80 



for the survival of the individual may occur — if one may 

 put this interpretation on the phenomena of some cases that 

 have been recorded by Sir William Osler/« cases presenting 

 in striking fashion the external features associated with the 

 occurrence of fibrillation. Referring to sudden death in 

 some anginal subjects, he writes : 



" Possibly in some act combining intense emotion with muscular 

 effort there is a rapid change, a sudden unconsciousness, a stony 

 stare, a slight change in the facial expression, and then with two 

 or three gasps all is over ; no pulse is felt at the wrist ; the respira- 

 tion stops; but even when the patient is apparently dead a feeble 

 heart impulse may be felt or faint heart sounds heard." 



In one of these cases where slowly recurring respiratory 

 gasps occurred over some minutes, cardio-puncture with a 

 long thin aspirator needle showed movements indicating 

 heart beats at gradually diminishing rates — 52, 44, 32 per 

 minute — ceasing fifty minutes after collapse and forty-live 

 minutes after the last inspiratory gasp. (It may be 

 remarked that the phenomena here described by Osier were 

 not such as to be suggestive of reflex vagus inhibition.) 



Osier's description of such deaths may be compared with 

 what Sir Thomas Lewis' '^ says of deaths from ventricular 

 fibrillation, occurring in subjects of auricular fibrillation : 



" From time to time a sudden and unexpected catastrophe 

 happens; regarded as convalescent, the patient is sitting in bed, 

 chatting or feeding maybe. A nurse in charge, or perhaps a neigh- 

 bouring patient, hears a cry or choking sound ; the patient falls 

 back on the pillows intensely pale, there are a few gasping respira- 

 tions, a little convulsive movement, and the pulseless patient, 

 rapidly becoming livid, is still." 



Melation of the A-V Junctional Tissues to Ventricular 

 Fibrillation. 



Unlike auricular fibrillation, which, as is well known, may 

 go on over a long term of years, ventricular fibrillation is 

 promptly fatal, involving as it does an abrupt and complete 

 abolition of the pumping action of the ventricles and a 

 speedy cessation of the circulation. The effect of auricular 

 fibrillation is to impose a more or less extensive limitation 

 to the efficiency of the heart in two ways — by the absence of 

 the normal action of auricular systole in completing the 

 filling of the ventricular force-pump, and still more by the 

 rapid and disorderly lead given to the ventricles by the 

 rapid and irregular excitations transmitted from the 

 fibrillating auricles to the ventricles; the latter involves a 

 wasteful and exhausting expenditure of the energy of the 

 ventricular muscle, attended by relatively poor results in the 

 way of maintaining the circulation. 



Fortunately the structure and properties of the junctional 

 tissues between auricles and ventricles are such as to afford 

 a most important protection against transmission of the 

 fibrillation from the auricles to the ventricles. In default 

 of such protection the onset of auricular fibrillation would 

 necessarily be fatal by extension to the ventricles. It is 



