ACLS Study Guide

ACLS
STUDY GUIDE
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ACLS
STUDY GUIDE
Barbara Aehlert, MSEd, BSPA, RN
FIFTH EDITION
3251 Riverport Lane
St. Louis, Missouri 63043
ACLS STUDY GUIDE, FIFTH EDITION ISBN: 978-0-323-40114-2
Copyright © 2017, Elsevier Inc. All rights reserved.

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Notices
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PREFACE TO THE FIFTH EDITION
As Stiggins has observed, “Many of us grew up in classrooms in which our teachers believed that the way
you maximize learning is by maximizing anxiety. Assessment was always the intimidator. Many of our
teachers believed that if a little intimidation doesn’t work, turn up the heat—try a lot of intimidation.
This is why most adults today feel that being evaluated is a distinctly dangerous enterprise. It always left
us feeling vulnerable” (Stiggins, 2005, p. 18*).
I took my first Advanced Cardiac Life Support (ACLS) class many years ago. I felt terrified and lost
throughout the entire course. Although I had spent weeks studying before the course began, material now
seemed to be written in a foreign language. I could find no resources to “translate” the information into
something that was useful to me. The course consisted of very long lectures by instructors who read slides
and offered little useful insight. The most memorable part of the course was the “Patient Management”
station, in which each course participant was evaluated one-on-one by an instructor. (Those of you who
have been around a while are probably having flashbacks of those days.) I will never forget that experience.
Despite my preparation, as soon as the door closed behind me I was a mental wreck. The instructor
proceeded to methodically strip away any self-confidence I might have had in treating patients with car-
diac emergencies. I was able to answer the questions asked of me until I was presented with a patient who
had symptomatic bradycardia. Atropine had not worked (transcutaneous pacing was not readily available
back then), and the next drug recommended at that time was isoproterenol. I knew that. What I could
not recall was whether isoproterenol was given in mcg/min (correct) or mg/min. I took a “50/50” guess
and said mg/min. Because that was the wrong decision, I was told I had failed and would need to attend
another 2-day course.
Before driving home, I sat outside for a few minutes contemplating what had happened and what I
might have done to change the outcome. Then and there, promised myself I would become an ACLS
instructor someday and find a way to teach this information in a more user-friendly way. I vowed to teach
courses that were useful to practicing health care professionals and delivered in an environment in which
the participants looked forward to the class—instead of dreading it.
As the years passed, I did become an ACLS instructor and I loved it. At the conclusion of each course,
participants often wrote on their evaluation forms that a study guide would have been helpful in preparing
for class. Those suggestions resulted in my writing a few pages of information that ultimately became a
book—this book.
The ACLS Study Guide is a course preparation tool designed for paramedic, nursing, and medical
students, ECG monitor technicians, nurses, and other allied health personnel working in emergency
departments, critical care units, postanesthesia care units, operating rooms, and telemetry units. The fifth
edition of this book is based on the following scientific principles, treatment recommendations, and
guidelines:
• 2015 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care
• 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular
Care Science with Treatment Recommendations
• Other evidence-based treatment recommendations or sources cited in the references section of rele-
vant chapters.
*
Stiggins, R. J. (2005). An introduction to student-involved assessment for learning (5th ed.). Upper Saddle River, NJ: Pearson Prentice
Hall. v
vi Preface to the Fifth Edition
This book is designed for use with the American Safety and Health Institute (ASHI) ACLS Course.
It can also be used as supplementary material by those participating in ACLS courses offered by other
organizations.
I have made every attempt to provide information consistent with the current literature, including the
latest resuscitation guidelines; however, medicine is a dynamic field. Resuscitation guidelines change,
new medications and technology are being developed, and medical research is ongoing. As a result,
be sure to learn and follow local protocols as defined by your medical advisors. The author and publisher
assume no responsibility or liability for loss or damage resulting from the use of information contained
within.
I genuinely hope the content of this book is helpful to you, and I wish you success in your ACLS
course and clinical practice.
Sincerely,
Barbara Aehlert
ACKNOWLEDGMENTS
My sincerest thanks to Melissa Kinsey for her guidance throughout the development of this text. A spe-
cial thanks to the manuscript reviewers who provided insightful comments and suggestions.
A special thanks to these instructors, who share my ACLS teaching philosophy: Robert Aiken, CEP;
Andrew Baird, CEP; Eileen Blackstone, CEP; Lynn Browne-Wagner, RN; Randy Budd, CEP; Joanna
Burgan, CEP; Thomas Cole, CEP; Mike Connor, CEP; Paul Honeywell, CEP; James Johnson, CEP;
Stephen Knox, CEP; Bill Loughran, RN; Terence Mason, RN; Kevin McColm, CEP; Sean Newton,
CEP; Anthony Pino, RN; Jan Post, RN; Gary Smith, MD; Ed Tirone, CEP; and Maryalice
Witzel, RN.
vii
REVIEWERS FOR THE FIFTH EDITION
N.K. Alexander, EMT-P J.A. Nelson, DO, MS, FACOEP, FACEP

Instructor/Chief Operating Officer State EMS Medical Director
Wilton Emergency Squad, Inc Florida Department of Health
Saratoga Springs, New York Tallahassee, Florida
B. Cetanyan, RN S.L. Pinski, MD

Eastern Iowa Community College Head, Section of Cardiac Pacing and
Davenport, Iowa Electrophysiology
Robert and Suzanne Tomsich Department of
Cardiology
F.O. Garcia, EMT-P
Cleveland Clinic Florida
President
Weston, Florida
Professional EMS Education, LLC
Grand Junction, Colorado
B.R. Shade, EMT-P, EMS-I, AAS
AHA Program Instructor, Adjunct Faculty,
C. Horsfield, BA Firefighter
Paramedic Teaching Fellow Paramedic, retired Assistant Safety Director
School of Health Sciences Cleveland Clinic, Cuyahoga Community College,
University of Surrey Willoughby Fire Department, City of
Guildford, Surrey, UK Cleveland
Cleveland, Ohio
ix
ABOUT THE AUTHOR
Barbara Aehlert, MSEd, BSPA, RN, has been a registered nurse for more than 40 years, with clinical
experience in medical/surgical nursing, critical care nursing, prehospital education, and nursing educa-
tion. Barbara is an active CPR and ACLS instructor with a special interest in teaching basic dysrhythmia
recognition and ACLS to nurses and paramedics.
xi
CONTENTS
1 Emergency Cardiovascular Care 1

Introduction 1
Sudden Cardiac Death 2
Out-of-Hospital Cardiac Arrest 4
In-Hospital Cardiac Arrest 5
Chain of Survival 5
Out-of-Hospital Chain of Survival 5
In-Hospital Chain of Survival 8
Cardiopulmonary Resuscitation 10
Physiology of Chest Compressions 10
Barriers to Effective Cardiopulmonary Resuscitation 10
Feedback during Cardiopulmonary Resuscitation 11
Mechanical Chest Compression Devices 12
Patient Assessment 14
Primary Survey 15
Secondary Survey 17
Putting It All Together 18
Chapter Quiz 18
Chapter Quiz Answers 19
References 20
2 Airway Management 23
Introduction 23
Anatomy Review 25
Upper Airway 25
Lower Airway 27
The Patient with Respiratory Compromise 28
Patient Assessment 29
Oxygen Delivery Devices 32
Nasal Cannula 33
Simple Face Mask 34
Partial Rebreather Mask 35
Nonrebreather Mask 36
Manual Airway Maneuvers 37
Head Tilt–Chin Lift 37
Jaw Thrust 38
Suctioning 39
Airway Adjuncts 40
Oral Airway 40
Nasal Airway 42
xiii
xiv Contents
Positive Pressure Ventilation 44

Noninvasive Positive Pressure Ventilation 44
Mouth-to-Mask Ventilation 45
Bag-Mask Ventilation 47
Advanced Airways 49
Confirming Endotracheal Tube Placement 51
Chapter Quiz 53
References 60
3 Cardiac Anatomy and Electrophysiology 63

Introduction 63
Coronary Arteries 65
Cardiac Cells 66
Cardiac Action Potential 66
Depolarization 67
Repolarization 67
Phases of the Cardiac Action Potential 67
Refractory Periods 68
Conduction System 69
Sinoatrial Node 69
Atrioventricular Node and Bundle 70
Right and Left Bundle Branches 70
Purkinje Fibers 70
The Electrocardiogram 71
Electrodes 72
Leads 72
Electrocardiography Paper 76
Waveforms and Complexes 76
Segments and Intervals 77
Acute Coronary Syndromes 78
Chapter Quiz 79
References 81
4 Cardiac Arrest Rhythms 83

Introduction 83
Cardiac Arrest Rhythms 84
Ventricular Tachycardia 85
Ventricular Fibrillation 85
Asystole 88
Pulseless Electrical Activity 90
Defibrillation 91
Monophasic versus Biphasic Defibrillation 93
Transthoracic Impedance 94
Defibrillation Procedure 97
Automated External Defibrillation 99
Automated External Cardioverter-Defibrillators 100
Possible Complications 100
The Resuscitation Team 100
Team Leader Responsibilities 101
Team Member Responsibilities 102
Resuscitation Efforts 104
Helping the Caregivers 112
Contents xv

Chapter Quiz 113
References 125
5 Tachycardias 129
Introduction 129
Narrow-QRS Tachycardias 131
Sinus Tachycardia 131
Supraventricular Tachycardia 132
Wide-QRS Tachycardias 140
Ventricular Tachycardia 142
Irregular Tachycardias 143
Multifocal Atrial Tachycardia 143
Atrial Flutter 144
Atrial Fibrillation 145
Polymorphic Ventricular Tachycardia 148
Synchronized Cardioversion 150
Procedure 150
Chapter Quiz 153
References 165
6 Bradycardias 167
Introduction 167
Sinus Bradycardia 169
Junctional Escape Rhythm 169
Ventricular Escape Rhythm 171
Atrioventricular Blocks 172
First-Degree Atrioventricular Block 172
Second-Degree Atrioventricular Blocks 173
Third-Degree Atrioventricular Block 176
Transcutaneous Pacing 176
Indications 177
Procedure 178
Limitations 179
Possible Complications 180
Chapter Quiz 181
References 191
7 Acute Coronary Syndromes 193

Introduction 193
Pathophysiology of Acute Coronary Syndromes 194
Myocardial Ischemia, Injury, and Infarction 196
Myocardial Ischemia 196
Myocardial Injury 199
Myocardial Infarction 200
xvi Contents
Patient Evaluation 201

Patient History 201
Atypical Presentation 202
Physical Examination 203
Electrocardiogram Findings 204
Cardiac Biomarkers 214
Imaging Studies 215
Initial Management of Acute Coronary Syndromes 215
Prehospital Management 215
Emergency Department Management 216
Pharmacologic Therapies 217
Reperfusion Therapies 224
Chapter Quiz 227
References 235
8 Acute Ischemic Stroke 237

Introduction 237
Definition of Stroke 239
Anatomy Review 239
Stroke Types 240
Subarachnoid Hemorrhage 240
Intracerebral Hemorrhage 241
Ischemic Stroke 242
Transient Ischemic Attack 243
Stroke Systems of Care 243
Public Education 244
Emergency Medical Services 244
Stroke Centers 246
Chapter Quiz 251
References 256
9 Post Test 259

Post test Answers 269
References 276
Glossary 277
Index 281
CHAPTER 1
Emergency
Cardiovascular Care
INTRODUCTION
Heart disease is a broad term that refers to conditions that affect the heart, and it is a leading cause of
death for both men and women in the United States. Because someone in the United States experiences a
coronary event every 25 seconds, the likelihood of encountering a patient who requires basic life support
(BLS) or advanced cardiac life support (ACLS) care is high (Roger, et al., 2012).
Just as BLS is a systematic way of providing care to a choking victim or to someone who needs car-
diopulmonary resuscitation (CPR), ACLS is an orderly approach to providing advanced emergency care
to a patient who is experiencing a cardiac-related problem. This chapter discusses risk factors for coronary
artery disease (CAD), sudden cardiac death (SCD), the Chain of Survival, and a systematic approach to
patient assessment.
D E S I R E D RE S U L T S
G O A L Given a patient situation, and working in a team setting, direct or perform an initial patient
assessment, identify common barriers to effective CPR, and identify actions that can be taken to
overcome them.
LEARNING OBJECTIVES
After completing this chapter, you should be able to:
1. Define cardiovascular collapse, cardiac arrest, sudden cardiac death, and sudden cardiac
arrest.
2. Discuss the phases of a cardiac arrest.
3. Discuss the prearrest factors that influence survival in out-of-hospital cardiac
arrest (OHCA).
4. Identify the initial cardiac rhythms that are typically recorded in OHCA.
5. Discuss the prearrest factors that influence survival in in-hospital cardiac arrest (IHCA).
6. Identify the initial cardiac rhythms that are typically recorded in IHCA.
7. Describe the links in the Chain of Survival.
8. Discuss the requirements for performing high-quality CPR.
9. Discuss common barriers to effective CPR and possible actions that can be taken to
overcome them.
10. Explore the use of feedback devices during CPR. 1
2 CHAPTER 1 Emergency Cardiovascular Care
11. Discuss the use of continuous end-tidal carbon dioxide (EtCO2) monitoring during
resuscitation efforts.
12. Discuss the use of mechanical chest compression devices during resuscitation efforts.
13. State three areas to assess when forming a general impression of a patient.
14. Differentiate between the purposes and components of the primary and secondary
surveys.
15. Discuss a systematic approach to the initial emergency care of an unresponsive patient.
LEARNING PLAN
• Whether you are preparing for your first ACLS course or your tenth, schedule time to study
and review before the course. Studying in half-hour intervals with 10-minute breaks allows
a reasonable period for both learning and relaxation.
• Read this chapter before class. Take the time to highlight important concepts as you read.
• Develop and use flashcards, flowcharts, and mnemonics to help enhance your retention of
the information presented.
• Complete the chapter quiz and review the quiz answers provided.
KEY TERMS
Automated external defibrillator (AED) A machine with a sophisticated computer system
that analyzes a patient’s heart rhythm using an algorithm to distinguish shockable rhythms
from nonshockable rhythms and provides visual and auditory instructions to the rescuer to
deliver an electrical shock if a shock is indicated.
Cardiopulmonary (cardiac) arrest The absence of cardiac mechanical activity, which is
confirmed by the absence of a detectable pulse, unresponsiveness, and apnea or agonal,
gasping breathing.
Cardiovascular collapse A sudden loss of effective blood flow that is caused by cardiac and/
or peripheral vascular factors that may reverse spontaneously (eg, syncope) or only with
interventions (eg, cardiac arrest).
Cardiovascular disease (CVD) A collection of conditions that involve the circulatory system,
which contains the heart (cardio) and blood vessels (vascular), including congenital
cardiovascular diseases.
Chain of Survival The essential elements of a system of care that are necessary to link the
victim of sudden cardiac arrest with survival.
Coronary artery disease (CAD) Disease affecting the arteries that supply the heart muscle
with blood.
Coronary heart disease (CHD) Disease of the coronary arteries and resulting complications,
such as angina pectoris and acute myocardial infarction.
Heart disease A broad term that refers to conditions affecting the heart.
Risk factors Traits and lifestyle habits that may increase a person’s chance of developing a
disease.
Sudden cardiac death (SCD) A natural death of cardiac cause that is preceded by an abrupt
loss of consciousness within 1 hour of the onset of an acute change in cardiovascular
status; sudden cardiac arrest is a term commonly applied to such an event when the patient
survives.
SUDDEN CARDIAC DEATH

[Objectives 1, 2]
Cardiovascular disease (CVD) is a collection of conditions that involve the circulatory system, which
contains the heart (cardio) and blood vessels (vascular), including congenital CVD. More than one in
three American adults has one or more types of cardiovascular disease (Roger, et al., 2012). The preven-
tion of CVD requires the management of risk factors. Risk factors are traits and lifestyle habits that may
increase a person’s chance of developing a disease. Some risk factors can be modified by specific,
CHAPTER 1 Emergency Cardiovascular Care 3
preventable measures. Risk factors that cannot be modified are called nonmodifiable or fixed risk factors.
Contributing risk factors are thought to lead to an increased risk of heart disease, but their exact role has
not been defined (Table 1.1).
Coronary heart disease (CHD) refers to disease of the coronary arteries and resulting complications,
such as angina pectoris and acute myocardial infarction. Approximately one of every six deaths in the
United States was caused by CHD in 2008 (Roger, et al., 2012). Coronary artery disease (CAD) affects
the arteries that supply the heart muscle with blood. More than 90% of CAD events occur in individuals
who have at least one risk factor (Mack & Gopal, 2014). The relationships among CAD and its major
sequelae are shown in Fig. 1.1.
Cardiovascular collapse is a sudden loss of effective blood flow caused by cardiac factors, peripheral
vascular factors, or both, that may reverse spontaneously (eg, syncope) or only with interventions
(eg, cardiac arrest) (Myerburg & Castellanos, 2012). Cardiopulmonary (cardiac) arrest is the absence
of cardiac mechanical activity, which is confirmed by the absence of a detectable pulse, unresponsiveness,
and apnea or agonal, gasping breathing. Gasping is abnormal breathing, is common during the first few
minutes of primary cardiac arrest, and is a sign of adequate blood flow to the brainstem (Ewy, 2012).
Respiratory efforts can persist for 1 minute or longer after the onset of a cardiac arrest (Myerburg &
Castellanos, 2012).
TABLE 1.1 Cardiovascular Disease Risk Factors

Nonmodifiable (Fixed) Factors Modifiable Factors Contributing Factors
• Age • Diabetes mellitus • Alcohol intake
• Family history of cardiovascular • Elevated serum cholesterol levels • Inflammatory markers
disease • Hypertension • Psychosocial factors
• Gender • Metabolic syndrome • Sleep apnea
• Race • Obesity • Stress
• Physical inactivity
• Tobacco exposure
• Unhealthy dietary habits
CORONARY ARTERY DISEASE
Acute plaque Myocardial ischemia

Myocardial
change; coronary of increased severity
ischemia
artery thrombosis and duration
MYOCARDIAL INFARCTION
with muscle loss
and arrhythmias
Infarct Ventricular Hypertrophy,

healing remodeling dilation of
viable muscle
Chronic ischemic heart disease
Congestive heart failure
SUDDEN CARDIAC DEATH
Fig. 1.1 The relationships among coronary artery disease and its major sequelae. (From Kumar V, Abbas AK, Aster JC: Rob-
bins basic pathology, ed 9, Philadelphia, 2013, Saunders.)
TABLE 1.2 Phases of Cardiac Arrest

Phase Interval Focus of Care
Prearrest Period before the arrest Identify, anticipate, and manage factors that may result in
cardiac arrest (eg, use of rapid response teams to
recognize and treat patients at risk of deterioration)
No flow Untreated cardiac arrest Prompt initiation of basic life support upon recognition of the
arrest by a bystander or health care professional
Low flow Onset of cardiopulmonary Delivery of high-quality chest compressions to optimize
resuscitation myocardial and cerebral perfusion
Postresuscitation Return of spontaneous Identify and treat the cause of the arrest, preserve
circulation neurologic function, and support end organ perfusion and
function
Sudden cardiac death (SCD) is a natural death of cardiac cause that is preceded by an abrupt loss of
consciousness within 1 hour of the onset of an acute change in cardiovascular status (Myerburg &
Castellanos, 2012). SCD is often the patient’s first and only symptom of heart disease (O’Connor,
et al., 2010). For others, warning signs may be present up to 1 hour before the actual arrest. Sudden cardiac
arrest is a term commonly applied to such an event when the patient survives (Taniguchi, et al., 2012).
Four phases of cardiac arrest have been described, each with unique physiology and treatment strategies
(Topjian, et al., 2013) (Table 1.2).
Heart rhythms that may be observed in a cardiac arrest include the following:
1. Pulseless ventricular tachycardia (pVT), in which the electrocardiogram (ECG) displays a wide, reg-
ular QRS complex at a rate faster than 120 beats per minute (beats/min).
2. Ventricular fibrillation (VF), in which irregular chaotic deflections that vary in shape and height are
observed on the ECG but there is no coordinated ventricular contraction.
3. Asystole, in which no cardiac electrical activity is present.
4. Pulseless electrical activity (PEA), in which electrical activity is visible on the ECG but central pulses
are absent.
pVT and VF are shockable rhythms. This means that delivering a shock to the heart by means of a
defibrillator may result in termination of the rhythm. Asystole and PEA are nonshockable rhythms.
Out-of-Hospital Cardiac Arrest

[Objectives 3, 4]
Most nontraumatic OHCAs in the United States are the result of a primary cardiac arrest, rather than
secondary to respiratory arrest (Ewy & Bobrow, 2016). A primary cardiac arrest is an unexpected wit-
nessed (ie, seen or heard) collapse in an individual who is not responsive (Ewy, 2012). Seventy percent
of nontraumatic OHCAs occur in the home (Centers for Disease Control and Prevention, 2014). Of
these arrests, 50.3% are unwitnessed, 37.7% are witnessed by a bystander, and 12.1% are witnessed
by a 9-1-1 responder (Centers for Disease Control and Prevention, 2014).
Prearrest factors that influence survival in OHCA include the following (Boyd & Perina, 2012;
Martinez, 2012):
• Performance of bystander CPR
• Mode of arrest (ie, respiratory versus cardiac)
• Witnessed arrest
• Age (older age associated with worsened survival)
• Initial presenting rhythm of VF
• Short response times to defibrillation
• Location of the arrest (survival is 3 to 4 times more likely if an arrest occurs in a public place; survival is
6 times more likely if the arrest occurs in the workplace)
• Time of day (peak incidence occurs between 8 am and 10 am; survival to hospital discharge lowest for
arrests between midnight and 6 am)
When an OHCA occurs, the initial rhythm recorded by emergency personnel is generally considered
the electrical mechanism of the arrest (Myerburg & Castellanos, 2012). This information is important
because it affects patient outcome. Patients who are in sustained VT at the time of initial contact have the
best outcome, whereas those who present with a bradyarrhythmia or asystole at initial contact have the
worst prognosis (Myerburg & Castellanos, 2012). When the initial rhythm recorded is VF, the patient’s
outcome is intermediate between the outcomes associated with sustained VT and those of bradyarrhyth-
mia and asystole (Myerburg & Castellanos, 2012). Data from nontraumatic OHCAs in 2014 indicate
that asystole was the most common initial cardiac arrest rhythm (45.6%), followed by an idioventricular
rhythm/PEA (21.4%), VF/pVT/unknown shockable rhythm (20.4%), and an unknown nonshockable
rhythm (12.5%) (Centers for Disease Control and Prevention, 2014). Overall survival from nontraumatic
OHCA to hospital admission was 28.3%, and overall survival to hospital discharge was 10.8% (Centers
for Disease Control and Prevention, 2014).
In-Hospital Cardiac Arrest

[Objectives 5, 6]
The most common causes of IHCA include cardiac arrhythmia, acute respiratory insufficiency, and
hypotension (Morrison, et al., 2013) with predictable deterioration before the event (eg, tachypnea,
tachycardia) (Kronick, et al., 2015). Prearrest factors that influence survival in IHCA include the follow-
ing (Martinez, 2012):
• Initial presenting rhythm of VF
• Time to CPR and defibrillation (survival is 33% when CPR is started within 1 minute of arrest versus
14% if the time interval is greater than 1 minute; survival is 38% in pVT/VF arrests when defibrillation
is performed within 3 minutes versus 21% if the time interval is greater than 3 minutes)
• Location (survival is highest if an arrest occurs in an intensive care unit [ICU; witnessed and mon-
itored arrest, advanced life support {ALS} immediately available], better survival rates for wards that
have more than 5 cardiac arrests per year)
• Time of day (arrests that occur at night on general hospital wards have one-half the likelihood of
survival)
• AED use
With regard to adult IHCA, asystole and PEA are more common than VF or pVT as the initial
rhythm (Morrison, et al., 2013). In a large study of adult IHCA patients, only 23% presented with shock-
able rhythms (Wallace, et al., 2013). An analysis of multicenter IHCAs published in 2010 observed that
the onset of the IHCA was witnessed in 79.2% of instances and approximately 32% of IHCAs occurred
within 24 hours of admission, 34% occurred within 1 week of admission, and 23% occurred more than
1 week after admission (Larkin, et al., 2010). Generally, IHCA has a better outcome than OHCA with
22.3% to 25.5% of adult patients surviving to discharge (Kleinman, et al., 2015).
The terms code and code blue are often used in hospitals when a patient experiences a respiratory arrest,
a cardiac arrest, or a cardiac dysrhythmia that is associated with unresponsiveness. When a code blue is
called, usually by means of an overhead paging system, a predesignated team of health care professionals
is deployed to the patient’s bedside to provide lifesaving interventions. The configuration of the resus-
citation team and the responsibilities of each team member are discussed in Chapter 4.
CHAIN OF SURVIVAL
[Objective 7]
The Chain of Survival represents the essential elements of a system of care that are necessary to link the
victim of sudden cardiac arrest with survival. Although links of the Chain have been used for almost
25 years to depict the interrelated steps necessary with regard to an adult cardiac arrest both outside
and inside the hospital setting, the 2015 resuscitation guidelines depict two separate chains because there
are differences in these systems of care. Time is critical when dealing with a victim of sudden cardiac
arrest; a weak or missing link in either Chain of Survival can reduce the likelihood of a positive outcome.
Out-of-Hospital Chain of Survival

[Objective 7]
The links in the out-of-hospital Chain of Survival for adults include early recognition and activation,
early CPR, rapid defibrillation, effective ALS, and integrated post–cardiac arrest care.
Early Recognition and Activation

The first link in the out-of-hospital Chain of Survival is early recognition and activation of the emergency
medical services system (EMSS). When a cardiac emergency occurs, the patient (or a family member or
bystander) must identify his or her signs and symptoms, recognize that they are related to a heart con-
dition, and seek medical assistance in the hope of preventing cardiac arrest. Delays in seeking assistance
and delays in the arrival of assistance ultimately affect patient outcome.
Emergency dispatchers, who are located at public service access points, are the link between the
call for help and the arrival of medical assistance (Kronick, et al., 2015). Dispatchers are trained to
recognize the caller’s description of a potential heart attack or cardiac arrest and to provide real-time
CPR instructions over the phone if necessary while quickly sending appropriately trained and equipped
emergency medical services (EMS) personnel to the scene. Some emergency medical dispatch
protocols include telephone instructions for guiding an untrained rescuer in performing
compression-only CPR. In some areas, emergency dispatchers have used social media to summon
volunteer rescuers to the scene to provide bystander CPR until the arrival of EMS professionals
(Kronick, et al., 2015).
Early Cardiopulmonary Resuscitation

After recognizing that an emergency exists, the scene must be assessed to ensure that it is safe to enter. If
the scene is safe, the patient must be quickly assessed for life-threatening conditions and the nature of the
emergency determined.
CPR is a part of BLS. BLS includes the recognition of signs of cardiac arrest, heart attack, stroke, and
foreign body airway obstruction (FBAO); the relief of FBAO; CPR; and defibrillation with an AED.
BLS must be provided until advanced medical help arrives and assumes responsibility for the patient’s
care. Necessary care may include the following:
• Patient positioning
• CPR for victims of cardiac arrest
• Defibrillation with an AED
• Rescue breathing for victims of respiratory arrest
• Recognition and relief of FBAO
If CPR is necessary, compressions on adult victims of cardiac arrest should be performed at a rate of
100 to 120 compressions/minute with a compression depth of at least 2 inches (5 cm) but no more than
2.4 inches (6 cm) (Kleinman, et al., 2015).
Rapid Defibrillation
When an individual experiences a cardiac arrest, the likelihood of successful resuscitation is affected
by the speed with which CPR and defibrillation are performed. The goal for providing the first
shock for sudden cardiac arrest resulting from VF or pVT is within 3 minutes of collapse (Link,
et al., 2010).
The American Heart Association has promoted the development of AED programs to improve sur-
vival from sudden cardiac arrest since 1995. An automated external defibrillator (AED) is a machine
with a sophisticated computer system that analyzes the patient’s heart rhythm (Figs. 1.2 to 1.4). The AED
uses an algorithm to distinguish shockable rhythms from nonshockable rhythms. If the AED detects a
shockable rhythm, it provides visual and auditory instructions to the rescuer to deliver an electrical shock.
Defibrillation performed by citizens (such as flight attendants, casino security officers, athletic or golf club
employees, and ushers at sporting events) at the scene is called public access defibrillation.
Some AEDs:
• Have CPR pads available that are equipped with a sensor that detects the rate and depth of chest
compressions. If the rate or depth of compressions is inadequate, the machine provides voice prompts
to the rescuer.
• Provide voice instructions in adult and infant/child CPR at the user’s option. A metronome function
encourages rescuers to perform chest compressions at the recommended rate per minute.
• Are programmed to detect spontaneous movement by the patient or others.
• Have adapters available for many popular manual defibrillators, enabling the AED pads to remain on
the patient when patient care is transferred.
• Can be configured to allow ALS personnel to switch to a manual mode, allowing more decision-
making control.
• Are equipped with a small screen that allows the rescuer to view the patient’s cardiac rhythm, assisting
in identification of shockable versus nonshockable rhythms.
Fig. 1.2 The Philips HeartStart FR3 AED. (Courtesy of Philips Healthcare. All rights reserved.)
Fig. 1.3 The Cardiac Science Powerheart G3 Plus automated external defibrillator. (Courtesy Cardiac Science Corporation,
Waukesha, WI)
Fig. 1.4 The LIFEPAK® 1000 Defibrillator. (Courtesy Physio-Control, Inc., Redmond, WA)
• Can detect the patient’s transthoracic resistance through the adhesive pads applied to the patient’s
chest. The AED automatically adjusts the voltage and length of the shock, thus customizing how
the energy is delivered to that patient.
• Are equipped with a pediatric attenuator (ie, a pad-cable system or key). When the attenuator is
attached to the AED, the machine recognizes the pediatric cable connection and automatically adjusts
its defibrillation energy accordingly.
Defibrillation is discussed in more detail in Chapter 4.
Effective Advanced Life Support

Outside the hospital, early advanced care is provided by paramedics (and/or nurses) arriving on the scene.
Prehospital professionals work quickly to stabilize the patient by providing ventilation support, vascular
access, and giving emergency medications, among other interventions.
Integration of Post–Cardiac Arrest Care

Prehospital professionals transport and then transfer the patient to the closest most appropriate emergency
department (ED) or directly to a specialized cardiac arrest center where definitive care can be provided.
In-Hospital Chain of Survival

[Objective 7]
The links in the in-hospital Chain of Survival for adults include surveillance and prevention of cardiac
arrest, prompt notification and response when a cardiac arrest occurs, the performance of high-quality
CPR, prompt defibrillation, and intra-arrest and post–cardiac arrest care (Kronick, et al., 2015).
Surveillance and Prevention

A cardiac arrest experienced by a hospitalized adult is often preceded by warning signs and symptoms
that suggest physiologic deterioration such as tachypnea, tachycardia, and hypotension (Tibballs & van
der Jagt, 2008). Recognizing that early detection and treatment of the patient who demonstrates signs of
clinical deterioration may prevent cardiac arrest and improve patient outcome, the concept of a Rapid
Response System (RRS) emerged. The RRS is mobilized by other hospital staff based on predetermined
criteria for activation of the team. The Joint Commission National Patient Safety Goals require hospitals
to implement systems that enable health care workers to directly request additional assistance from spe-
cially trained individuals when the patient’s condition appears to be worsening (Joint Commission on
Accreditation of Healthcare Organizations, 2007).
Several types of responding teams exist, and large hospitals may require more than one response team.
It has been suggested that the term medical emergency team (MET) be used for teams that are generally led
by physicians and have the ability to: (1) prescribe therapy; (2) place central vascular lines; (3) initiate
ICU-level care at the bedside; and (4) perform advanced airway management (Devita, et al., 2006;
McCurdy & Wood, 2012). It is recommended that the term rapid response team (RRT) be used to
describe a team without all four of those abilities that performs a preliminary evaluation of a patient
and summons additional help or facilitates patient transfer to a higher level of care if warranted
(McCurdy & Wood, 2012). RRTs typically consist of multidisciplinary members such as a physician
(eg, critical care or hospitalist), a critical care nurse, and a respiratory therapist who respond to emergen-
cies, proactively identify and evaluate patients at risk for decompensation, educate and act as a liaison to
ward staff, and follow up on patients who have been discharged from the ICU. In addition to their role in
identifying prearrest conditions, studies have shown that MET and RRT services have also contributed
to the detection and management of medical errors, surgical postoperative morbidity, and clarification of
do not resuscitate status (Tibballs & van der Jagt, 2008).
Several scoring systems for detecting warning signs of patient deterioration exist, and they are used
as tools to assist in determining when the RRT should be activated. For example, with one type of scoring
system, the RRT is activated when a single vital sign or clinical abnormality is outside a predetermined
range (Box 1.1). With the Modified Early Warning Score (MEWS) points are assigned based on the
degree of derangement of ventilatory rate, heart rate, systolic blood pressure (BP), mental status, temper-
ature, and hourly urine output. Regardless of the type of scoring system used, the decision to activate the
RRT based on a score is ultimately the responsibility of the bedside clinician (McCurdy & Wood, 2012).
Adoption of an RRT necessitates teaching and staff empowerment because it usually “involves
substituting a traditional response reserved for cardiac or respiratory arrest (eg, Code Blue) with a system
that responds to the early onset of signs and symptoms that may lead to these conditions” (Tibballs & van
BOX 1.1 Rapid Response System Calling Criteria

• Abnormal or worsening respiratory symptoms • Progressive lethargy
• Acute change in mental status • Staff concern about the patient’s condition
• Chest pain or discomfort unrelieved by • Systolic blood pressure greater than 180 mm
nitroglycerin Hg or less than 90 mm Hg
• Heart rate greater than 140 beats/minute or • Threatened airway
less than 40 beats/minute • Urine output less than 50 mL over 4 hours
• Oxygen saturation less than 90% despite • Ventilatory rate greater than 28 breaths/
supplemental oxygen minute or less than 8 breaths/minute
der Jagt, 2008). Barriers to activation of the RRT by nurses have been identified and include the follow-
ing (McCurdy & Wood, 2012):
• The nurse may not know whom to contact when a patient’s condition deteriorates.
• The nurse may fear blame if activation of the RRS is later deemed unnecessary.
• Nurses often observe patients who briefly exhibit abnormal vital signs that spontaneously normalize.
Even when a dedicated response team exists within an institution, such teams are usually not imme-
diately available and most medical emergencies must be managed by ad-hoc teams (Monteleone & Lin,
2012). After-hours cardiac arrests (ie, evening and weekend) are associated with twice the mortality of
office-hour arrests, which is thought to be a result of both the availability and the experience of staff
(Herlitz, et al., 2002; Monteleone & Lin, 2012).
Studies show considerable variation in patient outcome data with regard to the use of RRTs. In adults,
some studies demonstrate reductions in both IHCA and mortality, others demonstrate reductions in
IHCA without a significant change in mortality, and still others show no significant differences in either
IHCA or mortality (McCurdy & Wood, 2012). The 2015 resuscitation guidelines note that for adult
patients, RRTs or MET systems can be effective in reducing the incidence of cardiac arrest, particularly
in general care wards; pediatric MET/RRT systems may be considered in facilities where children with
high-risk illnesses are cared for on general in-patient units; and the use of early warning sign systems may
be considered for adults and children (Kronick, et al., 2015).
Notification and Response

Every member of the hospital staff should know how to recognize a cardiac arrest and know how to sum-
mon assistance when such an event occurs. Prompt notification and activation of the code team may
include pressing a “code button” at the patient’s bedside, calling a specific phone extension, or use of a
“quick dial button” located on telephones within the facility. When the operator is reached, the type
of emergency and its location are stated. Once the operator is notified of the emergency, members of
the code team typically are activated by means of cell phones and/or a hospital-wide public address system.
Cardiopulmonary Resuscitation
Although cardiac arrests and the performance of CPR are relatively uncommon in in-hospital environ-
ments (Kronick, et al., 2015), it is essential that hospital staff be able to perform high-quality CPR.
Because training may not be adequate to ensure optimal performance, strategies such as timely access
to equipment, visual reminders, regular testing, and point-of-care feedback have been suggested as
methods to improve the translation of resuscitation guidelines into practice during cardiac arrest
(Morrison, et al., 2013).
Prompt Defibrillation
It has been estimated that about half of all IHCAs occur outside the ICU (Morrison, et al., 2013).
Because it can take several minutes for code team members to arrive with a defibrillator, the strategic
deployment of AEDs throughout the facility can aid in achieving prompt defibrillation, with the goal
being the delivery of the first shock within 3 minutes of collapse (Link, et al., 2010).
Intra-Arrest and Post–Cardiac Arrest Care

During the arrest, and under the direction of a team leader, the code team works to stabilize the patient by
continuing high-quality CPR, performing defibrillation for pVT/VF, obtaining vascular access and giv-
ing medications, performing advanced airway management procedures when warranted, and providing
ventilation support, among other interventions. If a return of spontaneous circulation (ROSC) is

achieved, post–cardiac arrest care, including advanced monitoring and targeted temperature manage-
ment, is provided by a multidisciplinary team in an ICU. Post–cardiac arrest care is discussed in more
detail in Chapter 4. After the resuscitation, a debriefing of the resuscitation team is recommended to
discuss areas such as psychomotor skill issues, cognitive issues, team issues, family emotional issues,
and professional staff emotional issues (Kronick, et al., 2015).
CARDIOPULMONARY RESUSCITATION
[Objective 8]
When an adult develops VF and suddenly collapses, his or her lungs, pulmonary veins, left heart, aorta,
and arteries contain oxygenated blood (Ewy, 2005; Meursing, et al., 2005). After recognizing that CPR
is indicated, chest compressions should be the initial action performed (instead of opening the airway or
giving ventilations) when starting CPR in victims of sudden cardiac arrest. Performing chest compres-
sions before ventilations enables better delivery of the oxygen that is already present in the lungs and
arterial circulation to the heart and brain (Kern & Mostafizi, 2009).
Physiology of Chest Compressions

[Objective 8]
During CPR, myocardial blood flow is dependent on coronary perfusion pressure, which is generated
when performing chest compressions. Coronary perfusion pressure is a key determinant of the success
of resuscitation, and adequate cerebral and coronary perfusion pressures are critical to neurologically nor-
mal survival (Ewy, 2005). During the low-flow phase of cardiac arrest, the only source of coronary and
cerebral perfusion pressures comes from the BP generated by high-quality chest compressions (Berg,
et al., 2010). High-quality chest compressions require compressing the chest at an adequate rate and
depth, allowing full chest recoil after each compression (enabling the heart to refill with blood), mini-
mizing interruptions in chest compressions, and avoiding excessive ventilation (Kleinman, et al., 2015).
Cardiac output is the product of stroke volume and heart rate. During CPR, the force of compressions
is a major determinant of stroke volume and the rate of compressions is the determinant of heart rate
(Berg, et al., 2010). Current resuscitation guidelines recommend a compression rate for adults of 100
to 120 per minute (Kleinman, et al., 2015). Because stroke volume also depends on preload, an adequate
blood volume is necessary for adequate perfusion. An adequate perfusion pressure cannot be obtained if
the patient’s blood volume is low, such as that caused by blood loss or significant venous dilation (eg,
hypovolemic shock, septic shock). These patients may require additional intravascular fluid volume to
generate an adequate stroke volume with chest compressions (Berg, et al., 2010).
During the compression (systolic) phase of chest compression, it is essential that the compressions
delivered be of sufficient depth to deliver adequate stroke volume and cerebral perfusion pressure
(Benner, et al., 2011). Current resuscitation guidelines recommend a compression depth for adults of
at least 2 inches (5 cm), not to exceed 2.4 inches (6 cm) (Kleinman, et al., 2015). During the release
(diastolic) phase of chest compression, intrathoracic pressure is low. This helps increase the return of
venous blood into the chest. If intrathoracic pressure is too high, venous return is inhibited.
ACLS Pearl
Hyperventilation is a common cause of excessive intrathoracic pressure during CPR. It is important
to ventilate a patient in cardiac arrest at an age-appropriate rate and with just enough volume to see
the patient’s chest rise gently. Ventilating a cardiac arrest patient too fast or with too much volume
results in excessive intrathoracic pressure, which results in decreased venous return into the chest,
decreased coronary and cerebral perfusion pressures, diminished cardiac output, and decreased
rates of survival.
Barriers to Effective Cardiopulmonary Resuscitation

[Objective 9]
Numerous studies have shown that the quality of CPR during actual resuscitation often falls short of
established resuscitation guidelines in both out-of-hospital and in-hospital settings. Possible factors
influencing these deficiencies include infrequent training, lack of awareness of the quality of CPR during
resuscitation, and inadequate team leadership during resuscitation efforts (Abella, et al., 2014).
Rescuer fatigue has been identified as an important potential contributor to poor CPR quality
(Brooks, et al., 2014). Rescuer fatigue contributes to an inadequate depth of compressions, compromises
coronary perfusion pressure, and also leads to inadequate chest recoil (Reynolds, et al., 2012). Research
has shown that the depth of compressions is compromised after just 1 minute of performing CPR
(Hightower, et al., 1995; Zhang, et al., 2013) and rescuers tend not to recognize their own fatigue until
after approximately 5 minutes of CPR (Reynolds, et al., 2012). To minimize fatigue, rescuers delivering
chest compressions should rotate every 2 minutes. Ideally, the switch should be accomplished in less than
5 seconds and should be done while another intervention is being performed (eg, defibrillation).
The brain and heart are sensitive to ischemic injury. Because it takes time to build up cerebral and
coronary perfusion pressures, even short pauses (4 to 5 seconds) in chest compressions have resulted
in a dramatic drop-off in cerebral and coronary perfusion pressures, thereby reducing blood flow to
the brain and heart (Ewy, 2005; Wik, et al., 2005). When chest compressions are stopped during cardiac
arrest, no blood flow is generated. Even after compressions are resumed, several chest compressions are
needed to restore coronary perfusion pressure.
ACLS Pearl
When caring for a patient in cardiac arrest it is essential that interruptions in chest compressions for
cardiac rhythm analysis, vascular access, airway management, and other interventions be kept to a
minimum. For example, charging the defibrillator before the end of a compression cycle in anticipa-
tion of delivering a shock is one technique that is often used to minimize compression interruptions.
It is important to allow the chest wall to rebound to its normal position after each compression. Incom-
plete chest wall recoil is common when performing CPR, particularly when rescuers are fatigued, and can
occur when a rescuer leans over the patient’s chest (Meaney, et al., 2013). Incomplete recoil results in
higher intrathoracic pressure, decreased coronary perfusion pressure, decreased myocardial blood flow,
decreased cerebral perfusion, and decreased cardiac output (Rajab, et al., 2011; Reynolds, et al., 2012).
Feedback during Cardiopulmonary Resuscitation

[Objectives 10, 11]
Feedback devices provide voice or visual cues about the quality of CPR that are measured and reported
by a defibrillator, a handheld device, or alternative technology (Morrison, et al., 2013). For example, a
metronome can be used to guide the rate and rhythm of chest compressions using auditory or visual
prompting at regular intervals. Timing lights may be used to prompt or time ventilations.
Some feedback devices enable information about CPR quality (eg, chest compression rate, depth, chest
wall recoil) to be fed back to the rescuer using a sternal force detector or accelerometer (or both) through an
external device placed between the rescuer’s hands and the patient’s sternum (Sutton, et al., 2012). With
some feedback-enabled defibrillators, audible voice prompts and visual messages on the monitor screen are
triggered when measured chest compressions or ventilations are interrupted or when they deviate from
preprogrammed resuscitation guideline parameters (Fig. 1.5). It is important that the chest compressor
have an unobstructed view of the monitor screen throughout a resuscitation effort to enhance the effec-
tiveness of audiovisual feedback (Bobrow, et al., 2013). Some defibrillators also possess technology that
filters CPR artifact, allowing the rescuer to analyze a patient’s cardiac rhythm without interrupting CPR
(Fig. 1.6). Although studies to date have not demonstrated a significant improvement in favorable
neurologic outcome or survival to hospital discharge with the use of CPR feedback devices during actual
cardiac arrest events, current resuscitation guidelines reflect that it may be reasonable to use audiovisual
feedback devices during CPR for real-time optimization of CPR performance (Kleinman, et al., 2015).
For intubated patients, continuous EtCO2 monitoring should be used to monitor the quality of com-
pressions during resuscitation efforts. When ventilation is constant, EtCO2 reflects lung perfusion and
therefore cardiac output (McGlinch & White, 2009). EtCO2 falls sharply with the onset of cardiac
arrest, increases when effective CPR is delivered (generally 10 to 20 millimeters of mercury [mm
Hg]), and returns to physiologic levels (35 to 40 mm Hg) with the ROSC (Abella, et al., 2014).
Low EtCO2 values (ie, less than 10 mm Hg) during resuscitation efforts indicate the need to explore
factors that are hindering effective CPR (eg, rescuer fatigue, cardiac tamponade, pneumothorax, bron-
chospasm, mucus plugging of the endotracheal tube (ETT), kinking of the ETT, alveolar fluid in the
Fig. 1.5 Several defibrillators, such as the MRx-QCPR shown here, are equipped with a chest compression pad that enables
monitoring of the quality of chest compressions and provides corrective feedback to rescuers. (Courtesy of Philips Healthcare.
All rights reserved.)
Fig. 1.6 This Zoll R Series Monitor defibrillator filters cardiopulmonary resuscitation artifact, enabling the rescuer to analyze a
patient’s cardiac rhythm without interrupting chest compressions. (Courtesy Zoll Medical Corporation, Chelmsford, MA)
ETT, an airway with an air leak, hyperventilation) (Kodali & Urman, 2014; Link, et al., 2015). As the
rescuer performing chest compressions tires, a gradual decrease in waveform height can be observed on
the monitor screen, indicating the need to change rescuer positions. A sudden sustained increase in
EtCO2 during CPR is an indicator of ROSC. In addition to improving the quality of CPR delivered,
EtCO2 monitoring allows clinicians to perform chest compressions without pausing for pulse checks
unless a sudden increase in EtCO2 is observed, at which time ROSC can be verified (Cunningham,
et al., 2012). When feasible, additional physiologic parameters that may be used to monitor and optimize
CPR quality, guide vasopressor therapy, and detect ROSC include arterial relaxation diastolic pressure,
arterial pressure monitoring, and central venous oxygen saturation (Link, et al., 2015).
Mechanical Chest Compression Devices

[Objectives 12]
The use of mechanical chest compression devices has been proposed as an alternative to manual
compressions to improve compression depth, rate, and consistency. When mechanical devices are used,
training should be provided to reduce the time needed for device deployment (Brooks, et al., 2014).
Training should also stress the importance of minimizing interruptions in chest compressions while
the device is in use (Morrison, et al., 2013).
Fig. 1.7 The AutoPulse uses a load-distributing band to compress the chest at a rate and depth consistent with resuscitation
guidelines. (Courtesy Zoll Medical Corporation, Chelmsford, MA)
Several mechanical chest compression devices are available. The AutoPulse (Zoll Medical Corpora-
tion, Chelmsford, MA) uses a load-distributing band that is attached to a backboard and battery-
powered motor (Fig. 1.7). The band encircles the patient’s chest and mechanically and rhythmically
shortens and lengthens to compress the chest at a rate and depth consistent with resuscitation guidelines.
The LUCAS Chest Compression System (Physio-Control, Jolife AB, Redmond, WA) uses a back
plate that is positioned underneath the patient as a support and a piston/suction cup to compress the
patient’s anterior chest. The LUCAS 1 is powered by compressed air from a wall outlet or cylinder
(Fig. 1.8). The LUCAS 2 is electrically powered (Fig. 1.9). A UK trial studied whether the introduction
of the LUCAS 2 device into front-line emergency response vehicles would improve survival from
OHCA (Perkins, et al., 2015). Results showed no evidence of improvement in 30-day survival with
the LUCAS 2 compared with manual compressions. The Life-Stat, formerly the Thumper (Michigan
Instruments, Grand Rapids, MI), is a gas-powered piston device that is equipped with an automatic
transport ventilator (Fig. 1.10).
Current resuscitation guidelines state that although manual chest compressions remain the standard
of care for the treatment of cardiac arrest, the use of mechanical chest compression devices may be a
reasonable alternative for use by properly trained personnel and “may be considered in specific settings
where the delivery of high-quality manual compressions may be challenging or dangerous for the pro-
vider (eg, limited rescuers available, prolonged CPR, during hypothermic cardiac arrest, in a moving
ambulance, in the angiography suite, during preparation for extracorporeal CPR), provided that rescuers
strictly limit interruptions in CPR during deployment and removal of the devices” (Brooks, et al., 2015).
Fig. 1.8 The LUCAS® 1 Chest Compression System is powered by compressed air from a wall outlet or cylinder. (Courtesy
Physio-Control, Inc., Redmond, WA; Jolife AB, Lund, Sweden)
Fig. 1.9 The LUCAS® 2 Chest Compression System is electrically powered. (Courtesy Physio-Control, Inc., Redmond, WA;
Jolife AB, Lund, Sweden)
Fig. 1.10 The Life-Stat is a gas-powered piston device that is equipped with an automatic transport ventilator. (Courtesy
Michigan Instruments, Grand Rapids, MI)
PATIENT ASSESSMENT
[Objectives 13]
Patient assessment is a systematic method of evaluating a patient’s condition and is the foundation of med-
ical care. The information obtained by the clinician when performing a patient assessment helps guide
treatment decisions. Recognizing when a patient’s condition becomes unstable requires good patient
assessment skills and is essential for improved patient outcomes.
Before approaching the patient, make sure that the scene is safe. Note any hazards or potential hazards
and any visible mechanism of injury or illness. Always use appropriate personal protective equipment.
Once you come into view of the patient, immediately begin to form a general impression, which is
an “across-the-room” or “from-the-doorway” assessment of the severity of the patient’s condition. Your
general impression should focus on three main areas that can be remembered by the mnemonic ABC:
Appearance, (work of) Breathing, and Circulation. As you finish forming your general impression, you
will have a good idea if the patient is sick (unstable) or not sick (stable).
• Appearance. The patient’s appearance reflects the adequacy of oxygenation, ventilation, and
central nervous system function. When forming a general impression, normal findings include a
patient who is aware of your approach and has normal muscle tone and equal movement of all
extremities.
• Breathing. Breathing reflects the adequacy of the patient’s oxygenation and ventilation. Normal find-
ings include breathing without excessive respiratory muscle effort that is quiet and regular with equal
rise and fall of the chest. Abnormal findings include use of accessory muscles to breathe, the presence
of retractions, and audible respiratory sounds that can be heard without a stethoscope such as stridor,
gasping, wheezing, snoring, or gurgling.
• Circulation. Circulation reflects the adequacy of cardiac output and perfusion of vital organs. When
forming a general impression, circulation refers to skin color. Skin color normally is some shade of
pink. Even patients who have heavy pigmentation have an underlying pink color to the skin. Abnor-
mal findings include pallor, mottling, and cyanosis.
An abnormal finding that is observed when assessing any of these areas suggests that the patient is sick
(unstable); move quickly and proceed immediately to the primary survey. If the patient’s condition does
not appear to be urgent, proceed systematically starting with the primary survey and then the secondary
survey.
Primary Survey
[Objectives 14]
The primary survey is a rapid hands-on patient assessment that focuses on basic life support interventions
and management. The purposes of the primary survey are to detect the presence of life-threatening prob-
lems and to immediately correct them. During this phase of patient assessment, assessment and man-
agement occur at the same time.
The ABCDE sequence of the primary survey is taught to physicians, nurses, and prehospital person-
nel in many types of educational courses. In programs other than cardiac-related courses, the primary
survey sequence stands for Airway, Breathing, Circulation, Disability (referring to a brief neurologic
exam), and Exposure. In cardiac-related courses, the “D” also stands for Defibrillation.
Repeat the primary survey:
• With any sudden change in the patient’s condition
• When interventions do not appear to be working
• When vital signs are unstable
• Before any procedures are performed
• When a change in rhythm is observed on the cardiac monitor
Begin the primary survey by assessing responsiveness. Start by asking, “Are you all right?” or “Can you
hear me?” If there is no response, then gently tap or squeeze the victim’s shoulder while repeating verbal
cues. Look at the chest for movement for 5 to 10 seconds. Call for help and ask someone to get an AED
or defibrillator.
ACLS Pearl
Use the AVPU acronym when evaluating level of responsiveness:
• A ¼ Alert
• V ¼ Responds to verbal stimuli
• P ¼ Responds to painful stimuli
• U ¼ Unresponsive
Responsive Patient
Ask the patient questions to determine his or her level of responsiveness and the adequacy of his or her
airway and breathing.
Airway
If the airway is not clear, clear it with suctioning or positioning as indicated. If the airway is open, move
on and assess the patient’s breathing.
Breathing
An open airway does not ensure adequate breathing. Evaluate the depth (tidal volume) and symmetry of
movement with each breath. Chest expansion should be adequate, with sufficient tidal volume to make
the chest rise, and equal, with no excessive use of accessory muscles during inspiration or expiration.
Assess the patient’s breathing with regard to rate, quality, and regularity. A patient who has breathing
difficulty often has a ventilatory rate outside the normal limits for his or her age. Normal, noisy, labored,
or shallow are terms used to describe the quality of ventilations. Note if breathing is quiet, absent, or
noisy (eg, stridor, gasping, wheezing, snoring, gurgling). Labored breathing is evident when a patient is
working hard to breathe. It is often evidenced by the use of accessory muscles to breathe, pursed-lip
breathing, retractions, leaning forward to inhale, or the patient’s inability to speak in full sentences with-
out pausing to take a breath. Shallow breathing may result in ineffective delivery of oxygen to the body’s
tissues and ineffective elimination of carbon dioxide, even when the ventilatory rate is normal. A bag-
mask device (BMD) is often used to provide assisted ventilation for the patient who has an inadequate
rate or depth of breathing (see Chapter 2). If the patient’s breathing is adequate, move on to assessment
of circulation.
Circulation
Quickly estimate the patient’s heart rate and determine the quality of the pulse (ie, fast or slow, regular or
irregular, weak or strong). Evaluate the patient’s skin temperature, color, and moisture to assess
perfusion.
Disability/Defibrillation
Perform a brief neurologic evaluation (ie, obtain a Glasgow Coma Scale score) and assess the need for a
defibrillator.
Exposure
Expose the patient for further evaluation.
Unresponsive Patient
[Objective 15]
If your assessment of responsiveness indicated that the patient is unresponsive, call for help and ask
someone to get an AED or defibrillator. Look at the chest for movement while simultaneously feeling
for a carotid pulse for no more than 10 seconds.
ACLS Pearl
If the patient is unresponsive but has normal breathing, CPR is not needed. Perform a primary survey
as you would for a responsive patient.
If a pulse is present, open the airway and begin rescue breathing, providing one breath every 5 to 6 sec-
onds, or about 10 to 12 breaths/min (Kleinman, et al., 2015). Recheck a pulse every 2 minutes for up to
10 seconds. If there is no pulse or if you are unsure if there is a pulse and the patient is an adult, begin
chest compressions, remembering to allow the chest wall to rebound after each compression. Minimize
interruptions of chest compressions. Rotate chest compressors at 2-minute intervals (ideally in less than
5 seconds) to avoid tiring. If an opioid overdose is suspected, administer naloxone if it is available (check
your agency’s protocol).
If there is no pulse, check for a shockable rhythm using a monitor-defibrillator or AED. Provide
shocks as indicated. Refer to the specific operating instructions of the AED model being used as
models may vary. After each shock, immediately resume CPR beginning with chest compressions for
2 minutes.
After 30 compressions, open the airway using a head tilt–chin lift (see Chapter 2). If head or neck
trauma is suspected, open the airway using the jaw thrust without neck extension maneuver. Next,
use a pocket mask or BMD and deliver 2 breaths, ensuring that the delivery of each breath takes about
1 second. Make sure the breaths are effective (the chest rises). If the chest does not rise, reposition
the head, make a better seal, and try again. Avoid excessive ventilation (ie, too many breaths, too large
a volume).
BOX 1.2 Secondary Survey Components

• Airway • Evaluate interventions and pain management
• Breathing • Facilitate family presence for invasive and
• Circulation resuscitative procedures
• Differential diagnosis and diagnostic
procedures
Secondary Survey
[Objectives 14]
The purpose of the physical examination during the secondary survey is to detect potentially life-
threatening conditions and to provide care for those conditions (Box 1.2). The secondary survey focuses
on advanced life support interventions and management. If the patient is responsive, obtain the patient’s
vital signs; attach a pulse oximeter, ECG, and BP monitor; and obtain a focused history. The history is
often obtained while the physical examination is being performed and emergency care is being given.
Reassess the effectiveness of initial airway maneuvers and interventions. If needed, insert an advanced
airway. If an advanced airway has been inserted, confirm proper placement using clinical assessment and
waveform capnography. Make sure the tube is adequately secured. Obtain a chest radiograph to confirm
proper placement. If bag-mask ventilation is adequate, advanced airway insertion may be deferred until
spontaneous circulation returns or the patient fails to respond to initial resuscitation efforts.
Reassess the adequacy of oxygenation (using pulse oximetry) and ventilation (using capnography).
Reassess chest rise. If oxygenation is inadequate, administer supplemental oxygen to achieve an oxygen
saturation of 94% or greater. If breathing is inadequate, assist ventilations with a BMD at an age-
appropriate rate.
If the patient has a pulse, check its rate and quality often. If not already done, attach ECG electrodes
and connect the patient to an ECG monitor. ECG monitoring allows continuous recording and reas-
sessment of the cardiac rhythm. Obtain a 12-lead ECG if appropriate. Perform defibrillation or cardio-
version as indicated. Establish vascular access and give medications appropriate for the cardiac rhythm/
clinical situation. Vascular access is usually established via a peripheral IV; however, intraosseous (IO)
access in cardiac arrest is safe, effective, and appropriate for patients of all ages. Consider limiting periph-
eral IV attempts to no more than two unsuccessful attempts before initiating IO access. During cardiac
arrest, establishing vascular access is important, but it should not interfere with CPR and the delivery of
shocks. Each medication given during a cardiac arrest should be followed with a 20 mL IV fluid bolus
and elevation of the extremity. These techniques help speed delivery of the medication to the central
circulation. During a cardiac arrest, medications should be given without interrupting CPR.
Search for, find, and treat reversible causes of the cardiac arrest, rhythm, or clinical situation. Reassess
the effectiveness of the care given thus far and troubleshoot as needed. If the patient is responsive and
complaining of discomfort, begin appropriate pain management if his or her BP and other vital signs will
tolerate it. Facilitate family presence for invasive and resuscitative procedures. Explain what is being done
for the patient to family members who are present.
PUTTING IT ALL TOGETHER

CHAPTER QUIZ
Multiple Choice
Identify the choice that best completes the statement or answers the question.
____ 1. Which of the following memory aids may be used when evaluating a patient’s level of
responsiveness?
A. CAB
B. AVPU
C. ABCDE
D. OPQRST
____ 2. Upon finding an unresponsive adult patient, you called for help and asked that
someone get an AED or defibrillator. Your next action should be to:
A. Begin chest compressions.
B. Reposition the patient’s head.
C. Open the airway and begin rescue breathing.
D. Simultaneously look for breathing and feel for a pulse.
____ 3. During which phase of a cardiac arrest is CPR performed?

A. No-flow phase
B. Prearrest phase
C. Low-flow phase
D. Postresuscitation phase
____ 4. The purpose of the primary survey is to:

A. Perform a detailed head-to-toe physical examination.
B. Determine the number of personnel needed to assist in the patient’s care.
C. Focus on the patient’s chief complaint/reason for seeking medical assistance.
D. Detect the presence of life-threatening problems that require rapid intervention.
____ 5. Shockable cardiac arrest rhythms include:

A. Asystole and PEA.
B. pVT and asystole.
C. PEA and VF.
D. VF and pVT.
____ 6. Which of the following is (are) the initial cardiac rhythm(s) typically recorded in an
out-of-hospital cardiac arrest?
A. Asystole
B. Idioventricular rhythm, PEA
C. VF, pVT
D. pVT, PEA
____ 7. During the primary survey, for what length of time should you assess for the presence
of a pulse?
A. Check for a pulse for no more than 3 seconds.
B. Check for a pulse for no more than 5 seconds.
C. Check for a pulse for at least 5 seconds but no more than 10 seconds.
D. Check for a pulse for at least 10 seconds but no more than 30 seconds.
____ 8. Which of the following is a common cause of excessive intrathoracic pressure during
CPR?
A. Hyperventilation
B. Inability to open the victim’s airway
C. Inadequate rate of chest compressions
D. Frequent interruptions for rhythm/pulse checks
Matching
Match the components of patient assessment with their descriptions.
A. General impression
B. Primary survey
C. Secondary survey
____ 9. Establish vascular access
____ 10. From a distance, assess the patient’s breathing effort
____ 11. Insert an advanced airway, if needed
____ 12. Open the airway if the patient is unresponsive
____ 13. From a distance, assess skin color
____ 14. Obtain a 12-lead ECG if appropriate
____ 15. Apply pads to the patient’s bare chest and defibrillate if indicated
____ 16. Obtain vital signs; attach a pulse oximeter, cardiac monitor, and BP monitor
CHAPTER QUIZ ANSWERS

Multiple Choice
1. B. The AVPU acronym is used to quickly assess a patient’s level of responsiveness. AVPU – Alert,
responds to verbal stimuli, responds to painful stimuli, unresponsive. ABCDE is an acronym that
reflects the components of the primary survey. OPQRST is an acronym that is used when evaluating
a patient’s complaint of pain. CAB is an acronym that emphasizes the importance of performing
chest compressions first, followed by opening the airway and assessing breathing, in victims of car-
diac arrest.
OBJ: Differentiate between the purposes and components of the primary and secondary surveys.
2. D. If you find an unresponsive patient, call for help and ask someone to get an AED or defibrillator.
Look at the chest for movement while simultaneously feeling for a carotid pulse for up to 10 seconds.
Gasping, if present, is abnormal breathing and should not be interpreted as a sign of effective breath-
ing. If the patient has no pulse, begin chest compressions. If the patient is breathing normally, con-
tinue monitoring until additional help arrives. If the patient is not breathing normally but a pulse is
present, provide rescue breathing and recheck for a pulse about every 2 minutes.
OBJ: Discuss a systematic approach to the initial emergency care of an unresponsive patient.
3. C. Four phases of cardiac arrest have been described: (1) the prearrest phase, (2) the no-flow phase,
(3) the low-flow phase, and (4) the postresuscitation phase (Berg, et al., 2010). The prearrest phase is
the period that precedes cardiac arrest. The no-flow phase reflects untreated cardiac arrest. The low-
flow phase begins with the onset of CPR. During this phase of cardiac arrest, the only source of cor-
onary and cerebral perfusion pressures comes from the BP generated by high-quality chest compres-
sions. The postresuscitation phase begins with the ROSC.
OBJ: Discuss the phases of a cardiac arrest.
4. D. The primary survey is a rapid hands-on assessment to detect the presence of life-threatening
problems and immediately correct them.
5. D. The four cardiac arrest rhythms are pVT, VF, asystole, and PEA. pVT and VF are shockable
rhythms. Defibrillation is not indicated for asystole or PEA.
OBJ: Differentiate between shockable and nonshockable cardiac arrest rhythms.
6. A. Data from nontraumatic OHCAs in 2014 indicate that asystole was the most common (45.6%)
initial cardiac arrest rhythm, followed by an idioventricular rhythm/PEA (21.4%), VF/pVT/
unknown shockable rhythm (20.4%), and an unknown nonshockable rhythm (12.5%) (Centers for
Disease Control and Prevention, 2014).
OBJ: Recognize the initial cardiac rhythms that are typically recorded in OHCA.
7. C. Check for a pulse for at least 5 seconds but no more than 10 seconds. If the patient has no pulse,
begin chest compressions.
8. A. Hyperventilation is a common cause of excessive intrathoracic pressure during CPR. It is impor-

tant to ventilate a patient in cardiac arrest at an age-appropriate rate and with just enough volume to
see the patient’s chest rise gently. Ventilating a cardiac arrest patient too fast or with too much volume
results in excessive intrathoracic pressure, which results in decreased venous return into the chest,
decreased coronary and cerebral perfusion pressures, diminished cardiac output, and decreased rates
of survival.
OBJ: Discuss common barriers to effective CPR and possible actions that can be taken to
overcome them.
Matching
9. C
10. A
11. C
12. B
13. A
14. C
15. B
16. C
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CHAPTER 2
Airway Management
INTRODUCTION
As a health care professional, it is essential that you be able to recognize if a patient has clinical signs and
symptoms of inadequate oxygenation, inadequate ventilation, or both, and know how to confidently pro-
vide appropriate emergency care in such situations. This chapter briefly describes respiratory system anat-
omy, reviews the devices used to deliver supplemental oxygen, discusses the techniques used for opening
the airway of an unresponsive patient, discusses the devices used for delivering positive pressure venti-
lation, and discusses methods used to confirm proper positioning of an endotracheal tube (ETT).
G O A L Given a patient situation, and working in a team setting, competently direct the initial emer-
gency care for a patient experiencing a respiratory arrest.
LEARNING OBJECTIVES
1. Differentiate among respiratory distress, respiratory failure, and respiratory arrest and
implement a treatment plan based on the severity of the patient’s respiratory compromise.
2. Discuss the evaluation of oxygenation and ventilation with the use of pulse oximetry and
capnography.
3. Describe the advantages, disadvantages, oxygen liter flow per minute, and estimated
oxygen percentage delivered with each of the following devices: nasal cannula, simple
face mask, partial nonrebreather mask, and nonrebreather mask.
4. Describe and demonstrate the steps needed to perform the head tilt–chin lift and the jaw
thrust without neck extension maneuvers and relate the mechanism of injury to the
opening of the airway.
5. Describe and demonstrate the procedure for suctioning the upper airway, and discuss
possible complications associated with this procedure.
6. Discuss the indications, contraindications, advantages, and disadvantages of oral and
nasal airways, and demonstrate how to correctly size and insert each of these airway
adjuncts.
7. Describe methods by which positive pressure ventilation is delivered.
8. Differentiate between continuous positive airway pressure (CPAP) and bilevel positive
airway pressure (BPAP).
9. Describe the oxygen liter flow per minute and the estimated inspired oxygen
concentration delivered with a pocket face mask and a bag-mask device (BMD). 23
24 CHAPTER 2 Airway Management
10. Describe and demonstrate how to ventilate a patient with a BMD and two rescuers.
11. Recognize the signs of adequate and inadequate bag-mask ventilation (BMV).
12. Differentiate between extraglottic airways and intraglottic airways.
13. Describe methods that are used to confirm correct ETT placement.
LEARNING PLAN
• Read this chapter before class. Take the time to highlight important concepts as you read.
• Master the following medications: O2.
• Master the following skills:
• Ensure scene safety and the use of personal protective equipment.
• Assign team member roles or perform as a team member in a simulated patient
situation.
• Direct or perform an initial patient assessment.
• Recognize signs and symptoms of respiratory compromise.
• Develop and implement a treatment plan on the basis of the severity of the patient’s
respiratory compromise, history, physical examination, and diagnostic test results.
• Obtain vital signs, establish vascular access, attach a pulse oximeter and blood
pressure and cardiac monitor, and give supplemental O2 if indicated.
• Demonstrate manual methods for opening the airway.
• Demonstrate the procedure for suctioning the upper airway.
• Demonstrate how to properly size and insert an oral airway and a nasal airway.
• Perform two-rescuer BMV when indicated.
• Demonstrate how to troubleshoot inadequate BMV.
• Demonstrate how to confirm the correct positioning of an ETT.
• Review your performance as a team leader or team member during a postevent
debriefing.
• Read the case study at the end of this chapter and answer each question that follows it.
Compare your answers with the answers provided at the end of the case study.
KEY TERMS
Capnography The continuous analysis and recording of carbon dioxide concentrations in
respiratory gases.
Carina The point where the trachea divides into the right and left primary bronchi.
Cricothyroid membrane A fibrous membrane located between the cricoid and thyroid
cartilages.
Epiglottis A small piece of cartilage located at the top of the larynx that prevents foreign
material from entering the trachea during swallowing.
Glottis The true vocal cords and the space between them.
Hard palate Bony portion of the roof of the mouth that forms the floor of the nasal cavity.
Nasal cannula A piece of plastic tubing with two soft prongs that project from the tubing;
used to deliver supplemental oxygen to a spontaneously breathing patient.
Oxygenation The process of getting oxygen into the body and to its tissues for metabolism.
Pulse oximeter A small instrument with a light sensor that quickly calculates the percentage
of hemoglobin that is saturated with oxygen in a pulsating capillary bed.
Respiration The exchange of oxygen and carbon dioxide during cellular metabolism.
Simple face mask An oxygen delivery device that consists of a plastic reservoir that fits over
a patient’s nose and mouth and a small diameter tube connected to the base of the mask
through which oxygen is delivered; also called a standard mask.
Soft palate The back part of the roof of the mouth that is made up of mucous membrane,
muscular fibers, and mucous glands.
CHAPTER 2 Airway Management 25
Uvula Fleshy tissue that hangs down from the soft palate and into the posterior portion of the
oral cavity.
Vallecula The space or “pocket” between the base of the tongue and the epiglottis.
Ventilation The mechanical movement of gas or air into and out of the lungs.
ANATOMY REVIEW
Upper Airway
The upper airway extends from the mouth and nose to the upper trachea. The upper airway functions as a
passageway for gas flow; for filtering, warming, and humidifying the air; and for protecting the surfaces of
the lower respiratory tract (Fig. 2.1). The upper airway also functions in phonation and in the senses of
smell and taste.
The nasal cavity and the mouth meet at the pharynx (ie, the throat). The pharynx extends from the
nasal cavities to the larynx, and it includes three parts: the nasopharynx, the oropharynx, and the laryn-
gopharynx or hypopharynx. The pharynx is a passageway that is common to both the respiratory and
digestive systems. The separation of the respiratory and digestive tracts occurs immediately below the
laryngopharynx.
The nasopharynx is located at the posterior end of the nasal cavity, and it extends to the tip of the
uvula. The mucous lining of the nasopharynx filters, warms, and moistens the air. The nasopharynx con-
tains two pharyngeal tonsils (also called adenoids) and the eustachian tube openings. Tissues of the naso-
pharynx are extremely delicate and vascular. The improper or overly aggressive placement of tubes or
airways may result in significant bleeding.
The oropharynx begins at the uvula, which is fleshy tissue that hangs down from the soft palate and
into the posterior portion of the oral cavity. The posterior portion of the oral cavity opens into the oro-
pharynx. The oropharynx extends to the upper rim of the epiglottis. The epiglottis is a small piece of
cartilage located at the top of the larynx that prevents foreign material from entering the trachea during
swallowing. The oropharynx functions in respiration and digestion. The anterior oropharynx opens into
the oral cavity, which comprises the lips, cheeks, teeth, tongue, and hard and soft palates (Fig. 2.2). The
Frontal sinus
Nasal bone
Nasal cartilage
Superior Sphenoidal sinus
nasal concha
Internal naris
Middle Pharyngeal tonsil
nasal concha
Opening for auditory tube
External naris
Inferior Nasopharynx
nasal concha Soft palate
Hard palate
Uvula
Oral cavity Palatine tonsil
Oropharynx
Tongue
Epiglottis
Mandible
Hyoid bone Laryngopharynx
Fauces
Lingual tonsil Larynx
Thyroid cartilage Vestibular folds

Cricoid cartilage True vocal folds
Trachea
Esophagus
Fig. 2.1 Structures of the upper airway. (From Applegate: The anatomy and physiology learning system, ed 4, 2011,
Saunders.)
Philtrum
Upper lip
Hard palate
Soft palate
Uvula
Palatine
tonsil
Tongue
Fauces
(opening)
Lower lip
Fig. 2.2 Frontal view into the open mouth showing the major structures within. (From Patton K, Thibodeau G: Anatomy &
physiology, ed 7, St. Louis, 2013, Mosby.)
anterior roof of the oral cavity is formed by the maxillary bone and is called the hard palate. The posterior
portion of the roof of the mouth is called the soft palate because it is made up of mucous membrane,
muscular fibers, and mucous glands. The cheeks form the walls, and the tongue dominates the floor of
the oral cavity. Located on the lateral walls of the oropharynx are a pair of palatine tonsils that can cause a
partial airway obstruction if they become excessively swollen. The space (or “pocket”) between the base of
the tongue and the epiglottis is called the vallecula. When performing orotracheal intubation, the epi-
glottis is lifted out of the way to visualize the area during the passage of the tracheal tube between the
vocal cords. The vallecula is an important anatomic landmark to identify when intubating a patient with
the use of a curved laryngoscope blade.
The laryngopharynx extends from the upper rim of the epiglottis to the glottis, which encompasses
the true vocal cords and the space between them (ie, the glottic opening). The glottis is the narrowest part
of the adult larynx. The laryngopharynx is connected to the esophagus, and the laryngopharynx functions
in respiration and digestion.
ACLS Pearl
In the unresponsive patient, a partial or complete airway obstruction can result when the muscles of
the tongue and laryngopharynx relax, thus allowing the tongue and other soft tissues to block the
opening of the laryngopharynx.
The larynx (ie, voice box) connects the pharynx to the trachea at the level of the cervical vertebrae. It
conducts air between the pharynx and the lungs; it prevents food and foreign substances from entering
the trachea; and it houses the vocal cords, which are involved in speech production. The larynx is a tubular
structure made up of muscles, ligaments, and nine cartilages (see Fig. 2.1). The thyroid cartilage (ie,
Adam’s apple) is the largest and most superior cartilage of the larynx. It is more pronounced in adult
males than adult females. The thyroid gland lies over the outer surface of the thyroid cartilage. The
pyramid-shaped arytenoid cartilages of the larynx serve as a point of attachment for the vocal cords.
The arytenoid cartilages often serve as an important landmark during intubation.
The cricoid cartilage is inferior to the thyroid cartilage. It is considered the first tracheal ring, and it
is the only complete ring of cartilage in the larynx. The other cartilages of the larynx are incomplete
C-shaped rings on the posterior surface. The C-shaped rings are open to permit the esophagus, which
lies behind the trachea, to bulge forward as food moves to the stomach. The narrowest diameter of the
airway in infants and children who are younger than age 10 is at the cricoid cartilage. The cricothyroid
membrane is a fibrous membrane that is located between the cricoid and thyroid cartilages. This site may
be used for surgical and alternative airway placement.
ACLS Pearl
Stimulation of the larynx by a laryngoscope blade, tracheal tube, or suction catheter can result in
bradycardia, hypotension, and a decreased ventilatory rate because the larynx is innervated with
nerve endings from the vagus nerves. Monitor the patient closely for these effects and discontinue
the treatment that is causing them if they appear.
Lower Airway
The lower airway extends from the lower trachea to the alveoli, and it functions in the exchange of oxygen
and carbon dioxide. Air moves from the larynx through the glottic opening and into the trachea. The
adult trachea is about twelve centimeters (cm) in length and has an inner diameter of about 2 cm. It
divides or bifurcates into two separate tubes called the left and right primary bronchi (Fig. 2.3). The point
where the trachea divides into the right and left primary bronchi is called the carina. The right bronchus
serves three lobes of the lung and the left bronchus serves two. The right primary bronchus is shorter,
wider, and straighter or less angled than the left, because the heart occupies space in the left chest cavity.
Fig. 2.3 An adult and infant trachea showing the different angles of primary bronchi bifurcation. (From Kacmarek R, Stoller J,
Heuer A: Egan’s fundamentals of respiratory care, ed 11, Elsevier, 2017.)
Therefore a tracheal tube that is inserted too far or foreign material that is aspirated is more likely to enter
the right primary bronchus than the left.
The walls of the trachea are supported and held open by a series of 16 to 20 C-shaped cartilaginous
rings. The area between the tracheal cartilages is composed of connective tissue and smooth muscle,
which allow for changes in the diameter of the trachea. Tracheal smooth muscle is innervated by the
parasympathetic division of the autonomic nervous system.
Internally, the trachea is lined with a mucous membrane that contains cilia as well as mucus-
producing cells. The cilia sweep foreign materials out of the airway and the mucus can also trap partic-
ulate matter that is then expelled during coughing. Obstruction of the trachea will result in death if not
corrected within minutes.
The primary bronchi branch into narrowing secondary and tertiary bronchi, which then branch into
bronchioles. As the bronchi continue to divide into the lung tissue and become smaller passageways, they
become bronchioles. Bronchioles are composed entirely of smooth muscle that is supported by connec-
tive tissue. Bronchioles are responsible for regulating the flow of air to the alveoli. The stimulation of
beta2 receptor sites in the bronchioles results in relaxation of bronchial smooth muscle. After multiple
subdivisions, the bronchioles divide into tiny tubes called alveolar ducts, where gas exchange first becomes
possible. These ducts end in alveoli, which are tiny, hollow air sacs. Each lung of an average adult con-
tains about 300 million alveoli, and each alveolus is surrounded by a pulmonary capillary. Oxygen diffuses
through the thin walls of the alveoli to the capillaries, and carbon dioxide diffuses from the capillaries to
the alveoli.
THE PATIENT WITH RESPIRATORY COMPROMISE

[Objective 1]
Respiratory complaints are common in patients of all ages. Respiratory distress, respiratory failure, and
respiratory arrest reflect increasing levels of severity of respiratory compromise. Signs of adequate ven-
tilation include the ability to breathe at a regular rate and within normal limits for the patient’s age, an
equal rise and fall of the chest with each breath, an adequate depth of breathing (ie, tidal volume), and the
ability to speak in full sentences without pausing. Signs of inadequate ventilation include the following:
• A breathing rate that is too fast or slow for the patient’s age
• Abnormal breath sounds (stridor, wheezing, crackles, silent chest, unequal)
• Abnormal work (effort) of breathing (retractions, accessory muscle use, sweating, tripod position,
flared nostrils, pursed lips)
• An irregular breathing pattern
• Anxious appearance, concentration on breathing
• Confusion, restlessness
• Depth of breathing that is unusually deep or shallow
• Inability to speak in complete sentences
• Inadequate chest wall movement (paradoxical, splinting, asymmetric)
• Pain with breathing
Signs of respiratory distress reflect an attempt to compensate for hypoxia and may include mental
status changes (eg, anxiety, restlessness, decreased ability to concentrate), nasal flaring, pallor or mottling,
retractions, stridor, tachypnea, wheezing, and the use of accessory muscles of breathing. Because the
causes of respiratory distress are many, possible therapeutic interventions include allowing the patient
to assume a position of comfort, the administration of supplemental oxygen if indicated, and pharma-
cologic therapy (eg, bronchodilators). Uncorrected respiratory distress may lead to respiratory failure.
Acute respiratory failure develops when the exchange of oxygen and carbon dioxide within the lungs is
inadequate. Hypoxemic respiratory failure refers to respiratory failure associated with failure to oxygenate,
whereas hypercarbic respiratory failure is the failure to ventilate (Casserly & Rounds, 2010). Signs of
impending respiratory failure include agitation, irritability, confusion, lethargy, accessory muscle use,
nasal flaring, pursed-lip breathing, retractions, tachypnea, and pallor, mottling, or cyanosis despite oxy-
gen therapy. Although tachycardia is often seen with early respiratory failure, the patient may become
bradycardic with impending respiratory arrest. Depending on its cause and severity, possible therapeutic
interventions for respiratory failure may include suctioning, administration of supplemental oxygen, non-
invasive positive pressure ventilation (NPPV), BMV, and treatment of specific contributing or causative
factors.
With respiratory arrest, the patient is unresponsive with no visible chest rise, no ventilatory effort, and
limp muscle tone. Therapeutic interventions include the use of manual maneuvers to open the airway, the
removal of a foreign body if present, insertion of an oral or nasal airway, suctioning, BMV with supple-
mental oxygen, possible insertion of an advanced airway by an appropriately trained clinician, and treat-
ment of specific contributing or causative factors.
Patient Assessment
[Objective 2]
As you approach the patient with a respiratory complaint, form a general impression to determine
whether the patient is sick (ie, unstable) or not sick (ie, stable) and to determine the urgency of further
assessment and care. When forming a general impression, an altered mental status, an inability to main-
tain ventilatory effort, and/or the presence of mottling or cyanosis are red flags that suggest imminent
respiratory arrest and warrant immediate intervention (McEvoy, 2013). Flaring nostrils and the use of
accessory muscles are signs that suggest the patient is struggling to breathe. Noting the patient’s position
may be helpful in assessing the severity of the patient’s respiratory problem. For example, a patient who is
sitting upright with his elbows braced on a table or with his hands on his knees and elbows out while
leaning forward is said to be tripoding or assuming a tripod position. If abnormal findings are present,
move quickly and proceed immediately to the primary survey and begin emergency care. If the patient’s
condition does not appear to be urgent, work at a reasonable pace and proceed systematically with your
patient assessment. Because his or her condition can quickly change, it is important to reassess the
patient often.
If the patient is responsive, ask the patient questions to determine his or her level of responsiveness
and the adequacy of his or her airway and breathing. Observe for agitation, confusion, restlessness, or
combativeness, which may be the result of hypoxia. Also observe if the patient is able to speak in sen-
tences before requiring a breath or if he or she experiences shortness of breath after speaking only a few
words. If the patient is unresponsive, manual maneuvers may be needed to open the patient’s airway.
Manual airway maneuvers are discussed later in this chapter.
The evaluation of a patient’s breathing should include an assessment of the patient’s tidal volume (ie,
depth of breathing), ventilation rate, and symmetry of movement with each breath. Ventilation (which is
often misnamed respiration) is the mechanical movement of air into and out of the lungs. Respiration is
the exchange of oxygen and carbon dioxide during cellular metabolism. During normal, quiet breathing,
an adult male moves an average of 500 mL (5 to 7 mL/kg) of air into and out of the respiratory tract with
each breath (Douce, 2009); this amount is called the tidal volume. Chest expansion should be adequate
with sufficient tidal volume to make the chest rise equally with no excessive use of accessory muscles
during inspiration or expiration. Look for signs of increased work of breathing such as pursed-lip breath-
ing, use of accessory muscles, leaning forward to inhale, or retractions. Frequently auscultate breath
sounds to detect decreased ventilation, crackles, wheezes, or rhonchi. If breathing is inadequate, provide
supplemental oxygen if indicated and, if necessary, provide positive pressure ventilation. Oxygen delivery
devices and techniques of positive pressure ventilation are discussed later in this chapter.
Assess the patient’s heart rate, pulse quality, and skin temperature, color, and moisture. Obtain a
Glasgow Coma Scale score, assess the need for a defibrillator, and expose pertinent areas of the patient
for further examination as necessary. Obtain the patient’s vital signs, attach a pulse oximeter, cardiac
monitor, and blood pressure monitor, and obtain a focused history.
Pulse Oximetry
[Objective 2]
Oxygenation is the process of getting oxygen into the body and to its tissues for metabolism. A pulse
oximeter, which is commonly called a pulse ox, is a small instrument with a light sensor that quickly
calculates the percentage of hemoglobin that is saturated with oxygen in a pulsating capillary bed. This
calculation is called the saturation of peripheral oxygen or SpO2. The oximeter displays this value as a per-
centage and the patient’s pulse rate on its screen. The oximeter’s sensor is typically applied to a finger
(Fig. 2.4), but the forehead, an earlobe, or a toe can also be used with the selection of a sensor that is
appropriate for the chosen site. For example, an adhesive or clip-on sensor can be used for a finger,
but a forehead sensor is usually adhesive.
Pulse oximetry sensors may be disposable or reusable. When using a disposable sensor, assess the site
every 2 to 4 hours and replace the sensor every 24 hours (Schutz, 2011). Assess the site for decreased
Fig. 2.4 Finger application of a pulse oximeter sensor. (From Bonewit-West K: Clinical procedures for medical assistants,
ed 9, St. Louis, 2015, Saunders.)
temperature, decreased peripheral pulse, cyanosis, and tissue integrity. Reusable clip-on sensors are gen-
erally used when spot-checking oximetry values, when monitoring continuously for less than 10 minutes,
and when monitoring patients who are immobile. When a reusable sensor is applied, assess the site every
2 hours and change the site every 4 hours (Schutz, 2011).
Possible indications for continuous pulse oximetry monitoring include the following:
• A patient with a critical or unstable airway
• A patient who requires oxygen therapy
• During the intrahospital and interhospital transfer of a critically ill patient
• During hemodialysis
• A patient who has a condition or who is undergoing a procedure that alters oxygen saturation or a
patient who has a condition or history that suggests a risk for significant desaturation
Pulse oximetry may be inaccurate in situations that involve poor capillary blood flow, an abnormal
hemoglobin concentration, or an abnormal shape of the hemoglobin molecule. Examples of conditions
that may give misleading results are listed in Box 2.1.
ACLS Pearl
A pulse oximeter is an adjunct to—not a replacement of—vigilant patient assessment. You must cor-
relate your assessment findings with pulse oximeter readings to determine appropriate treatment
interventions for the patient.
BOX 2.1 Factors Affecting the Accuracy of Pulse Oximetry Readings

• Anemia (conflicting evidence) • Dark or metallic nail polish (conflicting evidence)
• Artificial acrylic nails (conflicting evidence) • Dark skin pigmentation
• Bright ambient light such as sunlight, or sur- • Medications (eg, vasoconstrictors)
gical, fluorescent, or heating lamps (conflict- • Motion artifact
ing evidence) • Poor peripheral perfusion as a result of cardiac
• Carbon monoxide or cyanide poisoning or arrest, shock, hypotension, or hypothermia
presence of other molecules that bind to
hemoglobin
Carbon Dioxide Monitoring

