(Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities (Vectorial analysis pdf - The Heart

the vector is said to extend in the direction of 0 degrees, as shown in Figure

When a vector is exactly horizontal and directed toward the person’s left side,

Direction of a Vector Is Denoted in Terms of Degrees

current is considerable in quantity, the potential is large, and the vector is long.

cles in a direction from base toward apex. Furthermore, because the summated

black

instantaneous mean vector,

erated potential at this particular instant, called the

apex than in the upward direction. Therefore, the summated vector of the gen-

from the depolarized areas toward the still polarized areas. Overall, consider-

long elliptical arrows. Some current also flows inside the heart chambers directly

and the nondepolarized areas on the outside of the heart, as indicated by the

tation, electrical current flows between the depolarized areas inside the heart

of the apical endocardial walls of the two ventricles. At this instant of heart exci-

area and the negative signs, depolarization of the ventricular septum and parts

Figure 12–1 shows, by the shaded

“Resultant” Vector in the Heart at Any Given Instant.

convention, the length of the arrow is drawn

Also, by

with the arrowhead in the positive direction.

ated by the current flow,

particular direction in the heart at a given instant during the cardiac cycle. A

tours of the electrocardiogram, one must first become thoroughly familiar with

Use of Vectors to Represent Electrical Potentials

of Electrocardiograms

Principles of Vectorial Analysis

waves in the different electrocardiographic leads.

electrocardiogram. For this reason, almost all

consequently, alter the shapes of the waves in the

mission through the heart, it is obvious that any

From the discussion in Chapter 10 of impulse trans-

Abnormalities: Vectorial Analysis

131

Electrocardiographic

Interpretation of Cardiac Muscle

and Coronary Blood Flow

change in the pattern of this transmission can cause
abnormal electrical potentials around the heart and,

serious abnormalities of the heart muscle can be
diagnosed by analyzing the contours of the different

Before it is possible to understand how cardiac abnormalities affect the con-

the concept of vectors and vectorial analysis as applied to electrical potentials
in and around the heart.

Several times in Chapter 11 it was pointed out that heart current flows in a

vector is an arrow that points in the direction of the electrical potential gener-

proportional to the voltage of the

potential.

ably more current flows downward from the base of the ventricles toward the

is represented by the long

arrow drawn through the center of the ventri-

this chapter.

limb leads I, II, and III, to understand the remainder of

axes and their polarities, particularly for the bipolar

minus signs in the figure.

The

of the axes of all these leads are shown in Figure 12–3,

30 degrees. The directions

90 degrees; and aVL

aVF,

120 degrees; lead aVR,

By similar analysis, it can be seen that lead III has

60 degrees.

connects in the lower left-hand corner. Therefore, the

right arm and left leg. The right arm connects to the

In recording lead II, electrodes are placed on the

0 degrees.

the positive electrode to the left, the axis of lead I is

trodes lie exactly in the horizontal direction, with

placed respectively on the two arms. Because the elec-

of the lead. Lead I is recorded from two electrodes

ative electrode to positive electrode is called the “axis”

opposite sides of the heart, and the direction from neg-

unipolar limb leads are described. Each lead is actu-

In Chapter 11, the three standard bipolar and the three

in the chapter.

with respect to the base of the heart, as discussed later

ization wave, the apex of the heart remains positive

direction. This means that during most of the depolar-

through the center of Figure 12–2 in the

59 degrees, which is shown by vector

mean QRS vector,

through the ventricles, called the

In a normal heart, the average direction of the

270) degrees.

it extends straight upward, it has a direction of

180 degrees; and when

to right, it has a direction of

90 degrees; when it extends from the person’s left

from above and straight downward, it has a direction

vectors rotates clockwise: when the vector extends

12–2. From this zero reference point, the scale of

132

Unit III

The Heart

-90 (or

vector during spread of the depolarization wave

about

A drawn

+59-degree

Axis for Each Standard Bipolar Lead
and Each Unipolar Limb Lead

ally a pair of electrodes connected to the body on

torso in the upper right-hand corner and the left leg

direction of this lead is about

an axis of about

+210 degrees;

which is known as the hexagonal reference system.
polarities of the electrodes are shown by the plus and

The reader must learn these

- -

- - -

+ +

+ + + + + +

Mean vector through the partially depolarized ventricles.

Figure 12–1

∞

270

∞

180

∞

100

∞

120

∞

heart.

and the “axis” of the potential (expressed in degrees) for each

Vectors drawn to represent potentials for several different hearts,

Figure 12–2

∞

210

∞

aVR

aVF

aVL

III

120

∞

Axes of the three bipolar and three unipolar leads.

Figure 12–3

In Figure 12–6, vector

Vectorial Analysis of Potentials in the Three Standard

the entire voltage of the vector will be recorded.

almost exactly the same axis as the lead axis, essentially

Conversely,

is very low.

voltage recorded in the electrocardiogram of this lead

tion almost perpendicular to the axis of the lead, the

0.3 millivolts. This figure demon-

will be slight, about

in the electrocardiogram), and the voltage recorded

direction, indicating that at this particular instant, the

Vector

lead I, we draw a perpendicular line from the tip of

livolts. To determine the potential actually recorded in

direction of 100 degrees, and its voltage is again 2 mil-

right. In this instance, the instantaneous vector has a

analysis. In this example, vector

Figure 12–5 shows another example of vectorial

times 2 millivolts, or about

cardiogram of lead I is positive. And the instantaneous

the positive end of the lead I axis, which means that

I axis. The arrow of this projected vector points toward

to the lead I axis, and

in lead I, a line perpendicular to the axis of lead I is

axis of lead I in the 0-degree direction. To determine

is shown again, and a line is drawn to represent the

is 2 millivolts. In the diagram below the heart, vector

of the potential, represented by the length of vector

55 degrees, and the voltage

of current flow in the ventricles. In this instance, the

Figure 12–4 shows a partially depolarized heart;

follows.

gram of each lead for a given vector in the heart, as

vectors and, second, the axes of the leads, it is possible

Now that we have discussed, first, the conventions for

Recorded in Different Leads

Vectorial Analysis of Potentials

Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities

Chapter 12

133

representing potentials across the heart by means of

to use these together to determine the instantaneous
potential that will be recorded in the electrocardio-

vector A represents the instantaneous mean direction

direction of the vector is

how much of the voltage in vector A will be recorded

drawn from the tip of vector A
a so-called projected vector (B) is drawn along the lead

the record momentarily being recorded in the electro-

recorded voltage will be equal to the length of B
divided by the length of A
1 millivolt.

