider is Obstructed Airway
ready to assist or the AED is ready to analyze.
A patient who cannot cough, speak, cry or breathe
The CPR for Adults Skill Sheet provides step-by-step requires immediate care. If the patient does not receive
guidance for performing CPR on an adult. quick and effective care, an airway obstruction can lead to
respiratory arrest, which in turn can lead to cardiac arrest.
AED
When a patient experiences cardiac arrest, an AED
should be applied as soon as one is available (Figure
Responsive Adult
2-8). AEDs are programmed to deliver a shock to a
A patient who is choking typically has a panicked,
patient in cardiac arrest when they detect ventricular
confused or surprised facial expression. The patient may
fibrillation or ventricular tachycardia. Early use of an AED
place one or both hands on their throat (the “universal
greatly increases the patient’s chance for survival.
sign of choking”). Other behaviors may include running
If CPR is in progress and more than one provider is about, flailing the arms or trying to get another’s
present, do not stop CPR to apply the AED. If you are attention. You may hear stridor (high-pitched squeaking
alone and an AED is available, you should use it as soon noises) as the patient tries to breathe, or you may hear
as you have determined that the patient is in cardiac nothing at all. The patient’s skin may initially appear
arrest. flushed, but it will become pale or cyanotic as the body
is deprived of oxygen.
Use adult AED pads. Place one pad to the right of the
sternum and below the right clavicle, and the other Encourage the patient who is coughing forcefully
pad on the left side of the chest on the midaxillary line to continue coughing until they are able to breathe
a few inches below the left armpit. Remember to stay normally. If the patient cannot breathe or has a weak
clear of the patient while the AED is analyzing the or ineffective cough, summon additional resources
rhythm or delivering a shock, and resume compressions and obtain consent. Then, provide up to 5 back blows
immediately after a shock is a delivered or the AED until the obstruction is relieved. If the obstruction is not
advises that a shock is not indicated. Perform about 2 relieved, transition to up to 5 abdominal or chest thrusts.
minutes of CPR (about 5 cycles of 30 compressions If necessary, continue with cycles of 5 back blows followed
by 5 abdominal or chest thrusts until the obstruction is
relieved or the patient becomes unresponsive.

Back Blows
To perform back blows, position yourself to the side and
slightly behind the patient. For a patient in a wheelchair,
you may need to kneel. Provide support by placing one
arm diagonally across the patient’s chest. Then bend the
patient forward at the waist so that the patient’s upper
body is parallel to the ground (or as close as it can be).
Using the heel of your other hand, give firm back blows
between the scapulae (Figure 2-9). Make each blow a
separate and distinct attempt to dislodge the object.

Figure 2-8 | Use an AED as soon as one is available.

Chapter 2 | Basic Life Support Review | 11

 Figure 2-9 | For effective back blows, bend the patient Figure 2-10 | To perform abdominal thrusts, place the thumb
forward at the waist and use the heel of your hand to give side of your fist just above the navel, cover the fist with your
back blows between the scapulae. other hand and give quick inward and upward thrusts.

Abdominal Thrusts Unresponsive Adult

To perform abdominal thrusts, stand behind the patient,
with one foot in front of the other for balance and stability. If a patient who is choking becomes unresponsive,
If possible, place your front foot between the patient’s feet. carefully lower them to a firm, flat surface, while
If the patient is in a wheelchair, you may need to kneel protecting their head. Then, send someone to get an
behind them. AED and summon additional resources (if appropriate
and you have not already done so). Immediately begin
Wrap your arms around the patient’s waist. Use one or CPR, starting with chest compressions. Compressions
two fingers to find the navel. Make a fist with one hand may help clear the airway by moving the blockage into
and place the thumb side of your fist against the middle the upper airway and the oropharynx, where it can be
of the abdomen, just above the navel. Grab your fist seen and removed.
with your other hand and give quick inward and upward
thrusts (Figure 2-10). Make sure each thrust is a distinct After each set of chest compressions and before
attempt to dislodge the object. attempting ventilations, open the patient’s mouth and
look for the object. If you see the object in the patient’s
Chest Thrusts mouth, remove it using a finger sweep. If you do not see
Chest thrusts should be used instead of abdominal the object, do not perform a blind finger sweep. Next,
thrusts if you cannot reach around the patient, the attempt 2 ventilations. Never try more than 2 ventilations
patient might be pregnant, the patient is in a bed or a during one cycle of CPR, even if the chest does not rise.
wheelchair with features that make abdominal thrusts Continue CPR, checking for an object before each set of
difficult to do, or abdominal thrusts are not effective in ventilations. Health care professionals with appropriate
dislodging the object. To perform chest thrusts, position training may consider the use of Magill forceps to
yourself behind the patient as you would for abdominal remove a foreign body obstructing the airway.
thrusts. Place the thumb side of your fist against the
center of the patient’s chest on the lower half of the
sternum. Then cover your fist with your other hand and
pull straight back, providing a quick inward thrust into
the patient’s chest. Make sure each thrust is a distinct
attempt to dislodge the object.

Airway Management Techniques

If back blows, abdominal thrusts and/or chest thrusts are
not effective or practical, use a combination of basic or
advanced airway management techniques based on your
level of training and experience.

12 | American Red Cross | Advanced Life Support

BASIC LIFE SUPPORT: ADULTS AND ADOLESCENTS
BLS - 2020 VERSION
Shock

Perform rapid assessment

Assess for life-threatening bleeding. If at any

time the patient has life-threatening bleeding,
control the hemorrhage with any available
resource (including the use of tourniquet or Responsive? YES
hemostatic dressing as appropriate).

NO

• Activate EMS, rapid response or resuscitation team

• Check breathing and pulse for no more than 10 sec
• At the same time, scan the body for life-threatening bleeding

Breathing
and pulse?

Not breathing Not breathing

Breathing
(or ineffective ventilation) (or only gasping breaths)
Pulse present
Pulse present Pulse absent

Respiratory Arrest* • Perform primary assessment

Cardiac Arrest* (Airway, Breathing, Circulation,
Respiratory Failure*
Disability, Exposure)
and emergent/initial interventions
A
Deliver 1 ventilation every 6 sec Start CPR †‡ • Position patient as appropriate for
clinical condition
• Single and multiple providers 30:2
• Perform secondary assessment as
patient condition allows
• Perform primary assessment
(Airway, Breathing, Circulation, • Use AED as soon as it is available • Reassess patient, recognize issues
Disability, Exposure) and emergent/ and provide care as needed
initial interventions, if not already done • Continue CPR until AED is ready
to analyze
• Continue to check breathing and
pulse every 2 min; if pulse becomes
absent, go to A
• Position patient as appropriate for Shockable
clinical condition rhythm? YES
• Perform secondary assessment as
patient condition allows NO

• Reassess patient, recognize issues and

provide care as needed • Resume CPR immediately for about
2 min or until the AED is ready to
analyze
• Continue cycles of CPR/AED until:
- The team leader tells you to stop
*For a suspected or known opioid overdose, pregnant - Other trained providers arrive
patient or obstructed airway follow the appropriate to relieve you
code card.
- You see signs of ROSC
†
If drowning is the suspected cause of cardiac arrest,
deliver 2 initial ventilations before starting CPR. - You are presented with a valid
‡
If an advanced airway is in place, one provider delivers DNR order
1 ventilation every 6 seconds, while the other provider - You are too exhausted to continue
delivers continuous chest compressions without pausing
for ventilations. - The situation becomes unsafe

Copyright © 2021 The American National Red Cross

Chapter 2 | Basic Life Support Review | 13

 BASIC LIFE SUPPORT: ADULTS AND ADOLESCENTS
BLS - 2020 VERSION

CPR Technique

• Hand position: Centered on the lower half of the sternum

Compression-to-ventilation • Depth: At least 2 inches (5 cm)

ratio: 30:2 • Rate: 100 to 120 per min
Compressions
• Full chest recoil: Compression and recoil times should be approximately equal

• Open airway to past-neutral position. Use modified jaw-thrust maneuver

instead if you suspect head, neck or spinal injury.
Switch CPR compressors • Each ventilation should last about 1 sec and make the chest begin to rise;
• Every 2 min allow the air to exit before delivering next ventilation.
• During rhythm check
• If provider is fatigued Ventilations • If an advanced airway is in place, one provider delivers 1 ventilation every
6 seconds, while the other provider delivers continuous chest compressions
without pausing for ventilations.

Copyright © 2021 The American National Red Cross

14 | American Red Cross | Advanced Life Support

SKILL SHEET
Rapid Assessment for Adults
Step 1 Perform a visual survey
• Make sure the environment is safe—for you, your team and any
individuals present during the emergency.

• Gather an initial impression of the patient, which includes

looking for life-threatening bleeding.

• Quickly determine the need for additional resources.

Alert
If at any time the patient has life-threatening bleeding, control the
hemorrhage with any available resource (including the use of a
tourniquet or hemostatic dressing as appropriate).

Step 2 Check for responsiveness

• Shout, “Are you OK?” Use the patient’s name if you know it.
• Tap the patient’s shoulder and shout again (shout-tap-shout).
• If the patient is unresponsive and you are alone, call for help
to activate EMS, the rapid response team or the resuscitation
team, as appropriate, and call for an AED.

• If the patient is unresponsive and you are with another provider, the
first provider stays with the patient. Other providers activate EMS,
the rapid response team or the resuscitation team, as appropriate,
and retrieve the AED, BVM and other emergency equipment.

© 2021 The American National Red Cross. ALL RIGHTS RESERVED | 1

Chapter 2 | Basic Life Support Review | 15
 SKILL SHEET
Rapid Assessment for Adults (continued)
Step 3 Simultaneously check for breathing, a pulse,
and life-threatening bleeding
• Make sure the patient is in a supine (face-up) position. If they are face-down, you must roll them onto
their back, taking care not to create or worsen a suspected injury.

• Open the airway to a past-neutral position using the head-tilt/

chin-lift technique; or, use the modified jaw-thrust maneuver if
you suspect a head, neck or spinal injury.

• Simultaneously check for breathing and a pulse (carotid) for

no more than 10 seconds.

• At the same time, scan the body for life-threatening bleeding

or other signs and symptoms that might not have been seen
during the initial impression.

Practice Note
A-B-C Mnemonic

Use the A-B-C mnemonic to easily recall and perform assessment, including opening of the airway
(A), checking for the presence or absence of normal breathing (B), and simultaneously assessing
for circulation (C) by a pulse check. If necessary, CPR should then begin with delivery of chest
compressions.

Step 4 Provide care based on the conditions found

© 2021 The American National Red Cross. ALL RIGHTS RESERVED | 2

16 | American Red Cross | Advanced Life Support
SKILL SHEET
CPR for Adults
Step 1 Conduct a rapid assessment
• Perform a quick visual survey looking for life-threatening
bleeding.

• Check for responsiveness.

• Open the airway and simultaneously check for breathing and a
pulse (carotid) for no more than 10 seconds. At the same time,
scan the body again for life-threatening bleeding.

• If the patient is not breathing (or only gasping) and their central
pulse is absent, begin CPR.

Step 2 Place the patient on a firm, flat surface

• In a healthcare setting, use a bed with a CPR feature, or place
a CPR board under the patient.

• Adjust the bed to an appropriate working height or use a step

stool. Lower the bed side rail closest to you.

• In other settings, move the patient to the floor or ground and

kneel beside them.

Step 3 Position your hands correctly

• Expose the patient’s chest to ensure proper hand placement
and visualize chest recoil.

• Place the heel of one hand in the center of the patient’s chest
on the lower half of the sternum.

• Place your other hand on top of the first and interlace your
fingers or hold them up so that they are not resting on the
patient’s chest.

© 2021 The American National Red Cross. ALL RIGHTS RESERVED | 1

Chapter 2 | Basic Life Support Review | 17
 SKILL SHEET
CPR for Adults (continued)
Step 4 Position your body effectively
• Position yourself so your shoulders are directly over your hands.
This position lets you compress the chest using a straight up-
and-down motion.

• To help keep your arms straight, lock your elbows.

Practice Note
If drowning is the suspected cause of cardiac arrest, deliver 2
initial ventilations before starting CPR.

Step 5 Perform 30 chest compressions

• For an adult, compress the chest to a depth of at least 2 inches
(5 cm). If you are using a feedback device, make sure the
compressions are no more than 2.4 inches (6 cm) deep.

• Provide smooth compressions at a rate of 100 to 120 per minute.

• Allow the chest to fully recoil after each compression. Avoid
leaning on the patient’s chest at the top of the compression.
Compression and recoil times should be approximately equal
as this improves the circulation generated by CPR.

Practice Note
Consider the use of mechanical CPR (mCPR) devices for an adult patient in cardiac arrest, if the BLS
response team is practiced and adept at rapid application with less than a 10-second interruption in chest
compressions.

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18 | American Red Cross | Advanced Life Support
SKILL SHEET
CPR for Adults (continued)
Step 6 Seal the mask and open the airway
• Use an adult pocket mask for single-provider CPR or a BVM
for multiple-provider CPR. Remember, a two-person technique
for BVM ventilation is the preferred methodology.

• Seal the mask and simultaneously open the airway to a

past-neutral position using the head-tilt/chin-lift technique.

• Or, use the modified jaw-thrust maneuver if you suspect a

head, neck or spinal injury.

Practice Note
Attach supplemental oxygen to the BVM resuscitator as soon as appropriate and when enough resources
are available.

Step 7 Provide 2 ventilations

• While maintaining the mask seal and open airway, provide
smooth, effortless ventilations. Each ventilation should last
about 1 second and make the chest begin to rise; allow the
air to exit before delivering next ventilation. Avoid excessive
ventilation.

• If you do not have a pocket mask or BVM, provide mouth-to-

mouth or mouth-to-nose ventilations.

© 2021 The American National Red Cross. ALL RIGHTS RESERVED | 3

Chapter 2 | Basic Life Support Review | 19
 SKILL SHEET
CPR for Adults (continued)
Practice Note
If an advanced airway is in place, one provider delivers 1 ventilation every 6 seconds. If an advanced
airway is in place, the 30:2 ratio does not apply. In this case, one provider delivers 1 ventilation every 6
seconds, while the other provider delivers continuous chest compressions without pausing for ventilations.

Step 8 Switch positions every 2 minutes

• When providing CPR with multiple providers, smoothly switch

positions about every 2 minutes. This should take less than 10
seconds.

• The compressor calls for a position change by saying “switch”

in place of the number 1 in the compression cycle.

Step 9 Continue CPR

Continue providing CPR until:

• The team leader tells you to stop

• Other trained providers arrive to relieve you
• You see signs of ROSC
• You are presented with a valid DNR order
• You are too exhausted to continue
• The situation becomes unsafe

Practice Note
Upon achieving ROSC, supplemental oxygen should be used based on your facility’s protocols to maintain
a normal oxygen saturation level while avoiding hyperoxygenation. Providers should use a pulse oximeter to
monitor oxygen saturation.

© 2021 The American National Red Cross. ALL RIGHTS RESERVED | 4

20 | American Red Cross | Advanced Life Support
SKILL SHEET
AED Use for Adults
Step 1 Turn on the AED and follow the prompts
• Because AED models function differently, follow your
facility's protocols and the manufacturer’s instructions for the
AED you have.

Step 2 Expose the chest

• Expose the chest and wipe it dry, if necessary.

Step 3 Attach the pads

• Use an anterior/lateral pad placement, according to the
manufacturer instructions:

• Place one pad on the upper right chest, below the right
clavicle to the right of the sternum.

• Place the other pad on the left side of the chest along the
midaxillary line a few inches below the armpit.

• Or, use an anterior/posterior placement, according to the

manufacturer instructions:

• Place one pad to the center of the patient’s chest—on the

sternum.

• Place one pad to the patient’s back between the scapulae.

Alert
Do not use pediatric AED pads or pediatric levels of energy on
an adult or on a child older than 8 years or weighing more than
55 pounds.

© 2021 The American National Red Cross. ALL RIGHTS RESERVED | 1

Chapter 2 | Basic Life Support Review | 21
 SKILL SHEET
AED Use for Adults (continued)
Practice Note
It is safe to use an AED on a pregnant patient. However, AED
pads should not incorporate any breast tissue.

Step 4 Prepare to let the AED analyze the heart’s rhythm

• If necessary, plug in the connector and push the analyze button.
• Instruct everyone to stand clear while the AED analyzes. No
one, including you, should be touching the patient.

• If you are working as a team, prepare to smoothly switch

positions to prevent fatigue. The provider giving compressions
should hover their hands above the patient’s chest.

Practice Note
When the AED is analyzing the rhythm, pause compressions
and ventilations, even when using devices with artifact-filtering
algorithms.

Step 5 Deliver a shock, if the AED determines one is needed

• If the AED advises a shock, again instruct everyone to stand
clear. The compressor should continue to hover their hands
over the patient’s chest in preparation for CPR.

• Press the shock button to deliver the shock.

© 2021 The American National Red Cross. ALL RIGHTS RESERVED | 2

22 | American Red Cross | Advanced Life Support
SKILL SHEET
AED Use for Adults (continued)
Step 6 After the AED delivers the shock, or if no shock is needed
• Immediately begin CPR.
• Continue for about 2 minutes until:
• The AED prompts that it is reanalyzing.
• The patient shows signs of return of spontaneous circulation.
• The team leader or other trained providers instruct you to stop.
• If you are working as a team, smoothly switch positions
approximately every 2 minutes (which usually occurs at the time
of AED analysis) to prevent fatigue.

Practice Note
After a shock is delivered, immediately resume CPR for 2 minutes before pausing compressions
for the AED to analyze the heart rhythm. However, based on the clinical situation, you may consider
performing rhythm analysis after defibrillation, recognizing that this may not be possible on all AEDs.

© 2021 The American National Red Cross. ALL RIGHTS RESERVED | 3

Chapter 2 | Basic Life Support Review | 23
 CHAPTER
3

Tools and Therapies

Introduction
As a member of a high-performance resuscitation team, you must be familiar with the
equipment and interventions that are used most frequently when caring for a patient
who is experiencing a cardiovascular, cerebrovascular or respiratory emergency. This
chapter reviews equipment and interventions commonly used to assess and stabilize an
acutely ill patient.
Airway Management Basic Airways

Suctioning An oropharyngeal airway (OPA) or nasopharyngeal

airway (NPA) can be used to maintain an open airway.
Suctioning is used to clear the airway of excessive
secretions, vomitus or blood. Suctioning can be Practice Note
performed through the nose or mouth and when a basic
or advanced airway is in place. When providing ventilations to a patient with an OPA
or NPA in place, maintain an open airway using the
Suctioning is performed using a flexible or rigid catheter head-tilt/chin-lift technique or the jaw-thrust maneuver.
that is attached via tubing to a suction unit, which may
be wall-mounted or portable. The suction unit has a
Oropharyngeal Airway
pressure gauge to indicate the amount of negative
pressure (suction force) and a collection canister. An OPA provides a channel for air movement and
suctioning. The curved body of the airway fits over the
■ Flexible catheters are inserted through the mouth
tongue and holds it up and away from the posterior wall
or nose and are best suited for removing thin, fluid
secretions from the oropharynx or nasopharynx. A sterile of the pharynx (Figure 3-1).
flexible catheter is used to suction an endotracheal tube.
An OPA is only indicated for use in an unconscious
■ Rigid (Yankauer) catheters are inserted through
patient. Do not use an OPA in a conscious or
the mouth and are best suited for removing thick or
particulate matter from the oropharynx. semiconscious patient with intact cough or gag reflexes.
In addition, avoid using an OPA in patients with oral
trauma or who have recently undergone oral surgery.
Practice Note
The Inserting an Oropharyngeal Airway (OPA) Skill
Use appropriate personal protective equipment (e.g., Sheet provides step-by-step guidance for inserting an
face shield, gown, gloves) when suctioning a patient. OPA.

Nasopharyngeal Airway
An NPA is a soft rubber tube with a flange on one end
Practice Note and a beveled tip on the other. NPAs are available in a
Suctioning can induce hypoxia and bradycardia (as range of diameters. The NPA is inserted through the nose
a result of vagal stimulation). Always monitor the and extends to the posterior pharynx to provide a channel
patient’s oxygen saturation, heart rate and rhythm for air movement and suctioning (Figure 3-2).
and appearance while suctioning. If the patient An NPA may be used in a conscious, semiconscious
shows signs of compromise (e.g., decreased oxygen or unconscious patient. Do not use an NPA in a patient
saturation, bradycardia, arrhythmia, cyanosis), stop with a possible skull or facial fracture. Exercise caution if
suctioning immediately, administer high-flow oxygen considering use of an NPA in a patient with suspected
and provide ventilation assistance as needed. head trauma.

Curved body

Bite block

Flange

Figure 3-1 | Oropharyngeal airway

26 | American Red Cross | Advanced Life Support

 Flange

Beveled
tip

Figure 3-2 | Nasopharyngeal airway

The Inserting a Nasopharyngeal Airway (NPA) Skill Sheet Types of Advanced Airways
provides step-by-step guidance for inserting an NPA.
Advanced airway options include supraglottic airways
and transglottic airways (Table 3-1). Supraglottic
Advanced Airways airways, such as laryngeal mask airways and laryngeal
tubes, do not pass through the vocal cords, whereas
Placement of an advanced airway is indicated when: transglottic airways, such as endotracheal tubes, do.
■ An open airway cannot be maintained using manual The choice of advanced airway depends on the patient’s
techniques or a basic airway. condition, the available resources and the provider’s
■ Airway protection is necessary because of impaired capabilities and scope of practice.
airway reflexes (e.g., as a result of impaired level of
consciousness). Laryngeal Mask Airway
■ Continuous ventilation management is required. The laryngeal mask airway consists of an airway tube
The risks of placing an advanced airway must be weighed and a mask with an inflatable cuff at the distal end. The
against the potential benefits. Improper placement of an mask is advanced along the contour of the pharynx
advanced airway can lead to complications that further with the aperture of the mask facing the tongue until
destabilize the patient. Additionally, although it is possible resistance is met. Properly positioned, the mask
to place supraglottic airways while CPR is in progress opening overlies the glottis, while the bottom rim
without pausing compressions, endotracheal intubation wedges up against the upper esophageal sphincter,
may require pausing compressions briefly. If it is possible creating a seal. Once the cuff of the mask is inflated, the
to maintain adequate ventilation with a bag-valve-mask glottis is isolated, permitting air from the tube to enter
(BVM) resuscitator, consider delaying placement of an the trachea (Figure 3-3).
advanced airway.

Figure 3-3 | Laryngeal mask airway

Chapter 3 | Tools and Therapies | 27

 Table 3-1 | Advanced Airways
Advanced Airway Advantages Limitations Precautions
■ Laryngeal mask airway ■ Trained providers more ■ Does not offer ■ Improper placement
readily available; easier protection of the airway may cause suboptimal
to learn how to insert from aspiration as an ventilation, gastric
(as compared with an endotracheal tube does distension or
endotracheal tube) ■ May not be effective for laryngospasm/
■ Alternative to patients requiring higher obstruction of the
endotracheal intubation ventilation pressures airway
when patient access is (e.g., those with lung ■ Head movement and
limited or positioning disease) suctioning of the
of the patient for pharynx can cause
endotracheal intubation displacement of the
is impossible device
■ Lower risk for ■ Tissue damage may
regurgitation (as occur with prolonged
compared with BVM use
ventilation)
■ Can be inserted
during CPR without
interrupting chest
compressions
■ Laryngeal tube ■ Trained providers more ... ...
readily available; easier
to learn how to insert
(as compared with an
endotracheal tube)
■ Isolates the airway and
reduces the risk for
aspiration (as compared
with BVM ventilation)
■ Can be inserted
during CPR without
interrupting chest
compressions

■ Endotracheal tube ■ Offers protection of the ■ Training is more ■ Improper placement

airway from aspiration complex than for can result in severe
■ Facilitates tracheal supraglottic airways complications, including
suctioning ■ Skill is outside scope brain damage and death
■ Provides an alternate of practice for many
administration route for providers
some medications ■ Providers require a
■ Best choice when the great deal of practice
need for long-term and experience to
assisted ventilation is become proficient
anticipated ■ Requires laryngoscopy
■ High incidence of
complications when
placement is attempted
by inexperienced
providers

28 | American Red Cross | Advanced Life Support

 Figure 3-4 | Laryngeal tube

Laryngeal Tube nasotracheal intubation). The orotracheal route is used

The laryngeal tube consists of an airway tube with most often because it is faster and associated with fewer
a larger, proximal oropharyngeal cuff and a smaller, complications. Endotracheal intubation is facilitated by
distal esophageal cuff. The laryngeal tube is inserted direct visualization of the airway using a laryngoscope
against the hard palate and advanced down the midline equipped with a light source.
until resistance is met. When properly positioned and The endotracheal tube consists of an airway tube with
the cuffs are inflated, the proximal cuff isolates the an inflatable cuff and beveled tip at the distal end and
laryngopharynx from the oropharynx and nasopharynx, a connector at the proximal end. A stylet may be used
and the distal cuff isolates the laryngopharynx from the to stiffen and shape the endotracheal tube to facilitate
esophagus (Figure 3-4). insertion. The laryngoscope blade is used to displace the
epiglottis and the endotracheal tube is passed through the
Endotracheal Tube
vocal cords and into the trachea. When the endotracheal
Use of an endotracheal tube may be preferred over a tube is properly inserted and the cuff is inflated, the cuff
supraglottic airway when there is disease at or below the forms a seal against the walls of the trachea (Figure 3-5).
level of the glottis, when prolonged assisted ventilation is
needed or when higher ventilatory pressures are required. Laryngoscope blades (Figure 3-6) may be straight
Endotracheal intubation also protects the airway from (e.g., Miller blade) or curved (e.g., Macintosh blade)
aspiration of gastric contents, a protection that cannot be and are available in various sizes. Ensure that backup
ensured with supraglottic airways. blades a few sizes smaller and a few sizes larger than
the selected blade are available before beginning
The endotracheal tube may be inserted through the the procedure. Test the lightbulbs on the selected
mouth (i.e., orotracheal intubation) or the nose (i.e., and backup blades by attaching the blade to the

Figure 3-5 | Endotracheal tube

Chapter 3 | Tools and Therapies | 29

 placement of an advanced airway is verified using both
physical assessment techniques and confirmation
devices, such as capnography, a colorimetric or other
nonwaveform exhaled carbon dioxide detector or an
A
esophageal detector device.

Practice Note
Nonwaveform exhaled carbon dioxide detectors are
not effective for confirming correct airway placement
in low-perfusion states (e.g., cardiac arrest, shock).

B
Physical Assessment
Always assess the patient after placing an advanced
airway for clinical indications of correct placement. These
include bilateral chest rise with ventilations, bilateral
Figure 3-6 | Laryngoscope blades. (A) Straight (Miller) blade. breath sounds and an absence of gurgling sounds on
(B) Curved (Macintosh) blade.
auscultation of the epigastric region.

laryngoscope handle. Tighten each lightbulb to prevent Capnography

dislodgement during intubation.
Capnography is considered the most reliable means of
quickly confirming and monitoring endotracheal tube
Practice Note placement. Although studies have not yet validated
capnography’s effectiveness for confirming and monitoring
To minimize interruptions to chest compressions during placement of other types of advanced airways, it stands
endotracheal intubation, be prepared to insert the to reason that effective ventilations when a supraglottic
laryngoscope blade and advance the endotracheal airway is in use would also produce the expected end-
tube as soon as compressions are paused. Pause tidal carbon dioxide (ETCO2) values and capnography
compressions only long enough to pass the waveforms.
endotracheal tube through the vocal cords.
To confirm endotracheal tube placement using
capnography:
■ Attach the capnography sampling device directly to
Practice Note the endotracheal tube and attach the ventilation bag
to the adapter.
Intubation of the right (most common) or left mainstem ■ Provide 1 full ventilation and wait for a waveform to
bronchus is a possibility if the endotracheal tube appear on the monitor. With some devices, this may
is advanced too far. In this case, only one lung will take up to 3 seconds.
be ventilated, which can lead to hypoxemia and c A four-point square waveform indicates
overinflation of the ventilated lung. Clinical signs of tracheal intubation. Note that in cardiac arrest,
right or left mainstem bronchus intubation include capnography will only record a waveform when
unilateral chest expansion and breath sounds. compressions and ventilations are being given.
■ Equal bilateral breath sounds and three square
waveforms in a row on the monitor confirm correct
placement of the endotracheal tube.
Confirming Placement of an c Esophageal intubation will not produce a
Advanced Airway waveform, or it will produce a waveform that is not
When an advanced airway is in use, confirming its well defined.
correct placement initially is essential. In addition, airway c If the waveform is square but breath sounds

placement should be confirmed whenever the patient’s are absent on the left, right mainstem bronchus
intubation is likely.
position changes and on an ongoing basis. Correct

30 | American Red Cross | Advanced Life Support

■ After confirming correct placement, secure the bag and the mask prevents exhaled air from re-entering
endotracheal tube and control ventilations, keeping the bag. When an advanced airway is in place, the bag is
the ETCO2 level between 35 and 45 mmHg in normal attached to the advanced airway, rather than to a mask.
perfusion states.
The BVM resuscitator can be used with ambient air or
attached to supplemental oxygen. Most BVM resuscitators
Practice Note come with the oxygen reservoir already attached. When
When an advanced airway is in place, always monitor the BVM resuscitator is connected to a high-flow (15 L/
the patient for signs of compromise. Clinical signs min) supplemental oxygen source, the reservoir fills with
of compromise, a change in capnography waveform oxygen. The reservoir, which fills when the patient exhales,
appearance or a sudden decrease in the ETCO2 allows for the maximum concentration of oxygen to be
level may be signs of airway displacement or other delivered to the patient with each ventilation.
complications.
A BVM resuscitator can be used by one or two providers.
Performing BVM resuscitation as a two-person technique
Bag-Valve-Mask Ventilation is essential for providing adequate mask seal and thus
adequate ventilation. When there is only one provider
Ventilation is the mechanical process of moving air into to deliver ventilations, using a pocket mask provides
and out of the body. When spontaneous breathing is better ventilation volume. However, factors such as
absent or is insufficient to support adequate ventilation limited personnel or the need to perform other time-
and gas exchange, assisted ventilation is indicated. A critical interventions may preclude using two-person
BVM resuscitator is used to ventilate the patient while BVM technique. Additionally, the need for positive
awaiting placement of an advanced airway or when the end-expiratory pressure (PEEP), infection control
need for assisted ventilation is expected to be short- or supplemental oxygen may require use of a BVM
term. Using a BVM resuscitator correctly requires ample resuscitator over a pocket mask. In these situations, one-
training and practice. person BVM technique is allowable.

The BVM resuscitator consists of a cushioned mask that To minimize complications when using a BVM resuscitator,
fits over the patient’s mouth and nose and is connected depress the bag slowly (over 1 second) and only about
via a one-way valve to a self-inflating compressible halfway to deliver the minimal tidal volume. Complications
chamber, or bag (Figure 3-7). Squeezing the bag with the that can result from improper technique include:
mask properly sealed over the patient’s mouth and nose ■ Decreased cardiac output. Positive pressure
forces air into the lungs (positive pressure ventilation). ventilation increases the intrathoracic pressure, which
Releasing the bag causes it to self-inflate by drawing air in turn decreases venous return.
in from the other end. The one-way valve between the ■ Barotrauma. Delivering too much pressure can
damage the airways, lungs and other organs.
Intake Oxygen Volutrauma. Excessive volume can lead to tension
One-way valve reservoir
■
pneumothorax (especially in patients with lung
valve
disease).
■ Gastric insufflation. Increased airway pressure
can cause air to enter the stomach, leading to gastric
distension and increasing the risk for regurgitation
and aspiration.
Oxygen Pay close attention to any increasing difficulty when
Bag port providing ventilations using a BVM resuscitator. This
Face difficulty may indicate an increase in intrathoracic
mask pressure, inadequate airway opening or other
Oxygen
complications. Be sure to share this information with the
tubing
team for corrective actions.

The Using a Bag-Valve-Mask (BVM) Resuscitator—One

Provider Skill Sheet and the Using a Bag-Valve-Mask
Resuscitator—Two Provider Skill Sheet provide step-by-
Figure 3-7 | Parts of a bag-valve-mask (BVM) resuscitator step guidance for using a BVM resuscitator.

Chapter 3 | Tools and Therapies | 31

Supplemental Oxygen Bag-Valve-Mask Resuscitator
A BVM resuscitator can be used on a breathing or
The administration of supplemental oxygen is often nonbreathing patient. A BVM resuscitator with an
indicated for patients experiencing a cardiovascular, oxygen reservoir bag is capable of supplying an oxygen
cerebrovascular or respiratory emergency. Oxygen concentration of 90% or more when used at a flow rate of
delivery systems consist of an oxygen source (wall- 15 L/min or more. As when using a non-rebreather mask,
mounted or an oxygen cylinder), a flowmeter and a occlude the one-way valve before applying the mask to
delivery device. Oxygen cylinders also have a pressure allow the reservoir to fill with oxygen.
regulator, which reduces the pressure of the oxygen to a
safe level. Pulse Oximetry
Oxygen Delivery Devices Oxygen therapy is typically titrated to achieve an oxygen
saturation of 94% to 99% on pulse oximetry.
The maximum flow rate and concentration of oxygen
that can be delivered vary according to the delivery An oximeter consists of a clip-on probe with light-emitting
device (Table 3-2). Factors that influence the choice diodes on one side and a light detector on the other.
of delivery device include whether the patient When the probe is placed on a finger, toe or earlobe,
is spontaneously breathing or requires assisted beams of red and infrared light are passed through the
ventilation, the degree of oxygen desaturation, tissues to the light detector on the other side. Oxygenated
equipment availability and patient comfort. hemoglobin absorbs more infrared light, allowing more
red light to pass through, and deoxygenated hemoglobin
Nasal Cannula absorbs more red light, allowing more infrared light to
A nasal cannula is only suitable for use on a pass through. The ratio of red to infrared light that reaches
spontaneously breathing patient. The nasal cannula is the light detector is translated into a measurement of
commonly used for patients with only minor breathing how much oxygen the blood is carrying, referred to as
difficulty or for those who have a history of respiratory the peripheral capillary hemoglobin oxygen saturation, or
disease and is useful for patients who cannot tolerate SpO2.
a face mask. Patients experiencing a serious breathing
To establish pulse oximetry monitoring:
emergency generally breathe through the mouth and
need a device that can supply a greater concentration ■ Position an appropriately sized probe on a finger, toe
of oxygen. or earlobe. If using a finger or toe, remove any nail
polish from the nail. Avoid placing the probe on an
Simple Oxygen Face Mask extremity being used for blood pressure monitoring
because cuff inflation will interfere with pulse oximetry
Simple oxygen masks can deliver high-flow oxygen. readings.
However, because room air is entrained through the side ■ Connect the probe to the pulse oximeter and ensure
ports and, potentially, around the mask, delivered oxygen that the probe is working by confirming that it is
concentrations are in the range of 35% to 55%. emitting a red light.
■ After a few seconds, look for a pulse indicator or
Non-Rebreather Mask waveform on the monitor indicating that the probe
A non-rebreather mask is used to deliver high has detected a pulse; otherwise, the reading will be
inaccurate.
concentrations of oxygen to a breathing patient. The one-
way valve prevents exhaled air from mixing with the oxygen
in the reservoir bag. The patient inhales oxygen from the Practice Note
bag and exhaled air escapes through flutter valves on
the side of the mask. To inflate the reservoir bag, occlude Some factors may reduce the reliability of the pulse
the one-way valve with your gloved thumb before placing oximetry reading, including hypoperfusion (shock),
the mask on the patient’s face. The oxygen reservoir bag cardiac arrest, excessive patient motion, carbon
should be sufficiently inflated (about two-thirds full) so monoxide poisoning, hypothermia, sickle cell disease
it does not deflate when the patient inhales. If the bag or anemia, a history of smoking and edema.
deflates, increase the flow rate of the oxygen to refill the
reservoir bag.

32 | American Red Cross | Advanced Life Support

Table 3-2 | Oxygen Delivery Devices
Delivery Device Description Oxygen Flow Oxygen Appropriate
Rate, L/min Concentration, % for
Nasal cannula Held in place over the patient’s 1–6 24–44 Breathing
Low flow ears; oxygen is delivered through patients only
High flow two small prongs inserted into
the nostrils

Simple oxygen face mask Pliable, dome-shaped mask that 6–15 35–55 Breathing
fits over the mouth and nose with patients only
an oxygen inlet and side ports to
permit egress of exhaled gas

Non-rebreather mask Face mask with an attached 10–15 Up to 90 Breathing

oxygen reservoir bag and one- patients only
way valve between the mask and
bag; patient inhales oxygen from
the bag, and exhaled air escapes
through flutter valves on the side
of the mask

BVM resuscitator Handheld breathing device ≥ 15 ≥ 90 Breathing and

consisting of a self-inflating bag, nonbreathing
a one-way valve, a face mask and patients
an oxygen reservoir bag

Chapter 3 | Tools and Therapies | 33

 A B

Figure 3-8 | Three-electrode system. (A) The white electrode is placed under the right clavicle at the midclavicular line, the
black electrode is placed under the left clavicle at the midclavicular line, and the red electrode is placed on the lower left
abdomen. (B) The three-electrode system allows monitoring of leads I, II and III.

Cardiac Monitoring
For basic monitoring of heart rate and rhythm, most
Practice Note
cardiac monitors/defibrillators use a three- or five- Most cardiac monitors/defibrillators have a wide
electrode system. A three-electrode system (Figure 3-8) range of functions, including continuous monitoring
permits monitoring of the bipolar limb leads (i.e., leads I, capabilities (e.g., heart rate and rhythm, blood
II and III). A five-electrode system (Figure 3-9) uses four pressure, pulse oximetry and capnography), diagnostic
limb electrodes and one chest electrode to provide seven capabilities (i.e., 12-lead ECG) and therapeutic
views of the electrical activity of the heart. The four limb capabilities (i.e., modes for defibrillation, synchronized
electrodes produce six leads in the frontal plane: I, II, III, cardioversion and transcutaneous pacing). Make sure
augmented voltage of the right arm (aVR), augmented you are familiar with the features and functions of the
voltage of the left arm (aVL) and augmented voltage of the equipment in use at your facility.
left foot (aVF). The chest electrode produces one lead in
the horizontal plane: V1.

A B

Figure 3-9 | Five-electrode system. (A) In addition to the electrodes placed for a three-electrode system, the brown electrode
is placed in the fourth intercostal space along the right sternal border and the green electrode is placed on the lower right
abdomen. (B) The five-electrode system allows monitoring of leads V1, I, II, III, aVR, aVL and aVF.

