Guyton and Hall Physiology Chapter 12 - Electrocardiographic Interpretation of Cardiac Muscle.PDF

CHAPTER 12 UNIT III Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities: Vectorial Analysis...

CHAPTER 12 UNIT III Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities: Vectorial Analysis From the discussion in Chapter 10 of impulse transmis- THE DIRECTION OF A VECTOR IS DENOTED sion through the heart, it is obvious that any change in IN TERMS OF DEGREES the pattern of this transmission can cause abnormal elec- When a vector is exactly horizontal and directed toward trical potentials around the heart and, consequently, alter the person’s left side, the vector is said to extend in the the shapes of the waves in the electrocardiogram (ECG). direction of 0 degrees, as shown in Figure 12-2. From this For this reason, most serious abnormalities of the heart zero reference point, the scale of vectors rotates clock- muscle can be diagnosed by analyzing the contours of the wise; when the vector extends from above and straight waves in the different electrocardiographic leads. downward, it has a direction of +90 degrees, when it extends from the person’s left to right, it has a direction of VECTORIAL ANALYSIS OF +180 degrees, and when it extends straight upward, it has ELECTROCARDIOGRAMS a direction of −90 (or +270) degrees. In a normal heart, the average direction of the vec- VECTORS CAN REPRESENT ELECTRICAL tor during spread of the depolarization wave through POTENTIALS the ventricles, called the mean QRS vector, is about +59 To understand how cardiac abnormalities affect the con- degrees, which is shown by vector A drawn through the tours of the ECG, one must first become familiar with the center of Figure 12-2 in the +59-­degree direction. This concept of vectors and vectorial analysis as applied to elec- means that during most of the depolarization wave, the trical potentials in and around the heart. In Chapter 11, we apex of the heart remains positive with respect to the base pointed out that heart current flows in a particular direction of the heart, as discussed later in this chapter. in the heart at a given instant during the cardiac cycle. A vec- tor is an arrow that points in the direction of the electrical AXIS FOR EACH STANDARD BIPOLAR potential generated by the current flow, with the arrowhead LEAD AND EACH UNIPOLAR LIMB LEAD in the positive direction. Also, by convention, the length of the In Chapter 11, the three standard bipolar and the three arrow is drawn proportional to the voltage of the potential. unipolar limb leads are described. Each lead is actually a pair of electrodes connected to the body on opposite sides Resultant Vector in the Heart at Any Given Instant. of the heart, and the direction from negative electrode to The shaded area and the minus signs in Figure 12-1 show positive electrode is called the axis of the lead. Lead I is depolarization of the ventricular septum and of parts of recorded from two electrodes placed respectively on the the apical endocardial walls of the two ventricles. At the two arms. Because the electrodes lie exactly in the hori- instant of heart excitation, electrical current flows between zontal direction, with the positive electrode to the left, the the depolarized areas inside the heart and the nondepolar- axis of lead I is 0 degrees. ized areas on the outside of the heart, as indicated by the In recording lead II, electrodes are placed on the right long elliptical arrows. Some current also flows inside the arm and left leg. The right arm connects to the torso in heart chambers directly from the depolarized areas toward the upper right-­hand corner, and the left leg connects in the still polarized areas. Overall, considerably more current the lower left-­hand corner. Therefore, the direction of this flows downward from the base of the ventricles toward the lead is about +60 degrees. apex than in the upward direction. Therefore, the sum- By similar analysis, it can be seen that lead III has an mated vector of the generated potential at this particular axis of about +120 degrees, lead aVR, +210 degrees, lead instant, called the instantaneous mean vector, is represent- aVF, +90 degrees, and lead aVL, −30 degrees. The direc- ed by the long black arrow drawn through the center of tions of the axes of all these leads are shown in Figure the ventricles in a direction from the base toward the apex. 12-3, which is known as the hexagonal reference system. Furthermore, because the summated current is quite large, The polarities of the electrodes are shown by the plus the potential is large, and the vector is long. 143 UNIT III The Heart + + ++ A a se + + B− − − + − − + + − − + + ++ − − + + + − − + − + + + + − − I B I + − − + + – + + + − − − + + − − + − −− + + + + ++ − + + +− − + A + + x + + e + ++ Ap + + + + + + + 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 12-1 Mean vector through the partially depolarized ventricles and minus signs in the figure. The reader must learn goes from the base of the left ventricle towards the apex. these axes and their polarities, particularly for the bipo- lar limb leads I, II, and III, to understand the remainder of this chapter. VECTORIAL ANALYSIS OF POTENTIALS –90° RECORDED IN DIFFERENT LEADS +270° Figure 12-4 shows a partially depolarized heart, with vector A representing the instantaneous mean direc- tion of current flow in the ventricles. In this case, the direction of the vector is +55 degrees, and the voltage 180° 0° of the potential, represented by the length of vector A, A is 2 millivolts. In the diagram below the heart, vector A is shown again, and a line is drawn to represent the axis 120° 59° of lead I in the 0-­degree direction. To determine how much of the voltage in vector A will be recorded in lead I, a line perpendicular to the axis of lead I is drawn from +90° the tip of vector A to the lead I axis, and a so-­called pro- jected vector (B) is drawn along the lead I axis. The arrow Figure 12-2 Vectors drawn to represent potentials for several dif- of this projected vector points toward the positive end ferent hearts and the axis of the potential (expressed in degrees) for of the lead I axis, which means that the record momen- each heart. tarily being recorded in the ECG of lead I is positive. 