# 07 - 247 Electrocardiography

### 247 Electrocardiography

Fang LC et al: History, physical examination, and the virtual visit. 

An evidence-based approach, in Braunwald’s Heart Disease. A 
Textbook of Cardiovascular Medicine, 12th ed, RO Bonow et al  (eds). 
Philadelphia, Elsevier/Saunders, 2022, p. 123.
Jani V et al: The discerning ear: Cardiac auscultation in the era of 
artificial intelligence and telemedicine. Eur Heart J Digit Health 
2:456, 2021.
PART 6
Disorders of the Cardiovascular System
Ary L. Goldberger

Electrocardiography
An electrocardiogram (ECG or EKG) is a graphical representation 
of electrical activity generated by the heart. The signals, detected by 
means of metallic electrodes attached to the extremities and chest wall, 
are amplified and recorded by the electrocardiograph device. ECG leads 
are configured to display the instantaneous differences in electrical 
potentials between specific sets of electrodes. The utility of the ECG 
derives from its immediate availability as a noninvasive, inexpensive, 
and highly versatile test. In addition to its use in detecting arrhythmias, 
conduction disturbances, and myocardial ischemia/infarction, the 
ECG may reveal findings related to life-threatening metabolic distur­
bances, drug toxicities, and increased susceptibility to sudden cardiac 
arrest (see also Chaps. 317 and 420). The importance of electrocar­
diologic abnormalities in the diagnosis, prognosis, and management of 
muscular dystrophies and other hereditary neuromuscular diseases is 
discussed separately (see Chap. 360).
■
■ELECTROPHYSIOLOGIC BACKGROUND
Depolarization of the heart is the initiating event for cardiac contrac­
tion. The electrical currents that spread through the heart are produced 
by three components: cardiac pacemaker cells, specialized conduction 
tissue, and the heart muscle itself. The ECG records only the depolar­
ization (stimulation) and repolarization (recovery) electrical activity 
generated by the “working” atrial and ventricular myocardium (see also 
Chaps. 251 and 253).
The stimulus initiating the normal heartbeat originates in the 
sinoatrial (SA) node (Fig. 247-1), which possesses spontaneous auto­
maticity. Spread of the depolarization wave through the right and 
left atria induces contraction of these chambers. Next, the impulse 
LA
Sinoatrial (SA)
node
Ventricular
myocardium
AV junction
AV node
RA
His bundle
LV
Purkinje
fibers
RV
Left bundle
branch
Right bundle branch
Ventricular septum
FIGURE 247-1  Schematic of the cardiac conduction system. AV, atrioventricular; 
LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

stimulates specialized conduction tissues in the atrioventricular (AV) 
nodal and His-bundle areas; together, these two regions constitute the 
AV junction. The bundle of His bifurcates into two main divisions, 
the right and left bundle branches, which rapidly transmit depolariza­
tion wavefronts in a synchronous way to the right and left ventricu­
lar myocardium via the Purkinje fibers. The main left bundle fans 
out into left anterior and left posterior fascicular subdivisions. The 
depolarization wavefronts then spread through the ventricular wall, 
from endocardium to epicardium, triggering coordinated ventricu­
lar contraction. Since the cardiac depolarization and repolarization 
wavefronts have direction and magnitude, they can be represented 
by vectors.
■
■BASIC ECG WAVEFORMS AND INTERVALS
The ECG waveforms are labeled alphabetically, beginning with the P 
wave, which represents atrial depolarization (Fig. 247-2). The QRS 
complex represents ventricular depolarization; the ST-T-U complex 
(ST segment, T wave, and U wave) represents ventricular repolariza­
tion. The J point is the junction between the end of the QRS complex 
and the beginning of the ST segment. Atrial repolarization waveforms 
(ST-Ta) are usually too low in amplitude to be detected, but they may 
become apparent in acute pericarditis, atrial infarction, and AV heart 
block syndromes.
The QRS-T waveforms of the surface ECG correspond to sequential 
phases of simultaneously obtained ventricular action potentials, the 
intracellular recordings from single myocardial fibers (Chap. 251). 
The rapid upstroke (phase 0) of the action potential corresponds to 
the onset of QRS. The plateau (phase 2) corresponds to the isoelectric 
ST segment, and active repolarization (phase 3) corresponds to the 
inscription of the T wave. Factors that decrease the slope of phase 0 
by impairing the influx of Na+ (e.g., hyperkalemia and drugs such as 
flecainide) tend to increase QRS duration. Factors that prolong phase 
2 or 3 (e.g., amiodarone, hypocalcemia) increase the QT interval. In 
contrast, factors (e.g., hypercalcemia, digoxin) associated with short­
ening of ventricular repolarization duration abbreviate the QT. The 
hereditary short QT syndrome and its relationship to sudden cardiac 
arrest are discussed in Chap. 262.
The ECG is usually recorded on graph paper divided into a grid 
of 1-mm2 boxes. When the recording (sweep) speed is 25 mm/s, the 
smallest (1 mm) horizontal divisions correspond to 40 ms (0.04 s), 
with heavier lines at intervals of 200 ms (0.20 s). Vertically, the ECG 
graph measures the amplitude of a specific wave or deflection (1 mV = 
10 mm with standard calibration; the voltage criteria for hypertrophy 
mentioned below are given in millimeters). There are four major sets 
of ECG intervals: RR, PR, QRS, and QT/QTc (Fig. 247-2). The instan­
taneous heart rate (beats per minute) can be computed from the inter­
beat (RR) interval by dividing the number of large (0.20 s) time units 
QRS
T
P
ST
U
J
PR interval
QRS interval
QT interval
FIGURE 247-2  Basic ECG waveforms and intervals. Not shown is the RR interval, 
the time between consecutive QRS complexes.