[Objective 2]
Carbon dioxide is produced during cellular metabolism, carried to the lungs by the circulatory system,
and excreted by the lungs during ventilation. Capnography is the continuous analysis and recording of
CO2 concentrations in respiratory gases. Capnography provides health care professionals with breath-to-
breath patient information, thereby enabling the early recognition of hypoventilation, apnea, or airway
obstruction and thus preventing hypoxic episodes. The monitoring of exhaled carbon dioxide with either
capnometry or capnography can detect changes in metabolism, circulation, respiration, the airway, or the
respiratory system.
Exhaled carbon dioxide detection devices are used in conjunction with the history and clinical assess-
ment of the patient, which may include mental status, lung sounds, pulse rate, and skin color. Examples
of situations in which exhaled CO2 monitoring is commonly used include the following:
• Assessment of the adequacy of ventilation in patients with altered mental status, bronchospasm,
asthma, chronic obstructive pulmonary disease (COPD), anaphylaxis, heart failure, drug overdose,
stroke, shock, or circulatory compromise
• Confirmation of correct tracheal tube placement (capnography should not be used as the only means of
assessing tracheal tube placement) and continuous monitoring of tracheal tube position (including
during patient transport)
• Evaluation of the effectiveness of chest compressions during resuscitation efforts and the detection of
the return of spontaneous circulation
• Monitoring of exhaled CO2 levels in patients with suspected increased intracranial pressure
• Procedural sedation and analgesia
Alveolar CO2 and arterial CO2 (PaCO2) values are closely related in patients with normal cardiopul-
monary function, and they usually range between 35 and 45 millimeters of mercury (mm Hg). In patients
with normal lung and cardiac function, normal values for end-tidal carbon dioxide (EtCO2) range
between 33 mm Hg and 43 mm Hg. This is dependent on adequate ventilation and adequate perfusion:
a change in either factor will increase or decrease the amount of exhaled CO2.
Digital capnometers use infrared technology to analyze exhaled gas. These devices provide a quan-
titative measurement of the exhaled CO2, in that they provide the exact amount of CO2 exhaled
(Fig. 2.5). This is beneficial as trends in CO2 levels can be monitored and the effectiveness of treatment
can be determined. In conjunction with clinical assessment, continuous waveform capnography is the
preferred method for confirming tracheal tube placement, for the continuous monitoring of tracheal tube
position (including during patient transport), and for the evaluation of chest compressions during resus-
citative efforts and detection of the return of spontaneous circulation.
ACLS Pearl
Interpreting capnograms should be done with the use of a systematic approach that includes the
evaluation of height, contour, baseline, frequency, and rhythm. Capnogram interpretation is beyond
the scope of this text and the Advanced Cardiac Life Support course.
A colorimetric capnometer functions through a pH change that occurs with the breath of a patient.
The patient’s breath causes a chemical reaction on pH-sensitive litmus paper housed in the detector.
The capnometer is placed between a tracheal tube or advanced airway device and a ventilation
Fig. 2.5 A combination handheld capnograph and pulse oximeter. (Copyright ©2016 Medtronic. All rights reserved. Used
with the permission of Medtronic.)
Fig. 2.6 Colorimetric exhaled carbon dioxide detector. (Copyright ©2016 Medtronic. All rights reserved. Used with the per-
mission of Medtronic.)
device (Fig. 2.6). The presence of CO2, which is evidenced by a color change on the colorimetric device,
suggests placement of the tube in the trachea. A colorimetric capnometer is qualitative in that it simply
shows the presence of CO2. It has no ability to provide an actual CO2 reading or to indicate the presence
of hypercarbia, and it provides no opportunity for ongoing monitoring to ensure that the tube remains in
the trachea. A lack of CO2 (ie, no color change) suggests tube placement in the esophagus, particularly in
patients with a perfusing rhythm (ie, not in cardiac arrest). Some manufacturers of colorimetric cap-
nometers recommend ventilating the patient at least six times before attempting to use an exhaled
CO2 detector to assess tracheal tube placement. The rationale for this action is to quickly wash out
any retained CO2 that is present in the stomach or esophagus as a result of BMV. Any CO2 that is
detected after six positive pressure ventilations can be presumed to be from the lungs (Ornato, et al.,
1992; Sum Ping, et al., 1992). Colorimetric capnometers are susceptible to inaccurate results as a result
of the age of the paper and exposure of the paper to the environment. A colorimetric capnometer may not
change color if the paper is contaminated with patient secretions (eg, vomitus) or acidic drugs (eg, tra-
cheally administered epinephrine) (Cantineau, et al., 1994). When CO2 is not detected, an alternative
method should be used to confirm tracheal tube placement, such as direct visualization or the use of an
esophageal detector device (EDD).
ACLS Pearl
Pulse oximetry provides important information about oxygenation, but does not provide information
about the effectiveness of a patient’s ventilation. Capnography provides information about the effec-
tiveness of ventilation, but does not measure oxygenation.
OXYGEN DELIVERY DEVICES

The fraction of inspired gas that is oxygen is abbreviated as FiO2 and is often expressed as a percentage.
Research has shown that routine use of supplemental oxygen in cardiac patients may have unto-
ward effects, including increased coronary vascular resistance, reduced coronary blood flow, and
increased risk of mortality (Amsterdam, et al., 2014). Indications for supplemental oxygen administra-
tion include clinically significant hypoxemia (ie, oxygen saturation less than 90%), heart failure, dyspnea,
cyanosis, or when other high-risk features of hypoxemia are present (Amsterdam, et al., 2014;
O’Gara, et al., 2013).
Nasal Cannula
[Objective 3]
A nasal cannula, which is also called nasal prongs, is a piece of plastic tubing with two soft prongs that
project from the tubing. The prongs are inserted into the patient’s nostrils, and the tubing is then secured
to the patient’s face (Fig. 2.7). Oxygen flows from the cannula into the patient’s nasopharynx, which acts
as an anatomic reservoir. Factors that influence the FiO2 delivered by a nasal cannula include the oxygen
flow rate, the patient’s ventilatory rate and tidal volume, and the anatomy and geometry of the patient’s
nasal cavity, nasopharynx, and oropharynx (Ward, 2013).
For many years it was thought that for every liter-per-minute (L/min) increase in oxygen flow when
using a nasal cannula, the effective FiO2 increased by about 4 percentage points. For example, giving
supplemental O2 at 1 L/min by cannula would raise the FiO2 to about 24%, 2 L/min would raise it
to 28%, and up to 6 L/min would raise it to 44% (Markovitz, et al., 2010). Research has shown these
estimates of cannula performance to be overly optimistic (Ward, 2013). In a 2010 study, the FiO2 levels
produced in the trachea at oxygen flow rates of 1, 3, and 5 L/min were measured while subjects breathed
at a normal rate and pattern. Researchers found the delivered FiO2 to be about 23% at 1 L/min, about
28% at 3 L/min, and about 32% at 5 L/min (Markovitz, et al., 2010). Delivered FiO2 decreases consid-
erably during conditions associated with dyspnea (Ward, 2013). Advantages and disadvantages of using a
nasal cannula are shown in Box 2.2.
Fig. 2.7 Low-flow nasal cannula. (From Potter PA & Perry AG: Fundamentals of nursing: Concepts, process, and practice,
ed 8, St. Louis, 2013, Mosby.)
BOX 2.2 Low-Flow Nasal Cannula—Advantages and Disadvantages

ADVANTAGES DISADVANTAGES
• Comfortable and well tolerated by most • Can only be used in a spontaneously
patients breathing patient
• Does not interfere with patient assessment or impede • Easily displaced
patient communication with health care personnel • Nasal passages must be open
• Allows for talking and eating • Drying to mucous membranes; may cause
• No rebreathing of expired air sinus pain
• Can be used with mouth breathers • Tubing may cause skin breakdown or
• Useful for patients who are predisposed to carbon irritation
dioxide retention • Deviated septum and mouth breathing may
• Can be used for patients who require oxygen but who reduce FiO2
cannot tolerate a nonrebreather mask • Oxygen flow rates of more than 6 L/min
do not enhance delivered oxygen
concentration
High-flow nasal cannula (HFNC) systems are being used with increasing frequency for some critically
ill patients. Components needed to provide HFNC oxygen include a nasal cannula that can accommo-
date high inlet flow, a high-flow oxygen flowmeter, and a humdifier (Ward, 2013). Commercially avail-
able humidified HFNC systems use flow rates of 5 to 40 L/min and deliver an FiO2 of close to 100%
(Reardon, et al., 2014a).
Simple Face Mask

[Objective 3]
A simple face mask, which is also called a standard mask, is a plastic reservoir that has been designed
to fit over the nose and mouth of a spontaneously breathing patient. The mask is secured around
the patient’s head by means of an elastic strap. The internal capacity of the mask produces a reservoir
effect. Small holes on each side of the mask allow for the passage of inspired and expired air.
Supplemental oxygen is delivered through a small-diameter tube connected to the base of the mask
(Fig. 2.8).
When using a simple face mask, the oxygen flow rate must be higher than 5 L/min to flush the
buildup of the patient’s exhaled carbon dioxide from the mask. At 5 to 10 L/min, the simple face mask
can deliver an inspired oxygen concentration of approximately 35% to 60%. The patient’s actual inspired
oxygen concentration will vary, because the amount of air that mixes with supplemental oxygen is depen-
dent on the patient’s inspiratory flow rate. Advantages and disadvantages of using a simple face mask are
shown in Box 2.3.
Exhalation ports
Oxygen inlet
Fig. 2.8 Simple face mask. (From Kacmarek, Stoller, Heuer: Egan's fundamentals of respiratory care, ed 10, St. Louis, 2013,
Mosby.)
BOX 2.3 Simple Face Mask—Advantages and Disadvantages

• Higher oxygen concentration delivered • Can only be used in a spontaneously breathing patient
than by nasal cannula • Not tolerated well by severely dyspneic patients
• Can be uncomfortable
• Difficult to hear the patient speaking when the device is in
place
• Must be removed at meals
• Requires a tight face seal to prevent the leakage of oxygen
• Side holes in the mask permit inhalation of room air
• Oxygen flow rates of more than 10 L/min do not enhance
delivered oxygen concentration
Partial Rebreather Mask

[Objective 3]
A partial rebreather mask is similar to a simple face mask, but it has an attached oxygen-collecting device
(ie, reservoir) at the base of the mask that is filled before patient use (Fig. 2.9A). When the patient
breathes in, 100% oxygen is drawn into the mask from the reservoir (bag). When the patient breathes
out, oxygen enters the bag from the oxygen source and some of the patient’s exhaled air enters the bag (ie,
an amount that is approximately equal to the volume of the patient’s anatomic dead space). The amount
of CO2 that is rebreathed is negligible as long as the oxygen flow keeps the bag from collapsing more than
about one-third during inhalation (Heuer, 2013).
Valves
Reservoir bag Reservoir bag
A B
Fig. 2.9 A, Partial rebreather mask. B, Nonrebreather mask. (From Kacmarek, Stoller, Heuer: Egan's fundamentals of respi-
ratory care, ed 10, St. Louis, 2013, Mosby.)
BOX 2.4 Partial Rebreather Mask—Advantages and Disadvantages

• Higher oxygen concentration delivered than by • Can only be used in a spontaneously breathing
nasal cannula patient
• Not tolerated well in severely dyspneic patients
• Can be uncomfortable
• Difficult to hear the patient speaking when the
device is in place
• Requires a tight face seal to prevent the leakage of
oxygen
• May cause skin irritation
• Lacks inspiratory valve; thus exhaled air mixes with
inspired air
The oxygen concentration of the patient’s exhaled air, in combination with the supply of 100% oxy-
gen, allows for the use of oxygen flow rates that are lower than those that are necessary for a nonrebreather
mask. Depending on the patient’s breathing pattern, the mask fit, and the oxygen flowmeter setting,
oxygen concentrations of 35% to 60% can be delivered when an oxygen flow rate is used that prevents
the reservoir bag from completely collapsing on inspiration (ie, typically 6 to 10 L/min). Advantages and
disadvantages of using a partial rebreather mask are shown in Box 2.4.
Nonrebreather Mask
[Objective 3]
A nonrebreather mask, also called a nonrebreathing mask, is similar to a partial rebreather mask, but it does
not permit the mixing of the patient’s exhaled air with 100% oxygen. A one-way valve between the mask
and the reservoir bag and a flap over one of the exhalation ports on the side of the mask prevent the
inhalation of room air (Fig. 2.9B). When the patient breathes in, oxygen is drawn into the mask from
the reservoir (ie, bag) through the one-way valve that separates the bag from the mask. When the patient
breathes out, the exhaled air exits through the open side port on the mask. The one-way valve prevents
the patient’s exhaled air from returning to the reservoir bag (thus the name nonrebreather). This ensures a
supply of 100% oxygen to the patient, with minimal dilution from room air.
A nonrebreather mask is the delivery device of choice when high concentrations of oxygen are needed
for the spontaneously breathing patient. Depending on the patient’s breathing pattern, the fit of the
mask, and the oxygen flowmeter setting, oxygen concentrations of 60% to 80% can be delivered when
an oxygen flow rate (typically a minimum of 10 L/min) is used that prevents the reservoir bag from col-
lapsing completely on inspiration (Heuer, 2013). Inflate the reservoir bag with oxygen before placing the
nonrebreather mask on the patient. Advantages and disadvantages of using a nonrebreather mask are
shown in Box 2.5. A summary of oxygen percentages by device is shown in Table 2.1.
ACLS Pearl
When using a partial rebreather or nonrebreather mask, make sure that the bag does not collapse
when the patient inhales. Should the bag collapse, increase the delivered oxygen by 2 L increments
until the bag remains inflated during inhalation. The reservoir bag must remain at least two-thirds full
so that sufficient supplemental oxygen is available for each breath.
BOX 2.5 Nonrebreather Mask—Advantages and Disadvantages

• Higher oxygen concentration delivered than by • Can only be used with a spontaneously
nasal cannula, simple face mask, and partial breathing patient
rebreather mask • Not tolerated well in severely dyspneic patients
• Inspired oxygen is not mixed with room air • Can be uncomfortable
• Difficult to hear the patient speaking when the
device is in place
• Mask must fit snugly on the patient’s face to
prevent room air from mixing with oxygen inhaled
from the reservoir bag
• May cause skin irritation
TABLE 2.1 Oxygen Percentage Delivery by Device

Approximate Inspired Oxygen
Device Concentration Liter Flow (Liters/Minute)
Nasal cannula 23% to 32% 1 to 5
Simple face mask 35% to 60% 5 to 10
Partial rebreather mask 35% to 60% Typically, 6 to 10 to prevent bag collapse on
inspiration
Nonrebreather mask 60% to 80% Typically, a minimum of 10 to prevent bag
collapse on inspiration
MANUAL AIRWAY MANEUVERS

The most common cause of a partial airway obstruction in an unresponsive patient is the result of a loss of
muscle tone, which causes the tongue to fall back into the pharynx and block airflow. Manual airway
maneuvers are performed to lift the tongue off the back of the throat and open the airway.
If the unresponsive patient is breathing, snoring sounds are a sign of airway obstruction from displace-
ment of the tongue. If the patient is not breathing, airway obstruction from the tongue may go undetected
until positive pressure ventilation is attempted. Ventilating a nonbreathing patient with an airway
obstruction is difficult. If the airway obstruction is caused by the tongue, repositioning the patient’s head
and jaw may be all that is needed to open the airway.
Head Tilt–Chin Lift

[Objective 4]
The head tilt–chin lift is the preferred technique for opening the airway of an unresponsive patient with-
out suspected cervical spine injury (Kleinman, et al., 2015). Follow these steps to perform a head tilt–chin
lift:
1. Place the patient in a supine position.
2. Place one hand on the patient’s forehead, and apply downward pressure with your palm to gently tilt
the patient’s head back (Fig. 2.10).
3. Place the tips of the fingers of your other hand under the bony part of the patient’s chin, and gently lift
up and pull the jaw forward. Positioning your fingers under the bony part of the patient’s chin is
important because compression of the soft tissue under the patient’s chin can obstruct the airway.
4. If needed, open the patient’s mouth by pulling down on the patient’s lower lip using the thumb of the
same hand used to lift the chin.
Fig. 2.10 Opening the airway with a head tilt–chin lift maneuver. (From Kacmarek, Stoller, Heuer: Egan's fundamentals of
respiratory care, ed 10, St. Louis, 2013, Mosby.)
Jaw Thrust
[Objective 4]
A jaw thrust maneuver may be performed with or without an accompanying head tilt. For patients who
are unresponsive without any risk of spinal injury, perform the following technique:
1. With the patient supine, position yourself above the patient’s head or at his or her side, looking at
the face.
2. Place your fingers on each side of the lower jaw at the angle of the jaw near the bottom of the
patient’s ears.
3. Lift the jaw forward toward the patient’s face and gently open the mouth.
4. Gently tilt the patient’s head while maintaining displacement of the lower jaw.
The jaw thrust without neck extension maneuver (also called the modified jaw thrust) is the technique
that is recommended for opening the airway when cervical spine injury is suspected. Perform the follow-
ing for a jaw thrust without neck extension maneuver:
1. Ensure that the patient is in a supine position.
2. While stabilizing the patient’s head in a neutral position, grasp the angles of the patient’s lower jaw
with your fingertips (Fig. 2.11).
3. Displace the lower jaw forward.
The jaw thrust without neck extension maneuver is a difficult technique for one person to manage. In
most cases, one rescuer is needed to displace the patient’s lower jaw forward while a second rescuer ven-
tilates the patient. Health care professionals should use the head tilt–chin lift maneuver to open the air-
way if use of the jaw thrust without neck extension maneuver is unsuccessful (Kleinman, et al., 2015).
Manual airway maneuvers are summarized in Table 2.2.
Fig. 2.11 The jaw thrust without neck extension maneuver is used to open the airway when cervical spine injury is sus-
pected. (From Kacmarek, Stoller, Heuer: Egan's fundamentals of respiratory care, ed 10, St. Louis, 2013, Mosby.)
TABLE 2.2 Manual Airway Maneuvers

Considerations Head Tilt–Chin Lift Jaw Thrust without Neck Extension
Indications • Unresponsive patient with no mechanism for • Unresponsive patient with possible
cervical spine injury cervical spine injury
Advantages • Simple to perform • No equipment required
• No equipment required • Noninvasive
• Noninvasive
Disadvantages • Does not protect the lower airway from • Difficult to maintain
aspiration • Second rescuer needed for bag-mask
• May cause spinal movement ventilation
• Does not protect the lower airway
from aspiration
• May cause spinal movement
SUCTIONING
[Objective 5]
Suctioning is performed for the following reasons:
• To remove vomitus, saliva, blood, or foreign material from the patient’s airway
• To maintain patency of an artificial airway (eg, ETT, tracheostomy tube)
• To improve gas exchange by allowing air to pass through to the lower airway
• To obtain secretions for diagnosis
Rigid suction catheters, also called tonsil tip or Yankauer catheters, are made of hard plastic and angled
to help with the removal of secretions from the mouth and throat (Fig. 2.12). Because of its size, a rigid
suction catheter is not used to suction the nares, except externally. The catheter typically has one large and
several small holes at the distal end through which particles may be suctioned. The HI-D Big Stick suc-
tion tip (SSCOR, Inc., Sun Valley, CA) is a large-bore suction tip that is effective in clearing vomitus and
secretions from the upper airway (Fig. 2.13).
Soft suction catheters are also called whistle tip, flexible, or French catheters. They are long, narrow,
flexible pieces of plastic that are used to clear blood or mucus from the oropharynx or nasopharynx, an
ETT, or a tracheostomy tube (Fig. 2.14). When suctioning the lower airway, the outer diameter of the
suction catheter should be no more than half the internal diameter of the tracheal or tracheostomy tube to
minimize the risk of atelectasis and hypoxemia when suction is applied (Tiffin, et al., 1990).
Fig. 2.12 A rigid suction catheter is used to remove secretions from the mouth and throat. (From Perry, Potter: Clinical
nursing skills & techniques, ed 8, St. Louis, 2013, Mosby.)
HI-D Big Stick suction tip
5/16”
suction tubing
Fig. 2.13 The HI-D Big Stick suction tip is effective in clearing vomitus and secretions from the upper airway. (From Roberts J:
Roberts and Hedges’ clinical procedures in emergency medicine, ed 6, Philadelphia, 2014, Saunders.)
Fig. 2.14 A soft suction catheter is used to remove secretions from the lower airway. (From Perry, Potter: Clinical nursing
skills & techniques, ed 8, St. Louis, 2013, Mosby.)
A suction catheter is inserted without applying suction. Suction is applied as the catheter is withdrawn
and should not be applied for more than 10 seconds to avoid hypoxia. After suctioning, reevaluate airway
patency and auscultate lung sounds. Document the amount, color, and consistency of any secretions that
are obtained. Possible complications of suctioning are shown in Box 2.6.
ACLS Pearl
Although microorganisms are present throughout the airway, the mouth and throat are considered
“clean” areas and the portion of the airway below the glottis is considered “sterile” because the
upper airway contains more microorganisms than the lower airway. When a patient requires both
upper and lower airway suctioning, change catheters after suctioning the upper airway and before
suctioning the lower airway. Alternately, the same suction catheter may be used if lower airway suc-
tioning is performed before upper airway suctioning. Suctioning the lower airway first leads to less
potential for transmission of microorganisms to the lungs.
BOX 2.6 Suctioning—Possible Complications

• Arrhythmias • Hypoxia
• Bradycardia and hypotension from vagal • Increased intracranial pressure
stimulation • Local swelling
• Bronchospasm • Tachycardia
• Hemorrhage • Tracheal infection
• Hypertension • Tracheal trauma
AIRWAY ADJUNCTS
Manual maneuvers facilitate the opening of an airway. Airway adjuncts, such as pharyngeal airways, are devices
that assist in keeping the airway open by keeping the tongue away from the posterior wall of the pharynx.
Oral Airway
[Objective 6]
An oral airway, also called an oropharyngeal airway or OPA, is a J-shaped plastic device that is used to
create an air passage between the patient’s mouth and the posterior wall of the pharynx. Because oral
airway insertion may provoke vomiting and thus increase the risk of aspiration in a patient with an intact
gag reflex, indications for insertion include patients who are unresponsive and have no gag reflex. An oral
airway may be used as a bite block after the insertion of a tracheal tube or an orogastric tube.
Oral airways are available in a variety of sizes that range from 0 for neonates up to 6 for large adults.
The size of the airway is based on the distance, in millimeters, from the flange to the distal tip.
There are two main oral airway designs. The Guedel airway has a tubular design with a single center chan-
nel that allows for ventilation and the passage of a suction catheter (Fig. 2.15A). The Berman airway has two
Oropharyngeal tube in place
Body (2)
Flange (1)
Channel (3)
A Flange (1)
Body (2)
Channel (3)
B C
Fig. 2.15 A, Guedel oral airway. B, Berman oral airway. C, Oral airway in place. (From Kacmarek, Stoller, Heuer: Egan's
fundamentals of respiratory care, ed 10, St. Louis, 2013, Mosby.)
airway channels along each side of the device through which a suction catheter can be passed to remove secre-
tions from the back of the throat (Fig. 2.15B). When correctly positioned, the flange of the device rests on the
patient’s lips or teeth. The distal tip lies between the base of the tongue and the back of the throat, thereby
preventing the tongue from blocking the airway (Fig. 2.15C). Air passes around and through the device.
Proper oral airway size is determined by holding the device against the side of the patient’s face and
selecting an airway that extends from the corner of the mouth to the tip of the earlobe or to the angle of
the jaw (Fig. 2.16). To prevent inaccurate measurements for patients who experience facial drooping after
a stroke, some experts recommend measuring from the first incisor or from the center of the lips to the tip
of the earlobe or to the angle of the jaw. If an oral airway is too long, it may press the epiglottis against the
entrance of the larynx, which may result in a complete airway obstruction (Fig. 2.17). If the airway is too
short, it will not displace the tongue, and it may advance out of the mouth (Fig. 2.18).
When inserting an oral airway into a patient’s mouth, hold the device at its flange end and insert it
with the tip pointing toward the roof of the mouth (Fig. 2.19). As the distal end nears the back of the
throat, rotate the airway 180 degrees so that it is positioned over the tongue. Alternatively, the airway can
be inserted sideways and rotated 90 degrees into position. When the oral airway is inserted properly, the
flange should rest comfortably on the patient’s lips or teeth. The proper placement of the device is con-
firmed by ventilating the patient. If the airway is placed correctly, chest rise should be visible and breath
sounds should be present on auscultation of the lungs during ventilation. If the patient is not breathing or
if his or her breathing is inadequate, begin positive pressure ventilation.
Another method of oral airway insertion requires the use of a tongue blade to depress the tongue. If
this method is used, the airway is inserted with its tip facing the floor of the patient’s mouth (ie, curved
side down). With the use of the tongue blade to depress the tongue, the oral airway is advanced gently
into place over the tongue.
If the patient’s gag reflex returns or if he or she spontaneously attempts to displace the airway, remove
the airway to minimize the risk of aspiration.
Fig. 2.16 Select an oral airway of appropriate size. (From Roberts J: Roberts and Hedges’ clinical procedures in emergency
medicine, ed 6, Philadelphia, 2014, Saunders.)
Fig. 2.17 An oral airway that is too long may press the epiglottis against the entrance of the larynx, which may result in a
complete airway obstruction. (From McSwain N, Paturas J: The basic EMT, ed 2, 2003, Mosby.)
Fig. 2.18 An oral airway that is too short will not displace the tongue, and it may advance out of the mouth. (From McSwain
N, Paturas J: The basic EMT, ed 2, 2003, Mosby.)
Fig. 2.19 Open the patient’s mouth and insert the oral airway with the tip pointing toward the roof of the mouth. (From
Roberts J: Roberts and Hedges’ clinical procedures in emergency medicine, ed 6, Philadelphia, 2014, Saunders.)
Nasal Airway
[Objective 6]
A nasal airway (also called a nasopharyngeal airway, NPA, or nasal trumpet) is a soft, uncuffed tube made
from rubber or plastic polymers that is designed to keep the tongue away from the back of the throat.
Indications for the use of a nasal airway include unresponsive patients or those with an altered level of
consciousness who continue to have an intact gag reflex but who need assistance with maintaining an
Fig. 2.20 Nasal airways. (From Harkreader, Hogan, Thobaben: Fundamentals of nursing: caring and clinical judgment, ed 3,
St. Louis, 2007, Saunders.)
open airway. A nasal airway should not be used with patients who have sustained trauma to the nasal area
or when space-occupying lesions or foreign objects block the nasal passages (Barnes, 2013).
Nasal airways are available in many sizes varying in length and internal diameter (Fig. 2.20). Proper
airway size is determined by holding the device against the side of the patient’s face and selecting an
airway that extends from the tip of the nose to the angle of the jaw or to the earlobe (Fig. 2.21). A nasal
airway that is too long may stimulate the gag reflex; one that is too short may not be inserted far enough to
keep the tongue away from the back of the throat.
Before inserting a nasal airway, lubricate the distal tip of the device liberally with a water-soluble lubri-
cant to minimize resistance and to decrease the irritation of the nasal passage. Hold the nasal airway at its
flange end like a pencil, and slowly insert it into the larger of the patient’s two nares, with the bevel facing
the nasal septum (Fig. 2.22). During insertion, do not force the airway, because it may cut or scrape the
nasal mucosa; this may result in significant bleeding, which increases the risk of aspiration. Bleeding can
occur in up to 30% of patients after nasal airway insertion (Link, et al., 2015). If resistance is encountered,
a gentle back-and-forth rotation of the device between your fingers may ease insertion. If resistance con-
tinues, withdraw the nasal airway, reapply lubricant, and attempt insertion in the patient’s other nostril.
Advance the airway along the floor of the nostril, following the natural curvature of the nasal passage
until the flange is flush with the nostril. If blanching of the nostril is observed after placement of the
Fig. 2.21 A nasal airway of proper size extends from the tip of the patient’s nose to the angle of the jaw or to the earlobe.
(From Roberts J: Roberts and Hedges’ clinical procedures in emergency medicine, ed 6, Philadelphia, 2014, Saunders.)
Fig. 2.22 Nasal airway insertion. (From Roberts J: Roberts and Hedges’ clinical procedures in emergency medicine, ed 6,
Philadelphia, 2014, Saunders.)
TABLE 2.3 Oral and Nasal Airways

Considerations Oral Airway Nasal Airway
Indications • Helps maintain an open airway in an • To aid in maintaining an airway when
unresponsive patient with no gag reflex use of an oral airway is contraindicated
who is not intubated or difficult to place such as when the
• Helps maintain an open airway in an patient’s jaw is clenched during a
unresponsive patient with no gag reflex seizure or if oral trauma is present
who is being ventilated with a bag-mask
or other positive pressure device
• May be used as a bite block after
insertion of a tracheal tube or orogastric
tube
Contraindications • Responsive patient with an intact gag • Severe craniofacial trauma
reflex • Patient intolerance
Sizing • Corner of the mouth to the tip of the • Tip of nose to the angle of the jaw or the
earlobe or the angle of the jaw earlobe
Advantages • Positions the tongue forward and away • Provides a patent airway
from the back of the throat • Tolerated by responsive patients
• Easily placed • Does not require the mouth to be open
Disadvantages • Does not protect the lower airway from • Does not protect the lower airway from
aspiration aspiration
• May produce vomiting if used in a • Improper technique may result in severe
responsive or semiresponsive patient bleeding; resulting epistaxis may be
with a gag reflex difficult to control
• Suctioning through the device is difficult
• Although tolerated by most responsive
and semiresponsive patients, can
stimulate the gag reflex in sensitive
patients, precipitating vomiting,
gagging, or laryngospasm
Precautions • Use of the device does not eliminate the • Use of the device does not eliminate the
need for maintaining proper head need for maintaining proper head
position position
adjunct, the diameter of the nasal airway is too big. The nasal airway should be removed and a smaller
airway should be inserted.
The proper placement of the device is confirmed by ventilating the patient. If the nasal airway is cor-
rectly placed, chest rise should be visible, and breath sounds should be present on auscultation of the
lungs during ventilation. If the patient is not breathing or if breathing is inadequate, begin positive pres-
sure ventilation. Indications, contraindications, advantages, and disadvantages of oral and nasal airways
are shown in Table 2.3.
POSITIVE PRESSURE VENTILATION

[Objective 7]
Adequate oxygenation requires an open airway and adequate air exchange. After the airway has been
opened, determine whether the patient’s breathing is adequate or inadequate. If ventilatory efforts are
inadequate, the patient’s breathing may be assisted by forcing air into the lungs (ie, delivering positive
pressure ventilations). NPPV, mouth-to-mask ventilation, and BMV are examples of methods that may
be used to deliver positive pressure ventilation.
Noninvasive Positive Pressure Ventilation

[Objectives 7, 8]
NPPV, also called noninvasive ventilation (NIV), is the delivery of ventilatory support to a spontaneously
breathing patient without using an invasive artificial airway (eg, ETT, tracheostomy tube). NPPV has
been effectively used to avoid or decrease the rates of endotracheal intubation and to improve outcomes
(eg, reduce rates of mortality, decrease duration of hospital stays) in patients with severe exacerbations of
COPD or acute cardiogenic pulmonary edema, in immunosuppressed patients with acute respiratory
distress or failure, and as an adjunct to early liberation from mechanical ventilation in patients who have
COPD (Keenan, et al., 2011). In general, the best candidates for NPPV are cooperative, able to protect
their airway, and are hemodynamically stable (Liesching, et al., 2003).
Although a number of interfaces are available, the patient typically wears a nasal mask, oronasal mask,
or full face mask equipped with straps to hold the mask firmly in place. Ventilatory support is provided by
means of a portable or standard ventilator.
The term noninvasive positive pressure ventilation encompasses various modes of positive pressure ven-
tilation including CPAP and BPAP, but these modes of NPPV are distinctly different. With noninva-
sive CPAP, a continuous pressure that is greater than atmospheric pressure is delivered throughout the
respiratory cycle. CPAP provides airway support by splinting open the upper airway, increasing lung
volume, and increasing intrathoracic pressure, but it does not decrease the workload of the patient’s inspi-
ratory muscles during breathing (Hess, 2013). Because CPAP is helpful in improving alveolar oxygen-
ation, it is more effective in hypoxemic conditions (eg, heart failure) than in hypercapnic states. When
BPAP is administered, two levels of pressure are applied; a higher pressure is used during inspiration (ie,
inspiratory positive airway pressure) and a lower pressure is used during expiration (expiratory positive
airway pressure), thus decreasing the patient’s inspiratory muscle workload. BPAP is useful in hypercap-
nic failure (eg, exacerbations of COPD) as well as in mixed hypoxic and hypercapnic failure. Contrain-
dications for NPPV are shown in Box 2.7.
ACLS Pearl
Because BPAP is the most common mode used with NPPV, some clinicians use the terms BPAP and
NPPV synonymously.
BOX 2.7 Noninvasive Positive Pressure Ventilation—Contraindications

• Cardiac arrest • Inability to fit mask
• Complete upper airway obstruction • Inability to protect airway
• Excessive secretions • Recent facial, esophageal, or gastric surgery
• Facial trauma or deformity • Respiratory arrest
• Hemodynamic instability • Uncontrolled vomiting
• High risk for aspiration • Uncooperative patient
Mouth-to-Mask Ventilation
[Objectives 7, 9]
The device used for mouth-to-mask ventilation is commonly called a pocket mask, pocket face mask, ven-
tilation face mask, or resuscitation mask. A pocket face mask is a clear, semirigid mask that is sealed around
Fig. 2.23 Pocket mask. (Courtesy Laerdal Medical.)

the patient’s mouth and nose (Fig. 2.23). Masks used for ventilation should be made of transparent mate-
rial to allow assessment of the patient’s lip color and detection of vomitus, secretions, or other substances
and they should be equipped with an oxygen inlet and a standard connector that enables connection to a
bag-mask (or other ventilation) device.
When ventilating with a patient using a pocket mask, connect a one-way valve to the ventilation port
on the mask. If an oxygen inlet is present on the mask and oxygen is available, connect oxygen tubing to
the oxygen inlet, and set the flow rate at 10 to 12 L/min.
Position yourself at the patient’s head or side. Positioning yourself directly above the patient’s head
allows you to watch the patient’s chest while delivering ventilations. This position is used if the patient is
in respiratory arrest (but not cardiac arrest) or when two-rescuer cardiopulmonary resuscitation (CPR) is
being performed. If you are by yourself, positioning yourself at the patient’s side allows you to maintain
the same position for both rescue breathing and chest compressions.
Open the patient’s airway. If needed, clear the patient’s airway of secretions or vomitus. If the
patient is unresponsive and has no gag reflex, insert an oral airway. Select a mask of appropriate size
and place it on the patient’s face. A mask of correct size should extend from the bridge of the nose to the
groove between the lower lip and chin. If the mask is not properly positioned and a tight seal main-
tained, air will leak from between the mask and the patient’s face, thereby resulting in the delivery of
less tidal volume to the patient. Less tidal volume results in less lung inflation, which means less
oxygenation.
The E-C clamp technique, also called the E-C grip, can be used to create a good face-to-mask seal and
provide effective ventilation (Fig. 2.24). Apply the narrow portion (ie, apex) of the mask over the bridge of
the patient’s nose and stabilize it in place with your thumbs. Lower the mask over the patient’s face and
mouth. Use your index fingers to stabilize the wide end (ie, base) of the mask over the groove between
the patient’s lower lip and chin. When properly positioned, your thumb and index finger will create a
“C.” Gently push down on the mask to establish an adequate mask seal. Position your remaining fingers
along the angle of the jaw to form an “E.” Use these fingers to lift the jaw and pull the patient’s chin into
the mask. Ventilate the lungs through the one-way valve on the top of the mask at a rate of one breath every 5
to 6 seconds, or about 10 to 12 breaths/min. Deliver each breath over 1 second and stop ventilation when
gentle chest rise is observed.
Fig. 2.24 The E-C clamp technique for mouth-to-mask or BMV. (From Roberts J: Roberts and Hedges’ clinical procedures in
emergency medicine, ed 6, Philadelphia, 2014, Saunders.)
ACLS Pearl
Gastric distention is a complication of positive pressure ventilation that can lead to vomiting and
subsequent aspiration. Gastric distention also restricts movement of the diaphragm, impeding ven-
tilation, and decreases the effectiveness of CPR if the patient is in cardiac arrest.
Another method used for ventilation is the thenar eminence (TE) technique, also called the TE grip.
When the TE method is used, the TEs of both hands are used to hold the mask in place (Fig. 2.25). The
rescuer’s fingers are positioned under the angle of the patient’s mandible to perform a jaw lift (Fig. 2.26).
Research has shown that use of the TE technique is easier for inexperienced providers and results in
improved ventilation compared with the E-C clamp technique (Gerstein, et al., 2013). Indications,
advantages, and disadvantages of mouth-to-mask ventilation are shown in Table 2.4.
Fig. 2.25 The thenar eminences of both hands of the re- Fig. 2.26 The rescuer’s fingers are positioned under the angle
scuer hold the face mask firmly in place. (From Roberts J: of the patient’s mandible to perform a jaw lift. (From Roberts J:
Roberts and Hedges’ clinical procedures in emergency Roberts and Hedges’ clinical procedures in emergency medicine,
medicine, ed 6, Philadelphia, 2014, Saunders.) ed 6, Philadelphia, 2014, Saunders.)
TABLE 2.4 Mouth-to-Mask Ventilation

Inspired Oxygen • Without supplemental oxygen equals about 16% to 17% (exhaled air)
Concentration • Mouth-to-mask breathing combined with supplemental oxygen at a minimum flow rate of
10 L/min equals about 50%
Advantages • Esthetically more acceptable than mouth-to-mouth ventilation
• Easy to teach and learn
• Physical barrier between the rescuer and the patient’s nose, mouth, and secretions
• Reduces (but does not prevent) the risk of exposure to infectious diseases
• Use of a one-way valve at the ventilation port decreases exposure to the patient’s
exhaled air
• If the patient resumes spontaneous breathing, the mask can be used as a simple face
mask to deliver 40% to 60% oxygen by giving supplemental oxygen through the oxygen
inlet on the mask (if so equipped)
• Can deliver a greater tidal volume compared with a BMD
• Rescuer can feel the compliance of the patient’s lungs (compliance refers to the
resistance of the patient’s lung tissue to ventilation)
Disadvantages • Rescuer fatigue
• Possible gastric distention
Bag-Mask Ventilation
[Objective 7]
A BMD is a self-inflating bag with a nonrebreathing valve mechanism (Fig. 2.27). A BMD may also be referred
to as a bag-mask, bag-valve-mask device or bag-mask resuscitator (when the mask is used), or as a bag-valve device
(when the mask is not used [ie, when ventilating a patient with a tracheal tube or tracheostomy tube in place]).
The BMD should be equipped with a transparent disposable plastic mask with a high-volume, low-pressure
cuff; standard fittings to allow for attachment of the device to a standard mask, advanced airway, or other ven-
tilation device; and an oxygen-collecting device (ie, reservoir) to allow delivery of high concentrations of oxygen.
Oxygen Delivery
[Objective 9]
When using a BMD, the amount of delivered O2 is dependent on the ventilatory rate, the volume deliv-
ered during each breath, the O2 flow rate into the ventilating bag, the filling time for the reservoir bag,
Fig. 2.27 Bag-mask devices. (Courtesy Laerdal Medical.)

and the type of reservoir used (Reardon, et al., 2014a). Delivered tidal volumes vary with bag type, hand
size, and patient body characteristics (Rouse & Frakes, 2010).
A BMD that is used without supplemental oxygen will deliver 21% oxygen (ie, room air) to the
patient. The BMD should be connected to an oxygen source. To do this, attach one end of a piece
of oxygen connecting tubing to the oxygen inlet on the BMD and the other end to an oxygen regulator.
A BMD that is used with supplemental oxygen set at a flow rate of 10 to 15 L/min delivers approximately
40% to 60% oxygen to the patient when a reservoir is not used.
Ideally, an oxygen reservoir should be attached to the bag-mask to deliver a high concentration
of oxygen. The reservoir collects a volume of 100% oxygen that is equal to the capacity of the bag.
After squeezing the bag, it reexpands and draws 100% oxygen from the reservoir into the bag.
A BMD that is used with supplemental oxygen set at a flow rate of 10 to 15 L/min and with an attached
reservoir delivers approximately 90% to 100% oxygen to the patient. Advantages and disadvantages of
BMV are shown in Box 2.8.
Ventilating with a Bag-Mask Device

[Objectives 7, 10]
Performing positive pressure ventilation with a BMD can be difficult. Several reasons contribute to this,
but none as much as the inability to create a good seal with the mask while simultaneously generating an
adequate tidal volume by squeezing the bag. BMV should be a two-rescuer operation. With two people,
one is assigned the responsibility of opening and maintaining the airway while creating a good seal with
the mask. That frees a second person to squeeze the bag.
To ventilate a patient with a BMD, position yourself at the top of the supine patient’s head and
open the patient’s airway. If needed, clear the patient’s airway of secretions or vomitus. If the patient
is unresponsive, insert an oral airway. Next, select a bag and mask of appropriate size for the patient.
Connect the bag to the mask if this has not already been done. Connect the bag to oxygen at a flow rate
of 15 L/min, and attach a reservoir. Place the mask on the patient’s face. Create a good face-to-mask seal
with the mask positioned over the patient’s mouth and nose.
Although single-rescuer BMV is not recommended during CPR (Link, et al., 2015), if you find your-
self in this situation, press the mask firmly against the patient’s face with one hand using the E-C clamp
technique previously described (and simultaneously use it to maintain the patient’s proper head position),
and then squeeze the bag with the other hand (Fig. 2.28). If a second rescuer is present, the E-C clamp
technique or the TE technique can be used.
If an assistant is available, ask him or her to squeeze the bag until the patient’s chest rises while you
press the mask firmly against the patient’s face with both hands and simultaneously maintain the patient’s
proper head position (see Fig. 2.26). Observe the rise and fall of the patient’s chest with each ventilation.
Deliver each breath over 1 second and stop ventilation when gentle chest rise is observed. Ventilate the
adult patient at a rate of one breath every 5 to 6 seconds, or about 10 to 12 breaths/min.
ACLS Pearl
Assessment of chest rise, breath sounds, oxygen saturation, and capnography should be used to
evaluate the effectiveness of oxygenation and ventilation (Reardon, et al., 2014a).
A reliable indicator of adequate ventilation is the rise and fall of the patient’s chest wall with each
ventilation at an age-appropriate rate. Another indication that the patient is being well ventilated is
BOX 2.8 Bag-Mask Ventilation

Advantages • Provides a means for delivery of an oxygen-enriched mixture to the patient
• Can be used with the spontaneously breathing patient as well as with the
nonbreathing patient
• Conveys a sense of compliance of the patient’s lungs to the BMD operator
• Provides a means for immediate ventilatory support
Disadvantages • Requires practice to be used effectively
• Delivery of inadequate tidal volumes
• Causes rescuer fatigue
• Can lead to possible gastric distention
Fig. 2.28 Single-rescuer bag-mask ventilation using the E-C clamp. (From Sole ML, Klein DG, Moseley MJ: Introduction to
critical care nursing, ed 6, St Louis, 2013, Saunders.)
an improvement of the patient’s condition as evidenced by improvements in color, pulse oximeter read-
ings, heart rate, and responsiveness.
During BMV, avoid excessive ventilation (either by rate or volume) and allow adequate time for
exhalation to occur. Excessive ventilation decreases coronary perfusion pressure and may decrease the like-
lihood for return of spontaneous circulation in patients in cardiopulmonary arrest (Aufderheide, et al.,
2004). Also, feel for compliance when ventilating the patient’s lungs. Pulmonary compliance refers to
the resistance of the patient’s lung tissue to ventilation. The lungs are normally pliable and expand easily.
If the lungs feel stiff or inflexible, lung compliance is said to be poor. Upper airway obstruction, lower airway
obstruction, severe bronchospasm, and tension pneumothorax are examples of conditions that can cause
poor lung compliance and an inability to ventilate. If at any time you sense poor compliance, reassess the
patient to ensure that the airway remains unobstructed and that lung sounds are clear and equal.
Troubleshooting Bag-Mask Ventilation

[Objective 11]
The most frequent problems with BMV are the inability to deliver adequate ventilatory volumes and
gastric inflation (Reardon, et al., 2014a). The delivery of an inadequate ventilatory volume may be
the result of difficulty with providing a leak-proof seal to the face while simultaneously maintaining
an open airway, incomplete bag compression, or both. Gastric inflation may result if excessive force
and volume are used during ventilation.
If the chest does not rise and fall with BMV, reassess the patient in the following manner:
• Begin by reassessing the patient’s head position. Reposition the airway, and try to ventilate
again.
• Inadequate tidal volume delivery may be the result of an improper mask seal or incomplete bag com-
pression. If air is escaping from under the mask, reposition your fingers and the mask, and reevaluate
the effectiveness of bag compression.
• Check for an airway obstruction. Lift the jaw, and suction the airway as needed. If the chest still does
not rise, select an alternative method of positive pressure ventilation.
ADVANCED AIRWAYS
[Objective 12]
Extraglottic airway devices, formerly called supraglottic airways, are advanced airways that are blindly
inserted. They may be used in areas where tracheal intubation is not permitted, or in communities in
which health care providers have little opportunity to obtain experience with the technique of orotracheal
intubation as a result of having few patients. They may also be used by anesthesiologists for short, low-risk
procedures. Extraglottic airways are available in a range of sizes and can be placed while CPR is in pro-
gress, thereby minimizing interruptions when performing chest compressions (Anders, et al., 2014).
Examples of extraglottic airway devices include the esophageal-tracheal Combitube (Nellcor, Pleasanton,
CA), laryngeal mask airway (LMA) (Laryngeal Mask Company, Singapore) (Fig. 2.29), air-Q (Cookgas,
St. Louis, MO), i-gel (Intersurgical LTD, Wokingham, Berkshire, UK), laryngeal tube (King Airway-
LTS-D, King Systems, Noblesville, IN), and R€usch EasyTube (Teleflex Medical, Limerick, PA).
Endotracheal intubation is an example of an intraglottic airway procedure in which a tube is placed
directly into the trachea (Fig. 2.30). This procedure requires special training, equipment, and supplies
and may be performed for a variety of reasons including for the delivery of anesthesia, to assist a patient’s
breathing with positive pressure ventilation, and to protect the patient’s airway from aspiration.
Fig. 2.29 The laryngeal mask airway is an example of an extraglottic airway. (From Rothrock: Alexander's care of the patient
in surgery, ed 15, St. Louis, 2015.)
Fig. 2.30 Endotracheal intubation is an example of an intraglottic airway procedure. (From Pfenninger JL, Fowler GC: Pfen-
ninger and Fowler's Procedures for Primary Care, ed 3, Philadelphia, 2011, Saunders.)
ACLS Pearl
Advanced airway insertion requires a high degree of skill and knowledge as well as regular practice to
maintain proficiency. Regular practice, continuing education programs, and an effective quality
management program to monitor skill performance are essential for all health care professionals
who perform this skill.
Current resuscitation guidelines reflect that there is inadequate evidence to show a difference in sur-
vival or favorable neurologic outcome with the use of BMV compared with endotracheal intubation or
other advanced airway devices; further, the ideal timing of advanced airway placement to maximize out-
come has not been adequately studied (Link, et al., 2015). Therefore either a BMD or an advanced air-
way may be used for oxygenation and ventilation during CPR in both the in-hospital and out-of-hospital
setting (Link, et al., 2015). For health care providers trained in their use, either an extraglottic airway or
an ETT may be used as the initial advanced airway during CPR (Link, et al., 2015).
In cardiac arrest situations, members of the resuscitation team may opt to delay insertion of an
advanced airway until after several minutes of cardiac arrest management or until there is a return of
spontaneous circulation. If an advanced airway is not inserted, the patient should be ventilated at a rate
of 10 to 12 breaths per minute. If the decision is made to insert an advanced airway during the
resuscitation effort, ventilation does not require interruption (or even pausing) of chest compressions
once the advanced airway is in place—unless ventilation is inadequate when compressions are not paused
(Link, et al., 2015). After insertion of an advanced airway, the patient should be ventilated at a rate of one
breath every 6 seconds (10 breaths/min) (Link, et al., 2015). Avoid delivering an excessive number or
volume of ventilations.
ACLS Pearl
Remember that ventilating a cardiac arrest patient too fast or with too much volume results in exces-
sive intrathoracic pressure, which results in decreased venous return into the chest, decreased cor-
onary and cerebral perfusion pressures, diminished cardiac output, and decreased rates of survival.
Confirming Endotracheal Tube Placement

[Objective 13]
Methods that are used to verify the proper placement of an ETT include the following:
• Visualizing the passage of the tracheal tube between the vocal cords
• Auscultating the presence of bilateral breath sounds
• Confirming the absence of sounds over the epigastrium during ventilation
• Observing adequate chest rise with each ventilation
• Determining the absence of vocal sounds after the placement of the tracheal tube
• Measuring the level of EtCO2 (continuous waveform capnography is preferred)
• Verifying tube placement with the use of an EDD
• Obtaining a chest radiograph
In addition to these methods, some institutions use ultrasound imaging as an adjunct to monitor
proper ETT position. Do not rely exclusively on one method or device to detect and monitor for inadvertent
esophageal intubation.
Current resuscitation guidelines recommend the use of continuous waveform capnography in
addition to clinical assessment as the most reliable method of confirming and monitoring correct
placement of an ETT (Link, et al., 2015). A nonwaveform CO2 detector, EDD, or ultrasound used by
an experienced operator are reasonable alternatives if continuous waveform capnometry is not available
(Link, et al., 2015).
ACLS Pearl
An advanced airway that is misplaced or that becomes dislodged can be fatal. Make it a habit to
recheck the placement of an advanced airway immediately after insertion, after securing the tube,
during intrafacility or interfacility transport, and whenever the patient is moved. Be certain to docu-
ment the cm position of the tube at the patient’s teeth/lips. Capnography can be used to immediately
alert you to a misplaced or dislodged tube.
Esophageal Detector Devices

[Objective 13]
EDDs, also called esophageal intubation detectors, are used to help determine whether a tracheal tube is in
the trachea or the esophagus. There are two types of esophageal detectors: syringes and bulbs.
The syringe device is connected to a tracheal tube with the plunger fully inserted into the barrel of the
syringe. If the tube is in the trachea, the plunger can be easily withdrawn from the syringe barrel. If the
tracheal tube is in the esophagus, resistance will be felt when the plunger is withdrawn because the walls
of the esophagus will collapse when negative pressure is applied to the syringe. The EDD should be
checked for air leaks before use. If any connections are loose, the leak may allow the syringe to be easily
withdrawn, thus mimicking tracheal location of the tube (Reardon, et al., 2014b).
The bulb device is compressed before it is connected to a tracheal tube (Fig. 2.31). A vacuum is created
as the pressure on the bulb is released. If the tube is in the trachea, the bulb will refill easily when pressure
is released, thereby indicating proper tube placement. If the tracheal tube is in the esophagus, the bulb
will remain collapsed, which indicates improper tube placement. Conditions in which the trachea tends
to collapse can result in misleading findings. Examples of these conditions include morbid obesity, late
pregnancy, status asthmaticus, and the presence of profuse tracheal secretions.
Fig. 2.31 Bulb-type esophageal detector device. (From Sandberg, Urman, Ehrenfeld: The MGH textbook of anesthetic equip-
ment, Philadelphia, 2011, Saunders.)
If an EDD is used to confirm the placement of the tube, apply the device to the tube before the infla-
tion of the distal cuff. Inflating the cuff moves the distal end of the tracheal tube away from the walls of
the esophagus. If the tube was inadvertently inserted into the esophagus, this movement will cause the
detector bulb to reexpand, which falsely suggests that the tube is in the trachea.

The chapter quiz and case study that follow are provided to help you integrate the information presented
in this chapter. As you work through the case study, remember that there may be alternative actions that
are perfectly acceptable, yet not presented in the case study.
CHAPTER QUIZ
Multiple Choice
_____ 1. If no head or neck trauma is suspected, which of the following techniques should
health care professionals use to open the airway?
A. Tongue–jaw lift
B. Head tilt–chin lift
C. Head tilt–neck lift
D. Jaw thrust without neck extension
_____ 2. An oral airway:

A. May result in an airway obstruction if improperly inserted.
B. Is usually well tolerated in the responsive or semiresponsive patient.
C. Should be lubricated with a petroleum-based lubricant before insertion.
D. May inadvertently enter the cranial vault if used in a patient with a craniofacial injury.
_____ 3. Which of the following devices may be used to deliver positive pressure ventilation?
A. Nasal cannula
B. Pocket face mask
C. Simple face mask
D. Nonrebreather mask
_____ 4. Which of the following statements is true about a nasal airway?

A. A nasal airway can be placed in either nostril to help maintain an open airway.
B. A nasal airway should only be used in unresponsive patients who do not have a gag
reflex.
C. A correctly sized nasal airway extends from the corner of the patient’s mouth to the
tip of the ear lobe.
D. When properly positioned, the distal tip of the nasal airway rests in the patient’s
trachea.
_____ 5. Pulmonary compliance refers to:

A. The resistance of the patient’s lung tissue to ventilation.
B. The amount of gas inhaled or exhaled during a normal breath.
C. The exchange of oxygen and carbon dioxide during cellular metabolism.
D. The amount of air moved in and out of the respiratory tract in 1 minute.
_____ 6. You and a coworker arrive to find a 78-year-old woman unresponsive in bed. She is
not breathing but does have a pulse. You have a pocket face mask on hand that is
equipped with an oxygen inlet. After quickly connecting oxygen tubing to the inlet on
the mask, you should set the oxygen flow rate at:
A. 1 to 2 L/min.
B. 4 to 6 L/min.
C. 8 to 10 L/min.
D. 10 to 12 L/min.
_____ 7. Which of the following will deliver the highest oxygen concentration?
A. A nasal cannula with an oxygen flow rate of 4 L/min
B. A pocket mask with an oxygen flow rate of 10 L/min
C. A simple face mask with an oxygen flow rate of 8 L/min
D. A nonrebreather mask with an oxygen flow rate of 10 L/min
_____ 8. Signs of adequate ventilation when delivering ventilations with a BMD include:
A. The presence of gurgling sounds during ventilation.
B. The rise and fall of the patient’s chest wall with each ventilation.
C. The collapse of the oxygen reservoir on the BMD with each ventilation.
D. The BMD becomes progressively more difficult to compress with each ventilation.
_____ 9. Which of the following is not an example of an extraglottic airway device?

A. Laryngeal tube
B. ETT
C. LMA
D. Esophageal-tracheal Combitube
______ 10. A 19-year-old man is unresponsive and not breathing. A slow, weak pulse is present.
Your best course of action will be to:
A. Begin chest compressions.
B. Insert an advanced airway.
C. Administer oxygen by nasal cannula.
D. Insert an oral airway and begin BMV.
_____ 11. Tracheal intubation:

A. Is contraindicated in unresponsive patients.
B. Eliminates the risk of aspiration of gastric contents.
C. Should be preceded by efforts to ventilate by another method.
D. When attempted, should be performed in less than 60 seconds.
____ 12. When ventilating a patient by means of a BMD, rescuers can successfully deliver about
__ oxygen without the use of supplemental oxygen.
A. 16%
B. 21%
C. 50%
D. 80%
CASE STUDY 2-1

Your patient is an 85-year-old woman who presents with difficulty breathing. She has a long history of
COPD and has experienced increasing shortness of breath since yesterday. You have a sufficient number
of advanced life support personnel available to assist you and carry out your instructions. Emergency
equipment is available.
1. As you approach the patient, you observe that she is supine on a stretcher. Her eyes are
closed, her lips are blue, and her skin is pale. You see no signs of breathing. What should be
done next?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
2. The patient is unresponsive. What should be done next?

_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
3. The patient is not breathing but a carotid pulse is present. The rate is slow, weak, and regular. What
should be done now?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
4. How will you open the patient’s airway?

_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
5. A significant amount of mucus is observed in the patient’s mouth. How will you remedy this
problem?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
6. The patient’s airway is clear. You have asked a team member to insert an oral airway. How is proper
oral airway size determined?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
7. When is the use of an oral airway contraindicated?

_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
8. An oral airway has been inserted. The patient is still not breathing. What should be done now?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
9. Differentiate between the E-C clamp technique and the TE technique when performing BMV.
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
10. What are the most common problems associated with the use of BMV?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
11. The patient’s chest does not rise despite attempts to ventilate the patient with a BMD. What is the
first thing you should do to remedy this problem?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
12. Equal chest rise is now present with BMV. Breath sounds reveal clear upper lobes and diminished
sounds in the lower lobes bilaterally. The patient’s blood pressure is 108/74 mm Hg. She has been
placed on the cardiac monitor, which reveals the rhythm shown. What is the rhythm on the monitor?
What should be done now?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
(From Aehlert: ECGs made easy, ed 4, St. Louis, 2011, Mosby.)
13. Vascular access has been established with normal saline. An ETT has been inserted and the cuff
inflated. How will you confirm placement of the ETT?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
14. Waveform capnography confirms the presence of CO2. The ETT has been secured. What should be
done now?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________

1. B. The head tilt–chin lift is the preferred technique for opening the airway of an unresponsive patient
without suspected cervical spine injury. If trauma is suspected, the jaw thrust without neck extension
maneuver should be used. Health care professionals should use the head tilt–chin lift maneuver to
open the airway if use of the jaw thrust without neck extension maneuver is unsuccessful.
OBJ: Describe and demonstrate the steps needed to perform the head tilt–chin lift and jaw thrust
without neck extension maneuvers and relate the mechanism of injury to the opening of the airway.
2. A. An oral airway should only be used in unresponsive patients who have no cough or gag reflex
because it may stimulate vomiting or laryngospasm in responsive or semiresponsive patients. If
the airway is too long, it may press the epiglottis against the entrance of the larynx resulting in a
complete airway obstruction. If the airway is too short, it will not displace the tongue and may
advance out of the mouth. A petroleum-based lubricant should never be used because it may damage
the airway device and cause tissue inflammation. A nasal airway (not an oral airway) may inadver-
tently enter the cranial vault if it is inserted into the nose of a patient who has sustained a craniofacial
injury.
OBJ: Discuss the indications, contraindications, advantages, and disadvantages of oral and nasal
airways, and demonstrate how to correctly size and insert each of these airway adjuncts.
3. B. NPPV, mouth-to-mask ventilation, and BMV are examples of methods that may be used to
deliver positive pressure ventilation. The remaining devices listed (nasal cannula, simple face mask,
and nonrebreather mask) do not deliver a tidal volume; they are oxygen delivery devices and require a
spontaneously breathing patient.
OBJ: Describe methods by which positive pressure ventilation is delivered.
4. A. A nasal airway can be used in an unresponsive patient and may be useful in semiresponsive
patients who have a gag reflex. It can be placed in either nostril to help maintain an open airway.
To select a nasal airway of proper size, hold the device against the side of the patient’s face. Select an
airway that extends from the tip of the patient’s nose to the angle of the jaw or the earlobe. When a
nasal airway of the proper size is correctly positioned, the tip rests in the back of the throat.
5. A. Pulmonary compliance refers to the resistance of the patient’s lung tissue to ventilation. The lungs
are normally pliable and expand easily. If the lungs feel stiff or inflexible during positive pressure
ventilation, lung compliance is said to be poor. Upper airway obstruction, lower airway obstruction,
severe bronchospasm, and tension pneumothorax are examples of conditions that can cause poor
lung compliance and an inability to ventilate. If at any time you sense poor compliance, reassess
the patient to ensure that the airway remains unobstructed and that lung sounds are clear and equal.
Tidal volume is the amount of gas inhaled or exhaled during a normal breath. Respiration is the
exchange of oxygen and carbon dioxide during cellular metabolism. Minute volume is the amount
of air moved in and out of the respiratory tract in 1 minute.
OBJ: Recognize the signs of adequate and inadequate BMV.
6. D. If not already attached, connect a one-way valve to the ventilation port on the pocket face mask
and connect oxygen tubing to the oxygen inlet on the mask. Set the oxygen flow rate at 10 to
12 L/min.
OBJ: Describe the oxygen liter flow per minute and the estimated inspired oxygen concentration
delivered with a pocket face mask and a BMD.
7. D. Of the oxygen delivery devices listed, a nonrebreather mask with an oxygen flow rate of 10 L/min
will deliver the highest oxygen concentration.
OBJ: Describe the advantages, disadvantages, oxygen liter flow per minute, and estimated oxygen
percentage delivered with each of the following devices: nasal cannula, simple face mask, partial non-
rebreather mask, and nonrebreather mask.
8. B. A reliable indicator of ventilation adequacy is the rise and fall of the patient’s chest wall. Gurgling
sounds are abnormal and indicate the need for suctioning. If the oxygen reservoir on the BMD col-
lapses with each ventilation, it may indicate that the oxygen flow is too low or the ventilation rate is
too rapid. If the BMD becomes progressively more difficult to squeeze when ventilating a patient,
assess the need to suction, ensure that proper airway opening procedures are in use, suspect that there
may be excessive air in the stomach (anticipate vomiting), and suspect a possible pneumothorax.
9. B. An ETT is an intraglottic airway device that is placed directly into the trachea. Extraglottic airway
devices, formerly called supraglottic airways, are advanced airways that are blindly inserted. Examples
of extraglottic airway devices include the esophageal-tracheal Combitube, LMA, air-Q, i-gel, laryn-
geal tube, and R€ usch EasyTube.
OBJ: Differentiate between extraglottic airways and intraglottic airways.
10. D. The patient has experienced a respiratory arrest. Your best course of action will be to insert an oral
airway and begin positive pressure ventilation with a BMD. Chest compressions are not indicated
because the patient has a pulse. Although insertion of an advanced airway is appropriate, it must be
preceded by another form of ventilation (such as BMV) while preparations are made to insert the
airway. Use of a nasal cannula is inappropriate because it can only be used in a spontaneously breath-
ing patient.
OBJ: Differentiate among respiratory distress, respiratory failure, and respiratory arrest and
11. C. Tracheal intubation should be preceded by attempts to ventilate by another method. Tracheal
intubation is indicated in situations where the patient is unable to protect his/her own airway. Tra-
cheal intubation reduces (but does not eliminate) the risk of aspiration of gastric contents and, when
attempted, should be performed in less than 30 seconds.
OBJ: Describe methods that are used to confirm correct ETT placement.
12. B. A BMD that is used without supplemental oxygen will deliver 21% oxygen (ie, room air, not
expired air) to the patient. A BMD that is used with supplemental oxygen set at a flow rate of
10 to 15 L/min delivers approximately 40% to 60% oxygen to the patient when a reservoir is not
used. A BMD that is used with supplemental oxygen set at a flow rate of 10 to 15 L/min and with
an attached reservoir delivers approximately 90% to 100% oxygen to the patient.
CASE STUDY 2-1 ANSWERS

1. Your general impression should focus on three main areas that can be remembered by the mnemonic
ABC: Appearance, (work of) Breathing, and Circulation. As you finish forming your general
impression, you will have a good idea if the patient is sick (ie, unstable) or not sick (ie, stable). Begin
the primary survey by assessing responsiveness. Start by asking, “Are you all right?” or “Can you hear
me?” If there is no response, then gently tap or squeeze the patient’s shoulder while repeating
verbal cues.
2. Call for help and ask someone to get an automated external defibrillator (AED) or defibrillator.
Look at the chest for movement while simultaneously feeling for a pulse for 5 to 10 seconds.
3. If the patient had no pulse, you would direct your team to start chest compressions and attach an
AED to the patient. In this situation, chest compressions are not indicated because a pulse is present.
Open the airway and begin rescue breathing.
4. Because there is no evidence of trauma, open the patient’s airway using a head tilt–chin lift. If there
was anything that suggested trauma in this situation, you would open the airway with a jaw thrust
without neck extension maneuver. Look in the mouth for blood, broken teeth or loose dentures,
gastric contents, and foreign objects.
OBJ: Describe and demonstrate the steps needed to perform the head tilt–chin lift and jaw thrust
without neck extension maneuvers and relate the mechanism of injury to the opening of the airway.
5. Ask a team member to suction the patient’s upper airway. Suction should be applied as the catheter is
withdrawn and should not be applied for more than 10 seconds to avoid hypoxia.
OBJ: Describe and demonstrate the procedure for suctioning the upper airway, and discuss pos-
sible complications associated with this procedure.
6. Proper oral airway size is determined by holding the device against the side of the patient’s face and
selecting an airway that extends from the corner of the mouth to the tip of the earlobe or to the angle
of the jaw. To prevent inaccurate measurements for patients who experience facial drooping after a
stroke, some experts recommend measuring from the first incisor or from the center of the lips to the
tip of the earlobe or to the angle of the jaw.
7. The use of an oral airway is contraindicated in responsive patients who have an intact gag reflex. An
oral airway should only be used in unresponsive patients who have no gag reflex because it may stim-
ulate vomiting or laryngospasm in responsive or semiresponsive patients.
8. Begin positive pressure ventilation with a BMD connected to 100% oxygen. Ideally, two team mem-
bers should be assigned this task. Ask one team member to open and maintain the airway while
creating a good seal with the mask. Ask the other team member to squeeze the bag at an age-
appropriate rate. Ask a team member to assess baseline breath sounds while the patient is being
ventilated.
OBJ: Describe and demonstrate how to ventilate a patient with a BMD and two rescuers.
9. The E-C clamp technique can be used when performing mouth-to-mask or BMV. The rescuer’s
thumb and index finger form a “C” around the mask and the remaining fingers form an “E” on
the inferior portion of the patient’s mandible. If the rescuer is alone, one hand is used to form
the E-C clamp while the other is used to squeeze the bag. If a second rescuer is present, the first
rescuer uses both hands to form the E-C clamp while the second rescuer squeezes the bag. When
the TE method of ventilation is used, the TEs of both hands are used to hold the mask in place and
the rescuer’s fingers are positioned under the angle of the patient’s mandible to pull the jaw upward
toward the mask. A second rescuer is needed to squeeze the BMD.
10. The most frequent problems with BMV are the inability to deliver adequate ventilatory volumes and
gastric inflation. The delivery of an inadequate ventilatory volume may be the result of difficulty with
providing a leak-proof seal to the face while simultaneously maintaining an open airway, incomplete
bag compression, or both. Gastric inflation may result if excessive force and volume are used during
ventilation.
11. If the chest does not rise and fall with BMV, your first action should be to reposition the patient’s
head and try to ventilate again.
12. The rhythm is a sinus bradycardia. Ask a qualified team member to prepare to intubate the patient.
Ask another team member to start an IV with normal saline. Order a 12-lead electrocardiogram
(ECG) and portable chest radiograph and perform a focused physical examination. Resist the temp-
tation to treat the patient’s bradycardia with atropine. The most likely cause of the patient’s brady-
cardia is hypoxia. Make sure the patient is adequately oxygenated and ventilated before considering
other possible causes of the patient’s respiratory arrest or the use of atropine.
13. Attach a ventilation device to the ETT and ventilate the patient. Confirm proper placement of the
tube by visualizing the passage of the tracheal tube between the vocal cords. Next, auscultate over the
epigastrium (should be silent) and then in the midaxillary and anterior chest line on the right and left
sides of the patient’s chest. Observe the patient’s chest for adequate chest rise with ventilation. After
confirming proper tube position with the use of capnography, note the cm markings on the tracheal
tube and then secure the tube in place with a commercial tube holder or tape. Waveform capnogra-
phy is recommended for the continuous monitoring of proper tube placement. After securing the
tube, recheck and record the tube depth at the patient’s teeth. This value is typically between
the 19 and 23 cm marks on the tube at the front teeth. Average tube depth in men is 23 cm at
the lips, 22 cm at the teeth; average tube depth in women is 22 cm at the lips, 21 cm at the teeth.
OBJ: Describe methods that are used to confirm correct ETT placement.
14. Repeat the primary survey and obtain another set of vital signs. Order laboratory studies, evaluate the
patient’s 12-lead ECG and chest radiograph results, and attempt to determine possible causes of the
patient’s respiratory arrest. Transfer the patient for continued monitoring and care.
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CHAPTER 3
Cardiac Anatomy
and Electrophysiology
INTRODUCTION
A prerequisite to participation in most Advanced Cardiac Life Support (ACLS) courses is completion of
a basic electrocardiogram (ECG) recognition course. This requirement exists because there simply is not
time in an ACLS course to cover detailed information about rhythm recognition. A basic ECG course
teaches you how to identify cardiac rhythms. An ACLS course quickly reviews cardiac rhythms, but
focuses on teaching how to recognize serious signs and symptoms related to those rhythms and how
to manage them.
Normally, the heart beats at a very regular rate and rhythm. If this pattern is interrupted, an abnormal
heart rhythm can result. Although arrhythmia technically means “absence of rhythm” and dysrhythmia
means “abnormal heart rhythm,” these terms are used interchangeably by health care professionals to
refer to disturbances in cardiac rhythm. To help you understand and recognize cardiac dysrhythmias,
this chapter reviews the heart’s blood supply and normal conduction pathways; normal waveforms
and intervals; lead systems; and ECG changes associated with myocardial ischemia, injury, and
infarction.
G O A L Given a patient situation, correlate electrophysiologic, physiologic, and pathophysiologic
cardiac events with the patient’s presentation; direct or perform accurate placement for monitoring
leads and a standard 12-lead ECG; and associate coronary artery blood flow with areas of myo-
cardial ischemia, injury, and infarction.
LEARNING OBJECTIVES
1. Name the primary branches and areas of the heart supplied by the right and left coronary
arteries.
2. Define the events of the cardiac action potential and correlate them with the waveforms
produced on the ECG.
3. Define the absolute, effective, relative refractory, and supernormal periods and their
locations in the cardiac cycle.
4. Describe the normal sequence of electrical conduction through the heart.
63
64 CHAPTER 3 Cardiac Anatomy and Electrophysiology
5. Describe the location, function, and, where appropriate, intrinsic rate of the following
structures: the sinoatrial (SA) node, the atrioventricular (AV) bundle, and the Purkinje fibers.
6. Differentiate between the frontal plane and the horizontal plane leads.
7. Relate the cardiac surfaces or areas represented by the ECG leads.
8. Define and describe the significance of each of the following as they relate to cardiac
electrical activity: the P wave, the QRS complex, the T wave, the U wave, the PR
segment, the TP segment, the ST segment, the PR interval, the QRS duration, and
the QT interval.
9. Recognize the changes on the ECG that may reflect evidence of myocardial ischemia,
injury, and infarction.
LEARNING PLAN
• Read this chapter before class.
• Application of ECG monitoring leads.
• Recognition of myocardial ischemia, injury, and infarction on an ECG.
KEY TERMS
Absolute refractory period (ARP) Corresponds with the onset of the QRS complex to
approximately the peak of the T wave on the ECG; cardiac cells cannot be stimulated to
conduct an electrical impulse, no matter how strong the stimulus.
Accessory pathway An extra bundle of working myocardial tissue that forms a connection
between the atria and ventricles outside the normal conduction system.
Action potential A five-phase cycle that reflects the difference in the concentration of
charged particles across the cell membrane at any given time.
Acute coronary syndromes (ACSs) A group of conditions that are caused by an abrupt
reduction in coronary artery blood flow; ACSs consist of three major syndromes: unstable
angina, non–ST segment elevation myocardial infarction (NSTEMI), and ST segment–
elevation myocardial infarction (STEMI).
Atrioventricular (AV) junction AV node and the bundle of His.
AV node Specialized cells located in the lower portion of the right atrium; delays the electrical
impulse to allow the atria to contract and complete filling of the ventricles.
Bundle of His Fibers located in the upper portion of the interventricular septum that conduct
an electrical impulse through the heart.
Conduction system A system of pathways in the heart composed of specialized electrical
(ie, pacemaker) cells.
Depolarization Movement of ions across a cell membrane, causing the inside of the cell to
become more positive; an electrical event expected to result in contraction.
Effective refractory period (ERP) Period of the cardiac action potential that includes the
ARP and the first half of the relative refractory period.
Electrocardiogram (ECG) A recording of the heart’s electrical activity from the body surface
that appears on ECG paper as specific waveforms and complexes.
Electrode Adhesive pad that contains a conductive gel and is applied at a specific location on
the patient’s chest wall or extremities and is connected by cables to an ECG machine.
His-Purkinje system Portion of the conduction system consisting of the bundle of His,
bundle branches, and Purkinje fibers.
Interval On the ECG, a waveform and a segment.
Lead A record (ie, tracing) of electrical activity between two electrodes.
Myocardial cells Working cells of the myocardium that contain contractile filaments and form
the muscular layer of the atrial walls and the thicker muscular layer of the ventricular walls.
Pacemaker cells Specialized cells of the heart’s electrical conduction system capable of
spontaneously generating and conducting electrical impulses.
CHAPTER 3 Cardiac Anatomy and Electrophysiology 65
Refractoriness A term used to describe the period of recovery that cells need after being
discharged before they are able to respond to a stimulus.
Relative refractory period (RRP) Corresponds with the downslope of the T wave on the
ECG; cardiac cells can be stimulated to depolarize if the stimulus is strong enough.
Repolarization Movement of ions across a cell membrane in which the inside of the cell is
restored to its negative charge.
Segment On the ECG, a line between waveforms that is named by the waveform that
precedes or follows it.
Supernormal period (SNP) Period during the cardiac cycle when a weaker than normal
stimulus can cause cardiac cells to depolarize.
CORONARY ARTERIES
[Objective 1]
The right coronary artery (RCA) originates from the right side of the aorta. It travels along the groove
between the right atrium and right ventricle (Fig. 3.1). Blockage of the RCA can result in inferior wall
myocardial infarction (MI), disturbances in AV conduction, or both.
The left coronary artery (LCA) originates from the left side of the aorta. The first segment of the LCA
is called the left main coronary artery (LMCA). The LMCA supplies oxygenated blood to its two primary
branches: the left anterior descending artery (LAD), which is also called the anterior interventricular
artery, and the circumflex (CX) artery. Blockage of the proximal LAD coronary artery has been referred
to as the widow maker because of its association with sudden cardiac arrest when it is blocked.
The major branches of the LAD are the septal and diagonal arteries. Blockage of the septal branch of
the LAD can result in a septal MI. Blockage of the diagonal branch of the LAD can result in an anterior
wall MI. Blockage of the LAD can also result in pump failure, intraventricular conduction delays,
or both.
The CX coronary artery circles around the left side of the heart. Blockage of the CX artery can result in
a lateral wall MI. In some patients, the CX artery may also supply the inferior portion of the left ventricle.
A posterior wall MI may occur because of blockage of the RCA or the CX artery.
Superior vena cava Superior vena cava

Aortic arch
Pulmonary artery
Left atrium
Left main coronary artery

Left circumflex
coronary artery
Left anterior
descending
coronary
artery (LAD)
Diagonal
branch of LAD
Right ventricle
Left ventricle
Right coronary artery Right coronary artery
Fig. 3.1 Major coronary arteries and some of their branches. (From Benjamin I, Griggs RC, Wing EJ, Fitz JG, Andreoli TE:
Andreoli and Carpenter's Cecil essentials of medicine, ed 8, Philadelphia, 2011, Saunders.)
ACLS Pearl
A common cause of MI is an obstructed coronary artery. When viewing the patient’s 12-lead ECG, an
understanding of the coronary artery anatomy makes it possible to predict which coronary artery is
blocked.
CARDIAC CELLS
In general, cardiac cells have either a mechanical (ie, contractile) or an electrical (ie, pacemaker) function.
Myocardial cells are also called working cells or mechanical cells, and they contain contractile filaments.
When these cells are electrically stimulated, these filaments slide together and cause the myocardial cell to
contract. These myocardial cells form the thin muscular layer of the atrial walls and the thicker muscular
layer of the ventricular walls (ie, the myocardium). These cells do not normally generate electrical
impulses, and they rely on pacemaker cells for this function.
Pacemaker cells are specialized cells of the electrical conduction system. Pacemaker cells also may
be referred to as conducting cells or automatic cells. They are responsible for the spontaneous generation
and conduction of electrical impulses. The heart’s pacemaker cells can generate an electrical impulse
without being stimulated by a nerve. The ability of cardiac pacemaker cells to create an electrical impulse
without being stimulated by another source is called automaticity. Increased blood concentrations of cal-
cium (Ca++) increase automaticity. Decreased concentrations of potassium (K +) in the blood decrease
automaticity. The heart’s normal pacemaker (ie, the SA node) usually prevents other areas of the heart
from assuming this function because its cells depolarize more rapidly than other pacemaker cells.
CARDIAC ACTION POTENTIAL

[Objective 2]
Human body fluids contain electrolytes, which are elements or compounds that break into
charged particles (ie, ions) when melted or dissolved in water or another solvent. Cell membranes contain
pores or channels through which specific electrolytes and other small, water-soluble molecules can cross the
cell membrane from the outside to the inside (Fig. 3.2). A slight difference in the concentrations of charged
particles across the membranes of cells is normal. Potential energy (ie, voltage) exists because of the imbal-
ance of charged particles. This imbalance makes the cells excitable. The energy expended by the cells to
move electrolytes across the membranes of cells creates a flow of current. This flow of current is measured in
volts or millivolts (mV). Voltage appears on an ECG as spikes or waveforms.
ACLS Pearl
Differences in the composition of ions between the body’s intracellular and extracellular fluid com-
partments are important for normal function. The main electrolytes that affect the function of the
heart are Na +, K +, Ca++, and chloride (Cl ).
Membrane
channels
Open Closed
Fig. 3.2 Cell membranes contain membrane channels. These channels are pores through which specific ions or other small,
water-soluble molecules can cross the cell membrane from outside to inside. (From Patton KT, Thibodeau GA: Anatomy &
physiology, ed 8, St. Louis, 2013, Mosby.)
Depolarization
[Objective 2]
When a cell is stimulated, the cell membrane changes and becomes permeable to sodium (Na +) and K +,
allowing the passage of electrolytes once it is open. Na + rushes into the cell through Na + channels. This
causes the inside of the cell to become more positive relative to the outside. A spike (ie, a waveform) is
then recorded on the ECG. The stimulus that alters the electrical charges across the cell membrane may
be electrical, mechanical, or chemical.
When opposite charges come together, energy is released. When the movement of electrolytes
changes the electrical charge of the inside of the cell from negative to positive, an impulse is generated.
The impulse causes channels to open in the next cell membrane and then the next. The movement of
charged particles across a cell membrane that causes the inside of the cell to become positive is called
depolarization. Depolarization, which is an electrical event, must take place before the heart can contract
and pump blood, which is a mechanical event.
An impulse normally begins in the pacemaker cells found in the SA node of the heart. A chain reac-
tion occurs from cell to cell in the heart’s electrical conduction system until all the cells have been stim-
ulated and depolarized. This chain reaction is a wave of depolarization that proceeds from the innermost
layer of the heart (ie, endocardium) to the outermost layer (ie, epicardium). Eventually the impulse is
spread from the pacemaker cells to the working myocardial cells, which contract when they are stimu-
lated. When the atria are stimulated, a P wave is recorded on the ECG; thus the P wave represents atrial
depolarization. When the ventricles are stimulated, a QRS complex is recorded on the ECG; thus the
QRS complex represents ventricular depolarization.
ACLS Pearl
Depolarization is not the same as contraction. Depolarization is an electrical event that is expected to
result in contraction, which is a mechanical event. It is possible to see organized electrical activity on
the cardiac monitor, even when the assessment of the patient reveals no palpable pulse. This clinical
situation is called pulseless electrical activity (PEA).
Repolarization
[Objective 2]
After the cell depolarizes, it quickly begins to recover and restore its electrical charges to normal. The
movement of charged particles across a cell membrane in which the inside of the cell is restored to
its negative charge is called repolarization. The cell membrane stops the flow of Na + into the cell
and allows K + to leave it. Negatively charged particles are left inside the cell; thus the cell is returned
to its resting state. This causes contractile proteins in the working myocardial cells to separate (ie, relax).
The cell can be stimulated again if another electrical impulse arrives at the cell membrane. Repolarization
proceeds from the epicardium to the endocardium. On the ECG, the ST segment and T wave represent
ventricular repolarization.
Phases of the Cardiac Action Potential

[Objective 2]
The action potential of a cardiac cell reflects the rapid sequence of voltage changes that occur across the
cell membrane during the electrical cardiac cycle. The configuration of the action potential varies
depending on the location, size, and function of the cardiac cell (Fig. 3.3).
There are two main types of action potentials in the heart. The first type, the fast response action
potential, occurs in normal atrial and ventricular myocardial cells and in the Purkinje fibers, which are
specialized conducting fibers found in both ventricles that conduct an electrical impulse through the
heart. The second type of cardiac action potential, the slow response action potential, occurs in the heart’s
normal pacemaker (ie, the SA node) and in the AV node, which is the specialized conducting tissue that
carries an electrical impulse from the atria to the ventricles.
CARDIAC ACTION POTENTIALS
Ventricle Atrium Sinoatrial node

+20 1 1
Membrane potential (mV)

2
2
0
–20 0
3 0 3
–40 0
3
–60 4
–80 4 4
–100
A 100 msec B 100 msec C 100 msec
Fig. 3.3 Cardiac action potentials in the ventricle, atrium, and sinoatrial (SA) node. The numbers correspond to the phases
of the action potentials. A, Ventricle. B, Atrium. C, SA node. (From Costanzo LS: Physiology, ed 5, Philadelphia, 2014, Saunders.)
ACLS Pearl
Although there is no universally accepted classification scheme for antiarrhythmic agents, a com-
monly used system is to classify the medications by their effects on the cardiac action potential.
For example, Class I antiarrhythmic medications such as procainamide and lidocaine block sodium
channels, interfering with phase 0 depolarization. Class IV antiarrhythmics (ie, Ca++ channel
blockers) such as verapamil and diltiazem slow the rate at which calcium passes through the cells,
interfering with phase 2 in the cells of the atria, ventricles, and Purkinje fibers.
Refractory Periods
[Objective 3]
Refractoriness is a term that is used to describe the period of recovery that cells need after being dis-
charged before they are able to respond to a stimulus. During the ventricular absolute refractory period
(ARP), the cell will not respond to further stimulation within itself (Fig. 3.4). This means that the myo-
cardial working cells cannot contract and that the pacemaker cells cannot conduct an electrical impulse,
no matter how strong the internal electrical stimulus.
+20
0
Membrane potential (mV)
–20
RRP
ARP
–40
SNP
–60 ERP
–80
–100
Fig. 3.4 Refractory periods of the ventricular action potential. The effective refractory period (ERP) includes the absolute
refractory period (ARP) and the first half of the relative refractory period (RRP). The RRP begins when the ARP ends and includes
the last portion of the ERP. The supernormal period (SNP) begins when the RRP ends. (From Costanzo LS: Physiology, ed 5,
The effective refractory period (ERP) includes the ARP and the first half of the RRP (see Fig. 3.4).
“The distinction between the absolute and effective refractory periods is that absolute means absolutely no
stimulus is large enough to generate another action potential; effective means that a conducted action
potential cannot be generated (ie, there is not enough inward current to conduct to the next site).”
(Costanzo, 2014, p. 135)
The relative refractory period (RRP) begins at the end of the ARP and ends when the cell mem-
brane is almost fully repolarized. During the RRP, some cardiac cells have repolarized to their threshold
potential and thus can be stimulated to respond (ie, depolarize) to a stronger-than-normal stimulus.
After the RRP is a supernormal period (SNP). Because the cell is more excitable than normal during
this period, a weaker-than-normal stimulus can cause cardiac cells to depolarize and cause the develop-
ment of dysrhythmias (see Fig. 3.4).
CONDUCTION SYSTEM
The heart’s pacemaker cells are arranged in a system of interconnected pathways called the conduction
system. The conduction system makes sure that the chambers of the heart contract in a coordinated
fashion.
Sinoatrial Node
[Objectives 4, 5]
The normal heartbeat is the result of an electrical impulse (ie, an action potential) that begins in the SA
node. The SA node is normally the primary pacemaker of the heart because it has the fastest firing rate of
all of the heart’s normal pacemaker sites (Fig. 3.5). The built-in (ie, intrinsic) rate of the SA node is 60 to
100 beats per minute (beats/min).
The SA node is richly supplied by sympathetic and parasympathetic nerve fibers. Although the SA
node normally fires at a rate of 60 to 100 beats/min, this rate can increase to about 180 beats/min,
primarily through sympathetic stimulation. Heart rates faster than 150 beats/min can be problematic
Sinoatrial node
Right Left
atrium atrium
Atrioventricular node
Bundle of His
(common bundle)
Right Left Left bundle branch

Right bundle branch
ventricle ventricle
Purkinje fibers
Fig. 3.5 Conduction pathways through the normal heart. (From Costanzo LS: Physiology, ed 5, Philadelphia, 2014,
Saunders.)
because: (1) the duration of diastole shortens as heart rate increases, reducing ventricular filling time and,
potentially, stroke volume, and (2) the heart’s workload and oxygen requirements are increased, but the
time for coronary artery filling, which occurs during diastole, is decreased (DeBeasi, 2003).
Areas of the heart other than the SA node can initiate beats and assume pacemaker responsibility
under special circumstances. The term ectopic, which means out of place, or latent is used to describe
an impulse that originates from a source other than the SA node. Ectopic pacemaker sites include
the cells of the AV bundle and Purkinje fibers, although their intrinsic rates are slower than that of
the SA node.
ACLS Pearl
Although the presence of ectopic pacemakers provides a backup or safety mechanism in the event
of SA node failure, ectopic pacemaker sites can be problematic if they fire while the SA node is still
functioning. For example, ectopic sites may cause early (ie, premature) beats or sustained rhythm
disturbances.
Atrioventricular Node and Bundle

[Objectives 4, 5]
Conduction through the AV node begins before atrial depolarization is completed. The AV node is sup-
plied by both sympathetic and parasympathetic nerve fibers.
The bundle of His, also called the common bundle or the AV bundle, is located in the upper portion
of the interventricular septum and connects the AV node with the bundle branches. When the AV
node and bundle are bypassed by an abnormal pathway, the abnormal route is called an accessory
pathway.
The AV bundle has pacemaker cells that have an intrinsic rate of 40 to 60 beats/min. The AV node
and the AV bundle are called the AV junction. The term His-Purkinje system or His-Purkinje network
refers to the bundle of His, bundle branches, and Purkinje fibers.
ACLS Pearl
Abnormal cardiac rhythms that develop near or within the AV node are called junctional dysrhyth-
mias. Those that develop above the bundle of His or activate the ventricles through an accessory
pathway are called supraventricular dysrhythmias. Dysrhythmias that develop below the bundle
of His are called ventricular dysrhythmias.
Right and Left Bundle Branches

[Objective 4]
The right bundle branch innervates the right ventricle. The left bundle branch spreads the electrical
impulse to the interventricular septum and left ventricle. The left bundle branch divides into fascicles,
which are small bundles of nerve fibers that allow electrical innervation of the larger, more muscular left
ventricle.
Purkinje Fibers
[Objectives 4, 5]
The right and left bundle branches divide into smaller and smaller branches and then into a special net-
work of fibers called the Purkinje fibers. The Purkinje fibers have pacemaker cells that have an intrinsic
rate of 20 to 40 beats/min. The electrical impulse spreads rapidly through the right and left bundle
branches and the Purkinje fibers to reach the ventricular muscle. The electrical impulse spreads from
the endocardium to the myocardium, finally reaching the epicardial surface. The conduction system
is summarized in Table 3.1.
TABLE 3.1 Summary of the Conduction System

Intrinsic
Pacemaker Rate
Structure Function (beats/min)
Sinoatrial (SA) node Primary pacemaker; initiates impulse that is normally 60 to 100
conducted throughout the left and right atria
Atrioventricular (AV) node Receives impulse from SA node and delays relay of
the impulse to the bundle of His, allowing time for
the atria to empty their contents into the ventricles
before the onset of ventricular contraction.
Bundle of His (AV bundle) Receives impulse from AV node and relays it to right 40 to 60
and left bundle branches
Right and left bundle branches Receives impulse from bundle of His and relays it to
Purkinje fibers
Purkinje fibers Receives impulse from bundle branches and relays it 20 to 40
to ventricular myocardium
THE ELECTROCARDIOGRAM
The electrocardiogram (ECG) is a graphic display of the heart’s electrical activity. When electrodes
are attached to the patient’s limbs or chest and connected by cables to an ECG machine, the ECG
machine functions as a voltmeter, detecting and recording the changes in voltage (ie, action poten-
tials) generated by depolarization and repolarization of the heart’s cells. The voltage changes are
displayed as specific waveforms and complexes (Fig. 3.6). Practice standards for ECG monitoring
are shown in Box 3.1.
Sinoatrial
(SA) node Atrial excitation
Excitation of ventricles begins
(initial downward deflection is
a Q wave)
Pulmonary artery
R
Left
atrium
Right
atrium
Internodal
pathways T
Septum P
Left Q S
Atrioventricular ventricle
(AV) node
AV bundle Right
(bundle of His) ventricle
Fig. 3.6 Schematic drawing of the conducting system of the heart. An impulse normally is generated in the SA node and
travels through the atria to the atrioventricular (AV) node, down the bundle of His and Purkinje fibers, and to the ventricular
myocardium. Recording of the depolarizing and repolarizing currents in the heart with electrodes on the surface of the body
produces characteristic waveforms. (From Copstead-Kirkhorn LE, Banasik JL: Pathophysiology, ed 5, St Louis, 2013,
Saunders.)
BOX 3.1 Practice Standards for Cardiac Monitoring