A represents the elec-

trical potential and its axis at a given instant during
ventricular depolarization in a heart in which the left
side of the heart depolarizes more rapidly than the

vector A to the lead I axis and find projected vector B.

B is very short and this time in the negative

recording in lead I will be negative (below the zero line

strates that when the vector in the heart is in a direc-

when the heart vector has

Bipolar Limb Leads.

A depicts the

vector A represents the instantaneous potential in the ventricles.

Determination of a projected vector B along the axis of lead I when

Figure 12–4

when vector A represents the instantaneous potential in the

Determination of the projected vector B along the axis of lead I

Figure 12–5

ventricles.

III

vector A represents the instantaneous potential in the ventricles.

Determination of projected vectors in leads I, II, and III when

Figure 12–6

about 0.15 second later, repolarization begins and

Repolarization—The T Wave

Electrocardiogram During

deflection is the S wave.

Figure 12–7 is the R wave, and the final negative

vector occurs. The major positive deflection shown in

side, which creates a weak vector from left to right for

the Q wave. When it occurs, it is caused by initial depo-

which is not shown in Figure 12–7; this depression is

depression at its beginning in one or more of the leads,

three standard bipolar limb leads.

Thus, the QRS complexes are completed in the

zero.

becomes zero, and the voltages in all leads become

and no electrical potential is generated. The vector

depolarized, so that no current flows around the heart

depolarization, the entire ventricular muscle mass is

In Figure 12–7

voltage of lead I is still positive.

both negative—that is, below the line—whereas the

this time, the voltages recorded in leads II and III are

ized positive. Because of the direction of the vector at

of the left ventricle, and it is short because only a

depolarization, the heart vector points toward the base

In Figure 12–7

voltage in lead I to that in lead III is increasing.

to depolarize than the right. Therefore, the ratio of the

the other epicardial surfaces of the heart. Also, the axis

electronegative, neutralizing much of the positivity on

depolarization, the heart vector is becoming shorter

In Figure 12–7

become depolarized. Therefore, the voltages in all

after onset of depolarization, the heart vector is long

In Figure 12–7

of the leads. The voltage in lead II is greater than the

fore, all electrocardiographic voltages are low, as

of the ventricles—the septum—is depolarized. There-

time, the vector is short because only a small portion

0.01 second after the onset of depolarization. At this

begun to be depolarized, representing an instant about

In Figure 12–7

summary of this sequence follows.

in detail by the procedure given here. A short

understood. Each of these analyses should be studied

successive normal vectors presented in Figure 12–7 be

vectorial analysis, it is essential that this analysis of the

will cause recording below the zero line.

diogram above the zero line, whereas a negative vector

vector in a lead will cause recording in the electrocar-

Keep in mind that a positive

electrocardiographic leads. To the right in each figure

the ventricle in each figure. Each of these vectors is

At each stage in Figure 12–7, parts

C, D,

Figure 12–7

the outside of the heart, as shown progressively in

Finally, it spreads through the ventricular muscle to

der of the two ventricles, as shown in Figure 12–7

. Next, depolarization

of the ventricle in Figure 12–7

the septum, as demonstrated by the shaded portion

cardial surface of the septum. Then depolarization

through the atrioventricular bundle, the first part of

When the cardiac impulse enters the ventricles

Ventricles—The QRS Complex

Intervals During Depolarization of the

Vectors That Occur at Successive

Normal Electrocardiogram

Vectorial Analysis of the

limb lead axes used for Figure 12–6.

Figure 12–3) are used in place of the standard bipolar

potentials recorded in augmented limb leads, except

), it is about one third that in the

), it is almost equal to that in the heart; and

); in lead

The potential in lead I (vector

positive directions along the axes of all the leads.

the electrocardiogram is positive—that is, above the

potential in lead III. In each of these, the record in

potential in lead II, and projected vector

at that instant in lead I, projected vector

The projected vector

three different standard leads, as shown in the figure.

the three standard bipolar limb leads, perpendicular

larized heart. To determine the potential recorded at

134

Unit III

The Heart

instantaneous electrical potential of a partially depo-

this instant in the electrocardiogram for each one of

lines (the dashed lines) are drawn from the tip of
vector A to the three lines representing the axes of the

B depicts the potential recorded

C depicts the

D depicts the

zero line—because the projected vectors point in the

B) is about one half that

of the actual potential in the heart (vector A
II (vector C
in lead III (vector D
heart.

An identical analysis can be used to determine

that the respective axes of the augmented leads (see

the ventricles to become depolarized is the left endo-

spreads rapidly to involve both endocardial surfaces of

spreads along the endocardial surfaces of the remain-

B and

and E.

A to E, the

instantaneous mean electrical potential of the ventri-
cles is represented by a red vector superimposed on

then analyzed by the method described in the preced-
ing section to determine the voltages that will be
recorded at each instant in each of the three standard

is shown progressive development of the electrocar-
diographic QRS complex.

Before proceeding with further consideration of

A, the ventricular muscle has just

recorded to the right of the ventricular muscle for each

voltages in leads I and III because the heart vector
extends mainly in the same direction as the axis of lead
II.

B, which represents about 0.02 second

because much of the ventricular muscle mass has

electrocardiographic leads have increased.