between consecutive R waves into 300 or the number 
of small (40 ms) segments into 1500. The PR interval 
measures the time (normally 120–200 ms) between 
atrial and ventricular depolarization, which includes the 
physiologic delay imposed by stimulation of cells in the 
AV junction area. The QRS interval (normally 100–110 
ms or less) reflects the duration of ventricular depo­
larization. The QT interval subtends both ventricular 
depolarization and (primarily) repolarization times and 
varies inversely with the heart rate. A variety of formulas 
has been proposed for computing a rate-corrected QT 
interval, termed QTc, but without formal consensus. The 
classic “square root” formula (QTc = QT/√RR, computed 
in second units) has been criticized for systematic errors 
at both lower and higher heart rates. One alternative is 
the Framingham formula (given here for units of mil­
liseconds): QTc = QT + 0.154 (1000 – RR). The following 
upper normal limits (based visually on the longest QT) 
have been proposed: QTc of 460 ms in women and 450 ms in men. 
Lower limits are less well defined. Visual or electronic QT/QTc mea­
surements should be assessed in light of inherent limitations in their 
precise determination from standard ECGs waveforms.
Right
Left
A
FIGURE 247-3  The six frontal plane (A) and six horizontal plane (B) leads provide a threedimensional representation of cardiac electrical activity.
■
■ECG LEADS
The 12 conventional ECG leads are divided into two groups: six 
limb (extremity) leads and six chest (precordial) leads. The limb 
leads record potentials transmitted onto the frontal plane (Fig. 247-3A); 
the chest leads record potentials transmitted onto the horizontal 
plane (Fig. 247-3B).
The orientation and polarity of the frontal plane leads are repre­
sented on a hexaxial diagram (Fig. 247-4). The six chest leads are 
obtained by exploring electrodes as shown in Fig. 247-5.
Each lead is analogous to a different video camera angle “look­
ing” at the same events—atrial and ventricular depolarization and 
repolarization—from different spatial orientations. The 12-lead ECG 
can be supplemented with additional leads in special circumstances. 
For example, right precordial leads V3R to V6R are useful in detect­
ing evidence of acute right ventricular ischemia/infarction. Bedside 
monitors and ambulatory ECGs (e.g., Holter monitors, event recorders, 
patch electrode and other medical wearable devices) usually employ 
   
   
   
  
Le
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 d
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ia
is
–90°
–aVF
–60°
–III
ti
ax
on
–120°
–II
e 
m
e
tr
Ex
–150°
+aVR
–30°
+aVL
   
   
   
   
   
   
0°
+I
180°
–I
   
   
   
+30°
–aVR
+150°
–aVL
   
Ri
gh
t 
ax
s
+60°
+II
+90°
+aVF
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is
+120°
+III
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 d
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FIGURE 247-4  The frontal plane (limb or extremity) leads are represented on a 
hexaxial diagram. Each ECG lead has a specific spatial orientation and polarity. The 
positive pole of each lead axis (solid line) and the negative pole (hatched line) are 
designated by their angular position relative to the positive pole of lead I (0°). The 
mean electrical axis of the QRS complex is measured with respect to this display.

Posterior
Superior
CHAPTER 247
–
–
–
–
–
Right
Left
+
aVR
aVL
–
–––
+
+
V6
–
I
+
–
–
+
V5
Electrocardiography
+
+
+
+
+
+
+
V4
V3
V2
V1
II
III
aVF
B
Anterior
Inferior
only one or two modified leads. The standard ECG leads are config­
ured such that a positive (upright) deflection is recorded in a lead if a 
wave of depolarization spreads toward the positive pole of that lead, 
and a negative deflection is recorded if the wave spreads toward the 
negative pole. If the mean orientation of the depolarization vector is at 
right angles to a particular lead axis, a biphasic (equally positive and 
negative) deflection will be inscribed.
GENESIS OF THE NORMAL ECG
■
■P WAVE
The normal atrial depolarization vector is oriented downward and 
toward the subject’s left, reflecting the spread of depolarization from 
the sinus node to the right and then the left atrial myocardium. Since 
this vector points toward the positive pole of lead II and toward the 
negative pole of lead aVR, the sinus-generated P wave will be positive in 
lead II and negative in aVR. By contrast, activation of the atria from an 
ectopic pacemaker in the lower part of either atrium or in the AV junc­
tion region may produce retrograde P waves (negative in II, positive in 
aVR). The normal P wave in lead V1 may be biphasic with a positive 
component reflecting right atrial depolarization, followed by a small 
(<1 mm2) negative component reflecting left atrial depolarization.
■
■QRS COMPLEX
Normal ventricular depolarization proceeds as a rapid, continuous 
spread of activation wave fronts. This complex process can be divided 
V1
V2
V3R
V3
V4
V5
V6
V4R
FIGURE 247-5  The horizontal plane (chest or precordial) leads are obtained with 
electrodes in the locations shown. Additional posterior leads are sometimes placed 
on the same horizontal plane as V4 to facilitate detection of acute posterolateral 
infarction (V7, midaxillary line; V8, posterior axillary line; and V9, posterior scapular 
line). Right chest leads (V3R–V6R) may enhance detection of right ventricular 
involvement in the context of inferior infarction.