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 12-5 shows another example of vectorial analy- sis. In this example, vector A represents the electrical potential and its axis at a given instant during ventricular + aVR aVL + depolarization in a heart in which the left side of the heart 210° depolarizes more rapidly than the right side. In this case, –30° the instantaneous vector has a direction of 100 degrees, 0° I and its voltage is again 2 millivolts. To determine the – + potential actually recorded in lead I, we draw a perpen- dicular line from the tip of vector A to the lead I axis and find projected vector B. Vector B is very short, and this 60° time it is in the negative direction, indicating that at this – – III II particular instant, the recording in lead I will be negative 120° 90° (below the zero line in the ECG), and the voltage recorded + + will be small, about −0.3 millivolts. This figure demon- aVF strates that when the vector in the heart is in a direction + almost perpendicular to the axis of the lead, the voltage Figure 12-3 Axes of the three bipolar and three unipolar leads. recorded in the ECG of this lead is very low. Conversely, 144  Chapter 12 Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities equal to that in the heart and, in lead III (vector D), it is about one-third that in the heart. An identical analysis can be used to determine poten- tials recorded in augmented limb leads, except that the respective axes of the augmented leads (see Figure 12-3) UNIT III are used in place of the standard bipolar limb lead axes used for Figure 12-6. I B I – + VECTORIAL ANALYSIS OF THE NORMAL ELECTROCARDIOGRAM A VECTORS THAT OCCUR AT SUCCESSIVE INTERVALS DURING DEPOLARIZATION OF THE VENTRICLES—THE QRS COMPLEX Figure 12-5 Determination of the projected vector B along the axis When the cardiac impulse enters the ventricles through of lead I when vector A represents the instantaneous potential in the the atrioventricular bundle, the first part of the ventricles 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 shown by the – II III – darker shaded portion of the ventricle in Figure 12-7A. Next, depolarization spreads along the endocardial sur- faces of the remainder of the two ventricles, as shown in Figure 12-7B and C. Finally, it spreads through the ven- tricular muscle to the outside of the heart, as shown pro- gressively in Figure 12-7C to E. I B I – + At each stage in Figure 12-7, A to E, the instantaneous D mean electrical potential of the ventricles is represented A by a red vector superimposed on the ventricle in each fig- C ure. Each of these vectors is then analyzed by the method described in the preceding section to determine the volt- III ages that will be recorded at each instant in each of the II three standard electrocardiographic leads. To the right + + in each Figure is shown progressive development of the Figure 12-6 Determination of projected vectors in leads I, II, and III electrocardiographic QRS complex. Keep in mind that a when vector A represents the instantaneous potential in the ventricles. positive vector in a lead will cause recording in the ECG above the zero line, whereas a negative vector will cause when the heart vector has almost exactly the same axis as recording below the zero line. the lead axis, essentially the entire voltage of the vector will Before proceeding with further consideration of be recorded. vectorial analysis, it is essential that this analysis of the successive normal vectors presented in Figure 12-7 be Vectorial Analysis of Potentials in the Three Stand- understood. Each of these analyses should be studied in ard Bipolar Limb Leads. In Figure 12-6, vector A de- detail by the procedure given here. A short summary of picts the instantaneous electrical potential of a partially this sequence follows. depolarized heart. To determine the potential recorded at In Figure 12-7A, the ventricular muscle has just begun this instant in the ECG for each one of the three standard to be depolarized, representing an instant about 0.01 second bipolar limb leads, perpendicular lines (the dashed lines) after the onset of depolarization. At this time, the vector is are drawn from the tip of vector A to the three lines rep- short because only a small portion of the ventricles—the resenting the axes of the three different standard leads, as septum—is depolarized. Therefore, all electrocardiographic shown in the figure. The projected vector B depicts the voltages are low, as recorded to the right of the ventricular potential recorded at that instant in lead I, projected vec- muscle for each of the leads. The voltage in lead II is greater tor C depicts the potential in lead II, and projected vec- than the voltages in leads I and III because the heart vector tor D depicts the potential in lead III. In each of these, extends mainly in the same direction as the axis of lead II. the record in the ECG is positive—that is, above the zero In Figure 12-7B, which represents about 0.02 sec- line—because the projected vectors point in the positive ond after onset of depolarization, the heart vector is long directions along the axes of all the leads. The potential in because much of the ventricular muscle mass has become lead I (vector B) is about half of that of the actual potential depolarized. Therefore, the voltages in all electrocardio- in the heart (vector A), in lead II (vector C), it is almost graphic leads have increased. 145 UNIT III The Heart − − − − II III II III I I I I I I − + − + II II III II III II + + + + III III A B − − − − II III II III I I I I I I − + − + II II III II III II + + + + III III C D − − II III I I I − + II III II + + III E Figure 12-7 Shaded areas of the ventricles are depolarized (−); nonshaded areas are still polarized (+). Shown are 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). In Figure 12-7C, about 0.035 second after onset of In Figure 12-7E, about 0.06 second after onset of depo- depolarization, the heart vector is becoming shorter, and larization, the entire ventricular muscle mass is depolarized the recorded electrocardiographic voltages are lower, so that no current flows around the heart and no electrical because the outside of the heart apex is now electronega- potential is generated. The vector becomes zero, and the tive, neutralizing much of the positivity on the other epi- voltages in all leads become zero. cardial surfaces of the heart. Also, the axis of the vector is Thus, the QRS complexes are completed in the three beginning to shift toward the left side of the chest because standard bipolar limb leads. the left ventricle is slightly slower to depolarize than the Sometimes the QRS complex has a slight negative right ventricle. Therefore, the ratio of the voltage in lead I depression at its beginning in one or more of the leads, to that in lead III is increasing. which is not shown in Figure 12-7; this depression is In Figure 12-7D, about 0.05 second after onset of depo- the Q wave. When it occurs, it is caused by initial depo- larization, the heart vector points toward the base of the larization of the left side of the septum before the right left ventricle, and it is short because only a minute por- side, which creates a weak vector from left to right for a tion of the ventricular muscle is still polarized positive. fraction of a second before the usual base to apex vector Because of the direction of the vector at this time, the volt- occurs. The major positive deflection shown in Figure ages recorded in leads II and III are both negative—that is, 12-7 is the R wave, and the final negative deflection is below the line—whereas the voltage of lead I is still positive. the S wave. 146  Chapter 12 Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities + + ++ P T − ++ − − −+ + + − − + + I + − − + ++ − − + + − − + + + II III + + SA UNIT III + + − − II II III I I − + I I III III II − + + + I III II + + II Figure 12-9 Depolarization of the atria and generation of the P wave showing the maximum vector through the atria and the resultant III vectors in the three standard leads. At the right are the atrial P and T waves. SA, Sinoatrial node. Figure 12-8 Generation of the T wave during repolarization of the ventricles, also showing vectorial analysis of the first stage of repolari- zation. The total time from the beginning of the T wave to its end is approximately 0.15 second. 