Sotalol prolongs the QT interval and can precipitate torsades de pointes. A distinctive feature of its class III action, which distinguishes it from amiodarone's electrophysiology, is:

• A Reverse use dependence: action potential prolongation is greater at slow heart rates ✓
• B Use dependence: block increases progressively at higher heart rates
• C Frequency-independent block of inward rectifier potassium current
• D Enhancement of IKr at rapid rates, shortening refractoriness

Explanation

Sotalol blocks IKr (rapid delayed rectifier potassium current) in a reverse use-dependent manner: channel blockade and QT prolongation are greatest when heart rate is low. This paradoxically means bradycardic pauses carry the highest torsades risk, unlike sodium channel blockers where use dependence makes tachycardia the risky state. Amiodarone shows much weaker reverse use dependence, contributing to its lower torsades incidence despite marked QT prolongation. Options B and D invert the actual property, and sotalol blocks rather than enhances IKr.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.