404 



Dr. E. H. Embley. 



[June 13, 



exceed 20 per cent, in the air inspired the slowing of the heart rate from 

 vagus inhibition is the cause of that fall. When a strength of vapour 

 of 30 per cent, and upwards is administered the fall of blood-pressure is in 

 part due to cardio-vascular paralysis, but a fall of blood-pressure occurring 

 without slowing of the heart rate is due wholly to cardio-vascular paralysis. 



These statements apply to dogs. They, moreover, apply for short periods — 

 not more than 14' periods, which, however, are longer than those during 

 which ethyl chloride is generally used in clinical administrations. 



In comparing the cases of inhibition of the heart produced by chloroform 

 in my previous experimental work (11), I find that 2'5 per cent, chloroform 

 vapour in the air administered produces approximately the same degree 

 of cardiac inhibition as 10 per cent, ethyl chloride. 



There is, however, a difference of vast clinical interest between the inhibi- 

 tion produced by chloroform and that by ethyl chloride, since inhibition due 

 to chloroform is liable to prove fatal, whereas I have not succeeded, in 

 this investigation, in causing a fatal case of cardiac inhibition with ethyl 

 chloride. Furthermore, I have never succeeded in fatally arresting the heart 

 by faradic stimulation of the peripheral ends of the divided vagi under any 

 depth of ethyl chloride narcosis. Whereas, with chloroform, faradic stimulation 

 under like conditions and deep degree of narcosis easily brought about this 

 result (11). 



If, however, we compare the results of chloroform (5) and of ethyl 

 chloride upon the heart alone (p. 393), and upon the vagus mechanism alone, 

 it is seen that whilst it requires approximately (p. 401) four times more 

 ethyl chloride to produce the same degree of inhibition as is produced by 

 chloroform in a given time, it requires approximately 19 (p. 396) times as 

 much ethyl chloride to produce the same degree of cardiac depression in 

 the same period of time as is produced by chloroform. Hence it is that in 

 these experiments cardiac inhibition has come on early — before the spontaneous 

 excitability of the heart has been much depressed. Herein, therefore, appears 

 to lie the reason why 30 per cent, and upwards of ethyl chloride vapour in 

 the air inspired has not produced fatal cardiac inhibition in the experiments 

 with ethyl chloride. Herein, too, lies the cause of the relative safety of ethyl 

 chloride. 



That the slowing of the heart under the influence of ethyl chloride is due to 

 vagus inhibition is proved by its prompt cessation upon section of these nerves, 

 as is shown in fig. 9. This experiment also proves that the inhibition is not 

 a reflex arising from stimulation of the sensory nerve ends in the mucous 

 membrane of the nose, trachea, or bronchi, or in the alveoli of the lungs, but 

 to direct central stimulation, for in this experiment defibrinated blood 



