The ECG records extracellular currents generated by the spread of depolarization and repolarization through the myocardium. When a region of myocardium becomes ischemic, its resting membrane potential is less negative and its action potential is altered, so a voltage gradient exists between ischemic and normal tissue. This gradient produces an injury current that shifts the ST segment: ST elevation when the injured region faces the recording electrode, ST depression when the electrode records the opposite side. As ischemia progresses to necrosis, the dead tissue no longer generates a depolarization wave, so the electrode over that region records the electrical activity of the opposite wall — a deep, wide Q wave. T-wave inversion reflects altered repolarization in ischemic but still viable tissue. The sequence of ST elevation, then T-wave inversion, then Q-wave development tracks the progression from reversible injury to completed infarction.
A key principle is that the ECG lead reflects the region of myocardium it faces. Leads II, III, and aVF view the inferior wall; V1–V4 view the anterior and septal walls; I, aVL, V5, and V6 view the lateral wall. A territorial pattern of ST elevation therefore localizes the occluded vessel and the region at risk.