Abstract
Increasing doses of quinidine cause increased slowing of the auricular rate in flutter of circus movement origin, and maximally tolerated doses cause reversion to sinus rhythm. Quinidine lengthens conduction time in the nonfluttering auricle, and the effect increases as the dose is increased. Refractory period is lengthened equally by small and large doses. Experimental results suggest that the effects of quinidine on the auriculoventricular conducting mechanisms are of three types, (1) direct depressant, (2) vagal block, and (3) reflex sympathetic stimulation, and that these effects are manifest to different degrees depending upon dose and the state of innervation to the heart.