Electrocardiography of Arrhythmias A Comprehensive
Review A Companion to Cardiac Electrophysiology 2nd
Edition
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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, Ruchi, Mohineesh, Kriti, and Avyukt
—MKD
To my wife, Joan,
and my children, Debra, Jeffrey, and David
—DPZ
PREFACE
Clinical cardiac electrophysiology continues to play a critically important role in the care of patients
of all ages. Being able to interpret the electrocardiogram (ECG) accurately is vital for their evaluation
and treatment. As more people live to older ages, arrhythmias become an ever-increasing component
to their health and well-being. We have thoroughly revised and updated this second edition to
facilitate learning the fundamental aspects of arrhythmia interpretation. Similar to the first edition,
we have designed the book for learners at all levels of training, including internists with an interest
in cardiology, trainees in cardiology and electrophysiology, and experienced cardiologists. This
volume also continues as a companion to the well-known text, Cardiac Electrophysiology: From
Cell to Bedside, soon in its eighth edition. We hope you find it a useful addition to help with your
ECG reading skills.
Mithilesh K. Das, MD
Douglas P. Zipes, MD
vii
CONTENTS
1 Important Concepts, 1
2 Sinus Node Dysfunction, 37
3 Atrioventricular Conduction Abnormalities, 61
4 Junctional Rhythm, 99
5 Atrioventricular Nodal Reentrant Tachycardia, 125
6 Atrioventricular Reentrant Tachycardias, 151
7 Atrial Tachycardia, 179
8 Atrial Flutter, 223
9 Atrial Fibrillation, 273
10 Wide Complex Tachycardia, 297
11 Ventricular Tachycardia in the Absence of Structural Heart
Disease, 329
12 Ventricular Tachycardia in Structural Heart Disease, 361
13 Polymorphic Ventricular Tachycardia and Ventricular Fibrillation in
the Absence of Structural Heart Disease, 411
Index, 463
ix
1
Important Concepts
A normal 12-lead electrocardiogram (ECG) includes P, QRS, T, and Sinus P waves have prolonged duration and generally have a low ampli-
sometimes the U waves (Fig. 1.1). The P wave is generated by activation tude after a maze surgery for atrial fibrillation (Fig. 1.6).
of the atria, the P-R segment represents the duration of atrioventricular
(AV) conduction, the QRS complex is produced by the activation of
P-R INTERVAL AND P-R SEGMENT
the two ventricles, and the ST-T wave reflects ventricular recovery.
Normal values for the various intervals and waveforms of the ECG are The P-R segment is usually the isoelectric region beginning with the
shown in Table 1.1. The range of normal values of these measurements end of the P wave to the onset of the QRS complex. The P-R interval is
reflects the substantial interindividual variability related to (among measured from the onset of the P wave to the onset of the QRS com-
other factors) differences in age, sex, body habitus, heart orientation, plex. The P-R interval represents the initiation of atrial depolarization
and physiology. In addition, significant differences in electrocardio- to the initiation of ventricular depolarization. It is the time taken by the
graphic patterns can occur in an individual’s ECGs recorded days, sinus impulse to travel to the ventricles by way of the atrium, AV node,
hours, or even minutes apart. These intraindividual variations may be bundle of His, and bundle branches. A delay in any part of the conduc-
caused by technical issues (e.g., changes in electrode position) or the tion will prolong the P-R interval. Prolonged P-R interval results
biologic effects of changes in posture, temperature, autonomics, or eat- mostly from AV nodal disease and His-Purkinje disease but can occur
ing habits, and may be sufficiently large to alter diagnostic evidence for due to atrial myopathy causing prolonged intra- or interatrial conduc-
conditions, such as chamber hypertrophy. tion. His-Purkinje disease is almost always associated with a bundle
branch block (BBB). PR prolongation (.200 ms) caused by AV nodal
disease or severe His-Purkinje disease represents a potential substrate
P WAVE
for various degrees of heart block (see Chapter 3). A short P-R interval
Normal P waves (duration equal to ,110 ms and amplitude ,0.25 mV) (,120 ms) can result from enhanced AV nodal conduction (Fig. 1.7),
are generated in the sinus node, which depolarizes in the direction from ventricular preexcitation (Fig. 1.8), or an atrial rhythm. Isorhythmic
right to left atria and superior to inferior. P wave patterns in the precor- AV dissociation can also falsely appear as short P-R interval (Fig. 1.9).
