Electrophysiologic effects of quinidine. Studies using chronically implanted electrodes in awake dogs with and without cardiac denervation.

Abstract

Experiments were performed on awake dogs with chronic recording electrodes implanted on the SA node, His bundle, and right bundle branch. Quinidine at serum concentrations of 5 to 10 mg/liter had little effect on AV conduction, but slowed conduction in Purkinje tissue, prolonged ventricular activation, decreased the excitability of atrium and ventricle, and prolonged the atrial refractory period without a consistent effect on the ventricular refractory period. In awake dogs that had previously undergone cardiac denervation, quinidine decreased the excitability and prolonged the refractory period of atrium and ventricle. The effects of quinidine on excitability were dependent on the duration of the stimulus used to test excitability. The actions of quinidine on intraventricular conduction and excitability were enhanced at rapid rates of stimulation. These data indicate that slowing of intraventricular conduction is observed consistently at serum quinidine concentrations that are generally considered to be within the therapeutic range, but changes of the refractory period of the ventricle are not observed consistently. Although the vagolytic properties of quinidine may contribute to changes of heart rate, they do not appear to influence significantly the effects of quinidine on atrial refractoriness and AV conduction.