Electrocardiography
in Emergency Medicine
Amal Mattu, MD, FACEP
Associate Professor of Emergency Medicine
Program Director, Emergency Medicine Residency
Program Co-Director, Emergency Medicine/Internal Medicine Combined Residency
Department of Emergency Medicine
University of Maryland School of Medicine
Baltimore, Maryland
Jeffrey A. Tabas, MD, FACEP
Associate Professor
UCSF School of Medicine
Emergency Services
San Francisco General Hospital
San Francisco, California
Robert A. Barish, MD, FACEP
Professor of Emergency Medicine and Medicine
Department of Emergency Medicine
Vice Dean for Clinical Affairs, Office of the Dean
University of Maryland School of Medicine
Baltimore, Maryland
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materials contained herein are not intended to establish policy, procedure, or a standard of care.
Copyright 2007, American College of Emergency Physicians, Dallas, Texas. All rights reserved. Except as
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First printing, October 2007
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About the Editors
Amal Mattu, MD, FACEP
Dr. Mattu is an associate professor and residency director in emergency medicine
at the University of Maryland. He has received more than a dozen teaching awards
including national teaching awards from the American College of Emergency
Physicians. In 2000, he was selected Teacher of the Year from among the entire
faculty of the University of Maryland at Baltimore. Dr. Mattu has rapidly become
a leading educator in emergency cardiology and electrocardiography. He has
conducted workshops and lectures pertaining to electrocardiography nationally
and internationally, and he has authored or edited three other texts pertaining
to emergency electrocardiography and high-risk emergency medicine. He was
the first emergency physician to serve as primary Guest Editor for Cardiology
Clinics of North America. Dr. Mattu completed an emergency medicine residency
at Thomas Jefferson University Hospital in Philadelphia, after which he completed
a teaching fellowship with a special focus on emergency cardiology.
Jeffrey A. Tabas, MD, FACEP
Dr. Tabas is an attending physician in the emergency department at San
Francisco General Hospital and director of cardiac quality assurance. He is
an associate professor of clinical medicine at the University of California, San
Francisco School of Medicine. He has lectured and published extensively on
cardiovascular emergencies and procedural education, and his ECG training
workshops have received national acclaim. He is active within the American College
of Emergency Physicians in planning and teaching cardiovascular emergency
education. Dr. Tabas received his undergraduate degree from Brown University
and his medical degree from the University of Pennsylvania. He completed
both an internal medicine residency and an emergency medicine residency at
University of California, Los Angeles and received board certification in both.
Robert A. Barish, MD, FACEP
Dr. Barish is the vice dean for clinical affairs at the University of Maryland
School of Medicine. He was recruited out of residency to establish the University’s
emergency medicine program and was the first emergency physician at the University
of Maryland to be granted the rank of full professor. Dr. Barish has served as a
lieutenant colonel and flight surgeon in the 104th Fighter Squadron of the Maryland
Air National Guard. In 1992, he was one of the finalists in a group of prospective
astronauts at NASA’s Johnson Space Center. Currently, he is a Colonel (MD) and
Commander of the 10th Medical Regiment in the Maryland Defense Force. Dr.
Barish has also been involved with volunteer initiatives that brought medical care to
refugees in Thailand and Somalia, American Indians in Minnesota, Kuwaiti citizens
during the Gulf War, residents of a Louisiana community devastated by Hurricane
Katrina, and civilian victims of the military conflict in Bosnia-Herzegovina.
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Contributors
Benjamin S. Abella, MD, MPhil Suzanne Doyon, MD
Department of Emergency Medicine Medical Director
Center for Resuscitation Science Maryland Poison Center
University of Pennsylvania Baltimore, Maryland
Philadelphia, Pennsylvania
Barbara J. Drew, RN, PhD
Fredrick M. Abrahamian, DO, FACEP Department of Physiological Nursing
Department of Emergency Medicine University of California
Olive View-UCLA Medical Center San Francisco, California
Sylmar, California
Gus M. Garmel, MD, FACEP
Edward B. Bolgiano, MD, FACEP Co-Program Director
Chairman, Emergency Department Stanford/Kaiser Emergency Medicine Residency
Bon Secours Hospital Clinical Associate Professor of Surgery
Assistant Professor of Emergency Medicine
Department of Emergency Medicine (Emergency Medicine)
University of Maryland School of Medicine Stanford University School of Medicine
Baltimore, Maryland Senior Staff Emergency Physician
The Permanente Medical Group
Michael C. Bond, MD Clerkship Director for Medical
Instructor, Department of Emergency Medicine
University of Maryland School of Medicine Students and Rotating Interns
Baltimore, Maryland Kaiser Permanente Medical Center
Santa Clara, California
William J. Brady, MD, FACEP
Professor of Emergency Medicine Chris A. Ghaemmaghami, MD, FACEP
Associate Professor of Emergency
and Internal Medicine
Departments of Emergency Medicine Medicine and Internal Medicine
Departments of Emergency Medicine
and Internal Medicine
Vice Chair, Department of Emergency Medicine and Internal Medicine
Medical Director, Life Support Learning Center Program Director, Emergency Medicine Residency
University of Virginia School of Medicine Medical Director, Chest Pain Center
Charlottesville, Virgina Department of Emergency Medicine
University of Virginia School of Medicine
Kevin R. Brown, MD, MPH, FACEP Charlottesville, Virginia
Director of Emergency Medicine
Greenwich Hospital Malkeet Gupta, MD, MS
Greenwich, Connecticut UCLA Medical Center
Assistant Clinical Professor of Los Angeles, California
Emergency Medicine Luis H. Haro, MD
New York Medical College Assistant Professor of Emergency Medicine
New York, New York Mayo Clinic College of Medicine
Consultant, Department of Emergency Medicine
Mayo Clinic Rochester
Rochester, Minnesota
Richard A. Harrigan, MD Andrew D. Perron, MD, FACEP
Associate Professor of Emergency Medicine Residency Program Director and
Department of Emergency Medicine
Temple University School of Medicine Associate Professor
Philadelphia, Pennsylvania Department of Emergency Medicine
Maine Medical Center
Tarlan Hedayati, MD Portland, Maine
Director, Chest Pain Observation Unit
Clinical Instructor Christopher H. Ross, MD, FACEP,
Department of Emergency Medicine FAAEM, FRCPC
Los Angeles County/USC Medical Center
Keck School of Medicine of the Department of Emergency Medicine
Cook County Hospital
University of Southern California Chicago, Illinois
Los Angeles, California
Theresa M. Schwab, MD
Salem Kim, BA Department of Emergency Medicine
Clinical Research Assistant Advocate Christ Medical Center
Department of Emergency Medicine Oak Lawn, Illinois
Center for Resuscitation Science
University of Pennsylvania Ghazala Q. Sharieff, MD, FACEP
Philadelphia, Pennsylvania Associate Clinical Professor
Children’s Hospital and Health Center/
Stephen Y. Liang, MD
Resident Physician University of California San Diego
Department of Emergency Medicine Director of Pediatric Emergency Medicine
University of Maryland School of Medicine Palomar-Pomerado Hospitals/California
Baltimore, Maryland
Emergency Physicians
Douglas D. Mayo, MD San Diego, California
Assistant Professor of Emergency Medicine
Department of Emergency Medicine Stuart P. Swadron, MD, FRCPC, FACEP
University of Maryland School of Medicine Director, Residency in Emergency Medicine
Baltimore, Maryland Assistant Professor
Department of Emergency Medicine
Steven A. Pace, MD, FACEP Los Angeles County/USC Medical Center
Clinical Assistant Professor Keck School of Medicine of the
Department of Medicine
University of Washington University of Southern California
Seattle, Washington Los Angeles, California
Attending Physician
Department of Emergency Medicine Jeffrey A. Tabas, MD, FACEP
Madigan Army Medical Center Associate Professor
Fort Lewis, Washington University of California, San
vi Francisco School of Medicine
Emergency Services
San Francisco General Hospital
San Francisco, California
David Whetstone, MD
Chief Resident
Department of Emergency Medicine
University of Virginia School of Medicine
Charlottesville, Virginia
Table of Contents
Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ix
Fundamentals
1. The ECG and Clinical Decision Making in the Emergency Department. . . . . . . . . . . . . . . . . . . . 1
Abnormalities of Rhythm and Conduction
2. Intraventricular Conduction Abnormalities. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13
3. Bradycardias and Heart Blocks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27
4. Narrow Complex Tachycardias. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45
5. Wide Complex Tachycardias . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59
Acute Coronary Syndromes and Mimics
6. Acute Coronary Ischemia and Infarction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73
7. Additional-Lead Testing in Electrocardiography. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 95
8. New ECG Technologies for Detection of Acute Myocardial Ischemia
and Infarction in the Emergency Department . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105
9. ACS Mimics: Non–AMI Causes of ST-Segment Elevation . . . . . . . . . . . . . . . . . . . . . . . . . . . 119
10. ACS Mimics: Non–ACS Causes of ST-Segment Depression and T-Wave Abnormalities. . . . 133
Other Cardiac Conditions
11. Pericarditis, Myocarditis, and Pericardial Effusions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141
12. Preexcitation and Accessory Pathway Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155
13. Inherited Syndromes of Sudden Cardiac Death. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 165
14. Pacemakers and Pacemaker Dysfunction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 179
15. Metabolic Abnormalities: Effects of Electrolyte Imbalances and
Thyroid Disorders on the ECG. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 193
16. The ECG in Selected Noncardiac Conditions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 203
17. ECG Manifestations of Drug Overdose. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 223
Pediatric Considerations
18. The Pediatric ECG. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 247
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viii
Preface
We are pleased to present this first edition of what we hope will be the consummate
“practitioners’ guide” to electrocardiography for acute care medicine. The text is geared toward
clinicians who evaluate ECGs in real time and make decisions based on those assessments.
Much of the knowledge and inspiration for this book has come from our extensive experience
teaching ECG evaluation to acute care physicians, as well as to medical students, residents,
and allied health personnel interested in emergency care. From these experiences, we
have learned what works and doesn’t work, what clinicians want and don’t want.
The emergency practitioner must be the expert in emergency interpretation of the ECG. The
“over-read,” which is performed hours or days after the acute care visit, with the luxury of subsequent
clinical information or prior ECGs, and without the distraction of multiple other patients calling for
your attention, is rarely available at the time that rapid diagnostic and therapeutic decisions are made.
There is increasing evidence of the importance of ECG interpretation by emergency practitioners
and their role in operationalizing acute cardiac care. For example, studies have shown that initiation
of reperfusion therapy by emergency practitioners, based on the ECG and clinical interpretation
of acute ST elevation myocardial infarction, decreases “door-to-balloon” time for activation of the
catheterization laboratory team and “door-to-needle” time for initiation of fibrinolytic therapy.
Our goal is to provide an easily understood, highly visual resource that is readable from cover to
cover. While this text can be used as a “bookshelf reference,” this is somewhat at odds with the goal
of cover-to-cover readability, and other texts may provide a more detailed and comprehensive body of
knowledge. For example, it is not clear to us that an explanation of “Einthoven’s triangle” is essential or
even helpful to emergency practitioners. Similarly, we provide an abbreviated discussion of algorithms
used to differentiate a ventricular from a supraventricular source in the patient with wide complex
tachycardia, given that application of such approaches has been shown to be inaccurate and, at times,
even dangerous in the acute setting. We place greater emphasis on reviewing the pitfalls of such
algorithms and focus on the few instances where distinctions can be made that do affect management.
We hope you enjoy your reading and look forward to any and all of your feedback. We would
especially like to thank Linda Kesselring, MS, ELS, copy editor at University of Maryland, and
Mary Anne Mitchell, ELS, copy editor at ACEP, whose persistence and insight saw this project
through to completion and excellence. We would also like to thank our families for their
patience and understanding while we worked on this project, and we thank our colleagues,
students, and residents who have been a constant source of inspiration for our work.
Amal Mattu
Jeffrey A. Tabas
Robert A. Barish
April 2007
ix
C h apter o n e
The ECG and Clinical Decision Making in
the Emergency Department
William J. Brady, MD, David Whetstone, MD, and Chris A. Ghaemmaghami, MD
Electrocardiography is performed widely within the context of the presentation, assisted
throughout emergency medicine, not only in ruling out various syndromes.1 Chest pain
in emergency departments and observation and dyspnea were the most frequent reasons
units but also in prehospital and other out- for obtaining an ECG (Figure 1-1).1 In this
of-hospital medical deployments. In fact, same investigation, the ECG influenced the
electrocardiographic (ECG) monitoring is diagnostic approach in one third of patients;
one of the most widely applied diagnostic additions to the evaluation included repeat
tests in clinical emergency medicine today. ECGs, serum markers, and initiation of rule-out
Electrocardiography itself includes a rhythm- myocardial infarction (MI) protocol. Treatment
monitoring technique using single- or was altered almost as often, with the addition
multiple-lead analysis as well as the 12-lead of antiplatelet, anticoagulant, anti-anginal, and
electrocardiogram (ECG) applied in patients reperfusion therapies. Disposition was changed
with a range of primary and secondary in approximately 15% of cases when the ECG
cardiopulmonary illnesses. Numerous interpretation became available. The effect of
situations in the emergency department can the 12-lead ECG on diagnostic, therapeutic, and
necessitate an ECG evaluation, either rhythm disposition issues in the emergency department
monitoring or 12-lead ECG assessment. population is summarized in Figure 1-2.1
The ECG can assist in establishing a diagnosis, Interpreting the ECG in
ruling out various ailments, guiding diagnostic the Context of the Clinical
and management strategies, providing indication Presentation
for certain therapies, determining inpatient
disposition, and assessing end-organ impact ECGs, just like other clinical investigations,
of a syndrome (Table 1-1). In the emergency must be interpreted within the context
department, the ECG less often provides a of a patient’s clinical presentation. An
specific diagnosis. In a study of ECGs obtained in understanding of this concept and its application
an emergency,1 only 8% of applications provided at the bedside is crucial for appropriate
a specific diagnosis yet, when interpreted use of the ECG in clinical practice.
