ACTION OF CHLOROFORM UPON THE HEART AND ARTERIES. 333 
For convenience of description, this may be termed “ primary ” inhibition. It is prob- 
able that it occurs but rarely in man, and some altogether deny that it can produce 
a fatal result; it is, however, impossible to explain the well-authenticated instances 
of sudden heart failure at the very commencement of administration without assuming 
- that under certain conditions such primary inhibition, which, when it occurs in other 
cases, is usually quite evanescent, is occasionally persistent and fatal.* 
(2) At a somewhat later stage of administration death is liable to occur from 
sudden heart failure due to inhibition produced by the action of the drug on the 
eardio-inhibitory centre, aided by its action on the neuro-muscular end-apparatus of 
the heart itself, and also by increasing venosity of blood caused by failing respiration. 
The liability to this form of inhibition, which may be termed “secondary” (as well 
as to that mentioned under 1), can be removed by the prior exhibition of a moderate 
dose of atropine, which, by diminishing or abolishing the effect upon the heart of 
excitation of the cardio-inhibitory centre by chloroform, deprives it of the power to 
produce sudden cardiac arrest. This precautionary measure was long ago suggested,t 
and all recent work on the subject emphasises the importance of its adoption. 
That the prolonged administration of chloroform itself tends to diminish its 
excitatory effect upon the cardio-inhibitory centre in the medulla oblongata is probable 
from the fact that a dosage of chloroform can be given with impunity at the later 
stages of a long operation which would be highly dangerous if given at earlier stages. 
The respiration in these “secondary ” cases of inhibition may stop simultaneously 
with, or shortly before, or immediately after the heart. We have frequently succeeded 
in effecting resuscitation by artificial respiration in animals, in which both heart and 
respiration had completely stopped at this stage of poisoning after even a minute or 
two of cessation of heart-beats, and in two cases as long as three and five minutes 
respectively after complete cessation ; but in other instances we have failed to obtain 
recovery after three minutes or more of cessation. 
The two cases just referred to are of exceptional interest. In the one the animal had been under ether 
for about an hour (the anesthetic being inhaled through a Y-shaped trachea tube), when chloroform, at first 
with considerable intermixture of air, was substituted for the ether. The effect was to produce a gradual 
fall of blood-pressure from 100 mm. Hg. to about 40 mm., after which both it and the respiration, which was 
much shallower than under ether, remained nearly constant. After five minutes the lateral air-inlet was cut 
off, and the dog received a much stronger dose of chloroform. The result of this was immediately apparent 
in a further fall of blood-pressure, and a slowing and irregularity of the respirations, which ceased altogether 
about two minutes later, although the heart continued to beat regularly and the blood-pressure was maintained 
and even rose slightly. About one minute twenty seconds after cessation of respiration the heart suddenly 
* This mode of producing inhibition has been especially emphasised by ARLoING (These, Paris, 1879), who describes 
the effect of chloroform in producing heart failure in terms very similar to those which we have employed. 
+ PirHa (1861, quoted by Dasrre); J. Harry, Brit. Med. Journ., vol. i., 1868, p. 320; ScHAFER, Brit. Med. 
Jowrn., vol. ii., 1880, p. 620. Fraser (Brit. Med. Journ., vol. ii., 1880, p. 715), Brown-Sfquarp (C. r. Soc. Biol., 1883, 
p. 289), and DastrE and Morar (Lyon Meéd., 1882, and C. r. Soc. Biol., 1883, pp. 242 and 259) have made a similar 
recommendation, but have suggested the addition of morphia, and this combination has often been used (first 
systematically by AuBERt, C. r. Soc. Biol., 1883, p. 626). But morphia is in some ways antagonistic to atropine, and 
‘tends by itself to exalt the irritability of the cardio-inhibitory centre. Without atropine it would undoubtedly 
. 
: 
increase the danger of heart-arrest in chloroform administration. 