r
RV
LV

q
V6
V1
PART 6
Disorders of the Cardiovascular System
A
V1
R
r
RV
LV
V1
V6

q
B
S
–
–
–
–
–
–

+

V6
+
V5
+
+
+
+
V1
V2
V3
V4
C
FIGURE 247-6  Ventricular depolarization can be divided into two major phases, 
each represented by a vector. A. The first phase (arrow 1) denotes depolarization 
of the ventricular septum, beginning on the left side and spreading to the right. This 
process is represented by a small “septal” r wave in lead V1 and a small septal 
q wave in lead V6. B. Simultaneous depolarization of the left and right ventricles 
(LV and RV) constitutes the second phase. Vector 2 is oriented to the left and 
posteriorly, reflecting the electrical predominance of the LV. C. Vectors (arrows) 
representing these two phases are shown in reference to the horizontal plane 
leads. (Reproduced with permission from AL Goldberger et al: Goldberger’s Clinical 
Electrocardiography: A Simplified Approach, 10th ed. Philadelphia, Elsevier, 2024.)
into two major sequential phases, and each can be represented by a 
mean vector (Fig. 247-6). The first and shortest phase is depolarization 
of the interventricular septum, proceeding from the left to the right 
and anteriorly (vector 1). The second and major phase results from 
the simultaneous depolarization of the 
right and left ventricles (vector 2). This 
phase is normally dominated by the 
more massive left ventricle, so that vec­
tor 2 points leftward and posteriorly. 
Therefore, a right precordial lead (V1) 
will record this biphasic depolarization 
process with a small positive deflection 
(septal r wave) followed by a larger 
negative deflection (S wave). A left 
precordial lead, for example, V6, will 
record the same sequence with a small 
negative deflection (septal q wave) fol­
lowed by a relatively tall positive deflec­
tion (R wave). Intermediate leads show 
a relative increase in R-wave amplitude 
(normal R-wave progression) and a 
decrease in S-wave amplitude progress­
ing across the chest from right to left. 
The lead where the R and S waves are 
of about equal amplitude is referred to 
as the transition zone (usually V3 or V4) 
(Fig. 247-7).
aVR
I
II
III
FIGURE 247-7  Normal electrocardiogram from a healthy male subject. Sinus rhythm is present with a heart rate of 75 
beats per minute. PR interval is 160 ms; QRS interval (duration) is 80 ms; QT interval is 360 s; QTc (Framingham formula) 
is about 390 ms; the mean QRS axis is about +70°. The precordial leads show normal R-wave progression with the 
transition zone (R wave ≈ S wave) in lead V3.

The QRS pattern in the extremity leads may vary considerably 
from one normal subject to another depending on the electrical axis 
of the QRS, which describes the mean orientation of the QRS vector 
with reference to the six frontal plane leads. Normally, the QRS axis 
ranges from –30° to +100° (Fig. 247-4). An axis more negative than 
–30° is referred to as left axis deviation, and an axis more positive than 
+90 to +100° is referred to as right axis deviation. Left axis deviation 
may occur as a normal variant but is more commonly associated with 
left ventricular hypertrophy, a block in the anterior fascicle of the left 
bundle system (left anterior fascicular block or hemiblock), or inferior 
myocardial infarction. Right axis deviation also may occur as a normal 
variant (particularly in children and young adults), as a spurious find­
ing due to reversal of the left and right arm electrodes, or in conditions 
such as right ventricular overload (acute or chronic), lateral infarction, 
dextrocardia, left pneumothorax, and left posterior fascicular block.
■
■T WAVE AND U WAVE
Normally, the mean T-wave vector is oriented roughly concordant with 
the mean QRS vector (within about 45° in the frontal plane). Since 
depolarization and repolarization are electrically opposite processes, this 
normal QRS–T-wave vector concordance indicates that repolarization 
normally must proceed in the reverse direction from depolarization 
(i.e., from ventricular epicardium to endocardium). The normal U wave 
is a small, rounded deflection (≤1 mm) that follows the T wave and 
usually has the same polarity as the T wave. An abnormal increase in 
U-wave amplitude is most commonly due to hypokalemia or drugs (e.g., 
dofetilide, amiodarone, sotalol, quinidine). Very prominent U waves, as 
part of prolonged ventricular repolarization syndromes, are a marker of 
increased susceptibility to torsades de pointes (Chap. 253).
MAJOR ECG ABNORMALITIES
■
■CARDIAC ENLARGEMENT AND HYPERTROPHY
Right atrial overload (acute or chronic) may lead to an increase in 
P-wave amplitude (≥2.5 mm) (Fig. 247-8), previously referred to as 
“P-pulmonale.” Left atrial overload typically produces a biphasic P wave in 
V1 with a broad negative component or a broad (≥120 ms), often with 
a notched P wave in one or more limb leads (Fig. 247-8). This pattern, 
historically referred to as “P-mitrale,” may occur with interatrial con­
duction delays in the absence of actual atrial enlargement, leading to the 
more general designation of left atrial abnormality.
Right ventricular hypertrophy due to a sustained, severe pressure 
load (e.g., with pulmonic valve stenosis or certain pulmonary artery 
hypertension syndromes) is characterized by a relatively tall R wave 
in lead V1 (R ≥ S wave), usually with right axis deviation (Fig. 247-9); 
alternatively, there may be a qR pattern in V1 or V3R. ST depression 
and T-wave inversion in the right to mid-precordial leads are also 
V1
V4
V2
V5
aVL
V3
V6
aVF

