Effects of lidocaine and quinidine on post-repolarization refractoriness after the basic and premature action potentials: consideration of aim of antiarrhythmic drug therapy.

Antiarrhythmic drugs are often more effective in suppressing ventricular tachycardias than are background premature extrasystoles. The mechanism of action of these agents was examined by studies on the effects of lidocaine and quinidine on post-repolarization refractoriness of both basic and premature action potentials. In the absence of antiarrhythmic drugs, the excitability threshold was relatively constant after the end of repolarization of both basic and premature action potentials. In the presence of lidocaine or quinidine, the strength-interval curves were shifted to the right and superiorly, and the two drugs had different effects on the course of the strength-interval curve and Vmax recovery, presumably due to use-dependent V max block. Moreover, depressions of Vmax and excitability were more marked after the premature action potential than after the basic action potential. These results suggest that lidocaine and quinidine cause more depression of the excitability of second premature contractions than of first premature contractions, and also indicate that for protection against sustained ventricular tachycardias, it may not be necessary to suppress chronic premature ventricular contractions.