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American Heart

Association~,
Fighting Heart Disease
and Stroke

The Electrocardiogram
Examination of the Heart
Part5
Examination of the Heart Part 5
The Electrocardiogram

Prepared on behalf of the


Council on Clinical Cardiology
of the American Heart Association

Masood Akhtar, MD
Professor of Medicine
University of Wisconsin Medical School
Milwaukee Clinical Campus
Director, Arrhythmia Services
Sinai Samaritan Medical Center
Milwaukee, Wisconsin
Contents

2 Cardiac Conduction System


Examination of the Heart 3 Standard Signals and Measurements
A Series of Booklets 5 Theoretical Basis
6 Vectorial Concept of Cardiac Activation
Part 1
The Clinical History 7 Einthoven’s Triangle
Mark E. Silverman, MD 8 Unipolar Limb Leads
11 Unipolar Precordial Leads and Horizontal Reference Frame
Part 2 12 Construction of Mean Vectors
Inspection and Palpation of
Venous and Arterial Pulses 14 The Normal Electrocardiogram
Michael H. Crawford, MD 16 Hypertrophy, Bundle Branch Blocks, and Preexcitations
16 Right Atrial Enlargement
Part 3 16 Left Atrial Enlargement
Examination of the Precordium:
Inspection and Palpation 16 Left Ventricular Hypertrophy
Robert C. Schlant, MD, and J. Willis Hurst, MD 19 Right Ventricular Hypertrophy
22 Bundle Branch Block
Part 4 23 Right Bundle Branch Block
Auscultation of the Heart
James A. Shaver, MD, James J. Leonard, MD,
24 Left Bundle Branch Block
and Donald F. Leon, MD 27 Nonspecific Intraventricular Conduction Defect
28 Fascicular Blocks or Hemiblocks
Part 5
29 Left Anterior-Superior Fascicular Block or Hemiblock
The Electrocardiogram
Masood Akhtar, MD 30 Left Posterior Fascicular Block or Hemiblock
32 Ventricular Preexcitation
Available from your local American Heart Association 35 Myocardial Ischemia, Injury, and Infarction
35 Subendocardial Ischemia
35 Subepicardial or Transmural Ischemia
38 Injury
39 Myocardial Infarction
41 Site of Infarction
44 ST-Segment Elevation and T-Wave Abnormalities

©1972, 1978, 1990 American Heart Association


47 Cardiac Arrhythmias
47 Mechanisms
48 Approach
48 Recognition of the Site of Origin
48 Atrial Arrhythmias
50 Atrioventricular Junctional Arrhythmias
51 Ventricular Arrhythmias The scalar electrocardiogram (ECG) continues to be an effective,
inexpensive, and widely used clinical tool that is easily acquired. Any
51 Electrocardiographic Diagnosis of Specific Arrhythmias student of electrocardiography (physician, nurse, or medical student) can
52 Isolated Premature Beats learn to interpret the essentials of electrocardiography. Even though
52 Atrial Beats computer interpretations of ECGs are readily available, the clinician’s role
53 Atrioventricular Junctional Beats as overseer and final interpreter has not and must not be diminished.
Fundamental principles and commonly encountered abnormalities of
53 Ventricular
conduction patterns and arrhythmias are covered in this publication, which
53 Sustained Tachyarrhythmias is not a substitute for standard textbooks on electrocardiography but rather
54 Atrial Tachycardias an introduction to this time-honored and well-established diagnostic tool.
54 Multifocal Atrial Tachycardias The reader is urged to consult more extensive texts and periodicals for
specific details. A list of suggested reading is provided at the back of this
54 Atrial Flutter publication.
54 Atrial Fibrillation
56 Atrioventricular Junctional Tachycardias
56 Nonparoxysmal Junctional Tachycardias
59 Accelerated Idioventricular Rhythm
60 Ventricular Tachycardia
63 Bradyarrhythmias
63 Sinus Bradycardia
64 Sinus Arrest and Sinoatrial Exit Block
64 Bradycardia-Tac hycardia Syndrome
64 Atrioventricular Block
64 First-Degree Atrioventricular Block
65 Second-Degree Atrioventricular Block
66 2:1 Block
66 Third-Degree Atrioventricular Block
68 Functional or Physiologic Blocks
70 Atrioventricular Dissociation
71 Electrocardiogram of the Paced Rhythms
73 Suggested Reading
Cardiac Conduction System recovery of the ventricular myocardium, which follows the QRS complex, is
clearly recorded as a T wave on the surface ECG (Figure 1). It should be
stressed that electrical depolarization of the atrial and ventricular
myocardium is not synonymous with atrial and ventricular contraction. As a
rule, electrical depolarization of these structures must precede the
corresponding mechanical contraction; however, mechanical contraction
occasionally may not follow the electrical events, as, for example, during
To understand propagation of electrical impulses throughout the heart,
electrical-mechanical dissociation.
two types of cardiac tissue (Figure 1, left) must be considered:
Ordinary myocardium (atrial and ventricular)
CARDIAC CONDUCTION SYSTEM
Specialized cardiac conduction system, which includes the following: AND ELECTRICAL CYCLE
sinoatrial node; anterior, middle, and posterior internodal tracts;
R
atrioventricular (AV) node; bundle of His; right and left bundle
branches; anterior-superior and posterior-inferior divisions of the left SEGMENTp N ~]SEGMENT T~U
P-R S-T
bundle; and the Purkinje network
Both the ordinary myocardium and the specialized conduction system
allow conduction of electrical impulses. Most cells in the specialized
cardiac conduction system also depolarize spontaneously, which enables
these cells to function as cardiac pacemakers. The inherent spontaneous RIGHT BUNDLE
rate of depolarization is progressively slower from the sinus node down to BRANCH {RB8) INTERVAL ~ INTERVAL
the Purkinje fibers. The normal rate of spontaneous depolarization in the qRs
DURATION
sinus node ranges from 60 to 100 beats/min, which is faster than other I I
Q - T INTERVAL
cardiac pacemakers (i.e., His bundle, Purkinje network, etc.); therefore, it is
the dominant pacemaker. 1 ) SINUS NODE FIRING - NOT RECORDABLE
2 } ATRIAL MUSCLE DEPOLARIZATION-P WAVE
Depolarization of the heart from sinus impulse suppresses other 3) A-V NODAL; HIS BUNDLE, RBB AND LBB, AND PURKINJE NET~NORK (~e RIS-PURKINJE SYSTEM)
ACTIVATION - NOT RECORDED, OCCURING DURING ISOELECTRIC P - R INTERVAL
potential pacemakers; their activity is normally recognized only when sinus 4) VENTRICULAR MUSCLE DEPOLARIZATION QRS COMPLEX
5) VENTRICULAR MUSCLE REPOLARIZATION-T WAVE
rates fall below those of other pacemakers. The emergence of lower 6) U WAVE-TERMINAL VENTRICULAR OR PURKINJE SYSTEM REPOLARIZATION
pacemakers to sustain a heart rate when the dominant pacemaker fails is
called an escape mechanism. During an escape mechanism, the heart Figure 1. At left, cardiac conduction system. All pertinent structures are labeled. Typical
deflection of surface electrocardiogram (ECG) and relevant intervals are seen at right.
rate is obviously slower than the dominant pacemaker.
Sinus node automaticity (or firing) is not recorded on the surface ECG.
Sinus impulse activates the internodal tracts as well as the atrial
myocardium. Activation of the atrial myocardium produces the so-called P
wave on the surface ECG (Figure 1). During sinus rhythm, the initial part
of the P wave represents right atrial activation, whereas the terminal part Standard Signals and Measurements
of the P wave represents activation of the left atrium with some overlap in
the middle. The impulse then depolarizes the AV node, the His bundle, the The ECG is generally recorded at a paper speed of 25 mm/sec. At this
bundle branches, the Purkinje network, and the ventricular myocardium. speed, one small square of ECG paper in the horizontal direction depicts
Propagation of impulse through the AV node, His bundle branch-Purkinje an interval of 40 msec or 0.04 second; the large square represents a total
system is also not recorded on the surface ECG and occurs during the of 200 msec or one fifth of a second (Figure 2). In the vertical direction,
isoelectric PR segment. Ventricular muscle depolarization produces the the amplitude of ECG signals is measured in millivolts; standardization of
QRS complex (Figure 1). Atrial depolarization is followed by atrial 1 mV is routine. Amplitude of 1 mV is equivalent to the height of two large
repolarization, called Tp or Ta, but is generally not discernible. However, squares (10 small squares or 10 mm) of ECG paper. The electrical cardiac

2
3
QT interval depends on the heart rate. Rate-corrected QT intervals are
generally expressed as QTc intervals, which can be calculated from the
ECG PAPER TIME & AMPLITUDE SCALE formula K\ RR where K equals 0.397 in men and 0.415 in women.
However, a QTc exceeding 450 msec is considered abnormal for any age,
gender, or heart rate.
jim
III
III
III Theoretical Basis
III 10 m.m. OR 1 m.V.
III Understanding of cardiac electrical force requires complex recording
III and analytic techniques not offered by the standard surface ECG. Yet the
III
III standard 12-lead ECG using only the "centrally located, fixed dipole-
homogeneous medium" concept yields valuable clinical information that
......... :11 - - - Jrll has been strengthened by clinical experience.
As the impulse is propagated during cardiac depolarization, electrical
activity is recorded by an electrode, based on its location relative to
direction and magnitude of forces. Figure 3 shows an electrode (EA)
msec. located opposite to the direction of propagation of the impulse. It records a

PAPER SPEED = 25 mm / sec. VARIATIONS IN QRS MORPHOLOGY


Figure 2. Electrocardiogram (ECG) paper grid, At normal speed of 25 msec/sec, small AT DIFFERENT ELECTRODE (E) SITES
square represents 40 msec time interval; large square represents 200 msec. Height and
depth of ECG waveforms are measured in millivolts (mV). Each small square is 1 mm high
(10=1 mV). Routine ECGs are recorded with 1 mV standard amplitude scale. Unless CELLULAR DEPOLARIZATION
otherwise indicated, all tracings were recorded with 1 mV standardization. DIPOLE

cycle begins with the P wave, which normally has a duration of less than
m,,,~ + m’-~" + ~,~,- -I- F EB

120 msec and a maximum amplitude of 0.25 mV. The normal PR interval TIME 1 TIME 2 TIME 3
measured from beginning of the P to onset of the QRS complex ranges
from 120 to 200 msec. During inscription of the QRS complex, the first
downward deflection is called a Q or q wave, the first upward deflection an
R or r wave, the second downward deflection an S or s wave, and a EC
second upward deflection an R or r prime. Capital or lowercase letters
designate the size of these deflections in relation to each other.
The isoelectric segment recorded between P and QRS is called the PR
segment; the isoelectric segment recorded between the end of the QRS
complex and the beginning of the T wave is called the STsegment. The
Figure 3. Electrocardiogram (ECG) signal configuration depends on location of electrode
ST segment is normally at the same level as the baseline, and its deviation (E) relative to direction of current flow. Positive signal is recorded when impulse approaches
above and below the baseline is considered abnormal. T waves are electrode (EB). Negative signal is registered at electrode A (EA) since current is flowing
generally upright in most ECG Leads; their amplitude and duration varies. away. Biphasic waveform is recorded (Ec) if electrode is perpendicular to direction of
The QT interval, measured from onset of the QRS complex to the end of impulse propagation rather than parallel, as seen with electrodes A and B.
the T wave, includes ventricular activation and reDolarization. The overall

5
4
negative deflection, one directed below the baseline. An electrode located
in the direction of the wave of impulse propagation (EB) records a positive DESIGNATIONS OF QRS ACCORDING TO
deflection (above the baseline). An electrode perpendicular to the direction SIZE OF COMPONENT WAVES
of impulse propagation (Ec) records a positive signal as the impulse
approaches it and a negative deflection as the impulse passes by,
resulting in a biphasic deflection. The magnitude of the electrical signal
recorded on the surface ECG depends on the current generated within
the myocardium at any moment, minus the cancellation of forces by
electrical wavefronts traveling in opposite directions. Two electrical forces of
qR qRs Qr qrS QS rS RS Rs RSr" rSr" rSR" rsR" rsR’s"
equal magnitude and strength moving in opposite directions should
produce a zero potential. A large number of electrical signals generated Figure 4. Various QRS morphologic appearances with corresponding conventional
within the myocardium are lost before reaching the surface leads because designations. Smaller deflections are indicated by lowercase letters. A second R (r) or S (s)
of intervening tissues of the lungs, chest wall, etc. deflection is generally labeled R’ (r’) or S’ (s’). Configuration of the first and sixth QRS
complexes depicted are often referred to as monophasic, 2-5, 7-9 as biphasic, and the
subsequent three as triphasic. Last complex is multiphasic.