Cardiac monitoring is indicated in most, if not all, a pacemaker lead and who are considered
of the following: pacemaker dependent
• Patients resuscitated from sudden cardiac • Patients with a temporary pacemaker or
death transcutaneous pacing pads
• Patients in the early phase of ACSs • Patients with AV block
• Patients with unstable coronary syndromes • Patients with arrhythmias and Wolff-
and newly diagnosed high-risk coronary Parkinson-White syndrome
lesions • Patients with long-QT syndrome and
• Adults and children who have undergone arrhythmias
cardiac surgery • Patients with intra-aortic balloon pumps
• Patients who have undergone nonurgent per- • Patients with acute heart failure
cutaneous coronary intervention with • Patients with indications for intensive care
complications • Patients undergoing conscious sedation
• Patients who have undergone implantation • Patients with unstable arrhythmias
of an automated defibrillator lead or • Pediatric patients with symptoms of
arrhythmia
(Drew, et al., 2004)
Fig. 3.7 Electrodes are adhesive pads applied at specific locations on the patient’s chest wall and limbs. (Courtesy Bruce R.
Shade, EMT-P, EMS-I, AAS.)
Electrodes
Electrode refers to an adhesive pad containing a conductive substance in the center that is applied to the
patient’s skin (Fig. 3.7). The conductive media of the electrode conducts skin surface voltage changes
through wires to a cardiac monitor (ie, electrocardiograph). Electrodes are applied at specific locations
on the patient’s chest wall and extremities to view the heart’s electrical activity from different angles and
planes.
One end of a monitoring cable, which is also called a lead wire, is attached to the electrode and the
other end to an ECG machine. The cable conducts current back to the cardiac monitor. Three-lead wire
systems are often used with portable monitor defibrillators. Five-lead wire systems allow viewing of the
six limb leads (ie, I, II, III, aVR, aVL, and aVF) and one chest lead.
Leads
[Objective 6]
A lead is a record (ie, tracing) of electrical activity between two electrodes. Each lead records the average
current flow at a specific time in a portion of the heart. A 12-lead ECG provides views of the heart in
both the frontal and horizontal planes and views the surfaces of the left ventricle from 12 different angles.
From this, ischemia, injury, and infarction affecting areas of the heart can be identified. The 12-lead
ECG is an essential part of the diagnostic workup of patients with a suspected ACS.
Frontal Plane Leads

[Objectives 6, 7]
Six leads view the heart in the frontal plane. Leads I, II, and III are called standard limb leads. Leads aVR,
aVL, and aVF are called augmented limb leads.
A bipolar lead is an ECG lead that has a positive and negative electrode. Each lead records the dif-
ference in electrical potential (ie, voltage) between two selected electrodes. Although all ECG leads are
technically bipolar, leads I, II, and III use two distinct electrodes, one of which is connected to the pos-
itive input of the ECG machine and the other to the negative input (Wagner, et al., 2009).
Leads I, II, and III make up the standard limb leads. If an electrode is placed on the right arm, left arm,
and left leg, three leads are formed (Fig. 3.8). The positive electrode is located at the left wrist in lead I,
while leads II and III both have the positive electrode located at the left foot. The difference in electrical
potential between the positive pole and its corresponding negative pole is measured by each lead.
Leads aVR, aVL, and aVF are limb leads that record measurements at a specific electrode with respect
to a reference electrode (see Fig. 3.8). The “a” in aVR, aVL, and aVF refers to augmented. The “V” refers
to voltage, and the last letter refers to the position of the positive electrode. The “R” refers to the right arm,
the “L” to left arm, and the “F” to left foot (ie, leg). A summary of the limb leads appears in Table 3.2.
Horizontal Plane Leads

[Objectives 6, 7]
Six chest (ie, precordial or “V”) leads view the heart in the horizontal plane. This allows a view of the front
and left side of the heart. The chest leads are identified as V1, V2, V3, V4, V5, and V6. Each electrode
placed in a “V” position is a positive electrode (Fig. 3.9). A summary of the chest leads can be found in
Table 3.3.
ACLS Pearl
Lead V1 is particularly useful for analyzing dysrhythmias that have a wide QRS complex (eg, bundle
branch blocks, ventricular pacemaker rhythms, wide-QRS tachycardias).
Fig. 3.8 View of the standard limb leads and augmented leads. LA, left arm; LL, left leg; RA, right arm. (From Boron WF:
Medical physiology, ed 2 updated edition, Philadelphia, 2011, Saunders.)
TABLE 3.2 Limb Leads

Lead Positive Electrode Position Negative Electrode Position Heart Surface Viewed
I Left arm Right arm Lateral
II Left leg Right arm Inferior
III Left leg Left arm Inferior
aVR Right arm Reference electrode None
aVL Left arm Reference electrode Lateral
aVF Left foot (ie, leg) Reference electrode Inferior
Midclavicular Anterior axillary

line line
Midaxillary
line
X X
X X X
X
V1 V3 V5
V2 V4 V6
Fig. 3.9 Chest (ie, precordial) leads V1 through V6. (From Copstead-Kirkhorn LE, Banasik JL: Pathophysiology, ed 5, St Louis,
2013, Saunders.)
TABLE 3.3 Chest Leads

Lead Positive Electrode Position Heart Area Viewed
V1 Right side of sternum, fourth intercostal space Interventricular septum
V2 Left side of sternum, fourth intercostal space Interventricular septum
V3 Midway between V2 and V4 Anterior surface
V4 Left midclavicular line, fifth intercostal space Anterior surface
V5 Left anterior axillary line; same level as V4 Lateral surface
V6 Left midaxillary line, fifth intercostal space Lateral surface
Right chest leads are used to evaluate the right ventricle (Fig. 3.10). The placement of right chest leads
is identical to the placement of the standard chest leads except that it is done on the right side of the chest.
If time does not permit obtaining all of the right chest leads, the lead of choice is V4R. A summary of the
right chest leads can be found in Table 3.4.
Leads V7, V8, and V9 permit viewing of the posterior surface of the heart (Fig. 3.11). All of the leads
are placed on the same horizontal line as V4 to V6. Lead V7 is placed at the posterior axillary line. Lead V8
is placed at the angle of the scapula (ie, the posterior scapular line), and lead V9 is placed over the left
border of the spine.
ACLS Pearl
Multiple-lead ECGs are used to help spot infarctions of the right ventricle and the posterior wall of
the left ventricle. The 15-lead ECG uses all of the leads of a standard 12-lead ECG plus leads V4R, V8,
and V9 or a standard 12-lead plus posterior leads V7, V8, and V9. A 16-lead ECG machine allows
recording of a standard 12-lead plus leads V3R, V4R, V5R, and V6R. An 18-lead ECG uses all of
the leads of a standard 12-lead ECG plus leads V4R, V5R, V6R, V7. V8, and V9.
Midclavicular line
Anterior axillary line
Midaxillary line Angle of Louis

RIGHT CHEST LEADS
1 V1R: Fourth intercostal space (ICS) at

left sternal border (same as V2)
2
3
V2R: Fourth ICS at right sternal border
4 (same as V1)
5
V3R: Halfway between V2R and V4R
6
V4R: Right midclavicular line in the fifth ICS
7
8 V5R: Right anterior axillary line at the fifth ICS
9
V6R: Right midaxillary line at the fifth ICS
V6R V5R V4R V3R V2R V1R
Fig. 3.10 Electrode locations for recording a right chest electrocardiogram (ECG). Right chest leads are not part of a standard
12-lead ECG but are used when a right ventricular infarction is suspected. (From Drew BJ, Ide B: Right ventricular infarction,
Prog Cardiovascular Nurs 10:46, 1195.)
TABLE 3.4 Right Chest Leads and Their Placement

Lead Placement
V1R Left side of sternum, fourth intercostal space
V2R Right side of sternum, fourth intercostal space
V3R Midway between V2R and V4R
V4R Right midclavicular line, fifth intercostal space
V5R Right anterior axillary line; same level as V4R
V6R Right midaxillary line, fifth intercostal space
Posterior axillary line Left paraspinal
Midaxillary line
1
2 LEFT POSTERIOR LEADS
3
V7: Posterior axillary line at
4 the same level as V4 to V6
5
6
V8: Halfway between V7 and V9
7
8 V9: Left paraspinal line at
the same level as V4 to V6
9
V6 V7 V8 V9
Fig. 3.11 Posterior chest lead placement. (From Drew BJ, Ide B: Right ventricular infarction, Prog Cardiovascular Nurs 10:46,
1195.)
1 mm = 0.1 mV
5 mm = 0.20 s
Amplitude (voltage)
5 mm = 0.5 mV
1 mm = 0.04 s
Duration (time)
Fig. 3.12 ECG strip showing the markings for measuring amplitude and duration of waveforms, using a standard recording
speed of 25 mm/sec. (From Copstead-Kirkhorn LE, Banasik JL: Pathophysiology, ed 5, St Louis, 2013, Saunders.)
Electrocardiography Paper
ECG paper is graph paper made up of small and large boxes measured in millimeters (mms). The
smallest boxes are 1 mm wide and 1 mm high (Fig. 3.12). The horizontal axis of the paper corresponds
with time, which is stated in seconds. ECG paper normally records at a constant speed of 25 mm/second.
Thus each horizontal 1 mm box represents 0.04 second (25 mm/sec 0.04 second ¼ 1 mm). The lines
after every five small boxes on the paper are heavier. The heavier lines indicate one large box, which
represents 0.20 second.
The vertical axis of the graph paper represents the voltage or amplitude of the ECG waveforms or deflec-
tions. Voltage is measured in mV. Amplitude is measured in mm. When properly calibrated, a small box is
1 mm high (ie, 0.1 mV), and a large box, which is equal to five small boxes, is 5 mm high (ie, 0.5 mV).
Waveforms and Complexes

[Objective 8]
An ECG waveform (ie, a deflection) is movement away from the baseline (ie, isoelectric line) in either a
positive (ie, upward) or negative (ie, downward) direction. Waveforms are named alphabetically, begin-
ning with P, QRS, and T (Fig. 3.13).
The P wave is the first waveform in the cardiac cycle and represents atrial depolarization and the
spread of the electrical impulse throughout the right and left atria. A P wave is normally positive (ie,
upright) in standard leads and precedes each QRS complex.
Atria Ventricles
+1 RR interval
R wave
T wave PR interval ST segment
P wave
Voltage
0
(mV)
S wave
SA AV
node node Q wave
QRS
Bundle of His The ECG cannot show duration
Bundle branches the electrical activity of
Purkinje network these five structures. QT interval
–1
0 0.2 0.4 0.6 0.8 1.0 1.2 1.4 1.6 1.8 2.0
Time (sec)
Fig. 3.13 Components of the ECG recording. AV, atrioventricular; SA, sinoatrial. (From Boron WF: Medical physiology, ed 2
updated edition, Philadelphia, 2011, Saunders.)
The QRS complex consists of the Q wave, R wave, and S wave. It represents the spread of the elec-
trical impulse through the ventricles (ie, ventricular depolarization). A QRS complex normally follows
each P wave. In adults, the normal duration of the QRS complex is 0.11 second or less (Surawicz, et al.,
2009). When viewing the chest leads in a normal heart, the R wave becomes taller (ie, increases in ampli-
tude) and the S wave becomes smaller as the electrode is moved from right to left. This pattern is called
R-wave progression. The transition zone is the area at which the amplitude of the R wave begins to
exceed the amplitude of the S wave (Ganz, 2012). This usually occurs in the area of leads V3 and V4.
Poor R-wave progression is a phrase used to describe R waves that decrease in size from V1 to V4. Possible
causes include right or left ventricular hypertrophy and left bundle branch block, among other causes.
Poor R-wave progression may also be a nonspecific indicator of anterior wall infarction. Electrode place-
ment in the correct intercostal space is critical when evaluating R-wave progression.
Ventricular repolarization is represented on the ECG by the ST segment (discussed later) and the
T wave. The direction of the T wave is normally the same as the QRS complex that precedes it.
A U wave is a small waveform that, when seen, follows the T wave. The U wave is thought to represent
repolarization of the Purkinje fibers in the papillary muscle of the ventricular myocardium.
Segments and Intervals

[Objectives 8, 9]
A segment is a line between waveforms. It is named by the waveform that precedes or follows it. An
interval is made up of a waveform and a segment.
The PR segment is the horizontal line between the end of the P wave and the beginning of the QRS
complex. The P wave plus the PR segment equals the PR interval. The PR interval normally measures
0.12 to 0.20 second in adults.
The TP segment is the portion of the ECG tracing between the end of the T wave and the beginning
of the next P wave, during which there is no electrical activity (Fig. 3.14). When the heart rate is within
normal limits, the TP segment is usually isoelectric and is used as the reference point from which to
estimate the position of the isoelectric line and determine ST segment displacement. With rapid heart
rates, the TP segment is often unrecognizable because the P wave encroaches on the preceding T wave.
When the TP segment is unrecognizable, the PR segment is used as the reference point from which to
estimate the position of the isoelectric line.
The portion of the ECG tracing between the QRS complex and the T wave is the ST segment (see
Fig. 3.13). The ST segment represents the early part of repolarization of the right and left ventricles.
In the limb leads, the normal ST segment is isoelectric (ie, flat) but may normally be slightly elevated
or depressed. The point where the QRS complex and the ST segment meet is called the ST junction
or the J point. The ST segment is considered elevated if the segment is deviated above the baseline
and is considered depressed if the segment deviates below it. Various conditions may cause the displace-
ment of the ST segment from the isoelectric line in either a positive or a negative direction. Some
displacement of the ST segment from the isoelectric line is normal and dependent on age, gender,
and ECG lead.
When looking for ST segment elevation or depression, first locate the J point. Next use the TP seg-
ment to estimate the position of the isoelectric line. Then compare the level of the ST segment to the
isoelectric line. Deviation is measured as the number of mm of vertical ST segment displacement from
the isoelectric line or from the patient’s baseline at the J point (Thygesen, et al., 2012). Proper machine
P T P
QS TP-segment
PR-segment
Fig. 3.14 The TP segment is used as the reference point for the isoelectric line. (From Aehlert B: ECGs made easy, ed 3,
St. Louis, 2006, Mosby.)
BOX 3.2 Systematic Rhythm Interpretation

1. Assess regularity (atrial and ventricular). 4. Assess intervals (eg, PR, QRS, QT) and
2. Assess rate (atrial and ventricular). examine ST segments.
3. Identify and examine waveforms. 5. Interpret the rhythm and assess its clinical
significance.
calibration is critical when analyzing ST segments. The ST segment criteria described here apply only
when the monitor is adjusted to standard calibration.
The QT interval is the period from the beginning of the QRS complex to the end of the T wave (see
Fig. 3.13). It represents total ventricular activity; this is the time from ventricular depolarization (ie, acti-
vation) to repolarization (ie, recovery). The QT interval is measured from the beginning of the QRS
complex to the end of the T wave. In the absence of a Q wave, the QT interval is measured from
the beginning of the R wave to the end of the T wave. The term QT interval is used regardless of whether
the QRS complex begins with a Q wave or an R wave.
The duration of the QT interval varies in accordance with age, gender, and heart rate. As the heart
rate increases, the QT interval shortens (ie, decreases). As the heart rate decreases, the QT interval
lengthens (ie, increases). Because of the variability of the QT interval with the heart rate, it can be
measured more accurately if it is corrected (ie, adjusted) for the patient’s heart rate. The corrected
QT interval is noted as QTc. The QT interval is considered short if it is 0.39 second or less and
prolonged if it is 0.46 second or longer in women or 0.45 second or longer in men (Rautaharju,
et al., 2009). A prolonged QT interval may be congenital or acquired and indicates a lengthened
RRP. A QTc of more than 0.50 second in either gender has been correlated with a higher risk for
life-threatening dysrhythmias (eg, torsades de pointes [TdP]). A systematic approach to rhythm
analysis appears in Box 3.2.
ACUTE CORONARY SYNDROMES

Acute coronary syndromes (ACSs) are a group of conditions that are caused by an abrupt reduction
in coronary artery blood flow (Amsterdam, et al., 2014). Myocardial ischemia, injury, and infarction
are among the causes of ST segment deviation. When ECG changes of myocardial ischemia, injury,
or infarction occur, they are not found in every lead of the ECG. Indicative changes are ECG findings
that are seen in leads that look directly at the area fed by the blocked vessel. Reciprocal changes, also called
mirror image changes, are ECG findings that are seen in leads opposite the affected area. Indicative
changes are significant when they are seen in two anatomically contiguous leads. Two leads are contiguous
if they look at the same or adjacent areas of the heart or if they are numerically consecutive chest leads.
ST segment depression of 0.5 mm or more in a patient who is experiencing an ACS is suggestive
of myocardial ischemia when it is viewed in two or more anatomically contiguous leads (Amsterdam,
et al., 2014). Evidence of myocardial injury can be seen on the ECG as ST segment elevation
(see Chapter 7).
ACLS Pearl
The LMCA perfuses a large area of the anterior wall of the heart. Research has shown that ST seg-
ment elevation in lead aVR can predict occlusion of the LMCA (Lawner, et al., 2012).

CHAPTER QUIZ
Multiple Choice
____ 1. In the heart’s conduction system, the ___ receive(s) an electrical impulse from the right
and left bundle branches and relay(s) it to the ventricular myocardium.
A. Purkinje fibers
B. SA node
C. AV node
D. Atrial pacemaker cells
____ 2. When the heart rate is within normal limits, which of the following is used as the
reference point from which to estimate the position of the isoelectric line and
determine ST segment displacement?
A. PR segment
B. TP segment
C. QT interval
D. QRS complex
____ 3. Which of the following represent ventricular repolarization on the ECG?

A. P wave and PR interval
B. ST segment and T wave
C. PR interval and ST segment
D. QRS complex and ST segment
____ 4. The period during the cardiac cycle when cells cannot respond to a stimulus, no matter
how strong, is called the:
A. Supernormal period.
B. Depolarized period.
C. Relative refractory period.
D. Absolute refractory period.
____ 5. Which of the following are the main branches of the left coronary artery?
A. Marginal and oblique arteries
B. CX and marginal arteries
C. Anterior descending and oblique arteries
D. CX and anterior descending arteries
____ 6. Which of the following leads view the heart in the frontal plane?
A. I, II, III, V1, V2, and V3
B. V1, V2, V3, V4, V5, and V6
C. I, II, III, aVR, aVL, and aVF
D. aVR, aVL, aVF, V4, V5, and V6
____ 7. What does the QRS complex represent?

A. Atrial depolarization
B. Ventricular contraction
C. Ventricular depolarization
D. Ventricular repolarization
Matching
Match each description with its corresponding answer.
A. TP segment E. P wave
B. PR segment F. Interval
C. QT interval G. QRS complex
D. ST segment H. PR interval
____ 8. Represents atrial depolarization
____ 9. A waveform and a segment
____ 10. Normally measures 0.11 second or less in adults
____ 11. Horizontal line between the end of the P wave and the beginning of the QRS complex
____ 12. Portion of the ECG tracing between the end of the T wave and the beginning of the
next P wave
____ 13. Normally measures 0.12 to 0.20 second in adults
____ 14. Portion of the ECG tracing between the QRS complex and the T wave
____ 15. Represents total ventricular activity: the time from ventricular depolarization (ie,
stimulation) to repolarization (ie, recovery)

Multiple Choice
1. A. The right and left bundle branches divide into smaller and smaller branches and then into a special
network of fibers called the Purkinje fibers. These fibers spread from the interventricular septum into
the papillary muscles. They continue downward to the apex of the heart, making up an elaborate web
that penetrates about one-third of the way into the ventricular muscle mass. The fibers then become
continuous with the muscle cells of the right and left ventricles. The Purkinje fibers have pacemaker
cells that have an intrinsic rate of 20 to 40 beats/min.
OBJ: Describe the normal sequence of electrical conduction through the heart.
2. B. When the heart rate is within normal limits, the TP segment is usually isoelectric and used as the
reference point from which to estimate the position of the isoelectric line and determine ST segment
displacement. With rapid heart rates, the TP segment is often unrecognizable because the P wave
encroaches on the preceding T wave. When the TP segment is unrecognizable, the PR segment
is used as the reference point from which to estimate the position of the isoelectric line.
OBJ: Define and describe the significance of each of the following as they relate to cardiac elec-
trical activity: the P wave, the QRS complex, the T wave, the U wave, the PR segment, the TP seg-
ment, the ST segment, the PR interval, the QRS duration, and the QT interval.
3. B. On the ECG, the ST segment and T wave represent ventricular repolarization.

4. D. During the ARP, the cell will not respond to further stimulation within itself. This means that the
myocardial working cells cannot contract and the cells of the electrical conduction system cannot con-
duct an electrical impulse, no matter how strong the internal electrical stimulus. As a result, tetanic (ie,
sustained) contractions cannot be provoked in cardiac muscle.
OBJ: Define the absolute, effective, relative refractory, and supernormal periods and their loca-
tions in the cardiac cycle.
5. D. The CX and anterior descending arteries are the main branches of the LCA.
OBJ: Name the primary branches and areas of the heart supplied by the right and left coronary
arteries.
6. C. Frontal plane leads view the heart from the front of the body as if it were flat. Directions in the
frontal plane are superior, inferior, right, and left. Six leads view the heart in the frontal plane. Leads I,
II, and III are called standard limb leads. Leads aVR, aVL, and aVF are called augmented limb leads. Six
chest (ie, precordial or “V”) leads view the heart in the horizontal plane. The chest leads are identified
as V1, V2, V3, V4, V5, and V6.
OBJ: Differentiate between the frontal plane and the horizontal plane leads.
7. C. When the ventricles are stimulated, a QRS complex is recorded on the ECG. Thus the QRS com-
plex represents ventricular depolarization.
Matching
8. E
9. F
10. G
11. B
12. A
13. H
14. D
15. C
REFERENCES
Amsterdam, E. A., Wenger, N. K., Brindis, R. G., Casey, D. E., Ganiats, T. G., Holmes, D. R.,et al. (2014). 2014
AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes. J Am
Coll Cardiol, 1–150.
Costanzo, L. S. (2014). Cardiovascular physiology. In Physiology (5th ed., pp. 113–184). Philadelphia: Saunders.
DeBeasi, L. C. (2003). Physiology of the cardiovascular system. In S. A. Price, & L. M. Wilson (Eds.), Pathophys-
iology: Clinical concepts of disease processes (6th ed., pp. 416–428). St. Louis: Mosby.
Drew, B. J., Califf, R. M., Funk, M., Kaufman, E. S., Krucoff, M. W., Laks, M. M.,et al. (2004). Practice standards
for electrocardiographic monitoring in hospital settings: An American Heart Association scientific statement
from the Councils on Cardiovascular Nursing, Clinical Cardiology, and Cardiovascular Disease in the Young.
Circulation, 110, 2721–2746.
Ganz, L. (2012). Electrocardiography. In L. Goldman, & A. I. Schafer (Eds.), Goldman’s Cecil medicine (24th ed.,
Lawner, B. J., Nable, J. V., & Mattu, A. (2012). Novel patterns of ischemia and STEMI equivalents. Cardiol Clin, 30
(4), 591–599.
Surawicz, B., Childers, R., Deal, B. J., & Gettes, L. S. (2009). AHA/ACCF/HRS recommendations for the
standardization and interpretation of the electrocardiogram: Part III: Intraventricular conduction disturbances:
A scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee.
J Am Coll Cardiol, 53(11), 976–981.
Thygesen, K., Alpert, J. S., Jaffe, A. S., Simoons, M. L., Chaitman, B. R., & White, H. D. (2012). Third universal
definition of myocardial infarction. Circulation, 126(16), 2020–2035.
Wagner, G. S., Macfarlane, P., Wellens, H., Josephson, M., Gorgels, A., Mirvis, D. M.,et al. (2009). AHA/ACCF/
HRS recommendations for the standardization and interpretation of the electrocardiogram: Part VI: Acute ische-
mia/infarction: A scientific statement from the American Heart Association Electrocardiography and Arrhyth-
mias Committee. J Am Coll Cardiol, 53, 1003–1011.
CHAPTER 4
Cardiac Arrest Rhythms
INTRODUCTION
Evaluation of your ability to manage a patient who is experiencing a cardiac arrest and your ability to
manage the team who will assist you in providing patient care is part of the Advanced Cardiac Life
Support (ACLS) course. This chapter discusses the cardiac arrest rhythms and their management;
defibrillation; and the roles and responsibilities of each member of the resuscitation team.
gency care (including mechanical, pharmacologic, and electrical therapy where applicable) for a
patient experiencing a cardiac arrest.
LEARNING OBJECTIVES
1. Identify four cardiac rhythms that are associated with cardiac arrest.
2. Differentiate between shockable and nonshockable cardiac arrest rhythms.
3. Given a patient situation, describe the electrocardiogram (ECG) characteristics and initial
emergency care for cardiac arrest rhythms, including mechanical, pharmacologic (ie,
indications, contraindications, doses, and route of administration of applicable
medications), and electrical therapy, where applicable.
4. Explain defibrillation, its indications, proper pad or paddle placement, relevant
precautions, and the steps required to perform this procedure with a manual defibrillator
and an automated external defibrillator (AED).
5. Differentiate between monophasic and biphasic defibrillation.
6. Identify the energy levels that are currently recommended, and indicate if the shock
delivered should be a synchronized or unsynchronized countershock, for pulseless
monomorphic ventricular tachycardia (VT), polymorphic VT (PMVT), and ventricular
fibrillation (VF).
7. Describe the role of each member of the resuscitation team.
8. Discuss the events of a typical resuscitation effort.
9. Discuss immediate post–cardiac arrest care upon return of spontaneous
circulation (ROSC).
10. Recognize the opportunities provided when a postevent debriefing is held.
11. Discuss the use of the SPIKES protocol when conveying bad news.
83
84 CHAPTER 4 Cardiac Arrest Rhythms
LEARNING PLAN
• Master identification of the following rhythms: VF, monomorphic VT, PMVT, asystole, and
pulseless electrical activity (PEA).
• Master the following medications: O2, epinephrine, amiodarone, and lidocaine.
• Assign team member roles or perform as a team member in a simulated patient situation.
• Quickly recognize cardiopulmonary arrest.
• Demonstrate familiarity with the cardiac arrest algorithm.
• Ensure the performance of high-quality cardiopulmonary resuscitation (CPR) when
indicated.
• Demonstrate safe operation of a manual defibrillator and an AED if electrical therapy is
indicated.
• Demonstrate an understanding of the actions, indications, dosages, adverse effects,
and contraindications for the medications used in the treatment of cardiac arrest.
• Consider the possible reversible causes of a cardiac emergency.
• Direct the performance of appropriate airway management throughout a resuscitation
effort.
• Recognize the ROSC and direct the performance of immediate post–cardiac
arrest care.
debriefing.
• Read the case studies at the end of this chapter and compare your answers with the
answers provided.
KEY TERMS
Automated external defibrillation The placement of paddles or pads on a patient’s chest
and interpretation of the patient’s cardiac rhythm by the defibrillator’s computerized
analysis system. Depending on the type of AED used, the machine will deliver a shock (if a
shockable rhythm is detected) or instruct the operator to deliver a shock.
Defibrillation Delivery of an electrical current across the heart muscle over a very brief period to
terminate an abnormal heart rhythm; also called unsynchronized countershock or asynchronous
countershock because the delivery of current has no relationship to the cardiac cycle.
Defibrillator A device used to administer an electrical shock at a preset energy level to
terminate a cardiac dysrhythmia.
Manual defibrillation The placement of paddles or pads on a patient’s chest, interpretation of
the patient’s cardiac rhythm by a trained health care professional, and the health care
professional’s decision to deliver a shock (if indicated).
Transthoracic impedance (resistance) The resistance of the chest wall to current.
CARDIAC ARREST RHYTHMS

[Objectives 1, 2]
The initial rhythms that may be observed in a cardiac arrest include the following:
1. Pulseless VT (pVT), in which the ECG displays a wide, regular QRS complex at a rate faster than 120
beats per minute (beats/min)
2. VF, in which irregular chaotic deflections that vary in shape and height are observed on the ECG but
there is no coordinated ventricular contraction
CHAPTER 4 Cardiac Arrest Rhythms 85
3. Asystole, in which no cardiac electrical activity is present

4. PEA, in which electrical activity is visible on the ECG but central pulses are absent
VF and pVT are shockable rhythms. This means that delivering a shock to the heart by means of a
defibrillator may result in termination of the rhythm. Asystole and PEA are nonshockable rhythms.
Survival when a patient presents in a shockable rhythm is up to 6 times as high as when they have a
nonshockable rhythm (Herlitz, et al., 2002; Martinez, 2012).
Ventricular Tachycardia
VT exists when three or more ventricular complexes occur in immediate succession at a rate greater than
100 beats/min. VT may occur with or without pulses, and the patient may be stable or unstable with this
rhythm.
When the QRS complexes of VT are of the same shape and amplitude, the rhythm is called mono-
morphic VT (Table 4.1, Fig. 4.1). When the QRS complexes of VT vary in shape and amplitude from beat
to beat, the rhythm is called polymorphic VT (PMVT). In PMVT, the QRS complexes appear to twist
from upright to negative, or negative to upright, and back. PMVT is a dysrhythmia of intermediate sever-
ity between monomorphic VT and VF. If monomorphic VT or PMVT is present without a pulse, the
rhythm is treated as VF (discussed later). Monomorphic VT is discussed in more detail in Chapter 5 with
wide-QRS tachycardias. PMVT is discussed in Chapter 5 with irregular tachycardias.
TABLE 4.1 Characteristics of Monomorphic Ventricular Tachycardia

Rhythm Ventricular rhythm essentially regular
Rate 101 to 250 (121 to 250 per some cardiologists) beats/min
P waves Usually not seen; if present, they have no set relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS duration 0.12 sec or greater; often difficult to differentiate between the QRS and the T wave
Fig. 4.1 When the QRS complexes of ventricular tachycardia (VT) are of the same shape and amplitude, the rhythm is called
monomorphic VT. (From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)
Ventricular Fibrillation
[Objective 3]
VF is a chaotic rhythm that begins in the ventricles (Table 4.2). With VF, there is no organized depo-
larization of the ventricles. The ventricular muscle quivers, and as a result, there is no effective myocardial
contraction and no pulse. The resulting rhythm looks chaotic with deflections that vary in shape and
amplitude; no normal-looking waveforms are visible. The amplitude of VF waveforms decreases over
TABLE 4.2 Characteristics of Ventricular Fibrillation

Rhythm Rapid and chaotic with no pattern or regularity
Rate Cannot be determined because there are no discernible waves or complexes to measure
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
C
1 sec
Fig. 4.2 Ventricular tachydysrhythmias. A, Rhythm strip showing monomorphic VT. B, Example of polymorphic VT (PMVT).
C, Example of ventricular fibrillation (VF). All tracings are from lead V1. (From Goldman L, Ausiello DA, Arend W, et al.: Cecil
medicine, ed 23, Philadelphia, 2007, Saunders.)
time as myocardial blood flow and energy metabolism diminishes (Li & Tang, 2012). VF with waves that
are 3 or more millimeters (mm) high is called coarse VF. VF with low amplitude waves (ie, less than
3 mm) is called fine VF. Survival to hospital discharge increases with VF waveforms of 3 to 4 mm
and is best for VF of 5 mm or greater (Li & Tang, 2012). Fig. 4.2 illustrates a comparison of ventricular
dysrhythmias.
Factors that increase the susceptibility of the myocardium to fibrillate include the following:
• Acute coronary syndromes
• Dysrhythmias
• Electrolyte imbalance
• Environmental factors (eg, electrocution)
• Hypertrophy
• Increased sympathetic nervous system activity
• Proarrhythmic effect of antiarrhythmics and other medications
• Severe heart failure
• Vagal stimulation
The patient in VF is unresponsive, apneic, and pulseless. The priorities of care in cardiac arrest
because of pVT or VF are high-quality CPR and defibrillation. When pVT or VF persists or recurs
after one or more shocks it is called refractory pVT/VF (Link, et al., 2015). Use the memory aids
PATCH-4-MD and the Five Hs and Five Ts to recall possible reversible causes of cardiac emergencies
(Boxes 4.1, 4.2).
Medications that may be used in the treatment of pVT/VF include epinephrine (Table 4.3) and amio-
darone. Epinephrine is a vasopressor. A vasopressor is administered during cardiac arrest to increase the
perfusion pressure of (1) the myocardium, for increased chance of ROSC; and (2) the brain, for increased
chance of neurologically intact survival (Sunde & Steen, 2012). Epinephrine is a potent medication that
stimulates both alpha- and beta-adrenergic receptors. It should be given by the intravenous (IV) or
intraosseous (IO) route in cardiac arrest. Because the effects of epinephrine do not last long, epinephrine
should be repeated every 3 to 5 minutes as long as the patient is in cardiac arrest. Although epinephrine
has been used in the management of cardiac arrest for more than 40 years, there is some concern that
BOX 4.1 PATCH-4-MD

Pulmonary embolism—anticoagulants? Fibrino- Heat/cold (hyperthermia/hypothermia)—cool-
lytics? Surgery? ing/warming methods
Acidosis—ventilation, correct acid-base Hypokalemia/hyperkalemia (and other electro-
disturbances lytes)—monitor serum glucose levels closely
Tension pneumothorax—needle in concert with correcting electrolyte distur-
decompression bances
Cardiac tamponade—pericardiocentesis Myocardial infarction—reperfusion therapy
Hypovolemia—replace intravascular volume Drug overdose/accidents—antidote/specific
Hypoxia—ensure adequate oxygenation and therapy
ventilation
BOX 4.2 Five Hs and Five Ts

Hypovolemia Tamponade, cardiac
Hypoxia Tension pneumothorax
Hypothermia Thrombosis: lungs (ie, massive pulmonary embolism)
Hypokalemia/Hyperkalemia Thrombosis: heart (ie, acute coronary syndromes)
Hydrogen ion (acidosis) Tablets/toxins: drug overdose
TABLE 4.3 Epinephrine (Adrenalin)

Class Natural catecholamine; sympathomimetic; adrenergic agonist
Mechanism of Binds with alpha- and beta-adrenergic receptors, increasing heart rate and force of
Action contraction, causing vasoconstriction, and relaxing bronchial smooth muscle
Indications • Cardiac arrest: VF, pVT, asystole, PEA
• Symptomatic bradycardia
• Hypotension
Dosage Cardiac arrest
• IV/IO: 1 mg (10 mL) of 1:10,000 solution IV push, follow with 20 mL fluid flush; may
repeat 1 mg dose every 3 to 5 min (Link, et al., 2015)
• Tracheal: 2 to 2.5 mg diluted in 5 to 10 mL of sterile water or normal saline
Post–cardiac arrest care: Continuous IV infusion of 0.1 to 0.5 mcg/kg/min (Callaway, et al.,
2015)
Symptomatic bradycardia or hypotension: Continuous infusion at 2 to 10 mcg/min (Link,
et al., 2015)
Considerations • Epinephrine is available in different concentrations and in different medication
containers. Read the label carefully before giving epinephrine to ensure that you are
giving the right dose and using the right concentration of the drug.
• Increases myocardial oxygen demand; may cause postresuscitation myocardial
dysfunction and ventricular dysrhythmias (Attaran & Ewy, 2010).
• Administer an epinephrine infusion via an infusion pump.
• Check IV site frequently for evidence of tissue sloughing.
• Should not be administered in the same IV line as alkaline solutions: this inactivates
epinephrine.
• According to the Institute for Safe Medication Practices, ratio expressions no longer
appear on single entity drug products as of May 1, 2016. Epinephrine 1:1000 is
displayed as 1 mg/mL and epinephrine 1:10,000 is displayed as 0.1 mg/mL.
ECG, electrocardiogram; IO, intraosseous; IV, intravenous; PEA, pulseless electrical activity; pVT, pulseless ventricular
tachycardia; VF, ventricular fibrillation
epinephrine administration during cardiac arrest may negatively affect patient outcomes. In a study that
compared patients given epinephrine versus no epinephrine, the investigators concluded that although
patients receiving epinephrine experienced ROSC more frequently and had a statistically significant
improvement for survival to hospital admission, the final outcome was not significantly affected
(Herlitz, et al., 1995). A more recent study found that although the rate of ROSC increased with epi-
nephrine, there was no statistically significant difference in hospital discharge rate (Jacobs, et al., 2011).
After its administration, epinephrine can have unwanted effects including increased myocardial oxygen
consumption and postdefibrillation ventricular dysrhythmias (Attaran & Ewy, 2010). Noting that the
value and safety of its beta-adrenergic effects are controversial because they may increase myocardial work
and reduce subendocardial perfusion, current resuscitation guidelines reflect that standard-dose epineph-
rine (ie, 1 mg every 3 to 5 minutes) may be reasonable for patients in cardiac arrest (Link, et al., 2015).
With regard to the timing of epinephrine administration during cardiac arrest, current guidelines state
that it may be reasonable to administer epinephrine as soon as feasible after the onset of cardiac arrest
associated with an initial nonshockable rhythm (Link, et al., 2015). However, because optimal timing may
vary based on patient factors and resuscitation conditions, there is insufficient evidence to make a rec-
ommendation as to the optimal timing of epinephrine, particularly in relation to defibrillation, when
cardiac arrest is associated with a shockable rhythm (Link, et al., 2015).
ACLS Pearl
An agonist is a drug or substance that produces a predictable response (ie, stimulates action). An
antagonist is an agent that exerts an action opposite to another (ie, blocks action). A chronotrope is a
substance that affects the heart rate: positive chronotrope ¼ " heart rate; negative chronotrope ¼ #
heart rate. A dromotrope is a substance that affects AV conduction velocity: positive dromotrope ¼ "
AV conduction velocity; negative dromotrope ¼ # AV conduction velocity. An inotrope is a substance
that affects myocardial contractility: positive inotrope ¼ " force of contraction; negative inotrope ¼ #
force of contraction.
ACLS Pearl
Sympathetic (ie, adrenergic) receptors are located in different organs and have different physiologic
actions when stimulated. Adrenergic receptors have been categorized into the following main types:
alpha1, alpha2, beta1, beta2, and beta3. Alpha1 receptors are found in the eyes, peripheral small arter-
ies and arterioles, bladder, gastrointestinal sphincters, and male reproductive organs. Stimulation of
alpha1 receptor sites primarily causes constriction of vascular smooth muscle. Alpha2 receptor sites
are found on platelets, blood vessels, and both presynaptically and postsynaptically on neurons in
the brain (Wecker, et al., 2010). Stimulation results in suppression of further norepinephrine release.
Both alpha1 and alpha2 receptors have been found in the myocardium but their physiologic function
remains more clearly defined in the peripheral blood vessels than in the heart (Opie & Hasenfuss,
2012). Beta receptor sites are divided into beta1, beta2, and beta3. Beta1 receptors are found in
the heart and kidneys. In the heart, stimulation of beta1 receptor sites results in an increase in heart
rate (ie, positive chronotropy), an increase in the strength of cardiac contraction (ie, positive inotropy),
and, ultimately, irritability of cardiac cells. Beta2 receptor sites are found in several locations in
the body. In the lungs, stimulation of these receptors causes bronchodilation. Beta2 receptors have
also been found in the heart and account for about 20% of beta receptors in the left ventricle and
about 40% in the atria (Opie & Hasenfuss, 2012). Beta3 receptors are localized in fat cells.
Consider administration of an antiarrhythmic if pVT/VF continues despite CPR, defibrillation, and

giving a vasopressor. Although some antiarrhythmics have been associated with increased rates of ROSC
and hospital admission, none has proved to increase long-term survival or survival with a good neurologic
outcome (Link, et al., 2015). Further, the ideal sequence and timing of antiarrhythmic administration
during cardiac arrest in relation to the delivery of shocks is not known (Link, et al., 2015). Amiodarone is
an antiarrhythmic that blocks sodium channels, inhibits sympathetic stimulation, and blocks potassium
channels as well as calcium channels (Table 4.4). The administration of lidocaine may be considered as an
alternative to amiodarone for pVT/VF that is unresponsive to CPR, defibrillation, and vasopressor ther-
apy (Link, et al., 2015). Lidocaine is a Class 1B antiarrhythmic that inhibits the influx of sodium through
the fast channels of the myocardial cell membrane and decreases conduction in ischemic cardiac tissue
without adversely affecting normal conduction (Table 4.5). Although the routine use of lidocaine after
cardiac arrest is not supported by current resuscitation guidelines, the initiation or continuation of lido-
caine may be considered immediately after ROSC from cardiac arrest associated with pVT/VF (Link,
et al., 2015).
Asystole
[Objective 3]
Asystole, which is also called ventricular asystole, is a total absence of ventricular electrical activity
(Table 4.6, Fig. 4.3). There is no ventricular rate or rhythm, no pulse, and no cardiac output. Some atrial
electrical activity may be evident. If atrial electrical activity is present, the rhythm is called “P-wave”
asystole or ventricular standstill (Fig. 4.4).
The memory aids PATCH-4-MD and the Five Hs and Five Ts may be used to recall possible revers-
ible causes of asystole. In addition, ventricular asystole may occur temporarily after termination of a
tachycardia with medications, defibrillation, or synchronized cardioversion.
When asystole is observed on a cardiac monitor, confirm that the patient is unresponsive and has no
pulse, and then begin high-quality CPR. Additional care includes establishing vascular access, consid-
ering possible reversible causes of the arrest, administering epinephrine, and possibly inserting an
advanced airway. For intubated patients, use continuous end-tidal carbon dioxide (EtCO2) monitoring
to assess the quality of compressions during the resuscitation effort and to monitor the ROSC.
TABLE 4.4 Amiodarone (Cordarone)
Class Class III antiarrhythmic
Mechanism of • Directly depresses the automaticity of the SA and AV nodes
Action • Slows conduction through the AV node and in the accessory pathway of patients with
Wolff-Parkinson-White preexcitation pattern
• Inhibits alpha- and beta-adrenergic receptors
• Possesses both vagolytic and calcium channel blocking properties
• Coronary and peripheral vasodilator
• Mild decrease in myocardial contractility; however, cardiac output may actually increase
because of decreased afterload
Indications • pVT/VF (after CPR, defibrillation, and a vasopressor)
• Stable narrow-QRS tachycardias if the rhythm persists despite vagal maneuvers or
adenosine, or the tachycardia is recurrent
• To control ventricular rate in atrial fibrillation
• To control ventricular rate in preexcited atrial dysrhythmias with conduction over an
accessory pathway
• Stable monomorphic VT
• PMVT with normal QT interval
Dosage • pVT/VF: Initial bolus of 300 mg IV/IO; can be followed by 1 dose of 150 mg (Link, et al.,
2015). If ROSC, can consider continuous IV infusion (1 mg/min infusion for 6 hours and
then a 0.5 mg/min maintenance infusion over 18 hours). Maximum daily dose 2.2 g IV
per 24 hours.
• Other indications: Loading dose of 150 mg IV over 10 min. May repeat every 10 min if
needed. After conversion, follow with a 1 mg/min infusion for 6 hours and then a 0.5 mg/
min maintenance infusion over 18 hours. Maximum cumulative dose 2.2 g IV per
24 hours (Link, et al., 2015).
Considerations • In the United States, amiodarone is available in two formulations. One formulation
contains polysorbate 80, which is a vasoactive solvent that can produce hypotension.
The other contains cyclodextrin (Captisol), which possesses no vasoactive effects (Link,
et al., 2015).
• Hypotension, bradycardia, and AV block are adverse effects of amiodarone
administration. Slow the infusion rate or discontinue if seen.
• Prolongs the PR, QRS, and QT intervals, and has an additive effect with other
medications that prolong the QT interval (eg, procainamide, phenothiazines, some
tricyclic antidepressants, thiazide diuretics, sotalol). Although prolongation of the QRS
duration and QT interval may be beneficial in some patients, it may also increase the risk
for TdP.
AV, atrioventricular; CPR, cardiopulmonary resuscitation; IV, intravenous; PMVT, polymorphic ventricular tachycardia; pVT,
pulseless ventricular tachycardia; ROSC, return of spontaneous circulation; SA, sinoatrial; TdP, torsades de pointes; VF,
ventricular fibrillation; VT, ventricular tachycardia
TABLE 4.5 Lidocaine (Xylocaine)

Class Class 1B antiarrhythmic
Mechanism of Decreases conduction in ischemic cardiac tissue without adversely affecting normal
Action conduction
Indications • Stable monomorphic VT
• May be considered as an alternative to amiodarone for pVT/VF that is unresponsive to
CPR, defibrillation, and vasopressor therapy (Link, et al., 2015)
Dosage • Initial dose: 1 to 1.5 mg/kg IV/IO bolus; consider repeat dose (0.5 to 0.75 mg/kg) at 5 to
10 min intervals
• Cumulative IV/IO bolus dose should not exceed 3 mg/kg
• Maintenance infusion: 1 to 4 mg/min
• Tracheal dose: 2 to 3 mg/kg (2 to 2.5 times IV dose)
Considerations • Lidocaine may be lethal for a patient with a bradycardia with a ventricular escape
rhythm.
• The initiation or continuation of lidocaine may be considered immediately after a ROSC
from cardiac arrest associated with pVT or VF (Link, et al., 2015).
IO, intraosseous; IV, intravenous; pVT, pulseless ventricular tachycardia; ROSC, return of spontaneous circulation; VF,
ventricular fibrillation; VT, ventricular tachycardia
TABLE 4.6 Characteristics of Asystole

Rhythm Ventricular not discernible; atrial may be discernible
Rate Ventricular not discernible but atrial activity may be observed (ie, “P-wave” asystole)
P waves Usually not discernible
PR interval Not measurable
QRS duration Absent
Fig. 4.3 Asystole. (From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)
Fig. 4.4 “P-wave” asystole. (From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)
Pulseless Electrical Activity

[Objective 3]
PEA is a clinical situation, not a specific dysrhythmia. PEA exists when organized electrical activity
(other than VT) is observed on the cardiac monitor but the patient is unresponsive and not breathing,
and a pulse cannot be felt (Fig. 4.5). PEA was formerly called electromechanical dissociation. The term was
changed because research using ultrasonography and indwelling pressure catheters revealed that the elec-
trical activity seen in some of these situations is indeed associated with mechanical contractions; however,
the contractions are simply too weak to produce a palpable pulse or measurable blood pressure.
PEA has a poor prognosis unless the underlying cause can be rapidly identified and appropriately
managed. Emergency care includes high-quality CPR, establishing vascular access, an aggressive search
for possible reversible causes of the arrest, the administration of epinephrine, and considering the inser-
tion of an advanced airway. Point of care ultrasound (POCUS) can be useful in identifying mechanical
causes of PEA. The cardiac arrest algorithm is shown in Fig. 4.6.
ACLS Pearl
Although memory aids can be used to recall possible reversible causes of PEA, an approach that
focuses on differentiation between narrow- or wide-QRS complexes on the cardiac monitor has
been suggested (Littmann, et al., 2014). This approach requires study, and it does not apply to
trauma settings. Narrow-QRS PEA is often the result of a mechanical problem caused by right ven-
tricular inflow or outflow obstruction (eg, cardiac tamponade, tension pneumothorax, mechanical
hyperinflation, pulmonary embolism). The presence of wide-QRS PEA suggests a metabolic (ie, left
ventricular) problem such as severe hyperkalemia with or without metabolic acidosis, or sodium
channel blocker toxicity. When used in conjunction with POCUS, this approach could help guide
initial treatment decisions when managing PEA.
A F
II
B G
C H
II II
D I
II
E J
Fig. 4.5 Pulseless electrical activity (PEA) requires the absence of detectable mechanical activity in the heart (ie, absence of a
pulse) with some form of organized electrical activity in the heart (ie, a rhythm). The most typical dysrhythmias seen in patients
with PEA include both narrow- and wide-QRS complex rhythms. A, Sinus bradycardia. B, Junctional rhythm. C, Atrial fibrillation
with slow ventricular response. D, Third-degree AV block. E, Idioventricular bradycardia. F, Idioventricular rhythm. G, Accel-
erated idioventricular rhythm. H, Accelerated idioventricular rhythm. I, Atrial tachycardia. J, Sinus tachycardia with bundle
branch block morphology. (From Adams JG: Emergency Medicine, ed 2, Philadelphia, 2013, Saunders.)
DEFIBRILLATION
[Objective 4]
Defibrillation is the delivery of an electrical current across the heart muscle over a very brief period to
terminate an abnormal heart rhythm. Defibrillation is also called unsynchronized countershock or asynchro-
nous countershock, because the delivery of current has no relationship to the cardiac cycle. Indications for
defibrillation include pulseless monomorphic VT, sustained PMVT, and VF. Recall that the goal for
providing the first shock for sudden cardiac arrest resulting from VF or pVT is within 3 minutes of
patient collapse (Link, et al., 2010).
Manual defibrillation refers to the following: placement of paddles or pads on a patient’s chest,
the interpretation of the patient’s cardiac rhythm by a trained health care professional, and the
health care professional’s decision to deliver a shock, if indicated. Automated external defibrilla-
tion refers to the following: placement of pads on a patient’s chest and the interpretation of the
patient’s cardiac rhythm by the defibrillator’s computerized analysis system. Depending on the type
of AED used, the machine will deliver a shock (if a shockable rhythm is detected) or instruct the
operator to deliver a shock. AEDs are discussed in more detail later in this chapter. In the hospital
setting, it is recommended that manual defibrillators or AEDs should be readily accessible in any
patient area and that all staff should know the location of this equipment and how to use it
(Morrison, et al., 2013).
Defibrillation does not “jump start” the heart. The shock attempts to deliver a uniform electrical cur-
rent of sufficient intensity to depolarize myocardial cells (including fibrillating cells) at the same time,
thereby briefly “stunning” the heart. This provides an opportunity for the heart’s natural pacemakers
to resume normal activity. When the cells repolarize, the pacemaker with the highest degree of automa-
ticity should assume responsibility for pacing the heart.
Fig. 4.6 Cardiac arrest algorithm. (Reprinted with permission. 2015 American Heart Association Guidelines for Cardio-
pulmonary Resuscitation and Emergency Cardiovascular Care—Part 7: Adult Advanced Cardiovascular Life Support.
ECCguidelines.heart.org. © 2015 American Heart Association, Inc.)
A defibrillator is a device that is used to deliver a shock to eliminate an abnormal heart rhythm
(Fig. 4.7). It consists of the following:
• A capacitor that stores energy (ie, electrons) at a particular voltage: think of voltage as the electrical
pressure that drives a flow of electrons (ie, current) through a defibrillator circuit (eg, the chest).
• An energy select button or dial: The shocks that are used for defibrillation and cardioversion are
expressed in joules (J) of energy.
• A charge switch/button that allows the capacitor to charge.
• Discharge buttons that allow the capacitor to discharge.
Fig. 4.7 A defibrillator is used to deliver an electrical shock to terminate an abnormal heart rhythm. (Courtesy Physio-Control,
Redmond, WA.)
• Handheld paddles, which require the use of conductive media, or combination pads through
which current is delivered from the defibrillator to the patient. Combination pads consist of a
flexible metal “paddle,” a layer of conductive gel, and an adhesive ring that holds them in place
on the patient’s chest. They are disposable and have multiple functions. Combination pads are
applied to a patient’s bare chest for ECG monitoring and then used for defibrillation, synchro-
nized cardioversion, and, in some cases, pacing. Combination pads physically separate the oper-
ator from the patient. Instead of leaning over the patient with handheld paddles, the operator
delivers a shock to the patient by means of a discharge button that is located on a remote cable,
an adapter, or on the defibrillator itself.
ACLS Pearl
Combination pads have multiple names including combo pads, multipurpose pads, multifunction elec-
trode pads, combination electrodes, therapy electrodes, and self-adhesive monitoring/defibrillation
pads. Not all combination pads are alike. Some pads can be used for defibrillation, synchronized
cardioversion, ECG monitoring, and pacing. Others can be used for defibrillation, synchronized car-
dioversion, and ECG monitoring, but not for pacing. Some pads have a built-in sensor that provides
feedback with regard to the proper rate and depth of compressions during CPR. Be sure that you are
familiar with the capabilities of the pads that you are using.
When the charge button on the defibrillator is pushed, the capacitor charges. Once the capacitor is
charged and the shock control is pressed, voltage pushes a flow of electrons (ie, current) to the patient by
means of handheld paddles or combination pads. Current passes through the heart in “waveforms” that
travel from one paddle/pad, through the chest, and to the other paddle/pad over a brief period.
Monophasic versus Biphasic Defibrillation

[Objective 5]
Different types of defibrillation waveforms exist. Waveforms are classified by whether the current flow
delivered is in one direction, two directions, or multiple directions.
When a monophasic waveform is used, current passes through the heart in one (ie, mono) direction
(Fig. 4.8). Although few monophasic waveform defibrillators are manufactured today, many are still in
use. With biphasic waveforms, energy is delivered in two (ie, bi) phases. The current moves in one direc-
tion for a specified period, stops, and then passes through the heart a second time in the opposite
Fig. 4.8 When a monophasic waveform is used, current Fig. 4.9 With biphasic waveforms, energy is delivered in
passes through the heart in one direction. two phases. The current moves in one direction for a spec-
ified period, stops, and then passes through the heart a sec-
ond time in the opposite direction.
direction during a very short period (ie, milliseconds) (Fig. 4.9). Today’s manual defibrillators and AEDs
use biphasic truncated exponential (BTE), rectilinear biphasic (RLB), or pulsed biphasic waveforms.
These waveforms deliver different peak currents at the same programmed energy setting and may adjust
their energy output with regard to patient impedance (discussed later) in differing ways (Link,
et al., 2015).
Defibrillators using biphasic waveforms (ie, BTE or RLB) are preferred to monophasic defibrillators
for treatment of both atrial and ventricular dysrhythmias because of their greater success with dysrhyth-
mia termination (Link, et al., 2015). Both escalating (ie, increasing energy levels) and nonescalating (ie,
no increase in energy level) biphasic waveform defibrillators are available. When preparing to deliver elec-
trical therapy to a patient, knowledge of the type of device that you are using (ie, monophasic versus biphasic)
and the manufacturer’s recommended energy levels for the dysrhythmia you are treating is essential.
Transthoracic Impedance
Although the energy selected for defibrillation or cardioversion is expressed in J, it is current that delivers
energy to the patient and that depolarizes the myocardium. Transthoracic impedance (resistance) refers
to the resistance of the chest wall to the flow of current at the interface between the patient’s chest wall
and combination pads or defibrillation paddles. If transthoracic resistance is high, the amount of current
that is actually delivered to the myocardium can be compromised, leading to failed shocks. Transthoracic
impedance varies greatly among individuals. Some of the factors known to affect transthoracic impedance
are discussed below.
ACLS Pearl
When a biphasic defibrillator is used, the patient’s transthoracic impedance is measured through the
paddles or combination pads in contact with the patient’s chest. The biphasic defibrillator compen-
sates for transthoracic impedance before the delivery of the shock, allowing the defibrillator to
deliver the actual amount of energy selected by the clinician.
Chest Hair
Chest hair can cause significant increases in transthoracic resistance (Sado, et al., 2004). It may be dif-
ficult to ensure good electrode-to-skin contact in a patient who has a hairy chest. However, if good con-
tact is not ensured, transthoracic impedance will be high and the effectiveness of the shocks delivered will
be reduced. (Bissing & Kerber, 2000; Sado, et al., 2004). There is an increased risk of burns from arcing
(ie, sparks) from electrode to skin and from electrode to electrode; ECG identification and analysis can
also be inhibited.
ACLS Pearl
If excessive chest hair is present and if time permits, quickly clip or shave the hair in the areas of
intended electrode placement to ensure the proper adhesion of the pads. If this is not feasible (or
if a razor is not available), check to see if an extra set of electrodes is available. If so, apply one
set to the patient’s chest and then quickly remove them. This should remove some hair and improve
electrode-to-skin contact when you apply a second set of pads.
Paddle/Pad Size
Studies have shown that adult paddles or pads should be used for patients weighing more than 10 kg
(22 lb.) (ie, generally older than age 1) (de Caen, et al., 2015). Avoid using pediatric electrodes for adult
defibrillation because myocardial injury can occur (Dahl, et al., 1974). Because the optimum pad sizes for
defibrillation and pacing on the basis of patient age and weight vary by manufacturer, it is important to
carefully follow all manufacturer instructions.
When applying paddles or pads, remove the patient’s clothing and expose his or her chest. Do not use
alcohol, tincture of benzoin, or antiperspirant when preparing the skin for paddle or pad placement. Look
at the patient’s chest for transdermal patches or disks, which may be used to deliver medications such as
nitroglycerin, nicotine, analgesics, hormones, or antihypertensives. Do not apply paddles or pads directly over
the medication patch or disk, because the patch may prevent good electrode contact, thereby hindering
the delivery of energy from the defibrillation paddle or pad to the heart (Wrenn, 1990). A lack of good contact
can cause arcing and may cause skin burns (Panacek, et al., 1992). If a medication patch, disk, or ointment
is located at or near the site of paddle or pad placement, remove it and wipe the area clean (do not use
alcohol or alcohol-based cleansers) before applying the defibrillation paddles or pads (Wrenn, 1990).
Because some patients wear jewelry in various body locations, take a moment to look for metal body
piercings after the patient’s chest is exposed. Although the presence of these materials is not a contra-
indication to defibrillation, it is possible that their presence can divert the defibrillating current from the
myocardium and decrease defibrillation effectiveness. If feasible and if time permits, the metal object
should be removed to minimize the potential for burn injuries across the chest.
Paddle/Pad Position
Handheld paddles or combination pads should be placed on the patient’s bare chest in accordance with
the manufacturer’s instructions. Paddles or pads may be labeled according to their intended position on
the chest (eg, sternum/apex, front/back) or according to their polarity (eg, positive, negative).
The typical paddle or pad position that is used during resuscitation is the sternum–apex position,
which is also called the anterolateral or apex–anterior position. This position is often used because the
anterior chest is usually easy to get to and placement of the paddles or pads in this position approximates
ECG electrode positioning in lead II. Place the sternum paddle or pad lateral to the right side of the
patient’s sternum, just below the clavicle. Place the center of the left (ie, apex) paddle or pad in the mid-
axillary line, lateral to the patient’s left nipple (Fig. 4.10). If the patient is a woman, elevate the left breast
and place the apex paddle or pad lateral to or underneath the breast. Placing defibrillation paddles or pads
directly on breast tissue results in higher transthoracic impedance, thereby reducing current flow (Pagan-
Carlo, et al., 1996).
Anterior Sternum Sternum
Lateral Apex Apex
Quick-combo Fast-patch Standard

electrodes electrodes paddles
Fig. 4.10 Combination pads and standard paddles in a sternum–apex position.
Another common position used for paddle or pad placement is the anterior–posterior position. In this
position, one paddle or pad is placed over the patient’s the left chest with the upper edge of the pad below
the nipple. The other is placed on the back, just below his or her left scapula (Fig. 4.11). Alternative
positions (eg, anterior–left infrascapular, anterior–right infrascapular) may be considered based on indi-
vidual patient characteristics (Link, et al., 2015).
Use of Conductive Material

When using handheld paddles, the use of gels, pastes, or pre-gelled defibrillation pads aids the passage of
current at the interface between the defibrillator paddles/electrodes and the body surface (Fig. 4.12). Fail-
ure to use conductive material results in increased transthoracic impedance, a lack of penetration of cur-
rent, and burns to the skin surface. Combination pads are pre-gelled and do not require the application of
additional gel to the patient’s chest.
When applying adhesive pads to the patient’s bare chest, press from one edge of the pad across the
entire surface to remove all air and to avoid the development of air pockets. A hands-free defibrillation
cable is used to attach the pads to the monitor/defibrillator.
When using pre-gelled pads with handheld paddles, make sure that the pads cover the entire paddle
surface to avoid arcing current and potential burns. Do not use saline-soaked gauze or alcohol-soaked
pads for defibrillation. Excess saline on the chest may cause arcing and burns. Alcohol-soaked pads
may ignite. Do not use gels or pastes that are not specifically made for defibrillation (eg, ultrasound
gel). The use of improper pastes, creams, gels, or pads can cause burns or sparks and may pose a risk of
fire in an oxygen-enriched environment (Hummel III, et al., 1988). If too much gel is used, the
Anterior Posterior
Fig. 4.11 Combination pads in an anterior–posterior position.
A B
Fig. 4.12 Use of conductive material is essential when performing defibrillation or cardioversion to lower the impedance to
flow of current at the electrode-chest interface. A, If standard paddles are being used, electrode gel must be applied before the
procedure. B, Self-adhesive pads have conductive material incorporated into the adhesive. Use of gel with these pads is
unnecessary. (From Roberts and Hedges’ clinical procedures in emergency medicine, ed 6, Philadelphia, 2014, Saunders.)
material may spread across the chest wall during resuscitation. This can lead to the arcing of the current
from one paddle to another and away from the heart, and this can also produce a potentially dangerous
spark or burn.
Paddle Pressure
When using handheld paddles for adult defibrillation, apply firm pressure (ie, about 25 lbs.) to each
paddle. This lowers transthoracic impedance by improving contact between the skin surface and the
paddles and by decreasing the amount of air in the lungs. No pressure is applied when combination
pads are used.
Selected Energy
When electrical therapy is used to treat an abnormal heart rhythm, it is important to select the appro-
priate energy level (ie, the right amount of J). If the energy level selected and the current delivered are too
low, the shock will not eliminate the abnormal rhythm. During adult cardiac arrest, use 360 J for all
shocks when using a monophasic defibrillator (Link, et al., 2015). When using a biphasic defibrillator,
use the energy level recommended by the manufacturer for the initial shock (eg, 120 to 200 J). If you do
not know what the recommended energy level is, consider defibrillation at the maximal dose (Link, et al.,
2015). The second and subsequent energy doses should be equivalent and higher doses may be
considered (Link, et al., 2015).
Defibrillation Procedure
[Objectives 4, 6]
The procedure described next assumes that the patient is an adult and confirmed to be unresponsive,
apneic, and pulseless. It also assumes that the patient’s cardiac rhythm is pVT or VF and that team
members are available to assist with procedures during the resuscitation effort.
Be sure that high-quality CPR is continued as the defibrillator is readied for use (Fig. 4.13). While
CPR continues, instruct a team member to expose the patient’s chest and to remove any transdermal
medication patches or ointment from the patient’s chest, if present. If handheld paddles are used, apply
conductive material (eg, gel) to the defibrillator paddles or apply disposable pre-gelled defibrillator pads
to the patient’s bare chest. If combination pads are used, remove the pads from their sealed package.
Check the pads for the presence of adequate gel. Attach the pads to the hands-free defibrillation cable,
and then attach the combination pads to the patient’s chest in the position recommended by the
manufacturer (Fig. 4.14).
Turn the power to the monitor/defibrillator on and verify the presence of a shockable rhythm on the
monitor (Fig. 4.15). Select an appropriate energy level (Fig. 4.16). Charge the defibrillator (Fig. 4.17).
If handheld paddles are used, press the “Charge” button on the machine or the button located on the apex
paddle. If combination pads are used, press the “Charge” button on the machine.
ACLS Pearl
When a shockable rhythm is present in cardiac arrest, give one shock and then immediately resume
CPR, starting with chest compressions. The reason for this is that lengthy interruptions in chest com-
pressions are associated with a decreased probability of conversion of a shockable rhythm to a per-
fusing rhythm. Resuming CPR immediately after a shock is more likely to be beneficial than
another shock.
All team members, with the exception of the chest compressor, should immediately clear the patient as
the machine charges. Listen as the machine charges. The sound usually changes when it reaches its
full charge. To help minimize interruptions in chest compressions, the person who is performing chest
compressions should continue CPR while the machine is charging. When the defibrillator is charged,
the chest compressor should immediately clear the patient. If a shockable rhythm is still present, call
“Clear!” Look around you (360 degrees) to be sure that everyone—including you—is clear of the patient,
the bed, and any equipment that is connected to the patient. Be sure oxygen is not flowing over the
patient’s chest.
ACLS Pearl
Remove supplemental oxygen sources from the area of the patient’s bed before defibrillation
attempts are made, and place them at least 3.5 to 4 feet away from the patient’s chest. Examples
of supplemental oxygen sources include masks, nasal cannulae, resuscitation bags, and ventilator
tubing.
Press the “Shock” control to defibrillate the patient (Fig. 4.18). Release the shock control after the
shock has been delivered. Instruct the team to resume chest compressions immediately without pausing
for a rhythm or pulse check.
Fig. 4.13 Continue CPR while the defibrillator is read- Fig. 4.14 Attach the combination pads to the
ied for use. (From Roberts and Hedges’ clinical proce- patient’s chest. (From Roberts and Hedges’ clinical
dures in emergency medicine, ed 6, Philadelphia, 2014, procedures in emergency medicine, ed 6, Philadel-
Saunders.) phia, 2014, Saunders.)
Fig. 4.15 Verify the presence of a shockable rhythm on Fig. 4.16 Select an appropriate energy level using the
the cardiac monitor. (From Roberts and Hedges’ clinical manufacturer’s recommended energy dose. (From Rob-
procedures in emergency medicine, ed 6, Philadelphia, erts and Hedges’ clinical procedures in emergency med-
2014, Saunders.) icine, ed 6, Philadelphia, 2014, Saunders.)
Fig. 4.17 Charge the defibrillator and clear everyone Fig. 4.18 After ensuring that everyone is clear of the
from the patient. (From Roberts and Hedges’ clinical patient, press the “Shock” control to defibrillate. (From Rob-
procedures in emergency medicine, ed 6, Philadelphia, erts and Hedges’ clinical procedures in emergency medicine,
2014, Saunders.) ed 6, Philadelphia, 2014, Saunders.)
ACLS Pearl
When defibrillating or cardioverting a patient with a permanent pacemaker or an implantable
cardioverter-defibrillator (ICD), be careful to not place the defibrillator paddles or combination pads
directly over the pulse generator (there will be a bulge under the patient’s skin). The anterior–
posterior and anterolateral paddle or pad positions are considered acceptable in these patients.
Depending on the manufacturer, the ICD may deliver a maximum of six shocks for VF. A shock
of about 2 J is delivered at the body surface when the ICD discharges internally. Rescuers who
are in contact with the patient may feel a tingling sensation when the ICD delivers a shock. Although
the energy is enough to be felt by the rescuer, it is not enough to cause physiologic harm. Because
some of the defibrillation current flows down the pacemaker leads, a patient who has a permanent
pacemaker or ICD should have the device checked to ensure proper function after defibrillation.
Automated External Defibrillation

An AED is an external defibrillator that has a computerized cardiac rhythm analysis system. AEDs are
easy to use. Voice prompts and visual indicators guide the user through a series of steps that may include
defibrillation. When the adhesive electrodes are attached to the patient’s chest, the AED examines the
patient’s cardiac rhythm and analyzes it. Some AEDs require the operator to press an “Analyze” control
to initiate rhythm analysis, whereas others automatically begin analyzing the patient’s cardiac rhythm
when the electrode pads are attached to the patient’s chest. Safety filters check for false signals (eg, radio
transmissions, poor electrode contact, 60-cycle interference, loose electrodes).
When the AED analyzes the patient’s cardiac rhythm, it “looks” at multiple features of the rhythm,
including the QRS width, rate, and amplitude. If the AED detects a shockable rhythm, it then charges its
capacitors. If the machine is a fully automated AED and a shockable rhythm is detected, it will signal
everyone to stand clear of the patient and then deliver a shock by means of the adhesive pads that were
applied to the patient’s chest. If the machine is a semiautomated AED and a shockable rhythm is
detected, it will instruct the AED operator (by means of voice prompts and visual signals) to press
the shock control to deliver a shock.
Use a standard AED for a patient who is unresponsive, apneic, pulseless, and age 8 or older. If the
patient is between age 1 and 8 and a pediatric attenuator is unavailable for the AED, use a standard AED
(Atkins, et al., 2015). For infants, defibrillation with a manual defibrillator is preferred (Atkins, et al.,
2015). If a manual defibrillator is not available, an AED equipped with a pediatric attenuator is desirable.
If neither is available, use a standard AED.
Operation
[Objective 4]
• Assess responsiveness. If the patient is unresponsive, quickly check for breathing while simultaneously
checking for a pulse for no more than 10 seconds. If a pulse is absent or if you are not certain that a
pulse is present, begin chest compressions.
• Turn on the power to the AED. Depending on the brand of AED, this is achieved by either pressing
the “On” button or lifting up the monitor screen or lid.
• Open the package containing the adhesive pads. If the gel in the pads is dried out, use a new set of
pads. Connect the pads to the AED cables (if not preconnected), and then apply the pads to the
patient’s chest in the locations specified by the AED manufacturer. Most models require connection
of the AED cable to the AED before use.
• Analyze the ECG rhythm. If several “looks” confirm the presence of a shockable rhythm, the AED
will signal that a shock is indicated. Listen for the voice prompts. The chest compressor and ventilator
should switch positions during rhythm analysis.
• Clear the area surrounding the patient. Be sure to look around you. Ensure that everyone is clear of the
patient, the bed, and any equipment that is connected to the patient. Make sure that oxygen is not
flowing over the patient’s chest.
• If the area is clear and the AED advises a shock, confirm that all team members are clear and then press
the shock control to deliver the energy to the patient when prompted to do so by the AED. After
delivering the shock, immediately resume CPR, beginning with chest compressions. After about
2 minutes of CPR, reanalyze the rhythm. Continue to provide care as indicated by the AED’s voice
and screen prompts.
Automated External Cardioverter-Defibrillators

Automated external cardioverter-defibrillators (AECDs), such as the Powerheart Cardiac Rhythm Module
(CRM) (Cardiac Science Inc., Irvine, CA), differ from AEDs. AECDs are being used with increased
frequency in hospitals to reduce the interval between the onset of sustained pVT/VF and the first
defibrillation.
The Powerheart CRM combines biphasic defibrillation technology, noninvasive external pacing, and
ECG monitoring technology. Dysrhythmia detection criteria and therapy protocols are programmed and
customized for individual patients by hospital staff. Once programmed and attached to the patient by
means of its disposable adhesive pads, the CRM can continuously monitor the patient’s cardiac rhythm,
detect the onset of life-threatening dysrhythmias using rhythm analysis software, and advise or automat-
ically deliver defibrillation therapy to patients upon detection of a shockable rhythm. The CRM can also
be used as a manual defibrillator or cardioverter.
Possible Complications
Possible complications of electrical therapy include the following:
• Injury to the operator or other team members if improper technique is used
• Risk of fire from the combination of electrical and oxygen sources
• Myocardial damage or dysfunction
• Embolic episodes
• Dysrhythmias including asystole, atrioventricular (AV) block, bradycardia, or VF after cardioversion
• Skin burns to the patient as a result of a lack of conductive material or of gel “bridging” (ie, the gel
forms a “bridge” on the skin) when using handheld paddles
THE RESUSCITATION TEAM

[Objective 7]
During a resuscitation effort, an interdisciplinary team works together to provide coordinated patient
care. Teamwork helps to ensure that the patient’s many needs are met throughout the resuscitation effort.
Regardless of where a cardiac arrest occurs, the primary goals of resuscitation are to restore spontaneous
circulation and meaningful neurologic recovery and to preserve vital organ function.
The size of a resuscitation team, also called a code team, and the skills of each team member
vary. Essential tasks that must be coordinated during a resuscitation effort include chest compressions,
ECG monitoring and defibrillation, airway management, vascular access and medication administration,
and documentation of the events of the code. The American College of Critical Care Medicine
recommends that a family support person be a recognized member of the code team (Davidson,
et al., 2007).
In the prehospital setting, emergency medical technicians (EMTs) and paramedics often work in
teams of two to four. The number varies depending on the environment in which the EMT or paramedic
works. For example, a fire department crew that responds to an emergency medical services (EMS) call
may be staffed with two EMTs and two paramedics on the vehicle. Although staffing may differ, the
ambulance that arrives on the scene is typically staffed with two EMTs, an EMT and a paramedic,
or an EMT and a registered nurse. A helicopter flight crew is typically staffed with a registered nurse
and a paramedic.
In the hospital setting, a predesignated resuscitation team should be available 24 hours a day, 7 days
a week. It is estimated that 77% of U.S. hospitals have a predesignated resuscitation team, but nearly
one-quarter do not (Kronick, et al., 2015). It is essential that health care facilities have policies and pro-
cedures in place for activating the code team. Just as it is important to know how to use a piece of equip-
ment before using it in an emergency, you must know your facility’s procedure for activating the team.
It is important to know, learn, and practice your facility’s code procedure and to learn what is expected
of you as a member of the resuscitation team. Frequent (eg, monthly) practice using methods such
as simulation-based mock codes is needed to minimize errors, maintain skills, and optimize patient
outcome (Morrison, et al., 2013).
ACLS Pearl
Knowledge of the algorithms is essential to successful completion of an ACLS course. During an
ACLS course, your knowledge of the ACLS algorithms is evaluated in simulated situations and
on the course posttest. The simulations (also called cases) are evaluated by an ACLS instructor.
The cardiac arrest algorithms are evaluated in the Cardiac Arrest Management (also called the Mega
Code) station. In this station, you work in teams of four or five persons. Each person takes a turn as
the team leader and as individual resuscitation team members, performing each of the critical tasks
of resuscitation. The team leader is evaluated on his or her knowledge of the ACLS algorithms, ability
to manage the resuscitation team, and his or her decisions regarding patient management. Although
the team leader is responsible for directing the overall actions of the team, a resuscitation effort
requires teamwork. Each member of the team must know his or her responsibilities and should
be able to anticipate the team leader’s instructions. This is true in real life, as well as in simulated
situations.
Team Leader Responsibilities

[Objective 7]
Every resuscitation effort must have someone who assumes responsibility for overseeing the actions of the
code team. If more than one person attempts to make decisions regarding the patient’s care, confusion
reigns and chaos will most likely result. The person in charge of the resuscitation effort is typically called
the code director or team leader.
In the prehospital setting, resuscitation efforts are usually led by a paramedic or nurse who operates
under standing physician orders, local protocols, or both. In the hospital setting, the team leader is usually
a physician who is experienced in cardiac arrest management. In most institutions, ACLS is considered
the standard of care in a cardiac arrest situation and, in the absence of a physician, emergency care may be
initiated by appropriately trained nurses per that institution’s policy.
The team leader guides the members of the code team and uses rapid, dynamic reasoning that con-
siders several things at once. Because research has shown that team leaders who perform hands-on tasks
in an emergency are less likely to be efficient leaders, the team leader should be in a position to “stand
back” to view and direct the resuscitation effort (Hunziker, et al., 2011).
It is likely that anyone who has been involved in, or simply observed, a resuscitation effort can recall at
least one chaotic event where the team leader shouted at everyone and the team members became flus-
tered, not knowing what to anticipate next. As the team leader, it is essential that your manner, attitude,
words, and skills be professional throughout the resuscitation effort. A modified autocratic leadership
style that allows for team feedback and knowledge sharing is necessary during a code. It is best to speak
in a calm and confident tone to the members of your team using terms that are known and shared by all
team members. Generally, speaking in a normal, composed tone has a calming effect on those present. A
good team leader values his or her team members, fosters an environment in which team members feel
comfortable speaking up, and encourages a respectful exchange of ideas.
During the resuscitation effort, the team leader:
• Instructs a team member to perform the primary and secondary surveys and to relay his or her findings
to the team leader.
• Receives a concise history of the event and care given, when applicable. For example, a first responder
relays information to arriving paramedics. Paramedics relay information to the emergency department
nurse or physician. In the hospital, the nurse who was providing patient care relays important prearrest
information to the team leader.
• Instructs the team to perform high-quality chest compressions and evaluates the adequacy of chest
compressions including hand position, depth of cardiac compressions, proper rate, and ratio of com-
pressions to ventilations.
• Directs the team to administer appropriate oxygen therapy to the patient throughout the resuscitation effort.
• Instructs the team to perform defibrillation, when indicated, and ensures that it is performed safely
and correctly.
• Instructs the team to establish vascular access (IV or IO).
• Orders the administration of the correct medications, doses, and routes for the dysrhythmia.
• Considers placement of an advanced airway; if the decision is made to insert an advanced airway,
directs a qualified team member to insert it and instructs the team to confirm proper positioning
of the device.
• Considers baseline laboratory values and other relevant data if necessary.
• Directs reassessment of the patient’s response to interventions.
• Monitors the performance of team members.
• Ensures family notification of resuscitation events.
• Problem-solves (including evaluating possible causes of the arrest and recognizing malfunctioning
equipment and misplaced or displaced tubes or lines).
• Considers special resuscitation protocols (eg, asthma, anaphylaxis, pregnancy, toxic ingestion, trauma,
accidental hypothermia, submersion incident, electric shock or lightning strike), when appropriate.
• Directs post–cardiac arrest care when there is a ROSC.
• Decides when to terminate resuscitation efforts (in consultation with team members), when there is no
response to resuscitation efforts after a reasonable period.
• Provides an opportunity for team members to be involved in a team debriefing or reflection on the
resuscitation effort after the event.
Remember that during a cardiac arrest, the most important priorities are the performance of high-quality
CPR and, if a shockable rhythm is present, defibrillation. Obtaining vascular access, giving medications, and
inserting an advanced airway are of secondary importance. The rhythm present on the cardiac monitor will
guide the sequence of procedures that need to be done next. For example, if the patient is in cardiac arrest
and the cardiac monitor shows no electrical activity, asystole is present. If the monitor shows an organized
rhythm despite no central pulse when you assess the patient, PEA is present. Defibrillation is not indicated
for asystole or PEA. If the monitor shows VF or pVT, defibrillation is indicated.
Throughout the resuscitation effort, keep in mind that a change in the patient’s cardiac rhythm or
pulse status (eg, pulseless to pulse present) usually results in a change in the recommended treatment
sequence (ie, algorithm). For instance, if defibrillation of pVT/VF results in the observation of an orga-
nized rhythm on the monitor, a pulse check should be performed (Link, et al., 2015). If the patient has a
pulse, the algorithm changes because of the rhythm change as well as the presence of a pulse. If the orga-
nized rhythm on the monitor does not produce a pulse, PEA exists and treatment continues using the
cardiac arrest algorithm; however, the treatment sequence changes from the shockable rhythm segment
of the algorithm to the nonshockable rhythm segment. If the organized rhythm on the monitor does pro-
duce a pulse, supportive measures must be taken to maintain the perfusing rhythm. This is called post-
resuscitation support or post–cardiac arrest care. Assess the patient’s vital signs upon the return of a pulse. If
defibrillation of pVT results in VF (or vice versa), there is no change in the algorithm because pVT and
VF are treated in the same way.
Team Member Responsibilities

[Objective 7]
Each member of the resuscitation team must have clear roles and responsibilities, must know his or her
limitations, must be knowledgeable about current resuscitation algorithms, must be practiced in resus-
citation skills, and must be prepared to question other team members if an action is about to occur that
may be inappropriate. Nurses who respond to a cardiac arrest must be familiar with the layout of the code
cart, which is also called a crash cart, and the location of all items contained therein. In the prehospital
setting, paramedics must be familiar with the location of all medications in their drug box and the
resuscitation-related equipment in their emergency bags and vehicles, if applicable.
The team member responsible for CPR must be able to properly perform CPR and provide chest
compressions of adequate rate, force, and depth in the correct location.
The team member responsible for ECG monitoring and defibrillation should know how to do the
following:
• Operate an AED and a manual defibrillator.
• Properly place handheld defibrillator paddles and combination adhesive pads.
• Consider the necessary safety precautions when performing electrical therapy.
• Solve problems with regard to equipment failure.
The team member responsible for airway management should know how to do the following:
• Perform the head tilt–chin lift maneuver and the jaw thrust without neck extension maneuver.
• Correctly size and insert an oral airway and a nasal airway.
• Correctly apply and understand the indications, contraindications, advantages, disadvantages, com-
plications, liter flow ranges, and concentrations of delivered oxygen for oxygen delivery devices,
including the nasal cannula, the simple face mask, the pocket mask, the nonrebreathing mask, and
the bag-mask device (BMD).
• Suction the upper airway by selecting an appropriate suction device and catheter and by using correct
technique.
• Know the indications, contraindications, advantages, disadvantages, complications, equipment,
and techniques for the insertion of an advanced airway, if this is within his or her scope of practice.
• Know how to confirm the placement of an advanced airway.
• Know how to use waveform capnography, an exhaled carbon dioxide detector, and an esophageal
detector device.
• Know how to properly secure an advanced airway.
ACLS Pearl
In the hospital, an anesthesiologist or nurse anesthetist typically assumes responsibility for the
patient’s oxygenation and ventilation and is aided by a respiratory therapist who assists with suc-
tioning, equipment set up, and manual ventilation of the patient. In some institutions, the respiratory
therapist performs tracheal intubation.
The team member responsible for vascular access and medication administration must be familiar
with the location of the emergency medications, IV fluids, and related supplies that may be used during
a resuscitation effort. This team member prepares and labels the medications and IV fluids used during
the code as directed by the team leader.
During circulatory collapse or cardiac arrest, the preferred vascular access site is the largest, most
accessible vein that does not require the interruption of resuscitation efforts. If no IV is in place before
the arrest, establish IV access using a peripheral vein—preferably the antecubital or external jugular
vein. Normal saline is the preferred IV fluid because it expands intravascular volume better than dex-
trose. During cardiac arrest, give IV drugs rapidly by bolus injection. Follow each drug with a 20 mL
bolus of IV fluid and briefly raise the extremity during and after drug administration to aid delivery of
the drug(s) to the central circulation (Link, et al., 2015). If peripheral IV access is unsuccessful during
cardiac arrest, consider an IO infusion before considering placement of a central line. To improve flow
rates during an IO infusion, the use of a pressure bag or infusion pump may be necessary. Current
resuscitation guidelines note that an appropriately trained provider can consider placement of an inter-
nal jugular or subclavian central line during cardiac arrest, unless there are contraindications (Link,
et al., 2015).
The vascular access and medication administration team member should know the following:
• The antecubital fossa is the site of first choice for vascular access if no IV catheter is in place at the time
of cardiac arrest.
• The procedure for performing IO access in an adult.
• The importance of following each medication given during a cardiac arrest with a 20 mL IV fluid
bolus and brief elevation of the extremity.
• The routes of administration and appropriate dosages for IV, IO, and tracheal resuscitation
medications.
ACLS Pearl
The tracheal route of drug administration is not preferred because multiple studies have shown that
giving drugs (eg, lidocaine, epinephrine, atropine, naloxone, vasopressin) tracheally results in lower
blood concentrations than the same dose given intravascularly (Link, et al., 2015). Intravascular drug
administration provides more predictable drug delivery and pharmacologic effect (Link, et al., 2015).
The recommended dose of some medications that can be given via the tracheal route is generally 2
to 2.5 times the intravascular dose, although the optimal tracheal dose of most drugs is unknown.
Support Roles
[Objective 7]
There are many support roles in a resuscitation effort. In the hospital, a nursing supervisor often assumes
responsibility for contacting the patient’s attending physician, limiting the number of people present to
those necessary (ie, crowd control), ensuring that a critical care bed is available, and coordinating the
transfer of the patient to the intensive care unit (ICU). Another nurse typically assumes responsibility
for bringing the patient’s chart to the bedside or referring to the patient’s electronic chart for pertinent
patient information (eg, code status, allergies, most recent laboratory results) and relaying that informa-
tion to the team leader.
Support staff is needed to remove excess furniture or equipment from the room (eg, overbed table,
wheelchair), to assist the patient’s roommate (if applicable), and to provide ongoing care to other patients
on the ward. Pastoral care, social workers, or other nursing staff are needed for family support. The use of
a professional language interpreter may be needed to explain the patient’s condition to the family.
Resuscitation Efforts
[Objective 8]
It is important that resuscitation efforts be performed with the patient on a firm surface. In the field, care
should begin where the patient is found unless EMS personnel do not have enough space in which to
resuscitate the patient or conditions exist that may be hazardous to them or to the patient. In the hospital,
a team member must ensure that a code board is placed under the patient. Most hospital beds have a
“code” feature that quickly places the bed flat and deflates cushioning devices at the same time. Simu-
lation studies have demonstrated that even with the use of a backboard, mattress compression can
account for as much as 40% of measured compression depth in patients with in-hospital cardiac arrest
(IHCA); thus deeper chest compressions in the IHCA setting may be needed to compensate for mattress
movement if it cannot be neutralized by the use of a backboard (Morrison, et al., 2013).
ACLS Pearl
Although not always available, information related to the arrest should be sought, including the
following:
• When and where did the arrest occur?
• Was the arrest witnessed?
• Was CPR performed? If yes, how long was the patient down before CPR was started?
• What was the patient’s initial cardiac rhythm? If VF or pVT, when was the first shock delivered?
• Are there any special circumstances to consider such as hypothermia, trauma, drug overdose, or
do-not-attempt-resuscitation (DNAR) orders?
• What treatment has been given?
• What information is available regarding the patient’s past medical history?
CPR should be continued by the caregivers who recognized the patient’s arrest. The team leader
assigns team member roles as the team members are assembled, if the roles of each member of the team
have not been preassigned. Several tasks are performed simultaneously as the members of the code team
converge and position themselves around the patient to begin or continue resuscitation efforts. For exam-
ple, the code cart is positioned at the patient’s bedside for easy access to the defibrillator, oxygen, suction
equipment, medications, and supplies, as well as for viewing the ECG monitor. The patient is attached to
a cardiac monitor and to a continuous EtCO2 monitor (if available), combination pads are applied to the
patient’s bare chest, an oxygen source is attached to a BMD, and suction is set up. Pertinent information
from the patient’s caregiver should be quickly obtained such as patient age, weight (this allows rescuers to
anticipate weight-based drug dosages), estimated time of arrest, the circumstances surrounding the
arrest, and the presence of a DNAR order.
ACLS Pearl
Originally developed as a communication technique by the U.S. Navy, SBAR is an acronym for
Situation, Background, Assessment, and Recommendation that is often used by health care person-
nel as a tool to ensure rapid, effective communication when transferring patient care. The Reason,
Story, Vital Signs, Plan (RSVP) system is another communication tool that is used to convey patient
information.
Closed-Loop Communication
It is important that the team leader, team members, and the event recorder communicate clearly through-
out the resuscitation effort. Because there are often a large number of persons present during a code,
sidebar conversations among team members that can be distracting to other team members must be
avoided. To avoid information overload and to help ensure that what is said by the team leader is what
is heard by the team members, the team leader should state his or her instructions one at a time using
terms that are known and shared by all team members. The team member’s name should be used, if
known. For example, “Aubree, please charge the defibrillator to 150 joules” or “Andrew, please insert
an oral airway.”
To avoid the need for repetitious instructions, team members must clearly acknowledge when pro-
cedures and medications are complete. For example, if a team member was directed to establish an IV or
give a medication, he or she should respond by saying something like, “IV started, left antecubital vein” or
“epinephrine 1 mg of 1:10,000 solution given IV” when the task is completed. This practice allows those
sending and receiving messages an opportunity to recognize and correct errors and helps to ensure accu-
rate documentation of the interventions performed, the timing of those interventions, and the patient’s
response to them by the designated event recorder.
Because safe practice includes the verification of orders, it is important that team members request
clarification of any orders that are unclear. Team members must also verbalize any change in the status
of the patient’s pulse, cardiac rhythm, oxygenation, or ventilation to the team leader. For example,
“Dr. __, the rhythm on the monitor has changed” or “Dr. __, bag-mask ventilation is becoming increas-
ingly difficult.”
ACLS Pearl
Regardless of your role in a resuscitation effort or your level of certification or licensure, it is important
to tactfully voice your concerns and question an intervention if you know a mistake is being made or
is about to occur.
Shockable Rhythms
[Objectives 2, 7, 8]
When pVT/VF is present, defibrillation is indicated. Be sure that the CPR team member con-
tinues chest compressions as the defibrillator is readied for use. The airway team member should
coordinate ventilations with the CPR team member until an advanced airway is placed and its posi-
tion confirmed.
While high-quality CPR continues, instruct the defibrillation team member to expose the patient’s
chest and to attach the combination pads to the patient’s chest, if not already done. Verify the presence of
a shockable rhythm on the monitor and select an appropriate energy level. While the defibrillator is read-
ied, instruct the IV/medication team member to prepare the initial medications that will be used and to
establish vascular access after the first shock is delivered.
When it is time to deliver a shock, instruct all team members with the exception of the person per-
forming chest compressions to immediately clear the patient. The airway team member must make sure
that oxygen is not flowing over the patient’s chest. Once the defibrillator is charged, the chest compressor
should clear the patient. In this way, chest compressions are interrupted for the least amount of time
possible during the resuscitation effort. Check to be certain that everyone is clear and then instruct
the defibrillation team member to defibrillate the patient.
Once the shock is delivered, instruct the team to resume chest compressions immediately without
pausing for a rhythm or pulse check. Instruct the airway team member to coordinate ventilations with
the chest compressor. Assuming that vascular access has been established, instruct the IV/medications
team member to give the patient a vasopressor during CPR.
After five cycles of CPR (about 2 minutes), recheck the rhythm. Pauses in chest compressions for
rhythm checks should not exceed 10 seconds. If a shockable rhythm is present, charge the defibrillator
and then call “Clear!” Check to be certain that everyone is clear, and then defibrillate. Resume chest com-
pressions immediately. While continuing CPR, consider giving an antiarrhythmic (eg, amiodarone).
Consider placement of an advanced airway. After intubation, initiate capnography to determine the
adequacy of CPR. Use the memory aids PATCH-4-MD or the Five Hs and Five Ts to help identify
possible reversible causes of the arrest or factors that may be complicating the resuscitation effort.
ACLS Pearl
Current resuscitation guidelines note that although there is insufficient evidence to recommend the
use of extracorporeal CPR (ECPR) for patients with cardiac arrest, in settings where it can be rapidly
implemented, ECPR may be considered for select cardiac arrest patients for whom the suspected
cause of the arrest is potentially reversible. Examples given include acute coronary artery occlusion,
pulmonary embolism, refractory VF, profound hypothermia, cardiac injury, myocarditis, cardiomy-
opathy, heart failure, and drug intoxication. ECPR can serve as a bridge for left ventricular assist
device implantation or cardiac transplantation during a limited period of mechanical cardiorespira-
tory support (Link, et al., 2015).
If defibrillation restores an organized rhythm, check for a pulse (Link, et al., 2015). If you are not sure
if a pulse is present, resume CPR. If a pulse is present, repeat the primary survey, ask a team member to
obtain the patient’s vital signs, and begin post–cardiac arrest care. If a spontaneous pulse has returned,
efforts of the code team should be focused on the following:
• Repeating the primary and secondary surveys
• Anticipating changes in the patient’s condition (and preventing deterioration)
• Stabilizing vital signs
• Securing tubes and lines
• Troubleshooting any problem areas
• Preparing the patient for transport or transfer
• Accurately documenting the events that took place during the resuscitation effort
• Drawing blood for laboratory tests and treating the patient as needed on the basis of results
If defibrillation successfully terminated pVT/VF but the rhythm recurs, begin defibrillation at the last
energy level used that resulted in successful defibrillation.
Nonshockable Rhythms
If a rhythm check reveals a nonshockable rhythm, continue high-quality CPR. Establish vascular access
and give epinephrine every 3 to 5 minutes. Consider placement of an advanced airway and the use of cap-
nography after intubation. Because hypoxemia is a possible reversible cause of cardiac arrest, advanced air-
way placement is theoretically more important during a cardiac arrest associated with PEA or asystole than
with pVT/VF and may be necessary to achieve adequate oxygenation or ventilation (Link, et al., 2015).
Reassess the patient’s cardiac rhythm. If an organized rhythm is present, perform a pulse check. If a
pulse is present, begin post–cardiac arrest care. If a nonshockable rhythm persists, resume high-quality
CPR. Search for and treat reversible causes of the arrest or factors that may be complicating the resus-
citation effort during each 2-minute period of CPR (Link, et al., 2015). If PEA is present and ultrasound
equipment and a qualified sonographer are available, this technology can be useful in identifying poten-
tially treatable causes of cardiac arrest and guiding patient management decisions. For example, ultra-
sound can be used to recognize cardiac tamponade and pneumothorax, to identify the presence of
tumors or clots, to assess myocardial contractility during CPR, and to assess ventricular volume. The
use of cardiac or noncardiac ultrasound should not interfere with standard cardiac arrest treatment pro-
tocols (Link, et al., 2015).
Continue CPR for 2 minutes before performing another rhythm check. Remember to switch chest
compressors every 2 minutes to avoid rescuer fatigue. If there is no response to appropriately performed
interventions after a reasonable period, consider termination of efforts after consultation with the mem-
bers of the resuscitation team. Examples of factors that are considered when deciding to terminate in-
hospital resuscitative efforts include the following:
• The time from patient collapse to CPR
• The patient’s initial cardiac rhythm at the time of the arrest
• The time from collapse to the first defibrillation attempt (if a shockable rhythm was present)
• The existence of special circumstances (eg, traumatic injury, asthma, pregnancy, poisoning, hypother-
mia, submersion injury, electrical/lightning injury)
• The presence of comorbid disease
• The patient’s response to resuscitative measures, including physiologic parameters such as quantitative
waveform capnography, arterial relaxation diastolic pressure, arterial pressure monitoring, and central
venous oxygen saturation (Link, et al., 2015)
ACLS Pearl
For intubated patients, continuous EtCO2 monitoring should be used to monitor the quality of com-
pressions during resuscitation efforts. Failure to achieve an EtCO2 of greater than 10 mm Hg imme-
diately after intubation and after 20 minutes of CPR is associated with extremely poor chances for
ROSC and survival (Link, et al., 2015). This finding, in combination with other factors, may be con-
sidered when deciding when to terminate resuscitation (Link, et al., 2015).
Special Resuscitation Situations