34 | American Red Cross | Advanced Life Support

Electrocardiography and aVF. The six chest electrodes produce six leads in
the horizontal plane: V1, V2, V3, V4, V5 and V6. In some
Most cardiac monitors/defibrillators can also be used to clinical situations, obtaining a 15-lead ECG may be
obtain a 12-lead ECG, which is necessary for accurately necessary, which is done by obtaining a 12-lead ECG
diagnosing arrhythmias, acute coronary syndromes and then repositioning some of the electrodes to obtain
(ACS) and other conditions affecting the electrical the additional three views (Figure 3-11).
activity of the heart. The 12-lead ECG uses four limb
Preparing the skin where the electrodes will be placed
electrodes and six chest electrodes to provide 12 views
is important to minimize artifact. The skin should be
of the heart (Figure 3-10). The four limb electrodes
clean, dry and free of excess hair. In addition, proper
produce six leads in the frontal plane: I, II, III, aVR, aVL
electrode placement is essential for accurate rhythm
A identification. Misplacement of an electrode by as little as
one intercostal space can cause waveform morphology to
change, potentially leading to misdiagnosis.

Figure 3-11 | The 15-lead ECG uses three additional

electrodes to obtain three additional views of the heart. (A)
Lead V4R is placed over the fifth intercostal space at the
midclavicular line on the right side. (B) Leads V8 and V9 are
placed posteriorly. V8 is placed over the fifth intercostal space
Figure 3-10 | The 12-lead ECG uses (A) four limb
at the midscapular line on the left side and V9 is placed over
electrodes and six chest electrodes to provide (B) 12 views
the fifth intercostal space between V8 and the spine.
of the electrical activity of the heart.

Chapter 3 | Tools and Therapies | 35

The Placing Electrodes for Electrocardiography Skill A
Sheet provides step-by-step guidance for placing
electrodes for a 12-lead and 15-lead ECG.

Electrical Therapies
Commonly used electrical therapies include manual
defibrillation, synchronized cardioversion and
transcutaneous pacing.

Manual Defibrillation
Defibrillation is indicated for shockable cardiac arrest
rhythms (i.e., ventricular fibrillation and pulseless
ventricular tachycardia). Defibrillation involves the
administration of direct-current electricity. The delivery of
electricity is not synchronized in any way with the cardiac
cycle. The electricity depolarizes the myocardial cells,
B
making them unresponsive to abnormal pacemakers in
the heart and ideally allowing the sinoatrial (SA) node to
resume its normal pacemaker function, terminating the
arrhythmia.

Electricity is delivered to the patient via two adhesive

pads that contain a conductive gel layer. The conductive Figure 3-12 | Defibrillation pad placement. (A) Anterolateral
gel layer helps to overcome transthoracic impedance placement. (B) Anterior-posterior placement.
(the body’s resistance to current flow that is caused
by the thoracic structures, including soft tissue and ■ If using a monophasic defibrillator, set the
bone, between the defibrillation pads and the heart) and energy dose at 360 joules. Use this energy dose for
each subsequent shock.
minimizes the risk for burns.

The pads may be placed using anterolateral placement

Practice Note
or anterior-posterior placement:
■ Anterolateral placement (Figure 3-12A): Place the To minimize interruptions to chest compressions, continue
sternal pad on the patient’s right side adjacent to the providing compressions while placing the pads on the
upper sternum, below the clavicle. Place the apical patient’s chest and charging the cardiac monitor/defibrillator.
pad on the patient’s left side over the fourth and fifth
intercostal spaces, with the center of the pad at the
midaxillary line.
Anterior-posterior placement (Figure 3-12B):
■
Place the anterior pad on the patient’s left side over Practice Note
the fourth and fifth intercostal spaces, with the center Always precede the delivery of a shock by announcing
of the pad at the midaxillary line. Place the posterior
the intention to shock in a clear, succinct manner.
pad in the left infrascapular region.
Before delivering a shock, perform a visual scan to
The energy dose depends on the type of defibrillator. ensure that no one is touching the patient, the bed or
■ If using a biphasic defibrillator, follow the the stretcher and that oxygen delivery devices have
manufacturer’s recommendations for the initial dose been removed and set aside, away from the patient.
(usually between 120 and 200 joules). Subsequent When delivering the shock, continue to face the team,
doses should be the same as or higher than the initial rather than the defibrillator.
dose. If the manufacturer’s recommendations for the
initial dose are not known, use the highest energy
dose available for the first and all subsequent shocks.

36 | American Red Cross | Advanced Life Support

The Manual Defibrillation Skill Sheet provides step-by- it is necessary to press and hold the shock button
step guidance for manual defibrillation. until the shock is delivered. Table 3-3 summarizes
the key differences between synchronized
Synchronized Cardioversion cardioversion and defibrillation.

Synchronized cardioversion is first-line therapy for

patients with tachyarrhythmia with a pulse and signs of
Practice Note
hemodynamic compromise and may also be indicated If the sync markers are hard to see, try selecting
for refractory wide-complex tachyarrhythmia in patients another lead on the monitor.
without signs of hemodynamic compromise.

Synchronized cardioversion involves the delivery of a low

Because synchronized cardioversion can be
dose of direct-current electricity that is timed to correlate
uncomfortable for the patient, administer sedation or
with the peak of the R wave. This avoids delivery of
analgesia unless the patient’s condition is deteriorating
electricity during the refractory phase of the cardiac cycle
rapidly. Energy doses depend on the arrhythmia and the
(represented by the T wave on the ECG), which could
type of defibrillator. After delivering the shock, reassess
precipitate ventricular fibrillation or torsades de pointes.
the rhythm and the patient:
As in defibrillation, a cardiac monitor/defibrillator is ■ If the rhythm did not convert, reset the cardiac
used for synchronized cardioversion, and shocks monitor/defibrillator to synchronous mode, increase
are delivered through adhesive pads placed on the energy level in a stepwise fashion, charge the
the patient’s chest. However, the cardiac monitor/ pads and deliver a shock.
defibrillator must be set to synchronous mode ■ If the rhythm did convert, check the patient’s vital signs
(indicated by the appearance of sync markers at the and ensure adequate airway, breathing and circulation.
top of each R wave on the monitor). Additionally,

Table 3-3 | Key Differences Between Synchronized Cardioversion and Manual Defibrillation
Feature Synchronized Cardioversion Manual Defibrillation
Mechanism Delivery of electricity timed with QRS complex Delivery of electricity not timed with any part of
on ECG the cardiac cycle

Indications ■ Tachyarrhythmias with a pulse and signs of ■ Ventricular fibrillation

hemodynamic compromise ■ Pulseless ventricular tachycardia
■ Refractory wide-complex tachyarrhythmia
with a pulse and no hemodynamic
compromise

Use ■ Must select synchronous mode prior to ■ No need to select mode prior to delivering
delivering shock shock
■ Must press and hold the shock button to ■ No need to hold the shock button to deliver
deliver the shock the shock

Chapter 3 | Tools and Therapies | 37

 Intravenous Access
Practice Note
Peripheral veins are commonly used for vascular access
Most cardiac monitor/defibrillators revert to defibrillation during emergencies. The best site for peripheral access
mode after delivering a shock. This is because is that which permits placement of the largest-diameter
cardioversion may induce ventricular fibrillation, in which catheter possible without interfering with other resuscitative
case immediate defibrillation is necessary. Always efforts, such as airway maneuvers or chest compressions.
ensure that the cardiac monitor/defibrillator is returned Common peripheral sites for intravenous (IV) catheter
to synchronous mode before each subsequent attempt insertion include the large surface veins in the antecubital
at synchronized cardioversion. fossa and the dorsum of the hands and wrists.

Factors to consider when selecting the site for peripheral

The Synchronized Cardioversion Skill Sheet provides IV access include the duration of, and indication for,
step-by-step guidance for synchronized cardioversion. treatment, the types of solutions to be infused and vein
availability.
Transcutaneous Pacing
Practice Note
Transcutaneous pacing involves delivering an electrical
current through the skin to stimulate the heart to contract. If upper extremity peripheral venous access cannot
Transcutaneous pacing is indicated for patients with be achieved, consider central venous access (e.g.,
bradyarrhythmia and signs of hemodynamic compromise the femoral vein) or lower extremity peripheral venous
that is not responsive to pharmacologic therapy. access (e.g., the saphenous vein or the veins of the
dorsum of the foot).
Like synchronized cardioversion, transcutaneous pacing
can be uncomfortable for the patient, so administer
sedation or analgesia if the patient’s condition permits. Set When administering IV therapies in an emergency, keep
the cardiac monitor/defibrillator to pacing mode, and then the following points in mind:
set the demand rate and the current milliamperes output. ■ Use the largest-diameter catheter possible (at least
Gradually increase the current milliamperes output until 18 gauge in an adult).
electrical capture (wide QRS complexes and tall, broad ■ Because strict aseptic technique may be breached
T waves following each pacing spike) is observed on the during an emergency, replace the original catheter using
monitor. Confirm mechanical capture by assessing the strict aseptic technique after the patient is stabilized.
patient for clinical signs such as an improved peripheral ■ Ensure that the extremity with IV access is at or above
pulse, an increase in blood pressure, an improved level of the level of the heart.
consciousness and improved skin color and temperature. ■ When providing care for a patient in cardiac arrest,
follow each peripherally administered drug dose with
The Transcutaneous Pacing Skill Sheet provides step-by- a 10- to 20-mL normal saline flush to ensure that the
step guidance for transcutaneous pacing. medication reaches the central circulation.
■ Monitor the patient for local and systemic
complications of IV therapy.
Practice Note
Intraosseous Access
Check for a pulse using the right radial artery or the
right or left femoral artery. During transcutaneous In emergency situations, intraosseous (IO) access should
pacing, skeletal muscle contractions can mimic a only be used for adults when IV access is unsuccessful or
pulse in the left radial artery or in the carotid arteries. not feasible. IO access has been associated with lower
rates of return of spontaneous circulation (ROSC) and
Vascular Access should not be used as first-line access.
Quick access to the circulation is often needed for IO access uses the bone marrow as the vascular space
delivery of medications and other therapies and for and typically involves a needle rather than a catheter. As
sampling of blood. The best access technique is one with IV access, IO access can be used to administer
that is rapid and does not interfere with CPR. medications, fluids and blood products and to collect blood

38 | American Red Cross | Advanced Life Support

for laboratory analysis. Medication dosing is the same for Table 3-4 | Sites for Intraosseous (IO) Access
IO and IV routes, and all medications administered to a
patient in cardiac arrest should be followed by a 10- to 20- IO Drill Bone Injection
mL normal saline flush. Because the IO needle should not Device
be left in place for more than 24 hours, IV access should be Anterior proximal X X
established as soon as possible, ideally within a few hours. tibia (medial
aspect)
Sites for IO needle insertion vary according to the device
Proximal humerus X X
used to achieve access (Table 3-4).
Distal tibia X
The most commonly used sites are the medial aspect of the
anterior proximal tibia and the proximal humerus. These sites extravasation and compartment syndrome. Remove the
provide a flat surface with a relatively thin outer layer of bone, IO needle as soon as IV access can be established,
a large marrow cavity and easily identifiable landmarks to ideally within a few hours.
facilitate placement. Other sites for IO access include the
The Intraosseous Access (Drill) Skill Sheet and the
distal femur, distal radius, anterior-superior iliac spine, medial
Intraosseous Access (Manual Insertion) Skill Sheet
malleolus and sternum.
provide step-by-step guidance for achieving IO access
IO needle placement should not be attempted in using an IO drill and manually, respectively. Always follow
patients with bone fractures at the site or disorders that the manufacturer’s instructions when using a device to
predispose to fracture (e.g., osteoporosis). Relative insert an IO needle.
contraindications to IO needle placement include
infection or burns of the overlying skin and previous
attempts to establish access at the same IO access site; Fluid Therapy
however, IO placement may still be considered in these
Fluid resuscitation is often indicated for patients
instances when there is no other vascular access during
experiencing a cardiovascular emergency and as part
an emergency.
of post–cardiac arrest care. Along with the use of
IO needles can be inserted using a device (such as a vasoconstrictors or inotropic agents, the administration of
drill or injection device) or manually (Figure 3-13). After fluids can help to maintain cardiac output, blood pressure
insertion, monitor the insertion site and the extremity and perfusion.
for swelling, which may indicate that the needle is
Isotonic crystalloid solutions, such as 0.9% normal saline
out of place. Dislodging of the needle can lead to
or lactated Ringer’s solution, are the primary solutions
complications, including infection, medication or fluid
used for fluid resuscitation. Isotonic fluids are used

A
Hub
5 mm
mark Stylet

B C

Figure 3-13 | Equipment for intraosseous (IO) access. (A) IO drill and needle. (B) Bone injection device. (C) Jamshidi needle for
manual insertion.

Chapter 3 | Tools and Therapies | 39

instead of hypotonic fluids (e.g., 0.45% normal saline) lost when capillary membranes are “leaky,” as they are in
because isotonic solutions allow a greater proportion of various shock states.
the administered volume to remain in the intravascular
Large peripheral IV catheters are adequate for most types
space. In most situations, normal saline and lactated
of fluid resuscitation, as are central and IO catheters.
Ringer’s solution are equally effective options for fluid
Infusion pumps typically allow infusion of 1 liter of
resuscitation. Because of the association between
crystalloid solution in approximately 10 to 15 minutes.
repeated normal saline boluses and hyperchloremic
metabolic acidosis, which may obscure an ongoing
or developing acidosis secondary to impaired tissue
perfusion, use of a “balanced” solution such as lactated
Drug Therapy
Ringer’s solution may be preferred in some situations. A good working knowledge of the drugs most
Colloid solutions, such as albumin, dextran and commonly used in the management of cardiovascular,
hydroxyethyl starch, may also be used for fluid cerebrovascular and respiratory emergencies is
resuscitation in shock. Historically, colloids were proposed essential. Table 3-5 summarizes the action, indications,
to be a more effective option for fluid resuscitation than administration and precautions for drugs that are
crystalloid solutions, based on the assumption that a commonly administered via the IV or IO route in
greater proportion of colloid solution remains in the resuscitation situations. Table 3-6 summarizes other drugs
vascular space. However, this property appears to be that are referenced throughout the course materials and
their uses.

Table 3-5 | Commonly Used IV/IO Drugs in Resuscitation Situations

Drug Action Indications Administration Precautions

Adenosine Slows ■ Regular narrow- ■ Has an extremely short ■ Therapeutic effects
conduction complex half-life; administer can be blocked by the
of impulses tachyarrhythmias/ over 1–2 s, at a site as presence of caffeine
through the AV no hemodynamic close to the heart as or theophylline
compromise possible ■ VF possible if
node
■ Regular narrow- ■ 6 mg by rapid IV/IO adenosine is
complex push follow by 10- to administered for
tachyarrhythmias/ 20-mL NS flush unstable, irregular or
hemodynamic ■ If not effective after polymorphic wide-
compromise (do not 1–2 min, 12 mg by complex tachycardias
delay cardioversion) rapid IV/IO push ■ Can temporarily evoke
■ Regular monomorphic followed by 10- to a transiently slow
wide-complex 20-mL NS flush ventricular rate or
tachyarrhthmias/ complete cessation
no hemodynamic of electrical activity;
compromise as drug is eliminated,
electrical activity
resumes

40 | American Red Cross | Advanced Life Support

Table 3-5 | Commonly Used IV/IO Drugs in Resuscitation Situations (continued)

Drug Action Indications Administration Precautions

Amiodarone Class III ■ Shock-refractory VF/ For VF/pVT: ■ Do not use with other
antiarrhythmic; pVT drugs that prolong
■ First dose: 300 mg IV/
delays Refractory QT interval
■ IO bolus
repolarization tachyarrhythmia with ■ Second dose: 150 mg
and prolongs the a pulse/hemodynamic after 3–5 min
compromise
QT interval
■ Wide-complex For tachyarrhythmia with
tachyarrhythmia/ a pulse:
no hemodynamic
■ 150 mg IV over
compromise
10 min; may repeat as
needed if arrhythmia
recurs
■ Maintenance infusion:
1 mg/min for first 6
hours
Atropine Blocks the effect ■ Bradyarrhythmia/ ■ 1 mg IV bolus every ■ Use in patients
of acetylcholine hemodynamic 3–5 min, up to a max with acute coronary
released by the compromise dose of 3 mg ischemia or
vagus nerve myocardial infarction
may have negative
at muscarinic
outcomes because
receptors, thereby of increased heart
increasing the rate rate and myocardial
of firing of the oxygen demand
SA node and ■ IV/IO doses of less
conduction than 0.1 mg may
through the AV cause paradoxical
node bradycardia
Dopamine Has positive ■ Bradyarrhythmia/ For bradyarrhythmia: ■ Can increase
chronotropic hemodynamic myocardial oxygen
■ 5–20 mcg/kg/min
and inotropic compromise (second- demand
titrated to effect
effects, resulting line agent) ■ Can cause
■ After cardiac arrest For post–cardiac arrest ventricular
in an increase in
care: arrhythmias
heart rate and
contractility ■ 5–20 mcg/kg/min IV/
IO

Chapter 3 | Tools and Therapies | 41

 Table 3-5 | Commonly Used IV/IO Drugs in Resuscitation Situations (continued)

Drug Action Indications Administration Precautions

Epinephrine Acts on ■ Cardiac arrest (VF, For VF/pVT/pulseless ■ Increased blood
both α- and pVT, pulseless electrical activity/asystole: pressure, heart rate
ß-adrenergic electrical activity, and myocardial
■ 1 mg IV/IO followed
receptors; asystole) oxygen demand may
by 10- to 20-mL NS
■ After cardiac arrest cause myocardial
induces flush every 3–5 min
■ Bradyarrhythmia/ ischemia
systemic
hemodynamic For post–cardiac arrest
vasoconstriction
compromise (second- care:
and increases line agent) ■ 2–10 mcg/min IV/IO
heart rate and
contractility For bradyarrhythmia:
■ 2–10 mcg/min titrated
to effect
Note: 1:1000 concentration
= 1.0 mg/mL; 1:10,000
concentration = 0.1 mg/mL
Lidocaine Class Ib ■ VF/pVT ■ First dose: 1–1.5 mg/ ■ Do not use
antiarrhythmic kg IV/IO followed by prophylactically in
(sodium channel 10- to 20-mL NS flush patients with acute
blocker); delays ■ Subsequent doses: myocardial infarction
repolarization 0.5–0.75 mg/kg IV/ ■ Monitor patient for
IO followed by 10- to lidocaine toxicity
and slightly
20-mL NS flush every ■ Reduce maintenance
increases the 5–10 min, up to a max dose in patients
QT interval dose of 3 mg/kg with hepatic disease
or left ventricular
dysfunction
■ Do not alternate
between amiodarone
and lidocaine

Naloxone Competitively ■ Opioid overdose ■ 0.4–2 mg IV/IO/IM/ ■ May precipitate

binds to μ-opioid IN/SC repeated every opioid withdrawal
receptors 2–3 min syndrome (rarely life
threatening)
Norepinephrine Acts on ■ After cardiac arrest ■ 0.1–0.5 mcg/kg/min ■ Potent
both α- and IV/IO vasoconstrictor;
ß-adrenergic extravasation can
receptors lead to necrosis
to increase
heart rate,
contractility and
vasoconstriction;
increases
systemic blood
pressure and
coronary blood
flow

42 | American Red Cross | Advanced Life Support

Table 3-5 | Commonly Used IV/IO Drugs in Resuscitation Situations (continued)

Drug Action Indications Administration Precautions

Procainamide Class Ia ■ Refractory ■ 20–50 mg/min ■ May induce torsades
antiarrhythmic tachyarrhythmia with a until arrhythmia de pointes
(sodium channel pulse/ hemodynamic is suppressed, ■ Avoid in prolonged
blocker); delays compromise hypotension develops, QT or congestive
■ Wide-complex QRS duration heart failure
repolarization
tachyarrhythmia/ increases by more
and prolongs the than 50% or max dose
no hemodynamic
QT interval compromise of 17 mg/kg is given
■ Maintenance infusion:
1–4 mg/min
Sotalol Prolongs ■ Refractory ■ 100 mg (1.5 mg/kg) ■ Avoid in prolonged
repolarization; tachyarrhythmia with a over 5 min QT
also acts as a pulse/ hemodynamic
ß-blocker compromise
■ Wide-complex
tachyarrhthmia/
no hemodynamic
compromise

Table 3-6 | Other Drugs Used in the Treatment of Cardiovascular and Cerebrovascular Disorders

Drug Used for

Aspirin Acute coronary syndromes, stroke
β-Blockers (e.g., metoprolol, atenolol, propranolol, esmolol, Acute coronary syndromes, tachyarrhythmias, stroke
labetalol)
Bivalirudin Acute coronary syndromes
Calcium channel blockers
■ Diltiazem Tachyarrhythmias
■ Verapamil Tachyarrhythmias
■ Nicardipine Stroke
■ Clevidipine Stroke
Glycoprotein IIb/IIIa inhibitors Acute coronary syndromes
Anticoagulants (e.g., unfractionated heparin, enoxaparin, Acute coronary syndromes
fondaparinux)
Morphine Acute coronary syndromes
Nitroglycerin Acute coronary syndromes
Nitroprusside Stroke
P2Y12 inhibitors Acute coronary syndromes
Tissue plasminogen activators
■ Recombinant tissue plasminogen activator (alteplase) Acute coronary syndromes, stroke
■ Reteplase Acute coronary syndromes
■ Tenecteplase Acute coronary syndromes

Chapter 3 | Tools and Therapies | 43

 SKILL SHEET
Inserting an Oropharyngeal Airway (OPA)
Step 1 Select the proper size
Measure the OPA from the corner of the patient’s mouth to the
angle of the jaw.

Step 2 Open the patient’s airway

Open the airway to a past-neutral position using the head-tilt/chin-lift technique, or use the
modified jaw-thrust maneuver.

Step 3 Open the patient’s mouth

Open the patient’s mouth using the cross-finger technique.

44 | American Red Cross | Advanced Life Support

SKILL SHEET
Inserting an Oropharyngeal Airway (OPA) (continued)
Step 4 Insert the OPA
• Insert the OPA upside down, with the tip pointing up.
• As the tip approaches the posterior pharynx, rotate the OPA
180 degrees into the proper position.

Step 5 Ensure correct placement

The flange should rest on the patient’s lips.

Chapter 3 | Tools and Therapies | 45

 SKILL SHEET
Inserting a Nasopharyngeal Airway (NPA)
Step 1 Select the proper size
• Select an NPA that is smaller in diameter than the inner
aperture of the patient’s nostril.
• Measure the NPA from the nostril to the angle of the jaw.

Step 2 Apply a water-soluble lubricant

Lubricate the NPA and the opening of the nostril.

46 | American Red Cross | Advanced Life Support

SKILL SHEET
Inserting a Nasopharyngeal Airway (NPA) (continued)
Step 3 Insert the NPA
• Right nostril: Insert the NPA with the bevel toward the
septum. Gently advance the NPA straight in, following the floor
of the nose and avoiding excessive force.
• Left nostril: Insert the NPA with the bevel toward the septum.
Gently advance the NPA, rotating it as you advance it past the
nasal cavity.

Step 4 Ensure correct placement

The flange should rest on the nostril.

Chapter 3 | Tools and Therapies | 47

 SKILL SHEET
Using a Bag-Valve-Mask (BVM) Resuscitator—One
Provider
Step 1 Select an appropriately sized resuscitator
The mask should not cover the patient’s eyes or extend below the patient’s chin. Assemble the
equipment as needed.

Step 2 Place the mask

Position yourself behind the patient’s head (cephalic position). Place the mask at the bridge of the
nose and then lower it over the nose, mouth and chin.

Step 3 Seal the mask and open the airway

• Place one hand around the mask, forming a C with your thumb
and index finger around the side of the mask and an E with the
last three fingers under the patient’s jaw.

• Simultaneously seal the mask and open the airway to the past-
neutral position by lifting the patient’s jaw up into the mask.

Step 4 Provide ventilations

• While maintaining the mask seal and an open airway with one hand, use the other hand to
depress the bag about halfway to deliver a tidal volume of 400 to 700 mL.

• Watch for chest rise.

• Continue providing smooth and effortless ventilations that last about 1 second and cause the
chest to just begin to rise.

48 | American Red Cross | Advanced Life Support

SKILL SHEET
Using a Bag-Valve-Mask (BVM) Resuscitator—Two
Providers
Step 1 Select an appropriately sized resuscitator
The mask should not cover the patient’s eyes or extend below the patient’s chin. Assemble the
equipment as needed.

Step 2 Place the mask

Provider 1 gets into position behind the patient’s head (cephalic position). Provider 1 places the
mask at the bridge of the nose and then lowers it over the nose, mouth and chin.

Step 3 Seal the mask and open the airway

Provider 1:
• Places both hands around the mask, forming a C with the thumb
and index finger around the sides of the mask and an E with the
last three fingers of each hand under the patient’s jaw.
• Simultaneously seals the mask and opens the airway to the past-
neutral position by lifting the patient’s jaw up into the mask.

Step 4 Provide ventilations

• Provider 1 maintains the mask seal and an open airway.
• Provider 2 depresses the bag about halfway to deliver a tidal volume of 400 to 700 mL.
Provider 2 provides smooth and effortless ventilations that last about 1 second and cause the
chest to just begin to rise.

• Both providers watch for chest rise.

Chapter 3 | Tools and Therapies | 49

 SKILL SHEET
Placing Electrodes for Electrocardiography
12-Lead ECG
Step 1 Prepare the skin where the electrodes will be placed
• Make sure the skin is clean, dry and free of excess hair.
• Using a skin prep pad, gently abrade the skin to remove dead
skin cells.

Step 2 Prepare equipment

Attach electrodes to the cables.

Step 3 Apply the limb electrodes

• On the arms, place the electrodes between the shoulders and
the elbows.

• On the legs, place the electrodes on the thighs or calves,

avoiding bony areas.

50 | American Red Cross | Advanced Life Support

SKILL SHEET
Placing Electrodes for Electrocardiography (continued)
Step 4 Apply the chest electrodes
• V1: Palpate the jugular notch, then palpate down to identify
the sternal angle (angle of Louis), which is adjacent to the
second rib. Palpate along the right sternal border to identify
the second, third and fourth intercostal spaces. Place the
electrode for V1 over the fourth intercostal space at the right
sternal border.

• V2: Place the electrode for V2 over the fourth intercostal space
at the left sternal border.

• V4: Place the electrode for V4 over the fifth intercostal space at
the midclavicular line on the patient’s left side.

• V3: Place the electrode for V3 halfway between electrodes V2 and V4.
• V5: Place the electrode for V5 at the anterior axillary line on the patient’s
left side, even with electrode V4.

• V6: Place the electrode for V6 at the midaxillary line on the patient’s left
side, even with electrodes V4 and V5.

Note: If necessary, lift breast tissue to place electrodes as close to the

chest wall as possible.

15-Lead ECG
Step 1 Obtain a 12-lead ECG
Run a standard 12-lead ECG.

Chapter 3 | Tools and Therapies | 51

 SKILL SHEET
Placing Electrodes for Electrocardiography (continued)
Step 2 Place additional electrodes
• V4R: Place the electrode for V4R over the fifth intercostal space
at the midclavicular line on the patient’s right side.

• V8: Place the electrode for V8 over the fifth intercostal space
at the midscapular line on the patient’s left side.

• V9: Place the electrode for V9 over the fifth intercostal space
between V8 and the spine.

Step 3 Move cables to obtain additional views

Detach the cables for leads V4, V5 and V6.

• Place the cable from V4 on V4R.

• Place the cable from V5 on V8.
• Place the cable from V6 on V9.

Step 4 Obtain a second 12-lead ECG

• Run a second 12-lead ECG to capture the three additional leads.
• Re-label the three additional leads on the rhythm strip.

52 | American Red Cross | Advanced Life Support

SKILL SHEET
Manual Defibrillation
Step 1 Select appropriately sized pads
Choose the largest adult pad available.

Step 2 Apply the pads to the patient’s chest

Apply the pads to the patient’s chest, pressing firmly and making
good skin contact.
• Anterolateral placement: Place the sternal pad on the
patient’s right side adjacent to the upper sternum, below the
clavicle. Place the apical pad on the patient’s left side over the
fourth and fifth intercostal spaces, with the center of the pad at
the midaxillary line.
• Anterior-posterior placement: Place the anterior pad on the
patient’s left side over the fourth and fifth intercostal spaces,
with the center of the pad at the midaxillary line. Place the
posterior pad in the left infrascapular region.

Step 3 Set the energy dose

• Biphasic defibrillator: Follow the manufacturer’s
recommendations for the initial dose (usually between 120
and 200 joules). Subsequent doses should be the same
as or higher than the initial dose. If the manufacturer’s
recommendations for the initial dose are not known, use
the highest energy dose available for the first and all
subsequent shocks.

• Monophasic defibrillator: Set the energy dose at 360 joules.

Use this energy dose for each subsequent shock.

Step 4 Charge the pads

Press the “charge” button on the cardiac monitor/defibrillator.

Chapter 3 | Tools and Therapies | 53

 SKILL SHEET
Manual Defibrillation (continued)
Step 5 Deliver the shock
• Instruct the team to “clear.”
• Conduct a visual check to ensure that no one is touching the
patient or the bed/stretcher and that oxygen delivery devices
have been removed and set aside, away from the patient.

• Press the “shock” button on the cardiac monitor/defibrillator

to deliver the shock.

Step 6 Resume CPR

Immediately resume CPR and then reassess the rhythm in 2 minutes. If a shockable rhythm
persists, deliver another shock, using an energy dose that is the same as or higher than the
initial dose.

54 | American Red Cross | Advanced Life Support

SKILL SHEET
Synchronized Cardioversion
Step 1 Identify the rhythm
Attach the cardiac monitoring leads and ensure that the patient’s cardiac rhythm is shown on
the monitor.

Step 2 Select appropriately sized pads

Choose the largest adult pad available.

Step 3 Apply the pads to the patient’s chest

Apply the pads to the patient’s chest, pressing firmly and making good skin contact.

• Anterolateral placement: Place the sternal pad on the patient’s right side adjacent to the
upper sternum, below the clavicle. Place the apical pad on the patient’s left side over the fourth
and fifth intercostal spaces, with the center of the pad at the midaxillary line.

• Anterior-posterior placement: Place the anterior pad on the patient’s left side over the
fourth and fifth intercostal spaces, with the center of the pad at the midaxillary line. Place the
posterior pad in the left infrascapular region.

Step 4 Select synchronous mode

Verify that sync markers are visible at the top of each R wave.

Chapter 3 | Tools and Therapies | 55

 SKILL SHEET
Synchronized Cardioversion (continued)
Step 5 Set the energy dose
• Use the device manufacturer's recommended energy dose for
the type of rhythm.

Step 6 Charge the pads

Press the “charge” button on the cardiac monitor/defibrillator.

Step 7 Deliver the shock

• Instruct the team to “clear.”
• Conduct a visual check to ensure that no one is touching the
patient or the bed/stretcher and that oxygen delivery devices
have been removed and set aside, away from the patient.

• Press and hold the “shock” button on the cardiac monitor/

defibrillator to deliver the shock.

Step 8 Reassess
Reassess the rhythm and the patient.

• If the rhythm did not convert, reset the cardiac monitor/

defibrillator to synchronous mode, increase the energy level in
a stepwise fashion, charge the pads and deliver a shock.

• If the rhythm did convert, check the patient’s vital signs and
ensure adequate airway, breathing and circulation.

56 | American Red Cross | Advanced Life Support

SKILL SHEET
Transcutaneous Pacing
Step 1 Identify the rhythm
Attach the cardiac monitoring leads and ensure that the patient’s
cardiac rhythm is shown on the monitor.

Step 2 Apply the pacing pads to the patient’s chest

Apply the pacing pads to the patient’s chest, pressing firmly and making good skin contact.
• Anterolateral placement: Place the sternal pad on the patient’s right side adjacent to the
upper sternum, below the clavicle. Place the apical pad on the patient’s left side over the
fourth and fifth intercostal spaces, with the center of the pad at the midaxillary line.
• Anterior-posterior placement: Place the anterior pad on the patient’s left side over the
fourth and fifth intercostal spaces, with the center of the pad at the midaxillary line. Place the
posterior pad in the left infrascapular region.

Step 3 Select pacing mode

Set the cardiac monitor/defibrillator to pacing mode.

Chapter 3 | Tools and Therapies | 57

 SKILL SHEET
Transcutaneous Pacing (continued)
Step 4 Set the demand rate
Set the demand rate to approximately 60 beats per minute. Once
pacing is established, the demand rate can be adjusted according
to the patient’s clinical response.

Step 5 Set the current milliamperes output

Set the current milliamperes output by starting low and gradually
increasing it until consistent electrical capture is observed on the
monitor (wide QRS complexes with tall, broad T waves).

Step 6 Check for mechanical capture

Check for mechanical capture (evidenced by clinical signs such as an improved peripheral pulse
and an increase in blood pressure).

58 | American Red Cross | Advanced Life Support

SKILL SHEET
Intraosseous Access (Drill)
Step 1 Stabilize the target site
Stabilize the target site on a firm surface.

Step 2 Select the correct needle size

Palpate the site to determine tissue depth.

Step 3 Disinfect the skin

Disinfect the skin overlying the insertion site.

Step 4 Consider pain control

If the patient is awake, consider infiltration of the skin and periosteum with 1% lidocaine.

Step 5 Attach the needle

Attach the needle to the IO drill.

Chapter 3 | Tools and Therapies | 59

 SKILL SHEET
Intraosseous Access (Drill) (continued)
Step 6 Position the needle
Aim the IO drill with the needle at a 90-degree angle to the
insertion site. Push the needle through the skin until the tip is
against the bone. The 5-mm mark on the needle must be visible
above the skin when the needle is resting on the bone.

Step 7 Drill the needle into the bone

Pressing the trigger on the device, lightly drill the needle into the
bone until you feel a decrease in resistance.

Step 8 Remove the drill

Hold the needle securely in place as you pull the drill straight off.
When inserted correctly, the needle should feel like it is firmly in the
bone and should remain upright without support.

60 | American Red Cross | Advanced Life Support

SKILL SHEET
Intraosseous Access (Drill) (continued)
Step 9 Remove the stylet
Remove the stylet by twisting it counterclockwise, and dispose of it
properly.

Step 10 Position the stabilizer dressing

Place the stabilizer dressing over the needle.

Step 11 Attach the primed tubing

Hold the needle securely and attach the primed tubing to
the needle.

Chapter 3 | Tools and Therapies | 61

 SKILL SHEET
Intraosseous Access (Drill) (continued)
Step 12 Confirm placement
Confirm correct placement of the needle by using one of the
following methods:

• Aspirate bone marrow or blood through the needle.

• Flush the needle with a small amount of saline and check for
extravasation.

• Administer fluids by free flow through the needle.

Step 13 Secure the dressing

Peel the adhesive tabs off the stabilizer dressing and press the
dressing firmly onto the skin.

Step 14 Monitor the insertion site

Monitor the insertion site and the extremity for swelling.

62 | American Red Cross | Advanced Life Support

SKILL SHEET
Intraosseous Access (Manual Insertion)
Step 1 Stabilize the target site
Stabilize the target site on a firm surface.

Step 2 Select the correct needle size

Palpate the site to determine tissue depth.

Step 3 Disinfect the skin

Disinfect the skin overlying the insertion site.

Step 4 Consider pain control

If the patient is awake, consider infiltration of the skin and periosteum with 1% lidocaine.

Step 5 Position the needle

Position the needle at a 90-degree angle to the insertion site.
Push the needle through the skin until the tip is against the bone.

Chapter 3 | Tools and Therapies | 63

 SKILL SHEET
Intraosseous Access (Manual Insertion) (continued)
Step 6 Insert the needle into the bone
Once the needle reaches the periosteum, apply pressure in a back-
and-forth twisting motion until you feel a decrease in resistance.
When inserted correctly, the needle should feel like it is firmly in the
bone and should remain upright without support.

Step 7 Remove the stylet

Remove the stylet by twisting it counterclockwise, and dispose of
it properly.

Step 8 Attach the primed tubing

Hold the needle securely and attach the primed tubing to the needle.

Step 9 Confirm placement

Confirm correct placement of the needle by using one of the following methods:

• Aspirate bone marrow or blood through the needle.

• Flush the needle with a small amount of saline and check for extravasation.
• Administer fluids by free flow through the needle.

64 | American Red Cross | Advanced Life Support

SKILL SHEET
Intraosseous Access (Manual Insertion) (continued)
Step 10 Secure the needle
Tape the flange to the skin and add a gauze dressing for support.

Step 11 Monitor the insertion site

Monitor the insertion site and the extremity for swelling.

Chapter 3 | Tools and Therapies | 65

 CHAPTER
4

Working Well Together in an Emergency

Introduction
Working well together as a team when caring for a patient experiencing a
cardiovascular, cerebrovascular or respiratory emergency is vital. Poor teamwork can
lead to poor outcomes in emergency situations. Conversely, effective teamwork can be
the difference between life and death for the patient who requires emergency care.
Rapid Response and
Resuscitation Teams
Many healthcare facilities have implemented systems
designed to improve patient outcomes by decreasing
the likelihood of cardiopulmonary arrest in unstable
patients and reducing mortality when cardiopulmonary
arrest does occur. These systems rely on teams of highly
trained and skilled personnel, known as rapid response
teams and resuscitation teams. The goal of the rapid
response team is to intervene quickly and effectively to
address the warning signs of impending cardiopulmonary
arrest so that the arrest can be prevented. The goal
of the resuscitation team is to respond quickly and
effectively to provide advanced life support care to a
patient in respiratory or cardiac arrest.