Einthoven’s Triangle
Vectorial Concept of Cardiac Activation
The bipolar limb leads are treated as if the left and right shoulder
A vector quantity has both direction and magnitude, whereas a scalar electrodes and left leg electrode constitute the apices of an equilateral
quantity has magnitude but no direction. Because of the many triangle (Figure 5). The axis is divided by the midpoint of each bipolar lead
simultaneous electrical forces of differing magnitudes and direction that into positive and negative halves. Perpendicular lines drawn through the
occur during cardiac activation, it has been customary to determine the centers of the lead axis of leads I, II, and III intersect the center of the
mean or resultant vector of electrical activity in cardiac activation. equilateral triangle. For simplicity, the equilateral triangle can be
It may be imagined that the infinite number of small electromotive forces rearranged into a triaxial reference figure by superimposing the lead axes
generated within the heart, if resolved into a single equivalent force, can of leads I, II, and III so that the midpoints coincide. Projection of the
be represented by a resultant or mean cardiac vector. For example, bipolar limb leads on a 360° scale will show a 60° angle between leads I
instant-to-instant changes in direction and magnitude of such a mean and II and II and III.
vector determine the configuration of the ventricular complex (QR, QRS, Standard limb leads allow recording of a difference of electrical
RS) (Figure 4). A mean instantaneous vector can be constructed by potential between the two points. In a bipolar limb lead system, the left
analysis of the surface ECG. For a three-dimensional view of the mean arm is electropositive relative to the right arm (lead I); similarly, the left leg
vector of ventricular activation, frontal and horizontal planes, projections of is positive relative to the right arm for lead II, and the left leg is
cardiac depolarization must be analyzed. The frontal plane is represented electropositive relative to the left arm in lead III. On a 360° scale, the
by limb leads and allows projection and determination of superior and positive end of lead I is considered to be at 0O, whereas the negative end
inferior forces and those directed to the left and right, but not anteriorly or is considered to be at +180°. Values for the positive ends of leads II and
posteriorly. Horizontal forces can be determined by using the precordial III are +60° and +120O, respectively. The negative ends of leads II and III
lead system (Vl through V6). Horizontal plane projection permits analysis lie at -120° and -60°, respectively.
of right, left, anterior, and posterior electrical forces but does not pick up
superior and inferior forces. The frontal plane mean QRS vector (the
cardiac axis) can be constructed from standard (bipolar) limb leads (I, II,
and III), using the triaxial modification of Einthoven’s triangle.

6 7
STANDARD BIPOLAR LIMB LEADS- GOLDBERGER’S AUGMENTED (a) UNIPOLAR (V)
FRONTAL PLANE LIMB LEADS RELATED TO EINTHOVEN’S
TRIANGLE AND IN TRIAXIAL
- 120° - 6O° REFERENCE FRAME FRONTAL PLANE
RA LA
LEAD I ,~, ~t,
aVR aVL

- IoF_; " ’, oO
¯
I
I
LEAD I aVR + 150° I - 30°
+ aVL
+1 O°
LEAD II LEAD III -

+ 60°
+ 150 +30°
+V+ + LEAD III LEAD II

LL
+ 90°
EINTHOVEN’S TRIAXIAL REFERENCE aVF
TRIANGLE FRAME CTG= CENTRAL TERMINAL + aVF
OF GOLDBERGER
Figure 5. Standard limb leads and Einthoven’s triangle. As can be seen in lead I, left arm
(LA) is positive compared with right arm (RA), while in leads II and III, left leg (LL) is Figure 6. Unipolar limb leads. By connecting limb leads to common terminal (CTG),
electropositive compared to other end of lead. Using a 360° scale, positive and negative unipolar limb leads can be obtained by placing exploring electrode over right arm (VR), left
ends of leads can be projected and a numeric value designated. Conventionally, positive arm (VL), and left or right leg (VF). Lowercase "a" prefix (aVR, aVL, and aVF) designates
end of lead I is considered at 0° and negative at +180°. Positive ends of leads II and III are augmentation for greater amplitude. On 360° scale, aVL is placed at -30°, aVR at -150°,
at +60° and +120°, respectively. and aVF at +90°, implying that predominantly positive P or QRS complex in aVR is due to
P or QRS vector pointing -150° on scale. In contrast, totally negative aVR suggests a
vector near +30° on scale.
Unipolar Limb Leads
By connecting electrodes attached to the arms and the left leg, an On a circular scale, the positive ends of aVL, aVR, and aVF can be
indifferent central terminal at a zero potential can be obtained (Figure 6). projected as -30°, -150°, and +90°, respectively. By producing the leads
An exploring electrode can then be applied to the extremities to obtain on negative halves, all six limb leads can be obtained on a hexaxial
local electrical potentials. In clinical electrocardiography, such unipolar reference frame system. Scale values for positive and negative ends of
limb leads can be obtained by placing electrodes on the right arm (VR), these leads are shown in Figure 7, right. In a frontal projection, lead I is
left arm (VL), and left leg (VF). On a triaxial frame system, VR, VL, and VF divided into positive and negative halves by aVF (Figure 7, left). Similarly,
can be projected by connecting the apices of Einthoven’s triangle with the aVF is divided into positive and negative halves by lead I. Negative and
center of the equilateral triangle. Unipolar leads generally register lower positive hemispheres for other limb leads can also be obtained.
voltages compared with bipolar leads and thus need a correction factor.
Goldberger* augmented the small amplitude deflections obtained with
Wilson’s unipolar leads by removing resistors from the central terminal and
designating them modified unipolar leads or augmented limb leads by
adding the prefix "a" to VR, VL, and VF (aVR, aVL, and aVF).

*Goldberger E: Simple indifferent, electrocardiographic electrode of zero potential and


technique of obtaining augmented, unipolar, extremity leads. Am Heart J 1942;23:483-492.

8 9
Unipolar Precordial Leads and Horizontal Reference Frame
_ 90° The precordial lead system, leads V1 through V6, permits detection of
- 90° °
-120°
forces along the horizontal plane (Figure 8). A 360° scale can also be
- 60
aVR ~ ~ #. aVL
-,6oo -30° devised for the horizontal plane system but is seldom used in routine
~ m ~
clinical electrocardiography.
0° I
±180° mmmmmm

+ 150
STANDARD PRECORDIAL LEADS
-}-90° +120° +60 °
+90°
+ aVF III II
i:i:!:!:!:!:::’: NEGATIVE HEMISPHERE OF LEAD I aVF

NEGATIVE HEMISPHERE OF aVF HEXAXlAL REFERENCE FRAME OF THE


FRONTAL PLANE

Figure 7. Determination of axis on hexaxial frame. All six limb leads and positive (solid
lines, at right) and negative (dotted lines, at right) halves are shown. Each lead is divided
into negative and positive hemicircles by another lead (lead II divided into positive and
negative halves by aVL and vice versa), if equiphasic lead is found (P or QRS), axis will be 4 th INTERCOSTAL
perpendicular to that lead. In perpendicular lead, positive or negative direction of SPACE
complexes can be easily identified. For example, if aVF is equiphasic, axis is along lead I. If
lead I is positive, axis is 0°; if negative, it will be near +180°.

PLACEMENT OF
POSITIVE EXPLORING
ELECTRODE MID -AXlLLARY LINE
ANTERIOR AXILLARY LINE

MID- CLAVICULAR LINE


Figure 8. Usual placement of precordial leads that provide information about cardiac
electrical forces along horizontal plane, which is sensitive to forces directed anteriorly,
posteriorly, right, and left but not as much to superior or inferior, seen primarily by limb
leads of 12-lead ECG.

11
10
Construction of Mean Vectors providing the mean QRS axis. A more practical method of finding the axis
is to inspect the six limb leads and find the lead with the most equiphasic
The frontal plane mean QRS vector, or the mean electrical axis of the
QRS complex, is constructed from the standard bipolar limb leads I, II, complex (i.e., equally positive and negative) (Figure 9). The mean vector of
and III using the triaxial reference frame figure derived from Einthoven’s the QRS complex should be perpendicular to the lead with the equiphasic
triangle. Although there are several ways to calculate the axis, an easy complex. Orientation of the mean vector can be determined by examining
method for constructing the mean axis is to use the net amplitude of QRS the lead perpendicular to that with an equiphasic complex. If it is positive
complexes in the bipolar leads. Positive or negative voltage in any lead or negative, the axis will point in the corresponding direction. Any of the
six limb leads can be taken if an equiphasic complex is available.
can be measured and projected in millivolts or millimeters on the
corresponding side of the lead. By drawing perpendiculars on two leads, a However, when determining the axis based on height or depth of a lead,
only leads I, II, or III should be taken because relative voltage and
point can be determined and then connected to the center of the terminal,
magnitude of the bipolar and augmented unipolar limb leads are not the
same. Normal values and various axis orientations are seen in Figure 10.
aVR V1 V4 Values from -30° to +100° are considered normal, whereas values
between -30° and -90° are designated as left axis deviation. Axes
between +110° and +180° are labeled right. Values between -90° and
+180° are categorized as extreme left axis.

EXTREME LEFT } LEFTAXIS }


AXIS -90° to + 180° _90° DEVIATION -30° to -90°
-120° -60°

II aVL V2 V5
aVR -150° -30° aVL

±180° 0° I

+ 150° ~, +30°

III aVF V3 V6 Ill + 120°


+90°
+60° II

aVF NORMAL }
RIGHT AXIS +110° to +180° -30° to +100 o
DEVIATION AXIS

Figure 10. Axis orientation (frontal plane) and ranges of various axis orientation. Normal
axis range is -30° to +100°. Abnormal ranges are shown. Various terminologies are used
when axis is -90° to +180°, including extreme left axis. When axis is difficult to determine
due to biphasic examples in several leads, it is called indeterminate axis.
Figure 9. Determination of QRS axis. Both leads III and aVF show equiphasic complex.
Axis will be perpendicular to leads III and aVF, respectively. Since aVR is predominantly
negative, axis will be around +30°. Similarly, lead I is positive. Axis should be
approximately 0°. In this case, both leads III and aVF are equiphasic; orientation most likely
is around +15°.

