Electrocardiography of Arrhythmias: A Comprehensive Review

492 Pages·2016·51.47 MB·English

by  Das M.

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ELECTROCARDIOGRAPHY
OF ARRHYTHMIAS:
A Comprehensive Review
A Companion to CARDIAC ELECTROPHYSIOLOGY: From Cell to Bedside
ELECTROCARDIOGRAPHY
OF ARRHYTHMIAS:
A Comprehensive Review
A Companion to CARDIAC ELECTROPHYSIOLOGY: From Cell to Bedside
MITHILESH K. DAS, MD
Associate Professor of Clinical Medicine
Krannert Institute of Cardiology
Indiana University School of Medicine
Chief, Cardiac Arrhythmia Service
Roudebush Veterans Affairs Medical Center
Indianapolis, Indiana
DOUGLAS P. ZIPES, MD
Distinguished Professor
Professor Emeritus of Medicine, Pharmacology,
and Toxicology
Director Emeritus, Division of Cardiology and
the Krannert Institute of Cardiology
Indiana University School of Medicine
Editor, HeartRhythm
Indianapolis, Indiana
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ELECTROCARDIOGRAPHY OF ARRHYTHMIAS: ISBN: 978-1-4377-2029-7
A COMPREHENSIVE REVIEW
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Library of Congress Cataloging-in-Publication Data
Das, Mithilesh K.
Electrocardiography of arrhythmias : a comprehensive review / Mithilesh K. Das, Douglas P. Zipes. –
1st ed.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-4377-2029-7 (pbk. : alk. paper)
I. Zipes, Douglas P. II. Title.
[DNLM: 1. Arrhythmias, Cardiac–diagnosis. 2. Electrocardiography. WG 330]
616.1′207547–dc23
2011053492
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To our wives and families, without whose support we could not have accomplished a fraction of what we have achieved
To my parents, Ganpati Lal Das and Bimla Das; my wife, Rekha; and my children, Awaneesh and Mohineesh
—MKD
To my wife, Joan, and my children, Debra, Jeffrey, and David
—DPZ
PREFACE
Many books, both clinical and basic, have been written about the field of cardiac electrophysiology. Similarly, a multitude
of texts have been published on the interpretation of the clinical electrocardiogram (ECG). In this text we have combined
the two skill sets: the content is electrocardiography of arrhythmias, but we have approached the topic from an understand-
ing of both clinical and basic electrophysiology. As a result, this book should be useful to a broad spectrum of physicians,
from internists with an interest in cardiology and trainees in cardiology and electrophysiology to experienced cardiologists.
This book is also the first companion to the well-known text, Cardiac Electrophysiology: From Cell to Bedside, now in its
fifth edition. We hope you find it a useful addition to help with your ECG reading skills.
We wish to thank John C. Bailey, MD, who provided several key electrocardiographic images used in this book.
MITHILESH K. DAS
DOUGLAS P. ZIPES
vii
ELECTROCARDIOGRAPHY OF ARRHYTHMIAS
A Comprehensive Review
By Mithilesh K. Das and Douglas P. Zipes
CHAPTER 1 IMPORTANT CONCEPTS
CHAPTER 2 SINUS NODE DYSFUNCTION
CHAPTER 3 ATRIOVENTRICULAR CONDUCTION ABNORMALITIES
CHAPTER 4 JUNCTIONAL RHYTHM
CHAPTER 5 ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA
CHAPTER 6 ATRIOVENTRICULAR REENTRANT TACHYCARDIAS
CHAPTER 7 ATRIAL TACHYCARDIA
CHAPTER 8 ATRIAL FLUTTER
CHAPTER 9 ATRIAL FIBRILLATION
CHAPTER 10 WIDE COMPLEX TACHYCARDIA
CHAPTER 11 VENTRICULAR TACHYCARDIA IN STRUCTURAL HEART DISEASE
CHAPTER 12 VENTRICULAR TACHYCARDIA IN THE ABSENCE OF STRUCTURAL
HEART DISEASE
CHAPTER 13 POLYMORPHIC VENTRICULAR TACHYCARDIA AND VENTRICULAR
FIBRILLATION IN THE ABSENCE OF STRUCTURAL HEART DISEASE
ix
1
IMPORTANT CONCEPTS
1
A normal 12-lead electrocardiogram (ECG) includes P, and intermittently changing P wave morphology from sinus
QRS, T, and sometimes the U waves (Figure 1-1). The P to nonsinus represents wandering atrial pacemakers (Figure
wave is generated by activation of the atria, the P-R segment 1-4). Frequent premature atrial complexes can provoke
represents the duration of atrioventricular (AV) conduc- atrial tachyarrhythmia (atrial tachycardia, atrial fibrillation,
tion, the QRS complex is produced by the activation of the and atrial flutter). Paroxysmal atrial fibrillation often is
two ventricles, and the ST-T wave reflects ventricular triggered by premature atrial complexes generated in the
recovery. Normal values for the various intervals and wave- muscle sleeves of one or more of pulmonary veins. Electri-
forms of the ECG are shown in Table 1-1. The range of cal isolation of these veins prevents the recurrence of atrial
normal values of these measurements reflects the sub- fibrillation (Figure 1-5). P waves can enlarge in right and
stantial interindividual variability related to (among other left atrial hypertrophy or enlargement. Sinus P waves have
factors) differences in age, gender, body habitus, heart ori- prolonged duration and generally have a low amplitude
entation, and physiology. In addition, significant differences after a maze surgery for atrial fibrillation (Figure 1-6).