Patients in respiratory distress or shock tend to

decompensate quickly, and respiratory and cardiac arrest
may result. In critical care settings such as a critical care Figure 4-1 | Rapid response teams intervene early to
unit or emergency department, highly trained teams are prevent a patient’s condition from worsening.
already in place and advanced life support care will be
implemented quickly. However, patients outside of these quickly address the symptoms and underlying cause
settings are also at risk for experiencing respiratory or when a patient is in distress to prevent the occurrence of
cardiac arrest. Thus all healthcare providers should be respiratory or cardiac arrest.
trained to recognize early signs of clinical deterioration in
Any healthcare provider can call for a rapid response
patients and should know how to initiate the emergency
team; often the nurse providing direct patient care makes
response as quickly as possible.
the call. Regardless, guidelines are always in place for
calling a team. Each facility uses its own, often very
Rapid Response Systems specific, criteria to activate the rapid response system.
These criteria may be called “triggers,” or an early warning
Rapid response systems became commonly integrated in score system may be used. In general, the rapid response
hospitals in the mid-2000s as a response to the 100,000 system would be activated for the following reasons:
Lives Campaign initiated by the Institute for Healthcare
■ An acute change in respiratory rate, pattern or status
Improvement, which aimed to reduce the percentage
from baseline (especially acute onset or worsening
of preventable in-hospital deaths. Today, all hospitals in respiratory distress)
the United States are required by the Joint Commission ■ Airway compromise
National Patient Safety Goals to have a system in place
■ A respiratory rate greater than 28 breaths/min or less
to better recognize and respond to significant changes than 8 breaths/min
in a patient’s status. Thus, all hospitals, and some other ■ An oxygen saturation less than 90% despite
types of healthcare facilities, have some form of a rapid supplementation
response system in place. Rapid response teams (also ■ A heart rate greater than 140 bpm or less than 40 bpm
called multidisciplinary medical emergency teams) ■ A systolic blood pressure greater than 180 mmHg or
work together to care for the patient when signs and less than 90 mmHg
symptoms of cardiopulmonary compromise or shock ■ An acute change in urine output or a urine output of
are noted (Figure 4-1). The specific composition of less than 50 mL over 4 hours
the team may vary, but generally rapid response teams ■ An acute change in mental status
include critical care nurses, respiratory therapists, and ■ An acute change in pain status (or uncontrolled pain)
a critical care physician or hospitalist, nurse practitioner ■ Seizure activity (new onset or prolonged)
or physician assistant. No matter the composition of ■ Staff or family concern
the team, the goal of every rapid response team is to

68 | American Red Cross | Advanced Life Support

Resuscitation Teams Communication
Resuscitation teams, like rapid response teams, are Communication is essential when caring for a patient
multidisciplinary teams of highly trained and skilled who is experiencing a cardiovascular, cerebrovascular or
healthcare professionals. Team members may vary, but respiratory emergency. You need to communicate with
teams often include a critical care physician, a critical your colleagues, the patient and the patient’s family.
care nurse, a respiratory therapist, a hospitalist, a
Communication involves four essential components
pharmacist and a chaplain. The goal of the resuscitation
(Figure 4-3):
team is singular and focused: to provide resuscitative
care when a patient experiences respiratory or cardiac ■ Sender: The person initiating the communication
arrest (Figure 4-2). ■ Message: The content of the communication; this
must be expressed clearly so that everyone involved
knows exactly what the message is
Functioning as a Team ■ Receiver: The person for whom the message is
intended
Healthcare providers on rapid response and ■ Feedback: The confirmation by the receiver that the
resuscitation teams must work together in a message is received and understood; an essential
coordinated effort to achieve the best possible element of closed-loop communication
outcomes for each patient. Teamwork refers to Communication includes spoken words (verbal
a group of people with well-defined roles and messages) and nonverbal messages conveyed through
responsibilities working toward a common goal. body language, such as gestures and facial expressions.
Teamwork is crucial during rapid response and
resuscitation because the ultimate goal is to save a Communicating with the Team
life, and effective team care requires a coordinated The foundation of effective teamwork is clear and effective
effort by the team leader and the team members. communication among team members. When a team
To achieve the best possible outcomes, every team is working to provide care, a designated team leader
leader and team member must exhibit key skills including directs the efforts of the other team members. When
communication, critical thinking and problem solving. communicating information or assigning tasks to team
Implementing effective and efficient teamwork and exhibiting members, the team leader must be sure to speak clearly
these critical key skills allows the team to respond efficiently and deliberately, to convey information in an organized
and effectively, and it improves patient outcomes. fashion and to “close the loop” by waiting for feedback from
the team member responsible for carrying out the action.
If feedback is not provided, the team leader should seek it
before continuing. Similarly, team members must provide
confirmation that they have received the message and that
they understand it by repeating the task back to the team
leader and acknowledging initiation and completion of the

Message

Feedback

Sender Receiver

Figure 4-3 | Clear communication among team members

is essential. The sender initiates the communication,
sending a clear message. The receiver provides feedback,
Figure 4-2 | The resuscitation team provides resuscitative confirming that the message was understood and the task
care to patients in cardiac or respiratory arrest. has been completed.

Chapter 4 | Working Well Together in an Emergency | 69

task. No matter what your role is on the team, speak clearly in ■ Consistently re-evaluate the situation for changes,
a calm tone of voice, and take care not to speak over others. interpret these changes and apply them to the
patient’s care and treatment.
Communicating with the Family ■ Modify your actions based on the changes you observe.
Patients who require resuscitation are unresponsive, Problem Solving
making communication with the family very important.
Remember, during emergencies, families are stressed and Problem solving refers to the ability to use readily
may not always hear what you are saying. Speak slowly available resources to find solutions to challenging or
and in terms the family can understand. Build rapport complex situations or issues that arise. In emergency
and establish trust. Be prepared to repeat information, situations, problems or issues can occur at any point.
if necessary. Be open and honest, especially about the For example, a team member may be unable to find a
patient’s condition. Minimize family members’ fears, as vein adequate for achieving vascular access. Another
necessary, but avoid giving misleading information or false emergency might occur, leaving the team short-staffed.
hope. Reassure the family that everything that can be An upset family member may interfere with care.
done is being done. In doing so, you need to demonstrate Problem solving also requires creativity in finding
credibility and trustworthiness, confidence and empathy. solutions. Use whatever resources are at hand,
In advanced life support situations, patients may not including equipment, other team members or other
survive, despite the team’s best resuscitation efforts. As a healthcare facility staff.
healthcare provider, you may be involved in communicating
with the family about a patient’s death. In this situation:
Working as a High-
■ Provide information honestly and with compassion,
in a straightforward manner, and include information Performance Team
about events that may follow.
■ Allow the family to begin processing the information. Your role on an advanced life support team may vary
■ Allow time for the family to begin the grief process. Ask according to your training and areas of expertise. In
whether they would like to contact or have you contact addition to understanding your own role on the team,
anyone, such as other family members or clergy. it is important to understand the roles of other team
■ Anticipate emotional reactions, which may include members as well. This knowledge will help you function
crying, sobbing, shouting, anger, screaming or effectively in an advanced life support situation.
physically lashing out.
■ Wait and answer any questions that the family may have. Members of effective teams keep their skills and
knowledge current, and they practice together
Critical Thinking regularly (Figure 4-4A). In addition, effective teams
hold debriefing sessions after each resuscitation event
Critical thinking refers to thinking clearly and rationally (Figure 4-4B). The debriefing session is an opportunity
to identify the connection between information and to review successes, as well as areas where
actions. When you use critical thinking, you are constantly improvement is needed.
identifying new information, adapting to the information
logically in order to determine your best next actions and Team Leader Responsibilities
anticipating how those actions will affect the patient.
The team leader oversees the entire emergency situation
Critical thinking is an essential skill in healthcare and and organizes and runs the response. The team leader
especially in advanced life support situations. You use does not perform a particular task but is responsible for
critical thinking when you: making sure all team members perform necessary tasks
■ Obtain an initial impression. according to their roles. The coordination of all involved is
■ Determine a course of action. necessary to:
■ Anticipate roles and functions as part of a team ■ Ensure that everyone works as a team to help
based on the patient’s presentation and condition. promote the best possible outcome for the patient.
■ Promote effective perfusion to vital organs.
■ Minimize interruptions of chest compressions, which
improves patient survival.

70 | American Red Cross | Advanced Life Support

 A B

Figure 4-4 | Effective teams (A) practice together regularly and (B) hold debriefing sessions after every resuscitation event.

The team leader: Coordinated Team Response

■ Assigns and understands team roles.
■ Sets clear expectations. When the team leader and all of the team members,
■ Prioritizes, directs and acts decisively. in their assigned roles, work together as a high-
■ Encourages and allows team input and interaction. performance team, expert care is delivered and
■ Focuses on the big picture. outcomes are improved. In a highly effective team
■ Monitors performance while providing support. working together in an emergency situation, the team
■ Acts as a role model. leader will assign the team roles. These roles may differ
■ Coaches the team. according to healthcare facility policy. A typical six-
■ Re-evaluates and summarizes progress. person high-performance resuscitation team includes
■ Facilitates a debriefing session. team members who perform CPR/defibrillator roles,
as well as team members who perform leadership and
Team Member Responsibilities supportive roles (Figure 4-5). All team members should
be trained and able to perform multiple roles on the
Team members provide care with skill and expertise. team, within their scope of practice.
Team members:
CPR/Defibrillator Roles
■ Have the necessary knowledge and skills to perform
The CPR/defibrillator roles include the following:
their assigned role.
■ Stay in their assigned role but assist others as ■ Compressor. One team member is responsible for
needed, as long as they are able to maintain their own chest compressions.
assigned responsibilities. ■ AED/defibrillator operator. One team member
■ Communicate effectively with the team leader if they: is responsible for managing the AED or defibrillator
c Feel they are lacking any knowledge or skills.
and for establishing any other monitoring. This team
member also relieves the team member who is giving
c Identify something that the team leader may
compressions.
have overlooked.
■ Airway manager/ventilator. One team member is
c Recognize a dangerous situation or need for
responsible for managing the airway and providing
urgent action. ventilations. A trained respiratory therapist, if available,
■ Share information with other team members. would fill this role.
■ Focus on achieving the goals.
■ Ask pertinent questions and share pertinent observations.
■ Participate in the debriefing session.

Chapter 4 | Working Well Together in an Emergency | 71

 Leadership/Supportive Roles

CPR/Defibrillator Roles

Airway manager/
ventilator

Data manager

AED/
Compressor
defibrillator operator

Medication
Team leader XXX
XX administrator

Figure 4-5 | A resuscitation team usually includes six people.

Leadership and Supportive Roles efficient teamwork. When following the principles of
crew resource management, all members of the team
The leadership and supportive roles include the following:
demonstrate respect for one another and use clear,
■ Team leader. One team member functions as the closed-loop communication.
team leader.
■ Medication administrator. One team member Crew resource management centers around the team
is responsible for establishing vascular access and leader, who coordinates the actions and activities of
administering medications. team members so that the team functions effectively and
■ Data manager. One team member is responsible efficiently. For example, when team members switch roles
for keeping track of elapsed time and communicating during an emergency, the team leader is responsible for
and recording key data during the resuscitation effort,
coordinating these activities. Crew resource management
such as the nature and timing of interventions.
also guides team members to communicate directly and
effectively with the team leader about dangerous or time-
Crew Resource Management critical decisions. Being a member of the team is just as
important as being a team leader. Everyone on the team
Crew resource management is a concept that helps to needs to have a voice and be encouraged to speak up if
promote effective and efficient teamwork and reduce the a problem arises. When a problem arises, team members
likelihood of errors. Originally developed by the aviation must get the attention of the team leader, state their
industry in the 1970s in response to several airline concern, describe the problem as they see it and suggest
disasters where human error and poor communication a solution. The team leader then provides direction,
were found to be contributing factors, crew resource enabling the team to work together to resolve the issue.
management has been adapted for use as a tool in the
healthcare setting as well. Crew resource management
emphasizes using all available resources (including
Phased Response Approach
people, equipment and procedures) to reduce the
likelihood of human error and promote effective and The phased response approach, first introduced in
1987 by Burkle and Rice, can be used to describe

72 | American Red Cross | Advanced Life Support

the process of a resuscitation team in action during a Family Notification
resuscitation event. The phased response approach
Although listed as a phase, family notification is actually
refers to how a group of people, working as a team,
an ongoing process throughout the resuscitation or
reacts to and handles an emergency using crew resource
emergency care event. Ideally, one member of the team
management and the key skills of communication, critical
is dedicated to this role so that family members are kept
thinking and problem solving. This response approach
informed throughout the process.
consists of seven phases.
Transfer
Anticipation
After the rapid response team, the resuscitation team or
In the anticipation phase, the team leader gathers any
both provide care, the patient is likely to be transferred
preliminary information about the emergency (e.g., the
to a critical care unit or other unit capable of providing
patient’s age and present illness, significant medical
specialized care. The team leader, with input from the
history, and events leading up to the emergency) and
team members, determines the appropriate level of care
plans for the resuscitation or emergency response
required for each situation.
by assigning team roles and gathering the equipment
needed to handle the situation. If the emergency care Debrief
will take place in a location other than where the team is
As soon as possible after the resuscitation is over, the
located, the leader and team members go the site of the
team should review their performance. The debriefing
emergency as quickly as possible.
session is an opportunity to reflect on and analyze the
Entry care that was provided and to learn from mistakes, as well
as successes. The purpose of the debriefing session is
In this phase, the patient is brought to the emergency
not to place blame; rather, it is to take a closer look at the
department or the team arrives at the patient’s location
decisions that were made and the actions that were taken
in the healthcare facility. The team members assess the
with the goal of identifying opportunities for improvement
patient and collect vital signs, transfer the patient as
at the system, team and individual level. The debriefing
needed (e.g., from bed to bed) and ensure that the patient
phase is also a time for team members to decompress.
is positioned properly for the emergency interventions
Some resuscitations can be very traumatic or emotionally
taking place. One team member quickly and efficiently
laborious; this phase can be a time for the team to grieve.
obtains information from the person who identified the
emergency and called for “the code.” The team leader leads the debriefing session, which
typically follows a consistent format. For example:
Resuscitation
■ Review: The team leader provides a brief recap of
Resuscitation is the most critical phase of the approach. the emergency and the interventions that were used.
During this phase, the team leader directs the team ■ Analyze: The team reviews and evaluates the
members to perform actions per therapeutic protocols; objective data obtained during the resuscitation
communication is essential in this phase. The team effort.
members must also report any changes in the patient’s ■ Reflect: The team reflects on the actions they took
clinical condition, such as changes in heart rhythm, and why, discusses the pros and cons of those
decreasing oxygen saturation or changes in blood actions and identifies changes that could be made to
pressure. If resuscitation efforts are successful, a patient improve future outcomes.
in cardiac arrest will achieve return of spontaneous ■ Summarize: The team recaps the main takeaway
points and develops a list of action items.
circulation (ROSC).

Maintenance Practice Note

In the maintenance phase, the team focuses on
Participating in a resuscitation effort, even a
stabilizing the patient’s vital signs and using intelligent
successful one, can have a psychological impact on
intuition to predict any potential problems that may
team members. Mental health treatment provided
occur. The primary assessment is repeated during this
by a qualified mental health professional can benefit
phase, any required laboratory samples are collected
providers following a resuscitation or other stressful
and the care provided is documented. If the patient must
event.
be transferred, preparation for the transfer takes place in
this phase.

Chapter 4 | Working Well Together in an Emergency | 73

 CHAPTER
5

Assessment
Introduction
The data you gather through ongoing assessment of the patient informs the decisions
that you make in order to provide appropriate care. Taking a systematic approach to
assessment allows you and the team to focus on identifying and addressing the most
critical problems first, and helps to ensure that important details about the patient’s
condition and underlying causes are not overlooked.
Assess, Recognize and Care situation and care needs. This understanding enables
you to determine your next steps.
Assess, Recognize and Care (ARC) is a concept that
describes the ongoing process of gathering data about Care
the patient’s condition, using that data to identify a
problem and then intervening to address the problem Based on your understanding of the patient’s condition,
(Figure 5-1). Because an acutely ill patient’s condition implement appropriate care. Without effective
can change rapidly (for better or for worse), you must assessment and accurate recognition of the patient’s
continuously assess the patient, recognize what is condition, proper care cannot be provided.
happening with the patient and provide care accordingly.

Assess Systematic Approach to

Assessment
Assessment is the process of gathering the data
that helps you to determine what is happening with A systematic approach to assessment includes a rapid
the patient. In order to ensure that the most pressing assessment, a primary assessment and a secondary
problems are addressed first, take a phased, systematic assessment. The Adult Systematic Assessment
approach to assessment: perform a rapid assessment, Code Card summarizes the approach to systematic
a primary assessment and (when the patient’s condition assessment of an adult.
allows) a secondary assessment. In an emergency
situation, assessment is ongoing. Rapid Assessment
Recognize The rapid assessment is a quick survey to ensure safety,
form an initial impression about the patient’s condition
After you gather assessment data, use critical (including looking for life-threatening bleeding), and
thinking, your past clinical experience and your general determine the need for additional resources.
knowledge to correctly interpret the meaning of the
data and gain an understanding of the patient’s clinical You can gain a great deal of preliminary information very
quickly just by looking at the patient. For example:
■ Does the patient appear to be unresponsive?
■ Is the patient speaking?
■ Does the patient appear to be working to breathe?
■ Does the patient’s skin appear to be its normal color,
or does it seem pale, ashen, cyanotic or flushed?
■ Does the patient appear to be diaphoretic?
■ Is there any fluid or blood coming from, on or near the
patient?
■ Is there life-threatening bleeding?

Practice Note
If you see life-threatening bleeding immediately use
any available resources to control the hemorrhage,
including a tourniquet or hemostatic dressing if one
is available.

If the patient appears to be unresponsive, check for

Figure 5-1 | Assess, Recognize and Care (ARC) is a responsiveness.
concept that describes the ongoing process of gathering
data about the patient’s condition, using that data to identify
a problem, and then intervening to address the problem.

76 | American Red Cross | Advanced Life Support

Responsive Patient Primary Assessment
If the patient is responsive, perform the primary
assessment and provide emergent/initial interventions. The primary assessment structures the approach to
Position the patient as appropriate for their clinical patient assessment around the mnemonic ABCDE
condition, and perform the secondary assessment as (Airway, Breathing, Circulation, Disability, Exposure). The
the patient’s condition allows. Continually reassess the goal of the primary assessment is to identify potentially
patient, recognize issues and provide care as needed. life-threatening conditions and correct them immediately,
in order to prevent the patient’s condition from
Unresponsive Patient deteriorating further (Figure 5-2). Provide interventions
If the patient is unresponsive, call for additional as needed and as resources permit, delegating care to
resources, the rapid response or resuscitation team appropriate team members as needed.
and the resuscitation equipment or cart. Simultaneously
check for breathing and a central pulse for no more than
Airway
10 seconds. While completing the breathing and pulse Assess airway patency and maintainability. If the patient
check, look a second time for life-threatening bleeding. is able to speak to you in a normal voice, then the airway
Quickly scan down the patient’s body, looking for blood is patent. Signs that the upper airway may not be patent
or other signs of life-threatening bleeding that you might include:
not have seen initially. ■ Abnormal sounds (e.g., stridor, wheezing, gurgling or
snoring).
■ An obstruction or foreign body (including secretions,
Practice Note blood or vomit) in the upper airway.
Remember A-B-C: open the airway (A), check for the ■ Increased work of breathing or respiratory distress
(e.g., nasal flaring, retractions).
presence or absence of normal breathing (B), and
■ Altered level of consciousness.
simultaneously assess for circulation (C) by doing a
pulse check. ■ Cyanosis.
If the patient’s airway is not open and clear, patency
must be restored immediately and maintained. Methods
Provide care based on your findings. of ensuring and maintaining a patent airway include:
■ If the patient is not breathing (or only has gasping ■ Patient positioning.
breaths) and there is no pulse present, provide care ■ Manual maneuvers, such as the head-tilt/chin-lift
for cardiac arrest. Begin CPR immediately. technique and the jaw-thrust maneuver.
■ If the patient is not breathing or ventilation is
ineffective but there is a pulse, provide care for
respiratory arrest or failure. Ensure an adequate
airway and support oxygenation and ventilation
as needed with bag-valve-mask (BVM)-assisted
ventilation, noninvasive ventilation or invasive
ventilation. Perform the primary assessment and
provide emergent/initial interventions. Position the
patient as appropriate for their clinical condition, and
then perform a secondary assessment as the patient’s
condition allows. Continually reassess the patient,
recognize issues and provide care as needed.
■ If the patient is breathing and there is a pulse,
perform a primary assessment and provide
emergent/initial interventions. Position the patient as
appropriate for their clinical condition, and perform
the secondary assessment as the patient’s condition
allows. Continually reassess the patient, recognize
Figure 5-2 | During the primary assessment, assessment
issues and provide care as needed. and intervention take place concurrently to identify and
address potentially life-threatening problems related to
airway, breathing, circulation, disability (neurologic status)
and exposure.

Chapter 5 | Assessment | 77
■ Techniques for clearing an airway obstruction (e.g.,
abdominal thrusts or foreign body removal using
forceps with direct laryngoscopy). Practice Note
■ Suctioning.
Capnography allows rapid, objective and reliable
■ Placement of an oropharyngeal airway (OPA) or assessment of airway, breathing and circulation.
nasopharyngeal airway (NPA).
An ETCO2 value in the normal range and a square
■ Placement of an advanced airway.
waveform indicates that the patient’s airway,
If placement of an advanced airway is indicated, confirm breathing and circulation are intact:
proper placement using capnography and secure the ■ There is no obstruction to carbon dioxide emptying.
device to prevent it from becoming dislodged. ■ Ventilation is adequate. An ETCO2 value in the
normal range correlates closely with the arterial
pressure of carbon dioxide (PaCO2), which means
Breathing that ventilation is adequate.
Assess breathing rate, depth and rhythm and observe ■ Perfusion is adequate. In low-perfusion states, it is
for chest rise. Auscultate for the presence or absence impossible to achieve a normal ETCO2 value.
of breath sounds, the presence of abnormal breath
sounds (e.g., wheezes, rales, rhonchi or stridor) and for
Disability
bilateral equality. Establish pulse oximetry to monitor
oxygen saturation and if necessary, provide the minimal Perform quick assessments to gain information about the
level of supplemental oxygen needed to maintain an patient’s neurologic status:
oxygen saturation of at least 94% but not more than ■ Assess the patient’s level of consciousness using
99%. Establish capnography to monitor the adequacy the AVPU (Alert, Verbal responsive, Pain responsive,
of ventilation. End-tidal carbon dioxide (ETCO2) values Unresponsive) model:
in the range of 35 to 45 mmHg confirm adequacy of c Awake: The patient is fully awake (but may still be

ventilation. If necessary, support ventilation with BVM- confused).

assisted ventilation, noninvasive ventilation or invasive c Verbal responsive: The patient responds to verbal

ventilation. stimuli.
c Pain responsive: The patient responds to painful
Circulation stimuli (e.g., a tap on the shoulder).
c Unresponsive: The patient does not respond to
Assess the pulse rate, quality and rhythm, and establish
any stimuli.
cardiac monitoring. Assess the adequacy of perfusion by
■ Assess orientation to person, place and time.
assessing blood pressure and capillary refill time, assessing
■ Check the pupils for size, equality and reactivity to light.
for signs of shock and noting skin color, appearance and
■ Measure the patient’s blood glucose level.
temperature. Signs of compromised perfusion include a
Hypoglycemia can cause changes in level of
prolonged capillary refill time (greater than 2 seconds); consciousness and is easily corrected.
cool, pale or cyanotic skin in the extremities; an altered level ■ If stroke is suspected, conduct a neurologic
of consciousness; and abnormally low ETCO2 readings examination using the National Institutes of Health
(i.e., less than 30 mmHg). If time and resources permit, Stroke Scale (NIHSS) or similar assessment tool.
obtain a 12-lead ECG.
Exposure
Determine whether the patient needs defibrillation, As the last step of the primary assessment, check the
cardioversion or pacing. Establish vascular access for patient’s body for obvious signs of injury or illness, such
the administration of fluids, medications or both. as bleeding, bruises, rashes and deformities. Note skin
color, appearance and temperature. Remove clothing as
needed to inspect the head, ears, face, and neck; the
anterior and posterior trunk; and the upper and lower
extremities. If the patient has a suspected head, neck,
spinal or pelvic injury, remember to consider spinal
motion restriction while turning the patient over.

78 | American Red Cross | Advanced Life Support

 P: Past medical history
L: Last intake and output
Practice Note E: Events
Older adults do not thermoregulate as well as Signs and Symptoms
younger adults; they can lose core body temperature
Interview the patient (and, if necessary, family members
much faster when their skin is exposed. Be sure to
or other healthcare providers) to identify signs and
keep the areas not being actively assessed covered.
symptoms that occurred at the onset of the illness or
injury. Ask follow-up questions as needed. For example,
if the patient reports pain, ask the patient where the pain
Practice Note is located, when the pain started, and what the pain feels
like.
Bruises at various stages of healing or an inconsistent
patient history or a history that does not align with Allergies
the presenting injuries may indicate nonaccidental Determine whether the patient has any known allergies
trauma. Follow your local and institutional policies for to medications, foods, latex, or environmental items.
reporting suspected abuse. If the patient does report an allergy, ask what type of
reaction the patient had in the past when exposed to the
allergen, and what care the patient received. Even if the
Secondary Assessment patient does not report an allergy, inquire about possible
exposures to substances that are known to be allergens
When the patient’s condition has been stabilized, or toxins.
perform a secondary assessment. The secondary
assessment includes a focused history, a focused Medications
physical examination and diagnostic tests. The goal of Check what medications the patient is taking. This
the secondary assessment is to gather more detailed includes prescription medications, over-the-counter
information that will allow you to narrow the list of medications, vitamins, herbal supplements and any
differential diagnoses and discover underlying, treatable “home remedies.” Also explore the possibility of
causes (Figure 5-3). unintentional poisoning in a confused older adult or
when polypharmacy may be a concern.
Focused History
The focused history can be obtained by collecting data Past Medical History
following the SAMPLE mnemonic: Ask about hospitalizations, surgeries, previous illnesses
S: Signs and symptoms and significant chronic diseases that may be pertinent to
A: Allergies the patient’s current illness. Also inquire about nutritional
M: Medications status and immunization status.

Last Intake and Output

Establish when the patient last had something to
eat or drink, either by mouth or via enteral feeding.
Accurately establishing the time of the last intake
is important because the risk for aspiration may be
increased with some advanced treatment interventions,
such as intubation or general anesthesia. Note other
pertinent details about the patient’s last intake, such
as the amount, the patient’s willingness to eat or drink,
and whether or not the patient was having difficulty
with eating or drinking. Finally, ask about any changes
Figure 5-3 | During the secondary assessment, conducted that could cause fluid imbalance, such as changes
after the patient has been stabilized, information is gathered in urination or bowel elimination, vomiting, significant
with the aim of narrowing the differential diagnosis list, bleeding or fever.
identifying underlying causes and determining candidacy for
planned interventions.

Chapter 5 | Assessment | 79
Events The following diagnostic tests are often indicated in the
Gather details about the patient’s activities prior to the evaluation of patients experiencing a cardiovascular,
onset of signs and symptoms. Note the time between cerebrovascular or respiratory emergency:
the events leading up to the patient’s illness or injury ■ Blood tests, including arterial blood gases
and the onset of signs and symptoms. Also note any (ABGs), a complete blood count (CBC),
treatments the patient may have received prior to arriving an electrolyte panel, a blood glucose level,
coagulation studies, a lipid profile, serum cardiac
at the healthcare facility.
markers and toxicology screens.
Focused Physical Examination ■ Imaging studies, including chest radiography,
computed tomography (CT) of the chest or brain,
The information gathered from the rapid and primary magnetic resonance imaging (MRI) of the brain,
assessments, as well as the focused history, will assist vascular imaging of the brain and ultrasound of
you in determining the primary area of concern and the chest.
the extent of the focused physical assessment. For ■ Electrocardiography (12-lead).
example, if the primary area of concern is respiratory,
then the areas of focus may include the head, neck
and chest. In addition to completing a focused physical
exam, a complete head-to-toe assessment should also
be performed.

Diagnostic Tests
Diagnostic tests may be ordered to:
■ Assist in identifying underlying causes, including
potentially reversible causes.
■ Narrow the list of differential diagnoses.
■ Aid in determining candidacy for, or contraindications
to, planned therapeutic interventions.

80 | American Red Cross | Advanced Life Support

ADULT SYSTEMATIC ASSESSMENT
ALS - 2020 VERSION

Perform rapid assessment

Assess for life-threatening bleeding. If at any

time the patient has life-threatening bleeding,
control the hemorrhage with any available
resource (including the use of tourniquet or Responsive? YES
hemostatic dressing as appropriate).

NO

• Activate EMS, rapid response or resuscitation team

• Check breathing and pulse for no more than 10 sec
• At the same time, scan the body for life-threatening bleeding

Breathing
and pulse?

Not breathing Not breathing

Breathing
(or ineffective ventilation) (or only gasping breaths)
Pulse present
Pulse present No pulse present

Respiratory Arrest*
Cardiac Arrest*
Respiratory Failure*
• Perform primary assessment
(Airway, Breathing,
Circulation, Disability,
• Ensure adequate airway • Begin CPR immediately Exposure) and emergent/initial
• Support oxygenation and • Follow Adult Cardiac Arrest interventions
ventilation as needed (BVM, code card • Refer to applicable condition-
noninvasive or invasive) specific code cards
• Position patient as appropriate
for clinical condition
• Perform secondary assessment
as patient condition allows

• Reassess patient
• Recognize issues
• Provide care as needed

*Asappropriate,followcondition-specificcodecards.

Copyright © 2021 The American National Red Cross

Chapter 5 | Assessment | 81
 CHAPTER
6

Respiratory Emergencies
Introduction
A patient who is having difficulty breathing requires immediate care. Respiratory
distress can quickly progress to respiratory failure, respiratory arrest and cardiac arrest.
Respiratory Anatomy The pharynx has three regions (see Figure 6-1), the:
Nasopharynx, which extends from the base of the
and Physiology ■
skull to the soft palate and is located posterior to the
nasal cavities.
The overall function of the respiratory system is to
■ Oropharynx, which extends from the hard palate to
provide the body’s cells with oxygen and to remove
the level of the hyoid bone and is located posterior to
the byproduct of cellular metabolism, carbon dioxide. the oral cavity.
Respiration (the process of moving oxygen and carbon ■ Laryngopharynx (hypopharynx), which extends
dioxide between the atmosphere and the body’s cells) from the oropharynx to the level of the cricoid
includes ventilation (the mechanical process of moving cartilage.
air into and out of the body) and gas exchange (the
The larynx contains the vocal cords, is covered by the
molecular process of adding oxygen to, and removing
epiglottis (a leaf-shaped cartilaginous structure that
carbon dioxide from, the blood). Effective respiration
closes over the opening of the larynx during the act
relies on effective functioning of the respiratory system,
of swallowing) and is supported by the thyroid and
the cardiovascular system and the nervous system.
cricoid cartilages. The larynx serves as the “gatekeeper”
between the upper and lower airways. The structures
Respiratory System Anatomy of the upper airway can be categorized according to
where they lie in relation to the larynx (see Figure 6-1):
The respiratory system includes the upper and lower
■ Supraglottic: used to describe structures above
airways, the lungs and the muscles of respiration, including the larynx (e.g., the nasal and oral cavities, the
the diaphragm and intercostal muscles (Figure 6-1). nasopharynx and oropharynx)
■ Glottic: variably used to describe the space
Upper Airway between the vocal cords or the structures
The upper airway consists of the nasal passages, surrounding the larynx
pharynx, larynx and upper portion of the trachea, and ■ Subglottic: used to describe structures below the
ends at the level of the thoracic inlet. larynx (i.e., the upper portion of the trachea)

Figure 6-1 | The respiratory system

84 | American Red Cross | Advanced Life Support

Lower Airway Alveoli, located at the very end of the smallest
bronchioles, are arranged into clusters and surrounded
The lower airway encompasses the lower trachea,
by a rich network of capillaries. The alveoli provide a
bronchi, bronchioles and alveoli (see Figure 6-1). The
thin surface for gas exchange between the lungs and
trachea, bronchi and bronchioles serve as conduits
the blood (Figure 6-2). The walls of the alveoli contain
for the air entering and leaving the lungs. The trachea,
elastin fibers that allow them to stretch and then
which is supported by C-shaped rings of cartilage,
return to their normal shape. The inside of the alveolar
extends from the larynx to the carina (i.e., the point
membrane is coated with surfactant, which allows
where the trachea bifurcates into the right and left
reinflation and prevents atelectasis (alveolar collapse).
main bronchi). The right mainstem bronchus has three
intrapulmonary branches, whereas the left mainstem
bronchus has two, corresponding with the number of Respiratory Physiology
lobes on each side. Once inside the lobes of the lungs,
the bronchi divide into progressively narrower branches, Respiration involves the processes of ventilation and
called bronchioles. gas exchange.

Ventilation
Practice Note The diaphragm is the primary muscle responsible for
The right mainstem bronchus is more vertically ventilation. On inspiration, the diaphragm contracts
oriented relative to the trachea, whereas the left downward, increasing space for lung expansion. The
mainstem bronchus is more horizontally oriented. external intercostal muscles, located between the ribs,
Additionally, the left mainstem bronchus is short synergistically act with the diaphragm during inspiration
and narrow, and the right mainstem bronchus is to expand the rib cage. When ventilation demands
comparatively longer and wider. These anatomical increase, the body recruits accessory muscles for
features make the right mainstem bronchus assistance. The sternocleidomastoid, scalene and upper
easier to access and increase the risk for its trapezius muscles are the body’s accessory muscles of
accidental intubation. inspiration.

Figure 6-2 | Gas exchange occurs between the air in the alveolus and the red blood cells in the pulmonary capillary.

Chapter 6 | Respiratory Emergencies | 85

 Expiration is a passive action that occurs when the ■ Right shift. When there is acidosis, carbon dioxide
diaphragm and external intercostal muscles relax. is elevated or the body temperature is elevated,
During active (forced) expiration, the internal intercostal hemoglobin’s affinity for oxygen is decreased. It is
muscles, the rectus abdominis and the external and harder for oxygen to bind with the hemoglobin, but
it is easier for the hemoglobin to offload the oxygen
internal oblique muscles are recruited as accessory
that it is carrying. This causes the curve to shift to the
muscles of ventilation. right. Hypoventilation leads to acidosis and a right
shift of the oxygen–hemoglobin dissociation curve.
The impulse to breathe is controlled by respiratory
This rightward shift helps to provide oxygen to the
centers in the brain stem that regulate nerve impulses tissues during times of increased need, decreased
to the diaphragm and intercostal muscles. The delivery or both (such as during exercise or shock).
respiratory centers receive input from chemoreceptors ■ Left shift. When there is alkalosis, carbon dioxide
located throughout the body. These chemoreceptors is decreased or the body temperature is decreased,
detect changes in arterial oxygen and carbon dioxide hemoglobin’s affinity for oxygen is increased. Oxygen
content and in arterial pH, all of which affect the rate binds to the hemoglobin easily, but offloading is
and depth of breathing. Other physiologic parameters difficult. For example, hyperventilation leads to
that affect ventilation include core body temperature, alkalosis and a left shift of the oxygen–hemoglobin
dissociation curve. As a result, it is more difficult for
muscle activity (e.g., during exercise) and activity of the
oxygen to be released at the cellular level. In the lungs
sympathetic nervous system, which increases during under normal conditions, this is what leads to the
times of stress. higher affinity and binding of oxygen.
Gas Exchange Gas exchange relies on pulmonary circulation. The
The oxygen-hemoglobin dissociation curve, shown main function of the pulmonary circulation is to bring
in Figure 6-3, depicts the relationship between the deoxygenated blood to the lungs, perfuse the alveolar-
partial pressure of oxygen (PaO2) and the arterial oxygen capillary membrane and deliver oxygenated blood to the
saturation (SaO2). As more oxygen molecules bind left side of the heart for systemic circulation (Figure 6-4).
with the hemoglobin molecule, hemoglobin’s affinity for Pulmonary circulation begins with the main pulmonary
oxygen increases until the hemoglobin molecule reaches artery, which receives oxygen-depleted blood from the right
its maximum oxygen-carrying capacity. Many factors can ventricle. The main pulmonary artery divides into the right
affect hemoglobin’s affinity for binding with oxygen and and left pulmonary arteries. Once in the lungs, the pulmonary
the strength of the bond. These factors can cause the arteries branch into progressively smaller arteries and
curve to shift to the right or to the left. arterioles to carry the oxygen-depleted blood to the capillary
beds surrounding the alveoli. Because the concentration
of oxygen is greater in the alveoli (as compared with the
100
concentration of oxygen in the blood in the capillaries),
Left shift
90 (increased affinity) oxygen diffuses across the alveolar-capillary membrane into
the blood. Similarly, because the concentration of carbon
80
dioxide is greater in the blood, carbon dioxide diffuses
70 across the alveolar-capillary membrane into the alveoli, to be
SaO 2 (mmHg)

removed from the body on exhalation.

60
Right shift The oxygenated blood is carried through a network of
50 (reduced affinity)
pulmonary venules and veins until it reaches the right and
40 left pulmonary veins, which empty into the left atrium. From
the left atrium, the oxygenated blood is pumped into the
30 left ventricle and out to the rest of the body.
20

10

0 10 20 30 40 50 60 70 80 90 100
PaO 2 (mmHg)
Figure 6-3 | The oxygen-hemoglobin dissociation curve

86 | American Red Cross | Advanced Life Support

 airways (i.e., the distal trachea, bronchi and
bronchioles). Lower airway obstruction may be due
to inflammation, constriction or mucus plugging
of the airways themselves. It may also be due to
external compression, for example, by interstitial
fluid in pulmonary edema. Obstruction at the level
of the upper airway makes it difficult for air to get in,
potentially impeding alveolar ventilation. Obstruction
of the lower airway makes it difficult for air to get
out, potentially leading to a greater volume of air, or
“air trapping,” in the lungs at the end of expiration.
Air trapping ultimately increases the inspiratory work
of breathing.
■ Neuromuscular conditions. Conditions such
as amyotrophic lateral sclerosis (ALS), myasthenia
gravis, Guillain-Barré syndrome and muscular
dystrophy impair neural signaling to the respiratory
muscles, and over time, respiratory weakness and
fatigue develop, impairing ventilation.
■ Central nervous system conditions. Overdose of
certain substances (such as opioids and alcohol) can
Figure 6-4 | The pulmonary circulation transports suppress the respiratory drive, leading to impaired
deoxygenated blood to the lungs and oxygenated blood back ventilation. Similarly, certain medications may
to the heart for distribution to the rest of the body. suppress the respiratory drive.
■ Chronic lung disease. In restrictive lung disease,
Pathophysiologic Mechanisms such as pulmonary fibrosis and interstitial lung
disease, lung compliance (i.e., the ability of the lung
Contributing to Respiratory to stretch and expand) is reduced. In obstructive
Emergencies lung disease, such as chronic obstructive pulmonary
disease (COPD), obstruction of the airways leads
Respiratory emergencies arise due to problems with to increased airway resistance. Both types of lung
disease are associated with impaired ventilation and
ventilation, diffusion (gas exchange) or perfusion.
increased work of breathing.
Problems with these processes may have many different
■ Trauma. Blunt or penetrating trauma to the chest
sources. Remember, for effective respiration, the
wall and traumatic brain injury (TBI) can lead to
following must be present: impaired ventilation.
■ Intact neuromuscular control of breathing
■ A patent airway Inadequate Diffusion and Perfusion
■ An intact alveolar-capillary membrane
■ Oxygen-rich blood When diffusion is impaired, the exchange of oxygen
■ Functioning pulmonary and systemic circulatory and carbon dioxide between the alveoli and the
systems pulmonary capillaries is affected. Diffusion defects
■ Adequate blood pressure to promote diffusion and may result from obstruction of the smaller airways in
perfusion the lungs or from conditions that create an increased
barrier to diffusion (e.g., interstitial lung disease).
Inadequate Ventilation Diffusion defects may also occur when alveoli are
filled with fluid or collapsed (e.g., due to pneumonia,
Problems with ventilation occur in the presence of pulmonary edema or COPD). Ventilation-perfusion
conditions that affect the body’s ability to move air in and mismatch refers to an imbalance between the air that
out of the lungs. Conditions that can lead to impaired reaches the alveoli (i.e., ventilation) and blood flow
ventilation include: to the alveoli (i.e., perfusion) in a portion of the lung
■ Airway obstruction. Obstruction of the upper (Figure 6-5). Cardiac disorders, pulmonary embolism
airway can result from a foreign body, fluids or and tension pneumothorax can affect blood flow
secretions. Lower airway obstruction may result from to the pulmonary capillary beds, resulting in “dead
pathologic processes involving the intrathoracic space ventilation” (i.e., ventilation without perfusion).