12 13
The Normal Electrocardiogram

From the sinus node, the electrical impulse spreads rapidly through the
right and left atria (Figure 1). The internodal tracts may be involved in
conduction from the sinus to the AV node, although this does not appear
to be essential. Initially, during right atrial activation, electrical forces are
II aVL V2 V5
directed anteriorly, inferiorly, and to the left. The last portion of atrial
depolarization occurs entirely in the left atrium, and the vectors are
directed inferiorly, to the left, and more posteriorly, with the net effect being
that the P wave is positive in leads II, III, and aVF, and positive isoelectric
or biphasic in I and aVL (Figures 9 and 11). The P wave is usually inverted
in aVR. Typically in V~, the P wave is initially positive and the terminal
portion is negative (Figures 9 and 11).
The ventricular myocardium is activated via the Purkinje network, the
III aVF V3 V6
impulse traveling from the endocardium toward the epicardium. Onset of
left ventricular activation only slightly precedes right ventricular activation.
The initial dominant vector of left ventricular activation is due to left septal
activation and is directed to the right, anteriorly, inferiorly, or superiorly,
typically producing a small r wave in V~ and a small q wave in leads I and
V6. However, when the QRS axis is near +90°, the septal q wave may be
more obvious in the inferior leads (11, III, and aVF). Activation of the free Figure 11. Normal 12-lead electrocardiogram (ECG). Normal P, QRS, and T-wave
wall of the left ventricle and the right ventricle soon follows. Since left orientations are evident. P wave is positive in leads II and aVF, biphasic in Vl, and negative
in aVR. P axis is +60° since it is isoelectric in aVL (lead perpendicular to II, which is
ventricular forces are greater than their right ventricular counterparts, the positive). QRS complex shows normal transition from small r and large S (rS) in Vl to qRs
resultant vector essentially represents left ventricular activity. The overall pattern in V6. Note progressively larger R wave from V~-V6. T wave is upright in most leads
direction of left ventricular activation is leftward, posterior, and generally and negative in aVR, as expected. All waves (P, QRS, and T) should be negative in aVR
inferior. A mean QRS complex axis between -30° and +100° results (i.e., since both atrial and ventricular forces normally point away from right arm and are oriented
normal QRS axis). ECG changes produced by such a vector include the to left. QRS axis is approximately +100’~
deep S wave in lead V~ and the tall R wave in leads I and V6. The terminal
portion of ventricular activation is due to depolarization of the thick of 0°, leads I and aVL may show more classic left ventricular complex
posterolateral and basilar wall of the left ventricle and the area of the patterns. Normally, aVR shows a negative QRS complex. Ventricular
outflow tract of the right ventricle. Normally, a transition of QRS recovery follows ventricular depolarization; the T wave is normally upright
morphology is noted when proceeding from V~ to V6; that is, an initially in all leads except aVR. Occasionally, however, leads III, aVL, V1, and V2
small R wave in V~ gradually increases and results in a taller R wave until may show a biphasic or inverted T wave under normal circumstances. A
morphology of V6 is achieved (Figures 9 and 11). Similarly, the S wave in small, low-amplitude wave frequently follows the T wave and is particularly
V~ gradually diminishes until it practically disappears at the V6 level. prominent in left precordial leads; termed a U wave, its exact origin is still
Morphology of the QRS complex in the limb leads depends on the overall uncertain. The possibilities include His-Purkinje system recovery or
axis of the complex; thus, in a vertically oriented heart where the axis is recovery of ventricular myocardium in areas devoid of the Purkinje system.
around the +90° range, leads II, III, and aVF may show more typical QRS Nonetheless, the U wave may be prominent in such clinical situations as
complexes like V6. In a horizontal position with the axis more in the region hypokalemia.

14 15
Hypertrophy, Bundle Branch Blocks,
and Preexcitations aVR V1 ~ Sfd. V4

Right Atrial Enlargement II aVL V2 V5


Since the initial part of the P wave is due to right atrial depolarization,
enlargement of the right atrium produces a P-wave prominence (peaked P
waves) in leads II and aVF without necessarily increasing P-wave duration.
P-wave voltage of more than 0.25 mV in the limb leads or Vl suggests right
atrial enlargement.

Left Atrial Enlargement III aVF V3 V6


Left atrial enlargement is suggested by P-wave duration of 120 msec or
more, definite notching and prominence of the terminal portion of the P
wave, and prominent negativity of the terminal portion of the P wave in Vl.
It should be pointed out that conduction delay in the atria without
hypertrophy can prolong P-wave duration. However, conduction delay is
secondary to hypertrophy or dilation in most instances.
Figure 12. Left ventricular hypertrophy. Increased QRS voltage can be appreciated in
Left Ventricular Hypertrophy several limb leads (I, III, and aVL). Precordial leads were recorded at half-standard to
accommodate large amplitude of QRS complex within confines of electrocardiogram paper.
Electrical forces generated during left ventricular activation ordinarily In addition to QRS voltage, ST and T changes due to hypertrophy are also noted.
produce the normal QRS complex. With an increase in the thickness of
left ventricular myocardium (left ventricular hypertrophy), electrical V6 exceeding 26 mm, or a sum of R wave in V5 or V6 and S wave in V2 of
preponderance of left ventricle over right ventricle is further accentuated. more than 35 mm are generally considered sufficient for diagnosis of left
The mean vector of the left ventricle becomes more posterior and leftward, ventricular hypertrophy (Figure 12). The presence of ST depression and T-
increasing QRS complex voltage and ventricular activation time. wave inversion in the presence of adequate voltage criteria improves the
Secondary ST and T-wave abnormalities are not uncommon in the later diagnostic accuracy of left ventricular hypertrophy by ECG (Figure 12).
stages of left ventricular hypertrophy. On voltage criteria alone, standards Additional ECG clues to diagnosis of left ventricular hypertrophy are left
have been established for different leads. Left ventricular hypertrophy may axis deviation, increased QRS duration, and the presence of left atrial
be diagnosed in the extremity leads if the sum of the R wave in lead I and enlargement. Due to the increased voltage of QRS complexes, many or all
the S wave in lead Ill equals or exceeds 25 mm (Figure 12). An R wave of leads may have to be recorded at half the usual standardization scale of 1
11 mm in aVL or 20 mm in aVF is considered high voltage and adequate mV (Figure 12).
for diagnosis of left ventricular hypertrophy in extremity leads. For
precordial leads, an S wave in V~ exceeding 24 mm, an R wave in V5 or

16 17
Right Ventricular Hypertrophy
aVR Vl V4 With right ventricular hypertrophy, electrical voltage generated at the
right ventricular level is increased. Consequently, there is characteristic
alteration in the balance of electrical forces between the ventricles.
However, it should be pointed out that the increase in right ventricular
forces must be sufficient to either reduce or abolish the left ventricular
preponderance. Increasing hypertrophy of the right ventricle produces
progressive anterior and rightward displacement of the QRS vector. These
changes become more pronounced as the degree of hypertrophy
increases. Progressive hypertrophy of the right ventricle causes an
increase in amplitude of the R wave and a corresponding decrease in the
S wave in lead V1. Therefore, the R:S ratio gradually increases. The most
severe right ventricular hypertrophy is manifested by a tall R wave in lead
il aVL V2 V5 V1 (Figure 13).
In the extremity leads, the diagnostic criteria for right ventricular
hypertrophy include an R wave in aVR of more than 5 mm. In the
precordial leads, an R wave in V1 exceeding 7 mm or an S wave in V~ of
less than 2 mm suggests right ventricular hypertrophy. An R:S ratio of
more than 1 in V~, or the sum of R in V1 and S in V5 of more than 10 mm,
or an R:S ratio in V5 or V6 of less than 1 suggest right ventricular
hypertrophy. Conventionally, right ventricular hypertrophy has been
classified as one of three types. Type A usually produces a tall R wave in
V~ and represents concentric hypertrophy of the right ventricle, usually
associated with right ventricular outflow obstruction of congenital origin
III aVF V3 V6 (Figure 13). An R:S pattern is produced in type B and usually anatomically
reflects a moderately severe hypertrophy of the right ventricle. Type C
produces an rSr pattern that represents a moderate-to-mild hypertrophy of
the crista supraventricularis and the outflow tract of the right ventricle. It is
commonly seen in atrial septal defect, mitral stenosis, and cor pulmonale.
Right atrial enlargement, right axis deviation, and ST and T-wave
abnormalities in leads showing the R prominence may accompany
right ventricular hypertrophy and generally support the diagnosis. Right
ventricular hypertrophy can mimic posterior myocardial infarction. Changes
produced by the latter are limited to the right precordial leads, and
prominent S waves are seldom seen in leads I and V6. Posterior infarction
Figure 13. Severe (type A) right ventricular hypertrophy. Note prominent R wave in V1 and is often accompanied by inferior (Figure 14) or lateral wall infarction or
deep S wave in V6 and lead I, a pattern opposite to that seen in normal ECG (see Figure both. Other conditions that produce prominent R waves in V~ include right
11). QRS axis location of around -110° also suggests right ventricular predominance bundle branch block (see below) and left ventricular preexcitation (Figure
possibly due to congenital heart disease.
15), which is preceded by a short PR interval. Right bundle branch block
should not be diagnosed in the absence of prolonged QRS duration.

18 19
aVR V1 V4 aVR Vl V4

II aVL V2 V5

III aVF V3 V6

III aVF V3 V6

Figure 14. Prior or healed myocardial infarction. Pathological Q waves in leads II, III, and
aVF with normal ST and T waves are shown. These inferior wall changes are also
accompanied by prominent R wave in V1 and V2, which is best explained by posterior
extension of inferior wall infarction, a common occurrence. (See text for more detail.)

Figure 15. Type A ventricular preexcitation. Note short PR, delta wave, which is positive in
V1, negative in I and aVL, typical of left free wall accessory pathway (AP).