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 ELECTROCARDIOGRAM DURING VENTRI- decreases. These changes also demonstrate that the vec- CULAR REPOLARIZATION—THE T WAVE tor is greatest when about half the heart is in the polarized After the ventricular muscle has become depolarized, state and about half is depolarized. about 0.15 second later, repolarization begins and pro- The changes in the ECGs of the three standard limb ceeds until complete, at about 0.35 second. This repolar- leads during repolarization are noted under each of the ization causes the T wave in the ECG. ventricles, depicting the progressive stages of repolariza- Because the septum and endocardial areas of the tion. Thus, over about 0.15 second, the period of time ventricular muscle depolarize first, it seems logical that required for the entire process to take place, the T wave of these areas should repolarize first as well. However, the ECG is generated. this is not the usual case, because the septum and other endocardial areas have a longer period of contraction ATRIAL DEPOLARIZATION—THE P WAVE than most of the external surfaces of the heart. There- Depolarization of the atria begins in the sinus node and fore, the greatest portion of ventricular muscle mass spreads in all directions over the atria. Therefore, the point to repolarize first is the entire outer surface of the ven- of original electronegativity in the atria is at about the point tricles, especially near the apex of the heart. The endo- of entry of the superior vena cava where the sinus node cardial areas, conversely, normally repolarize last. This lies, and the direction of initial depolarization is denoted sequence of repolarization is postulated to be caused by the black vector in Figure 12-9. Furthermore, the vector by the high blood pressure inside the ventricles during remains generally in this direction throughout the process contraction, which greatly reduces coronary blood flow of normal atrial depolarization. Because this direction is to the endocardium, thereby slowing repolarization in generally in the positive directions of the axes of the three the endocardial areas. standard bipolar limb leads I, II, and III, the ECGs recorded Because the outer apical surfaces of the ventricles from the atria during depolarization are also usually posi- repolarize before the inner surfaces, the positive end of tive in all three of these leads, as shown in Figure 12-9. This the overall ventricular vector during repolarization is record of atrial depolarization is known as the atrial P wave. toward the apex of the heart. As a result, the normal T wave in all three bipolar limb leads is positive, which is Repolarization of the Atria—the Atrial T Wave. Spread also the polarity of most of the normal QRS complex. of depolarization through the atrial muscle is much slower In Figure 12-8, five stages of repolarization of the ven- than in the ventricles because the atria have no Purkinje tricles are denoted by progressive increase of the light tan system for fast conduction of the depolarization signal. areas—the repolarized areas. At each stage, the vector Therefore, the musculature around the sinus node be- extends from the base of the heart toward the apex until it comes depolarized a long time before the musculature in disappears in the last stage. At first, the vector is relatively distal parts of the atria. Consequently, the area in the atria small because the area of repolarization is small. Later, that also becomes repolarized first is the sinus nodal re- the vector becomes stronger because of greater degrees gion, the area that had originally become depolarized first. 147 UNIT III The Heart Thus, when repolarization begins, the region around the sinus node becomes positive with respect to the remain- der of the atria. Therefore, the atrial repolarization vector is backward to the vector of depolarization. (Note that this is 1 2 3 4 5 opposite to the effect that occurs in the ventricles.) There- 4 fore, as shown to the right in Figure 12-9, the so-­called atri- al 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 5 line from the P wave; that is, it is normally negative rather 1 than positive in the three standard bipolar limb leads. 3 In a normal ECG, 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 2 the large ventricular QRS complex, although in some very Depolarization Repolarization QRS T abnormal states it does appear in the recorded ECG. Figure 12-10 QRS and T vectorcardiograms. Vectorcardiogram As noted previously, the vector of current flow through the heart changes rapidly as the impulse spreads through the III – –60 myocardium. It changes in two aspects. First, the vector in- I creases 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 vectorcardiogram – + I I II depicts these changes at different times during the cardiac 180 0 cycle, as shown in Figure 12-10. 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 120 59 III polarized between heartbeats, the positive end of the vec- + tor remains at the zero point because there is no vectorial III electrical potential. However, as soon as current begins to Figure 12-11 Plotting the mean electrical axis of the ventricles from flow through the ventricles at the beginning of ventricu- two electrocardiographic leads (leads I and III). lar depolarization, the positive end of the vector leaves the zero reference point. When the septum first becomes depolarized, the vector of ventricular depolarization, the direction of the electrical extends downward toward the apex of the ventricles, but potential (negative to positive) is from the base of the it is relatively weak, thus generating the first portion of the ventricles toward the apex. This preponderant direction ventricular vectorcardiogram, as shown by the positive end of the potential during depolarization from the base to the of vector 1. As more of the ventricular muscle becomes de- apex of the heart is called the mean electrical axis of the polarized, the vector becomes stronger and stronger, usual- ventricles. The