dial leads correspond to the direction of atrial activation wave fronts in
the horizontal plane. Atrial activation early in the P wave is over the
QRS WAVE
right atrium and is oriented primarily anteriorly; later, it shifts poster-
iorly as activation proceeds over the left atrium. Therefore P waves are Normal QRS complexes represent the depolarization of both ventricles
positive in lead I and inferior in leads. The P wave in the right precordial (normal QRS duration 5 60120 ms). This is represented by the
leads (V1 and, occasionally, V2) is upright or, often, biphasic, with an beginning of the Q wave and end of the S wave. Ventricular depolariza-
initial positive deflection followed by a later negative deflection. In the tion begins at the left side of the interventricular septum near the AV
more lateral leads, the P wave is upright and reflects continual right to junction and progresses across the interventricular septum from left to
left spread of the activation fronts. Variations in this pattern may reflect right. The impulse then travels simultaneously to both the ventricles
differences in pathways of interatrial conduction. endocardially by way of the right and left bundle branches. It also pro-
P waves with prolonged duration usually denote atrial conduction gresses from the endocardial surface through the ventricular wall to the
abnormalities and occur in atrial enlargement or myopathy, which can epicardial surface. The normal Q wave is the first negative deflection of
be a substrate for reentrant atrial tachycardia (Fig. 1.2 and Table 1.2). the QRS, which is not preceded by any R wave and represents interven-
Negative P waves in lead I represent lead arm reversal or dextrocardia tricular depolarization. The R wave is the first positive deflection in the
(Fig. 1.3). Isolated dextrocardia is not a precursor for arrhythmias, but QRS complex. Subsequent positive deflection in the QRS above the base-
when dextrocardia is associated with congenital heart disease, atrial line represents a bundle branch delay or bundle branch block (BBB)
arrhythmias caused by atrial myopathy or scarring related to cardiac called R0 (R prime). The S wave is the first negative deflection (below the
surgery can occur. An abnormal P wave axis denotes an ectopic atrial baseline) after an R wave. The QS wave is a QRS complex that is entirely a
rhythm, and intermittently changing P wave morphology from sinus to negative wave without any positive deflection (R wave) above the baseline.
nonsinus represents wandering atrial pacemakers (Fig. 1.4). Frequent The larger waves that form a major deflection in QRS complexes are
premature atrial complexes can provoke atrial tachyarrhythmia (atrial usually identified by uppercase letters (QS, R, S), whereas smaller waves
tachycardia, atrial fibrillation, and atrial flutter). Paroxysmal atrial fibril- with amplitude less than the half of the major positive (R wave) or
lation often is triggered by premature atrial complexes generated in the negative (S wave) deflection are denoted by lowercase letters (q, r, s).
muscle sleeves of one or more pulmonary veins. Electrical isolation of Therefore notches in R, S, or QS waves can be defined as qR, Rs, RSR,
these veins prevents the recurrence of atrial fibrillation (Fig. 1.5). P QrS, or rS patterns. The QRS morphology on a particular ECG lead
waves can enlarge in right and left atrial hypertrophy or enlargement. depends on the sum vector of depolarization toward or away from that
1
2 CHAPTER 1 Important Concepts
due to scarring from a myocardial infarction. Noninfarction Q waves
(pseudoinfarction pattern) are also encountered in ventricular
hypertrophy, fascicular blocks, preexcitation, cardiomyopathy, pneu-
QRS mothorax, pulmonary embolus, amyloid heart disease, primary and
metastatic tumors of the heart, traumatic heart disease, intracranial
hemorrhage, hyperkalemia, pericarditis, early repolarization, and car-
diac sarcoidosis.