2O
21
Right Bundle Branch Block
Bundle Branch Block
Since the initial part of the QRS complex is inscribed as a result of left-
Normally, ventricular activation is completed in approximately 60-80 to-right forces in the septal mass (Figure 9) supplied by fibers of the left
msec and is due to rapid simultaneous activation of the ventricles via the bundle branch, the occurrence of right bundle branch block does not alter
Purkinje system. In bundle branch block, QRS duration may be prolonged the initial part of the QRS complex (Figures 16, panel A, and 17). Similarly,
due to 1) sequential rather than simultaneous activation of the ventricles since the left bundle branch is intact, the remainder of the left ventricle
(activation time of the ventricle contralateral to the blocked bundle branch continues to activate normally. However, soon after ventricular activation
is tagged onto depolarization of the chamber supplied by the normally begins, transseptal muscle-to-muscle conduction from left to right
conducting bundle branch) and 2) a significant amount of muscle-to- generates significant electrical forces. The first 20-40 msec of ventricular
muscle conduction, including transseptal conduction, which is much activation is not altered by the presence of right bundle branch block.
slower than Purkinje-to-muscle conduction. However, ventricular activation later becomes oriented to the right and
anterior. The rightward forces become particularly prominent when left
A, RIGHT BUNDLE BRANCH BLOCK C. LEFT ANTERIOR HEMIBLOCK ventricular activation ceases (after 60-80 msec). Hence, the terminal
( RBBB ) ( LAH )

aVR V1 V4

12 3

II aVL V2 V5
Bo LEFT BUNDLE BRANCH BLOCK Do LEFT POSTERIOR HEMIBLOCK
(LBBB) (LPH)

1 2 3
III aVF V3 V6
Vl V6

Figure 16. Electrical forces in various conduction abnormalities. Right bundle branch
block (panel A) shows normal initial septal fomes that are altered in left bundle branch
block (panel B). Transseptal and sequential ventricular activation prolong QRS complex in
both right and left bundle branch block. In hemiblock, QRS widening is minimal because
transseptal conduction is not necessary and activation is simultaneous in both ventricles.
Terminal forces in hemiblock point toward area supplied by fascicle with blo(~k (panels C Figure 17. Typical 12-lead electrocardiogram in right bundle branch block. Note normal q
and D). in leads I, aVL, and V6, widening of QRS (160 msec), and rsR’ in V1. Most delay is in latter
part of QRS complex.

22 23
vector is directed to the right and anterior. After the initial normally directed
septal forces, the QRS vector is directed anteriorly and to the right,
resulting in a positive terminal R pattern in V1 and a terminal S wave in aVR Vl V4
leads I and Vs. Because of a significant amount of muscle-to-muscle
conduction, slurring is seen in the terminal portion of the QRS complex,
which is a characteristic feature of right bundle branch block. As a result
of unopposed right ventricular activation time in addition to normal left
ventricular activation time, the QRS complex is prolonged and generally
exceeds 120 msec. The term complete right bundle branch block is used
when the QRS complex equals or exceeds 120 msec; the term incomplete
right bundle branch block is used when QRS duration is 100-120 msec.
Secondary changes in the ST and T segments usually accompany altered II aVL V2 V5
QRS morphology during right bundle branch block.

Left Bundle Branch Block


During this disturbance of intraventricular conduction, septal and left
ventricular activation is altered from onset (Figures 16, panel B, and 18).
Since left septal mass cannot activate via the left bundle, septal activation
occurs through the right bundle from the opposite direction, that is, to the
left. This results in the absence of a q wave in leads I and V6. However, an
r wave may persist in V1 because of the anterior component of right-to-left III aVF V3 V6
septal activation. The activation wave moves transseptally toward the left
ventricle. The ventricular activation vector therefore is directed posteriorly
and to the left. Due to a considerable amount of muscle-to-muscle
conduction during ventricular depolarization, QRS duration frequently
exceeds 120 msec. In addition to the QRS complex widening, small
notching is frequently seen during R-wave inscription. Electrocardio-
graphically, the QRS complex typically shows the absence of a q as well
as a slurred R wave in leads I and Vs. V1 shows a srrlall r wave or none
followed by an S wave, with total QRS duration of more than 120 msec. Figure 18. Typical 12-lead electrocardiogram in left bundle branch block. Note absence of
q in leads I and V6 and wide QRS complex (170 msec) delay throughout inscription of QRS
Secondary ST segment and T-wave abnormalities are universal. In fact, the complex. Deep S in V1 and V2 and broad R in V~ and V6 are also typical, as is orientation of
ST and T vectors are oriented in the opposite direction, compared with the T opposite to QRS complex.
QRS complex (Figure 18). Due to the abnormal vector throughout
ventricular activation, ischemia, injury, and infarction usua.lly cannot be
detected with confidence in the presence of left bundle branch block. On
the other hand, since the initial part of the QRS complex is not altered in
right bundle branch block, the abnormal Q waves of myocardial infarction
can be accurately diagnosed in the presence of right bundle branch block
(Figure 19).

24 25
Nonspecific Intraventricular Conduction Defect
aVR V1 V4 The term nonspecific intraventricular conduction defect is used when no
characteristic pattern of right or left bundle branch block exists, although
QRS duration is prolonged (Figure 20). Such abnormalities are frequently
seen with previous myocardial infarction and scar formation. Prolonged
QRS duration without a specific bundle branch block pattern can also
occur due to intramyocardial conduction slowing from class I
antiarrhythmic drugs, left ventricular hypertrophy, and hyperkalemia.

aVR V1 V4
II aVL V2 V5

II aVL V2 V5
III aVF V3 V6
....

i....i

III aVF V3 V6
Figure 19. Q-wave (transmural) myocardial infarction and right bundle branch block.
Despite right bundle branch block, transmural myocardial infarction in anteroseptal region
(abnormal Q wave in V1-V4) can be clearly identified.

Figure 20. Nonspecific intraventricular conduction defect. Markedly slurred and broad
QRS (190 msec) is seen but septal forces, q wave in I and V6, are preserved, in this case,
due to extensive myocardial scarring. Nonspecific QRS widening may also occur with class
I antiarrhythmic drugs and hyperkalemia.

26 27
Fascicular Blocks or Hemiblocks Left Anterior-Superior Fascicular Block or Hemiblock
Thus far, discussion of the left bundle branch system has been based Like the main left bundle, a variety of conditions can produce a block in
on the assumption that it represents a single fascicle like the right bundle this division, including arteriosclerotic heart disease, aortic stenosis,
branch. In actuality, the left bundle branch is divided into the so-called hypertension, and cardiomyopathy. Sometimes a block is not associated
anterior-superior division, or fascicle, and posterior-inferior division, or with obvious structural heart disease. Septal activation generally occurs in
fascicle. These fascicles activate the corresponding portion of the left a normal left-to-right direction. However, there frequently is inferior
ventricular mass (Figure 16, panels C and D). Septal activation occurs orientation of initial forces because activation from inferior divisional fibers
from fibers of variable origin that generally arise from the left posterior is unopposed by fibers from the superior fascicle. Due to the block in
division. fibers supplying the anterior-superior portion of the left ventricle, the initial
forces are directed inferiorly, producing an initial r wave in leads II, III, and
aVF, and a q wave in leads I and aVL (Figures 16, panel C, and 21).
aVR V1 V4 However, the mean QRS vector is directed superiorly and to the left

aVR V1 V4

II aVL V2 V5
II aVL V2 V5

III aVF V3 V6
III aVF V3 V6

Figure 21. Left anterior fascicular block and hemiblock. Typical tracing with QRS axis of
-60° without significant QRS prolongation. (See also Figure 16, panel C.) Figure 22. Left posterior fascicular block or hemiblock. QRS axis of +120° can be
appreciated. (See also Figure 16, panel D.) Electrocardiogram also shows incidental
abnormalities such as marked ST depression, T-wave inversion, and prolonged QT interval.

28 29
(toward the area supplied by the anterior-superior division), resulting in a wave in leads I and aVL and a q wave in leads II, III, and aVE The major
tall R wave in leads I and aVL as well as deep S waves in leads II, III, and QRS vector points to the left and inferiorly as well as posteriorly. The QRS
aVE Since right and left ventricular activation proceeds simultaneously, abnormality therefore is the presence of tall R waves in leads II, III, and
QRS duration is generally not significantly prolonged. The main ECG aVF, and the presence of an S wave in lead I, the axis generally being
abnormality produced by a left anterior fascicular block is marked left axis around 120° (Figures 16, panel D, and 22). Again, the QRS complex
deviation located between -45° and -75°. usually does not widen because of simultaneous activation of the
ventricles. Right bundle branch block commonly coexists with either left
Left Posterior Fascicular Block or Hemib!ock anterior hemiblock or left posterior hemiblock (Figures 23, panels A and B,
and 24), a combination also called bifascicular block.
Isolated block in this division is uncommon. The same diseases that
produce the anterior fascicular block are frequently responsible for this
abnormality as well. Since the posterior-inferior fascicle is interrupted (the
initial activation vector is directed superiorly and to the left), producing an r aVR V1 V4
:=....i....::....::....i
A. RBBB and LAH C. WOLFF-PARKINSON-WHITE :: :: :: i i
SYNDROME
( WPW ) TYPE A

1 2 3

aVL V2 V5

B. RBBB and LPH D= WPW TYPE B ~~

III aVF V3 V6
V1 V6

Figure 23. A combination of right bundle branch block with left anterior hemiblock (LAH)
(panel A) or left posterior hemiblock (LPH) (panel B). Main electrocardiographic leads
showing abnormal pattern are drawn. Panels C and D depict left and right atrioventricular
accessory pathway (AP) connections (dotted line), respectively. Note short PR due to early
arrival of sinus impulses at ventricular level by AR Initial ventricular activation is along AP Figure 24. Combination of right bundle branch block and left anterior hemiblock (leads II,
and is muscle to muscle, producing initial slurring and the characteristic delta wave. (See III, and aVF). This is often termed bifascicular block. There is also prolonged PR interval (1°
also Figure 25.) AV block).

30 31
Ventricular Preexcitation
Normally, the atrial impulses conduct to the ventricles by the AV node- VENTRICULAR ORTHODROMIC
His-Purkinje system. Most conduction delay accounting for the normal PR PREEXCITATION TACHYCARDIA
interval is located in the AV node. On occasion, however, additional
pathways connecting the atria with the ventricles may exist, and these are
called accessory pathways. The most common of these, the Kent bundle,
is a direct muscle-to-muscle bridge, anatomically separate from the normal
conduction system (Figure 23, panels C and D). This type of accessory
pathway forms the anatomic basis for Wolff-Parkinson-White syndrome.
The Kent bundle can be located anywhere around the AV junction,
connecting the right atrium and right ventricle or the left atrium and left
ventricle. Sometimes these bypass tracts are located within the septum.
Conduction velocity is often faster in these tracts compared with the
normal AV node; therefore, sinus impulses usually activate ~he ventricle ECG
through these pathways, resulting in a short PR interval. Initial ventricular
activation by the accessory pathway is muscle to muscle; thus, the first
part of the QRS complex, the delta wave, is slurred (Figure 25, panel A). ANTIDROMIC PRE EXCITATION
These patients also have an intact normal pathway through which sinus TAC HYCARDIA DURING A- Fib
impulses reach and activate the remainder of the myocardium beyond
what has been depolarized via the accessory pathway (Figure 25, panel
A). Thus, the resulting QRS is a fusion complex, which is initially activated
through the accessory pathway and finally via the normal pathway. In left D
atrioventricular connections, ventricular activation from the accessory
pathway proceeds anteriorly and produces a positive R wave in V1
(positive delta), the so-called type A ventricular preexcitation (Figures 23,
panel C, and 15). In right atrioventricular connection, activation is directed
posteriorly, producing a predominantly negative wave in lead V1 (negative
delta), and called type B ventricular preexcitation (Figure 23, panel D).
This is an oversimplification; such terminology should be abandoned since
accessory pathways can be located anywhere at the AV junction, and Figure 25. Various electrocardiographic (ECG) patterns seen in patients with Wolff-
designation of types A and B alone does not serve a useful purpose. Parkinson-White syndrome. Panel A: Typical fusion complex. Short PR and initial slurring of
Depending on the relative conduction properties of the normal versus QRS is due to activation via accessory pathway (AP), and latter part of QRS is due to
accessory pathway, the QRS complex can be normal to totally preexcited. activation of ventricle along normal pathway. Panel B: Circuit of so-called orthodromic
tachycardia. Ventricular depolarization occurs exclusively over normal pathway. Note narrow
The presence of the short PR interval and the delta wave constitute the QRS and no evidence of preexcitation or delta wave. This is the most common arrhythmia
basic ECG abnormality. Since these patients have two potential pathways, in patients with Wolff-Parkinson-White syndrome. Panel C: Regular wide QRS tachycardia
the impulses can conduct by one and return by the other, making them due to reversed direction of impulse propagation. This tachycardia, called antidromic, is
prone to paroxysmal AV junctional reentrant tachycardias (Figure 25, relatively uncommon. In contrast, atrial fibrillation is common in patients with Wolff-
panels B and C; see section on cardiac arrhythmias). The combination of Parkinson-White syndrome. If AP has short refractory period, rapid conduction will occur via
AP, producing a rapid, wide QRS tachycardia with characteristic irregularity (panel D).
ECG abnormality and a history of recurrent palpitation constitutes the
Wolff-Parkinson-White syndrome.