mean electrical axis of the normal ventricles ly swinging slightly to one side. Thus, vector 2 of Figure 12- is 59 degrees. In many pathological conditions of the heart, 10 represents the state of depolarization of the ventricles about 0.02 second after vector 1. After another 0.02 second, this direction changes markedly, sometimes even to opposite vector 3 represents the potential, and vector 4 occurs in poles of the heart. another 0.01 second. Finally, the ventricles become totally depolarized, and the vector becomes zero once again, as DETERMINING THE ELECTRICAL AXIS FROM shown at point 5. STANDARD LEAD ELECTROCARDIOGRAMS The elliptical figure generated by the positive ends of the vectors is called the QRS vectorcardiogram. Clinically, the electrical axis of the heart is usually estimated from the standard bipolar limb lead ECGs rather than from the vectorcardiogram. Figure 12-11 shows a method for performing this estimation. After recording MEAN ELECTRICAL AXIS OF the standard leads, one determines the net potential and THE VENTRICULAR QRS AND ITS polarity of the recordings in leads I and III. In lead I of SIGNIFICANCE Figure 12-11, the recording is positive, and in lead III, The vectorcardiogram during ventricular depolarization the recording is mainly positive but negative during part (the QRS vectorcardiogram) shown in Figure 12-10 is of the cycle. If any part of a recording is negative, this that of a normal heart. Note that during most of the cycle negative potential is subtracted from the positive part of 148  Chapter 12 Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities 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 UNIT III shown in Figure 12-11. To determine the vector of the total QRS ventricular I II III mean electrical potential, one draws perpendicular lines III (the dashed lines in the figure) from the apices of leads – I and III, respectively. The point of intersection of these two perpendicular (dashed) lines represents, by vectorial analysis, the apex of the mean QRS vector in the ventri- cles, and the point of intersection of the lead I and lead I – +I 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 III the length of this mean QRS vector, and the mean electri- Figure 12-12 Left axis deviation in a hypertensive heart (hypertroph- cal axis is represented by the direction of the mean vec- ic left ventricle). Note the slightly prolonged QRS complex as well. tor. Thus, the orientation of the mean electrical axis of the normal ventricles, as determined in Figure 12-11, is 59 through the hypertrophied ventricle than through the degrees positive (+59 degrees). normal ventricle. Consequently, the normal ventricle becomes depolarized considerably in advance of the hy- pertrophied ventricle, and this situation causes a strong ABNORMAL VENTRICULAR CONDITIONS vector from the normal side of the heart toward the THAT CAUSE AXIS DEVIATION hypertrophied side, which remains strongly positively Although the mean electrical axis of the ventricles aver- charged. Thus, the axis deviates toward the hypertro- ages about 59 degrees, this axis can swing, even in a nor- phied ventricle. mal heart, from about 20 degrees to about 100 degrees. The causes of the normal variations are mainly anatomical Vectorial Analysis of Left Axis Deviation Resulting differences in the Purkinje distribution system or in the from Hypertrophy of the Left Ventricle. Figure 12-12 musculature itself of different hearts. However, a number shows the three standard bipolar limb lead ECGs. Vec- of abnormal conditions of the heart can cause axis devia- torial analysis demonstrates left axis deviation, with the tion beyond the normal limits, as described below. mean electrical axis pointing in the −15-­degree direc- tion. This is a typical ECG caused by increased muscle Change in the Position of the Heart in the Chest. If mass of the left ventricle. In this case, the axis deviation the heart is angulated to the left, the mean electrical axis was caused by hypertension (high arterial blood pres- of the heart also shifts to the left. Such shift occurs (1) at sure), which caused the left ventricle to hypertrophy the end of deep expiration, (2) when a person lies down, so that it could pump blood against elevated systemic because the abdominal contents press upward against arterial pressure. A similar picture of left axis deviation the diaphragm, and (3) quite frequently in obese peo- occurs when the left ventricle hypertrophies as a result ple, whose diaphragms normally press upward against of aortic valvular stenosis, aortic valvular regurgitation, the heart all the time as a result of increased visceral or congenital heart conditions in which the left ventricle adiposity. enlarges while the right ventricle remains relatively nor- Likewise, angulation of the heart to the right causes the mal in size. mean electrical axis of the ventricles to shift to the right. This shift occurs (1) at the end of deep inspiration, (2) Vectorial Analysis of Right Axis Deviation Resulting when a person stands up, and (3) normally in tall lanky from Hypertrophy of the Right Ventricle. The ECG of people whose hearts hang downward. Figure 12-13 shows intense right axis deviation, to an electrical axis of 170 degrees, which is 111 degrees to the Hypertrophy of One Ventricle. When one ventricle right of the normal 59-­degree mean ventricular QRS axis. hypertrophies greatly, the axis of the heart shifts toward The right axis deviation demonstrated in this figure was the hypertrophied ventricle for two reasons. First, there caused by hypertrophy of the right ventricle as a result of is more muscle on the hypertrophied side of the heart congenital pulmonary valve stenosis. Right axis deviation than on the other side, which allows for the generation also can occur in other congenital heart conditions that of greater electrical potential on that side. Second, more cause hypertrophy of the right ventricle, such as tetralogy time is required for the depolarization wave to travel of Fallot and interventricular septal defect. 