C, about 0.035 second after onset of

and the recorded electrocardiographic voltages are
lower because the outside of the heart apex is now

of the vector is beginning to shift toward the left side
of the chest because the left ventricle is slightly slower

D, about 0.05 second after onset of

minute portion of the ventricular muscle is still polar-

E, about 0.06 second after onset of

Sometimes the QRS complex has a slight negative

larization of the left side of the septum before the right

a fraction of a second before the usual base-to-apex

After the ventricular muscle has become depolarized,

repolarization is small. Later, the vector becomes

first, the vector is relatively small because the area of

the apex until it disappears in the last stage. At

white areas—the repolarized areas. At each stage,

In Figure 12–8, five stages of repolarization of the

T wave in all three bipolar limb leads is positive, which

As a result, the normal

repolarize before the inner surfaces, the positive end

tion in the endocardial areas.

flow to the endocardium, thereby slowing repolariza-

contraction, which greatly reduces coronary blood

dial areas, conversely, normally repolarize last. This

The endocar-

cles, especially near the apex of the heart.

repolarize first is the entire outer surface of the ventri-

fore,

than most of the external surfaces of the heart. There-

these areas should repolarize first as well. However,

ventricular muscle depolarize first, it seems logical that

larization causes the T wave in the electrocardiogram.

proceeds until complete at about 0.35 second.This repo-

Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities

Chapter 12

135

Because the septum and endocardial areas of the

this is not the usual case because the septum and other
endocardial areas have a longer period of contraction

the greatest portion of ventricular muscle mass to

sequence of repolarization is postulated to be caused
by the high blood pressure inside the ventricles during

Because the outer apical surfaces of the ventricles

of the overall ventricular vector during repolarization
is toward the apex of the heart.

is also the polarity of most of the normal QRS complex.

ventricles are denoted by progressive increase of the

the vector extends from the base of the heart toward

−

III

−

III

−

III

−

III

−

III

Shaded areas of the ventricles are depolarized (–); nonshaded areas are still polarized (

Figure 12–7

+). 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).

Second, the vector changes direction because of

increasing and decreasing voltage of the vector.

myocardium. It changes in two aspects: First, the

Vectorcardiogram

complex, although in some very abnormal states, it

of the ventricles appears. Therefore, it is almost always

In the normal electrocardiogram, the

limb leads.

ence line from the P wave; that is, it is normally nega-

this T wave is on the opposite side of the zero refer-

follows about 0.15 second after the atrial P wave, but

the right in Figure 12–9, the so-called atrial T wave

that occurs in the ventricles.) Therefore, as shown to

backward to the vector of

itive with respect to the rest of the atria. Therefore, the

begins, the region around the sinus node becomes pos-

Thus, when repolarization

become depolarized first.

is the sinus nodal region, the area that had originally

the area in the atria that also becomes repolarized first

musculature in distal parts of the atria. Because of this,

tion signal. Therefore, the musculature around the

slower than in the ventricles

much

Repolarization of the Atria—The Atrial T Wave.

depolarization is known as the atrial P wave.

leads, as shown in Figure 12–9. This record of atrial

standard bipolar limb leads I, II, and III, the electro-

depolarization. Because this direction is generally

12–9. Furthermore, the vector remains generally in this

depolarization is denoted by the black vector in Figure

where the sinus node lies, and the direction of initial

and spreads in all directions over the atria. Therefore,

The P Wave

Depolarization of the Atria—

take place, the T wave of the electrocardiogram is

stages of repolarization. Thus, over about 0.15 second,

under each of the ventricles, depicting the progressive

The changes in the electrocardiograms of the three

that the total quantity of current flow decreases. These

Finally, the vector becomes weaker again because the

136

Unit III

The Heart

stronger because of greater degrees of repolarization.

areas of depolarization still persisting become so slight

changes also demonstrate that the vector is greatest
when about half the heart is in the polarized state and
about half is depolarized.

standard limb leads during repolarization are noted

the period of time required for the whole process to

generated.

Depolarization of the atria begins in the sinus node

the point of original electronegativity in the atria is
about at the point of entry of the superior vena cava

direction throughout the process of normal atrial

in the positive directions of the axes of the three

cardiograms recorded from the atria during depolar-
ization are also usually positive in all three of these

Spread of

depolarization through the atrial muscle is

because the atria have no

Purkinje system for fast conduction of the depolariza-

sinus node becomes depolarized a long time before the

atrial repolarization vector is
depolarization. (Note that this is opposite to the effect

tive rather than positive in the three standard bipolar

atrial T wave

appears at about the same time that the QRS complex

totally obscured by the large ventricular QRS

does appear in the recorded electrocardiogram.

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

vector increases and decreases in length because of

III

approximately 0.15 second.

The total time from the beginning of the T wave to its end is

showing also vectorial analysis of the first stage of repolarization.

Generation of the T wave during repolarization of the ventricles,

Figure 12–8

+ +

+ + +

III

the three standard leads. At the right are the atrial P and T waves.

the maximum vector through the atria and the resultant vectors in

Figure 12–9

Depolarization of the atria and generation of the P wave, showing

SA, sinoatrial node.

for that lead, as shown by the

recording is negative,

negative during part of the cycle. If any part of a

and in lead III, the recording is mainly positive but

III. In lead I of Figure 12–11, the recording is positive,

recording the standard leads, one determines the net

Figure 12–11 shows a method for doing this. After

Clinically, the electrical axis of the heart usually is esti-

Determining the Electrical Axis from

tions of the heart, this direction changes markedly—

ventricles is 59 degrees. In many pathological condi-

The mean electrical axis of the normal

ventricles.

This preponderant direction of the potential during

most of the cycle of ventricular depolarization, the

mainly toward the apex of the heart. That is, during

12–10 is that of a normal heart. Note from this vec-

tion (the QRS vectorcardiogram) shown in Figure

The vectorcardiogram during ventricular depolariza-

of the Ventricular QRS—

vector, thus inscribing the vectorcardiogram on the

the vector changes, the spot of light on the oscilloscope

each side of the heart to the horizontal plates. When

Vectorcardiograms can be recorded on an oscilloscope

QRS vectorcardiogram.

The elliptical figure generated by the positive ends

zero once again, as shown at point 5.

become totally depolarized, and the vector becomes

occurs in another 0.01 second. Finally, the ventricles

second, vector 3 represents the potential, and vector 4

about 0.02 second after vector 1. After another 0.02

slightly to one side. Thus, vector 2 of Figure 12–10 rep-

becomes stronger and stronger, usually swinging

ventricular muscle becomes depolarized, the vector

by the positive end of vector 1. As more of the

portion of the ventricular vectorcardiogram, as shown

tricles, but it is relatively weak, thus generating the first

When the septum first becomes depolarized, the

cles at the beginning of ventricular depolarization, the

there is no vectorial electrical potential. However,

muscle is polarized between heartbeats, the positive

ative end of all the successive vectors. While the heart

zero reference point,

In the large vectorcardiogram of Figure 12–10, point

the cardiac cycle, as shown in Figure 12–10.

vectorcardio-

potential from the heart. The so-called

Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities

Chapter 12

137

changes in the average direction of the electrical

gram depicts these changes at different times during

5 is the

and this point is the neg-

end of the vector remains at the zero point because

as soon as current begins to flow through the ventri-

positive end of the vector leaves the zero reference
point.

vector extends downward toward the apex of the ven-

resents the state of depolarization of the ventricles

of the vectors is called the

by connecting body surface electrodes from the neck
and lower abdomen to the vertical plates of the oscil-
loscope and connecting chest surface electrodes from

follows the course of the positive end of the changing

oscilloscopic screen.

