210 



Prof. J. A. Mc William. 



[May 17, 



When vagus stimulation does not cause complete standstill, but 

 only a marked slowing, the strength of the slow ventricular beats is 

 usually much less than the normal. 



The reduction in contraction force does not bear any constant rela- 

 tion to the degree of slowing. While all the slow beats are weakened in 

 some degree, a beat occurring after a long pause is sometimes decidedly 

 stronger than one occurring after a shorter pause ; on the other hand, 

 the converse more often holds good — a beat occurring after a long 

 pause is weaker than a beat occurring after a shorter pause. 



The depression of contraction force does not appear to depend on 

 over-disfcension of the ventricles during the slowing or standstill ; nor 

 upon the fall of arterial pressure that occurs and involves a dimi- 

 nished resistance to the ventricular systole and a change in the coro- 

 nary circulation. 



The force-depressing effects of vagus stimulation can still be seen 



(1) when the superior and inferior venae cavse have been clamped ; or 



(2) when the pulmonary artery or (3) the aorta has been clamped ; or 

 (4) when all these vessels have been clamped before the vagus stimu- 

 lation. 



2. When slowing or arrest of the ventricular aetion occurs as a 

 result of vagus stimulation, there is a marked change in the shape and 

 duration of the ventricular curves ; the degree of change stands in 

 close relation to the length of the pause preceding each beat. The 

 curves become broader near the top, and their duration is increased. 

 The longer the interval preceding a curve the broader the curve is, 

 and the more markedly is it prolonged. These features are not 

 abolished when the superior and inferior venae cavae have been clamped 

 before the vagus stimulation ; nor when the aorta or the pulmonary 

 artery, or all these vessels, have been clamped. 



3. The vagus appears to inhibit the spontaneous rhythmic tendency 

 inherent in the ventricles ; the ventricular standstill does not appear 

 to be due simply to the standstill of the rest of the heart. 



4. At the same time the absence of auricular beats of any consider- 

 able strength is usually a necessary condition for the occurrence of a 

 protracted ventricular standstill. It commonly but not invariably 

 happens that if the auricles are artificially excited to contract during 

 the period of cardiac standstill, the ventricles beat also in sequence to 

 the artificially excited auricular contraction. 



5. When the heart begins to beat after a period of inhibition, the 

 order of contraction most commonly seen is that which obtains 

 normally — ostial parts of the great veins ; auricles ; ventricles. But 

 sometimes the ventricles recommence, and give one or more beats 

 before any contraction occurs in the other parts of the heart. 



6. There are sometimes seen evidences of the occurrence under 

 vagus influence of a block in the propagation of the contraction from 



