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.
Acute Anterior Wall Infarction. Figure 12-19 shows the electrocardiogram in the three standard bipolar limb
J point as the zero reference potential of the electrocardiograms for leads I and II. Also, the method for plotting the axis of the injury potential is shown by the lowermost panel.
Current of injury in acute anterior wall infarction. Note the intense injury potential in lead V2.
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
Injury potential in acute posterior wall, apical Infarction.
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
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.
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