T
P Q J point
U
INTRAVENTRICULAR CONDUCTION
ABNORMALITIES
P-R interval QRS prolongation can be because of the conduction system abnormal-
ity resulting from a right bundle branch block (RBBB) or a left bundle
QRS interval branch block (LBBB). When the QRS duration is prolonged, often
called wide ( . 120 ms), and its morphology does not qualify for a BBB,
then it is called an interventricular conduction defect (IVCD). IVCD
can result from myocardial disease, such as coronary artery disease or
Q-T interval
cardiomyopathy. IVCD can also result from electrolyte abnormalities,
such as hypokalemia or antiarrhythmic drug therapy, mainly with the
Fig. 1.1 Normal QRS waves and baseline intervals. use of class I drugs (sodium channel blockers), which prolong the
conduction velocity of the myocardial depolarizing waves (Fig. 1.10).
IVCD can represent a substrate for ventricular arrhythmias. Other
TABLE 1.1 Normal Electrocardiogram causes of a wide QRS include premature ventricular complexes, ventri-
Parameters cular preexcitation, or a paced ventricular rhythm.
Electrocardiogram Waves
or Intervals Duration in MS FRAGMENTED QRS COMPLEXES
P wave duration ,110 Fragmented QRS is defined as the presence of one or more notches in
P-R interval 120 to ,200 ms the R wave or S wave without any BBB in two contiguous leads.
Fragmented wide QRS is defined as QRS duration greater than 120 ms
QRS duration ,100 ms with 2 or more notches in the R wave or the S wave in two contiguous
QTc (corrected Q-T interval) a
#460 for men and #470 for women leads. QRS fragmentation and Q waves represent myocardial infarction
scarring and can indicate a substrate for reentrant ventricular arrhyth-
b
U wave N/A mias (Figs. 1.111.14).
N/A, Not applicable.
a
The QTc is traditionally reported in units of ms; however, the units of the BUNDLE BRANCH BLOCK AND FASCICULAR BLOCKS
QTc will vary with the formula used for the rate correction. The commonly
applied Bazett formula is a ratio of Q-T interval in ms to the square root of Conduction block or delay in one of the bundle branches results in the
R-R interval in seconds. Fridericia formula: QTc 5 QT/3 ORR. depolarization of the corresponding ventricle by way of the contralat-
eral bundle (Table 1.3). The RBBB has rSR0 pattern in lead V1-V2,
b
U waves may normally be present in midprecordial leads in a few
individuals. The normal range of amplitude and duration is not well whereas LBBB has rSR0 pattern in lead V6 and lead I (Figs. 1.151.17).
defined. The QRS duration between 100 ms and less than 120 ms is called
incomplete BBB, and greater than 120 ms is called a complete BBB.
lead. Usually, the R waves are upright in limb leads and augmented limb Narrow QRS at baseline and a physiologic delay in one of the bundle
leads except for lead aVR. A QS pattern in lead V1-V2 may represent nor- branches at higher heart rates can cause BBB and is called ventricular
mal myocardial depolarization, but a Q wave in lead V3 represents myo- aberrancy (see Chapter 6). A wide complex tachycardia is more com-
cardial scarring, usually caused by a septal myocardial infarction. QRS monly a ventricular tachycardia but can also be a supraventricular
transition is seen in lead V3-V4 with R wave amplitude larger than S tachycardia with BBB or ventricular aberrancy.
wave amplitude. R waves are upright in lead V5-V6 because of a positive
net vector toward these precordial leads. Poor progression of R wave
MULTIFASCICULAR BLOCK
amplitude across the precordial leads represents severe myocardial dis-
ease. It is seen in severe nonischemic and ischemic cardiomyopathy with Conduction delay in any two fascicles is called a bifascicular block, and
severely reduced left ventricular ejection fraction. delay in all three fascicles is termed a trifascicular block (Table 1.4). The
term bilateral bundle branch block has been used to refer to concomi-
tant conduction abnormalities in both the left and right bundle branch
Q WAVES
systems. Trifascicular block involves conduction delay in the right bun-
The normal Q wave duration is less than 40 ms with amplitude less dle branch plus delay in the main left bundle branch or in both the left
than one-fourth of the amplitude of the succeeding R wave. Q waves in anterior and the left posterior fascicles.
the baseline ECG of a patient with palpitations can be a clue to Rate-dependent conduction block or ventricular aberrancy, BBB,
reentrant ventricular arrhythmias. Q waves more than 40 ms may be fascicular block, or IVCD can occur with changes in the heart rate.
