A patient with ventricular tachycardia is given amiodarone. The primary electrophysiological mechanism responsible for its broad-spectrum antiarrhythmic efficacy is:

• A Predominantly class III action via IKr (hERG) blockade that uniformly prolongs action potential duration in all cardiac tissues, plus class I, II, and IV effects ✓
• B Potent sodium channel blockade (class I) and mild potassium channel blockade prolongs action potential in a frequency-dependent manner
• C Alpha and beta adrenoceptor blockade (non-competitive) reducing triggered activity in ischemic myocardium
• D Selective inhibition of L-type calcium channels in AV node reducing automaticity without affecting ventricular myocardium

Explanation

Amiodarone has multi-class effects (I, II, III, IV) but the dominant chronic mechanism is class III — prolongation of action potential duration and effective refractory period via IKr (hERG channel) and IKs blockade. Unlike pure class III agents, amiodarone does NOT show reverse use-dependence (ERP prolongation is maintained at high heart rates), making it effective during tachyarrhythmias. The iodinated benzofuran ring is structurally similar to thyroid hormone, also explaining thyroid toxicity. The broad-spectrum efficacy comes from this multi-class profile. Torsades de pointes risk is paradoxically low despite QT prolongation.

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

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Written and medically reviewed by the StethoPrep medical team.