A patient develops torsades de pointes arrhythmia after starting a class IA antiarrhythmic. This proarrhythmic complication is due to excessive blockade of which ion channel?

• A Inward rectifier potassium channel (IK1) causing depolarization
• B Voltage-gated sodium channels causing intraventricular conduction delay
• C Rapid delayed rectifier potassium channel (IKr), prolonging QT interval and enabling early afterdepolarizations ✓
• D L-type calcium channels causing negative inotropy

Explanation

Class IA antiarrhythmics (quinidine, procainamide, disopyramide) block both sodium channels (reducing Vmax) and the rapid delayed rectifier potassium channel (IKr, encoded by hERG). IKr blockade prolongs action potential duration and QT interval. When QT prolongation is excessive, early afterdepolarizations (EADs) can arise during the prolonged repolarization, triggering polymorphic ventricular tachycardia — torsades de pointes. This is why class IA agents are contraindicated in patients with baseline QT prolongation.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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