in electrocardiographic patterns can occur in an individual’s
P-R INTERVAL AND P-R SEGMENT
ECGs recorded days, hours, or even minutes apart. These
intraindividual variations may be caused by technical issues
(e.g., changes in electrode position) or the biologic effects The P-R segment is usually the isoelectric region beginning
of changes in posture, temperature, autonomics, or eating with the end of the P wave to the onset of the QRS complex.
habits and may be sufficiently large to alter diagnostic The P-R interval is measured from the onset of the P wave
evidence for conditions such as chamber hypertrophy. to the onset of the QRS complex. The P-R interval repre-
sents the initiation of atrial depolarization to the initiation
P WAVE
of ventricular depolarization. It is the time taken by the
sinus impulse to travel to the ventricles by way of the atrium,
Normal P waves (duration = <110 ms and amplitude AV node, bundle of His, and bundle branches. A delay in
<0.25 mV) are generated in the sinus node, which depolar- any part of the conduction will prolong the P-R interval.
izes in the direction from right to left atria, as well as supe- Prolonged P-R interval results mostly from AV nodal
rior to inferior. P wave patterns in the precordial leads disease and His-Purkinje disease but can occur due to atrial
correspond to the direction of atrial activation wave fronts myopathy causing prolonged intra- or interatrial conduc-
in the horizontal plane. Atrial activation early in the P wave tion. His-Purkinje disease is almost always associated with
is over the right atrium and is oriented primarily anteriorly; a bundle branch block. PR prolongation (>200 ms) caused
later, it shifts posteriorly as activation proceeds over the left by AV nodal disease or severe His-Purkinje disease repre-
atrium. Therefore P waves are positive in lead I and inferior sents a potential substrate for various degrees of heart block
in leads. The P wave in the right precordial leads (V1 and, (see Chapter 3). A short P-R interval (<120 ms) can result
occasionally, V2) is upright or, often, biphasic, with an from enhanced AV nodal conduction (Figure 1-7), ven-
initial positive deflection followed by a later negative deflec- tricular preexcitation (Figure 1-8), or an atrial rhythm. Iso-
tion. In the more lateral leads, the P wave is upright and rhythmic AV dissociation can also falsely appear as short
reflects continual right to left spread of the activation fronts. P-R interval (Figure 1-9).
Variations in this pattern may reflect differences in path-
QRS WAVE
ways of interatrial conduction.
P waves with prolonged duration usually denote atrial
conduction abnormalities and occur in atrial enlargement Normal QRS complexes represent the depolarization of
or myopathy, which can be a substrate for reentrant atrial both ventricles (normal QRS duration = 60 ms to 100 ms).
tachycardia (Figure 1-2 and Table 1-2). Negative P waves This is represented by the beginning of the Q wave and end
in lead I represent lead arm reversal or dextrocardia of the S wave. Ventricular depolarization begins at the left
(Figure 1-3). Isolated dextrocardia is not a precursor for side of interventricular septum near the AV junction and
arrhythmias, but when dextrocardia is associated with con- progresses across the interventricular septum from left to
genital heart disease, atrial arrhythmias caused by atrial right. The impulse then travels simultaneously to both the
myopathy or scarring related to cardiac surgery can occur. ventricles endocardially by way of the right and left bundle
An abnormal P wave axis denotes an ectopic atrial rhythm, branches. It also progresses from the endocardial surface
3
4 CHAPTER 1 Important ConCepts
TABLE  1-1 Normal electrocardiogram parameters letters (q, r, s). Therefore notches in R, S, or QS waves can
be defined as qR, Rs, RSR, QrS, or rS patterns. The QRS
ECG WAVES OR INTERVALS DURATION IN MS morphology on a particular ECG lead depends on the sum
p wave duration <110 vector of depolarization toward or away from that lead.
