Electrocardiographic
Interpretation of Cardiac Muscle
and Coronary Blood Flow
Abnormalities: Vectorial Analysis
From the discussion in Chapter 10 of impulse transmission through the heart, it is obvious that any
change in the pattern of this transmission can cause
abnormal electrical potentials around the heart and,
consequently, alter the shapes of the waves in the
electrocardiogram. For this reason, almost all
serious abnormalities of the heart muscle can be
diagnosed by analyzing the contours of the different
waves in the different electrocardiographic leads.
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Unit III
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The Heart
aVF
III
aVL +
+ aVR
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-30
aVL
aVR
III
Figure 121
120
90
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II
Figure 123
Axes of the three bipolar and three unipolar leads.
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+270
-100
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59
-90
Figure 122
Vectors drawn to represent potentials for several different hearts,
and the axis of the potential (expressed in degrees) for each
heart.
Chapter 12
133
Figure 125
Determination of the projected vector B along the axis of lead I
when vector A represents the instantaneous potential in the
ventricles.
II
III
A
C
-
III
+
II
+
Figure 124
Determination of a projected vector B along the axis of lead I when
vector A represents the instantaneous potential in the ventricles.
Figure 126
Determination of projected vectors in leads I, II, and III when
vector A represents the instantaneous potential in the ventricles.
134
Unit III
instantaneous electrical potential of a partially depolarized heart. To determine the potential recorded at
this instant in the electrocardiogram for each one of
the three standard bipolar limb leads, perpendicular
lines (the dashed lines) are drawn from the tip of
vector A to the three lines representing the axes of the
three different standard leads, as shown in the figure.
The projected vector B depicts the potential recorded
at that instant in lead I, projected vector C depicts the
potential in lead II, and projected vector D depicts the
potential in lead III. In each of these, the record in
the electrocardiogram is positivethat is, above the
zero linebecause the projected vectors point in the
positive directions along the axes of all the leads.
The potential in lead I (vector B) is about one half that
of the actual potential in the heart (vector A); in lead
II (vector C), it is almost equal to that in the heart; and
in lead III (vector D), it is about one third that in the
heart.
An identical analysis can be used to determine
potentials recorded in augmented limb leads, except
that the respective axes of the augmented leads (see
Figure 123) are used in place of the standard bipolar
limb lead axes used for Figure 126.
The Heart
Electrocardiogram During
RepolarizationThe T Wave
After the ventricular muscle has become depolarized,
about 0.15 second later, repolarization begins and
Chapter 12
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135
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E
Figure 127
Shaded areas of the ventricles are depolarized (); nonshaded areas are still polarized (+). The ventricular vectors and QRS complexes
0.01 second after onset of ventricular depolarization (A); 0.02 second after onset of depolarization (B); 0.035 second after onset of
depolarization (C); 0.05 second after onset of depolarization (D); and after depolarization of the ventricles is complete, 0.06 second after
onset (E).
proceeds until complete at about 0.35 second.This repolarization causes the T wave in the electrocardiogram.
Because the septum and endocardial areas of the
ventricular muscle depolarize first, it seems logical that
these areas should repolarize first as well. However,
this is not the usual case because the septum and other
endocardial areas have a longer period of contraction
than most of the external surfaces of the heart. Therefore, the greatest portion of ventricular muscle mass to
repolarize first is the entire outer surface of the ventricles, especially near the apex of the heart. The endocardial areas, conversely, normally repolarize last. This
sequence of repolarization is postulated to be caused
by the high blood pressure inside the ventricles during
contraction, which greatly reduces coronary blood
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Unit III
The Heart
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Figure 129
III
Figure 128
Generation of the T wave during repolarization of the ventricles,
showing also vectorial analysis of the first stage of repolarization.
The total time from the beginning of the T wave to its end is
approximately 0.15 second.
Vectorcardiogram
It has been noted in the discussion up to this point that
the vector of current flow through the heart changes
rapidly as the impulse spreads through the
myocardium. It changes in two aspects: First, the
vector increases and decreases in length because of
increasing and decreasing voltage of the vector.
Second, the vector changes direction because of
Chapter 12
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I
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0
180
Depolarization
QRS
120
Repolarization
T
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III
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III
Figure 1210
QRS and T vectorcardiograms.