Chapter 6 | Respiratory Emergencies | 87

 A B C

Figure 6-5 | Ventilation-perfusion mismatch refers to an imbalance between the air that reaches the alveoli and blood flow to
the alveoli in a portion of the lung. (A) In the normal state, ventilation matches perfusion. (B) When blood flow to the alveolus
is blocked, ventilation is adequate, but perfusion is not. (C) Shunting occurs when blood flow to the alveolus is adequate, but
ventilation is not.

Disorders that result in pulmonary edema or atelectasis, using compensatory mechanisms to maintain adequate
such as pneumonia, can cause perfusion to exceed oxygenation and ventilation. The patient’s work of
ventilation. The result is a physiologic shunt, in which breathing is increased, but physiologically, oxygenation
poorly oxygenated blood coming back from these areas and ventilation are adequate to meet metabolic
mixes with fully oxygenated blood returning from the demands. However, if the patient’s respiratory distress
rest of the lungs, ultimately resulting in the delivery of is not relieved, these compensatory mechanisms will
desaturated blood to the body. soon become inadequate, at which point the patient may
develop respiratory failure.

Respiratory Distress, Signs and symptoms of respiratory distress may include:

Dyspnea.
Respiratory Failure and ■
■ Speech dyspnea (i.e., the need to pause between
Respiratory Arrest words to take a breath), speaking in short one- or
two-word sentences, or an inability to speak.
Respiratory compromise manifests along a continuum ■ Changes in breathing rate or depth.
(Figure 6-6). ■ Tachycardia or bradycardia.
■ Decreasing SaO2 levels (however, SaO2 levels may
Respiratory Distress be unaffected in some patients).
■ End-tidal carbon dioxide (ETCO2) levels that are
Respiratory distress represents the earliest stage initially low (less than 35 mmHg) but with increasing
on the continuum. A patient in respiratory distress is

Respiratory distress Respiratory arrest

1 2 3
2
Respiratory failure

Figure 6-6 | Respiratory compromise occurs along a continuum.

88 | American Red Cross | Advanced Life Support

 distress move into the normal range (35 to 45 mmHg) respiratory failure (characterized by a PaO2 less
and then become elevated (greater than 45 mmHg). than 60 mmHg) and hypercapnic respiratory failure
■ Decreased, absent or abnormal breath sounds (e.g., (characterized by a PaCO2 greater than 50 mmHg).
wheezes, crackles, rhonchi). Patients may also have a combined form. Hypoxic failure
■ Use of accessory muscles to assist in breathing, is most often associated with ventilation-perfusion
evidenced by supraclavicular, suprasternal, intercostal mismatch, whereas hypercapnic failure is most often
or substernal retractions. associated with decreased tidal volume or increased
■ Tripod positioning (leaning forward with the hands dead space. Signs of respiratory failure could include:
supported on the thighs or other surface).
■ Diaphoresis (the skin is often cool and clammy). ■ Changes in level of consciousness.
■ Irritability, restlessness or anxiety. ■ Cyanosis.
■ Changes in level of consciousness. ■ SaO2 values less than 90%.
■ Cyanosis. ■ ETCO2 values greater than 50 mmHg.
■ Tachycardia.
Early on in respiratory distress, the patient will tend ■ A decreased or irregular respiratory rate.
to hyperventilate, which leads to hypocapnia and is
reflected by a low ETCO2 value (i.e., less than 35
mmHg). As the patient’s respiratory distress increases Practice Note
and the patient begins to tire, the ETCO2 value may
An SaO2 of less than 90% (PaO2 of less than 50
return to the normal range (35 to 45 mmHg). But
mmHg) or a low PaO2 despite compensation and/or
with the onset of respiratory failure, the ETCO2 level
an ETCO2 value greater than 50 mmHg or a PaCO2
will increase to greater than 45 mmHg, indicating
that is elevated and not reflective of ventilatory effort
hypoventilation.
is indicative of respiratory failure.

Practice Note
Respiratory Arrest
Capnography can provide an objective assessment
of the severity of the patient’s respiratory distress.
Respiratory arrest is complete cessation of the
Arterial carbon dioxide (PaCO2) values can also
breathing effort. The body can tolerate respiratory
be used and are more accurate than capnography,
arrest for only a very short time before the heart stops
but require arterial sampling and do not provide
functioning as well, leading to cardiac arrest.
a continuous output. Some respiratory conditions
can make the absolute values or even capnography
unreliable. For this reason, it is good clinical practice
to correlate capnography with PaCO2 values.
Capnography in Respiratory
When and how often to obtain an arterial sample to Emergencies
correlate depends on clinical judgment, resources
Quantitative capnometry is the measurement of ETCO2
and the patient’s condition. In conditions where the
expressed as a value, and quantitative capnography
absolute value may not match the PaCO2 value, the
is the measurement of ETCO2 expressed as a value and
trend in capnography values is usually accurate.
as a waveform. Capnography is useful for assessing the
severity of the patient’s clinical condition, discerning the
underlying pathophysiology and evaluating the patient’s
Respiratory Failure response to interventions.

Respiratory failure occurs when the respiratory system Normal Waveform

can no longer meet metabolic demands. Respiratory
failure usually represents a progression from respiratory The capnography waveform is a graphical representation
distress, but patients may also initially present in of the movement of carbon dioxide through the
respiratory failure. Respiratory failure must be addressed respiratory system. The normal waveform has four
quickly to prevent respiratory arrest. phases (Figure 6-7).

There are two types of respiratory failure: hypoxic

Chapter 6 | Respiratory Emergencies | 89

 Waveform Interpretation
To evaluate a capnography waveform, take a five-step
C D approach:

A B E 1. Look at the waveform. Is there a waveform? Even

an abnormal waveform is an indication that carbon
dioxide is present.

2. Look at the respiratory baseline. Is the

respiratory baseline flat and consistent from breath
Figure 6-7 | Phases of the normal capnography waveform.
to breath? A respiratory baseline that slopes upward
A–B: respiratory baseline; B–C: respiratory upstroke; C–D:
expiratory plateau; D–E: inspiratory downslope. and increases with each breath suggests that the
patient is rebreathing carbon dioxide (Figure 6-8A).
■ Phase I (A–B): This is the respiratory baseline,
representing the beginning of exhalation. During this 3. Look at the respiratory upstroke. Is the
phase, “dead space” air is exhaled from the body. respiratory upstroke nearly vertical? A sloping,
This is the air in the airways from the bronchioles to prolonged respiratory upstroke that is not vertical
the nasal cavity that does not contain carbon dioxide. represents uneven alveolar emptying as a result of
■ Phase II (B–C): This is the respiratory upstroke, bronchospasm (see Figure 6-8B).
representing air from the alveoli that contains carbon
dioxide being exhaled from the body. For most 4. Look at the expiratory plateau. Is the expiratory
patients, the respiratory upstroke should be nearly plateau flat? Loss of plateau (see Figure 6-8C) is
vertical. produced by uneven alveolar emptying secondary to
■ Phase III (C–D): This is the expiratory plateau. severe bronchospasm that leads to air trapping. An
During this phase, the last of the carbon dioxide–
laden air from the most distal alveoli is exhaled from A
the body. The ETCO2 value is measured at the end of
exhalation (point D), which represents the peak level.
ETCO2 mmHg

50
40
■ Phase IV (D–E): This is the inspiratory downslope. 30
20
During this phase, inhalation occurs and the carbon 10

dioxide is rapidly purged from the airways and alveoli. 0

Time

A normal capnogram is square with a flat respiratory B

baseline, a flat expiratory plateau and an ETCO2 value
between 35 and 45 mmHg. The square waveform
indicates that carbon dioxide flow is not obstructed. The
flat respiratory baseline means that the patient is not
rebreathing carbon dioxide. The flat expiratory plateau
means that the patient is exhaling carbon dioxide to the
peak level.

Practice Note C

58
In inflammatory conditions, the waveform may still
be square, despite narrowing of the airway, because CO2
the alveoli still empty at the same rate. However,
in conditions that cause bronchospasm, alveolar 0
emptying is uneven, producing abnormal respiratory
upstroke and expiratory plateau morphology. Figure 6-8 | Abnormal capnography waveform morphology.
(A) Upward sloping respiratory baselines indicate that
the patient is rebreathing carbon dioxide. (B) A sloping,
prolonged respiratory upstroke indicates uneven alveolar
emptying. (C) A loss of expiratory plateau indicates
bronchospasm and air trapping.

90 | American Red Cross | Advanced Life Support

 absent plateau suggests dynamic hyperinflation, ■ Ensure a patent airway.
also called auto–positive end-expiratory pressure ■ Assist with ventilation as necessary. Patients who
(auto–PEEP). Auto–PEEP occurs when exhalation cannot ventilate adequately despite an open airway
time is insufficient and the lungs do not completely or who have insufficient respiratory effort require
empty before the next breath, preventing the assisted ventilation, which is initially provided using a
bag-valve-mask (BVM) resuscitator.
respiratory system from returning to its resting
■ Establish pulse oximetry and provide the minimal
end-expiratory equilibrium volume between breath
level of supplemental oxygen needed to maintain an
cycles. This is a serious condition because the oxygen saturation of 94% to 99%.
patient’s ETCO2 level is much higher than the value
■ Establish capnography and adjust ventilations
recorded by capnography. as needed to maintain carbon dioxide levels in
physiologic range (PaCO2 between 35 and 45 mmHg
5. Read the ETCO2 value. Finally, evaluate the or monitored using ETCO2) unless another target is
ETCO2 measurement. An ETCO2 measurement clinically indicated.
greater than 45 mmHg suggests hypercapnia, ■ Establish vascular access.
which may be caused by respiratory failure.
An ETCO2 measurement less than 35 mmHg
suggests hypocapnia, which may be caused by Practice Note
hyperventilation or hypoperfusion.
Some patients with end-stage COPD may have
chronically elevated arterial carbon dioxide levels and
Practice Note chronically low arterial oxygen levels. In these patients,
the stimulus to breathe becomes dependent on the
To interpret a waveform accurately, print it out in peripheral chemoreceptors, which respond to arterial
real time on paper. The waveform displayed on oxygen levels rather than arterial carbon dioxide levels.
the monitor is compressed and cannot be used Provide the minimal level of supplemental oxygen
for diagnostic purposes, other than for noting the needed to maintain an oxygen saturation of 94% and
presence of a square waveform or a flat line (apnea). carefully monitor the patient for inadequate ventilation,
which may necessitate providing a lower level of
supplemental oxygen.
Patient Assessment
Data gathered during the rapid, primary and secondary
assessments can help you to determine where the Secondary Assessment
patient is on the continuum of respiratory compromise
and may offer clues as to the underlying cause.
The secondary assessment will often help to further discern
the underlying cause of the respiratory compromise and
Rapid Assessment evaluate the severity of the patient’s condition. Although
there are many potential differential diagnoses for respiratory
Signs of respiratory compromise that you may observe compromise, the acute onset of respiratory distress is
during the rapid assessment include retractions and the frequently pulmonary or cardiac in origin (Box 6-1).
use of accessory muscles to breathe; tripod positioning;
an inability to speak in complete sentences (or at all); pale, History
ashen or cyanotic skin; diaphoresis; and restlessness, Conduct a focused history. If the patient is having
agitation or an altered level of consciousness. difficulty speaking or has an altered level of
consciousness, you may need to obtain the history
A patient in respiratory arrest or failure has a pulse but
from other healthcare providers, family members or
is not breathing (arrest) or has ineffective ventilation
bystanders. Ask about the patient’s medical history
(failure).
and whether they have experienced similar episodes in
the past. Information about the onset of the respiratory
Primary Assessment distress (was it acute, or did it develop over time?),
associated signs and symptoms (such as chest pain,
Conduct a primary assessment following the ABCDE nausea or fever) and medications can also provide
approach and provide initial interventions as needed: valuable insight into the underlying cause.

Chapter 6 | Respiratory Emergencies | 91

Box 6-1 | Pulmonary and Cardiac Differential Diagnoses for is a single level of positive pressure during all phases
Acute-Onset Respiratory Distress of breathing. BiPAP may be preferred for patients with
ventilatory failure in addition to oxygenation issues
Pulmonary because this method of noninvasive ventilation provides
■ Pulmonary embolism support to ventilation during inspiration and support of
■ Chronic obstructive pulmonary disease alveoli during other phases of respiration.
(COPD) exacerbation
After any intervention, reassess the patient to determine
■ Asthma exacerbation
response and adjust the treatment plan as necessary.
■ Pneumonia
Monitor the patient for signs of worsening respiratory
■ Pneumothorax
function, such as increased work of breathing, an
■ Noncardiogenic pulmonary edema/acute
increase or decrease in respiratory rate, hypoxemia or
respiratory distress syndrome (ARDS)
mental status changes. Pulse oximetry and capnography
Cardiac provide ongoing data about the patient’s respiratory
■ Cardiogenic pulmonary edema/congestive heart function and should be monitored closely.
failure (CHF)
■ Acute coronary syndromes (ACS) Respiratory Arrest
■ Cardiac tamponade
■ Acute valvular insufficiency Assess and Recognize
A patient in respiratory arrest is not breathing but has a
Physical Examination pulse.
Perform a physical examination of the patient. For
patients with respiratory compromise, a detailed Care
pulmonary examination is essential. Ensure a patent airway and deliver 1 ventilation every 6
seconds. Provide ventilations by BVM initially; provide
Diagnostic Tests mechanical ventilation as indicated. Provide high-flow
Diagnostic tests that may be ordered in the initial supplemental oxygen, titrating to achieve and maintain
evaluation of a patient with respiratory compromise an oxygen saturation of 94% to 99%, a PaO2 in the
include blood gases (arterial or venous); serum cardiac physiologic range or both. Adjust ventilations as needed
markers; a basic metabolic panel; a toxicology screen; to keep carbon dioxide levels in physiologic range
chest radiography, chest computed tomography (CT), or (PaCO2 between 35 to 45 mmHg or monitored using
both; a 12-lead ECG; and bedside echocardiography or ETCO2). While supporting ventilation, consider and
ultrasonography. address potential underlying causes.

Perform a primary assessment and provide emergent/

initial interventions, if not already done. Continue to
Approach to the Patient check breathing and pulse every 2 minutes; if the pulse
For a patient with respiratory compromise, interventions becomes absent, begin CPR immediately. Position
depend on the underlying cause. Common interventions the patient as appropriate for their clinical condition,
include supplemental oxygen, medications specific to and perform a secondary assessment as the patient’s
the underlying cause (e.g., bronchodilators, diuretics) condition allows. Reassess the patient, recognize issues
and assisted ventilation (BVM-assisted ventilation, and provide care as needed.
noninvasive ventilation or invasive ventilation).

A continuous positive airway pressure (CPAP) device

Opioid Overdose
“splints” the alveoli open and allows for better gas
Opioid overdose suppresses the central respiratory
exchange, which improves oxygenation and may reduce
drive and can quickly induce respiratory arrest or cardiac
the work of breathing. A bilevel positive airway pressure
arrest. The Adult Suspected or Known Opioid Toxicity
(BiPAP) device provides two levels of pressure—one for
Code Card summarizes the approach to a patient with
the inspiratory positive airway pressure (IPAP) and one
known or suspected opioid toxicity.
for the expiratory positive airway pressure (EPAP). The
same device is also often able to provide CPAP, which

92 | American Red Cross | Advanced Life Support

Assess and Recognize hours after the last dose of naloxone is given. Longer
observation times may be indicated if the cause of
Respiratory depression is a hallmark feature of opioid
the overdose was an extended-release or long-acting
toxicity, especially when accompanied by altered mental
opioid. Because respiratory depression may recur with
status (including unconsciousness) and miosis.
an extended-release or long-acting opioid, consider
Care admission to the critical care unit and initiation of
a continuous naloxone infusion at two-thirds of the
For patients with respiratory arrest or failure as a result of
effective dose per hour, titrated to patient response.
suspected or known opioid toxicity, ensure an adequate
airway and support oxygenation and ventilation as When opioid toxicity is the suspected or known cause of
needed. Administer naloxone as soon as it is available. cardiac arrest, naloxone should be administered as soon
Naloxone may be administered via the intravenous as possible without disrupting or delaying CPR and AED
(IV), intraosseous (IO), intramuscular (IM), intranasal use. For a patient in cardiac arrest, high-quality CPR
(IN) or subcutaneous (SC) route. For intravenous and AED use are prioritized over the administration of
administration, the dose is 0.4 mg IV. For administration naloxone.
via an auto-injector or nasal delivery device (such as
those used in public access and community programs), If the patient is responsive but has altered mental
the dose is 0.4 mg IM or 2 mg IN. All naloxone dosing status, or is not responsive but is breathing normally
may be repeated after 2 to 3 minutes. Reassess and has a pulse, consider naloxone. If not already done,
responsiveness and breathing and administer additional perform a primary assessment, position the patient as
doses of naloxone as needed. If not already done, appropriate for their clinical condition, and perform a
perform a primary assessment, position the patient secondary assessment as the patient’s condition allows.
appropriately for their clinical condition, and perform a Continuously reassess the patient, recognize issues, and
secondary assessment as the patient’s condition allows. provide care. If naloxone was given, monitor the patient
for 4 to 6 hours after the last dose.
Continue to reassess the patient, recognize issues
and provide care. Monitor the patient for at least 4 to 6

Chapter 6 | Respiratory Emergencies | 93

 ADULT SUSPECTED OR KNOWN OPIOID TOXICITY
ALS - 2020 VERSION

Suspected or known opioid overdose

Medications Responsive? YES

Naloxone
NO
• Healthcare: 0.4 to 2 mg IV/IO/IM/IN/SC; repeat
every 2 to 3 min as needed
• Activate EMS, rapid response or resuscitation team
• Public access and community programs (auto-
injector and nasal delivery devices): 0.4 mg IM • Check breathing and pulse for no more than 10 sec
or 2 mg IN; repeat every 2 to 3 min as needed • At the same time, scan the body for life-threatening bleeding

Breathing and pulse?

Not breathing Not breathing Breathing normally

(or ineffective ventilation) (or only gasping breaths) Pulse present
Pulse present No pulse

Respiratory Arrest
Cardiac Arrest Consider naloxone
Respiratory Failure

If not already done: • Begin CPR immediately If not already done:

following the Adult Cardiac • Perform primary assessment
• Ensure adequate airway Arrest code card (Airway, Breathing,
• Support oxygenation and ventilation as • Administer naloxone as soon Circulation, Disability,
needed (BVM, noninvasive or invasive) as available* Exposure) and emergent/
initial interventions
• Position patient as
Administer naloxone as soon as available*
appropriate for clinical
condition
• Reassess responsiveness and breathing • Perform secondary
assessment as patient
• Administer additional dose(s) of naloxone as needed condition allows

If not already done:

• Reassess patient
• Perform primary assessment (Airway, Breathing, Circulation,
Disability, Exposure) and emergent/initial interventions • Recognize issues

• Position patient as appropriate for clinical condition • Provide care as needed

• Perform secondary assessment as patient condition allows

If naloxone given:
• Reassess patient • Monitor for 4 to 6 hours after
• Recognize issues last dose of naloxone
• Provide care as needed - Consider longer
observation times if
extended-release or long-
Monitor for 4 to 6 hours after last dose of naloxone acting opioid
• Consider longer observation times if extended-release or - Consider admission and
long-acting opioid initiation of a continuous
naloxone infusion if
• Consider admission and initiation of a continuous naloxone potential for recurrence of
infusion if potential for recurrence of respiratory depression respiratory depression due
due to opioid to opioid

*Prioritize care for respiratory arrest/respiratory failure or cardiac arrest over the administration of naloxone.

Copyright © 2021 The American National Red Cross

94 | American Red Cross | Advanced Life Support

 CHAPTER
7

Arrhythmias
Introduction
A cardiac arrhythmia is a deviation from the normal heart rate, electrical activity pattern
or rhythm that varies from normal sinus rhythm. Although not every arrhythmia is
dangerous to the patient, many can be serious, and some require immediate treatment
to prevent sudden death. For this reason, ALS providers must be able to identify
abnormal rhythms accurately and interpret them within the overall clinical context.
Electrical Conduction Features of an ECG Tracing

Cardiac Conduction System An ECG tracing is a graphical representation of the

electrical impulse as it travels through the conduction
system, causing depolarization and then repolarization
The cardiac conduction system is a group of
of the myocardium. The waveforms and intervals seen
specialized myocardial cells that generate and transmit
on an ECG tracing correspond to events in the cardiac
the electrical signals that cause the heart muscle
cycle (Figure 7-2):
to contract. A well-functioning conduction system
is essential for ensuring the rhythmic, coordinated ■ P wave. The P wave represents depolarization of the
contraction of the heart that is necessary to maintain atrial myocardial cells.
cardiac output. ■ QRS complex. The QRS complex represents
depolarization of the ventricular myocardial cells.
The cardiac conduction system consists of the sinoatrial The normal duration of the QRS complex is less than
(SA) node, the atrioventricular (AV) node, the bundle of 120 milliseconds (0.12 second).
His, the left and right bundle branches and the Purkinje ■ T wave. The T wave represents repolarization of
fibers (Figure 7-1). Normally, the SA node, located in the ventricular myocardial cells. (Atrial repolarization
the upper right atrium, generates the electrical impulses occurs during ventricular depolarization and is
not seen on the ECG; it is overshadowed by the
that initiate the rhythm and rate of the heart. The impulse
depolarization of the larger ventricles.)
generated by the SA node travels via specialized
■ PR interval. The PR interval represents the time
pathways across the walls of the atria, causing the atria from the beginning of atrial depolarization to the
to contract, until it reaches the AV node at the base of beginning of ventricular depolarization. It is measured
the right atrium. The AV node, which briefly slows the from the beginning of the P wave to the beginning
transmission of the impulse, plays an important role in of the QRS complex. The normal duration of the
coordinating and maintaining appropriate AV conduction. PR interval is 120 to 200 milliseconds (0.12 to 0.2
From the AV node, the impulse travels through the second).
bundle of His, which descends the membranous aspect ■ QT interval. The QT interval is measured from
of the interventricular septum before dividing into the the beginning of the QRS complex to the end of
the T wave. This encompasses the time from the
right and left bundle branches. The impulse continues
beginning of ventricular depolarization to the end of
down the bundle branches and through the Purkinje ventricular repolarization. Because the QT interval
fibers, causing the ventricles to contract. varies normally with the heart rate, the corrected
QT interval (QTc) is used to give a value that is
The SA node is the primary pacemaker of the heart. theoretically independent of rate. The QTc adjusts
However, in the event of SA node dysfunction or failure, for heart rate differences by dividing the QT interval
the AV node can function as a backup pacemaker. by the square root of the RR interval (i.e., one
Similarly, the cells of the atrioventricular (AV) junction cardiac cycle). In general, a QTc greater than 460
(the zone of tissue surrounding the AV node), the bundle milliseconds (0.46 second) is considered to be
branches and the ventricles can generate impulses to prolonged.
maintain some level of contraction and cardiac output.
Practice Note
If the heart rate is faster than 120 bpm or slower than
50 bpm, the formula for calculating the QTc is not
considered valid and should not be used.

■ ST segment. The ST segment represents the time

between the end of ventricular depolarization and the
beginning of ventricular repolarization. It is measured
from the end of the QRS complex to the beginning
of the T wave.
■ J point. The J point is the point where the QRS
complex ends and the ST segment begins.
Figure 7-1 | The cardiac conduction system

96 | American Red Cross | Advanced Life Support

 R

T
P

Isoelectric line J point

Q ST segment
PR
interval S
QT
interval

Figure 7-2 | Features of an ECG tracing

Approach to Evaluating an 4. QRS complex. Measure the QRS complex. Is it

within the normal range? (QRS complexes that
ECG Tracing exceed 0.12 second in duration are abnormal.) Do
all the QRS complexes have the same morphology?
Taking a methodical approach to evaluating the rhythm
strip ensures that you gather relevant details that can 5. PR interval. Measure the PR interval. Is it within
help you to identify the rhythm accurately. the normal range (0.12 to 0.2 second)? Is it
consistent throughout the tracing? If it varies, is the
1. Regularity. Look at the rhythm to see whether it variation predictable?
is regular. Is the amount of time between each P
wave the same? What about the amount of time 6. Clinical significance. Determine the rhythm
between each QRS complex (i.e., the RR interval)? and its clinical significance. Is the patient showing
signs or symptoms? Is the rhythm potentially life-
2. Rate. To estimate the atrial rate, count the number threatening?
of P waves over a 6-second period and multiply
by 10. To estimate the ventricular rate, do the
same with the QRS complexes. Alternatively, if Normal Sinus Rhythm
the rhythm is regular, divide 300 by the number of
large squares between two P waves (to get the In normal sinus rhythm (Figure 7-3):
atrial rate) and between two R waves (to get the ■ The rhythm is regular (but may vary slightly during
ventricular rate). If the heart rate is very fast, divide respirations).
1500 by the number of small squares between two ■ The rate ranges between 60 and 100 bpm.
P waves (to get the atrial rate) and between two ■ The P waves are uniform in shape, indicating that
R waves (to get the ventricular rate). Are the atrial the SA node is the only pacemaker driving atrial
and ventricular rates the same or different? Are depolarization.
they within normal limits? ■ Each P wave is linked in a 1:1 fashion to each QRS
complex (i.e., atrial depolarization is always linked to
3. P waves. Look at the P wave morphology. Is it ventricular depolarization).
consistent? Is there one—and only one—P wave
associated with each QRS complex? Note that in
lead II, the P waves are usually upright but in lead
V1, the P waves may be inverted or biphasic.

Chapter 7 | Arrhythmias | 97
 Signs and Symptoms
Sinus bradycardia may not cause signs or symptoms.
However, when sinus bradycardia significantly affects
cardiac output, signs and symptoms may include:
■ Dizziness or light-headedness.
■ Syncope.
Regularity: regular ■ Fatigue.
Rate: 60–100 bpm
■ Shortness of breath.
P wave: upright and uniform; one for every QRS complex
■ Confusion or memory problems.
QRS complex: < 0.12 second
PR interval: 0.12–0.20 second ECG Findings
Figure 7-3 | Sinus rhythm On ECG, sinus bradycardia appears the same as
sinus rhythm, except the heart rate is less than
60 bpm (Figure 7-4).
Recognizing Bradyarrhythmias
Bradyarrhythmias described in this chapter include
sinus bradycardia, first-degree AV block, second-
degree AV block (types I and II) and third-degree
(complete) AV block.

Practice Note Regularity: regular

Rate: < 60 bpm
Bradycardia is defined as a heart rate less than 60 P wave: upright and uniform; one for every QRS complex
bpm. In most cases, patients present with symptoms QRS complex: < 0.12 second
when the heart rate is less than 50 bpm. PR interval: 0.12–0.20 second
Figure 7-4 | Sinus bradycardia

Sinus Bradycardia
Atrioventricular Block
Sinus bradycardia is identical to normal sinus rhythm, except
the rate is less than 60 bpm. Cardiac activation starts at the AV block is partial or complete interruption of impulse
SA node but is slower than normal. Sinus bradycardia may transmission from the atria to the ventricles. The
be a normal finding in some patients, particularly healthy block may occur at the AV node, the bundle of His,
young adults and trained athletes. In other patients, however, the bundle branches or the Purkinje fibers. Common
sinus bradycardia is a pathologic finding. causes of AV block include fibrosis and scarring of the
conduction system and myocardial infarction. Other
Causes
causes include medications (such as β-blockers, calcium
Causes of sinus bradycardia include: channel blockers, digoxin and amiodarone), electrolyte
■ Vagal stimulation. abnormalities, myocardial ischemia, infectious or
■ Myocardial infarction. inflammatory disorders and congenital heart conditions.
■ Hypoxia. Depending on the cause, AV block can be transient or
■ Medications (e.g., β-blockers, calcium channel persistent. AV blocks are classified as first, second or
blockers, digoxin). third degree. Figure 7-5 summarizes how to differentiate
■ Coronary artery disease. AV blocks according to ECG findings.
■ Hypothyroidism.
First-Degree Atrioventricular Block
■ Iatrogenic illness.
■ Inflammatory conditions. First-degree AV block is characterized by a prolonged
delay in conduction at the AV node or bundle of His. The
impulse is conducted normally from the sinus node through
the atria, but upon reaching the AV node, it is delayed for

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 Second-Degree Atrioventricular Block
NO
More P waves than
QRS complexes?
PR interval greater
than 200 ms? Type I
YES YES In second-degree AV block type I (also called Mobitz type
First-degree AV block I or Wenckebach block), impulses are delayed and some
YES
PR interval constant? Second-degree AV block type II are not conducted through to the ventricles. After three
or four successive impulse delays, the next impulse is
NO
blocked. After the blocked impulse, the AV node resets,
RR interval constant? YES
Third-degree AV block and the pattern repeats. Second-degree AV block type I
usually occurs at the AV node but may be infranodal.
NO
Second-degree AV block type I Causes
Figure 7-5 | Approach to differentiating atrioventricular (AV) Because the block usually occurs above the bundle
blocks according to ECG findings of His, conditions or medications that affect the AV
node (such as myocarditis, electrolyte abnormalities,
longer than the usual 200 milliseconds (0.2 second). In
inferior wall myocardial infarction or medications such as
first-degree AV block, although the impulses are delayed,
digoxin) can cause second-degree AV block type I. This
each atrial impulse is eventually conducted through the AV
type of arrhythmia can also be physiologic.
node to cause ventricular depolarization.
Signs and Symptoms
Causes
Second-degree AV block type I rarely produces symptoms.
First-degree AV block may be a normal finding in athletes
Some patients may have signs and symptoms similar to sinus
and young patients with high vagal tone. It can also be an
bradycardia.
early sign of degenerative disease of the conduction system
or a transient manifestation of myocarditis or drug toxicity. ECG Findings
Signs and Symptoms Because some impulses are not conducted through to
the ventricles, the ratio of P waves to QRS complexes
First-degree AV block rarely produces symptoms.
is greater than 1:1 (Figure 7-7). Because each impulse
ECG Findings is delayed a little more than the last until eventually one
impulse is completely blocked, the ECG shows progressive
First-degree AV block (Figure 7-6) is characterized by
lengthening of the PR interval with each beat, then a P wave
normal P waves that are each followed by QRS complexes,
that is not followed by a QRS complex (a “dropped beat”).
but because the impulse is delayed at the AV node or
In most cases, the RR interval decreases before each
bundle of His, the PR interval is longer than normal (i.e., it
dropped beat. After the dropped beat, impulse conduction
exceeds 0.2 second). QRS complexes of normal duration
through the AV node resumes and the sequence repeats.
suggest that the delay is occurring at the level of the AV
node, whereas wide QRS complexes suggest that the delay
is infranodal (distal to the node).

Regularity: irregular in a pattern

Rate: variable; usually < 100 bpm
P wave: upright and uniform; more P waves than
Regularity: regular QRS complexes
Rate: variable; can occur with normal rate, QRS complex: < 0.12 second
bradycardia or tachycardia PR interval: becomes progressively longer until a P
P wave: upright and uniform: one for every QRS complex wave is not conducted, then cycle repeats
QRS complex: < 0.12 second
Figure 7-7 | Second-degree atrioventricular (AV) block type I
PR interval: > 0.20 second

Figure 7-6 | First-degree atrioventricular (AV) block

Chapter 7 | Arrhythmias | 99
Second-Degree Atrioventricular Block contract, usually at a rate of 30 to 45 bpm. This
Type II means that the atria and ventricles are being driven
by independent pacemakers and are contracting
In second-degree AV block type II (Mobitz type II), the
at their own intrinsic rates, a situation known as
block occurs below the AV node, in the bundle of His.
atrioventricular (AV) dissociation.
As with second-degree AV block type I, some atrial
impulses are conducted through to the ventricles, and Causes
others are not. However, there are no progressive
Degenerative disease of the conduction system is the
delays. The blocked impulses may be chaotic or occur
leading cause of third-degree AV block. This arrhythmia
in a pattern (e.g., 2:1, 3:1 or 4:1). In high-grade second-
may also result from damage caused by myocardial
degree AV block type II, the ratio is greater than 2:1 (i.e.,
infarction, Lyme disease or antiarrhythmic medications.
3:1, 4:1, or variable).
Signs and Symptoms
Causes
If ventricular contraction is stimulated by pacemaker
Second-degree AV block type II is always pathologic. It
cells above the bifurcation of the bundle of His, the
is usually caused by fibrotic disease of the conduction
ventricular rate is relatively fast (40 to 60 bpm) and
system or anterior wall myocardial infarction.
reliable, and symptoms may be mild (such as fatigue,
Signs and Symptoms orthostatic hypotension and effort intolerance). However,
if ventricular contraction is stimulated by pacemaker cells
Patients may present with light-headedness or syncope,
in the ventricles, the ventricular rate will be slower (20 to
or they may be asymptomatic. The clinical presentation
40 bpm) and less reliable, and symptoms of decreased
varies, depending on the ratio of conducted to blocked
cardiac output may be more severe.
impulses.
ECG Findings
ECG Findings
In third-degree AV block, there is no electrical
Second-degree AV block type II is characterized by a
communication between the atria and ventricles, so there
constant PR interval (Figure 7-8). Because impulses
is no relationship between P waves and QRS complexes
are intermittently blocked, there are more P waves than
(Figure 7-9). The RR interval is usually constant. The PP
QRS complexes.
interval is constant or slightly irregular. If pacemaker cells
in the AV junction stimulate ventricular contraction, the
QRS complexes will be narrow (less than 0.12 second
in duration). Impulses that originate in the ventricles
produce wide QRS complexes.

Regularity: regular (2:1), unless conduction ratio varies

Rate: usually < 100 bpm, tendency for bradycardia
P wave: upright and uniform; more P waves than
QRS complexes (2:1, 3:1, 4:1 or variable)
QRS complex: < 0.12 second
PR interval: < 0.20 second or prolonged; constant Regularity: usually regular RR interval, regular PP interval
for every QRS complex Rate: varies depending on escape focus; junctional
(40–60 bpm) and ventricular (< 40 bpm)
Figure 7-8 | Second-degree atrioventricular (AV) block type II P wave: upright and uniform, more P waves than
QRS complexes
QRS complex: < 0.12 second if junctional escape,
≥ 0.12 second if ventricular escape
Third-Degree Atrioventricular Block
PR interval: total dissociation from QRS complexes
In third-degree (complete) AV block, no impulses
are conducted through to the ventricles. The block Figure 7-9 | Third-degree atrioventricular (AV) block
can occur at the level of the AV node but is usually
infranodal. Pacemaker cells in the AV junction, bundle
of His or the ventricles stimulate the ventricles to

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Recognizing Causes
Tachyarrhythmias Atrial flutter is often seen in patients with heart
disease (such as heart failure, rheumatic heart disease
Tachyarrhythmias can be categorized as narrow complex or coronary artery disease) or as a postoperative
or wide complex. complication.
■ Narrow-complex tachyarrhythmias include sinus
Signs and Symptoms
tachycardia, atrial flutter, supraventricular tachycardia
(SVT) and atrial fibrillation. These arrhythmias usually Patients may be asymptomatic or present with shortness
originate above the ventricles in the atria or AV node of breath, palpitations, effort intolerance, chest
and run normally through the bundle branches, constriction, weakness or syncope.
producing a normal QRS complex.
■ Wide-complex tachyarrhythmias originate in the ECG Findings
ventricles and include monomorphic and polymorphic
In atrial flutter, atrial contraction occurs at such a
ventricular tachycardia, torsades de pointes (a form of
polymorphic ventricular tachycardia) and ventricular rapid rate that discrete P waves separated by a flat
fibrillation. Supraventricular tachycardia with aberrant baseline cannot be seen (Figure 7-11). Instead, the
conduction can also produce a wide-complex baseline continually rises and falls, producing the
tachyarrhythmia. “flutter” waves. In leads II and III, the flutter waves may
be quite prominent, creating a “sawtooth” pattern.
Sinus Tachycardia Because of the volume of atrial impulses, the AV node
allows only some of the impulses to pass through to
Sinus tachycardia, the most common tachyarrhythmia, the ventricles. In atrial flutter, a 2:1 ratio is the most
is identical to normal sinus rhythm, except the rate common (i.e., for every two flutter waves, only one
is between 100 and 150 bpm (Figure 7-10). Sinus impulse passes through the AV node to generate
tachycardia is a normal physiologic response when the a QRS complex). Ratios of 3:1 and 4:1 are also
body is under stress (such as that caused by exercise, frequently seen.
illness or pain). It may also be seen in patients with heart
failure, lung disease, shock or hyperthyroidism.