Electrocardiography in Emergency Medicine
The “clinical presentation” includes age, benign, ground-level fall will be assessed and
sex, chief complaint, comorbid medical illness, treated in a different manner than a block on an
and results of the physical examination. For ECG from a 19-year-old man presenting after
instance, a 12-lead ECG demonstrating normal a large ingestion of metoprolol. The same ECG
sinus rhythm with normal ST segments and T finding suggests significantly different levels
waves (ie, a normal ECG) will be interpreted of cardiovascular risk and mandates markedly
and the interpretation used very differently different clinical management strategies. The
depending on the patient under scrutiny. Patient- basic, vital message is as follows: Interpret the
based issues are likely the most important and ECG within the context of the particular clinical
frequently encountered considerations in the presentation evolving before your eyes. This
interpretation of an ECG. A normal ECG (Figure statement captures the message of this chapter.
1-3) from a stable 34-year-old man with a pleuritic
chest pain syndrome will be interpreted very Clinical Scenarios and the
differently from one obtained from a 64-year- ECG
old diaphoretic woman with chest pressure,
dyspnea, and pulmonary congestion. The first The ECG is regularly employed in numerous
patient in this scenario causes less concern situations in the emergency department, eg,
than does the second, who is in the early stages to assess patients with chest pain, dyspnea,
of a significant acute coronary event. Based in syncope, palpitations, or altered mentation
part on these identical ECG interpretations, and following toxic ingestion or resuscitation
additional evaluation and management after cardiac arrest. It can also perform many
decisions will be made along different pathways functions for a particular patient. For instance,
for these markedly dissimilar patients. in a patient with chest pain who is suspected
of experiencing an acute coronary syndrome
The appearance of an ECG abnormality also (ACS), the ECG is used to help distinguish
must be interpreted within the context of the between a coronary and a noncoronary ailment.
clinical scenario. For example, the presence of a It can indicate the extent of an illness and help
first-degree atrioventricular block (Figure 1-4) identify appropriate therapy, such as helping
can induce widely different levels of concern identify a patient’s candidacy for fibrinolysis or
and influence subsequent medical management percutaneous coronary intervention. It is also
very differently. A block on an ECG from a used to determine the response to treatments
37-year-old woman undergoing evaluation administered in the emergency department.
for operative “clearance” after sustaining a Lastly, the ECG can help predict the risk of
trimalleolar fracture of the ankle in an otherwise cardiovascular complications and death.
Table 1-1. Symptom-based considerations are the most
Clinical applications of the ECG common reasons for obtaining a 12-lead ECG.
The most frequent indication for obtaining an
Establishing a diagnosis ECG in the emergency department is chest pain.
Ruling out a syndrome Other common indications for ECG are dyspnea
Assessing end-organ effect of syndrome and syncope. A typical emergency department
Guiding additional diagnostic studies patient undergoing a 12-lead ECG has three
Continuous/intermittent cardiac monitoring simultaneous indications for electrocardiography.1
Providing an indication for certain therapies For example, the adult patient with chest pain
Guiding management (the presence of chest pain is the first indication)
Assessing the effects of therapy is evaluated with an ECG in the “rule-out MI”
Predicting risk of cardiovascular complication protocol (the rule-out protocol application is the
Determining inpatient disposition second indication) in the consideration of ACS
(evaluation of ACS is the third indication).
Additional indications for obtaining an ECG
the ecg and clinical decision making in the emergency department
can be either diagnosis based (eg, ACS and ST-segment elevation of 1 mm or more in two
suspected pulmonary embolism) or system or more anatomically contiguous standard limb
related (eg, rule-out MI protocol, admission leads and 2 mm or more elevation in two or
purposes, and operative clearance).1 These more contiguous precordial leads or 2) new or
applications involve the consideration of a presumed new left bundle-branch block (LBBB).
complaint, yet the ECG is performed in a No evidence of benefit from fibrinolytic therapy
process, as in the rule-out MI protocol. Although is found in patients with ACS presentations who
it has not been studied, it is reasonable to lack either appropriate ST-segment elevation
assume that ECG rhythm monitoring is more or the new development of LBBB. Large
frequently performed during the evaluation of randomized trials involving fibrinolytic therapy
emergency patients, particularly early in the and/or percutaneous coronary intervention have
evaluation of an ill or potentially ill individual. demonstrated that mortality rates are reduced
in some patients with STEMI. For instance, the
Chest Pain Fibrinolytic Therapy Trialists Collaborative
Group analyzed all randomized fibrinolytic
The most frequent clinical scenario in which therapy trials of more than 1,000 patients and
a 12-lead ECG is obtained involves an adult with found that fibrinolytic therapy benefited only
chest pain—either to assess the patient for ACS patients with ST-segment elevation or LBBB.2
(indicated by significant ST-segment and T-wave Patients with acute myocardial infarction
abnormalities) or to implement the rule-out MI (AMI) in anterior, inferior, or lateral anatomic
protocol.1 In addition, the 12-lead ECG can be locations benefit from fibrinolytic therapy if it is
used to diagnose other disorders originating administered within 12 hours after event onset.
in the chest such as acute myopericarditis. Benefit was greatest in patients with LBBB and
anterior AMI and least in those with inferior
The ECG plays a central role in the AMI. Patients with inferior AMI and right
evaluation of these patients. In fact, an ECG precordial ST-segment depression (presumably
demonstrating an anatomically oriented ST- acute posterior wall STEMI) or elevation in right
segment abnormality is a major contributor ventricular leads (the right ventricular STEMI)
to the diagnosis of ST-segment elevation acute have a worse prognosis and benefit more from
MI (STEMI). In non-STEMI and unstable fibrinolytic agents than patients with isolated
angina presentations, the ECG provides inferior ST-segment elevation.3-12 Patients with
diagnostic information that is important inferior AMI and co-existing right ventricular
but less straightforward than in the case of infarctions, as detected by additional-lead
STEMI because the range of abnormality ECGs, are likely to benefit because of the large
is quite broad (from minimal, nonspecific amount of jeopardized myocardium. Acute,
ST-segment abnormality to obvious ST- isolated posterior wall myocardial infarction,
segment depression and T-wave inversion). diagnosed by posterior leads, may represent
yet another ECG indication for fibrinolysis, for
Therapeutic interventions can be suggested the same reason—although this statement is
or indicated by interpretation of a 12-lead tracing unproven in large fibrinolytic agent trials.3-12
from a patient with chest pain suspected of ACS.
For instance, the individual with chest discomfort Risk stratification is of great importance to
who demonstrates anatomically oriented T-wave emergency physicians. In broad terms, low-risk
inversion or ST-segment depression can be a patients may be safely discharged for outpatient
candidate for anticoagulant, antiplatelet, and evaluation, and high-risk patients generally
anti-anginal therapies. In fact, ECG information require more extensive assessment. A more
influences emergency department management challenging category is presented by patients
strategies for one third of chest pain patients.1 at moderate (or intermediate) risk for ACS. In
chest pain patients with or without coronary
In the STEMI patient, the ECG indications
for acute reperfusion therapy (fibrinolysis or
percutaneous coronary intervention) are 1)
Electrocardiography in Emergency Medicine
artery disease, high-risk features include new wave inversion is noted; the presence of these
ECG abnormality, positive cardiac marker, abnormalities may factor into the decision
or acute congestive heart failure.13 The ECG making for patients at risk for coronary disease.15
plays a central role in this risk assessment.
To further evaluate the risk for ACS,
The initial ECG correlates well with the some authors have used standardized ECG
prognosis of patients who have sustained AMI, classification systems based on the initial
based on heart rate, QRS duration, and infarct ECG. One example was drafted by the
location, as well as the amount of ST-segment Standardized Reporting Criteria Working Group
deviation.14-16 The initial 12-lead ECG obtained of the Emergency Medicine Cardiovascular
in the emergency department can be a helpful Research and Education Group to determine
guide for determination of cardiovascular risk whether the initial ECG could predict risk
and thus the choice of in-hospital admission of death, AMI, or need for revascularization
location. Brush and colleagues17 used the initial at 30 days after presentation. The efforts of
ECG to classify patients into high- and low-risk this group have demonstrated that an ECG
groups. The low-risk ECG group was defined as reliably and accurately identifies patients
those with absolutely normal ECGs, nonspecific at higher risk of an adverse outcome.16,19
ST/T-wave changes, or no change from a previous
ECG. The high-risk group was defined by ECGs Dyspnea
showing significant abnormality or confounding
pattern, such as pathologic Q waves, ischemic Dyspnea represents the second most
ST-segment or T-wave changes, left ventricular frequent indication for obtaining an ECG in
hypertrophy, LBBB, or ventricular paced the emergency department. In this complaint-
rhythm. Patients with initial ECGs classified based situation, the clinician is considering not
as low risk had a 14% incidence of AMI, 0.6% only the anginal-equivalent ACS presentation
incidence of life-threatening complications, and but also other cardiorespiratory ailments
0% mortality rate. Patients with initial ECGs such as pulmonary embolism (PE). ECG
classified as high risk had a 42% incidence manifestations that raise suspicion for ACS are
of AMI, 14% incidence of life-threatening reviewed above in the “Chest Pain” section.
complications, and 10% mortality rate.
The diagnosis of PE relies predominantly
Another approach to risk prediction involves on the magnitude of clinical suspicion and the
counting the number of ECG leads with ST- interpretation of various diagnostic investigations
segment deviation (elevation or depression). Risk in light of that level of concern. In patients
increases with the number of leads showing with unexplained dyspnea, certainly, the acute
deviation. Along similar lines, clinicians can onset of additional symptoms such as pleuritic
predict risk by adding up the total millivolts chest pain and hemoptysis suggests PE. Yet,
of ST-segment deviation; once again, higher as with most classic symptom constellations,
totals are associated with greater risk.17 these complaints seldom occur simultaneously.
A myriad of tests may be performed, including
The simple presence of left ventricular initial “screening” studies (chest radiography, 12-
hypertrophy (LVH) on the ECG is associated, lead ECG, arterial blood gas) and more advanced
long-term, with increased incidence of sudden diagnostic investigations (chest computed
death, congestive heart failure, angina, and tomography with angiography, ventilation-
AMI.18 The ECG has also been shown to predict perfusion imaging). The chest radiograph and
adverse cardiac events as well as the release the ECG are usually the initial diagnostic tests.
of cardiac serum markers in patients with Despite this widespread application of the ECG,
chest pain and new LBBB, ST elevation, or ST its diagnostic performance in the suspected
depression. More recent studies involving risk PE patient is inadequate. The most appropriate
have also raised awareness about the potential use of the ECG in this patient presentation is
for adverse events if pathologic Q waves or T- to exclude other diagnoses such as ACS. The
the ecg and clinical decision making in the emergency department
ECG should not be used as a primary study to Syncope
rule in PE because its sensitivity is quite low.
Syncope is another common indication
The ECG can be entirely normal in patients for electrocardiography in the emergency
with PE; alternatively, it could show any number department. Most patients with syncope have
of rhythm and/or morphologic abnormalities. a favorable outcome; a significant minority,
The abnormal ECG might show alterations in however, will ultimately be diagnosed with
rhythm; in intraventricular and interventricular a life- or limb-threatening event or will die.
conduction; in the axis of the QRS complex; Several clinical variables have demonstrated
and in the morphology of the P wave, QRS utility in the evaluation of the patient with
complex, and ST segment/T wave. The “classic” syncope; the ECG is one of these variables.
ECG finding of PE was first reported in 1935
by McGinn and White,20 who described the Certain obvious ECG presentations in patients
traditional S1Q3T3 pattern in acute cor pulmonale. with syncope will not only provide a reason
In fact, this finding is rarely seen in the PE for the loss of consciousness but also guide
patient and is not uncommonly seen in patients early therapy and disposition. Bradycardia,
without PE; therefore, its diagnostic power is atrioventricular block, intraventricular
quite poor. The ECG findings associated with PE conduction abnormality, and tachyarrhythmia
are numerous: arrhythmias (sinus tachycardia, in the appropriate clinical setting provide a
atrial flutter, atrial fibrillation, atrial tachycardia, reason for the syncopal event. Morphologic
and atrial premature contractions), nonspecific findings suggesting the range of cardiovascular
ST-segment/T-wave changes, T-wave inversions maladies are also encountered; these entities
in the right precordial leads, rightward QRS- include the various ST-segment and T-wave
complex axis shift and other axis changes, S1Q3 abnormalities of ACS, ventricular hypertrophy
or S1Q3T3 pattern, right bundle-branch block suggestive of hypertrophic cardiomyopathy,
(RBBB), and acute cor pulmonale (defined ventricular preexcitation as seen in Wolff-
by S1Q3T3 pattern, right axis deviation, and Parkinson-White syndrome, prolonged QT
RBBB).21 The most common ECG abnormalities interval common in the diverse long-QT-interval
are extremely nonspecific ST-segment/T- presentations, and Brugada syndrome with
wave changes with sinus tachycardia.22 the associated tendency for sudden death.