Mean Electrical Axis

And Its Significance

torcardiogram that the preponderant direction of the
vectors of the ventricles during depolarization is

direction of the electrical potential (negative to posi-
tive) is from the base of the ventricles toward the apex.

depolarization is called the mean electrical axis of the

sometimes even to opposite poles of the heart.

Standard Lead Electrocardiograms

mated from the standard bipolar limb lead electrocar-
diograms rather than from the vectorcardiogram.

potential and polarity of the recordings in leads I and

this negative potential is sub-

tracted from the positive part of the potential to deter-
mine the net potential
arrow to the right of the QRS complex for lead III.

Depolarization

QRS

Repolarization

QRS and T vectorcardiograms.

Figure 12–10

III

∞

180

∞

120

∞

trocardiographic leads (leads I and III).

Plotting the mean electrical axis of the ventricles from two elec-

Figure 12–11

deviation, to an electrical axis of 170 degrees, which is

cardiogram of Figure 12–13 shows intense right axis

The electro-

from Hypertrophy of the Right Ventricle.

Vectorial Analysis of Right Axis Deviation Resulting

relatively normal in size.

aortic valvular stenosis, aortic valvular regurgitation,

sure. A similar picture of left axis deviation occurs

(high arterial blood pressure), which

tricle. In this instance, the axis deviation was caused by

15-degree direction. This is a typical electrocardio-

grams. Vectorial analysis demonstrates left axis devia-

Figure 12–12 shows

Hypertrophy of the Left Ventricle.

Vectorial Analysis of Left Axis Deviation Resulting from

hypertrophied ventricle.

positively charged. Thus, the axis deviates toward the

toward the hypertrophied side, which remains strongly

ventricle, and this causes

than through the normal ventricle. Consequently, the

Second, more time is required for the depolarization

excess generation of electrical potential on that side.

side of the heart than on the other side, and this allows

for two reasons. First, a far

the axis of the heart shifts toward the

hypertrophies,

When one ventricle greatly

Hypertrophy of One Ventricle.

(2) when a person stands up, and (3) normally in tall,

This occurs (1) at the end of deep inspiration,

Likewise, angulation of the heart to the right causes

upward against the heart all the time.

stocky, fat people whose diaphragms normally press

against the diaphragm, and (3) quite frequently in

down, because the abdominal contents press upward

at the end of deep expiration, (2) when a person lies

. Such shift occurs (1)

itself is angulated to the left, the mean electrical axis

limits, as follows.

hearts. However, a number of abnormal conditions of

100 degrees. The causes of the normal variations are

averages about 59 degrees, this axis can swing even

Cause Axis Deviation

Abnormal Ventricular Conditions That

as determined in Figure 12–11, is 59 degrees positive

of the mean electrical axis of the normal ventricles,

the direction of the mean vector. Thus, the orientation

vector, and the mean electrical axis is represented by

between these two points. The approximate average

mean vector. Therefore, the

ventricles, and the point of intersection of the lead I

rial analysis, the apex of the

of these two perpendicular lines represents, by vecto-

leads I and III, respectively. The point of intersection

lar mean electrical potential, one draws perpendicular

To determine the vector of the total QRS ventricu-

along the line depicting lead III. If it is negative, it is

and, if positive, it is plotted in the positive direction

a negative direction. Also, for lead III, the net poten-

Conversely, if this potential is negative, it is plotted in

If the net potential of lead I is positive, it is plotted

shown in Figure 12–11.

potential at the point of intersection of the axes, as

on the axes of the respective leads, with the base of the

Then each net potential for leads I and III is plotted

138

Unit III

The Heart

in a positive direction along the line depicting lead I.

tial is placed with its base at the point of intersection,

plotted in the negative direction.

lines (the dashed lines in the figure) from the apices of

mean QRS vector in the

and lead III axes represents the negative end of the

mean QRS vector is drawn

potential generated by the ventricles during depolar-
ization is represented by the length of this mean QRS

(

+59 degrees).

Although the mean electrical axis of the ventricles

in the normal heart from about 20 degrees to about

mainly anatomical differences in the Purkinje distri-
bution system or in the musculature itself of different

the heart can cause axis deviation beyond the normal

Change in the Position of the Heart in the Chest.

If the heart

of the heart also shifts to the left

the mean electrical axis of the ventricles to shift to the
right.

lanky people whose hearts hang downward.

hypertrophied ventricle
greater quantity of muscle exists on the hypertrophied

wave to travel through the hypertrophied ventricle

normal ventricle becomes depolarized considerably in
advance of the hypertrophied
a strong vector from the normal side of the heart

the three standard bipolar limb lead electrocardio-

tion with mean electrical axis pointing in the
-
gram caused by increased muscle mass of the left ven-

hypertension
caused the left ventricle to hypertrophy so that it could
pump blood against elevated systemic arterial pres-

when the left ventricle hypertrophies as a result of

any number of congenital heart conditions in which the
left ventricle enlarges while the right ventricle remains

III

. Note the slightly prolonged QRS complex as well.

