Abstract
In the normal heart several centers of rhythm formation are potentially active, but the sinus node, which generates the impulse most rapidly, sets the pace of the heart. Observations on experimental animals indicate that there is considerable variation in the rhythmic efficiency of other portions of the heart. Cohn, Kessel and Mason, 1 after removing the sinus node in dogs, found a transitory quiescence of the heart varying from 4 seconds to 3 minutes, the interval being less than 30 seconds in most instances. The period of the quiescence was interpreted as representing the time required for some other portion of the heart to take on the pacemaking function. Rothberger and Winterberg 2 demonstrated in dogs that depression of the sinus node by stimulation of the right vagus nerve usually resulted in cardiac standstill. After eliminating the sinus node by vagus stimulation these observers studied the influence of various procedures in inducing new centers of impulse initiation. Thus they found that upon stimulation of the left sympathetic nerve, cardiac standstill was prevented by the development of new rhythmic centers in the ventricles. The addition of barium chloride or calcium chloride further increased the automaticity of the ventricles.
The purpose of this report is to point out that the above experiments may be reproduced in man, permitting a study of the rhythmic property of the human heart and also a direct method for the investigation of the action of drugs on this function. Utilizing the carotid sinus reflex of Hering, 3 pressure over the right carotid artery in the neck induces a reflex stimulation of the vagus nerve. In most individuals the degree of vagal stimulation is such that only a moderate slowing of the heart occurs.
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