The relatively low sensitivities of these Investigators have studied ECGs from patients
ECG presentations of PE limit the usefulness with syncope, with the aim of identifying
of electrocardiography as a sole diagnostic individuals at risk for adverse outcome. For
tool. The ECG changes are most frequently instance, Martin and colleagues,24 in a two-
seen in patients with massive or submassive step analysis, reviewed the presentations of
embolization; smaller PEs less often produce 612 patients with syncope and found that an
significant abnormality on ECG. Various studies abnormal ECG was associated with arrhythmia
have shown that approximately 15% to 30% of or death with an odds ratio (OR) of 3.2; other
ECGs are normal in patients with established factors suggestive of a poor outcome included
PE. Perhaps as a partial explanation of this a history of congestive heart failure (OR 3.2) or
relatively high rate of “normal” ECGs, it has of ventricular arrhythmia (OR 4.8). Additional
been noted that the range of ECG findings in work performed by Sarasin et al25 considered
PE is transient, usually appearing during the the subset of patients with unexplained syncope
acute phase of the illness.23 The transient nature after an initial emergency department evaluation.
of ECG abnormalities and the often nonspecific In 344 patients, an abnormal ECG predicted
changes reduce the utility of ECGs in the arrhythmia with an OR of 8.1; other factors
evaluation of patients suspected of having PE. of significance associated with arrhythmic
syncope included older age (OR 5.4) and a
history of congestive heart failure (OR 5.3). In
patients with one risk factor, arrhythmia was
Electrocardiography in Emergency Medicine
encountered rarely (0% to 2%); in patients with stable cardiac rhythm) and, in addition to
identified risk factors, arrhythmia occurred at rhythm interpretation, it will be reviewed
the following frequencies: one risk factor, 0% for abnormalities of the various structures,
to 2%; two, 35% to 41%; and three, 27% to 60%. intervals, complexes, and axes. Beyond rhythm
The San Francisco Syncope Rule26 incorporates considerations, the primary ECG determinants
the ECG into the evaluation of the patient of impending or established cardiotoxicity
with syncope. Quinn et al26 considered 684 include the PR interval, the QRS complex, the
presentations of syncope and reviewed clinical T wave, the ST segment, and the QT interval.
variables with the intent of identifying patients
at risk of poor short-term outcomes. They found Numerous authorities have explored ECGs
that an abnormal ECG was associated with an from patients with suspected or known
increased risk of a short-term adverse event and poisoning (tricyclic antidepressant [TCA]
that dyspnea, low hematocrit, and hypotension ingestion or digoxin exposure). However, little
were also predictors of poor outcome. clinical information addressing the general
use of the ECG in the assessment of poisoned
The most appropriate ECG approach to patients can be found in the literature. Homer
syncopal patients is an initial review aimed at and associates27 reviewed the range of ECG
the detection of malignant dysrhythmia; this abnormalities encountered in poisoned patients.
first ECG evaluation most often involves the All patients evaluated for poisoning by the
rhythm strip. Detection of dysrhythmia at this toxicology service at a tertiary referral center
stage is diagnostic and will mandate therapy. who underwent ECG analysis within 6 hours
If the rhythm strip does not yield an answer, after ingestion were entered in the study. Each
then a 12-lead ECG may be obtained. The 12- ECG was reviewed for rhythm and morphologic
lead ECG can provide a more detailed review diagnosis as well as interval/complex durations.
of a challenging rhythm presentation and can Of the 277 patients who underwent ECG
reveal the various morphologic findings as evaluation, 32% of them had a normal ECG. Of
discussed in this section. Of course, a “negative” the patients with abnormal ECGs (68%), 62% had
ECG does not rule out cardiac pathology. a rhythm abnormality and 38% had morphologic
abnormality. Rhythm disturbances included
Toxic Ingestion sinus tachycardia (51%), sinus bradycardia (7%),
atrioventricular block (7%), non-sinus atrial
Clinicians approach the evaluation of a tachycardias (3%), and nodal bradycardia (3%).
poisoned patient with numerous important Morphologic abnormalities included abnormal
diagnostic tools, including the history of QRS configuration (35%), QRS-complex
the ingestion, the physical examination widening (33%), QT-interval prolongation (33%),
demonstrating various toxidromic findings, and PR-interval prolongation (12%), ST-segment
selected investigations. Another investigative abnormality (9% elevated, 25% depressed),
tool is the ECG. In poisoned patients, the and T-wave inversion (20%). Interestingly, the
ECG assessment is based on both the rhythm degree of abnormality was directly related to the
strip and a 12-lead ECG. The ECG is used to number of toxins ingested, yet cardiovascular
establish the diagnosis, assess for end-organ agents (β-adrenergic blockers or calcium-channel
toxicity, and guide therapeutic interventions. antagonists) were no more likely to produce
Not unlike syncopal patients, individuals ECG abnormality than were noncardiovascular
presenting with significant cardiotoxicity substances (sedative-hypnotic medications or
manifested by dysrhythmia are assessed with stimulants). Importantly, this analysis did not
the ECG monitor; further diagnostic and include patients who underwent ECG rhythm
management decisions are suggested by the analysis via a monitor and thus would have likely
bedside interpretation of the rhythm strip. missed the more malignant rhythm presentations
such as ventricular tachycardia or complete
A 12-lead ECG will be obtained from
“stable” patients (ie, patients with a perfusing,
the ecg and clinical decision making in the emergency department
atrioventricular block. This study demonstrates applied in collective fashion, they demonstrate
that the ECG is, in fact, frequently abnormal less-than-reliable sensitivity and specificity for
in poisoned patients. The investigators did not both the diagnosis as well as the occurrence of
explore the effect of an abnormal ECG on medical convulsion or malignant dysrhythmia—meaning
decision making and patient management. that the clinician should not employ these
criteria alone as the reason to either “rule-
The ECGs of patients who have ingested in” or “rule-out” TCA poisoning. In a meta-
sedative-hypnotic or psychotropic medications analysis of ECG prognostic indicators, Baily and
have been thoroughly explored, and their colleagues33 reported the frequent occurrence
influence on clinical decisions has been reviewed. of these various ECG abnormalities in the ill
For instance, TCA poisoning can cause a range TCA-poisoned patient. Unfortunately, these
of ECG abnormalities, including dysrhythmia, abnormalities were not entirely predictive for the
QRS-complex widening, alterations in the QRS- development of significant end-organ toxicity,
complex configuration (prominent, terminal with sensitivities and specificities ranging from
R wave in lead aVR and S wave in lead I), and 69% to 81% and 46% to 69%, respectively.
QT-interval prolongation. Specific ECG findings
have specific clinical utility. For instance, sinus When these findings are interpreted within
tachycardia, which is present in many TCA- the context of the clinical presentation, they are
poisoned patients, is a nonspecific finding. markedly more powerful. In the TCA-poisoned
Widening of the QRS complex, a more specific patient who is fully alert and oriented, sinus
finding suggestive of TCA cardiotoxicity, is tachycardia is an abnormal but nonspecific
a more useful abnormality; QRS complexes finding that is not necessarily indicative of
longer than 100 milliseconds (msec) are impending cardiotoxicity. This same ECG in
predictive of convulsion.28 Conversely, a QRS a lethargic TCA-overdose patient, while not
complex of normal duration is not “protective”; predictive of a significant adverse event, certainly
convulsions and malignant dysrhythmia can does not rule out impending toxicity. Now, with
occur in patients with normal complexes sinus tachycardia complicated by a widened
as well.28,29 In general, with increasing QRS- QRS complex and prominent R' wave in lead
complex duration, the patient is more likely to aVR, either mental status presentation (normal
have significant end-organ toxicity. Rightward or altered) does not significantly influence the
deviation of the terminal 40 msec of the QRS interpretation of the ECG. In both instances, the
complex frontal plane axis is associated with patient is at extreme risk of an adverse event.
both neurotoxicity and cardiotoxicity. This
rightward axis of the terminal QRS complex The 12-lead ECG can be applied in serial
is easily detected on the 12-lead ECG as a fashion as a screening tool for the patient
prominent R' wave in lead aVR and a deep who is asymptomatic (ie, fully alert, with
S wave in lead I. This finding is reasonably normal mentation, and without tachycardia)
predictive of seizure and/or ventricular at presentation to aid the clinician in
arrhythmia, with an observed sensitivity of 81%. ruling out significant TCA poisoning. An
As with increasingly wider QRS complexes, asymptomatic patient can be monitored over
progressively larger R' waves are associated with a 6-hour period; if serial ECGs do not reveal
greater toxicity.30 QTc-interval prolongation is tachycardia, QRS-complex widening, terminal
also seen in these poisoned patients but is not QRS-complex rightward axis shift, or QT-
necessarily indicative of TCA cardiotoxicity interval prolongation, then the patient is at
or predictive of an impending adverse event. low risk for significant TCA poisoning.34
Numerous investigators31,32 have noted that Other Scenarios
these and other ECG abnormalities occur not
infrequently in the TCA-poisoned patient. They Patients who present to an emergency
also point out that, when these findings are department with metabolic abnormality, altered
mentation, cardiorespiratory arrest, or blunt
Electrocardiography in Emergency Medicine
chest trauma are evaluated with numerous The remaining patients have ECGs that are
diagnostic studies. In the renal failure patient, entirely normal, nonspecifically abnormal, or
hyperkalemia can be diagnosed early with the clearly abnormal yet without pathologic ST-
ECG, even before the return of serum laboratory segment elevation indicative of STEMI. Lee et al37
study results; obviously, abnormalities of the T reported that a significant portion of emergency
wave and/or QRS complex suggest the diagnosis department patients in whom ACS was suspected
and allow potentially life-saving therapy to be had a normal or minimally abnormal ECG yet
delivered expeditiously. The ECG provides the were ultimately diagnosed with an ACS (unstable
reason for altered mental status in 7% of patients angina, 4%–20%, and AMI, 1%–4%). Pope and
presenting to an emergency department with colleagues,18 in a description of emergency
abnormal mentation.35 Patients experiencing department patients in whom the diagnosis of
cardiorespiratory arrest are managed with the ACS was missed (2.1% unstable angina and 2.3%
ECG while in active arrest and, once they have AMI), noted a number of factors that could have
been resuscitated, the ECG continues to guide contributed to the initial incorrect assessment.
therapy. After the patient is stabilized, the 12- One was a normal ECG on presentation to the
lead ECG can yield clues as to the cause of the emergency department. Overreliance on a normal
hemodynamic collapse such as STEMI or PE. or nonspecifically abnormal ECG in a patient
Unexplained hypotension in the blunt trauma with potential ACS who is currently pain free
patient can result from myocardial contusion; should also be avoided. The total elapsed time
the ECG can confirm the diagnosis during from chest pain onset in patients with these
the early phase of the trauma evaluation.36 nondiagnostic ECG patterns does not assist
in “ruling out” AMI with a single ECG.38
Limitations of the ECG
The single initial ECG obtained in the
The ECG has numerous limitations when emergency department is merely a “snapshot” in
used in patients suspected of ACS or other acute time as to the status of coronary perfusion and
event. For instance, an adult with chest pain its effect on the myocardium, ie, the presence
who is ultimately diagnosed with STEMI can of ECG abnormality suggesting ACS. Patients
demonstrate a normal or minimally abnormal with nondiagnostic ECGs might have presented
ECG on presentation; the ECG then evolves at an early phase of the syndrome. ACS is a
over subsequent minutes to hours to reveal the dynamic, evolving process; it follows that the
STEMI. In non-ACS scenarios, the initial ECG ECG will change and evolve over time as the
after ingestion of TCA might not reveal pathologic syndrome progresses. The history and other
abnormality in a patient with impending toxicity; clinical data must be relied on heavily in patients
alternatively, the ECG in a patient found to have with either normal or minimally abnormal ECGs
a PE could reveal only nonspecific findings such and a convincing description of ischemic chest
as sinus tachycardia. In each of these clinical discomfort. In these patients, serial ECGs might
situations and others, a sound understanding of reduce this initial relatively poor sensitivity for
these limitations will guide emergency physicians AMI. Management and disposition decisions
in the appropriate application of the 12-lead ECG. must be based on the total clinical picture and
not necessarily on a nondiagnostic ECG.
In a patient who may have ACS, the ECG
has numerous shortcomings: “normal” and A rather broad range of ECG abnormalities
“nondiagnostic” ECG presentations; evolving, are encountered in adult patients with chest
confounding, and mimicking syndromes; and pain—some of whom are presenting to the
the electrocardiographically “silent” areas of the emergency department with ACS while others
heart (eg, isolated acute posterior wall STEMI). have a noncoronary ailment. The emergency
Only half of patients ultimately diagnosed physician must be able to identify changes
with AMI have an ECG that is diagnostic for related to ACS early in the evaluation such that
AMI at emergency department presentation. appropriate therapy is offered as expeditiously
the ecg and clinical decision making in the emergency department
as possible. Certain ECG syndromes will mimic must be made with this caveat in mind.
ACS presentations; these syndromes include The limitations of the ECG in the ACS
benign early repolarization, acute pericarditis,
left ventricular hypertrophy, and bundle- patient are well known and reasonably well
branch block. Although it may not be possible elucidated in the literature. Other clinical
to reliably distinguish among these various scenarios, as described in the “Clinical
causes of ECG abnormality based on a single Scenarios” section, demonstrate similar
ECG, emergency physicians should attempt to limitations, ranging from major to minor
do this as rapidly as possible. For instance, the shortcomings. For instance, the 12-lead ECG
presence of ST-segment elevation in an adult in the patient in whom PE is suspected offers
with chest pain does not equate with STEMI. little diagnostic information; conversely, the
In fact, the minority of chest pain patients with ECG in the patient with hyperkalemia provides
ST-segment elevation are diagnosed with STEMI; evidence of the degree of cardiotoxicity in most
the majority are ultimately diagnosed with non- instances, whether it demonstrates prominent
STEMI syndromes. This observation has been T waves or QRS-complex abnormalities.
noted in prehospital, emergency department,
and coronary care unit populations.39-42 A The important issue to consider is the presence
sound, thorough understanding of the various of these limitations and their magnitude. With
ECG syndromes encountered in the emergency this knowledge, clinicians will be able to use
department is crucial in the initial evaluation the ECG appropriately in patient evaluation.
and subsequent management of these patients.43
References
The ECG abnormalities associated with
AMI can be masked by the altered patterns of 1. Brady WJ, Adams M, Burry SD, Perron AD. The impact
ventricular conduction encountered in patients of the 12-lead ECG on ED evaluation and management
with confounding patterns, including LBBB, [abstract 168]. Ann Emerg Med. 2002;40:S47.
ventricular paced rhythm, and LVH. These
syndromes produce ST-segment and T-wave 2. Fibrinolytic Therapy Trialists (FTT) Collaborative Group.
changes—the new “normal” findings in these Indications for thrombolytic therapy in suspected acute
patients. These findings might obscure and/ myocardial infarction: collaborative overview of early mortality
or mimic the typical ECG findings of ACS, and major morbidity results from all randomized trials of
including STEMI. Emergency physicians must more than 1000 patients. Lancet. 1994;343:311-322.
approach these patients knowing that the ECG
will be of considerably less diagnostic power. 3. Bates ER, Clemmensen PM, Califf RM, et al.