(hypertrophic left ven-

Left axis deviation in a hypertensive heart

Figure 12–12

tricle)

rapidly than the right ventricle, so that the left side of

is blocked, the left ventricle depolarizes far more

When the right bundle branch

Vectorial Analysis of Right Axis Deviation in Right

caused by hypertrophy.

the chapter. This extremely prolonged QRS complex

Figure 12–14. This is discussed in greater detail later in

in the affected side of the heart. One can see this by

ation, the duration of the QRS complex is greatly pro-

the Purkinje system is blocked, in addition to axis devi-

demonstrated in Figure 12–14, which shows typical left

the vector points toward the left ventricle. This is

ventricle. In other words, there is intense left axis devi-

during most of the depolarization process, and a strong

Thus, the right ventricle becomes electronegative,

the left ventricle. Consequently, much of the left ven-

blocked, cardiac depolarization spreads through the

When the left bundle branch is

Vectorial Analysis of Left Axis Deviation in Left Bundle

ation occurs as follows.

tials do not neutralize each other. As a result, axis devi-

nearly simultaneously, and the depolarization poten-

before it spreads through the other. Therefore, depo-

the major bundle branches is blocked, the cardiac

heart) almost neutralize each other. But if only one of

the same instant. As a result, the potentials generated

Ordinarily, the

tetralogy of Fallot

phy of the right ventricle, such as

valve stenosis.

ventricular QRS axis. The right axis deviation demon-

Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities

Chapter 12

139

111 degrees to the right of the normal 59-degree mean

strated in this figure was caused by hypertrophy of the
right ventricle as a result of congenital pulmonary

Right axis deviation also can occur in

other congenital heart conditions that cause hypertro-

and

interventricular septal defect.

Bundle Branch Block Causes Axis Deviation.

lateral walls of the two ventricles depolarize at almost
the same instant because both the left and the right
bundle branches of the Purkinje system transmit the
cardiac impulse to the two ventricular walls at almost

by the two ventricles (on the two opposite sides of the

impulse spreads through the normal ventricle long

larization of the two ventricles does not occur even

Branch Block.

right ventricle two to three times as rapidly as through

tricle remains polarized for as long as 0.1 second after
the right ventricle has become totally depolarized.

whereas the left ventricle remains electropositive

vector projects from the right ventricle toward the left

ation of about

-50 degrees because the positive end of

axis deviation resulting from left bundle branch block.

Because of slowness of impulse conduction when

longed because of extreme slowness of depolarization

observing the excessive widths of the QRS waves in

differentiates bundle branch block from axis deviation

Bundle Branch Block.

the ventricles becomes electronegative as long as

III

ation and a slightly prolonged QRS complex also are seen.

with right ventricular hypertrophy. Intense right axis devi-

congenital pulmonary valve

High-voltage electrocardiogram in

Figure 12–13

stenosis

III

the greatly prolonged QRS complex.

Figure 12–14

Left axis deviation caused by left bundle branch block. Note also

electricity around the heart, so that the voltages at the

to a lesser extent, also can “short-circuit” the

reach the outside surfaces of the body.

dial fluid. Thus, this effusion effectively “short-circuits”

trical currents with great ease, a large portion of the

pericardium.

Decreased Voltage Caused by Conditions Surrounding the

of muscle mass throughout the ventricles.

QRS complex, which is common after multiple small

decreased voltage. Figure 12–16 shows a typical low-

once. Consequently, this condition causes some pro-

This

diminished muscle mass.

old myocardial artery

Decreased Voltage Caused by Cardiac Myopathies.

Decreased Voltage of the

shown in Figures 12–12 and 12–13.

graphic leads are considerably greater than normal, as

quantities of electricity around the heart. As a result,

when a person has high blood pressure. The increased

monary valve, and the left ventricle hypertrophies

the other. For example, the right ventricle hypertro-

often is increased muscle mass of the heart, which

The cause of high-voltage QRS complexes most

4 millivolts, the patient is considered to have a high-

general, when the sum of the voltages of all the QRS

tions are not invariable, even for the normal heart. In

voltage and lead II the highest. However, these rela-

millivolts, with lead III usually recording the lowest

to the bottom of the S wave, vary between 0.5 and 2.0

limb leads, as measured from the peak of the R wave

Normally, the voltages in the three standard bipolar

Increased Voltage in the Standard

Abnormal Voltages of the QRS

12–15, which shows an axis of about 105 degrees

demonstrated, and its vector is analyzed, in Figure

other words, intense right axis deviation occurs. Right

cle and its positive end toward the right ventricle. In

develops, with its negative end toward the left ventri-

0.1 second before the right. Therefore, a strong vector

140

Unit III

The Heart

axis deviation caused by right bundle branch block is

instead of the normal 59 degrees and a prolonged QRS
complex because of slow conduction.

Conditions That Cause

Complex

Bipolar Limb Leads

complexes of the three standard leads is greater than

voltage electrocardiogram.

ordinarily results from hypertrophy of the muscle in
response to excessive load on one part of the heart or

phies when it must pump blood through a stenotic pul-

quantity of muscle causes generation of increased

the electrical potentials recorded in the electrocardio-

Electrocardiogram

One of

the most common causes of decreased voltage of the
QRS complex is a series of
infarctions with resultant
also causes the depolarization wave to move through
the ventricles slowly and prevents major portions of
the heart from becoming massively depolarized all at

longation of the QRS complex along with the

voltage electrocardiogram with prolongation of the

infarctions of the heart have caused local delays of
impulse conduction and reduced voltages due to loss

Heart.

One of the most important causes of decreased

voltage in electrocardiographic leads is fluid in the

Because extracellular fluid conducts elec-

electricity flowing out of the heart is conducted from
one part of the heart to another through the pericar-

the electrical potentials generated by the heart,
decreasing the electrocardiographic voltages that

Pleural effu-

sion,

III

also the greatly prolonged QRS complex.

Figure 12–15

Right axis deviation caused by right bundle branch block. Note

III

previous myocardial infarction

Low-voltage electrocardiogram following local damage through-

Figure 12–16

out the ventricles caused by

of lead III, the voltage of the current of injury in lead

so that the record is positive. Furthermore, because the

of the lead. In lead III, the projected vector points in

lead II, the record is above the line because the pro-

points toward the negative end of the lead I axis. In

record in lead I below the zero potential line,

the QRS complex begins,

shown in the lower portions of the figure, even before

toward the injured muscle. As

vector, the

direction of about 125 degrees, with the base of the

injury,” as shown in the first heart in the figure, is in a

rest of the ventricles. The vector of this “current of

Therefore, during the T-P interval—that is, when the

In Figure 12–17, a small area in the base of the left ven-

Effect of Current of Injury on the

current of injury in the heart. During ischemia, not

occlusions,

of local areas of heart muscle caused by local coronary

ischemia

that damage the muscle membranes; and (3)

larization cannot take place; (2)

mechanical trauma,

neutral or positive polarity.