Regularity: usually regular (could be irregular with

variable conduction)
Regularity: regular Rate: varies with conduction; < 100 bpm is
controlled; > 100 bpm is uncontrolled (rapid
Rate: 100–150 bpm ventricular response); usually has ventricular rates
P wave: upright and uniform; one for every QRS complex of 75 bpm (4:1), 100 bpm (3:1) or 150 bpm (2:1),
QRS complex: < 0.12 second, regular depending on conduction ratio
PR interval: 0.12–0.20 second P wave: none; flutter (F) waves; characteristic
“sawtooth” baseline
Figure 7-10 | Sinus tachycardia
QRS complex: < 0.12 second
PR interval: not discernible

Atrial Flutter Figure 7-11 | Atrial flutter

Atrial flutter is caused by an ectopic focus in the atria that

causes the atria to contract at a rate of 250 to 350 bpm. Supraventricular Tachycardia
The underlying mechanism of atrial flutter is most often a
reentrant circuit that encircles the tricuspid valve annulus. Supraventricular tachycardia (SVT) is an arrhythmia
originating above the ventricles. In general, the rate is
greater than 150 bpm, which helps to differentiate SVT
from sinus tachycardia. SVT can be classified as AV

Chapter 7 | Arrhythmias | 101

nodal reentrant tachycardia (AVNRT), AV-reciprocating Causes
tachycardia (AVRT) and atrial tachycardia.
Atrial fibrillation can occur in young patients with no
Causes history of cardiac disease. Acute alcohol toxicity can
precipitate an episode of atrial fibrillation in otherwise
SVT is seen in patients with low potassium and healthy patients. However, atrial fibrillation commonly
magnesium levels, a family history of tachycardia, occurs in the presence of underlying heart disease, lung
structural abnormalities of the heart, adverse reactions disease, hyperthyroidism or myocardial infarction.
from certain pharmacologic agents (e.g., antihistamines,
theophylline, cough and cold preparations, appetite Signs and Symptoms
suppressants), certain medical conditions (e.g.,
Patients with atrial fibrillation may be asymptomatic.
cardiovascular disease, long-term respiratory disease,
However, ventricular rates greater than 100 bpm are
diabetes, anemia, cancer) and illicit drug use.
usually not tolerated well because the filling time for
Signs and Symptoms the ventricles is significantly reduced. Symptoms may
include shortness of breath, palpitations, chest pain,
Patients may present without symptoms or with dizziness light-headedness, dizziness and fatigue. Hypotension,
or light-headedness, dyspnea, palpitations (including syncope and heart failure can occur.
pulsations in the neck area), diaphoresis, ischemic chest
pain, hypotension, fatigue, vision changes and syncope. ECG Findings
ECG Findings The two key features of atrial fibrillation on ECG are
the absence of discrete P waves and the presence of
In SVT, the P waves may be absent or abnormal. There is irregularly irregular QRS complexes (Figure 7-13). The
minimal to no beat-to-beat variability and the heart rate is baseline appears flat or undulates slightly, producing
usually greater than or equal to 150 bpm (Figure 7-12). fibrillatory waves.

Regularity: regular; minimal beat-to-beat variability

Rate: typically > 150 bpm Regularity: irregularly irregular
P wave: absent or not clearly identifiable Rate: varies with conduction; < 100 bpm is
controlled; > 100 bpm is uncontrolled (rapid
QRS complex: < 0.12 second ventricular response)
PR interval: if P waves are visible, PR interval P wave: none; fibrillation (f) waves; chaotic baseline
may be shortened or lengthened depending on QRS complex: < 0.12 second
mechanism PR interval: not discernible
Figure 7-12 | Supraventricular tachycardia
Figure 7-13 | Atrial fibrillation

Atrial Fibrillation Ventricular Tachycardia

Atrial fibrillation is caused by multiple ectopic foci in Ventricular tachycardia occurs when a ventricular
the atria that cause the atria to contract at a rate of focus below the bundle of His becomes the new
350 to 600 bpm. Rarely, the atrial rate may be as high pacemaker. The ventricles contract rapidly (usually at
as 700 bpm. The AV node only allows some of the a rate faster than 100 bpm) and usually with a regular
impulses to pass through to the ventricles, generating an rhythm. The rapid ventricular rate significantly diminishes
irregularly irregular rhythm that is completely chaotic and cardiac output and can only be sustained for a short
unpredictable. period before the patient becomes hemodynamically
compromised. Ventricular tachycardia can quickly turn
into ventricular fibrillation, leading to cardiac arrest.

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Torsades de pointes is a highly unstable form of A
polymorphic ventricular tachycardia that may revert to
sinus rhythm or degenerate into pulseless ventricular
tachycardia or ventricular fibrillation.

Causes
Ventricular tachycardia usually occurs in the presence Regularity: regular
of heart disease or damage, such as that caused by Rate: > 100 bpm
acute or remote myocardial infarction or cardiomyopathy. P wave: not discernible
There is a significant risk for ventricular tachycardia QRS complex: ≥ 0.12 second, uniform in shape
after myocardial infarction, and this risk can last for PR interval: not discernible
weeks, months or years. Ventricular tachycardia may
also be precipitated by medications that prolong the QT
interval, including amiodarone or other antiarrhythmics B
and certain antibiotics and antidepressants. Electrolyte
derangements (including hypocalcemia, hypomagnesemia
and hypokalemia) can also be involved.

Torsades de pointes most often accompanies prolonged

QT intervals, which may be the result of a congenital Regularity: irregular (can appear regular due to
condition, acute myocardial infarction, medications fast rate)
or drug–drug interactions. The risk for torsades de Rate: > 100 bpm
pointes is increased when the QTc is greater than 500 P wave: not discernible
milliseconds (0.5 second). QRS complex: ≥ 0.12 second, variable in shape
PR interval: not discernible
Signs and Symptoms
With sustained ventricular tachycardia, signs and C
symptoms of reduced cardiac output and hemodynamic
compromise develop, including chest pain, hypotension
and loss of consciousness.

ECG Findings
In ventricular tachycardia, the QRS complexes are wide Regularity: regular or irregular
(lasting longer than 0.12 second). When there is only Rate: > 200 bpm
one ectopic focus in the ventricles, monomorphic P wave: not discernible
ventricular tachycardia is seen on the ECG (i.e., QRS complex: ≥ 0.12 second, variable in shape
the QRS complexes are generally the same shape; PR interval: not discernible
Figure 7-14A). When there are two or more ectopic Figure 7-14 | Ventricular tachycardia. (A) Monomorphic
foci, polymorphic ventricular tachycardia is seen. In ventricular tachycardia. (B) Polymorphic ventricular
polymorphic ventricular tachycardia, the QRS complexes tachycardia. (C) Torsades de pointes.
vary in shape and rate (see Figure 7-14B).

When the QRS complexes in ventricular tachycardia are

Practice Note
polymorphic and wide, the rhythm may be torsades de
pointes. In torsades de pointes (“twisting of the points”), Monomorphic ventricular tachycardia is more likely
the QRS complexes appear to pivot around the isoelectric caused by a chronic condition, such as scarring from
line, deflecting upward and then downward, with their a healed infarction. It may also be seen with reentrant
amplitude becoming smaller and larger, then smaller rhythms. Polymorphic ventricular tachycardia is more
again (see Figure 7-14C). The rhythm may be regular or likely caused by an acute condition, such as ischemia,
irregular. The rate is faster than 200 bpm. P waves are not current infarction or profound electrolyte disturbance.
visible, and the QRS complexes are wide (lasting longer
than 0.12 second) and difficult to measure.

Chapter 7 | Arrhythmias | 103

Patient Assessment Diagnostic Tests
A 12-lead ECG aids in further identifying the arrhythmia.
Rapid Assessment Additionally, a complete blood count, comprehensive
metabolic panel, arterial blood gases and cardiac markers
The patient’s appearance on rapid assessment can may be considered.
vary widely, depending on the arrhythmia. The patient
may appear to be in minimal distress, show signs
of hemodynamic compromise (e.g., pale, mottled or Approach to the Patient
cyanotic skin) or show signs related to the underlying
cause of the arrhythmia (e.g., pain, diaphoresis). Bradyarrhythmia

Primary Assessment The Adult Bradyarrhythmia Code Card summarizes the

approach to a patient with a bradyarrhythmia.
Conduct a primary assessment following the ABCDE
Assess and Recognize
approach and provide care as needed. Obtain and monitor
the patient’s vital signs. Establish cardiac monitoring, pulse When bradyarrhythmia is suspected, the team takes
oximetry and vascular access, and be prepared to provide actions to ensure adequate airway, breathing and
CPR and defibrillation if the patient’s condition deteriorates. circulation, including obtaining and monitoring vital signs,
Provide the minimal level of supplemental oxygen needed establishing cardiac monitoring and pulse oximetry,
to maintain an oxygen saturation of at least 94% to 99% administering supplemental oxygen if needed and ensuring
and provide assistance with ventilation if needed. Assess vascular access. If time and resources permit, a 12-lead
level of consciousness in patients who appear to have ECG should be obtained. Because the rhythm may change
changes in mental status. Obtain a 12-lead ECG if time to a cardiac arrest rhythm, the team should be prepared to
and resources permit. initiate CPR and defibrillation.

Because care depends on whether the patient has

Secondary Assessment adequate perfusion or is hemodynamically compromised,
assessing indicators of perfusion status (such as mental
The goals of the secondary assessment are to: status, blood pressure and pulses) is key. Findings that
■ Identify signs and symptoms and determine whether they may suggest that the patient is experiencing hemodynamic
are being caused by the arrhythmia or another condition. compromise include changes in mental status, ischemic
■ Further determine the severity of the signs and chest discomfort, hypotension, signs of shock or acute
symptoms. heart failure.
■ Identify the arrhythmia, if not done as part of the
primary assessment. Care
■ Identify potentially reversible causes of the arrhythmia. Throughout treatment, work to determine the underlying
cause of the bradycardia and continually reassess the
History
patient’s condition. Clinical signs of improved cardiac
Key information to elicit during the history includes: output include an improved peripheral pulse, an increase
■ A description of the patient’s symptoms, including a full in blood pressure, an improved level of consciousness,
description of symptoms such as chest pain or syncope. and improved skin color and temperature.
■ A medical history of arrhythmias, cardiac disorders or
cardiac surgery. Treatment pathways depend on whether the patient has
■ The presence of comorbid conditions, including adequate perfusion or hemodynamic compromise.
cardiovascular disease, pulmonary disease and
thyroid disease. Bradyarrhythmia/No Hemodynamic
■ Current medications, including antiarrhythmic agents. Compromise
If the patient is not showing signs and symptoms of
Physical Examination hemodynamic compromise, the patient’s condition should
Obtain and monitor the patient’s vital signs and perform be monitored (cardiac monitoring, noninvasive blood
a physical examination. pressure monitoring, vital signs). A 12-lead ECG may
be obtained and an effort should be made to identify and

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address the underlying cause of the bradyarrhythmia. Atropine
Consider expert consultation. Atropine is an anticholinergic drug that increases SA node
Bradyarrhythmia/Hemodynamic Compromise firing by counteracting vagus nerve action to increase the
heart rate. It is the first-line therapy for bradyarrhythmia
If the patient has signs of hemodynamic compromise, with hemodynamic compromise. Administer a 1-mg bolus
initiate treatment immediately (Figure 7-15). It may be intravenously every 3 to 5 minutes, up to a maximum dose of
necessary to implement multiple treatment measures 3 mg. If the atropine is having no effect, do not wait to reach
simultaneously. First-line therapy is with atropine. the maximum dose of atropine before initiating second-line
therapies.
Practice Note
If at any point atropine is not effective, consider Practice Note
transcutaneous pacing or β-adrenergic agonist therapy.
Use atropine with caution in patients with acute
Also consider transcutaneous pacing or β-adrenergic
coronary ischemia or myocardial infarction because
agonist therapy immediately if the patient has second-
in these patients, atropine can cause adverse effects,
degree AV block type II or third-degree AV block.
including ventricular tachycardia or ventricular fibrillation.
Second-line therapies include transcutaneous pacing
and β-adrenergic agonists. Consider expert consult and Transcutaneous Pacing
transvenous pacing if first- and second-line therapies are
not effective. If at any point atropine is not effective, consider initiating
transcutaneous pacing as a second-line therapy. Consider
implementing transcutaneous pacing immediately if
vascular access is difficult to achieve. Transcutaneous
A pacing can be painful. If the patient’s clinical condition
permits, administer sedation or analgesia before pacing.
After initiating pacing, verify electrical capture (evidenced
by wide QRS complexes and tall, broad T waves following
each pacing spike on the monitor). Confirm mechanical
capture by assessing the patient for clinical signs of
improved cardiac output.

β-Adrenergic Agonists
Epinephrine or dopamine may be administered to patients
with symptomatic bradycardia as an alternative second-
line therapy. These medications may also be considered
when the cause of the bradyarrhythmia is an overdose
B
with a β-blocker or calcium channel blocker. The initial
dose is 2 to 10 mcg/min by IV infusion for epinephrine or
5 to 20 mcg/kg/min by IV infusion for dopamine, and then
the dose is titrated to the patient’s response.

Tachyarrhythmia
The Adult Tachyarrhythmia Code Card summarizes the
approach to a patient with a tachyarrhythmia.

Assess and Recognize

When tachyarrhythmia is suspected, the team takes
Figure 7-15 | Interventions for bradyarrhythmia with
actions to ensure adequate airway, breathing and
hemodynamic compromise. (A) Atropine is considered first-
line therapy. (B) Transcutaneous pacing is a second-line circulation, including obtaining and monitoring vital
therapy. signs, establishing cardiac monitoring and pulse

Chapter 7 | Arrhythmias | 105

oximetry, administering supplemental oxygen if needed and an effort should be made to identify and address the
and ensuring vascular access. If time and resources underlying cause of the tachycardia.
permit, a 12-lead ECG should be obtained. Because the
rhythm may change to a cardiac arrest rhythm, the team Tachyarrhythmia with a Pulse/Hemodynamic
should be prepared to initiate CPR and defibrillation. Compromise
When a patient with tachyarrhythmia with a pulse has
When a patient is found to have tachyarrhythmia with signs of hemodynamic compromise, synchronized
a pulse, take a three-step approach to determining cardioversion is indicated (Figure 7-16). If the patient’s
appropriate care. condition allows, administer sedation before initiating
■ First, look at the heart rate. Tachycardia caused cardioversion. Follow the device manufacturer’s
by a systemic condition is usually associated with recommendations for energy doses. Consider adenosine
a heart rate between 100 and 150 bpm, whereas (6 mg via rapid IV push followed by a rapid 10- to 20-mL
tachyarrhythmias are usually associated with heart
normal saline flush) before synchronized cardioversion
rates greater than 150 bpm. If the heart rate is
between 100 and 150 bpm, the tachycardia is most for a narrow-complex regular rhythm if vascular access
likely sinus tachycardia. Search for an underlying is readily available. Do not delay cardioversion to
systemic cause (such as dehydration, blood loss, administer adenosine.
fever, infection or anxiety) and treat that first. If the
heart rate is 150 bpm or more, the tachycardia is If the tachyarrhythmia is refractory, consider the need to
likely caused by an arrhythmia. increase the energy level for the next cardioversion and
the use of an antiarrhythmic medication (procainamide,
amiodarone or sotalol.) Also consider underlying causes
Practice Note and expert consultation.
Even when a patient’s heart rate is between 100 and Narrow-Complex Supraventricular
150 bpm, signs of hemodynamic compromise should Tachycardia/No Hemodynamic Compromise
be sought and, if found, treatment for tachyarrhythmia
If the patient is not showing signs of hemodynamic
with hemodynamic compromise should be initiated.
compromise, the QRS complex is narrow and the rhythm
is regular, attempt vagal maneuvers (Table 7-1) to break
■ Next, if the patient’s heart rate is greater than 150
bpm and the tachycardia is not presumed to be the tachyarrhythmia. Consider adenosine (6 mg via rapid
sinus tachycardia, determine whether the patient IV push followed by a 10- to 20-mL normal saline flush)
has adequate perfusion or is hemodynamically if the rhythm is regular. An additional 12-mg dose of
compromised. A patient who is showing signs and adenosine (followed by a normal saline flush) may be
symptoms of hemodynamic compromise despite given if the rhythm does not convert. Consider a calcium
initial management of airway and breathing requires channel blocker or β-blocker if the rhythm is not regular,
immediate therapy with synchronized cardioversion.
adenosine is ineffective or the tachyarrhythmia recurs.
■ Finally, if the patient’s heart rate is greater than 150 Consider expert consultation.
bpm, the tachycardia is not presumed to be sinus
tachycardia and the patient is not showing signs of
hemodynamic compromise, determine whether the
QRS complexes are narrow (< 0.12 second) or wide
(≥ 0.12 second).
Care
Throughout treatment, work to determine the underlying
cause of the tachycardia and continually reassess the
patient’s clinical condition.

Sinus Tachycardia
If the patient’s heart rate is between 100 and 150 bpm
and the patient is not showing signs of hemodynamic
compromise, the patient’s condition should be monitored
(e.g., cardiac monitoring, noninvasive blood pressure Figure 7-16 | If a patient with tachyarrhythmia and a pulse
has signs of hemodynamic compromise, the treatment is
monitoring, vital signs). A 12-lead ECG may be obtained
synchronized cardioversion.

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Table 7-1 | Vagal Maneuvers supraventricular tachycardia with aberrant conduction.
In this case, consider adenosine (6 mg via rapid IV push
Maneuver Method followed by a 10- to 20-mL normal saline flush). For a
Valsalva Instruct the patient to exhale forcefully patient without signs of hemodynamic compromise and
maneuver against a closed airway or blow a wide rhythm, consider an antiarrhythmic medication
through an occluded straw. (procainamide, amiodarone or sotalol).
Cold stimulus Apply a cold stimulus (e.g., an ice pack ■ Procainamide: Avoid in patients with known prolonged
or a washcloth soaked in cold water) QT intervals or congestive heart failure. Administer
to the patient’s nose and mouth for 10 20 to 50 mg/min until the arrhythmia is suppressed,
seconds. hypotension develops, the QRS duration increases
by more than 50% or a maximum dose of 17 mg/kg is
Gagging Touch a tongue depressor to the back given. The maintenance infusion is 1 to 4 mg/min.
of the patient’s throat to stimulate the ■ Amiodarone: Administer 150 mg over 10 minutes.
gag reflex. Repeat as needed if the tachyarrhythmia recurs. The
Carotid With the patient’s neck extended and maintenance infusion is 1 mg/min for the first 6 hours.
massage the head turned away, apply pressure ■ Sotalol: Avoid in patients with known prolonged
underneath the angle of the jaw in a QT intervals. Administer 100 mg (1.5 mg/kg) over 5
circular motion for 10 seconds (not minutes.
recommended for patients with carotid If the tachyarrhthmia is refractory, consider the
artery stenosis or a history of smoking). underlying cause, cardioversion, a change to the
antiarrhythmic medication (e.g., adjustment of the dose,
Wide-Complex Ventricular Tachycardia/No a change to a different antiarrhythmic medication or the
Hemodynamic Compromise addition of another antiarrhythmic medication) and expert
consultation.
If the rhythm is wide (QRS complex ≥ 0.12 second),
regular and monomorphic and the patient does not have
signs of hemodynamic compromise, the rhythm may be

Chapter 7 | Arrhythmias | 107

 ADULT BRADYARRHYTHMIA
ALS - 2020 VERSION

Bradyarrhythmia
• HR < 50
• Relative bradycardia for patient’s
condition may also warrant treatment

• Maintain airway and breathing

• Establish pulse oximetry
• Administer supplemental oxygen (target SpO2 of 94%
to 99%) if clinically indicated
• Establish cardiac monitoring
• Monitor blood pressure and perfusion
• Obtain IV access (IO access if necessary)
• Obtain 12-lead ECG if time and resources permit

Signs of hemodynamic
compromise?
YES NO

• Administer atropine* • Monitor patient (e.g., cardiac

• If atropine is ineffective: monitoring, noninvasive blood
pressure, vital signs)
- Provide transcutaneous pacing OR
• Obtain 12-lead ECG if not already done
- Initiate β-adrenergic agonist
infusion (dopamine or epinephrine) • Identify and treat underlying causes
• Consider expert consultation

• Consider expert consultation

• Consider transvenous pacing

Medications Signs of Hemodynamic Compromise

Atropine
• 1 mg IV bolus every 3 to 5 min, up to a max dose of 3 mg • Changes in mental status
• Ischemic chest discomfort
Dopamine
• 5 to 20 mcg/kg/min titrated to effect • Hypotension
• Signs of shock
Epinephrine
• Acute heart failure
• 2 to 10 mcg/min titrated to effect

*Consider implementing transcutaneous pacing or β-adrenergic agonist therapy immediately for patients with second-degree AV block type II or third-degree AV block.
Consider implementing transcutaneous pacing immediately if vascular access is difficult to achieve.

Copyright © 2021 The American National Red Cross

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ADULT TACHYARRHYTHMIA
ALS - 2020 VERSION

Tachyarrhythmia
• HR ≥ 150
• Relative tachycardia for patient’s condition may also warrant treatment

• Maintain airway and breathing; establish pulse oximetry

• Administer supplemental oxygen (target SpO2 of 94% to 99%) if
clinically indicated
• Establish cardiac monitoring; monitor blood pressure and perfusion
• Obtain 12-lead ECG if time and resources permit
• Obtain IV access (IO access if necessary)

Probable sinus tachycardia

Evaluate rhythm
• HR usually < 150

• Monitor patient (e.g., cardiac monitoring, Signs of hemodynamic

noninvasive blood pressure, vital signs) compromise?
• Obtain 12-lead ECG if not already done YES NO
• Identify and treat underlying cause
(e.g., dehydration, blood loss, fever,
infection, anxiety)
Wide QRS (≥ 0.12 sec)?

YES NO
• Immediate synchronized cardioversion
(pre-sedate if possible)
• Consider adenosine (do not delay
cardioversion) for narrow-complex and • Obtain IV access and 12-lead ECG • Obtain IV access and 12-lead ECG
regular rhythm if not already done and time and if not already done and time and
• If refractory, consider: resources permit resources permit
- Need to increase energy level for next • Consider adenosine if regular • Attempt vagal maneuver if rhythm
cardioversion and monomorphic is regular
- Antiarrhythmic medication • Consider antiarrhythmic • Consider adenosine if rhythm is
(procainamide, amiodarone OR sotalol) medication (procainamide, regular
- Underlying cause amiodarone OR sotalol) • Consider calcium channel blocker
• If refractory, consider: OR β-blocker if rhythm is not
- Expert consultation regular, adenosine is ineffective or
- Underlying cause tachyarrhythmia recurs
- Cardioversion • Consider expert consultation
Medications
- Adjustment of dose or
Adenosine change/addition of another
• First dose: 6 mg via rapid IV push antiarrhythmic medication
• Second dose: 12 mg if needed (procainamide, amiodarone OR
NOTE: Follow each dose with a rapid 10- to 20-ml NS sotalol)
flush - Expert consultation
Amiodarone
• 150 mg IV over 10 min; repeat as needed if arrhythmia
recurs
• Maintenance infusion: 1 mg/min for first 6 hours Synchronized Cardioversion Energy Doses Signs of Hemodynamic Compromise
Procainamide (avoid if prolonged QT or congestive heart Follow device manufacturer’s recommendations for • Changes in mental status
failure) energy doses • Ischemic chest discomfort
• 20 to 50 mg/min until arrhythmia is suppressed, • Hypotension
hypotension develops, QRS duration increases by more Vagal Maneuvers
than 50% or max dose of 17 mg/kg is given • Signs of shock
• Valsalva maneuver • Acute heart failure
• Maintenance infusion: 1 to 4 mg/min
• Cold stimulus
• Gagging
Sotalol (avoid if prolonged QT)
• Carotid massage (use with caution in those with
• 100 mg (1.5 mg/kg) over 5 min
vascular disease, older adults)

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Chapter 7 | Arrhythmias | 109

 CHAPTER
8

Cardiac Arrest
Introduction
In the United States, approximately 200,000 cases of in-hospital cardiac arrest and
approximately 395,000 cases of out-of-hospital cardiac arrest occur annually. No
matter where cardiac arrest occurs, patient outcomes are improved when each link in
the Cardiac Chain of Survival is implemented swiftly and properly.
Recognizing Cardiac Arrest sustain sufficient cardiac output.

Rhythms Causes
The underlying causes of pulseless ventricular
Rhythms associated with cardiac arrest include
tachycardia are the same as for ventricular tachycardia
ventricular fibrillation, pulseless ventricular tachycardia,
(see Chapter 7) and include heart disease or damage
pulseless electrical activity (PEA) and asystole. The
(as from myocardial infarction), certain medications and
first step in recognizing a cardiac arrest rhythm is
electrolyte imbalances.
establishing that the patient does not have a pulse by
checking for a carotid pulse. ECG Findings
In pulseless ventricular tachycardia, the ventricular rate is
Ventricular Fibrillation usually greater than 180 bpm, and the QRS complexes
are very wide (Figure 8-2).
Ventricular fibrillation is characterized by erratic,
rapid and completely ineffective depolarization of the
ventricles. Rather than contracting, the ventricles quiver.
This rhythm is fatal if not corrected quickly.

Causes
Precipitating causes of ventricular fibrillation include
myocardial ischemia or infarction, shock, electrocution, Regularity: regular or irregular
stimulant overdose and ventricular tachycardia (including Rate: usually > 180 bpm
torsades de pointes). P wave: not discernible
QRS complex: ≥ 0.12 second
ECG Findings
PR interval: not discernible
The rhythm is irregular and there are no discernible P
waves, QRS complexes or T waves (Figure 8-1). The Figure 8-2 | Pulseless ventricular tachycardia
waveforms that are seen may vary in amplitude, from
coarse to fine. As ventricular fibrillation progresses,
the waveforms may change from coarse to fine and Pulseless Electrical Activity
eventually disappear (asystole).
Pulseless electrical activity (PEA) is a term used to
describe several rhythms that are organized on ECG
(i.e., the QRS complexes are similar in appearance)
but the patient has no palpable pulse. The heart’s
conduction system is functioning, but the myocardium is
not contracting (or contracting too weakly) to produce
cardiac output, or volume is not sufficient to maintain
Regularity: irregular cardiac output.
Rate: not measurable
P wave: not discernible Causes
QRS complex: chaotic, not discernible PEA may be seen immediately after successful
PR interval: not discernible defibrillation of a patient with ventricular fibrillation or
pulseless ventricular tachycardia. But when PEA is the
Figure 8-1 | Ventricular fibrillation
presenting rhythm (“primary PEA”), the underlying cause
is usually a condition that either affects contractility
or ejection (e.g., hypoxia, acidosis, anterior wall
Pulseless Ventricular Tachycardia myocardial infarction) or leads to inadequate preload
(e.g., severe hypovolemia, pulmonary embolism, tension
Patients in ventricular tachycardia may or may not have pneumothorax, cardiac tamponade, right ventricular
a pulse. Pulseless ventricular tachycardia occurs when infarction).
the ventricles are not contracting effectively enough to

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ECG Findings
In PEA, the monitor shows an identifiable rhythm but no Practice Note
pulse can be palpated. The rhythm may be sinus, atrial,
junctional or ventricular in origin. The rate may be fast or Although asystole is said to have a “flatline” appearance
slow. The QRS complexes are similar in appearance and on ECG, there is some fluctuation from the baseline in
may be narrow or wide. When the cause of the PEA is asystole. A completely flat baseline is likely the result of
cardiac in origin, it is most common to see a slow rate disconnected leads or equipment problems.
and wide QRS complexes. Noncardiac causes of PEA
are often associated with a rapid rate and narrow QRS
complexes.
Reversible Causes of Cardiac
Asystole Arrest (Hs and Ts)
When caring for a patient in cardiac arrest, it is important to
In asystole, there is no electrical activity and therefore no
recognize reversible causes for the arrest and address them
contraction.
(Figure 8-4). This is especially important with PEA and
Causes asystole, which often have reversible underlying causes.
The mnemonic Hs and Ts can help you to remember the
Asystole is often the terminal rhythm in untreated
reversible causes of cardiac arrest (Box 8-1).
pulseless ventricular tachycardia or ventricular fibrillation
or when resuscitation efforts are unsuccessful. Other While resuscitation is underway, review the patient’s
causes include narcotic drug overdose, hypothermia, medical history with the providers who were caring for
myocardial infarction, pulmonary embolism, hyperkalemia, the patient at the time of the arrest or family members
hypoxia (drowning, suffocation) and indirect lightning to identify details that could point to one of the Hs or
strike. Ts as an underlying cause (Table 8-1). Of particular
importance are changes in the patient’s clinical condition
ECG Findings leading up to the arrest, disorders or situations that
Asystole is characterized by a lack of discernible could predispose a patient to developing one of the Hs
electrical activity on ECG, which results in a “flatline” or Ts, risk factors for cardiac and pulmonary conditions
appearance (Figure 8-3). Very rarely, the sinoatrial and medication use.
(SA) node may generate impulses that cause atrial
depolarization but are completely blocked at the
atrioventricular (AV) node, resulting in “P-wave asystole.”

Practice Note
Care must be taken to differentiate asystole from fine
ventricular fibrillation. To do this, quickly look at another
lead to evaluate the electrical activity in a different plane.

Regularity: not discernible

Rate: not discernible
P wave: usually absent
QRS complex: not discernible
PR interval: not discernible Figure 8-4 | While resuscitation is underway, consider
possible underlying causes for the cardiac arrest (Hs and Ts)
Figure 8-3 | Asystole with the team.

Chapter 8 | Cardiac Arrest | 113

Box 8-1 | Reversible Causes of Cardiac Arrest: Hs and Ts
Practice Note
Hs
Ultrasonography can be a useful tool for recognizing
■ Hypovolemia several underlying causes of cardiac arrest, including
■ Hypoxia pulmonary embolism, tension pneumothorax,
■ Hydrogen ion excess (acidosis) cardiac tamponade and hypovolemia. Consider use
■ Hyper- or hypokalemia of ultrasonography if the equipment and a skilled
■ Hypothermia technician are readily available, and if doing so will
Ts not impede or delay resuscitation efforts. Point-
of-care ultrasonography should not have a role in
■ Toxins
prognostication for cardiac arrest.
■ Tamponade
Tension pneumothorax
■
Hypovolemia
■ Thrombosis (pulmonary embolism)
■ Thrombosis (myocardial infarction) Hypovolemia (a reduction of fluid volume in the circulatory
system) develops because of excessive blood or fluid
Diagnostic studies that may prove useful for identifying loss (for example, because of trauma, internal bleeding or
underlying causes of the cardiac arrest include a 12- severe dehydration). A fluid challenge can aid in determining
lead ECG, arterial blood gases, a serum electrolyte whether hypovolemia is contributing to the cardiac arrest.
panel, chest radiography and bedside ultrasonography.
Although some diagnostic studies can be done while Hypoxia
resuscitation efforts are underway, others (such as a
Suspect hypoxia in any patient who had respiratory
12-lead ECG) should be delayed until after return of
difficulties preceding cardiac arrest. To address hypoxia
spontaneous circulation (ROSC) is achieved.
as a cause of cardiac arrest, ensure that the patient’s
airway is patent and provide adequate ventilation and
supplemental oxygen.

Table 8-1 | Clinical Clues to Underlying Causes of Cardiac Arrest (Hs and Ts)

Reversible History May Be Significant for: Monitoring and Diagnostic Tests

Cause
Hypovolemia Internal or external bleeding, dehydration, diabetes 12-lead ECG: narrow-complex
insipidus, diarrhea/vomiting, peritonitis, profound ventricular tachycardia
preload compromise (e.g., right ventricular infarction)
15-lead ECG: ST-segment elevation in
Peri-arrest signs and symptoms: hypotension; lead V4R
oliguria; cyanosis; rapid, shallow breathing;
confusion
Hypoxia Trauma, chronic or acute respiratory disorder Peri-arrest ETCO2: > 50 mmHg

Peri-arrest signs and symptoms: respiratory distress, Peri-arrest arterial oxygen saturation: <
respiratory failure, respiratory arrest 90%
Hydrogen ion Metabolic acidosis Arterial blood gases: pH < 7.35
excess Diabetes, sepsis, renal disease, alcoholism
ETCO2: < 29 mmHg in metabolic
Peri-arrest signs and symptoms: lethargy, drowsiness, acidosis, > 50 mmHg in respiratory
hyperventilation, headache acidosis

Respiratory acidosis
Chronic or acute respiratory disorder

Peri-arrest signs and symptoms: tachycardia,

tachypnea, hypercapnia, hypertension, hypoxemia,
hypercarbia, confusion, headache

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Table 8-1 | Clinical Clues to Underlying Causes of Cardiac Arrest (Hs and Ts) (continued)

Reversible History May Be Significant for: Monitoring and Diagnostic Tests

Cause
Hyper- or Hyperkalemia Hyperkalemia
hypokalemia Renal disease, trauma, burns, potassium 12-lead ECG: wide QRS complexes
supplementation and tall, pointed T waves

Peri-arrest signs and symptoms: cramps, muscle Hypokalemia

twitching, hypotension 12-lead ECG: flat T waves, prominent
U waves and possibly prolonged QT
Hypokalemia intervals
Renal disease, diuretics, eating disorder, diarrhea/
vomiting

Peri-arrest signs and symptoms: muscle weakness or

spasms, confusion, drowsiness
Hypothermia Exposure, drowning, fluid resuscitation ...
Toxins Drug abuse, medications ...
Tamponade Chest trauma, pericarditis (lung/breast cancer, PEA rhythm with narrow QRS
radiation therapy, post–myocardial infarction, infection, complexes, electrical alternans
connective tissue disorders, chronic renal disease,
postoperative complication)
Bedside ultrasonography can aid in
Peri-arrest signs and symptoms: dyspnea, tachypnea,
diagnosis
tachycardia, anxiety, changes in mental status,
hypotension, muffled heart sounds, jugular venous
distension, pericardial friction rub, pulsus paradoxus
Tension Chest trauma, thoracentesis, central venous catheter PEA rhythm with narrow QRS
pneumothorax insertion complexes

Peri-arrest signs and symptoms: tachypnea, diminished

or absent breath sounds, unequal chest expansion,
Bedside ultrasonography can aid in
tracheal deviation (late sign), jugular venous distension,
diagnosis
hypotension, anxiety, diaphoresis, cyanosis, high peak
inspiratory pressures (in patients receiving mechanical
ventilation)
Thrombosis Abnormal clotting (cancer/cancer treatment, Bedside ultrasonography can aid in
(pulmonary inherited disorder, cardiovascular disease, stroke, diagnosis
embolism) hormone therapy, history of deep venous thrombosis,
anticoagulant therapy); stasis (bed rest, travel); vessel
injury (post-surgical, central venous catheter, trauma)

Peri-arrest signs and symptoms: dyspnea,

tachycardia, pleuritic chest pain, hemoptysis, anxiety,
diaphoresis, syncope
Thrombosis Coronary artery disease 12-lead ECG: ST-segment changes,
(myocardial T-wave inversion
Peri-arrest signs and symptoms: chest pain/
infarction)
discomfort; dizziness, light-headedness or syncope;
nausea or vomiting; dyspnea; diaphoresis; cyanosis

Chapter 8 | Cardiac Arrest | 115

Hydrogen Ion Excess (Acidosis) cocaine, methamphetamines, opioids (heroin, fentanyl),
β-blockers, calcium channel blockers, digoxin and
Acidosis can impair cardiac function, in some cases tricyclic antidepressants. Reversal agents are specific to
to the point of cardiac arrest. Acidosis can occur in a the toxin (e.g., glucagon for β-blocker overdose, sodium
multitude of conditions, including shock, diabetes and bicarbonate for tricyclic antidepressant overdose,
acute or chronic renal failure. Arterial blood gases are naloxone for opioid overdose).
used to confirm the diagnosis of acidosis. In patients
with metabolic acidosis, the administration of an Tamponade
initial dose of sodium bicarbonate (1 mEq/kg) may be
indicated. If administering sodium bicarbonate, ensure Cardiac tamponade occurs when fluid accumulates
adequate ventilation for removal of carbon dioxide or in the pericardial sac, compressing the heart and
sodium bicarbonate may worsen intracellular and tissue preventing it from pumping effectively. Causes of
acidosis. cardiac tamponade include trauma, cancer, renal
failure, infections and idiopathic pericarditis. Cardiac
Hyperkalemia or Hypokalemia tamponade may also be seen postoperatively.

Pre-arrest physical examination findings may include the

Potassium imbalances can precipitate cardiac arrest. three cardinal signs of cardiac tamponade (Beck’s triad):
Suspect hyperkalemia in patients with acute or chronic hypotension (weak pulse or narrow pulse pressure),
renal failure and in those who had wide QRS complexes muffled heart sounds and jugular venous distension. In a
and tall, peaked T waves on ECG prior to the arrest. patient with PEA, narrow QRS complexes and electrical
Several measures may be taken to reduce potassium alternans (i.e., beat-to-beat variation in the amplitude of
levels, including administering sodium bicarbonate, the QRS complexes) may be seen.
glucose and insulin, or nebulized albuterol. Sodium Treatment is pericardiocentesis (needle aspiration of
bicarbonate is the preferred method of addressing fluid from the pericardial sac).
hyperkalemia in patients in cardiac arrest because it
causes a rapid shift in serum potassium level. Other
therapies take much longer to work.
Tension Pneumothorax
Suspect hypokalemia in patients with dehydration Tension pneumothorax occurs when air accumulates in
or overuse of diuretics. In hypokalemia, flat T waves, the pleural space, causing the lung on the affected side
prominent U waves and possibly prolonged QT to collapse and the mediastinum to shift, compressing
intervals may be seen on ECG before arrest. Treatment the heart and vena cava. Compression of the vena cava
is intravenous administration of a dilute solution of leads to impaired venous return and decreased cardiac
potassium chloride. output. Penetrating chest trauma is a common cause
of tension pneumothorax, but the condition can also
Hypothermia develop in older patients with underlying lung disease
and in patients who smoke.
For patients with severe hypothermia (body temperature Pre-arrest physical examination findings may include
less than 86° F [30° C]) and cardiac arrest, core hypotension, tachycardia, absent breath sounds on the
rewarming (with cardiopulmonary bypass, extracorporeal affected side, jugular venous distension, hyperresonance
blood warming with partial bypass or thoracic lavage on percussion and tracheal deviation away from the
with warmed fluids) is indicated. Warmed fluids and affected side (a late sign). Difficulty ventilating the
warmed humidified oxygen may be administered as patient may also be a sign of tension pneumothorax.
adjunctive therapies. In a patient with PEA, narrow QRS complexes should
raise suspicion for tension pneumothorax as a possible
Toxins underlying cause.

Overdoses (of both illicit and therapeutic drugs) Initial treatment is with needle chest decompression or
and poisoning can induce cardiac arrest. Drugs that thoracostomy.
are frequently implicated in cardiac arrest include

116 | American Red Cross | Advanced Life Support

Thrombosis (Pulmonary Embolism) Care
In massive pulmonary embolism, obstruction of the When a patient is in cardiac arrest, treatment focuses
pulmonary artery and the release of vasoconstrictive on providing high-quality CPR (see Chapter 2),
mediators from the thrombus lead to cardiogenic shock, providing shocks (if the rhythm is shockable) or early
which can quickly lead to cardiac arrest. Conditions epinephrine (if the rhythm is nonshockable) and, if
in the patient history associated with prolonged possible, determining and addressing the underlying
immobilization or venous stasis, hypercoagulability or cause. For nonshockable rhythms, epinephrine should
damage to the veins should increase suspicion for be administered as early as possible. For shockable
pulmonary embolism as a potential cause of cardiac rhythms, medication administration should be
arrest. Witnessed cardiac arrest and respiratory distress delayed until after at least 2 shocks have been given.
before arrest also may point to pulmonary embolism as Placement of an advanced airway and establishment
the cause. PEA is the initial rhythm in one-third to one- of capnography should be delayed until after at least
half of patients with cardiac arrest caused by pulmonary 2 shocks have been administered (in the case of a
embolism. Fibrinolytic therapy may be initiated for shockable rhythm) or CPR has been provided for at least
patients with known or suspected pulmonary embolism. 2 minutes (in the case of a nonshockable rhythm).

