Guyton and Hall Textbook of Medical Physiology, 12th Ed


Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities

Vectorial Analysis

imageFrom 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, most serious abnormalities of the heart muscle can be diagnosed by analyzing the contours of the waves in the different electrocardiographic leads.

Principles of Vectorial Analysis of Electrocardiograms

Use of Vectors to Represent Electrical Potentials

Before it is possible to understand how cardiac abnormalities affect the contours of the electrocardiogram, one must first become thoroughly familiar with 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 particular direction in the heart at a given instant during the cardiac cycle. A vector is an arrow that points in the direction of the electrical potential generated by the current flow, with the arrowhead in the positive direction. Also, by convention, the length of the arrow is drawn proportional to the voltage of the potential.

“Resultant” Vector in the Heart at Any Given Instant

Figure 12-1 shows, by the shaded area and the negative signs, depolarization of the ventricular septum and parts of the apical endocardial walls of the two ventricles. At this instant of heart excitation, electrical current flows between the depolarized areas inside the heart and the nondepolarized areas on the outside of the heart, as indicated by the long elliptical arrows. Some current also flows inside the heart chambers directly from the depolarized areas toward the still polarized areas. Overall, considerably more current flows downward from the base of the ventricles toward the apex than in the upward direction. Therefore, the summated vector of the generated potential at this particular instant, called the instantaneous mean vector, is represented by the long black arrow drawn through the center of the ventricles in a direction from base toward apex. Furthermore, because the summated current is considerable in quantity, the potential is large and the vector is long.


Figure 12-1 Mean vector through the partially depolarized ventricles.

Direction of a Vector Is Denoted in Terms of Degrees

When a vector is exactly horizontal and directed toward the person’s left side, the vector is said to extend in the direction of 0 degrees, as shown in Figure 12-2. From this zero reference point, the scale of vectors rotates clockwise: when the vector extends from above and straight downward, it has a direction of +90 degrees; when it extends from the person’s left to right, it has a direction of +180 degrees; and when it extends straight upward, it has a direction of −90 (or +270) degrees.


Figure 12-2 Vectors drawn to represent potentials for several different hearts, and the “axis” of the potential (expressed in degrees) for each heart.

In a normal heart, the average direction of the vector during spread of the depolarization wave through the ventricles, called the mean QRS vector, is about +59 degrees, which is shown by vector A drawn through the center of Figure 12-2 in the +59-degree direction. This means that during most of the depolarization wave, the apex of the heart remains positive with respect to the base of the heart, as discussed later in the chapter.

Axis for Each Standard Bipolar Lead and Each Unipolar Limb Lead

In Chapter 11, the three standard bipolar and the three unipolar limb leads are described. Each lead is actually a pair of electrodes connected to the body on opposite sides of the heart, and the direction from negative electrode to positive electrode is called the “axis” of the lead. Lead I is recorded from two electrodes placed respectively on the two arms. Because the electrodes lie exactly in the horizontal direction, with the positive electrode to the left, the axis of lead I is 0 degrees.

In recording lead II, electrodes are placed on the right arm and left leg. The right arm connects to the torso in the upper right-hand corner and the left leg connects in the lower left-hand corner. Therefore, the direction of this lead is about +60 degrees.

By similar analysis, it can be seen that lead III has an axis of about +120 degrees; lead aVR, +210 degrees; aVF, +90 degrees; and aVL −30 degrees. The directions of the axes of all these leads are shown in Figure 12-3, which is known as the hexagonal reference system. The polarities of the electrodes are shown by the plus and minus signs in the figure. The reader must learn these axes and their polarities, particularly for the bipolar limb leads I, II, and III, to understand the remainder of this chapter.


Figure 12-3 Axes of the three bipolar and three unipolar leads.

Vectorial Analysis of Potentials Recorded in Different Leads

Now that we have discussed, first, the conventions for representing potentials across the heart by means of vectors and, second, the axes of the leads, it is possible to use these together to determine the instantaneous potential that will be recorded in the electrocardiogram of each lead for a given vector in the heart, as follows.

Figure 12-4 shows a partially depolarized heart; vector A represents the instantaneous mean direction of current flow in the ventricles. In this instance, the direction of the vector is +55 degrees, and the voltage of the potential, represented by the length of vector A, is 2 mv. In the diagram below the heart, vector A is shown again, and a line is drawn to represent the axis of lead I in the 0-degree direction. To determine how much of the voltage in vector Awill be recorded in lead I, a line perpendicular to the axis of lead I is drawn from the tip of vector A to the lead I axis, and a so-called projected vector (B) is drawn along the lead I axis. The arrow of this projected vector points toward the positive end of the lead I axis, which means that the record momentarily being recorded in the electrocardiogram of lead I is positive. And the instantaneous recorded voltage will be equal to the length of B divided by the length of A times 2 millivolts, or about 1 millivolt.


Figure 12-4 Determination of a projected vector B along the axis of lead I when vector A represents the instantaneous potential in the ventricles.