Subsequent diagnostic and management decisions Precordial ST-segment depression predicts a worse
prognosis in inferior infarction despite reperfusion
therapy. J Am Coll Cardiol. 1990;16:1538-1544.
4. Willems JL, Willems RJ, Willems GM, et al. Significance
of initial ST-segment elevation and depression for the
management of thrombolytic therapy in acute myocardial
infarction. Circulation. 1990;82:1147-1158.
5. Wong C, Freedman B, Bautovich G, et al. Mechanism
and significance of precordial ST-segment depression
associated with severe narrowing of the dominant right
coronary artery. Am J Cardiol. 1993;71:1025-1030.
Key Facts
• The ECG must be interpreted within the context of the clinical presentation, including information
such as the patient’s age, chief and secondary complaints, findings from the physical examination,
and other diagnostic test results.
• Clinical judgment plays a very important role in the interpretation of the ECG within the context of
the individual clinical event.
• The ECG can provide information to confirm a diagnosis, rule out a diagnosis, assess the effect of
an event, provide an indication for therapy, and predict the risk of complications.
• The ECG has numerous limitations in the various clinical scenarios in which it is used. An
awareness of these limitations is vital to the correct application of the ECG in clinical care.
Electrocardiography in Emergency Medicine
6. Zehender M, Kasper W, Kauder E, et al. Right ventricular 26. Quinn JV, Stiell IG, McDermott DA, et al. Derivation of the
infarction as an independent predictor of prognosis after acute San Francisco Syncope Rule to predict patients with short-
inferior myocardial infarction. N Engl J Med. 1993;328:981-988. term serious outcomes. Ann Emerg Med. 2004;43:224-232.
7. Zehender M, Kasper W, Kauder E, et al. Eligibility for and 27. Homer A, Brady WJ, Holstege C. The association of
benefit of thrombolytic therapy in inferior myocardial toxins and ECG abnormality in poisoned patients.
infarction: focus on the prognostic importance of right Paper presented at: Mediterranean Emergency Medicine
ventricular infarction. J Am Coll Cardiol. 1994;24:362-369. Congress, September 2005; Nice, France.
8. Edmonds JJ, Gibbons RJ, Bresnahan JF, et al. Significance 28. Boehnert MT, Lovejoy FH. Value of the QRS complex
of anterior ST depression in inferior wall acute myocardial duration versus the serum drug level in predicting seizures
infarction. Am J Cardiol. 1994;73:143-148. and ventricular arrhythmias after an acute overdose of
tricyclic antidepressants. N Engl J Med. 1985;313:474-479.
9. Wong C, Freedman SB. Precordial ST change and site of the
infarct-related lesion in right coronary artery-related inferior wall 29. Foulke GE, Albertson TE. QRS complex interval in tricyclic
acute myocardial infarction. Am J Cardiol. 1995;75:942-943. antidepressant overdose: inaccuracy as a toxicity indicator
in emergency settings. Ann Emerg Med. 1987;16:160-163.
10. Birnbaum Y, Herz I, Sclarovsky S, et al. Prognostic
significance of precordial ST-segment depression on 30. Liebelt EL, Francis PD, Woolf AD. ECG lead aVR
admission electrocardiogram in patients with inferior wall versus QRS complex interval in predicting seizures
myocardial infarction. J Am Coll Cardiol. 1996;28:313-318. and arrhythmias in acute tricyclic antidepressant
toxicity. Ann Emerg Med. 1995;26:195-201.
11. Peterson ED, Hathaway WR, Zabel KM, et al. Prognostic
significance of precordial ST-segment depression during 31. Lavoie FW, Gansert GG, Weiss RE. Value of initial ECG
inferior myocardial infarction in the thrombolytic era: results findings and plasma drug levels in cyclic antidepressant
in 16,521 patients. J Am Coll Cardiol. 1996;28:305-312. overdose. Ann Emerg Med. 1990;19:696-700.
12. Schroder K, Wegscheider K, Neuhaus KL, et al. Significance 32. Buckley NA, Chevalier S, Leditschke IA, et al. The limited utility
of initial ST-segment changes for thrombolytic treatment in of electrocardiography variables used to predict arrhythmia
first inferior myocardial infarction. Heart. 1997;77:506-511. in psychotropic drug overdose. Crit Care. 2003;7:R101-R107.
13. Braunwald E, Mark DB, Jones RH, et al. Unstable angina: 33. Baily B, Buckley NA, Amre DK. A meta-analysis of
diagnosis and management. Rockville, MD: Agency for electrocardiographic prognostic indicators to predict
Health Care Policy and Research and the National Heart, seizures, arrhythmias, or death after tricyclic antidepressant
Lung, and Blood Institute, US Public Health Service, US overdose. J Toxicol Clin Toxicol. 2004;42:877-888.
Department of Health and Human Services; 1994.
34. Banaham BF, Schelkum PH. Tricyclic antidepressant overdose:
14. Hathaway WR, Peterson ED, Wagner GS, et al. Prognostic conservative management in a community hospital with
significance of the initial electrocardiogram in patients with cost-saving implications. J Emerg Med. 1990;8:451-458.
acute myocardial infarction. JAMA. 1998;279(5):387-391.
35. Kanich W, Brady WJ, Huff JS, et al. Altered mental
15. Blomkalns AL, Lindsell CJ, Chandra A, et al. Can status: evaluation and etiology in the emergency
electrocardiographic criteria predict adverse cardiac events and department. Am J Emerg Med. 2002;20:613-617.
positive cardiac markers? Acad Emerg Med. 2003;10(3):205-210.
36. Plautz CU, Perron AD, Brady WJ. Electrocardiographic
16. Zalenski R, Sloan E, Chen E, et al. The emergency ST-segment elevation in the blunt trauma patient:
department ECG and immediately life-threatening acute myocardial infarction vs myocardial contusion.
complications in initially uncomplicated suspected Am J Emerg Med. 2005;23(4):510-516.
myocardial ischemia. Ann Emerg Med. 1988;17:221-226.
37. Lee TH, Rouan GW, Weisberg MC, et al. Clinical
17. Brush JE, Brand DA, Acamparo D, et al. Use of the initial characteristics and natural history of patients with acute
electrocardiogram to predict in-hospital complications of acute myocardial infarction sent home from the emergency
myocardial infarction. N Engl J Med. 1985;312:1137-1141. department. Am J Cardiol. 1987;60:219-224.
18. Pope JH, Ruthazer R, Kontos MC, et al. The impact 38. Singer AJ, Brogan GX, Valentine SM, et al. Effect of
of left ventricular hypertrophy and bundle branch duration from symptom onset on the negative predictive
block on the triage and outcome of ED patients with value of a normal ECG for exclusion of acute myocardial
a suspected acute coronary syndrome: a multicenter infarction. Ann Emerg Med. 1997;29:575-582.
study. Am J Emerg Med. 2004;22(3):156-163.
39. Otto LA, Aufderheide TP. Evaluation of ST segment elevation
19. Forest RS, Shofer FS, Sease KL, Hollander JE. Assessment criteria for the prehospital electrocardiographic diagnosis of
of the standardized reporting guidelines ECG acute myocardial infarction. Ann Emerg Med. 1994;23:17-24.
classification system: the presenting ECG predicts 30-
day outcomes. Ann Emerg Med. 2004;44(3):206-212. 40. Brady WJ, Syverud SA, Beagle C, et al. Electrocardiographic
ST-segment elevation: the diagnosis of acute
20. McGinn S, White PD. Acute cor pulmonale resulting myocardial infarction by morphologic analysis of the
from pulmonary embolism. JAMA. 1935;104:1473. ST segment. Acad Emerg Med. 2001;8:961-967.
21. Ullman E, Brady WJ, Perron AD, et al. 41. Brady WJ, Perron AD, Martin ML, et al. Electrocardiographic
Electrocardiographic manifestations of pulmonary ST segment elevation in emergency department chest
embolism. Am J Emerg Med. 2001;19:514-519. pain center patients: etiology responsible for the ST
segment abnormality. Am J Emerg Med. 2001;19:25-28.
22. Petruzzelli S, Palla A, Pieraccini F, et al. Routine
electrocardiography in screening for pulmonary 42. Miller DH, Kligfield P, Schreiber TL, Borer JS. Relationship
embolism. Respiration. 1986;50:233-243. of prior myocardial infarction to false-positive
electrocardiographic diagnosis of acute injury in patents
23. Panos RJ, Barish RA, Whye DW, Groleau G. The with chest pain. Arch Intern Med. 1987;147:257-261.
electrocardiographic manifestations of pulmonary
embolism. J Emerg Med. 1988;6:301-307. 43. Michelson EA, Brady WJ. Emergency physician interpretation
of the electrocardiogram. Acad Emerg Med. 2002;9;317-319.
24. Martin TP, Hanusa BH, Kapoor WN. Risk stratification of
patients with syncope. Ann Emerg Med. 1997;29:459-466.
25. Sarasin FP, Hanusa BH, Perneger T, et al. A risk score
to predict arrhythmias in patients with unexplained
syncope. Acad Emerg Med. 2003;10:1312-1317.
10
the ecg and clinical decision making in the emergency department
Figures
Figure 1-1.
Clinical reasons for obtaining a 12-lead ECG.1
Figure 1-2.
Effect of the 12-lead ECG on diagnostic, therapeutic, and dispositional issues in the emergency department.
Note that all changes in evaluation and therapy were additions.1
11
Electrocardiography in Emergency Medicine
Figures
Figure 1-3.
A normal 12-lead ECG demonstrating normal sinus rhythm with no evidence of ST-segment or T-wave
abnormality.
Figure 1-4.
Normal sinus rhythm with first-degree atrioventricular block.
12
C h apter t w o
Intraventricular Conduction
Abnormalities
Richard A. Harrigan, MD
Recognizing the ECG manifestations of block would be a widening and distortion of the
intraventricular conduction abnormalities begins QRS complex. It also makes interpretation of
with an understanding of the basics of cardiac the ECG more difficult, demanding a working
impulse conduction and the realization that a knowledge of the expected changes of bundle-
delay in a phase of the conduction sequence branch block to recognize abnormalities such
will lead to a lengthening, and distortion, of the as acute cardiac ischemia (Figure 2-1).
corresponding portion of the ECG waveform.
Normally, the cardiac impulse begins at the All intraventricular conduction abnormalities
sinuatrial node and then depolarizes the atria feature widening and distortion of the QRS
(right before left); on the surface ECG, this complex; it is the degree of widening and the
event is manifested by the P wave. Internodal variations in distortion that make them distinct.
fibers connect the sinuatrial node to the Bundle-branch blocks are the widest and are of
atrioventricular (AV) node, which serves as the two varieties: right and left. Fascicular blocks do
gateway to the ventricles. Conduction through not significantly prolong the QRS duration but
the AV node, the bundle of His, the right and are important because they can cause changes
left bundle branches, and the Purkinje fibers is that mimic previous infarction. Because only the
represented by the PR interval (which includes left bundle branch splits into two fascicles, there
the P wave and the PR segment). Ventricular are only two fascicular blocks: the more common
activation, or depolarization, is represented on left anterior and the relatively rare left posterior.
the ECG by the QRS complex.1 Thus, a delay in Finally, delays in ventricular conduction
impulse conduction down a part of the bundle- can occur that do not meet the morphologic
branch system will lead to a partial delay in criteria of the four major intraventricular
ventricular activation; the impulse will reach the conduction abnormalities. These are classified as
ventricles via the bundle branches at different nonspecific intraventricular conduction delays.
times, leading to asynchronous activation
of the ventricles. It follows that the cardinal The appearance of an intraventricular
manifestation of any complete bundle-branch conduction abnormality on the ECG must
be both recognized and interpreted. An
intraventricular conduction abnormality
13
Electrocardiography in Emergency Medicine
signals a new or important disease process. In right bundle-branch block (RBBB), the
It also makes interpretation of the ECG more septum depolarizes normally from left to
difficult, because clinicians must be comfortable right, but the duration is prolonged. Next, left
with how an intraventricular conduction ventricular depolarization proceeds relatively
abnormality “normally” manifests so as to normally, but the resultant wave is diminished
recognize changes on the ECG (eg, identifying by the prolonged septal depolarization in the
acute cardiac ischemia, injury, or infarction in opposite direction. The delayed right ventricle
the presence of a bundle-branch block) (Figure then depolarizes unopposed. In lead V1 this
2-1). The causes of intraventricular conduction generates a normal, initial, small R wave, a
abnormalities are myriad1,2 (Table 2-1) and should subsequent S wave that can be small or even
be considered in medical decision making. absent if significantly diminished, and a terminal
R' wave. In V6 there is a small initial Q wave from
Bundle-Branch Blocks the septum, a significant R wave from the close
proximity of the left ventricle, and a wide S wave
Bundle-branch block should be considered from the delayed right ventricle. Recognition
whenever the QRS complex exceeds 0.12 of a dominant R wave in lead V1 should trigger
second; however, there are other triggers consideration of RBBB, although other entities are
to consider when scanning the ECG for an associated with this phenomenon of “R >S wave
intraventricular conduction abnormality. amplitude in V1” (Table 2-2). The key morphologic
changes in RBBB, therefore, are the appearance
Right Bundle-Branch Block of a widened QRS complex (>0.12 sec), usually
The normal QRS complex seen in the with an rSR' pattern in the right precordial leads
(V1 and V2) and a prominent, wide S wave in
precordial leads results from 1) depolarization the left precordial leads (V5 and V6). See Table
of the septum from left to right and then 2-3 for the ECG criteria for RBBB (Figure 2-2).