Some situations require basic life support (BLS) or advanced life support modifications during resusci-
tative efforts. Cardiac arrest in patients with known or suspected opioid overdose and cardiac arrest in
pregnancy are discussed below.
Known or Suspected Opioid Overdose

Recognizing that opioid overdose became the leading cause of unintentional injurious death in people
aged 25 to 60 years in the United States in 2012 (Lavonas, et al., 2015), the 2015 resuscitation guidelines
address cardiac or respiratory arrest associated with known or suspected opioid overdose. It is reasonable
for appropriately trained lay rescuers and BLS providers to administer intramuscular (IM) or intranasal
(IN) naloxone in addition to providing standard BLS care for the patient who is unresponsive, is not
breathing normally or is only gasping, who has a clearly palpable pulse, and who is suspected of having
an opioid overdose (Lavonas, et al., 2015). Naloxone should be given as soon as it is available and may be
repeated after 4 minutes.
The unresponsive patient who is not breathing and who has no pulse may be in cardiac arrest or may
have a pulse that is too weak or too slow to be detected (Lavonas, et al., 2015). Standard resuscitative
measures, including high-quality CPR, should be used to manage these patients. Naloxone administra-
tion may be considered after CPR is begun if opioid overdose is suspected (Kleinman, et al., 2015).
Cardiac Arrest and Pregnancy

Common causes of common maternal cardiac arrest include hemorrhage, cardiovascular diseases, amni-
otic fluid embolism, sepsis, aspiration pneumonitis, pulmonary embolism, and eclampsia (Lavonas, et al.,
2015). In the latter half of pregnancy, cesarean delivery may be considered part of maternal resuscitation,
regardless of fetal viability (Lavonas, et al., 2015).
At 20 weeks’ gestation, the fundal height is typically at the level of the umbilicus. The weight of the
pregnant uterus on the inferior vena cava and aorta can hinder venous return and cardiac output when
the patient is supine. During cardiac arrest, the uterus should be manually displaced to the left when the
fundal height is at or above the level of the umbilicus to shift the weight of the uterus off these major
blood vessels and improve cardiac output. High-quality CPR should be performed with the patient in
this position. If manual uterine displacement is unsuccessful and a firm wedge is immediately available,
consider placing the patient in a left lateral tilt of 27 to 30 degrees, using the wedge to support the
patient’s thorax and pelvis (Lavonas, et al., 2015).
Cesarean delivery should be considered at 4 minutes after the onset of maternal cardiac arrest or resusci-
tative efforts (for the unwitnessed arrest) if there is no ROSC (Lavonas, et al., 2015). Factors to consider
with regard to the decision to perform a cesarean delivery include the availability of appropriately trained per-
sonnel, gestational age, etiology of the arrest, and available equipment and resources (Lavonas, et al., 2015).
Patient Transfer
The resuscitation team’s responsibility to the patient continues until patient care is transferred to a health
care team with equal or greater expertise. Transfer the patient with oxygen, ECG monitoring, and resus-
citation equipment and ensure that trained personnel accompany the patient. When transferring care,
provide information that is well organized, concise, and complete. Make certain that the family has been
updated regarding events.
Post–Cardiac Arrest Care

[Objective 9]
Care of the patient with ROSC after cardiac arrest has a strong impact on patient morbidity and mor-
tality (Boutsikaris & Winters, 2012). Best practices include a multidisciplinary team approach that
includes personnel from cardiology, interventional cardiology, cardiac electrophysiology, intensive care,
and neurology (Morrison, et al., 2013). The components of post–cardiac arrest syndrome are shown in
Table 4.7. The post–cardiac arrest algorithm is shown in Fig. 4.19.
Oxygenation and Ventilation

Immediately after the ROSC, repeat the primary survey, and then perform a thorough physical exam-
ination and assess vital signs.
Reassess the effectiveness of initial airway maneuvers and interventions. Apply a pulse oximeter and
assess oxygen saturation. To avoid hypoxia during the period immediately after ROSC, the highest avail-
able oxygen concentration may be used until the arterial oxyhemoglobin saturation or the partial pressure
of arterial oxygen can be measured (Callaway, et al., 2015). When resources are available to titrate the
fraction of inspired gas that is oxygen (FiO2) and to monitor oxyhemoglobin saturation, it is reasonable to
decrease the FiO2 when the oxyhemoglobin saturation is 100%, provided that a blood oxygen saturation
level (SpO2) of 94% or greater can be maintained (Callaway, et al., 2015).
Assess and monitor the effectiveness of ventilations with capnography. Mechanical ventilation may be
necessary for absent or inadequate spontaneous breathing and to minimize acute lung injury and poten-
tial oxygen toxicity (Callaway, et al., 2015). Avoid hyperventilation, which increases intrathoracic pres-
sure and can potentially worsen hemodynamic instability (Boutsikaris & Winters, 2012). Avoid
hypoventilation, which can contribute to hypoxia and hypercarbia. The 2015 resuscitation guidelines
state that it is reasonable to maintain the partial pressure of carbon dioxide (PaCO2) within a normal phys-
iologic range, taking into account any temperature correction, unless patient factors prompt more indi-
vidualized treatment (Callaway, et al., 2015). If tolerated, elevate the head of the bed 30 degrees to reduce
the incidence of cerebral edema, aspiration, and ventilatory-associated pneumonia (Peberdy, et al., 2010).
Obtain a chest radiograph to confirm advanced airway placement and identify potential breathing causes
or complications of resuscitation such as pneumothorax, rib fractures, sternal fractures, pneumonitis,
pneumonia, or pulmonary edema (Callaway, et al., 2015). The administration of fibrinolytics may be
considered for the post‒cardiac arrest patient with arrest resulting from presumed or known pulmonary
embolism (Callaway, et al., 2015).
TABLE 4.7 Components of Post–Cardiac Arrest Syndrome

Component Clinical Manifestations Possible Interventions
Brain injury Coma TTM
Seizures Seizure control
Myoclonus
Varying degrees of neurocognitive dysfunction
(ranging from memory deficits to a persistent
vegetative state)
Stroke
Brain death
Myocardial Circulatory collapse Coronary reperfusion
dysfunction Dysrhythmias Hemodynamic support
Hypotension Mechanical support (eg, left
ventricular assist device,
intraaortic balloon pump)
Systemic Circulatory collapse Hemodynamic support
ischemia/ Hypotension Temperature control
reperfusion Hypovolemia
response Multiorgan failure
Persistent Cause-specific (eg, acute coronary syndrome, Disease-specific interventions
precipitating asthma, hemorrhage, hypovolemia, overdose,
cause pulmonary embolism, sepsis, stroke)
TTM, Targeted temperature management

Fig. 4.19 The post–cardiac arrest algorithm. (Reprinted with permission. 2015 American Heart Association Guidelines for
Cardiopulmonary Resuscitation and Emergency Cardiovascular Care—Part 8: Post–Cardiac Arrest Care. ECCguidelines.
heart.org. © 2015 American Heart Association, Inc.)
Cardiovascular Care
Heart rate and blood pressure are extremely variable immediately after ROSC. After ROSC, all patients
should receive continuous ECG monitoring and a 12-lead ECG should be obtained as soon as possible
to determine whether acute ST segment elevation is present (Callaway, et al., 2015).
Emergent coronary angiography is recommended for out-of-hospital cardiac arrest (OHCA) patients
with a presumed cardiac cause of arrest and with ST segment elevation (Callaway, et al., 2015). Emergent
coronary angiography is considered reasonable for electrically or hemodynamically unstable patients who are
comatose after OHCA of suspected cardiac origin but without ST segment elevation (Callaway, et al., 2015).
Coronary angiography is reasonable in post–cardiac arrest patients for whom coronary angiography is indi-
cated regardless of whether the patient is comatose or awake (Callaway, et al., 2015).
Establish IV access with normal saline or lactated Ringer’s solution if not already done. Hypotonic
fluids should be avoided because they may increase edema, including cerebral edema (Peberdy, et al.,
2010). If IO access was used during the arrest, establish an IV line to replace it when time permits. Insert
a nasogastric tube and urinary catheter to monitor intake and output.
Dysrhythmias that occur during the post‒cardiac arrest period should be treated in the same way as
that for a patient who has not had a cardiac arrest (Boutsikaris & Winters, 2012). Current guidelines
consider it reasonable to avoid and to immediately correct hypotension (ie, systolic blood pressure
less than 90 millimeters of mercury [mm Hg], mean arterial pressure less than 65 mm Hg) during
post‒cardiac arrest care (Callaway, et al., 2015). Administration of IV/IO fluid boluses, about 1 to 2 liters
of normal saline or lactated Ringer’s solution, may be necessary to restore intravascular volume, and the
administration of vasoactive medications may be necessary to maintain perfusion if hypotension persists
(Callaway, et al., 2015). For example, chronotropic agents may be needed to improve heart rate, inotropic
agents may be necessary to enhance myocardial contractility, vasoconstrictive medications may be needed
to increase arterial pressure, or vasodilators may be necessary to reduce afterload (Callaway, et al., 2015).
Neurologic Care
Targeted temperature management (TTM), formerly known as therapeutic hypothermia, is recom-
mended for adult patients who lack a meaningful response to verbal commands after ROSC
(Callaway, et al., 2015). Selecting and maintaining a constant temperature between 32 ºC and 36 ºC
is recommended and it is reasonable that TTM be maintained for at least 24 hours after cardiac arrest
after achieving target temperature (Callaway, et al., 2015). The routine prehospital cooling of patients
after ROSC with rapid infusion of cold intravascular fluids is not recommended (Callaway, et al., 2015).
Clinical manifestations of post–cardiac arrest brain injury include coma, seizures, myoclonus, various
degrees of neurocognitive dysfunction (ranging from memory deficits to a persistent vegetative state), and
brain death (Callaway, et al., 2015). Because seizures after a cardiac arrest may be caused by, as well as
worsen, post–cardiac arrest brain injury, an electroencephalogram should be promptly performed and
interpreted and then should be monitored frequently or continuously in comatose survivors of cardiac
arrest (Callaway, et al., 2015). Current evidence does not support the routine administration of anticon-
vulsant medications for patients after cardiac arrest without seizure activity. If seizures are present, the
same anticonvulsant regimens for the treatment of status epilepticus associated with other etiologies may
be considered after cardiac arrest (Callaway, et al., 2015).
Debriefing
[Objective 10]
Regardless of the outcome of a resuscitation effort or its length, the team leader is responsible for making
sure that a postevent debriefing takes place. Data from the defibrillator, the code sheet, feedback devices,
and other sources that captured data during the resuscitation effort should be collected and provided for
feedback to the code team.
During a debriefing, each member of the code team has an opportunity to engage in honest dialogue
to gain understanding and to identify lessons learned in a nonpunitive environment. Ideally, the indi-
vidual who leads the debriefing should have training and experience as a facilitator. A debriefing provides
the following:
• An opportunity for each team member to reflect on what they did, when they did it, how they did it,
why they did it, and how they can improve (Phrampus & O’Donnell, 2013)
• An opportunity to identify and address performance gaps (ie, the gap between desired and actual per-
formance) and perception gaps (ie, the difference between the team member’s perception of their per-
formance and actual performance as defined by objective measures) (Phrampus & O'Donnell, 2013)
• An opportunity to review the clinical judgments made and actions performed during the event and
compare them with current resuscitation algorithms, professional standards, institution policies, and
local protocols
• An opportunity to address emotional responses related to the event
• An opportunity for self-reflection that can be translated to actionable knowledge to guide future deci-
sions and actions, and ultimately improve patient care
• An opportunity to identify and discuss the elements of the resuscitation that went well, those areas that
could be improved, and recommendations for future resuscitation efforts
Although there are many debriefing techniques, the structured and supported debriefing model is a
method that is commonly used in advanced life support courses. This model consists of the following
phases: (Phrampus & O’Donnell, 2013)
1. Gather phase. This phase is used for gauging the reaction of the team to the event, clarifying facts,
describing what happened, and creating an environment for reflective learning. During this phase
of the debriefing, the team leader is asked to provide a synopsis of what occurred and supplemental
information is requested from team members. Using open-ended questions, the facilitator listens to
the team members describe their perceptions of their behaviors.
2. Analysis phase. During this phase, the record of the event (eg, code sheet, data from feedback-enabled
devices) is reviewed and the observations of team members are reported. The facilitator asks questions
to assist with self-reflection and analysis of each team member’s actions, changes in the patient’s
condition that may have occurred during the event, and how individual and team actions may have
influenced the outcome of the event. The actions of the team can be compared with current resus-
citation algorithms, professional standards, institution policies, best evidence, and local protocols to
enhance understanding.
3. Summary phase. The debriefing concludes with a review of the lessons learned and a summary of the
main take-home messages and needed performance improvements.
Family Notification
Several surveys have revealed that most relatives of patients who require CPR would like to be offered the
possibility of being present during a resuscitation attempt. According to follow-up surveys with family
members who had witnessed a resuscitation effort, most felt that their adjustment to the death or grieving
was facilitated by their witnessing the resuscitation and that their being present was beneficial to the
dying family member.
If family members are not present during the resuscitation effort, they should be told that resuscitation
efforts have begun and they should be periodically updated. The result of the resuscitation effort, whether
successful or unsuccessful, should be relayed to the family promptly with honesty and compassion.
When speaking with the family, speak slowly and in a quiet, calm voice. Use simple terms rather than
medical terms. Pause every few seconds to ask if they understand what is being said. You may need to
repeat information several times. Generally, you should make eye contact with the family members,
except where cultural differences may exist. Enlist the assistance of a social worker, a clergy member,
or grief support personnel, as needed.
Conveying Bad News

[Objective 11]
Health care professionals may not receive sufficient training regarding how the death of a loved one
should be conveyed to survivors. Family members often do not remember what was said to them when
the news of a death was relayed as much as they remember the attitude and empathy of the person who
spoke to them (Schmid, et al., 2005).
SPIKES is an acronym for a six-step protocol that is used for conveying distressing information to
patients and families (Box 4.3) (Baile, et al., 2000). Using the SPIKES protocol can help ease the distress
felt by the patient or family who is receiving the news and the health care professional who is breaking the
news (Kaplan, 2010).
1. Setting. Organize your thoughts about the information that you will need to convey and anticipate
questions that family members will ask. Select a location that provides for privacy with all appropriate
people present. Sit down, face the family, and minimize interruptions by putting your pager on silent
and putting your cell phone on vibrate. If language is a barrier, arrange for a translator to be present
and part of the discussion.
2. Perception. Before conveying information, use open-ended questions to find out what the family
already knows. Asking, “What have you been told so far?” or “What is your understanding of what
has happened?” allows an opportunity to gauge how the family perceives the current situation—what
it is and its seriousness (Baile, et al., 2000). It also provides an opportunity to correct misinformation.
3. Invitation. Ask the family how they prefer to receive the information that you have to share and how
much they want to know. For example, “Would you like me to tell you more about what happened?”
Keep in mind that ethnic and cultural values play a significant role in the need for information.
Although families are often clear about how much information they are ready to hear, it is possible
that they may be too emotionally upset or overwhelmed to hear and comprehend the information that
you are about to convey.
BOX 4.3 SPIKES Protocol

S—Setting K—Knowledge (ie, relaying medical facts)
P—Perception of what the patient/family E—Emotions (ie, address with empathetic
understand about the situation responses)
I—Invitation from the patient/family to give S—Summary
information
4. Knowledge. Beginning with a warning statement that unfavorable news is coming may lessen the
shock that can follow the disclosure of bad news (Baile, et al., 2000). Say something like, “I am sorry
to tell you that …” or “I have some bad news to tell you” and then pause. This allows the family time to
grasp what has been said. While speaking slowly, proceed to convey the news in small chunks and in a
straightforward manner. To reduce the potential for misunderstanding, use words that the family will
easily comprehend. Avoid the use of medical jargon and avoid excessive bluntness. Assume nothing as
to how the news is going to be received. If the resuscitation effort was unsuccessful, allow time for the
shock to be absorbed and as much time as necessary for questions and discussion. Recognize that the
initial shock experienced by the family may prevent them from knowing what questions to ask. It may
be necessary to repeat answers or explanations to make sure they are understood.
5. Emotions. Give the family time to respond. Be sensitive and respectful of cultural differences.
The family’s reaction may be anger, shock, withdrawal, disbelief, extreme agitation, guilt, or sorrow.
An expected death may elicit a response of acceptance and relief. The resuscitation efforts may have
given the family time to accept the terminal outcome. In some cases, there may be no observable
response, or the response may seem inappropriate. A statement such as, “You have my (our) sincere
sympathy” may be used to express your feelings. However, there are times that silence is appropriate.
Silence respects the family’s feelings and allows them to regain composure at their own pace.
6. Summarize. Offer to contact the patient’s physician and to be available if there are further questions.
Arrange for follow-up and continued support during the grieving period. Allow the family the oppor-
tunity to see their relative. In cases involving severe traumatic cardiac arrest, this may not be advisable.
If equipment is still connected to the patient, prepare the family for what they will see. The patient
should be gowned before the family views the body. Accompany them if necessary. Some caregivers
may prefer not to view the body. If this is their preference, do not attempt to force them to do so.
Helping the Caregivers

An unsuccessful resuscitation effort is difficult for the family as well as the health care professionals
involved in the resuscitation. Although each health care professional may deal with stress differently,
reactions suggesting a need for assistance include persistent feelings of anger, self-doubt, sadness, depres-
sion, or a desire to withdraw from others. It is important to recognize the warning signs of stress in your-
self and others and know how to deal with them. Strategies for dealing with stress may include engaging
in exercise, practicing relaxation techniques, talking with family or friends, or meeting with a qualified
mental health professional.

The chapter quiz and case studies presented on the following pages are provided to help you integrate the
information presented in this chapter. As you work through the case studies, remember that there may be
alternative actions that are perfectly acceptable, yet not presented in the case study.
CHAPTER QUIZ
True/False
Indicate whether the statement is true or false.
____ 1. Transthoracic impedance is significantly increased when defibrillation is performed

without the use of conductive material.
____ 2. Vasopressin can be substituted for the first or second dose of epinephrine in cardiac
arrest.
____ 3. Current resuscitation guidelines recommend the routine use of lidocaine after cardiac
arrest.
____ 4. For intubated patients, failure to achieve an EtCO2 of greater than 10 mm Hg after
20 minutes of CPR is associated with extremely poor chances for ROSC and survival.
____ 5. When a monophasic defibrillator is used for shockable cardiac arrest rhythms, the
initial recommended energy dose is 120 to 150 J; 360 J is recommended for all
subsequent shocks.
____ 6. Patients in cardiac arrest associated with PEA or asystole should receive epinephrine
early during the resuscitative effort.
Multiple Choice
____ 7. What is meant by the term PEA?

A. PEA refers to a flat line on the cardiac monitor.
B. PEA refers to a slow rhythm with a wide-QRS complex.
C. PEA refers to a chaotic rhythm that is likely to degenerate into cardiac arrest.
D. PEA refers to an organized rhythm on the cardiac monitor (other than VT),
though a pulse is not present.
____ 8. Defibrillation is indicated in the management of:

A. VF and asystole.
B. PEA and asystole.
C. pVT and VF.
D. pVT and PEA.
____ 9. A patient is in cardiac arrest. CPR is in progress. Two attempts to establish peripheral
IV access have been unsuccessful. To administer medications to this patient, your best
course of action in this situation will be to:
A. Proceed with insertion of a central line.
B. Continue attempts to establish peripheral IV access.
C. Intubate the patient and administer drugs via the tracheal tube.
D. Establish vascular access by means of an IO infusion.
____ 10. In which of the following situations would an epinephrine IV bolus be indicated?
A. Junctional rhythm, pVT, and asystole
B. Sinus bradycardia, junctional rhythm, and a ventricular escape rhythm
C. PEA, pVT, and asystole
D. PEA, VF, and a ventricular escape rhythm
____ 11. Establishing vascular access is part of:

A. “A” in the primary survey.
B. “B” in the secondary survey.
C. “C” in the secondary survey.
D. “D” in the primary survey.
____ 12. The first medication used in the management of PEA is:
A. Lidocaine.
B. Epinephrine.
C. Amiodarone.
D. Atropine or epinephrine.
____ 13. Which of the following statements about lidocaine dosing during cardiac arrest is correct?
A. Lidocaine is given as a continuous IV infusion of 2 to 10 mcg/min.
B. Lidocaine is given as a continuous IV infusion of 10 to 20 mcg/kg/min.
C. The initial dose is 1 mg IV push, which may be repeated twice to a maximum dose
of 3 mg.
D. The initial dose is 1 to 1.5 mg/kg IV push; repeat doses of 0.5 to 0.75 mg/kg IV
push may be given at 5- to 10-minute intervals, to a maximum dose of 3 mg/kg.
____ 14. A 49-year-old man is found unresponsive, not breathing, and pulseless. The cardiac
monitor reveals monomorphic VT. The most important actions in the management of
this patient are:
A. CPR and defibrillation.
B. Defibrillation and resuscitation medications.
C. CPR and prompt insertion of an advanced airway.
D. Synchronized cardioversion and resuscitation medications.
____ 15. A 75-year-old man is on the telemetry floor recovering from an inferior wall
myocardial infarction. The nursing staff arrives in the patient’s room in response to an
alarm from his cardiac monitor, which reveals a sinus bradycardia at 40 beats/min. The
patient is unresponsive, pulseless, and apneic. An IV is in place. You should now:
A. Defibrillate immediately.
B. Begin transcutaneous pacing.
C. Begin CPR, ventilate with a bag-mask, and give epinephrine IV.
D. Begin CPR, insert an advanced airway, and give atropine IV.
Completion
Complete each statement.
16. Identify the following rhythm (lead II):
(From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)
Identification _____________________________________
Identification: _____________________________________
Identification _____________________________________
Identification: _____________________________________
Matching
Match the cardiac rhythms with their descriptions by placing the letter of each correct answer in the space
provided.
A. VF
B. Monomorphic VT
C. PMVT
D. Asystole
____ 20. A total absence of ventricular electrical activity
____ 21. Chaotic rhythm with no discernible waveforms, complexes, pattern, or regularity
____ 22. Rapid rhythm in which the QRS complex is wide and usually regular; QRS
complexes are of same shape and amplitude
____ 23. Rapid rhythm in which the QRS complexes are wide and appear to twist from
upright to negative or negative to upright and back
Short Answer
24. What is the purpose of defibrillation?

_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
CASE STUDY 4-1

Your patient is a 52-year-old woman who was found unresponsive on her kitchen floor by a neighbor.
You have a sufficient number of advanced life support personnel available to assist you and carry out your
instructions. Emergency equipment, including a biphasic AED, is available.
1. As you approach the patient, you observe that she is supine on a stretcher. Her eyes are closed, her
lips are blue, and her skin is pale. You see no signs of breathing. What should be done next?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
2. The patient is unresponsive. How would you like to proceed?

_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
3. The patient is not breathing and a pulse cannot be felt. Her skin is cool, pale, and dry. How should
you proceed?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
4. How will you ensure the performance of high-quality chest compressions throughout this
resuscitation effort?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
5. What is the difference between manual defibrillation and automated external defibrillation?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
6. The AED pads are in place on the patient’s chest and rhythm analysis is complete. The AED advises
a shock. What should be done next?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
7. The patient has been defibrillated and high-quality CPR is ongoing. How will you open the patient’s
airway?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
8. The patient’s airway is clear. What should be done now?

_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
9. Chest compressions are ongoing. An oral airway has been inserted. The patient is being ventilated
with a BMD. You see gentle chest rise with bagging. Vascular access has been established. What
should be done next?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
10. After 2 minutes of CPR, the defibrillation team member reanalyzed the patient’s rhythm with the
AED, which indicated, “No shock advised.” How would you like to proceed?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
11. A carotid pulse is present. The patient is breathing about 8 times/min but remains unresponsive.
What should be done now?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
12. The Five Hs and Five Ts are memory aids used to recall possible reversible causes of cardiac
emergencies. Explain the meaning of each of the Five Hs and Five Ts.
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
13. The patient’s heart rate is strong and regular. Her blood pressure is 98/60 mm Hg and she has been
placed on the cardiac monitor, which shows a sinus tachycardia at 118 beats/min. Ventilations are
being assisted with a BMD. The following information has been obtained:
Signs/Symptoms: Found unresponsive by neighbor
Allergies: Unknown
Medications: Azithromycin (Zithromax), alendronate (Fosamax), aspirin
Past history: Osteoporosis, heart attack 3 months ago
Last oral intake: Unknown
Events prior: Found unresponsive on the kitchen floor by a neighbor who had last
spoken to the patient about 25 minutes prior
What would you like to do next?

_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
CASE STUDY 4-2

Your patient is a 40-year-old man who was found unresponsive in the street. Paramedics have placed the
patient on a backboard with cervical spine stabilization. An IV of normal saline is infusing when the
patient arrives in the emergency department. You have a sufficient number of advanced life support
personnel available to assist you and carry out your instructions. Emergency equipment, including a
biphasic manual defibrillator, is available.
1. As you approach the patient, you see that he is supine on a backboard. His eyes are closed and his skin
is pale. You observe blood dripping from the patient’s right ear. What should be done next?
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
2. The patient has occasional gasping breaths occurring at a rate of 4 breaths/min. There is no pulse. His
skin is warm, pale, and moist. What should be done now?
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
3. As the patient’s chest is exposed to apply the combination pads, you observe multiple abrasions, a
partial thickness laceration in the area of the right nipple, and what looks like footprints on the
patient’s chest and abdomen. What should be done next?
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
4. The monitor reveals the following rhythm:
Identification _____________________________________
5. Information from the paramedics has been obtained and your physical examination findings are
noted.
Signs/Symptoms: Possible assault by unknown persons with unknown
weapons
Allergies: Unknown
Medications: Unknown
Past history: Unknown
Last oral intake: Unknown
Events prior: Found unresponsive in the street
Focused Physical Examination

Head/face: Blood dripping from right ear, bruising of left orbit, frontal bone contusion, left
temporal area contusion; both pupils deviated to left side
Neck: Unremarkable
Thorax: Partial thickness laceration near right nipple; abrasions and footprints noted
Abdomen: Markedly distended and firm; abrasions and footprints noted
Pelvis: Unremarkable
Back: Unremarkable
Extremities: Multiple abrasions on upper extremities
You estimate the patient’s weight to be 70 kg. What would you like to do next?
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
6. Chest compressions are ongoing. An oral airway has been inserted and the patient is being ventilated
with a BMD. What should be done next?
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
7. Although the monitor remains unchanged, a team member informs you that a weak pulse is present.
How would you like to proceed?
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
8. The patient is unresponsive and there are no signs of spontaneous breathing. His heart rate is 125
beats/min and his blood pressure is 53/30 mm Hg. What should be done next?
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________

True/False
1. T. When using handheld paddles, the use of gels, pastes, or pre-gelled defibrillation pads aids the
passage of current at the interface between the defibrillator paddles/electrodes and the body surface.
Failure to use conductive material results in increased transthoracic impedance, a lack of penetration
of current, and burns to the skin surface. Combination pads are pre-gelled and do not require the
application of additional gel to the patient’s chest.
OBJ: Explain defibrillation, its indications, proper pad or paddle placement, relevant precautions,
and the steps required to perform this procedure with a manual defibrillator and an AED.
2. F. Epinephrine and vasopressin, which are vasopressors, have been shown to improve ROSC after
administration during cardiac arrest. Because current evidence has revealed that the efficacy of these
medications are similar and that there is no demonstrable benefit from administering both epineph-
rine and vasopressin compared with epinephrine alone, vasopressin has been removed from the adult
cardiac arrest algorithm (Link, et al., 2015).
OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for
cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications,
doses, and route of administration of applicable medications), and electrical therapy, where
applicable.
3. F. Although there is inadequate evidence to support the routine use of lidocaine after cardiac arrest,
the initiation or continuation of lidocaine may be considered immediately after a ROSC from car-
diac arrest associated with pVT or VF (Link, et al., 2015).
OBJ: Discuss immediate post–cardiac arrest care upon ROSC.
4. T. For intubated patients, continuous EtCO2 monitoring should be used to monitor the quality of
compressions during resuscitation efforts. Failure to achieve an EtCO2 of greater than 10 mm Hg
immediately after intubation and after 20 minutes of CPR is associated with extremely poor chances
for ROSC and survival (Link, et al., 2015). This finding, in combination with other factors, may be
considered when deciding when to terminate resuscitation (Link, et al., 2015).
OBJ: Discuss the use of continuous EtCO2 monitoring during resuscitation efforts.
5. F. When a monophasic defibrillator is used for shockable cardiac arrest rhythms, the recommended
energy dose is 360 J for all shocks (Link, et al., 2015).
OBJ: Identify the energy levels that are currently recommended, and indicate if the shock deliv-
ered should be a synchronized or unsynchronized countershock, for pulseless monomorphic VT,
PMVT, and VF.
6. T. Current guidelines state that it may be reasonable to administer epinephrine as soon as feasible
after the onset of cardiac arrest associated with an initial nonshockable rhythm (Link, et al., 2015).
However, because optimal timing may vary based on patient factors and resuscitation conditions,
there is insufficient evidence to make a recommendation as to the optimal timing of epinephrine,
particularly in relation to defibrillation, when cardiac arrest is associated with a shockable rhythm
(Link, et al., 2015).
doses, and route of administration of applicable medications), and electrical therapy, where applicable.
Multiple Choice
7. D. PEA is a clinical situation, not a specific dysrhythmia. PEA exists when organized electrical
activity (other than VT) is observed on the cardiac monitor, but the patient is unresponsive, not
breathing, and a pulse cannot be felt.
OBJ: Identify four cardiac rhythms that are associated with cardiac arrest.
8. C. Defibrillation is indicated in the management of pVT and VF. It is not indicated in the man-
agement of PEA. Remember: defibrillation is performed to depolarize the myocardial cells at one
time and provide an opportunity for one of the heart’s natural pacemakers to take over. In PEA, an
organized rhythm is present on the monitor. Thus pacemaker activity is already present but there is
inadequate cardiac output and no pulse. PEA is not shocked because a shock could disrupt the orga-
nized rhythm and cause chaos (ie, VF). Defibrillation is not indicated in asystole.
9. D. When peripheral IV cannulation is unsuccessful or is taking too long, an IO infusion is an

alternative method of gaining access to the vascular system and should be considered before
considering placement of a central line. To improve flow rates during an IO infusion, the use
of a pressure bag or infusion pump may be necessary. If IV or IO access cannot be achieved to
give drugs during a cardiac arrest, the tracheal route can be used to give selected medications; how-
ever, intravascular drug administration provides more predictable drug delivery and pharmacologic
effect (Link, et al., 2015).
cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses,
and route of administration of applicable medications), and electrical therapy, where applicable.
10. C. An IV bolus of epinephrine is indicated in cardiac arrest. Cardiac arrest rhythms include PEA,
asystole, pVT, and VF. Epinephrine is not given as an IV bolus to patients who have a pulse.
Although epinephrine may be given to patients for symptomatic bradycardia, it is given as an IV
infusion, not an IV bolus.
11. C. The primary survey focuses on BLS assessment and intervention. The secondary survey focuses
on advanced life support assessment and interventions. Thus establishing vascular access is part of
“C” (ie, Circulation) in the secondary survey.
OBJ: List the purpose and components of the primary and secondary surveys.
12. B. The first medication used in the management of PEA is epinephrine. Amiodarone, atropine, and
lidocaine are not indicated in the management of PEA.
applicable.
13. D. The initial dose of lidocaine is 1 to 1.5 mg/kg IV push. Repeat doses of 0.5 to 0.75 mg/kg IV
push may be given at 5- to 10-minute intervals, to a maximum dose of 3 mg/kg.
14. A. CPR and defibrillation are the most important treatments for the patient in cardiac arrest asso-
ciated with pVT or VF. Insertion of advanced airways and administration of resuscitation medica-
tions are of secondary importance. Although synchronized cardioversion may be used in the
treatment of an unstable patient in monomorphic VT with a pulse, it is not indicated for pVT.
15. C. Although an organized rhythm is present on the monitor, the patient has no pulse. This clinical situation
is PEA. You should begin CPR immediately, ventilate the patient with a BMD, and give epinephrine
1 mg IV. Transcutaneous pacing, defibrillation, and atropine administration are not indicated for PEA.
Completion
16. Sinus rhythm to monomorphic VT

17. PMVT
applicable.
18. Sinus rhythm with a run of monomorphic VT

19. Coarse VF
Matching
20. D
21. A
22. B
23. C
Short Answer
24. The purpose of defibrillation (ie, unsynchronized countershock) is to deliver a uniform electrical
current of sufficient intensity to depolarize myocardial cells (including fibrillating cells) at the same
time, briefly “stunning” the heart. This provides an opportunity for the heart’s natural pacemakers to
resume normal activity. When the cells repolarize, the pacemaker with the highest degree of auto-
maticity should assume responsibility for pacing the heart.

1. Your general impression should focus on three main areas that can be remembered by the mnemonic
ABC: Appearance, (work of) Breathing, and Circulation. As you finish forming your general
impression, you will have a good idea if the patient is sick (ie, unstable) or not sick (ie, stable). Begin
the primary survey by assessing responsiveness. Start by asking, “Are you all right?” or “Can you hear
me?” If there is no response, then gently tap or squeeze the patient’s shoulder while repeating
verbal cues.
2. Call for help and ask someone to get an AED or defibrillator. Look at the chest for movement while
simultaneously feeling for a pulse for 5 to 10 seconds. While your fingers are in contact with the
patient’s skin, note the patient’s skin temperature, color, and moisture.
3. Direct a team member to start chest compressions. Ask another team member to turn on the AED
and apply the AED pads to the patient.
4. High-quality chest compressions require compressing the chest at an adequate rate and depth, allow-
ing full chest recoil after each compression (enabling the heart to refill with blood), minimizing
interruptions in chest compressions, and avoiding excessive ventilation. To avoid tiring, the chest
compressor and airway team member should rotate positions (ideally in less than 5 seconds) when
chest compressions are interrupted (eg, while the AED is analyzing the patient’s cardiac rhythm,
when the AED is delivering a shock).
OBJ: Discuss the requirements for performing high-quality chest compressions.
5. Manual defibrillation refers to the placement of paddles or pads on a patient’s chest, interpretation of
the patient’s cardiac rhythm by a trained health care professional, and the health care professional’s
decision to deliver a shock, if indicated. Automated external defibrillation refers to the placement of
pads on a patient’s chest and interpretation of the patient’s cardiac rhythm by the defibrillator’s com-
puterized analysis system.
OBJ: Explain defibrillation, its indications, proper pad or paddle placement, relevant pre-
cautions, and the steps required to perform this procedure with a manual defibrillator and
an AED.
6. When the defibrillation team member indicates that he is ready to shock, ensure that all
team members clear the patient. After the shock is delivered, instruct the team to resume
CPR without pausing for a pulse or rhythm check. Ask a team member to establish vascular
access.
7. Although there are no visible signs of trauma, open the patient’s airway with the use of a jaw thrust
without neck extension maneuver because the patient was found on the floor and you cannot rule out
trauma because of a possible fall injury. Look in the mouth for blood, broken teeth or loose dentures,
gastric contents, and foreign objects.
OBJ: Describe and demonstrate the steps needed to perform the head tilt–chin lift and jaw
thrust without neck extension maneuvers and relate the mechanism of injury to the opening of
the airway.
8. While continuing chest compressions, ask the airway team member to size and insert an oral
airway. With the help of an assistant, ask the airway team member to begin positive pressure
ventilation with a BMD connected to 100% oxygen. Ventilate the patient with just enough force
to produce gentle chest rise. Assess the patient’s baseline breath sounds while the patient is being
ventilated.
applicable.
9. While CPR continues, instruct a team member to administer epinephrine 1 mg or

vasopressin 40 units IV/IO. Consider the need for placement of an advanced airway and waveform
capnography.
applicable.
10. Check for a pulse and repeat the primary survey. If a pulse is present, obtain the patient’s vital signs.
applicable.
11. Ask a team member to attach a pulse oximeter, ECG monitor, and blood pressure monitor.
Ask the airway team member to continue to assist the patient’s breathing with a BMD connected
to O2. Obtain a 12-lead ECG and order laboratory tests. Find out if there is someone available
who can provide additional information about the patient so that factors that may have
caused the arrest can be identified and treated. Because the patient remains unresponsive,
consider TTM.
12. Hypovolemia Tamponade, cardiac

Hypoxia Tension pneumothorax
Hypothermia Thrombosis: lungs (ie, massive pulmonary embolism)
Hypokalemia/Hyperkalemia Thrombosis: heart (ie, acute coronary syndromes)
Hydrogen ion (acidosis) Tablets/toxins: drug overdose
applicable.
13. Arrange for a cardiology consult and continue to monitor the patient’s vital signs and ECG every
5 minutes as you prepare to transfer the patient for continued care. Request a team debriefing after
the patient’s transfer is complete.

1. Look at the chest for movement while assessing for a carotid pulse for up to 10 seconds, and assess
the patient’s skin, noting the patient’s skin temperature, color, and moisture.
2. Direct a team member to start chest compressions. While CPR continues, instruct a team member
to attach combination pads to the patient’s bare chest in the position recommended by the
manufacturer. Turn the power to the monitor/defibrillator on and identify the patient’s cardiac
rhythm.
3. While CPR continues, perform a focused physical examination, looking for possible clues as to the
cause of the arrest. Obtain, or direct a team member to obtain, additional information from the para-
medics with regard to the circumstances in which the patient was found.
applicable.
4. The monitor shows a sinus tachycardia; however, because the patient has no pulse with this rhythm
the clinical situation is PEA.
5. Activate the trauma team, if not already done, and consider the possible causes of the patient’s car-
diac arrest. On the basis of the information provided, hypovolemia (ie, firm distended abdomen) is
one possible cause. Ask the IV team member to establish a second IV line and give a fluid challenge
of normal saline. The amount given often varies depending on agency policy/local protocol. For the
purposes of this scenario, we will give a 20 mL/kg fluid challenge of normal saline to start with.
Because this patient weighs about 70 kg, our initial fluid challenge will be 1400 mL.
applicable.
6. While CPR continues, ask the IV team member to give 1 mg of 1:10,000 epinephrine IV push now
and repeat the same dose every 3 to 5 minutes as long as the patient has no pulse.
applicable.
7. Check the patient’s other vital signs and repeat the primary survey.
applicable.
8. Ask the airway team member to continue to assist the patient’s breathing with a BMD connected to
100% oxygen. Continue to monitor the patient’s vital signs and ECG every 5 minutes as you prepare
to transport the patient to the operating room (OR). Weigh the decision to place an advanced airway
and giving additional IV fluids now (delaying definitive care) versus transporting the patient to the
OR and having these interventions performed by the anesthesiologist. Request a team debriefing
after the patient’s transfer is complete.
applicable.
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CHAPTER 5
Tachycardias
INTRODUCTION
The tachycardia algorithm is a treatment guideline that is used when providing care to patients who have
a tachycardia with a pulse. You must be able to recognize if a patient is asymptomatic, symptomatic but
stable, symptomatic but unstable, or pulseless. Care of the pulseless patient with a tachycardia is provided
using the cardiac arrest algorithm, which was discussed in Chapter 4. Familiarity with the tachycardia
algorithm requires patient assessment, rhythm recognition, and knowledge of medications, vagal maneu-
vers, and electrical therapy.
The signs and symptoms that are experienced by a patient with a tachycardia depend on the ventric-
ular rate, how long the tachycardia lasts, the patient’s general health, and the presence of underlying heart
disease. The faster the heart rate, the more likely the patient is to have signs and symptoms resulting from
the rapid rate.
When a patient presents with signs and symptoms related to a tachycardia, ask yourself these
questions:
1. Is the patient asymptomatic, symptomatic but stable, symptomatic and unstable, or pulseless?
2. Is the QRS wide or narrow? If it is wide, is it monomorphic or polymorphic?
3. Is the ventricular rhythm regular or irregular?
The answers to these questions will help to guide your treatment decisions. Most tachycardias do not
cause serious signs and symptoms until the ventricular rate exceeds 150 beats per minute (beats/min)
unless the patient has impaired ventricular function (Link, et al., 2015).
Serious signs and symptoms are those that affect vital organ function. Examples of serious signs and
symptoms are shown in Box 5.1. If the patient is symptomatic but does not have serious signs and symp-
toms because of the rapid rate, the patient is considered to be stable. For example, a patient who has
symptoms such as lightheadedness or palpitations with stable vital signs is symptomatic, but he or
she is not in imminent danger of cardiac arrest. After their airway, breathing, and circulation (ie, ABCs)
have been assessed, stable but symptomatic patients are given oxygen (if indicated), intravenous (IV)
access is established, and medication therapy is begun. Frequent patient reassessment is essential. If
the tachycardia produces serious signs and symptoms, typically with heart rates of 150 beats/min or more,
the patient is considered unstable. Unstable patients who have a pulse and serious signs and symptoms
caused by the tachycardia should receive immediate synchronized cardioversion.
The management of patients who present with a tachycardia is often complex. As an advanced cardiac
life support provider, it is important for you to recognize when to consult expert advice with regard to
rhythm interpretation, medications, or patient-management decisions.
129
130 CHAPTER 5 Tachycardias
BOX 5.1 Signs and Symptoms of Hemodynamic Compromise

Acute changes in mental status Hypotension
Chest pain Pulmonary congestion
Cold, clammy skin Shortness of breath
Fall in urine output Signs of shock
Heart failure
DESIRED RESULTS
patient experiencing a tachycardia.
LEARNING OBJECTIVES
1. Differentiate among narrow-QRS tachycardias, wide-QRS tachycardias, and irregular
tachycardias.
2. Given a patient situation, describe the electrocardiogram (ECG) characteristics and initial
emergency care for narrow-QRS tachycardias, wide-QRS tachycardias, and irregular
tachycardias, including mechanical, pharmacologic, and electrical therapy, where
applicable.
3. Identify a patient who is experiencing a tachycardia as asymptomatic, symptomatic but
stable, symptomatic but unstable, or pulseless.
4. Explain synchronized cardioversion, describe its indications, and list the steps required to
perform this procedure safely.
5. For each of the following rhythms, identify the energy levels that are currently
recommended: monomorphic ventricular tachycardia (VT), narrow-QRS tachycardia, atrial
fibrillation (AFib), and atrial flutter.
LEARNING PLAN
• Read this chapter before class. Remember to highlight important concepts as you read.
the information presented. Flashcards can be particularly helpful with the recall of
medication dosages and rhythm recognition.
• Master identification of the following rhythms: sinus tachycardia, atrial tachycardia (AT),
atrioventricular (AV) nodal reentrant tachycardia (AVNRT), AV reentrant tachycardia (AVRT),
monomorphic VT, and polymorphic VT (PMVT).
• Master the following medications: O2, adenosine, amiodarone, beta-blockers, diltiazem,
magnesium sulfate, procainamide, sotalol, and verapamil.
• Assign team member roles or performing as a team member in a simulated patient
situation.
pressure and cardiac monitor, give supplemental O2 if indicated, and order a
12-lead ECG.
• Quickly identify an ECG rhythm, determining whether the QRS is narrow or wide (and if
it is wide, if the QRS is monomorphic or polymorphic), regular or irregular.
• Quickly recognize if a patient is asymptomatic, symptomatic but stable, symptomatic
but unstable, or pulseless.
CHAPTER 5 Tachycardias 131
• Demonstrate familiarity with the tachycardia algorithm.

• Demonstrate an understanding of what vagal maneuvers are and when they are
indicated.
and contraindications for the medications used in the treatment of a narrow-QRS or
wide-QRS tachycardia.
• Deliver the correct type of energy (synchronized cardioversion versus defibrillation) and
the correct energy level for the tachycardia if electrical therapy is indicated.
• Demonstrate safe operation of the defibrillator if electrical therapy is indicated.
• Recognize the need to change from synchronized cardioversion to defibrillation if the
rhythm changes to pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VF).
• Verbalize when it is best to seek expert consultation.
debriefing.
answers provided.
KE Y T ERMS
Delta wave Slurring of the beginning portion of the QRS complex, caused by preexcitation.
Supraventricular arrhythmias Rhythms that begin in the sinoatrial (SA) node, atrial tissue, or
the AV junction.
Synchronized cardioversion The timed delivery of a shock during the QRS complex.
NARROW-QRS TACHYCARDIAS
Supraventricular arrhythmias begin above the bifurcation of the bundle of His. This means that su-
praventricular arrhythmias include rhythms that begin in the SA node, the atrial tissue, or the AV
junction.
Sinus Tachycardia
If the SA node fires at a rate faster than normal for the patient’s age, the rhythm is called sinus tachycardia.
In adults, the rate associated with sinus tachycardia is usually between 101 and 180 beats/min; however,
some experts calculate the upper rate as about 220 beats/min, minus the patient’s age in years (Link, et al.,
2015) (Table 5.1, Fig. 5.1).
Sinus tachycardia is a normal response to the body’s demand for increased cardiac output, which
results from many conditions (Box 5.2). The patient is often aware of an increase in heart rate. Some
patients complain of palpitations, a racing heart, or a feeling of pounding in their chests.
In a patient with coronary artery disease, any tachycardia can cause problems. The heart’s demand for
oxygen increases as the heart rate increases. As the heart rate increases, there is less time for the ventricles
to fill and less blood for the ventricles to pump out with each contraction, which can lead to decreased
TABLE 5.1 Characteristics of Sinus Tachycardia

Regularity R to R and P to P intervals are regular
Rate Usually between 101 and 180 beats/min; some experts calculate the upper rate as about
220 beats/min, minus the patient’s age in years
P waves Positive (ie, upright) in lead II; one precedes each QRS complex; P waves look alike
PR interval 0.12 to 0.20 sec and constant from beat to beat
QRS duration 0.11 sec or less unless abnormally conducted
Fig. 5.1 Sinus tachycardia. (From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)
BOX 5.2 Causes of Sinus Tachycardia

• Acute MI • Hypoxia
• Caffeine-containing beverages • Infection
• Dehydration, hypovolemia • Medications (eg, epinephrine, atropine,
• Drugs (eg, cocaine, amphetamines, dopamine)
“ecstasy,” cannabis) • Nicotine
• Exercise • Pain
• Fear and anxiety • Pulmonary embolism
• Fever • Shock
• Heart failure • Sympathetic stimulation
• Hyperthyroidism
cardiac output. Because the coronary arteries fill when the ventricles are at rest, rapid heart rates decrease
the time available for coronary artery filling. This decreases the heart’s blood supply. Chest discomfort
can result if the supplies of blood and oxygen to the heart are inadequate. Sinus tachycardia in a patient
who is having an acute myocardial infarction (MI) may be an early warning signal for heart failure, car-
diogenic shock, and more serious dysrhythmias.
Treatment for sinus tachycardia is directed at correcting the underlying cause. Sinus tachycardia in a
patient experiencing an acute MI may be treated with medications to slow the heart rate and decrease
myocardial oxygen demand (eg, beta-blockers), provided there are no signs of heart failure or other
contraindications.
ACLS Pearl
Some dysrhythmias with very rapid ventricular rates (ie, above 150 beats/min) require the delivery of
medications or a shock to stop the rhythm. However, it is important to remember that shocking a
sinus tachycardia is inappropriate; rather, treat the cause of the tachycardia.
Supraventricular Tachycardia
[Objectives 1, 2]
Supraventricular tachycardias (SVTs) involve tissue within the bundle of His or above and are associated
with ventricular rates faster than 100 beats/min at rest (Page, et al., 2015). Three examples of SVTs are
shown in Fig. 5.2.
ACLS Pearl
Some SVTs need the AV node to sustain the rhythm and some do not. For example, AVNRT
and AVRT require the AV node as part of the reentry circuit to continue the tachycardia. Other
SVTs use the AV node only to conduct the rhythm to the ventricles. For example, AT, atrial flutter,
and AFib arise from a site (or sites) within the atria; they do not need the AV node to sustain the
rhythm.
Atrial Tachycardia
AT consists of a series of regular rapid beats from an irritable site in the atria at a rate faster than 100
beats/min (Ellenbogen & Stambler, 2014). Although the P waves preceding each QRS complex appear
upright, they tend to look different from those seen when the impulse is initiated from the SA node
(Table 5.2, Fig. 5.3).
The term paroxysmal is used to describe a rhythm that starts or ends suddenly. AT that starts or ends
suddenly is called paroxysmal supraventricular tachycardia (PSVT), once called paroxysmal AT (PAT)
(Fig. 5.4). PSVT may last for minutes, hours, or days. If the onset or end of PSVT is not observed
on the ECG, the dysrhythmia is simply called SVT.
Atrioventricular nodal reentrant Atrioventricular reentrant

Normal sinus rhythm Atrial tachycardia (AT) tachycardia (AVNRT) tachycardia (AVRT)
X BT
SA SA SA SA
AV AV AV AV
A B C D
II II II II
Fig. 5.2 Types of SVTs. A, Normal sinus rhythm is shown here as a reference. B, With AT, a focus (X) outside the SA node fires off
automatically at a rapid rate. C, With AVNRT, the cardiac stimulus originates as a wave of excitation that spins around the AV
junctional area. As a result, P waves may be buried in the QRS or appear immediately before or just after the QRS complex (arrows)
because of nearly simultaneous activation of the atria and ventricles. D, A similar type of reentrant (circus movement) mechanism in
Wolff-Parkinson-White (WPW) syndrome. This mechanism is referred to as AVRT. Note the P wave in lead II somewhat after the QRS
complex. BT, bypass tract. (From Goldberger AL: Clinical electrocardiography: a simplified approach, ed 7, St. Louis, 2006, Mosby.)
TABLE 5.2 Characteristics of Atrial Tachycardia

Regularity Regular
Rate 101 to 250 beats/min
P waves One P wave precedes each QRS complex in lead II; these P waves differ in shape from sinus
P waves; an isoelectric baseline is usually present between P waves; if the atrial rhythm
originates in the low portion of the atrium, P waves will be negative in lead II; with rapid rates,
it may be difficult to distinguish P waves from T waves.
PR interval May be shorter or longer than normal; may be difficult to measure because P waves may
be hidden in the T waves of preceding beats
Atrial tachycardia Sinus rhythm
P' P
Fig. 5.3 An AT (a type of SVT) that ends spontaneously with the abrupt resumption of sinus rhythm. The P waves of the
tachycardia (rate: about 150 beats/min) are superimposed on the preceding T waves. (From Goldberger AL: Clinical electro-
cardiography: a simplified approach, ed 7, St. Louis, 2006, Mosby.)
Fig. 5.4 PSVT. (From Clochesy J: Critical care nursing, ed 2, Philadelphia, 1996, Saunders.)
Focal AT is a type of AT that begins in a small area (ie, focus) within the atria. Its atrial rate is often
between 100 and 250 beats/min (Page, et al., 2015). A patient with focal AT often presents with PSVT.
Automatic AT, which is also called ectopic AT, is another type of focal AT in which a small cluster of cells
with altered automaticity fire. Vagal maneuvers do not usually stop the tachycardia, but they may slow the
ventricular rate. Multifocal AT is discussed later in this chapter with irregular tachycardias.
A rhythm that lasts from three beats up to 30 seconds is a nonsustained rhythm. A sustained rhythm is
one that lasts more than 30 seconds. Focal AT can be sustained or nonsustained. If episodes of AT are
short, the patient may be asymptomatic. Nonsustained focal AT typically does not require treatment
(Page, et al., 2015). If AT is sustained and the patient is symptomatic because of the rapid rate, treatment
should include applying a pulse oximeter and administering oxygen (if indicated), obtaining the patient’s
vital signs, and establishing IV access. A 12-lead ECG should be obtained. If the patient is not hypo-
tensive, vagal maneuvers may be tried. Although AT will rarely stop with vagal maneuvers, they are used
to try to better identify the mechanism of the SVT (ie, automatic, triggered activity, reentry) (Page, et al.,
2015). Vagal maneuvers are discussed in the next section of this chapter.
If vagal maneuvers fail, antiarrhythmic medications should be tried. Adenosine is the drug of choice
for regular narrow-QRS complex tachycardias (Link, et al., 2015) (Table 5.3, Fig. 5.5). If needed, cal-
cium channel blockers (Table 5.4) or beta-blockers (Table 5.5) may be used to slow the ventricular rate.
TABLE 5.3 Adenosine (Adenocard)

Class Endogenous chemical, antiarrhythmic
Mechanism of Action • Naturally present throughout the body
• Rapidly metabolized in the blood vessels
• Slows sinus rate
• Slows conduction time through AV node
• Can interrupt reentry pathways through AV node
• Half-life is less than 10 sec; doses of 12 mg or less terminate 92% of SVTs,
usually within 30 sec (Miller & Zipes, 2012)
Indications (Link, • Stable narrow-QRS regular tachycardias
et al., 2015) • Unstable narrow-QRS regular tachycardia while preparations are made for
synchronized cardioversion
• Stable, regular, monomorphic wide-QRS tachycardia
Dosage (Link, Initial dose is 6 mg rapid IV push over 1 to 3 sec. If no response within 1 to 2 min, give
et al., 2015) 12 mg rapid IV push. May repeat 12 mg dose once in 1 to 2 min. Follow each
adenosine dose immediately with a 20 mL normal saline flush.
Considerations • Constant ECG monitoring is essential.
• Use with caution in patients with reactive airway disease.
• Contraindicated in WPW pattern (Page, et al., 2015).
• Adverse effects (eg, flushing, dyspnea, chest pressure) common but transient
and usually resolve within 1 to 2 min. Discontinue in any patient who develops
severe respiratory difficulty.
• If the dysrhythmia is not caused by reentry involving the AV node or sinus node
(ie, AFib, AT, or VT), adenosine will not terminate the dysrhythmia but may
produce transient AV block that may clarify the diagnosis.
• After administration, many patients report a feeling of impending doom or feel
that they are about to die (Appelboam, et al., 2015).
• Reduce the dose by one-half in patients on dipyridamole (Persantine),
carbamazepine (Tegretol), those with transplanted hearts, or if given via a
central IV line (Page, et al., 2015).
AT, atrial tachycardia; AV, atrioventricular; ECG, electrocardiogram; IV, intravenous; SVT, supraventricular tachycardia; VT,
ventricular tachycardia; WPW, Wolff-Parkinson-White
Flush Adenosine
Fig. 5.5 Because of adenosine’s extremely short half-life, start the IV line as proximal to the heart as possible, such as the
antecubital fossa. Follow each adenosine dose immediately with a 20 mL normal saline flush. (From Roberts and Hedges’
clinical procedures in emergency medicine, ed 6, Philadelphia, 2014, Saunders.)
TABLE 5.4 Calcium Channel Blockers

Mechanism of Action • Inhibit movement of calcium ions across cell membranes in the heart and vascular
smooth muscle
• Slow conduction through the AV node and prolong the refractory period of the
AV node
• Decrease myocardial contractility
Indications (Link, • Stable narrow-QRS tachycardia if the rhythm persists despite vagal maneuvers or
et al., 2015) adenosine or if the tachycardia is recurrent
• To control the ventricular rate in patients with AFib or atrial flutter
Dosage (Link, • Diltiazem: Initial dose is 15 to 20 mg (0.25 mg/kg) IV over 2 min. If needed, follow
et al., 2015) in 15 min with 20 to 25 mg (0.35 mg/kg) IV over 2 min. Subsequent IV bolus
doses should be individualized for each patient.
• Verapamil: 2.5 to 5 mg slow IV push over 2 min (give over 3 to 4 min in older
adults or when BP is within the lower range of normal). May repeat with 5 to
10 mg in 15 to 30 min (if no response and BP remains normal or elevated).
Maximum total dose 20 to 30 mg.
Considerations • Can worsen hypotension and should not be given to patients with a systolic BP of
less than 90 mm Hg. Use with caution in patients with mild to moderate
hypotension. Monitor BP, heart rate, and ECG closely.
• Avoid in patients with impaired ventricular function or heart failure (Link, et al.,
2015).
• Avoid in patients with wide-QRS tachycardia and preexcited AFib/atrial flutter
(Mottram & Svenson, 2011).
• IV calcium channel blockers and IV beta-blockers should not be given together
or in close proximity (within a few hours); may cause severe hypotension.
AFib, atrial fibrillation; AV, atrioventricular; BP, blood pressure; ECG, electrocardiogram; IV, intravenous
TABLE 5.5 Beta-Blockers

Mechanism of • Slow sinus rate
Action • Depress AV conduction
• Reduce blood pressure
• Decrease myocardial oxygen consumption
Indications • Stable narrow-QRS tachycardias if the rhythm persists despite vagal maneuvers or
(Link, adenosine or if the tachycardia is recurrent
et al., 2015) • For ventricular rate control in AFib and atrial flutter if no signs of heart failure
• Specific forms of PMVT (eg, ischemic PMVT, congenital long-QT syndrome PMVT,
catecholaminergic PMVT)
Considerations • In general, patients with reactive airway disease should not receive beta-blockers.
• Some beta-blockers should be used with caution in patients with impaired renal or
liver function.
• Adverse effects include hypotension, bradycardia, and the precipitation of heart failure.
• Avoid in patients with wide-QRS tachycardia, preexcited AFib, and atrial flutter
(Mottram & Svenson, 2011).
AFib, atrial fibrillation; AV, atrioventricular; PMVT, polymorphic ventricular tachycardia

If AT is sustained at a rate faster than 150 beats/min and it is causing persistent signs of hemodynamic
compromise, sedation should be administered and synchronized cardioversion should be performed.
Synchronized cardioversion is most likely to be successful for ATs caused by reentry; it may or may
not be successful for ATs that result from triggered activity, and it is unlikely to be effective for automatic
ATs (Page, et al., 2015). Synchronized cardioversion is discussed later in this chapter.
ACLS Pearl
Calcium channel blockers inhibit the entry of calcium into vascular smooth muscle cells and myo-
cardial cells, which inhibits both myocardial and vascular smooth muscle contraction. By inhibiting
the contractility of vascular smooth muscle and coronary vessels, vascular resistance is reduced,
thereby reducing blood pressure.
There are two major categories of calcium channel blockers: the dihydropyridines (including
amlodipine and nifedipine) and the nondihydropyridines (including diltiazem and verapamil). The
dihydropyridines primarily affect the peripheral vasculature, resulting in peripheral vasodilation, with
little or no effect on the SA or AV nodes. The nondihydropyridines decrease heart rate and myocar-
dial contractility, slow conduction through the AV node, and have some peripheral arterial dilatory
effects as well. The major adverse effects of calcium channel blockers include hypotension, wors-
ening heart failure, bradycardia, and AV block.
Vagal Maneuvers
Vagal maneuvers are methods that are used to stimulate baroreceptors located in the internal carotid
arteries and the aortic arch. The stimulation of these receptors results in reflex stimulation of the vagus
nerve and the release of acetylcholine. Acetylcholine slows conduction through the AV node, thereby
resulting in the slowing of the heart rate. Vagal maneuvers have been shown to be successful in converting
AVRT or AVNRT to sinus rhythm 17.9% to 54% of the time (Pandya & Lang, 2015).
Common vagal maneuvers include the following:
• Application of a cold stimulus to the face for up to 10 seconds (eg, a washcloth soaked in iced water, a
cold pack, or crushed ice mixed with water in a plastic bag or glove). This method is often effective in
children, but seldom effective in adults. When using this method, do not obstruct the patient’s mouth
or nose or apply pressure to the eyes.
• The Valsalva maneuver is the forced expiration of air against a closed glottis (ie, deep cough, bearing
down). A 2010 study showed improved success rates with the patient supine while forcefully exhaling
for at least 15 seconds (Walker & Cutting, 2010). A more recent study showed improved success with
a modified Valsalva maneuver during which the patient was placed in a semirecumbent position and
asked to blow into a 10 mL syringe until the plunger moved (Appelboam, et al., 2015). The patient
was then immediately moved to a supine position with passive leg elevation by a staff member at 45
degrees for 15 seconds, and then returned to a semirecumbent position for 45 seconds before reassess-
ment of the patient’s cardiac rhythm. Study results showed that conversion to sinus rhythm was sig-
nificantly more common in the modified-maneuver group (43%) versus the control group (17%)
(Appelboam, et al., 2015).
• Carotid sinus massage (CSM), which is also called carotid sinus pressure. This procedure is performed
with the patient’s neck extended. The carotid pulse is palpated and then steady pressure is applied to
the right or left carotid sinus for 5 to 10 seconds (Page, et al., 2015) (Fig. 5.6). Carotid sinus pressure
should be avoided in older adults and in patients who have a history of stroke, known carotid artery
stenosis, or a carotid artery bruit on auscultation (Olgin, 2008). Simultaneous, bilateral carotid pres-
sure is not recommended.
ACLS Pearl
Before performing a vagal maneuver, place the patient on a cardiac monitor, apply a pulse oximeter
and blood pressure monitor, and establish IV access. Ensure that a defibrillator with pacing capa-
bility and antiarrhythmic medications are at the bedside.
Reentrant Tachycardias
Reentry is the spread of an impulse through tissue already stimulated by that same impulse; an electrical
impulse is delayed, blocked, or both, in one or more areas of the conduction system while the impulse is
External
carotid artery
Angle of
Internal mandible
cartoid
artery
Carotid
sinus
Thyroid
cartilage
Sternocleidomastoid
muscle
Fig. 5.6 Location of the carotid sinus. (From Roberts and Hedges’ clinical procedures in emergency medicine, ed 6,
conducted normally through the rest of the conduction system. This results in the delayed electrical
impulse entering cardiac cells that have just been depolarized by the normally conducted impulse. Reen-
try is a common mechanism for AVNRT, which is also called AV nodal reciprocating tachycardia, and
AVRT, which is also called AV reciprocating tachycardia. With AVNRT, the electrical circuit or loop
(ie, the reentrant circuit) exists within the AV node. With AVRT, an accessory AV conduction pathway
and either the AV node or another accessory pathway form the two parts of the electrical circuit or loop
(Goel, et al., 2013).
Atrioventricular Nodal Reentrant Tachycardia

AVNRT is the most common SVT (Page, et al., 2015). Typical AVNRT is usually caused by a prema-
ture atrial complex (PAC) that is spread by the electrical circuit. This allows the impulse to spin around in
a circle indefinitely and to reenter the normal electrical pathway with each pass around the circuit. The
result is a very rapid and regular ventricular rhythm that ranges from 150 to 250 beats/min (Table 5.6,
Fig. 5.7).
Because AVNRT may be short-lived or sustained, treatment depends on the duration of the tachy-
cardia and severity of the patient’s signs and symptoms. Assessment findings and symptoms that may be
associated with rapid ventricular rates may include the following:
• Chest pain or pressure • Nervousness, anxiety
• Dizziness • Palpitations (common)
• Dyspnea • Signs of shock
• Heart failure • Syncope
• Lightheadedness • Weakness
• Nausea
TABLE 5.6 Characteristics of Atrioventricular Nodal Reentrant Tachycardia

Regularity Ventricular rhythm is usually very regular
Rate 150 to 250 beats/min; typically 180 to 200 beats/min in adults
P waves P waves are often hidden in the QRS complex; if the ventricles are stimulated first and then
the atria, a negative (ie, inverted) P wave will appear after the QRS in leads II, III, and aVF;
when the atria are depolarized after the ventricles, the P wave typically distorts the end of the
QRS complex
PR interval P waves are not seen before the QRS complex, therefore the PR interval is not measurable
Fig. 5.7 AVNRT.
If the patient is stable but symptomatic and the symptoms are the result of the rapid heart rate, apply a
pulse oximeter and administer supplemental oxygen, if indicated. Obtain the patient’s vital signs, estab-
lish IV access, and consider possible reversible causes of the tachycardia. A 12-lead ECG should be
obtained to assist with rhythm identification; if the patient is unstable, do not delay cardioversion to
obtain a 12-lead ECG (Link, et al., 2015). While continuously monitoring the patient’s ECG, attempt
a vagal maneuver if there are no contraindications. AVNRT is usually responsive to vagal maneuvers. If
vagal maneuvers do not slow the rate or cause conversion of the tachycardia to a sinus rhythm, the first
antiarrhythmic given is adenosine (Link, et al., 2015). Treatment with calcium channel blockers or beta-
blockers is indicated when AVNRT fails to convert to sinus rhythm, recurs, or when treatment with vagal
maneuvers or adenosine reveals AFib or atrial flutter (Mottram & Svenson, 2011).
An unstable patient is one who has signs and symptoms of hemodynamic compromise. Examples of
these signs and symptoms include acute changes in mental status, chest pain or discomfort, hypotension,
shortness of breath, pulmonary congestion, heart failure, acute MI, or signs of shock. If the patient is
unstable, treatment should include application of a pulse oximeter and administration of supplemental
oxygen (if indicated), IV access, and sedation (if the patient is awake and time permits), followed by
synchronized cardioversion. In clinical practice, health care practitioners sometimes consider a trial of
adenosine before cardioversion for patients who are mildly unstable with a narrow-QRS SVT that is
not a sinus tachycardia. This practice is based on retrospective evidence that has shown that adenosine
may promptly convert an unstable narrow-QRS SVT and resolve hemodynamic instability (Mottram &
Svenson, 2011).
Atrioventricular Reentrant Tachycardia

AVRT is caused by the presence of an abnormal accessory pathway that serves as a conduit for impulses
that originate from the SA node and allows rapid conduction, bypassing the AV node either on its way to
the ventricles or on its return to the atria, resulting in a reentrant circuit (Mottram & Svenson, 2011).
Ventricular preexcitation occurs when a supraventricular impulse travels by means of an accessory path-
way and excites the ventricles earlier than would be expected if the impulse traveled only by way of the
normal AV conduction system (Hamdan, 2010). The number of atrial impulses reaching the ventricles
may approach 300 to 350 beats/min, which significantly increases the risk of development of VF.
The most common form of preexcitation is the Wolff-Parkinson-White (WPW) pattern, which
includes a triad of findings that consist of the following: (1) a short PR interval, (2) a delta wave,
and (3) a wide-QRS complex (Fig. 5.8). A delta wave is the initial slurred deflection at the beginning
of the QRS complex. It represents the relatively slow ventricular depolarization over the accessory path-
way (Fig. 5.9) (Mark, et al., 2009). The QRS is wide because it reflects a fusion complex created by ven-
tricular activation through both the AV node and the accessory pathway (Hamdan, 2010). A patient is
said to have WPW syndrome when a WPW preexcitation pattern is present on the ECG and a tachy-
dysrhythmia occurs that is related to the accessory pathway (Olgin & Zipes, 2012). An example of the
WPW pattern is shown in Fig. 5.10, and its ECG characteristics are summarized in Table 5.7.
Although some people with AVRT never have symptoms, common signs and symptoms associated
with AVRT and a rapid ventricular rate include anxiety, chest discomfort, dizziness, lightheadedness,
palpitations (common), shortness of breath during exercise, signs of shock, and weakness. Consultation
with a cardiologist is recommended when caring for a patient with AVRT. If a delta wave is noted on the
ECG but the patient is asymptomatic, no specific treatment is required (Hamdan, 2010). If the patient is
symptomatic because of the rapid ventricular rate, treatment will depend on how unstable the patient is,
Normal Sinus Rhythm
SA
AV
LEAD II
WPW: Sinus Rhythm WPW: Atrioventricular
Reentrant
Tachycardia
SA (AVRT)
SA
BT BT
AV AV
LEAD II LEAD II
Delta Wave P Wave
Fig. 5.8 Conduction during sinus rhythm in the normal heart (top) spreads from the SA node to the AV node and then
down the bundle branches. The jagged line indicates physiologic slowing of conduction in the AV node. With WPW syndrome
(bottom left), an abnormal accessory conduction pathway called a bypass tract (BT) connects the atria and ventricles.
With WPW, during sinus rhythm the electrical impulse is conducted quickly down the BT, preexciting the ventricles before
the impulse arrives via the AV node. Consequently, the PR interval is short and the QRS complex is wide, with slurring at
its onset (ie, delta wave). WPW predisposes patients to develop an AVRT (bottom right) in which a premature atrial beat
may spread down the normal pathway to the ventricles, travel back up the BT, and recirculate down the AV node again. This
reentrant loop can repeat itself, resulting in a tachycardia. Notice the normal QRS complex and often negative P wave in lead II
during this type of BT tachycardia. (From Goldberger AL: Clinical electrocardiography: a simplified approach, ed 7, St. Louis,
2006, Mosby.)
Normal conduction WPW
or
A
Delta
B Delta or
Fig. 5.9 Characteristic WPW pattern (ie, short PR interval, QRS widening, and delta wave) compared with normal conduction.
A, The usual appearance of WPW in leads where the QRS complex is mainly upright. B, The usual appearance of WPW when
the QRS is predominantly negative. Negative delta waves may simulate pathologic Q waves—mimicking MI. (From Grauer K:
A practical guide to ECG interpretation, ed 2, St Louis, 1998, Mosby.)
Fig. 5.10 This rhythm strip shows an example of intermittent preexcitation. The first three beats show preexcitation. This is
followed by abrupt normalization of the QRS complex in the next two beats. The preexcitation pattern returns for the final
three beats. (From Zipes DP, Jalife J: Cardiac electrophysiology: from cell to bedside, ed 3, Philadelphia, 2000, Saunders.)
TABLE 5.7 Characteristics of the Wolff-Parkinson-White Preexcitation Pattern

Regularity Regular, unless associated with AFib
Rate Usually 60 to 100 beats/min, if the underlying rhythm is sinus in origin
P waves Normal and positive in lead II unless WPW is associated with AFib
PR interval 0.12 sec or less if P waves are observed because the impulse travels very quickly across
the accessory pathway, bypassing the normal delay in the AV node
QRS duration Usually more than 0.12 sec; slurred upstroke of the QRS complex (ie, delta wave) may be
seen in one or more leads
AFib, atrial fibrillation; AV, atrioventricular; WPW, Wolff-Parkinson-White
the width of the QRS complex (ie, wide or narrow), and the regularity of the ventricular rhythm. Obtain
the patient’s vital signs, apply a pulse oximeter, and administer supplemental oxygen, if indicated. Estab-
lish IV access and obtain a 12-lead ECG. If the tachycardia persists, the patient is stable, and the QRS is
regular and narrow, current resuscitation guidelines recommend the use of adenosine (Link, et al., 2015).
Because adenosine can precipitate AFib with a rapid ventricular rate in a patient with WPW, it is prudent
to have a defibrillator readily available for cardioversion before giving adenosine (Page, et al., 2015).
ACLS Pearl
Medications such as adenosine, digoxin, diltiazem, and verapamil should be avoided for preexcited
AFib or atrial flutter (Link, et al., 2015). These medications are contraindicated because they slow or
block conduction across the AV node but they may speed up conduction through the accessory
pathway, thereby resulting in a further increase in the ventricular rate. If the patient is unstable, prep-
arations should be made for synchronized cardioversion.
WIDE-QRS TACHYCARDIAS
[Objectives 1, 2]
The QRS duration of a wide-QRS tachycardia is 0.12 second or more. Most wide-complex tachycardias
are VT. Some wide-complex tachycardias are actually SVT with a bundle branch block (BBB) or aberrant
conduction. Still others are ventricular-paced rhythms or a tachycardia with AV conduction associated
with or mediated by an accessory pathway (ie, preexcited tachycardia). It is best to seek expert consul-
tation when treating a patient who has a wide-complex tachycardia.
If the patient is stable, the QRS is wide, the rhythm is regular, and the QRS complexes are of similar
shape (ie, monomorphic), adenosine is administered to try to identify the origin of the tachycardia while
continuously monitoring the patient’s ECG (Link, et al., 2015). With few exceptions, adenosine will
generally have no effect if the rhythm is VT. If the wide-QRS rhythm is actually SVT with aberrancy,
adenosine administration will usually result in a transient slowing or conversion to a sinus rhythm. For
the pharmacologic termination of a stable wide-QRS tachycardia that is most likely VT, procainamide
(Table 5.8), amiodarone, or sotalol (Table 5.9) can be used (Link, et al., 2015). These medications are
considered first-line antiarrhythmics for monomorphic VT, and they have complex mechanisms of
action. They are used for both atrial and ventricular dysrhythmias. Although lidocaine is a ventricular
antiarrhythmic, it is considered a second-line antiarrhythmic for the management of monomorphic
VT because it is reportedly less effective for the termination of VT than the first-line agents. If the deci-
sion is made to administer procainamide, amiodarone, or sotalol, it is recommended that expert consul-
tation be sought before another drug is administered (Link, et al., 2015). If the diagnosis of SVT cannot
be proved or cannot be made easily, then the patient should be treated as if VT were present.
TABLE 5.8 Procainamide (Pronestyl)

Class Class IA antiarrhythmic
Mechanism • Blocks sodium and potassium channels, prolonging the effective refractory period and
of Action action potential duration in the atria, the ventricles, and the His-Purkinje system
• Suppresses ectopy in atrial and ventricular tissue
• Prolongs the PR and QT intervals
• Exerts a peripheral vasodilatory effect
Indications • To control the ventricular rate in the patient with preexcited AFib
• Stable monomorphic VT with a normal QT interval
Dosage • 20 mg/min IV infusion or 100 mg every 5 min until one of the following occurs:
dysrhythmia resolves, hypotension ensues, QRS prolongs by more than 50% of original
width, or total cumulative dose of 17 mg/kg is administered (Link, et al., 2015)
• Up to 50 mg/min may be used in urgent situations (Gahart, et al., 2016b)
• Maintenance infusion of 1 to 4 mg/min
Considerations • During administration, carefully monitor the patient’s ECG and BP. If the BP falls 15 mm
Hg or more, temporarily discontinue administration. Watch the ECG closely for
increasing PR and QT intervals, widening of the QRS complex, heart block, and/or
onset of TdP.
• Reduce the maintenance infusion rate in patients with impaired or reduced renal
function.
• Avoid use in patients with QT prolongation or heart failure.
AFib, atrial fibrillation; BP, blood pressure; ECG, electrocardiogram; IV, intravenous; TdP, torsades de pointes; VT, ventricular
tachycardia
TABLE 5.9 Sotalol (Betapace)

Mechanism • Slows heart rate
of Action • Decreases AV nodal conduction
• Increases AV nodal refractoriness
• Prolongs the effective refractory period of atrial muscle, ventricular muscle, and AV
accessory pathways (where present) in both anterograde and retrograde directions
• Negative inotrope
Indications Stable monomorphic VT (Link, et al., 2015)
Dosage 1.5 mg/kg IV over 5 min; however, U.S. package labeling recommends any dosage should
be infused slowly over a period of 5 hours (Link, et al., 2015)
Considerations • Sotalol is not a first-line antiarrhythmic.
• Use with caution in patients with bronchospastic disease.
• Monitor carefully for bronchospasm, bradycardia, hypotension, and new
dysrhythmias, including TdP.
• Closely monitor the QT interval every 2 to 4 hours after each dose; if the QT interval
lengthens to 0.5 sec or greater, reduce the dose or discontinue the drug (Page,
et al., 2015).
• Avoid in patients with a prolonged QT interval, those taking other QT-prolonging
drugs, those with uncontrolled heart failure, and those with hypokalemia.
AV, atrioventricular; BP, blood pressure; IV, intravenous; TdP, torsades de pointes; VT, ventricular tachycardia
Ventricular Tachycardia
VT exists when three or more sequential premature ventricular complexes (PVCs) occur at a rate of more
than 100 beats/min. VT may occur as a short run that lasts less than 30 seconds and spontaneously ends
(ie, nonsustained VT) (Fig. 5.11). Sustained VT persists for more than 30 seconds and may require ther-
apeutic interventions to terminate the rhythm. VT may occur with or without pulses, and the patient may
be stable or unstable with this rhythm.
VT, like PVCs, may originate from an ectopic focus in either ventricle. When the QRS complexes of
VT are of the same shape and amplitude, the rhythm is called monomorphic VT. When the QRS com-
plexes of VT vary in shape and amplitude from beat to beat, the rhythm is called polymorphic VT. In
PMVT, the QRS complexes appear to twist from upright to negative or negative to upright and back.
PMVT is discussed later in this chapter with irregular tachycardias.
Signs and symptoms associated with VT vary. The patient who has sustained monomorphic VT may
be stable for long periods. However, when the ventricular rate is very fast, or when myocardial ischemia is
present, monomorphic VT can deteriorate to PMVT or VF. Syncope or near-syncope may occur because
of an abrupt onset of VT. The patient’s only warning symptom may be a brief period of lightheadedness.
ACLS Pearl
An SVT with an intraventricular conduction delay may be difficult to distinguish from VT. Keep in mind
that VT is considered a potentially life-threatening dysrhythmia. If you are unsure whether a regular,
wide-QRS tachycardia is VT or SVT with an intraventricular conduction delay, treat the rhythm as VT
until proven otherwise. Obtaining a 12-lead ECG may help differentiate VT from SVT, but do not delay
treatment if the patient is symptomatic.
During VT, the severity of the patient’s symptoms is related to a number of factors, including how
rapid the ventricular rate is, how long the tachycardia has been present, the presence and extent of under-
lying heart disease, and the presence and severity of peripheral vascular disease (Martin & Wharton,
2001). Hemodynamic stability should not be used to differentiate between VT and SVT with an intra-
ventricular conduction delay (Mottram & Svenson, 2011).
Signs and symptoms of hemodynamic instability related to VT may include the following:
• Acute altered mental status
• Chest pain or discomfort
• Hypotension
• Pulmonary congestion
• Shock
• Shortness of breath
ACLS Pearl
VT may occur in a patient who has an implantable cardioverter-defibrillator (ICD) in place. If the rate of
the VT is below the programmed tachycardia detection rate, the ICD will not treat it. It is important to
identify this situation and request expert consultation immediately. It is possible that the VT can be
terminated painlessly with the use of the programmer that corresponds with the implanted device.
Fig. 5.11 Nonsustained VT. (From Crawford MV, Spence MI: Commonsense approach to coronary care, rev ed 6, St Louis,
1994, Mosby.)
Treatment is based on the patient’s signs, symptoms, and the type of VT. If the rhythm is monomor-
phic VT (and the patient’s symptoms are caused by the tachycardia):
• Cardiopulmonary resuscitation (CPR) and defibrillation are used to treat the pulseless patient
with VT.
• Stable but symptomatic patients are treated with oxygen (if indicated), IV access, and ventricular anti-
arrhythmics (eg, procainamide, amiodarone, sotalol) to suppress the rhythm. Procainamide should be
avoided if the patient has a prolonged QT interval or signs of heart failure. Sotalol should also be
avoided if the patient has a prolonged QT interval.
• Unstable patients (usually a sustained heart rate of 150 beats/min or more) are treated with oxygen, IV
access, and sedation (if the patient is awake and time permits), followed by synchronized
cardioversion.
In all cases, an aggressive search must be made for the cause of the VT. For example, VT that occurs in
the presence of hypokalemia may be terminated by treatment with replacement potassium.
ACLS Pearl
A rapid, wide-QRS rhythm associated with pulselessness, shock, or heart failure should be pre-
sumed to be VT until proven otherwise.
IRREGULAR TACHYCARDIAS
The severity of signs and symptoms associated with an irregular tachycardia varies depending on the
ventricular rate, how long the rhythm has been present, and the patient’s cardiovascular status. The
patient may be asymptomatic and not require treatment or may experience serious signs and symptoms.
It is best to seek expert consultation when treating a patient who has an irregular tachycardia.
Multifocal Atrial Tachycardia

Multifocal AT (MAT) is an automatic tachycardia that is the result of the random and chaotic firing of
multiple ectopic sites in the atria. At least three different P wave configurations (seen in same lead) are
required for a diagnosis of MAT (Table 5.10, Fig. 5.12). MAT is an irregular rhythm with a ventricular
rate faster than 100 beats/min; it is most often found in patients with advanced pulmonary disease.
Because MAT can be difficult to treat, it is best to consult a cardiologist before starting treatment.
Apply a pulse oximeter and administer supplemental oxygen, if indicated. Obtain the patient’s vital signs,
establish IV access, and obtain a 12-lead ECG.
The treatment of MAT is directed at the underlying cause (eg, hypoxia, acidosis, electrolyte distur-
bances). If the rhythm persists, evaluate the clinical significance of the tachycardia before considering the
use of antiarrhythmics (Mottram & Svenson, 2011). Because MAT does not involve reentry through the
AV node, it is unlikely that vagal maneuvers or giving adenosine will terminate the rhythm. Metoprolol
has been shown to be effective for rate control, but it should be avoided in patients with impaired left
ventricular function or bronchospastic pulmonary disease; in such cases, amiodarone may be preferred
(Mottram & Svenson, 2011; Olgin & Zipes, 2012). MAT is unresponsive to cardioversion (Link,
et al., 2015).
TABLE 5.10 Characteristics of Multifocal Atrial Tachycardia

Regularity Irregular; the pacemaker site shifts from the SA node to ectopic atrial locations or the AV
junction
Rate Ventricular rate faster than 100 beats/min
P waves Size, shape, and direction may change from beat to beat; at least three different P wave
configurations (seen in same lead) are required for a diagnosis of MAT
PR interval Varies; the pacemaker site shifts from the SA node to ectopic atrial locations or the AV junction
AT, atrial tachycardia; AV, atrioventricular; MAT, multifocal atrial tachycardia; SA, sinoatrial.
Fig. 5.12 MAT. (From Braunwald E, Libby P, Zipes DP, et al.: Heart disease: a textbook of cardiovascular medicine, ed 6, St.
Louis, 2001, Mosby.)
Atrial Flutter
Atrial flutter is a macroreentrant AT in which an irritable site within the atria fires regularly at a very rapid
rate (Table 5.11). Because of this extremely rapid stimulation, atrial waveforms are produced that resem-
ble the teeth of a saw, or a picket fence; these are called flutter waves or F waves (Fig. 5.13).
Typical atrial flutter is caused by reentry in which an impulse circles around a large area of tissue, such
as the entire right atrium in a counterclockwise direction. F waves are predominantly negative in leads II,
III, and aVF, and positive in V1 (January, et al., 2014). The atrial rate is typically 240 to 300 beats/min
(January, et al., 2014).
It is best to consult a cardiologist when considering treatment options. Apply a pulse oximeter and
administer supplemental oxygen, if indicated. Obtain the patient’s vital signs, establish IV access, and
obtain a 12-lead ECG. Vagal maneuvers may help to identify the rhythm by temporarily slowing AV
conduction and revealing the underlying flutter waves (see Fig. 5.13). When vagal maneuvers are used
in the management of atrial flutter, the response is usually sudden slowing and then a return to the former
rate. Vagal maneuvers will not usually convert atrial flutter because the reentry circuit is located in the
atria, not the AV node.
ACLS Pearl
The two primary treatment strategies used to control symptoms associated with atrial flutter or AFib
are rate control and rhythm control. With rate control, the patient remains in atrial flutter or AFib but
the ventricular rate is controlled to decrease acute symptoms, reduce signs of ischemia, and reduce
or prevent signs of heart failure from developing. With rhythm control, sinus rhythm is reestablished.
When a rate control strategy is considered for the patient with atrial flutter and a rapid ventricular
response, medications such as beta-blockers or nondihydropyridine calcium channel blockers (eg, verap-
amil, diltiazem) are the drugs of choice (Link, et al., 2015). When a rhythm control strategy is consid-
ered, it is best to consult a cardiologist (Link, et al., 2015). The short-acting antiarrhythmic ibutilide
(Table 5.12) may be ordered for pharmacologic rhythm control, provided there are no contraindications
to its use (Bontempo & Goralnick, 2011). Successful pharmacologic cardioversion with ibutilide has
reportedly occurred in 60% to 90% of episodes of atrial flutter (Olgin & Zipes, 2012). Excessive QT
TABLE 5.11 Characteristics of Atrial Flutter

