ACTION OF CHLOROFORM UPON THE HEART AND ARTERIES. 327 
remain quiescent, the ventricles escape from the inhibition and resume contracting, at first 
very slowly, afterwards more quickly, although often somewhat irregularly, so that the 
blood-pressure again rises. On ceasing to excite the vagus, the heart beats more rapidly 
and more strongly, and there may be a temporary rise of blood-pressure above the 
normal average just before the excitation. This characteristic effect is shown in fig. 18. 
In chloroform anesthesia the effect upon the heart of vagal excitation is more 
pronounced and permanent.* ‘The complete arrest of cardiac action may last long 
enough to cause a concomitant arrest of respiration, and when this occurs, even if the 
JU AI a AOR 
sia ee eC 
i 
it 
ui 
aa 
OU tg ns 
DAV 
1 WN TILL WV, . 
vi UN MALNIAM AM AMAAAN Ny ananen, 2 
Fic. 16.—Shows a tracing of respiration and blood-pressure under inhalation of air strongly charged with chloroform vapour. 
This tracing illustrates the type of result obtained when cardiac inhibition does not occur to the extent of causing 
complete arrest of the heart, but merely a slowing (which may be suddenly increased), the heart failing quite gradually. 
The chloroform inhalation lasted 44 minutes, at the end of which period respiration had ceased, and was not again 
renewed until the heart had nearly stopped, when a ‘staircase’ group of 25 slow gasping respirations showed them- 
selves—the so-called ‘respirations of the death-agony.’ The lid reflex, which was present immediately before the 
inhalation began, disappeared within one minute. 
ventricles resume action, their rhythm is very slow, and their force insufficient to 
raise the blood-pressure much, so that, as a rule, respirations are not spontaneously 
resumed although artificial respiration may effect recovery. Or it may happen, 
_ especially with a strong excitation, that the recovery of the ventricles does not occur 
at all, and even heart massage, which can be effected by compressing the chest, to 
which the ventricle may at first respond, may be incapable of causing it permanently 
to resume its action. 
* DastreE states that this increase of vagal excitability under chloroform was first noted by Vunpran (C. 7. Soc. 
Biol., 1883, p. 243). According to FRANGoIS-FRANCK (ibid., p. 255), it disappears with increase of anesthesia, but this 
is not in accordance with our experience so far as concerns direct excitation. 
TRANS. ROY. SOC. EDIN., VOL. XLI. PART II. (NO. 12.) 49 