LA
RA
V1
Normal
Right
Left
RA
LA
RA
RA
LA
LA
II
RA
RA
RA
V1
LA
LA
LA
FIGURE 247-8  Right atrial (RA) overload may cause tall, peaked P waves in the 
limb or precordial leads. Left atrial (LA) abnormality may cause broad, often 
notched P waves in the limb leads and a biphasic P wave in lead V1 with a prominent 
negative component representing delayed depolarization of the LA. (Reproduced 
with permission from MK Park, WG Guntheroth: How to Read Pediatric ECGs, 4th ed. 
St. Louis, Mosby/Elsevier, 2006.)
often present. This pattern, formerly called right ventricular “strain,” 
is attributable to repolarization abnormalities in acutely or chroni­
cally overloaded muscle. Prominent S waves may occur in the left 
lateral precordial leads. Right ventricular hypertrophy due to ostium 
secundum atrial septal defects, with the accompanying right ventricu­
lar volume overload, is commonly associated with an incomplete or 
complete right bundle branch block pattern in concert with a right­
ward QRS axis.
Main QRS vector
QRS in hypertrophy
V1
V6
V1
Normal
LVH
RVH
or
or
FIGURE 247-9  Left ventricular hypertrophy (LVH) increases the amplitude of 
electrical forces directed to the left and posteriorly. In addition, repolarization 
abnormalities may cause ST-segment depression and T-wave inversion in leads 
with a prominent R wave. Right ventricular hypertrophy (RVH) may shift the QRS 
vector to the right; this effect usually is associated with an R, RS, or qR complex in 
lead V1. T-wave inversions may be present in right precordial leads.

Acute cor pulmonale due to pulmonary thromboembolism 
(Chap. 290) or acute respiratory distress syndromes (e.g., COVID-19) 
may be associated with a normal ECG or a variety of abnormalities. 
Sinus tachycardia is the most common arrhythmia, although other 
tachyarrhythmias, such as atrial fibrillation or flutter, may occur. The 
QRS axis may shift to the right, sometimes in concert with the so-called 
S1Q3T3 pattern (prominence of the S wave in lead I and the Q wave 
in lead III, with T-wave inversion in lead III). Acute right ventricular 
dilation also may be associated with slow R-wave progression and ST-T 
abnormalities in V1 to V4 simulating acute anterior infarction. A right 
ventricular conduction disturbance may appear.

CHAPTER 247
Electrocardiography
Chronic cor pulmonale due to obstructive lung disease (Chap. 307) 
usually does not produce the classic ECG patterns of right ventricular 
hypertrophy noted above. Instead of tall right precordial R waves, 
emphysema is more typically associated with diminished r waves in 
right to mid-precordial leads (slow R-wave progression) due in part to 
downward displacement of the diaphragm and the heart. Low-voltage 
complexes are commonly present, owing to hyperaeration.
Multiple voltage criteria for left ventricular hypertrophy (Fig. 247-9) have 
been proposed based on the presence of tall left precordial R waves and 
deep right precordial S waves (e.g., SV1 + [RV5 or RV6] >35 mm). Repolar­
ization abnormalities (ST depression with T-wave inversions, formerly 
called the left ventricular “strain” pattern) may appear in leads with 
prominent R waves. However, prominent precordial voltages occur as 
a common normal variant, especially in athletic or young individu­
als. Left ventricular hypertrophy may increase limb lead voltage with 
or without increased precordial voltage (e.g., RaVL + SV3 >20 mm in 
women and >28 mm in men). The presence of left atrial abnormality 
increases the likelihood of underlying left ventricular hypertrophy in 
cases with borderline voltage criteria. Left ventricular hypertrophy 
often progresses to incomplete or complete left bundle branch block. 
The sensitivities of conventional voltage criteria for left ventricular 
hypertrophy are low in middle age to older adults and may be decreased 
further in obese persons and smokers, as well as with right bundle 
branch block. ECG evidence for left ventricular hypertrophy is a major 
noninvasive marker of increased risk of cardiovascular morbidity and 
mortality rates, including sudden cardiac death. However, because of 
false-positive and false-negative diagnoses, the ECG is of limited util­
ity in diagnosing atrial or ventricular enlargement. More definitive 
anatomic and functional information is provided by echocardiographic 
and cardiac magnetic resonance imaging studies (Chaps. 248 and A9).
V6
■
■BUNDLE BRANCH BLOCKS AND RELATED 
PATTERNS
Intrinsic impairment of conduction in either the right or the left bundle 
system (intraventricular conduction disturbances) leads to prolonga­
tion of the QRS interval. With complete bundle branch blocks, the 
widest QRS interval is ≥120 ms in duration; with incomplete blocks, the 
QRS interval is between about 110 and 120 ms. The QRS vector usually 
is oriented in the direction of the myocardial region where depolariza­
tion is delayed (Fig. 247-10). Thus, with right bundle branch block, the 
terminal QRS vector is oriented to the right and anteriorly (rSR′ in V1 
and qRS in V6, typically). Left bundle branch block alters both early 
and later phases of ventricular depolarization. The major QRS vector is 
directed to the left and posteriorly. In addition, the normal early left-toright pattern of septal activation is disrupted such that septal depolar­
ization proceeds from right to left as well. As a result, left bundle branch 
block generates wide, predominantly negative (QS) complexes in lead 
V1 and entirely positive (R) complexes in V6. Waveform patterns identi­
cal to those of left bundle branch block, preceded by a sharp (sometimes 
very low amplitude) spike, are seen in most cases of electronic right 
ventricular pacing due to the relative delay in left ventricular activation.
Bundle branch block may occur in a variety of conditions. In sub­
jects without structural heart disease, right bundle branch block is seen 
more commonly than left bundle branch block. Right bundle branch 
block also occurs with heart disease, both congenital (e.g., atrial septal 
defect) and acquired (e.g., valvular, ischemic). Left bundle branch block 
is often a marker of one of four underlying conditions associated with 
increased risk of cardiovascular morbidity and mortality rates: coronary