Regularity Atrial: regular; ventricular: regular or irregular, depending on AV conduction and blockade
Rate The atrial rate generally ranges from 240 to 300 beats/min; the ventricular rate varies and is
determined by AV blockade; the ventricular rate will usually not exceed 180 beats/min as
a result of the intrinsic conduction rate of the AV junction
P waves No identifiable P waves; saw-toothed “flutter” waves are present
QRS duration 0.11 sec or less but may be widened if flutter waves are buried in the QRS complex or if
abnormally conducted
AV, atrioventricular
II
A
II
B
CSM
II
C
Fig. 5.13 Atrial flutter. A, This rhythm strip shows a narrow-QRS tachycardia with a ventricular rate just under 150
beats/min. B, The same rhythm shown in A with arrows added indicating possible atrial activity. C, When CSM is performed,
the rate of conduction through the AV node slows, revealing atrial flutter. (From Grauer K: A practical guide to ECG interpre-
tation, ed 2, St Louis, 1998, Mosby.)
interval prolongation, which can cause torsades de pointes (TdP), is a potential complication that can
occur during and shortly after ibutilide administration. Because most episodes of ibutilide-induced
TdP occur within 1 hour after treatment and almost all occur within 6 hours, continuous ECG
monitoring is essential throughout ibutilide administration and for 6 to 8 hours thereafter
(Bontempo & Goralnick, 2011; Olgin & Zipes, 2012). Other medications that are useful for the phar-
macologic cardioversion of atrial flutter or AFib include flecainide, dofetilide, and propafenone (January,
et al., 2014).
Prompt synchronized cardioversion should be considered for any patient who is hemodynamically
unstable (Link, et al., 2015). If synchronized cardioversion is performed, atrial flutter can be successfully
converted to a sinus rhythm with the use of low energy levels. Sedation should be considered when cir-
cumstances permit.
Atrial Fibrillation
AFib is a SVT characterized by uncoordinated atrial activation and consequently ineffective atrial con-
traction (January, et al., 2014). It occurs because of altered automaticity in one or several rapidly firing
sites in the atria or reentry involving one or more circuits in the atria (Table 5.13, Fig. 5.14). Cardiac
output is decreased because of various mechanisms including the loss of effective atrial contraction, irreg-
ular cardiac cycle length, rapid heart rates, and decreased coronary blood flow (Goel, et al., 2013).
Patients who experience AFib are at increased risk of atrial thrombus formation, leading to stroke,
peripheral thromboembolism, or both (January, et al., 2014).
TABLE 5.12 Ibutilide (Corvert)

Mechanism of • Potassium channel blocker; prolongs action potential duration and QT interval
Action • Mild slowing of the sinus rate and AV conduction
• Rhythm conversion usually occurs within 30 min but may take up to 90 min after
the start of the infusion (Gahart, et al., 2016a)
Indications Rapid conversion of recent onset AFib or atrial flutter to sinus rhythm
Dosage 1 mg IV over 10 min; if the dysrhythmia does not terminate within 10 min after the end
of the initial dose, a repeat dose of 1 mg may be administered 10 min after completion
of the first infusion (Olgin & Zipes, 2012)
Considerations • Avoid if the QTc is longer than 0.44 sec or when uncorrected hypokalemia or
bradycardia exists (Olgin & Zipes, 2012)
• Should not be given concurrently with Class IA antiarrhythmics or other Class III
antiarrhythmics (eg, amiodarone, sotalol).
• Lengthens the QT interval, increasing the risk of ventricular dysrhythmias, including
TdP and monomorphic VT
• During administration, resuscitation equipment must be immediately available and
continuous ECG monitoring is essential; ECG monitoring should be continued for at
least 4 hours after administration (January, et al., 2014).
• Pretreatment with IV magnesium may reduce the risk of ventricular dysrhythmias
(January, et al., 2014).
AFib, atrial fibrillation; AV, atrioventricular; ECG, electrocardiogram; IV, intravenous; QTc, corrected QT interval; TdP, torsades
de pointes; VT, ventricular tachycardia
TABLE 5.13 Characteristics of Atrial Fibrillation

Regularity Ventricular rhythm usually irregularly irregular
Rate Atrial rate usually 400 to 600 beats/min; ventricular rate variable
P waves No identifiable P waves; fibrillatory waves present; erratic, wavy baseline
II
MCLI
Fig. 5.14 AFib. (From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)
Atrial flutter or AFib that has a rapid ventricular rate is described as uncontrolled (Figs. 5.15, 5.16).
Atrial flutter or AFib with a rapid ventricular response is commonly called Aflutter with RVR or AFib
with RVR.
Obtaining a thorough medical history and patient assessment are important. When obtaining the
patient’s history, asking about the number of episodes of AFib, their frequency, the nature of the patient’s
symptoms, and possible triggers may help to determine the pattern of the dysrhythmia.
It is best to consult a cardiologist when considering specific therapies. Apply a pulse oximeter and
administer supplemental oxygen, if indicated. Obtain the patient’s vital signs, establish IV access, and
obtain a 12-lead ECG.
II
Fig. 5.15 AFib with a rapid ventricular response. (From Aehlert B: ECGs made easy study cards, St. Louis, 2004, Mosby.)
Lead I
Fig. 5.16 AFib with a rapid ventricular response and left BBB. (From Goldberger AL: Clinical electrocardiography: a simplified
approach, ed 7, St. Louis, 2006, Mosby.)
With a rate control strategy, the ventricular rate associated with the AFib is slowed without termi-
nation of the AFib and it is achieved using medications that prolong the refractory period of the AV node
or catheter ablation (Fuster, et al., 2011; Bontempo & Goralnick, 2011). Treatment of precipitating or
reversible causes of AFib is recommended before starting antiarrhythmic therapy (Wann, et al., 2011).
IV administration of beta-blockers (eg, esmolol, metoprolol, propranolol) or nondihydropyridine cal-
cium channel blockers (eg, verapamil, diltiazem) is recommended to slow the ventricular response to
AFib (Anderson, et al., 2013; January, et al., 2014). These medications must be used with caution in
patients with hypotension or heart failure. IV amiodarone can be useful for rate control in critically
ill patients without preexcitation, but it is less effective than nondihydropyridine calcium channel
blockers (January, et al., 2014).
Rhythm control, that is, termination of AFib and restoring sinus rhythm, is achieved using a com-
bination of approaches including pharmacologic or electric cardioversion and radiofrequency catheter
ablation. Because pharmacologic or electric cardioversion carries a risk of thromboembolism, anticoagu-
lation is recommended before attempting conversion of AFib to a sinus rhythm when the duration of the
AFib exceeds 48 hours (January, et al., 2014). Shorter durations of AFib do not exclude the possibility of
thromboembolism (Link, et al., 2015). For patients who are symptomatic and stable, but the duration of
atrial flutter or AFib is unknown, issues with regard to anticoagulation are important. Rate control can be
attempted while expert consultation is sought.
Patients who are hemodynamically unstable (eg, angina, heart failure, symptomatic hypotension,
ongoing myocardial ischemia, shock, pulmonary edema) should receive prompt synchronized cardiover-
sion (January, et al., 2014). Sedation should be considered when circumstances allow. Anticoagulation
should be started as soon as possible and continued for at least 4 weeks after cardioversion unless contra-
indicated (January, et al., 2014).
Although atrial flutter often converts to a sinus rhythm with the use of low energy levels during syn-
chronized cardioversion, higher energy levels are required for AFib (Fuster, et al., 2011). Although resus-
citation guidelines have traditionally recommended that the energy used during the cardioversion of
AFib be increased in successive increments, experts state that the initial use of a higher-energy shock
is more effective and may minimize the number of shocks required, as well as the duration of sedation
(January, et al., 2014). Pretreatment with selected antiarrhythmic medications such as ibutilide can be
useful to enhance the success of synchronized cardioversion, prevent recurrent AFib, and increase the
likelihood of maintenance of sinus rhythm (January, et al., 2014). For cardioversion of AFib, a biphasic
waveform is more effective than a monophasic waveform (January, et al., 2014). Some, but not all, studies
have shown anterior–posterior electrode placement superior to anterolateral placement. If cardioversion

is attempted using one electrode placement and fails, experts recommend using the alternative placement
before attempting another shock (January, et al., 2014).
Polymorphic Ventricular Tachycardia

With PMVT, the QRS complexes vary in shape and amplitude from beat to beat and appear to twist
from upright to negative or negative to upright and back, resembling a spindle (Fig. 5.17). The ECG
characteristics of PMVT are shown in Table 5.14.
Several types of PMVT and their possible causes have been identified. PMVT that occurs in the pres-
ence of a long QT interval (generally, 0.50 second or more) is called torsades de pointes (TdP). A long QT
interval may be congenital, acquired (typically precipitated by antiarrhythmic drug use or hypokalemia,
which are typically associated with bradycardia), or idiopathic (neither familial nor with an identifiable
acquired cause). PMVT that occurs in the presence of a normal QT interval is simply referred to as poly-
morphic VT or normal-QT PMVT.
The signs and symptoms associated with PMVT are usually related to the decreased cardiac output
that occurs because of the fast ventricular rate. Signs of shock are often present. The patient may expe-
rience a syncopal episode or seizures. The rhythm may occasionally terminate spontaneously and recur
after several seconds or minutes, or it may deteriorate to VF. The patient with sustained PMVT is rarely
hemodynamically stable.
Apply a pulse oximeter and administer supplemental oxygen, if indicated. Obtain the patient’s vital
signs, establish IV access, and obtain a 12-lead ECG. It is best to seek expert consultation when treating
the patient with PMVT because of the diverse mechanisms of PMVT, for which there may or may not be
clues as to its specific cause at the time of the patient’s presentation. Treatment options vary and can be
contradictory. For example, a medication that may be appropriate for the treatment of TdP may be con-
traindicated when treating another form of PMVT. In general, if the patient is symptomatic because of
the tachycardia, treat ischemia (if it is present) and correct electrolyte abnormalities. If the QT interval is
prolonged, the cause of the long QT should be determined and corrected, if possible (Olgin & Zipes,
2012). Discontinue any medications that the patient may be taking that prolong the QT interval. Gen-
erally, IV magnesium (Table 5.15) is the initial treatment for the stable patient with PMVT associated
with a long QT interval (ie, TdP). Beta-blockers may be effective for certain forms of PMVT
Fig. 5.17 When the QRS complexes of VT vary in shape and amplitude, the rhythm is called PMVT. (From Aehlert B: ECGs
made easy study cards, St. Louis, 2004, Mosby.)
TABLE 5.14 Characteristics of Polymorphic Ventricular Tachycardia

Regularity Ventricular rhythm may be regular or irregular
Rate Ventricular rate is 150 to 300 beats/min; typically 200 to 250 beats/min
P waves None
PR interval None
QRS duration 0.12 sec or more; there is a gradual alteration in the amplitude and direction of the QRS
complexes; a typical cycle consists of 5 to 20 QRS complexes
TABLE 5.15 Magnesium Sulfate

Class Antiarrhythmic, electrolyte
Mechanism • Essential for activity of many enzyme systems
of Action • Plays an important role with regard to neurochemical transmission and muscular
excitability
Indications PMVT with prolonged QT interval
Dosage • If pulseless, give 1 to 2 g IV diluted in 10 mL D5W.
• If pulse present, give 1 to 2 g IV diluted in 50 to 100 mL D5W over 15 min.
Considerations • Use with caution in patients receiving digitalis, patients with impaired renal function,
and patients with preexisting heart blocks.
• Calcium is the antidote for magnesium toxicity.
D5W, dextrose 5% in water; IV, intravenous; PMVT, polymorphic ventricular tachycardia
(eg, ischemic PMVT, congenital long-QT syndrome PMVT, catecholaminergic PMVT). Amiodarone
may be effective for PMVT with a normal QT interval. PMVT that is associated with Brugada syndrome
may be responsive to isoproterenol (Link, et al., 2015). Adenosine should not be given for PMVT
because it may cause degeneration of the dysrhythmia to VF (Link, et al., 2015).
Because the QRS complexes of PMVT are disorganized (ie, they differ in amplitude and direction),
synchronized cardioversion is generally not possible when managing an unstable patient with this
rhythm. Therefore if the patient with PMVT is unstable or has no pulse, proceed with defibrillation
as for VF. The tachycardia algorithm is shown in Fig. 5.18.
Fig. 5.18 Tachycardia algorithm. (American Heart Association tachycardia algorithm. Reprinted with permission. 2015
American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care—Part 7: Adult
Advanced Cardiovascular Life Support. ECC guidelines.heart.org. © Copyright 2015 American Heart Association, Inc.)
SYNCHRONIZED CARDIOVERSION
[Objectives 4, 5]
Synchronized cardioversion is a type of electrical therapy during which a shock is timed or programmed
for delivery during ventricular depolarization (ie, the QRS complex). When the “Sync” control is pressed,
a synchronizing circuit in the machine searches for the QRS complex and delivers the shock a few mil-
liseconds after the QRS. The delivery of a shock during this portion of the cardiac cycle reduces the
potential for the delivery of current during ventricular repolarization, which includes the vulnerable
period of the T wave (ie, the relative refractory period).
Because the machine must be able to detect a QRS complex so that it can “sync,” synchronized car-
dioversion is used to treat rhythms that have a clearly identifiable QRS complex and a rapid ventricular
rate (eg, some narrow-QRS tachycardias, monomorphic VT). Synchronized cardioversion is not used
to treat disorganized rhythms (eg, PMVT) or those that do not have a clearly identifiable QRS
complex (eg, VF).
Procedure
[Objectives 4, 5]
Before performing synchronized cardioversion, take appropriate standard precautions and obtain a 12-
lead ECG. Identify the rhythm on the cardiac monitor and verify that the procedure is indicated. Print an
ECG strip to document the patient’s rhythm, and assess the patient for serious signs and symptoms from
the tachycardia. Make sure that suction and emergency medications are available. Give supplemental
oxygen, if indicated, and start an IV. If the patient is awake, explain the procedure and obtain an
informed consent. If time and the patient’s clinical condition permit, sedation should be administered
before performing the procedure.
Place the patient in a supine position and remove clothing from the patient’s upper body. With gloves,
remove transdermal medication patches, bandages, jewelry, and any other materials from the sites that
will be used for paddle or pad placement; do not attempt to administer shocks through them. Keep mon-
itoring electrodes and wires well away from the area where paddles or combination pads will be placed.
Contact may cause electrical arcing and patient skin burns during defibrillation or cardioversion.
Turn the power to the defibrillator on. If using combination pads, place them in proper position on
the patient’s bare chest. If using handheld paddles, remember to use appropriate conductive gel or dis-
posable gel pads between the paddle electrode surface and the patient’s skin.
Press the “Sync” control on the defibrillator to select the synchronized mode (Fig. 5.19). Select a lead
with an optimum QRS complex amplitude and no artifact. Make sure the machine is marking or flagging
each QRS complex and that no artifact is present. The sense marker should appear near the middle of
each QRS complex. If sense markers do not appear or are seen in the wrong place (eg, on a T wave), adjust
the ECG size, or select another lead.
Select the energy level appropriate for the patient’s rhythm on the defibrillator (Fig. 5.20). Turn on the
ECG recorder for a continuous printout. Next, press the “Charge” button on the defibrillator and recheck
the ECG rhythm (Fig. 5.21). If using handheld paddles, place the paddles on pre-gelled defibrillator
pads on the patient’s chest and apply firm pressure. If the rhythm is unchanged, call “Clear!” and look
around you. Make sure that everyone is clear of the patient, the bed, and any equipment that is connected
to the patient. Make sure oxygen is not flowing over the patient’s chest to decrease the risk of combustion
in the presence of electrical current. After confirming that the area is clear, depress the “Shock” control
until the energy is delivered (Fig. 5.22). If using handheld paddles, simultaneously depress both buttons
on the paddles and hold until the shock is delivered. A slight delay may occur while the machine detects
the next QRS complex. Release the “Shock” control after the shock has been delivered.
Reassess the rhythm and the patient (Fig. 5.23). If the tachycardia persists, make sure that the
machine is in “Sync” mode before delivering another shock. This is important because many defibrillators
default to the unsynchronized mode after cardioversion. If the rhythm changes to VF, confirm that the
patient has no pulse while another team member quickly verifies that all electrodes and cable connections
are secure. If no pulse is present, ensure that the machine is not in “Sync” mode and defibrillate (see
Chapter 4). See Table 5.16 for a summary of cardioversion.
Fig. 5.19 Place combination pads in proper position on Fig. 5.20 Select the appropriate energy level on the defi-
the patient’s bare chest according to the defibrillator man- brillator. (From Roberts and Hedges’ clinical procedures in
ufacturer’s instructions. Press the “Sync” control on the emergency medicine, ed 6, Philadelphia, 2014, Saunders.)
defibrillator. Make sure the machine is marking each
QRS complex and that no artifact is present. (From Roberts
and Hedges’ clinical procedures in emergency medicine,
ed 6, Philadelphia, 2014, Saunders.)
Fig. 5.21 Press the “Charge” button on the defibrillator Fig. 5.22 Depress the “Shock” button until the energy is
and recheck the ECG rhythm. (From Roberts and Hedges’ delivered. (From Roberts and Hedges’ clinical procedures in
clinical procedures in emergency medicine, ed 6, Philadel- emergency medicine, ed 6, Philadelphia, 2014, Saunders.)
phia, 2014, Saunders.)
Fig. 5.23 Reassess the rhythm and the patient. (From Roberts and Hedges’ clinical procedures in emergency medicine, ed 6,
TABLE 5.16 Synchronized Cardioversion—Summary*

Rhythm Recommended Energy Doses
Unstable narrow regular tachycardia The biphasic dose is typically 50 to 100 J initially; increase in a
(ie, atrial flutter, other SVTs) stepwise fashion if the initial shock fails
Unstable narrow irregular tachycardia The biphasic dose is typically 120 to 200 J initially; increase in a
(ie, AFib) stepwise fashion if the initial shock fails; begin with 200 J if using
monophasic energy, and increase if unsuccessful
Unstable wide regular tachycardia The monophasic or biphasic dose is typically 100 J initially; it is
(ie, monomorphic VT) reasonable to increase in a stepwise fashion if the initial
shock fails
*Use energy doses recommended by the device manufacturer.

AFib, atrial fibrillation; J, Joule; SVT, supraventricular tachycardia; VT, ventricular tachycardia

CHAPTER QUIZ
Multiple Choice
____ 1. A 72-year-old man is anxious and complaining of palpitations. His blood pressure is
110/64 millimeters of mercury (mm Hg), his pulse is 190 beats/min, and his
ventilatory rate is 16 breaths/min. The patient denies chest pain. Breath sounds are
clear. The cardiac monitor reveals monomorphic VT. Recommended treatment
in this situation includes:
A. Beginning CPR and defibrillating immediately.
B. ABCs, O2, IV, and epinephrine 1 mg rapidly IV.
C. ABCs, O2, IV, and procainamide 20 to 50 mg/min IV.
D. ABCs, O2, IV, sublingual nitroglycerin, and adenosine 6 mg rapidly IV.
____ 2. With which type of tachycardia does the impulse begin above the ventricles but travel
via a pathway other than the AV node and bundle of His?
A. Sinus tachycardia
B. AT
C. AVRT
D. AVNRT
____ 3. Which of the following reflects the correct initial dosage of adenosine?
A. 6 mg IV bolus over 1 to 2 minutes
B. 3 mg rapid IV bolus over 1 to 3 seconds followed by a 20 mL saline flush
C. 6 mg rapid IV bolus over 1 to 3 seconds followed by a 20 mL saline flush
D. 12 mg rapid IV bolus over 1 to 3 seconds followed by a 20 mL saline flush
____ 4. Synchronized cardioversion:

A. Is used only for atrial dysrhythmias.
B. Delivers a shock during the QRS complex.
C. Delivers a shock between the peak and end of the T wave.
D. Is used only to treat rhythms with a ventricular rate of less than 60/min.
____ 5. The most common type of SVT is:

A. AT.
B. Ventricular escape rhythm.
C. AVRT.
D. AVNRT.
____ 6. A 29-year-old man presents with acute altered mental status. His blood pressure is
50/P, ventilations 14 breaths/min. The cardiac monitor reveals PMVT. Your best
course of action in this situation will be to:
A. Give adenosine rapid IV push.
B. Give diltiazem IV push over 2 minutes.
C. Consider sedation and defibrillate immediately.
D. Perform immediate synchronized cardioversion.
____ 7. Examples of irregular tachycardias include:

A. Sinus tachycardia, accelerated junctional rhythm, and atrial flutter.
B. PMVT, asystole, and sinus tachycardia.
C. AFib, atrial flutter, and PMVT.
D. Accelerated idioventricular rhythm, AFib, and accelerated junctional rhythm.
____ 8. Select the incorrect statement regarding vagal maneuvers.

A. Carotid sinus pressure should be avoided in older patients.
B. Carotid sinus pressure should be avoided if carotid bruits are present.
C. An ECG monitor should be used when a vagal maneuver is performed.
D. Simultaneous bilateral carotid pressure is recommended to ensure slowing of the
heart rate.
____ 9. Which of the following correctly describes MAT?

A. In MAT, at least three different P wave configurations are observed.
B. MAT is an irregularly irregular rhythm with no normal looking waveforms.
C. Waveforms resembling teeth of a saw or picket fence are observed before each
QRS complex.
D. P waves are uniform in appearance, positive (ie, upright) in lead II, and one
precedes each QRS complex.
____ 10. A 68-year-old man is complaining of chest pain. His level of responsiveness is rapidly
decreasing. His blood pressure is 50/32 mm Hg, his pulse is 230 beats/min, and his
ventilatory rate is 6 breaths/min. The cardiac monitor reveals a regular, narrow-QRS
tachycardia. Your best course of action will be to:
A. Defibrillate with 360 J.
B. Begin immediate transcutaneous pacing.
C. Sedate and perform synchronized cardioversion with 50 J.
D. Sedate and perform synchronized cardioversion with 120 J.
____ 11. When administering procainamide, the maximum dose is ____ and the maintenance
infusion dose is ____.
A. 0.25 mg/kg, 5 to 15 mg/hour
B. 0.5 mg/kg, 50 mcg/kg/min
C. 17 mg/kg, 1 to 4 mg/min
D. 150 mg, 0.5 mg/min
____ 12. A 73-year-old woman is complaining of palpitations and chest pain. Her blood
pressure is 72/50 mm Hg, her heart rate is 188 beats/min, and her ventilatory rate is 16
breaths/min. The cardiac monitor reveals a wide-QRS tachycardia. Your best course
of action will be to:
B. Begin immediate transcutaneous pacing.
C. Perform synchronized cardioversion with 100 J.
D. Begin CPR and ventilate using a bag-mask device.
____ 13. A 56-year-old woman is complaining of palpitations. When questioned, she denies
chest pain or shortness of breath. Her blood pressure is 134/82 mm Hg, pulse 180,
ventilations 18 breaths/min. The cardiac monitor shows a regular narrow-QRS
tachycardia without visible P waves. Which of the following reflects your best course of
action to take at this time?
A. O2, IV, vagal maneuvers, and adenosine 6 mg rapid IV bolus
B. O2, IV, vagal maneuvers, and verapamil 2.5 mg slow IV bolus
C. O2, IV, sedate and perform synchronized cardioversion with 50 J
D. O2, IV, and atropine 0.5 mg IV every 3 to 5 minutes to a maximum of 3 mg
____ 14. A 62-year-old man is complaining of palpitations that came on suddenly after
walking up a short flight of stairs. His symptoms have been present for about
20 minutes. He denies chest pain and is not short of breath. His skin is warm and dry;
breath sounds are clear. His blood pressure is 144/88 mm Hg, pulse 186, ventilations
18 breaths/min. The cardiac monitor reveals sustained monomorphic VT. An IV has
been established. Which of the following medications is most appropriate in this
situation?
A. Dopamine or sotalol
B. Furosemide or atropine
C. Nitroglycerin or morphine
D. Procainamide or amiodarone
CASE STUDY 5-1

A 72-year-old man presents with complaints of palpitations and chest heaviness. You have a sufficient
number of advanced life support personnel available to assist you and carry out your instructions.
Emergency equipment, including a biphasic manual defibrillator, is available.
1. As you approach the patient, you observe that he is sitting upright on a stretcher. He appears
anxious, his breathing is not labored, and his skin is pink. The patient speaks hurriedly, telling
you that his heart is “racing and feels like it is going to pound out of my chest.” What should be
done next?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
2. The patient’s ventilatory rate is 18 breaths/min and unlabored. His radial and carotid pulses are
strong but too fast to count accurately. You estimate the rate to be about 200 beats/min. His
skin is warm, pink, and dry. How would you like to proceed?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
3. The patient’s vital signs are as follows: Blood pressure: 142/90 mm Hg; heart rate 214 beats/
min; and ventilatory rate 18 breaths/min. Breath sounds are clear and equal. The patient’s
SpO2 on room air is 96%, and he has been placed on the cardiac monitor, which reveals
the following rhythm:
II
The following information has been obtained from the patient:

Signs/Symptoms: Palpitations and chest “heaviness” began 1 hour ago when the patient began feeling as if
everything was spinning around him and felt heaviness in his chest at the same time;
says this has happened once before but only lasted a minute or two; rates his chest
discomfort at 1/10
Allergies: None
Medications: Lisinopril, hydrochlorothiazide
Past history: Hypertension
Last oral intake: Lunch 1 hour ago
Events prior: Patient was walking from his kitchen to his living room when his symptoms began
The physical examination reveals no abnormalities. What is the rhythm shown on the monitor?
What should be done next?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
4. An IV has been started in the right antecubital vein. A 12-lead ECG has been ordered. On the basis
of the information provided, would you categorize this patient as asymptomatic, symptomatic but
stable, symptomatic but unstable, or pulseless? How would you like to proceed?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
5. A cardiology consult has been requested. The patient has complied with your instructions, but no
change is observed on the cardiac monitor. What would you like to do next?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
6. After administering the initial dose of the ordered medication, a team member tells you that the
patient’s blood pressure is now 74/52 mm Hg and he is difficult to arouse. The rhythm on the
monitor remains unchanged. What action(s) should be taken at this time?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
7. Intubation equipment, suction, and resuscitation medications are within arm’s reach. Sedation
has been administered. Will you perform synchronized cardioversion or will you defibrillate the
patient?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
8. A biphasic manual defibrillator is available to you. What initial energy setting will you use?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
9. What precautions should be observed to ensure that this procedure is performed safely?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
10. A shock was delivered as instructed. The cardiologist has arrived. The cardiac monitor reveals this
rhythm. What is the rhythm?
II
Identification: _____________________________________
11. The patient is awake and alert. Strong carotid and radial pulses are present. His ventilatory rate is 14
breaths/min. Breath sounds are clear and equal. The patient’s blood pressure is 108/88 mm Hg, and
his SpO2 is 98% on room air. What should be done now?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
CASE STUDY 5-2

A 61-year-old man presents with dizziness and difficulty breathing. You have a sufficient number of
advanced life support personnel available to assist you and carry out your instructions. Emergency equip-
ment, including a biphasic manual defibrillator, is available.
1. The patient is sitting upright on a stretcher and he is aware of your approach. His breathing is slightly
labored, and his skin is pale. Are these general impression findings normal or abnormal? If abnormal,
what are the abnormal findings?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
2. On the basis of the information provided, would you categorize this patient as sick (ie, unstable) or
not sick (ie, stable)?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
3. The patient is alert and oriented to person, place, time, and event. He reports several episodes of
dizziness since 5:30 am today and says that during these episodes he can feel his heart beating
faster than normal. The patient is allergic to codeine. He has a history of high cholesterol and
hypertension for which he takes Lipitor and lisinopril. How would you like to proceed?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
4. The patient’s vital signs are as follows: Blood pressure: 63/40 mm Hg; heart rate 150 beats/min;
and ventilatory rate 20 breaths/min. Breath sounds are clear and equal and his skin is cool, pale,
and dry. The patient’s SpO2 on room air is 88%, and he has been placed on the cardiac monitor,
which reveals the following rhythm:
Identification: _____________________________________
5. How would you like to proceed?

_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
6. Supplemental oxygen is being administered and an IV has been started. A cardiology consult has
been requested. What would you like to do next?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
7. Will you perform synchronized cardioversion or will you defibrillate the patient?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
8. A biphasic manual defibrillator is available to you. What initial energy setting will you use?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
9. A shock was delivered as instructed. You observe this rhythm on the cardiac monitor. What is the
rhythm?
Identification: _____________________________________
10. What should be done now?

_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
11. Chest compressions are being performed. What additional actions should be performed at this time?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
12. What actions can be taken during cardiac arrest to help ensure the delivery of medications from an
extremity to the central circulation?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
13. Chest compressions are continuing, bag-mask ventilation is being performed, and a vasopressor has
been administered. The patient’s cardiac rhythm remains unchanged. How would you like to
proceed?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
14. The patient has been defibrillated a second time. The IV team member is preparing to administer
amiodarone while chest compressions are being performed. What are the initial and repeat doses of
this medication during cardiac arrest?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
15. Despite the efforts of your team, the resuscitation effort is unsuccessful. Discuss the use of the
SPIKES protocol when conveying bad news to the patient’s family.
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________

Multiple Choice
1. C. Because the patient has a pulse, CPR, defibrillation, and epinephrine are not indicated. The
patient denies chest pain so nitroglycerin is not indicated. Procainamide, amiodarone, or sotalol
can be considered for a stable patient in monomorphic VT.
narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechan-
ical, pharmacologic, and electrical therapy, where applicable.
2. C. The AV node is normally the only electrical connection between the atria and ventricles. Pre-
excitation is a term used to describe rhythms that originate from above the ventricles but in which
the impulse travels via a pathway other than the AV node and bundle of His. Thus the supraven-
tricular impulse excites the ventricles earlier than would be expected if the impulse traveled by way of
the normal conduction system. Patients with preexcitation syndromes are prone to AVRT. When
the AV junction is bypassed by an abnormal pathway, the abnormal route is called an accessory path-
way. An accessory pathway is an extra bundle of working myocardial tissue that forms a connection
between the atria and ventricles outside the normal conduction system.
OBJ: Differentiate among narrow-QRS tachycardias, wide-QRS tachycardias, and irregular
tachycardias.
3. C. The initial dose of adenosine is 6 mg rapid IV push over 1 to 3 seconds. If there is no response
within 1 to 2 minutes, give 12 mg rapid IV push. The 12 mg dose may be repeated once in 1 to
2 minutes. Follow each adenosine dose immediately with a 20 mL normal saline flush. Reduce
the dose of adenosine by one-half in patients on dipyridamole (Persantine), carbamazepine (Tegre-
tol), those with transplanted hearts, or if given via a central IV line.
4. B. Synchronized cardioversion is the timed delivery of a shock during the QRS complex. It is indicated
in the management of a patient with a pulse who is exhibiting serious signs and symptoms related to a
tachycardia. It is used to treat rhythms that have a clearly identifiable QRS complex and a rapid ven-
tricular rate (such as some narrow-QRS tachycardias and monomorphic VT).
OBJ: Explain synchronized cardioversion, describe its indications, and list the steps required to
5. D. AT, AVNRT, and AVRT are types of SVT. The most common type of SVT is AVNRT. The
next most common is AVRT. A ventricular escape rhythm is a bradycardia (ie, 20 to 40 beats/min),
not a tachycardia, and it is a ventricular, not a supraventricular, rhythm.
6. C. The patient is unstable (acute altered mental status, hypotension). Consider sedation and defi-
brillate immediately. Although synchronized cardioversion is an appropriate treatment for unstable
patients with a tachycardia and a pulse, it is used for tachycardias that have a relatively uniform
amplitude. Because the amplitude of the waveforms in PMVT varies, defibrillation should be used
instead. Adenosine and diltiazem are not indicated.
7. C. Examples of irregular tachycardias include AFib, atrial flutter, MAT, and PMVT. Asystole,
accelerated idioventricular rhythm, and accelerated junctional rhythm are not tachycardias.
tachycardias.
8. D. When using vagal maneuvers, make sure oxygen, suction, a defibrillator, and emergency
medications are available before attempting the procedure. Continuous monitoring of the patient’s
ECG is essential and a 12-lead ECG recording is desirable. Carotid sinus pressure should be
avoided in older adults and in patients who have a history of stroke, known carotid artery stenosis,
or a carotid artery bruit on auscultation. Simultaneous, bilateral carotid pressure is not
recommended.
9. A. Wandering atrial pacemaker is a rhythm in which the size, shape, and direction of the P waves
vary, sometimes from beat to beat. The difference in the look of the P waves is a result of the gradual
shifting of the dominant pacemaker between the SA node, the atria, and/or the AV junction. When
a wandering atrial pacemaker is associated with a ventricular rate greater than 100 beats/min, the
rhythm is called multifocal atrial tachycardia (MAT). MAT is also called chaotic AT. At least three
different P wave configurations (seen in the same lead) are required for a diagnosis of wandering
atrial pacemaker or MAT. The rhythm may be irregular as the pacemaker site shifts from the
SA node to ectopic atrial locations and the AV junction.
tachycardias.
10. C. The patient’s chest pain, decreasing level of responsiveness, and hypotension indicate that he is
clearly unstable. Your best course of action will be to administer sedation and perform synchronized
cardioversion. The initial biphasic energy level is typically 50 to 100 J (use energy levels recom-
mended by the defibrillator manufacturer). Transcutaneous pacing is not indicated. Defibrillation
with an initial shock of 360 J is warranted for pulseless VT, VF, and unstable, sustained PMVT
(when using a monophasic defibrillator).
OBJ: For each of the following rhythms, identify the energy levels that are currently recom-
mended: monomorphic VT, narrow-QRS tachycardia, AFib, and atrial flutter.
11. C. The initial dose of procainamide is 20 to 50 mg/min IV. The maximum dose is 17 mg/kg, and
the maintenance infusion dose is 1 to 4 mg/min.
12. C. The patient’s chest discomfort and hypotension indicate that her condition is unstable. You
should administer sedation and perform synchronized cardioversion. The initial biphasic energy
level is typically 100 J (use energy levels recommended by the defibrillator manufacturer). Transcu-
taneous pacing and CPR are not indicated. Defibrillation is warranted for pulseless VT, VF, and
unstable (ie, sustained) PMVT.
13. A. The patient appears stable but symptomatic because of the rapid rate. Treatment usually includes
oxygen (if indicated), IV access, and vagal maneuvers. Vagal maneuvers are used to try to stop
the rhythm or slow conduction through the AV node. If vagal maneuvers fail, antiarrhythmic
medications should be tried. Adenosine is the drug of choice, except for patients with severe
asthma.
14. D. From the information provided, the patient appears to be clinically stable at this time. Procain-
amide would be appropriate to consider in this situation. Acceptable alternatives include amiodarone
and sotalol. Dopamine increases the force of myocardial contraction, heart rate, and blood pressure.
Because this patient is not hypotensive and he has a rapid heart rate, dopamine is not indicated.
Nitroglycerin is a vasodilator. The patient has no complaint of chest pain and shows no signs of
heart failure so nitroglycerin is not indicated. Furosemide (Lasix) is also not indicated because there
are no signs of pulmonary congestion. Atropine is not indicated because the patient has a tachycar-
dia, not a bradycardia.

1. Assess the patient’s breathing with regard to rate, quality, and regularity. Quickly estimate the
patient’s heart rate and determine the quality of the pulse (ie, fast or slow, regular or irregular, weak
or strong). Evaluate the patient’s skin temperature, color, and moisture to assess perfusion. Perform a
brief neurologic evaluation (ie, obtain a Glasgow Coma Scale score), and assess the need for a
defibrillator.
2. Ask a team member to attach a pulse oximeter, ECG monitor, and blood pressure monitor. Ask the
airway team member to administer supplemental O2 if indicated. Ask a team member to obtain the
patient’s baseline vital signs while you obtain, or direct a team member to obtain, a SAMPLE history
and perform a focused physical examination.
3. The monitor shows a narrow-QRS tachycardia with ST segment depression. Ask the IV team mem-
ber to start an IV of normal saline and order a 12-lead ECG.
tachycardias.
4. On the basis of the patient’s history and physical findings, the patient is symptomatic but stable at
this time. Order a cardiology consult. Ask the patient to perform a vagal maneuver.
OBJ: Identify a patient who is experiencing a tachycardia as asymptomatic, symptomatic but sta-
ble, symptomatic but unstable, or pulseless.
5. Because the patient is stable and the rhythm is a narrow-QRS tachycardia, ask the IV team member
to give adenosine 6 mg rapid IV bolus over 1 to 3 seconds and to follow with a 20 mL IV normal
saline flush.
6. The patient’s change in mental status and blood pressure indicates that he is now symptomatic and
unstable. Electrical therapy is warranted. Ensure that the code cart, including intubation equipment,
suction, and resuscitation medications, is within arm’s reach. Ask the defibrillation team member to
apply combination pads to the patient’s bare chest. While preparing to shock the patient, ask the IV
team member to sedate the patient.
OBJ: Identify a patient who is experiencing a tachycardia as asymptomatic, symptomatic but
7. Because the patient has a pulse and the rhythm is a narrow-QRS tachycardia, ask the defibrillation
team member to perform synchronized cardioversion.
8. The biphasic energy setting is typically 50 to 100 J initially for an unstable patient with a narrow-
QRS tachycardia; increase in a stepwise fashion if the initial shock fails.
9. Ensure that the energy level appropriate for the patient’s rhythm has been selected on the
defibrillator. If the rhythm is unchanged, call “Clear!” and make sure that everyone is clear of
the patient, the bed, and any equipment that is connected to the patient. Make sure oxygen is
not flowing over the patient’s chest to decrease the risk of combustion in the presence of electrical
current. After confirming that the area is clear, depress the “Shock” control until the shock is
delivered.
10. The monitor shows a sinus rhythm.

11. Repeat the primary survey and monitor the patient’s vital signs every 5 minutes for the next
30 minutes. Transfer patient care to the cardiologist. Request a team debriefing after the transfer
of patient care is complete.

1. The general impression findings are abnormal (Appearance: normal; Breathing: abnormal; Circu-
lation: abnormal skin color).
OBJ: State three areas to assess when forming a general impression of a patient.
2. An abnormal finding that is observed when assessing any of the general impression areas (ie, appear-
ance, work of breathing, circulation) suggests that the patient is sick (ie, unstable); move quickly and
proceed immediately to the primary survey.
3. Ask a team member to attach a pulse oximeter, ECG monitor, and blood pressure monitor and
obtain the patient’s baseline vital signs while you perform a focused physical examination.
4. The monitor shows monomorphic VT.

tachycardias.
5. Ask the airway team member to administer supplemental O2 by nonrebreather mask for now and to
monitor the patient’s oxygen saturation. Direct the IV team member to start an IV of normal saline.
Order a 12-lead ECG and cardiology consult as soon as possible.
6. Because the patient is symptomatic and unstable, ask the defibrillation team member to apply com-
bination pads to the patient’s bare chest and prepare to shock the patient. Ensure that the code cart,
including intubation equipment, suction, and resuscitation medications, is within arm’s reach.
While preparing to shock the patient, ask the IV team member to sedate the patient.
7. Because the patient has a pulse and the rhythm is a monomorphic VT, ask the defibrillation team
member to perform synchronized cardioversion.
8. The initial monophasic or biphasic energy dose is typically 100 J for an unstable patient with mono-
morphic VT. Use the energy setting recommended by the manufacturer.
9. The monitor shows VF.

10. It is important to recognize that VF is a shockable cardiac arrest rhythm. Instruct the defibrillation
team member to ensure that the “Sync” control is off and to prepare to defibrillate the patient, using
the energy levels recommended by the manufacturer. Ensure that all team members are clear of the
patient and that oxygen is not flowing over the patient’s chest before the shock is delivered. Instruct
the team to resume chest compressions immediately without pausing for a rhythm or pulse check
after the shock is delivered.
OBJ: Differentiate between shockable and nonshockable cardiac arrest rhythms.
11. Instruct the airway team member to remove the nonrebreather mask, insert an oral airway, and begin
ventilating the patient with a bag-mask device connected to 100% oxygen. Consider placement of an
advanced airway. Direct the IV team member to prepare and administer epinephrine 1 mg (1:10,000
solution) every 3 to 5 minutes as long as the patient is in cardiac arrest. Remember to rotate the
compressor every 2 minutes to avoid tiring.
applicable.
12. During cardiac arrest, ensure that the IV team member follows each drug administered with a 20 mL
bolus of IV fluid and brief (ie, about 10 to 20 seconds) elevation of the extremity during and after
drug administration to aid delivery of the drug into the central circulation.
applicable.
13. Direct the defibrillation team member to clear the patient, ensure oxygen is not flowing over the
patient’s chest, and then defibrillate the patient. After the shock has been delivered, instruct the team
to immediately resume CPR. Direct the IV team member to prepare and administer amiodarone or
lidocaine IV while chest compressions are being performed. Consider reversible causes of the arrest
using the Five Hs and Five Ts.
applicable.
14. Amiodarone is an antiarrhythmic that may be considered for VF or pulseless VT unresponsive to

CPR, defibrillation, and vasopressor therapy. The initial dose is 300 mg IV/IO, which can be fol-
lowed by one dose of 150 mg IV/IO.
applicable.
15. SPIKES is an acronym for a six-step protocol that is used for conveying distressing information to
patients and families. Following the SPIKES protocol can help ease the distress felt by the patient or
family who is receiving the news and the health care professional who is breaking the news.
• S—Setting (Select a location that provides for privacy with all appropriate people present)
• P—Perception of what the family understands about the situation (Find out what the family
already knows by asking, “What have you been told so far?” or “What is your understanding
of what has happened?”)
• I—Invitation from the family to give information (Ask the family how they prefer to receive the
information that you have to share and how much they want to know; keep in mind that ethnic
and cultural values play a significant role in the need for information)
• K—Knowledge (Begin with a warning statement that unfavorable news is coming and then
pause; “I am sorry to tell you that …”)
• E—Emotions (Give the family time to respond; be sensitive and respectful of cultural differences)
• S—Summarize (Offer to contact the patient’s physician and to be available if there are further
questions, arrange for follow-up support, allow the family the opportunity to see their relative
if they wish to do so)
OBJ: Discuss the use of the SPIKES protocol when conveying bad news.
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824). Philadelphia: Saunders.
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CHAPTER 6
Bradycardias
INTRODUCTION
[Objectives 1, 2]
The bradycardia algorithm is a treatment guideline that is used when providing care to patients who are
symptomatic with a bradycardia. You must be able to recognize if a patient is asymptomatic, symptom-
atic but stable, symptomatic but unstable, or pulseless. Familiarity with the bradycardia algorithm
requires patient assessment, rhythm recognition, knowledge of medications, and transcutaneous
pacing (TCP).
Cardiac output ¼ Stroke volume Heart rate. Therefore a decrease in either stroke volume or heart
rate may result in a decrease in cardiac output. An absolute bradycardia is a heart rate of less than 60
beats per minute (beats/min). When a patient has a relative bradycardia, his or her heart rate may be
more than 60 beats/min. This may occur when a hypotensive patient needs a tachycardia (as in
hypovolemia) but is unable to increase his or her heart rate because of sinoatrial (SA) node disease,
beta-blockers, or other medications. A patient with an unusually slow heart rate may complain of weak-
ness, or dizziness and fainting (ie, syncope) can occur. Decreasing cardiac output will eventually produce
hemodynamic compromise.
If a patient presents with a bradycardia, assess how the patient is tolerating the rhythm. If the patient
has no symptoms, no treatment is necessary but he or she should be observed closely. Many patients
tolerate a heart rate of 50 to 60 beats/min but become symptomatic when the rate drops below
50 beats/min. The term symptomatic bradycardia is used to describe a patient who experiences signs
and symptoms of hemodynamic compromise related to a slow heart rate. Examples of common signs and
symptoms associated with symptomatic bradycardia are shown in Box 6.1.
Treatment of a symptomatic bradycardia should include assessment of the patient’s oxygen saturation
level and determining whether signs of increased work of breathing are present (eg, retractions, tachyp-
nea, paradoxical abdominal breathing). Give supplemental oxygen if oxygenation is inadequate, and
assist breathing if ventilation is inadequate. Establish intravenous (IV) access and obtain a 12-lead elec-
trocardiogram (ECG). Atropine, administered IV, is the drug of choice for symptomatic bradycardia
(Link, et al., 2015). Reassess the patient’s response and continue monitoring the patient. Other inter-
ventions that may be used in the treatment of symptomatic bradycardia include epinephrine, dopamine,
or isoproterenol IV infusions, or TCP (discussed later in this chapter).
patient experiencing a bradycardia.
167
168 CHAPTER 6 Bradycardias
BOX 6.1 Symptomatic Bradycardia—Common Signs and Symptoms

• Acute altered mental status • Ongoing ischemic chest discomfort
• Diaphoresis • Pulmonary congestion
• Dizziness • Shortness of breath
• Fatigue • Signs of shock
• Heart failure • Syncope
• Hypotension • Weak pulses
• Lightheadedness • Weakness
LEARNING OBJECTIVES
1. Given a patient situation, describe the ECG characteristics and initial emergency care for
symptomatic bradycardia, including mechanical, pharmacologic (ie, indications,
contraindications, doses, and route of administration of applicable medications), and
electrical therapy, where applicable.
2. Identify a patient who is experiencing a bradycardia as asymptomatic, symptomatic but
3. Discuss the procedure for TCP, as well as its indications and possible complications.
LEARNING PLAN
• Master identification of the following rhythms: sinus bradycardia, junctional rhythm,
ventricular escape rhythm, and atrioventricular (AV) blocks: first-degree, second-degree
type I, second-degree type II, 2:1 AV block, and third-degree AV block.
• Master the following medications: O2, atropine, dopamine, epinephrine, and isoproterenol.
• Master the following skills: primary and secondary surveys, supplemental O2 delivery
devices, attachment and use of ECG monitoring leads, IV access, IV medication
administration, and operation of a transcutaneous pacemaker.
situation.
pressure and cardiac monitor, give supplemental O2 if indicated, and order a
12-lead ECG.
• Quickly recognize if a patient is asymptomatic, symptomatic but stable, symptomatic
but unstable, or pulseless.
• Demonstrate familiarity with the bradycardia algorithm.
and contraindications for the medications used in the treatment of a symptomatic
bradycardia.
• Administer medications and perform TCP when indicated.
• Consider reperfusion therapy if the patient’s signs and symptoms are consistent with
an acute coronary syndrome (ACS) and there are no contraindications.
• Verbalize when it is best to seek expert consultation.
debriefing.
answers provided.
CHAPTER 6 Bradycardias 169
KE Y T ERMS
Absolute bradycardia A heart rate of less than 60 beats/min.
Relative bradycardia A term that refers to a situation in which a patient’s heart rate may be
more than 60 beats/min but, physiologically, the patient needs a tachycardia (as in
hypovolemia) and is unable to increase his or her heart rate because of SA node disease,
beta-blockers, or other medications.
Symptomatic bradycardia A term used to describe a patient who experiences signs and
symptoms of hemodynamic compromise related to a slow heart rate.
SINUS BRADYCARDIA
[Objectives 1, 2]
If the SA node fires at a rate that is slower than normal for the patient’s age, the rhythm is called sinus
bradycardia. In adults and adolescents, a sinus bradycardia has a heart rate of less than 60 beats/min
(Table 6.1, Fig. 6.1). The term severe sinus bradycardia is sometimes used to describe a sinus bradycardia
with a rate of less than 40 beats/min.
Assess how the patient tolerates the rhythm at rest and with activity. If the patient has no symptoms,
no treatment is necessary. If the patient is symptomatic because of the slow rate, initial treatment gen-
erally includes supplemental oxygen (if indicated), starting an IV, obtaining a 12-lead ECG, and giving
IV atropine if the bradycardia persists despite adequate oxygenation and ventilation (Table 6.2).
ACLS Pearl
In the setting of a myocardial infarction (MI), sinus bradycardia is often temporary. A slow heart rate
can be beneficial in the patient who has had an MI if no symptoms are caused by the slow rate. This is
because the heart’s demand for oxygen is less when the heart rate is slow.
TABLE 6.1 Characteristics of Sinus Bradycardia

Regularity R to R and P to P intervals are regular
Rate Less than 60 beats/min
P waves Positive (ie, upright) in lead II; one precedes each QRS complex; P waves look alike
PR interval 0.12 to 0.20 sec and constant from beat to beat
Fig. 6.1 Sinus bradycardia with ST segment depression.
JUNCTIONAL ESCAPE RHYTHM

[Objectives 1, 2]
Because a junctional rhythm starts from above the ventricles, the QRS complex is usually narrow and its
rhythm is very regular at a rate of 40 to 60 beats/min (Table 6.3, Fig. 6.2). If the AV junction paces the
heart at a rate slower than 40 beats/min, the resulting rhythm is called a junctional bradycardia. This may
TABLE 6.2 Atropine Sulfate

Class Vagolytic, parasympatholytic, antimuscarinic, muscarinic antagonist, anticholinergic,
parasympathetic antagonist, parasympathetic blocker
Mechanism of • Competes with acetylcholine at muscarinic receptor sites
Action • Increases heart rate and AV conduction velocity by blocking the effects of the vagus
nerve on the SA and AV nodes
• Relaxes bronchial smooth muscle
• Dilates pupils
• Decreases secretion from salivary glands, sweat glands, bronchial glands, and acid-
secreting cells of the stomach
• Decreases motility of the gastrointestinal tract
Indications First-line drug for symptomatic bradycardia (eg, sinus bradycardia, sinus arrest, AV block
at the level of the AV node) (Link, et al., 2015)
Dosage 0.5 mg IV every 3 to 5 min to a total dose of 3 mg (Link, et al., 2015)
Precautions • Second-degree AV block type II and third-degree AV blocks are unlikely to respond to
atropine. In these situations, an IV infusion of a beta-adrenergic drug (ie, dopamine,
epinephrine, or isoproterenol) or TCP is preferred while preparing for transvenous
pacing (Link, et al., 2015).
• Do not push slowly or in smaller than recommended doses; may cause paradoxical
slowing of the heart rate.
• May result in tachycardia, palpitations, and ventricular ectopy.
• Use with caution in acute coronary syndromes; excessive increases in heart rate
may further worsen ischemia or increase size of infarction.
• Transplanted hearts do not usually respond to atropine because they lack vagal
nerve innervation.
AV, atrioventricular; IV, intravenous; SA, sinoatrial; TCP, transcutaneous pacing
TABLE 6.3 Characteristics of Junctional Escape Rhythm

Regularity Very regular
Rate 40 to 60 beats/min
P waves May occur before, during, or after the QRS; if visible, the P wave is inverted in leads II, III,
and aVF
PR interval If a P wave occurs before the QRS, the PR interval will usually be 0.12 sec or less; if no
P wave occurs before the QRS, there will be no PR interval
Fig. 6.2 Junctional escape rhythm with ST segment elevation. (From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)
seem confusing because the AV junction’s normal pacing rate is bradycardic; however, the term junctional
bradycardia refers to a rate slower than normal for the AV junction.
The patient may be asymptomatic with a junctional escape rhythm, or he or she may experience signs
and symptoms that may be associated with the slow heart rate and decreased cardiac output. Treatment
depends on the cause of the dysrhythmia and the patient’s presenting signs and symptoms. If the patient’s
signs and symptoms are related to the slow heart rate, treatment should include application of a pulse
oximeter and administration of supplemental oxygen if indicated. Establish IV access, obtain a 12-lead
ECG, and administer IV atropine. Reassess the patient’s response and continue monitoring the patient.
TABLE 6.4 Dopamine (Intropin, Dopastat)

Class Direct- and indirect-acting sympathomimetic; cardiac stimulant and vasopressor;
natural catecholamine
Mechanism • Naturally occurring immediate precursor of norepinephrine in the body
of Action • Effects of dopamine are dose-related (there is some overlap of effects). At low
doses, causes renal vasodilation. Moderate doses increase cardiac contractility and
stroke volume. Higher doses increase peripheral resistance, BP, and renal
vasoconstriction.
Indications • Temporizing measure in the management of symptomatic bradycardia that has not
responded to atropine, or for which atropine is inappropriate, while waiting for a
pacemaker
• Hypotension that occurs after return of spontaneous circulation
• Hemodynamically significant hypotension in the absence of hypovolemia
Dosage Give as a continuous IV infusion of 2 to 20 mcg/kg/min (Link, et al., 2015); titrate
infusion rate according to BP and other clinical responses.
Precautions • Monitor the BP, ECG, and drip rate closely.
• Correct hypovolemia before beginning dopamine therapy for the treatment of
hypotension and shock.
• Administer using an infusion pump.
• Extravasation into surrounding tissue may cause necrosis and sloughing.
• Gradually taper this drug before discontinuing the infusion.
BP, blood pressure; ECG, electrocardiogram; IV, intravenous
TABLE 6.5 Isoproterenol (Isuprel)

Class Sympathomimetic, cardiac stimulant, antiarrhythmic
Mechanism • Increases heart rate and causes bronchodilation
of Action • Onset of action is immediate and lasts 1 to 2 hours
Indications Temporizing measure in the management of symptomatic bradycardia that has not
responded to atropine, or for which atropine is inappropriate, while waiting for
a pacemaker
Dosage Give as a continuous IV infusion of 2 to 10 mcg/min (Link, et al., 2015); titrate infusion
rate according to heart rate and rhythm response.
Precautions • Administer using an infusion pump.
• Monitor the BP, ECG, and drip rate closely.
BP, blood pressure; ECG, electrocardiogram; IV, intravenous
Other interventions that may be considered for the treatment of symptomatic bradycardia include epi-
nephrine, dopamine (Table 6.4), or isoproterenol (Table 6.5) IV infusions, or TCP (discussed later in
this chapter).
ACLS Pearl
Recognizing the similarities and differences among dopamine, epinephrine, and isoproterenol
administration is important when treating a symptomatic bradycardia. Although these drugs are
given by continuous IV infusion, their dosing differs. Because the correct infusion rate for dopamine
depends on the patient’s weight, its dose range is 2 to 10 mcg/kg/min. An isoproterenol infusion is
not based on the patient’s weight and it is infused at 2 to 10 mcg/min. With symptomatic bradycar-
dia, an epinephrine infusion is administered at a dose range of 2 to 10 mcg/min; however, during
post–cardiac arrest care, epinephrine is infused at a rate of 0.1 to 0.5 mcg/kg/min. In all cases,
the infusion is titrated to the desired clinical response.
VENTRICULAR ESCAPE RHYTHM

[Objectives 1, 2]
A ventricular escape rhythm, which is also called an idioventricular rhythm, occurs at a rate of 20 to
40 beats/min. The QRS complexes seen with this rhythm are wide because the impulses begin in the
TABLE 6.6 Characteristics of Ventricular Escape Rhythm

Regularity Ventricular rhythm is essentially regular
Rate Ventricular rate is 20 to 40 beats/min
P waves Usually absent or with retrograde conduction to the atria; may appear after the QRS (usually
upright in the ST segment or T wave)
PR interval None
QRS duration 0.12 sec or greater; the T wave is frequently in the opposite direction of the QRS complex
Fig. 6.3 Ventricular escape rhythm. (From Aehlert B: ECGs made easy, ed 3, St. Louis, 2006, Mosby.)
ventricles, bypassing the normal conduction pathway. When the ventricular rate slows to a rate of less
than 20 beats/min, some clinicians refer to the rhythm as an agonal rhythm or dying heart. The charac-
teristics of a ventricular escape rhythm are described in Table 6.6, and an example is shown in Fig. 6.3.
If the patient has a pulse and is symptomatic because of the slow rate, treatment should include appli-
cation of a pulse oximeter and administration of supplemental oxygen if indicated. Establish IV access,
obtain a 12-lead ECG, and administer IV atropine. Reassess the patient’s response and continue
monitoring the patient. TCP or a dopamine, epinephrine, or isoproterenol IV infusion may be tried
if atropine is ineffective. Ventricular antiarrhythmics (eg, lidocaine) should be avoided during the man-
agement of this rhythm because they may abolish ventricular activity, possibly causing asystole in a
patient with a ventricular escape rhythm.
If the patient is not breathing and has no pulse despite the appearance of organized electrical activity
on the cardiac monitor, pulseless electrical activity (PEA) exists. PEA was discussed in Chapter 4. The
management of PEA should include high-quality cardiopulmonary resuscitation, giving oxygen,
establishing vascular access, possible placement of an advanced airway, and an aggressive search for
the underlying cause of the situation.
ATRIOVENTRICULAR BLOCKS
An AV block is a delay or block in the transmission of an impulse from the atria to the ventricles.
AV blocks occur in 12% to 25% of patients with acute MI (Issa, et al., 2012). They are classified into
(1) first-degree AV block, (2) second-degree AV block, and (3) third-degree AV block. With first-
degree AV block, impulses from the SA node to the ventricles are delayed; they are not blocked. With
second-degree AV blocks, there is an intermittent disturbance in the conduction of impulses between the
atria and the ventricles. With third-degree AV block, there is a complete block in the conduction of
impulses between the atria and the ventricles.
First-Degree Atrioventricular Block

[Objectives 1, 2]
A first-degree AV block is associated with a delay in impulse conduction that results in a constant PR
interval of more than 0.20 second in duration (Table 6.7, Fig. 6.4). First-degree AV block may be per-
manent or transient (Latcu & Nadir, 2010). When the QRS complex associated with a first-degree AV
block is narrow, the conduction abnormality is most commonly in the AV node (Hamdan, 2010). When
the QRS complex associated with a first-degree AV block is wide, the conduction abnormality may be
located in the AV node, the bundle of His, or the bundle branches.
TABLE 6.7 Characteristics of First-Degree Atrioventricular Block

Regularity Regular
Rate Usually within normal range, but depends on underlying rhythm
P waves Every positive (ie, upright) P wave is followed by a QRS complex
PR interval Fixed duration of more than 0.20 sec
QRS duration Usually 0.11 sec or less unless abnormally conducted
Fig. 6.4 Sinus rhythm with a first-degree AV block, ST-segment depression. (From Aehlert B: ECG study cards, St. Louis,
2004, Mosby.)
The patient with a first-degree AV block is often asymptomatic; however, marked first-degree AV
block can lead to symptoms even in the absence of higher degrees of AV block (Barold, 1996). First-
degree AV block that occurs with acute MI should be monitored closely to detect progression to
higher-degree AV block (Blank, et al., 2014). If first-degree AV block accompanies a symptomatic bra-
dycardia, treat the bradycardia.
Second-Degree Atrioventricular Blocks

The term second-degree AV block is used when one or more, but not all, sinus impulses are blocked from
reaching the ventricles. Intermittent AV conduction is reflected on the ECG as more P waves than QRS
complexes.
Second-degree AV block is classified as type I or type II, depending on the behavior of the PR inter-
vals associated with the dysrhythmia. The type I or type II designation is used to describe the ECG pat-
tern of the PR intervals and should not be used to describe the anatomic site (ie, location) of the AV block
(Issa, et al., 2012). At least two consecutively conducted PR intervals must be observed to determine their
pattern.
Second-Degree Atrioventricular Block Type I

[Objectives 1, 2]
Blockage of the right coronary artery resulting in an inferior MI or right ventricular infarction can result
in conduction delays such as first-degree AV block and second-degree AV block type I. Second-degree
AV block type I is also known as type I block, Mobitz I, or Wenckebach. The term Wenckebach phenomenon is
used to describe a progressive lengthening of conduction time in any cardiac conducting tissue that even-
tually results in the dropping of a beat or a reversion to the initial conduction time. It is generally rec-
ognized that all of the classic Wenckebach features are found in less than 50% of cases (Latcu &
Nadir, 2010).
Second-degree AV block type I is associated with a cyclic pattern that consists of conducted P waves
(ie, each P wave is followed by a QRS) and then a P wave that is not conducted (ie, the P wave is not
followed by a QRS) (Table 6.8, Fig. 6.5). The P wave that is not conducted ends a group of beats. The
cycle then begins again. The repetition of this cyclic pattern is called grouped beating.
The patient with this type of AV block is usually asymptomatic because the ventricular rate often
remains nearly normal, and cardiac output is not significantly affected. If the patient is symptomatic
and the dysrhythmia is a result of medications (eg, digoxin, beta-blockers), these substances should
be withheld. When it is associated with an acute inferior MI, this dysrhythmia is usually transient
and resolves within 48 to 72 hours as the effects of parasympathetic stimulation disappear.
TABLE 6.8 Characteristics of Second-Degree Atrioventricular Block Type I

Regularity Ventricular irregular; atrial regular; grouped beating may be present
Rate Atrial rate is greater than the ventricular rate
P waves Normal in size and shape; some P waves are not followed by a QRS complex
PR interval Progressive prolongation of the PR interval (although lengthening may be very slight) until a
P wave appears without a QRS complex; the PR interval after a nonconducted P wave is
shorter than the interval preceding the nonconducted beat
QRS duration Usually 0.11 sec or less; complexes are periodically dropped
Fig. 6.5 Second-degree AV block type I. (From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)
If the heart rate is slow and serious signs and symptoms occur because of the slow rate, treatment
should include applying a pulse oximeter and administering oxygen (if indicated), obtaining the patient’s
vital signs, and establishing IV access. A 12-lead ECG should be obtained. Atropine, administered IV, is
the drug of choice. Reassess the patient’s response and continue monitoring the patient. When this
rhythm occurs in conjunction with acute MI, the patient should be observed closely for increasing
AV block and expert consultation should be sought with regard to patient management decisions.
Second-Degree Atrioventricular Block Type II

[Objectives 1, 2]
Second-degree AV block type II is also called type II block or Mobitz II AV block (Table 6.9, Fig. 6.6).
The site of block in type II block is most often in the bundle branches (Issa, et al., 2012). Although
second-degree AV block type II is less common than type I, type II is more serious and it is associated
TABLE 6.9 Characteristics of Second-Degree Atrioventricular Block Type II

Regularity Ventricular irregular; atrial regular
Rate Atrial rate is greater than the ventricular rate; ventricular rate is often slow
PR interval Within normal limits or prolonged, but constant for the conducted beats; the PR intervals
before and after a blocked P wave are constant
QRS duration Within normal limits if the block occurs above or within the bundle of His; greater than
0.11 sec if the block occurs below the bundle of His; complexes are periodically absent
after P waves
Lead II
Fig. 6.6 Second-degree AV block type II. (From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)
with an increased risk of mortality because it has a relatively high risk of progression to advanced or third-
degree AV block (Blank, et al., 2014).
Because second-degree AV block type II may abruptly progress to third-degree AV block, the patient
should be closely monitored for increasing AV block. If the heart rate is slow and serious signs and symp-
toms occur because of the slow rate, treatment should include obtaining the patient’s vital signs, applying
a pulse oximeter and administering oxygen (if indicated), and establishing IV access. Although atropine
is the first-line drug for acute symptomatic bradycardia, it is unlikely to be effective when the site of an
AV block is below the AV node. In situations such as this, pacing or the administration of beta-
adrenergic medications is preferable (Link, et al., 2015). The choice of transcutaneous versus temporary
transvenous pacing varies by institution and equipment availability. If TCP is available, it should be read-
ied for immediate use should the patient’s condition deteriorate and become unstable. A 12-lead ECG
should be obtained and a cardiology consult should be sought.
2:1 Atrioventricular Block

With second-degree AV block in the form of 2:1 AV block, there is one conducted P wave followed by a
blocked P wave; thus two P waves occur for every one QRS complex (ie, 2:1 conduction) (Table 6.10).
Because there are no two PQRST cycles in a row from which to compare PR intervals, 2:1 AV block
cannot be conclusively classified as type I or type II. To determine the type of block with certainty, it is
necessary to continue close ECG monitoring of the patient until the conduction ratio of P waves to QRS
complexes changes to 3:2, 4:3, and so on, which would enable PR interval comparison. If the QRS com-
plex measures 0.11 second or less, the block is likely to be a form of second-degree AV block type I. A 2:1
AV block associated with a wide QRS complex (ie, more than 0.11 second) is usually a type II block. The
causes and emergency management for 2:1 AV block are those of type I or type II block previously
described. A comparison of the types of second-degree AV blocks is shown in Fig. 6.7.
TABLE 6.10 Characteristics of Second-Degree 2:1 Atrioventricular Block

Regularity Ventricular regular; atrial regular
Rate Atrial rate is twice the ventricular rate
P waves Normal in size and shape; every other P wave is not followed by a QRS complex
PR interval Constant
QRS duration May be narrow or wide; complexes are absent after every other P wave
Lead II
Lead II
Lead II
C
Fig. 6.7 Types of second-degree AV block. A, Second-degree AV block type I. B, Second-degree AV block type II. C, 2:1
AV block. (From Grauer K: A practical guide to ECG interpretation, ed 2, St Louis, 1998, Mosby.)
Third-Degree Atrioventricular Block

[Objectives 1, 2]
With third-degree AV block, there is a complete block in conduction of impulses between the atria and
the ventricles (Table 6.11, Fig. 6.8). The site of block may occur at the level of the AV node, the bundle of
His, or distal to the bundle of His. A secondary pacemaker (either junctional or ventricular) stimulates
the ventricles; therefore the QRS may be narrow or wide, depending on the location of the escape pace-
maker and the condition of the intraventricular conduction system.
If the patient is symptomatic because of the slow rate, treatment should include obtaining the patient’s
vital signs, applying a pulse oximeter, administering oxygen (if indicated), establishing IV access, and
obtaining a 12-lead ECG. Because atropine is unlikely to be effective in the management of a third-
degree AV block, TCP may be used as a temporizing measure to provide immediate stabilization while
preparations are made for transvenous pacing. Other interventions that may be used in the treatment of
third-degree AV block include epinephrine, dopamine, or isoproterenol IV infusions (Link, et al., 2015).
Frequent patient reassessment is essential. Most patients with third-degree AV block have an indication
for permanent pacemaker placement. The bradycardia algorithm is shown in Fig. 6.9.
ACLS Pearl
Although calcium administration is not part of the symptomatic bradycardia algorithm, IV calcium is
useful in the treatment of many types of bradydysrhythmias, especially those that occur because of
an overdose of a calcium channel blocker (eg, verapamil, diltiazem) or because of hyperkalemia.
TABLE 6.11 Characteristics of Third-Degree Atrioventricular Block

Regularity Ventricular regular; atrial regular; no relationship between the atrial and ventricular rhythms
(ie, AV dissociation is present)
Rate The ventricular rate is determined by the origin of the escape pacemaker; the atrial rate is
greater than (and independent of) the ventricular rate
PR interval None: the atria and the ventricles beat independently of each other, thus there is no true
PR interval
QRS duration Narrow or wide, depending on the location of the escape pacemaker and the condition of
the intraventricular conduction system
AV, atrioventricular
Fig. 6.8 Third-degree AV block with ST segment depression and inverted T waves. (From Aehlert B: ECG study cards,
St. Louis, 2004, Mosby.)
TRANSCUTANEOUS PACING
TCP is the use of electrical stimulation through pacing pads that are positioned on a patient’s torso to
stimulate the contraction of the heart. TCP is also called temporary external pacing or noninvasive pacing.
TCP requires attaching two pacing electrodes to the skin surface of the patient’s outer chest wall.
Although TCP is a type of electrical therapy, the current delivered is considerably less than that
used for cardioversion or defibrillation. The stimulating current selected for TCP is measured in
Fig. 6.9 Bradycardia algorithm. (American Heart Association bradycardia algorithm. Reprinted with permission. 2015 Amer-
ican Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care—Part 7: Adult
Advanced Cardiovascular Life Support. ECC guidelines.heart.org. ©2015 American Heart Association, Inc.)
milliamperes (mA). The power delivered during each pacing impulse is less than 1⁄1000 of that delivered
during defibrillation (Bessman, 2013). The range of output current of a transcutaneous pacemaker varies
depending on the manufacturer. Because TCP is painful in conscious patients, sedation, analgesia, or
both may be needed to minimize the patient’s discomfort associated with this procedure.
Indications
[Objective 3]
TCP is indicated for symptomatic bradycardias unresponsive to atropine therapy or when atropine is
not immediately available or indicated. It may also be used as a bridge until transvenous pacing can be
accomplished or until the cause of the bradycardia is reversed (as in cases of drug overdose or hyper-
kalemia). Some clinicians prophylactically apply pacing electrodes to all critically ill patients with
bradycardia to facilitate immediate TCP should decompensation occur (Bessman, 2013). Whether
or not TCP is effective, the patient should be prepared for transvenous pacing and expert consultation
sought.
Procedure
[Objective 3]
Take appropriate standard precautions, and verify that the procedure is indicated. Place the patient on
oxygen, if indicated. Assess the patient’s vital signs and establish IV access. Because continuous mon-
itoring of the patient’s ECG is essential throughout the procedure, apply ECG electrodes. Position the
ECG electrodes as far away as possible from where the pacing pads will be applied to minimize distortion
of the ECG signal by the pacing current (Boehm, 2007; Del Monte, 2006). Identify the rhythm on the
cardiac monitor. Record a rhythm strip and verify the presence of a paceable rhythm.
To improve electrode adherence and maximize the delivery of energy through the chest wall, prepare
the skin on the patient’s chest (and back if the anterior–posterior pad position will be used) by washing
with a nonemollient soap and water (Spotts, 2011). When preparing the skin, avoid the use of flammable
liquids (eg, alcohol, benzoin) because of the increased potential for burns (Spotts, 2011). Remove any
transdermal medication patches that may be present and wipe away any residue.
Apply adhesive pacing pads to the patient according to the manufacturer’s recommendations
(Fig. 6.10). Do not place the pads over open cuts, sores, drains, dressings, or over an implanted pace-
maker or defibrillator. Avoid placing the pacing pads over bone (eg, sternum, spine, scapula) because this
increases the level of energy needed to achieve capture, increases patient discomfort, and increases the
possibility of noncapture (Spotts, 2011). When using the anterior–posterior position for pad placement,
the anterior electrode is placed between the xiphoid process and the left nipple, which corresponds
with the V2 to V3 ECG electrode position (Boehm, 2007; Del Monte, 2006). Ensure that the upper
edge of the electrode is below the nipple. If the patient is female, place the electrode beneath the breast
and against the chest wall (Bessman, 2013). The posterior electrode is placed beneath the left scapula and
lateral to the spine at the level of the heart. Some clinicians recommend placing the posterior pad first to
prevent buckling of the anterior electrode when rolling the patient to the side (Boehm, 2007). When
using the anterolateral position for pad placement, which is also called the sternum–apex position, the
lateral (ie, apex) pad is placed lateral to the left nipple in the left midaxillary line, which corresponds with
the V6 ECG electrode position. The anterior electrode is placed to the right of the sternum and below the
clavicle. Do not reverse placement of the pacing pads; doing so can result in the need for more current to
achieve capture, which can result in increased patient discomfort (Del Monte, 2006).
Next, connect the pacing cable to the pacemaker and to the adhesive pads on the patient. Turn the
power to the pacemaker on. Set the pacing rate to the desired number of paced pulses per minute (ppm)
(Fig. 6.11). Generally, a rate that is between 60 and 90 pulses/min will maintain an adequate blood pres-
sure and cerebral perfusion in an adult (Del Monte, 2006).
After the rate has been regulated, start the pacemaker (Fig. 6.12). Slowly increase the stimulating
current (ie, output or mA) until pacer spikes are visible before each QRS complex (ie, capture). This
control is usually labeled “Current,” “Pacer output,” or “mA.” Electrical capture occurs when a pacing
stimulus leads to ventricular depolarization and is achieved in many patients between 50 and 100 mA
(Del Monte, 2006). Although the amount of current necessary to achieve capture varies among individ-
uals, it does not appear to correlate with body surface area or patient weight (Boehm, 2007; Del Monte,
2006). Electrical capture usually is seen in the form of a wide QRS and a broad T wave on the ECG
(Fig. 6.13). The captured QRS complex may be deflected in a positive or negative direction (Del
Fig. 6.10 Apply adhesive pacing pads to the patient Fig. 6.11 Turn the pacemaker on and set the pacing rate
according to the manufacturer’s recommendations. (From to the desired number of ppm. (From Roberts and Hedges’
Roberts and Hedges’ clinical procedures in emergency clinical procedures in emergency medicine, ed 6, Philadel-
medicine, ed 6, Philadelphia, 2014, Saunders.) phia, 2014, Saunders.)
Fig. 6.12 After the rate has been regulated, start the pace- Fig. 6.13 After electrical capture is achieved, assess for
maker and slowly increase the current output until electrical mechanical capture by palpating for a pulse. (From Roberts
capture is achieved. (From Roberts and Hedges’ clinical pro- and Hedges’ clinical procedures in emergency medicine, ed
cedures in emergency medicine, ed 6, Philadelphia, 2014, 6, Philadelphia, 2014, Saunders.)
Saunders.)
Monte, 2006). For some patients, electrical capture is less obvious; it may only be indicated as a change in
the shape of the QRS.
ACLS Pearl
During TCP, the muscle twitching that occurs with skeletal muscle contraction is not an indicator of
electrical or mechanical capture (Boehm, 2007).
Assess mechanical capture. Mechanical capture refers to contraction of the myocardium and occurs
when pacing produces a response that can be measured, such as a palpable pulse. Other signs of increased
cardiac output resulting from mechanical capture include an improved level of responsiveness, a rise in
blood pressure, and improved oxygen saturation and skin color (Boehm, 2007; Del Monte, 2006).
To minimize confusion between the presence of an actual pulse and skeletal muscle contractions caused
by the pacemaker, assess mechanical capture by assessing the patient’s femoral pulse, right brachial pulse,
or right radial pulse. If available, bedside ultrasound may be useful in determining mechanical capture
(Bessman, 2013). After capture is achieved, continue pacing at an output level slightly higher than the
threshold of initial electrical capture.
Assess the patient’s level of responsiveness, oxygen saturation, blood pressure, and other vital signs.
Closely monitor the patient, and assess the skin under the pacing electrodes for irritation after the first
30 minutes of pacing and periodically thereafter (Boehm, 2007). Documentation should include the
following (Boehm, 2007; Del Monte, 2006):
• The date and time pacing was initiated (including baseline and pacing rhythm strips)
• The current required to obtain capture
• The pacing rate selected
• The patient’s response with capture (ie, mental status, blood pressure, oxygen saturation)
• Medications administered during the procedure
• The date, time, and reason pacing was terminated, if applicable
Limitations
The main limitation of TCP is patient discomfort. The discomfort is proportional to the intensity of
skeletal muscle contraction and the direct electrical stimulation of cutaneous nerves (Box 6.2). Patients
have described the sensations associated with skeletal muscle contractions as tapping, twitching, or thud-
ding (Boehm, 2007; Del Monte, 2006). Sensations associated with cutaneous nerve stimulation have
been described as tingling, stinging, pinching, or burning (Boehm, 2007; Del Monte, 2006). When
using the anterior–posterior position for pacing pad placement, discomfort may be reduced in some
patients by moving the anterior electrode from its V2 to V3 position more laterally to a V6 position, rec-
ognizing that pacing will be temporarily discontinued during the period in which the pacing pad is moved
(Boehm, 2007; Del Monte, 2006).
Another possible limitation of TCP is the use of incompatible pacing electrodes. For example, TCP
electrodes used in the out-of-hospital setting may be incompatible with those used in the emergency
BOX 6.2 Patient Responses to Current

with Transcutaneous Pacing*
OUTPUT (mA) RESPONSE
20 Prickly sensation on skin
30 Slight thump on chest
40 Definite thump on chest
50 Coughing
60 Diaphragm pacing and coughing
70 Coughing and knock on chest
80 More uncomfortable than 70 mA
90 Strong, painful knock on chest
100 Leaves bed because of pain
*Responses with Zoll transcutaneous pacemaker.
From Flynn, JB: Introduction to critical care skills. St. Louis, 1993, Mosby-Year Book.
department. Similarly, TCP electrodes/connectors used in the emergency department may be incompat-
ible with those used in other areas of the hospital (Bessman, 2013).
Capture may be difficult to achieve or it may be inconsistent for some patients. Increased stimulating
current may be required for patients with increased chest wall muscle mass, chronic obstructive pulmo-
nary disease, pleural effusions, dilated cardiomyopathy, hypoxia, or metabolic acidosis because of the
extremely high current thresholds required.
Possible Complications
[Objective 3]
Possible complications of TCP include the following:
• Coughing
• Skin burns
• Interference with sensing from patient agitation or muscle contractions
• Discomfort as a result of the electrical stimulation of the skin and muscles
• Failure to recognize that the pacemaker is not capturing
• Tissue damage, including third-degree burns, with improper or prolonged TCP
• When pacing is prolonged, pacing threshold changes, thereby leading to capture failure

CHAPTER QUIZ
Multiple Choice
____ 1. An ECG rhythm strip shows a regular ventricular rhythm at a rate of 30 beats/min,
more P waves than QRS complexes (the P waves occur regularly), a variable
PR interval, and a QRS duration of 0.14 second. This rhythm is:
A. 2:1 AV block.
B. Third-degree AV block.
C. Second-degree AV block type I.
D. Second-degree AV block type II.
____ 2. Depending on the severity of the patient’s signs and symptoms, management of slow
rhythms may require intervention including:
A. Defibrillation.
B. IV atropine.
C. Synchronized cardioversion.
D. Vagal maneuvers and/or adenosine.
____ 3. With 2:1 AV block, the PR interval:

A. Is absent.
B. Shortens.
C. Lengthens.
D. Remains constant.
____ 4. Which of the following dysrhythmias has the greatest potential for sudden,
third-degree AV block?
A. Junctional rhythm
B. Sinus bradycardia
C. First-degree AV block
D. Second-degree AV block type II
____ 5. Which of the following best describes a ventricular escape rhythm?

A. Rapid, chaotic rhythm with no pattern or regularity
B. Gradual alteration in the amplitude and direction of the QRS; atrial
rate indiscernible; ventricular rate 150 to 250 beats/min
C. Essentially regular ventricular rhythm with QRS complexes measuring 0.12 second
or greater; atrial rate not discernible; ventricular rate 20 to 40 beats/min
D. Regular ventricular rhythm with QRS complexes measuring less than
0.10 second; P waves may occur before, during, or after the QRS; ventricular
rate 40 to 60 beats/min
____ 6. With second-degree and third-degree AV blocks:

A. P waves occur regularly.
B. Every other P wave is dropped.
C. P waves are periodically dropped.
D. There are more QRS complexes than P waves.
____ 7. TCP may be useful in which of the following situations?

A. Asystole
B. Ventricular fibrillation
C. Sinus tachycardia; blood pressure 108/70 millimeters of mercury
(mm Hg), unresponsive
D. Second-degree AV block type II; blood pressure 64/42 mm Hg, altered
mental status
____ 8. Which of the following medications increases heart rate by accelerating the rate at
which the SA node discharges and by blocking the vagus nerve?
A. Digitalis
B. Atropine
C. Amiodarone
D. Beta-blocker
____ 9. Which of the following best describes third-degree AV block?

A. Absent P waves, wide QRS, ventricular rate 40 beats/min or less
B. Rapid rhythm in which the QRS complexes are wide and appear to twist
from upright to negative or negative to upright and back
C. More P waves than QRSs, P waves occur regularly, regular ventricular
rhythm, no pattern to PR intervals, QRS narrow or wide
D. Rapid rhythm in which the QRS complex is wide and usually regular;
QRS complexes are of same shape and amplitude
____ 10. A 47-year-old man is complaining of dizziness, nausea, and chest discomfort that he
rates 4 out of 10. His blood pressure is 74/40 mm Hg; ventilations 16 breaths/min.
The patient’s breath sounds are clear. The cardiac monitor displays the rhythm shown.
Recommended treatment for this patient includes:

A. ABCs, O2, IV, and atropine IV push.
B. ABCs, O2, IV, and adenosine rapid IV push.
C. ABCs, O2, IV, and morphine titrated to pain relief.
D. ABCs, O2, IV, sublingual nitroglycerin, and TCP.
____ 11. How would you differentiate a junctional escape rhythm at 40 beats/min from a
ventricular escape rhythm at the same rate?
A. It is impossible to differentiate a junctional escape rhythm from a ventricular
escape rhythm.
B. The junctional escape rhythm will have a narrow QRS complex; the
ventricular escape rhythm will have a wide QRS complex.
C. The rate (40 beats/min) would indicate a junctional escape rhythm,
not a ventricular escape rhythm.
D. The junctional escape rhythm will have a wide QRS complex; the ventricular
escape rhythm will have a narrow QRS complex.
Completion
Complete each statement.
Identification: _____________________________________
Identification: _____________________________________
Identification: _____________________________________
Identification: _____________________________________
Identification: _____________________________________
CASE STUDY 6-1

A 75-year-old man presents with dizziness and generalized weakness. You have a sufficient number of
advanced life support personnel available to assist you and carry out your instructions. Emergency
equipment, including a biphasic manual defibrillator with TCP capability, is available.
1. The patient is lying supine on a stretcher and is aware of your approach. His breathing is not labored,
and his skin is pale. Are these general impression findings normal or abnormal? If abnormal, what are
the abnormal findings?
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________

______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
3. The patient’s blood pressure is 72/44 mm Hg and his ventilatory rate is 18 breaths/min. Breath
sounds are clear and equal and his skin is cool, pale, and dry. The patient’s blood oxygen
saturation level (SpO2) on room air is 94% and he has been placed on the cardiac monitor, which
reveals the following rhythm:
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
II
(From Aehlert B: ECGs made easy, ed 3, St. Louis, 2006, Mosby.)
Identification: _____________________________________
4. The patient is alert and oriented to person, place, time, and event. He reports that while preparing
breakfast he felt as if he was going to “pass out” and promptly sat down until his symptoms passed.
The patient has no known allergies. He has a history of chronic obstructive pulmonary disease, for
which he occasionally uses a Combivent Respimat inhaler, and hypertension, for which he takes
captopril daily. The patient denies chest pain and shortness of breath. How would you like to proceed?
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
5. IV access has been established, a cardiology consult has been requested, and a 12-lead ECG has been
obtained. On the basis of the information provided, would you classify this patient as asymptomatic,
symptomatic but stable, symptomatic but unstable, or pulseless?
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________

______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
7. The patient’s blood pressure is now 114/63 mm Hg and his ventilatory rate is 16 breaths/min. His
skin is warm, pink, and dry. The cardiac monitor reveals a sinus rhythm at 75 beats/min. The patient
states that he is feeling much better. What would you like to do next?
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
CASE STUDY 6-2

A 70-year-old man presents with nausea and dizziness. His symptoms began about 15 minutes ago while
at rest. You have a sufficient number of advanced life support personnel available to assist you and carry
out your instructions. Emergency equipment, including a biphasic manual defibrillator with TCP
capability, is available.
1. The patient is semireclined on a stretcher and is aware of your approach. You can see equal rise and fall
of his chest and his skin is pale. How would you like to proceed?
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
2. The patient is alert and oriented to person, place, time, and event, but he is slow to respond to your
questions. You are unable to palpate a radial pulse. A slow carotid pulse is present. The patient denies
chest pain and has no known allergies. He has a history of diabetes, an abdominal aneurysm, and has
had an angioplasty three times (he is uncertain of dates). His medications include furosemide,
nitroglycerin (NTG), trazodone, warfarin, and hydrocodone.
The patient’s blood pressure is 57/32 mm Hg and his ventilatory rate is 16 breaths/min. Breath
sounds are clear and equal and his skin is cool, pale, and moist. The patient’s SpO2 on room air is 96%.
The cardiac monitor reveals the following rhythm:
Identification: _____________________________________
3. On the basis of the information provided, would you classify this patient as asymptomatic,
symptomatic but stable, symptomatic but unstable, or pulseless?
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________

______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
5. IV access has been established, a cardiology consult has been requested, a 12-lead ECG has been
obtained, and laboratory results are pending. What factors must be considered when determining
the next steps in the management of this patient?
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
6. On the basis of the patient’s ECG rhythm, you elect to begin TCP. Pacing pads have been applied to
the patient’s chest and the procedure has been explained to the patient. At what rate should the
pacemaker be set? What current (ie, output) settings should be used?
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
7. The cardiac monitor reveals a 100% ventricular paced rhythm at 70 pulses/min. The patient’s blood
pressure is now 104/60 mm Hg and his ventilatory rate is 16 breaths/min. His skin is warm, pink, and
dry. What would you like to do next?
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________

Multiple Choice
1. B. With a third-degree block, the ventricular and atrial rhythms are regular; however, AV dissoci-
ation is present. The ventricular rate is determined by the origin of the escape rhythm. Based on the
description provided (ie, a QRS duration of 0.14 second and a ventricular rate of 30 beats/min), the
escape pacemaker is probably ventricular in origin. P waves are normal in size and shape, but some P
waves are not followed by a QRS complex. There is no true PR interval because the atria and the
ventricles beat independently of each other. The QRS may be narrow or wide, depending on the
location of the escape pacemaker and the condition of the intraventricular conduction system.
symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications,
2. B. Atropine, administered IV, is the drug of choice for symptomatic bradycardia. Defibrillation,
synchronized cardioversion, vagal maneuvers, and adenosine are not indicated in the treatment
of bradycardias.
applicable.
3. D. Second-degree 2:1 AV block is characterized by P waves that are normal in size and shape, but
every other P wave is not followed by a QRS. The atrial rate is twice the ventricular rate. The PR
interval for the conducted beats is constant.
applicable.
4. D. Second-degree AV block type II is often associated with anteroseptal MI. It is associated with an
increased risk of mortality because it has a relatively high risk of progression to advanced or third-
degree AV block.
5. C. A ventricular escape rhythm, which is also called an idioventricular rhythm, exists when three or
more ventricular beats occur in a row at a rate of 20 to 40 beats/min (ie, the intrinsic firing rate of the
Purkinje fibers). The QRS complexes seen with this rhythm are wide because the impulses begin in
the ventricles, bypassing the normal conduction pathway. When the ventricular rate slows to a rate of
less than 20 beats/min, some clinicians refer to the rhythm as an agonal rhythm or dying heart.
6. A. With second-degree and third-degree AV blocks there are more P waves than QRS complexes
and the P waves occur regularly.
7. D. TCP may be useful for symptomatic bradycardias when the patient’s signs and symptoms are
caused by the slow heart rate. TCP is not indicated for any of the other rhythms listed.
OBJ: Discuss the procedure for TCP, as well as its indications and possible complications.
8. B. Atropine is a vagolytic drug that is used to increase the heart rate. Vago refers to the vagus nerves
(right and left), which are the main nerves of the parasympathetic division of the autonomic nervous
system. Lytic refers to “lyse,” which means “to interfere with.” Atropine works by blocking acetylcho-
line at the endings of the vagus nerves. The vagus nerves innervate the heart at the SA and AV nodes.
Thus atropine is most effective for narrow-QRS bradycardias. By blocking the effects of acetylcholine,
atropine allows more activity from the sympathetic division of the autonomic nervous system. As a
result, the rate at which the SA node can fire is increased. Areas of the heart that are not innervated
or that are minimally innervated by the vagus nerves (eg, the ventricles) will not respond to atropine.
Thus atropine is usually ineffective for the treatment of wide-QRS bradycardias.
9. C. A third-degree AV block has more P waves than QRSs, P waves occur regularly, there is a regular
ventricular rhythm, there is no pattern to PR intervals, and the QRS may be narrow or wide. Absent
P waves, wide QRS, and a ventricular rate 40 beats/min or less describes a ventricular escape (idio-
ventricular) rhythm. A rapid rhythm in which the QRS complexes are wide and appear to twist from
upright to negative or negative to upright and back describes polymorphic ventricular tachycardia.
A rapid rhythm in which the QRS complex is wide and usually regular and QRS complexes are of the
same shape and amplitude describes monomorphic ventricular tachycardia.
10. A. The cardiac monitor displays a junctional bradycardia. Atropine is often effective in increasing the
heart rate in symptomatic narrow-QRS bradycardias. Because atropine will likely result in an
increase in heart rate, the resulting increased rate will also increase myocardial oxygen demand. This
must be considered when giving atropine to a patient who may be experiencing an acute MI. Aden-
osine is used to slow the heart rate in symptomatic narrow-QRS tachycardias. Because this patient
has a bradycardia, adenosine is not indicated. Sublingual nitroglycerin should not be given at this
time because the patient’s heart rate is less than 50 beats/min and his blood pressure is
low. Nitrates are contraindicated in patients with hypotension (ie, systolic blood pressure less
than 90 mm Hg, or 30 mm Hg or more below baseline). Although morphine is used to relieve pain,
the patient’s blood pressure is very low. Because the patient’s breath sounds are clear, consider
a 250 mL IV fluid challenge of normal saline to try to increase the patient’s blood pressure. Give
nitroglycerin and morphine as needed for pain relief if the patient’s systolic blood pressure rises
above 90 to 100 mm Hg (check your local protocols) and the heart rate increases to more than
50 beats/min.
OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care
for symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications,
11. B. Although junctional and ventricular rhythms are ectopic pacemaker sites, their rhythms can gen-
erally be differentiated by the width of their QRS complexes. The junctional escape rhythm will have
a narrow QRS complex; the ventricular escape rhythm will have a wide QRS complex.
OBJ: Given a patient situation, describe the ECG characteristics and initial emergency
care for symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications,
Completion
12. 100% ventricular paced rhythm

13. 2:1 AV block with ST segment depression

14. Ventricular escape rhythm

15. Sinus rhythm with first-degree AV block

applicable.
16. Third-degree (ie, complete) AV block with ST segment elevation


1. The general impression findings are abnormal (Appearance: normal; Breathing: normal; Circula-
tion: abnormal skin color).
obtain the patient’s baseline vital signs while you perform a focused physical examination.
3. The monitor shows sinus bradycardia at 33 beats/min changing to junctional bradycardia at

32 beats/min.
4. Ask the airway team member to monitor the patient’s oxygen saturation. Direct the IV team member
to start an IV of normal saline. Order a 12-lead ECG, a cardiology consult, laboratory studies, and a
portable chest radiograph.
5. This patient is symptomatic but unstable because he is hypotensive and his symptoms appear to be
directly related to his bradycardia. Although the patient’s mental status is normal, a blood pressure of
72/44 mm Hg is a concern for a patient who is being treated for hypertension.
OBJ: Identify a patient who is experiencing a bradycardia as asymptomatic, symptomatic but
6. Instruct the IV team member to administer atropine 0.5 mg IV. This dose may be repeated every 3 to
5 minutes to a total dose of 3 mg. Closely monitor the patient’s cardiac rhythm and vital signs after
each atropine dose. Although sinus bradycardia and junctional escape rhythms typically respond well
to atropine, it is prudent to ask the defibrillation team member to prepare for TCP in the event that
atropine is ineffective.
7. Continue to closely monitor the patient’s ECG and vital signs. Review the results of the patient’s
12-lead ECG and laboratory studies to try to determine the cause of the patient’s bradycardia.
Arrange for the patient’s transfer for continued care and request a team debriefing after the transfer
of patient care is complete.

obtain the patient’s baseline vital signs while you perform a primary survey and obtain a focused
history.
2. The rhythm shown is a third-degree AV block at 46 beats/min.

