A patient develops proarrhythmia after initiation of flecainide for paroxysmal atrial fibrillation. Which specific arrhythmia mechanism is flecainide most likely to have unmasked or facilitated?
- A Torsades de pointes due to QTc prolongation from pure IKr blockade
- B Ventricular fibrillation triggered by triggered activity from early afterdepolarizations
- C Complete AV block due to concomitant AV nodal sodium channel blockade
- D Conversion of AF to organized atrial flutter with 1:1 AV conduction causing rapid ventricular rate ✓
Explanation
Flecainide is a class IC antiarrhythmic that potently blocks fast sodium channels. When used for AF, it can slow atrial conduction and flutter rate, but paradoxically organize AF into atrial flutter — often at a flutter rate of 220–250 bpm rather than the usual 300 bpm. This organized flutter can conduct 1:1 through the AV node (since class IC agents do not significantly block the AV node), producing a sudden ventricular rate of 200–250 bpm — a life-threatening tachycardia. This is why an AV nodal blocking agent (beta-blocker or verapamil) must be co-prescribed with flecainide if used for atrial fibrillation. The CAST trial established that IC agents increase mortality in patients with structural heart disease, limiting their use to structurally normal hearts.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.