In summary, myocardial ischemia and infarction cause a series of metabolic, ionic neurohumeral and anatomic changes that influence the electrophysiologic properties of individual cells, impact on conduction and refractoriness and cause changes in all portions of the electrocardiographic waveform. Within the ischemic region, the resting membrane potential becomes less negative and the rate of rise of the action potential upstroke becomes slower, As the myocardial fibers within the ischemic region become inexcitable and irreversibly damaged, conduction within the ischemic region is slowed and then blocked, currents of injury are created across the ischemic borders causing ST segment elevation and/or depression, changes in the sequence of depolarization develop leading to Q waves and/or notches in the QRS complex, and changes in repolarization occur leading to changes in the T wave.
It is important to recognize that the ECG changes associated with ischemia and infarction are neither uniquely sensitive nor specific and can occur in a variety of other clinical settings. It is also important to recogn1ze that if the area of infarction is very small or is located in an area not well represented in the 12 lead body surface ECG (such as the posterior wall), the associated ECG changes may be minimal or absent, i.e, may be electrocardiographically silent. An understanding of these ECG changes and the ability to discriminate between those due to ischemia/infarction and those due to other causes requires an appreciation of the mechanisms underlying the ECG changes, and as always (and this is most important), the correlation of the changes appearing on the body surface electrocardiogram to the clinical setting in which they occur.