Figure 12-5 shows another example of vectorial analysis. In this example, vector A represents the electrical 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 right. In this instance, the instantaneous vector has a direction of 100 degrees, and its voltage is again 2 millivolts. To determine the potential actually recorded in lead I, we draw a perpendicular line from the tip of vector A to the lead I axis and find projected vector B. Vector B is very short and this time in the negative direction, indicating that at this particular instant, the recording in lead I will be negative (below the zero line in the electrocardiogram), and the voltage recorded will be slight, about −0.3 millivolts. This figure demonstrates that when the vector in the heart is in a direction almost perpendicular to the axis of the lead, the voltage recorded in the electrocardiogram of this lead is very low. Conversely, when the heart vector has almost exactly the same axis as the lead axis, essentially the entire voltage of the vector will be recorded.


Figure 12-5 Determination of the projected vector B along the axis of lead I when vector A represents the instantaneous potential in the ventricles.

Vectorial Analysis of Potentials in the Three Standard Bipolar Limb Leads

In Figure 12-6, vector A depicts the 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 positive—that is, above the zero line—because 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.


Figure 12-6 Determination of projected vectors in leads I, II, and III when vector A represents the instantaneous potential in the ventricles.

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 12-3) are used in place of the standard bipolar limb lead axes used for Figure 12-6.

Vectorial Analysis of the Normal Electrocardiogram

Vectors That Occur at Successive Intervals during Depolarization of the Ventricles— the QRS Complex

When the cardiac impulse enters the ventricles through the atrioventricular bundle, the first part of the ventricles to become depolarized is the left endocardial surface of the septum. Then depolarization spreads rapidly to involve both endocardial surfaces of the septum, as demonstrated by the darker shaded portion of the ventricle in Figure 12-7A. Next, depolarization spreads along the endocardial surfaces of the remainder of the two ventricles, as shown in Figure 12-7B and C. Finally, it spreads through the ventricular muscle to the outside of the heart, as shown progressively in Figure 12-7C, D, and E.


Figure 12-7 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).

At each stage in Figure 12-7, parts A to E, the instantaneous mean electrical potential of the ventricles is represented by a red vector superimposed on the ventricle in each figure. Each of these vectors is then analyzed by the method described in the preceding section to determine the voltages that will be recorded at each instant in each of the three standard electrocardiographic leads. To the right in each figure is shown progressive development of the electrocardiographic QRS complex. Keep in mind that a positive vector in a lead will cause recording in the electrocardiogram above the zero line, whereas a negative vector will cause recording below the zero line.

Before proceeding with further consideration of vectorial analysis, it is essential that this analysis of the successive normal vectors presented in Figure 12-7 be understood. Each of these analyses should be studied in detail by the procedure given here. A short summary of this sequence follows.

In Figure 12-7A, the ventricular muscle has just begun to be depolarized, representing an instant about 0.01 second after the onset of depolarization. At this time, the vector is short because only a small portion of the ventricles—the septum—is depolarized. Therefore, all electrocardiographic voltages are low, as recorded to the right of the ventricular muscle for each of the leads. The voltage in lead II is greater than the voltages in leads I and III because the heart vector extends mainly in the same direction as the axis of lead II.

In Figure 12-7B, which represents about 0.02 second after onset of depolarization, the heart vector is long because much of the ventricular muscle mass has become depolarized. Therefore, the voltages in all electrocardiographic leads have increased.

In Figure 12-7C, about 0.035 second after onset of depolarization, the heart vector is becoming shorter and the recorded electrocardiographic voltages are lower because the outside of the heart apex is now electronegative, neutralizing much of the positivity on the other epicardial surfaces of the heart. Also, the axis of the vector is beginning to shift toward the left side of the chest because the left ventricle is slightly slower to depolarize than the right. Therefore, the ratio of the voltage in lead I to that in lead III is increasing.

In Figure 12-7D, about 0.05 second after onset of depolarization, the heart vector points toward the base of the left ventricle, and it is short because only a minute portion of the ventricular muscle is still polarized positive. Because of the direction of the vector at this time, the voltages recorded in leads II and III are both negative—that is, below the line—whereas the voltage of lead I is still positive.

In Figure 12-7E, about 0.06 second after onset of depolarization, the entire ventricular muscle mass is depolarized so that no current flows around the heart and no electrical potential is generated. The vector becomes zero, and the voltages in all leads become zero.

Thus, the QRS complexes are completed in the three standard bipolar limb leads.

Sometimes the QRS complex has a slight negative depression at its beginning in one or more of the leads, which is not shown in Figure 12-7; this depression is the Q wave. When it occurs, it is caused by initial depolarization of the left side of the septum before the right side, which creates a weak vector from left to right for a fraction of a second before the usual base-to-apex vector occurs. The major positive deflection shown in Figure 12-7 is the R wave, and the final negative deflection is the S wave.

Electrocardiogram during Repolarization—the T Wave

After the ventricular muscle has become depolarized, about 0.15 second later, repolarization begins and 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 flow to the endocardium, thereby slowing repolarization in the endocardial areas.

Because the outer apical surfaces of the ventricles repolarize before the inner surfaces, the positive end of the overall ventricular vector during repolarization is toward the apex of the heart. As a result, the normal T wave in all three bipolar limb leads is positive, which is also the polarity of most of the normal QRS complex.