Figure 1211
Plotting the mean electrical axis of the ventricles from two electrocardiographic leads (leads I and III).
138
Unit III
The Heart
side of the heart than on the other side, and this allows
excess generation of electrical potential on that side.
Second, more time is required for the depolarization
wave to travel through the hypertrophied ventricle
than through the normal ventricle. Consequently, the
normal ventricle becomes depolarized considerably in
advance of the hypertrophied ventricle, and this causes
a strong vector from the normal side of the heart
toward the hypertrophied side, which remains strongly
positively charged. Thus, the axis deviates toward the
hypertrophied ventricle.
Vectorial Analysis of Left Axis Deviation Resulting from
Hypertrophy of the Left Ventricle. Figure 1212 shows
the three standard bipolar limb lead electrocardiograms. Vectorial analysis demonstrates left axis deviation with mean electrical axis pointing in the
-15-degree direction. This is a typical electrocardiogram caused by increased muscle mass of the left ventricle. In this instance, the axis deviation was caused by
hypertension (high arterial blood pressure), which
caused the left ventricle to hypertrophy so that it could
pump blood against elevated systemic arterial pressure. A similar picture of left axis deviation occurs
when the left ventricle hypertrophies as a result of
aortic valvular stenosis, aortic valvular regurgitation, or
any number of congenital heart conditions in which the
left ventricle enlarges while the right ventricle remains
relatively normal in size.
Vectorial Analysis of Right Axis Deviation Resulting
from Hypertrophy of the Right Ventricle. The electro-
II
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III
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I-
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Figure 1212
Left axis deviation in a hypertensive heart (hypertrophic left ventricle). Note the slightly prolonged QRS complex as well.
100
5
12
6
4
LA
RA
V4
V 4
DI A
R
VT
R
LL
FIGURE 4.27 How the six precordial ECGs are obtained from the chest.
II and III, V1, V3 and aVR. Note the inverted QRS spike in leads V1 and aVR (also
seen in V2; not shown).
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V II (mV)
1.0R
0.8
0.6
0.4
T
0.2
P
SPR
SST
I PR
I QT
TH
FIGURE 4.28 A normal Lead II ECG cycle, showing intervals and amplitudes used in
diagnosis.
rally, the frontal ECG vector tip locus depends on the state of the cardiac cycle. The
ECG Leads I, II and III, or aVR, aVL and aVF define a set of three vector axes
spaced 60 apart, lying in the frontal plane. The three ECG voltages are treated as
three vectors that, at any time, are resolved by vector addition to a vector or point
at the vector + tip in the frontal plane. An example of a vector sum of VI, VII and
VIII in the frontal plane at some time t1 is shown in Figure 4.30. This is V(t1) = VI
(t1) + VII (t1) + VIII (t1). The vector axes are at 0, 60, and 120. The (positive)
tip of the vector V(t1) defines a point. If the voltage vectors VI, VII and VIII are
sampled throughout the cardiac cycle, we can generate a closed curve connecting
the points at the end of V(tk). This curve is the frontal plane vector cardiogram
(VCG). This type of vector cardiogram is easily calculated by computer. The voltages
VI, VII and VIII, are sampled and converted into X and Y components:
Vx(tk) = VI (tk) + VII (tk)cos(60) + VIII(tk)cos(120)
4.77A
4.77B
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Lead I
t
R
Lead II
P
Lead III
Lead V3
LeadV1
Lead aVR
FIGURE 4.29 A summary of typical normal ECG wave-shapes recorded from various
defined leads.
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V I (t 1)
(t 1 )
V II I (t 1 )
V II (t 1)
(V I + V II )
(V I + V II + V III )
@ t1
III
II
FIGURE 4.30 The vector addition of ECG waveforms from leads I, II and III in the frontal
plane. Notice the three, fixed vector axes are spaced 60 apart.
Next, we put the net vector into polar form. Its magnitude is:
V(t k ) = Vx2 (t k ) + Vy2 (t k )
4.78
(tk) = tan1{Vy(tk)/Vx(tk)}
4.79
4.80
Note that, in this vector convention, positive (tk) is measured clockwise from the
+ x-axis.
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Actually, there are three loops in the VCG, a very small one for the P-wave,
another large one for the QRS complex, and a third small one for the T wave.