Thrombosis (Myocardial Infarction) Practice Note

Myocardial infarction can lead to cardiac arrest. If a pre- When a patient is receiving CPR, use capnography
arrest 15-lead ECG shows an inferior wall myocardial to monitor the effectiveness of compressions and for
infarction with right ventricular involvement (evidenced ROSC.
by ST-segment elevation in lead V4R), then impaired
preload is likely the cause of cardiac arrest and fluid
bolus therapy should be provided during resuscitation.
If a pre-arrest 12-lead ECG shows anterior wall Practice Note
myocardial infarction, then impaired contractility is the
If the airway and adequate ventilations can be
likely cause of cardiac arrest. When myocardial infarction
maintained without placing an advanced airway,
is the suspected cause of cardiac arrest, a 12-lead ECG
consider delaying placement until after ROSC is
should be obtained after ROSC is achieved to guide
achieved. After placing an advanced airway, verify
therapy and inotropic support may be needed to address
correct placement using clinical parameters and
cardiogenic shock.
capnography, and secure the device.

Approach to the Patient

The Adult Cardiac Arrest Code Card summarizes the Practice Note
approach to a patient in cardiac arrest. When an advanced airway has been placed in a
patient who is in cardiac arrest, compressions should
Assess and Recognize be delivered continuously (100 to 120 per minute)
with no pauses for ventilations.
After determining that the patient is not responsive,
not breathing and has no pulse, call for additional
resources, the rapid response or resuscitation team and Shockable Rhythms
the resuscitation equipment or cart and initiate CPR
Ventricular fibrillation and pulseless ventricular
immediately. Without interrupting high-quality CPR,
tachycardia require defibrillation as soon as possible.
attach the cardiac monitor/defibrillator and identify the
Because shocks may not be successful or, in the case of
arrest rhythm.
successful defibrillation, the resultant rhythm may not be
adequate to sustain perfusion or a pulse, resume CPR
immediately after each shock. After every 2 minutes of

Chapter 8 | Cardiac Arrest | 117

CPR, reassess the rhythm (while minimizing interruptions and measurable blood pressure, a sudden and sustained
to chest compressions; Figure 8-5) to determine next increase in ETCO2 or an arterial pulse waveform on an
actions: arterial line when no compressions are being delivered.
■ If the rhythm is shockable, resume CPR immediately Additional signs (such as patient movement, normal
and administer 1 shock as soon as the defibrillator is breathing or coughing) may be present.
charged.
■ If the rhythm is nonshockable and organized, attempt
Defibrillation
to palpate a pulse. If a definitive pulse is palpated, the The energy dose depends on whether the defibrillator
patient has achieved ROSC and post–cardiac arrest is biphasic or monophasic. Providers should familiarize
care should be initiated. If a definitive pulse cannot themselves with the equipment used in their facility.
be palpated, resume CPR immediately and follow the
code card pathway for a nonshockable rhythm. ■ If using a biphasic defibrillator, follow the
manufacturer’s recommendations for the initial dose
(usually between 120 and 200 joules). Subsequent
Practice Note doses should be the same as or higher than the initial
dose. If the manufacturer’s recommendations for the
Pause compressions for rhythm analysis, even when initial dose are not known, use the highest energy
using a device with artifact-filtering technology. dose available for the first and all subsequent shocks.
■ If using a monophasic defibrillator, set the energy
dose at 360 joules. Use this energy dose for each
subsequent shock.
Practice Note If defibrillation is initially successful in terminating
the cardiac arrest rhythm but ventricular fibrillation or
Check the pulse only if an organized rhythm is
pulseless ventricular tachycardia resumes, use the
present.
energy dose that successfully terminated the rhythm for
subsequent shocks.

Always precede the delivery of a shock by announcing

Practice Note the intention to shock in a clear, succinct manner. Before
delivering a shock, perform a visual scan to ensure that
During rhythm and pulse checks, pause
no one is touching the patient or the bed and that oxygen
compressions for no more than 10 seconds.
delivery devices have been removed and set aside, away
from the patient.

Repeat cycles of 2 minutes of CPR, rhythm check, When delivering the shock, face the team, rather than
shock and medication as appropriate until the rhythm the defibrillator (Figure 8-6).
check reveals a nonshockable rhythm, ROSC is
When administering shocks, minimize interruptions to
achieved or the resuscitation effort is terminated. Clinical
CPR.
indications of ROSC include a palpable central pulse
■ Continue providing compressions while placing the
defibrillator pads on the patient’s chest.
■ If the rhythm check reveals a shockable rhythm,
resume compressions as soon as the charging
sequence begins and continue until immediately
before the shock button is pushed and the shock is
delivered.
■ Immediately after the shock is delivered, resume
CPR for 2 minutes before pausing compressions to
conduct a rhythm check. In some clinical situations,
it may be appropriate to conduct a rhythm check
after the shock is delivered and prior to immediately
resuming compressions.

Figure 8-5 | Minimize pauses in compressions to less than

10 seconds during rhythm and pulse checks.

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 Nonshockable Rhythms
Defibrillation is not indicated when the rhythm is PEA
or asystole. Management of these rhythms involves
providing continuous high-quality CPR, administering
epinephrine (1 mg IV/IO repeated every 3 to 5 minutes)
as early as possible and performing rhythm checks
after every 2 minutes of CPR. In addition, it is extremely
important to look for and address potential underlying
causes of the cardiac arrest. PEA and asystole often
have an underlying cause, and unless that cause is
addressed, the resuscitative effort will not be successful.

Repeat cycles of 2 minutes of CPR, rhythm check

Figure 8-6 | Ensure that all providers are clear of the patient and medication as appropriate until the rhythm check
and the bed before delivering a shock. When delivering the
reveals a shockable rhythm, ROSC is achieved or the
shock, face the team, rather than the defibrillator.
resuscitation effort is terminated.
Medications
Various medications may be used in the treatment of Terminating the
ventricular fibrillation or pulseless ventricular tachycardia.
Remember that in cardiac arrest, all medications
Resuscitation Effort
administered through the IV or IO route should be If it seems unlikely that ROSC will be achieved, the team
followed by a 10- to 20-mL normal saline flush. leader may decide to terminate the resuscitation effort.
Epinephrine Many factors are considered when deciding to terminate
the resuscitation effort, including:
After 2 shocks have been delivered, epinephrine (1
mg IV/IO every 3 to 5 minutes) may be administered. ■ How much time elapsed before CPR was initiated
and the first shock was provided.
The vasoconstrictive and positive ionotropic effects
■ The patient’s health status before the cardiac arrest
of epinephrine help to increase cerebral and coronary
and the presence of comorbidities.
perfusion. Evidence suggests that epinephrine is most
■ The initial cardiac arrest rhythm.
effective when administered early.
■ The duration of the resuscitation effort.
Amiodarone or Lidocaine ■ Physiologic data, such as an ETCO2 level less than
10 mmHg after 20 minutes of high-quality CPR.
After 3 shocks have been delivered, consider
administering an antiarrhythmic agent. In general, the longer a patient is in cardiac arrest,
■ Amiodarone: The initial dose of amiodarone is 300 the less likely the patient is to survive (or to survive
mg administered as an IV/IO bolus. If the arrest with neurological function intact). However, in some
rhythm persists, consider giving a second dose of situations it may be appropriate to consider prolonging
150 mg as an IV/IO bolus 3 to 5 minutes later. the resuscitation effort, using specialized interventions or
■ Lidocaine: Alternatively, lidocaine may be used. The both. For example, it may be appropriate to prolong the
initial dose is 1 to 1.5 mg/kg IV/IO, followed by 0.5 resuscitation effort when more time is needed to address
to 0.75 mg/kg IV/IO every 5 to 10 minutes, up to a the underlying cause of the cardiac arrest (for example,
maximum dose of 3 mg/kg. drug overdose, hypothermia, pulmonary embolism).
Specialized interventions, such as extracorporeal
Practice Note cardiopulmonary resuscitation (ECPR) may also
be considered. In ECPR, large-bore cannulas are
Choose one antiarrhythmic agent (amiodarone inserted into a major artery (e.g., the femoral artery)
or lidocaine) and use it for the duration of the and the corresponding vein. Deoxygenated blood is
resuscitation effort. Do not alternate between removed from the body, passed through a membrane
the two. that removes the carbon dioxide and adds oxygen,
warmed, filtered, and then pumped back into the body.
For patients who are good candidates for the procedure,

Chapter 8 | Cardiac Arrest | 119

survival and neurological outcomes may be improved When the gestational age is known to be equal to or
with the use of ECPR (compared with outcomes greater than 20 weeks or the fundus is at or above the
associated with standard CPR). ECPR may also be umbilicus, resuscitative cesarean delivery (RCD) should
considered for organ procurement in a post–cardiac be performed within 5 minutes from the time of arrest.
arrest patient with circulatory determination of death. RCD may be performed earlier than 5 minutes from the
time of arrest and as soon as possible when the rhythm
is nonshockable or ROSC has not been achieved or is
Cardiac Arrest in Pregnancy intermittent after 2 cycles of CPR. In a pregnant patient
with out-of-hospital cardiac arrest, RCD should be
The Cardiac Arrest in Pregnancy Code Card performed immediately upon the patient’s arrival to the
summarizes the approach to a pregnant patient in emergency department if the patient has not achieved
cardiac arrest. ROSC.
Management of cardiac arrest during pregnancy presents The provision of high-quality CPR is essential to a
unique challenges and considerations for resuscitation. successful resuscitative effort. For a pregnant patient in
Because the likelihood of a positive outcome for the cardiac arrest, at least three (and preferably four) team
fetus is increased when there is a positive outcome for members are needed to perform high-quality CPR:
the pregnant patient, the resuscitation team should stay one to provide compressions, one (preferably two) to
focused on resuscitation of the pregnant patient. Fetal manage the airway and breathing, and one to provide
monitors, if present, should be removed immediately after continuous left uterine displacement (LUD; Box 8-2)
pulselessness in cardiac arrest. when the fundus is at or above the umbilicus. As in non-
Gestational age is an important consideration when pregnant patients, ECG rhythm interpretation guides the
determining the approach to a pregnant patient in management of cardiac arrest in the pregnant patient.
cardiac arrest. If the gestational age is not known and Pad placement, timing and doses for defibrillation (for
point-of-care ultrasound is available and able to be shockable rhythms) and medication administration (for
performed without impeding or delaying the resuscitation shockable and nonshockable rhythms) are the same for
effort, it can be used to quickly estimate gestational age pregnant patients as for non-pregnant patients. Because
and to guide decision-making. physiologic changes of pregnancy alter hemodynamics
in the pregnant patient, IV access should be obtained
Box 8-2 | Left Uterine Displacement

When the fundus is at or above the umbilicus, left uterine displacement (LUD) must be provided continuously
throughout the resuscitation effort and until the infant is delivered, even if return of spontaneous circulation
(ROSC) is achieved. LUD relieves pressure placed on the inferior vena cava by the gravid uterus, increasing
venous return to the heart to maximize cardiac output. In most cases, two hands are needed to achieve the
necessary displacement.

To provide LUD from the patient’s left side: To provide LUD from the patient’s right side:

■ Position yourself on the patient’s left side. ■ Position yourself on the patient’s right side.
■ Reach across the patient, place both hands on the ■ Place both hands on the right side of the uterus,
right side of the uterus, and pull the uterus to the and push the uterus to the left and up.
left and up.

120 | American Red Cross | Advanced Life Support

above the level of the diaphragm. If IV access cannot ECPR may be considered when there is no ROSC after
be established, IO access should be obtained in the RCD, or for refractory cardiac arrest when the uterus
proximal humerus. It is important to consider and has not yet reached the umbilicus and the patient is in a
address underlying causes for the cardiac arrest in a facility that is capable of providing ECPR and caring for
pregnant patient, just as it is for a non-pregnant patient. critically ill patients. As in non-pregnant patients, ECPR
The mnemonic BAACC TO LIFE™ can be used to may also be considered to facilitate organ procurement
remember causes of cardiac arrest in pregnancy (see following circulatory determination of death.
the Cardiac Arrest in Pregnancy Code Card).

Chapter 8 | Cardiac Arrest | 121

 ADULT CARDIAC ARREST
ALS - 2020 VERSION
Shock Defibrillation Energy Doses
• Start CPR
Biphasic: Per manufacturer’s
Epinephrine
• Attach monitor/defibrillator recommendations (e.g., 120 to 200 J) or
if unknown, max available; subsequent
doses equal to or greater than first dose
Monophasic: 360 J for all doses

Shockable Medications
YES NO
rhythm?
Epinephrine
• 1 mg IV/IO bolus every 3 to 5 min
VF/pVT Asystole/PEA
Amiodarone
• First dose: 300 mg IV/IO bolus
Epinephrine ASAP
• Second dose: 150 mg after 3 to 5 min
C
• 2 min CPR • 2 min CPR Lidocaine
• IV/IO access • IV/IO access • First dose: 1 to 1.5 mg/kg IV/IO
• Subsequent doses: 0.5 to 0.75 mg/
• Administer epinephrine every kg IV/IO every 5 to 10 min, up to a
3 to 5 min max dose of 3 mg/kg
• Consider advanced airway,
High-Quality CPR
Shockable capnography
NO
rhythm? • Compress at a rate of 100 to 120
compressions per min and a depth of
YES at least 2 inches (5 cm); allow for full
chest recoil
Shockable • Minimize interruptions to chest
YES
A rhythm? compressions to less than 10 sec
• 2 min CPR • Avoid excessive ventilations. Each
• Administer epinephrine NO ventilation should last about 1 sec
and make the chest begin to rise
every 3 to 5 min
• Without advanced airway: 30
• Consider advanced compressions: 2 ventilations
airway, capnography YES ROSC? With advanced airway: continuous
compressions; deliver 1 ventilation
every 6 sec without pausing
NO compressions
Shockable
NO D • Rotate compressor every 2 min
rhythm?
• 2 min CPR • Monitor CPR quality with ETCO2 or
YES • Treat reversible causes arterial blood pressure (if available)
(Hs and Ts)
What Is ROSC?
• Pulse and blood pressure
B
• 2 min CPR • Sudden and sustained increase in
Shockable YES ETCO2
• Administer amiodarone OR rhythm?
lidocaine • Arterial pulse waveform on an a-line
when no compressions are being
• Treat reversible causes NO delivered
(Hs and Ts)
• Additional signs, including patient
movement, normal breathing or
YES ROSC? coughing, may be present

ROSC? Hs and Ts
NO • Hypovolemia
NO YES • Hypoxemia
• Hydrogen ion excess (acidosis)
Follow Adult Post–Cardiac • Hyperkalemia/hypokalemia
Go to C or D Go to C or D Go to A or B • Hypothermia
Arrest Care code card
• Hyperglycemia/hypoglycemia
• Tamponade (cardiac)
• Tension pneumothorax
• Thrombosis (pulmonary embolism)
• Thrombosis (myocardial infarction)
• Toxins

Copyright © 2021 The American National Red Cross

122 | American Red Cross | Advanced Life Support

CARDIAC ARREST IN PREGNANCY Supported by science reviews and guidelines
of Obstetric Life Support™ (OBLS™)

ALS - 2020 VERSION

Shock
• Start Obstetric Life SupportTM (OBLSTM)
Epinephrine • High-quality CPR
• Activate maternal cardiac arrest and neonatal teams
• Remove fetal monitors (if present)

NO
Is fundus at or above umbilicus or
Below umbilicus Not palpable/uncertain fetal age known to be ≥ 20 weeks?
Continuous
high-quality CPR
and LUD*
YES
NO Able to perform
POC-US?
YES
Follow Adult Shockable NO
YES
Cardiac Arrest YES rhythm?
code card
Is FL ≥ 30 mm or BPD VF/pVT Asystole/PEA
NO
≥ 45 mm?
Epinephrine ASAP
B
• 2 min CPR • 2 min CPR
• IV access above diaphragm • IV access above diaphragm (IO proximal
(IO proximal humerus if necessary) humerus if necessary)
Goals of Care
• Administer epinephrine every 3 to 5 min
• Focus on maternal • Consider advanced airway, capnography
resuscitation A
• Early transport as opposed to • 2 min CPR
care on the scene
of arrest (for OHCA) • Administer epinephrine every 3 to 5 min

• High-quality CPR • Consider advanced airway, capnography • 2 min CPR

• Early involvement of • Treat causes (BAACC TO LIFE™)
obstetrical and neonatal teams

Defibrillation Energy Doses

• Perform RCD if trained provider (goal is no later than 4 min CPR/2 cycles)†
Biphasic: Per manufacturer’s
recommendations (e.g., 120 to 200 – If no trained provider, continue care and perform as soon as available
J) or if unknown, max available; • Care for infant using neonatal resuscitation protocols
subsequent doses equal to or
greater than first dose
Monophasic: 360 J for all doses
Follow Adult
Medications • 2 min CPR
ROSC? YES Post–Cardiac Arrest
Epinephrine • Administer Care code card
• 1 mg IV/IO bolus every 3 amiodarone OR
to 5 min lidocaine NO

Amiodarone • Treat causes (BAACC

• First dose: 300 mg IV/IO TO LIFE™) Shockable
YES
bolus rhythm?
• Second dose: 150 mg after 3
to 5 min NO
Consider ECLS
Lidocaine
• First dose: 1 to 1.5 mg/kg Consider ECLS
IV/IO
• Subsequent doses: 0.5 to
0.75 mg/kg IV/IO every 5 to
10 min, up to a max dose of Go to A Go to B
3 mg/kg
*Provide continuous LUD until the infant is delivered, even if ROSC is achieved.
†
Although RCD should be performed at 4 min CPR/2 cycles, preparation needs to start as early in resuscitation as possible to allow this goal to be met.
Copyright © 2021 The American National Red Cross

Chapter 8 | Cardiac Arrest | 123

 CARDIAC ARREST IN PREGNANCY
ALS - 2020 VERSION

Prehospital Assessment and Care

• Prioritize transport over care at the scene (follow local protocols for destination decision)
• Provide high-quality CPR, including airway management and continuous LUD during transport. Provide continuous LUD until the
infant is delivered, even if ROSC is achieved
• Alert receiving hospital and follow protocols for maternal cardiac arrest arrival

Causes of Cardiac Arrest in Pregnancy (BAACC TO LIFE™)

B: bleeding T: trauma L: lung injury/acute respiratory distress syndrome

A: anesthesia O: overdose I: ions (glucose, potassium)
(opioids, magnesium sulfate, other)
A: amniotic fluid embolism F: fever (sepsis)
C: cardiovascular/cardiomyopathy E: eclampsia/emergency hypertension
C: clot/cerebrovascular

Indications for Resuscitative Cesarean Delivery (RCD)

• No ROSC after 2 cycles of CPR in a pregnant patient with a fundus at or above umbilicus or fetal age known to be ≥ 20 weeks
• Intermittent ROSC after 2 cycles of CPR
• Nonshockable rhythm
• Immediately upon arrival to an emergency department without ROSC (for OHCA)

High-Quality CPR

• Compress at a rate of 100 to 120 compressions per min and a depth of at least 2 inches (5 cm); allow for full chest recoil
• Minimize interruptions to chest compressions to less than 10 sec
• Avoid excessive ventilations. Each ventilation should last about 1 sec and make the chest begin to rise
• Without advanced airway: 30 compressions: 2 ventilations
With advanced airway: continuous compressions; deliver 1 ventilation every 6 sec without pausing compressions
• Rotate compressor every 2 min
• Monitor CPR quality with ETCO2 or arterial blood pressure (if available)

Left Uterine Displacement (LUD)

• When the fundus is at or above the umbilicus, provide continuous LUD until the infant is Fig 1.
delivered, even if return of spontaneous circulation (ROSC) is achieved
• LUD relieves pressure placed on the inferior vena cava by the gravid uterus, increasing
venous return to the heart to maximize cardiac output
• In most cases, two hands are needed to provide the necessary displacement
• From the patient’s left side, reach across the patient, place both hands on the right side
of the uterus, and pull the uterus to the left and up (Fig. 1)
• From the patient’s right side, place both hands on the right side of the uterus and push Fig 2.
the uterus to the left and up (Fig. 2)

Copyright © 2021 The American National Red Cross

124 | American Red Cross | Advanced Life Support

 CHAPTER
9

Post–Cardiac Arrest Care

Introduction
Expert post–cardiac arrest care delivered by a multidisciplinary team can reduce
both short- and long-term morbidity and mortality following the return of spontaneous
circulation (ROSC). Post–cardiac arrest care includes interventions aimed at optimizing
oxygenation, ventilation and perfusion; minimizing the systemic consequences of
cardiac arrest; preventing future cardiac arrest; and assessing the patient’s prognosis
for recovery.
Pathophysiologic Consequences
of Cardiac Arrest
Among patients who achieve ROSC, the short-term
mortality rate (i.e., within the first 24 hours of arrest) is
high. This is largely a result of the global consequences
of hypoxemia and the ischemia/reperfusion response,
in addition to the precipitating cause of the cardiac
arrest itself. Blood flow must be restored to tissues that
have been deprived of oxygen in order to prevent tissue
death; however, reperfusion of previously ischemic
tissues can induce an inflammatory response that
causes cellular injury in addition to that caused by the
ischemia itself. This is known as the ischemia/reperfusion
response.
Figure 9-1 | Expert care during the immediate post–cardiac
Sometimes referred to as post–cardiac arrest arrest period can improve outcomes for the post–cardiac
syndrome, the pathophysiologic consequences of arrest patient.
cardiac arrest comprise four key areas:
■ Brain injury. Brain injury, caused by ischemia and
Assess and Recognize
cerebral edema, is a significant cause of morbidity
and mortality in patients who achieve ROSC. Clinical indications of ROSC include a palpable
■ Myocardial dysfunction. Myocardial stunning central pulse, a measurable blood pressure, a sudden
secondary to the ischemia/reperfusion response and sustained increase in ETCO2, an arterial pulse
causes systolic and diastolic dysfunction, leading to waveform on an arterial line when no compressions are
hemodynamic instability in the immediate post-arrest being delivered and additional signs, such as patient
period.
movement, breathing or coughing. Upon recognizing
■ Systemic dysfunction. The ischemia/reperfusion
ROSC, the team assesses and supports the patient’s
response can trigger a systemic inflammatory
response, which can lead to multiple organ airway, breathing and circulation; assesses the patient’s
dysfunction. In addition, organs that are sensitive to level of consciousness and institutes neuroprotective
changes in perfusion pressure, such as the kidneys, interventions.
are at increased risk for reperfusion injury.
■ Persistent precipitating conditions. The Care
underlying cause of the cardiac arrest may continue
to have pathophysiologic consequences during the
post-arrest period. Interventions during the immediate post–cardiac
arrest period focus on ensuring optimal ventilation and
The duration of the cardiac arrest (i.e., from collapse oxygenation, managing hemodynamics, providing cardiac
through ROSC) directly affects the severity of the post– interventions and support as necessary, promoting
cardiac arrest syndrome. neurologic recovery and addressing underlying causes
After ROSC, survival outcomes are improved when a (Figure 9-2).
multidisciplinary team of providers works to stabilize the
Initial Stabilization
patient, minimize complications, and diagnose and treat
the underlying cause (Figure 9-1). Optimizing Ventilation and Oxygenation
If not already done, place an endotracheal tube. If an
endotracheal tube is already in place, confirm proper
Approach to the Patient position and patency. Start ventilations at a rate of 10
breaths per minute and adjust as necessary to keep
The Adult Post–Cardiac Arrest Care Code Card
carbon dioxide levels in physiologic range (PaCO2
summarizes the approach to caring for a patient during
between 35 and 45 mmHg or monitored using ETCO2),
the immediate post–cardiac arrest period.
unless another target is clinically indicated. Provide
100% oxygen (FiO21.0) until the oxygen saturation can

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 Optimizing ventilation
and oxygenation

Addressing underlying
causes

Managing
hemodynamics

Promoting neurologic
recovery
Providing cardiac
interventions
and support

Figure 9-2 | During the immediate post–cardiac arrest period, interventions are focused on ensuring optimal ventilation and
oxygenation, managing hemodynamics, addressing underlying causes, providing cardiac interventions and support and promoting
neurologic recovery.

be measured, an arterial blood gas is obtained or both, Ongoing Management

and then provide the minimal level of oxygen needed
Obtain a 12–lead ECG expediently. As time and
to maintain an oxygen saturation (SaO2) of 94% to
resources permit, obtain a medical history and complete
99% and (if obtained) a PaO2 in the physiologic range.
focused physical and neurologic examinations.
Continuously monitor the patient using capnography
Maintain euglycemia and identify treatable underlying
and pulse oximetry and, as available, PaCO2 and PaO2
causes (including Hs and Ts). Diagnostic studies aid
to ensure ventilation and oxygenation levels are in the
in determining the pathophysiologic consequences
physiologic range.
of cardiac arrest, identifying the underlying cause and
Managing Hemodynamics monitoring the patient’s response to interventions (Table
9-2).
To ensure the best outcome, perfusion must be
adequate and maintained. Blood pressure can be Providing Cardiac Interventions and Support
extremely labile during the post–cardiac arrest period.
Addressing ST-segment elevation myocardial infarction
As such hypotension should be treated aggressively.
(STEMI) and non–ST-segment elevation acute
Current recommendations are to target a minimum
coronary syndromes (NSTE-ACS) and providing
systolic blood pressure of 90 mmHg or a mean arterial
mechanical cardiac support if needed may improve
pressure (MAP) of 65 mmHg. Initially treat hypotension
neurological outcomes. Consider the need for emergent
with a 1- to 2-L intravenous (IV) isotonic crystalloid fluid
cardiac interventions such as reperfusion therapy
bolus. If the patient fails to respond to fluid, consider
starting an IV vasopressor infusion (Table 9-1). The
Table 9-1 | Vasopressor Infusion for the Post–Cardiac Arrest Patient
choice of agent is based on the clinical situation. Once
therapy is initiated, the drug infusion rate can be titrated Vasopressor Dosage
according to hemodynamic parameters and physical Epinephrine 2 to 10 mcg/min IV/IO
examination findings. Norepinephrine 0.1 to 0.5 mcg/kg/min IV/
IO
Dopamine 5 to 20 mcg/kg/min IV/IO

Chapter 9 | Post—Cardiac Arrest Care | 127

Table 9-2 | Diagnostic Tests That May Be Ordered in the Evaluation of the Post–Cardiac Arrest Patient
Diagnostic Test Purpose
Comprehensive Detecting metabolic and electrolyte derangements and assessing acute renal injury
metabolic panel
Serial lactate Monitoring perfusion status (decreasing lactate levels suggest improved perfusion)
Serum glucose Detecting hyperglycemia (associated with poor neurological outcomes) and
hypoglycemia
Arterial blood gases Monitoring for acidosis, hypoxia and hypercapnia; tailoring ventilation and oxygenation

Serum cardiac markers Detecting myocardial infarction

12-lead ECG Detecting myocardial infarction, arrhythmias

Chest radiograph Verifying placement of endotracheal tube; detecting underlying causes of cardiac arrest
Ultrasonography Detecting underlying causes of cardiac arrest
Echocardiography Evaluating myocardial stunning and cardiac functioning; detecting ventricular wall
abnormalities (suggestive of focal ischemia) and structural abnormalities
Coronary angiography Evaluating coronary artery disease; diagnosing coronary thrombosis; performing
percutaneous coronary intervention (PCI)
Brain imaging Assessing brain injury and prognosis

Continuous EEG Identifying seizures and epileptiform activity

monitoring

and mechanical circulatory support and obtain a considered when determining the target temperature;
cardiology consultation. Patients with STEMI require for example, a temperature at the lower end of the range
immediate reperfusion therapy with percutaneous may be preferred for patients with seizures or cerebral
coronary intervention (PCI), fibrinolytic therapy or both. edema. Various methods of inducing hypothermia
Emergency coronary angiography is recommended may be used, including administering an ice-cold IV
for all patients, awake or comatose, who have ECG fluid bolus (30 mL/kg), using endovascular catheters
and laboratory findings suggestive of acute myocardial or employing surface cooling strategies (e.g., cooling
infarction. Both reperfusion therapy and mechanical blankets, ice packs). The patient’s core body temperature
circulatory support can be initiated in patients who are should be continuously monitored throughout therapy
comatose and concurrently with targeted temperature using an esophageal, rectal or bladder core temperature
management (TTM). monitoring device.

Promoting Neurologic Recovery

Targeted temperature management (TTM) should Practice Note
be considered for all patients who remain comatose Providers should not initiate TTM in the prehospital setting.
after ROSC, as indicated by an inability to follow verbal
commands. TTM may reduce global oxygen demand and
improve overall outcomes after cardiac arrest. Other measures for promoting neurologic recovery
in patients who remain comatose following cardiac
In TTM, a target temperature between 32° C (89.6° F)
arrest include obtaining brain imaging and establishing
and 36° C (96.8° F) is established, the patient’s body
continuous EEG monitoring to help identify seizures
temperature is maintained at the targeted temperature
that might not be detected by other clinical parameters.
for at least 24 hours, and then the patient’s body
Seizures or epileptiform activity on EEG occur in
temperature is slowly brought back up at a rate of
approximately 20% to 30% of comatose patients in
0.25° C per hour. Patient-specific factors should be

128 | American Red Cross | Advanced Life Support

the post–cardiac arrest period. If detected, post– A multimodal approach to predicting neurologic outcome
cardiac arrest seizures must be treated; however, is recommended and includes clinical examination,
anticonvulsants should not be used prophylactically imaging, biomarkers and electrophysiology (see the
during the post–cardiac arrest period. Adult Post–Cardiac Arrest Care Code Card). Clinical
examination findings that may be used to predict
outcome include pupillary light reflex, quantitative
Post—Cardiac Arrest pupillometry and corneal reflex (at 72 hours or later
Prognostication after ROSC) and myoclonus or status myoclonus
(within 96 hours of ROSC). Imaging studies used for
Accurate neuroprognostication in patients who remain neuroprognostication in the post–cardiac arrest patient
comatose after cardiac arrest is essential for decision- include brain computed tomography (CT) and magnetic
making related to the continuation or withdrawal of resonance imaging (MRI). The biomarker neuron-specific
life-sustaining treatments. Because results of many of endolase (NSE) may be evaluated within 72 hours
the assessments used for neuroprognostication can of ROSC but should be considered in conjunction
be affected by medications (e.g., sedation, analgesia), with other tests as part of a multimodal approach to
temperature, organ dysfunction or a combination neuroprognostication. Electroencephalography (EEG)
of these factors, neuroprognostication should be and somatosensory evoked potential (SSEP) may also
multimodal and delayed until 72 hours after ROSC and be considered as part of a multimodal approach to
following return to normothermia (although individual predicting neurological outcome. Neither background
assessments that may not be affected by these factors reactivity alone nor seizures on EEG or status
may be completed prior to this). epilepticus should be used to predict poor outcome.

Chapter 9 | Post—Cardiac Arrest Care | 129

 ADULT POST–CARDIAC ARREST CARE
ALS - 2020 VERSION

Return of spontaneous circulation (ROSC)

Optimize Ventilation and Oxygenation

• If not already done, place ETT; if ETT already in place, confirm proper position and patency
• Provide minimal level of supplemental oxygen to maintain SpO2 of 94% to 99%
• Support ventilations to keep carbon dioxide levels in physiologic range (PaCO2 between
35 and 45 mmHg or monitored using ETCO2) unless clinical condition warrants carbon
dioxide level above or below this range; avoid hypercarbia

Manage Hemodynamics (SBP > 90 mmHg, MAP > 65 mmHg)

• Administer as indicated:
- IV/IO fluid bolus
- Inotrope/inodilator/vasopressor infusion (as clinically indicated)

• Obtain 12-lead ECG

• As time and resources permit:
- Medical history and focused physical and neurologic examinations
- Maintain euglycemia
• Identify treatable causes (including Hs and Ts)

YES STEMI or further cardiac NO

support needed?

• Consider reperfusion therapy

• Consider mechanical
Able to follow
circulatory support
verbal commands?
• Cardiology consultation YES NO

Admit to critical care unit • Initiate TTM*

• Brain imaging
• EEG monitoring

Medications Ventilation and Oxygenation Goals Hs and Ts Targeted Temperature Management*

IV/IO fluid bolus Maintain core body temperature 32° C to 36° C

Ventilation • Hypovolemia for at least 24 hours
• 1 to 2 L NS or LR solution • Hypoxemia
• Start at 10 breaths/min; adjust as
needed • Hydrogen ion excess (acidosis) Methods include:
Dopamine • PaCO2: 35 to 45 mmHg • Hyperkalemia/hypokalemia • Ice-cold IV fluid bolus (30 mL/kg)
• 5 to 20 mcg/kg/min IV/IO • Hypothermia • Endovascular catheters
• Hyperglycemia/hypoglycemia • Surface-cooling strategies (e.g., cooling
Epinephrine • Tamponade (cardiac) blankets, ice packs)
• 2 to 10 mcg/min IV/IO Oxygenation • Tension pneumothorax
• Provide minimal level needed to • Thrombosis (pulmonary embolism) Continuously monitor core temperature via
Norepinephrine maintain SpO2 of 94% to 99% • Thrombosis (myocardial infarction) esophageal, rectal or bladder catheter
• 0.1 to 0.5 mcg/kg/min IV/IO • Toxins
Monitor for negative consequences of
hypothermic temperature
*Providers should not initiate TTM in the prehospital setting. The evidence for TTM is constantly evolving.
Defer to institutional protocols and clinician judgment based on the latest evidence.

Copyright © 2021 The American National Red Cross

130 | American Red Cross | Advanced Life Support

ADULT POST–CARDIAC ARREST CARE
ALS - 2020 VERSION

Prognostication Following Return of Spontaneous Circulation (ROSC)

TTM (if indicated) 0 to 30 hours post-ROSC

Clinical management Rewarming (if indicated) 30 to 54 hours post-ROSC

Minimize sedation and analgesia as possible; controlled normothermia 54 to 72+ hours post-ROSC

Multimodal prognostication in the post–cardiac arrest period should not be determined before 72 hours after ROSC and following return to normothermia.

Modality Predictor Timeframe Post-ROSC

Brain computed tomography (CT) 0 to 24 hours

• Gray-to-white matter ratio (GWR)
Imaging
Brain diffusion-weighted MRI (DWMRI) 24 to 72+ hours
• Apparent diffusion coefficient (ADC)

Somatosensory evoked potentials (SSEPs) 24 to 72+ hours

• Bilaterally absent N20 SSEPs

Electrophysiology Electroencephalography (EEG) 72+ hours

• Seizure activity
• Burst suppression

Myoclonus or status myoclonus* 24 to 72 hours

Pupillary light reflexes 72+ hours

Clinical examination
Quantitative pupillometry 72+ hours

Corneal reflexes 72+ hours

Serum biomarkers Serum neuron-specific enolase (NSE) 24 to 72 hours

* Obtain EEG with myoclonic jerks.

Copyright © 2021 The American National Red Cross

Chapter 9 | Post—Cardiac Arrest Care | 131

 CHAPTER
10

Acute Coronary Syndromes

Introduction
Acute coronary syndromes (ACS) is a general term for a group of life-threatening
conditions that occur because of a sudden reduction in blood flow to the heart. Each
year in the United States, an estimated 660,000 people require hospitalization for
myocardial infarction related to coronary artery disease. Quickly identifying and triaging
patients with ACS is critical because ACS carries a significantly increased risk of death
and complications associated with myocardial ischemia.
Classification of Acute ■ Determine and manage risk for major adverse cardiac
events, including death, new or recurrent myocardial
Coronary Syndromes infarction or severe recurrent ischemia requiring
urgent revascularization.
Based on 12-lead ECG findings, the ischemic
conditions that comprise ACS can be subdivided into
two categories (Figure 10-1): Pathophysiology of Acute
■ STEMI, or ST-segment elevation myocardial Coronary Syndromes
infarction, which is characterized by new ST-segment
elevation that suggests myocardial infarction. The underlying cause of ACS is a sudden reduction
■ NSTE-ACS, or non–ST-segment elevation ACS, in the blood supply to the myocardium. In most cases,
which can be further classified as high-risk and the precipitating cause of the reduced blood supply is
low- or intermediate-risk. Patients with ECG findings rupture of a vulnerable atherosclerotic plaque. Disruption
highly suspicious for ischemia, a high risk score on of the lipid-laden plaque results in transient platelet
a risk-stratification tool or both are considered to
aggregation and the release of vasoactive substances
have high-risk NSTE-ACS. Patients with a normal
or nondiagnostic ECG or a low risk score on a risk- from the diseased endothelium, causing vasospasm,
stratification tool are considered to have low- or plaque erosion and eventually the development of an
intermediate-risk NSTE-ACS. occlusive intracoronary thrombus. The thrombus and
associated inflammatory changes lead to partial or
complete occlusion of the coronary artery, producing
Goals for Management a spectrum of ACS (Figure 10-2). In about 70% of
patients who present with ACS each year, arterial
When ACS is determined to be the cause of a patient’s
occlusion results in myocardial ischemia without
chest pain or discomfort, the goals for management are
persistent ST-segment elevation (NSTE-ACS). In the
to:
other approximately 30% of patients who present with
■ Identify those patients with STEMI and determine ACS, arterial occlusion results in STEMI.
candidacy for early reperfusion therapy with either
percutaneous coronary intervention (PCI) or
fibrinolytic therapy.
■ Relieve ischemic chest pain and discomfort.
■ Manage complications, such as ischemia-induced
arrhythmias that can lead to cardiac arrest and death.

Plaque disruption
and platelet aggregation
ACUTE CORONARY SYNDROMES

Vulnerable
plaque

STEMI NSTE-ACS Thrombus

formation

High-risk Low- or
NSTE-ACS intermediate-risk
ACS
ACUTE CORONARY SYNDROMES

Figure 10-1 | Acute coronary syndromes (ACS) are Non–ST-segment elevation acute coronary syndromes (NSTE-ACS)
subdivided into two main categories, ST-segment elevation
myocardial infarction (STEMI) and non–ST-segment
elevation ACS (NSTE-ACS). NSTE-ACS can be further ST-segment elevation myocardial infarction (STEMI)
divided into high-risk and low- or intermediate-risk
NSTE-ACS. Figure 10-2 | Pathogenesis of acute coronary syndromes (ACS)

134 | American Red Cross | Advanced Life Support

STEMI Chain of Survival Rapid In-Hospital Assessment
The STEMI Chain of Survival illustrates how a
and Diagnosis
coordinated effort among members of the community,
After the patient arrives at the receiving facility, providers
prehospital providers and in-hospital providers can
work to obtain a definitive diagnosis and initiate
increase the patient’s likelihood of surviving STEMI
appropriate care.
(Figure 10-3).