2) depolarization of the left ventricle from
right to left (overshadowing the smaller right In addition to the classic “rabbit ear” rSR'
ventricle). In lead V1, the right chest lead, pattern, lead V1 can demonstrate a “qR” pattern
this generates a small R wave followed by a (Figure 2-3). The qR variant of RBBB should be
large S wave. In V6, the left chest lead, this differentiated from a qR complex in V1 signaling
generates a small initial Q wave (termed a right ventricular hypertrophy; although the ECG
“septal” Q wave) followed by a large R wave. is not sensitive for the latter, other findings such
as right QRS axis deviation (>110°), right atrial
Table 2-1. enlargement, S wave greater than 0.7 mV in lead
Causes of intraventricular conduction V6, and R:S ratio less than 1 in V5 or V6 all favor
abnormalities1,2 right ventricular hypertrophy. Alternatively,
RBBB could appear as a notched R wave in the
Atherosclerotic heart disease
Infiltrative cardiomyopathy (eg, sarcoidosis, Table 2-2.
hemochromatosis, amyloidosis) Causes of R-wave amplitude greater than S-wave
Fibrotic heart disease (eg, Lev syndrome; Lenègre amplitude in ECG lead V11
syndrome)
Electrolyte abnormalities (eg, hyperkalemia) RBBB
Infectious disease (eg, Lyme disease, Chagas disease, Right ventricular hypertrophy
myocarditis) True posterior myocardial infarction
Connective tissue disease (eg, scleroderma) Wolff-Parkinson-White syndrome
Toxicologic (eg, tricyclic antidepressant poisoning) Duchenne-type pseudohypertrophic muscular dystrophy
Pulmonary embolism Hypertrophic cardiomyopathy
Congenital heart disease Normal variant (especially children and adolescents)
Iatrogenic (eg, right heart catheterization/RBBB)
Normal variant
14
Intraventricular conduction abnormalities
right precordial leads. In these cases, the S Left Bundle-Branch Block
wave has been reduced to a mere hitch in the In left bundle-branch block (LBBB), septal
ascending limb of the R' wave1,3 (Figure 2-4).
depolarization is delayed and proceeds
It is important to recognize the ST-segment abnormally from right to left. Ventricular wall
and T-wave changes that are a normal depolarization is also delayed but proceeds in
consequence of RBBB. They occur in the the normal right-to-left direction. The right-
right precordial leads with primarily positive to-left depolarizations of both the septum and
QRS complexes (V1 to V3). In these leads, the ventricular free wall generate wide and
repolarization changes result in ST segments and primarily monophasic complexes in LBBB—a
T waves that are opposite to (discordant with) QS wave in V1 and a monophasic R wave in V6.
the overall direction of the QRS. Any elevation Large negative QRS complexes in lead V1, V2,
in these leads is highly suggestive of acute or V3 are seen in only a few ECG entities (Table
myocardial injury (Figures 2-1 and 6-18). The ST 2-4). The key morphologic findings with LBBB
segments in other leads are unaffected by RBBB, are a wide, slurred R wave in the left-sided leads
and any deviations should be assessed as usual. (some combination of I, aVL, V5, and V6) as
well as a QS (single negative deflection) or an
ECGs that demonstrate the morphologic rS complex in the right precordial leads (V1 and
changes of RBBB yet do not feature a QRS V2). Also characteristic of LBBB is the absence
complex width of more than 0.12 second are of the customary q wave in lead V6. Since this
classified as having incomplete RBBB or right- q wave results from normal left-to-right septal
sided conduction delay (Figure 2-5). Incomplete depolarization (thus a negative, or rightward,
RBBB is a relatively common and benign spike in this left precordial lead), which is lost
finding in children and young adults. Liao et with LBBB, V6 will demonstrate only an initial
al4 found middle-aged men with incomplete R wave in uncomplicated LBBB. See Table 2-5
RBBB to be roughly seven times more likely for the ECG criteria for LBBB (Figure 2-6).
to develop complete RBBB over 11 years of
followup; however, 95% of those patients found Variations in this typical pattern can occur.
to have incomplete RBBB did not progress to For example, the slurred monophasic R wave
complete RBBB during that time. Incomplete in V5 and occasionally V6 might be absent but
RBBB might also arise as an artifact if the will typically be present in leads I and aVL.
precordial leads V1 and V2 are inadvertently Left QRS axis deviation is not a prerequisite for
placed one interspace too high on the chest.5 diagnosis of LBBB but can occur with it (Figure
2-7). It has been suggested that such a finding,
Table 2-3. especially if the axis is quite superior (leftward
ECG criteria for RBBB and more toward –90°), is suggestive of LBBB
with a preexisting or coincident left anterior
QRS complex longer than 0.12 sec fascicular block.6 Other clinicians have found
Abnormal QRS morphology in right precordial leads (V1, that patients with LBBB plus left axis deviation
V2)
• rSR' / rsr' / RsR' wave (“rabbit ear” or “M-shaped” Table 2-4.
QRS complex) Differential diagnosis of large-amplitude negative
• qR variant QS or rS complexes in leads V1 and V2 (right
• single R-wave variant (wide and notched) precordial leads)
Deep, wide S wave in left precordial leads (V5, V6) and
possibly left-sided leads I and aVL LBBB
Late intrinsicoid deflection (time to peak of R wave) in Left ventricular hypertrophy
lead V1 (>0.5 sec) Right ventricular paced rhythm
Ventricular tachycardia
Athlete’s heart
15
Electrocardiography in Emergency Medicine
are more likely to have organic heart disease left anterior fascicle courses toward the anterior-
than those with LBBB and a normal QRS axis.1,7 superior papillary muscle; the left posterior
fascicle runs toward the posterior-inferior
It is important to recognize the expected papillary muscle. A conduction delay that occurs
ST-segment changes that occur with LBBB. ST- in these fascicles was previously referred to as
segment deviation is opposite to (discordant with) either a left anterior or left posterior hemiblock;
the predominant direction of the QRS. Therefore, the term “fascicular block” is now used more
in leads with a predominantly positive QRS, the commonly. Fascicular blocks are rarely of vital
ST segments (and T waves) are isoelectric or clinical significance to emergency physicians,
depressed. In leads with a predominantly negative but they should be recognized to avoid
QRS, the ST segments are isoelectric or elevated misinterpretation of associated ECG findings.
(Figure 2-6). Only the transition leads, in which
the overall QRS is neutral, do not necessarily Left Anterior Fascicular Block
follow this pattern. Deviations from this expected This is the more common of the two fascicular
pattern of ST-segment change reliably predict
acute myocardial ischemia (see Chapter 6). blocks, owing to the more delicate nature of
the left anterior fascicle. Delayed conduction
ECGs that demonstrate the morphologic down this fascicle means that the left ventricle
changes of LBBB yet do not feature a QRS is depolarized in an asynchronous fashion.
complex width larger than 0.12 second are The anterior fascicle activates the anterior and
classified as having incomplete LBBB or left-sided lateral walls of the left ventricle. In left anterior
conduction delay (Figure 2-8). This finding can fascicular block, this means the depolarization
be difficult to distinguish from Wolff-Parkinson- wave courses from an inferoposterior region (the
White syndrome (type B—no prominent R wave posterior fascicle’s territory) in an anterolateral
in lead V1). This difficulty is not surprising, direction.1 Therefore, the inferior leads show
considering the pathophysiology. In incomplete an initial upward deflection followed by a
LBBB, the left ventricle is activated in a delayed larger downward deflection, as depolarization
fashion; in type B Wolff-Parkinson-White spreads first in an inferoposterior direction
syndrome, the right ventricle is preexcited. A (along the left posterior fascicle and toward the
shortened PR interval favors the latter diagnosis, inferior leads) and then subsequently toward
whereas a normal PR segment is more consistent the anterior and lateral walls of the left ventricle
with incomplete LBBB (or the relatively rare (and toward the lateral leads and away from
normal PR variant of Wolff-Parkinson-White).8 the inferior leads). This should shift the overall
QRS axis leftward. These concepts should be
Fascicular Blocks kept in mind when reviewing the criteria for
left anterior fascicular block (Table 2-6).
The left bundle branch splits into two fascicles
soon after it arises from the bundle of His. The The trigger is recognition of a leftward QRS
axis deviation; indeed, it is a criterion for the
Table 2-5.
ECG criteria for LBBB Table 2-6.
ECG criteria for left anterior fascicular block
QRS complex longer than 0.12 sec
Abnormal QRS morphology in left precordial leads (V5, Left QRS axis deviation (generally considered to
V6) and left limb leads (I, aVL) be >–45°)
• monophasic, slurred, or notched R wave Slightly widened QRS complex (but <0.12 sec unless
• absence of septal q wave (although may be seen in coincident RBBB)
aVL) rS pattern in the inferior leads (II, III, and aVF)
QS or rS pattern in right precordial leads (V1, V2) qR pattern in the lateral limb leads (I and aVL)
Late intrinsicoid deflection (or time to peak of R wave) in Delayed intrinsicoid deflection in lead aVL (>0.045 sec)
V5 and V6 (>0.6 sec)
16
Intraventricular conduction abnormalities
ECG diagnosis of left anterior fascicular block. with hypertensive heart disease, aortic valvular
The critical degree of left QRS axis deviation disease, cardiomyopathy, and degenerative
necessary for left anterior fascicular block is disease of the cardiac conduction system.1,3
debatable. In fact, the concept that some number
exists that serves as the criterion threshold Left Posterior Fascicular Block
between those with and those without left
anterior fascicular block does not make clinical This entity is relatively rare, owing to the
sense. It is generally accepted that the degree dual blood supply of the left posterior fascicle.
of left QRS axis deviation should exceed –45°, The posterior fascicle activates the inferior and
although a more liberal definition would begin posterior walls of the left ventricle. Delayed
at –30°.1 The key morphologic changes include conduction along this fascicle means the left
this leftward QRS axis deviation plus an rS ventricle is again depolarized in an asynchronous
(small r, deep S wave) pattern inferiorly (leads fashion. In left posterior fascicular block, this
II, III, and aVF) and a qR (small-to-absent q, tall means the depolarization wave spreads from
R wave) in the lateral leads (I and aVL). The key the anterolateral region (the domain of the left
to the diagnosis of left anterior fascicular block anterior fascicle) in an inferoposterior direction.1
(and later, left posterior fascicular block) lies The ECG findings are perhaps best remembered
in the limb leads, not in the precordial leads. as the “opposite” of left anterior fascicular
block. The lateral limb leads (I and aVL) show
Nonetheless, a key result of the presence of an initial upward deflection followed by a larger
left anterior fascicular block is poor precordial downward deflection, as depolarization spreads
R-wave progression, or displacement of the first in an anterolateral direction (along the left
transition zone (where R = S in amplitude, as one anterior fascicle and toward the lateral leads)
moves across the precordium) toward the left. and then subsequently toward the inferior and
This simulates age-indeterminate anteroseptal posterior walls of the left ventricle (and toward
myocardial infarction (Figure 2-9). The strong the inferior leads [II, III, and aVF] and away from
shift in the lateral direction of ventricular the lateral leads). This should shift the overall
depolarization forces also causes the R wave QRS axis rightward. These concepts should
in lead aVL to be bigger than normal. Thus, be kept in mind when reviewing the criteria
left ventricular hypertrophy should not be for left posterior fascicular block (Table 2-7).
diagnosed by aVL R-wave amplitude (>11 mm)
in the presence of left anterior fascicular block.1 Just as the trigger to look for left anterior
fascicular block is a left QRS axis deviation, the
Although left anterior fascicular block is key with its “opposite,” left posterior fascicular
the most common intraventricular conduction block, is the appearance of a rightward QRS axis
abnormality seen in acute myocardial infarction, deviation—between +90° and +180°. The key
isolated left anterior fascicular block has been morphologic changes include this rightward
found in only 4% of acute myocardial infarctions. QRS axis deviation plus an rS (small r, deep
Left anterior fascicular block is also associated S wave) pattern laterally (I and aVL) and a qR
(small-to-absent q, tall R wave) inferiorly (III,
Table 2-7. and perhaps II and aVF). As with left anterior
ECG criteria for left posterior fascicular block fascicular block, left posterior fascicular block
is defined by findings in the limb leads, not
Right QRS axis deviation (between +90° and +180°; the precordial leads. Again, the precordial
usually >+120°) transition zone may be displaced to the left
Slightly widened QRS complex (but <0.12 sec, unless as the left ventricle is activated sequentially,
coincident RBBB) simulating an age-indeterminate anteroseptal
qR pattern in lead III; q waves may or may not be myocardial infarction (Figure 2-10).
present in leads II and aVF
rS pattern in the lateral limb leads (I and aVL) Right QRS axis deviation—the trigger to
look for left posterior fascicular block—is
17
Electrocardiography in Emergency Medicine
itself rather rare, and there are other more Multifascicular Blocks
common causes of this hallmark finding. The
differential diagnosis includes right ventricular By definition, a bifascicular block involves
hypertrophy, lateral wall myocardial infarction a conduction delay in two fascicles, and a
(indicated by large Q waves in leads I and aVL), trifascicular block involves three. A definitive
dextrocardia, ventricular tachycardia, limb diagnosis of the latter requires that recordings
electrode misconnection, and pulmonary disease be made from the bundle of His.1 LBBB can
(including acute pulmonary embolism as well as be thought of as a bifascicular block if the
other diseases that could increase pressure in the conduction delay occurs in both the anterior
pulmonary circuit, such as chronic obstructive and posterior fascicles; it can be considered
pulmonary disease and primary pulmonary a unifascicular block if the delay is more
hypertension). Right QRS axis deviation might proximal.3 RBBB occurring with left anterior
be a normal finding in younger populations. fascicular block is the most common type of
Overdose with cyclic antidepressants and other bifascicular block (Figure 2-12), whereas RBBB
sodium channel blocking agents can also cause plus left posterior fascicular block—although
a rightward shift in the QRS axis. Although more common than left posterior fascicular
the key to recognizing this toxicologic entity block alone—is the rarest.1,3 In one series of
is a large R wave in lead aVR with or without 277 patients with bifascicular block, 196 had
a widening of the QRS complex,9 a deep S RBBB plus left anterior fascicular block, 60
wave can emerge in lead I as well, causing a had LBBB, and 21 had RBBB with left posterior
rightward shift in the QRS axis, if it exceeds fascicular block.10 Multifascicular block is a
the amplitude of the R wave in lead I and the marker of advanced disease of the cardiac
major QRS vector in lead aVF remains upright. conduction system and is associated with higher
rates of sudden cardiac death over time.1,3,10
Left posterior fascicular block is the least
likely intraventricular conduction abnormality Nonspecific Intraventricular
to be found in acute myocardial infarction. It Conduction Delay
is associated with hypertensive heart disease,
aortic valvular disease, and fibrotic changes of When the QRS complex duration exceeds
the heart. It is seldom seen in isolation, more 0.11 sec, yet the criteria for LBBB or RBBB
commonly occurring with RBBB1,3 (Figure 2-11). are not met, a nonspecific intraventricular
conduction delay exists.1 This entity might
be encountered as is, or it could manifest
secondary to a disease process or syndrome
Key Facts
• All bundle-branch blocks feature QRS complexes with a duration of more than 0.12 sec.
