Serum Alkalinization Affects Elimination of Flecainide in Chronic Toxicity: A Case Report

Abstract

Background: Supratherapeutic flecainide concentrations may result in wide complex cardiac dysrhythmias, which are normally treated with hypertonic sodium bicarbonate therapy. Previous cases have suggested that in acute toxicity, serum alkalinization may impair the elimination of flecainide. Case summary: We present a single case of chronic flecainide toxicity. A 69-year-old patient began taking oral flecainide 1 month prior and developed recurrent wide complex tachycardia (WCT) that was refractory to treatment with sodium bicarbonate and repeated defibrillations. Further arrhythmias stopped after the resolution of alkalosis and treatment with lidocaine. Serum flecainide concentrations were notable for an apparent rise from initial levels following serum alkalinization. Discussion: Medication interactions and pharmacodynamic testing could not account for increasing serum flecainide concentrations following treatment. No evidence of supratherapeutic ingestion was identified. Tissue redistribution as a result of serum alkalinization likely contributed to impaired elimination in a patient with chronic flecainide toxicity. Conclusions: Serum alkalinization from sodium bicarbonate administration has implications in the length of stay and need for adjunctive therapies in the treatment of flecainide toxicity.