149 UNIT III The Heart I II III I II III III – III – I – +I I – +I + III Figure 12-14 Left axis deviation caused by left bundle branch block. + III Note also the greatly prolonged QRS complex. Figure 12-13 A high-­voltage electrocardiogram for a person with Because of slowness of impulse conduction when the congenital pulmonary valve stenosis with right ventricular hypertro- Purkinje system is blocked, in addition to axis devia- phy. Intense right axis deviation and a slightly prolonged QRS com- plex are also seen. tion, the duration of the QRS complex is greatly pro- longed as a result of extreme slowness of depolarization in the affected side of the heart. One can see this effect Bundle Branch Block Causes Axis Deviation. Ordi- by observing the excessive widths of the QRS waves in narily, the lateral walls of the two ventricles depolarize at Figure 12-14 (discussed in greater detail later in this almost the same instant because both the left and right chapter). This extremely prolonged QRS complex differ- bundle branches of the Purkinje system transmit the car- entiates bundle branch block from axis deviation caused diac impulse to the two ventricular walls at almost the by hypertrophy. same time. As a result, the potentials generated by the two ventricles (on the two opposite sides of the heart) almost Vectorial Analysis of Right Axis Deviation in Right neutralize each other. However, if only one of the major Bundle Branch Block. When the right bundle branch bundle branches is blocked, the cardiac impulse spreads is blocked, the left ventricle depolarizes far more rapidly through the normal ventricle before it spreads through than the right ventricle, and thus the left side of the ven- the other ventricle. Therefore, depolarization of the two tricles becomes electronegative as long as 0.1 second be- ventricles does not occur, even nearly at the same time, fore the right. Therefore, a strong vector develops, with its and the depolarization potentials do not neutralize each negative end toward the left ventricle and its positive end other. As a result, axis deviation occurs as follows. toward the right ventricle. In other words, intense right axis deviation occurs. In Figure 12-15, right axis devia- Vectorial Analysis of Left Axis Deviation in Left B ­ undle tion caused by right bundle branch block is demonstrated, Branch Block. When the left bundle branch is blocked, and its vector is analyzed; this analysis shows an axis of cardiac depolarization spreads through the right ventricle about 105 degrees instead of the normal 59 degrees and a two to three times as rapidly as through the left ventricle. prolonged QRS complex because of slow conduction. Consequently, much of the left ventricle remains polar- ized for as long as 0.1 second after the right ventricle has become totally depolarized. Thus, the right ventricle be- CONDITIONS THAT CAUSE ABNORMAL comes electronegative, whereas the left ventricle remains VOLTAGES OF THE QRS COMPLEX electropositive during most of the depolarization process, INCREASED VOLTAGE IN THE STANDARD and a strong vector projects from the right ventricle toward BIPOLAR LIMB LEADS the left ventricle. In other words, intense left axis deviation of about −50 degrees occurs because the positive end of Normally, the voltages in the three standard bipolar the vector points toward the left ventricle. This situation limb leads, as measured from the peak of the R wave is demonstrated in Figure 12-14, which shows typical left to the bottom of the S wave, vary between 0.5 and 2.0 axis deviation resulting from left bundle branch block. millivolts, with lead III usually recording the lowest 150  Chapter 12 Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities III I – I– +I UNIT III II I II III + III Figure 12-15 Right axis deviation caused by right bundle branch block. Note also the greatly prolonged QRS complex. III Figure 12-16 A low-­voltage electrocardiogram following local damage throughout the ventricles caused by a previous myocardial infarction. voltage and lead II the highest voltage. However, these relationships are not invariable, even for the normal Decreased Voltage Caused by Conditions Surrounding heart. In general, when the sum of the voltages of the Heart. One of the most important causes of decreased all the QRS complexes of the three standard leads is voltage in electrocardiographic leads is excessive fluid in the greater than 4 millivolts, the patient is considered to pericardium (pericardial effusion). Because extracellular flu- have a high-­voltage ECG. id easily conducts electrical currents, a large portion of the The cause of high-­ voltage QRS complexes is usu- electricity flowing out of the heart is conducted from one ally increased muscle mass of the heart, which ordinar- part of the heart to another through the pericardial fluid. ily results from hypertrophy of the muscle in response to Thus, this effusion effectively “short-­circuits” the electrical excessive load on one part of the heart or the other. For potentials generated by the heart, decreasing the electro- example, the right ventricle hypertrophies when it must cardiographic voltages that reach the outside surfaces of pump blood through a stenotic pulmonary valve or when the body. Pleural effusion, to a lesser extent, also can short- the pulmonary arterial pressure is elevated, and the left circuit the electricity around the heart so that the voltages ventricle hypertrophies when a person has high systemic at the surface of the body and in the ECGs are decreased. arterial blood pressure. The increased quantity of muscle Pulmonary emphysema can decrease the electrocar- generates increased electricity around the heart. As a diographic potentials, but for a different reason than result, the electrical potentials recorded in the electrocar- that of pericardial effusion. In persons with pulmonary diographic leads are considerably greater than normal, as emphysema, conduction of electrical current through the shown in Figures 12-­12 and 12-­13. lungs is depressed considerably because of an excessive quantity of air in the lungs. Also, the chest cavity enlarges, and the lungs tend to envelop the heart to a greater extent DECREASED VOLTAGE OF THE than normal. Therefore, the lungs act as an insulator to ELECTROCARDIOGRAM prevent the spread of electrical voltage from the heart to Decreased Voltage Caused by Cardiac Myopathies. the surface of the body, which results in decreased elec- One of the most common causes of decreased voltage trocardiographic potentials in the various leads. of the QRS complex is a series of old myocardial in- farctions with resultant diminished muscle mass. This PROLONGED AND BIZARRE PATTERNS condition also causes the depolarization wave to move OF THE QRS COMPLEX through the ventricles slowly and prevents major por- CARDIAC HYPERTROPHY OR DILATION tions of the heart from becoming massively depolar- PROLONG THE QRS COMPLEX ized all at once. Consequently, this condition causes some prolongation of the QRS complex, along with the The QRS complex lasts as long as depolarization con- decreased voltage. Figure 12-16 shows a typical low-­ tinues to spread through the ventricles—that is, as long voltage ECG with prolongation of the QRS complex, as part of the ventricles is depolarized and part is still which is common after multiple small infarctions of polarized. Therefore, prolonged conduction of the impulse the heart have caused local delays of impulse conduc- through the ventricles always causes a prolonged QRS tion and reduced voltages due to loss of muscle mass complex. Such prolongation often occurs when one or throughout the ventricles. Infiltrative myocardial dis- both ventricles are hypertrophied or dilated because of eases also cause low ECG voltage. For example, in car- the longer pathway that the impulse must then travel. The diac amyloidosis, abnormal proteins infiltrate the myo- normal QRS complex lasts 0.06 to 0.08 second, whereas cardium, leading to reduced voltages, particularly in in hypertrophy or dilation of the left or right ventricle, the the limb leads. QRS complex may be prolonged to 0.09 to 0.12 second. 