Key result
Combined beta-sympathomimetic, physostigmine, and sodium loading restores sinus rhythm in severe flecainide overdose.
Why the study?
Flecainide acetate can cause life-threatening ventricular tachyarrhythmias and severe bradycardia, with toxicity correlating closely with plasma drug levels.
Does infusion of a beta-sympathomimetic agent, physostigmine, and a sodium load improve life-threatening arrhythmias in a patient with flecainide overdose?
Case Report (n=1)
Does infusion of a beta-sympathomimetic agent, physostigmine, and a sodium load improve life-threatening arrhythmias in a patient with flecainide overdose?
Life-threatening arrhythmias and ECG interval prolongation from flecainide overdose can be successfully managed with a combination of a beta-sympathomimetic agent, physostigmine, and sodium loading.
ECG prolongation flags flecainide toxicity tied to plasma levels; leaves open prospective validation for routine monitoring.
Ventricular tachyarrhythmias and severe bradycardia, flecainide acetate's most serious side effects, occur in patients with chronic heart disease or in healthy persons after frank overdose. Toxic effects appear to correlate closely with drug levels in plasma. The surface electrocardiogram can indicate toxicity by demonstrating this drug's electrophysiologic potency to depress all major cardiac conduction pathways with marked prolongation of the PR and QRS intervals. We report the clinical course of a young, healthy person who developed polymorphous ventricular tachycardia after taking a 3800-mg dose of flecainide acetate. Sinus rhythm was restored without pacing or cardioversion after infusion of a beta-sympathomimetic agent, physostigmine, and a sodium load. The initial flecainide serum levels were five times greater than the usual upper therapeutic level. Electrocardiography showed that the lengthened electrocardiographic time intervals decreased in correlation with falling drug levels. Flecainide-associated life-threatening arrhythmias and available therapeutic interventions are discussed.
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Bernhard Rudolf Winkelmann (1987) conducted a case report in Flecainide toxicity (n=1). Flecainide acetate was evaluated. A 3800-mg overdose of flecainide acetate induced polymorphous ventricular tachycardia in a young person, with sinus rhythm restored via a beta-sympathomimetic agent, physostigmine, and sodium load.
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