• Bundle-branch block typically features discordant ST/T-wave changes in certain leads: the ST
segment is depressed and the T wave is inverted in the leads that show the classic bundle-branch
block findings.
• RBBB typically has an rSR′ in leads V1 and V2; qR and notched R variants can occur.
• Signs of incomplete RBBB might result from incorrect positioning of leads V1 and V2.
• LBBB might not show the characteristic slurred monophasic R wave in all lateral leads.
• The PR interval is used to differentiate incomplete LBBB from Wolff-Parkinson-White syndrome.
• RBBB plus left anterior fascicular block is the most common bifascicular block.
• Left posterior fascicular block is rare and resembles right ventricular hypertrophy on the ECG.
18
Intraventricular conduction abnormalities
that delays ventricular depolarization, such
as left ventricular hypertrophy with QRS
complex widening, functioning artificial
cardiac pacemaker with isoelectric (ie,
undetectable) spikes, preexcitation syndromes
(eg, Wolff-Parkinson-White), ventricular
tachycardia, hypothermia, hyperkalemia,
and sodium channel blocker poisoning.
References
1. Surawicz B, Knilans TK. Chou’s Electrocardiography
in Clinical Practice: Adult and Pediatric. 5th ed.
Philadelphia, PA: WB Saunders; 2001.
2. Mattu A, Rogers RL. Intraventricular conduction
abnormalities. In: Chan TC, Brady WJ, Harrigan RA,
et al, eds. ECG in Emergency Medicine and Acute Care.
Philadelphia, PA: Elsevier Mosby; 2005:89-95.
3. Mirvis DM, Goldberger AL. Electrocardiography.
In: Braunwald E, Zipes DP, Libby P, eds. Heart
Disease: A Textbook in Cardiovascular Medicine. 6th ed.
Philadelphia, PA: WB Saunders; 2001:82-125.
4. Liao Y, Emidy LA, Dyer A, et al. Characteristics and
prognosis of incomplete right bundle-branch block: an
epidemiologic study. J Am Coll Cardiol. 1986;7:492-499.
5. Harper RJ, Richards CF. Electrode misplacement
and artifact. In: Chan TC, Brady WJ, Harrigan RA,
et al, eds. ECG in Emergency Medicine and Acute Care.
Philadelphia, PA: Elsevier Mosby; 2005:16-21.
6. Lichstein E, Mahapatra B, Gupta PK, Chadda KD.
Significance of complete left bundle-branch block with
left axis deviation. Am J Cardiol. 1979;44:239-242.
7. Parharidis G, Nouskas G, Efthimiadis J, et al. Complete left
bundle-branch block with left QRS axis deviation: defining
its clinical importance. Acta Cardiol. 1997;52:295-303.
8. Barold SS, Linhart JW, Hildner FJ, et al. Incomplete left
bundle-branch block: a definite electrocardiographic
entity. Circulation. 1968;38:702-710.
9. Liebelt EL, Francis PD, Woolf AD. ECG lead aVR versus QRS
interval in predicting seizures and arrhythmias in acute tricyclic
antidepressant toxicity. Ann Emerg Med. 1995;26:195-201.
10. Denes P, Dhingra RC, Wu D, et al. Sudden cardiac
death in patients with chronic bifascicular block.
Arch Intern Med. 1977;137:1005-1010.
19
Electrocardiography in Emergency Medicine
Figures
Figure 2-1.
Acute myocardial infarction in a patient with RBBB. One of the keys to recognizing the acute anteroseptal
ST-segment elevation myocardial infarction on this ECG is being comfortable with the appearance of RBBB
at baseline. Note the qR pattern (with a notched R) in leads V1 to V3—consistent with RBBB. However, the ST
segment is not depressed in V3 as is expected in RBBB; it is elevated, signaling an injury current. Leads V3
through V5 have ST-segment elevation, which is consistent with ST-segment elevation myocardial infarction.
During cardiac catheterization, this patient was found to have a left anterior descending coronary artery
occlusion.
Figure 2-2.
RBBB. This tracing features the rSR' and discordant (principally downward deflection of the) ST/T-wave
complex classic for RBBB. The relatively deep and wide S waves appearing in leads I and V6 are also typical of
RBBB.
20
Intraventricular conduction abnormalities
Figures
Figure 2-3.
RBBB—qR variant. RBBB can appear without the characteristic rSR' in lead V1. In this tracing, there is a qR
complex in lead V1 or, at most, there is an almost indistinguishable nubbin of an r wave preceding the initial
negative deflection in that lead. Note the discordant ST/T complex in the right-sided precordial leads and the
deep, wide S wave laterally (both classic for RBBB).
Figure 2-4.
RBBB—notched R wave variant. RBBB can present as a notched R wave in lead V1 rather than the classic rSR'.
Note the discordant ST/T complex in the right-sided precordial leads and the deep, wide S wave laterally (both
classic for RBBB). This patient also has a left anterior fascicular block; the axis approaches –90°, and there is a
small r wave followed by a deep S wave in the inferior leads.
21
Electrocardiography in Emergency Medicine
Figures
Figure 2-5.
Incomplete RBBB. The QRS complex is less than the requisite 0.12 sec, so, despite the rSR' morphology in lead
V1, this is merely an incomplete RBBB. At times, incomplete RBBB will show discordant ST/T complexes and a
significant left-sided S wave as well.
Figure 2-6.
LBBB. The left-sided leads (I, aVL, V5, and V6) in this tracing feature the widened, slurred R wave seen in LBBB,
as well as the discordant (principally downward deflection of the) ST/T-wave complex classic for LBBB. The
relatively deep and wide S waves following the small r waves in leads V1 and V2 are also typical of LBBB. Note
the absence of septal q waves in the left-sided leads.
22
Intraventricular conduction abnormalities
Figures
Figure 2-7.
LBBB plus left QRS axis deviation. Again, the classic widened QRS complex is evident, as well as the notched
upright QRS complex in the left-sided leads (I, aVL, V5, and V6); note that these leads also do not demonstrate
an initial q wave. The right-sided precordial leads (and indeed all the way through lead V4) show QS (V1, V2)
or rS (V3, V4) patterns typical of LBBB. The ST/T-wave complexes are appropriately discordant in the affected
leads. Lastly, there is left QRS axis deviation (roughly –45°). Two pseudo-infarct patterns are evident on this
tracing. The QS pattern in leads V1 and V2 is caused by LBBB but, taken out of context, could be misconstrued
as an age-indeterminate septal infarct. The left axis deviation can be mistaken for an age-indeterminate
inferior infarction as well.
Figure 2-8.
Incomplete LBBB. This tracing does not show complete LBBB, because the QRS complex is not wider than
0.12 sec. The ST/T-wave changes seen in leads I, aVL, V5, and V6 should invoke the differential diagnosis
of incomplete LBBB, left ventricular hypertrophy with repolarization abnormality, and coronary ischemia.
The delayed intrinsicoid deflection (time to peak height of the R wave) in the left-sided leads—a feature of
incomplete LBBB—bears a resemblance to the slurred upstroke of the QRS complex (the delta wave) of Wolff-
Parkinson-White syndrome; note, however, that the PR interval is not less than 0.12 sec, as would be expected
in patients with Wolff-Parkinson-White syndrome.
23
Electrocardiography in Emergency Medicine
Figures
Figure 2-9.
Left anterior fascicular block. The ECG trigger is the leftward deviation of the QRS axis in the frontal plane,
here seen to be approximately –75° degrees. The rS pattern inferiorly (leads II, III, and aVF) and the qR pattern
laterally (leads I and especially aVL) are part of the ECG definition of left anterior fascicular block. The poor R-
wave progression across the precordium simulates age-indeterminate anteroseptal myocardial infarction.
Figure 2-10.
Left posterior fascicular block. The ECG trigger is the rightward deviation of the QRS axis in the frontal plane,
here seen to be approximately +120°. The rS wave laterally (leads I and aVL) and the qR pattern inferiorly
(leads II, III, and aVF) are typical of left posterior fascicular block. It is difficult to discern if there has been a
prior anteroseptal myocardial infarction or if the poor R-wave progression is a result of the fascicular block.
An echocardiogram looking for wall motion abnormality would be helpful in this regard.
24
Intraventricular conduction abnormalities
Figures
Figure 2-11.
Left posterior fascicular block plus RBBB. This is a relatively uncommon bifascicular block. Note the rightward
axis—a cue to look for left posterior fascicular block. Notice also the ST-segment elevation myocardial
infarction manifesting anteriorly. On cardiac catheterization, this patient was found to have critical stenosis of
the left anterior descending artery.
Figure 2-12.
Left anterior fascicular block plus RBBB. This is the most common variety of bifascicular block. The trigger is
to see RBBB morphology together with a left QRS axis deviation, here between –60° and –90°. The criteria for
left anterior fascicular block are also met (rS wave inferiorly; qR wave in lead aVL).
25
Electrocardiography in Emergency Medicine
26
C h apter T h ree
Bradycardias and Heart Blocks
Kevin R. Brown, MD, MPH
Dysrhythmias can be sorted into three Bradycardias
main types: those going too fast, those going
too slow, and those that are too irregular. Bradycardic ventricular rates in
Bradyarrhythmias involve conduction and rhythm adults are those less than 60 beats/min.
abnormalities that are “too slow” and might Unstable bradycardias are those that have
also be “too irregular.” Clinically significant ventricular rates below 45 beats/min and
bradydysrhythmias (Table 3-1) usually have rates cause tissue hypoperfusion, resulting in
below 45 beats/min; rates faster than this seldom lightheadedness, chest pain, syncope,
have hemodynamic consequences. This chapter generalized weakness, fatigue, shortness
describes the significant bradycardias that should of breath, or other signs of shock.
be addressed by emergency physicians and those
that are clinically less serious and do not need ECG Manifestations
urgent attention but warrant careful monitoring.
The ECG clues that can help sort out the
The prognosis of a patient with atrioventricular various dysrhythmias that result in bradycardia
(AV) heart block caused by AMI is related to the can be found in the P waves and QRS complexes.
site of the infarction (whether the block occurred Finding P waves in association with bradycardia
at the AV node or below), the type of escape is useful in identifying the origin of the slow
rhythm, and the hemodynamic response to the rhythm. Fixed P waves before each QRS-T
escape rhythm. Treatment is warranted when the complex indicate a sinus (or supraventricular)
rate remains persistently slow, when the person rhythm. P waves with progressive PR interval
is symptomatic, and when the cardiac output is prolongation indicate Wenckebach AV heart
inadequate to meet the body’s needs. The degrees block. P waves occurring “helter skelter” across
of AV heart block and their clinical significance, the QRS-T complexes point toward a complete
as well as sinuatrial (S-A) blocks, are also heart block or AV dissociation. Fixed PR intervals
discussed in this chapter. before intermittently or regularly dropped QRS
complexes indicate a non-Wenckebach form of
second-degree block.
27
Electrocardiography in Emergency Medicine
The width and shape of the QRS complex patients experiencing severe visceral pain.
help determine whether the rhythm originated Regularly blocked premature atrial complexes
from a supraventricular focus or a ventricular
site. QRS duration of 0.1 second or less arises (PACs) (eg, every other or every third PAC
from a supraventricular focus (that is, above is not conducted) commonly masquerade as
the bifurcation of the AV bundle). However, either sinus bradycardia or sinus block (Figure
some supraventricular impulses follow aberrant 3-2). Nonconducted PACs have no clinical
paths, leading to an abnormally prolonged significance, yet the ECG can mimic a serious
QRS duration (≥0.12 sec). QRS duration of 0.12 rhythm disorder. PACs are blocked when they
second or more with wide and distorted shapes occur so early during the cardiac cycle that the
indicates an ectopic pacemaker in the ventricle. AV node is still refractory and unable to transmit
the premature impulse. The ST segments and T
Sinus Bradycardia waves of the sinus beats preceding the cardiac
Sinus bradycardia is a benign variant of pauses hold the clue to hidden P waves. The
following Marriott1 adage should be kept in
normal sinus rhythm, consisting of normal P- mind: blocked PACs are the most common
QRS-T complexes at a rate below 60 beats/min cause of pauses—not a sinus block/arrest.