rounding fluids, whereas the remainder of the heart is

depolarized and emits negative charges into the sur-

of the heart is negative, because this is the part that is

current of injury.

ized areas even between heartbeats. This is called a

When this occurs, current flows between

all the time.

depolarized

that damage the heart muscle itself, often cause part

Many different cardiac abnormalities, especially those

Current of Injury

as those shown in Figure 12–14.

peaks in some of the electrocardiographic leads, such

axis deviations. This often causes double or even triple

becomes irregular, causing rapid shifts in voltages and

system. As a result, cardiac impulse conduction

scar tissue, and (2) multiple small local blocks in the

ventricular system, with replacement of this muscle by

are caused by two conditions: (1) destruction of

Figures 12–14 and 12–15.

where in the ventricular conduction system, as shown

when it lasts more than 0.12 second, the prolongation

In general, a QRS complex is considered to be

greater.

one of the bundle branches occurs, the duration of the

one third of normal. Therefore, if complete block of

muscle instead of by way of the Purkinje system. This

When the Purkinje fibers are blocked, the cardiac

from Purkinje System Blocks

the left or right ventricle, the QRS complex may be

to 0.08 second, whereas in hypertrophy or dilatation of

must then travel. The normal QRS complex lasts 0.06

dilated, owing to the longer pathway that the impulse

longed QRS complex. Such prolongation often occurs

still polarized. Therefore,

tinues to spread through the ventricles—that is, as long

The QRS complex lasts as long as depolarization con-

of Cardiac Hypertrophy or Dilatation

Patterns of the QRS Complex

Prolonged and Bizarre

electrocardiographic potentials in the various leads.

to the surface of the body, and this results in decreased

than normally. Therefore, the lungs act as an insulator

of air in the lungs. Also, the chest cavity enlarges, and

that of pericardial effusion. In pulmonary emphysema,

diographic potentials, but by a different method from

Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities

Chapter 12

141

surface of the body and in the electrocardiograms are
decreased.

Pulmonary emphysema can decrease the electrocar-

conduction of electrical current through the lungs is
depressed considerably because of excessive quantity

the lungs tend to envelop the heart to a greater extent

to prevent spread of electrical voltage from the heart

Prolonged QRS Complex as a Result

as part of the ventricles is depolarized and part is

prolonged conduction of the

impulse through the ventricles always causes a pro-

when one or both ventricles are hypertrophied or

prolonged to 0.09 to 0.12 second.

Prolonged QRS Complex Resulting

impulse must then be conducted by the ventricular

decreases the velocity of impulse conduction to about

QRS complex usually is increased to 0.14 second or

abnormally long when it lasts more than 0.09 second;

is almost certainly caused by pathological block some-

by the electrocardiograms for bundle branch block in

Conditions That Cause Bizarre QRS
Complexes

Bizarre patterns of the QRS complex most frequently

cardiac muscle in various areas throughout the

conduction of impulses at many points in the Purkinje

of the heart to remain partially or totally

the pathologically depolarized and the normally polar-

Note especially that the injured part

Some abnormalities that can cause current of injury

are (1)

which sometimes makes

the membranes remain so permeable that full repo-

infectious processes

which is by far the most common cause of

enough nutrients from the coronary blood supply are
available to the heart muscle to maintain normal mem-
brane polarization.

QRS Complex

tricle is newly infarcted (loss of coronary blood flow).

normal ventricular muscle is totally polarized—abnor-
mal negative current still flows from the infarcted area
at the base of the left ventricle and spreads toward the

negative end,

this vector causes an initial

because

the projected vector of the current of injury in lead I

jected vector points more toward the positive terminal

the same direction as the positive terminal of lead III,

vector lies almost exactly in the direction of the axis

III is much greater than in either lead I or lead II.

segment. In the figure, a horizontal line has been

trocardiograms is not on the same line as the T-P

In other words, the J point of each of these two elec-

an injured heart. Both records show injury potentials.

Figure

Use of the J Point in Plotting Axis of Injury Potential.

zero potential level

the level of the J point. This horizontal line is then the

potential caused by a current of injury, a horizontal

Then, for analysis of the electrical axis of the injury

gram, as shown in Figure 12–18.

point is known as the “J point” in the electrocardio-

electrocardiogram at this instant is at zero voltage.This

disappears at this point. Therefore, the potential of the

is flowing around the heart. Even the current of injury

damaged parts and the normal parts, so that no current

cles have become depolarized, including both the

complex. At exactly this point, all parts of the ventri-

the exact point at which the

tial level: First, one notes

electrocardiogram. For these reasons, the following

leg, these stray currents make it impossible for one to

fluids of the body. Therefore, when two electrodes are

such as currents resulting from “skin potentials” and

heart. However, many stray currents exist in the body,

Potential for Analyzing Current

in each lead, as noted at the far right in Figure 12–17.

larization in the injured base of the left ventricle. Thus,

finally repolarizes, except the area of permanent depo-

Next, as repolarization takes place, all of the heart

in the electrocardiogram, no current flows from the

muscle is in a negative state. Therefore, at this instant

next-to-last stage in Figure 12–17), all the ventricular

When the heart becomes totally depolarized, at the

lower part of Figure 12–17.

can be constructed graphically, as demonstrated in the

manently depolarized. By vectorial analysis, the suc-

depolarized is the base of the right ventricle, because

The last portion of the ventricles to become totally

the apex and back toward the bases of the ventricles.

depolarized; then the depolarization spreads down to

process of depolarization, the septum first becomes

142

Unit III

The Heart

As the heart then proceeds through its normal

the base of the left ventricle is already totally and per-

cessive stages of electrocardiogram generation by the
depolarization wave traveling through the ventricles

end of the depolarization process (as noted by the

ventricles to the electrocardiographic electrodes
because now both the injured heart muscle and the
contracting muscle are depolarized.

repolarization causes a return of the current of injury

The J Point—The Zero Reference

of Injury

One would think that the electrocardiograph
machines for recording electrocardiograms could
determine when no current is flowing around the

from differences in ionic concentrations in different

connected between the arms or between an arm and a

predetermine the exact zero reference level in the

procedure must be used to determine the zero poten-

wave of depolarization just completes its passage
through the heart, which occurs at the end of the QRS

line is drawn in the electrocardiogram for each lead at

in the electrocardiogram from

which all potentials caused by currents of injury must
be measured.