CHAPTER 1 Important Concepts 3
Fig. 1.2 Biatrial enlargement in a 32-year-old patient with complex congenital heart disease with pulmonary atresia, double inlet ventricle, and
multiple cardiac shunts (A). Lead II shows tall P waves greater than 0.25 mV, and lead V1 shows deep inverted T waves. The patient suffered from
atrial arrhythmias. (B) Biatrial enlargement with left bundle branch block in a patient with nonischemic dilated cardiomyopathy with severely
reduced left ventricular systolic function.
TABLE 1.2 Right and Left Atrial Enlargement
Left Atrial Abnormality Right Atrial Abnormality
P wave duration .120 ms in lead II Peaked P waves with amplitudes in lead II .0.25 mV (P pulmonale)
Prominent notching of P wave, usually most obvious in lead II, with Prominent initial positivity in lead V1 or V2 .0.15 mV
interval between notches of 0.40 ms (P mitrale)
Ratio between the duration of the P wave in lead II and duration of the Increased area under initial positive portion of the P wave in lead V1 to
PR segment .1.6 .0.06 mm-sec
Increased duration and depth of terminal-negative portion of P wave in Rightward shift of mean P wave axis to more than 175
lead V1 (P terminal force) so that area subtended by .0.04 mm-sec
Leftward shift of mean P wave axis to between 230 and 245
4 CHAPTER 1 Important Concepts
Fig. 1.3 Electrocardiogram showing inverted P and QRS waves in lead I along with poor progression of R wave. This is due to dextrocardia. The
arm lead reversal is also associated with similar P and QRS axis in lead I, but the QRS progression in precordial leads is unaffected.
1. Ashman phenomenon: The duration of the refractory period of the point elevation. The amplitude of the normal J point and ST segment
ventricular myocardium is a function primarily of the immediately varies with race, sex, autonomic input, and age. The upper limits of J
preceding cycle length(s). If the preceding cycle length is long, the point elevation in leads V2 and V3 are 0.2 mV for men older than 40
refractory period of the subsequent QRS complex is long and may years, 0.25 mV for men younger than 40 years, and 0.15 mV for
conduct with BBB aberrancy (Ashman phenomenon) as part of a women. In other leads the accepted upper limit is 0.1 mV.
long cycleshort cycle sequence, often when there is an abrupt The J wave can be prominent as a normal variant called early repo-
prolongation of the immediately preceding cycle. The RBBB larization (Figs. 1.24 and 1.25). However, the incidence of early repo-
aberrancy is more common than LBBB aberrancy because the larization abnormality in the inferolateral leads is higher in patients
refractory period of the right bundle is usually longer than that of who were resuscitated after sudden cardiac death, and therefore it may
the left bundle at slower heart rates (Fig. 1.18). not always be benign, as was previously believed. In addition, the J
2. Acceleration (tachycardia)-dependent block or conduction delay: It is wave can be seen in systemic hypothermia (Osborn wave), Brugada
manifest as either RBBB or LBBB, which occurs when the heart rate pattern, coronary artery disease, and electrolyte abnormalities and dur-
exceeds a critical value. At the cellular level, this aberration is the result ing vagal stimulation. Its origin has been related to a prominent notch
of encroachment of the impulse on the relative refractory period (phase 1) of the action potentials on the epicardium but not on the
(sometime during phase 3 of the action potential) of the preceding endocardium (Figs. 1.261.28).
impulse, which results in slower conduction (Figs. 1.191.23).
