A 64-year-old with CKD stage 4 (eGFR 22 mL/min) receives sotalol after cardioversion of atrial fibrillation. Two days later she develops polymorphic ventricular tachycardia with a QT interval of 610 ms. The factor most responsible for precipitating this event is:

• A Hepatic first-pass metabolism reducing active drug levels
• B Antagonism at cardiac potassium channels being enhanced by coexisting anemia
• C Conversion of sotalol to an active cardiotoxic metabolite
• D Renal clearance of the parent drug leading to accumulation and dose-dependent QT prolongation ✓

Explanation

Sotalol combines nonselective beta-blockade with class III IKr blocking activity and is excreted unchanged by the kidney. Renal impairment causes accumulation, dose-dependent QT prolongation, and torsades de pointes, so dosing must follow creatinine clearance and initiation usually requires hospital monitoring. It has no active metabolites and negligible hepatic metabolism, which eliminates the other options and explains why renal function governs its safety.

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

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Written and medically reviewed by the StethoPrep medical team.