In Figure 12-8, five stages of repolarization of the ventricles are denoted by progressive increase of the light tan areas—the repolarized areas. At each stage, the vector extends from the base of the heart toward the apex until it disappears in the last stage. At first, the vector is relatively small because the area of repolarization is small. Later, the vector becomes stronger because of greater degrees of repolarization. Finally, the vector becomes weaker again because the areas of depolarization still persisting become so slight that the total quantity of current flow decreases. These changes also demonstrate that the vector is greatest when about half the heart is in the polarized state and about half is depolarized.


Figure 12-8 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.

The changes in the electrocardiograms of the three standard limb leads during repolarization are noted under each of the ventricles, depicting the progressive stages of repolarization. Thus, over about 0.15 second, the period of time required for the whole process to take place, the T wave of the electrocardiogram is generated.

Depolarization of the Atria—the P Wave

Depolarization of the atria begins in the sinus node and spreads in all directions over the atria. Therefore, the point of original electronegativity in the atria is about at the point of entry of the superior vena cava where the sinus node lies, and the direction of initial depolarization is denoted by the black vector in Figure 12-9. Furthermore, the vector remains generally in this direction throughout the process of normal atrial depolarization. Because this direction is generally in the positive directions of the axes of the three standard bipolar limb leads I, II, and III, the electrocardiograms recorded from the atria during depolarization are also usually positive in all three of these leads, as shown in Figure 12-9. This record of atrial depolarization is known as the atrial P wave.


Figure 12-9 Depolarization of the atria and generation of the P wave, showing the maximum vector through the atria and the resultant vectors in the three standard leads. At the right are the atrial P and T waves. SA, sinoatrial node.

Repolarization of the Atria—the Atrial T Wave

Spread of depolarization through the atrial muscle is much slower than in the ventricles because the atria have no Purkinje system for fast conduction of the depolarization signal. Therefore, the musculature around the sinus node becomes depolarized a long time before the musculature in distal parts of the atria. Because of this, the area in the atria that also becomes repolarized first is the sinus nodal region, the area that had originally become depolarized first. Thus, when repolarization begins, the region around the sinus node becomes positive with respect to the rest of the atria. Therefore, the atrial repolarization vector is backward to the vector of depolarization. (Note that this is opposite to the effect that occurs in the ventricles.) Therefore, as shown to the right in Figure 12-9, the so-called atrial T wave follows about 0.15 second after the atrial P wave, but this T wave is on the opposite side of the zero reference line from the P wave; that is, it is normally negative rather than positive in the three standard bipolar limb leads.

In the normal electrocardiogram, the atrial T wave appears at about the same time that the QRS complex of the ventricles appears. Therefore, it is almost always totally obscured by the large ventricular QRS complex, although in some very abnormal states, it 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 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 changes in the average direction of the electrical potential from the heart. The so-called vectorcardiogram depicts these changes at different times during the cardiac cycle, as shown in Figure 12-10.


Figure 12-10 QRS and T vectorcardiograms.

In the large vectorcardiogram of Figure 12-10, point 5 is the zero reference point, and this point is the negative end of all the successive vectors. While the heart muscle is polarized between heartbeats, the positive end of the vector remains at the zero point because there is no vectorial electrical potential. However, as soon as current begins to flow through the ventricles at the beginning of ventricular depolarization, the positive end of the vector leaves the zero reference point.

When the septum first becomes depolarized, the vector extends downward toward the apex of the ventricles, but it is relatively weak, thus generating the first portion of the ventricular vectorcardiogram, as shown by the positive end of vector 1. As more of the ventricular muscle becomes depolarized, the vector becomes stronger and stronger, usually swinging slightly to one side. Thus, vector 2 of Figure 12-10represents the state of depolarization of the ventricles about 0.02 second after vector 1. After another 0.02 second, vector 3 represents the potential, and vector 4 occurs in another 0.01 second. Finally, the ventricles become totally depolarized, and the vector becomes zero once again, as shown at point 5.

The elliptical figure generated by the positive ends of the vectors is called the QRS vectorcardiogram. Vectorcardiograms can be recorded on an oscilloscope by connecting body surface electrodes from the neck and lower abdomen to the vertical plates of the oscilloscope and connecting chest surface electrodes from each side of the heart to the horizontal plates. When the vector changes, the spot of light on the oscilloscope follows the course of the positive end of the changing vector, thus inscribing the vectorcardiogram on the oscilloscopic screen.

Mean Electrical Axis of the Ventricular QRS—and Its Significance

The vectorcardiogram during ventricular depolarization (the QRS vectorcardiogram) shown in Figure 12-10 is that of a normal heart. Note from this vectorcardiogram that the preponderant direction of the vectors of the ventricles during depolarization is mainly toward the apex of the heart. That is, during most of the cycle of ventricular depolarization, the direction of the electrical potential (negative to positive) is from the base of the ventricles toward the apex. This preponderant direction of the potential during depolarization is called the mean electrical axis of the ventricles. The mean electrical axis of the normal ventricles is 59 degrees. In many pathological conditions of the heart, this direction changes markedly, sometimes even to opposite poles of the heart.

