Inadequate blood supply to the myocardium can result in myocardial ischemia, injury or infarction, or all three. Atherosclerosis of the larger coronary arteries is the most common anatomic condition to reduce coronary blood flow. The branches of coronary arteries arising from the aortic root are distributed on the epicardial surface of the heart. These in turn provide intramural branches that supply the cardiac muscle. Myocardial ischemia generally appears first and is more extensive in the subendocardial region since these deeper myocardial layers are farthest from the blood supply, with greater intramural tension and need for oxygen.
Ischemia in subendocardial area prolongs local recovery time. Since repolarization normally proceeds in an epicardial-to-endocardial direction, delayed recovery in the subendocardial region due to ischemia does not reverse the direction of repolarization but merely lengthens it. This generally results in increased amplitude of the T wave as recorded by the electrodes overlying the subendocardial ischemic section.
Transmural ischemia has a more visible effect on recovery of subepicardial cells compared with subendocardial cells. Upturn is more delayed in the subepicardial layers, and the subendocardial muscle fibers seem to recover first. Repolarization is endocardial-to-epicardial, resulting in inversion of the T waves in leads overlying the ischemic regions, but in opposite area one can see increased amplitude of the T wave.
Injury to the myocardial cells results when the ischemic process is more severe. Subendocardial damage on a surface ECG is manifested by ST segment depression, and subepicardial or transmural injury is manifested as ST segment elevation. In patients with ischemic heart disease, ischemia, injury and myocardial infarction of different areas commonly coexist, producing mixed and complex ECG examples.
When the blood supply to part of the myocardium is interrupted, there are profound changes in the myocardium that lead to irreversible changes and death of muscle cells. The ECG is very useful for diagnosing and locating areas of infarction. The underlying electrical events and the resulting electrocardiographic changes are complex. The left ventricle is the predominant site for infarction. The appearance of pathological Q waves is the most characteristic ECG finding of transmural myocardial infarction of the left ventricle.
Figure 53 — Different zones around necrotic area
A pathological Q wave is defined as an initial downward deflection of duration of 0.04 s. or longer in any lead. The Q wave appears when the infarcted muscle is electrically lifeless and the loss of forces normally generated by the infarcted area leaves unbalanced forces of variable magnitude in the opposite direction from the remote region, for example, an opposite wall. These forces can be represented by a vector directed away from the site of infarction and seen as a negative Q wave by electrodes overlying the necrotic region.
The standard 12 lead ECG does not directly examine the right ventricle, and is relatively poor at examining the posterior basal and lateral walls of the left ventricle. In particular, acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG. The use of additional ECG leads like right-sided leads V3R and V4R and posterior leads V7, V8, and V9 may improve sensitivity for right ventricular and posterior myocardial infarction. In spite of these limitations, the 12 lead ECG stands at the center of risk stratification for the patient with suspected acute myocardial infarction. Mistakes in interpretation are relatively common, and the failure to identify high risk features has a negative effect on the quality of patient care.
During acute myocardial infarction, the central area of necrosis is generally surrounded by an area of injury, which in turn is surrounded by an area of ischemia. As a result, various stages of myocardial damage can develop. The distinction between ischemia and necrosis is whether the phenomenon is reversible. Transient myocardial ischemia that produces T wave, and sometimes ST segment abnormalities, can be reversible without producing permanent injury and is not gone together with by serum enzyme elevation. Two types of developing myocardial infarction (acute coronary syndrome) can be observed electrocardiographically in early stage:
With ST segment elevation or new bundle branch block (suspicious for transmural infarction and a possible candidate for acute reperfusion therapy with thrombolytics)
With ST segment depression or T wave inversion (suspicious for ischemic injury).
The first change during infarction, abnormally rapid repolarization after discharge of the infarcted muscle fibers as a result of accelerated opening of K+ channels, develops seconds after occlusion of a coronary artery in experimental animals. It lasts only a few minutes, but before it is over the resting membrane potential of the infarcted fibers declines because of the loss of intracellular K+. Starting about 30 minutes later, the infarcted fibers also begin to depolarize more slowly than the surrounding normal fibers.
All three of these changes cause current flow that produces elevation of the ST segment in electrocardiographic leads recorded with electrodes over the infarcted area. Because of the rapid repolarization in the infarct, the membrane potential of the area is greater than it is in the normal area during the latter part of repolarization, making the normal region negative relative to the infarct. Extracellularly, current therefore flows out of the infarct into the normal area (since, by convention, current flow is from positive to negative). This current flows toward electrodes over the injured area, causing increased positivity between the S and T waves of the ECG. Similarly, the delayed depolarization of the infarcted cells causes the infarcted area to be positive relative to the healthy tissue during the early part of repolarization, and the result is also ST segment elevation. The remaining change, the decline in resting membrane potential during diastole, causes a current flow into the infarct during ventricular diastole. The result of this current flow is a depression of the TQ segment of the ECG. However, the electronic arrangement in electrocardiographic recorders is such that a TQ segment depression is recorded as an ST segment elevation. As a result, the main ECG sign of acute myocardial infarction in early stage is elevation of the ST segments in the leads overlying the area of infarction. The leads on the opposite side of the heart show ST segment depression.
In latest stages we can distinguish:
Q wave infarction, which is diagnosed by the presence of pathological Q waves and is also called transmural infarction. However, transmural infarction is not always present; hence, the term Q-wave infarction may be preferable for ECG description
Non-Q wave infarction, which is diagnosed in the presence of ST depression and T wave abnormalities. This infarct is less severe, but there is a high incidence of subsequent reinfarction.
Stages of acute myocardial infarction evolution are represented in fig.54.
Figure 54 — Evolution of acute myocardial infarction
A) Illustrates the normal QRS complex in a lead.
B & C) Within 0.5 to 6 hours of the clinical onset of an MI. There is essential ST segment elevation. At this stage no QRS or T wave changes have occurred. This signifies large myocardial damage only, but not definitive evidence of infarction. This gives to physician a time for coronary artery reocclusion.
D) Within 48 days, the R wave voltage falls and abnormal Q waves appear. This is sufficient evidence of an infarction. In addition, T wave inversion will also have appeared but the ST segment elevation may be less noticeable than before.
E) After four weeks, the ST segment changes revert completely to normal. The R wave voltage remains low and the abnormal Q waves persist. Deep, symmetrical negative T wave may develop at this stage.
F) Months after the Q-myocardial infarction, the T waves may progressively return to normal. The abnormal Q waves and reduced R wave voltage persists often all life of the patient.
The ECG is useful to localize the site of ischemia and infarction. Some leads depict certain areas; the location of the infarct can be detected fairly accurately from analysis of the 12-lead ECG. Leads that best detect changes in commonly described locations are classified as follows: inferior (or diaphragmatic) wall: II, II and aVF; septal: V1 and V2; anteroseptal: V1, V2, V3 and sometimes V4; anterior: V3, V4 and sometimes V2; apical: V3, V4 or both lateral: I, aVL, V5 and V6; extensive anterior: I, aVL and V1 through V6.
Since the electrical characteristics of the infarcted tissue change, arrhythmias are a frequent complication. The re-entry phenomenon may cause rapid heart rates (ventricular tachycardia and even ventricular fibrillation), and ischemia in the electrical conduction system of the heart may cause a complete heart block (when the impulse from the sinoatrial node, the normal cardiac pacemaker, does not reach the heart chambers).
Figure 55 — Anterior localization of Q wave infarction
Figure 56 — Inferior localization of myocardial infarction
