flecainide

Flecainide is a Vaughan-Williams Class IC sodium channel blocker. Mechanism: strongly blocks fast Na+ channels with slow dissociation kinetics ('slow off' drug), causing marked slowing of phase 0 depolarization and conduction velocity in atrial, ventricular, and His-Purkinje tissue. It has minimal effect on action potential duration and refractory period compared to Class IA drugs, and no significant effect on QT interval. It widens the QRS complex on ECG in a use-dependent manner (effect more pronounced at faster heart rates).

Clinical uses: Paroxysmal atrial fibrillation/flutter and SVT (including AVNRT/AVRT via accessory pathways, e.g., WPW) in patients with structurally normal hearts ('pill-in-the-pocket' approach for AF). Also used for refractory ventricular arrhythmias.

Key contraindication: Structural or ischemic heart disease. This stems from the landmark CAST trial (Cardiac Arrhythmia Suppression Trial), which showed increased mortality when flecainide (and other Class IC agents) was used post-MI to suppress asymptomatic PVCs, due to proarrhythmic effects (can precipitate sustained ventricular tachycardia by facilitating reentry through areas of slow, non-uniform conduction in scarred/ischemic myocardium).

Adverse effects: Proarrhythmia (including incessant VT), negative inotropy (can worsen heart failure), and can convert atrial fibrillation to atrial flutter with 1:1 AV conduction (dangerous rapid ventricular rates) - often combined with an AV nodal blocker (beta-blocker or calcium channel blocker) to prevent this.

Pharmacokinetics: Hepatically metabolized (CYP2D6), renally excreted; requires dose adjustment in renal impairment.

High-yield board points: Remember mnemonic 'Class IC drugs = flecainide, propafenone' - 'Can Cause Cardiac Death' post-MI (CAST trial). No effect on QT interval (unlike Class IA/III). Contraindicated in structural heart disease.