A 55-year-old man started on sotalol for paroxysmal atrial fibrillation develops syncope three days after initiation. ECG shows polymorphic ventricular tachycardia with a twisting QRS axis. Which property of sotalol most directly explains this event?

• A Strong sodium channel blockade causing wide QRS complexes
• B Selective beta-1 antagonism producing severe bradycardia
• C Dose-related prolongation of the action potential duration via IKr blockade ✓
• D Calcium channel blockade at the AV node

Explanation

Sotalol combines nonspecific beta-blockade with class III activity by blocking the rapid component of the delayed rectifier potassium current (IKr). This prolongs repolarization and the QT interval in a dose-dependent manner, creating a substrate for torsades de pointes, particularly early after initiation or after dose escalation. It has no meaningful sodium channel blocking activity, ruling out option A. Beta-blockade slows sinus rate but causes bradycardia, not polymorphic VT, and sotalol lacks calcium channel blocking properties.

Reference: Goodman & Gilman's The Pharmacological Basis of Therapeutics, 14th ed.

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