A 58-year-old man from Delhi presents to the emergency department with acute onset chest pain radiating to the left arm for 2 hours. He is diaphoretic and anxious. Blood pressure is 145/92 mmHg, heart rate 102/min. His ECG shows ST-segment elevation in leads II, III, and aVF, with reciprocal ST depression in leads I and aVL. The PR interval measures 0.16 seconds, QRS duration 0.08 seconds, and QT interval 0.38 seconds (corrected QT 0.40 seconds). What is the primary pathophysiological basis for the ST-segment elevation observed in this patient?

Explanation

## Pathophysiology of ST-Segment Elevation in Acute STEMI ### Mechanism of ST Elevation **Key Point:** ST-segment elevation in acute transmural myocardial infarction results from loss of the resting membrane potential in the acutely ischaemic zone, creating a current of injury between the ischaemic (depolarized, ~−60 mV) and normal (polarized, ~−85 mV) myocardium. ### Current of Injury Concept During acute transmural ischaemia: 1. The affected myocardium loses ATP-dependent Na^+^/K^+^ ATPase function 2. Resting membrane potential depolarizes from −85 mV toward −60 mV 3. A potential difference develops between ischaemic and normal zones 4. Current flows from normal (negative) to ischaemic (positive) tissue 5. The ECG electrode "sees" this as ST elevation in the territory of the infarct **High-Yield:** The **location of ST elevation** identifies the coronary artery involved: - **Inferior MI (II, III, aVF)** → Right coronary artery (RCA) or left circumflex (LCx) - **Anterior MI (V1–V4)** → Left anterior descending (LAD) - **Lateral MI (I, aVL, V5–V6)** → LCx or diagonal branches This patient has **inferior STEMI**, most commonly due to RCA occlusion. ### Reciprocal Changes **Clinical Pearl:** Reciprocal ST depression in opposite leads (I, aVL in this case) reflects the same electrical event viewed from the opposite direction—further evidence of transmural injury. ### ECG Intervals in Context The normal intervals (PR 0.16 s, QRS 0.08 s, QTc 0.40 s) rule out conduction abnormalities or prolonged repolarization as the primary mechanism. ### Differential Pathophysiology | Finding | Mechanism | ECG Pattern | |---------|-----------|-------------| | **Transmural ischaemia** | Loss of resting potential in affected zone | ST elevation in infarct territory + reciprocal depression | | **Subendocardial ischaemia** | Unopposed epicardial current (normal epicardium vs depolarized endocardium) | ST depression (not elevation) | | **LVH** | Increased muscle mass, prolonged repolarization | LVH voltage criteria + T-wave changes, no ST elevation | | **Pericarditis** | Diffuse epicardial inflammation | Diffuse ST elevation (all leads) + PR depression, no reciprocal changes | **Warning:** Do not confuse **subendocardial ischaemia** (ST depression) with **transmural ischaemia** (ST elevation). The location and pattern of current flow determine the ECG appearance.