A 58-year-old man from Delhi presents to the emergency department with palpitations and syncope. His ECG shows a prolonged QT interval (520 ms) with a heart rate of 45 bpm. On examination, he is pale and diaphoretic. His serum potassium is 2.1 mEq/L (normal 3.5–5.0), serum calcium is 7.2 mg/dL (normal 8.5–10.5), and serum magnesium is 1.4 mg/dL (normal 1.7–2.2). He has a history of chronic diarrhea. Which phase of the cardiac action potential is most significantly prolonged in this patient?

Explanation

## Clinical Context This patient presents with **long QT syndrome secondary to electrolyte abnormalities** (hypokalemia, hypocalcemia, hypomagnesemia). The ECG finding of prolonged QT interval directly reflects prolongation of ventricular repolarization. ## Cardiac Action Potential Phases | Phase | Duration | Ion Channels | Membrane Potential | Pathophysiology in This Case | |-------|----------|--------------|-------------------|------------------------------| | Phase 0 | ~1 ms | Fast Na^+^ influx | −90 to +20 mV | Normal; not affected | | Phase 1 | ~10 ms | K^+^ efflux | +20 to 0 mV | Normal; brief repolarization | | Phase 2 | 200–300 ms | Ca^2+^ influx vs K^+^ efflux (balance) | 0 to −20 mV | **Prolonged** due to impaired K^+^ efflux | | Phase 3 | 150–200 ms | Delayed K^+^ rectifier channels (I~K~) | −20 to −90 mV | **MOST PROLONGED** — hypokalemia & hypomagnesemia impair K^+^ channel function | | Phase 4 | Variable | Leak channels, Na^+^/K^+^ ATPase | −90 mV (stable) | Normal; not affected | **Key Point:** The QT interval on ECG represents the duration of the **action potential from Phase 0 through Phase 3**. Prolongation of Phase 3 (repolarization) is the primary mechanism of long QT syndrome in electrolyte disturbances. ## Mechanism of Electrolyte-Induced Long QT 1. **Hypokalemia** → ↓ extracellular K^+^ → ↓ driving force for K^+^ efflux → delayed repolarization 2. **Hypomagnesemia** → impaired function of delayed rectifier K^+^ channels (I~K~) → prolonged Phase 3 3. **Hypocalcemia** → ↓ Ca^2+^ influx during Phase 2 → secondary effects on repolarization timing **Clinical Pearl:** The combination of prolonged QT + bradycardia + syncope in this patient suggests risk of **torsades de pointes** (polymorphic ventricular tachycardia), a life-threatening arrhythmia triggered by early afterdepolarizations (EADs) during prolonged Phase 2–3 junction. **High-Yield:** Electrolyte abnormalities prolong the **plateau phase (Phase 2) and repolarization phase (Phase 3)**, NOT depolarization (Phase 0) or resting potential (Phase 4). The QT interval = QRS duration + ST segment + T wave = Phases 0–3 duration. ## Management Implications - Correct hypokalemia (target K^+^ >3.5 mEq/L, ideally 4.0–4.5 in long QT) - Correct hypomagnesemia (target Mg^2+^ >2.0 mg/dL) - Correct hypocalcemia (target Ca^2+^ >8.5 mg/dL) - Avoid QT-prolonging drugs (antiarrhythmics, antipsychotics, macrolides) - Monitor ECG for QT shortening as electrolytes normalize