3. This patient is symptomatic but unstable because he is hypotensive.

OBJ: Identify a patient who is experiencing a bradycardia as asymptomatic, symptomatic but
4. Ask the airway team member to monitor the patient’s oxygen saturation. Direct the IV team member
to start an IV of normal saline. Order a 12-lead ECG, a cardiology consult, laboratory studies, and a
portable chest radiograph. Instruct the defibrillation team member to prepare for TCP.
5. When a patient experiences a bradycardia and the bradycardia is the cause of serious signs and symptoms,
the patient needs immediate emergency care. Several factors must be considered, such as the use of phar-
macologic therapy, electrical therapy, or both. Because atropine is unlikely to be effective when the site of
an AV block is below the AV node, pacing or the use of beta-adrenergic agents is preferable (Link, et al.,
2015). The choice of transcutaneous versus temporary transvenous pacing varies by institution and
equipment availability. Some clinicians prefer to administer IV atropine while external pacing pads
are simultaneously placed on the patient.
In the setting of bradycardia and coronary ischemia or MI, consideration must be given to
atropine’s effects. For example, if the bradycardia is responsive to atropine administration, the result-
ing increased heart rate may increase myocardial oxygen demand, resulting in worsened ischemia or
extension of the infarction. Additional considerations in the setting of MI include the administration
of aspirin, completion of a reperfusion checklist, and reperfusion therapy (ie, percutaneous coronary
intervention or fibrinolytics). Consultation with a cardiologist is advised.
6. Set the pacing rate to the desired number of ppm. Generally, a rate that is between 60 and 90 pulses/
min will maintain an adequate blood pressure and cerebral perfusion in an adult. After the rate has
been regulated, start the pacemaker. Titrate the stimulating current (ie, output or mA) slowly but
steadily until pacer spikes are visible before each QRS complex. After capture is achieved, continue
pacing at an output level slightly higher than the threshold of initial electrical capture.
OBJ: Discuss the procedure for TCP, as well as its indications and possible complications.
7. Continue to closely monitor the patient’s ECG and vital signs. Assess the skin under the pacing
electrodes for irritation after the first 30 minutes of pacing and periodically thereafter. Review the
results of the patient’s 12-lead ECG and laboratory studies to try to determine the cause of the
patient’s bradycardia. Arrange for patient transfer for continued care and request a team debriefing
after the transfer of patient care is complete.
REFERENCES
Barold, S. S. (1996). Indications for permanent cardiac pacing in first-degree AV block: Class I, II, or III? PACE,
19(5), 745–751.
Bessman, E. S. (2013). Emergency cardiac pacing. In J. R. Roberts (Ed.), Roberts and Hedges’ clinical procedures in
emergency medicine (6th ed., pp. 277–297). Philadelphia: Saunders.
Blank, A. C., Loh, P., & Vos, M. A. (2014). Atrioventricular block. In D. P. Zipes, & J. Jalife (Eds.), Cardiac elec-
trophysiology: From cell to bedside (6th ed., pp. 1043–1049). Philadelphia: Saunders.
Boehm, J. (2007, Jul). Tried and true: Noninvasive transthoracic pacing. Retrieved Jan 28, 2015, from Zoll Code Com-
munications: www.zoll.com/CodeCommunicationsNewsletter/CCNLPacing/CCNLPacing.htm.
Del Monte, L. (2006). Noninvasive pacing: What you should know. Redmond, WA: Medtronic Emergency Response
Systems.
Hamdan, M. H. (2010). Cardiac arrhythmias. In T. E. Andreoli, I. J. Benjamin, R. C. Griggs, & E. J. Wing (Eds.),
Andreoli and Carpenter’s Cecil essentials of medicine (8th ed., pp. 118–144). Philadelphia: Saunders.
Issa, Z. F., Miller, J. M., & Zipes, D. P. (2012). Atrioventricular conduction abnormalities. In Clinical arrhythmology
and electrophysiology: A companion to Braunwald’s heart disease (2nd ed., pp. 175–193). Philadelphia: Saunders.
Latcu, D.-G., & Nadir, S. (2010). Atrioventricular and intraventricular conduction disorders. In M. H.
Crawford, J. P. DiMarco, & W. J. Paulus (Eds.), Cardiology (3rd ed., pp. 725–739). Philadelphia: Elsevier.
In Web-based integrated guidelines for cardiopulmonary resuscitation and emergency cardiovascular care—
part 7: Adult advanced cardiovascular life support: Eccguidelines.heart.org.
Spotts, V. (2011). Temporary transcutaneous (external) pacing. In D. J. Lynn-McHale Wiegand (Ed.), AACN
procedure manual for critical care (6th ed., pp. 413–420). St. Louis: Saunders.
CHAPTER 7
Acute Coronary Syndromes
INTRODUCTION
Acute coronary syndromes (ACSs), also called acute ischemic coronary syndromes (AICSs), are a group of
conditions that are caused by an abrupt reduction in coronary artery blood flow (Amsterdam, et al.,
2014). The sequence of events that occurs during an ACS results in conditions that range from myo-
cardial ischemia (ie, unstable angina pectoris) to infarction (with or without associated ST segment ele-
vation [STE] on the electrocardiogram [ECG]). This chapter discusses the pathophysiology, history and
clinical presentation, patient evaluation, and initial management of the patient experiencing an ACS.
gency care for a patient experiencing an ACS.
LEARNING OBJECTIVES
1. Explain the pathophysiology of ACSs.
2. Describe the forms of ACSs.
3. Discuss the typical clinical presentation of the patient with a suspected ACS.
4. Identify key components that should be included in the history and physical examination
of the patient with a suspected ACS.
5. Explain and give examples of anginal equivalents.
6. Explain atypical presentation and its significance in ACSs.
7. Identify the ECG changes that are associated with myocardial ischemia, injury, and
infarction.
8. Identify the ECG leads that view the anterior wall, the inferior wall, the lateral wall, the
septum, the inferobasal wall, and the right ventricle.
9. Explain the clinical and ECG features of a right ventricular infarction (RVI).
10. Describe the initial management of a patient who is experiencing an ACS.
11. Explain the importance of the 12-lead ECG for the patient with an ACS.
12. Discuss the three groups that are used when categorizing the 12-lead ECG findings of the
patient experiencing an ACS.
193
194 CHAPTER 7 Acute Coronary Syndromes
LEARNING PLAN
• Master identification of the following rhythms: sinus rhythm, sinus bradycardia, sinus
tachycardia, atrial fibrillation (AFib), atrial flutter; atrioventricular (AV) blocks: first-degree,
second-degree type I, second-degree type II, third-degree; premature atrial complexes,
premature ventricular complexes (PVCs).
• Master the following medications: O2, nitroglycerin (NTG), morphine sulfate, aspirin.
situation.
• Recognize signs and symptoms of ACSs.
• Recognize signs of myocardial ischemia, injury, and infarction on an ECG.
• Develop and implement a treatment plan on the basis of the patient’s presentation,
history, physical examination, and diagnostic test results.
• Know the actions, indications, dosages, adverse effects, and contraindications for the
medications used in the treatment of ACSs.
• If applicable, use a reperfusion checklist to evaluate the patient’s candidacy for
fibrinolytic therapy.
debriefing.
• Read the case studies at the end of this chapter and answer the questions within each case
study. Compare your answers with the answers provided.
KEY TERMS
Anginal equivalent Symptom other than chest pain or discomfort resulting from myocardial
ischemia that may occur either alone or in combination in a patient with ischemic heart
disease (IHD).
Arteriosclerosis A chronic disease of the arterial system characterized by abnormal
thickening and hardening of the vessel walls.
Atherosclerosis A form of arteriosclerosis in which the thickening and hardening of the
vessel walls are caused by a buildup of fat-like deposits in the inner lining, specifically of
large- and middle-sized muscular arteries.
Atypical presentation Uncharacteristic signs and symptoms experienced by some
patients.
PATHOPHYSIOLOGY OF ACUTE CORONARY

SYNDROMES
[Objective 1]
Arteriosclerosis is a chronic disease of the arterial system characterized by abnormal thickening and loss
of elasticity of the vessel walls. Atherosclerosis is a form of arteriosclerosis in which the thickening and
hardening of the vessel walls are caused by a buildup of fat-like deposits in the inner lining of large- and
middle-sized muscular arteries. The speed of progression of atherosclerosis is unpredictable and varies
among individuals (Bentzon & Falk, 2011). The usual cause of an ACS is the rupture of an atheroscle-
rotic plaque (Fig. 7.1).
CHAPTER 7 Acute Coronary Syndromes 195
FIBROUS CAP
(smooth muscle cells, macrophages,
foam cells, lymphocytes, collagen,
elastin, proteoglycans, neovascularization)
NECROTIC CENTER
(cell debris, cholesterol crystals,
foam cells, calcium)
MEDIA
Fig. 7.1 The basic structure of an atheromatous plaque. (From Kumar V, Abbas AK, Aster JC: Robbins basic pathology, ed 9,
Types of atherosclerotic lesions include the fatty streak, the fibrous plaque, and the advanced (ie, com-
plicated) lesion (Fig. 7.2). Although not all fatty streaks evolve into plaques (Kumar, et al., 2013a), pro-
gression from a fatty streak to an advanced lesion is associated with injured endothelium that activates the
inflammatory response. As the inflammatory response continues, the fatty streak becomes a fatty plaque,
then a fibrous plaque, and finally an advanced lesion. Initially the walls of the blood vessel outwardly
expand (ie, remodel) as plaque builds up inside of it. This occurs so that the size of the vessel stays rel-
atively constant, despite the increased size of the plaque. When the plaque fills about 40% of the inside of
the vessel, remodeling stops because the vessel can no longer expand to make room for the increase in
plaque size. As an atherosclerotic plaque increases in size, the vessel becomes severely narrowed (ie, ste-
nosed). Generally, arterial stenosis of 70% of the vessel’s diameter is required to produce anginal symp-
toms (Kumar, et al., 2013a). The extent of arterial narrowing and the amount of reduction in blood flow
are critical determinants of coronary artery disease (CAD).
Atherosclerotic plaques differ with regard to their makeup, their vulnerability to rupture, and their ten-
dency to form a blood clot. A “stable” or “nonvulnerable” atherosclerotic plaque has a relatively thick fibrous
cap that separates it from contact with the blood and that covers a core that contains a large amount of
collagen and smooth muscle cells but a relatively small lipid pool (Fig. 7.3). A stable plaque may produce
significant luminal obstruction, but it has a lower tendency to rupture or erode (Sapin & Muller, 2003).
A plaque that is prone to rupture is called a “vulnerable” plaque because it has a thin cap of fibrous
tissue over a large, soft, fatty center that separates it from the opening of the blood vessel. If the fibrous
cap erodes or ruptures, the contents of the plaque (ie, collagen, smooth muscle cells, tissue factor, inflam-
matory cells, and lipid material) are exposed to flowing blood, activating the clotting cascade, promoting
thrombus formation, and disrupting blood flow (Shah, 2003).
Although a thrombus is the most common cause of the blockage of a coronary artery, less commonly,
an ACS may occur as a result of coronary artery spasm (eg, with cocaine abuse), severe luminal narrowing
Fig. 7.2 The natural history, morphologic features, main pathogenic events, and clinical complications of atherosclerosis.
ECM, extracellular matrix; SMC, smooth muscle cell. (From Kumar V, Abbas AK, Aster JC: Robbins basic pathology, ed 9,
Vulnerable plaque Stable plaque
Media Media
Lumen Lumen
Lipid core Fibrous cap Lipid core Fibrous cap

Fig. 7.3 Vulnerable and stable atherosclerotic plaques. (From Kumar V, Abbas AK, Aster JC: Robbins basic pathology, ed 9,
from atherosclerosis or restenosis after percutaneous coronary intervention (PCI), coronary dissection,
hypercoagulation, trauma to the coronary arteries, or coronary artery emboli (rare) (Basra, et al.,
2014; Karve, et al., 2007).
MYOCARDIAL ISCHEMIA, INJURY, AND

INFARCTION
[Objective 2]
When a temporary or permanent blockage occurs in a coronary artery, the blood supply to the heart muscle is
impaired and myocardial cells distal to the site of the blockage are starved for oxygen and other nutrients.
IHD is a consequence of reduced coronary blood flow as a result of obstructive atherosclerotic vascular dis-
ease in more than 90% of cases (Kumar, et al., 2013b). Clinical presentations of IHD may include angina
pectoris, silent myocardial ischemia, acute myocardial infarction (AMI), or sudden cardiac death.
Partial or intermittent blockage of a coronary artery by a thrombus may result in no clinical signs and
symptoms (ie, silent ischemia), unstable angina (UA), non–ST elevation MI (NSTEMI), or, possibly,
sudden death. Complete blockage of a coronary artery may result in ST elevation MI (STEMI) or
sudden death.
The area supplied by a blocked coronary artery goes through a sequence of events that have been iden-
tified as zones of ischemia, injury, and infarction. Each zone is associated with characteristic ECG
changes (Fig. 7.4).
Myocardial Ischemia
[Objective 3]
Myocardial ischemia can occur because of increased oxygen demand (ie, demand ischemia), reduced
myocardial oxygen supply (ie, supply ischemia), or both. If the cause of the ischemia is not reversed
and blood flow restored to the affected area of the heart muscle, ischemia may lead to cellular injury
and, ultimately, cellular death (ie, infarction). Early assessment and emergency care are essential to pre-
vent worsening ischemia. Because ischemia affects repolarization, its effects can be viewed on the ECG as
ST segment depression (STD) and T wave changes in the leads that face the affected area of the ventricle
(see Fig. 7.4). Methods to reduce the heart’s oxygen demand include resting or slowing the patient’s heart
rate with medications such as beta-blockers. Methods to increase blood flow to the ischemic myocardium
include giving medications such as NTG.
ACLS Pearl
The complete blockage of a coronary artery may cause an MI. However, because a plaque usually
increases in size over months and years, other vascular pathways may enlarge as portions of a cor-
onary artery become blocked. These vascular pathways (ie, collateral circulation) serve as an alter-
native route for blood flow around the blocked artery to the heart muscle. Thus the presence of
collateral arteries may prevent infarction despite complete blockage of the artery.
Zone of ischemia
Zone of injury
Zone of infarction
T
Q
Left ventricle
Fig. 7.4 Zones of ischemia, injury, and infarction showing indicative ECG changes and reciprocal changes corresponding to each-
zone. (From Urden LD, Stacy KM, Lough ME: Critical care nursing: diagnosis and management, ed 6, St. Louis, 2010, Mosby.)
Angina pectoris is chest discomfort that occurs when the heart muscle does not receive enough oxygen
(ie, myocardial ischemia). The discomfort that is associated with angina occurs because of the stimulation
of nerve endings by lactic acid and carbon dioxide that build up in ischemic tissue. Angina most often
occurs in patients with CAD that involves at least one coronary artery. However, it can be present in
patients with normal coronary arteries. Angina also occurs in persons with uncontrolled high blood pres-
sure or valvular heart disease. Chest discomfort associated with myocardial ischemia usually begins in the
central or left chest and then radiates to the arm (especially the little finger [ulnar] side of the left arm), the
wrist, the jaw, the epigastrium, the left shoulder, or between the shoulder blades (Fig. 7.5). Common
words used by patients experiencing angina to describe the sensation they are feeling are shown in
Box 7.1.
ACLS Pearl
Monitoring of ST segment changes can provide useful diagnostic and predictive information in the
patient experiencing an ACS.
Stable Angina
[Objective 3]
Stable (ie, classic) angina remains relatively constant and predictable in terms of severity, signs and symp-
toms, precipitating events, and response to treatment. It is characterized by brief episodes of chest dis-
comfort related to activities that increase the heart’s need for oxygen such as emotional upset, exercise or
exertion, and exposure to cold weather. Possible related signs and symptoms are shown in Box 7.2.
Symptoms usually last less than 5 minutes and are typically relieved within 5 minutes with rest,
short-acting NTG, or both (Amsterdam, et al., 2014).
A B C D
E F G H
Fig. 7.5 Common sites for anginal discomfort. A, Upper part of chest. B, Beneath the sternum radiating to neck and jaw.
C, Beneath the sternum radiating down left arm. D, Epigastric. E, Epigastric radiating to the neck, jaw, and arms. F, Neck and
jaw. G, Left shoulder and arm. H, Interscapular. (From Urden LD, Stacy KM, Lough ME: Critical care nursing: diagnosis and
management, ed 6, St. Louis, 2010, Mosby.)
BOX 7.1 Common Terms Patients Use to Describe Angina

• “A band across my chest” • “Grip-like”
• “A vise tightening around my chest” • “Heaviness”
• “A weight in the center of my chest” • “Pressing”
• “Burning” • “Squeezing”
• “Bursting” • “Strangling”
• “Constricting” • “Suffocating”
BOX 7.2 Stable Angina

Common Precipitating Events Related Signs and Symptoms
• Emotional upset • Nausea or vomiting
• Exercise or exertion • Palpitations
• Exposure to cold weather • Shortness of breath
• Sweating
Unstable Angina
[Objective 3]
UA, which is also known as preinfarction angina, accelerating or crescendo angina, intermediate coronary
syndrome, and preocclusive syndrome, is a condition of intermediate severity between stable angina and
AMI. It is characterized by symptoms that occur at rest or with minimal exertion and last for 10 minutes
or more (Amsterdam, et al., 2014). The chest discomfort associated with UA may be described as painful
and be accompanied by dyspnea, diaphoresis, nausea, syncope, or dysrhythmias.
UA and NSTEMI may occur when blood flow through a coronary artery is partially or intermittently
blocked. The clinical presentations of patients with these conditions are similar, and it is often difficult to
distinguish between them. UA and NSTEMI are often grouped together as non–ST elevation acute cor-
onary syndromes (NSTE-ACSs) because ECG changes associated with these conditions usually include
STD and T wave inversion in the leads that face the affected area. UA and NSTEMI differ primarily by
whether myocardial ischemia is severe enough to cause cellular damage leading to detectable quantities of
cardiac biomarkers (Amsterdam, et al., 2014). Cardiac biomarkers, discussed later in this chapter, are
elevated when an infarction is present. Biomarkers are not elevated in patients with UA because there
is no tissue death.
Prinzmetal’s Angina
Prinzmetal’s angina, which is also called Prinzmetal’s variant angina or variant angina, is the result of
intense spasm of a segment of a coronary artery. This variant angina may occur in otherwise healthy
individuals (usually in their 40s or 50s) with no demonstrable coronary heart disease or in patients with
a nonobstructive atheromatous plaque. Although the episode of coronary artery spasm can be precip-
itated by exercise, emotional stress, hyperventilation, or exposure to cold, it usually occurs at rest, often
occurs between midnight and 8 am, and may awaken the patient from sleep (Kawano, et al., 2002).
Episodes may occur in clusters of two or three within 30 to 60 minutes. Although episodes usually
last only a few minutes, this may be long enough to produce serious dysrhythmias including AV block
and ventricular tachycardia (VT), as well as sudden death. If the spasm is prolonged, infarction may
result.
It can be difficult to suspect Prinzmetal’s angina from the patient’s clinical presentation. Patients
with Prinzmetal’s angina are generally younger and have fewer coronary risk factors (except for smok-
ing) compared with patients with chronic stable angina. The patient with Prinzmetal’s angina com-
plains of chest pain that is often described as severe and may be accompanied by syncope. Chest
discomfort is usually relieved by NTG. Although typical angina produces ST segment depression, Prinz-
metal’s angina produces ST segment elevation during periods of chest pain. After the episode of chest
discomfort is resolved, ST segments usually return to the baseline. Because NTG is effective at relieving
the coronary spasm, the ECG evidence of Prinzmetal’s angina may be lost if no pretreatment ECG is
obtained.
ACLS Pearl
Obtain a baseline 12-lead ECG before initiating treatment in any patient presenting with a
possible ACS.
Myocardial Injury
Ischemia that is prolonged by more than just a few minutes can result in myocardial injury. Myocardial
injury refers to myocardial tissue that has been cut off from, or experienced a severe reduction in, its blood
and oxygen supply. Myocardial injury can be extensive enough to produce a decrease in pump function or
electrical conductivity in the affected cells.
On the ECG, epicardial injury may cause elevation of the ST segment (in the leads that face the
affected area) and depression of the baseline, whereas endocardial injury may cause depression of the
ST segment and elevation of the baseline (Surawicz & Knilans, 2008). “It must be emphasized that acute
injury is not synonymous with acute MI. Acute injury pattern can appear in the absence of MI, as a pre-
cursor of MI, concomitant with the pattern of acute MI, or in the presence of a preexisting MI pattern.
The hallmark of acute injury is STE, which is usually accompanied by reciprocal STD. An acute injury
pattern can also produce a primary STD (eg, a subendocardial or posterior wall injury)” (Surawicz &
Knilans, 2008, p. 126).
Although injured myocardial cells are still alive, they will die (ie, infarct) if the blood flow is not quickly
restored to the injured area. Methods to restore blood flow include giving fibrinolytics or performing a
PCI, among others.
Myocardial Infarction
An MI occurs when blood flow to the heart muscle stops or is suddenly decreased long enough to cause myo-
cardial cell death and necrosis of the myocardium (Kurz, et al., 2014). Chest discomfort associated with acute
MI usually lasts more than 20 minutes (Thygesen, et al., 2012). The discomfort is often diffuse and may be
accompanied by diaphoresis, dyspnea, nausea, abdominal pain, or syncope (Amsterdam, et al., 2014).
The walls of the ventricles consist of an outer layer (ie, the epicardium), middle layer (ie, the myo-
cardium), and an inner layer (ie, the endocardium). The myocardium is subdivided into two areas. The
innermost half of the myocardium is called the subendocardial area and the outermost half is called the
subepicardial area. The main coronary arteries lie on the epicardial surface of the heart. The endocardial
and subendocardial areas of the myocardial wall are the least perfused areas of the heart and the most
vulnerable to ischemia because these areas have a high demand for oxygen and are fed by the most distal
branches of the coronary arteries. Transmural is a term that is used to describe ischemia, injury, or infarc-
tion that extends from the endocardium through the myocardium to the epicardium. For example, an
infarction that involves the entire thickness of the left ventricular wall is called a transmural MI. Possible
locations of infarctions in the ventricular wall are shown in Fig. 7.6.
When a coronary artery is blocked, the region of the heart supplied by the affected artery is called the
area at risk (Fig. 7.7). Ischemia occurs immediately in the area supplied by the affected artery. Anaerobic
metabolism ensues and lactic acid accumulates in the cardiac cells, which quickly results in a loss of myo-
cardial contractility (Schoen & Mitchell, 2010). Diastolic and systolic dysfunction appear within 30 to
45 seconds of blood flow deprivation (Blanc-Brude, 2011). Ischemia also contributes to dysrhythmias,
probably by causing electrical instability of ischemic areas of the heart (Schoen & Mitchell, 2010).
If blood flow is not restored to the affected artery, myocardial cells within the subendocardial area
begin to reveal signs of injury within 20 to 40 minutes. If blood flow is quickly restored, the area at risk
can potentially be salvaged; aerobic metabolism resumes, cellular repair begins, and myocardial contrac-
tility is restored.
Death of myocardial cells occurs when the area at risk has been deprived of blood flow for an extended
interval, usually 2 to 4 hours or longer, depending on factors such as the presence of collateral circulation
to the ischemic area, persistent or intermittent coronary vessel blockage, the metabolic/oxygen needs of
the myocardium at risk, and the sensitivity of the myocardial cells to ischemia (Schoen & Mitchell, 2010;
Thygesen, et al., 2012). Without clinical intervention (ie, reperfusion therapy), the infarction can expand
to involve the entire thickness of the myocardial wall. Because time is muscle when caring for patients
with an ACS, the benefits of reperfusion therapy are greatest when it is performed early.
Subendocardial
infarction
Endocardium
Transmural
infarction
Epicardium
Intramural
infarction
Subepicardial
infarction
Fig. 7.6 Possible locations of infarctions in the ventricular wall. (From Urden LD, Stacy KM, Lough ME: Critical care nursing:
diagnosis and management, ed 6, St. Louis, 2010, Mosby.)
Aorta
Pulmonary
artery
Left circumflex coronary

artery
Right
coronary Left anterior descending
artery coronary artery
Acute coronary
arterial occlusion
Zone of perfusion
(area at risk)
Completed infarct
Cross-section involving nearly the
of myocardium entire area at risk
Obstructed
coronary
artery
Endocardium
Zone of perfusion Zone of Zone of

(area at risk) necrosis necrosis
0 hr 2 hr 24 hr
Fig. 7.7 Progression of myocardial necrosis after coronary artery occlusion. A transmural segment of myocardium that is
dependent on the occluded vessel for perfusion constitutes the area at risk (outlined). Necrosis begins in the subendocardial
region in the center of the ischemic zone and with time expands to involve the entire wall thickness. Note that a very narrow
zone of myocardium immediately beneath the endocardium is spared from necrosis because it can be oxygenated by diffusion
from the ventricle. (From Kumar V, Abbas AK, Aster JC: Robbins basic pathology, ed 9, Philadelphia, 2013, Saunders.)
PATIENT EVALUATION
[Objective 4]
Because not all chest discomfort is cardiac-related, patients with suspected ACS must be evaluated rap-
idly to identify those with an emergent condition versus those with a less urgent condition. The answers
to two questions must be sought during the initial patient evaluation: (1) What is the likelihood that the
patient’s signs and symptoms represent an ACS, and (2) What is the likelihood of an adverse clinical
outcome? (Amsterdam, et al., 2014) Several risk assessment scores and clinical algorithms have been
developed that encompass the patient’s history, physical examination, ECG, and cardiac biomarkers
to help identify patients with ACS who are at increased risk of adverse outcomes and to help guide clin-
ical decision making (Amsterdam, et al., 2014).
Patient History
Obtaining an accurate history is important to help determine whether a patient’s signs and symptoms are
most likely related to ischemia as a result of CAD. It is important to ask targeted questions to determine
the patient’s probability of an ACS and to not delay reperfusion therapy, if indicated.
ACLS Pearl
When obtaining the patient’s history, use the patient’s words for the discomfort. For example, the
patient may not consider his or her symptom “discomfort” or “pain” but instead have another appro-
priately descriptive term to describe his or her symptom. Whatever term the patient uses, continue to
use that term when interacting with the patient.
SAMPLE History
• Signs and Symptoms. Ask the patient what prompted him or her to seek medical assistance.
• Allergies. Ask the patient about allergies to medications, food, environmental elements (eg, pollen),
and products (eg, latex).
• Medications. Ask the patient about the prescription and over-the-counter medications he or she
is currently taking. Find out if the patient has taken any medication for erectile dysfunction in
the past 24 to 48 hours. Ask about the use of any herbal supplements or recreational drugs, such
as cocaine.
• Past medical history. Ask if the patient has a history of a heart attack, angina, heart failure, high blood
pressure, or abnormal heart rhythm. If the patient answers yes to this question, ask how the current
symptoms compare with the previous episode. Ask if the patient has ever had a heart-related medical
procedure such as a bypass (ie, open-heart surgery), cardiac catheterization, angioplasty, transplant,
valve replacement, or pacemaker implantation. Determine whether the patient has a history of stroke;
diabetes; lung, liver, or kidney disease; or other medical condition. Find out the patient’s risk factors
for heart disease. Ask the patient if he or she smokes. If the answer is yes, ask how many packs per day.
Ask the patient if a history of heart disease is in the family. If the answer is yes, ask whether anyone
died of heart disease and at what age. Ask about a family history of high blood pressure, diabetes, and
high cholesterol. Also, ask about any recent hospitalizations and any recent surgeries.
• Last oral intake. Ask the patient when he or she last had anything to eat or drink and if any recent
changes in eating patterns or fluid intake (or output) have occurred.
• Events leading to the incident. Try to find out what precipitated the patient’s current symptoms. For
example, did an event or activity cause the patient’s symptoms, such as strenuous exercise, sexual activ-
ity, or unusual stress?
OPQRST History
The OPQRST mnemonic is used to explore the characteristics of the patient’s symptoms.
• Onset. When did your symptoms begin? Did they begin suddenly or gradually? Have you ever had this
discomfort before? When? How long did it last? Were you seen, evaluated, or treated for it? If so, what
was the diagnosis? How does the discomfort you are feeling right now compare with that?
• Provocation/Palliation/ Position. What were you doing when your symptoms started? What makes the
discomfort better or worse? What have you tried to relieve the problem? Does a change in position
lessen the discomfort?
• Quality. What does your discomfort feel like?
• Region/Radiation/Referral. Where is your discomfort? Does it stay in one area? Do you have symptoms
in a different area of your body?
• Severity. On a scale of 0 to 10, with 0 being the least and 10 being the worst, what number would you
assign your discomfort?
• Timing. Is your discomfort still present? Is it getting better, worse, or staying about the same? Does it
come and go or is it constant?
Atypical Presentation
[Objectives 5, 6]
Not all patients experiencing an ACS present similarly. Although chest pain is a common symptom of an
ACS, in a study of nearly 435,000 patients who were ultimately diagnosed with acute MI, 33% did not
have chest pain on presentation (Canto, et al., 2000). Anginal equivalent symptoms are symptoms other
than chest pain or discomfort resulting from myocardial ischemia that may occur either alone or in com-
bination in a patient with IHD (Box 7.3). Being mindful of anginal equivalents is essential to recognizing
atypical presentations of ACS. Atypical presentation refers to the uncharacteristic signs and symptoms
that are experienced by some patients.
The American College of Cardiology (ACC) and American Heart Association (AHA) guidelines list
the following as pain descriptions uncharacteristic of myocardial ischemia (Amsterdam, et al., 2014):
• Pleuritic pain (ie, sharp or knife-like pain provoked by breathing or coughing)
• Primary or sole location of the discomfort in the middle or lower abdominal region
• Pain that may be localized by the tip of one finger, particularly over the left ventricular apex or
costochondral junction
• Pain reproduced with movement or palpation of the chest wall or arms
BOX 7.3 Examples of Anginal Equivalent Symptoms

• Difficulty breathing • Indigestion
• Dizziness • Isolated arm, back, jaw, or neck discomfort
• Dysrhythmias • New dyspnea on exertion
• Epigastric pain or burning • Palpitations
• Excessive sweating • Syncope or near-syncope
• Fatigue • Unexplained nausea or vomiting
• Generalized weakness
• Brief episodes of pain that last a few seconds or less

• Pain that is of maximal intensity at onset
• Pain that radiates into the lower extremities
Although typical characteristics increase the probability of CAD, features that are not characteristic of
ischemic chest pain do not exclude the possibility of ACS (Amsterdam, et al., 2014).
Patients who are experiencing an ACS and who are most likely to present atypically include older
adults, diabetic individuals, women, patients with impaired renal function, patients with dementia,
patients with prior cardiac surgery, and patients during the immediate postoperative period after non-
cardiac surgery (Amsterdam, et al., 2014; Karve, et al., 2007).
Older adults may have atypical symptoms such as dyspnea, shoulder or back pain, weakness, fatigue, a
change in mental status, syncope, unexplained nausea, and abdominal or epigastric discomfort. They are
also more likely than a younger patient to present with more severe preexisting conditions, such as hyper-
tension, heart failure, or a previous acute MI.
Three-quarters of all deaths among patients with diabetes mellitus are related to CAD (O’Gara, et al.,
2013). Diabetic individuals may present atypically because of autonomic dysfunction. Signs and symp-
toms may include a change in mental status, fatigue, nausea or vomiting, dyspnea, generalized weakness,
or lightheadedness.
It is estimated that 30% of patients with STEMI are women (O’Gara, et al., 2013). Although chest
pain or discomfort is the most common symptom of an ACS, it is less common in women than in men
(Woo & Schneider, 2009). When chest discomfort is present, it may be located in the front neck, jaw,
right arm or shoulder, or upper back. Studies reveal that women refer to their chest discomfort differently
from men using descriptors such as “sharp,” “stabbing,” “aching,” or “tightness” (McSweeney, et al.,
2003; Woo & Schneider, 2009). When experiencing an ACS, women may report symptoms that include
shortness of breath, weakness, unusual fatigue, cold sweats, sleep disturbance, loss of appetite, nausea or
vomiting, abdominal discomfort, and dizziness or fainting (McSweeney, et al., 2003).
Physical Examination
[Objective 4]
Although the physical examination for patients who are being evaluated for possible ACS is often nor-
mal, performing a physical examination is important to identify potential precipitating causes of
myocardial ischemia (eg, uncontrolled hypertension, gastrointestinal [GI] bleeding), to assess the hemo-
dynamic effect of the ischemic event, to identify coexisting conditions (eg, pulmonary disease, malignan-
cies) that could influence treatment decisions (Anderson, et al., 2007), and to evaluate the patient for
complications related to ACS (O’Connor, et al., 2015). Because the goals of reperfusion therapy for
STEMI are to give fibrinolytics within 30 minutes of patient arrival or to provide PCI within 90 minutes
of arrival (O’Connor, et al., 2015), the targeted history and focused physical examination must be per-
formed quickly and efficiently. The physical examination should include the following:
• Measurement of vital signs (obtain blood pressure readings in both arms if dissection is suspected)
• Auscultation of breath sounds for crackles (ie, rales)
• Auscultation of cardiac sounds for murmurs, gallops, and friction rubs
• Assessment for jugular venous distention (JVD), peripheral pulse deficits, and the presence of bruits
• Neurologic evaluation
• Identification of contraindications to antiplatelet or fibrinolytic therapy
Electrocardiogram Findings
[Objective 7]
Obtaining and reviewing a 12-lead ECG is important when evaluating a patient presenting with symp-
toms suggestive of ACS. The first 12-lead ECG should be obtained and interpreted within 10 minutes
of patient contact (Amsterdam, et al., 2014). Because it may be normal or initially nondiagnostic, the
ECG should be repeated at 15- to 30-minute intervals during the first hour, especially if symptoms recur
(Amsterdam, et al., 2014).
Indicative changes, which are ECG findings that are seen in leads that look directly at the area fed by
the blocked vessel, are significant when they are seen in two anatomically contiguous leads. Two leads are
contiguous if they look at the same or adjacent areas of the heart or if they are numerically consecutive
chest leads (Fig. 7.8). Reciprocal ECG changes may be seen in leads opposite (ie, about 180 degrees away
from) the leads that show the indicative change.
Hyperacute T Waves
[Objective 7]
Within minutes of an interruption of coronary blood flow, hyperacute T waves may be observed on the
ECG in the leads facing the affected area. The presence of hyperacute T waves has been reported as early
as 30 minutes after the onset of chest pain, and hyperacute T waves usually appear before elevation in
cardiac biomarkers or ST changes on the ECG (Sovari, et al., 2007). Hyperacute T waves are tall, pos-
itive, peaked, and broad-based (Sovari, et al., 2007). Clinically, hyperacute T waves are often not
observed because these ECG changes have typically resolved by the time the patient seeks medical assis-
tance. In addition to acute myocardial ischemia and infarction, possible causes of tall T waves include
hyperkalemia, left ventricular hypertrophy, left BBB, acute pericarditis, acute central nervous system
events (eg, intracranial hemorrhage), and benign early repolarization, among others.
ST Segment Changes
[Objective 7]
As the ACS progresses, changes in the ST segment (eg, elevation, depression) may be evident on the
ECG. Recognizing these ECG changes and communicating these findings is important when caring
for the patient with a suspected ACS.
In a patient who is experiencing an ACS, new horizontal or downsloping STD of 0.5 mm or more is
highly suggestive of myocardial ischemia when it is viewed in two or more anatomically contiguous leads
(Thygesen, et al., 2012). Negative (ie, inverted) T waves may also be present.
Lateral
I, aVL, V5, V6
Inferior
II, III, aVF
Anteroseptal
V1, V2, V3, V4
Fig. 7.8 The surfaces of the heart. The posterior surface is not shown. (From Wesley K: Huszar’s ECG and 12-lead inter-
pretation, ed 5, St. Louis, 2016, Mosby JEMS.)
Evidence of myocardial injury can be seen on the ECG as STE. New or presumed new STE of 1 mm
or more at the J point in all leads other than V2 and V3 in a patient who is experiencing an ACS is sug-
gestive of myocardial injury when observed in two or more anatomically contiguous leads (O’Gara, et al.,
2013). For leads V2 and V3, STE is considered significant if it is elevated 2 mm or more in men older
than 40 years or elevated 1.5 mm or more in women (O’Gara, et al., 2013). Continuous ST segment
monitoring can be helpful for detecting ST segment changes that confirm the diagnosis of an ACS
as well as for detecting silent or unrecognized myocardial ischemia.
ACLS Pearl
A 2007 study evaluated the ability of clinicians in the emergency department, coronary care unit, and
telemetry unit to differentiate ischemic from nonischemic ECG patterns and to detect the affected
ECG leads and the location of ischemia (Stephens, et al., 2007). Only 19% of the clinicians correctly
identified the presence or absence of ischemia on all 12-lead ECG test strips. Of the three ECGs with
an acute MI pattern, none was able to determine the correct leads, location, or amplitude of STE.
These findings emphasize the importance of continuing education and ECG interpretation practice.
QRS Changes
[Objective 7]
In the past, an MI was classified according to its location (eg, anterior, inferior) and whether or not it
produced Q waves on the ECG over several days. A Q wave infarction was generally considered to be
synonymous with transmural infarction and a non–Q wave infarction was referred to as a subendocardial
infarction (Scirica & Morrow, 2015). This terminology has been replaced because a pathologic Q wave
may take hours to develop (and, in some cases, never develop) and because cardiac magnetic resonance
studies indicate that the development of a Q wave on the ECG is determined more by the size of the
infarction than by the depth of mural involvement (Scirica & Morrow, 2015).
Today, the 12-lead ECG is used to differentiate between those patients with STE and those without
STE and guide treatment decisions with regard to reperfusion therapy. If the ST segments are elevated in
two contiguous leads and elevated cardiac biomarkers are present, the diagnosis is STEMI. Most patients
with STEMI will develop ECG evidence of pathologic Q waves (O’Gara, et al., 2013). If STE is not
present but biomarker levels are elevated, the diagnosis is NSTEMI. If the ST segments are not elevated
and cardiac biomarkers are not elevated, the diagnosis is UA (Thygesen, et al., 2012). An MI may be
further classified into five types, depending on the circumstances in which the MI occurs (Table 7.1).
T Wave Inversion
[Objective 7]
In a patient experiencing an ACS, inverted T waves suggest possible myocardial ischemia. T wave inver-
sion may precede ST segment changes, or they may occur at the same time. Inverted T waves associated
with ischemia and infarction are usually narrow and symmetrically inverted (Kurz, et al., 2014). They
may remain inverted for varying periods ranging from days, weeks, or months, or they may remain
permanently (Wagner, et al., 2009).
TABLE 7.1 Classification of Myocardial Infarction

Classification Description
Type 1 Spontaneous MI related to ischemia
Type 2 MI secondary to an ischemic imbalance
Type 3 MI resulting in death when biomarker values are unavailable
Type 4a MI associated with PCI
Type 4b MI associated with stent thrombosis
Type 4c MI associated with restenosis
Type 5 MI associated with coronary artery bypass grafting
Source: Thygesen, et al., 2012.

MI, myocardial infarction; PCI, percutaneous coronary intervention
Anatomic Location of a Myocardial Infarction

[Objective 8]
Anatomic regions of the left ventricle include the septal, anterior, lateral, inferior, and inferobasal (ie,
posterior) surfaces (see Fig. 7.8). The areas of the heart supplied by the three major coronary arteries
are shown in Fig. 7.9.
Leads that view the same surfaces of the heart can be grouped together and analyzed for ECG evi-
dence of myocardial ischemia, injury, or infarction. Because ECG evidence must be found in at least two
contiguous leads, assessing lead groupings for indicative changes is helpful in determining the location of
the area at risk and predicting which coronary artery is affected (Table 7.2). In general, the more proximal
the blockage in the vessel, the larger the infarction and the greater the number of leads showing indicative
changes (Morris & Brady, 2002). It is important to mention that localization of an infarction works rea-
sonably well for STEMI. However, STD and T wave changes that suggest the presence of myocardial
ischemia, as in NSTE-ACS, are less reliable in localizing the culprit vessel because these ECG changes
reflect subendocardial rather than transmural ischemia (Halim, et al., 2010). Factors including the ana-
tomic position and size of the heart, the patient’s unique pattern of coronary artery distribution, the loca-
tion of the occlusion along the length of the coronary artery, the presence of collateral circulation,
RCA LAD LAD

RCA LAD Cx or or or
Cx Cx RCA
1. Four chamber 2. Two chamber 3. Long axis
4. Base 5. Mid 6. Apex

Fig. 7.9 Typical myocardial segments supplied by the right coronary artery (RCA), left anterior descending artery (LAD), and
circumflex (CX) coronary arteries. The coronary anatomy is shown on the left with the corresponding wall segments in standard
echocardiographic views on the right. The arterial distribution varies between patients. Some segments have variable coronary
perfusion as indicated by the hatched regions. (From Lang RM, Bierig M, Devereux RB, et al.: Recommendations for chamber
quantification: A report from the American Society of Echocardiography’s Guidelines and Standards Committee and the Cham-
ber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the
European Society of Cardiology. J Am Soc Echocardiogr 18(12):1440-1463, 2005.)
TABLE 7.2 Relationships among Ventricular Surfaces, Facing Leads, and

Coronary Arteries
Ventricular Surface Indicative Changes (Facing Leads) Affected Coronary Artery
Anterior V3, V4 LAD
Inferior II, III, aVF RCA (most common) or CX
Lateral I, aVL, V5, V6 CX
Septal V1, V2 LAD
Inferobasal (posterior) V7, V8, V9 RCA or CX
Right ventricle V1R to V6R RCA
CX , circumflex; LAD, left anterior descending; RCA , right coronary artery

TABLE 7.3 Contiguous Electrocardiographic Leads

I Lateral aVR --------- V1 Septum V4 Anterior
II Inferior aVL Lateral V2 Septum V5 Lateral
III Inferior aVF Inferior V3 Anterior V6 Lateral
Inter- Y Left
ventricular ventricle
septum
V6
Right X
atrium
V5 Lateral
chest
Right leads
ventricle
V4
V1 V2 V3
Septal Anterior
leads leads
Fig. 7.10 The areas of the heart as seen by the chest leads. Leads V1, V2, and V3 are contiguous. Leads V3, V4, and V5 are
contiguous, as well as V4, V5, and V6. Note that neither the right ventricular wall (X) nor the inferobasal (posterior) surface of the
left ventricle (Y) is well visualized by any of the usual six chest leads. (From Grauer K: A practical guide to ECG interpretation, ed
2, St. Louis, 1998, Mosby.)
previous infarctions, and concomitant drug- and electrolyte-related ECG changes may also affect the
perceived location of an infarction versus its actual location.
When viewing the 12-lead ECG of a patient who is experiencing an ACS, look at each lead for
the presence of ST segment displacement (ie, elevation or depression). If ST segment displacement
is present, note its displacement in mm. Inspect the T waves for any changes in orientation, shape,
and size. Examine each lead for the presence of a Q wave. If a Q wave is present, measure its duration.
The area of the left ventricle viewed by each lead of a standard 12-lead ECG is shown in Table 7.3.
Leads II, III, and aVF are contiguous leads because they view the inferior wall of the left ventricle; thus
they appear the same color in Table 7.3. Leads I, aVL, V5, and V6 are contiguous because they all look at
adjoining tissue in the lateral wall of the left ventricle. Numerically consecutive chest leads are also con-
tiguous leads (Fig. 7.10).
Anterior Infarction
[Objective 8]
The left anterior descending artery (LAD) supplies the anterior wall of the heart by means of its diagonal
branches and the anterior two-thirds of the interventricular septum by means of its septal perforating
branches (Fig. 7.11). Evidence of an anterior infarction can be seen in leads V3 and V4, which face
the anterior wall of the left ventricle. Septal involvement is evidenced by changes in leads V1 and V2
(Fig. 7.12). If an infarction involves the anterior wall and septum, ECG changes will be visible in
V1, V2, V3, and V4, and the descriptive name anteroseptal MI is used (Fig. 7.13).
Because the LAD supplies a large portion of the left ventricle, a blockage in this area can lead to com-
plications such as left ventricular dysfunction, including left-sided heart failure and cardiogenic shock.
Aorta
Left main
occlusion
Proximal
LAD occlusion
Septal artery
Circumflex artery
Obtuse
marginal artery Diagonal artery
Mid-LAD
Left anterior occlusion
descending artery (LAD)
I V1 V4
Lateral aVR Septum Anterior
II aVL V2 V5
Inferior Lateral Septum Lateral
III aVF V3 V6
Inferior Inferior Anterior Lateral
Fig. 7.11 Anterior wall infarction. Occlusion of the midportion of the LAD results in an anterior infarction. Proximal occlusion
of the LAD may become an anteroseptal infarction if the septal branch is involved or an anterolateral infarction if the marginal
branch is involved. If the occlusion occurs proximal to both the septal and diagonal branches, an extensive anterior infarction
will result. (From Phalen T, Aehlert BJ: The 12-lead ECG in acute coronary syndromes, ed 3, St. Louis, 2012, Mosby.)
Aorta
Left main
coronary artery
Right coronary
artery (RCA)
Circumflex
artery
Left anterior
descending
artery (LAD)
I V1 V4
aVR
Lateral Septum Anterior
II aVL V2 V5
III aVF V3 V6
Fig. 7.12 Septal infarction. (From Phalen T, Aehlert BJ: The 12-lead ECG in acute coronary syndromes, ed 3, St. Louis, 2012,
Mosby.)
I aVR V1 V4
aVL V2 V5
II
V3 V6
III aVF
Fig. 7.13 Anteroseptal infarction. (From Phalen T, Aehlert BJ: The 12-lead ECG in acute coronary syndromes, ed 3, St. Louis,
2012, Mosby.)
Aorta
Left main
coronary artery
Right coronary Circumflex
artery (RCA) artery
a Obtuse marginal
b c
Right ventricular Diagonal artery

marginal branch Left anterior
Posterior descending
descending artery artery (LAD)
I V1 V4
aVR
Lateral Septum Anterior
II aVL V2 V5
III aVF V3 V6
Fig. 7.14 Lateral wall infarction. Coronary artery anatomy shows (a) blockage of the circumflex artery, (b) blockage of the
proximal LAD, and (c) blockage of the diagonal artery. (From Phalen T, Aehlert BJ: The 12-lead ECG in acute coronary syn-
dromes, ed 3, St. Louis, 2012, Mosby.)
An anterior MI may cause dysrhythmias including PVCs, atrial flutter, or AFib. A blockage in the area of
the septum, which contains the bundle branches, may result in right or left bundle branch block (BBB),
second-degree AV block type II, and third-degree AV block.
Lateral Infarction
[Objective 8]
Lateral wall infarctions often occur as extensions of anterior or inferior infarctions because the lateral wall
of the left ventricle may be supplied by the circumflex (CX) artery, the LAD, or a branch of the right
coronary artery (RCA) (Fig. 7.14). Because the lateral wall of the left ventricle is viewed by a combination
of chest (V5 and V6) and limb (I and aVL) leads, evidence of a lateral wall infarction may be seen in some
or all of the following leads: I, aVL, V5, and V6. An example of an infarction involving the lateral wall is
shown in Fig. 7.15.
Inferior Infarction
[Objective 8]
The inferior wall of the left ventricle is perfused by the RCA in most individuals (Fig. 7.16); however, in
some patients the CX artery supplies the inferior wall through the posterior descending artery (Fig. 7.17).
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 7.15 Lateral wall infarction. Lead I shows a small Q wave with STE. A larger Q wave with STE can be seen in lead aVL.
This patient had an anterior NSTEMI 4 days earlier with STE and T wave inversion in leads V2 through V6. A coronary arte-
riogram at that time showed a blocked LAD distal to its first large septal perforator. The STE evolved and the T waves in all of
the chest leads had become upright the day before this tracing was recorded. The patient then had another episode of chest
pain associated with the appearance of signs of acute lateral infarction as shown in this tracing. A repeat coronary arteriogram
showed new blockage of the obtuse marginal branch of the circumflex artery. (From Surawicz B, Knilans TK: Chou's elec-
trocardiography in clinical practice: adult and pediatric, ed 5, Philadelphia, 2001, Saunders.)
Examine limb leads II, III, and aVF for ECG evidence of an ACS involving the inferior wall. STE in
lead V1 in the presence of an inferior STEMI (with elevation greater in lead III than in lead II) suggests
SA RVI (Kurz, et al., 2014).
Parasympathetic nervous system hyperactivity is common with inferior wall MIs, resulting in brady-
dysrhythmias, hypotension, or both (Scirica & Morrow, 2015). Conduction delays such as first-degree
AV block and second-degree AV block type I are common and usually transient. An example of an
infarction involving the inferior wall is shown in Fig. 7.18.
Aorta
Left main
coronary artery
Dominant right
coronary artery (RCA) Septal artery
a Circumflex artery
b Obtuse
marginal artery
Right ventricular
marginal branch Diagonal artery
Posterior Left anterior

descending artery descending
artery (LAD)
Posterolateral branch
of the circumflex artery
Fig. 7.16 Inferior wall infarction. Coronary anatomy shows a dominant RCA. A blockage at point a results in an inferior
infarction and RVI. A blockage at point b involves only the inferior wall, sparing the right ventricle. (From Phalen T, Aehlert
BJ: The 12-lead ECG in acute coronary syndromes, ed 3, St. Louis, 2012, Mosby.)
Aorta
Left main
coronary artery
Nondominant
right coronary Dominant
artery (RCA) circumflex artery I V1 V4
Lateral aVR Septum Anterior
b Obtuse marginal
artery II aVL V2 V5
a Inferior Lateral Septum Lateral
Diagonal artery
Right ventricular III aVF V3 V6
marginal branch Inferior Inferior Anterior Lateral
Left anterior
descending
Posterior artery (LAD)
descending artery
Fig. 7.17 Inferior wall infarction. Coronary anatomy shows a dominant CX artery. A blockage at point a results in an inferior
infarction. A blockage at b may result in a lateral and inferobasal infarction. (From Phalen T, Aehlert BJ: The 12-lead ECG in
acute coronary syndromes, ed 3, St. Louis, 2012, Mosby.)
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 7.18 STE in leads II, III, and aVF suggests an inferior wall injury pattern. Reciprocal STD is seen in leads I and aVL. (From
Johnson R, Schwartz M: A simplified approach to electrocardiography, Philadelphia, 1986, Saunders.)
Inferobasal Infarction
[Objective 8]
Posterior wall MIs reportedly occur in 15% to 20% of acute MIs (Lawner, et al., 2012). Current expert
opinion recommends that the term inferobasal wall be used instead of posterior wall (Thygesen, et al.,
2012). The inferobasal wall of the left ventricle is supplied by the CX coronary artery in most patients;
however, in some patients it is supplied by the RCA (Fig. 7.19). Although isolated inferobasal infarctions
do occur, an inferobasal infarction more commonly occurs with lateral wall or inferior wall infarctions. If
the inferobasal wall is supplied by the RCA, complications may include dysrhythmias that involve the SA
node, the AV node, and the bundle of His.
Because no leads of a standard 12-lead ECG directly view the inferobasal wall of the left ventricle,
posterior chest leads V7, V8, and V9 should be used to detect evidence of an inferobasal infarction. Indic-
ative changes of an inferobasal infarction include ST elevation in these leads. In a small study published in
2012, a 15-lead ECG (adding leads V4R, V8, and V9 to the standard 12 leads) was obtained for patients
presenting with STEMI. Forty percent of patients with inferior or lateral MI had an associated right or
posterior infarction that was not directly detected by a standard 12-lead ECG (Pickham & Sickler,
2012). Placement of additional posterior chest leads in the right midscapular line (V10), right paraspinal
line (V11), and left scapular line (V12) has been suggested and may increase the likelihood of identifying
an inferobasal infarction (Vasaiwala & Schreiber, 2008). An example of an inferobasal infarction is
shown in Fig. 7.20.
Aorta
Left coronary
artery
Circumflex
artery
Obtuse Posterior
marginal artery descending
artery
Left anterior
descending Right coronary
A branch artery
Aorta
Left coronary
artery
Circumflex
artery I V1 V4 V7
Posterior aVR
Lateral Septum Anterior Posterior
Obtuse descending
marginal artery artery II aVL V2 V5 V8
Inferior Lateral Septum Lateral Posterior
Left anterior
descending III aVF V3 V6 V9
branch Right Inferior Inferior Anterior Lateral Posterior
coronary
B artery
Fig. 7.19 Inferobasal (posterior) infarction. A, Coronary anatomy shows a dominant RCA. Blockage of the RCA commonly
results in an inferior and inferobasal infarction. B, Coronary anatomy shows a dominant CX artery. Blockage of a marginal
branch is the cause of most isolated inferobasal infarctions. (From Phalen T, Aehlert BJ: The 12-lead ECG in acute coronary
syndromes, ed 3, St. Louis, 2012, Mosby.)
I aVR V1 V4
RV4
V5
II aVL V1
V8
III aVF V1 V6
V9
Fig. 7.20 Fifteen-lead ECG with inferior, lateral, posterior, and right ventricular acute myocardial infarction (AMI). The stan-
dard 12-lead ECG reveals the typical STE in the inferior and lateral leads as well as STD with prominent R wave in the right
precordial leads. Posterior AMI is indicated by both the right precordial STD with a prominent R wave and the STE in posterior
leads V8 and V9. Note that the degree of STE is less pronounced than that seen in the inferior leads because of a relatively
longer distance from the posterior epicardium to surface leads. The RVI is noted in this case, using the simplified approach with
only RV4, which demonstrates STE of relatively small magnitude. (From Marx JA, Hockberger RS, Walls RM: Rosen’s emer-
gency medicine—concepts and clinical practice, ed 8, Philadelphia, 2014, Saunders.)
ACLS Pearl
If a patient presents with a possible ACS and the only ST segment change seen on a standard
12-lead ECG is depression (particularly in leads V1 through V4), strongly consider obtaining posterior
chest leads V7 through V9 to assess for a possible inferobasal (ie, posterior) infarction.
Right Ventricular Infarction

[Objective 9]
When a RVI occurs, it is most often the result of an occlusion of the RCA (Fig. 7.21). However, the CX
artery supplies a significant proportion of the right ventricle in about 10% of patients (Hutchinson &
Rudakewich, 2009).
Because about one-third of patients with inferior STEMI have RVI, all patients with inferior STEMI
should be evaluated for evidence of RVI (O’Gara, et al., 2013). The most sensitive ECG signs of right
ventricular injury include 1 mm ST elevation in lead V1 and in lead V4R (O’Gara, et al., 2013). Leads V2
and V3 may also show ST elevation in some patients. Some researchers have found that the sensitivity of
V4R in detecting RVI is greater when measured 0.06 second after the J point than when measured at the J
point (Seo, et al., 2011). The finding of ST elevation in V4R is often temporary, lasting only 24 to
48 hours and normalizing in half of cases within 10 hours (Hutchinson & Rudakewich, 2009). An exam-
ple of an infarction involving the right ventricle is shown in Fig. 7.22.
It has been estimated that only 25% of patients with RVI develop clinically evident hemodynamic
manifestations (Goldstein, 2012). Patients may present with, or subsequently develop, hypotension
caused by bradydysrhythmias or caused by a reduction in preload after the administration of vasodilators
such as NTG (Goldstein, 2012). Complications associated with RVI include bradydysrhythmias, AV
blocks, ventricular dysrhythmias, hypotension, right ventricular rupture, right ventricular papillary mus-
cle rupture, and right ventricular thrombi (Hutchinson & Rudakewich, 2009). Right BBB, observed in
up to 48% of cases of RVI, is associated with a poor prognosis (Hutchinson & Rudakewich, 2009).
Lead aVR
Lead aVR has been called “the forgotten lead” because many clinicians believe that lead aVR reflects
reciprocal changes from leads aVL, II, V5, and V6 (Gorgels, et al., 2001). However, research has shown
Aorta
Left main
coronary artery
Right coronary
artery (RCA)
Circumflex
a artery
b
Right ventricular
marginal branch Left anterior
descending
Posterior artery (LAD)
descending artery
Posterolateral branch
of the circumflex artery
I V1 V4 V4R
aVR
Lateral Septum Anterior Rt ventricle
II aVL V2 V5 V5R
Inferior Lateral Septum Lateral Rt ventricle
III aVF V3 V6 V6R
Inferior Inferior Anterior Lateral Rt ventricle
Fig. 7.21 RVI. At a, blockage of the RCA proximal to the right ventricular marginal branch results in an inferior infarction and
RVI. At b, blockage of the right ventricular marginal branch results in an isolated RVI. (From Phalen T, Aehlert BJ: The 12-lead
ECG in acute coronary syndromes, ed 3, St. Louis, 2012, Mosby.)
Right-sided leads
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
V1
II
V5
Fig. 7.22 The right-sided chest leads in a patient with acute inferior STEMI show STE in leads V4R and V5R, consistent with
concomitant RVI. (From Adams JG, Emergency medicine, ed 2, Philadelphia, 2013, Saunders.)
value in the use of lead aVR in evaluating CAD and clinical situations including pericarditis, pulmonary
embolism, tricyclic antidepressant toxicity, tension pneumothorax, stress-induced cardiomyopathy, and
as a means of differentiating atrial tachydysrhythmias (Vorobiof & Ellestad, 2011). Lead aVR has also
been used to differentiate between left main coronary artery (LMCA) disease and disease of the proximal
LAD. STE in lead aVR that is greater than or equal to that in V1 suggests LMCA disease; conversely,
STE that is greater in V1 than in aVR suggests disease of the proximal LAD (Yamaji, et al., 2001).
Cardiac Biomarkers
Injured myocardial cells release enzymes and proteins that pass through broken cell membranes and leak
into the bloodstream. Examples include myoglobin, cardiac troponins T (TnT) and I (TnI), creatine
kinase (CK) and its myocardial band (MB) isoform, and lactate dehydrogenase, among others
(Halim, et al., 2010). The presence of these substances in the blood, which are called cardiac biomarkers,
serum cardiac markers, or serum biomarkers, can subsequently be measured by means of blood tests to verify
the presence of an infarction. Cardiac biomarkers are useful for confirming the diagnosis of MI for
patients with STEMI. They are also useful for confirming the diagnosis of MI when patients present
without STE on their ECG, when the diagnosis may be unclear, and to distinguish patients with
UA from those with NSTEMI.
Cardiac troponins (ie, TnI and TnT) are components of the contractile apparatus of myocardial cells
and are the biomarkers of choice for diagnosing MI because of their increased specificity and sensitivity
compared with CK-MB (Amsterdam, et al., 2014; O’Connor, et al., 2015; Thygesen, et al., 2012).
Because the ranges of normal biomarker levels vary among laboratories, current clinical practice guide-
lines define an increased cardiac troponin concentration as a value that exceeds the 99th percentile com-
pared with a normal reference population (Amsterdam, et al., 2014).
Current resuscitation guidelines recommend against using high-sensitivity TnT and TnI alone mea-
sured at 0 and 2 hours (without performing clinical risk stratification) to identify patients at low risk for
ACS (O’Connor, et al., 2015). High-sensitivity TnI measurements that are less than the 99th percentile,
measured at 0 and 2 hours, may be used together with low-risk stratification (Thrombolysis in MI
[TIMI] score of 0 or 1, or low risk per Vancouver rule) to predict a less than 1% chance of 30-day major
adverse cardiac event (MACE) (O’Connor, et al., 2015). Negative TnI or TnT measurements obtained
at the patient’s initial presentation and again between 3 and 6 hours after symptom onset may be used
together with very low-risk stratification (TIMI score of 0, low-risk score per Vancouver rule, North
American Chest Pain score of 0 and age less than 50 years, or low-risk HEART score) to predict a less
than 1% chance of 30-day MACE (O’Connor, et al., 2015).
Troponin levels remain elevated for several days after myocardial necrosis and may remain elevated for
up to 2 weeks with a large infarction (Amsterdam, et al., 2014). Elevated troponins may also occur after
recent catheter ablation of a dysrhythmia because of direct cardiac trauma. CK-MB may be used to esti-
mate the size of an MI (Amsterdam, et al., 2014) and is the preferred alternative when cardiac troponin
markers are unavailable (Thygesen, et al., 2012).
It is important to recognize that elevated cardiac troponin levels may be present with a number of
conditions other than MI. For example, abnormal elevations have been observed with heart failure,
chronic kidney disease, pulmonary embolism, myocarditis, pericarditis, sepsis, transplant rejection, che-
motherapy, and direct or indirect cardiac trauma (Giugliano, et al., 2015; Ibrahim, et al., 2014).
Imaging Studies
A portable chest radiograph should be obtained for patients with a suspected ACS within 30 minutes of
patient presentation. Two-dimensional transthoracic echocardiography is useful for the evaluation of left
and right ventricular function, including the assessment of myocardial thickness, thickening, and motion
at rest. Echocardiography is also helpful for detecting mechanical complications of acute MI including
acute mitral regurgitation, pericardial effusion, myocardial free wall rupture, acute ventricular septal
defect, and intracardiac thrombus formation. Limitations of the two-dimensional echocardiogram
include the inability to distinguish between an acute MI and previous MI (Bolooki & Askari, 2010)
and the inability to distinguish regional wall motion abnormalities caused by myocardial ischemia from
that caused by infarction (Thygesen, et al., 2007).
Other imaging studies such as transesophageal echocardiography, a contrast-enhanced computed
tomography scan of the chest, or magnetic resonance imaging are useful for excluding some of the non-
ischemic causes of acute chest pain, such as valvular heart disease, aortic dissection, and pulmonary
embolism.
INITIAL MANAGEMENT OF ACUTE CORONARY

SYNDROMES
Treatment of the patient with a suspected ACS is time sensitive and it must be done efficiently. Ther-
apeutic interventions are aimed at improving myocardial tissue oxygen supply, reducing myocardial oxy-
gen demand, protecting ischemic myocardium, restoring coronary blood flow, and preventing
reocclusion of the artery (Brown, 2013).
Prehospital Management
When arriving on the scene of a patient who is complaining of chest discomfort or an anginal equivalent,
quickly perform a primary survey and stabilize the patient’s airway, breathing, and circulation (ABCs) as
necessary. Allow the patient to assume a position of comfort. Assess vital signs and oxygen saturation.
Supplemental oxygen is warranted if the patient is having difficulty breathing, has obvious signs of heart
failure, or if he or she is hypoxemic (ie, oxygen saturation less than 90%) (Amsterdam, et al., 2014;
O’Connor, et al., 2015; O’Gara, et al., 2013). Titrate oxygen therapy to maintain an oxygen saturation
of 94% or greater (O’Connor, et al., 2015). Because the usefulness of supplemental oxygen therapy has
not been established in patients with normal oxygen saturation, the withholding of supplemental oxygen
may be considered for normoxic patients with known or suspected ACS in the prehospital, emergency
department, and hospital settings (O’Connor, et al., 2015).
ACLS Pearl
Results of the Air Versus Oxygen in ST-Elevation Myocardial Infarction (AVOID) trial, which were pub-
lished after the systematic review by the International Liaison Committee on Resuscitation (ILCOR),
found that supplemental oxygen therapy in patients with STEMI but without hypoxia may increase
early myocardial injury and was associated with larger myocardial infarct size assessed at 6 months
(Stub, et al., 2015).
Obtain a focused history, including the time of symptom onset. Assess and document the degree of
the patient’s pain or discomfort using a 0-to-10 scale. Give aspirin if no contraindications are present.
Establish cardiac monitoring and obtain a diagnostic-quality 12-lead ECG as soon as possible
(O’Connor, et al., 2015). Perform a secondary survey during transport as dictated by the patient’s
condition.
STEMI alert programs have been implemented in many emergency medical services (EMS) systems
and hospitals across the country in an attempt to minimize total ischemic time, which is defined as the time
from onset of symptoms of STEMI to successful reperfusion (O’Gara, et al., 2013).
If the prehospital 12-lead ECG clearly shows evidence of STEMI, alert the receiving hospital and
begin completing a reperfusion checklist. Establish intravenous (IV) lines in transit and give medications
for pain control per local or system protocol. Experts encourage the development of local protocols that
allow preregistration and direct transport to the catheterization laboratory of a PCI-capable hospital
(bypassing the emergency department) for patients who do not require emergent stabilization upon
arrival (O’Gara, et al., 2013). Although prehospital fibrinolytic therapy is not used in most U.S. com-
munities, multiple studies have demonstrated its safety (O’Gara, et al., 2013). In communities where
prehospital fibrinolysis is part of a STEMI system of care, current guidelines state that prehospital fibri-
nolysis is reasonable when transport time is more than 30 minutes and in-hospital fibrinolysis is the alter-
native treatment strategy (O’Connor, et al., 2015). In communities where prehospital fibrinolysis is
available and transport directly to a PCI-capable hospital is available, transport directly to the PCI facility
may be preferred because the incidence of intracranial hemorrhage, although relatively rare, is greater
with fibrinolysis (O’Connor, et al., 2015).
Emergency Department Management

Although patients experiencing ischemic chest pain symptoms may arrive in the emergency department
by ambulance, many arrive by means of private vehicle. Patients who arrive by private vehicle should be
triaged immediately.
Quickly assess the patient’s ABCs, and ensure that the patient has a secure airway and adequate
breathing. Frequent assessment of the patient’s mental status, vital signs, and oxygen saturation level
is important and continuous ECG monitoring is essential during the prehospital, emergency depart-
ment, and early hospital phases of care. Administer supplemental oxygen if indicated. If not already done,
give aspirin if no contraindications are present and establish IV access. While completing a reperfusion
checklist, obtain a chest radiograph within 30 minutes and draw initial laboratory tests including cardiac
biomarkers, electrolytes, and coagulation studies.
Obtain a targeted history and physical examination. This can be done at the same time as other pro-
cedures. Assess and document the character of the patient’s chest discomfort, the presence of risk factors
for CAD, and the presence of associated signs and symptoms. Consider the possibility of other condi-
tions that mimic acute MI such as aortic dissection, acute pericarditis, acute myocarditis, and pulmonary
embolism. Continually reassess the degree of the patient’s pain or discomfort using a 0-to-10 scale, and
reassess the patient’s response to medications given. Risk assessment tools should be used to determine
the patient’s risk of death and ischemia in STEMI and NSTE-ACS (Kurz, et al., 2014).
An initial 12-lead ECG should be obtained and interpreted within 10 minutes of patient contact
(Amsterdam, et al., 2014). Obtain a repeat 12-lead ECG with each set of vital signs, when the patient’s
symptoms change, and as often as necessary. After the 12-lead has been obtained, it should be reviewed
carefully for ECG evidence of an ACS. Patients experiencing a STEMI are considered the most emer-
gent, followed by those with NSTE-ACS, and then persons experiencing chest pain of probable cardiac
origin. On the basis of the 12-lead ECG findings, categorize the patient into one of the three following
groups:
1. STE. Patients with ST elevation in two or more contiguous leads are classified as having a STEMI
and should be evaluated for immediate reperfusion therapy by means of pharmacologic reperfusion
(ie, fibrinolytics) or mechanical perfusion (ie, PCI) (discussed later in this chapter). The goals of
reperfusion are to administer fibrinolytics within 30 minutes of arrival or to provide PCI within
90 minutes of arrival (O’Connor, et al., 2015). Patients with obvious STE in leads II, III, and/or
aVF should also be evaluated for a possible RVI.
2. STD. ST depression or transient ST segment/T wave changes that occur with chest pain or discom-
fort suggest myocardial ischemia. Patients with obvious STD in leads V1 and V2 should be evaluated
for possible inferobasal MI. Patients presenting with NSTE-ACS, including those with recurrent
symptoms, ischemic ECG changes, or positive cardiac troponins should be admitted to a monitored
bed for further evaluation (Amsterdam, et al., 2014). Stabilized patients with NSTE-ACS should be
admitted to an intermediate (or step-down) care unit (Amsterdam, et al., 2014). Patients with con-
tinuing angina, hemodynamic instability, uncontrolled dysrhythmias, or a large MI should be admit-
ted to a coronary care unit (Amsterdam, et al., 2014). Treatment options for NSTE-ACS are based
on risk stratification and include antianginal, antiplatelet, and anticoagulant therapy (O’Connor,
et al., 2015). Because the presence of depressed left ventricular function can influence pharmacologic
therapies and can influence revascularization choices (ie, PCI versus coronary artery bypass graft sur-
gery), assessment of left ventricular function is recommended (Amsterdam, et al., 2014).
3. Normal or nondiagnostic ECG. A normal ECG or nonspecific ST- and T wave changes are nondiag-
nostic and should prompt consideration for further evaluation. Consider admission of the patient with
signs and symptoms suggesting an ACS and a nondiagnostic ECG to the emergency department
chest pain unit or to an appropriate bed (O’Connor, et al., 2015). Obtaining serial ECGs at 5- to
10-minute intervals or continuous monitoring of the ST segment should be performed to detect
the potential development of ST elevation if the initial ECG is not diagnostic of STEMI but the
patient remains symptomatic and there is a high clinical suspicion of STEMI. Noninvasive tests
(eg, computed tomography angiography, cardiac magnetic resonance, myocardial scintigraphy, stress
echocardiography) can be useful in identifying patients suitable for discharge from the emergency
department (O’Connor, et al., 2015). The ACSs algorithm appears in Fig. 7.23.
Pharmacologic Therapies
[Objective 10]
Relief of cardiac-related discomfort is a priority for the management of a patient who is experiencing an
ACS and often requires a combination of oxygen, NTG, and opioid analgesics. The relief of pain
decreases anxiety, myocardial oxygen demand, and the risk of dysrhythmias.
Nitroglycerin
NTG dilates the capacitance vessels (ie, veins), which causes a reduction in ventricular filling and cardiac
preload. NTG also dilates normal and atherosclerotic epicardial coronary arteries and increases coronary
collateral flow (Amsterdam, et al., 2014).
Before giving NTG, assess the degree of the patient’s pain or discomfort with the use of a 0-to-10
scale. Also record the pain’s duration, time of onset, the activity that was being performed, and the pain
quality. Reassess and document the patient’s vital signs and level of discomfort after each dose. Common
adverse effects of NTG administration include headache, flushing, tachycardia, dizziness, and orthostatic
hypotension. Hypotension usually responds to supine positioning and the administration of IV fluids.
Make sure that the patient has not used a phosphodiesterase inhibitor such as sildenafil (eg, Viagra)
within 24 hours or tadalafil (eg, Cialis) within 48 hours before NTG administration (Table 7.4). The
combination of a phosphodiesterase inhibitor and nitrates may result in severe hypotension. NTG should
be avoided in inferior wall MI with a possible associated RVI. Consider the presence of RVI if the patient
with an inferior wall MI becomes hypotensive after nitrate administration.
Analgesic Therapy
Morphine sulfate is a potent narcotic analgesic and anxiolytic (Table 7.5). It causes venodilation, and it
can lower heart rate (through increased vagal tone) and systolic blood pressure, thereby reducing myo-
cardial oxygen demand. The adverse effects of morphine administration include nausea and vomiting,
bradycardia, and respiratory depression. Hypotension may occur, particularly among patients who are
volume depleted or who have received vasodilators. Some studies have demonstrated increased adverse
events associated with the use of morphine sulfate in patients with ACS and acute decompensated heart
failure (Amsterdam, et al., 2014). Supine positioning or IV boluses of normal saline are used to restore
blood pressure. Respiratory depression or excessive morphine-related bradycardia may require adminis-
tration of a narcotic antagonist (eg, naloxone). Other narcotics may be considered for patients who are
allergic to morphine.
Before giving morphine, assess the degree of the patient’s pain or discomfort with the use of a 0-to-10
scale. Also determine the duration, the time of onset, the activity being performed, and the pain quality.
Reassess and document the patient’s vital signs and level of discomfort after each morphine dose.
Fig. 7.23 American Heart Association acute coronary syndromes algorithm. (Reprinted with permission. 2015 American
Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care—Part 9: Acute Coronary
Syndromes. ECCguidelines.heart.org. © 2015 American Heart Association, Inc.)
Because of the increased risk of MACEs (eg, reinfarction, hypertension, heart failure, myocardial rup-
ture) associated with the use of nonsteroidal antiinflammatory drugs (NSAIDs), these drugs (except for
aspirin) should not be initiated in the acute phase of care and should be discontinued in patients using
them before hospitalization (Amsterdam, et al., 2014; O’Connor, et al., 2015; O’Gara, et al., 2013).
Many health care professionals are using fentanyl (ie, Sublimaze) for pain relief as well as vasodilation
in place of morphine in patients experiencing an ACS. Fentanyl is a lipid-soluble synthetic opioid that
has minimal cardiovascular effects, as well as a more rapid onset and shorter duration of action than mor-
phine. The adverse effects of fentanyl are similar to those of morphine.
TABLE 7.4 Nitroglycerin

NSTE-ACS STEMI
Sublingual Class I recommendation: Patients with ongoing ischemic discomfort
Indications (Amsterdam, et al., 2014) should receive sublingual NTG (0.4 mg)
and Dosage Sublingual NTG may be given at 5-min every 5 min up to three doses as BP
intervals to a maximum of three doses. allows (O’Gara, et al., 2013).
IV Indications Class I recommendation: May be useful to treat patients with STEMI
(Amsterdam, et al., 2014) and hypertension or HF (O’Gara, et al.,
IV NTG is indicated for patients with NSTE-ACS 2013)
for treatment of persistent ischemia, HF, or
hypertension.
Notes Nitrates should not be administered to patients with a systolic BP less than 90 mm Hg or
30 mm Hg or more below baseline, marked bradycardia or tachycardia, phosphodiesterase
inhibitor use within the previous 24 to 48 hours, or suspected RVI (O’Gara, et al., 2013).
BP, blood pressure; HF, heart failure; IV, intravenous; mm Hg, millimeters of mercury; NSTE-ACS, non–ST elevation acute
coronary syndrome; NTG, nitroglycerin; RVI, right ventricular infarction; STEMI, ST elevation myocardial infarction
TABLE 7.5 Morphine Sulfate

NSTE-ACS STEMI
Indications Class IIb recommendation: Morphine sulfate (4 to 8 mg IV initially [use
and Morphine sulfate (1 to 5 mg IV) may be lower doses in the elderly] with increments
Dosage reasonable for patients with NSTE-ACS if of 2 to 8 mg IV repeated at 5- to 15-min
there is continued ischemic chest pain intervals if needed) is the analgesic of
despite maximally tolerated antiischemic choice for patients with STEMI, especially
therapy (Amsterdam, et al., 2014). Repeat those whose course is complicated by
every 5 to 30 min as needed to relieve acute pulmonary edema (O’Gara, et al.,
symptoms and maintain patient comfort. 2013).
Notes • Ensure that a narcotic antagonist and airway equipment is readily available before
administration.
• Factors such as patient age, body size, BP, and heart rate influence the dose of morphine
needed to achieve adequate pain control (O’Gara, et al., 2013).
• When indicated, administer naloxone 0.1 to 0.2 mg IV every 15 min to reverse the
narcotic effects of morphine (O’Gara, et al., 2013).
• Excessive morphine-related bradycardia may require the administration of atropine 0.5 to
1.5 mg IV (O’Gara, et al., 2013).
BP, blood pressure; IV, intravenous; NSTE-ACS, non–ST elevation acute coronary syndrome; STEMI, ST elevation myocardial
infarction
Beta-Blockers
The inhibition of beta1-adrenergic receptor sites decreases heart rate and the force of myocardial
contraction, thereby reducing myocardial oxygen demand (Table 7.6). It is essential to closely monitor
the patient’s heart rate, blood pressure, pulmonary status, and ECG rhythm during treatment with a
beta-blocker. Simultaneous IV administration with IV calcium channel blockers (CCBs) (eg, verapamil,
diltiazem) can cause severe hypotension.
Calcium Channel Blockers

Nondihydropyridine CCBs (eg, verapamil, diltiazem) decrease heart rate and myocardial contractility,
slow conduction through the AV node, and have some peripheral arterial dilatory effects (Table 7.7).
Although CCBs may be useful in relieving ischemia or lowering BP in patients who are intolerant of
beta-blockers, randomized controlled trials have demonstrated no beneficial effect on infarct size or
the rate of reinfarction when CCB therapy was initiated during either the acute or convalescent phase
of STEMI (O’Gara, et al., 2013).
TABLE 7.6 Beta-Blockers

NSTE-ACS STEMI
Indications Class I recommendation: (Amsterdam, Class I recommendation:
et al., 2014) (O’Gara, et al., 2013)
• Initiate oral beta-blockers within • Oral beta-blockers should be initiated in the first
the first 24 hours in the absence of 24 hours in patients with STEMI who do not have
HF, low output state, risk for any of the following: signs of HF, evidence of a low
cardiogenic shock, or other. output state, increased risk for cardiogenic shock, or
contraindications to beta blockade other contraindications to use of oral beta-blockers
• Use of sustained-release (PR interval more than 0.24 sec, second- or third-
metoprolol succinate, carvedilol, or degree heart block, active asthma, or reactive
bisoprolol is recommended for airway disease).
beta-blocker therapy with • Beta-blockers should be continued during and after
concomitant NSTE-ACS, stabilized hospitalization for all patients with STEMI and with
HF, and reduced systolic function. no contraindications to their use.
• Reevaluate to determine • Patients with initial contraindications to the use of
subsequent eligibility in patients beta-blockers in the first 24 hours after STEMI
with initial contraindications to should be reevaluated to determine their
beta-blockers. subsequent eligibility.
Class IIa recommendation: Class IIa recommendation:
(Amsterdam, et al., 2014) (O’Gara, et al., 2013)
• It is reasonable to continue beta- • It is reasonable to administer IV beta-blockers at the
blocker therapy in patients with time of presentation to patients with STEMI and no
normal LV function with NSTE-ACS. contraindications to their use who are hypertensive
or have ongoing ischemia.
Notes • Risk factors for cardiogenic shock are age greater than 70 years, systolic BP less than
120 mm Hg, heart rate greater than 110 beats/min, or increased time since onset of STEMI
symptoms (O’Gara, et al., 2013).
• Carefully monitor the patient’s blood pressure, heart rate, and cardiac rhythm after
beta-blocker administration.
BP, blood pressure; HF, heart failure; IV, intravenous; LV, left ventricular; mm Hg, millimeters of mercury; NSTE-ACS, non–ST
elevation acute coronary syndrome; STEMI, ST elevation myocardial infarction
TABLE 7.7 Calcium Channel Blockers

NSTE-ACS STEMI
Indications Class I recommendations (Amsterdam, et al., 2014): May be useful to relieve
• In patients with NSTE-ACS, continuing or frequently recurring ischemia, lower BP, or
ischemia, and a contraindication to beta-blockers, a control the ventricular
nondihydropyridine CCB should be given as initial therapy in the response rate to AFib in
absence of clinically significant LV dysfunction, increased risk patients who are
for cardiogenic shock, PR interval greater than 0.24 sec, or intolerant of beta-
second- or third-degree AV block without a cardiac pacemaker. blockers (O’Gara, et al.,
• Oral nondihydropyridine calcium antagonists are recommended 2013).
in patients with NSTE-ACS who have recurrent ischemia in the
absence of contraindications, after appropriate use of
beta-blockers and nitrates.
• CCBs are recommended for ischemic symptoms when
beta-blockers are not successful, are contraindicated, or cause
unacceptable side effects.
• Long-acting CCBs and nitrates are recommended in patients
with coronary artery spasm.
AFib, atrial fibrillation; AV, atrioventricular; BP, blood pressure; CCB, calcium channel blocker; HF, heart failure; IV, intravenous;
LV, left ventricular; NSTE-ACS, non–ST elevation acute coronary syndrome; STEMI, ST elevation myocardial infarction
TABLE 7.8 Lipid Management

Statin
Therapy NSTE-ACS STEMI
Indications Class I recommendation (Amsterdam, et al., 2014): Class I and Class IIa recommendations
High-intensity statin therapy should be initiated or same as for NSTE-ACS (O’Gara, et al.,
continued in all patients with NSTE-ACS and no 2013)
contraindications to its use
Class IIa recommendation (Amsterdam, et al.,
2014):
It is reasonable to obtain a fasting lipid profile in
patients with NSTE-ACS, preferably within
24 hours of presentation
NSTE-ACS, non–ST elevation acute coronary syndrome; STEMI, ST elevation myocardial infarction
Lipid Management
Several studies have demonstrated that in patients stabilized after an ACS, treatment with statin drugs
lowers the risk of coronary heart disease death, stroke, recurrent MI, and the need for coronary revas-
cularization (Amsterdam, et al., 2014; O’Gara, et al., 2013) (Table 7.8). High-dose atorvastatin (ie,
80 mg daily) has been shown to reduce death and ischemic events among patients with ACS
(O’Gara, et al., 2013).
Renin-Angiotensin-Aldosterone System Inhibitors

Angiotensin-converting enzyme (ACE) inhibitors produce vasodilation by blocking the conversion of
angiotensin I into angiotensin II (Table 7.9). Because angiotensin is a potent vasoconstrictor, limiting
its production decreases peripheral vascular resistance, thereby reducing the pressure that the heart must
pump against and decreasing the myocardial workload. ACE inhibitors also increase renal blood flow,
which helps rid the body of excess sodium and fluid accumulation. ACE inhibitors have been shown to
reduce fatal and nonfatal major cardiovascular events in patients with STEMI (O’Gara, et al., 2013). An
angiotensin receptor blocker (eg, valsartan) may be substituted for patients who are intolerant of ACE
inhibitors (O’Gara, et al., 2013).
Antiplatelet Therapy
Antiplatelet and anticoagulant therapies are important components of ACS patient management because
exposure of a ruptured plaque’s contents triggers activation of the coagulation cascade. Antiplatelet
medications target specific platelet functions at different levels in the pathway of platelet aggregation
(Fig. 7.24, Table 7.10).
Aspirin is an antiplatelet agent that inhibits cyclooxygenase, an enzyme required by platelets to syn-
thesize thromboxane A2. Non–enteric-coated aspirin (162 mg to 325 mg) should be administered to
patients experiencing an ACS as soon as possible after symptom onset, unless contraindicated
(Amsterdam, et al., 2014; O’Gara, et al., 2013). Recommendations with regard to the use of aspirin
in NSTE-ACS and STEMI are shown in Table 7.11.
The thienopyridines (eg, clopidogrel, prasugrel, ticlopidine) are drugs that target P2Y12 receptors,
which are key adenosine diphosphate (ADP) receptors on the platelet surface (Weitz, 2013). By blocking
P2Y12 receptor sites, ADP is inhibited from activating additional platelets. Clopidogrel, prasugrel, and
ticlopidine are irreversible platelet inhibitors that impede platelet function for the life of the platelet. Pra-
sugrel, a newer thienopyridine, has more rapid and consistent platelet inhibition than clopidogrel
(Amsterdam, et al., 2014). Unlike the thienopyridines, ticagrelor binds reversibly to P2Y12 receptors
and has a more rapid and consistent onset of action compared with clopidogrel (Amsterdam, et al.,
2014). ADP inhibitors have a synergistic effect when used with aspirin because they inhibit different
platelet-activating pathways. For patients with suspected STEMI intending to undergo primary PCI
(PPCI), current resuscitation guidelines note that it may be reasonable to begin ADP inhibition in either
the prehospital or in-hospital setting (O’Connor, et al., 2015).
Glycoprotein (GP) IIb/IIIa receptors are the most abundant receptors on the platelet surface (Weitz,
2013). GP IIb/IIIa inhibitors are potent antiplatelet medications that inhibit the final common pathway
of platelet aggregation (Mistry & Vesely, 2012). These agents are used in patients undergoing PCIs,
TABLE 7.9 Renin-Angiotensin-Aldosterone System Inhibitors

Renin-
Angiotensin-
Aldosterone
System Inhibitors NSTE-ACS STEMI
ACE inhibitors Class I recommendation: Class I recommendation:
(eg, lisinopril, (Amsterdam, et al., 2014) (O’Gara, et al., 2013)
captopril, An ACE inhibitor should be started and An ACE inhibitor should be administered
ramipril) continued indefinitely in all patients within the first 24 hours to all patients with
with a LVEF less than 0.40 and in STEMI with anterior location, HF, or LVEF
those with hypertension, diabetes less than or equal to 0.40, unless
mellitus, or stable chronic kidney contraindicated.
disease unless contraindicated. Class IIa recommendation:
(O’Gara, et al., 2013)
ACE inhibitors are reasonable for all patients
with STEMI and no contraindications to
their use.
ARBs (eg, Class I recommendation: Class I recommendation:
valsartan) (Amsterdam, et al., 2014) (O’Gara, et al., 2013)
ARBs are recommended in patients An ARB should be given to patients with
with HF or MI with LVEF less than STEMI who have indications for but are
0.40 who are ACE inhibitor intolerant. intolerant of ACE inhibitors.
Aldosterone Class I recommendation: Class I recommendation:
antagonists (eg, (Amsterdam, et al., 2014) (O’Gara, et al., 2013)
eplerenone) Aldosterone blockade is recommended An aldosterone antagonist should be given to
in patients post–MI without patients with STEMI and no
significant renal dysfunction or contraindications who are already
hyperkalemia who are receiving receiving an ACE inhibitor and beta-blocker
therapeutic doses of an ACE inhibitor and who have a LVEF less than or equal to
and beta-blocker and have a LVEF of 0.40 and either symptomatic HF or
0.40 or less, diabetes mellitus, or HF. diabetes mellitus.
Notes ACE inhibitors may cause a profound drop in BP after the first dose or if used with
diuretics. ACE inhibitors and ARBs should be avoided in patients with hypotension, renal
failure, or hyperkalemia.
ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blockers; BP, blood pressure; HF, heart failure; LVEF, left
ventricular ejection fraction; MI, myocardial infarction; NSTE-ACS, non–ST elevation acute coronary syndrome; STEMI, ST
elevation myocardial infarction
particularly those with STEMI (Weitz, 2013). GP IIb/IIIa inhibitors are administered IV. When the use
of any of these medications is planned, minimize arterial and venous punctures; intramuscular injections;
and the use of urinary catheters, nasotracheal intubation, and nasogastric tubes. When establishing IV
access, avoid noncompressible sites (eg, the subclavian or jugular veins).
Anticoagulant Therapy
Anticoagulants have been a mainstay in the management of patients with ACS, in the prevention of
stroke in patients with AFib, and in the prevention and treatment of venous thromboembolism, among
other conditions (Garg & Halperin, 2013). Older anticoagulants typically require frequent coagulation
monitoring to ensure that a therapeutic response is achieved. For example, warfarin requires coagulation
monitoring because its anticoagulant effects are influenced by dietary vitamin K intake, other medica-
tions, and various disease states (Weitz, 2013). Dabigatran (Pradaxa), rivaroxaban (Xarelto), and apix-
aban (Eliquis) are newer oral anticoagulants that have a wide therapeutic window, fewer drug–drug
interactions, an absence of major dietary effects, and less risk of intracranial bleeding than warfarin. Rou-
tine coagulation monitoring is not required in the majority of patients with these new agents; however,
strict compliance is critical because missing even one dose could result in a period without protection
from thromboembolism (January, et al., 2014). Examples of anticoagulants appear in Table 7.12.
For patients with NSTE-ACS, anticoagulation, in addition to antiplatelet therapy, is recommended
for all patients regardless of whether an invasive or conservative treatment strategy is planned
Plaque disruption
Platelet adhesion
and aggregation
A
Activation of
coagulation
cascade
B
Thrombin
formation
Stable thrombus
Fibrinogen Fibrin
Clot dissolution
Plasminogen Plasmin
C
Degradation
products
Fig. 7.24 Site of action of medications used in the treatment of ACSs. A, Site of action of antiplatelet agents such as aspirin,
thienopyridines, and GP IIb/IIIa inhibitors. B, Heparin bonds with antithrombin III and thrombin to create an inactive complex.
C, Fibrinolytic agents convert plasminogen to plasmin, an enzyme responsible for degradation of fibrin clots. (From Urden LD,
Stacy KM, Lough ME: Critical care nursing: diagnosis and management, ed 6, St. Louis, 2010, Mosby.)
TABLE 7.10 Antiplatelet Medications

Category Action Example(s) Route
Cyclooxygenase inhibitors Inhibit cyclooxygenase, an enzyme Aspirin Oral
required by platelets to synthesize
thromboxane A2
ADP P2Y12 receptor inhibitors Bind to ADP P2Y12 receptors on the platelet Clopidogrel (Plavix) Oral
surface, thereby inhibiting ADP from Prasugrel (Effient)
activating additional platelets Ticagrelor (Brilinta)
Ticlopidine (Ticlid)
GP IIb/IIIa receptor inhibitors Act on the GP IIb/IIIa receptors on the Abciximab (ReoPro) IV
platelet membrane to inhibit platelet Eptifibatide
aggregation and to prevent platelets (Integrilin)
from binding with fibrinogen Tirofiban
(Aggrastat)
ADP, adenosine diphosphate; GP, glycoprotein; IV, intravenous
(Amsterdam, et al., 2014). For patients with STEMI who are undergoing PPCI, Class I anticoagulant
therapy recommendations include the use of unfractionated heparin (UFH) with or without a GP IIb/
IIIa inhibitor, or bivalirudin (O’Gara, et al., 2013). Current resuscitation guidelines recommend that
EMS systems that do not currently administer heparin to suspected STEMI patients do not add this
treatment, whereas those that do administer it may continue their current practice (O’Connor, et al.,
TABLE 7.11 Aspirin

NSTE-ACS STEMI
Indications Class I recommendations: (Amsterdam, et al., 2014) Class I recommendations:
and (O’Gara, et al., 2013)
Dosage • Non–enteric-coated, chewable aspirin (162 mg to • Aspirin 162 to 325 mg should be
325 mg) should be given to all patients with NSTE- given before primary PCI.
ACS without contraindications as soon as possible • After PCI, aspirin should be
after presentation, and a maintenance dose of continued indefinitely.
aspirin (81 mg/d to 162 mg/d) should be continued • A loading dose of a P2Y12 receptor
indefinitely. inhibitor should be given as early
• In patients with NSTE-ACS who are unable to take as possible or at the time of
aspirin because of hypersensitivity or major GI primary PCI to patients with STEMI.
intolerance, a loading dose of clopidogrel followed • P2Y12 inhibitor therapy
by a daily maintenance dose should be (maintenance doses) should be
administered. given for 1 year to patients with
• A P2Y12 inhibitor (either clopidogrel or ticagrelor) in STEMI who receive a stent during
addition to aspirin should be administered for up to primary PCI.
12 months to all patients with NSTE-ACS without
contraindications who are treated with either an
early invasive or ischemia-guided strategy.
GI, gastrointestinal; NSTE-ACS, non–ST elevation acute coronary syndrome; PCI, percutaneous coronary intervention; STEMI,
ST elevation myocardial infarction
TABLE 7.12 Anticoagulants

Anticoagulant Action Route
Apixaban (Eliquis) Factor Xa inhibitor Oral
Argatroban (Acova) Direct thrombin inhibitor IV
Bivalirudin (Angiomax) Direct thrombin inhibitor IV
Dabigatran (Pradaxa) Direct thrombin inhibitor Oral
Dalteparin (Fragmin)* Indirect thrombin inhibitor SC; IV if rapid anticoagulant
response needed
Desirudin (Iprivask) Direct thrombin inhibitor SC
Enoxaparin (Lovenox)* Indirect thrombin inhibitor SC; IV if rapid anticoagulant
response needed
Fondaparinux (Arixtra) Factor Xa inhibitor SC
Rivaroxaban (Xarelto) Factor Xa inhibitor Oral
Unfractionated heparin Indirect thrombin inhibitor IV or SC
Warfarin (Coumadin) Vitamin K antagonist Oral
*Low-molecular-weight heparin
IV, intravenous; SC, subcutaneous
2015). Administration of UFH can occur either in the prehospital or in-hospital setting for STEMI
patients for whom there is a planned PPCI reperfusion strategy (O’Connor, et al., 2015).
Reperfusion Therapies
Of the patients who are experiencing ACSs, those who are experiencing a STEMI are most likely to
benefit from reperfusion therapy. The primary choices for reperfusion therapy are fibrinolysis and
PCI. Fibrinolytics (“clot-busters”) are medications that work by activating the conversion of plasminogen
to plasmin, which then breaks down fibrinogen and fibrin clots. A PCI is a procedure in which a catheter
is used to open a coronary artery that has been blocked or narrowed by CAD. The term primary PCI is
used when PCI is done alone as the primary treatment after diagnostic angiography. PPCI is the recom-
mended reperfusion strategy when it can be performed in a timely manner by experienced personnel
(O’Gara, et al., 2013). Current clinical practice guidelines with regard to PPCI in STEMI are shown
in Box 7.4.
BOX 7.4 Primary PCI in STEMI Recommendations

Class I Recommendations • Primary PCI should be performed in patients
• Primary PCI should be performed in patients with STEMI and cardiogenic shock or acute
with STEMI and ischemic symptoms of less severe HF, irrespective of time delay from
than 12 hours’ duration. MI onset.
• Primary PCI should be performed in
patients with STEMI and ischemic symptoms Class IIa Recommendation
of less than 12 hours’ duration who have • Primary PCI is reasonable in patients with
contraindications to fibrinolytic therapy, irres- STEMI if there is clinical and/or ECG evidence
pective of the time delay from first medical of ongoing ischemia between 12 and 24 hours
contact. after symptom onset.
Source: O’Gara, et al., 2013, p. e90.

