Flecainide (Tambocor) is a class I cardiac antiarrhythmic agent with electrophysiologic properties similar to lidocaine, quinidine, procainamide, and tocainide. Flecainide produces a dose-related decrease in intracardiac conduction in all parts of the heart, with the greatest effect on the His-Purkinje system. Atrial effects are limited. Flecainide causes a dose-related and plasma concentration-related decrease in single and multiple premature ventricular contractions and can suppress recurrence of ventricular tachycardia.
Flecainide is eliminated from blood by hepatic metabolism as well as renal clearance; significant changes in either organ system will cause impaired clearance. During preclinical trials, patients with congestive heart failure were observed to have radically altered clearance properties. Cardiac toxicity attributed to flecainide is related to its cardiac conduction slowing properties. Excessive prolongation of PR, QRS, and QT intervals occurs with increased amplitude of the T wave. Reductions in myocardial rate, contractility, as well as conduction disturbances, are also associated with excessive dose and plasma concentration of flecainide.
Death can occur from hypotension, respiratory failure, and asystole.
Flecainide is contraindicated in patients with sick sinus syndrome. It causes sinus bradycardia, sinus pause, or sinus arrest.
Flecainide is most effective in premature ventricular contractions suppression at plasma concentrations in the range of 0.2 to 1.0 mcg/mL.
Plasma concentrations >1.0 mcg/mL are associated with a high rate of cardiac adverse experiences such as conduction defects or bradycardia.
Therapeutic concentration: 0.2 to 1.0 mcg/mL.
Toxic concentration: >1.0 mcg/mL
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