Determining the Electrical Axis from Standard Lead Electrocardiograms

Clinically, the electrical axis of the heart is usually estimated from the standard bipolar limb lead electrocardiograms rather than from the vectorcardiogram. Figure 12-11 shows a method for doing this. After recording the standard leads, one determines the net potential and polarity of the recordings in leads I and III. In lead I of Figure 12-11, the recording is positive, and in lead III, the recording is mainly positive but negative during part of the cycle. If any part of a recording is negative, this negative potential is subtracted from the positive part of the potential to determine the net potential for that lead, as shown by the arrow to the right of the QRS complex for lead III. Then each net potential for leads I and III is plotted on the axes of the respective leads, with the base of the potential at the point of intersection of the axes, as shown in Figure 12-11.


Figure 12-11 Plotting the mean electrical axis of the ventricles from two electrocardiographic leads (leads I and III).

If the net potential of lead I is positive, it is plotted in a positive direction along the line depicting lead I. Conversely, if this potential is negative, it is plotted in a negative direction. Also, for lead III, the net potential is placed with its base at the point of intersection, and, if positive, it is plotted in the positive direction along the line depicting lead III. If it is negative, it is plotted in the negative direction.

To determine the vector of the total QRS ventricular mean electrical potential, one draws perpendicular lines (the dashed lines in the figure) from the apices of leads I and III, respectively. The point of intersection of these two perpendicular lines represents, by vectorial analysis, the apex of the mean QRS vector in the ventricles, and the point of intersection of the lead I and lead III axes represents the negative end of the mean vector. Therefore, the mean QRS vector is drawn between these two points. The approximate average potential generated by the ventricles during depolarization is represented by the length of this mean QRS vector, and the mean electrical axis is represented by the direction of the mean vector. Thus, the orientation of the mean electrical axis of the normal ventricles, as determined in Figure 12-11, is 59 degrees positive (+59 degrees).

Abnormal Ventricular Conditions That Cause Axis Deviation

Although the mean electrical axis of the ventricles averages about 59 degrees, this axis can swing even in the normal heart from about 20 degrees to about 100 degrees. The causes of the normal variations are mainly anatomical differences in the Purkinje distribution system or in the musculature itself of different hearts. However, a number of abnormal conditions of the heart can cause axis deviation beyond the normal limits, as follows.

Change in the Position of the Heart in the Chest

If the heart itself is angulated to the left, the mean electrical axis of the heart also shifts to the left. Such shift occurs (1) at the end of deep expiration, (2) when a person lies down, because the abdominal contents press upward against the diaphragm, and (3) quite frequently in obese people whose diaphragms normally press upward against the heart all the time due to increased visceral adiposity.

Likewise, angulation of the heart to the right causes the mean electrical axis of the ventricles to shift to the right. This occurs (1) at the end of deep inspiration, (2) when a person stands up, and (3) normally in tall, lanky people whose hearts hang downward.

Hypertrophy of One Ventricle

When one ventricle greatly hypertrophies, the axis of the heart shifts toward the hypertrophied ventricle for two reasons. First, a far greater quantity of muscle exists on the hypertrophied side of the heart than on the other side, and this allows generation of greater 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 normalventricle 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 12-12 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.


Figure 12-12 Left axis deviation in a hypertensive heart (hypertrophic left ventricle). Note the slightly prolonged QRS complex as well.

Vectorial Analysis of Right Axis Deviation Resulting from Hypertrophy of the Right Ventricle

The electrocardiogram of Figure 12-13 shows intense right axis deviation, to an electrical axis of 170 degrees, which is 111 degrees to the right of the normal 59-degree mean ventricular QRS axis. The right axis deviation demonstrated in this figure was caused by hypertrophy of the right ventricle as a result of congenital pulmonary valve stenosis. Right axis deviation also can occur in other congenital heart conditions that cause hypertrophy of the right ventricle, such as tetralogy of Fallot and interventricular septal defect.


Figure 12-13 High-voltage electrocardiogram in congenital pulmonary valve stenosis with right ventricular hypertrophy. Intense right axis deviation and a slightly prolonged QRS complex also are seen.

Bundle Branch Block Causes Axis Deviation

Ordinarily, the 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 the same instant. As a result, the potentials generated by the two ventricles (on the two opposite sides of the heart) almost neutralize each other. But if only one of the major bundle branches is blocked, the cardiac impulse spreads through the normal ventricle long before it spreads through the other. Therefore, depolarization of the two ventricles does not occur even nearly simultaneously, and the depolarization potentials do not neutralize each other. As a result, axis deviation occurs as follows.

Vectorial Analysis of Left Axis Deviation in Left Bundle Branch Block

When the left bundle branch is blocked, cardiac depolarization spreads through the right ventricle two to three times as rapidly as through the left ventricle. Consequently, much of the left ventricle remains polarized for as long as 0.1 second after the right ventricle has become totally depolarized. Thus, the right ventricle becomes electronegative, whereas the left ventricle remains electropositive during most of the depolarization process, and a strong vector projects from the right ventricle toward the left ventricle. In other words, there is intense left axis deviation of about −50 degrees because the positive end of the vector points toward the left ventricle. This is demonstrated in Figure 12-14, which shows typical left axis deviation resulting from left bundle branch block.


Figure 12-14 Left axis deviation caused by left bundle branch block. Note also the greatly prolonged QRS complex.