V6
V1
Normal
PART 6
Disorders of the Cardiovascular System
R′
R
r
RBBB
T
q
S
S
LBBB
T
FIGURE 247-10  Comparison of typical QRS-T patterns in right bundle branch block 
(RBBB) and left bundle branch block (LBBB) with the normal pattern in leads V1 and V6. 
Note the secondary T-wave inversions (arrows) in leads with an rSR′ complex with 
RBBB and in leads with a wide R wave with LBBB.
heart disease (frequently with impaired left ventricular function), hyper­
tensive heart disease, aortic valve disease (including after transcatheter 
aortic valve replacement), and cardiomyopathy. Bundle branch blocks 
may be chronic or intermittent. A bundle branch block may be raterelated, most commonly observed when the heart rate exceeds some 
critical value.
Bundle branch blocks and depolarization abnormalities second­
ary to artificial pacemakers not only affect ventricular depolariza­
tion (QRS) but also are characteristically associated with secondary 
repolarization (ST-T) abnormalities. With bundle branch blocks, the 

T wave is typically opposite in polarity to the last deflection of the QRS 
(Fig. 247-10). This discordance of the QRS–T-wave vectors is caused 
by the altered sequence of repolarization that occurs as a consequence 
of altered depolarization. In contrast, primary repolarization abnor­
malities are independent of QRS changes and are related instead to 
actual alterations in the electrical properties of the myocardial fibers 
themselves (e.g., in the resting membrane potential or action potential 
duration), not just to changes in the sequence of repolarization. Isch­
emia, electrolyte imbalance, and drugs such as digoxin all cause such 
primary ST–T-wave changes. Primary and secondary T-wave changes 
may coexist. For example, T-wave inversions in the right precordial 
leads with left bundle branch block or in the left precordial leads with 
right bundle branch block may be important markers of underlying 
ischemia or other abnormalities. A distinctive abnormality simulating 
right bundle branch block with ST-segment elevations in the right chest 
leads is seen with the Brugada pattern (Chap. 262).
Partial blocks in the left bundle system (left anterior or posterior 
fascicular blocks; formerly called hemiblocks) generally do not prolong 
ST
V5
ST
A
B
FIGURE 247-11  Acute ischemia causes a current of injury. A. With predominant subendocardial ischemia, the resultant ST vector will be directed toward the inner layer of 
the affected ventricle and the ventricular cavity. Overlying leads therefore will record ST depression. B. With ischemia involving the outer ventricular layer (transmural or 
epicardial injury), the ST vector will be directed outward. Overlying leads will record ST elevation.