12–18 shows electrocardiograms (leads I and III) from

drawn through the J point to represent the zero

III

Current

of injury

Injured area

Current
of injury

III

the electrocardiogram.

Effect of a current of injury on

Figure 12–17

Figure 12–19 shows the

Acute Anterior Wall Infarction.

current of injury.

Figures 12–19 and 12–20. Therefore, one of the most

the T-P interval between heartbeats, as shown in

coronary occlusion, and a strong current of injury

(the T-P portion) of each heart cycle.

membranes. As long as this state exists, an injury

Consequently, repolarization of the muscle membrane

dioxide, and (3) lack of sufficient food nutrients.

lack of oxygen, (2) excess accumulation of carbon

the metabolism of the muscle for three reasons: (1)

again until he or she understands it thoroughly. No

This analysis is obviously complex. However, it is

right ventricle.

In the example shown in Figure 12–18,

the ventricles.

toward the permanently depolarized, “injured” area of

the ventricles,

30 degrees. If one

upward, with an axis of about

instance, the resultant vector extends from the right

is determined by vectorial analysis as described. In this

nates of these leads, and the resultant vector of the

At the bottom in Figure 12–18, the respective injury

therefore, is negative.

and is, therefore, positive. Conversely, in lead III, the

mined from the J point. In lead I, the recorded voltage

voltage level in each of the two recordings. The injury

Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities

Chapter 12

143

potential in each lead is the difference between the
voltage of the electrocardiogram immediately before
onset of the P wave and the zero voltage level deter-

of the injury potential is above the zero potential level

injury potential is below the zero voltage level and,

potentials in leads I and III are plotted on the coordi-

injury potential for the whole ventricular muscle mass

side of the ventricles toward the left and slightly

places this vector for the injury potential directly over

the negative end of the vector points

the injured area would be in the lateral wall of the

essential that the student go over it again and

other aspect of electrocardiographic analysis is more
important.

Coronary Ischemia as a Cause
of Injury Potential

Insufficient blood flow to the cardiac muscle depresses

cannot occur in areas of severe myocardial ischemia.
Often the heart muscle does not die because the blood
flow is sufficient to maintain life of the muscle even
though it is not sufficient to cause repolarization of the

potential continues to flow during the diastolic portion

Extreme ischemia of the cardiac muscle occurs after

flows from the infarcted area of the ventricles during

important diagnostic features of electrocardiograms
recorded after acute coronary thrombosis is the

electrocardiogram in the three standard bipolar limb

“J” point

III

potential is shown by the lowermost panel.

for leads I and II. Also, the method for plotting the axis of the injury

J point as the zero reference potential of the electrocardiograms

Figure 12–18

III

injury potential in lead V

acute anterior wall infarction

Current of injury in

Figure 12–19

. Note the intense

terior wall infarction, demonstrating changes in the

shows a V

Figure 12–21

Recovery from Acute Coronary Thrombosis.

portion of the heart that is emitting the current of injury.

muscle, and the negative end points toward the injured

potential vector points toward the normal cardiac

is involved. In making such vectorial analyses, it must

current of injury, regardless of which part of the heart

anterior and posterior wall infarctions, it is possible to

the apex on the posterior wall of the left ventricle.

the heart, one would suspect that this infarct is near

potentials in leads II and III, is in the apical portion of

rior wall of the heart and, as indicated by the injury

infarct, as indicated by the chest lead, is on the poste-

the positive end pointing upward. Thus, because the

degrees, with the negative end pointing downward and

analysis, as shown in the figure, one finds that the

injury potential is negative in both leads. By vectorial

and III of Figure 12–20, it is readily apparent that the

of the heart opposite to the anterior chest wall, which

words, the current of injury is coming from the back

of the vector) points away from the chest wall. In other

anterior chest wall, and the negative end (injured end

the current of injury is positive. This means that the

apparent that during the T-P interval, the potential of

is drawn through the J point of this lead, it is readily

also in the chest lead. If a zero potential reference line

) from a patient with posterior wall infarction. The

Figure 12–20 shows the three

Posterior Wall Infarction.

nary artery.

heart. Therefore, one would conclude that this anterior

gram, the current of injury is coming mainly from the

right ventricle. Thus, in this particular electrocardio-

degrees, with the negative end pointing toward the left

potential in lead III. This means that the resultant

from the anterior wall of the ventricles, which diag-

This means that the current of injury is emanating

other words, the negative end of the injury potential

heart is in an area of strongly negative potential. In

injury potential during the T-P interval is found, which

the J point of this electrocardiogram, a strong

diogram is the intense injury potential in chest lead V

patient with acute anterior wall cardiac infarction. The

leads and in one chest lead (lead V

144

Unit III

The Heart

) recorded from a

most important diagnostic feature of this electrocar-

If one draws a zero horizontal potential line through

negative

means that the chest electrode over the front of the

vector in this heart is against the anterior chest wall.

noses this condition as anterior wall infarction.

Analyzing the injury potentials in leads I and III,

one finds a negative potential in lead I and a positive

vector of the injury potential in the heart is about

+150

ventricle and the positive end pointing toward the

left ventricle as well as from the anterior wall of the

wall infarction almost certainly is caused by thrombo-
sis of the anterior descending branch of the left coro-

standard bipolar limb leads and one chest lead (lead
V

major diagnostic feature of this electrocardiogram is

positive end of the vector is in the direction of the

is the reason this type of electrocardiogram is the basis
for diagnosing posterior wall infarction.

If one analyzes the injury potentials from leads II

resultant vector of the injury potential is about

-95

Infarction in Other Parts of the Heart.