Because of slowness of impulse conduction when the Purkinje system is blocked, in addition to axis deviation, the duration of the QRS complex is greatly prolonged because of extreme slowness of depolarization in the affected side of the heart. One can see this by observing the excessive widths of the QRS waves in Figure 12-14. This is discussed in greater detail later in the chapter. This extremely prolonged QRS complex differentiates bundle branch block from axis deviation caused by hypertrophy.

Vectorial Analysis of Right Axis Deviation in Right Bundle Branch Block

When the right bundle branch is blocked, the left ventricle depolarizes far more rapidly than the right ventricle, so the left side of the ventricles becomes electronegative as long as 0.1 second before the right. Therefore, a strong vector develops, with its negative end toward the left ventricle and its positive end toward the right ventricle. In other words, intense right axis deviation occurs. Right axis deviation caused by right bundle branch block is demonstrated, and its vector is analyzed, in Figure 12-15, which shows an axis of about 105 degrees instead of the normal 59 degrees and a prolonged QRS complex because of slow conduction.


Figure 12-15 Right axis deviation caused by right bundle branch block. Note also the greatly prolonged QRS complex.

Conditions That Cause Abnormal Voltages of the QRS Complex

Increased Voltage in the Standard Bipolar Limb Leads

Normally, the voltages in the three standard bipolar limb leads, as measured from the peak of the R wave to the bottom of the S wave, vary between 0.5 and 2.0 millivolts, with lead III usually recording the lowest voltage and lead II the highest. However, these relations are not invariable, even for the normal heart. In general, when the sum of the voltages of all the QRS complexes of the three standard leads is greater than 4 millivolts, the patient is considered to have a high-voltage electrocardiogram.

The cause of high-voltage QRS complexes most often is increased muscle mass of the heart, which ordinarily results from hypertrophy of the muscle in response to excessive load on one part of the heart or the other. For example, the right ventricle hypertrophies when it must pump blood through a stenotic pulmonary valve, and the left ventricle hypertrophies when a person has high blood pressure. The increased quantity of muscle causes generation of increased quantities of electricity around the heart. As a result, the electrical potentials recorded in the electrocardiographic leads are considerably greater than normal, as shown in Figures 12-12 and 12-13.

Decreased Voltage of the Electrocardiogram

Decreased Voltage Caused by Cardiac Myopathies

One of the most common causes of decreased voltage of the QRS complex is a series of old myocardial infarctions with resultant diminished muscle mass. This also causes the depolarization wave to move through the ventricles slowly and prevents major portions of the heart from becoming massively depolarized all at once. Consequently, this condition causes some prolongation of the QRS complex along with the decreased voltage. Figure 12-16 shows a typical low-voltage electrocardiogram with prolongation of the QRS complex, which is common after multiple small infarctions of the heart have caused local delays of impulse conduction and reduced voltages due to loss of muscle mass throughout the ventricles.


Figure 12-16 Low-voltage electrocardiogram following local damage throughout the ventricles caused by previous myocardial infarction.

Decreased Voltage Caused by Conditions Surrounding the Heart

One of the most important causes of decreased voltage in electrocardiographic leads is fluid in the pericardium. Because extracellular fluid conducts electrical currents with great ease, a large portion of the electricity flowing out of the heart is conducted from one part of the heart to another through the pericardial fluid. Thus, this effusion effectively “short-circuits” the electrical potentials generated by the heart, decreasing the electrocardiographic voltages that reach the outside surfaces of the body. Pleural effusion, to a lesser extent, also can “short-circuit” the electricity around the heart so that the voltages at the surface of the body and in the electrocardiograms are decreased.

Pulmonary emphysema can decrease the electrocardiographic potentials, but for a different reason than that of pericardial effusion. In pulmonary emphysema, conduction of electrical current through the lungs is depressed considerably because of excessive quantity of air in the lungs. Also, the chest cavity enlarges, and the lungs tend to envelop the heart to a greater extent than normally. Therefore, the lungs act as an insulator to prevent spread of electrical voltage from the heart to the surface of the body, and this results in decreased electrocardiographic potentials in the various leads.

Prolonged and Bizarre Patterns of the QRS Complex

Prolonged QRS Complex as a Result of Cardiac Hypertrophy or Dilatation

The QRS complex lasts as long as depolarization continues to spread through the ventricles—that is, as long as part of the ventricles is depolarized and part is still polarized. Therefore, prolonged conductionof the impulse through the ventricles always causes a prolonged QRS complex. Such prolongation often occurs when one or both ventricles are hypertrophied or dilated, owing to the longer pathway that the impulse must then travel. The normal QRS complex lasts 0.06 to 0.08 second, whereas in hypertrophy or dilatation of the left or right ventricle, the QRS complex may be prolonged to 0.09 to 0.12 second.

Prolonged QRS Complex Resulting from Purkinje System Blocks

When the Purkinje fibers are blocked, the cardiac impulse must then be conducted by the ventricular muscle instead of by way of the Purkinje system. This decreases the velocity of impulse conduction to about one third of normal. Therefore, if complete block of one of the bundle branches occurs, the duration of the QRS complex is usually increased to 0.14 second or greater.

In general, a QRS complex is considered to be abnormally long when it lasts more than 0.09 second; when it lasts more than 0.12 second, the prolongation is almost certainly caused by pathological block somewhere in the ventricular conduction system, as shown by the electrocardiograms for bundle branch block in Figures 12-14 and 12-15.