151 UNIT III The Heart PURKINJE SYSTEM BLOCK PROLONGS CURRENT OF INJURY THE QRS COMPLEX Many different cardiac abnormalities, especially those that When the Purkinje fibers are blocked, the cardiac impulse damage the heart muscle, may cause part of the heart to must then be conducted by the ventricular muscle instead remain partially or totally depolarized all the time. When of through the Purkinje system. This action decreases this condition occurs, current flows between the patho- the velocity of impulse conduction to about one-third of logically depolarized and normally polarized areas, even normal. Therefore, if complete block of one of the bundle between heartbeats. This condition is called a current of branches occurs, the duration of the QRS complex is usu- injury. Note especially that the injured part of the heart is ally increased to 0.14 second or longer. negative, because this is the part that is depolarized and In general, a QRS complex is considered to be abnor- emits negative charges into the surrounding fluids, whereas mally long when it lasts more than 0.09 second. When the remainder of the heart is neutral or in positive polarity. it lasts more than 0.12 second, the prolongation is Some abnormalities that can cause a current of injury almost certainly caused by a pathological block some- are as follows: (1) mechanical trauma, which sometimes where in the ventricular conduction system, as shown makes the membranes remain so permeable that full by the ECGs for bundle branch block in Figures. 12-­14 repolarization cannot take place; (2) infectious processes and 12-­15. that damage the muscle membranes; and (3) ischemia of local areas of heart muscle caused by local coronary occlu- sions, which is the most common cause of a current of CONDITIONS THAT CAUSE BIZARRE QRS injury in the heart. During ischemia, not enough nutri- COMPLEXES ents from the coronary blood supply are available to the Bizarre patterns of the QRS complex are usually caused heart muscle to maintain normal membrane polarization. by two conditions: (1) destruction of cardiac muscle in various areas throughout the ventricular system, EFFECT OF CURRENT OF INJURY ON THE with replacement of this muscle by scar tissue; and QRS COMPLEX (2) multiple small local blocks in the conduction of In Figure 12-17, a small area in the base of the left ven- impulses at many points in the Purkinje system. As a tricle is newly infarcted (i.e., there is loss of coronary result, cardiac impulse conduction becomes irregular, blood flow). Therefore, during the T-­P interval—that is, causing rapid shifts in voltages and axis deviations. when the normal ventricular muscle is totally polarized— This irregularity often causes double or even triple abnormal negative current still flows from the infarcted peaks in some of the electrocardiographic leads, such area at the base of the left ventricle and spreads toward as those shown in Figure 12-14. the rest of the ventricles. Injured area − − II III I I − + III II + + I J II Current Current of injury of injury J III J Figure 12-17 Effect of a current of injury on the electrocardiogram. 152  Chapter 12 Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities The vector of this current of injury, as shown in the the end of the QRS complex. At exactly this point, all first heart in Figure 12-17, is in a direction of about 125 parts of the ventricles have become depolarized, includ- degrees, with the base of the vector, the negative end, ing both the damaged parts and the normal parts, so no toward the injured muscle. As shown in the lower por- current is flowing around the heart. Even the current of tions of the figure, even before the QRS complex begins, injury disappears at this point. Therefore, the potential UNIT III this vector causes an initial record in lead I below the zero of the electrocardiogram at this instant is at zero voltage. potential line, because the projected vector of the current This point is known as the J point in the ECG, as shown of injury in lead I points toward the negative end of the in Figure 12-18. lead I axis. In lead II, the record is above the line because Then, for analysis of the electrical axis of the injury the projected vector points more toward the positive ter- potential caused by a current of injury, a horizontal line minal of the lead. In lead III, the projected vector points is drawn in the ECG for each lead at the level of the J in the same direction as the positive terminal of lead III so point. This horizontal line is then the zero potential level that the record is positive. Furthermore, because the vec- in the ECG from which all potentials caused by currents tor lies almost exactly in the direction of the axis of lead of injury must be measured. III, the voltage of the current of injury in lead III is much greater than in either lead I or lead II. Use of the J Point in Plotting Axis of Injury Potential. As the heart then proceeds through its normal process Figure 12-18 shows ECGs (leads I and III) from an in- of depolarization, the septum first becomes depolarized; jured heart. Both records show injury potentials. In other then the depolarization spreads down to the apex and words, the J point of each of these two ECGs is not on the back toward the bases of the ventricles. The last portion same line as the T-­P segment. In the figure, a horizontal of the ventricles to become totally depolarized is the base line has been drawn through the J point to represent the of the right ventricle because the base of the left ventricle zero voltage level in each of the two recordings. The injury is already totally and permanently depolarized. By vecto- potential in each lead is the difference between the voltage rial analysis, the successive stages of electrocardiographic of the ECG immediately before onset of the P wave and generation by the depolarization wave traveling through the zero voltage level determined from the J point. In lead the ventricles can be constructed graphically, as demon- I, the recorded voltage of the injury potential is above the strated in the lower part of Figure 12-17. zero potential level and is therefore positive. Conversely, When the heart becomes totally depolarized, at the in lead III, the injury potential is below the zero voltage end of the depolarization process (as noted by the next level and therefore is negative. to last stage in Figure 12-17), all the ventricular muscle is At the bottom in Figure 12-18, the respective injury in a negative