Lidocaine to stop fast heart rhythm in dogs with OAVRT

Abstract

BACKGROUND: Typical atrioventricular accessory pathways (APs) are composed of myocardial cells. They provide electrical connections between atria and ventricles separate from the normal conduction system. Accessory pathways can participate in a macroreentrant circuit resulting in orthodromic atrioventricular reciprocating tachycardia (OAVRT). HYPOTHESIS: Because of ultrastructural similarities of typical AP cells to ventricular myocardial cells, we hypothesized lidocaine would be effective in blocking AP conduction, thus terminating OAVRT. ANIMALS: Thirty-two consecutive client-owned dogs presenting with narrow complex tachyarrhythmias were confirmed to have OAVRT by electrophysiologic study (EPS). METHODS: Prospective, nonrandomized, single-arm study with lidocaine administered IV to dogs during OAVRT in 2 mg/kg boluses to a cumulative dose of 8 mg/kg or development of adverse effects. Electrocardiograms were monitored continuously. Subsequent EPS was performed to confirm OAVRT and the absence of other tachycardia mechanisms. RESULTS: Twenty-seven dogs experienced OAVRT cardioversion with lidocaine, before or at the time of adverse effects. Orthodromic atrioventricular reciprocating tachycardia in 5 dogs did not cardiovert before adverse effects, precluding additional dosing. Median total lidocaine dose for cardioversion was 2 mg/kg (interquartile range, 2-5.5 mg/kg). Dogs with right free wall APs had a significantly higher rate of cardioversion than did dogs with right posteroseptal APs. CONCLUSIONS AND CLINICAL IMPORTANCE: Lidocaine successfully cardioverted OAVRT in 84.4% of dogs in our study before adverse effects precluded additional dosing. In 5 dogs with dose limited by adverse effects, it is unknown whether cardioversion would have occurred at a higher cumulative dose.