ECG, electrocardiogram; HF, heart failure; MI, myocardial infarction; PCI, percutaneous coronary intervention; STEMI, ST ele-
vation myocardial infarction
The first physician who encounters a patient with STEMI should determine the need for reperfusion
therapy and determine the means by which it is performed (pharmacologic versus mechanical)
(O’Connor, et al., 2015). Because consultation delays therapy, routine consultation with a cardiologist
or other physician is not recommended except in equivocal or uncertain cases (O’Connor, et al., 2015).
Several factors must be considered when deciding to use fibrinolytic therapy versus PPCI including
the time from onset of symptoms, the patient’s clinical presentation and hemodynamic status, the
patient’s age, the location of the infarction, the duration of STEMI at the time of initial emergency
department presentation, patient comorbidities, the risk of bleeding, the presence of contraindications,
the time delay to PCI, and the abilities of the PCI cardiologist and hospital (O’Connor, et al., 2015;
O’Gara, et al., 2013). For adult patients who present with STEMI at a non–PCI capable hospital, cur-
rent guidelines recommend the immediate transfer of the patient without fibrinolysis to a PCI center
(O’Connor, et al., 2015). Fibrinolytic therapy with routine transfer for angiography may be an acceptable
alternative to immediate transfer to PPCI when a STEMI patient cannot be transferred to a PCI-capable
hospital in a timely manner (O’Connor, et al., 2015).
Strategies that have been suggested for decreasing door-to-balloon time include the following
(Bradley, et al., 2006; O’Gara, et al., 2013):
• Use of the prehospital 12-lead ECG to diagnose STEMI; activation of the reperfusion team while the
patient is in transit to the hospital
• Activation of the reperfusion team by the emergency physician without waiting to consult a
cardiologist
• Activation of the reperfusion team by means of a single call from the emergency department to a cen-
tral page operator, who then pages the interventional cardiologist and the catheterization
laboratory staff
• Goal established for the reperfusion team to arrive in the catheterization laboratory within 20 minutes
of being paged
• Prompt feedback and analysis provided from a multidisciplinary quality improvement team to mem-
bers of the STEMI care team
Although mechanical catheter-based intervention has been proven to produce better outcomes when
performed in a timely manner, fibrinolytic therapy continues to play a major role in the treatment of
STEMI because only a minority of U.S. hospitals have PCI capabilities (O’Gara, et al., 2013). In the
absence of contraindications, fibrinolytic therapy should be administered to patients with STEMI
and an onset of ischemic symptoms within the previous 12 hours when it is anticipated that primary
PCI cannot be performed within 120 minutes of first medical contact (O’Gara, et al., 2013). Fibrinolytic
therapy is generally not recommended for patients presenting between 12 and 24 hours after onset of
symptoms unless ischemic pain persists with continuing STE; fibrinolytic therapy should not be admin-
istered to patients who present more than 24 hours after symptom onset (O’Connor, et al., 2015).
STEMI patients with contraindications to fibrinolytic therapy and who are in cardiogenic shock are
not candidates for fibrinolytic therapy (O’Connor, et al., 2015). PCI or a coronary artery bypass graft
is the preferred reperfusion strategy for STEMI patients who present in shock (O’Connor, et al.,
2015). There is no role for fibrinolytic therapy in patients with NSTE-ACS (Amsterdam, et al.,
2014; O’Connor, et al., 2015).
Before starting fibrinolytic therapy, choose an ECG monitoring lead that shows clear evidence of ST
elevation. During fibrinolytic therapy, monitor the ECG and the patient’s vital signs closely. Watch for
ST changes, dysrhythmias, and hypotension, and question the patient about chest discomfort. When
reperfusion occurs, the patient’s chest discomfort typically stops abruptly as blood flow to the ischemic
myocardium is restored. Watch for reperfusion dysrhythmias (eg, PVCs, bradycardias, heart block, VT,
ventricular fibrillation [VF]) as blood flow is reestablished through the infarct-related artery. Previously
elevated ST segments should quickly return to baseline as blood flow is restored to the affected myocar-
dium. Reocclusion may occur. Pay careful attention to all potential bleeding sites (including catheter
insertion sites, arterial and venous puncture sites, cutdown sites, and needle puncture sites).

information presented in this chapter. As you work through the case study, remember that there may be
CHAPTER QUIZ
Multiple Choice
____ 1. Which of the following is the most common cause of the blockage of a coronary artery?
A. A thrombus
B. Coronary artery spasm
C. Coronary artery trauma
D. Coronary artery dissection
____ 2. Beta-blockers:
A. Increase heart rate.
B. Decrease the force of myocardial contraction.
C. Block the conversion of angiotensin I into angiotensin II.
D. Are contraindicated in patients experiencing an ACS.
____ 3. Indicative changes, which are ECG findings that are seen in leads that look directly at
the area fed by a blocked coronary artery, are significant when they are seen in two
anatomically contiguous leads. Which of the following reflects a pair of contiguous
leads?
A. I and aVF
B. V1 and V6
C. V2 and V3
D. II and aVL
____ 4. Which of the following patients is most likely to present atypically with an ACS?
A. A 34-year-old man with no history of heart disease
B. A 56-year-old woman with a history of type 1 diabetes
C. A 65-year-old man with a history of two previous MIs
D. A 58-year-old man with angina and a strong family history of CAD
____ 5. ECG changes characteristic of myocardial ischemia include temporary changes in the:
A. P wave and ST segment.
B. ST segment and T wave.
C. P wave and QRS complex.
D. QRS complex and T wave.
____ 6. A 66-year-old woman presents in acute distress. She describes a sudden onset of severe
chest discomfort and nausea that have been present for 2 hours. An initial 12-lead
ECG should be obtained within __ minutes of contact with this patient.
A. 10
B. 30
C. 60
D. 90
____ 7. Which of the following is preferred for the relief of persistent chest discomfort
associated with a STEMI?
A. Aspirin
B. Morphine
C. Midazolam
D. NSAIDs
____ 8. Which of the following is (are) the preferred cardiac biomarker(s) for diagnosing MI?
A. Myoglobin
B. TnI and TnT
C. Ischemia-modified albumin
D. CK-MB
____ 9. The recommended initial dose of aspirin is:

A. 35 to 81 mg.
B. 81 to 162 mg.
C. 162 to 325 mg.
D. 325 to 500 mg.
____ 10. A 52-year-old woman is complaining of chest pain. The cardiac monitor reveals a
sinus rhythm at 68 beats/min. Her blood pressure is 88/60 millimeters of mercury
(mm Hg) and her ventilatory rate is 14 breaths/min. Breath sounds are clear. There are
no signs of pedal edema. A standard 12-lead ECG is obtained that reveals 3-mm STE
in leads II, III, and aVF. The patient is being given oxygen at 2 L/min by nasal
cannula. An IV has been established. You should now:
A. Give sublingual NTG and aspirin.
B. Give morphine sulfate and a calcium channel blocker.
C. Attach right-sided chest leads to rule out RVI.
D. Give a beta-blocker and determine the patient’s eligibility for reperfusion therapy.
Matching
Match each description with its corresponding answer
A. The zone of ischemia produces ST segment _____ in the leads facing the affected area
B. View the anterior wall of the left ventricle
C. Indication for supplemental oxygen administration
D. Blood tests used to help verify the presence of a MI
E. View the inferior wall of the left ventricle
F. The period from STEMI symptom onset to successful reperfusion
G. Phosphodiesterase inhibitor use within the previous 24 to 48 hours
H. This type of angina is the result of intense spasm of a segment of a coronary artery
I. View the interventricular septum
J. Examples of ACE inhibitors
K. A procedure in which a catheter is used to open a coronary artery blocked or narrowed by CAD
L. View the lateral wall of the left ventricle
M. UA and NSTEMI
N. The zone of injury produces ST segment _____ in the leads facing the affected area
O. Components of the treatment plan for NSTE-ACS
P. Example of an antiplatelet agent
Q. View the inferobasal wall of the left ventricle
R. Example of a condition that can mimic an acute MI
S. PR interval more than 0.24 seconds, second- or third-degree heart block, reactive airway disease
T. Examples of beta-blockers
____ 11. Elevation
____ 12. PCI
____ 13. II, III, and aVF
____ 14. Atenolol, metoprolol
____ 15. NSTE-ACSs

____ 16. Cardiac biomarkers
____ 17. Leads V7, V8, and V9
____ 18. Contraindications for beta-blocker administration
____ 19. Depression
____ 20. Leads I, aVL, V5, and V6
____ 21. Prinzmetal’s
____ 22. Total ischemic time
____ 23. Oxygen saturation level of less than 90%
____ 24. Clopidogrel (Plavix)
____ 25. Leads V1 and V2
____ 26. Pericarditis
____ 27. Lisinopril, captopril, ramipril
____ 28. Leads V3 and V4
____ 29. Contraindication for nitrate administration
____ 30. Antianginal, antiplatelet, and anticoagulant therapy

CASE STUDY 7-1

Your patient is a 68-year-old man who is complaining of chest discomfort. The patient is hospitalized at a
PCI-capable facility. You have a sufficient number of advanced life support personnel available to assist
you and carry out your instructions. Emergency equipment, including a biphasic manual defibrillator, is
available.
1. You see the patient sitting upright on a stretcher with beads of sweat visible on his forehead. He is
awake and watches as you approach. The patient appears anxious and his skin is pale. His breathing
does not appear to be labored. Are these general impression findings normal or abnormal? If
abnormal, what are the abnormal findings?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________

_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
3. The patient’s blood pressure is 168/94 mm Hg and his ventilatory rate is 22 breaths/min. Breath
sounds are clear and equal and his skin is cool, pale, and moist. The patient’s SpO2 on room
air is 95%. He has been placed on the cardiac monitor, which reveals a sinus tachycardia at 110
beats/min. The following information has been obtained from the patient:
Signs/Symptoms: Discomfort located in the center of his chest and radiates to his left arm;
rates his chest discomfort at 9 out of 10
Allergies: None
Medications: Aspirin 81 mg daily
Past history: Heart attack at age 45, RCA stent inserted
Last oral intake: Lunch 2 hours ago
Events prior: Patient was reading the newspaper when his discomfort began
about 1½ hours ago.
The physical examination reveals no abnormalities. What should be done next?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
4. Should aspirin be administered to this patient?

_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
5. IV access has been established and a 12-lead ECG has been obtained. Which components of the
ECG should be carefully examined to determine the most appropriate treatment course for this
patient?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
6. When viewing the ECG of a patient experiencing an ACS, what does the presence of STE in the
leads facing the affected area suggest?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
7. The patient’s 12-lead ECG is shown here (Fig. 7.25). Are there any significant findings on this 12-
lead ECG?
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 7.25 (From Phalen T, Aehlert BJ: The 12-lead ECG in acute coronary syndromes, ed 3, St. Louis, 2012, Mosby.)
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
8. What complications should be reasonably anticipated with this type of infarction?

_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
9. Sublingual NTG is ordered for this patient. What is the rationale for giving NTG in this situation?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
10. What precautions should be taken before giving NTG?

_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
11. After three doses of sublingual NTG, the patient rates his discomfort as 7/10. His vital signs are
essentially unchanged. What should be done now?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
12. Cardiac biomarkers and the 12-lead ECG confirm a STEMI. What should be done next?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________

Multiple Choice
1. A. A thrombus is the most common cause of the blockage of a coronary artery. Less common causes
of an ACS include coronary artery spasm (eg, with cocaine abuse), severe luminal narrowing from
atherosclerosis or restenosis after PCI, coronary dissection, hypercoagulation, trauma to the coronary
arteries, or coronary artery emboli (rare).
OBJ: Explain the pathophysiology of ACSs.
2. B. The inhibition of beta1-adrenergic receptor sites decreases heart rate and the force of myocardial
contraction, thereby reducing myocardial oxygen demand. ACE inhibitors block the conversion of
angiotensin I into angiotensin II. In the absence of contraindications to their use, oral beta-blockers
should be initiated in the first 24 hours in patients experiencing an ACS.
OBJ: Describe the initial management of a patient experiencing an ACS.
3. C. Two leads are contiguous if they look at the same or adjacent areas of the heart or if they are
numerically consecutive chest leads. Examples of contiguous leads include V1 and V2, V2 and
V3, V3 and V4, V4 and V5, V5 and V6, I and aVL, II and aVF, and II and III, among others.
OBJ: Identify the ECG changes that are associated with myocardial ischemia, injury, and
infarction.
4. B. Patients who are experiencing an ACS who are most likely to present atypically include older
patients with prior cardiac surgery, and patients during the immediate postoperative period after
noncardiac surgery.
OBJ: Explain atypical presentation and its significance in ACSs.
5. B. The effects of myocardial ischemia can be viewed on the ECG as STD and T wave changes in the
leads that face the affected area of the ventricle.
OBJ: Identify the ECG changes associated with myocardial ischemia, injury, and infarction.
6. A. Obtaining and reviewing a 12-lead ECG is part of the initial assessment of the patient presenting
with ischemic chest discomfort and important in determining an appropriate treatment plan. Obtain
the first 12-lead ECG within 10 minutes of patient contact. Obtain a repeat 12-lead ECG with each
set of vital signs, when the patient’s symptoms change, and as often as necessary.
OBJ: Explain the importance of the 12-lead ECG for the patient with an ACS.
7. B. Morphine is the preferred analgesic for patients with STEMI who experience persistent chest
discomfort unresponsive to nitrates. Other narcotics may be considered in patients allergic to mor-
phine. NSAIDs are contraindicated in patients with STEMI.
8. B. Cardiac biomarkers include CK-MB, myoglobin, TnI, and TnT. Cardiac troponins are the bio-
markers of choice for diagnosing MI because of their increased specificity and sensitivity compared
with CK-MB. Ischemia-modified albumin has been recognized as a marker of inflammation and
myocardial ischemia but has been less well studied than those previously mentioned.
OBJ: Describe the initial management of a patient who is experiencing an ACS.
9. C. Non–enteric-coated chewable aspirin should be given as early as possible after presentation to

patients with an ACS, assuming there are no contraindications to its use. The initial dose is 162
to 325 mg.
10. C. RVI should be suspected when ECG changes suggesting an inferior infarction (ST elevation in
leads II, III, and/or aVF) are observed. The most sensitive ECG signs of right ventricular injury
include 1 mm ST elevation in lead V1 and in lead V4R. Patients with RVI may present with, or
subsequently develop, hypotension caused by bradydysrhythmias or caused by a reduction in preload
after the administration of vasodilators such as NTG.
OBJ: Explain the clinical and ECG features of a RVI.
Matching
11. N 21. H
12. K 22. F
13. E 23. C
14. T 24. P
15. M 25. I
16. D 26. R
17. Q 27. J
18. S 28. B
19. A 29. G
20. L 30. O

1. The general impression findings are abnormal (Appearance: normal; Breathing: normal; Circula-
tion: abnormal skin color).
2. Assess the patient’s breathing with regard to rate, quality, and regularity. Quickly estimate
the patient’s heart rate and determine the quality of the pulse (ie, fast or slow, regular or irregular,
weak or strong). Evaluate the patient’s skin temperature, color, and moisture to assess perfusion.
Perform a brief neurologic evaluation (ie, obtain a Glasgow Coma Scale score) and assess the need
for a defibrillator. Ask a team member to attach a pulse oximeter, ECG monitor, and blood pressure
monitor. Ask the airway team member to administer supplemental O2 if indicated. Ask a team
member to obtain the patient’s baseline vital signs while you obtain, or direct a team member to
obtain, a SAMPLE history and perform a focused physical examination.
3. When a patient presents with symptoms suggestive of ischemia or infarction, initial care should
include primary and secondary surveys and administration of supplemental oxygen (if indicated).
Direct the IV team member to start an IV of normal saline. Because it should be obtained within
10 minutes of patient contact, order a 12-lead ECG. In addition, order laboratory studies including
cardiac biomarkers, electrolytes, and coagulation studies, and a portable chest radiograph.
4. Yes. Non–enteric-coated chewable aspirin should be given as early as possible after presentation to
patients with an ACS, assuming there are no contraindications to its use. Although the patient cur-
rently takes 81 mg of aspirin daily, the recommended initial dose is 162 to 325 mg.
5. Once the 12-lead ECG has been obtained, it should be reviewed carefully. Look at each lead for the
presence of ST segment displacement (ie, elevation or depression). If ST segment displacement is
present, note its displacement in mm. Inspect the T waves for any changes in orientation, shape, and
size. Examine each lead for the presence of a Q wave. If a Q wave is present, measure its duration.
Assess for areas of ischemia or injury by assessing lead groupings. Remember: ECG evidence must
be found in at least two contiguous leads.
OBJ: Explain the importance of the 12-lead ECG for the patient with an ACS.
6. When viewing the ECG of a patient experiencing an ACS, the presence of STE in the leads facing
the affected area suggests myocardial injury.
OBJ: Identify the ECG changes that are associated with myocardial ischemia, injury, and
infarction.
7. STE is seen in leads V1, V2, V3, and V4. STE in these leads suggests an anteroseptal MI. STD is
seen in leads II, III, aVF, V5, and V6.
OBJ: Identify the ECG leads that view the anterior wall, the inferior wall, the lateral wall, the
8. Because the LAD supplies a large portion of the left ventricle, a blockage in this area can lead to
complications such as left ventricular dysfunction, including left-sided heart failure and cardiogenic
shock. An anterior infarction may cause dysrhythmias including PVCs, atrial flutter, or AFib. A
blockage in the area of the septum, which contains the bundle branches, may result in right
BBB, left BBB (this is more common), second-degree AV block type II, and third-degree AV block.
9. NTG dilates the capacitance vessels (ie, veins), which causes a reduction in ventricular filling and
cardiac preload. NTG also dilates normal and atherosclerotic epicardial coronary arteries and
increases coronary collateral flow.
10. Before giving NTG, assess the degree of the patient’s pain/discomfort using a 0-to-10 scale, dura-
tion, time started, activity being performed, and pain quality. Reassess (and document) the patient’s
vital signs and level of discomfort after each dose. Make sure that the patient has not used a phos-
phodiesterase inhibitor such as sildenafil (Viagra) within 24 hours or tadalafil (Cialis) within
48 hours before NTG administration. The combination of a phosphodiesterase inhibitor and
nitrates may result in severe hypotension. Nitrates should not be administered to patients with a
systolic blood pressure less than 90 mm Hg or 30 mm Hg or more below baseline, severe bradycardia
or tachycardia, or suspected RVI.
11. Morphine, which is generally given in 2 mg increments, should be administered for pain relief. Give
additional doses at 5- to 15-minute intervals. Reassess and document the patient’s vital signs and
level of discomfort after each morphine dose.
12. Reperfusion therapy is recommended for all eligible patients with STEMI who present within
12 hours of symptom onset. Primary PCI is the recommended method of reperfusion when it
can be performed in a timely fashion by experienced professionals. When the patient has a STEMI,
is a candidate for reperfusion, and is initially seen at a PCI-capable hospital, he or she should be sent
to the cardiac catheterization laboratory for primary PCI, which should be accomplished within
90 minutes (O’Gara, et al., 2013).
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CHAPTER 8
Acute Ischemic Stroke
INTRODUCTION
[Objective 1]
Stroke is the fourth leading cause of death in the United States, after heart disease, cancer, and chronic
lower respiratory disease (Jauch, et al., 2013). The American Heart Association (AHA) estimates that on
average, someone in the United States experiences a stroke every 40 seconds (Mozaffarian, et al., 2015).
Of the 795,000 strokes that occur in the United States each year, about 610,000 of these are first attacks,
and 185,000 are recurrent attacks (Mozaffarian, et al., 2015). Nearly half of stroke survivors have residual
deficits, including weakness or cognitive dysfunction, 6 months after stroke (Bushnell, et al., 2014). In
the United States women are more often institutionalized after stroke and have poorer recovery from
stroke than men (Bushnell, et al., 2014).
Before the introduction of fibrinolytic therapy in the treatment of stroke, a stroke was not always viewed
as a medical emergency as there was little to offer patients to stop the process (Saunorus Baird & Bethel,
2011). It is now recognized that early identification of a stroke is essential so that emergency care can be
initiated as rapidly as possible. Like the Chain of Survival that is used to describe the sequence of events
needed to survive sudden cardiac arrest, the Stroke Chain of Survival is a metaphor for the series of events
that must occur during the emergency care of the possible stroke patient to optimize his or her chances of
full recovery (Table 8.1). The chain consists of eight links, which are also referred to as the “Ds of stroke
care”: detection, dispatch, delivery, door, data, decision, drug, and disposition (Jauch, et al., 2013).
Types of strokes, stroke systems of care, and the initial emergency care for acute ischemic stroke are
discussed in this chapter.
ACLS Pearl
A stroke is also called a brain attack. The public is familiar with the phrase heart attack. Because a
stroke happens in the brain rather than in the heart, the phrase brain attack may convey the events
involved in a stroke more clearly to the public than the word stroke. The term brain attack and its
application to stroke are credited to Vladimir C. Hachinski, MD, and John Norris, MD, who are neu-
rologists from Canada. The NSA began using the term in 1990. The term cerebrovascular accident,
which was used for many years as a synonym for the word stroke, has lost favor, because strokes are
not really accidents (Zivin, 2012).
G O A L Given a patient situation, and working in a team setting, competently direct the initial
emergency care for a patient experiencing an acute ischemic stroke.
237
238 CHAPTER 8 Acute Ischemic Stroke
TABLE 8.1 Stroke Chain of Survival

Chain Link Description
Detection Recognition of stroke signs and symptoms by the patient, family, or bystanders
Dispatch Activation of the EMSS, priority EMSS dispatch, and prompt EMSS response
Delivery Prompt transport to an appropriate stroke hospital while providing appropriate prehospital
assessment and care as well as prearrival notification
Door Immediate ED triage
Data ED evaluation, stroke team activation, laboratory studies, and brain imaging
Decision Decision about potential therapies made on the basis of the data gathered and stroke type,
location (eg, carotid, vertebrobasilar), and stroke severity
Drug Administration of appropriate medications and postadministration monitoring
Disposition Prompt admission to a stroke unit, intensive care unit, or transfer for ongoing care and close observation
ED, emergency department; EMSS, emergency medical services system
LEARNING OBJECTIVES
1. Discuss the links in the Stroke Chain of Survival.
2. Discuss the brain’s arterial blood supply.
3. Describe the major types of stroke.
4. Explain what a transient ischemic attack (TIA) is and how it differs from stroke.
5. Explain why rapid identification of stroke is critical.
6. Differentiate between the hyperacute and acute phases of stroke care.
7. Describe the initial emergency care for acute ischemic stroke.
8. Compare elements of acute stroke care facilities in the United States.
9. State the recommended target times for key interventions during the hyperacute phase of
acute stroke care.
10. Give examples of medical conditions that mimic stroke.
LEARNING PLAN
• Master identification of the following rhythms: sinus rhythm and atrial fibrillation
• Master the following medications: O2, dextrose, fibrinolytics
• Assign team member roles or perform as a team member in a simulated patient situation.
• Recognize signs and symptoms of acute ischemic stroke.
• Develop and implement a treatment plan on the basis of the patient’s presentation,
history, physical examination, and diagnostic test results.
• Know the actions, indications, dosages, adverse effects, and contraindications for the
medications used in the treatment of acute ischemic stroke.
• If applicable, use a reperfusion checklist to evaluate the patient’s candidacy for
fibrinolytic therapy.
debriefing.
• Read the case study at the end of this chapter and answer the questions within the case
study. Compare your answers with the answers provided.
CHAPTER 8 Acute Ischemic Stroke 239
KE Y T ERMS
Stroke system of care A comprehensive, diverse system that addresses all aspects of stroke
care in a coordinated fashion.
Transient ischemic attack (TIA) A transient episode of neurologic dysfunction caused by
focal brain, spinal cord, or retinal ischemia, without acute infarction.
DEFINITION OF STROKE
In 2013, the Stroke Council of the American Heart Association/American Stroke Association (AHA/
ASA) developed an updated definition of stroke for the 21st century (Sacco, et al., 2013). The expert
consensus document generated by this group notes that the term stroke should be broadly used to include
all of the following (Sacco, et al., 2013):
• Definition of central nervous system (CNS) infarction: CNS infarction is brain, spinal cord, or retinal cell
death attributable to ischemia, based on
1. Pathological, imaging, or other objective evidence of cerebral, spinal cord, or retinal focal ischemic
injury in a defined vascular distribution; or
2. Clinical evidence of cerebral, spinal cord, or retinal focal ischemic injury based on symptoms per-
sisting 24 hours or more or until death, and other etiologies excluded. (Note: CNS infarction
includes hemorrhagic infarctions, types I and II.)
• Definition of ischemic stroke: An episode of neurological dysfunction caused by focal cerebral, spinal, or
retinal infarction. (Note: Evidence of CNS infarction is defined above.)
• Definition of silent CNS infarction: Imaging or neuropathological evidence of CNS infarction, without
a history of acute neurological dysfunction attributable to the lesion.
• Definition of intracerebral hemorrhage: A focal collection of blood within the brain parenchyma or ven-
tricular system that is not caused by trauma. (Note: Intracerebral hemorrhage includes parenchymal
hemorrhages after CNS infarction, types I and II.)
• Definition of stroke caused by intracerebral hemorrhage: Rapidly developing clinical signs of neurological
dysfunction attributable to a focal collection of blood within the brain parenchyma or ventricular
system that is not caused by trauma.
• Definition of silent cerebral hemorrhage: A focal collection of chronic blood products within the brain
parenchyma, subarachnoid space, or ventricular system on neuroimaging or neuropathological
examination that is not caused by trauma and without a history of acute neurological dysfunction
attributable to the lesion.
• Definition of subarachnoid hemorrhage: Bleeding into the subarachnoid space (ie, the space between the
arachnoid membrane and the pia mater of the brain or spinal cord).
• Definition of stroke caused by subarachnoid hemorrhage: Rapidly developing signs of neurological
dysfunction and/or headache because of bleeding into the subarachnoid space (ie, the space between
the arachnoid membrane and the pia mater of the brain or spinal cord), which is not caused by trauma.
• Definition of stroke caused by cerebral venous thrombosis: Infarction or hemorrhage in the brain, spinal
cord, or retina because of thrombosis of a cerebral venous structure. Symptoms or signs caused by
reversible edema without infarction or hemorrhage do not qualify as stroke.
• Definition of stroke, not otherwise specified: An episode of acute neurological dysfunction presumed to
be caused by ischemia or hemorrhage, persisting 24 hours or more or until death, but without suffi-
cient evidence to be classified as one of the above.
ANATOMY REVIEW
[Objective 2]
The brain makes up about 2% of an adult’s total body weight, it receives 15% to 17% of the total cardiac
output, and it consumes about 20% of the oxygen used by the body (Haines & Lancon, 2013). The brain
is supplied with blood by the internal carotid and vertebral arteries (Fig. 8.1). The internal carotid arteries
branch into the anterior and middle cerebral arteries. Strokes involving the carotid arteries are called ante-
rior circulation strokes or carotid territory strokes. They usually involve the cerebral hemispheres. After
Right anterior cerebral

Anterior communicating
Right middle cerebral

Left internal carotid
Left posterior
Right posterior cerebral communicating
Left superior cerebellar
Basilar
Left vertebral
Anterior spinal
Fig. 8.1 Arterial blood supply to the brain. (From Solomon EP. Introduction to human anatomy and physiology, ed 3, St. Louis,
2009, Mosby.)
passing through the foramen magnum, the vertebral arteries join to form the basilar artery, which divides
into right and left posterior cerebral arteries (Haines & Lancon, 2013). Strokes affecting the vertebral arter-
ies are called posterior circulation strokes or vertebrobasilar territory strokes. They usually affect the brainstem
or cerebellum. The anterior and posterior circulations form a circular connection of arteries called the circle
of Willis, which is located at the base of the brain. Because anatomic variations are frequent, particularly in
the vertebral artery system, the area supplied with blood by a given artery is not entirely predictable; as a
result, stroke syndromes do not always correlate well with the location of the vascular injury (Zivin, 2012).
ACLS Pearl
Most individuals will lose consciousness if the brain is deprived of blood and oxygen for 10 to
12 seconds; in the absence of hypothermia, irreparable brain damage or death may result after
3 to 5 minutes (Haines & Lancon, 2013).
STROKE TYPES
ACLS Pearl
For many years, the primary types of stroke were categorized as either ischemic or hemorrhagic.
Experts now recommend that the term hemorrhagic stroke be discontinued because the term is
confusing; it can refer to primary subarachnoid hemorrhage (SAH), primary intracerebral hemorrhage
(ICH), or hemorrhage after infarction that occurs spontaneously or because of antithrombotic or fibri-
nolytic therapy (Sacco, et al., 2013).
Subarachnoid Hemorrhage
[Objective 3]
SAH is bleeding into the subarachnoid space. Blood in the subarachnoid space may be the result of trauma or
nontraumatic causes such as a ruptured cerebral aneurysm or an arteriovenous malformation (Fig. 8.2). About
3% of all strokes are the result of SAH (Mozaffarian, et al., 2015).
Patients often report a sudden onset of a severe headache or describe the feeling as “the worst headache
of my life.” Associated signs and symptoms vary and may include vomiting, focal neurologic deficits, neck
stiffness, dizziness, visual disturbances (eg, blurry or double vision), loss of consciousness, and seizures.
Subarachnoid Intracerebral
hemorrhage hemorrhage
Ruptured cerebral Ruptured Cerebral thrombosis Cerebral embolism

A aneurysm blood vessel B
Fig. 8.2 A, SAH, ICH. B, Ischemic stroke. (From Brooks ML, Brooks DL. Exploring medical language, a student-directed
approach, ed 9, St. Louis, 2014, Mosby.)
Warning or sentinel signs and symptoms can occur minutes to weeks before a rupture because of blood
leakage or because of nerve compression as the aneurysm expands. The sudden onset of a severe head-
ache, vision problems, and nausea and vomiting are examples of possible warning signs and symptoms.
Misdiagnosis or delayed diagnosis in patients with SAH is common because of the variability in types of
headaches and associated symptoms (Nentwich & Veloz, 2012).
Frequent vital sign checks including oxygen saturation readings, electrocardiogram (ECG) monitor-
ing, and neurologic assessments are essential. ECG changes that may be observed in the acute phase of
SAH include peaked or deeply inverted T waves and increased U wave amplitude. The patient should be
admitted to a neurologic intensive care unit for continuous monitoring for bleeding, hydrocephalus,
vasospasm, and other potential complications.
Intracerebral Hemorrhage
[Objective 3]
About 10% of all strokes are the result of an ICH (Mozaffarian, et al., 2015). Patients who experience an
ICH have a 30-day mortality rate of 30% to 50%, with 75% of patients severely disabled or deceased at
1 year (Brouwers & Goldstein, 2012). Chronic hypertension and aging are among the risk factors asso-
ciated with ICH.
ICH is most often caused by the spontaneous rupture of small arteries within the substance of the
brain. Less common causes of ICH include aneurysm, arteriovenous malformation, hemorrhagic trans-
formation of ischemic stroke, and neoplasms (Brouwers & Goldstein, 2012). Signs and symptoms may
include a severe headache, vomiting, neck stiffness, seizures, and coma or decreased level of conscious-
ness. Symptoms may progress over minutes or hours. Because none of these findings are specific for ICH,
neuroimaging is essential to establish a definitive diagnosis (Brouwers & Goldstein, 2012). Rapid diag-
nosis and appropriate management are important because neurologic deterioration is common in the first
few hours of ICH onset (Morgenstern, et al., 2010).
ACLS Pearl
It is estimated that more than 20% of patients who experience an ICH will experience a decrease in
the GCS score of two points or more between the prehospital assessment and the patient’s initial
evaluation in the emergency department (Morgenstern, et al., 2010).
About 73% of patients with ICH experience ongoing bleeding after hospital arrival (Brouwers &
Goldstein, 2012). Admission to a neurologic intensive care unit is recommended with monitoring of
intracranial pressure and cerebral perfusion pressure, in addition to vital sign and oxygen saturation
monitoring (Morgenstern, et al., 2010). During the acute phase of care, strategies to minimize ongoing
bleeding may include reversal of anticoagulation and modest blood pressure reduction (Brouwers &
Goldstein, 2012). Selected patients may benefit from hematoma evacuation or external ventricular drain-
age (Brouwers & Goldstein, 2012).
Ischemic Stroke
[Objective 3]
Statistics indicate that 87% of strokes are ischemic (Mozaffarian, et al., 2015). An ischemic stroke, also
described as an occlusive stroke, is an infarction of CNS tissue that occurs when a blood vessel supplying
the brain is blocked. The middle cerebral artery is the blood vessel most often involved in ischemic stroke
(Zivin, 2012). It is estimated that about 20% of ischemic strokes are caused by atherosclerosis of the
extracranial or intracranial segments of the carotid or vertebrobasilar arteries, about 25% are caused
by penetrating artery disease, another 20% are caused by cardiogenic emboli, and the stroke cause is
unknown in about 30% of cases (Summers, et al., 2009). Ischemic strokes may be symptomatic or silent
(ie, asymptomatic) (Easton, et al., 2009). Signs and symptoms of ischemic stroke are shown in Table 8.2.
A thrombotic stroke is the most common cause of ischemic stroke. With a thrombotic stroke, a
thrombus (ie, blood clot) develops in arteries that perfuse the brain (see Fig. 8.2). When the blood clots
are of sufficient size to block blood flow through the artery, the area that was previously supplied by that
artery becomes ischemic. Ischemia is poorly tolerated by the brain because the brain is unable to store the
glucose it needs to function. The patient’s signs and symptoms depend on the location of the artery
affected and the areas of brain ischemia.
With an embolic stroke, material from an area outside of the brain (eg, heart, aorta, other major artery)
becomes dislodged and travels through the bloodstream to the brain (ie, cerebral embolism). Embolic
TABLE 8.2 Signs and Symptoms of Ischemic Stroke

Affected Artery Clinical Signs and Symptoms
Anterior cerebral Behavioral changes, emotional lability, impaired decision-making ability (especially
if bilateral infarction)
Contralateral hemiparesis
Contralateral sensory loss
Loss of coordination
Urinary incontinence
Basilar and vertebral Amnesia
Disturbances in gait, speech, swallowing, vision
Quadriplegia or hemiplegia
Vertigo
Internal carotid Altered level of responsiveness
Headaches
Ipsilateral blindness
Profound aphasia
Weakness, paralysis, numbness, sensory changes, and visual deficits (eg, blurring) on
the affected side
Middle cerebral Contralateral hemiparesis
Contralateral sensory loss
Contralateral visual field deficits
Deviation of the eyes to the side of the lesion
Language deficit (dominant hemisphere)
Spatial-perceptual deficit (nondominant hemisphere)
Posterior cerebral Contralateral sensory impairment or loss
Inability to recognize familiar faces
Ipsilateral visual field deficits
Memory impairment
Area of permanent damage
Penumbra, area of salvageable damage

Normal brain external to penumbra
Fig. 8.3 After an occlusive stroke, the penumbra is an interface between a region of permanent tissue damage and an area
that will most likely survive. Rapid and appropriate treatment, with reperfusion of the penumbra, may salvage this region and
reduce the neurologic deficits suffered by the patient. (From Haines DE. Fundamental neuroscience for basic and clinical
applications, ed 4, Philadelphia, 2013, Saunders.)
material may consist of fragments of tumors or plaques; air; fat; amniotic fluid; a foreign body; or a blood
clot. An embolus tends to become lodged where arteries branch, because blood flow is most turbulent in
these areas. Fragments of the embolus may become lodged in smaller vessels. Atrial fibrillation is the
cardiac source of emboli in 50% of cardioembolic strokes (Babarro, et al., 2009). As with thrombotic
strokes, the patient’s signs and symptoms depend on the location of the artery affected and the areas of
brain ischemia.
Lacunar strokes, also called lacunar infarcts, are small infarctions caused by the blockage of a pene-
trating branch of a large cerebral artery. Lacunar strokes are usually associated with chronic hypertension,
diabetes, and hyperlipidemia, and they most often occur in the basal ganglia, thalamus, cerebellum, white
matter of the internal capsule, and pons.
Blockage of a cerebral artery usually results in a core area that is irreversibly damaged within minutes or
hours (Nolte, 2009). The area of dead tissue is often surrounded by an area of hypoperfused tissue called
the ischemic penumbra or the transitional zone (Fig. 8.3). The penumbra is supplied with blood by col-
lateral arteries that connect with branches of the blocked vessel. Brain cells in the penumbra may be sal-
vaged depending on how quickly blood flow is restored. The earlier the treatment for stroke is given, the
more favorable the results are likely to be.
Transient Ischemic Attack

[Objective 4]
A transient ischemic attack (TIA), also called a ministroke, a warning stroke, or a transient stroke, is “a
transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without
acute infarction” (Easton, et al., 2009). A TIA is one of the most important warning signs of acute
stroke. It is estimated that about 15% of all strokes are preceded by a TIA (Mozaffarian, et al.,
2015). Most TIAs last less than 2 hours, but prolonged episodes do occur (Easton, et al., 2009).
STROKE SYSTEMS OF CARE

[Objectives 5, 6]
For several years, organizations such as the Brain Attack Coalition (BAC), the AHA/ASA, and the National
Stroke Association (NSA) have been active in the development of initiatives designed to optimize stroke care
in the United States. In 2000 the BAC recommended the establishment of primary stroke centers (PSCs) as
an approach to improve the medical care of patients with stroke (Alberts, et al., 2000). In 2005 the BAC
published recommendations for comprehensive stroke centers (CSCs) (Alberts, et al., 2005). During the
same year, the AHA/ASA published recommendations with regard to the establishment of a stroke
system of care, recognizing that U.S. citizens should have access to the full range of activities and services
associated with stroke prevention and the timely identification, transport, treatment, and rehabilitation of
stroke patients regardless of geographic location, geopolitical boundaries, or socioeconomic disparities
(Schwamm, et al., 2005). A stroke system of care is a comprehensive, diverse system that addresses all aspects
of stroke care in a coordinated fashion (Silva & Schwamm, 2013). It includes the spectrum of stroke care from
primary prevention to activation of emergency medical services (EMS), acute care, secondary prevention,
rehabilitation and return to the community (Silva & Schwamm, 2013).
In acute stroke management, the phrase “time is brain” or “time lost is brain lost” reflects the need for
rapid assessment and intervention, because delays in diagnosis and treatment may leave the patient neu-
rologically impaired and disabled (Gorelick, et al., 2008). The hyperacute phase of stroke care refers to the
key interventions involved in the assessment, stabilization, and treatment in the first hours after stroke
onset (Casaubon & Suddes, 2013). During this time-sensitive phase, which encompasses all prehospital
and initial emergency care for TIA and stroke, attention is focused on identifying stroke symptoms and
stroke type, identifying treatment options, and executing the treatment plan as quickly as possible. The
acute phase of stroke care refers to key interventions involved in the assessment, treatment or management,
and early recovery in the first days after stroke onset (Casaubon & Suddes, 2013). This phase focuses on
confirming the cause of stroke and preventing medical complications, preparing the patient and family
for discharge, and establishing long-term secondary prevention measures (Summers, et al., 2009).
Public Education
The recognition of stroke signs and symptoms by the patient, family, or bystanders is critical. According to
the AHA, a study was conducted of patients admitted to an emergency department with possible stroke to
determine their knowledge of the signs, symptoms, and risk factors of stroke. Of the patients who were able
to respond, 39% did not know a single sign or symptom and 43% did not know a single risk factor
(Mozaffarian, et al., 2015). Despite public education programs with regard to stroke warning signs
(Box 8.1), data show that fewer than half of 9-1-1 calls for stroke events were made within 1 hour of symptom
onset, and fewer than half of those callers thought stroke was the cause of their symptoms (Jauch, et al., 2013).
The intravenous (IV) administration of tissue plasminogen activator (tPA) has proved to be an effec-
tive cerebral reperfusion therapy. Currently, the window of opportunity for the use of IV tPA for the
treatment of ischemic stroke is within 3 hours of symptom onset in a broad range of patients and between
3 and 4.5 hours of symptom onset in a more selective spectrum of patients. Unfortunately, delay in seek-
ing treatment is a common reason for ineligibility for tPA. The main causes for delayed patient presen-
tation to an emergency department include a lack of patient and public awareness of stroke signs and
symptoms, the urgency of immediate care, and the need to call 9-1-1 for EMS activation
(Higashida, et al., 2013). Despite efforts to educate the public about the importance of calling 9-1-1
upon recognition of stroke signs and symptoms, a significant percentage of patients (up to 50% in some
studies) with an acute or subacute stroke present at a hospital by means of a private car, taxi, or another
mode of transportation (other than an ambulance) (Higashida, et al., 2013).
Emergency Medical Services

Emergency medical services systems (EMSSs) play a critical role in optimizing stroke care (Jauch, et al.,
2013). Activation of the EMSS, priority EMS dispatch, prompt EMS response, triage and stabilization
in the field, and ground or air ambulance transport are important components with regard to EMS and
BOX 8.1 Stroke Warning Signs – The Five “Suddens”

• Sudden difficulty speaking (eg, an inability to • Sudden visual changes in one or both eyes
say what is meant, slurred speech) • Sudden weakness or numbness of the face,
• Sudden dizziness arm, or leg (particularly on one side
• Sudden severe headache with no known cause of the body)
the care of the stroke patient. Advance notification of stroke patient arrival by EMS personnel shortens
the time to be seen for initial evaluation by an emergency physician, shortens the time to brain imaging,
and increases the use of IV tPA (Jauch, et al., 2013).
A 2007 AHA/ASA policy statement addressed specific parameters with regard to EMS and stroke
systems of care, including the following (Acker, et al., 2007):
• All 9-1-1 call centers should use dispatch guidelines that prioritize patients experiencing stroke as
requiring a high-priority EMS response at the highest care level available.
• The period between the receipt of the call and the dispatch of the response team should be less than
90 seconds for 90% of calls involving stroke.
• To rapidly and accurately identify acute stroke patients, EMS personnel should use validated stroke
screening algorithms for the prehospital setting (eg, Cincinnati Prehospital Stroke Scale [CPSS], Los
Angeles Prehospital Stroke Screen [LAPSS]). After identifying a stroke patient using a validated
screening form, EMS personnel should use validated stroke severity scales developed specifically
for prehospital use (eg, Los Angeles Motor Scale, Shortened National Institutes of Health Stroke
Scale [NIHSS]).
• The EMSS response time should be less than 9 minutes at least 90% of the time for suspected acute
stroke patients. Response time reflects the amount of time elapsed from the receipt of the call by the
dispatch entity to the arrival on the scene of a properly equipped and staffed ambulance.
• The dispatch time, which is the interval between the time a call is received at the EMS answering point
and the time the EMS unit is selected and notified of the need to respond, should be less than 1 minute.
• The turnout time, which is the interval between the time the EMS unit is notified of the need to
respond and the time the EMS unit starts moving (ie, wheels turning), should be less than 1 minute.
• The on-scene time, which is the amount of time spent with the patient before the start of transport,
should be less than 15 minutes (unless there are extenuating circumstances or extrication difficulties).
• Stroke system transport protocols should be developed collaboratively with prehospital and hospital
providers, as well as with other stakeholders. Transport destination protocols should reflect optimal
patient care with transport to a stroke center. Protocols for the transfer of stroke patients from non–
stroke center hospitals to stroke centers should be established. Stroke patients should be transported to
stroke-ready hospitals regardless of the patients’ geopolitical location.
• Prearrival notification of hospitals should be provided for all suspected stroke patients.
Prehospital Assessment and Management

[Objective 7]
Prehospital professionals should quickly perform a primary survey and stabilize the patient’s airway, breathing,
and circulation (ABCs) as necessary. A focused history should be obtained and the patient’s normal baseline
mental status determined. Because families often confuse the type of symptom onset with the time the patient
was found, the patient, patient’s family, coworkers, or others at the scene should be asked when the patient was
last known to be symptom-free (ie, last known normal or last known-well time) (Demaerschalk, et al., 2016).
Determining and documenting the time of symptom onset is critical and the single most important determi-
nant of treatment options during the hyperacute phase of stroke care (Summers, et al., 2009). All medications
that the patient is currently taking should be collected and documented. Medications that are particularly
important include anticoagulants, antiplatelet agents, antihypertensives, insulin, oral hypoglycemics, and
sympathomimetics. Ascertain if the patient has a history of conditions that increase the likelihood that his
or her symptoms are caused by stroke such as previous TIAs and their frequency, prior stroke, seizures, diabetes
mellitus, hypertension, and atrial fibrillation (Jauch, et al., 2013).
A neurologic assessment should be performed using a validated prehospital stroke screening tool.
Three commonly used screening tools include the CPSS, the LAPSS, and the Face Arm Speech Test
(FAST). The CPSS is taught as the three Ds of “drift (arm), droop (facial weakness), and dysarthria
(slurred speech).” The FAST assesses facial droop, arm drift, and speech (dysarthria and aphasia),
and the time of symptom onset. If stroke is suspected, use a validated stroke severity scale to rate the
severity of the stroke. The Los Angeles Motor Scale, which assigns point values to the LAPSS items
of facial weakness, arm strength, and grip, is often used for this purpose. More recently, the Rapid Arte-
rial oCclusion Evaluation (RACE) scale has been used to help identify large vessel occlusions (Perez de la
Ossa, et al., 2014). The RACE scale, which is based on the NIHSS, assesses the following areas in
patients with suspected acute ischemic stroke: facial palsy (scored 0 to 2), arm motor function (0 to
2), leg motor function (0 to 2), gaze (0 to 1), and aphasia (if right hemiparesis is present) or agnosia
(if left hemiparesis is present) (0 to 2).
Regardless of the stroke scale used, if the patient’s assessment findings and symptoms suggest an acute
stroke, immediately begin transport as soon as the patient’s condition is assessed as stable (ie, load and go) to a
stroke-ready hospital and notify the receiving facility that the patient is in transit. Consider air medical trans-
port when ground transport to the nearest stroke-ready hospital is longer than 1 hour (Jauch, et al., 2013).
Perform a secondary survey during transport as dictated by the patient’s condition. Monitor the
patient’s breathing effort and be prepared to assist ventilations. Apply a pulse oximeter and a cardiac
monitor. Use the least invasive method possible to maintain oxygen saturation above 94% (Jauch,
et al., 2013). Obtain a 12-lead ECG and establish IV access with normal saline. Avoid dextrose-
containing fluids in nonhypoglycemic patients because these solutions can worsen cerebral injury
(Jauch, et al., 2013). Check the patient’s serum glucose level; this helps to differentiate stroke from other
common causes of stroke symptoms (eg, hypoglycemia). Give dextrose if the patient is hypoglycemic. If
consistent with local protocols, obtain blood samples for laboratory testing and transfer the samples to
receiving facility staff on arrival. Do not delay transport to perform these procedures.
A supine position is recommended if the patient is not hypoxic and can tolerate it (Jauch, et al., 2013).
Elevate the head of the stretcher 15 to 30 degrees if the patient is at risk for airway obstruction or aspi-
ration or if increased intracranial pressure is suspected (Jauch, et al., 2013). Monitor vital signs at least
every 15 minutes and more frequently if any vital sign is abnormal. In general, hypertension should not be
treated in the prehospital setting. Hypotension should be treated in accordance with the underlying cause
of the hypotension.
Encourage family members or bystanders to accompany the patient to the hospital so they can provide
historical information to the stroke team and provide support to the patient. If the patient’s family cannot
go to the hospital, obtain a telephone number where they can be contacted, preferably a cell phone number,
and be certain to document this information for subsequent retrieval by other members of the health care team.
Because strokes are dynamic processes, reassess the patient often during transport. Document any
changes in the patient’s presentation from your initial assessment findings and relay this information
to the appropriate staff on arrival at the receiving facility.
Stroke Centers
[Objectives 8, 9]
At present, acute stroke care in the United States consists of a tiered system of hospitals: nonstroke hos-
pitals, acute stroke–ready hospitals (ASRHs), PSCs, and CSCs (Table 8.3). Acute stroke teams (ASTs)
are a key element for the delivery of stroke care within a stroke center. The AST is responsible for
TABLE 8.3 Comparison of Elements of Acute Stroke Care Facilities

Non-
Stroke
Element Center ASRH PSC CSC
Access to No Yes, available within Yes, available within Yes, 24/7 coverage
neurosurgical 3 hours or by 2 hours, in-house or by
services transfer transfer
AST available No At bedside within At bedside within 15 min At bedside within
15 min 15 min
IV tPA capability No 60-min or less door- 60-min or less door-to- 60-min or less
24/7 to-needle time needle time door-to-needle
time
Rapid brain No Completed and read Completed and read within Completed and read
imaging 24/7 within 45 min of 45 min of order within 45 min of
order order
Stroke unit No Not required unless Required for admitted Required for admitted
patient admitted patients patients
Typical bed 20 to 50 30 to 100 100 to 400 400 to 1500
count
ASRH, acute stroke–ready hospital; AST, acute stroke team; CSC, comprehensive stroke center; IV, intravenous; PSC, primary
stroke center; tPA, tissue plasminogen activator
Sources: (Alberts, et al., 2013; Higashida, et al., 2013)
responding to patients with an acute stroke and initiating diagnostic testing and immediate care (not
ongoing in-hospital care) (Alberts, et al., 2011).
The role of an ASRH is to stabilize the patient, provide specific acute stroke care therapies, and arrange
transportation of patients to the nearest PSC or CSC as determined by the patient’s clinical status
(Higashida, et al., 2013). Minimum staffing of the AST at an ASRH should include a nurse (or nurse
practitioner or physician assistant) and a physician who have received training in acute stroke care
(Alberts, et al., 2013). Stroke team members should be available 24 hours a day, 7 days a week, responding
within 15 minutes of patient arrival (Alberts, et al., 2013). An ASRH should establish a telemedicine link
to a PSC or CSC within 20 minutes of when it is deemed medically necessary (Alberts, et al., 2013). This
link can be used to obtain clinical stroke expertise, interpret brain imaging, initiate fibrinolytic therapy if
indicated, and address issues such as active bleeding or high intracranial pressures (Higashida, et al., 2013).
PSCs are able to care for the majority of stroke patients with typical ischemic strokes who do not require
endovascular therapy, neurosurgical interventions, or intensive care unit–level care or who have multisystem
disease (Higashida, et al., 2013). Intensive care unit–level care is offered by some PSCs (Higashida, et al., 2013).
CSCs are capable of providing care for the most complex stroke patients, including those with large
ischemic strokes, all types of hemorrhagic strokes, or multisystem involvement, as well as those who
require surgical or endovascular interventions and intensive care unit–level care (Higashida, et al., 2013).
Established recommended target times for hospitals that receive acute stroke patients include the fol-
lowing: (1) emergency department physician evaluation within 10 minutes of arrival; (2) stroke team
notification within 15 minutes of arrival; (3) brain computed tomography (CT) scan within 25 minutes
of arrival; (4) interpretation of the CT scan within 45 minutes of arrival; (5) if indicated, door-to-drug
time of 60 minutes or less from arrival in the emergency department for at least 80% of patients; (6) and
door-to-stroke-unit admission within 3 hours of arrival (Jauch, et al., 2013).
Triage and Initial Evaluation

[Objective 7]
Proper triage of stroke patients requires that emergency nurses be familiar with both typical and unusual
stroke presentations (Summers, et al., 2009). Within minutes of the patient’s arrival, reassess the patient’s
ABCs and ensure that the patient has a secure airway and adequate breathing. Assess the patient’s tem-
perature, heart rate, blood pressure, ventilatory rate, and oxygen saturation. Give oxygen if needed to main-
tain an oxygen saturation above 94%; supplemental oxygen is not recommended in nonhypoxic patients
with acute ischemic stroke (Jauch, et al., 2013). Perform a fingerstick glucose test to assess for hypoglycemia
and administer dextrose if the blood glucose is less than 60 mg/dL (Jauch, et al., 2013).
A minimum of two IV lines should be established if it is anticipated that the patient will receive fibri-
nolytic therapy. One site is used for infusing IV fluids (ie, normal saline) and medications and the other is
used for the administration of tPA. Generally, normal saline is infused at a rate of 75 to 100 mL/hr to
maintain normovolemia (Summers, et al., 2009) unless contraindications exist (eg, renal failure, heart
failure, pulmonary edema).
All patients with suspected acute stroke should receive continuous ECG monitoring to detect myo-
cardial ischemia and cardiac dysrhythmias (eg, atrial fibrillation) and monitoring should be continued for
at least the first 24 hours after stroke (Jauch, et al., 2013). A 12-lead ECG should be obtained to evaluate
for preexisting cardiac disease and concurrent myocardial injury (Gorelick, et al., 2008).
Patient History
[Objective 7]
Verify the patient’s last known-well time. Was anyone with the patient with his or her symptoms started?
What was the patient doing when the symptoms began? Did the patient complain of a headache? Did he
or she have a seizure? Has there been a change in his or her level of responsiveness? Is there a history of
any recent trauma? Review the patient’s past medical history and determine the presence of stroke risk
factors. Ask if there is any history of drug abuse, migraine, seizure, infection, trauma, or pregnancy
(Jauch, et al., 2013). Find out the medications the patient is currently taking and his or her allergies
to medications.
Physical Examination
[Objectives 7, 10]
When performing a physical examination, consider the presence of conditions that mimic stroke
(Box 8.2). Examine the head and face for signs of trauma or recent seizure activity (eg, contusions, tongue
BOX 8.2 Conditions That Mimic Stroke

• Bell’s palsy • Encephalitis, meningitis
• CNS abscess or tumor • Hypertensive encephalopathy
• Complicated migraine • Metabolic disorders (eg, hyperglycemia,
hypoglycemia, hyponatremia)
• Concussion with head injury • Positional vertigo
• Conversion disorder • Seizures
• Drug toxicity (eg, carbamazepine, • Subdural hematoma
lithium, phenytoin)
• Eclampsia • Wernicke’s encephalopathy
laceration). Auscultate the neck for carotid bruits, which suggests the presence of carotid atherosclerotic
disease. Assess for jugular venous distention, which may be a sign of heart failure. Auscultate heart
sounds, which may reveal murmurs or gallops, and lung sounds. Examine the extremities for asymmetric
strength and movement and asymmetric or diminished pulses. Inspect the skin for petechiae, purpura, or
ecchymoses, which may be the result of trauma, a platelet disorder, or a coagulation disorder.
Neurologic Examination
[Objective 7]
Perform a brief neurologic screening assessment using a validated stroke scale. If the initial history, phys-
ical examination, and neurologic examination are suggestive of stroke, the stroke team should be
mobilized.
The NIHSS is widely used and takes less than 10 minutes to perform. Training is required to use the scale
accurately and to ensure interrater reliability. Use of the NIHSS is helpful in objectively rating stroke severity,
promoting comparisons with NIHSS examinations performed by other members of the stroke team
(Nye, et al., 2012), recognizing (and documenting) improvement or deterioration in the patient’s neurologic
status, improving communication among members of the health care team, providing prognostic informa-
tion, and influencing acute treatment decisions. The NIHSS assigns points for neurologic deficits with
possible scores ranging from 0 to 42; the lower the score, the less the impairment. A score of 0 indicates
no impairment, a score between 1 and 20 indicates mild to moderate impairment, and a score of more than
20 indicates severe impairment. An increase of 2 or more points on serially administered NIH stroke scales
suggests stroke progression, although smaller changes may be equally significant.
Diagnostic Tests
[Objective 7]
Diagnostic laboratory tests should be drawn immediately and before IV fluids are started. Of the labo-
ratory tests recommended during the initial emergency evaluation (see Box 8.3), only the assessment of
blood glucose must precede the initiation of IV tPA (Jauch, et al., 2013).
Additional diagnostic studies should be obtained in selected cases such as pregnancy testing, blood
alcohol level, blood and urine toxicology screen (for patients with possible substance abuse), blood
cultures (if endocarditis is suspected), liver function tests and ammonia level (for patients with an
unexplained altered level of consciousness), lumbar puncture (for suspected meningitis or if SAH is sus-
pected and CT is negative for blood), electroencephalogram (for suspected seizures), and arterial blood
gas tests (for suspected hypoxia).
The usefulness of chest radiography in the absence of clinical evidence of underlying pulmonary, car-
diac, or vascular disease is unclear; if chest radiographs are obtained, they should not delay administration
of IV tPA unless there are specific concerns about intrathoracic issues, such as aortic dissection (Jauch,
et al., 2013).
BOX 8.3 Laboratory Studies for Suspected Stroke

• Activated partial thromboplastin time • Renal function tests
• Cardiac biomarkers; troponin is preferred • Serum electrolytes
• Complete blood count, including platelet • Serum glucose
count
• Prothrombin time or international normalized
ratio
Brain Imaging
[Objective 7]
A noncontrast brain CT or brain magnetic resonance imaging (MRI) scan should be obtained for all
patients with suspected acute ischemic stroke to confirm or exclude the presence of cerebral hemorrhage
(Jauch, et al., 2013). Although MRI has been shown to be equivalent to CT in the detection of acute
hemorrhage, CT remains the traditional initial imaging modality for the evaluation of suspected stroke
because of its widespread availability, short acquisition time of 1 to 2 minutes, noninvasiveness, and gen-
eral safety for both stable and unstable patients (Nentwich & Veloz, 2012). In patients presenting with a
history and clinical examination consistent with acute stroke, brain imaging is useful in determining
stroke location and vascular distribution, the presence of bleeding, the severity of ischemic stroke,
and the presence of large-vessel occlusion (Jauch, et al., 2013). Brain imaging is also useful for identifying
the size of the core of irreversibly infarcted tissue and determining the amount of hypoperfused tissue at
risk for subsequent infarction unless adequate perfusion is restored, which can affect treatment decisions
(Nentwich & Veloz, 2012). Brain imaging should be completed within 25 minutes and interpreted
within 45 minutes of emergency department arrival (Jauch, et al., 2013).
Intravenous Fibrinolysis
[Objective 7]
Fibrinolytic therapy with IV tPA is recommended for selected patients who may be treated within 3 hours
of onset of ischemic stroke (American Stroke Association, 2014). IV tPA is recommended for admin-
istration to a select group of eligible patients who present within a 3- to 4.5-hour window after the onset
of acute stroke symptoms (American Stroke Association, 2014). The eligibility criteria for treatment in
this time frame are similar to those for patients treated within 3 hours of symptom onset, but with addi-
tional exclusion criteria. The AHA recommends that physicians review current inclusion and exclusion
criteria to determine patient eligibility (Jauch, et al., 2013). A recently published statement by the AHA/
ASA reflects the scientific rationale behind the eligibility criteria for the use of IV tPA in acute ischemic
stroke (Demaerschalk, et al., 2016).
Hospital and registry estimates of tPA treatment rates for stroke range from 20% to 30%, but national
estimates of tPA use have ranged only from 3% to 5% since 2004 (Demaerschalk, et al., 2016). Reasons
suggested for this low use include a lack of public education about stroke signs and symptoms and the
need for rapid response, the slow adoption of tPA by the medical community, the complex systems
within the hospital necessary for safe and timely tPA administration, and the low eligibility rate of ische-
mic stroke patients for tPA (Demaerschalk, et al., 2016). It is estimated that the eligibility for tPA within
a population of ischemic stroke patients range from 6% to 8% of all strokes, with the most common rea-
son for exclusion being delays in presentation for medical attention (Demaerschalk, et al., 2016). To
reduce symptom onset–to-treatment time, experts recommend that patients who are eligible for IV
tPA and who did not have intracranial vascular imaging as part of their initial evaluation should begin
receiving IV tPA before being transported for additional imaging and before being transferred for endo-
vascular treatment (Powers, et al., 2015).
IV tPA is a weight-based therapy. Although a small retrospective study found that documented esti-
mated weights for patients receiving tPA were not significantly different from actual weights, it is pref-
erable to obtain the patient’s actual weight before tPA administration (Graves, et al., 2013).The tPA dose
is 0.9 mg/kg, not to exceed 90 mg. Ten percent of the dose is given as an initial IV bolus over 1 minute
followed by the remaining 90% of the dose infused using an infusion pump during the next hour. Cal-
culate the desired dose, withdraw any excess amount from the vial, and then discard the excess amount to
prevent accidental overdose (Summers, et al., 2009).
Bleeding is the major complication of treatment with IV tPA. Although bleeding may occur from any
site, intracranial bleeding is of particular concern. Close monitoring of the patient is critical. In addition
to using the NIHSS scale to assess neurologic deficits, assess pupil size, and use the Glasgow Coma Scale
(GCS) to monitor the patient’s level of responsiveness. These assessments should be performed every
hour for the first 24 hours after tPA administration and more often if indicated (Summers, et al.,
2009). The physician should be notified, the tPA infusion stopped (if tPA is still infusing), and an emer-
gent CT scan obtained if the patient develops acute hypertension, nausea or vomiting, or severe head-
ache, or if the patient has a worsening neurologic examination (Jauch, et al., 2013).
Closely observe for swelling of the tongue, lips, or oropharynx (ie, orolingual angioedema). Although
this complication of tPA administration occurs in a small number of patients, it can lead to airway
obstruction. Patients taking angiotensin-converting enzyme inhibitors and those with infarctions that
involve the insular and frontal cortex appear to be at highest risk (Jauch, et al., 2013). Treatment includes
the administration of IV ranitidine, diphenhydramine, and methylprednisolone (Jauch, et al., 2013).
Measure the patient’s blood pressure (BP) every 15 minutes during and after the tPA infusion for
2 hours, then every 30 minutes for 6 hours, and then every hour until 24 hours after the infusion
(Jauch, et al., 2013). Assess the patient’s BP more frequently if his or her systolic BP is more than
180 millimeters of mercury (mm Hg) or if the diastolic BP is more than 105 mm Hg (Jauch, et al.,
2013). Administer antihypertensive medications per physician’s orders to maintain the patient’s BP
at or below these levels (Jauch, et al., 2013). Obtain a brain CT or MRI scan 24 hours postinfusion before
starting anticoagulants or antiplatelet agents (Jauch, et al., 2013).
Other Therapies
[Objective 7]
In addition to IV tPA, other therapies for acute ischemic stroke include invasive catheter-based reper-
fusion therapies that include intraarterial (IA) fibrinolysis, mechanical thrombectomy, or balloon angio-
plasty with or without stent placement (Ramee & White, 2014). Use of these therapies requires stroke
centers with the resources and physician expertise to safely perform these procedures (Jauch, et al., 2013).
Patients eligible for IV tPA should receive IV tPA even if endovascular treatments are being considered
(Powers, et al., 2015).
Best Practices
Although current stroke guidelines recommend a door-to-needle time of 60 minutes or less for tPA
administration to eligible ischemic stroke patients, research has shown that less than 30% of patients
are treated within this period in the United States (Fonarow, et al., 2014). Target: Stroke is a national
quality improvement program launched in 2010 by the AHA/ASA in partnership with other organiza-
tions. The program aims to assist hospitals in improving acute ischemic stroke care by reducing door-to-
needle time for eligible patients being treated with tPA.
The primary goal during phase I of the program was for participating hospitals to administer tPA to at
least 50% of their patients with acute ischemic stroke within 60 minutes of hospital arrival (American
Stroke Association, 2014). After the start of the Target: Stroke initiative, research has shown a marked
improvement in the timeliness of tPA administration, with the proportion of patients with a door-to-
needle time of 60 minutes or less increasing from 29.6% to 53.3% (Fonarow, et al., 2014). Study results
also showed that the improvement in timeliness in tPA administration was associated with improved
clinical outcomes including lower in-hospital mortality, more frequent discharge to a more indepen-
dently functioning environment, and lower rates of tPA complications, including symptomatic intracra-
nial hemorrhage (Fonarow, et al., 2014).
On the basis of the success of phase I, the AHA/ASA launched phase II to continue eliminating treatment
delays for people who suffer ischemic strokes by challenging hospitals to provide tPA to eligible patients even
more promptly (American Stroke Association, 2014). The primary goal of phase II of Target: Stroke is to
achieve a door-to-needle time within 60 minutes in 75% or more of acute ischemic stroke patients treated
with IV tPA; a secondary goal is to achieve a door-to-needle time within 45 minutes in 50% or more of acute
ischemic stroke patients treated with IV tPA (American Stroke Association, 2014).
Target: Stroke encourages participating hospitals to adopt 11 evidence-based best practice strategies
that can improve the speed with which tPA is administered in acute ischemic stroke. These strategies
include the following (American Stroke Association, 2014):
• Encouraging prenotification of receiving hospitals by EMS personnel
• Using stroke-specific order sets, guidelines, and stroke tools
• Using a rapid triage protocol to aid in the prompt recognition of stroke
• Activating the entire stroke team with a single call or page, including notification to ensure prompt
availability of the CT/MRI scanner
• When appropriate, transferring eligible stroke patients from the emergency department triage area
directly to the CT/MRI scanner for initial neurologic examination and brain imaging
• Rapid acquisition and interpretation of brain imaging
• Rapid laboratory testing, including point of care testing if indicated
• Premixing tPA for high likelihood candidates, even before brain imaging
• Prompt administration of IV tPA to eligible patients
• Using a stroke team–based approach
• Providing prompt and rapid feedback to the stroke team with regard to performance

information presented in this chapter. As you work through the case study, remember that there may be
CHAPTER QUIZ
Multiple Choice
____ 1. What is the most common cause of stroke?

A. A thrombus
B. An embolus
C. A ruptured cerebral aneurysm
D. An arteriovenous malformation
____ 2. Paramedics are at the home of a 62-year-old man presenting with signs and symptoms
suggestive of stroke. Which of the following is the most important question that
should be asked of this patient, family members, or others at the scene?
A. “When did you last see a physician?”
B. “When did your symptoms begin?”
C. “Do you have a history of hypertension?”
D. “Are you currently taking any blood thinners?”
____ 3. Which of the following dysrhythmias is most likely to precipitate a stroke?

A. Junctional rhythm
B. Atrial fibrillation
C. Sinus bradycardia
D. Ventricular escape rhythm
____ 4. A 52-year-old woman presents with a sudden onset of numbness and weakness in
her right arm and leg. Family members state her signs and symptoms began while the
patient was preparing breakfast 1 hour ago. Examination reveals unequal grips with
marked weakness on the patient’s right side. Her blood pressure is 174/86 mm Hg,
pulse 88 beats/min, and ventilatory rate 16 breaths/min. Her oxygen saturation on
room air is 96%. As you establish vascular access, you note improvement in the
patient’s symptoms. After 25 minutes, her grips become equal and there is no
weakness on the patient’s right side. You suspect:
A. Hypoglycemia
B. Acute ischemic stroke
C. TIA
D. SAH
____ 5. The acute phase of stroke care:

A. Includes prehospital care for stroke
B. Seeks to identify stroke symptoms and stroke type
C. Is a time-sensitive phase in the first hours after stroke onset
D. Focuses on confirming the cause of stroke and preventing complications
____ 6. During which of the following links of the Stroke Chain of Survival is immediate
emergency department triage performed?
A. Data
B. Drug
C. Door
D. Delivery
____ 7. For hospitals that receive acute stroke patients, a patient presenting with a possible
stroke should be seen by a physician within __ of his or her arrival.
A. 5 minutes
B. 10 minutes
C. 25 minutes
D. 45 minutes
____ 8. Which of the following must be performed before IV tPA is administered?

A. Serum glucose
B. Serum electrolytes
C. Cardiac biomarkers
D. Activated partial thromboplastin time
____ 9. Fibrinolytic therapy with IV tPA is recommended for selected patients who may be
treated within 3 hours of onset of ischemic stroke. Which of the following is a
contraindication to fibrinolytic therapy for this patient?
A. The patient’s age is 55.
B. The patient’s symptoms began 45 minutes ago.
C. The patient has an international normalized ratio of 2.2.
D. The patient has a history of a myocardial infarction in 1996.
____ 10. Which of the following is true of acute stroke care facilities in the United States?
A. Neurosurgical coverage is available 24/7 at ASRHs.
B. Acute stroke care facilities should have a stroke team at the patient’s bedside within
15 minutes of arrival.
C. Acute stroke care facilities should have IV tPA capability 24/7 with a 90-minute or
less door-to-needle time.
D. The results of brain imaging should be obtained within 60 minutes of the order at a
stroke-ready facility.
CASE STUDY 8-1

Paramedics are called to a private residence for a 78-year-old man with a “possible stroke.” The patient’s
wife is present.
1. The general impression reveals an elderly man sitting in a recliner. He is awake and aware of the
paramedics’ approach. His breathing appears unlabored and equal chest risk and fall is observed.
The patient’s skin color is pink. What should be done next?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
2. The patient attempts to answer questions, but his speech is garbled. His breathing is quiet
and unlabored at a rate of 16 breaths/min. The patient’s radial and carotid pulses are strong but
irregular. His skin is warm, pink, and dry. What should be done next?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
3. Differentiate between the CPSS and the Los Angeles Motor Scale.
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
4. The examination reveals the patient has left facial droop, left arm drift, slurred speech, and a weak
left grip. His symptoms began about 35 minutes ago while watching television with his wife. The
patient’s blood pressure is 180/94 mm Hg, his heart rate is irregular at 80 to 110 beats/min, and the
cardiac monitor reveals atrial fibrillation. The patient has a history of hypertension, for which he
takes lisinopril and hydrochlorothiazide daily, and has no known allergies. What should be done
now?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
5. The patient’s glucose level is within normal limits. Why should the serum glucose level be
determined during the initial management of a patient with suspected stroke?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
6. Describe the initial interventions that should be performed upon the patient’s arrival in the
emergency department.
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
7. The patient’s oxygen saturation level is 96% on room air. Should supplemental oxygen be
administered to this patient?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
8. Why is ECG monitoring recommended for patients with suspected acute stroke?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
9. The patient has a NIHSS score of 8. Shortly after physician evaluation and arrival of the stroke team,
a brain CT scan is obtained and the results revealed no evidence of bleeding. After reviewing the
inclusion and exclusion criteria for treatment with IV tPA, the decision is made to begin fibrinolytic
therapy. How is this medication administered?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
10. What assessments should be performed during and after treatment with tPA?
_____________________________________________________________________________
_____________________________________________________________________________
_____________________________________________________________________________
1. A. Most strokes are the result of blockages caused by blood clots that develop within the brain artery
itself (ie, cerebral thrombosis) or clots that arise elsewhere in the body and then migrate to the brain
(ie, cerebral embolism).
OBJ: Describe the major types of stroke.
2. B. Determining and documenting the time of symptom onset is critical and the single most
important determinant of treatment options during the hyperacute phase of stroke care
(Summers, et al., 2009). The patient, patient’s family, coworkers, or others at the scene should
be asked when the patient was last known to be symptom-free (ie, last known normal or last
known-well time).
OBJ: Describe the initial emergency care for acute ischemic stroke.
3. B. Atrial fibrillation is the cardiac source of emboli in 50% of cardioembolic strokes (Babarro,
et al., 2009).
OBJ: Describe the major types of stroke.
4. C. A TIA is a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or ret-
inal ischemia, without acute infarction. A TIA should be treated with the same urgency as a com-
pleted stroke.
OBJ: Explain what a transient ischemic attack (TIA) is and how it differs from stroke.
5. D. The hyperacute phase of stroke care refers to the key interventions involved in the assessment,
stabilization, and treatment in the first hours after stroke onset (Casaubon & Suddes, 2013).
During this time-sensitive phase, which encompasses all prehospital and initial emergency care
for TIA and stroke, attention is focused on identifying stroke symptoms and stroke type, identi-
fying treatment options, and executing the treatment plan as quickly as possible. The acute phase of
stroke care refers to key interventions involved in the assessment, treatment or management, and
early recovery in the first days after stroke onset (Casaubon & Suddes, 2013). This phase focuses
on confirming the cause of stroke and preventing medical complications, preparing the patient and
family for discharge, and establishing long-term secondary prevention measures (Summers,
et al., 2009).
OBJ: Differentiate between the hyperacute and acute phases of stroke care.
6. C. The door link in the Stroke Chain of Survival refers to immediate emergency department triage
upon the patient’s arrival.
OBJ: Discuss the links in the Stroke Chain of Survival.
7. B. For hospitals that receive acute stroke patients, a patient presenting with a possible stroke should
be seen by a physician within 10 minutes of his or her arrival (Jauch, et al., 2013).
OBJ: State the recommended target times for key interventions during the hyperacute phase of
acute stroke care.
8. A. Of the laboratory tests recommended during the initial emergency evaluation of a patient with a
possible stroke, only the assessment of blood glucose must precede the administration of IV tPA
(Jauch, et al., 2013).
9. C. Some of the contraindications to fibrinolytic therapy include a history of previous intracranial

hemorrhage, symptoms that suggest SAH, a patient who is anticoagulated and has an international
normalized ratio greater than 1.7, significant head trauma or prior stroke within the last 3 months,
and a systolic BP greater than 185 mm Hg or a diastolic BP greater than 110 mm Hg (Jauch,
et al., 2013).
10. B. Acute stroke care facilities should have a stroke team at the patient’s bedside within 15 minutes of
arrival. Neurosurgical coverage is available 24/7 at a CSC; it is available within 2 hours, in-house, or
by transfer at a PSC; and it is available within 3 hours or by transfer at an ASRH. Acute stroke care
facilities should have IV tPA capability 24/7 with a 60-minute or less door-to-needle time. Rapid
brain imaging should be completed within 25 minutes of patient arrival and the results obtained
within 45 minutes of the order.
OBJ: Compare elements of acute stroke care facilities in the United States.

1. The next step is to perform a primary survey. Ask the patient questions to determine his level of
responsiveness and the adequacy of his airway and breathing. Quickly estimate the patient’s heart
rate and determine the quality of his pulse (ie, fast or slow, regular or irregular, weak or strong).
Evaluate his skin temperature, color, and moisture to assess perfusion. Perform a brief neurologic
evaluation, assess the need for a defibrillator, and expose the patient for further evaluation.
2. A focused history should be obtained and the patient’s normal baseline mental status determined.
The patient, patient’s family, or others at the scene should be asked when the patient was last known
to be symptom-free (ie, last known normal or last known-well time). Determining and documenting
the time of symptom onset is critical and the single most important determinant of treatment
options during the hyperacute phase of stroke care (Summers, et al., 2009).
OBJ: Explain why rapid identification of stroke is critical.
3. The CPSS is a commonly used stroke screening tool. The CPSS is taught as the three Ds of “drift
(arm), droop (facial weakness), and dysarthria (slurred speech).” The Los Angeles Motor Scale is a
tool used to rate stroke severity in the field. It assigns point values to the LAPSS items of facial
weakness, arm strength, and grip.
4. Because the patient’s assessment findings suggest an acute stroke, transport should begin immediately to
a stroke-ready hospital. EMS personnel should notify the receiving facility that the patient is en route.
5. Assessment of the patient’s serum glucose level is important because it helps to differentiate stroke
from other common causes of stroke symptoms, such as hypoglycemia.
OBJ: Give examples of medical conditions that mimic stroke.
6. Within minutes of the patient’s arrival, reassess the patient’s ABCs and ensure that the patient has a
secure airway and adequate breathing. Assess the patient’s temperature, heart rate, blood pressure,
ventilatory rate, and oxygen saturation. If not already done, perform a fingerstick glucose test to
assess for hypoglycemia. Establish a minimum of two IV lines if it is anticipated that the patient
will receive fibrinolytic therapy.
7. No, not at this time. Give oxygen if needed to maintain an oxygen saturation above 94%; supple-
mental oxygen is not recommended in nonhypoxic patients with acute ischemic stroke (Jauch,
et al., 2013).
8. All patients with suspected acute stroke should receive continuous ECG monitoring to detect myo-
cardial ischemia and cardiac dysrhythmias (eg, atrial fibrillation) and monitoring should be contin-
ued for at least the first 24 hours after stroke (Jauch, et al., 2013). A 12-lead ECG should be obtained
to evaluate for preexisting cardiac disease and concurrent myocardial injury (Gorelick, et al., 2008).
9. IV tPA is a weight-based therapy. The tPA dose is 0.9 mg/kg, not to exceed 90 mg. Ten percent of
the dose is given as an initial IV bolus over 1 minute followed by the remaining 90% of the dose
infused using an infusion pump during the next hour. Calculate the desired dose, withdraw any
excess amount from the vial, and then discard the excess amount to prevent accidental overdose
(Summers, et al., 2009).
10. Use the NIHSS scale to assess neurologic deficits, assess the patient’s pupil size, and use the GCS to
monitor the patient’s level of responsiveness. These assessments should be performed every hour for
the first 24 hours after tPA administration and more often if indicated (Summers, et al., 2009). Mea-
sure the patient’s BP every 15 minutes during and after the tPA infusion for 2 hours, then every
30 minutes for 6 hours, and then every hour until 24 hours after the infusion (Jauch, et al.,
2013). Assess the patient’s BP more frequently if his or her systolic BP is more than 180 mm
Hg or if the diastolic BP is more than 105 mm Hg (Jauch, et al., 2013). Administer antihypertensive
medications per physician’s orders to maintain the patient’s BP at or below these levels (Jauch,
et al., 2013).
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CHAPTER 9
Post Test
Multiple Choice
____ 1. A 48-year-old man became unresponsive shortly after presenting to you with nausea
and generalized chest discomfort. You observe gasping breathing and are unsure if
you feel a pulse. You should now:
A. Call for help and begin chest compressions.
B. Wait until breathing stops and then check again for a pulse.
C. Begin chest compressions only if you are certain a pulse is absent.
D. Observe the patient for 2 minutes, then reassess his breathing and pulse.
____ 2. Which of the following is the most likely complication of inferior wall myocardial
infarction (MI)?
A. Cardiogenic shock
B. Ventricular rupture
C. Bradydysrhythmias
D. Tachydysrhythmias
____ 3. A 52-year-old man is complaining of palpitations that came on suddenly after

walking up a short flight of stairs. His symptoms have been present for about
20 minutes. He denies chest pain and is not short of breath. His skin is warm and
dry; breath sounds are clear. His blood pressure (BP) is 144/88 millimeters of
mercury (mm Hg), his heart rate is 186 beats per minute (beats/min), and his
ventilatory rate is 18 breaths/min. The cardiac monitor reveals the rhythm here.
Vascular access has been established. Which of the following medications is most
appropriate in this situation?
A. Dopamine or sotalol
B. Furosemide or atropine
C. Nitroglycerin (NTG) or morphine
D. Procainamide or amiodarone
259
260 CHAPTER 9 Post Test
____ 4. Your general impression of a 78-year-old woman reveals that her eyes are closed, she is
not moving, you can see no rise and fall of her chest or abdomen, and her skin
color is pale. When you arrive at the patient’s side, you confirm that she is
unresponsive. Your best action in this situation will be to:
A. Open her airway and give two breaths.
B. Apply an automated external defibrillator (AED).
C. Assess breathing and determine whether she has a pulse.
D. Prepare the necessary equipment to insert an advanced airway.
____ 5. A 60-year-old woman has suffered a cardiac arrest. A health care professional trained
in endotracheal intubation has intubated the patient. Which of the following
findings would indicate inadvertent esophageal intubation?
A. Jugular vein distention
B. Subcutaneous emphysema
C. Gurgling sounds heard over the epigastrium
D. Breath sounds heard on only one side of the chest
____ 6. Hypotension (ie, a systolic BP of less than 90 mm Hg) after the return of spontaneous
circulation (ROSC) may necessitate the use of:
A. Fluid boluses and isoproterenol.
B. Procainamide, epinephrine, or dopamine.
C. Epinephrine, dopamine, or norepinephrine.
D. Fluid boluses, procainamide, and isoproterenol.
____ 7. Which of the following is incorrect with regard to a postevent debriefing?