32 33
Negative orientation of the delta wave can mimic the ECG patterns of
prior myocardial infarction (a Q wave) (Figure 26) and can occur in both Myocardial Ischemia, Injury, and Infarction
the anterior and inferior leads (Figure 26). It is not uncommon to
erroneously diagnose prior myocardial infarction in patients with Wolff-
Parkinson-White syndrome. The presence of a short PR interval is
generally the clue to correct diagnosis and should certainly raise
suspicion.
Insufficient blood supply to the myocardium can result in myocardial
ischemia, injury, or infarction, or all three. Atherosclerosis of the larger
aVR V1 V4 coronary arteries is the most common anatomic condition to diminish
coronary blood flow. The branches of coronary arteries arising from the
aortic root are distributed on the epicardial surface of the heart. These in
turn provide intramural branches that supply the cardiac muscle. Myocar-
dial ischemia generally appears first and is more extensive in the sub-
endocardial region since these deeper myocardial layers are farthest from
the blood supply, with greater intramural tension and need for oxygen.
II aVL V2 V5 Subendocardial Ischemia
Ischemia in this area prolongs local recovery time. Since repolarization
normally proceeds in an epicardial-to-endocardial direction, delayed
recovery in the subendocardial region due to ischemia does not reverse
the direction of repolarization but merely lengthens it. This generally
results in a prolonged QT interval or increased amplitude of the T wave or
both as recorded by the electrodes overlying the subendocardial ischemic
III aVF V3 V6 region.

Subepicardial or Transmural Ischemia


Transmural ischemia is said to exist when ischemia extends
subepicardially. This process has a more visible effect on recovery of
subepicardial cells compared with subendocardial cells. Recovery is more
Figure 26. Type B ventricular preexcitation with negative delta in V1, III, and aVF in patient delayed in the subepicardial layers, and the subendocardial muscle fibers
with posteroseptal accessory pathway (AP). Changes in V1, III, and aVF can be
misinterpreted as evidence of prior anteroseptal and inferior wall infarcti,on, respectively.
seem to recover first. Repolarization is endocardial-to-epicardial, resulting
Short PR and delta waves are clues. In addition, these patients are usually young with in inversion of the T waves in leads overlying the ischemic regions
typical history of paroxysmal supraventricular tachycardia. (Figures 27 and 28).

34 35
aVR V1 V4 aVR Vl V4

II aVL V2 V5
II aVL V2 V5

III aVF V3 V6
III aVF V3 V6

Figure 28. Changes revert back to normal.

Figure 27. Acute myocardial ischemia in same patient during and after episode
of typical angina with typical T-wave inversions in anterolateral leads (I, aVL, V3-V6).

36 37
Injury Myocardial Infarction
Injury to the myocardial cells results when the ischemic process is more The term infarction describes necrosis or death of myocardial cells.
severe. Subendocardial injury on a surface ECG is manifested by ST- Atherosclerotic heart disease is the most common underlying cause of
segment depression, whereas subepicardial or transmural injury is myocardial infarction. The left ventricle is the predominant site for
manifested as ST-segment elevation (Figure 29). In patients with coronary infarction; however, right ventricular infarction occasionally coexists with
artery disease, ischemia, injury, and myocardial infarction of different areas infarction of the inferior wall of the left ventricle. The appearance of
frequently coexist, producing mixed and complex ECG patterns. pathological Q waves is the most characteristic ECG finding of transmural
myocardial infarction of the left ventricle (Figures 14 and 30). A patholog-
ical Q wave is defined as an initial downward deflection of a duration of 40
aVR V1 V4 msec or more in any lead except III and aVR. The Q wave appears when
the infarcted muscle is electrically inert and the loss of forces normally
generated by the infarcted area leaves unbalanced forces of variable

aVR V1 V4

II aVL V2 V5

II aVL V2 V5

III aVF V3 V6

III aVF V3 V6

Figure 29. Acute transmural injury of inferior wall and marked ST elevation in leads II, III,
and aVE ST depression in leads I, aVL, V2, and V3 could be reciprocal changes from
inferior wall injury vector or could represent independent ischemic process in anterolateral
region. These changes did not result in evolution of myocardial infarction and were
transient. Figure 30. Acute Q wave (transmural) myocardial infarction. Abnormal Q waves and ST
elevation can be identified in leads I, aVL, and V1-V~, suggesting relatively large
anteroseptal infarction of recent onset.

38 39
magnitude in the opposite direction from the remote region, for example, ¯ Q-wave infarction, which is diagnosed by the presence of pathological
an opposite wall. These forces can be represented by a vector directed Q waves (Figures 14, 30-32) and is also called transmural infarction.
away from the site of infarction and seen as a negative wave (Q wave) by However, transmural infarction is not always present; hence, the term
electrodes overlying the infarcted region. Q-wave infarction may be preferable for ECG description.
During acute myocardial infarction, the central area of necrosis is ¯ Non-Q-wave infarction, which is diagnosed in the presence of ST
generally surrounded by an area of injury, which in turn is surrounded by
depression and T-wave abnormalities (Figure 33).
an area of ischemia. Thus, various stages of myocardial damage can
coexist. The distinction between ischemia and necrosis is whether the Elevation of serum enzymes is expected in both types of infarction. In
phenomenon is reversible (Figures 27 and 28). Transient myocardial the absence of enzyme elevation, ST and T-wave abnormalities are
ischemia that produces T wave, and sometimes ST-segment abnormali- interpreted as due to injury or ischemia rather than infarction.
ties, can be reversible without producing permanent damage and is not
accompanied by serum enzyme elevation. Infarction resulting in cell death
is irreversible, however, and is accompanied by enzyme elevation. Two
types of myocardial infarction can be observed electrocardiographically:
Site of Infarction
aVR V1 V4 The ECG has been used to localize the site of ischemia and infarction.
Some leads depict certain areas; the location of the infarct can be
detected fairly accurately from analysis of the 12-lead ECG. Leads that
best detect changes in commonly described locations are classified as
follows:
Inferior (or diaphragmatic) wall: II, III, and aVF
Septal: Vl and V2
Anteroseptal: Vl, V2, V3, and sometimes V4
II aVL V2 V5 Anterior: V3, V4, and sometimes V2
Apical: V3, V4, or both
Lateral: I, aVL, V5, and V6
Extensive anterior: I, aVL, and Vl through V6
Posterior wall infarction does not produce Q-wave abnormalities in
conventional leads and is diagnosed in the presence of tall R waves in V~
and V2 (Figure 14). The classic changes of necrosis (Q wave), injury (ST
elevation), and ischemia (T-wave inversion) may all be seen during acute
infarction. In recovery, the ST segment is the earliest change that
normalizes, then the T wave; the Q wave usually persists. Therefore, the
age of the infarction can be roughly estimated from the appearance of the
ST segment and T wave. The presence of the Q wave in the absence of
ST and T-wave abnormality generally indicates prior or healed infarction.
Although the presence of a Q wave with a 40 msec duration is sufficient
Figure 31. Acute Q wave (transmural) myocardial infarction and development of for diagnosis, criteria defining the abnormal depth of Q waves in various
pathological Q waves in inferior leads along with ST elevation. Reciprocal changes are leads have been established. For example, in lead I, the abnormal Q wave
seen in leads I and aVE Possible infarction of posterior part of septum is suggested by must be more than 10% of QRS amplitude. In leads III and aVF, it should
absence of r wave, which is normally present in V~ and V2.

40 41
exceed 25%, whereas in aVL it should equal 50% of R-wave amplitude. Q
aVR Vl V4
waves in V2 through V6 are considered abnormal if greater than 25% of R-
wave amplitude.
The Q wave generally indicates myocardial necrosis, although similar
patterns may be produced by other conditions, such as Wolff-Parkinson-
White syndrome (Figure 26), corrected transposition of the great vessels,
etc. ST-segment elevation can be observed in conditions other than acute
myocardial infarction.

aVR V1 V4
II aVL V2 V5

II aVL V2 V5

Iil aVF V3 V6

III aVF V3 V6

Figure 32. Healed infarction of anteroseptal and inferior walls. Note abnormal Q waves
and normal T waves.
Figure 33. Extensive subendocardial changes of ST depression and T-wave inversion,
which occurred with typical chest pain and elevation of cardiac enzymes. Note absence of
abnormal Q waves. Anterolateral subendocardial infarction was diagnosed. Voltage criteria
for left ventricular hypertrophy are also present in limb leads. QT interval is significantly
prolonged due to concomitant subepicardial ischemia.

42 43
¯ Ventricular aneurysm: After acute myocardial infarction, the ST
ST-Segment Elevation and T-Wave Abnormalities segment normalizes (Figure 36). However, in the presence of a
Other causes of ST-segment elevation include the following: persistent aneurysm in the region of infarction, ST-segment elevation
may persist indefinitely.
¯ Acute pericarditis: ST elevation in acute pericarditis is generally
diffuse and does not follow the pattern of blood supply. As a rule, Abnormal T waves can be seen in a variety of conditions other than
these changes are not accompanied by reciprocal depression of the myocardial ischemia, including the following:
ST segment in other leads (Figure 34). Hyperventilation
¯ Early repolarization: In some patients without known heart disease, Cerebrovascular disease
particularly young patients, early takeoff of the ST segment is seen, Mitral valve prolapse
separated from the QRS by a notch (Figure 35).

aVR V1 V4
aVR V1 V4

II aVL V2 V5 II aVL V2 V5

III aVF V3 V6 III aVF V3 V6

Figure 34. Acute pericarditis. Changes in ST elevation in leads I, II, aVL, and V2-V6 can be
seen. ST elevation in leads I and II on ischemic basis due to different sources of blood
supply is unusual. Pericardial inflammation can occur from viral infection but is most Figure 35. Early repolarization. Early take-off of ST segment is common normal variant.
commonly caused by open heart surgery and consequent pericardial inflammation. Notch between end of QRS complex and beginning of ST segment is typical.

44 45
Right or left ventricular hypertrophy
Conduction abnormalities (right or left bundle branch block)
Cardiac Arrhythmias
Ventricular preexcitation
Myocarditis
Electrolyte imbalance
Cardioactive drugs such as digitalis and antiarrhythmic agents.
No obvious cause, particularly in women
Better understanding of certain basic anatomic and electrophysiologic
concepts facilitates diagnosis of cardiac arrhythmias. A knowledge of
aVR V1 V4 underlying mechanisms and the site of origin of arrhythmias is particularly
important.