the QRS duration substantially. Instead, they are associated with shifts 
in the frontal plane QRS axis (leftward or rightward, respectively). Left 
anterior fascicular block (QRS axis more negative than –45°) is prob­
ably the most common cause of marked left axis deviation in adults. 
In contrast, left posterior fascicular block (QRS axis more rightward 
than +110–120°) is extremely rare as an isolated finding and requires 
exclusion of other factors causing right axis deviation. Intraventricular 
conduction delays also can be caused by factors extrinsic (toxic) to 
the conduction system that slow ventricular conduction, particularly 
hyperkalemia or drugs (e.g., class 1 antiarrhythmic agents, tricyclic 
antidepressants, phenothiazines). Prolongation of QRS duration does 
not necessarily indicate a conduction delay but may be due to preexci­
tation of the ventricles via a bypass tract, as in Wolff-Parkinson-White 
(WPW) patterns (Chap. 256) and related variants.
■
■MYOCARDIAL ISCHEMIA AND INFARCTION
(See also Chap. 286) The ECG is central to the diagnosis of acute 
and chronic ischemic heart disease. Ischemia exerts complex timedependent effects on the electrical properties of myocardial cells. 
Severe, acute ischemia lowers the resting membrane potential and 
shortens the duration of the action potential. Such changes cause 
a voltage gradient between normal and ischemic zones. As a con­
sequence, current flows between those regions. These currents of 
injury are represented on the surface ECG by deviation of the ST 
segment (Fig. 247-11). When the acute ischemia is transmural, the 
ST vector usually is shifted in the direction of the outer (epicardial) 
layers, producing ST elevations and sometimes, in the earliest stages of 
ischemia, tall, positive so-called hyperacute T waves over the ischemic 
zone. With ischemia confined primarily to the subendocardium, the ST 
vector typically shifts toward the subendocardium and ventricular cav­
ity, so that overlying (e.g., anterior precordial) leads show ST-segment 
depression (with ST elevation in lead aVR). Multiple factors affect the 
amplitude of acute ischemic ST deviations. Profound ST elevation or 
depression in multiple leads usually indicates very severe ischemia. The 
division of acute myocardial infarction due to obstructive coronary 
artery disease into ST-segment elevation and non-ST elevation types 
is useful since the consistent efficacy of emergency (minutes to hours) 
reperfusion therapy is limited to the former group. Indications for 
acute reperfusion therapy in non-ST elevation myocardial infarction 
are a focus of ongoing investigation (Chap. 285). Takotsubo syndrome, 
as well as other causes of myocardial infarction without atherosclerotic 
coronary disease, can simulate the patterns of acute or evolving ST-seg­
ment elevation or non-ST-segment elevation infarction (Chap. 285).
The ECG leads are usually more helpful in localizing regions of ST 
elevation than non-ST elevation ischemia. For example, acute transmu­
ral anterior (including apical and lateral) wall ischemia is reflected by ST 
elevations or increased T-wave positivity in one or more of the precor­
dial leads (V1–V6) and leads I and aVL. Inferior wall ischemia produces 
changes in leads II, III, and aVF. “Posterior” wall ischemia (almost 
always associated with lateral or inferior involvement) may be indirectly 
recognized by reciprocal ST depressions in leads V1 to V3 (thus constitut­
ing an ST elevation “equivalent” acute coronary syndrome). Acute right 
ventricular ischemia usually produces ST elevations in right-sided chest 
leads (Fig. 247-5). When ischemic ST elevations occur as the earliest 
sign of acute infarction, they typically are followed within a period 
ranging from hours to days by evolving T-wave inversions and often by 
Q waves occurring in the same lead distribution. Reversible transmural 
ST
ST
V5

V1
V2
V4
V5
V6
V3
FIGURE 247-12  Severe anterior wall ischemia (with or without infarction) may cause prominent T-wave inversions in the precordial leads and in leads I and aVL. This 
pattern (sometimes referred to as the Wellens T wave sign) is usually associated with a high-grade stenosis of the left anterior descending coronary artery.
ischemia, for example, due to coronary vasospasm (Prinzmetal’s angina) 
may cause transient ST-segment elevations without development of Q 
waves. Depending on the severity and duration of ischemia, ischemic 
ST elevations may resolve completely in minutes or be followed by 
T-wave inversions that persist for hours or even days. Patients with 
ischemic chest pain who present with deep T-wave inversions in mul­
tiple precordial leads (e.g., V1–V4, and sometimes I and aVL) with or 
without cardiac enzyme elevations typically have severe obstruction in 
the left anterior descending coronary artery (Fig. 247-12).
With infarction, depolarization (QRS) changes often accompany 
repolarization (ST-T) abnormalities. Necrosis of sufficient myocardial 
tissue may lead to decreased R-wave amplitude or abnormal Q waves 
(even in the absence of transmural ischemia) in the anterior or inferior 
leads (Fig. 247-13). Abnormal Q waves were once considered markers 
of transmural myocardial infarction, whereas subendocardial infarcts 
were thought not to produce Q waves. However, transmural infarcts 
may occur without Q waves, and subendocardial (nontransmural) 
infarcts may be associated with Q waves. Therefore, evolving or chronic 
infarcts are more appropriately classified as “Q-wave” or “non-Q-wave” 
(Chap. A7). Loss of depolarization forces due to posterior or lateral 
infarction may cause reciprocal increases in R-wave amplitude in leads 
V1 and V2 without diagnostic Q waves in any of the conventional leads. 
(Additional leads V7–V9 may show acute changes.) In the weeks and 
months after infarction, these ECG changes may persist or begin to 
resolve. Complete normalization of the ECG after Q-wave infarction is 
uncommon but may occur, particularly with smaller infarcts. In con­
trast, ST-segment elevations that persist for several weeks or more after 
a Q-wave infarct usually correlate with a severe underlying wall motion 
disorder, although not necessarily a frank ventricular aneurysm.
A
ECG sequence with anterior ST-elevation/Q-wave infarction
I
II
III
Acute
Evolving
ECG sequence with inferior ST-elevation/Q-wave infarction
B
I
II
III
Acute
Evolving
FIGURE 247-13  Sequence of depolarization and repolarization changes with acute and evolving anterior (A) and (B) inferior ST-elevation/Q-wave infarctions. With 
anterior infarcts, ST elevation in leads I and aVL and the precordial leads may be accompanied by reciprocal ST depressions in leads II, III, and aVF. Conversely, acute 
inferior (or posterolateral) infarcts may be associated with reciprocal ST depressions in leads V1 to V3. (Reproduced with permission from AL Goldberger et al: Goldberger’s 
Clinical Electrocardiography: A Simplified Approach, 10th ed. Philadelphia, Elsevier, 2024.)