A. The facilitator should use open-ended questions to encourage discussion.
B. Team members are encouraged to identify lessons learned in a nonpunitive
environment.
C. The gather phase of the debriefing includes a comparison of the team’s actions
with current resuscitation algorithms.
D. Team members are given an opportunity to reflect on their performance and how
their performance can be improved.
____ 8. Assuming there are no contraindications, which of the following can be performed as
an initial intervention for a stable but symptomatic patient with the rhythm shown?
II
III
A. Defibrillation
B. Vagal maneuvers
C. Administration of intravenous (IV) diltiazem
D. Administration of IV epinephrine
CHAPTER 9 Post Test 261
____ 9. A 62-year-old man received IV tissue plasminogen activator (tPA) 2 hours ago
after a diagnosis of acute ischemic stroke. While assessing the patient’s vital signs,
you observe swelling of the patient’s lips and tongue. Your best course of action will
be to:
A. Administer aspirin and IV heparin.
B. Administer IV antihistamines and steroids.
C. Observe and reassess the patient every 15 minutes.
D. Request an emergent brain computed tomography scan.
____ 10. During a cardiac arrest, multiple attempts to establish a peripheral IV have proved
unsuccessful. Your best course of action at this time will be to:
A. Insert a central line.
B. Attempt intraosseous access.
C. Discontinue resuscitation efforts.
D. Continue peripheral IV attempts until successful.
____ 11. Synchronized cardioversion:

A. Is used only for atrial dysrhythmias.
B. Delivers a shock during ventricular depolarization.
C. Delivers a shock between the peak and end of the T wave.
D. Is used only for rhythms with a ventricular rate of less than 60 beats/min.
____ 12. An 84-year-old man presents with an acute onset of altered mental status. The
cardiac monitor shows the rhythm here. The patient’s BP is 58/30 mm Hg and
his ventilatory rate is 14 breaths/min. His skin is cool, moist, and pale. His
blood oxygen saturation level (SpO2) on room air is 95%. An IV has been
established.
II
On the basis of the information provided, your best course of action will be to:
A. Prepare for transcutaneous pacing.
B. Give amiodarone 300 mg IV push.
C. Give epinephrine 1 mg IV bolus and reassess.
D. Observe the patient and monitor for signs of deterioration.
Questions 13 through 23 pertain to the following scenario

Paramedics are on the scene with a 55-year-old man who is complaining of severe chest discomfort.
He describes his discomfort as a “heavy pressure” in the middle of his chest that has been present for
about 1 hour.
____ 13. Which of the following actions performed at the scene is most likely to reduce
subsequent treatment delays at the hospital?
A. Giving aspirin
B. Obtaining a 12-lead electrocardiogram (ECG)
C. Assessing vital signs and oxygen saturation
D. Assessing the patient’s degree of discomfort
____ 14. The patient rates his discomfort 9/10. His BP is 126/72 mm Hg and ventilations 14
breaths/min. His SpO2 on room air is 95%. The cardiac monitor shows a sinus rhythm
at 60 beats/min. Immediate management of this patient should include:
A. Giving aspirin and NTG.
B. Establishing IV access and giving aspirin.
C. Administering oxygen and establishing IV access.
D. Administering oxygen and obtaining a targeted history.
____ 15. Current guidelines recommend obtaining an initial 12-lead ECG within ____ of
patient contact when an acute coronary syndrome (ACS) is suspected.
A. 10 minutes
B. 30 minutes
C. 45 minutes
D. 60 minutes
____ 16. When the patient’s 12-lead ECG is reviewed, the results should be used to classify the
patient into one of three groups. Which of the following correctly reflects these categories?
A. ST elevation (STE), normal ECG, Q waves
B. Q waves, ST depression (STD), inconclusive ECG
C. STD, normal ECG, inconclusive ECG
D. STE, STD, normal or nondiagnostic ECG
____ 17. A 12-lead ECG has been obtained.
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
V1
II
V5
(From Phalen T, Aehlert B: The 12-lead ECG in acute coronary syndromes, ed 3, St. Louis, 2012, Mosby.)
The patient’s 12-lead ECG shows:

A. STE in leads II, III, and aVF.
B. STD in leads I, II, III, and aVL.
C. STE in leads I, aVL, and V2 to V6.
D. STD in leads V1, V4, V5, and V6.
____ 18. To be considered significant, ECG findings, such as STE or STD, need to be
viewed in two or more contiguous leads. Which of the following are contiguous
leads?
A. V1, V4, and V5
B. V2, V3, and V4
C. III, aVF, and V1
D. I, II, III, and aVL
____ 19. The patient’s 12-lead ECG findings suggest a(n) _____ MI.
A. Posterior
B. Inferolateral
C. Anterolateral
D. Non–ST elevation
____ 20. On the basis of the patient’s 12-lead ECG findings:

A. The patient should be classified as having a nondiagnostic ECG and discharged
with follow-up instructions.
B. The patient should be classified as having an ST elevation MI (STEMI) and should
be evaluated for immediate reperfusion therapy.
C. The patient should be classified as having a normal ECG; serial ECGs should be
obtained at 30-minute intervals to detect the development of ST elevation.
D. The patient should be classified as having a non–ST elevation ACS (NSTE-ACS)
and should be admitted to a monitored bed for further evaluation.
____ 21. Vascular access has been established. The patient’s BP is 130/70 mm Hg, his pulse is 60
beats/min, and his ventilatory rate is 14 breaths/min. Assuming there are no
contraindications for any of the following medications, which of the following would be
appropriate for this patient at this time?
A. Aspirin and NTG
B. Aspirin and a nonsteroidal antiinflammatory drug (NSAID)
C. An oral beta-blocker and an NSAID
D. Aspirin and a calcium channel blocker (CCB)
____ 22. NTG has been ordered for administration to this patient. NTG:
A. Is contraindicated in hypotensive patients.
B. Should be administered via the IV route for maximum benefit.
C. Should be used with caution in patients with anterior infarction.
D. Should be given every 15 to 20 minutes until chest discomfort is relieved.
____ 23. The patient’s chest discomfort was unrelieved after the maximum recommended dosage
of NTG tablets. Morphine sulfate was ordered and a 4 mg dose was given IV. The
patient’s BP is now 80/60 mm Hg and his skin is cool, moist, and pale. His breath
sounds are clear. You should:
A. Prepare a lidocaine infusion at 1 to 4 mg/min.
B. Prepare an epinephrine infusion at 2 mcg/min.
C. Give a 250 mL IV fluid bolus of normal saline.
D. Prepare a dopamine infusion at 2 to 10 mcg/kg/min.
____ 24. Which of the following is not recommended when performing defibrillation?
A. Check for a pulse immediately after defibrillation to determine next steps.
B. Visually check and ensure that everyone is clear of the patient before shock
delivery.
C. Remove transdermal medication patches or ointment from the patient’s chest
before the procedure.
D. All team members with the exception of the chest compressor should clear the
patient as the machine charges.
____ 25. Atypical symptoms of ACSs are more common in:

A. Older adults, women, and diabetic individuals.
B. Men, older adults, and individuals who have liver disease.
C. Women, diabetic individuals, and individuals who have liver disease.
D. Men, patients who have a history of coronary artery disease, and patients who have a
history of hypertension.
____ 26. A 53-year-old woman is unresponsive. The cardiac monitor initially showed a
narrow-QRS tachycardia at 220 beats/min. Her BP was 50 mm Hg by palpation
and her ventilatory rate was 10 breaths/min. Supplemental oxygen therapy was
initiated and an IV established before the patient’s collapse. You promptly delivered
a synchronized shock. Reassessment reveals the patient is not breathing and has no
pulse. The cardiac monitor now reveals the rhythm shown. What course of action
should you take at this time?
(From Aehlert B, ECGs made easy, ed 5, St. Louis, 2013, Mosby.)
B. Perform cardiopulmonary resuscitation (CPR) for 2 minutes and then prepare to
defibrillate.
C. Place an advanced airway and then begin transcutaneous pacing.
D. Press the “Sync” control and deliver another synchronized shock.
____ 27. An unstable patient with a narrow-QRS tachycardia requires electrical therapy.
You have a biphasic defibrillator available to you. Which of the following
correctly reflects the recommended energy dose that should be delivered in this
situation?
A. Defibrillate with 120 joules (J).
B. Defibrillate with 360 J.
C. Perform synchronized cardioversion with 50 to 100 J for the initial shock.
D. Perform synchronized cardioversion with 100 to 200 J for the initial shock.
____ 28. The preferred method used to verify the proper placement of an endotracheal tube is:
A. Obtaining a chest radiograph.
B. Using continuous waveform capnography.
C. Auscultating the presence of bilateral breath sounds.
D. Observing adequate chest rise with positive pressure ventilation.
____ 29. Which of the following is incorrect with regard to the events of a typical resuscitation
effort?
A. The team leader should state his or her instructions one at a time.
B. The team leader should encourage a respectful exchange of ideas.
C. Team members must be knowledgeable about current resuscitation algorithms.
D. Team members should be encouraged to confer among themselves throughout the
resuscitation effort.
____ 30. Which of the following statements is correct about the use of medications during
cardiac arrest?
A. Amiodarone is the drug of choice for cardiac arrest resulting from asystole.
B. Lidocaine is contraindicated in cardiac arrest associated with a shockable rhythm.
C. Epinephrine should be given as soon as feasible after the onset of cardiac arrest
associated with a nonshockable rhythm.
D. Vasopressin can be substituted for either the first or second dose of epinephrine in
the treatment of cardiac arrest.
____ 31. This 12-lead ECG is from a 50-year-old man complaining of chest discomfort.
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
(From Phalen T, Aehlert B: The 12-lead ECG in acute coronary syndromes, ed 3, St. Louis, 2012, Mosby.)
Which of the following is true regarding this 12-lead ECG?

A. This 12-lead reveals no significant findings.
B. STE is present in leads V1 to V4. An anterior STEMI is suspected.
C. STE is present in leads I, aVR, and V6. A lateral STEMI is suspected.
D. STD is present in leads III and aVF. An inferior STEMI is suspected.
Questions 32 and 33 pertain to the following scenario

A 65-year-old man is complaining of a sudden onset of dizziness. He is awake, alert, and diaphoretic.
The patient states that his symptoms began 45 minutes ago while cleaning his garage. He denies chest
pain, shortness of breath, and nausea. The patient’s breath sounds are clear bilaterally. His BP is
78/50 mm Hg, ventilations 18 breaths/min. His SpO2 on room air is 96%.
____ 32. The cardiac monitor reveals the following rhythm.
This rhythm is:

A. Junctional rhythm.
B. Sinus bradycardia.
C. Third-degree atrioventricular (AV) block.
D. Second-degree AV block (2:1 AV block).
____ 33. An IV is in place. Your best course of action will be to:

B. Administer atropine 0.5 mg IV.
C. Administer amiodarone 300 mg IV.
D. Administer vasopressin 40 units IV.
Questions 34 through 36 pertain to the following scenario

An 89-year-old man is complaining of a “racing heart.” He states his symptoms began while playing a
card game with friends. He had an MI 15 years ago and a coronary artery bypass graft 5 years ago. His BP
is 140/90 mm Hg and his ventilatory rate is 16 breaths/min. Breath sounds are clear and his tidal volume
is adequate. His SpO2 on room air is 88%.
____ 34. On the basis of the information provided, supplemental oxygen:

A. Is unnecessary at this time.
B. Is indicated and should be delivered using a nasal cannula.
C. Is indicated for all patients who are experiencing a tachycardia.
D. Should ideally be administered only after placement of an advanced airway.
____ 35. You have started an IV and placed the patient on the cardiac monitor, which reveals the
following rhythm:
This rhythm can best be described as a:

A. Regular, polymorphic, wide-QRS tachycardia.
B. Regular, monomorphic, wide-QRS tachycardia.
C. Irregular, polymorphic, wide-QRS tachycardia.
D. Irregular, monomorphic, wide-QRS tachycardia.
____ 36. Which of the following statements is true with regard to the management of this
patient?
A. The patient is unstable. Sedate the patient and defibrillate as quickly as
possible.
B. The patient is stable. Administration of IV verapamil is recommended for
termination of the rhythm.
C. The patient is stable. Administration of IV adenosine can be used as a therapeutic
and diagnostic maneuver.
D. The patient is unstable. Because there are recognizable QRS complexes on the
monitor, synchronized cardioversion should be performed.
Questions 37 and 38 pertain to the following scenario

A 72-year-old woman presented with a sudden onset of shortness of breath and collapsed. After
confirming the patient was unresponsive, apneic, and pulseless, CPR was begun.
____ 37. The cardiac monitor shows the following rhythm.
II
Which of the following ACLS treatment guidelines should be used in the initial
treatment of this patient?
A. Symptomatic bradycardia
B. Narrow-QRS tachycardia
C. Pulseless electrical activity (PEA)
D. ACSs
____ 38. An IV has been established and the patient is being ventilated with a bag-mask device
(BMD). You observe gentle bilateral chest rise with ventilations. Your next action
should be to:
B. Give 0.5 mg of atropine IV.
C. Give 1 mg of epinephrine IV.
D. Begin transcutaneous pacing.
____ 39. A 73-year-old woman presents with symptoms of acute stroke 3.5 hours after symptom
onset. She has a history of an acute MI 6 years ago, chronic atrial fibrillation, and diabetes
mellitus. The patient’s BP is 168/100 mm Hg, her heart rate is 88 to 100 beats/min, and her
ventilations are 12 breaths/min. Her National Institutes of Health Stroke Scale (NIHSS)
score is 22. Daily medications include lisinopril, metformin, and warfarin. Which of the
following statements with regard to fibrinolytic therapy for this patient is true?
A. This patient is not a candidate for fibrinolytic therapy because of her age.
B. This patient is not a candidate for fibrinolytic therapy because she is hypertensive.
C. This patient is not a candidate for fibrinolytic therapy because she is taking an oral
anticoagulant.
D. This patient is not a candidate for fibrinolytic therapy because too much time has
lapsed between symptom onset and hospital arrival.
____ 40. Which of the following is true with regard to procainamide?

A. Procainamide is a potent vasoconstrictor.
B. Procainamide may cause widening of the QRS complex.
C. Procainamide is indicated in the treatment of asystole and slow PEA.
D. Procainamide is a first-line drug in the management of torsades de pointes (TdP).
____ 41. A BMD that is used with supplemental oxygen set at a flow rate of 10 to 15 L/min
delivers about _____oxygen to the patient when a reservoir is not used.
A. 21%
B. 40% to 60%
C. 60% to 90%
D. 90% to 100%
____ 42. A 35-year-old woman presents with a narrow-QRS tachycardia. She is stable but
symptomatic. Vagal maneuvers and an initial dose of adenosine were ineffective. You
should now:
A. Perform synchronized cardioversion.
B. Administer 6 mg of adenosine rapid IV push.
C. Administer 12 mg of adenosine rapid IV push.
D. Administer diltiazem 0.25 mg/kg IV over 2 minutes.
____ 43. A patient is unresponsive with spontaneous ventilations at a rate of 4 per minute.
Chest movement is barely visible with each breath. A pulse is present. Which of the
following oxygen delivery devices would be most appropriate to use in this situation?
A. A nasal cannula at 4 L/min
B. A simple face mask at 6 L/min
C. A nonrebreather mask at 12 L/min
D. A BMD with a reservoir at 15 L/min
____ 44. If a patient wakes from sleep or is found with symptoms of a stroke, the time of onset of
symptoms is defined as the time:
A. Of awakening.
B. The patient retired for sleep.
C. The patient was last known to be symptom-free.
D. The patient was last seen by a health care professional.
____ 45. The most common adverse effects of giving amiodarone are:
A. Nausea and asystole.
B. Bradycardia and hypotension.
C. Tachycardia and hypertension.
D. Blurred vision and abdominal pain.
____ 46. A 49-year-old man is found unresponsive, not breathing, and pulseless. The cardiac
monitor reveals monomorphic ventricular tachycardia. The most important actions
in the management of this patient are:
A. CPR and defibrillation.
B. Defibrillation and resuscitation medications.
C. CPR and prompt insertion of an advanced airway.
D. Synchronized cardioversion and resuscitation medications.
____ 47. Diltiazem may be used:

A. Concurrently with IV beta-blockers.
B. In the management of symptomatic bradycardia.
C. In the management of a stable patient with a wide-QRS tachycardia.
D. To control the ventricular rate with atrial flutter or atrial fibrillation.
____ 48. CPR is ongoing for a 66-year-old man in cardiac arrest. The cardiac monitor
reveals asystole. Vascular access has been achieved and an advanced airway has been
inserted. Which of the following statements is correct with regard to this situation?
A. The depth of chest compressions should be 1.5 to 2 inches.
B. Chest compressions should be delivered at a rate of 100 per minute.
C. The ratio of chest compressions to ventilations delivered should be 30:2.
D. Ventilations should be delivered at a rate of one breath every 6 seconds.
____ 49. What precautions should be taken before giving NTG?

A. Make sure the patient’s heart rate is at least 70 beats/min.
B. Make sure there is no evidence of a right ventricular infarction.
C. Make sure the patient’s systolic BP is more than 140 mm Hg.
D. Make sure the patient has not used a diuretic or an antihypertensive medication in
the past 24 hours.
____ 50. A simple face mask:

A. Requires a minimum oxygen flow rate of 2 L/min.
B. Can only be used in a spontaneously breathing patient.
C. Does not permit the mixing of the patient’s exhaled air with 100% oxygen.
D. Delivers an oxygen concentration of 70% to 85% at recommended flow rates.
POST TEST ANSWERS

Multiple Choice
1. A. Gasping breathing is not effective breathing. After recognizing that the patient is unresponsive
and is not breathing normally, activate the emergency response system and check for a pulse for no
more than 10 seconds. If you do not feel a pulse or are unsure if you feel a pulse during that period,
begin chest compressions.
2. C. Parasympathetic nervous system hyperactivity is common with inferior wall MIs, resulting in
bradydysrhythmias. Ischemia of the AV node can result in first-degree or second-degree type I
AV block. These dysrhythmias are relatively common with an inferior infarction, usually transient
(resolving within 2 to 3 days), generally do not warrant treatment, and have a low mortality rate
unless associated with hypotension, heart failure, or both.
3. D. The rhythm shown is monomorphic ventricular tachycardia. From the information provided, the
patient appears to be clinically stable at this time. Procainamide would be appropriate to consider in
this situation. Acceptable alternatives include amiodarone and sotalol. Dopamine increases the force
of myocardial contraction, heart rate, and BP. Because this patient is not hypotensive and he has a
rapid heart rate, dopamine is not indicated. NTG is a vasodilator. The patient has no complaint of
chest pain so NTG is not indicated. Furosemide (Lasix) is also not indicated because there are no
signs of pulmonary congestion. Atropine is not indicated because the patient has a tachycardia, not a
symptomatic bradycardia.
4. C. After forming a general impression, you should approach the patient and assess her level of
responsiveness. If the patient is unresponsive, quickly determine whether the patient is not breathing
(or only gasping) and simultaneously check for a pulse for up to 10 seconds. If there is no pulse, begin
chest compressions.
5. C. Absence of chest wall expansion and gurgling heard over the epigastrium indicate misplacement
of the endotracheal tube into the esophagus. If breath sounds were present bilaterally with bag-mask
ventilation before placement of a tracheal tube, the presence of breath sounds on only one side of the
chest after placement of the tube suggests right primary bronchus intubation.
OBJ: Describe methods that are used to confirm correct endotracheal tube placement.
6. C. IV fluid boluses can be considered if the patient is hypotensive after the ROSC. Vasopressor IV
infusions such as epinephrine, dopamine, or norepinephrine may be started if necessary and
titrated to achieve a minimum systolic BP of less than 90 mm Hg. Isoproterenol is an alternative
agent that is primarily used to increase heart rate in a patient with a symptomatic bradycardia.
Because it is not a vasopressor, it is not used to treat hypotension. Procainamide is an antiarrhythmic
used to treat many atrial and ventricular dysrhythmias. Procainamide is not a vasopressor and
because an adverse effect of procainamide administration is hypotension, it would not be used to
treat hypotension.
OBJ: Discuss immediate postcardiac arrest care upon ROSC.
7. C. During a debriefing, each member of the code team has an opportunity to engage in honest
dialogue to gain understanding and to identify lessons learned in a nonpunitive environment.
An opportunity is provided for each team member to reflect on what they did, when they did it,
how they did it, why they did it, and how they can improve (Phrampus & O’Donnell, 2013).
The facilitator uses open-ended questions to encourage discussion and listens to the team members
describe their perceptions of their behaviors. The actions of the team can be compared with current
resuscitation algorithms, professional standards, institution policies, best evidence, and local
protocols to enhance understanding and support discussion during the analysis phase of the
debriefing.
OBJ: Recognize the opportunities provided when a postevent debriefing is held.
8. B. The rhythm shown is AV nodal reentrant tachycardia (AVNRT) at 167 beats/min. Vagal maneu-
vers are methods used to stimulate baroreceptors located in the internal carotid arteries and the aortic
arch. Stimulation of these receptors results in reflex stimulation of the vagus nerve and release of
acetylcholine. Acetylcholine slows conduction through the AV node, resulting in slowing of the
heart rate. Vagal maneuvers can be attempted as an initial intervention in a stable patient with a
regular narrow-QRS tachycardia. Defibrillation is not indicated. Diltiazem is a CCB that is used
in the treatment of stable, narrow-QRS tachycardias if the rhythm remains uncontrolled or uncon-
verted by adenosine or vagal maneuvers or if the tachycardia is recurrent. Epinephrine is not
indicated in the management of a stable patient with a tachycardia.
9. B. Orolingual angioedema is an uncommon complication of tPA administration, but it can lead to

airway obstruction. Patients taking angiotensin-converting enzyme inhibitors and those with infarc-
tions that involve the insular and frontal cortex appear to be at highest risk (Jauch, et al., 2013).
Treatment includes the administration of IV ranitidine, diphenhydramine, and methylprednisolone
(Jauch, et al., 2013).
10. B. If peripheral IV access is unsuccessful during cardiac arrest, consider an intraosseous infusion
before considering placement of a central line.
applicable.
11. B. Synchronized cardioversion is a type of electrical therapy in which a shock is “timed” or

“programmed” for delivery during ventricular depolarization (ie, the QRS complex). It is indicated
in the management of a patient who is exhibiting serious signs and symptoms related to a tachycar-
dia. Because the machine must be able to detect a QRS complex in order to “sync,” synchronized
cardioversion is used to treat rhythms that have a clearly identifiable QRS complex and a rapid
ventricular rate (such as some narrow-QRS tachycardias and ventricular tachycardia).
12. A. The rhythm shown is a third-degree AV block at a rate of about 30 beats/min. This patient is
clearly symptomatic and needs immediate emergency care. A reasonable course of action will be to
prepare for immediate transcutaneous pacing. Amiodarone is not indicated in the management of a
symptomatic bradycardia. Although epinephrine may be used in the management of a symptomatic
bradycardia, it is given as a continuous IV infusion, not as an IV bolus.
applicable.
13. B. Although it is not yet known if this patient is experiencing a STEMI or if he is a candidate for
reperfusion therapy, obtaining a prehospital 12-lead ECG is associated with shorter reperfusion
time and a lower mortality rate from STEMI (O’Gara, et al., 2013).
14. B. Frequent assessment of the patient’s mental status, vital signs, and oxygen saturation level is
important, and continuous ECG monitoring is essential. Supplemental oxygen is warranted if
the patient is having difficulty breathing, has obvious signs of heart failure or shock, or if his
oxygen saturation level declines below 90% (Amsterdam, et al., 2014; O’Gara, et al., 2013). Estab-
lish IV access, obtain a targeted history and physical examination, and consider the possibility of
other conditions that mimic acute MI. Give aspirin if no contraindications are present. NTG
should not be administered until a 12-lead ECG has been obtained and a right ventricular infarc-
tion has been ruled out.
15. A. An initial 12-lead ECG should be obtained and interpreted with 10 minutes of patient contact
(Amsterdam, et al., 2014). Obtain a repeat 12-lead ECG with each set of vital signs, when the
patient’s symptoms change, and as often as necessary.
16. D. The patient’s initial 12-lead ECG should be reviewed and the patient classified into one of three
categories: STE, STD, or normal or nondiagnostic ECG.
OBJ: Discuss the three groups used when categorizing the 12-lead ECG findings of the patient
experiencing an ACS.
17. C. The patient’s 12-lead ECG shows STE in leads I, aVL, and V2 to V6.
OBJ: Identify the ECG leads that view the anterior wall, the inferior wall, the lateral wall, the
18. B. Two leads are contiguous if they look at the same or adjacent area of the heart or if they are
numerically consecutive chest leads. V2, V3, and V4 are numerically consecutive chest leads.
OBJ: Relate the cardiac surfaces or areas represented by the ECG leads.
19. C. The patient’s 12-lead ECG shows STE in lead I, aVL, and V2 through V6. Because these leads
view the lateral and anterior surfaces of the left ventricle, an extensive anterolateral infarction is
suspected.
OBJ: Recognize the changes on the ECG that may reflect evidence of myocardial ischemia,
20. B. Patients with STE in two or more contiguous leads are classified as having a STEMI and should
be evaluated for immediate reperfusion therapy.
OBJ: Discuss the three groups used when categorizing the 12-lead ECG findings of the patient
experiencing an ACS.
21. A. Aspirin should be administered as soon as possible after symptom onset to patients with
suspected ACSs (if there are no contraindications). NTG relaxes vascular smooth muscle and
decreases myocardial oxygen consumption. An oral beta-blocker should be started within the first
24 hours after hospitalization in the absence of contraindications to beta blockade. Because of the
increased risk of major adverse cardiac events associated with the use of NSAIDs, these drugs should
not be initiated in the acute phase of care and should be discontinued in patients using them before
hospitalization (Amsterdam, et al., 2014; O’Gara, et al., 2013). Although CCBs may be useful in
relieving ischemia or lowering BP in patients who are intolerant of beta-blockers, randomized
controlled trials have demonstrated no beneficial effect on infarct size or the rate of reinfarction when
CCB therapy was initiated during either the acute or convalescent phase of STEMI (O’Gara,
et al., 2013).
22. A. Patients with ischemic discomfort should receive up to three doses of sublingual NTG
tablets or spray at 3- to 5-minute intervals until chest discomfort is relieved or hypotension
limits its use. Nitrates are contraindicated in patients with hypotension (systolic BP below
90 mm Hg or 30 mm Hg or more below baseline), marked bradycardia or tachycardia, phos-
phodiesterase inhibitor use within the previous 24 to 48 hours, or suspected right ventricular
infarction.
23. C. Your best course of action will be to place the patient supine and give a 250 mL IV fluid bolus of
normal saline. Reassess his BP (and other vital signs) and breath sounds after administration.
24. A. Be sure that high-quality CPR is continued as the defibrillator is readied for use. While
CPR continues, instruct a team member to expose the patient’s chest and to remove any
transdermal medication patches or ointment from the patient’s chest, if present. All team
members with the exception of the chest compressor should clear the patient as the
machine charges. When the defibrillator is charged, the chest compressor should immedi-
ately clear the patient. Call “Clear!” Look around you (360 degrees) to be sure that
everyone—including you—is clear of the patient, the bed, and any equipment that is
connected to the patient. Be sure oxygen is not flowing over the patient’s chest. Press
the “Shock” control to defibrillate the patient. Release the “Shock” control after the energy
dose has been delivered. Instruct the team to resume chest compressions immediately
without pausing for a rhythm or pulse check.
OBJ: Explain defibrillation; describe proper pad/paddle placement, indications, precautions, and
the steps in performing this procedure with a manual defibrillator and automated external
defibrillator.
25. A. Patients who are experiencing an ACS who are most likely to present atypically include older
patients with prior cardiac surgery, and patients during the immediate postoperative period after
noncardiac surgery.
OBJ: Explain atypical presentation and its significance in ACSs.
26. A. The cardiac monitor shows ventricular fibrillation (VF). Appropriate care at this time includes
immediate defibrillation. Transcutaneous pacing can be used in the management of symptomatic
bradycardia; it is not used for cardiac arrest rhythms such as VF. Synchronized cardioversion is
not used to treat disorganized rhythms (eg, polymorphic VT) or those that do not have a clearly
identifiable QRS complex (eg, VF).
OBJ: Explain defibrillation; describe proper pad/paddle placement, indications, precautions, and
the steps in performing this procedure with a manual defibrillator and automated external
defibrillator.
27. C. If an unstable patient with a narrow-QRS tachycardia requires electrical therapy and a
biphasic defibrillator is available, perform synchronized cardioversion using 50 to 100 J
initially (or the energy levels recommended by the defibrillator manufacturer), increasing in
stepwise fashion if the initial shock fails. For example, if the initial synchronized shock was
delivered using 50 J and failed, reasonable energy levels to use for the second and subsequent
shocks would be 100 J, then 200 J, 300 J, and 360 J (assuming the rhythm failed to convert
with each shock).
mended: monomorphic VT, narrow-QRS tachycardia, atrial fibrillation, and atrial flutter.
28. B. In addition to clinical assessment, continuous quantitative waveform capnography is recom-

mended as the most reliable method for confirmation and monitoring of endotracheal tube
placement.
OBJ: Describe methods that are used to confirm correct endotracheal tube placement.
29. D. Each member of the resuscitation team must have clear roles and responsibilities, must know his
or her limitations, must be knowledgeable about current resuscitation algorithms, must be practiced
in resuscitation skills, and must be prepared to question other team members if an action is about to
occur that may be inappropriate. To avoid information overload and to help ensure that what is said
by the team leader is what is heard by the team members, the team leader should state his or her
instructions one at a time using terms that are known and shared by all team members. The team
member’s name should be used, if known. A good team leader values his or her team members, fos-
ters an environment in which team members feel comfortable speaking up, and encourages a respect-
ful exchange of ideas. Team members must clearly acknowledge when procedures and medications
are complete. Because there are often a large number of persons present during a code, sidebar con-
versations among team members that can be distracting to other team members must be avoided.
OBJ: Discuss the events of a typical resuscitation effort.
30. C. Because research has shown an association among the early administration of epinephrine and
increased ROSC, survival to hospital discharge, and neurologically intact survival, current guidelines
consider it reasonable to administer epinephrine as soon as feasible after the onset of cardiac arrest
associated with a nonshockable rhythm (Link, et al., 2015). Amiodarone is an antiarrhythmic that
can be used for shockable cardiac arrest rhythms (ie, VF, pulseless ventricular tachycardia [pVT]).
It is not indicated for nonshockable cardiac arrest rhythms (ie, asystole and PEA). The initiation or
continuation of lidocaine may be considered immediately after ROSC from VF/pVT cardiac arrest
(Link, et al., 2015). Epinephrine and vasopressin are vasopressors that, when administered during
cardiac arrest, have been shown to improve ROSC (Link, et al., 2015). Because the efficacy of both
drugs is similar and research has shown no benefit from administering both drugs compared with
epinephrine administered alone, vasopressin was removed from the adult cardiac arrest algorithm
(Link, et al., 2015).
31. B. The rhythm shown is a sinus rhythm at 92 beats/min. STE is noted in V1 to V4; it is borderline in
V5. QS complexes (ie, pathologic Q waves) are noted in V1 to V5. An anterior STEMI is suspected.
STD is present in lead aVF.
OBJ: Recognize the changes on the ECG that may reflect evidence of myocardial ischemia,
32. D. The rhythm shown is second-degree AV block (2:1 AV block).

33. B. The drug of choice for symptomatic bradycardia is atropine. The initial dose is 0.5 mg, which may
be repeated every 3 to 5 minutes to a maximum dose of 3 mg. Defibrillation, amiodarone, and vaso-
pressin are not indicated in the management of symptomatic bradycardia.
applicable.
34. B. Administer supplemental oxygen as needed to maintain the patient’s oxygen saturation at 94% or
higher. Because it is generally better tolerated than a mask, it is reasonable to use a nasal cannula. If the
patient’s oxygen saturation does not adequately improve with the use of the cannula, it may be necessary
to switch to oxygen delivery by mask. Because the patient’s breathing is adequate, advanced airway place-
ment and positive pressure ventilation are not necessary at this time; however, if the patient becomes
unresponsive or his breathing becomes inadequate, administer oxygen by positive pressure ventilation.
percentage delivered for each of the following devices: nasal cannula, simple face mask, partial non-
35. B. Monomorphic is a term used to describe QRS complexes that are of the same shape and amplitude.
When the QRS complexes vary in shape and amplitude from beat to beat, the term polymorphic is
used. The rhythm shown is a regular, monomorphic, wide-QRS tachycardia. A 12-lead ECG
should be obtained. It is wise to seek expert consultation when treating a patient with a wide-
QRS tachycardia.
36. C. On the basis of the information provided, the patient is stable at this time. Administration of IV
adenosine can be used as a therapeutic and diagnostic maneuver. Verapamil is a CCB and should
only be given to patients with a narrow-QRS tachycardia. It should not be given to patients with a
wide-complex tachycardia. Because electrical therapy is used for unstable patients, neither synchro-
nized cardioversion nor defibrillation is indicated for this patient. If he were unstable, synchronized
cardioversion would be used because the patient has a pulse and there are recognizable QRS
complexes on the monitor. Defibrillation would be performed if the rhythm observed was polymor-
phic VT, pulseless monomorphic VT, or VF.
37. C. Despite the presence of an organized rhythm on the monitor, the patient has no pulse. This
situation is PEA.
OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care
for cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindi-
cations, doses, and route of administration of applicable medications), and electrical therapy, where
applicable.
38. C. Give 1 mg of 1:10,000 epinephrine IV. Defibrillation attempts to deliver a uniform

electrical current of sufficient intensity to depolarize myocardial cells (including fibrillating cells)
at the same time. This provides an opportunity for the heart’s natural pacemakers to resume
normal activity. In this situation, organized electrical activity is already present on the cardiac
monitor; therefore defibrillation is contraindicated. Atropine, although once used for asystole
and slow PEA, is no longer recommended. Transcutaneous pacing is not indicated in cardiac
arrest.
39. C. IV tPA is recommended for administration to a select group of eligible patients who present
within a 3- to 4.5-hour window after the onset of acute stroke symptoms (American Stroke
Association, 2014). The eligibility criteria for treatment in this time frame are similar to those
for patients treated within 3 hours of symptom onset, with the following additional exclusion criteria
(American Stroke Association, 2014; Jauch, et al., 2013): patients older than age 80, those taking
oral anticoagulants regardless of their international normalized ratio, those with a baseline NIHSS
score of more than 25, those with imaging evidence of ischemic injury involving more than one-third
of the middle cerebral artery territory, or those with a history of both prior ischemic stroke and
diabetes mellitus.
40. B. Procainamide exerts a peripheral vasodilatory effect; therefore hypotension is a potential adverse
effect. Procainamide may cause widening of the QRS complex. The drug should be discontinued if
the QRS widens more than 50% of its pretreatment width. Procainamide is used to control the
ventricular rate in the patient with preexcited atrial fibrillation and in the management of stable
monomorphic VT with a normal QT interval. It is not used in the treatment of asystole or
PEA. Because it can cause prolongation of the PR and QT intervals, procainamide is not used
in the management of TdP.
41. B. A BMD that is used with supplemental oxygen set at a flow rate of 10 to 15 L/min delivers about
40% to 60% oxygen to the patient when a reservoir is not used.
42. C. Vagal maneuvers are used to try to stop the rhythm or slow conduction through the AV node. If
vagal maneuvers fail, antiarrhythmic medications should be tried. Adenosine is the drug of choice,
except for patients with severe asthma. The initial dose is 6 mg rapid IV push over 1 to 3 seconds. If
there is no response within 1 to 2 minutes, give 12 mg rapid IV push. The 12 mg dose may be
repeated once in 1 to 2 minutes. If needed, CCBs or beta-blockers may be used to slow the ven-
tricular rate. If the tachycardia is sustained and causing persistent signs of hemodynamic compro-
mise, synchronized cardioversion should be performed.
43. D. Remember that an open airway does not ensure adequate ventilation. This patient’s breathing is
inadequate as evidenced by his rate and depth of ventilations. The patient with inadequate breathing
requires positive pressure ventilation with supplemental oxygen. Of the choices listed, the only
device that can provide positive pressure ventilation is the BMD. If readily available, an oral airway
should be inserted before beginning bag-mask ventilation (if the patient does not have a gag or cough
reflex).
44. C. For a patient with symptoms of stroke on awakening, the time of onset is assumed to be the time
the patient was last known to be symptom-free before retiring (last known-well time). If a patient
had mild impairments but then had worsening over the subsequent hours, the time the first symp-
tom began is assumed to be the time of onset.
45. B. Hypotension and bradycardia are most common adverse effects of amiodarone administration.
46. A. CPR and defibrillation are the most important treatments for the patient in cardiac arrest asso-
ciated with pVT or VF. Insertion of advanced airways and administration of resuscitation medica-
tions are of secondary importance. Although synchronized cardioversion may be used in the
treatment of an unstable patient in monomorphic VT with a pulse, it is not indicated for pVT.
applicable.
47. D. Diltiazem is a CCB that may be used in stable narrow-QRS tachycardias if the rhythm persists
despite vagal maneuvers or adenosine, if the tachycardia is recurrent, or to control the ventricular rate
in patients with atrial fibrillation or atrial flutter. IV CCBs and IV beta-blockers should not be given
together or in close proximity (within a few hours) because severe hypotension may result. CCBs
should be avoided in patients with wide-QRS tachycardia and preexcited atrial fibrillation/atrial flut-
ter (Mottram & Svenson, 2011).
48. D. After insertion of an advanced airway, chest compressions should be delivered continuously at a
rate of 100 to 120 per minute without pauses for ventilation, unless ventilation is inadequate when
compressions are not paused (Link, et al., 2015). Ventilations should be delivered at a rate of one
breath every 6 seconds (10 breaths/min). For an average adult, chest compressions should be
performed to a depth of at least 2 inches (5 cm) but not more than 2.4 inches (6 cm).
OBJ: Describe the role of each member of the resuscitation team.
49. B. Before giving NTG, assess the degree of the patient’s pain/discomfort using a 0-to-10 scale, dura-
tion, time started, activity being performed, and pain quality. Reassess (and document) the patient’s
vital signs and level of discomfort after each dose. Make sure that the patient has not used a phos-
phodiesterase inhibitor such as sildenafil (Viagra) within 24 hours or tadalafil (Cialis) within
48 hours before NTG administration. The combination of a phosphodiesterase inhibitor and
nitrates may result in severe hypotension. Nitrates should not be administered to patients with a
systolic BP less than 90 mm Hg or 30 mm Hg or more below baseline, severe bradycardia or tachy-
cardia, or suspected right ventricular infarction.
50. B. A simple face mask, which is also called a standard mask, is a plastic reservoir that has been
designed to fit over the nose and mouth of a spontaneously breathing patient. When using a simple
face mask, the oxygen flow rate must be higher than 5 L/min to flush the buildup of the patient’s
exhaled carbon dioxide from the mask. At 5 to 10 L/min, the simple face mask can deliver an
inspired oxygen concentration of about 35% to 60%. The patient’s actual inspired oxygen concen-
tration will vary, because the amount of air that mixes with supplemental oxygen is dependent on the
patient’s inspiratory flow rate. A nonrebreather mask, also called a nonrebreathing mask, does not
permit the mixing of the patient’s exhaled air with 100% oxygen. A one-way valve between the mask
and the reservoir bag and a flap over one of the exhalation ports on the side of the mask prevent the
inhalation of room air.
percentage delivered for each of the following devices: nasal cannula, simple face mask, partial non-
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2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes.
Jauch, E. C., Saver, J. L., Adams, Jr., H. P., Bruno, A., Connors, J. J., Demaerschalk, B. M., et al. (2013).
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professionals from the American Heart Association/American Stroke Association. Stroke, 44(3), 870–947.
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lar care—part 7: Adult advanced cardiovascular life support: Eccguidelines.heart.org.
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(pp. 73–84). New York: Springer Science.
GLOSSARY
Absolute bradycardia A heart rate of less than 60 beats/min.
Absolute refractory period Corresponds with the onset of the QRS complex to about the peak of the
T wave on the electrocardiogram; cardiac cells cannot be stimulated to conduct an electrical impulse,
no matter how strong the stimulus.
Accessory pathway An extra bundle of working myocardial tissue that forms a connection between the
atria and ventricles outside the normal conduction system.
Action potential A five-phase cycle that reflects the difference in the concentration of charged particles
across the cell membrane at any given time.
Acute coronary syndrome (ACS) A group of conditions that are caused by an abrupt reduction in cor-
onary artery blood flow; ACSs consist of three major syndromes: unstable angina, non–ST segment
elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction
(STEMI).
Anginal equivalent Symptom other than chest pain or discomfort resulting from myocardial ischemia
that may occur either alone or in combination in a patient with ischemic heart disease.
Arteriosclerosis A chronic disease of the arterial system characterized by abnormal thickening and
hardening of the vessel walls.
Atherosclerosis A form of arteriosclerosis in which the thickening and hardening of the vessel walls are
caused by a buildup of fat-like deposits in the inner lining, specifically of large- and middle-sized
muscular arteries.
Atypical presentation Uncharacteristic signs and symptoms experienced by some patients.
Atrioventricular (AV) junction AV node and the bundle of His.
Atrioventricular (AV) node Specialized cells located in the lower portion of the right atrium; delays the
electrical impulse to allow the atria to contract and complete filling of the ventricles.
Automated external defibrillation The placement of paddles or pads on a patient’s chest and interpre-
tation of the patient’s cardiac rhythm by the defibrillator’s computerized analysis system. Depending
on the type of automated external defibrillator (AED) used, the machine will deliver a shock (if a
shockable rhythm is detected) or instruct the operator to deliver a shock.
Automated external defibrillator (AED) A machine with a sophisticated computer system that ana-
lyzes a patient’s heart rhythm using an algorithm to distinguish shockable rhythms from nonshockable
rhythms and provides visual and auditory instructions to the rescuer to deliver an electrical shock, if a
shock is indicated.
Bundle of His Fibers located in the upper portion of the interventricular septum that conduct an elec-
trical impulse through the heart; also called the common bundle or the AV bundle.
Capnography The continuous analysis and recording of carbon dioxide concentrations in respiratory
gases.
Cardiopulmonary (cardiac) arrest The absence of cardiac mechanical activity, which is confirmed by
the absence of a detectable pulse, unresponsiveness, and apnea or agonal, gasping breathing.
Cardiovascular collapse A sudden loss of effective blood flow that is caused by cardiac and/or periph-
eral vascular factors that may reverse spontaneously (eg, syncope) or only with interventions (eg,
cardiac arrest).
Cardiovascular disease (CVD) A collection of conditions that involve the circulatory system, which
contains the heart (cardio) and blood vessels (vascular), including congenital cardiovascular diseases.
Carina The point where the trachea divides into the right and left primary bronchi.
Chain of Survival The essential elements of a system of care that are necessary to link the victim of
sudden cardiac arrest with survival. 277
278 Glossary
Conduction system A system of pathways in the heart composed of specialized electrical (ie, pace-
maker) cells.
Coronary artery disease (CAD) Disease affecting the arteries that supply the heart muscle with blood.
Coronary heart disease (CHD) Disease of the coronary arteries and their resulting complications, such
as angina pectoris and acute myocardial infarction.
Cricothyroid membrane A fibrous membrane located between the cricoid and thyroid cartilages.
Defibrillation Delivery of an electrical current across the heart muscle over a very brief period to ter-
minate an abnormal heart rhythm; also called unsynchronized countershock or asynchronous counter-
shock because the delivery of current has no relationship to the cardiac cycle.
Defibrillator A device used to administer an electrical shock at a preset energy level to terminate a car-
diac dysrhythmia.
Delta wave Slurring of the beginning portion of the QRS complex; caused by preexcitation.
Depolarization Movement of ions across a cell membrane, causing the inside of the cell to become more
positive; an electrical event expected to result in contraction.
Effective refractory period Period of the cardiac action potential that includes the absolute refractory
period and the first half of the relative refractory period.
Electrocardiogram (ECG) A recording of the heart’s electrical activity from the body surface that
appears on ECG paper as specific waveforms and complexes.
Electrode Adhesive pad that contains a conductive gel and is applied at a specific location on the
patient’s chest wall and extremities and is connected by cables to an ECG machine.
Epiglottis A small piece of cartilage located at the top of the larynx that prevents foreign material from
entering the trachea during swallowing.
Glottis The true vocal cords and the space between them.
Hard palate Bony portion of the roof of the mouth that forms the floor of the nasal cavity.
Heart disease A broad term that refers to conditions affecting the heart.
His-Purkinje system Portion of the conduction system consisting of the bundle of His, bundle
branches, and Purkinje fibers.
Interval On the ECG, a waveform and a segment.
Lead A record (ie, tracing) of electrical activity between two electrodes.
Manual defibrillation The placement of paddles or pads on a patient’s chest, interpretation of the
patient’s cardiac rhythm by a trained health care professional, and the health care professional’s deci-
sion to deliver a shock (if indicated).
Myocardial cells Working cells of the myocardium that contain contractile filaments and form the mus-
cular layer of the atrial walls and the thicker muscular layer of the ventricular walls.
Nasal cannula A piece of plastic tubing with two soft prongs that project from the tubing; used to
deliver supplemental oxygen to a spontaneously breathing patient.
Oxygenation The process of getting oxygen into the body and to its tissues for metabolism.
Pacemaker cells Specialized cells of the heart’s electrical conduction system, capable of spontaneously
generating and conducting electrical impulses.
Pulse oximeter A small instrument with a light sensor that quickly calculates the percentage of hemo-
globin that is saturated with oxygen in a pulsating capillary bed.
Refractoriness A term used to describe the period of recovery that cells need after being discharged
before they are able to respond to a stimulus.
Relative bradycardia A term that refers to a situation in which a patient’s heart rate may be more than
60 beats/min but, physiologically, the patient needs a tachycardia (as in hypovolemia) and is unable to
increase his or her heart rate because of sinoatrial node disease, beta-blockers, or other medications.
Relative refractory period Corresponds with the downslope of the T wave on the ECG; cardiac cells
can be stimulated to depolarize if the stimulus is strong enough.
Repolarization Movement of ions across a cell membrane in which the inside of the cell is restored to its
negative charge.
Respiration The exchange of oxygen and carbon dioxide during cellular metabolism.
Risk factors Traits and lifestyle habits that may increase a person’s chance of developing a disease.
Segment On the ECG, a line between waveforms that is named by the waveform that precedes or fol-
lows it.
Simple face mask An oxygen delivery device that consists of a plastic reservoir that fits over a patient’s
nose and mouth and a small diameter tube connected to the base of the mask through which oxygen is
delivered; also called a standard mask.
Glossary 279
Soft palate The back part of the roof of the mouth that is made up of mucous membrane, muscular
fibers, and mucous glands.
Stroke system of care A comprehensive, diverse system that addresses all aspects of stroke care in a
coordinated fashion.
Sudden cardiac death (SCD) A natural death of cardiac cause that is preceded by an abrupt loss of
consciousness within 1 hour of the onset of an acute change in cardiovascular status; sudden cardiac
arrest is a term commonly applied to such an event when the patient survives.
Supernormal period Period during the cardiac cycle when a weaker-than-normal stimulus can cause
cardiac cells to depolarize.
Supraventricular arrhythmias Rhythms that begin in the sinoatrial node, atrial tissue, or the atrioven-
tricular junction (ie, above the bifurcation of the His bundle).
Symptomatic bradycardia A term used to describe a patient who experiences signs and symptoms of
hemodynamic compromise related to a slow heart rate.
Synchronized cardioversion The timed delivery of a shock during the QRS complex.
Transient ischemic attack (TIA) A transient episode of neurologic dysfunction caused by focal brain,
spinal cord, or retinal ischemia, without acute infarction.
Transthoracic impedance (resistance) The resistance of the chest wall to current.
Uvula Fleshy tissue that hangs down from the soft palate and into the posterior portion of the oral cavity.
Vallecula The space or “pocket” between the base of the tongue and the epiglottis.
Ventilation The mechanical movement of gas or air into and out of the lungs.
INDEX
Note: Page numbers followed by f indicate figures, t indicate tables, b indicate boxes and ge indicate glossary.
A AHA/ASA. See American Heart Association/American

Stroke Association (AHA/ASA)
ABC mnemonic, for general impression, 14–15
AICSs. See Acute ischemic coronary syndromes
Absolute bradycardia, 167
(AICSs)
Absolute refractory period (ARP), 68
Airway(s)
ACC. See American College of Cardiology (ACC)
advanced, 49–59, 50–51b
Accelerating angina, 198–199
lower, 27–28
Accessory pathway, 70
management of, 23–62
ACE inhibitors. See Angiotensin-converting enzyme (ACE)
manual, maneuvers for, 37–38, 38t
inhibitors
primary survey assessment of, 15
ACSs. See Acute coronary syndromes (ACSs)
suctioning of, 39–40
Action potential, 67
upper, 25–27, 26–27b
cardiac, 66–69, 66b, 66f
Airway adjuncts, 40–44
Acute coronary syndromes (ACSs), 78–79, 78b, 193–236
nasal airway, 42–44, 43f, 44t
algorithm, 218f
oral airway, 40–41, 41–42f, 44t
analgesic therapy in, 217–218, 219t
Alveolar ducts, 28
anticoagulant therapy in, 222–224, 224t
American College of Cardiology (ACC), 202–203
atypical presentation of, 202–203
American Heart Association (AHA), 6, 202–203, 237
cause of, 194
American Heart Association/American Stroke Association
electrocardiogram findings of, 204–214
(AHA/ASA), 243–244
hyperacute T waves, 204–214
Amiodarone (Cordarone), 88, 89t
QRS changes, 205, 205t
Analgesic therapy, 217–218, 219t
ST segment changes, 204–205, 205b
Anesthesiologist, 103b
T wave inversion, 205
Angina
evaluation of, 201–215
Prinzmetal's, 199, 199b
patient history, 201–202, 201b
stable, 197, 198b
imaging studies for, 215
terminology for, 198b
initial management of, 215–226
unstable, 198–199
emergency department, 216–217
variant, 199
pharmacologic therapies, 217–224
Angina pectoris, 3, 197, 197–198b, 198f
prehospital, 215–216, 215b
Anginal equivalent, 202
pathophysiology of, 194–196, 195f
examples of, 203b
patient evaluation for, 201–215
Angiotensin-converting enzyme (ACE)
physical examination of, 203
inhibitors, 221
Acute ischemic coronary syndromes (AICSs), 193–194
Anterior circulation strokes, 239–240
Acute ischemic stroke, 237–258, 237b, 238t
Anterior interventricular artery, 65
Acute stroke, 243–244. See also Stroke
Anterior myocardial infarction, 207–209, 208–209f
Acute stroke-ready hospitals (ASRHs), 246–247
Anterior oropharynx, 25–26
Acute stroke teams (ASTs), 246–247
Anterolateral, 95
Adam's apple, 26
Anteroseptal myocardial infarction, 207
Adenoids, 25
Anticoagulant therapy, 222–224, 224t
Adenosine, 134–136, 134t, 140b
Antiplatelet therapy, 221–222, 223f, 223–224t
Advanced airways, 49–59, 50–51b
Apex-anterior position, 95
endotracheal tube placement, confirming, 51–59, 51b
Area at risk, myocardial infarction, 200, 201f
Advanced cardiac life support (ACLS), 1, 63
Arrhythmia, 63–65
Advanced life support, effective, 8
Arteriosclerosis, 194, 195–196f
AECDs. See Automated external cardioverter-defibrillators
Arytenoid cartilages, 26
(AECDs)
Aspirin, 221, 224t
AED. See Automated external defibrillator (AED)
ASRHs. See Acute stroke-ready hospitals (ASRHs)
AFib. See Atrial fibrillation (AFib)
ASTs. See Acute stroke teams (ASTs)
Agonist, 88b
Asynchronous countershock. See Defibrillation
AHA. See American Heart Association (AHA)
281
282 Index
Asystole, 4, 88–89, 90f BMD. See Bag-mask device (BMD)

cardiac arrest rhythms, 88–89, 90f Bradycardias, 167–192. See also specific types
characteristics of, 90t absolute, 167
P-wave, 88, 90f algorithm of, 177f
ventricular, 88 relative, 167
AT. See Atrial tachycardia (AT) sinus, 169, 169b, 169f, 169–170t
Atheromatous plaque, basic structure of, 195f symptomatic, 167, 168b
Atherosclerosis, 194 Brain, arterial blood supply to, 240f
Atherosclerotic lesions, types of, 195 Brain attack, 237b. See also Stroke
Atherosclerotic plaques, 195 Brain Attack Coalition (BAC), 243–244
Atrial fibrillation (AFib), 145–148, 146–147f, 146t Brain imaging, 249
Atrial flutter, 144–145, 144b, 144t, 145f Breathing, 16
Atrial tachycardia (AT), 133–136, 133f, 133t, 135f Bronchi
Atrioventricular blocks, 172–176 primary, left and right, 27–28
first-degree, 172–173, 173t, 173f secondary, 28
second-degree, 173–175, 175f tertiary, 28
2:1, 175, 175t Bronchioles, 28
type I, 173–174, 174f, 174t BTE waveform. See Biphasic truncated exponential (BTE)
type II, 174–175, 174f, 174t waveform
third-degree, 176, 176f, 176b, 176t Bulb-type esophageal detector devices, 51, 52f
Atrioventricular bundle. See Bundle of His Bundle branch block (BBB), 140, 147f, 207–209
Atrioventricular junction, 70 Bundle branches
atrioventricular node and, 70 left, 70
bundle of His and, 70 right, 70
Atrioventricular nodal reciprocating tachycardia, 136–137 Bundle of His, 70. See also Bundle branches
Atrioventricular nodal reentrant tachycardia (AVNRT),
137–138, 137t, 138f
Atrioventricular node, 70
C
Atrioventricular reciprocating tachycardia, 136–137 CAD. See Coronary artery disease (CAD)
Atrioventricular reentrant tachycardia (AVRT), 138–140, Calcium channel blockers, 135t, 136b, 219–220, 220t
139f Capacitor, 92
Atropine sulfate, 170t Capnograms, interpreting, 31b
Atypical presentation, of acute coronary syndromes, 202–203 Capnography, 30
Augmented limb leads, 73, 73f Capnometers, digital, 31
Automated external cardioverter-defibrillators (AECDs), 100 Carbon dioxide, monitoring of, 30–32
Automated external defibrillation, 91, 99 Cardiac action potential, 66–69, 66b, 66f
operation of, 99 phases of, 67–68, 68b, 68f
Automated external defibrillator (AED), 6 Cardiac anatomy, 63–82
Automatic atrial tachycardia, 134 Cardiac arrest, 3
Automatic cells. See Pacemaker cells algorithm, 90–91, 92f
Automaticity, 66 heart rhythms in, 4, 83–128
AVNRT. See Atrioventricular nodal reentrant tachycardia in-hospital, 5
(AVNRT) out-of-hospital, 4–5
AVRT. See Atrioventricular reentrant tachycardia (AVRT) phases of, 4t
pregnancy and, 107
primary, 4
B sudden, 4
BAC. See Brain Attack Coalition (BAC) Cardiac Arrest Management station, 101b
Bad news, conveying, resuscitation efforts and, Cardiac arrest rhythms, 83–128
111–112, 111b asystole, 88–89, 90f
Bag-mask device (BMD), 47, 47f pulseless electrical activity, 90–91, 90b, 91f
supplemental oxygen, with/without, 48 resuscitation team, 100–124, 101b
Bag-mask resuscitator. See Bag-mask device (BMD) ventricular fibrillation, 85–88
Bag-mask ventilation, 47–49, 47f, 48b, 49f ventricular tachycardia, 85
oxygen delivery, 47–48 Cardiac biomarkers, 214–215
troubleshooting, 49 Cardiac cells, 66
Bag-valve-mask device. See Bag-mask device (BMD) action potential of, 66–69, 66b, 66f
Basic life support (BLS), 1 Cardiac output, 10
cardiopulmonary resuscitation and, 6 Cardiac troponins, 214
BBB. See Bundle branch block (BBB) Cardiopulmonary arrest, 3. See also Cardiac arrest
Berman airway, 40–41, 41f Cardiopulmonary resuscitation (CPR), 1–2, 10–13
Beta-blockers, 135t, 219, 220t barriers to effective, 10–11, 11b
Biphasic defibrillation, 93–94 cardiac output associated with, 10
Biphasic defibrillators, 94 in Chain of Survival, 6, 9
Biphasic truncated exponential (BTE) waveform, 93–94 chest compressions
Biphasic waveforms, 93–94, 94f mechanical devices, 12–13, 13–14f
Bipolar lead, 73 physiology of, 10, 10b
BLS. See Basic life support (BLS) feedback during, 11–12, 12f
Index 283
Cardiovascular care, after ROSC, 109–110 Conduction system (Continued)

Cardiovascular collapse, 3 Purkinje fibers, 70, 71t
Cardiovascular disease (CVD), 2–3 sinoatrial node, 69–70, 69f, 70b
risk factors for, 2–3, 3t Conductive material, use of, 96–97, 96f
Cardioversion, synchronized, 150 Congenital cardiovascular disease, 2–3
Caregivers, assistance by resuscitation team, 112–124 Contributing risk factors, 2–3, 3t
Carina, 27–28 Coronary arteries, 65–66
Carotid sinus, location of, 137f Coronary artery disease (CAD), 3
Carotid sinus massage (CSM), 136, 137f Coronary heart disease (CHD), 3
Carotid sinus pressure. See Carotid sinus massage (CSM) Coronary perfusion pressure, 10
Carotid territory strokes, 239–240 CPR. See Cardiopulmonary resuscitation (CPR)
Centers for Disease Control and Prevention, 4 CPSS. See Cincinnati Prehospital Stroke Scale (CPSS)
Central nervous system (CNS) infarction, definition of, 239 Crash cart, 102
Cerebral hemorrhage, silent, 239 Crescendo angina, 198–199
Cerebral venous thrombosis, stroke caused by, 239 Cricoid cartilage, 26–27
Chain of Survival, 5–10 Cricothyroid membrane, 26–27
advanced life support, effective, 8 CRM. See Powerheart Cardiac Rhythm Module (CRM)
cardiopulmonary resuscitation and, 9 CSCs. See Comprehensive stroke centers (CSCs)
early, 6 CSM. See Carotid sinus massage (CSM)
defibrillation CT. See Computed tomography (CT)
prompt, 9 CVD. See Cardiovascular disease (CVD)
rapid, 6–8, 7f CX artery. See Circumflex (CX) artery
definition, 5 Cyclooxygenase inhibitors, 223t
in-hospital, 8–10
links in, 5
medical emergency team and, 8
D
notification and response, 9 Debriefing, resuscitation efforts, 110–111
out-of-hospital, 5–8 Defibrillation, 91–100, 93b
post-cardiac arrest care automated external, 91, 99
integration of, 8 biphasic, 93–94
intra-arrest and, 9–10 manual, 91
recognition and activation in, 6 monophasic, 93–94
surveillance and prevention, 8–9, 9b primary survey assessment of, 16
CHD. See Coronary heart disease (CHD) procedure for, 97–99, 97–99b, 98f
Chest compressions prompt, 9
mechanical devices for, 12–13, 13–14f rapid, 6–8
physiology of, 10, 10b transthoracic impedance, 94–97, 94b
Chest hair, 94–95, 95b Defibrillation waveforms, 93
Chest leads, 72–76 biphasic waveform, 93–94, 94f
augmented limb, 73, 73f monophasic waveform, 93–94, 94f
bipolar, 73 Defibrillators, 92–93, 93f. See also Defibrillation
frontal plane, 73, 73t automated external, 6
horizontal plane, 73–76, 73–74b, 74f, 74–75t biphasic, 94
standard limb, 73, 73f monophasic, 94
Chronotrope, 88b Delta wave, 131ge, 138
Cilia, 28 Depolarization, 67, 67b
Cincinnati Pre-hospital Stroke Scale (CPSS), 245 wave of, 67
Circle of Willis, 239–240 Digital capnometers, 31, 31f
Circulation, 16 Disability, primary survey assessment of, 16
Circumflex (CX) artery, 65 Dispatch time, 245
blockage of, 65–66 DNAR. See Do-not-attempt-resuscitation (DNAR)
Closed-loop communication, resuscitation efforts, Do-not-attempt-resuscitation (DNAR), 104
105, 105b Dopamine, 171t, 171b
“Coarse” ventricular fibrillation, 85–86 Dromotrope, 88b
Code, 5 Drug administration, 103, 103b
Code blue, 5 “Ds of stroke care”. See Stroke Chain of Survival
Code director, 101 Dysrhythmia, 63–65
Code team, 100
Colorimetric capnometer, 31–32, 32f
Common bundle, 70
E
Complexes of electrocardiogram, 76–77 E-C clamp technique, 46, 46f
Comprehensive stroke centers (CSCs), 247 E-C grip, 46, 46f
Computed tomography (CT), 249 ECG. See Electrocardiogram (ECG)
Conducting cells. See Pacemaker cells Ectopic AT. See Ectopic atrial tachycardia (ectopic AT)
Conduction system, 69–70, 71t Ectopic atrial tachycardia (ectopic AT), 134
atrioventricular node, 70 Ectopic pacemaker sites, 70, 70b
bundle branches, right and left, 70 EDDs. See Esophageal detector devices (EDDs)
bundle of His, 70 Effective refractory period (ERP), 68f, 69
284 Index
Electrical capture, 178–179, 179f Glottis, 26

Electrical therapy, possible complications of, 100 Glycoprotein (GP) IIb/IIIa receptor inhibitors, 221–222, 223t
Electrocardiogram (ECG), 71–78, 71f, 72b Guedel airway, 40–41, 41f
absolute refractory period on, 68
chest leads for, 72–76
complexes of, 76–77
H
electrodes, 72, 72f Hard palate, 25–26
waveforms of, 76–77, 76f Head tilt-chin lift, 37, 37f, 38t
Electrocardiography paper, 76, 76f Heart, surfaces of, 204f
Electrodes, 72, 72f Heart attack, 237b
Electromechanical dissociation, 90 Heart disease, 1
Electrophysiology, 63–82 Heart rhythms. See also specific types
cardiac cells, 66 in cardiac arrest, 83–128
conduction system, 69–70 asystole, 88–89, 90f
refractory periods, 68–69, 68f pulseless electrical activity, 90–91, 90b, 91f
Embolic ischemic stroke, 242–243 resuscitation team, 100–124, 101b
Emergency cardiovascular care, 1–22 ventricular fibrillation, 85–88
Chain of Survival, 5–10 ventricular tachycardia, 85
coronary artery disease, 3 nonshockable, 86–88, 106–107
patient assessment, 14–19 shockable, 86–88, 97b, 105–106, 106b
sudden cardiac death, 4 Hemorrhagic stroke, 240b
Emergency medical services (EMS), 6 HFNC systems. See High-flow nasal cannula (HFNC)
on stroke care, 244–246 systems
Emergency medical technicians (EMTs), 100 HI-D Big Stick suction tip, 39, 39f
EMS. See Emergency medical services (EMS) High-flow nasal cannula (HFNC) systems, 34
EMTs. See Emergency medical technicians (EMTs) His-Purkinje system, 70
Endotracheal intubation, 50, 50f Horizontal plane leads, 73–76, 73–74b, 74f, 74–75t
Epiglottis, 25–26 Hyperacute T waves, 204
Epinephrine, 86–88, 87t, 171b Hypercarbic respiratory failure, 28
ERP. See Effective refractory period (ERP) Hyperventilation, 10b
Esophageal detector devices (EDDs), 51–59 Hypopharynx, 25
Esophageal intubation detectors, 51 Hypoxemic respiratory failure, 28
Exposure, assessment of patient's, 16
Extracorporeal CPR, 106b
Extraglottic airway devices, 49–50
I
Ibutilide, 144–145, 146t
ICH. See Intracerebral hemorrhage (ICH)
F Idioventricular rhythm, 171–172. See also Ventricular escape
Face Arm Speech Test (FAST), 245 rhythm
Family notification, resuscitation efforts, 111–112 IHCA. See In-hospital cardiac arrest (IHCA)
FAST. See Face Arm Speech Test (FAST) In-hospital cardiac arrest (IHCA), 5
FBAO. See Foreign body airway obstruction (FBAO) In-hospital Chain of Survival, 8–10
Fibrinolytics, 224 Inferior myocardial infarction, 209–210, 210–211f
"Fine" ventricular fibrillation, 85–86 Inferobasal myocardial infarction, 211–213, 212f, 213b
First-degree atrioventricular block, 172–173, 173t, 173f Inferobasal wall myocardial infarction, 211
Five Hs, 86, 87b Inotrope, 88b
Five Ts, 86, 87b Intermediate coronary syndrome, 198–199
"Fixed" risk factors, 2–3, 3t Intervals, 77–78, 77f, 78b
Flexible suction catheters, 39 Intracerebral hemorrhage (ICH), 241–242, 241b
Flow rates definition of, 239
of nasal cannula, 33 stroke caused by, 239
of nonrebreather mask, 36b Intravenous fibrinolysis, 249–250
of partial rebreather mask, 36 Inverted T waves, 204–205
of simple face mask, 34 Irregular tachycardias, 143–149
Flutter waves, 144, 145f atrial fibrillation, 145–148, 146–147f, 146t
Focal AT. See Focal atrial tachycardia (focal AT) atrial flutter, 144–145, 144b, 144t, 145f
Focal atrial tachycardia (focal AT), 134 multifocal atrial tachycardia, 143, 143t, 144f
Foreign body airway obstruction (FBAO), 6 polymorphic ventricular tachycardia (PMVT), 148–149,
French suction catheters, 39 148–149f, 148–149t
Frontal plane leads, 73, 73t Ischemic penumbra, 243, 243f
Ischemic stroke, 241f, 242–243
acute, 237–258, 237b, 238t
G definition of, 239
Gasping, 3 embolic, 242–243
Gastric distention, 46b lacunar, 243
GCS. See Glasgow Coma Scale (GCS) signs and symptoms of, 242t
Glasgow Coma Scale (GCS), 249 thrombotic, 242
Glottic opening, 26 Isoproterenol, 171t, 171b
Index 285
J Myocardial infarction (MI), 65, 196–200, 200–201f

anatomic location of, 204f, 206–213, 206–207t, 206f
J point, 77 anterior, 207–209, 208–209f
Jaw thrust, 38, 38t, 38f inferior, 209–210, 210–211f
Joint Commission National Patient Safety Goals, 8 inferobasal (posterior), 211–213, 212f, 213b
Joint Commission on Accreditation of Healthcare lateral, 209, 209–210f
Organizations, 8 right ventricular, 213, 213–214f
Junctional bradycardia, 169–170 anteroseptal, 207
Junctional dysrhythmias, 70b classification of, 205t
Junctional escape rhythm, 169–171, 170t, 170f, 171b common cause of, 66b
coronary heart disease and, 3
L transmural, 200
Myocardial injury, 196–200
Lacunar infarcts, 243 Myocardial ischemia, 196–200, 196b, 197f, 198b
Lacunar strokes, 243 pain descriptions uncharacteristic of, 202–203
LAD artery. See Left anterior descending (LAD) artery
Laryngeal mask airway (LMA), 49–50, 50f
Laryngopharynx, 26
N
Larynx, 26 Narrow-QRS tachycardias, 131–140, 134–135t, 135f
Latent pacemaker, 70 atrial tachycardia, 133–136, 133f, 133t, 135f
Lateral myocardial infarction, 209, 209–210f atrioventricular nodal reentrant tachycardia (AVNRT),
LCA. See Left coronary artery (LCA) 137–138, 137t, 138f
Lead aVR, 213–214 atrioventricular reentrant tachycardia (AVRT), 138–140,
Lead wire, 72 139f
Leads. See Chest leads sinus tachycardia, 131–132, 131t, 132f, 132b
Left anterior descending (LAD) artery, 65, 207 Nasal airway, 42–44, 43f, 44t
Left coronary artery (LCA), 65 Nasal cannula, 33–34, 33b, 33f, 37t
Left main coronary artery (LMCA), 65 Nasal prongs, 33
Lidocaine (Xylocaine), 88, 89t Nasal trumpet. See Nasal airway
Life support, advanced. See also Basic life support (BLS) Nasopharyngeal airway (NPA). See Nasal airway
effective, 8 Nasopharynx, 25
Lipid management, 221, 221t National Institutes of Health Stroke Scale (NIHSS), 248
LMA. See Laryngeal mask airway (LMA) National Stroke Association (NSA), 243–244
LMCA. See Left main coronary artery (LMCA) Negative T waves, 204
Los Angeles Motor Scale, 245 Neurologic care, after ROSC, 110
Lower airway, 27–28 NIHSS. See National Institutes of Health Stroke Scale
(NIHSS)
M Nitroglycerin (NTG), 217, 219t
NIV. See Noninvasive ventilation (NIV)
MACE. See Major adverse cardiac event (MACE) Non-ST elevation acute coronary syndromes (NSTE-ACSs),
Magnesium sulfate, 149t 199
Magnetic resonance imaging (MRI), 249 Noninvasive pacing. See Transcutaneous pacing (TCP)
Major adverse cardiac event (MACE), 214–215 Noninvasive positive pressure ventilation (NPPV), 44–45, 45b
Manual airway maneuvers, 37–38, 38t Noninvasive ventilation (NIV), 44–45
head tilt-chin lift, 37, 37f, 38t "Nonmodifiable" risk factors, 2–3, 3t
jaw thrust, 38, 38t, 38f Nonrebreather mask, 35f, 36, 36b, 37t
Manual defibrillation, 91 Nonshockable rhythms, 86–88, 106–107
MAT. See Multifocal atrial tachycardia (MAT) Nonsustained rhythm, 134
Mechanical cells, 66 NPPV. See Noninvasive positive pressure ventilation (NPPV)
Mechanical chest compression devices, 12–13, 13–14f NSA. See National Stroke Association (NSA)
Medical emergency team (MET), 8 NSTE-ACSs. See Non-ST elevation acute coronary
Mega Code station, 101b syndromes (NSTE-ACSs)
MET. See Medical emergency team (MET) NTG. See Nitroglycerin (NTG)
MEWS. See Modified Early Warning Score (MEWS) Nurse anesthetist, 103b
MI. See Myocardial infarction (MI)
Ministroke. See Transient ischemic attack (TIA)
Modifiable risk factors, 2–3, 3t
O
Modified Early Warning Score (MEWS), 8 Occlusive stroke, 242
Modified jaw thrust, 38 OHCA. See Out-of-hospital cardiac arrest (OHCA)
Monomorphic ventricular tachycardia, 142 On-scene time, 245
Monophasic defibrillation, 93–94 OPA. See Oropharyngeal airway (OPA)
Monophasic defibrillators, 94 Opioid overdose, 107
Monophasic waveform, 93–94, 94f Oral airway, 40–41, 42f, 44t
Mouth-to-mask ventilation, 45–46, 47t, 47f Oropharyngeal airway (OPA), 40
MRI. See Magnetic resonance imaging (MRI) Oropharynx, 25–26
Multifocal atrial tachycardia (MAT), 143, 143t, 144f Orotracheal intubation, 25–26
Myocardial blood flow, 10 Out-of-hospital cardiac arrest (OHCA), 4–5
Myocardial cells, 66 Out-of-hospital Chain of Survival, 5–8
286 Index
Oxygen delivery devices, 32–36 Powerheart Cardiac Rhythm Module (CRM), 100
bag-mask ventilation, 47–49 Pregnancy, cardiac arrest and, 107
nasal cannula, 33–34, 33b, 33f, 37t Preinfarction angina, 198–199
nonrebreather mask, 35f, 36, 36b, 37t Premature atrial complex (PAC), 137
partial rebreather mask, 35–36, 35–36b, 35f, 37t Premature ventricular complexes (PVCs), 142
simple face mask, 34, 34f, 34b, 37t Preocclusive syndrome, 198–199
Oxygenation, 29 Primary bronchi, left and right, 27–28
pulse oximetry, 32b Primary bronchi bifurcation, 27f
ROSC and, 108 Primary cardiac arrest, 4
Primary percutaneous coronary intervention, 224
P in STEMI recommendations, 225b
Primary stroke centers (PSCs), 247
P-wave, asystole, 88, 90f Primary survey, on patient, 15–16, 15–16b
P2Y12 receptor inhibitors, 221, 223t Prinzmetal's angina, 199, 199b
PAC. See Premature atrial complex (PAC) Procainamide, 140–141, 141t
Pacemaker cells, 66 PSCs. See Primary stroke centers (PSCs)
Paddle/pad PSVT. See Paroxysmal supraventricular tachycardia (PSVT)
position, 95–96, 95–96f Public access defibrillation, 6
size, 95 Pulmonary compliance, 49
Paddle pressure, 97 Pulse ox. See Pulse oximeter
Palatine tonsils, 25–26 Pulse oximeter, 29, 30b
Paroxysmal, definition of, 133 Pulse oximetry, 29–30, 30f, 32b
Paroxysmal AT. See Paroxysmal atrial tachycardia (PAT) accuracy of, factors affecting, 30b
Paroxysmal atrial tachycardia (PAT), 133 Pulseless electrical activity (PEA), 4, 90–91, 90b, 91f
Paroxysmal supraventricular tachycardia (PSVT), 133, 134f Pulseless ventricular tachycardia (pVT), 4
Partial rebreather mask, 35–36, 35–36b, 35f, 37t Purkinje fibers, 67–68, 70, 71t
PAT. See Paroxysmal atrial tachycardia (PAT) PVCs. See Premature ventricular complexes (PVCs)
PATCH-4-MD, 86, 86b pVT. See Pulseless ventricular tachycardia (pVT)
Patient assessment, 14–19
general impression of condition, 14–15
primary survey, 15–16, 15b
Q
responsive patient, 15–16 QRS complexes
unresponsive patient, 16, 16b of polymorphic ventricular tachycardia, 148, 148f
with respiratory compromise, 29–32 of ventricular tachycardia, 85f
scene safety, 14 QT interval, 78
secondary survey, 17–19
components, 17b
Patient history, of acute coronary syndromes, 201–202, 201b
R
PCI. See Percutaneous coronary intervention (PCI) R-wave progression, 77
PEA. See Pulseless electrical activity (PEA) RACE. See Rapid Arterial Occlusion Evaluation (RACE)
Percutaneous coronary intervention (PCI), 224 Rapid Arterial Occlusion Evaluation (RACE), 245
Pharyngeal tonsils, 25 Rapid Response System (RRS), 8
Pharynx, 25 calling criteria, 9b
laryngopharynx, 26 Rapid response team (RRT), 8
nasopharynx, 25 RCA. See Right coronary artery (RCA)
oropharynx, 25–26 Rectilinear biphasic (RLB) waveform, 93–94
Physical examination, of acute coronary syndromes, 203 Reentrant tachycardias, 136–140
PMVT. See Polymorphic ventricular tachycardia (PMVT) Reentry, 136–137
Pocket face mask, 45–46 Refractoriness, 68
Pocket mask, 45–46, 45f Refractory periods, 68–69, 68f
POCUS. See Point of care ultrasound (POCUS) Relative bradycardia, 167
Point of care ultrasound (POCUS), 90–91 Relative refractory period (RRP), 69
Polymorphic ventricular tachycardia (PMVT), 148–149, Renin-angiotensin-aldosterone system inhibitors, 221, 222t
148–149f, 148–149t Reperfusion therapies, 224–226, 225b
Poor R-wave progression, 77 Repolarization, 67
Positive pressure ventilation, 44–49 Respiration, 29
bag-mask ventilation, 47–49, 48b, 49f Respiratory compromise, patient with, 28–32
mouth-to-mask ventilation, 45–46, 47t, 47f Respiratory failure
noninvasive positive pressure ventilation, 44–45, 45b hypercarbic, 28
Post-cardiac arrest care, 102, 108–110, 108t, 109f hypoxemic, 28
integration of, 8 Respiratory system, anatomy of, 25–28
intra-arrest and, 9–10 Response time, 245
Post-cardiac arrest syndrome, components of, 108t Resuscitation efforts, 104–112, 104b
Posterior chest lead, 75f caregivers, assisting, 112–124
Posterior circulation strokes, 239–240 closed-loop communication, 105, 105b
Posterior wall myocardial infarction, 211 debriefing, 110–111
Postresuscitation support, 102. See also POst-cardiac arrest family notification, 111–112
care conveying bad news, 111–112, 111b
Index 287
Resuscitation efforts (Continued) Stable angina, 197, 198b

nonshockable rhythms, 106–107, 107b Standard limb leads, 73, 73f
patient transfer, 107 Standard mask, 34. See also Simple face mask
post-cardiac arrest care, 108–110, 109f Stroke, 237b. See also specific types
cardiovascular care, 109–110 anatomy review, 239–240, 240b, 240f
neurologic care, 110 anterior circulation, 239–240
oxygenation and ventilation, 108 carotid territory, 239–240
shockable rhythms, 105–106, 106b cerebral venous thrombosis, caused by, 239
special resuscitation situations, 107 conditions mimicking, 248b
cardiac arrest and pregnancy, 107 definition of, 239
known/suspected opioid overdose, 107 hemorrhagic, 240b
Resuscitation mask, 45–46 intracerebral hemorrhage, caused by, 239
Resuscitation team, 100–124, 101b occlusive, 242
team leader, responsibilities of, 101–102 posterior circulation, 239–240
team member, responsibilities of, 102–104, 103b Stroke Chain of Survival for, 237, 238t
Return of spontaneous circulation (ROSC), 108 subarachnoid hemorrhage, caused by, 239
Right chest leads, 74, 75t, 75f types of, 240–243
Right coronary artery (RCA), 65, 65f intracerebral hemorrhage, 241–242, 241b
blockage of, 65 ischemic stroke, 241f, 242–243, 242t
Right ventricular infarction (RVI), 213, 213–214f subarachnoid hemorrhage, 240–241
Rigid suction catheters, 39, 39f transient ischemic attack, 243
Risk factors vertebrobasilar territory, 239–240
contributing, 2–3, 3t warning signs of, 244b
defined, 2–3 Stroke centers, 246–250, 246t
“fixed”, 2–3, 3t best practices, 250
modifiable, 2–3, 3t brain imaging, 249
“nonmodifiable”, 2–3, 3t diagnostic tests, 248, 248b
RLB waveform. See Rectilinear biphasic (RLB) waveform intravenous fibrinolysis, 249–250
ROSC. See Return of spontaneous circulation (ROSC) neurologic examination, 248
RRP. See Relative refractory period (RRP) other therapies, 250
RRS. See Rapid Response System (RRS) patient history, 247
RRT. See Rapid response team (RRT) physical examination, 247–248, 248b
RSVP system, 104b triage and initial evaluation, 247
RVI. See Right ventricular infarction (RVI) Stroke Chain of Survival, 237, 238t
Stroke systems of care, 243–250
S acute phase of, 244
emergency medical services on, 244–246
SAH. See Subarachnoid hemorrhage (SAH) hyperacute phase of, 244
Saturation of peripheral oxygen (SpO2), 29 prehospital assessment and management, 245–246
SBAR acronym, 104b public education, 244, 244b
SCD. See Sudden cardiac death (SCD) Subarachnoid hemorrhage (SAH), 240–241, 241f
Second-degree atrioventricular blocks, 173–175, 175f definition of, 239
2:1, 175, 175t stroke caused by, 239
type I, 173–174, 174f, 174t Subendocardial area, 200
type II, 174–175, 174f, 174t Subepicardial area, 200
Secondary bronchi, 28 Suction catheters
Secondary survey, on patient, 17–19 flexible, 39
Segments, 77–78, 77f, 78b French, 39
Selected energy, 97 rigid, 39, 39f
Serum biomarkers, 214 soft, 39, 40f
Serum cardiac markers, 214 tonsil tip, 39
Severe sinus bradycardia, 169 whistle tip, 39
Shockable rhythms, 86–88, 97b, 105–106, 106b Yankauer, 39
Silent central nervous system infarction, definition of, 239 Suctioning of airway, 39–40, 40b
Silent cerebral hemorrhage, definition of, 239 possible complications of, 40b
Simple face mask, 34, 34f, 34b, 37t Sudden cardiac arrest, 4
Sinoatrial node, 69–70, 69f, 70b Sudden cardiac death (SCD), 2–5, 3f
Sinus bradycardia, 169, 169b, 169f, 169–170t definition of, 4
Sinus tachycardia, 131–132, 131t, 132f, 132b Supernormal period (SNP), 69
SNP. See Supernormal period (SNP) Support roles, in resuscitation team, 103–104
Soft palate, 25–26 Supraglottic airways, 49–50
Soft suction catheters, 39, 40f Supraventricular arrhythmias, 131, 131ge
Sotalol, 140–141, 141t Supraventricular dysrhythmias, 70b
SPIKES protocol, 111–112, 111b Supraventricular tachycardia (SVT), 132–140, 132b, 133f
SpO2. See Saturation of peripheral oxygen (SpO2) Sustained rhythm, 134
ST junction, 77 SVT. See Supraventricular tachycardia (SVT)
ST segment, changes of, with acute coronary syndrome, Sympathetic receptors, 88b
204–205, 205b Symptomatic bradycardia, 167, 168b
288 Index
Synchronized cardioversion, 131ge, 150 Tripod position, 29

procedure in, 150, 151f, 152t TTM. See Targeted temperature management (TTM)
Syringe-type esophageal detector devices, 51 Turnout time, 245
T U
T waves UA. See Unstable angina (UA)
hyperacute, 204 Unstable angina (UA), 198–199
inversion, 205 Unsynchronized countershock. See Defibrillation
Tachycardias, 129–166, 130b Upper airway, 25–27, 26–27b
algorithm for, 149f structures of, 25–26f
irregular, 143–149 Uvula, 25–26
narrow-QRS, 131–140, 134–135t, 135f
wide-QRS, 140–143, 143b
Targeted temperature management (TTM), 110
V
TCP. See Transcutaneous pacing (TCP) Vagal maneuvers, 136, 136b
TdP. See Torsades de pointes (TdP) Vallecula, 25–26
TE grip, 46, 47f Valsalva maneuver, 136
Team leader, 101 Variant angina, 199
responsibilities in resuscitation team, 101–102 Ventilation, 29
Team member, responsibilities in resuscitation team, ROSC and, 108
102–104, 103b Ventilation face mask, 45–46
airway management, 102–103 Ventricular asystole, 88
cardiopulmonary resuscitation, 102 Ventricular dysrhythmias, 70b
electrocardiogram monitoring, 102 Ventricular escape rhythm, 171–172, 172t, 172f
support roles, 103–104 Ventricular fibrillation (VF), 4, 85–88
vascular access and medication administration, 103 characteristics of, 85t
Temporary external pacing. See Transcutaneous pacing (TCP) Ventricular standstill, 88
Tertiary bronchi, 28 Ventricular tachycardia (VT), 85, 142–143, 142f, 142b
Thenar eminence (TE) technique, 46, 47f monomorphic, 85
Therapeutic hypothermia, 110 characteristics of, 85t
Thienopyridines, 221 polymorphic, 85
Third-degree atrioventricular block, 176, 176f, 176b, 176t QRS complexes of, 85f
Thrombolysis in MI (TIMI), 214–215 Ventricular tachydysrhythmias, 86f
Thrombotic ischemic stroke, 242 Vertebrobasilar territory strokes, 239–240
Thyroid cartilage, 26 VF. See Ventricular fibrillation (VF)
Thyroid gland, 26 Voice box. See Larynx
TIA. See Transient ischemic attack (TIA) VT. See Ventricular tachycardia (VT)
Tidal volume, 29 "Vulnerable" plaque, 195
TIMI. See Thrombolysis in MI (TIMI)
Tonsil tip suction catheters, 39
Torsades de pointes (TdP), 148
W
Total ischemic time, 216 Warning stroke. See Transient ischemic attack (TIA)
Trachea, 27–28 Waveforms, 76–77, 76f
Tracheal tube, 27–28 biphasic, 93–94, 94f
Transcutaneous pacing (TCP), 176–180 biphasic truncated exponential, 93–94
indications for, 177 defibrillation, 93
limitations of, 179–180 monophasic, 93–94, 94f
possible complications in, 180 rectilinear biphasic, 93–94
procedure for, 178–179, 178f, 179b Wenckebach phenomenon, 173
responses to, 180b Whistle tip suction catheters, 39
Transient ischemic attack (TIA), 243 Wide-QRS tachycardias, 140–143, 143b
Transient stroke. See Transient ischemic attack (TIA) ventricular tachycardia, 142–143, 142f, 142b
Transition zone, 77 Widow maker, 65
Transitional zone, 243, 243f Wolff-Parkinson-White (WPW) pattern, 138, 139–140f,
Transmural myocardial infarction, 200 140t
Transthoracic impedance, 94–97, 94b Working cells, 66
chest hair, 94–95, 95b WPW pattern. See Wolff-Parkinson-White (WPW)
conductive material, use of, 96–97, 96f pattern
paddle/pad
position, 95–96, 95–96f
size, 95 Y
paddle pressure, 97 Yankauer suction catheters, 39
selected energy, 97

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ACLS

ACLS STUDY GUIDE, FIFTH EDITION ISBN: 978-0-323-40114-2

Copyright © 2017, Elsevier Inc. All rights reserved.

Content Strategist: Sandra Clark

N.K. Alexander, EMT-P J.A. Nelson, DO, MS, FACOEP, FACEP

B. Cetanyan, RN S.L. Pinski, MD

1 Emergency Cardiovascular Care 1

Positive Pressure Ventilation 44

3 Cardiac Anatomy and Electrophysiology 63

4 Cardiac Arrest Rhythms 83

Putting It All Together 113

7 Acute Coronary Syndromes 193

Patient Evaluation 201

8 Acute Ischemic Stroke 237

9 Post Test 259

SUDDEN CARDIAC DEATH

TABLE 1.1 Cardiovascular Disease Risk Factors

CORONARY ARTERY DISEASE

Acute plaque Myocardial ischemia

Infarct Ventricular Hypertrophy,

Chronic ischemic heart disease

Congestive heart failure

SUDDEN CARDIAC DEATH

TABLE 1.2 Phases of Cardiac Arrest

Out-of-Hospital Cardiac Arrest

In-Hospital Cardiac Arrest

Out-of-Hospital Chain of Survival

Early Recognition and Activation

Early Cardiopulmonary Resuscitation

Effective Advanced Life Support

Integration of Post–Cardiac Arrest Care

In-Hospital Chain of Survival

Surveillance and Prevention

BOX 1.1 Rapid Response System Calling Criteria

Notification and Response

Intra-Arrest and Post–Cardiac Arrest Care

ventilation support, among other interventions. If a return of spontaneous circulation (ROSC) is

Physiology of Chest Compressions

Barriers to Effective Cardiopulmonary Resuscitation

Feedback during Cardiopulmonary Resuscitation

Mechanical Chest Compression Devices

BOX 1.2 Secondary Survey Components

PUTTING IT ALL TOGETHER

____ 3. During which phase of a cardiac arrest is CPR performed?

____ 4. The purpose of the primary survey is to:

____ 5. Shockable cardiac arrest rhythms include:

____ 9. Establish vascular access

____ 10. From a distance, assess the patient’s breathing effort

____ 11. Insert an advanced airway, if needed

____ 12. Open the airway if the patient is unresponsive

____ 13. From a distance, assess skin color

____ 14. Obtain a 12-lead ECG if appropriate

CHAPTER QUIZ ANSWERS

8. A. Hyperventilation is a common cause of excessive intrathoracic pressure during CPR. It is impor-

Oral cavity Palatine tonsil

Thyroid cartilage Vestibular folds

THE PATIENT WITH RESPIRATORY COMPROMISE

BOX 2.1 Factors Affecting the Accuracy of Pulse Oximetry Readings

Carbon Dioxide Monitoring

OXYGEN DELIVERY DEVICES

BOX 2.2 Low-Flow Nasal Cannula—Advantages and Disadvantages

Simple Face Mask

BOX 2.3 Simple Face Mask—Advantages and Disadvantages

Partial Rebreather Mask