Early Recognition and Activation of Rapid Treatment

the Emergency Response System Reperfusion therapy in the form of PCI or fibrinolytic
therapy is recommended for all patients with STEMI who
Early recognition of signs and symptoms along with present within 12 hours of symptom onset.
activation of emergency medical services (EMS) is the
■ PCI. When the receiving facility is equipped to
first link in the STEMI Chain of Survival.
perform PCI, the procedure should be performed
within 90 minutes of the patient’s first medical
Rapid Dispatch, Rapid Transport contact. If transfer to a facility that is capable
of performing PCI is necessary, PCI should be
and Prearrival Notification performed within 120 minutes of the patient’s first
medical contact. As the time from first medical
The second link in the STEMI Chain of Survival entails contact to PCI increases, so does the mortality rate.
rapid dispatch of EMS professionals to the patient’s ■ Fibrinolytic therapy. When reperfusion will be
location, rapid transport of the patient to a facility achieved through fibrinolysis, infusion of fibrinolytic
capable of administering reperfusion therapies and agents should be initiated within 30 minutes of the
notification of the receiving facility in advance of the patient’s arrival.
patient’s arrival. During this stage, prehospital providers
initiate diagnostic and therapeutic measures, such as
obtaining a 12-lead ECG, administering oxygen and
Recognizing Acute Coronary
medications and completing a fibrinolytic checklist. Syndromes
Signs and symptoms of ischemia, especially in a patient
with risk factors for coronary artery disease, should raise
suspicion for ACS. The patient’s clinical presentation
and results from diagnostic tests (including the 12-
lead ECG and serum cardiac marker testing) aid in

Early Recognition Rapid Dispatch, Rapid Rapid In-Hospital Rapid Treatment

and Activation of Transport and Assessment and
the Emergency Prearrival Notification Diagnosis
Response System

Figure 10-3 | STEMI Chain of Survival

Chapter 10 | Acute Coronary Syndromes | 135

diagnosing ACS, assessing the patient’s risk for major Women, patients younger than 40 years or older than
adverse cardiac events and determining a management 75 years, and those with medical conditions such
strategy. as diabetes may present with atypical symptoms of
ischemia or infarction. For example, patients with
Clinical Presentation diabetes may experience ischemia without pain (“silent
ischemia”).
ACS should initially be considered in all patients who
present with chest pain or discomfort or other signs ECG Findings
or symptoms of ischemia or infarction (Figure 10-4).
Patients may report retrosternal pressure, squeezing, A 12-lead ECG is an essential component of the
tightness, aching or heaviness that may radiate to one evaluation of a patient presenting with chest pain (Figure
or both arms or shoulders, the back, the neck, the 10-5). ECG findings can support a diagnosis of ACS.
jaw or the epigastric region. The pain or discomfort is In addition, in patients thought to have ACS, ECG
persistent, lasting longer than 3 to 5 minutes, and may findings can be used to assign patients to one of three
be intermittent. clinical categories, which in turn helps to determine
risk and guide treatment decisions. For the purposes of
The pain or discomfort may or may not be accompanied
recognizing ACS, ECG changes must be noted in two
by other symptoms, including: or more contiguous leads. Normal or nonspecific ECG
■ Dizziness, light-headedness or syncope. findings do not rule out the possibility of ACS. For this
■ Sudden, unexplained dyspnea, which may occur in reason, ECG findings must always be evaluated in the
the absence of chest pain or discomfort. context of the patient’s overall clinical presentation.
■ Nausea or vomiting.
■ STEMI. New ST-segment elevation at the J point in
■ Pale, ashen or slightly cyanotic skin, especially on the leads V2 and V3 of at least 0.2 mV (≥ 2 mm) in men
face and fingers. older than 40 years, 0.25 mV (≥ 2.5 mm) in men 40
■ Diaphoresis. years or younger or 0.15 mV (≥ 1.5 mm) in women
■ Anxiety or a feeling of impending doom. is considered diagnostic of STEMI. Alternatively, new
■ Extreme fatigue. ST-segment elevation of at least 0.1 mV (≥ 1 mm) in
■ Loss of consciousness. two or more contiguous leads other than V2 and V3 is
diagnostic for STEMI, as is new or presumed new left
bundle branch block (LBBB). ST-segment depression
in reciprocal leads is a common feature of STEMI and
in some studies has been associated with a worse
prognosis.

Figure 10-4 | Pain or discomfort is a common symptom Figure 10-5 | ECG findings can support a diagnosis of ACS
associated with ACS. and assist in guiding treatment decisions.

136 | American Red Cross | Advanced Life Support

■ High-risk NSTE-ACS. Patients with high-risk NSTE- Rapid Assessment
ACS show changes suggestive of ischemia, such
as ST-segment depression or T-wave inversion, in
two or more contiguous leads. Transient ST-segment On initial impression, some patients with ACS appear
elevation, defined as ST-segment elevation of at acutely ill (e.g., anxious, pale, diaphoretic, dyspneic,
least 0.05 mV (≥ 0.5 mm) that lasts for less than 20 in pain). However, others may appear to be in minimal
minutes, may also be seen in patients with high-risk distress or show only subtle signs of discomfort, such as
NSTE-ACS. rubbing the upper arm or chest.
■ Low- or intermediate-risk NSTE-ACS. Patients
with low- or intermediate-risk NSTE-ACS show
nondiagnostic ST-segment or T-wave changes on
Primary Assessment
ECG, or no changes at all. ST-segment deviation
less than 0.05 mV (0.5 mm) in either direction or Conduct a primary assessment following the ABCDE
T-wave inversion of 0.2 mV (2 mm) or less may be approach and provide initial interventions as needed.
seen on ECG. These patients require additional Establish cardiac monitoring, pulse oximetry and
risk stratification supported by the results of other vascular access, and be prepared to provide CPR and
diagnostic tests, such as serum cardiac marker defibrillation if the patient’s condition deteriorates. If the
testing and functional testing.
oxygen saturation is less than 90%, provide the minimal
level of supplemental oxygen needed to maintain an
oxygen saturation greater than 90% but less than or
Serum Cardiac Markers equal to 99%. Avoid hyperoxia. Obtain a 12-lead ECG
expediently.
Levels of serum cardiac markers should be assessed in
all cases of suspected ACS. Cardiac troponin T (cTnT) Secondary Assessment
and cardiac troponin I (cTnI) biomarkers are preferred
for diagnosing myocardial injury. For diagnosis, it is The goals of the secondary assessment are to gather
important to assess both the peak troponin level and more historical and physical information to further
changes in troponin level over time, so cardiac troponin differentiate ACS from other causes of acute chest
levels should be measured at initial presentation and pain (Box 10-1) as needed, and to gather data for risk
then 3 to 6 hours later. For high-sensitivity markers, stratification. Risk-stratification tools such as the HEART
some protocols suggest measurement at initial (History, ECG, Age, Risk factors, initial Troponin) score
presentation and then 2 hours later. In patients who (Figure 10-6), Thrombolysis in Myocardial Infarction
present with normal troponin levels initially but who show (TIMI) score and Global Registry of Acute Coronary
ECG changes suggestive of intermediate- or high-risk Events (GRACE) score assign weights to various
NSTE-ACS, an additional cardiac troponin measurement predictive factors to calculate the patient’s risk for
beyond 6 hours may be indicated. In addition to being experiencing a major adverse cardiac event in the next 1
prognostic (for both short- and long-term outcomes), to 6 months.
cardiac troponin levels in combination with risk
stratification are useful to guide treatment decisions. History
Key information to elicit during the history includes:
A full description of the chest pain or discomfort,
Patient Assessment ■
including provoking and alleviating factors, qualities,
where it is located, its onset and duration, its severity
Chest pain or discomfort results in approximately 7 and any associated symptoms.
million emergency department visits each year. Among
these patients, approximately 1.6 million are admitted
with a diagnosis of ACS. To expedite appropriate therapy Box 10-1 | Life-Threatening Causes of Acute Chest Pain
for all patients presenting with chest pain or discomfort,
providers must be able to rapidly discern the underlying ■ Aortic dissection
cause. ■ Pulmonary embolism
■ Pneumothorax
■ Ruptured esophagus
■ Perforating peptic ulcer disease

Chapter 10 | Acute Coronary Syndromes | 137

 HEART SCORE FOR CHEST PAIN

History Highly suspicious 2

Moderately suspicious 1

Slightly or nonsuspicious 0

ECG Significant ST-segment depression 2

Nonspecific repolarization 1

Normal 0

Age 65 years or older 2

45 to 64 years 1

44 years or younger 0

Risk Factors 3 or more risk factors OR a history of 2

■ Diabetes mellitus coronary artery disease
■ Hypercholesterolemia 1 or 2 risk factors 1
■ Hypertension
■ Smoking
0 known risk factors 0
■ Family history of coronary artery disease
■ Obesity
Troponin > 3x normal limit 2

1–3x normal limit 1

≤ normal limit 0

Total:

Figure 10-6 | Risk stratification tools, such as the HEART score, assign weights to various predictive factors to calculate the patient’s
short-term risk for experiencing a major adverse cardiac event. Adapted with permission from Backus BE, Six AJ, Kelder JC, et al. A
prospective validation of the HEART score for chest pain patients at the emergency department. Int J Cardiol. 2013;168(3):2154.

■ Symptoms suggestive of heart failure or other Diagnostic Tests

complications of ischemia.
ACS cannot be diagnosed on the basis of history and
■ The presence of risk factors for cardiovascular
physical examination findings alone. Tests that are
disease.
routinely ordered in the assessment of a patient with
■ Relevant events from the medical history, including a
history of cardiovascular or cerebrovascular disease. possible ACS include a 12-lead ECG, serum cardiac
■ Contraindications to fibrinolysis. markers, a serum electrolyte panel and coagulation
studies. A chest radiograph is typically obtained at
Physical Examination presentation to rule out other causes of acute chest
Physical examination may reveal signs that aid in the pain and to identify pulmonary congestion (a negative
differential diagnosis or that assist in identifying the prognostic factor in patients with ACS).
hemodynamic consequences of ischemia. Findings
may include signs of left ventricular dysfunction (e.g., Approach to the Patient
hypotension, crackles, weak peripheral pulses) or
cardiogenic shock (e.g., cool, clammy skin). Other Prompt evaluation and intervention for all patients with
significant findings may include jugular venous suspected ACS is critical to limit ischemic damage to
distension, a third or fourth heart sound or murmurs. In the myocardium and prevent death. The Adult Acute
some patients with ACS, the physical examination does Coronary Syndromes Code Card summarizes the
not reveal anything of significance. approach to a patient with ACS.

138 | American Red Cross | Advanced Life Support

Assess and Recognize
Practice Note
When ACS is suspected, the team takes actions to
ensure adequate airway, breathing and circulation, Nitroglycerin must be used with caution or not at all in
including establishing cardiac monitoring and pulse certain situations. Conditions that may preclude the
oximetry, administering supplemental oxygen if needed use of nitroglycerin include inferior wall myocardial
and ensuring vascular access. infarction with right ventricular involvement, hypotension
(systolic blood pressure < 90 mmHg), significant
Additionally, the team works to gather information that bradycardia (heart rate < 50 bpm), tachycardia and
will aid in definitive diagnosis, risk stratification and use of phosphodiesterase inhibitors within the previous
treatment decisions. Actions include: 24 to 48 hours. Nitroglycerin is a vasodilator and its
■ Obtaining a 12-lead ECG within 10 minutes of the administration under these conditions may prevent the
patient’s arrival at the facility. patient from maintaining adequate cardiac output and
■ Ordering serum cardiac marker, complete blood blood pressure.
count, electrolyte and coagulation studies within 10
minutes of the patient’s arrival at the facility. ■ Morphine. Consider morphine (1 to 5 mg) for
■ Obtaining a brief medical history and conducting a patients who continue to experience chest pain
focused physical examination. despite antianginal therapy.
■ Reviewing or completing the fibrinolytic checklist.
■ Obtaining a chest radiograph within 30 minutes of
the patient’s arrival at the facility (without delaying Practice Note
cardiac interventions).
Morphine should not be administered to hypotensive
patients or those with right ventricular infarction.
Practice Note Additionally, morphine should be used with caution
in patients with NSTE-ACS because its use in these
For patients with suspected STEMI, do not delay
patients has been associated with increased mortality.
activation of the PCI team or initiation of fibrinolytic
therapy while awaiting the results of serum cardiac
marker or radiographic studies. Care
Initiate general drug therapy for patients with signs and
Assigning the patient to a clinical category (STEMI, high-
symptoms of ischemia or infarction as soon as possible
risk NSTE-ACS or low- or intermediate-risk NSTE-ACS)
after screening for contraindications.
helps to guide management decisions.
■ Aspirin. If not already administered by prehospital
providers, administer antiplatelet therapy in the STEMI
form of aspirin (162 to 325 mg) to patients without
contraindications (such as aspirin allergy or a history Treatment for STEMI depends on how much time has
of gastrointestinal bleeding). The patient should be passed since symptom onset. Patients who present
instructed to chew the aspirin. within 12 hours of symptom onset should receive early
reperfusion therapy (PCI or fibrinolysis) and adjuvant
drug therapy. Those who present more than 12 hours
Practice Note after symptom onset and are found to be at high risk
Except for aspirin, use of nonsteroidal anti-inflammatory for experiencing a major adverse cardiac event in the
agents (NSAIDs) is contraindicated for patients with next 1 to 6 months may benefit from an early invasive
STEMI. strategy (e.g., coronary angiography with or without
revascularization within 24 hours of admission).
■ Nitroglycerin. Administer nitroglycerin (0.4 or 0.8
mg every 5 minutes by sublingual tablet or spray, Reperfusion Therapy
up to three doses) to relieve ischemic chest pain, Reperfusion therapy is the standard of care for all
unless contraindicated. If the pain persists, consider patients with STEMI who are diagnosed within 12 hours
intravenous nitroglycerin.
of symptom onset and who have no contraindications.

PCI is performed in a cardiac catheterization suite

and entails balloon angioplasty, with or without stent

Chapter 10 | Acute Coronary Syndromes | 139

placement. When performed at a PCI-capable facility, early invasive strategy include:
primary PCI (i.e., PCI performed as first-line therapy ■ Refractory ischemic chest discomfort.
for STEMI) is associated with better patient outcomes, ■ Recurrent or persistent ST-segment deviation.
compared with outcomes following fibrinolytic therapy. ■ Ventricular tachycardia.
If primary PCI cannot be performed within 90 minutes ■ Hemodynamic instability.
of the patient’s first medical contact, fibrinolysis
■ Signs or symptoms of heart failure.
should be provided within 30 minutes of the patient’s
arrival. Fibrin-specific agents (such as recombinant Dual antiplatelet therapy (aspirin and a P2Y12 platelet
tissue plasminogen activator [rtPA], reteplase and receptor inhibitor) and anticoagulant therapy may also
tenecteplase) are preferred over non–fibrin-specific be considered. Provide adjuvant therapies and obtain a
agents (such as streptokinase). Following fibrinolysis, cardiology consultation.
angiography and PCI may be performed within 3 to 24
hours, if indicated.
Low- or Intermediate-Risk NSTE-ACS
For patients with low- or intermediate-risk NSTE-
Adjuvant Drug Therapy ACS, consider admission to a chest pain unit or other
In addition to reperfusion therapy, anticoagulant and monitored bed. The HEART score can be a useful
antiplatelet therapies are initiated to inhibit the formation adjunct to clinical judgment when deciding whether to
or recurrence of intracoronary thrombi, and medications admit or discharge a patient with suspected low- or
may be administered to support cardiac function (Box intermediate-risk NSTE-ACS. For those patients who
10-2). are admitted, monitor for the development of ischemia
through the use of serial serum cardiac markers and
High-Risk NSTE-ACS repeat ECG or continuous ST-segment monitoring.
Noninvasive imaging and functional testing may also be
An early invasive strategy should be considered for
indicated. Patients with low- or intermediate-risk NSTE-
patients with NSTE-ACS who have elevated troponin
ACS who are discharged should have outpatient follow-
levels or high risk-stratification scores. Indications for an
up and testing.

Box 10-2 | Adjuvant Drug Therapy

■ P2Y12 platelet receptor inhibitors. Two ■ β-Blockers. Treatment with β-blockers should be
P2Y12 platelet receptor inhibitors—clopidogrel initiated within 24 hours of presentation unless there
and ticagrelor—are approved for use in are contraindications (e.g., acute heart failure, low
combination with asprin for PCI for high-risk cardiac output, risk for cardiogenic shock).
patients, or for patients with aspirin allergy. ■ Intravenous nitroglycerin. In patients with
■ Glycoprotein IIb/IIIa inhibitors. Intravenous STEMI, intravenous nitroglycerin may be used when
glycoprotein IIb/IIIa inhibitors are recommended chest pain or discomfort is recurrent or refractory
for patients allergic to or intolerant of P2Y12 to nitroglycerin administered sublingually or by
inhibitors, those who are undergoing PCI in spray. STEMI that is complicated by pulmonary
combination with P2Y12 inhibitors and are at edema or hypertension may also warrant the use
high risk for thrombus formation, and those with of intravenous nitroglycerin. When used to relieve
aspirin allergy. refractory chest discomfort, titrate to maintain
■ Anticoagulants. Unfractionated heparin, a systolic blood pressure of 90 mmHg or more
enoxaparin or fondaparinux may be used for (or 30 mmHg below baseline in patients with
anticoagulation therapy following fibrinolytic hypertension). When used to improve pulmonary
therapy or PCI. Incorrect dosing or monitoring edema or hypertension, titrate to maintain a systolic
of heparin in patients with STEMI has been blood pressure that is 10% less than the baseline
associated with intracerebral bleeding and pressure in patients with blood pressure in the
hemorrhage. normal range, and 30 mmHg below baseline in
■ Bivalirudin. Bivalirudin is a direct thrombin patients with hypertension.
inhibitor that may be used as an alternative
to combination therapy with heparin and a
glycoprotein IIb/IIIa inhibitor for anticoagulation
following PCI.

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ADULT ACUTE CORONARY SYNDROMES
ALS - 2020 VERSION

Suspected or known ACS

Prehospital Assessment and Care

• Monitor and support airway, breathing, circulation
• Be ready to provide CPR and defibrillation as needed
• Administer aspirin; consider oxygen, nitroglycerin and morphine if needed
• Obtain IV access; do not delay transport for IV
• Obtain 12-lead ECG
- Transmit ECG or share findings with receiving hospital
- Receiving hospital activates STEMI team per protocol as appropriate
• If considering fibrinolysis, complete fibrinolytic checklist
• Transport to emergency department or catheterization suite per protocol

Immediate Assessment and General Treatment

Within 10 minutes: Immediate General Treatment
• If STEMI, activate STEMI team per protocol • Aspirin
• Assess and support airway, breathing, circulation • Nitroglycerin
• Obtain vital signs, oxygen saturation • Morphine (if discomfort not relieved by nitroglycerin)
- If SpO2 < 90%, provide supplemental oxygen to maintain SpO2 • Consider administration of P2Y12 platelet receptor inhibitors
> 90% and ≤ 99%; titrate as needed but avoid hyperoxia
• Obtain 12-lead ECG
• Order cardiac markers, complete blood count, electrolytes and
coagulation studies
• Obtain brief medical history
• Conduct focused physical examination
• Review/complete fibrinolytic checklist
• Obtain chest radiograph (<30 min; do not delay cardiac interventions)

STEMI
or new/presumably new LBBB Evaluate ECG NSTE-ACS

• Activate STEMI team if not already done Complete risk score using validated tool
• Provide adjuvant therapies †

≤ 12 hours since High risk

Low or intermediate risk
symptom onset?
NO ECG finding highly
Normal ECG, nondiagnostic
YES suspicious of ischemia and/
ECG or low risk score
or high risk score
Start reperfusion therapy
• PCI (goal: ≤ 90 min of first medical contact) Elevated troponin or high risk Consider:
• Fibrinolysis (goal: ≤ 30 min of arrival) • Consider early invasive strategy for: • Admission for monitoring,
- Refractory ischemic chest further testing and/or
Medications discomfort intervention
Aspirin - Recurrent or persistent • Outpatient follow-up/
• 162 to 325 mg, chewed (if not previousy taken or contraindicated) ST-segment deviation testing
- Ventricular tachycardia
Nitroglycerin
- Hemodynamic instability
• 0.4 or 0.8 mg SL every 5 min up to 3 times
- Signs/symptoms of heart failure
Morphine • Consider dual antiplatelet therapy
• 1 to 5 mg IV only if discomfort not relieved by nitroglycerin and anticoagulant therapy (aspirin,
P2Y12 inhibitor, anticoagulant)
†
See Adjuvant Drug Therapies table, on reverse side.
• Provide adjuvant therapies†
Copyright © 2021 The American National Red Cross
• Cardiology consultation

Chapter 10 | Acute Coronary Syndromes | 141

 ADULT ACUTE CORONARY SYNDROMES
ALS - 2020 VERSION

ECG Findings in Acute Coronary Syndromes

NSTE-ACS

STEMI (ST-segment elevation or new or High Risk

Intermediate or Low Risk
presumably new LBBB) (ST-segment depression, dynamic T-wave
(normal or nondiagnostic ST-segment
inversion or transient ST-segment elevation
or T-wave changes)
strongly suspicious of ischemia)
• New ST-segment elevation at the J point in leads V2 • Changes suggestive of ischemia, such as • No ECG changes, or nondiagnostic ST-segment
and V3 of: ST-segment depression or T-wave inversion, or T-wave changes
- ≥ 0.2 mV (≥ 2 mm) in men > 40 years in two or more contiguous leads • ST-segment deviation < 0.05 mV (0.5 mm) in either
- ≥ 0.25 mV (≥ 2.5 mm) in men ≤ 40 years • Transient ST-segment elevation ≥ 0.05 mV direction or T-wave inversion ≤ 0.2 mV (2 mm)
- ≥ 0.15 mV (≥ 1.5 mm) in women (≥ 0.5 mm) lasting < 20 min
• New ST-segment elevation ≥ 0.1 mV (≥ 1 mm) in two or
more contiguous leads other than V2 and V3
• New or presumed new left bundle branch block (LBBB)
Normal or nonspecific ECG findings do not rule out the possibility of acute coronary syndromes. Always evaluate ECG findings in the context of the patient’s overall clinical presentation.

Clinical Presentation of Acute Coronary Syndromes

Consider in all patients presenting with chest pain or discomfort: Other possible signs and symptoms:
• Retrosternal pressure, squeezing, tightness, aching or heaviness • Dizziness, light-headedness or syncope
• May radiate to one or both arms or shoulders, the back, neck, jaw or • Sudden, unexplained dyspnea, which may occur without chest pain or discomfort
epigastric region • Nausea or vomiting
• Persistent (more than 3 to 5 min); may be intermittent • Pale, ashen or slightly cyanotic skin, especially on the face and fingers
• Diaphoresis
• Anxiety or a feeling of impending doom
• Extreme fatigue
• Loss of consciousness
Note: Women, patients < 40 years or > 75 years, and those with medical conditions may present with atypical symptoms of ischemia (e.g., patients with diabetes may experience ischemia
without pain, or “silent ischemia”).

Adjuvant Drug Therapies

Drug Class Use
• P2Y12 platelet receptor inhibitors For use in combination with aspirin for PCI for high-risk patients, or for patients with aspirin allergy
- Clopidogrel
- Ticagrelor
Glycoprotein IIb/IIIa inhibitors For patients allergic or intolerant of P2Y12 inhibitors, or undergoing PCI in combination with P2Y12 inhibitors and high risk for
thrombus, and for aspirin allergy
• Anticoagulants For anticoagulation therapy following fibrinolytic therapy or PCI
- Unfractionated heparin
- Enoxaparin
- Fondaparinux
Bivalirudin An alternative to combination therapy with heparin and a glycoprotein IIb/IIIa inhibitor for anticoagulation after PCI
β-Blockers Initiate within the first 24 hours unless there are contraindications (e.g., acute heart failure, low cardiac output)
Intravenous nitroglycerin For recurrent or refractory chest pain, pulmonary edema or hypertension accompanying STEMI

Copyright © 2021 The American National Red Cross

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 CHAPTER
11

Stroke
Introduction
Among American adults, stroke is the fifth-leading cause of death and is a leading cause
of long-term disability. Each year approximately 795,000 Americans have a stroke, which
equates to about one stroke occurring every 40 seconds. Among people experiencing a
stroke, one third will die, one third will have long-term disability and one third will recover
with minimal or no disability. Early management of acute stroke is included in ALS training
because, just as with cardiac emergencies, time is a critical component of treatment. Timely
recognition, assessment and management of acute stroke can minimize brain injury and
improve patient outcomes.
Overview of Stroke Hemorrhagic Stroke
A stroke is a sudden neurologic deficit that occurs Hemorrhagic stroke occurs when a blood vessel in the
because of impaired blood flow to part of the brain. brain ruptures and pressure from the bleeding damages
Stroke is characterized by: the brain tissue. This type of stroke is frequently caused
■ A sudden onset of signs and symptoms. by hypertension or aneurysms. Hemorrhagic strokes
■ Primary involvement of the central nervous system. are less common than ischemic strokes, accounting for
■ An ischemic or hemorrhagic cause. about 13% of all strokes, but are responsible for about
40% of all stroke-related deaths. Hemorrhagic strokes
Ischemic Stroke can be classified as intracerebral or subarachnoid.
■ Intracerebral hemorrhage, the most common form
Ischemic stroke occurs when a blood vessel carrying of hemorrhagic stroke, occurs when an artery located
blood to the brain becomes obstructed. Ischemic within the brain bursts, causing bleeding into the
strokes account for about 87% of all strokes. Ischemic surrounding brain tissue. Causes of intracerebral
hemorrhage include arteriovenous malformation,
stroke is classified as thrombotic or embolic.
anticoagulant therapy and chronic hypertension.
■ A thrombotic stroke is most often caused by ■ Subarachnoid hemorrhage occurs when a blood
rupture of an atherosclerotic plaque in a cerebral vessel located on the surface of the brain ruptures,
artery, resulting in the formation of a thrombus that causing bleeding into the subarachnoid space.
occludes the artery. Patients frequently have a This type of hemorrhage is most often caused by a
history of hypercholesterolemia and atherosclerosis. ruptured aneurysm but can also be caused by an
Large vessel thrombosis, which occurs in the larger arteriovenous malformation, bleeding disorder, head
arteries of the brain, is the most common form of injury or anticoagulant therapy.
thrombotic stroke and is associated with a poor
prognosis. Lacunar infarction occurs when one of
the small, deep penetrating arteries of the brain Acute Stroke Chain
becomes obstructed and is associated with a more
favorable prognosis. of Survival
■ An embolic stroke occurs when a plaque fragment
or blood clot forms elsewhere within the circulatory The Acute Stroke Chain of Survival (Figure 11-1)
system and travels to the cerebral circulation. Often illustrates how a coordinated effort among members of
the source of the embolus is a blood clot that forms the community, out-of-hospital providers and in-hospital
in the heart or the large arteries in the upper chest or providers can optimize outcomes for patients with
neck. Between 15% and 20% of embolic strokes are stroke.
associated with atrial fibrillation.
For acute ischemic stroke, the goal of treatment is to Early Recognition and Activation of
relieve the obstruction and restore blood flow to the
the Emergency Response System
brain tissue. Acute ischemic stroke can be treated with
fibrinolytic therapy, endovascular therapy, or both, but
Because treatment of acute ischemic stroke is time
the window for treatment is narrow.
dependent, early recognition of signs and symptoms
■ Fibrinolytic therapy is ideally administered within 60 of stroke and activation of emergency medical services
minutes of the patient’s arrival and within 3 hours (EMS) is key.
of symptom onset, although this time frame may be
extended to 4.5 hours for some patients.
■ Endovascular therapy is ideally administered as soon Rapid Dispatch and Stroke
as possible and within 6 hours of symptom onset, Protocol Activation
although this time frame may be extended to 24
hours for some patients.
The second link in the Acute Stroke Chain of Survival
is rapid dispatch and stroke protocol activation. The
EMS dispatcher should handle all potential stroke calls
as critical. Assistance should be dispatched to these
patients with the highest level of priority.

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 Early Recognition Rapid Dispatch and Rapid Transport and Rapid In-Hospital
and Activation of Stroke Protocol Prearrival Notification Assessment,
the Emergency Activation Diagnosis and
Response System Treatment

Figure 11-1 | Acute Stroke Chain of Survival

Rapid Transport and Prearrival laboratory studies; measures blood glucose and
provides treatment if necessary; obtains a 12-lead
Notification ECG; and places the patient on NPO status.
■ Within 20 minutes of the patient’s arrival, the team
Rapid transport and prearrival notification is the third obtains a focused history; conducts a neurologic
link in the Acute Stroke Chain of Survival. The goal is assessment using the National Institutes of Health
to efficiently transport the patient to a facility where Stroke Scale (NIHSS) or similar stroke severity tool;
definitive assessment and treatment can take place, and determines the time of symptom onset or last known
to ensure that appropriate personnel and resources are normal time; and completes the CT or MRI scan.
assembled in anticipation of the patient’s arrival. The ■ Within 45 minutes of the patient’s arrival, the CT or
MRI scan is interpreted.
receiving facility should be capable of administering
■ Within 60 minutes of the patient’s arrival, fibrinolytic
reperfusion therapies and providing post-stroke care on
therapy is initiated for patients with ischemic stroke
a dedicated stroke unit (Box 11-1). who have no contraindications.
■ Within 3 hours of the patient’s arrival, the patient is
admitted to a monitored bed on a dedicated stroke
Practice Note unit or critical care unit.
Patients with potential acute ischemic stroke who present
to a facility that is not equipped to provide fibrinolytic or Practice Note
endovascular therapy should be treated according to
the facility’s highest level of care or scope of practice, If a patient with suspected stroke presents to a facility
stabilized as much as possible and then transported to the that does not have a dedicated stroke unit, protocols
closest facility with stroke treatment capabilities. should be in place to expedite patient transfer to the
nearest hospital capable of providing a higher level of
stroke care and post-treatment monitoring. If possible,
the receiving facility should initiate fibrinolytic therapy
Rapid In-Hospital Assessment,
before transferring the patient to a facility capable
Diagnosis and Treatment of providing a higher level of stroke care and post-
treatment monitoring. If the receiving facility is not
The final link of the Acute Stroke Chain of Survival is equipped to administer fibrinolytic therapy, the patient
rapid in-hospital assessment, diagnosis and treatment. should be immediately transfered to a primary or
Time frames have been established for these activities comprehensive stroke center.
to take place for a patient with acute ischemic stroke
(Figure 11-2).
■ Within 10 minutes of the patient’s arrival, the team
The 8 Ds of Stroke Care
supports airway, breathing and circulation; orders The “8 Ds of Stroke Care” highlight critical steps in
a noncontrast computed tomography (CT) or
the management of a patient with stroke (Box 11-2). A
magnetic resonance imaging (MRI) brain scan;
performs a neurologic screening assessment; orders delay in carrying out any of these critical actions can be
detrimental to the patient.

Chapter 11 | Stroke | 145

Box 11-1 | Stroke Care Facilities

Every hospital that provides emergency services should have a written document detailing its capabilities and
protocols for caring for patients with acute stroke and should share this information with the public and with the
local emergency medical services (EMS) system. This document should identify areas of expertise in stroke care;
identify capabilities with regard to neuroimaging, administering reperfusion therapies and providing post-stroke
care; and establish criteria and protocols for patient transfer or direct transport to a higher level of care.

For hospitals that hold Joint Commission accreditation, the Joint Commission offers four levels of stroke program certification.
■ Acute stroke–ready hospitals: These hospitals do not possess dedicated stroke units but have access
to providers with expertise in diagnosing and treating acute ischemic stroke with fibrinolytic therapy 24
hours a day, 7 days a week. Additionally, these hospitals have transfer agreements with local primary or
comprehensive stroke centers.
■ Primary stroke centers: These hospitals have staff with neurological expertise dedicated to stroke care
and are capable of administering fibrinolytic therapy. These facilities must have a dedicated stroke unit.
Additionally, these hospitals have transfer agreements with local comprehensive stroke centers.
■ Thrombectomy-capable stroke center: Like primary stroke centers, these hospitals have staff with
extensive neurological expertise dedicated to stroke care and are capable of administering fibrinolytic therapy,
but thrombectomy-capable stroke centers must also offer mechanical thrombectomy. These facilities must
have dedicated neurointensive care beds for complex stroke patients on site and available 24 hours a day, 7
days a week. Additionally, these hospitals have transfer agreements with local comprehensive stroke centers.
■ Comprehensive stroke center: These hospitals have staff with extensive neurological expertise dedicated
to stroke care and the ability to administer fibrinolytic therapy and perform mechanical thrombectomy,
endovascular coiling and microsurgical clipping procedures for aneurysms.

Neurologic assessment
completed
Brain CT or MRI Fibrinolytic therapy
obtained initiated

10 minutes 20 minutes 45 minutes 60 minutes 3 hours

General assessment Brain CT or MRI scan Patient admitted to a

completed interpreted monitored bed
Brain CT or MRI
ordered

Figure 11-2 | Critical time periods for in-hospital assessment and management of acute ischemic stroke

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Box 11-2 | The 8 Ds of Stroke Care Box 11-3 | Cincinnati Prehospital Stroke Scale (CPSS)

■ Detection: Early recognition of the signs and An abnormal finding in any one of the following three
symptoms of stroke areas is associated with a 72% probability of stroke.
■ Dispatch: Early activation of, and response by,
emergency medical services (EMS) professionals Facial Droop (ask patient to show teeth/smile)
■ Delivery: Prompt transport of the patient to a ■ Normal: both sides of face move equally
facility capable of providing acute stroke care, ■ Abnormal: one side of the face does not move as
with advanced notification to the receiving facility well as the other side
■ Door: Immediate triage by receiving staff
Arm Drift (ask patient to close eyes and extend both
■ Data: Prompt collection of the data necessary
to inform treatment decisions, including medical arms straight out with the palms up for 10 seconds)
history and physical examination data and data ■ Normal: both arms move the same, or both arms
obtained through laboratory and imaging studies do not move at all
■ Decision: Prompt and expert evaluation of the ■ Abnormal: one arm does not move, or one arm
data to inform treatment decisions drifts downward as compared with the other
■ Drug/device: Administration of fibrinolytic Abnormal Speech (ask patient to say “You can’t
therapy, endovascular therapy or both within
teach an old dog new tricks”)
recommended time frames
■ Disposition: Admission to a dedicated stroke ■ Normal: patient uses correct words without slurring
unit or critical care unit ■ Abnormal: patient uses incorrect words, slurs
words or is unable to speak
Recognizing Stroke stroke once they arrive at the receiving facility (Figure
11-4). The NIHSS evaluates level of consciousness,
Clinical Presentation best gaze, visual fields, facial palsy, motor function (arm
and leg), limb ataxia, sensation, language deficits and
Signs and symptoms of stroke include: extinction and inattention and helps to determine both
■ Sudden weakness, numbness or tingling on one side the location and the severity of the stroke. The NIHSS is
of the face or body. included at the end of this chapter.
■ Sudden onset of confusion.
■ Sudden difficulty with language, including difficulty
speaking, difficulty understanding or garbled speech. Patient Assessment
■ Sudden vision difficulties in one or both eyes.
■ Difficulty with walking, balance or coordination. Rapid Assessment
■ Sudden severe headache.
On initial impression, the patient may appear to be
Stroke Assessment Tools fully alert, have some degree of impaired level of

Cincinnati Prehospital Stroke Scale

A rapid stroke assessment tool, such as the Cincinnati
Prehospital Stroke Scale (CPSS), can be used to
screen for signs of stroke (Box 11-3). The CPSS
screens for three physical indicators of stroke: facial
droop (Figure 11-3), arm drift and abnormal speech. An
abnormal finding in any one of these areas is associated
with a 72% probability of a stroke and is sufficient
reason to activate the EMS system.

National Institutes of Health Stroke Scale

The National Institutes of Health Stroke Scale (NIHSS),
which can be used to both assess and quantify deficits,
should be administered to all patients with suspected Figure 11-3 | Facial droop

Chapter 11 | Stroke | 147

 cause of the stroke and gather additional information
that will aid in determining candidacy for planned
interventions.