3. Deceleration (bradycardia)-dependent block or conduction delay: It
U WAVE
occurs when the heart rate falls below a critical level. It is thought to
be due to abnormal phase 4 depolarization of cells so that activation In some patients the T wave can be followed by an additional low-
occurs at reduced resting potentials. Deceleration-dependent block is amplitude wave known as the U wave. This wave, usually less than
less common than acceleration-dependent block and usually occurs 0.1 mV in amplitude, normally has the same polarity as the preceding
in the setting of a significant conduction system disease (Fig. 1.23). T wave and is best seen in anterior precordial leads. It is most often
seen at slow heart rates. Its electrophysiologic basis is uncertain; it may
be caused by the late repolarization of the Purkinje fibers, by the long
FASCICULAR BLOCK action potential of midmyocardial M cells, or by delayed repolarization
Fascicular block is an abnormal delay or conduction block in one of the in areas of the ventricle that undergo late mechanical relaxation.
fascicles of the LBBB. This alters ventricular activation, and therefore Prominent U waves can be seen in hypokalemia (discussed later).
the axis of the QRS is altered. Isolated fascicular block (without any Inverted U waves are a sign of coronary ischemia.
BBB) does not prolong the QRS significantly. Left anterior fascicular
block is associated with qR pattern in lead aVL, QRS axis between
ST-T WAVES
245 and 290 , and the time to peak R wave in aVL 45 ms or more.
Left posterior fascicular block is associated with a qR pattern in lead III Normal ST segment is almost always isoelectric to the PR and TP seg-
and aVF, rS pattern in lead I and aVL, and QRS axis between 190 and ments. ST segment elevation can be defined morphologically as cov-
1180 . Other causes of QRS wave changes similar to that of left poster- ing, concavity upward, or downsloping. ST horizontal or coving
ior fascicular block include right ventricular hypertrophy and lateral segment elevation occurs in acute myocardial infarction, coronary
wall myocardial infarction. vasospasm, and left ventricular aneurysm (Box 1.1). ST segment ele-
vation with concavity upward is seen in acute pericarditis. Coved or
saddleback ST segment elevation with incomplete RBBB is called a
J POINT AND J WAVE
Brugada pattern ECG. Persistence of juvenile pattern of T wave
The J point is the junction between the end of QRS and initiation of the inversion in precordial adults is encountered in 1% to 3% of the
ST segment. A J wave is a dome- or hump-shaped wave caused by J population.
CHAPTER 1 Important Concepts 5
Fig. 1.4 Wandering atrial pacemaker. (A) Electrocardiogram depicts intermittent change in P wave morphology from sinus rhythm to low atrial
rhythm (inverted P waves in lead II, arrows). (B) Electrocardiogram shows P wave morphology and axis during sinus rhythm. Wandering atrial
pacemaker usually does not denote atrial pathology; however, this patient later developed atrial flutter with 2:1 atrioventricular block (C).
When ST segment or T wave changes (or both) occur without any depolarization and repolarization. Ventricular depolarization, and there-
cardiac pathology or abnormal physiologic state, they are called non- fore repolarization, does not occur instantaneously. Electrophysiologically,
specific ST-T changes. This includes slight ST depression or T wave the Q-T interval is therefore a summation of action potentials in
inversion or T wave flattening. both ventricles. It is measured from the onset of the QRS to the
end of the T wave. The Q-T interval duration will vary from lead
to lead in a normal ECG by as much as 50 to 60 ms. The difference
Q-T INTERVAL
between the longest and shortest Q-T interval is called Q-T
The Q-T interval extends from the onset of the QRS complex to the dispersion. Accurately measuring the Q-T interval is challenging for
end of the T wave. Thus it includes the total duration of ventricular several reasons, including identifying the beginning of the QRS
6 CHAPTER 1 Important Concepts
Sinus beat
APC Atrial fibrillation
Sinus rhythm
Fig. 1.5 Frequent atrial premature complexes (APCs) initiating atrial fibrillation in a 40-year-old male patient. Frequent APCs, mostly originating from
pulmonary veins, can trigger focal atrial fibrillation. (A) Electrocardiogram shows frequent monomorphic APCs with right bundle branch block
aberrancy initiating a short run of atrial tachycardia. The APC was mapped to be originating from the right superior pulmonary vein. (B) APC was
mapped by a circular decapolar catheter (Lasso 1,2 to Lasso 9,10) and an ablation catheter (Abl D and Abl P) placed at the ostium of the pulmonary
vein. (C) These APCs repeatedly initiated atrial fibrillation. All these rapid focal discharges in the right pulmonary veins do not reach the left atrium,
as shown by the coronary sinus recording (CS 1,2 [distal] to CS 9,10 [proximal]). Electrical isolation of the right superior pulmonary vein during
catheter ablation is confirmed because these focal discharges are still present in the pulmonary vein during the sinus rhythm but do not reach the
left atrium; therefore the initiation atrial fibrillation is prevented. Arrows indicate atrial premature complexes.
