A 52-year-old man with a history of paroxysmal supraventricular tachycardia (PSVT) is prescribed flecainide for rhythm control. Which of the following best describes the primary mechanism of action of flecainide in terminating PSVT?

Explanation

## Mechanism of Flecainide in PSVT Termination **Key Point:** Flecainide is a Class IC antiarrhythmic agent that works primarily by blocking fast sodium channels, which slows conduction velocity throughout the heart, including in the accessory pathway and AV node. ### Class IC Antiarrhythmics Flecainide and propafenone are Class IC agents characterized by: - **Marked slowing of conduction velocity** (Phase 0 depression) - Minimal effects on action potential duration or refractory period - High affinity for sodium channels in a use-dependent manner ### Mechanism in PSVT In paroxysmal SVT (often due to an accessory pathway in Wolff-Parkinson-White syndrome or AV nodal reentry), flecainide terminates the reentrant circuit by: 1. **Slowing conduction in the accessory pathway** — reduces the speed of impulse propagation 2. **Slowing AV nodal conduction** — increases the PR interval and AV nodal refractory period indirectly 3. **Breaking the reentrant loop** — by creating sufficient conduction delay that the retrograde impulse encounters refractory tissue **Clinical Pearl:** Flecainide is highly effective for PSVT because it preferentially slows conduction in the fastest-conducting tissue (the accessory pathway), which is essential for maintaining reentry. ### Why Class IC Over Other Classes for PSVT? | Class | Primary Effect | Use in PSVT | |-------|---|---| | **Ia** | Na^+^ block + K^+^ block | Moderate; prolongs QT | | **Ib** | Na^+^ block (mild) | Poor; shortens action potential | | **Ic** | Na^+^ block (marked) | **Excellent**; minimal QT prolongation | | **II** | β-blockade | Moderate; slower onset | | **III** | K^+^ block | Good; but more QT prolongation | | **IV** | Ca^2+^ block | Good for AV nodal reentry only | **High-Yield:** For accessory pathway-mediated PSVT (WPW), Class IC agents are preferred because they slow conduction in the accessory pathway itself, whereas beta-blockers and calcium channel blockers only slow the AV node. ### Flecainide Pharmacokinetics - Oral bioavailability: 90% - Hepatic metabolism (CYP2D6) - Half-life: 12–27 hours - Steady state: 3–5 days **Warning:** Flecainide is contraindicated in structural heart disease (especially post-MI) due to increased mortality risk (CAST trial), but is safe in patients with normal cardiac structure and function.