Lidocaine for chemical cardioversion of orthodromic atrioventricular reciprocating tachycardia in dogs

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.