CHAPTER 1 Important Concepts 7
Fig. 1.6 Low voltage and prolonged P waves in a patient with a history of maze procedure for atrial fibrillation (A). (B) Patient developed atrial
flutter 2 years after the procedure. Flutter waves are positive in inferior leads, negative in lead aVR and aVL, and isoelectric/negative in V1. Flutter
circuit was mapped at the right superior pulmonary vein ostium during electrophysiology study.
Fig. 1.7 Electrocardiogram showing short P-R interval with no evidence of preexcitation. This is called enhanced atrioventricular nodal conduction
because of the minimum normal delay at the atrioventricular nodal level for the atrial impulse to reach the ventricle by way of the His-Purkinje
system. This is not a precursor of arrhythmia but can conduct impulses rapidly from the atria to the ventricles during an atrial arrhythmia.
8 CHAPTER 1 Important Concepts
B
Fig. 1.8 Short P-R interval caused by preexcitation in a 19-year-old female patient. Electrocardiogram shows a short P-R interval of 80 ms resulting
from preexcitation (negative delta waves in lead V1 and inferior leads and positive delta waves in lead I and aVL) over a right posteroseptal
accessory pathway (A) that was successfully ablated. The P-R interval normalized after the ablation (B).
complex and end of the T wave; determining which lead(s) to use; Because the Bazett correction exaggerates the correction at faster
and adjusting the measured interval for rate, QRS duration, and heart rates and undercorrects at slower heart rates, the Fridericia
sex. The presence of U waves also complicates the measurement. correction is often preferred. It uses cube root of R-R interval
Q-T interval should be measured in the lead at which it is longest, instead of square root of R-R interval used in Bazett formula
and without a prominent U wave. In automated electrocardio- (QTc 5 Q-T/ 3 ORR).
graphic systems, the interval is typically measured from a compo-
site of all leads, with the interval beginning with the earliest onset
LEFT AND RIGHT VENTRICULAR HYPERTROPHY
of the QRS in any lead and ending with the latest end of the T wave
in any lead. ECG manifestation of left ventricular hypertrophy (LVH) includes
The Q-T interval changes with heart rates, shorter at faster increased amplitude of the QRS complex. R waves in lateral leads (I,
heart rates and longer at slower ones. Therefore numerous formulas aVL, V5, and V6) and S waves in right precordial leads are increased in
have been proposed to correct the measured Q-T interval for this LVH, whereas ST-T segment changes in LVH are varied. The common
rate effect to a rate of 60 bpm. The Bazett formula is commonly findings are downsloping ST segment from a depressed J point and
used in the clinical practice. The corrected Q-T interval (QTc) is asymmetrically inverted T waves. Apart from QRS wave changes, ven-
measured by the ratio of Q-T interval in seconds and the root square tricular hypertrophy is also associated with atrial abnormalities
of the R-R interval in seconds (QTc [ms] 5 Q-T/ ORR [sec]). (Table 1.5 and Box 1.2).
CHAPTER 1 Important Concepts 9
B
Fig. 1.9 Electrocardiogram depicting short P-R interval with P waves extending into the QRS waves in the first three sinus complexes followed by
short P-R interval (A). It is an isorhythmic atrioventricular dissociation. (B) Electrocardiogram showing normal sinus rhythm of the same patient with
a normal P-R interval of 164 ms.
chronic obstructive lung disease, and severe myopathy, such as cardiac
RIGHT-SIDED PRECORDIAL LEAD PLACEMENT
amyloidosis. Cardiac amyloidosis is a substrate for conduction block or
Right-sided lead placement is needed when dextrocardia or right ven- ventricular arrhythmias.