state. Therefore, at this instant in the ECG, potentials in leads I and III are plotted on the coordi- no current flows from the ventricles to the electrocardio- nates of these leads, and the resultant vector of the injury graphic electrodes because now both the injured heart potential for the whole ventricular muscle mass is deter- muscle and the contracting muscle are depolarized. mined by vectorial analysis as described. In this case, the Next, as repolarization takes place, all the heart finally repolarizes, except the area of permanent depolarization I in the injured base of the left ventricle. Thus, repolariza- + − 0 0 tion causes a return of the current of injury in each lead, as noted at the far right in Figure 12-17. J point J point THE J POINT IS THE ZERO REFERENCE III POTENTIAL FOR ANALYZING CURRENT OF INJURY 0 + 0 − One might think that the ECG machines could determine when no current is flowing around the heart. However, III − 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. There- fore, when two electrodes are connected between the I− +I arms or between an arm and a leg, these stray currents make it impossible to predetermine the exact zero refer- ence level in the ECG. + For these reasons, the following procedure must be III used to determine the zero potential level: First, one notes Figure 12-18 J point as the zero reference potential of the electro- the exact point at which the wave of depolarization just cardiograms for leads I and III. Also, the method for plotting the axis completes its passage through the heart, which occurs at of the injury potential is shown in the bottom panel. 153 UNIT III The Heart resultant vector extends from the right side of the ven- 12-­20. Therefore, one of the most important diagnostic tricles toward the left and slightly upward, with an axis of features of ECGs recorded after acute coronary thrombo- about −30 degrees. If one places this vector for the injury sis is the current of injury. potential directly over the ventricles, the negative end of the vector points toward the permanently depolarized, Acute Anterior Wall Infarction. Figure 12-19 shows the “injured” area of the ventricles. In the example shown in ECG in the three standard bipolar limb leads and in one Figure 12-18, the injured area would be in the lateral wall chest lead (lead V2) recorded from a patient with acute of the right ventricle. anterior wall cardiac infarction. The most important diag- This analysis is obviously complex. However, it is nostic feature of this ECG is the intense injury potential in essential that the student review it again and again until chest lead V2. If one draws a zero horizontal potential line it is thoroughly understood. No other aspect of electrocar- through the J point of this ECG, a strong negative injury po- diographic analysis is more important. tential during the T-­P interval is found, which means that the chest electrode over the front of the heart is in an area CORONARY ISCHEMIA AS A CAUSE OF of strongly negative potential. In other words, the negative INJURY POTENTIAL end of the injury potential vector in this heart is against the anterior chest wall. This means that the current of injury is Insufficient blood flow to the cardiac muscle depresses the emanating from the anterior wall of the ventricles, which metabolism of the muscle for at least three reasons: (1) lack diagnoses this condition as an anterior wall infarction. of oxygen; (2) excess accumulation of carbon dioxide; and When analyzing the injury potentials in leads I and (3) lack of sufficient food nutrients. Consequently, repolar- III, one finds a negative potential in lead I and a positive ization of the muscle membrane cannot occur in areas of potential in lead III. This finding means that the resultant severe myocardial ischemia. Often, the heart muscle does vector of the injury potential in the heart is about +150 not die because the blood flow is sufficient to maintain life degrees, with the negative end pointing toward the left of the muscle, even though it is not sufficient to cause nor- ventricle and the positive end pointing toward the right mal repolarization of the membranes. As long as this state ventricle. Thus, in this ECG, the current of injury is com- exists, an injury potential continues to flow during the dia- ing mainly from the left ventricle, as well as from the ante- stolic portion (the T-­P portion) of each heart cycle. rior wall of the heart. Therefore, one would conclude that Extreme ischemia of the cardiac muscle occurs after this anterior wall infarction almost certainly is caused by coronary occlusion, and a strong current of injury flows thrombosis of the anterior descending branch of the left from the infarcted area of the ventricles during the T-­P coronary artery. interval between heartbeats, as shown in Figs. 12-­19 and T-P segment I II III V2 I II III II III – – III – I– +I + III + + V2 III II Figure 12-19 Current of injury in acute anterior wall infarction. Note Figure 12-20 Injury potential in an acute posterior wall, apical infarc- the intense injury potential in lead V2. tion. 154  Chapter 12 Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities Posterior Wall Infarction. Figure 12-20 shows the three ter about 1 week, the injury potential has diminished con- standard bipolar limb leads and one chest lead (lead V2) siderably and, after 3 weeks, it is gone. After that, the ECG from a patient with a posterior wall infarction. The major does not change greatly during the next year. This is the diagnostic feature of this ECG is also in the chest lead. usual recovery pattern after an acute myocardial infarc- If a zero potential reference line is drawn through the J tion of moderate degree, showing that the new collateral UNIT III point of this lead, it is readily apparent that during the coronary blood flow develops enough to re-­establish ap- T-­P interval, the potential of the current of injury is posi- propriate nutrition to most of the infarcted area. tive. This means that the positive end of the vector is in In some patients who experience myocardial infarc- the direction of the anterior chest wall, and the negative tion, the infarcted area never redevelops adequate cor- end (the injured end of the vector) points away from the onary blood supply. Often, some of the heart muscle chest wall. In other words, the current of injury is coming dies but, if the muscle does not die, it will continue to from the back of the heart opposite to the anterior chest show an injury potential as long as the ischemia exists, wall, which is the reason this type of ECG is the basis for particularly during bouts of exercise when the heart is diagnosing posterior wall infarction. overloaded. If one analyzes the injury potentials from leads II and III of Figure 12-20, it is readily apparent that the injury Q Waves on an ECG Represent Old Myocardial Infarc- potential is