Abstract
Quinidine acts directly upon the myocardium and is a powerful cardiac depressant. The drug depresses auriculo-ventricular conduction and retards the rate of the sinus node in dogs. 1 Auricular irritability is definitely diminished in the terrapin's heart. 2 However, when applied to clinical cases of hyperactivity of the sinus node as in sinus tachycardia, quinidine does not consistently exhibit its depressor effect. The rate of the sinus rhythm is frequently increased rather than retarded.
Lewis and his associates 1 have demonstrated in dogs that in addition to its direct cardiac action, quinidine also modifies the response of the heart to vagus stimulation. The prolongation of auriculo-ventricular conduction time on vagus stimulation was markedly lessened under quinidine. In some instances vagus stimulation actually shortened the conduction period. The reaction of the sinus node to vagus stimulation was only slightly affected. In the cat, however, Dale 3 showed that the vagus effect on the sinus node was not only eliminated by quinidine, but a reversal of vagus action could be obtained with an acceleration of the sinus rate. In man it is possible to study the effect of vagus stimulation on the sinus node by application of the carotid sinus reflex. In some subjects an intense reflex stimulation of the vagus nerve is obtained 4 with temporary inactivity of the sinus node and cardiac standstill. This reaction can be abolished by atropine. Six subjects were selected in whom a prolonged cardiac standstill could be consistently induced by pressure on the right carotid sinus. These subjects were repeatedly tested to determine the consistency of the response.
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