317
the evidence afforded by my experiments goes, the slowing of the heart seems to be most
commonly due to asphyxial conditions; the Second Hyderabad Commission has urged that it is
always asphyxial. But I have seen facts which indicate that cardiac slowing is in some cases
due to causes other than aphyxia, for example, to sensory irritation when the state of the
anæsthesia is not such as to render the cardio-inhibitory centre inexcitable by afferent stimuli.
In any case the cardiac slowing is not due to a direct influence of chloroform on the
heart; it is entirely different in its nature and causation from the enfeeblement and dilatation of
the organ described in this paper. The latter, it has been seen, is a result of the direct action
of chloroform on the cardiac substance. On the other hand, the temporary slowing of the heart,
which occasionally occurs, is due to stimulation of the cardio-inhibitory centre in the medulla,
as I found at an early stage of this investigation. It is abolished by section of both vagi, and
its characters can be imitated by brief stimulation of the vagi.
Slowing of the cardiac action under chloroform does not, as far as I have seen, prove
dangerous in itself in healthy animals, whatever it may do in conditions of derangement and
disease. The mode of failure in the healthy animal is not by a slowing or sudden cessation of
the cardiac rhythm, but by an enfeeblement and dilatation of the organ while the rhythmic
(but ineffectual) contractions go on.
Relation of the Influence of Chloroform to the Occurrence of Fibrillar Contraction in the
Ventricles ("Here delirium" or Delirium Cordis).—I have
several times witnessed the super-
vention of fibrillar contraction or delirium cordis in the ventricles of the cat's heart from the
influence of chloroform. The normal beat was abolished, and the ventricles were thrown into
the wildly-irregular, inco-ordinated, ineffective action characteristie of this condition. But
such an accident never occurred in any of my experiments with anæsthetic dose of the drug,
but only when an overdose of strong chloroform vapour was pumped into the lungs. I have
seen no proof that such a mode of cardiac failure may result from the administration of chloro-
form in the ordinary way in healthy animals. At the same time it is that the occur-
rence of fibrillar contraction may be a cause of death in some abnormal conditions where the
ventricles become prone to assume this disastrous form of activity. The depression and dila-
tation of the heart induced by chloroform may terminate in a fatal onset of fibrillar contraction
or delirium cordis.
PART IV.
The Relation of c e r t a i n C h a n g e s i n t h e R e s p i r a t i o n
t o t h e E f f e c t s o f
C h l o r o f o r m — A l t e r a - t i o n s i n t h e r a t e a n d d e p t h o ft
h e b r e a t h i n g e x e r t a p r o f o u n d i n f l u e n c e o nt
h e
e f f e c t s p r o d u c e d
by chloroform. The results following the administration of a definite amount of the anæsthetic
depend largely upon the rapidity with which it is introduced into the circulation. A small
amount of chloroform quickly taken in produces vastly more potent effects than a large
quantity slowly absorbed over a considerable period of time. Hence the absolute amount of
the drug taken in by an animal—apart from consideration of the time spent in its introduction—
proves no guide at all as to the degree of influence produced by it upon the various systems.