Usually, the R waves are upright in limb leads and aug-
p-r interval 120 to <200 ms
mented limb leads except for lead aVR. A QS pattern in lead
Qrs duration <100 ms V1-V2 may represent normal myocardial depolarization,
but a Q wave in lead V3 represents myocardial scarring,
Qtc (corrected Q-t interval)* ≤440-450
usually caused by a septal myocardial infarction. QRS tran-
U wave† n/a sition is seen in lead V3-V4 with R wave amplitude larger
than S wave amplitude. R waves are upright in lead V5-V6
*the Qtc is traditionally reported in units of ms; however, the units  
because of a positive net vector toward these precordial
of the Qtc will vary with the formula used for the rate correction. the 
leads. Poor progression of R wave amplitude across the
commonly applied Bazett formula is a ratio of Q-t interval in ms to the 
square root of r-r interval in seconds. Fridericia formula: Qtc = Qt/3 √rr. precordial leads represents severe myocardial disease. It is
†U waves may normally be present in midprecordial leads in a few  seen in severe nonischemic and ischemic cardiomyopathy
individuals. the normal range of amplitude and duration is not well  with severely reduced left ventricular ejection fraction.
defined.
Q WAVES
The normal Q wave duration is <40 ms with amplitude less
TABLE  1-2 Right and left atrial enlargement than one fourth of the amplitude of the succeeding R wave.
Q waves in the baseline ECG of a patient with palpitations
RIGHT ATRIAL can be a clue to reentrant ventricular arrhythmias. Q waves
LEFT ATRIAL ABNORMALITY ABNORMALITY >40 ms may be due to scarring from a myocardial infarc-
p wave duration >120 ms in lead II peaked p waves with  tion. Noninfarction Q waves (pseudoinfarction pattern) are
amplitudes in lead II  also encountered in ventricular hypertrophy, fascicular
>0.25 mV (p pulmonale) blocks, preexcitation, cardiomyopathy, pneumothorax,
prominent notching of p wave,  prominent initial positivity  pulmonary embolus, amyloid heart disease, primary and
usually most obvious in lead II, with  in lead V or V >0.15 mV metastatic tumors of the heart, traumatic heart disease,
1 2
interval between notches of 0.40 ms  intracranial hemorrhage, hyperkalemia, pericarditis, early
(p mitrale) repolarization, and cardiac sarcoidosis.
ratio between the duration of the p  Increased area under initial 
wave in lead II and duration of the  positive portion of the p  INTRAVENTRICULAR CONDUCTION
pr segment >1.6 wave in lead V1 to  ABNORMALITIES
>0.06 mm-sec
Increased duration and depth of  rightward shift of mean p 
QRS prolongation can be due to the conduction system
terminal-negative portion of p wave  wave axis to more than +75°
abnormality resulting from a right bundle branch block
in lead V (p terminal force) so that 
1 (RBBB) or a left bundle branch block (LBBB). When the
area subtended by >0.04 mm-sec QRS duration is prolonged, often called wide (>120 ms),
Leftward shift of mean p wave axis  and its morphology does not qualify for a BBB, then it is
to between −30° and −45° called an interventricular conduction defect (IVCD). IVCD
can result from myocardial disease such as coronary artery
disease or cardiomyopathy. IVCD can also result from elec-
trolyte abnormalities such as hypokalemia or antiarrhy-
thmic drug therapy, mainly with the use of class I drugs
through the ventricular wall to the epicardial surface. The (sodium channel blockers), which prolong the conduction
normal Q wave is the first negative deflection of the QRS, velocity of the myocardial depolarizing waves (Figure 1-10).
which is not preceded by any R wave and represents inter- IVCD can represent a substrate for ventricular arrhythmias.
ventricular depolarization. The R wave is the first positive Other causes of a wide QRS include premature ventricular
deflection in the QRS complex. Subsequent positive deflec- complexes, ventricular preexcitation, or a paced ventricular
tion in the QRS above the baseline represents a bundle rhythm.
branch delay or block (BBB) called R′ (R prime). The S wave
FRAGMENTED QRS COMPLEXES
is the first negative deflection (below the baseline) after an
R wave. The QS wave is a QRS complex that is entirely a
negative wave without any positive deflection (R wave) Fragmented QRS (fQRS) is defined as the presence of one
above the baseline. The larger waves that form a major or more notches in the R wave or S wave without any BBB
deflection in QRS complexes are usually identified by in two contiguous leads. Fragmented wide QRS (f-WQRS)
uppercase letters (QS, R, S), whereas smaller waves with is defined as QRS duration >120 ms with >2 notches in the
amplitude less than the half of the major positive (R wave) R wave or the S wave in two contiguous leads. QRS frag-
or negative (S wave) deflection are denoted by lowercase mentation and Q waves represent myocardial infarction