Mechanisms
Although several mechanisms are involved in the genesis of
arrhythmias, reentry is the most common. Reentrant arrhythmias can
occur in any cardiac tissue; slow conduction is the underlying prerequisite.
All cardiac tissues have an inherent conduction velocity that is normally
faster in the His-Purkinje system compared with the atrial and ventricular
II aVL V2 V5 myocardium. Conduction velocity is slowest in the AV and sinoatrial nodes.
Abnormally slow or ineffective propagation of atrial impulses across the AV
junction can produce various degrees of AV block. Such a mechanism has
also been incriminated in production of sinoatrial exit block when
abnormalities exist at the sinoatrial junction. It is difficult to visualize
tachyarrhythmias due to slow conduction. However, slow conduction is
commonly encountered during propagation of premature impulses in
tissues downstream due to incomplete recovery, where conduction may be
normal during the resting state. If premature impulses block along certain
fibers or pathways and conduct slowly along others, the impulse can
III aVF V3 V6 return via fibers not previously used. If the tissue ahead of the
approaching wave front has recovered excitability, propagation of the
impulse can continue, starting a reentry process that produces either
single beats or sustained tachycardia. In clinical settings, many reentrant
arrhythmias are initiated by premature beats with abrupt onset and
termination. Reentrant tachyarrhythmias can occur in structurally normal
tissues such as the AV node as well as diseased tissues (ventricular
tachycardia arising in diseased myocardium).

Figure 36. Left ventricular aneurysm. Combination of prior myocardial infarction (Q, V1-V4),
ST elevation, and normal T wave suggests healed infarction. Persistent ST elevation
suggests constant current of injury due to aneurysm formation.

46 47
Approach be altered by disease or cardioactive drugs. The QRS morphology and
axis during atrial arrhythmias is generally similar to that of sinus beats
Disturbance of cardiac rhythm or arrhythmia implies a deviation from since the impulses travel over the same route, the AV node and His
the normal pattern such as sinus rhythm. Tachyarrhythmias are bundle branch-Purkinje system. A different and wider QRS complex is
accelerated atrial or ventricular rates that exceed what is considered sometimes noted during atrial arrhythmias. There are two common
normal. Rhythms producing cardiac slowing are frequently grouped mechanisms for this phenomena. First, the atrial impulse conducting over
together as bradyarrhythmias. When three consecutive complexes occur at the normal pathway encounters rate-related refractoriness along the
a rate exceeding 100 beats/min, the tachycardia terminology is used. For bundle branches or the Purkinje system (aberrant conduction), resulting in
proper ECG diagnosis of cardiac arrhythmias, particular attention should complete or incomplete bundle branch block or fascicular block patterns.
be given to the following: Aberrant conduction by virtue of premature impulse encroaching on
¯ Presence or absence of atrial depolarization (P wave, flutter waves, refractoriness of the bundle branches is often described as functional and
etc.). Diagnosis of cardiac arrhythmia cannot be considered complete is usually a physiological phenomenon (Figure 37, panel B). Second, the
without accounting for atrial activity. atrial impulses may use accessory pathways rather than the normal AV
¯ Ratio between atrial and ventricular activities node-His-Purkinje system to reach the ventricles.
¯ Rate and regularity of atrial and ventricular depolarizations
¯ Possible relation of atrial and ventricular depolarization and which is A
primary
¯ Site of origin

Recognition of the Site of Origin B


Atrial Arrhythmias
When electrical impulses originate in the atria, atrial activation (P wave,
flutter waves, etc.) always precedes the QRS complex (Figures 37, panels C
A and B, and 38, panel A). Recognition of atrial activity, however, is not
always possible and is particularly difficult in the following settings:
When the P-wave axis is perpendicular to the monitored lead, which
can be corrected by changing the lead or recording multiple
simultaneous ECG leads Figure 37. Atrial and ventricular premature beats. During sinus rhythms (panel A),
When atrial activation occurs during the QRS-T segment. The P wave premature beats arising from atria (narrow QRS complex) and ventricles (wide QRS
complex) are shown. P wave is marked by arrows and precedes narrow QRS complex but
cannot be directly identified if it occurs at the same {ime as the QRS follows wide QRS complex of ventricular origin. Note that atrial premature beat reaches
complex; however, it may be recognizable within the ST segment and sinus and resets it so that sinus to premature atrial beat and next sinus cycle (enclosed
T waves. The presence of P waves is often suspected by subtle area) are less than two sinus cycles (incomplete compensatory pause). Ventricular
alteration of the ST-T wave forms. premature beat does not reach sinus node; hence, there is full compensatory pause
(enclosed area is equal to two sinus cycles). Panel B: Three premature atrial beats. First
Since atrial events are primary and ventricular response is secondary, beat blocks, second and third conduct aberrantly. Panel C: A junctional premature beat (no
atrial rates equal or exceed ventricular rates during atrial arrhythmias. prior P wave). Next sinus beat is on time and conducts with longer PR interval (interpolated
Ventricular response depends on the state of AV conduction, which may junctional premature beat). Lead II or V1 was used and is indicated in this and all
subsequent rhythm traces.

48 49
Atrioventricular Junctional Arrhythmias Ventricular Arrhythmias
Tachyarrhythmias arising from the AV junction are common. When These arrhythmias arise from below bifurcation of the His bundle. Since
impulses are propagated through the AV node, the atrial activation occurs depolarization of the two ventricles occurs asynchronously, the resulting
retrogradely, and the P wave is therefore inverted in leads II, III, and aVE QRS complex is wide (Figure 38, panel C). Impulses arising from the left
However, the P wave is often inscribed simultaneously with or immediately ventricle generally exhibit a right bundle branch block pattern, while those
after the QRS complex, and determination of its presence and polarity from the right ventricle display a left bundle branch block pattern.
may be difficult. Ventricular activation during these arrhythmias proceeds Ventricular impulses originating in the interventricular septum often show a
normally; thus, QRS morphology is similar to sinus beats (Figures 37, left bundle branch block pattern. Since ventricular activation precedes
panel C, and 38, panel B). Like atrial arrhythmias, aberrant conduction atrial activation, the QRS complex precedes the P wave (Figure 37, panel
may also occur during AV junctional arrhythmias. All arrhythmias arising A). Retrograde conduction during ventricular beats depends on the state
from the AV junction or atria can also be collectively called supraventricular. of retrograde conduction across the AV node and His-Purkinje system.
Ventricular impulses may retrogradely block in the AV node, and the atria
may be dissociated or a variable ventriculoatrial response (i.e., 1:1, 3:2, or
A 2:1) may be noted.

B Electrocardiographic Diagnosis of Specific


Arrhythmias
The term sinus arrhythmia refers to sinus rhythm with physiologic
variations in sinus rates (Figure 39, panel A). In phasic sinus arrhythmia,
the change in sinus rates is related to respiratory cycles. No such relation
C is noted in the nonphasic variety.

Figure 38. Repetitive patterns of premature beats: atrial, .iunctional. and ventricular
bigeminy. Note premature QRS complex is similar to sinus beats in Panels A and B but
different in Panel C. B

Figure 39. Panel A: Sinus arrhythmia. Panel B: Sinus tachycardia. Typical P wave of sinus
origin is upright in lead I1.

50 51
Isolated Premature Beats Atrioventricular-Junctional Beats
Isolated premature beats usually originate in the region of the His
Atrial Beats bundle rather than the AV node, as frequently assumed. From the His
bundle, less time is needed to activate the ventricle than the atria;
The term atrial premature beat describes beats arising from the atrium therefore, the QRS complex is expected to precede the P wave. However,
and occurring before the expected sinus beats. Premature beats can in many cases, retrograde conduction across the AV node is absent, and
occur randomly or in a pattern (Figure 38). P-wave morphology differs from the junctional beat blocks in the AV node. In turn, the dissociated sinus
sinus beats and varies, depending on the origin of the impulse in the atria. impulse may block in the AV node or conduct with a longer PR interval
In general, beats arising in the high atria have upright P waves in leads II, due to the effect of retrograde concealed conduction of the preceding
III, and aVF, whereas those originating in the low atria have inverted P junctional beat in the AV node, which can result in the ECG pattern of
waves in those leads. Depending on the prematurity of the atrial impulse interpolated junctional beat (Figure 37, panel C).
and refractoriness of the AV node and His-Purkinje system, the P wave
may conduct with normal or prolonged PR interval with nar.row or aberrant Ventricular
QRS complex or may block and not be followed by a QRS complex.
Premature atrial beats generally depolarize and reset the sinus node so Ventricular beats may be single or multiple, early or late in the cardiac
that the next sinus beat occurs sooner than the expected sinus P wave. cycle, and have fixed or variable coupling intervals relative to the
Expressed differently, the interval from sinus to atrial premature beat plus preceding supraventricular beat. Unifocal beats show a constant
the next sinus beat measures less than two sinus cycles. This configuration, whereas multifocal beats have different QRS morphologies.
phenomenon, incomplete compensatory pause, is fairly common with Two ventricular premature beats in succession are couplets. Ventricular
atrial premature beats (Figure 37, panel A). premature beats may occur randomly or in a recurrent pattern. A
sequence of premature beats after every sinus beat is bigeminal (Figure
38); premature beats occurring after every two consecutive sinus beats are
trigeminal. The earliest ventricular premature beats occur near the peak or
A descending limb of the T wave, the ventricular myocardium being
refractory before this. Such early beats are an R-on-T phenomenon.

Sustained Tachyarrhythmias
B The usual sinus tachycardia (more than 100 beats/min) results from
enhanced automaticity of the sinus node secondary to sympathetic
stimulation during exercise, thyrotoxicosis, congestive heart failure, etc.,
and can be produced with sympathomimetic or parasympatholytic
pharmacological agents (Figure 39, panel B). In usual clinical settings, the
C rhythm is an appropriate response to increased demand for cardiac output
and oxygen supply and does not require therapy. Sinus tachycardia starts
and stops with the underlying primary process. AV conduction during
sinus tachycardia usually remains unaltered or the PR interval decreases
since the sympathetic stimulation that produces sinus acceleration also
facilitates AV nodal conduction. Atrial rates during sinus tachycardia
Figure 40. Panel A: Ectopic origin of P wave (P inverted in lead II). Rate is 73 beats/min; generally do not exceed 160 beats/min.
this arrhythmia is called a rhythm, not a tachycardia. Panel B: Unifocal atrial tachycardia;
PP rate is 160 beats/min. Degree of atrioventricular nodal block varies. Panel C: Runs of
multifocal atrial tachycardia. Note varying P morphology (arrows).

52 53
Atrial Tachycardias
Atrial tachycardias are sustained rhythms that occur in parts of the atria
other than the sinus node. Reentrant arrhythmias start and stop abruptly
and can be initiated and terminated with atrial premature beats. The
overall rates vary from 150 to 250 beats/min; the most common range is
160 to 200 beats/min. AV block of varying degree may coexist with atrial
tachycardia (Figure 40, panel B), particularly in digitalis intoxication.
Concomitant AV block facilitates recognition and polarity of the P wave. B
When all P waves have a uniform morphology, the term unifocal atrial
tachycardia is used (Figure 40, panel B).