(Figure 3-1). The S-A node depolarizes slower
than usual, primarily because of increased Escape Pacemakers
vagal tone or from the use of β-blocking or
calcium channel–blocking medication. In When the ventricles are not stimulated as a
the setting of a myocardial infarction (MI), result of conduction or automaticity problems,
slow rates are protective by lessening the a slower escape or back-up rhythm emerges to
myocardial oxygen demand and limiting the pace the heart (Table 3-2). Failure of an escape
size of the infarction. Sinus bradycardia is pacemaker leads to asystole. Fortunately,
relatively common in inferior-wall MI and is escape rhythms usually rescue the silent heart
often seen with prolonged PR intervals. Sinus unless there is diffuse heart disease. When
bradycardia is well tolerated unless the rate the sinus node fails to discharge or the AV
drops below 45 beats/min (Figure 3-1A). Sinus node fails to conduct sinus impulses, escape
bradycardias almost never need emergent rhythms discharge in the AV junction at a rate
treatment unless the patient is symptomatic; just below 60 beats/min. If the AV junctional
then atropine is usually effective because the back-up pacemaker also fails, a pacemaker
sinus node is innervated with parasympathetic located more distally in the conduction
nerves. Slow resting heart rates are normal in system, such as in the bundle branches or
well-conditioned individuals and frequent in His-Purkinje fibers, stimulates the heart
but at a rate much slower than normal.
Table 3-1.
Types of bradycardias AV junctional (nodal) escape rhythm (Figure
3-3), a narrow QRS complex bradycardia, is
Sinus bradycardia regular and occurs at a rate around 50 beats/min.
Sinus block/arrest (sick sinus syndrome or tachy-brady P waves either are missing or occur immediately
syndrome) following the QRS complex (retrograde) and
AV junctional escape rhythms (secondary to sinus
arrest) Table 3-2.
AV heart blocks with slow ventricular escape rhythm Escape pacemaker rhythms
Atrial fibrillation or flutter with slow ventricular response
Idioventricular escape rhythm (secondary to sinus arrest QRS Rate Pacemaker
and failure of an AV junctional escape)
Agonal idioventricular rhythm Site Complex (beats/min) Reliability
28 AV junctional Narrow 40 – 55 Good
Idioventricular Wide, 20 – 40 Poor
distorted
Bradycardias and Heart Blocks
are buried in the early ST segment. Retrograde complexes are coupled with missing P waves.
P waves can sometimes be found after the QRS The idioventricular pacemaker rate is between
in AV junctional complexes. Patients with AV 20 and 40 beats/min. Idioventricular escape
junctional rhythms are usually not symptomatic, rhythms typically result when a conduction
because the ventricular rate is fast enough (45 to disturbance occurs simultaneously in both
55 beats/min) to perfuse organs despite the loss of bundle branches or in three fascicles (the right
atrial filling “kick.” Junctional escape bradycardic bundle and both divisions of the left bundle).
rhythms are “secondary” cardiac rhythms that
develop as a result of sinus node depression. Idioventricular bradyarrhythmias
usually cause lightheadedness, dizziness,
Idioventricular escape rhythms (or beats) and near syncope because of inadequate
(Figure 3-4) occur in the setting of sinus tissue perfusion. An artificial pacemaker is
node failure coupled with failure of the AV generally required to stabilize this rhythm.
junctional escape to rescue the asystolic heart.
Idioventricular escape rhythms are considerably Agonal Idioventricular Rhythms
less dependable than junctional escape rhythms Distorted QRS-T complexes, in a slow,
and could fail abruptly; hence, the need for an
artificial pacemaker. These rhythms are easy to irregular pattern, are commonly observed
identify because their wide and distorted QRS during the final phase of cardiopulmonary
resuscitation. During agonal idioventricular
Table 3-3. rhythm, the pacemaker is unreliable. Its
Atrioventricular block findings isolated beats do not generate cardiac output
and degenerate abruptly into asystole.
First-degree AV block
• simple prolongation of PR interval Atrial Fibrillation or Flutter With a
• no dropped QRS complexes Bradycardic Ventricular Response
• all P waves are conducted
A bradycardic ventricular response in the
Second-degree AV block (intermittent P-wave blockage) setting of a tachycardic dysrhythmia occurs
• Mobitz type I (Wenckebach) secondary to the administration of medication
• PR interval progressively increases before that is intended to slow the ventricular
dropped QRS response but that overshoots the mark and
• intermittent dropping of the QRS induces AV nodal refractoriness (Figure 3-
• QRS is usually narrow, as the AV block is 5). As a result, most of the atrial waves are
intranodal blocked, inducing iatrogenic bradycardia.
• usually fixed AV conduction ratio (3:2 or 4:3 but Transient third-degree AV block can also occur
can be 7:6, etc.) in atrial fibrillation and is recognized by the
• QRS complexes crowd closer together before regular R-R intervals instead of the classically
dropped QRS irregularly irregular ventricular rhythm.
• Mobitz type II
• fixed PR interval before dropped QRS complex Heart Blocks
• grouped beating
• wide and distorted QRS complexes due to There are two types of heart blocks:
infranodal blockage atrioventricular and sinuatrial. AV heart
blocks are much more commonly encountered
Third-degree (complete) AV block than S-A blocks. In AV blocks (except for
• complete interruption of atrial conduction first-degree block), there are more P waves
• independent atrial and ventricular rhythms than QRS complexes because some of the
• P waves march through the QRS complexes QRS-T complexes are dropped. In S-A
• width and rate of QRS complexes indicate the blocks, entire cardiac cycles are missing.
escape pacemaker site
• narrow, normal shape, and 40–50/min: junctional 29
• wide, distorted, and 20–40/min: ventricular
Electrocardiography in Emergency Medicine
Atrioventricular Blocks having a PR interval prolonged beyond 0.2
AV heart blocks can be divided into incomplete second (Figure 3-6). P waves are not actually
blocked, so no QRS complexes are dropped.
(first and second degree) and complete (third Since the PR interval includes transmission in
degree) (Table 3-3). First-degree block and the the atria, AV node, and His-Purkinje system,
Mobitz type I (Wenckebach) form of second- increased refractoriness in any of these areas
degree AV block can occur in healthy individuals could cause first-degree block; however, in
and do not usually require emergent treatment, as most cases a prolonged PR interval involves
patients tolerate them well. The conduction delay delay, mainly in the AV node. First-degree
for first-degree and Wenckebach heart block block has no cardiovascular consequences
forms occurs mostly in the AV node, and the QRS and is simply a benign PR interval delay.
complexes are narrow (<0.12 sec). These forms are First-degree block is relatively common in
not likely to progress to more advanced blocks. interior wall MIs and resolves as AV nodal
edema subsides. First-degree AV block can
Second-degree Mobitz II (non-Wenckebach also be seen along with sinus bradycardia,
form) and third-degree (complete) blocks are especially when there is increased vagal tone.
clinically significant. Their causes are listed in First-degree block can also be seen along with
Table 3-4. These blocks are never normal and the Wenckebach second-degree AV block.
always require emergent treatment. Mobitz type
II and complete AV blocks cause slow heart rates Second-Degree Atrioventricular Heart Block
and induce effects due to hypoperfusion, such as
syncope, near syncope, and myocardial ischemia. Second-degree AV block involves intermittent
Stokes-Adams attacks are syncope caused by conduction failure between the atria and
transient heart blocks. High-grade AV heart ventricles. Some P waves fail to be conducted,
block refers to an advanced form of Mobitz type resulting in QRS complexes being dropped.
II, in which consecutive P waves are blocked. There are two forms of second-degree AV
block: Mobitz type I, which is less serious and
First-Degree Atrioventricular Heart Block typically does not require emergent treatment,
First-degree block involves a delay in the and Mobitz type II, which is serious and
does require emergent therapy (Table 3-5).
impulse conduction between the sinus node and Bradycardia can result from both forms of
the ventricles. The hallmark is a sinus rhythm second-degree AV block if a significant number
of (nonconducted) QRS complexes have been
Table 3-4. dropped. The ventricular rate depends on
Causes of clinically significant atrioventricular block the sinus rate and the AV conduction ratio.
For instance, 3:2 AV conduction will yield a
Myocardial ischemia/injury (especially inferior and ventricular rate of 40 beats/min if the sinus rate
anterior) is 60 beats/min. A more tolerable ventricular
Age-associated AV nodal degeneration fibrosis rate of 60 beats/min occurs if the sinus rate was
Age-associated His-Purkinje degeneration fibrosis 80 beats/min for the same conduction ratio.
Lyme carditis
Congenital heart disease Second-Degree AV Heart Block Mobitz
Calcific aortic stenosis Type I (Wenckebach Type). Mobitz type I is
Rheumatic heart disease characterized by cycles of intermittently dropped
Endocarditis QRS complexes that are preceded by increasing
Cardiomyopathy PR intervals. Most, but not all, cases of Mobitz
Drug toxicity (calcium channel blocker, digitalis, and type I are caused by a blockage in the AV node.
-blocker toxicity) The classic pattern shows grouped beats until
Aortic or mitral valve surgery (proximity to His-Purkinje a dropped QRS complex occurs and the cycle
fibers) begins over (Figure 3-7). After the dropped beat
Viral myocarditis
30
Bradycardias and Heart Blocks
of each cycle, the next PR interval is the shortest Second-degree AV block Mobitz type II is
of the bunch. The sinus impulse encounters a important to identify; it is associated with
progressively more refractory AV node in the advanced disease of the conduction system,
succeeding beats, eventually resulting in a causes symptoms, and often progresses to
dropped QRS complex. A pattern is observed complete AV block. It should be identified
as the QRS complexes fall further behind the P quickly, because an artificial pacemaker
waves, appearing as shortening RP intervals. The is needed to stabilize the rhythm.
most frequent AV conduction ratios are 3:2 or
4:3 but higher ratios, even 7:6 and 6:5, are seen. 2:1 AV Heart Block: A Special Form of
Second-Degree Conduction. There has been
Patients with Mobitz type I AV block are confusion over whether a 2:1 AV block is a Mobitz
usually asymptomatic. Wenckebach block occurs type I or II. Some have argued that 2:1 block is
in about 10% of patients with AMI, especially a Wenckebach form of block, while others cite
interior wall MI. Mobitz type I also occurs in it as an example of Mobitz type II (Figures 3-9
healthy individuals with high vagal tone. A and 3-10). This is not just an academic point, as
clue to the increased parasympathetic tone is a the two second-degree block, types represent
slow sinus rhythm along with the prolonged PR very different causes and prognoses. Depending
interval. Wenckebach does not usually cause on the circumstances, each advocate is right.
symptoms, have an adverse effect on cardiac
output, or progress to more serious forms of Because every other P wave is blocked, the
AV block. Marriott2 spoke of recognizing the surface ECG in 2:1 conduction does not show
“footprints” of Wenckebach: the grouped beating, two consecutive PR intervals, so it is not clear
the dropped QRS complexes, and the shortening whether the PR interval is increasing or staying
of R-R intervals as the QRS falls farther behind the same. As a result, the lack of PR progression
the P wave. Treatment is usually not needed. before the dropped beat could signify a Mobitz
type II block. This is the more serious of the
Second-Degree AV Heart Block Mobitz Type two forms and usually requires a permanent
II. This is the serious form of second-degree pacemaker. The most useful clinical clue is
block, in which there is a sudden blockage of obtained by inspecting the QRS complexes. A
AV conduction without prolongation of the PR Wenckebach type AV block is usually located
interval. Mobitz II is a partial block consisting in the AV node and has a normal QRS complex
of dropped QRS complexes with constant PR and QRS duration (<0.12 sec). Mobitz type II AV
intervals before the dropped QRS complexes block, in contrast, generally occurs below the
(Figure 3-8). Type II block is identified when AV node within the His-Purkinje system and has
at least two consecutive atrial impulses are wide (≥0.12 sec) and distorted QRS complexes.
conducted with constant PR intervals before
the dropped QRS complex occurs. The QRS Figure 3-10 allows us to apply the rule in 2:1
complexes are usually wide and distorted, block: the QRS complexes are narrow, indicating
since the conduction disturbance is located this is likely a Mobitz type I (Wenckebach). In
infranodally, within the His-Purkinje fibers. the author’s experience, most 2:1 AV conduction
cases are intranodal blocks with narrow QRS
Table 3-5.
Types of second-degree atrioventricular heart block
Likelihood of
Progressing to
Site of AV QRS Dependability Third-Degree
Block Type Block Complexes of Escape Heart Block Duration
Mobitz I (Wenckebach) AV node Narrow Reliable Infrequent Transient
Mobitz II Below bundle of His Wide, distorted Unreliable Frequent Permanent
31
Electrocardiography in Emergency Medicine
complexes. Therefore, they usually do not need rhythms range from 40 to 50 beats/min.
treatment, but if the patient is symptomatic, The most common causes of third-degree
atropine is usually successful, because increased
vagal tone is the offending agent. In Figure block are age-associated fibrosis of the AV
3-10, the QRS complexes are narrow and the conduction system and MI (inferior and
AV block is probably located in the AV node. anterior types). Fibrosis and an anterior wall
MI are permanent, whereas the heart block
High-Grade Second-Degree AV Heart Block. caused by an inferior wall MI may subside
Advanced AV block is present when two or more as the edema resolves in 24 to 48 hours.
consecutive P waves are blocked (Figure 3-11).
