Prolongation of refractoriness and activation time in normal canine ventricular myocardium following bolus administration of lidocaine.

This study examines the electrophysiologic effects of an intravenous bolus of lidocaine in the normal canine ventricle. In 14 open-chest dogs, left ventricular effective refractory period, ventricular repolarization time, and activation time were measured continuously during ventricular pacing (150/min) before, during, and after intravenous lidocaine given over 4 minutes. Lidocaine doses of 1.25, 2.5, and 5.0 mg/kg transiently prolonged the ventricular effective refractory period from 177 +/- 4 (X +/- standard error of the mean) to 185 +/- 5 msec (p less than 0.05), 176 +/- 3 to 188 +/- 6 msec (p less than 0.05), and 176 +/- 5 to 197 +/- 5 msec, (p less than 0.05), respectively, at 6 +/- 1.5 minutes from the onset of the bolus. Serum lidocaine levels obtained at the peak of the effective refractory period prolongation averaged 4.3 +/- 1.0, 9.0 +/- 3.0, and 22.3 +/- 4.7 micrograms/ml, respectively. Ventricular repolarization time was not prolonged. Activation time also transiently increased from 43 to 45 msec (p less than 0.05) and from 47 to 52 msec with the 2.5 mg/kg and 5.0 mg/kg doses, respectively. Cardiac denervation and administration of propranolol, 1 mg/kg intravenously, did not influence these responses to lidocaine. We conclude that a bolus of lidocaine transiently prolongs the effective refractory period and activation time in the normal canine ventricle because of its direct membrane rather than autonomic effects.