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The Pathophysiology of Myocardial Infarction: From Coronary Occlusion to Clinical Consequence

1Coronary Supply and the Myocardial Oxygen Balance2Atherosclerotic Plaque Rupture and Coronary Thrombosis3Ischemia: Metabolic and Functional Consequences of Oxygen Deprivation4From Reversible Injury to Irreversible Cell Death5Inflammation, Healing, and Infarct Remodeling6Clinical Manifestations: ECG, Biomarkers, and Pump Dysfunction
Clinical Manifestations: ECG, Biomarkers, and Pump Dysfunction

Reading the ECG as a Map of Tissue State

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Here you drive the heart yourself. The waveform panel shows a twelve-lead ECG, and the state control moves the tissue through normal, ischemia, injury, and necrosis. Watch what each state does to the trace. In injury, the ischemic cells sit at a less negative resting potential, so a steady injury current flows between the damaged and healthy muscle, and that current lifts the ST segment in the leads facing the injured wall while depressing it in the opposite leads. In ischemia, repolarization is altered, so the T wave flips downward even though the cells are still alive. Once necrosis is complete, the dead region no longer generates a depolarization wave, so the electrode over it records the far wall instead — a deep, wide Q wave. Now switch leads: II, III, and aVF look at the inferior wall, V1 to V4 at the anterior and septal wall, and I, aVL, V5, and V6 at the lateral wall. Step through the sequence and you will see ST elevation give way to T-wave inversion and then to a pathologic Q wave, and whichever lead group shows that pattern tells you which vessel is occluded and which territory is at risk.
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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.

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