Control of Fibrillation in the Mammalian Heart. 



317 



in the form of slowed auricular heats. This is to be ascribed to the vagus 

 acting more strongly than usual on excitability, in addition to the usual 

 effects on contraction force and conductivity. 



When the influence of the vagus iii converting a rapid tachycardia or 

 flutter into fibrillation was first studied, the question naturally arose as to 

 whether the changes visible on inspection and in the graphic records might 

 not be due simply to the cutting down of the force of the rapidly-recurring 

 contractions, the mechanical limitation of the range of movement associated 

 with distension of the auricular chambers, etc. But the clamping-off experi- 

 ment brings out there is an essential difference in the mechanisms in the two 

 cases. 



The vagus alters or depresses conductivity in the auricles in such a way 

 that the inter-fascicular connections are unable to functionate normally when 

 the succession of excitations is much accelerated. (Distinct from this is the 

 question of the power of the vagus to slow the conduction along the main 

 transmitting paths in the auricles.) Certain other depressant agencies have 

 an influence on the inter-fascicular connections in the ventricles (already 

 described), which resembles that of the vagus in the auricles, and these 

 agencies, when acting in great intensity, may have the further result of 

 causing obvious and striking retardation in the passage of the contraction 

 wave both in the ventricles and the auricles, even when the sequence is not 

 a rapid one, but may indeed be slower than the normal. 



Some Differences in the Behaviour of Auricles and Ventricles. 



While the analogies between the various phenomena are very close in tlie 

 auricles and ventricles, certain points of diff'erence may be noted. 



1. Electrical stimulation of strength adequate to give a sufficiently excessive 

 rate of beat is, by itself, a ready means of exciting ventricular fibrillation, 

 though, as has been stated, tlie .addition of some influence depressing con- 

 ductivity causes fibrillation to develop when the rate of beat is not nearly so 

 rapid as would otherwise be required. Auricular fibrillation, on the other 

 hand, is not, in most cases when the heart is in good condition, excited by 

 electrical stimulation per se, but requires an alteration of conductivity (in the 

 sense abeady defined) by some other agency, e.g., vagus influence, defective 

 nutrition, toxic substances, etc. The reason of this diff'erence is probably to 

 be found in conduction being less easily upset in the auricles with their 

 simpler structure and easier conditions of rapid conduction, as compared with 

 the highly elaborate ventricular architecture with the much slower rate of 

 conduction in the ventricular muscle proper — apart from the Purkinje 

 .system. 



VOL. xc. — B. 2 c 



