Class III Antiarrhythmics Mechanism of Action
Class III antiarrhythmics — amiodarone, sotalol, dofetilide, and ibutilide — block cardiac potassium channels, prolonging the action potential and QT interval. Mastering their mechanism is essential for USMLE Step 1 and Step 2 CK, where drug selection for ventricular and atrial arrhythmias is frequently tested. The flashcards here build the mental model linking K⁺ blockade to proarrhythmic risk and clinical indications.
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5 CardsWhat is the major adverse effect of Class III antiarrhythmics?
Why is amiodarone unique among Class III agents?
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What is the difference between Class I and Class III antiarrhythmics?
Class I agents block Na⁺ channels, slowing conduction velocity. Class III agents block K⁺ channels, prolonging repolarization and refractoriness without slowing conduction as the primary effect.
- Class I: flecainide, lidocaine
- Class III: amiodarone, sotalol
How many Class III antiarrhythmics are there?
There are 5 main Class III antiarrhythmics: amiodarone, sotalol, dofetilide, ibutilide, and dronedarone. Amiodarone and sotalol are most frequently tested on USMLE Step 1 and Step 2 CK.
Why does QT prolongation cause Torsades de pointes?
A prolonged QT interval indicates delayed repolarization, creating a vulnerable window during which an early afterdepolarization (EAD) can trigger a re-entry circuit — the hallmark of Torsades de pointes.
How do I memorize which antiarrhythmics cause QT prolongation?
Group them by class: Class IA (quinidine, procainamide), Class III (amiodarone, sotalol, dofetilide), plus non-cardiac drugs (macrolides, fluoroquinolones, antipsychotics). Any IKr blocker prolongs QT and risks Torsades.