Multifocal Atrial Tachycardias


C
The term multifocal atrial tachycardia is used when atrial-impulses show
at least three different P-wave morphologies (Figure 40, panel C). Multifocal
atrial tachycardia is frequently associated with chronic obstructive lung
disease or significant atrial disease. Ventricular response during multifocal
atrial tachycardia is often rapid because of high endogenous D
catecholamines in these patients due to stress, infection, and hypoxia, and
concomitant use of sympathomimetic agents.

Atrial Flutter
Atrial rates in untreated atrial flutter range from 250 to 350 beats/min.
Figure 41. In atrial flutter, 2:1 ratio (panel A) is difficult to appreciate since flutter waves
The P waves (so-called flutter waves or F waves) commonly have a (arrows) are obscured. Ventricular response of 150 beats/min should suggest atrial flutter
negative polarity with a saw-tooth appearance in leads II, III, and aVE since atrial rate is usually 300 beats/min. Transition of atrial flutter with varying
However, the F wave may be upright in these leads. At the usual atrial atrioventricular block to atrial fibrillation (arrow) and then sinus rhythm is evident in panel B.
rates of flutter, 1:1 AV response is unusual, and 2:1 (Figure 41, panel A), Atrial activity may not be recognizable in atrial fibrillation (panel C), and irregular RR may
3:1, or 4:1 AV ratios are far more common. During atrial flutter with 2:1 AV be the only clue to underlying atrial fibrillation. Panel D shows atrial fibrillation where two
QRS complexes are conducted aberrantly with right bundle branch block pattern.
block, flutter waves are generally obscured by the QRS-T segment (Figure
41, panel A). Higher degrees of AV block (Figure 41, panel B) facilitate
identification of flutter waves and reveal the nature of the underlying on the preexisting state of AV conduction, autonomic tone, and the
arrhythmia. Slowing of AV response can be readily accomplished with presence or absence of cardi.bactive drugs. As with atrial premature beats,
vagal maneuvers. closely coupled RR intervals during atrial fibrillation may also show
aberrant ventricular conduction (Figure 41, panel D). Aberrantly conducted
Atrial Fibrillation beats occur after a long-short sequence of RR interval and seldom occur
after a short-long RR sequence. The occurrence of aberrant conduction is
This arrhythmia is characterized by the absence of discrete P waves
favored by the longer preceding cycle lepgth and shorter coupling
and irregular ventricular response. Atrial rhythm is chaotic, with rates that intervals, and analysis of both is helpful in making the proper diagnosis.
can exceed 400 beats/min when fibrillation waves are identifiable. Aberrantly conducted beats can display either a right or left bundle branch
However, atrial activity frequently cannot be detected, and atrial fibrillation block pattern. In patients with accessory pathways such as the Kent
is diagnosed from irregular ventricular response (Figure 41, panel C). The bundle, rapid response over the accessory pathways can produce a rapid,
inherent capacity of the AV node to transmit impulses to the ventricle is wide QRS tachycardia with irregular RR intervals (Figure 25, panel D).
exceeded by rapid atrial impulses, and the ventricular response generally This could constitute a life-threatening arrhythmia in patients with Wolff-
ranges’from 110 to 160 beats/min. The ventricular response is dependent Parkinson-White syndrome.

54 55
Atrioventricular Junctional Tachycardias
The majority of AV junctional tachycardias are paroxysmal and reentrant aVR Vl M4
(Figure 42), with abrupt onset and termination. Reentry phenomena may
be entirely localized to the AV node, or the circuit may incorporate the AV
node and His-Purkinje system anterogradely and accessory pathway
retrogradely, as in patients with Wolff-Parkinson-White syndrome (Figures
25 and 43). Retrograde accessory pathway conduction may also be a pad
of the circuit when there is no evidence of preexcitation during sinus
rhythm, for instance, no shod PR interval or a delta wave. Since
anterograde conduction in most junctional tachycardias occurs over the
normal pathway, the QRS complex is normal and narrow even in patients
with Wolff-Parkinson-White syndrome, in whom a delta wave appears
during sinus rhythm (Figures 25, panel B, and 43, pane! C). A clear-cut II aVL V2 V5
distinction between AV nodal versus accessory pathway reer~try is difficult
with the surface ECG. However, location of the P wave is usually helpful.
In AV nodal reentry, the retrograde P wave is inscribed during the QRS
complex or early part of the ST segment and is difficult to detect (Figure
43, panel A). During junctional tachycardia using the accessory pathway,
the retrograde P wave occurs after the QRS complex, and the P wave may
be identifiable in the ST-T segment or even later (Figure 43, panel C).
Aberrant conduction during these arrhythmias is common, and, if not
sustained, normalization of the QRS complex during the arrhythmia
permits distinction from ventricular tachycardias. The usual atrial and III aVF V3 V6
ventricular rates range from 150 to 220 beats/min, with rates of 160-180
beats/min most common. Vagal maneuvers generally either terminate the
arrhythmias or have little effect. AV nodal block during these arrhythmias
ordinarily results in their termination. In other words, AV junctional
reentrant tachycardias cannot be sustained with concomitant AV nodal
block, which, if noted, should help distinguish AV junctional from atrial
tachycardia.

Nonparoxysmal Junctional Tachycardias


Enhanced automaticity in the region of the bundle of His is the most Figure 42. Twelve-lead electrocardiogram of narrow QRS tachycardia, which typically
probable underlying mechanism of nonparoxysmal junctional tachycardia arises in atrioventricular (AV) junction. Rate is approximately 200 beats/min. ST and T-wave
(Figure 44, panels A and B). Depending on retrograde conduction across changes in this setting do not necessarily indicate ischemia but are usually present. Pattern
the AV node, the atria may be dissociated or a 1:1 or 2:1 retrograde is compatible with AV nodal reentry, reentry by Kent bundle in retrograde direction (Figure
25, panel B), and, on occasion, atrial tachycardia.
response may be noted. The arrhythmia generally occurs in the setting of
acute myocardial infarction, after open head surgery, and sometimes with
digitalis intoxication.

56 57
Accelerated Idioventricular Rhythm
A The term accelerated idioventricular rhythm describes ventricular rates
slower than usual tachycardia rates but faster than the ventricular escape
rhythm. Rates of 75-100 beats/min are usual. Accelerated idioventricular
rhythm probably represents enhanced automaticity in the ventricles
(Figure 44, panel C) and manifests itself when sinus rates slow. The
B arrhythmia usually starts late in the cycle and frequently begins with a
fusion beat. It may spontaneously terminate or sinus rhythm acceleration
II may eventually capture the ventricle.

C A

B
Figure 43. Examples of atrioventricular (AV) junctional tachycardia. Panel A: No P wave
can be identified, suggesting AV nodal reentry. Panel B: Tachycardia is initiated by single
atrial premature beat (first arrow). Note 1:1 P-QRS relation. Final QRS complex of
tachycardia is not followed by P wave and arrhythmia terminates. Location of retrograde P
wave (end of QRS) is seen in nodal reentry but may occur with accessory pathway (AP)
reentry. Panel C: Ventricular preexcitation occurs during sinus rhythm. First atrial premature
beat (first arrow) conducts over AP and second atrial premature beat (second arrow) blocks
in AP (note normalization of QRS complex and loss of delta wave). Impulse reaches
ventricle via normal pathway and returns via AP to start orthodromic tachycardia.
Retrograde P wave can be identified in ST-T segment. (See also Figure 25, panel B.)

Figure 44. Panel A: Nonparoxysmal junctional tachycardia where sinus and junctional
pacemaker have similar rates. Panel B: Sinus impulse gradually captures ventricle in
patient who needed no treatment after open heart surgery. Impulse was intermittent only in
first days after surgery. Panel C: Typical example of accelerated idioventricular rhythm.
Ventricular pacemaker emerges after two sinus beats. Two fusion complexes can be
appreciated initially. Atrioventricular dissociation occurs during accelerated rhythms. Finally,
fusion beat is seen again before restoration of sinus rhythm. Such rhythms often emerge
when sinus rates are slower than subsidiary pacemaker rates, which are accelerated due to
acute states.

58 59
Ventricular Tachycardia
Three or more consecutive ventricular beats at a rate of more than 100
beats/min constitute the minimum criteria for diagnosis of ventricular
aVR V1 V4
tachycardia. The usual rates of well-tolerated ventricular tachycardia range
from 120 to 200 beats/min. ECG diagnosis of ventricular tachycardia is
suggested by wide QRS complexes (Figure 45); however, other criteria
should also be considered since a wide QRS complex tachycardia can
occur from impulses arising in the atria or the AV junction.
Surface ECG criteria for ventricular tachycardia include the following:
¯ Atrioventricular dissociation
¯ QRS axis between -90° and +180°
¯ Positive QRS concordance (positive QRS Vl-V6) II aVL V2 V5
¯ QRS duration of 140 msec or more with right bundle branch block
pattern and 160 msec or more with left bundle branch block pattern
¯ Combination of left bundle branch block pattern and right axis
¯ Monophasic or biphasic QRS complex with right bundle branch block
pattern and slurred or prolonged S wave in V1 with left bundle branch
block morphology
The term nonsustained designates spontaneous termination of
ventricular tachycardia in less than 30 seconds. The term sustained
ventricular tachycardia is used when the episodes are longer or require
III aVF V3 V6
immediate intervention for termination. Monomorphic tachycardia has an
identical beat-to-beat QRS appearance, whereas polymorphic ventricular
tachycardia is characterized by beat-to-beat QRS variation. Ventricular
tachycardia is usually seen with structural heart disease such as previous
myocardial infarction or primary myocardial disease. Ventricular tachycardia
is the underlying mechanism in the majority of those with structural heart
disease and wide QRS complex (120 msec or more). The differential
diagnosis includes impulses arising from the atria or AV junction with
associated anterograde preexisting or functional bundle branch block and Figure 45. Twelve-lead electrocardiogram of monomorphic ventricular tachycardia. QRS
impulses arising from the atria and anterogradely conducting over an complex is wide (200 msec), with right axis (+120°) and marked slurring of S wave on V2
accessory pathway. When impulses arise from the atria and ventricular and V3. Patient had history of prior myocardial infarction.
response is secondary, atrial impulses either equal or exceed ventricular
rates. A 1:1 AV response is usual in reentrant AV junctional tacjh,4,ycardias Torsade de pointes refers to a rapid polymorphic ventricular tachycardia
with bundle branch block. From an ECG standpoint, the presence of AV associated with congenital or acquired prolonged QT interval syndrome
dissooiation (Figure 46, panel A), fusion, or normal beats during a wide (Figure 46, panel B). This arrhythmia has a characteristic morphology that
QRS complex tachycardia suggest ventricular origin. However, intermittent varies from beat to beat, with progressive shift of the QRS axis around the
normalization and fusion beats may also occur during atrial fibrillation in baseline. In most clinical situations, torsade de pointes results from use of
patients with Wolff-Parkinson-White syndrome. At times, it is difficult to antiarrhythmic drugs, hypokalemia, hypomagnesemia, or a combination of
distinguish ventricular tachycardia from supraventricular tachycardia with these. Correct identification is essential since prompt correction of these
aberrant conduction. abnormalities is lifesaving.