The atrial rate must not be too fast (<140 bpm); Differentiating AV Dissociation from
otherwise, a physiologic non-conduction such as Complete AV Heart Block. Independent atrial and
atrial flutter with 3:1 AV conduction can occur ventricular rhythms occur in AV dissociation,
rather than a true heart block. High-grade AV but this does not imply that there is a complete
block is the most serious form of second-degree AV block. Third-degree block is only one of
AV block. Identification is important because several causes of a dissociated state between
the rhythm advances to complete AV block the atria and ventricles. Dissociation commonly
within a short period. This form of Mobitz type occurs in the absence of a heart block but in the
II occurs when two or more consecutive QRS presence of either of two conditions: 1) the sinus
complexes are dropped, leading to a pause in rhythm is slower than a backup pacemaker,
ventricular activity. Rather than every third or causing interference, or 2) the ventricular
fourth QRS being dropped, as in other forms of rhythm accelerates faster than normal and
second-degree block, two or more consecutive competes with the sinus node. In both cases,
P waves are blocked. High-grade AV block is a there is a lack of coordination between the atrial
highly unstable form of second-degree block. and ventricular rhythm but not heart block.
Third-Degree (Complete) Atrioventricular The most common form of AV dissociation is
Heart Block isorhythmic AV dissociation, which occurs when
the atria and ventricles are paced independently
With this block there is total interruption but at almost the same rate. The usual cause is
of AV conduction—no P waves are conducted when the sinus rate transiently falls below 60
(Figure 3-12). The hallmark findings of third- beats/min—usually around 50 beats/min—and
degree AV heart block are regular PP intervals an AV junctional escape rhythm occurs. As
that are unrelated to regular R-R intervals with a result, the P waves and QRS complexes are
P waves that appear to march through the briefly dissociated from one another; however,
QRS-T complexes. There are two independent there is no actual AV conduction disorder.
pacemakers: one in the S-A node and one either The dissociated rhythm results from close
in the AV junction or within the Purkinje fibers discharge rates of the sinus and junction escape
in the ventricles. The ventricular escape rhythm pacemakers. The dissociation subsides as soon as
must be slow enough (usually 45 bpm) to permit the sinus node accelerates. A less common cause
an atrial beat to be conducted if conduction was occurs when an accelerated junctional rhythm
possible. The ventricular rate depends on whether speeds up and overtakes a normally functioning
the block is in the AV junction (less common) sinus node. Patients with isorhythmic
or the bundle branches (more common). The dissociation are usually asymptomatic, unlike
more distal the blockage in the conduction those with complete AV heart block.
system, the lower the escape pacemaker rhythm
will be. Slow and wide idioventricular escape Sinuatrial Blocks
rhythms ranging from 20 to 40 beats/min are
generally caused by trifascicular blockage. An S-A block is characterized by the sudden
Narrow and normal-appearing AV junctional loss of sinus activity, recognized as missing
P-QRS-T complexes. The sinus node might
32 fail to fire, or it might fire but the impulse
is blocked. Sinus block is easy to identify Bradycardias and Heart Blocks
because of the dramatic disruption in cardiac
rhythm (Figures 3-13 and 3-14). Patients with retrograde P wave. Sinus block is classified as
sinus block typically have a history of sudden either incomplete, in which an occasional sinus
syncopal episodes, generalized weakness, or impulse is dropped, or complete, in which no P
lightheadedness. Sinus pauses are terminated waves are visible and an escape rhythm occurs.
by an escape beat or rhythm. Sinus node failure
has three possible mechanisms: the sinus Incomplete Sinuatrial Block
node generates the impulse but it fails to be Incomplete S-A block involves an occasionally
transmitted out of the node; the sinus node
impulse occurs but the atrial tissue fails to blocked P wave. It is sometimes possible to detect
respond because of increased refractoriness of a relationship to the underlying PP interval and
atrial tissue; or the sinus node fails to form an to determine that the pause consists of a multiple
impulse. Regardless of the mechanism, one or of PP cycles, but this is usually not the case. It
more P-QRS-T complexes are absent, resulting is best to describe the ECG findings rather than
in a pause in the cardiac rhythm. In most cases, trying to find the precise term. “Sinus rhythm
a junctional escape beat or rhythm ends the with a 3-and-a-half-second pause” conveys all
pause after a second or more and is recognized the crucial information that is needed when
by its narrow QRS complex and absent or discussing the ECG with a cardiologist.
Key Facts
• A blocked premature atrial complex is the most common cause of a pause—not a sinus block/
arrest.
• First-degree AV block is a benign finding.
• Mobitz type II, second-degree AV block, is never normal and often progresses to complete AV
block.
• Third-degree AV block causes marked symptoms and requires a pacemaker. The adequacy of
the escape pacemaker depends on the ventricular rate. Junction escape pacemakers are better
tolerated than idioventricular pacemaker rhythms.
• The most likely cause of bradycardia in atrial fibrillation and flutter is overtreatment of the rapid
ventricular response. Withholding the medication usually corrects the problem.
• Atrial fibrillation with a slow regular ventricular rhythm (R-R intervals) indicates complete AV block,
which is usually medication induced.
• Even though a sinus block is dramatic in appearance, patients are usually stable and mainly require
elective pacemaker insertion.
• No matter what the type of dysrhythmia, therapy is based on the adequacy of the ventricular rate.
Bradycardic rates above 45 beats/min do not cause hypotension.
• Atropine is ineffective in accelerating idioventricular escape rhythms, as there is little
parasympathetic innervation in the ventricles.
• Atropine may cause a paradoxical slowing of the heart rate if given too slowly or in an inadequate
dose (<0.5 mg).
• Mobitz type II AV block is never a normal variant and occurs only in a diseased conduction system.
When it occurs during an MI, usually an anterior wall MI, it is permanent.
• Mobitz type I (Wenckebach) AV block may occur in normal individuals without conduction system
disease. When it occurs in the setting of an MI, it is usually associated with an inferior wall MI and
is transient.
33
Electrocardiography in Emergency Medicine
Complete Sinuatrial Block (Arrest) causes ischemia, hypotension, or escape
ventricular rhythms. Atropine is also useful
In complete S-A block, there is a sustained for AV block that occurs at the AV nodal level
failure of the sinus node to pace the heart. (narrow QRS complexes). Infranodal blocks
Management of complete S-A block involves causing slow and wide QRS complexes are
applying an external pacemaker. Atropine generally unresponsive to atropine. Care must
may sometimes be helpful temporarily. An be used when administering atropine in the
epinephrine infusion is indicated for hypotensive setting of an acute MI, as the slow heart rate
cases that are refractory to external pacing limits infarct size and atropine may increase it.
and atropine, but it is rarely needed.
External pacemakers are indicated for
Sick Sinus Syndrome patients at risk of developing complete heart
block, ie, those with any of the following:
This interesting sounding dysrhythmia is
actually a group of dysrhythmias with the • Second-degree block Mobitz type II and
hallmarks of alternating bradycardia and high-grade AV heart block.
tachycardia. The sick sinus syndrome title is
applied when frequent periods of pronounced • New left bundle-branch block and
bradycardia, tachycardia, and sinus block bifascicular blocks.
occur. Sinus node dysfunction has also been
referred to as “tachy-brady syndrome” due • Left bundle-branch block with first-degree
to the alternating fast and slow rates. heart block.
Treatment of Slow Cardiac References
Rhythms
1. Wagner GS. Marriott’s Practical Electrocardiography. 10th ed.
Hollander3 provides a useful review of Baltimore, MD: Lippincott Williams & Wilkins; 2001.
bradyarrhythmias occurring during an acute
coronary event. The mortality rate is increased 2. Marriott HJL. Rhythm Quizlets: Self Assessment.
in AV heart block associated with an AMI; Philadelphia, PA: Lea & Febiger; 1985.
however, artificial pacing has not been shown to
improve survival. The heightened risk of death 3. Hollander J. Intervention strategies for acute coronary
is probably related to more extensive myocardial syndromes. In: Tintinalli JE, Kelen GD, Stapczynski JS, eds.
damage rather than the heart block itself. Emergency Medicine A Comprehensive Study Guide. 5th ed. Dallas,
TX: American College of Emergency Physicians; 1985.
The 2005 advanced cardiac life support
guidelines4 advise observation and monitoring in 4. 2005 American Heart Association guidelines for
the setting of slow cardiac rhythms with adequate cardiopulmonary resuscitation and emergency cardiovascular
perfusion. If the patient looks well, observation care. Part 7.3: management of symptomatic bradycardia and
is more appropriate than trying to accelerate tachycardia. Circulation. 2005;112(24 Suppl):IV67–IV77.
the rhythm. For patients with poor perfusion,
external pacing and permanent pacing are the
definitive treatments. Use of atropine, a vagolytic
drug that can temporarily reverse a slow heart
rate, can be considered while pacing equipment
is being prepared. If the patient fails to respond
to atropine, second-line medications to consider
are epinephrine and dopamine. In the setting of
β-blocker or calcium channel-blocker toxicity,
intravenous administration of glucagon may be
useful if atropine fails to raise the heart rate.
Atropine is indicated when sinus bradycardia
34
Bradycardias and Heart Blocks
Figures
Figure 3-1.
Sinus bradycardia. Normal P-QRS-T complexes occur at rates below 60 beats/min. A: The rate in this tracing is
30 beats/min, which is extremely slow for a sinus bradycardia and will cause the patient to be symptomatic. B:
In this tracing, the rate is 54 beats/min and will not cause symptoms.
A
B
Figure 3-2.
Nonconducted PACs. The ventricular rate is 32 beats/min because every other beat is a nonconducted
premature atrial complex. The blocked P' wave (indicated by arrows) of the bigeminal rhythm can be seen
immediately after the T waves. This rhythm occurred for a few seconds and was followed by a sinus rate of 64
beats/min.
35
Electrocardiography in Emergency Medicine
Figures
Figure 3-3.
AV junctional escape rhythms. In tracings A and B, the QRS complexes are narrow and lack P waves. The rate
in tracing A is 42 beats/min, and in B the rate is 60 beats/min. Retrograde P waves (arrows) can be seen just
following the QRS complexes in tracing B.
A
B
Figure 3-4.
Idioventricular escape rhythms. The QRS complexes are slow, wide, and grossly distorted in both tracings.
The rate is 42 beats/min in tracing A and between 20 and 30 beats/min in tracing B. Idioventricular escape
pacemakers are unreliable and can deteriorate abruptly into asystole. The escape pacemakers arise in the
distal portion of the His-Purkinje system.
A
B
36
Bradycardias and Heart Blocks
Figures
Figure 3-5.
Atrial fibrillation and flutter with bradycardic ventricular response. Tracings A and B show what would
normally be considered tachycardic supraventricular dysrhythmias. Tracing A shows atrial flutter, and tracing
B shows atrial fibrillation. However, in these tracings, the ventricular rates are slower than normal because of
increased AV nodal refractoriness caused by intravenous calcium channel-blocker medication given to slow
the rapid ventricular rate. The treatment overshot the therapy goal.
A
B
Figure 3-6.
First-degree AV block. Tracing A shows a sinus bradycardia in addition to prolonged PR intervals. Both
tracings point toward increased parasympathetic tone, which delays conduction and depresses automaticity.
Tracing B shows a PR interval of 0.32 second and a bradycardic rate of 55 beats/min. The ST segment
elevation is caused by AMI. AMIs, particularly inferior infarcts, are associated with transient AV conduction
problems and bradycardia.
A
B
37
Electrocardiography in Emergency Medicine
Figures
Figure 3-7.
Second-degree AV block; Mobitz type I (Wenckebach). The three tracings show the typical characteristics of
Mobitz type I: grouped beats, narrow QRS complexes indicating an intranodal block, increasing PR intervals
before the dropped QRS, and decreasing R-R intervals before the dropped QRS complexes (indicated by
arrows). Tracing A shows variable AV conduction of 6:5 and 4:3. The PR intervals slightly increase during each
cycle until a QRS is dropped. Following the dropped QRS, the next PR interval is the shortest of the cycle.
Tracing B shows 5:4 AV conduction in the center cycle, flanked by two pauses. Tracing C shows a Wenckebach
block with 5:4 AV conduction in the setting of an acute cardiac injury pattern. The fifth QRS-T complex is an
escape junctional beat that escapes to pace the heart after the 1.6-second pause.
A
B
C
38
Bradycardias and Heart Blocks
Figures
Figure 3-8.
A: This tracing shows a second-degree AV block Mobitz type II with variable AV conduction. All four QRS
complexes are conducted, and the QRS complexes are narrow and have a normal configuration. There are
many more P waves than QRS complexes, so some of them have not been conducted. The AV conduction
ratio shifts between 2:1 and 3:1. Only the third P wave between the first two QRS complexes is conducted.
The other two are blocked, The same pattern holds for the P wave relationship between the 3rd and 4th QRS
complexes. B: This tracing is a dual simultaneous recording of ECG leads II and MCL1. The conduction ratio
was the same as for tracing A, ie, 3:1. The hallmark findings of a second-degree AV block Mobitz type I are
dropped QRS complexes that have fixed PR intervals ahead of the block. The first nonconducted P wave that
occurs just after the QRS complex creates a notched T wave as the P waves fall and are superimposed on the
preceding T wave. There is also a right bundle-branch block (rSR' configuration in V1). (P waves are indicated
by double-headed arrows.)
A
B
39
Electrocardiography in Emergency Medicine
Figures
Figure 3-9.
Second-degree AV block with 2:1 AV conduction. Strip A shows two P waves occurring for each QRS complex.
The second P wave is seen just after the T wave. Tracings B and C are a continuous recording. Except for one
cycle, a 2:1 AV conduction occurs. The first grouped beating that is not 2:1 occurs as the first two complexes in
tracing C (arrow indicates the dropped QRS). This 3:2 conduction confirms that the 2:1 conduction with narrow
QRS complexes is usually a Wenckebach (Mobitz type I) form, even though the increasing PR interval during
2:1 conduction is not visible.
A
B
C
40
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