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increased diastolic filling due to more rapid inflow from the 

 venae oavae, etc. Similar changes attend emotional excite- 

 ment, with the exception of the greatly increased venous 

 return to the heart depending on the pumping action of the 

 working muscles during exertion driving on the blood in 

 the veins. 



While the normal heart is not injured by such changes, 

 and in virtue of its great reserve power easily responds to 

 increased demands on it, a heart that is temporarily or per- 

 manently in an abnormal condition of excessive susceptibility 

 is apt to be thrown into fibrillation. 



Susceptibility to Ventricular Fihrillation. 



Both in healthy and diseased animals notable differences 

 in the ease with which fibrillation may be induced were seen 

 under experimental conditions that were apparently similar. 

 And a heart may sometimes be seen, under altered con- 

 ditions, to pass from the susceptible condition to a stable 

 one, which may be exceedingly resistant to the induction of 

 fibrillation by various forms of stimulation that are usually 

 very effective. Or a change in the opposite sense may take 

 place ; or there may be variation from one phase to another 

 more than once in the course of a single experiment in the 

 case of a healthy heart subjected to certain abnormal 

 influences. On the other hand, there are many cases where 

 the abnormal susceptibility is a persistent one associated 

 with altered nutritive conditions, toxic agencies, etc., in the 

 muscle. 



In healthy animals, cats particularly, a great susceptibility 

 to fibrillation may be established by the administration of 

 chloroform; the relation of this condition to the phase of 

 light chloroform anaesthesia has been specially worked out 

 by Levy, most (though not the whole) of whose results are 

 in agreement with those obtained by the present writer over 

 a long series of years. It is after a deeper phase of chloro- 

 form anaesthesia that the lighter phase is apt to be attended 

 by the marked susceptibility referred to. 



In the latter condition fibrillation is often readily induced 

 by stimulation of afferent nerves in various ways — resulting 

 in reflex contraction of skeletal muscles, disturbance of 

 respiration, rise of blood pressure, increased rate and force 

 of the heart with increased return of blood through the 

 great veins, etc. — in short, the same group of changes that 

 occur in muscular effort, and brought about in similar 

 fashion through the instrumentality of the vagus and cardiac 

 augmentor nerves, excitation of the respiratory and vaso- 

 motor centres, and the mechanical action of the skeletal 

 muscles in propelling blood more rapidly back to the heart 

 by the veins — increasing the rate of its diastolic filling and 

 its output and work per minute very largely. 



It is plain that it is through these changes that the sudden 

 fibrillation of the ventricles is determined in a susceptible 

 heart under chloroform, and there is a strong a priori case 