60 61
Ventricular fibrillation is rapid, disorganized ventricular depolarization Bradyarrhythmias
accompanied by loss of pumping action of the heart (Figure 46, panels C
and D). It is generally initiated by ventricular premature beats occurring in
quick succession in chronically diseased myocardium, acute myocardial Sinus Bradycardia
ischemia, electrolyte imbalance, and prolonged QT interval. Without
prompt DC cardioversion, this arrhythmia is usually fatal. Sinus bradycardia is the term for a sinus rate of less than 60 beats/min
seen in the normal adult population. Sinus bradycardia during exercise,
fever, or congestive heart failure is abnormal. Rates of less than 45
beats/min are also considered abnormal (Figure 47, panel A), and in the
absence of drugs such as digitalis, I~-blockers, and calcium channel
blockers, reflect abnormality in the sinus node.

A
B

B
C

C
D

D
Figure 46. Panel A: Abrupt onset of monomorphic ventricular tachycardia. Atrioventricular
dissociation can be appreciated in first few beats (first and last arrows). Other arrows
indicate expected location of P waves based on sinus rate seen in first four beats. Panel B:
Classic examples of torsade de pointes with prolonged QT interval. Notice typical beat-to-
beat change in QRS configuration and gradual transition of QRS complex from negative to
positive complex relative to baseline. Panel C: Abrupt onset of ventricular fibrillation in Figure 47. Panel A: Sinus bradycardia (44 beats/rain). Panels B and C: Cessation of sinus
patient with both quinidine and digitalis toxicity. Panel D: Continuation of ventricular activity. However, in panel B, subsidiary pacemaker does not emerge, whereas junctional
fibrillation. escape rhythm is seen in panel C. Exact mechanism of loss of sinus P wave, sinus arrest
versus sinoatrial exit block, cannot be diagnosed with confidence in either trace. Panel D:
Blocked atrial premature beats (arrows) simulate sinus pauses. P waves in ST-T segment of
beat preceding pause can be suspected by comparison with other beats in tracing.

62 63
Sinus Arrest and Sinoatrial Exit Block Second-Degree Atrioventricular Block (Intermittent AV
Sudden disappearance of sinus P waves for variable intervals can Conduction)
produce different patterns (Figure 47, panels B and C). Since sinus node Traditionally, second-degree AV block has been categorized as one of
activity is not recorded on the surface ECG, it is difficult to determine if two types. Type I, also called the Wenckebach phenomenon and Mobitz
sinus node automaticity or sinoatrial conduction abnormalities are type I, is characterized by progressive prolongation of the PR interval until
responsible in a given patient. When PP intervals have a pattern or a P wave is blocked and the cycle is repeated (Figure 48, panel B).
multiple or both of the basic sinus cycle, the term sinoatrial block is Maximum increment of the PR interval usually takes place with the
generally used. Both types of sinoatdal block can be diagnosed from the second conducted beat. RR intervals decrease progressively despite
surface ECG. In type I (VVenckebach phenomenon), the PP cycle is increasing PR intervals. The Wenckebach phenomenon most frequently
progressively shortened until there is a pause and the cycle is repeated. occurs in the AV node; however, it is also common in the bundle branches
The pause is due to the dropped P wave and measures less than twice
the PP cycle. It is similar to the behavior of RR intervals in type I second-
degree AV block. Type II second-degree sinoatrial exit block is A
characterized by an unexpected drop of the P wave, and the resultant
pause is a multiple of the basic sinus cycle. Blocked atrial premature beats
sometimes mimic second-degree sinoatrial block (Figure 47, panel D).
Third-degree sinoatrial exit block cannot be distinguished from sinus arrest
when the sinus node ceases to fire. Under such circumstances, subsidiary B
pacemakers in the AV junction or ventricles may take over (Figure 47,
panel C).

Bradycardia-Tachycardia Syndrome
The term bradycardia-tachycardia syndrome is used when episodes of C
sinus bradycardia alternate with atrial or AV junctional tachyarrhythmias. It
is one part of the so-called sick sinus syndrome, the other being the
various sinus bradyarrhythmias listed above.

D
Atrioventricular Block
First-Degree Atrioventricular Block (Prolonged AV Conduction)
A prolonged PR interval (greater than 200 msec) is called first-degree
AV b/ock (Figure 48, panel A). The PR interval of the surface ECG can be Figure 48. First- and second-degree atrioventricular (AV) block. Panel A: Prolonged PR (1°
subdivided into intra-atrial, AV nodal, and His-Purkinje system conduction AV block), a 1:1 P-QRS ratio with narrow QRS complex of conducted beat. Panels B and C:
times. An increase in the PR interval can result from conduction delays in Two types of second-degree AV block. Type 1 (Wenckebach phenomenon) is characterized
by progressive PR increase before block (panel B) and Mobitz type II with abrupt block of
any of these areas. However, first-degree AV block most commonly results P wave without significant PR prolongation in prior beat (panel C). Mobitz type II block can
from prolonged AV nodal conduction time, particularly in the presence of a be unpredictable and can lead to abrupt onset of prolonged period of third-degree AV block
narrow QRS complex. Drugs such as digitalis, ~-blockers, and calcium (panel D). Ventricular escape mechanism emerges when P waves cannot conduct. In
channel blockers, which prolong AV nodal conduction, can also produce panels A and B, site of block is AV node, as suggested by long PR and narrow QRS of
first-degree AV block, whereas atropine and isoproterenol can shorten the conducted beat. His-Purkinje system is site of block in panels C and D, which is typical in
Mobitz type I1.
PR interval by enhancing AV nodal conduction. Less commonly, first-
degree AV block can result from delay distal to the AV node such as the
His-Purkinje system.
64 65
and the bundle of His. Electrocardiographically, AV nodal and intra-His the AV junction, with resultant narrow QRS complexes (Figure 49, panel
blocks are associated with a narrow QRS complex of conducted beats, B), whereas in third-degree AV block localized to the bundle branches,
whereas infra-Hisian block is generally seen with a bundle branch block ventricular rhythm is maintained by a pacemaker in the Purkinje fibers,
pattern of conducted beats. AV nodal blocks can be differentiated from with resultant wide QRS complexes (Figure 49, panel C). The junctional
infranodal blocks (His bundle and bundle branches) by observing the pacemaker rate is usually faster (40-60 beats/rain) compared with the
magnitude of PR change from beat to beat, best appreciated with the peripheral Purkinje network (20-40 beats/min).
beats immediately before and after the blocked P wave. In AV nodal type I
second-degree block, PR shortening after the blocked P wave frequently
exceeds 100 msec, whereas in infranodal blocks, this magnitude of A
change in the PR interval is unusual.
Type II (Mobitz type II) is characterized by a constant PR interval
preceding a blocked P wave (Figure 48, panel C). The site of block is
usually the His-Purkinje system. Conducted P waves may display a
normal QRS complex if the site of block is within the bundle of His, or a B
bundle branch block pattern if it is more distal, as in the bundle branches,
which is more common. On occasion, AV nodal block of a P wave may
also be preceded by a constant PR interval; however, the baseline PR in
such cases is long and a block of the P wave under such circumstances
is not totally unexpected. C
2:1 Block
The term 2:1 block indicates an AV block where the P wave is. not
propagated to the ventricles. As with all other forms, the site of block can
be intranodal or infranodal. A 2:1 block in the AV node or bundle of His is Figure 49. 2:1 ratio of P to QRS. Conducted complexes show right bundle branch block.
generally accompanied by normal QRS complexes of the conducted Site of block is likely to be His-Purkinje system. Panels B and C: Examples of third-degree
beats, whereas the conducted beats show a bundle branch block pattern AV block, where no P waves are conducted. Escape mechanism is from atrioventricular (AV)
when the site of block is more distal in the bundle branches (Figure 49, junction in panel B (narrow QRS) and most likely Purkinje system in panel C (wide QRS).
Note relatively slow rates of ventricular escape (panel C) as compared with AV junction
panel A). If the PR interval of conducted beats is significantly prolonged, (panel B). Findings in panel B are typical of AV nodal block, while panel C shows typical
the site is generally the AV node. Diagnosis is difficult in the presence of a findings of block within His-Purkinje system.
normal PR interval and a bundle branch block pattern of the conducted
beats. Analysis of previous tracings showing a transition from a Mobitz
type I or II to a 2:1 AV block is frequently helpful in determining the site of
block. This is important since patients with a block in the His-Purkinje
system invariably need a permanent pacemaker, regardless of the type
of block.

Third-Degree Atrioventricular Block


In third-degree AV block (complete AV block, no AV conduction), no
atrial impulses reach the ventricles, and ventricular rhythm is maintained
by a subsidiary pacemaker (Figure 48, panel D, and Figure 49, panels B
and C). Since subsidiary pacemakers must be below the level of block,
their location is in part determined by the site of block. In third-degree AV
nodal block, the ventricular rhythm is usually maintained by pacemakers in

66 67
Functional or Physiologic Blocks
The failure of P waves to depolarize the ventricle at sinus rates signifies
abnormal AV conduction. However, at faster atrial rates such as atrial aVR Vl V4
flutter or atrial tachycardia, the capacity of the AV node to conduct
impulses may be saturated and a varying degree of physiological block
may exist (Figure 41). Acceleration of sinus or atrial rates from sympathetic
stimulation as seen during exercise is not accompanied by such a block
since the sympathetic stimulation concomitantly also facilitates AV nodal
conduction.

V4 II aVL V2 V5

II aVL V2 V5

III aVF V3 V6

III aVF V3 V6

Figure 51. Atrioventricular (AV) sequential pacing from high right atrium (upright P wave in
leads II, III, and aVF, and usually from atrial appendage) is followed by QRS from right
ventricular apex as pacing site. PR (AV delay) is programmed in this case to 150 msec.
Large pacing spikes suggest unipolar pacing from both chambers.
Figure 50. Ventricular pacing is suggested by wide QRS, which begins with artificial
pacemaker stimulus artifact. Left axis in limb leads suggests apical pacing. Left bundle
branch block morphology in leads I and V1 indicates right ventricle as pacing site. Although
typically Vs and V6 should also show QRS similar to that in lead I, due to cardiac
enlargement in this and other cases, chest electrode position more posterior to Ve may be
needed for positive QRS complex. Small pacing artifacts suggest bipolar pacing.

68
69
Atrioventricular Dissociation Electrocardiogram of the Paced Rhythms
AV dissociation is a rhythm in which atrial and ventricular activation
occurs from different pacemakers. The atrial rhythm can be of sinus origin
or from any of the atrial arrhythmias listed previously. Ventricular activation
may be from either junctional or lower pacemakers. Third-degree AV block
is one form of AV dissociation. The latter, however, is common in the
presence of intact AV conduction. AV dissociation in the presence of intact
AV conduction can occur when rates of subsidiary pacemakers, junctional Since their introduction several decades ago, pacemakers have become
or ventricular, exceed the atrial and there is associated VA block, as seen progressively more complex. Consequently, a significant discussion of
in ventricular tachycardia. This contrasts with AV dissociation during third- paced rhythms is beyond the scope of this publication. However, 12-lead
degree AV block, where atrial rates usually exceed ventricular rates. ECGs of single-chamber ventricular pacing and dual-chamber (AV
sequential) pacing are presented in Figures 50 and 51, respectively.
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