By the same proce-

dures demonstrated in the preceding discussions of

determine the locus of any infarcted area emitting a

be remembered that the positive end of the injury

chest lead from a patient with acute pos-

electrocardiogram from the day of the attack to 1

III

acute posterior wall, apical infarction

Injury potential in

Figure 12–20

Same day

1 week

2 weeks

1 year

present on the first day after the infarction and still slightly present

tion, demonstrating disappearance of the injury potential that is

Recovery of the myocardium after moderate posterior wall infarc-

Figure 12–21

at 1 week.

would not begin at the apex as it normally does.

ened action potential, repolarization of the ventricles

mally short period of depolarization, that is, a short-

of T Wave Abnormalities

of the Ventricular Muscle as a Cause

Shortened Depolarization in Portions

delayed, the T wave is almost always of opposite polar-

trocardiogram. Thus, when conduction of the depolar-

oping. In other words, the mean axis of the T wave is

the left ventricle at the time that the T wave is devel-

to repolarize long before the left ventricle; this causes

from each other. Therefore, the right ventricle begins

However, the refractory periods of the right and left

second after depolarization of the right ventricle,

resulting from left bundle branch block. This causes

delayed conduction in the left ventricle

complex is considerably prolonged. The reason for this

Referring back to Figure 12–14, note that the QRS

Characteristics of the T Wave

Depolarization Wave on the

Effect of Slow Conduction of the

repolarization does not occur. Several factors can

of the intraventricular surfaces. That is, the T wave

Earlier in the chapter, it was pointed out that the T

Abnormalities in the T Wave

areas of the heart during diastole.

toris, because the coronary insufficiency becomes great

appears.

but as soon as he or she overworks the heart, the pain

Usually, no pain is felt as long as the person is quiet,

the left neck area and down the left arm. The pain typ-

of the upper chest. This pain usually also radiates into

“Angina pectoris”

Current of Injury in Angina Pectoris.

nent Q waves, for instance), decreased voltage, and

cases of old cardiac infarction. Local loss of muscle and

These configurations are certainly not found in all

apical part of the ventricle.

the left ventricle, but in posterior infarction, a Q wave

called the “ideal” configurations of the QRS complex

acute heart attack. The records show what might be

and leads I and

Figure 12–22 shows

ischemia exists, particularly during bouts of exercise

muscle dies, but if the muscle does not die, it will con-

coronary blood supply. Often, some of the heart

tion, the infarcted area never redevelops adequate

Conversely, in some patients with coronary infarc-

collateral coronary blood flow

infarction of moderate degree, showing that the

does not change greatly during the next year. This

3 weeks, it is gone. After that, the electrocardiogram

injury potential has diminished considerably, and after

the S-T segment). However, after about 1 week, the

acute attack (T-P segment displaced positively from

From this electrocardiogram, one can see that the

week later, 3 weeks later, and finally 1 year later.

Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities

Chapter 12

145

injury potential is strong immediately after the

is the usual recovery pattern after acute cardiac

new

develops enough

to re-establish appropriate nutrition to most of the
infarcted area.

tinue to show an injury potential as long as the

when the heart is overloaded.

Old Recovered Myocardial Infarction.

leads I and III after anterior infarction
III after posterior infarction about 1 year after the

in these types of recovered myocardial infarction.
Usually a Q wave has developed at the beginning of
the QRS complex in lead I in anterior infarction
because of loss of muscle mass in the anterior wall of

has developed at the beginning of the QRS complex
in lead III because of loss of muscle in the posterior

local points of cardiac signal conduction block can
cause very bizarre QRS patterns (especially promi-

QRS prolongation.

means pain from the heart felt in the pectoral regions

ically is caused by moderate ischemia of the heart.

An injury potential sometimes appears in the elec-

trocardiogram during an attack of severe angina pec-

enough to prevent adequate repolarization of some

wave is normally positive in all the standard bipolar
limb leads and that this is caused by repolarization of
the apex and outer surfaces of the ventricles ahead

becomes abnormal when the normal sequence of

change this sequence of repolarization.

prolongation is

the left ventricle to become depolarized about 0.08

which gives a strong mean QRS vector to the left.

ventricular muscle masses are not greatly different

strong positivity in the right ventricle and negativity in

now deviated to the right, which is opposite the mean
electrical axis of the QRS complex in the same elec-

ization impulse through the ventricles is greatly

ity to that of the QRS complex.

If the base of the ventricles should exhibit an abnor-

III

Posterior

III

infarction.

anterior wall infarction and a Q wave in lead III in posterior wall

occurred about 1 year previously, showing a Q wave in lead I in

Electrocardiograms of anterior and posterior wall infarctions that

Figure 12–22

liest signs of digitalis toxicity.

is shown in Figure 12–24. Therefore, changes in the T

or more of the electrocardiographic leads. A biphasic

wave inversion or biphasic T waves, may occur in one

other parts. As a result, nonspecific changes, such as T

given, depolarization duration in one part of the ven-

contraction. But when overdosages of digitalis are

insufficiency to increase the strength of cardiac muscle

22, digitalis is a drug that can be used during coronary

Effect of Digitalis on the T Wave.

ate coronary insufficiency.

tion to the rest of the heart, caused by mild to moder-

inversion, for instance, or a biphasic wave—is often

cific, because any change in the T wave in any lead—

waves. The changes in the T waves need not be spe-

trocardiogram, noting whether changes occur in the T

One means for detecting mild coronary insufficiency

exercise.

or relative coronary insufficiency that occurs during

gressive coronary occlusion; acute coronary occlusion;

place. The ischemia might result from chronic, pro-

As a result, definite changes in the T wave can take

decreases out of proportion to that in other portions.

area of the heart, the depolarization period of this area

sium channels. When the ischemia occurs in only one

shortening of depolarization of cardiac muscle,

Mild ischemia

in Figure 12–23.

extent of changing the entire T wave polarity, as shown

cause marked changes in the T wave, even to the

Thus, the simple fact that the base of the ventricles has

leads would be negative rather than the usual positive.

tion. Consequently, the T wave in all three standard

heart, opposite to the standard vector of repolariza-

ahead of the apex, and the vector of repolarization

Instead, the base of the ventricles would repolarize

146

Unit III

The Heart

would point from the apex toward the base of the

a shortened period of depolarization is sufficient to

is by far the most common cause of

because this increases current flow through the potas-

is to have the patient exercise and to record the elec-

evidence enough that some portion of the ventricular
muscle has a period of depolarization out of propor-

As discussed in Chapter

tricles may be increased out of proportion to that of

T wave caused by excessive administration of digitalis

wave during digitalis administration are often the ear-

References

See references for Chapter 13.

Inverted T wave resulting from mild

Figure 12–23

ischemia at the apex of the

ventricles.

Figure 12–24

Biphasic T wave caused by digitalis toxicity.