The normal myocardium depolarizes from endocardium to epicardium and repolarizes in the opposite direction. When injured, the myocardium remains electrically more positive than the uninjured area at the end of depolarization. The relatively positive potential in this area will result in ST elevation of electrocardiogram leads over this area. Conversely, if the electrode is located over uninjured myocardium opposite the injured area, ST depression will be noted (reciprocal changes). If the injury is limited to the subendocardial area, the electrode will be separated from the injured area by the normal epicardial layer. The epicardial layer becomes more electrically negative than the injured subendocardial layer at the end of depolarization, resulting in ST-segment depressions.
Transmural myocardial ischemia also delays the repolarization process. The ischemic area is electrically more negative than the uninjured area. The T-wave recording over the ischemic area will be negative or downward. In subendocardial ischemia, the delay in repolarization does not alter the direction of the recovery period because the normal repolarization process is from the epicardium to the endocardium. T-wave inversions will not be seen. Since the electrical potential generated by the delayed repolarization in the subendocardium is not opposed, the T wave will be larger than normal (hyperacute T waves).
After acute myocardial infarction (AMI), the area of necrosis is electrically silent. The resultant forces generated from the myocardium during repolarization (the QRS complex) will be affected by this electrically silent area. Electrodes facing the infarcted area will record an abnormal negative deflection during depolarization (pathologic Q waves).
The standard 12-lead electrocardiogram (ECG), is the single best test to identify patients with acute myocardial infarction upon ED presentation. 3 National guidelines require that it be obtained and interpreted within 10 min of presentation. 4 Although it is the best immediately available test in the ED, it still has relatively low sensitivity for detection of acute myocardial infarction. The ST-segment is elevated during an AMI in approximately 50 percent, 13 i.e., half of the patients who present to the ED with AMI would not be detected solely on the basis of the electrocardiogram. Most patients with AMI will have some nondiagnostic abnormalities on the ECG. 3 Some 1 to 5 percent of patients with AMI have an entirely normal ECG.345 and 6 These figures refer to myocardial infarction, not angina.
Standard diagnostic ECG criteria for AMI are shown in I§ble...4..7..-.5. ST-segment elevations in the distributions shown suggest acute transmural injury. ST-segment depressions in these distributions suggest subendocardial ischemia. All inferior wall acute myocardial infarctions should have a right-sided lead V 4 (rV4) obtained because ST-segment elevation in rV4 is highly suggestive of right ventricular infarction. There is no proven role for other right-sided leads.
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