Conditions That Cause Bizarre QRS Complexes

Bizarre patterns of the QRS complex most frequently are caused by two conditions: (1) destruction of cardiac muscle in various areas throughout the ventricular system, with replacement of this muscle by scar tissue, and (2) multiple small local blocks in the conduction of impulses at many points in the Purkinje system. As a result, cardiac impulse conduction becomes irregular, causing rapid shifts in voltages and axis deviations. This often causes double or even triple peaks in some of the electrocardiographic leads, such as those shown in Figure 12-14.

Current of Injury

Many different cardiac abnormalities, especially those that damage the heart muscle itself, often cause part of the heart to remain partially or totally depolarized all the time. When this occurs, current flows between the pathologically depolarized and the normally polarized areas even between heartbeats. This is called a current of injury. Note especially that the injured part of the heart is negative, because this is the part that is depolarized and emits negative charges into the surrounding fluids, whereas the remainder of the heart is neutral or positive polarity.

Some abnormalities that can cause current of injury are (1) mechanical trauma, which sometimes makes the membranes remain so permeable that full repolarization cannot take place; (2) infectious processesthat damage the muscle membranes; and (3) ischemia of local areas of heart muscle caused by local coronary occlusions, which is by far the most common cause of current of injury in the heart. During ischemia, not enough nutrients from the coronary blood supply are available to the heart muscle to maintain normal membrane polarization.

Effect of Current of Injury on the QRS Complex

In Figure 12-17, a small area in the base of the left ventricle is newly infarcted (loss of coronary blood flow). Therefore, during the T-P interval—that is, when the normal ventricular muscle is totally polarized—abnormal negativecurrent still flows from the infarcted area at the base of the left ventricle and spreads toward the rest of the ventricles.


Figure 12-17 Effect of a current of injury on the electrocardiogram.

The vector of this “current of injury,” as shown in the first heart in Figure 12-17, is in a direction of about 125 degrees, with the base of the vector, the negative end, toward the injured muscle. As shown in the lower portions of the figure, even before the QRS complex begins, this vector causes an initial record in lead I below the zero potential line, because the projected vector of the current of injury in lead I points toward the negative end of the lead I axis. In lead II, the record is above the line because the projected vector points more toward the positive terminal of the lead. In lead III, the projected vector points in the same direction as the positive terminal of lead III so that the record is positive. Furthermore, because the vector lies almost exactly in the direction of the axis of lead III, the voltage of the current of injury in lead III is much greater than in either lead I or lead II.

As the heart then proceeds through its normal process of depolarization, the septum first becomes depolarized; then the depolarization spreads down to the apex and back toward the bases of the ventricles. The last portion of the ventricles to become totally depolarized is the base of the right ventricle, because the base of the left ventricle is already totally and permanently depolarized. By vectorial analysis, the successive stages of electrocardiogram generation by the depolarization wave traveling through the ventricles can be constructed graphically, as demonstrated in the lower part of Figure 12-17.

When the heart becomes totally depolarized, at the end of the depolarization process (as noted by the next-to-last stage in Figure 12-17), all the ventricular muscle is in a negative state. Therefore, at this instant in the electrocardiogram, no current flows from the ventricles to the electrocardiographic electrodes because now both the injured heart muscle and the contracting muscle are depolarized.

Next, as repolarization takes place, all of the heart finally repolarizes, except the area of permanent depolarization in the injured base of the left ventricle. Thus, repolarization causes a return of the current of injury in each lead, as noted at the far right in Figure 12-17.

The J Point—the Zero Reference Potential for Analyzing Current of Injury

One might think that the electrocardiograph machines for recording electrocardiograms could determine when no current is flowing around the heart. However, many stray currents exist in the body, such as currents resulting from “skin potentials” and from differences in ionic concentrations in different fluids of the body. Therefore, when two electrodes are connected between the arms or between an arm and a leg, these stray currents make it impossible to predetermine the exact zero reference level in the electrocardiogram.

For these reasons, the following procedure must be used to determine the zero potential level: First, one notes the exact point at which the wave of depolarization just completes its passage through the heart,which occurs at the end of the QRS complex. At exactly this point, all parts of the ventricles have become depolarized, including both the damaged parts and the normal parts, so no current is flowing around the heart. Even the current of injury disappears at this point. Therefore, the potential of the electrocardiogram at this instant is at zero voltage. This point is known as the “J” point in the electrocardiogram, as shown in Figure 12-18.


Figure 12-18 J point as the zero reference potential of the electrocardiograms for leads I and III. Also, the method for plotting the axis of the injury potential is shown by the lowermost panel.

Then, for analysis of the electrical axis of the injury potential caused by a current of injury, a horizontal line is drawn in the electrocardiogram for each lead at the level of the J point. This horizontal line is then the zero potential levelin the electrocardiogram from which all potentials caused by currents of injury must be measured.

Use of the J Point in Plotting Axis of Injury Potential

Figure 12-18 shows electrocardiograms (leads I and III) from an injured heart. Both records show injury potentials. In other words, the J point of each of these two electrocardiograms is not on the same line as the T-P segment. In the figure, a horizontal line has been drawn through the J point to represent the zero voltage level in each of the two recordings. The injury 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 determined from the J point. In lead I, the recorded voltage of the injury potential is above the zero potential level and is, therefore, positive. Conversely, in lead III, the injury potential is below the zero voltage level and, therefore, is negative.

