106 CIRCULATION 



causes a marked increase in pulse rate. In some cases lesions 

 have been found in the atrioventricular bundle but in others 

 a cardio-inhibitory excitation of an already permanently 

 diminished conductivity of the bundle is responsible. It is 

 found that when a heart is subjected to a series of stimuli it 

 will respond regularly when the rate is slow, but when it be- 

 comes too rapid, the stimuli will not all be able to call forth 

 a response. The heart muscle loses its irritability during a 

 part of its systole, and regains it during the remainder of the 

 systole and the following diastole. During a part of the cardiac 

 cycle, therefore, it is refractory to stimuli. A stimulus falling 

 within the refractory period is without effect. A stimulus 

 falling within the non-refractory period calls out a contrac- 

 tion, but does not disturb the rhythm of the heart, because 

 it is followed by a pause of extra length. This is called the 

 compensatory pause. The first systole after an extra contraction 

 and a compensatory pause is of marked strength. 



The nerves of the heart are branches of the vagus and the 

 sympathetic. Some of the fibers of the vagus which are derived 

 from the spinal accessory terminate in end baskets which 

 surround sympathetic ganglion cells whose axis cylinder pro- 

 cesses end on the muscle fibers. Other fibers of the vagus end 

 in end brushes in the pericardium and endocardium. Fibers 

 of the sympathetic system arise from cells in the cord and 

 pass out through the white rami, ending in the inferior cervical 

 and stellate ganglia on cells whose axis cylinder processes in 

 turn pass either directly to the heart muscle or to a third neurojn 

 lying in the heart. 



Stimulation of the vagus fibers along any portion of their 

 path from the medulla to the heart inhibits the heart's action. 

 The effect is not immediate, but follows a latent period which 

 extends over a beat or two. The inhibition manifests itself 

 at first by a lengthening of the duration of the diastole with- 

 out any change in the systole. A stronger stimulation lengthens 

 the systole also, and may stop the beat of the heart altogether. 

 Inhibition is further shown by a lessening of the force of the 

 contraction; by an increase of pressure in the heart during dias- 

 tole; by an increase in the amount of residual blood; by a 

 decrease in the input and output of the ventricle, and by 

 diminished ventricular tonus. It may further be said that 