negative in both leads. By vectorial analysis, as tion. Figure 12-22 shows leads I and III after anterior shown in the figure, one finds that the resultant vector of and posterior infarctions about 1 year after the acute heart the injury potential is about −95 degrees, with the nega- attacks. Usually, a Q wave has developed at the beginning tive end pointing downward and the positive end pointing of the QRS complex in lead I in anterior infarction be- upward. Thus, because the infarct, as indicated by the chest cause of the loss of muscle mass in the anterior wall of the lead, is on the posterior wall of the heart and, as indicated left ventricle but, in a posterior infarction, a Q wave has by the injury potentials in leads II and III, it is in the apical developed at the beginning of the QRS complex in lead portion of the heart, one would suspect that this infarct III because of loss of muscle in the posterior apical part is near the apex on the posterior wall of the left ventricle. of the ventricle. These configurations are certainly not found in all Infarction in Other Parts of the Heart. Using the same cases of old myocardial infarction. Local loss of muscle procedures demonstrated in the preceding discussions of and local points of cardiac signal conduction block anterior and posterior wall infarctions, it is often possi- can cause very bizarre QRS patterns (e.g., especially ble to determine the locus of an infarcted area emitting prominent Q waves), decreased voltage, and QRS a current of injury. In making such vectorial analyses, it prolongation. should be remembered that the positive end of the injury potential vector points toward the normal cardiac muscle, Current of Injury in Angina Pectoris. The term angina and the negative end points toward the injured portion of pectoris means pain from the heart felt in the pectoral re- the heart that is emitting the current of injury. gions of the chest. This pain usually also radiates into the ECG Progression During and After Acute Coronary left neck area and down the left arm. The pain is typi- Thrombosis. Figure 12-21 shows a V3 chest lead from cally caused by moderate ischemia of the heart. Usually, a patient with an acute anterior wall infarction, demon- no pain is felt as long as the person is quiet, but as soon as strating changes in the ECG from the day of the attack to the heart is overworked, the pain appears. 1 week later, 3 weeks later and, finally. 1 year later. From An injury potential sometimes appears on the ECG this ECG, one can see that the injury potential is strong during an attack of severe angina pectoris because the immediately after the acute attack (the T-­P segment is coronary insufficiency becomes great enough to prevent displaced positively from the S-­T segment). However, af- adequate repolarization of some areas of the heart during diastole. Anterior Posterior Q Q I III I III Normal During 1 day Weeks Years Figure 12-22 Electrocardiograms of anterior and posterior wall in- Figure 12-21 Recovery of the myocardium after anterior wall infarc- farctions that occurred about 1 year previously, showing a Q wave tion, demonstrating the disappearance of the injury potential that is in lead I in an anterior wall infarction and a Q wave in lead III in a present on the first day after the infarction. posterior wall infarction. 155 UNIT III The Heart ABNORMALITIES IN THE T WAVE Earlier in the chapter, we noted that the T wave is nor- T T T T mally 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 Figure 12-23 An inverted T wave resulting from mild ischemia at the normal sequence of repolarization does not occur. Several base of the ventricles. factors, including myocardial ischemia, can change this sequence of repolarization. EFFECT OF SLOW CONDUCTION OF THE DEPOLARIZATION WAVE ON THE T T 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 delayed conduction causes Figure 12-24 A biphasic T wave caused by digitalis toxicity. 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, Mild ischemia is the most common cause of short- the refractory periods of the right and left ventricular ening of depolarization of cardiac muscle because this muscle masses are not greatly different from each other. condition increases current flow through the potas- Therefore, the right ventricle begins to repolarize long sium channels. When the ischemia occurs in only one before the left ventricle, which causes strong positivity in area of the heart, the depolarization period of this area the right ventricle and negativity in the left ventricle when decreases out of proportion to that in other portions. the T wave is developing. In other words, the mean axis of As a result, changes in the T-­wave morphology, such the T wave is now deviated to the right, which is opposite as inversion or biphasic waveforms, can be evidence of to the mean electrical axis of the QRS complex in the myocardial ischemia. The ischemia might result from same ECG. Thus, when conduction of the depolarization chronic, progressive coronary stenosis (narrowing), impulse through the ventricles is greatly delayed, the T acute coronary occlusion, coronary artery spasm, or rel- wave is almost always of opposite polarity to that of the ative coronary insufficiency that occurs during exercise QRS complex. or severe anemia. SHORTENED DEPOLARIZATION IN Effect of Digitalis on the T Wave. As discussed in PORTIONS OF THE VENTRICULAR MUSCLE Chapter 22, digitalis is a drug that can be used during CAN CAUSE T-WAVE ABNORMALITIES heart failure to increase the strength of cardiac muscle contraction. However, when an overdose of digitalis is If the base of the ventricles should exhibit an abnormally given, depolarization duration in one part of the ventri- short period of depolarization—that is, a shortened action cles may be increased out of proportion to that of other potential—repolarization of the ventricles would not begin parts. As a result, nonspecific changes, such as T-­wave in- at the apex, as it normally does. Instead, the base of the ven- version or biphasic T waves, may occur in one or more of tricles would repolarize ahead of the apex, and the vector of the electrocardiographic leads. A biphasic T wave caused repolarization would point from the apex toward the base by excessive administration of digitalis is shown in Figure of the heart, opposite to the standard vector of repolariza- 12-24. Therefore, changes in the T wave during digitalis tion. Consequently, the T wave in all three standard leads administration are often the earliest signs of digitalis tox- would be negative rather than the usual positive. Thus, icity. the simple fact that the base of the ventricles has a short- ened period of depolarization is sufficient to cause marked changes in the T wave, even to the extent of changing the Bibliography entire T-­wave polarity, as shown in Figure 12-23. See the bibliography for Chapter 13. 156