At the bottom in Figure 12-18, the respective injury potentials in leads I and III are plotted on the coordinates of these leads, and the resultant vector of the injury potential for the whole ventricular muscle mass is determined by vectorial analysis as described. In this instance, the resultant vector extends from the right side of the ventricles toward the left and slightly upward, with an axis of about −30 degrees. If one places this vector for the injury potential directly over the ventricles, the negative end of the vector points toward the permanently depolarized, “injured” area of the ventricles. In the example shown in Figure 12-18, the injured area would be in the lateral wall of the right ventricle.

This analysis is obviously complex. However, it is essential that the student go over it again and again until he or she understands it thoroughly. No other aspect of electrocardiographic analysis is more important.

Coronary Ischemia as a Cause of Injury Potential

Insufficient blood flow to the cardiac muscle depresses the metabolism of the muscle for three reasons: (1) lack of oxygen, (2) excess accumulation of carbon dioxide, and (3) lack of sufficient food nutrients. Consequently, repolarization of the muscle membrane 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 membranes. As long as this state exists, an injury potential continues to flow during the diastolic portion (the T-P portion) of each heart cycle.

Extreme ischemia of the cardiac muscle occurs after coronary occlusion, and a strong current of injury flows from the infarcted area of the ventricles during the T-P interval between heartbeats, as shown in Figures 12-19 and 12-20. Therefore, one of the most important diagnostic features of electrocardiograms recorded after acute coronary thrombosis is the current of injury.


Figure 12-19 Current of injury in acute anterior wall infarction. Note the intense injury potential in lead V2.


Figure 12-20 Injury potential in acute posterior wall, apical infarction.

Acute Anterior Wall Infarction

Figure 12-19 shows the electrocardiogram in the three standard bipolar limb leads and in one chest lead (lead V2) recorded from a patient with acute anterior wall cardiac infarction. The most important diagnostic feature of this electrocardiogram is the intense injury potential in chest lead V2. If one draws a zero horizontal potential line through the J point of this electrocardiogram, a strong negative injury potential during the T-P interval is found, which means that the chest electrode over the front of the heart is in an area of strongly negative potential. In other words, the negative end of the injury potential vector in this heart is against the anterior chest wall. This means that the current of injury is emanating from the anterior wall of the ventricles, which diagnoses 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 potential in lead III. This means that the resultant vector of the injury potential in the heart is about +150 degrees, with the negative end pointing toward the left ventricle and the positive end pointing toward the right ventricle. Thus, in this particular electrocardiogram, the current of injury is coming mainly from the left ventricle, as well as from the anterior wall of the heart. Therefore, one would conclude that this anterior wall infarction almost certainly is caused by thrombosis of the anterior descending branch of the left coronary artery.

Posterior Wall Infarction

Figure 12-20 shows the three standard bipolar limb leads and one chest lead (lead V2) from a patient with posterior wall infarction. The major diagnostic feature of this electrocardiogram is also in the chest lead. If a zero potential reference line is drawn through the J point of this lead, it is readily apparent that during the T-P interval, the potential of the current of injury is positive. This means that the positive end of the vector is in the direction of the anterior chest wall, and the negative end (injured end of the vector) points away from the chest wall. In other words, the current of injury is coming from the back of the heart opposite to the anterior chest wall, which is the reason this type of electrocardiogram is the basis for diagnosing posterior wall infarction.

If one analyzes the injury potentials from leads II and III of Figure 12-20, it is readily apparent that the injury potential is negative in both leads. By vectorial analysis, as shown in the figure, one finds that the resultant vector of the injury potential is about −95 degrees, with the negative end pointing downward and the positive end pointing upward. Thus, because the infarct, as indicated by the chest lead, is on the posterior wall of the heart and, as indicated by the injury potentials in leads II and III, is in the apical portion of the heart, one would suspect that this infarct is near the apex on the posterior wall of the left ventricle.

Infarction in Other Parts of the Heart

By the same procedures demonstrated in the preceding discussions of anterior and posterior wall infarctions, it is possible to determine the locus of any infarcted area emitting a current of injury, regardless of which part of the heart is involved. In making such vectorial analyses, it must be remembered that the positive end of the injury potential vector points toward the normal cardiac muscle, and the negative end points toward the injured portion of the heart that is emitting the current of injury.

Recovery from Acute Coronary Thrombosis

Figure 12-21 shows a V3 chest lead from a patient with acute posterior wall infarction, demonstrating changes in the electrocardiogram from the day of the attack to 1 week later, 3 weeks later, and finally 1 year later. From this electrocardiogram, one can see that the injury potential is strong immediately after the acute attack (T-P segment displaced positively from the S-T segment). However, after about 1 week, the injury potential has diminished considerably, and after 3 weeks, it is gone. After that, the electrocardiogram does not change greatly during the next year. This is the usual recovery pattern after acute myocardial infarction of moderate degree, showing that the new collateral coronary blood flow develops enough to re-establish appropriate nutrition to most of the infarcted area.


