Flecainide

Flecainide ( Na⁺ and K⁺ Channel Blocker)

• Overview:

  • Fluorinated local anesthetic analog of procainamide

  • More effective than quinidine gluconate or disopyramide in:

    • suppressing ventricular tachycardia

    • suppressing ventricular premature contractions

• Pharmacokinetics:

  • oral absorption: excellent

  • long elimination half-time (approximately 20 hours)

  • 25% flecainide: excreted unchanged (kidneys)

  • Hepatic metabolism: weakly active metabolites

  • Factors reducing flecainide elimination:

    • congestive heart failure

    • renal failure

• Cardiac Effects/Clinical Use:

  • Suppression ventricular tachycardia & ventricular premature contractions

  • Effective in management of atrial tachyarrhythmias

  • Effective in tachyarrhythmias associated with Wolff-Parkinson-White syndrome (suppression of conduction bypass tracts)

  • Chronic flecainide treatment following myocardial infarction not recommended:

    • increased incidence of sudden death in treated patients

      • In CAST, flecainide increased mortality in patients recovering from myocardial infarction.

    • Flecainide: should be reserved for management of life-threatening arrhythmias

  • Slight/moderate negative inotropic property

  • Proarrhythmic effects in patients with preexisting left ventricular function deficiency

• Electrophysiology:

• Prolongation of PR interval (ECG)

• Prolongation of QRS complex (> 25%)

• Sinoatrial nodal depression (similar to beta-adrenergic blockers and calcium channel blockers)

• Side-Effects/Toxicities

  • Most common:vertigo and difficulty in visual accommodation

  • Most serious of adverse effects is induction of potentially lethal arrhythmias such as reentrant ventricular tachyarrhythmias.

Stoelting, R.K., "Cardiac Antidysrhythmic Drugs", in Pharmacology and Physiology in Anesthetic Practice, Lippincott-Raven Publishers, 1999, 331-343

Category: Pharmacology Notes