History
Key information to elicit during the history includes:
■ The time of symptom onset and the events leading up
to the onset of signs and symptoms. If the patient was
asleep when the stroke occurred, consider the time of
onset to be the last time the patient was known to be
asymptomatic.
■ The presence of risk factors for stroke,
Figure 11-4 | A neurologic assessment using the National arteriosclerosis and cardiac disease.
Institutes of Health Stroke Scale (NIHSS) or a similar ■ Prior occurrences of migraine, seizure, infection,
assessment tool should be conducted when the patient
trauma or illicit drug use.
arrives at the facility.
■ The presence of comorbid conditions, including
consciousness or appear unresponsive. Other signs that hypertension, diabetes and atrial fibrillation.
may be immediately apparent include difficulty speaking ■ The use of medications, including anticoagulants,
or facial droop. antiplatelet agents, antihypertensive agents and
insulin.
■ Relevant events from the past medical history,
Primary Assessment including recent stroke or transient ischemic attack,
myocardial infarction, surgery, trauma or bleeding.
As with any acutely ill patient, the goal of the primary
assessment is to quickly assess the patient’s airway, Physical Examination
breathing, circulation, disability and exposure and Conduct a focused physical examination of the head
provide care as needed. Ensure an adequate airway and and neck, chest and extremities to identify potential
support ventilation as needed. If necessary, provide the causes of stroke and rule out stroke mimics. The head
minimal level of supplemental oxygen needed to maintain and neck examination may reveal signs of cardiovascular
an oxygen saturation of 94% to 99%, unless another disease (e.g., bruits, jugular venous distension) or injury
target is clinically indicated. Take care to avoid hyperoxia. as a result of trauma or seizure. The focus of the chest
Assess perfusion. If the patient is hypotensive, give fluids examination is to identify potential cardiac causes of
as needed to maintain adequate perfusion. Measure stroke, such as a valve disorder. Examination of the
blood glucose and provide treatment as needed. extremities may reveal signs of cardiac disorders or other
Conduct a neurologic assessment using the NIHSS or conditions, such as platelet disorders or coagulopathies.
similar assessment tool.
Additionally, obtain vital signs and repeat the neurologic
examination at frequent regular intervals.
Secondary Assessment
Diagnostic Tests
The goals of the secondary assessment are to further
rule out differential diagnoses (“stroke mimics”; Box Brain imaging is essential for evaluating patients
11-4) as appropriate, determine the potential underlying with suspected acute stroke. Brain imaging enables
differentiation of ischemic stroke from hemorrhagic
Box 11-4 | Common Stroke Mimics stroke and can reveal structural abnormalities that
may be causing the patient’s signs or symptoms or
■ Seizure that might be contraindications to fibrinolytic therapy.
■ Migraine Both noncontrast CT and MRI are acceptable imaging
■ Toxicity or metabolic disturbance (e.g., drug or options. Noncontrast CT is the most widely used tool for
alcohol intoxication, hypoglycemia) urgent brain imaging in the setting of acute stroke.
■ Intracranial tumor or infection
Other diagnostic studies that are routinely ordered
■ Infectious processes for patients with suspected acute ischemic stroke are
■ Somatoform or conversion disorder summarized in Box 11-5. These tests assist in making

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Box 11-5 | Recommended Diagnostic Tests for Patients with Suspected Acute Ischemic Stroke

All Patients Select Patients

■ Brain imaging (noncontrast CT or MRI) ■ Thrombin time and/or ecarin clotting time (for
■ Blood glucose level patients known or suspected to be on direct
■ Serum electrolyte panel with renal function tests* thrombin inhibitors or direct factor Xa inhibitors)
■ Complete blood count* ■ Hepatic function tests
■ Cardiac markers* ■ Toxicology screen
■ Prothrombin time and international normalized ratio* ■ Blood alcohol level
■ Activated partial thromboplastin time* ■ Pregnancy test
■ 12-Lead ECG ■ Arterial blood gases (in cases of suspected hypoxia)
■ Chest radiography (in cases of suspected lung disease)
■ Lumbar puncture (in cases where subarachnoid
hemorrhage is suspected, but CT scan results
are negative for blood)
■ Electroencephalography (in cases of suspected
seizures)

*Obtaining these tests and interpreting their results should not delay ordering and initiation of therapy unless there is clinical suspicion
of a bleeding abnormality or thrombocytopenia, the patient has received heparin or warfarin, the patient has received other anticoagulants
or laboratory results have revealed a platelet count of less than 100,000/mm³, an international normalized ratio (INR) greater than 1.7, an
activated partial thromboplastin time (aPTT) greater than 40 seconds or a prothrombin time (PT) greater than 15 seconds.

a definitive diagnosis, determining underlying causes necessary. Order laboratory studies (such as a complete
and evaluating candidacy for therapeutic interventions. blood count and coagulation studies) and obtain a
Additional tests may be ordered depending on history 12-lead ECG, but do not delay brain imaging to do
and physical examination findings. so. Place the patient on NPO status until the ability to
swallow can be assessed. Obtain a focused history
(including the time of symptom onset) and complete a
Practice Note neurologic screening assessment using the NIHSS or a
Obtaining laboratory studies and interpreting their results similar assessment tool.
should not delay ordering and initiation of therapy unless
there is clinical suspicion for conditions that would Care
increase the patient’s risk for bleeding.
Hemorrhagic Stroke
If brain imaging reveals hemorrhage, treatment depends
Approach to the Patient on the cause and severity of the bleeding. Measures
are taken to support the airway, oxygenation, ventilation
The Adult Acute Stroke Code Card summarizes the and perfusion. In addition, care entails measures to
approach to a patient with acute stroke. control the internal bleeding, including consideration of
reversal of anticoagulants, consideration of treatment of
Assess and Recognize hypertensive crisis, management of increased intracranial
pressure and treatment of seizures. A neurology or
When stroke is suspected on the basis of the rapid neurosurgical consult is necessary and the patient may
and primary assessments, activate the stroke team need to be transferred to a comprehensive stroke center
immediately per facility protocol. Order a noncontrast or a neurosurgical center for definitive care.
CT or MRI scan of the brain within 10 minutes of the
Ischemic Stroke
patient’s arrival. Results should be obtained within 20
minutes and interpreted within 45 minutes. Measure If brain imaging does not reveal hemorrhage, consider
blood glucose levels and provide treatment as fibrinolytic therapy, endovascular therapy, or both, based
on inclusion and exclusion criteria. If serial neurologic

Chapter 11 | Stroke | 149

examinations show that the patient’s neurologic function ■ No contraindications to initiation of endovascular
is improving toward normal, fibrinolytic therapy may not therapy (groin puncture) within 6 hours of the onset
be indicated. In this case, consider adjuvant therapies, of signs and symptoms
seek neurology/expert consult and admit or prepare the Endovascular therapy is ideally administered as soon as
patient for transfer to a stroke unit. possible and within 6 hours of the onset of symptoms,
although this time frame may be extended for some
Fibrinolytic Therapy
patients. If transfer is needed, the goal is to complete
For patients with ischemic stroke who meet the the transfer within 60 minutes of the patient’s arrival.
eligibility criteria (see the Adult Acute Stroke Code
Card), fibrinolytic therapy is the first-line treatment.
Administration of intravenous recombinant tissue Practice Note
plasminogen activator (rtPA) as soon as possible and
Intra-arterial fibrinolysis with rtPA is considered
within 3 hours of the onset of signs and symptoms is
beneficial for patients with ischemic stroke caused by
optimal (with a goal “door-to-needle” time of less than
occlusion of the middle cerebral artery who are not
60 minutes). For select patients, intravenous rtPA may
eligible for intravenous rtPA. Intra-arterial fibrinolysis
be administered within 4.5 hours after the onset of signs
should only be performed at a qualified stroke center,
and symptoms. Following the administration of rtPA,
and it should not delay mechanical thrombectomy.
therapy with anticoagulant or antiplatelet agents should
When performed in conjunction with mechanical
be stopped for 24 hours.
thrombectomy, intra-arterial fibrinolysis is considered
Endovascular Therapy to have the best overall success rate of recanalization
without having an appreciable effect on the rate of
Studies suggest that eligible patients should receive
intracranial hemorrhage. Intra-arterial administration
endovascular therapy in addition to fibrinolytic therapy.
of rtPA has not yet been approved by the Food and
Endovascular therapy entails the use of catheters
Drug Administration.
to deliver a clot-disrupting or a clot-retrieval device
directly to the site of the obstruction. In mechanical
thrombectomy, stent retrievers are preferred over coil
retrievers. In order to be eligible for endovascular therapy
Admission
with a stent retriever, patients must meet the following Within 3 hours of arriving at the facility, the patient
criteria: should be admitted to a monitored bed on a dedicated
■ A prestroke modified Rankin Scale (mRS) score of stroke unit or critical care unit. Care at this stage
0 to 1 includes supporting airway, breathing and circulation;
■ A diagnosis of acute ischemic stroke receiving initiating post-therapy protocols; monitoring for
intravenous rtPA within 4.5 hours of the onset of neurologic deterioration, complications of the stroke and
signs and symptoms its treatment (e.g., intracranial hemorrhage and other
■ Causative occlusion of the internal carotid artery or bleeding complications); and managing blood pressure
proximal middle cerebral artery and glucose according to facility protocols and the
■ Age 18 years or older provider’s clinical judgment.
■ An NIHSS score of 6 or greater
■ Alberta Stroke Programme Early Computed
Tomography (ASPECT) score of 6 or greater

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ADULT ACUTE STROKE
ALS - 2020 VERSION

Suspected or known acute stroke

Prehospital Assessment and Care

• Monitor and support airway, breathing, circulation
- Provide supplemental oxygen if needed to maintain SpO2 of 94% to 99%; provide ventilatory
support (BVM, noninvasive or invasive) as needed
• Perform prehospital stroke screen and severity assessment and record time of symptom onset/last
known normal
• Measure blood glucose; treat hypoglycemia as indicated
• Follow local protocols for destination decision
• Alert receiving hospital and follow protocols for stroke arrival

Activate stroke team per protocol

Immediate General Assessment*

Within 10 minutes: Within 20 minutes: Within 45 minutes:
• Ensure airway • Obtain focused history • Interpret imaging results
• Support oxygenation (maintain SpO2 of 94% to 99% • Conduct neurologic assessment
unless clinical condition warrants a different level) and (NIHSS or similar stroke severity
ventilation (BVM, noninvasive or invasive) as needed tool)
• Monitor and support circulation as needed • Determine time of symptom
• Order noncontrast CT or MRI† onset/last known normal
• Perform neurologic screening assessment • Complete CT/MRI of head
• Obtain vascular access and order laboratory studies‡
• Measure blood glucose and provide treatment as needed
• Obtain 12-lead ECG
• Place on NPO status

Ischemic Hemorrhagic

• Consider reversal and/or treatment

Eligible for fibrinolytic and/or if patient is on anticoagulants
endovascular therapy? • Consider treatment of
YES NO
hypertensive crisis
• Manage raised intracranial
Start fibrinolytic therapy, endovascular therapy Consider adjuvant therapies pressure
or both§ • Treat seizures
• Fibrinolytic therapy (≤ 60 min of arrival) • Seek expert consult (neurologist/
- < 3 hours of symptom onset (< 4.5 hours neurosurgeon)
Seek neurology/expert consult
for select patients)
• Endovascular therapy (if transfer needed,
goal is < 60 min from arrival to departure) Admit or prepare for transfer Prepare patient for admission/
- ≤ 6 hours of symptom onset (6 to 24 hours to stroke unit transfer to comprehensive stroke or
for select patients) neurosurgical unit/center

Admit or prepare for transfer to stroke unit *Can be done in emergency department or imaging location; best practice is to bring the patient directly from
arrival to imaging.
†
CTA with CTP or MRA with diffusion-weighted MRI with or without MR perfusion may be used for selected patients.
• Begin post-therapy protocols ‡
Serum electrolyte panel with renal function tests, complete blood count, cardiac markers, prothrombin time,
• Monitor for neurologic deterioration, international normalized ratio, activated partial thromboplastin time
complications of stroke/stroke therapy §
Discontinue therapy with anticoagulant or antiplatelet agents for 24 hours after rtPA administration.
• Manage blood pressure
• Manage glucose per protocol

Copyright © 2021 The American National Red Cross

Chapter 11 | Stroke | 151

 ADULT ACUTE STROKE
ALS - 2020 VERSION

Signs and Symptoms of Stroke

• Acute-onset mental status changes or confusion • Sudden difficulty with language (e.g., difficulty • Difficulty with walking, balance or coordination
• Sudden weakness or numbness on one side speaking, difficulty understanding, garbled speech) • Sudden severe headache
of the body • Sudden loss of vision in one or both eyes

Cincinnati Prehospital Stroke Scale (CPSS)

An abnormal finding in any one of the following three areas is associated with a 72% probability of stroke.

Facial Droop (ask patient to show teeth/smile) Arm Drift (ask patient to close eyes and extend both Abnormal Speech (ask patient to say “You can’t teach
• Normal: both sides of face move equally arms straight out with the palms up for 10 seconds) an old dog new tricks”)
• Abnormal: one side of the face does not move • Normal: both arms move the same, or both arms do • Normal: patient uses correct words without slurring
as well as the other side not move at all • Abnormal: patient uses incorrect words, slurs words
• Abnormal: one arm does not move, or one arm or is unable to speak
drifts downward as compared with the other

Eligibility Criteria for Intravenous rtPA Administration in Patients with Acute Ischemic Stroke

Treatment Timing Inclusion Criteria Absolute Exclusion Criteria Relative Exclusion Criteria

Within 3 hours of • Ischemic stroke diagnosis • Significant head trauma or stroke within last 3 months • Minor or rapidly improving
symptom onset or • Measurable neurologic • Symptoms suggestive of subarachnoid hemorrhage stroke symptoms
patient last known well deficit • Arterial puncture at noncompressible site within last 7 days (clearing spontaneously)
or at baseline state • ≥ 18 years of age • History of intracranial hemorrhage, intracranial tumor, AVM or aneurysm • Pregnancy
• Recent intracranial or intraspinal surgery • Seizure at onset
• Hypertension (systolic blood pressure > 185 mmHg or diastolic blood • Major surgery or serious
pressure > 110 mmHg) trauma within past 14 days
• Active internal bleeding • Gastrointestinal malignancy
• Risk factors for acute bleeding, including but not limited to: or recent gastrointestinal or
- Low platelet count (< 100,000/mm³) urinary tract hemorrhage
- Heparin administration within the last 48 hours, resulting in an aPTT within past 21 days
value greater than the upper limit of normal • Recent acute myocardial
- Current use of an anticoagulant with an INR > 1.7 or a PT > 15 sec infarction within past 3 months
- Current use of direct thrombin inhibitors or direct factor Xa inhibitors
with elevated results on sensitive laboratory tests (e.g., aPTT, INR,
platelet count or ECT; TT or appropriate factor Xa activity assays)
• Low blood glucose level (< 50 mg/dL or 2.7 mmol/L)
• Multilobar infarction on CT

Within 3 to 4.5 hours • Ischemic stroke diagnosis In addition to the exclusion criteria for treatment within 3 hours of symptom onset: • Patients ≥ 80 years of age
of symptom onset* or • Measurable neurologic • Current anticoagulant therapy (INR > 1.7) with a history of both diabetes
patient last known well deficit • History of ischemic stroke within previous 3 months mellitus and prior stroke
or at baseline state
*Intravenous rtPA administration may also be considered for a patient with acute ischemic stroke who awakens with stroke symptoms or who has an unclear time of symptom onset
greater than 4.5 hours from the last known well or baseline state who has a DW-MRI lesion smaller than one-third of the MCA territory and no visible signal change on FLAIR.
Blood Pressure Management
Patients who have elevated blood pressure and are otherwise eligible for treatment with intravenous rtPA (or mechanical thrombectomy) should have their blood pressure carefully lowered
so that their systolic blood pressure (SBP) is less than 185 mmHg and their diastolic blood pressure (DBP) is less than 110 mmHg before intravenous fibrinolytic therapy is initiated.

Management of blood pressure for a patient otherwise eligible for emergency Management of blood pressure during and after rtPA or other emergency reperfusion
reperfusion therapy except that blood pressure is greater than 185/110 mmHg therapy to maintain blood pressure at less than or equal to 180/105 mmHg
Labetalol Clevidipine Monitor blood pressure every 15 min for 2 h from the start of rtPA therapy, then every
• 10 to 20 mg IV over 1 to 2 min, • 1 to 2 mg/h IV, titrate by doubling 30 min for 6 h, and then every hour for 16 h.
may repeat 1 time OR the dose every 2 to 5 min until If SBP > 180 to 230 mmHg or DBP > 105 to 120 mmHg:
Nicardipine desired blood pressure reached
Labetalol Clevidipine
• 5 mg/h IV, titrate up by 2.5 mg/h every (maximum 21 mg/h)
• 10 mg IV followed by continuous IV • 1 to 2 mg/h IV; titrate by doubling the
5 to 15 min (maximum 15 mg/h); Other agents (e.g., hydralazine,
infusion 2 to 8 mg/min OR dose every 2 to 5 min until desired blood
when desired blood pressure reached, enalaprilat) may also be considered.
Nicardipine pressure reached (maximum 21 mg/h)
adjust to maintain proper blood If blood pressure is not maintained
• 5 mg/h IV; titrate up to desired effect If blood pressure is not controlled or
pressure limits OR at less than or equal to 185/110 mmHg,
by 2.5 mg/h every 5 to 15 min DBP > 140 mmHg, consider IV sodium
do not administer rtPA.
(maximum 15 mg/h) OR nitroprusside.

Copyright © 2021 The American National Red Cross

152 | American Red Cross | Advanced Life Support

National Institutes of Health Stroke Scale (NIHSS)

Chapter 11 | Stroke | 153

154 | American Red Cross | Advanced Life Support
Chapter 11 | Stroke | 155
Glossary
Acute coronary syndromes Critical thinking
A general term for a group of life-threatening conditions The process of thinking clearly and rationally to identify
that occur because of a sudden reduction in blood flow the connection between information and actions
to the heart
Dynamic hyperinflation
Arteriovenous malformation Auto–positive end-expiratory pressure (auto–PEEP);
A congenital vascular lesion, often found in the central occurs when exhalation time is insufficient and the
nervous system, consisting of a mass of entwined lungs do not completely empty before the next breath,
arteries and veins connected by fistulae preventing the respiratory system from returning to
its resting end-expiratory equilibrium volume between
Atelectasis breath cycles
Alveolar collapse
Electrical alternans
Atrioventricular (AV) dissociation Beat-to-beat variation in the amplitude of QRS
A situation that occurs when the atria and ventricles complexes
are being driven by independent pacemakers and are
contracting at their own intrinsic rates Embolic stroke
A type of ischemic stroke that occurs when a plaque
Atrioventricular (AV) junction fragment or blood clot forms elsewhere within the
The zone of tissue surrounding the atrioventricular (AV) circulatory system and travels to the cerebral circulation
node
Epiglottis
Capnography A leaf-shaped cartilaginous structure that closes over
A noninvasive way of measuring the end-tidal carbon the opening of the larynx during the act of swallowing
dioxide (ETCO2) level
Expiratory plateau
Carina The phase of the capnography waveform representing
The point where the trachea bifurcates into the right and exhalation of the last of the carbon dioxide–laden air
left main bronchi from the most distal alveoli
Chest compression fraction (CCF) Extracorporeal cardiopulmonary
An indicator of CPR quality; represents the percentage resuscitation (ECPR)
of time during the resuscitation effort spent performing A specialized intervention that uses venoarterial
chest compressions extracorporeal membrane oxygenation (ECMO) in
Closed-loop communication addition to standard CPR
A communication technique used to prevent Fibrillatory waves
misunderstandings; the receiver confirms that the The slight undulation of the baseline seen on the ECG in
message is received and understood atrial fibrillation
Coronary perfusion pressure (CPP) Fibrinolytic therapy
A reflection of myocardial blood flow; the difference Drug therapy to lyse blood clots
between the pressure in the aorta and the pressure in
the right atrium during diastole Gas exchange
The molecular process of adding oxygen to, and
Corrected QT interval (QTc) removing carbon dioxide from, the blood
A calculation used to give a QT value that is theoretically
independent of rate Hemorrhagic stroke
A sudden neurologic deficit caused by rupture of a blood
Crew resource management vessel in the brain
A concept that helps to promote effective and efficient
teamwork and reduce the likelihood of errors by Hyperventilation
encouraging problem solving and communication among The state of exhaling carbon dioxide at a faster rate than
team members the body can produce it

Glossary | 157
Hypoventilation saturation (SaO2)
The state of producing more carbon dioxide than can be
Percutaneous coronary intervention (PCI)
exhaled
A procedure that uses balloon angioplasty, with or
Infranodal without stent placement, to open occluded coronary
Distal to the node arteries

Inspiratory downslope Phased response approach

The phase of the capnography waveform representing A model that organizes the team response to an
inhalation emergency into seven phases and incorporates the
concept of crew resource management and the skills of
Intracerebral hemorrhage communication, critical thinking and problem solving
A type of hemorrhagic stroke that occurs when an artery
located within the brain bursts, causing bleeding into the Polymorphic ventricular tachycardia
surrounding brain tissue A wide-complex ventricular tachycardia characterized by
QRS complexes that vary in shape and rate; produced
Ischemia/reperfusion response by two or more ectopic foci in the ventricles
An inflammatory response induced by the reperfusion of
tissues previously deprived of blood flow, as in cardiac Post–cardiac arrest syndrome
arrest The pathophysiologic consequences of cardiac
arrest, comprising four areas (brain injury, myocardial
Ischemic stroke dysfunction, systemic dysfunction and persistent
A sudden neurologic deficit caused by obstruction of a precipitating conditions)
blood vessel supplying the brain
Primary percutaneous coronary intervention (PCI)
Laryngopharynx Percutaneous coronary intervention performed as the first-
The region of the pharynx that extends from the line therapy for ST-segment elevation myocardial infarction
oropharynx to the level of the cricoid cartilage; also (STEMI)
called the hypopharynx
Problem solving
Left uterine displacement (LUD) The ability to use readily available resources to find
A technique used during CPR in a pregnant patient to solutions to challenging or complex situations or issues
move the gravid uterus up and toward the left to relieve that arise
pressure on the inferior vena cava and maximize the
return of blood to the heart and cardiac output Pulseless electrical activity (PEA)
A term used to describe rhythms that are organized on
Lung compliance the monitor (i.e., all of the QRS complexes are similar in
The ability of the lung to stretch and expand appearance) but which fail to produce a palpable pulse
Monomorphic ventricular tachycardia Quantitative capnography
A wide-complex ventricular tachycardia characterized The measurement of end-tidal carbon dioxide (ETCO2)
by QRS complexes that are generally the same shape; expressed as a value and as a waveform
produced by one ectopic focus in the ventricles
Quantitative capnometry
Nasopharynx The measurement of end-tidal carbon dioxide (ETCO2)
The region of the pharynx that extends from the base of expressed as a value
the skull to the soft palate and is located posterior to the
nasal cavities Rapid response team
A team of highly trained and skilled personnel who
Oropharynx work together to care for a patient when signs of
The region of the pharynx that extends from the hard cardiopulmonary compromise or shock are noted
palate to the level of the hyoid bone and is located
posterior to the oral cavity Respiration
The process of moving oxygen and carbon dioxide between
Oxygen–hemoglobin dissociation curve the atmosphere and the body’s cells
A graphical depiction of the relationship between the
partial pressure of oxygen (PaO2) and the arterial oxygen

158 | American Red Cross | Advanced Life Support

Respiratory arrest Supraglottic airway
Complete cessation of the breathing effort An advanced airway that is not passed through the vocal
cords, such as the laryngeal mask airway and the laryngeal
Respiratory baseline tube
The phase on the capnography waveform representing the
beginning of exhalation Targeted temperature management (TTM)
A neuroprotective intervention that involves lowering and
Respiratory distress maintaining the core body temperature in the range of
The earliest stage on the continuum of respiratory 32° C to 36° C for a period of at least 24 hours
compromise; the patient is using compensatory
mechanisms to maintain oxygenation and ventilation Teamwork
adequate to meet metabolic demands The actions of a group of people with well-defined roles
and responsibilities making a coordinated effort to achieve a
Respiratory failure common goal
The intermediate stage on the continuum of respiratory
compromise; the respiratory system is no longer able to Thrombotic stroke
meet metabolic demands A type of ischemic stroke caused by rupture of an
atherosclerotic plaque in a cerebral artery that results in the
Respiratory upstroke formation of a thrombus
The phase on the capnography waveform representing the
exhalation of air containing carbon dioxide from the alveoli Transglottic airway
An advanced airway that is passed through the vocal cords,
Resuscitation team such as an endotracheal tube
A team of highly trained and skilled personnel who work
together to provide resuscitative care when a patient Transthoracic impedance
experiences respiratory or cardiac arrest The body’s resistance to current flow that is caused by the
thoracic structures, including soft tissue and bone, between
Resuscitative cesarean delivery (RCD) defibrillation pads or paddles and the heart
Surgical delivery of the fetus performed when a pregnant
patient is in cardiac arrest with the goals of resuscitating Ventilation
the pregnant patient and increasing the likelihood of fetal The mechanical process of moving air into and out of the
survival body

Subarachnoid hemorrhage Ventilation-perfusion mismatch

A type of hemorrhagic stroke that occurs when a blood An imbalance between the air that reaches the alveoli (i.e.,
vessel located on the surface of the brain ruptures, causing ventilation) and blood flow to the alveoli (i.e., perfusion) in a
bleeding into the subarachnoid space portion of the lung

Glossary | 159
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Chapter 8
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Warner, M., Trinidad, J. P., Bastian, B. A., Minino, A. M., and H. Hedegaard. 2016. Drugs most frequently involved in
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Chapter 9
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Chapter 10
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Marino, P. L. 2007. The ICU book. 3rd ed. Philadelphia: Lippincott Williams & Wilkins.

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Mozaffarian, D., Benjamin, E. J., Go, A. S., et al. 2016. Heart disease and stroke statistics—2016 update: A report
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Chapter 11
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American Heart Association and American Stroke Association. Quick stroke treatment for saving the brain. Accessed
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UCM_492017_SubHomePage.jsp.

Aminoff, M. J., Greenberg, D. A., and R. P. Simon. 2015. Stroke. In Clinical neurology. 9th ed. New York: McGraw-
Hill.

Centers for Disease Control and Prevention. Atrial fibrillation fact sheet. Accessed December 11, 2017. https://www.
cdc.gov/dhdsp/data_statistics/fact_sheets/fs_atrial_fibrillation.htm.

Centers for Disease Control and Prevention. Stroke fact sheet. Accessed December 11, 2017. https://www.cdc.gov/
dhdsp/data_statistics/fact_sheets/fs_stroke.htm.

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Bibliography | 173
 Index
Note: b indicates box; t indicates table Atrioventricular (AV) block
approach to differentiating, 99
8 Ds of Stroke Care, 145, 147b causes of, 99
classification of, 98–100
ABCDE mnemonic, 77-78, 91, 104, 137 Atropine, 41t, 105
Abdominal thrusts, 11–12, 78 Automated external defibrillator (AED), 10–11, 21–23
Acidosis, 40, 86, 112, 114b, 116, 128t coordinated team response and, 71–72
ACS. See Acute coronary syndromes AV block. See Atrioventricular block
Acute coronary syndromes (ACS), 135, 157
classification of, 134 ß-adrenergic agonists, 105
code card for, 141-142
ß-blockers
drug therapy for, 43t, 139
adjuvant drug therapy and, 140b
goals for management of, 134
in cardiac arrest, 98
pathophysiology of, 134
in the treatment of cardiovascular and
recognition of, 135-137
cerebrovascular disorders, 43t
treatment of, 138-140
Bag-valve-mask resuscitator (BVM), 31–32, 33t,
Adjuvant drug therapy, 140
48–49
AED. See Automated external defibrillator
complications from improper technique, 31
Airway
in respiratory arrest, 91
assessment of, 77-80
parts of, 31
methods of maintaining patent airway, 77-78
technique, 31
obstructed (care for), 11–12
use with advanced airway, 31
Airways, advanced
Bivalirudin, 43
confirming placement of, 27, 30-31, 77-78
Bradyarrhythmia
during CPR, 10-11, 27, 28t, 117
approach to patient with, 104
endotracheal tube, 28t, 29
code card for, 108
indications for, 30
Breathing, assessment of, 79
laryngeal mask airway, 27-28
BVM. See Bag-valve-mask resuscitator
laryngeal tube, 28t, 29
patient monitoring, 30-31
Capnography, 153
types of
and ROSC, 9
supraglottic, 27
evalution of the capnography waveform, 90
transglottic, 27
phases of the normal waveform, 90
Airways, basic
use in confirming advanced airway placement,
nasopharyngeal airway, 26-27
30–31
insertion of, 46-47
use in monitoring effectiveness of CPR, 9
oropharyngeal airway, 26
use in monitoring effectiveness of ventilations, 9, 30
insertion of, 44-45
use in respiratory emergencies, 89–92
Amiodarone, 41-42t, 103, 107, 119
Cardiac arrest
Antiarrhythmic agent, 41-43t, 104
approach to patient in, 117–119
in the treatment of cardiac arrest, 119
code card for, 122
in the treatment of tachycardia, 41-43t, 107
drug therapy for, 40–43t
patient history and, 104
pulse check in, 10, 118
Arrhythmias, drug therapy for, 105-107
recognition of, 112–113
Arterial blood gases, 80, 114, 116, 128
reversible causes (Hs and Ts) of, 113–117
Aspirin
rhythm check in, 118–119
in acute coronary syndromes, 139
rhythms, 112–113
Assess, Recognize and Care, 76
Cardiac arrest in pregnancy, 120
Assessment
code card for, 123
primary, 77–78
Cardiac Chain of Survival, 6–7
rapid, 76–77
In-Hospital Cardiac Chain of Survival, 6
secondary, 79–80
Out-of-Hospital Cardiac Chain of Survival, 6–7
systematic approach to, 85–87
Cardiac conduction system, 96
Asystole, 112–113, 118–119
Cardiac monitoring
Atrial fibrillation, 102–103
five-electrode system, 34
Atrial flutter, 101
three-electrode system, 34
Atrial rate, calculation of, 97
Cardiopulmonary resuscitation (CPR), 6–12, 17–20,
117–119

Index | 175
 compression-to-ventilation ratio in, 10 expected values in normal perfusion states, 9
coordinated team response and, 71–72 expected values in post–cardiac arrest, 9
monitoring effectiveness of, 8–9 for confirming adequacy of ventilation, 78
principles of high-quality, 7–8 in respiratory distress, 88
technique for, 8 in respiratory failure, 89
Endovascular therapy, 144–145, 150, 151
CCF. See Chest compression fraction indications for, 150, 151
Chest compression fraction (CCF), 9, 157 timing for, 144, 151
Chest compressions Exposure, assessment of, 78
compression-to-ventilation ratio, 10, 20 Extracorporeal cardiopulmonary resuscitation (ECPR),
depth of, 7 119, 157
minimizing interruptions to, 7–8, 30, 36, 70 Feedback devices, 9
technique, 7 Fibrillatory waves, 102, 157
Chest radiograph Fibrinolytic therapy, 134–135, 142, 144–146, 149–
use in acute coronary syndromes, 138, 139 150, 152
use in verifying advanced airway placement, 128t for treatment of myocardial infarction, 134–135,
Cincinnati Prehospital Stroke Scale (CPSS), 147, 147t 142
Circulation, assessment of, 78 for treatment of stroke, 144–145, 149, 151
Code cards eligibility criteria for, 151
Adult Acute Coronary Syndromes, 141–142 indications for, 145, 151–152
Adult Acute Stroke, 151–152 timing for, 144–145, 151–152
Adult Bradyarrhythmia, 108 First-degree atrioventricular (AV) block, 98–99
Adult Cardiac Arrest, 122 Fluid therapy, 39–40, 42–43t
Adult Post–Cardiac Arrest Care, 130–132 in post-cardiac arrest care, 39, 40–43t
Adult Suspected or Known Opioid Toxicity, 94 indications for, 39
Adult Systematic Assessment, 81 solutions used for, 40–43t
Basic Life Support: Adults and Adolescents, 13–14
Cardiac Arrest in Pregnancy, 123–124 Glucose (blood levels of), 128t, 151, 149, 145, 151
Communication in stroke, 149, 150, 151
essential components of, 69 post–cardiac arrest, 128t, 130
with team, 3, 65, 69–70 Glycoprotein IIb/IIIa inhibitors, 43t, 140b
with family members, 70
Coronary angiography, 128, 139 HEART score, 138, 140
Coronary perfusion pressure (CPP), 7, 157 Hemodynamic compromise, signs of, 103, 104, 106,
Continuous quality improvement, 8 108–109
Corrected QT interval (QTc), 96, 103, 157 Hemorrhage, subarachnoid, 144, 149b, 152, 159
CPP. See Coronary perfusion pressure Heparin, 43t, 140b, 142
CPR. See Cardiopulmonary resuscitation
CPSS. See Cincinnati Prehospital Stroke Scale Intraosseous access, 38–39, 59–65
Crew resource management, 72, 157 Intravenous (IV) access, 38
Critical thinking, 3, 70, 157 Ischemia/reperfusion response, 126, 158
IV access. See Intravenous access
Debriefing, 8, 70, 73
Defibrillation, 6, 36–38, 53–54, 118 J point, 96–97
energy doses for, 38, 53–54, 118
indications for, 37 MAP. See Mean arterial pressure
pad placement for, 36, 53–54 Mean arterial pressure (MAP), 127
technique, 36–38, 53–54, 118 MI. See Myocardial infarction
with AED, 6 Morphine, 43t, 139, 141
Disability, assessment of, 77–78, 81, 148 Myocardial infarction (MI), 117, 122, 127, 130, 134

ECG tracing, 96–97 Naloxone, 93, 94

approach to interpreting, 97 Nasopharyngeal airway (NPA), 26, 27
waveforms and intervals of, 96–97 indications for, 26
ECPR. See extracorporeal cardiopulmonary placement of, 26, 46-47
resuscitation National Institutes of Health Stroke Scale (NIHSS), 78,
Electrocardiography, 35–36, 50–52, 80 147, 153–155
12-lead ECG, 35–36, 50–52, 80 NIHSS. See National Institutes of Health Stroke Scale
15-lead ECG, 35–36, 50–52 Nitroglycerin
End-tidal carbon dioxide, 9, 78, 88 intravenous, 140b, 142
expected values in low perfusion states, 9 sublingual, 139

176 | American Red Cross | Advanced Life Support

Non–ST-segment elevation ACS (NSTE-ACS), 134, goals of, 76
137, 141–142 technique for, 15-16, 77
high-risk NSTE-ACS, 137 Rapid response team, 6, 10, 68, 73, 158
intermediate- or low-risk NSTE-ACS, 137 criteria for calling, 68
Nonshockable rhythm, 117–118, 124 goals for, 68
Normal sinus rhythm, 97 Reperfusion therapy, 127-128, 134, 135, 139
NPA. See nasopharyngeal airway Respiratory arrest, 10, 11, 69, 83, 88-92, 114t, 159
NSTE-ACS. See Non–ST-segment elevation ACS recognition of, 92
OPA. See oropharyngeal airway treatment of, 69, 88-92
Opioid overdose, 92–93, 94 Respiratory distress, 68, 77, 83, 88-92, 114t, 117, 159
recognition of, 92, 94 signs and symptoms of, 68, 88-92
treatment of, 92–93, 94 Respiratory failure, 83, 88-92, 114t, 159
Oropharyngeal airway (OPA), 26, 44–45 signs and symptoms of, 89, 91
Oxygen delivery devices, 32, 33t types of, 89
Oxygen-hemoglobin dissociation curve, 86, 158 Resuscitation team, 6, 9, 10, 25, 68-73
Oxygen therapy, 32 goals for, 68-73
bag-valve-mask resuscitator (BVM), 32, 33t team member responsibilities, 69-73
nasal cannula, 32, 33t team member roles, 69-73
non-rebreather mask, 32, 33t Return of spontaneous circulation (ROSC), 2, 6, 7, 9,
simple oxygen face mask, 32, 33t 20, 73, 114, 117-119, 125-127, 130
minimum arterial diastolic pressure for, 9
P wave, 96, 97 minimum CPP for, 7
P2Y12 platelet receptor inhibitors, 43t, 140b, 141, 142 recognition of, 73
PCI. See Percutaneous coronary intervention ROSC. See Return of spontaneous circulation
PEA. See Pulseless electrical activity
Percutaneous coronary intervention (PCI), 134-135, SAMPLE mnemonic, 79
139-140, 158 Second-degree atrioventricular (AV) block type I, 99
indications for, 134 Second-degree atrioventricular (AV) block type II, 100
primary, 140 Secondary assessment, 76, 77, 79, 91-92, 104, 137,
timing for, 135 148-149
Phased response approach, 72-73, 158 components of, 76, 77, 91-92, 104, 137-138,
Pneumothorax, 92b, 137b 148-149
differential diagnosis for ACS, 92b goals of, 76, 91, 104, 137, 148-149
Post–cardiac arrest care, 125-131, 127t, 128t Serum cardiac markers, 80, 92, 128t, 135, 137, 138,
code card for, 130 139, 140
identifying and treating myocardial infarction, 128 indications for, 137
management of hemodynamics in, 127 timing for, 137
optimization of ventilation and oxygenation in, Shockable rhythm, 54, 117-119
126-127 Shout-tap-shout sequence, 10, 15
promoting neurologic recovery, 128-129 Sinus bradycardia, 98
Post–cardiac arrest prognostication, 129 Sinus tachycardia, 101, 106
Post–cardiac arrest syndrome, 126 Skill sheets
PR interval, 96, 97 AED Use for Adults, 21-23
Primary assessment, 77-78, 81, 91, 104, 137, 148 CPR for Adults, 17-20
goals for, 77-78 Inserting a Nasopharyngeal Airway, 46-47
Problem solving, 3, 70 Inserting an Oropharyngeal Airway, 44-45
Procainamide, 107 Intraosseous Access (Drill), 59-62
Pulmonary embolism, 92b, 115t, 117 Intraosseous Access (Manual Insertion), 63-65
recognition of, 117 Manual Defibrillation, 53-54
treatment of, 117 Placing Electrodes for Electrocardiography, 50-52
Pulse oximetry, 32 Rapid Assessment for Adults, 15-16
Pulseless electrical activity (PEA), 112-113, 122, 158 Synchronized Cardioversion, 55-56
recognition of, 112-113 Transcutaneous Pacing, 57-58
treatment for, 122 Using a Bag-Valve-Mask Resuscitator—One
underlying causes of, 112 Provider, 48
Using a Bag-Valve-Mask Resuscitator—Two
QRS complex, 96, 97, 103, 106-107 Providers, 49
QT interval, 96, 97 Sotalol, 43t, 107
QTc. See Corrected QT interval STEMI. See ST-segment elevation myocardial
infarction
Rapid assessment, 10, 15-16, 76-77, 81, 91, 104, 137 STEMI Chain of Survival, 135

Index | 177
 ST segment, 96-97 causes of, 100, 104
ST-segment elevation myocardial infarction (STEMI), clinical signs of, 102
134-136, 139-140 treatment of, 104-105
recognition of, 135 pulseless ventricular tachycardia
treatment for, 135, 139-140 12-lead ECG criteria, 112
Stroke, 143, 144, 147 causes of, 112
Acute Stroke Chain of Survival, 144-145 clinical signs of, 112
code card for, 151-152 treatment of, 117-119
embolic, 144, 157
fibrinolytic therapy, 144, 150, 157
eligibility criteria for, 150
hemorrhagic, 144, 149, 157
intracerebral hemorrhage, 144, 158
ischemic, 144, 149-150, 158
mimics, 148, 148b
recommended diagnostic tests for patients with
suspected acute, 149b
stroke care facilities, 146b
thrombotic, 144, 159
Suctioning, 26
Supraventricular tachycardia, 101-102, 106
Synchronized cardioversion, 37-38
indications for, 37t

T wave, 96
Tachyarrhythmia, 101
approach to patient with, 105-107
code card for, 109
narrow complex, 101
wide complex, 101
Targeted temperature management (TTM), 128, 159
Teamwork, 3, 159
critical skills for, 69-70
importance of, 67
Tension pneumothorax, 116
as a cause of cardiac arrest, 115t
as a complication of BVM use, 31
Third-degree atrioventricular (AV) block, 100
Torsades de pointes, 103
Transcutaneous pacing, 38
indications for, 38
technique for, 57-58
TTM. See Targeted temperature management

Ultrasonography, in cardiac arrest, 114, 128t

Vagal maneuvers
indications for, 106
methods of performing, 107t
Vasopressor therapy, 127t
Ventilation-perfusion mismatch, 87-88, 159
Ventricular fibrillation, 112
Ventricular rate, calculation of, 97
Ventricular tachycardia, 102-103
monomorphic ventricular tachycardia, 158
12-lead ECG criteria, 103, 104
causes of, 100, 103
clinical signs of, 103
treatment of, 36-37, 106-107
polymorphic ventricular tachycardia, 158
12-lead ECG criteria, 103, 104

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