Figure 12-21 Recovery of the myocardium after moderate posterior wall infarction, demonstrating disappearance of the injury potential that is present on the first day after the infarction and still slightly present at 1 week.

Conversely, in some patients with myocardial infarction, the infarcted area never redevelops adequate coronary blood supply. Often, some of the heart muscle dies, but if the muscle does not die, it will continue to show an injury potential as long as the ischemia exists, particularly during bouts of exercise when the heart is overloaded.

Old Recovered Myocardial Infarction

Figure 12-22 shows leads I and III after anterior infarction and leads I and III after posterior infarction about 1 year after the acute heart attack. The records show what might be called the “ideal” configurations of the QRS complex 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 the left ventricle, but in posterior infarction, a Q wave has developed at the beginning of the QRS complex in lead III because of loss of muscle in the posterior apical part of the ventricle.


Figure 12-22 Electrocardiograms of anterior and posterior wall infarctions that occurred about 1 year previously, showing a Q wave in lead I in anterior wall infarction and a Q wave in lead III in posterior wall infarction.

These configurations are certainly not found in all cases of old cardiac infarction. Local loss of muscle and local points of cardiac signal conduction block can cause very bizarre QRS patterns (especially prominent Q waves, for instance), decreased voltage, and QRS prolongation.

Current of Injury in Angina Pectoris

“Angina pectoris” means pain from the heart felt in the pectoral regions of the upper chest. This pain usually also radiates into the left neck area and down the left arm. The pain is typically caused by moderate ischemia of the heart. Usually, no pain is felt as long as the person is quiet, but as soon as he or she overworks the heart, the pain appears.

An injury potential sometimes appears in the electrocardiogram during an attack of severe angina pectoris because the coronary insufficiency becomes great enough to prevent adequate repolarization of some areas of the heart during diastole.

Abnormalities in the T Wave

Earlier in the chapter, it was pointed out that the T 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 of the intraventricular surfaces. That is, the T wave becomes abnormal when the normal sequence of repolarization does not occur. Several factors can change this sequence of repolarization.

Effect of Slow Conduction of the Depolarization Wave on the Characteristics of the T Wave

Referring to Figure 12-14, note that the QRS complex is considerably prolonged. The reason for this prolongation is delayed conduction in the left ventricle resulting from left bundle branch block. This causes the left ventricle to become depolarized about 0.08 second after depolarization of the right ventricle, which gives a strong mean QRS vector to the left. However, the refractory periods of the right and left ventricular muscle masses are not greatly different from each other. Therefore, the right ventricle begins to repolarize long before the left ventricle; this causes strong positivity in the right ventricle and negativity in the left ventricle at the time that the T wave is developing. In other words, the mean axis of the T wave is now deviated to the right, which is opposite the mean electrical axis of the QRS complex in the same electrocardiogram. Thus, when conduction of the depolarization impulse through the ventricles is greatly delayed, the T wave is almost always of opposite polarity to that of the QRS complex.

Shortened Depolarization in Portions of the Ventricular Muscle as a Cause of T Wave Abnormalities

If the base of the ventricles should exhibit an abnormally short period of depolarization, that is, a shortened action potential, repolarization of the ventricles would not begin at the apex as it normally does. Instead, the base of the ventricles would repolarize ahead of the apex, and the vector of repolarization would point from the apex toward the base of the heart, opposite to the standard vector of repolarization. Consequently, the T wave in all three standard leads would be negative rather than the usual positive. Thus, the simple fact that the base of the ventricles has a shortened period of depolarization is sufficient to cause marked changes in the T wave, even to the extent of changing the entire T wave polarity, as shown in Figure 12-23.


Figure 12-23 Inverted T wave resulting from mild ischemia at the apex of the ventricles.

Mild ischemia is by far the most common cause of shortening of depolarization of cardiac muscle because this increases current flow through the potassium channels. When the ischemia occurs in only one area of the heart, the depolarization period of this area decreases out of proportion to that in other portions. As a result, definite changes in the T wave can take place. The ischemia might result from chronic, progressive coronary occlusion; acute coronary occlusion; or relative coronary insufficiency that occurs during exercise.

One means for detecting mild coronary insufficiency is to have the patient exercise and to record the electrocardiogram, noting whether changes occur in the T waves. The changes in the T waves need not be specific because any change in the T wave in any lead—inversion, for instance, or a biphasic wave—is often evidence enough that some portion of the ventricular muscle has a period of depolarization out of proportion to the rest of the heart, caused by mild to moderate coronary insufficiency.

Effect of Digitalis on the T Wave

As discussed in Chapter 22, digitalis is a drug that can be used during coronary insufficiency to increase the strength of cardiac muscle contraction. But when overdosages of digitalis are given, depolarization duration in one part of the ventricles may be increased out of proportion to that of other parts. As a result, nonspecific changes, such as T wave inversion or biphasic T waves, may occur in one or more of the electrocardiographic leads. A biphasic T wave caused by excessive administration of digitalis is shown in Figure 12-24. Therefore, changes in the T wave during digitalis administration are often the earliest signs of digitalis toxicity.


Figure 12-24 Biphasic T wave caused by digitalis toxicity.


See bibliography for Chapter 13.


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