Representative vector loops for the QRS and T waves in the frontal plane are shown
in Figure 4.31. The large VCG loop from the QRS complex has great utility in
diagnosing a multitude of cardiac problems, ranging from conduction blocks (bundle
branch blocks) to ventricular hypertrophy, various ventricular myopathies, coronary
artery ischemia, localization of infarctions, etc. (Guyton, 1991). VCG loops vary
from beat to beat, and the cardiologist must take this small normal variability into
consideration in making a diagnosis.
T Loop
QRS Loop
(Frontal plane)
III
(120)
II
(60)
FIGURE 4.31 A typical frontal vectorcardiogram derived from lead I, II and III ECG voltages. Note that there are two loops, both traversed counterclockwise, one from the QRS
complex, and the smaller one from the T-wave.
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Z
Horizontal plane
QRS
Frontal plane
X
P
T
T
QRS
Sagittal plane
Z
T
QRS
FIGURE 4.32 Frontal, sagittal and horizontal projections of a 3-D vector cardiogram
recorded using a multiple 3-D electrode array such as the Frank system.
The Frank VCG System using seven electrodes is shown in Figure 4.33. Note
the Frank axis convention where the positive x-axis points left, positive y is down,
and positive z is points dorsal. The Frank system uses a resistive summing circuit
to resolve the three orthogonal components of the VCG with 13% error, compared
with a gold standard system that summed the outputs of 150 electrodes. The nineelectrode precordial system had 10% error compared with the 150-electrode system,
and an experimental 30-electrode system gave only 1% error (Rawlings, 1991).
AND
DIAGNOSIS
An experienced cardiologist can read a standard set of ECG traces or a VCG and
make a diagnosis based on education and experience. When one considers the many
things that can go wrong with the heart, this diagnostic ability is remarkable.
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R
I
7.15R
Vx
DA
3.27R
Z
E
2.32R
M
I
A
E
3.74R
C
45
C
4.59R
Y
1.28R
A
13.3R
Vz
6.56R
DA
1.18R
M
2.90R
LL
Vy
1.53R
DA
H
FIGURE 4.33 Schematic of the Frank VCG electrode system. The DAs are medical isolation
amplifiers. The three analog voltages Vx, Vy and Vz are used to generate the 3-D VCG display.
Biomedical engineers, computer scientists, and cardiologists have tried since the
days of the DEC PDP-series computers in the 70s to design pattern recognition
software that could diagnose common cardiac pathologies, given various ECG lead
voltages as inputs. Early ECG diagnostic programs would measure waveform features such as the various intervals and segment lengths associated with the PQRST
elements of the lead II ECG waveform, and also examine peak heights and slopes,
and then compare them with a standard database for statistical analysis. Certain sets
of out-of-range ECG features could then be assigned probabilities for various cardiac
diseases. Such programs were good for gross screening, but were nothing you would
want to bet your life on.
More sophisticated techniques have now emerged for ECG analysis, including
the use of Fourier-transformed ECGs, time-frequency analysis of ECGs (Clayton et
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al., 1998), and 2-D frequency-domain analysis of VCG loops (Lei et al., 1997). Work
has also been done with trainable artificial neural networks (ANNs) for the diagnosis
of cardiac pathologies, applying the trainable ANN to recognizing anomalies in the
time-domain QRS complex (Barro et al., 1998).
4.4.5 DISCUSSION
As noninvasive diagnostic modalities, the ECG and VCG are probably among the more
cost-effective presently available. The electrodes are simple and inexpensive, the ECG
signals are conditioned by inexpensive differential isolation amplifiers, and their digitized outputs are easily processed by computer to form moving chart recorder displays
or vector displays. Much can be learned from the various waveforms of the different
ECG leads, and from the VCG about the state of the heart muscle over its surface, and
the state of the internal excitation conduction system of the heart.
OF
EMGS
There are several types of muscle in the body, e.g., cardiac, smooth, and striated.
Striated muscle in mammals can be further subdivided into fast and slow muscles
(Guyton, 1991). Fast muscles are used for fast movements; they include the two
gastrocnemii laryngeal muscles, extraocular muscles, etc. Slow muscles are used for
postural control against gravity; they include the soleus, abdominal muscles, back
muscles, neck muscles, etc. EMG recording is generally carried out on both slow
and fast skeletal muscles. It can also be done on less superficial muscles such as the