tricular infarction is suspected. In acute right ventricular infarction,
V4R shows ST elevation. Dextrocardia and arm reversal is suspected
when the P wave is negative in lead I. However, in dextrocardia, the
CORONARY ARTERY DISEASE
QRS morphology of the precordial leads shows poor progression of R Coronary artery disease is the second most common cause of con-
waves, whereas in arm lead reversal precordial progression of R wave is duction system disease and the most common cause of ventricular
unchanged. In dextrocardia, ECG placement can be corrected when the arrhythmias. The ECG plays a major role in the diagnosis of acute
left arm lead is placed on the right arm, the right arm lead is placed on and chronic coronary artery disease. ECG changes result from depo-
the left arm, and the V1 through V6 leads are placed in the V1, V2, and larization or repolarization abnormalities (or both). Acute ST eleva-
V3R through V6R positions. When Brugada syndrome is suspected tion myocardial infarction (STEMI) may be associated with serial
and the typical coving pattern of ST-T segment is present but J point changes: transient hyperacute (tall) T waves, ST elevation in two con-
elevation is less than 2 mm in a routine ECG, precordial leads V1 and tiguous leads, and later abnormal Q waves in two contiguous leads.
V2 can be placed in third or second intercostal spaces, which may elicit Non-ST elevation myocardial infarction (NSTEMI) is more difficult
typical Brugada pattern with more than 2 mm J point elevation and to diagnose, and the diagnosis depends on the elevation of cardiac
coved pattern spontaneously or with the use of a class I antiarrhythmic biomarkers. ECG signs of NSTEMI include T wave inversion, ST
drug. depression, and fragmentation of the QRS waves in two contiguous
leads. Atrial arrhythmias, such as atrial fibrillation, can occur during
an acute myocardial infarction (MI). Bifascicular block, when it
GENERALIZED LOW VOLTAGE
occurs with anterior MI, carries a poor prognosis. Complete heart
Generalized low voltage is defined when the amplitude of the QRS block during anterior MI also carries a poor prognosis because it
complexes in precordial leads is less than 1 mV and in the limb leads represents a large infarction with an extensive involvement of
are ,0.5 mV. This is commonly present in obesity, pericardial effusion, His-Purkinje system. AV block with an inferior MI usually results
10 CHAPTER 1 Important Concepts
Fig. 1.10 (A) Electrocardiogram (ECG) of a 59-year-old male patient with ischemic cardiomyopathy shows sinus rhythm with a long P-R interval
(270 ms) and intraventricular conduction delay (QRS duration 5 156 ms). (B) ECG of the same patient after 3 months shows long P-R interval, left
bundle branch block, and right axis deviation suggestive of a multifascicular block. (C) ECG showing wide complex tachycardia that is an atrial
tachycardia left bundle branch block with further prolongation of QRS waves.
CHAPTER 1 Important Concepts 11
III aVF
Fig. 1.11 (A) Fragmented QRS (fQRS) with inferior scar. fQRS is a sign of myocardial infarction. (B) fQRS (arrow) in lead III, and aVF signifies
inferior myocardial scar. (C) Electrocardiogram of the same patient shows a wide complex tachycardia, which is a ventricular tachycardia arising
from the inferoposterior wall of the left ventricle.
from a high vagal tone or ischemia to the AV nodal artery and gener- shows the baseline ECG showing fragmented QRS inferior leads,
ally carries a good prognosis (Fig. 1.29). Polymorphic ventricular which represents myocardial scar.
tachycardia and ventricular fibrillation can also be the presenting
manifestation of an acute MI (Fig. 1.30). Repetitive monomorphic
QRS ALTERNANS AND T WAVE ALTERNANS
idioventricular rhythm is encountered during the reperfusion phase
of MI (reperfusion arrhythmia) (Fig. 1.31). Sinus node dysfunction Beat-to-beat variation of QRS or T wave amplitude are called QRS and
and AV block can occur within the first few months of MI. Patients T wave alternans, respectively. QRS alternans can occur in pericardial
with a remote MI are at a risk for scar-related monomorphic, poly- tamponade, in severe myocardial disease, or during a supraventricular
morphic VT, and ventricular fibrillation (Fig. 1.32A). Fig. 1.32B or ventricular tachycardia (Figs. 1.33 and 1.34). Macroscopic T wave