CHAPTER 247
Electrocardiography
The ECG has important limitations in both sensitivity and speci­
ficity in the diagnosis of acute and chronic ischemic heart disease. 
Although a single normal ECG does not exclude ischemia or even acute 
infarction, a normal ECG throughout the course of an acute infarct is 
distinctly uncommon. Prolonged chest pain without diagnostic ECG 
changes therefore should always prompt a careful search for other non­
coronary causes of chest pain (Chap. 15). Furthermore, the diagnostic 
changes of acute or evolving ischemia are often masked by the presence 
of left bundle branch block, electronic ventricular pacemaker patterns, 
and WPW preexcitation. However, clinicians may also overdiagnose 
ischemia or infarction based on the presence of ST-segment elevations 
or depressions; T-wave inversions; tall, positive T waves; or Q waves not 
related to ischemic heart disease (pseudoinfarct patterns). For example, 
ST-segment elevations simulating acute ischemia/infarction may occur 
with acute pericarditis or myocarditis, including COVID-19 infections, 
as a normal variant (including the typical “early repolarization” pat­
tern), or in a variety of other conditions (Table 247-1). Similarly, tall 
T waves do not invariably represent hyperacute ischemic changes but 
may also be caused by normal variants, hyperkalemia, or cerebrovas­
cular injury, among other causes.
ST-segment elevations and tall, positive T waves are common find­
ings in leads V1 and V2 in left bundle branch block or left ventricular 
hypertrophy in the absence of ischemia. The differential diagnosis of 
Q waves includes physiologic or positional variants, ventricular hyper­
trophy, acute or chronic noncoronary myocardial injury, hypertrophic 
cardiomyopathy, and ventricular conduction disorders. Ventricular 
hypertrophy, hypokalemia, drugs such as digoxin, and a variety of 
other factors may cause ST-segment depression mimicking suben­
docardial ischemia. Prominent T-wave inversion may occur with 
aVR
aVL
aVF
V2
V4
V6
aVR
aVL
aVF
V2
V4
V6

TABLE 247-1  Differential Diagnosis of ST-Segment Elevations
Myocardial ischemia/infarction
  Noninfarction transmural ischemia (e.g., Prinzmetal’s syndrome)
  Acute myocardial infarction
    Due to atherosclerotic coronary occlusion
    Due to nonatherosclerotic causes (e.g., takotsubo syndrome, coronary 
PART 6
Disorders of the Cardiovascular System
dissection)
  Post-myocardial infarction (left ventricular motion abnormality/aneurysm)
Acute pericarditis
Normal variants (including benign “early repolarization” patterns)
  Left ventricular hypertrophy/left bundle branch blocka
Other (rarer)
  Acute pulmonary embolisma
  Brugada patterns (right bundle branch block–like morphology with ST 
elevations in right precordial leads)
  Class 1C antiarrhythmic drugsa
  DC cardioversion (transient)
  Hypercalcemiaa
  Hyperkalemiaa
  Hypothermia (J [Osborn] waves)
  Nonischemic myocardial injury
    Myocarditis syndromes (infectious and noninfectious)
    Tumor invading left ventricle
    Trauma to ventricles
aUsually localized to V1–V2 or V3.
Source: Modified from AL Goldberger et al: Goldberger’s Clinical 
Electrocardiography: A Simplified Approach, 10th ed. Elsevier, 2024.
ventricular hypertrophy, cardiomyopathies, myocarditis, and “stress 
cardiomyopathies” associated with takotsubo syndrome and cerebro­
vascular injury (particularly intracranial bleeds), among others causes. 
Diagnostic confusion may also occur when nonischemic T-wave inver­
sions (“cardiac memory” effect) appear in normally conducted beats in 
patients with intermittent wide QRS complexes, most commonly due 
to ventricular pacing or to left bundle branch block.
■
■METABOLIC FACTORS AND DRUG EFFECTS
A variety of metabolic abnormalities and pharmacologic agents alter 
the ECG and, in particular, cause changes in repolarization (ST-T-U) 
and sometimes QRS prolongation. Certain life-threatening electrolyte 
disturbances may be diagnosed initially and monitored from the ECG. 
Hyperkalemia produces a sequence of changes (Fig. 247-14), usually 
Hyperkalemia
Mild-Moderate
Moderate-Severe
Very Severe
T
V1
V1
P
T
V2
V2
P
FIGURE 247-14  The earliest ECG change with hyperkalemia is usually peaking (“tenting”) of the T waves. With further increases in the serum potassium concentration, 
the QRS complexes widen, the P waves decrease in amplitude and may disappear, and finally a sine-wave pattern leads to asystole unless emergency therapy is given. 
(Reproduced with permission from AL Goldberger et al: Goldberger’s Clinical Electrocardiography: A Simplified Approach, 10th ed. Philadelphia, Elsevier, 2024.)

beginning with narrowing and peaking (tenting) of the T waves. Fur­
ther elevation of extracellular K+ leads to AV conduction disturbances, 
diminution in P-wave amplitude, and widening of the QRS interval. 
Severe hyperkalemia eventually causes cardiac arrest with a slow sinu­
soidal type of mechanism (“sine-wave” pattern) followed by asystole. 
Hypokalemia (Fig. 247-15) prolongs ventricular repolarization, often 
with prominent U waves. Prolongation of the QT interval is also seen 
with drugs that increase the duration of the ventricular action poten­
tial: class 1A antiarrhythmic agents and related drugs (e.g., quinidine, 
procainamide, tricyclic antidepressants, phenothiazines) and class III 
agents (e.g., amiodarone [Fig. 247-15], dofetilide, sotalol, ibutilide). 
Systemic hypothermia (Fig. 247-15) also prolongs repolarization, usu­
ally with a distinctive convex elevation of the J point (Osborn wave) 
and bradycardia. Marked QT prolongation, sometimes with deep, wide 
T-wave inversions, may occur with intracranial bleeds, particularly 
subarachnoid hemorrhage (“CVA T-wave” pattern) (Fig. 247-15). 
Hypocalcemia typically prolongs the QT interval (ST portion), whereas 
hypercalcemia shortens it (Fig. 247-16). Digitalis glycosides also 
shorten the QT interval, often with a characteristic “scooping” of the 
ST–T-wave complex (digitalis effect).
■
■NONSPECIFIC ST-T CHANGES AND LOW QRS 
VOLTAGE
Many other factors are associated with ECG changes, particularly alter­
ations in ventricular repolarization. T-wave flattening, minimal T-wave 
inversions, or slight ST-segment depression (“nonspecific ST–T-wave 
changes”) may occur with a variety of electrolyte and acid-base distur­
bances, infectious or inflammatory processes, central nervous system 
disorders, endocrine abnormalities, many drugs, ischemia, hypoxia, 
and virtually any type of cardiopulmonary abnormality, in addition to 
physiologic changes (e.g., with posture or after meals). Low QRS volt­
age is arbitrarily defined as peak-to-trough QRS amplitudes of ≤5 mm 
in the six limb leads and/or ≤10 mm in the chest leads. Multiple factors 
may be responsible. Among the most serious include pericardial 
(Fig. 247-17) or pleural effusions, chronic obstructive pulmonary 
disease, cardiac amyloid, and anasarca.
■
■ELECTRICAL ALTERNANS SYNDROMES
Electrical alternans—a beat-to-beat alternation in one or more com­
ponents of the ECG signal—is a common type of nonlinear cardio­
vascular response to a variety of hemodynamic and electrophysiologic 
perturbations. Total electrical alternans (P-QRS-T) with sinus tachy­
cardia is a relatively specific sign of pericardial effusion, usually with 
cardiac tamponade (Fig. 247-17). In contrast, pure repolarization 
Lead I
Lead II
1mV
1s

Hypokalemia
Hypothermia
Amiodarone
V3
II
U
Tricyclic overdose
III
V3
V2
I
FIGURE 247-15  A variety of metabolic derangements, drug effects, and other factors may prolong ventricular repolarization with QT prolongation or prominent U waves. 
Prominent repolarization prolongation, particularly if due to hypokalemia, inherited “channelopathies,” or certain pharmacologic agents, indicates increased susceptibility 
to torsades des pointes ventricular tachycardia (Chap. 261). Marked systemic hypothermia is associated with a distinctive convex “hump” at the J point (Osborn wave, 
arrow) attributed to altered transmural ventricular action potential characteristics. Note QRS and QT prolongation along with sinus tachycardia in the case of tricyclic 
antidepressant overdose.
Hypocalcemia
Normal
Hypercalcemia
I
I
I
 II
 II
 II
QT=480 ms
QTc=500 ms
QT=360 ms
QTc=400 ms
QT=260 ms
QTc=350 ms
FIGURE 247-16  Prolongation of the Q-T interval (ST-segment portion) is typical of hypocalcemia. Hypercalcemia may cause abbreviation of the ST segment with relative or 
absolute shortening of the QT interval.
FIGURE 247-17  Classic triad of findings for pericardial effusion with cardiac tamponade: (1) sinus tachycardia; (2) low QRS voltages and (3) electrical alternans (best seen 
in leads V3 and V4 in this case; arrows). This triad is highly suggestive of pericardial effusion, usually with tamponade physiology, but is of limited sensitivity. (Adapted from 
LA Nathanson et al: ECG Wave-Maven. ecg.bidmc.harvard.edu.)

V5
V4
T
CHAPTER 247
Electrocardiography
Subarachnoid hemorrhage