ACTION OF CHLOROFORM UPON THE HEART AND ARTERIES. 331 
the heart has been administered, but this is a condition which no anesthetist has any 
right or occasion to produce. On the other hand, it can prevent the sudden cardiac 
arrest which may show itself even at a comparatively early stage of chloroformisation, 
and which may be produced by the drug itself acting on the cardio-inhibitory centre, 
with (or without) the assistance of an effect reflexly produced upon that centre by 
the operation which is proceeding ; or by some other concomitant, such as the incidental 
occurrence of dyspnoea, which is well known also to cause inhibition through the vagus.* 
Whether the vagi be cut or their terminal branches blocked by atropine, or whether 
they be left intact, the ultimate effect of chloroform upon the heart, if its inhalation be 
pushed, is to produce complete arrest in diastole, a condition being observed which has 
been termed “ paralytic dilatation.” The condition is a peculiar one, for the cardiac 
muscle is not.only paralysed and incapable of contracting spontaneously, but is in a 
permanently refractory condition, and incapable of responding ‘to stimuli of any sort.t 
To all forms of direct stimulation the heart gives no response, although the 
muscular tissue is not dead, and it suffices to remove the chloroform by producing a 
flow of unpoisoned blood or circulating fluid through the coronary vessels to restore its 
thythmic contractility and its power of responding to artificial stimuli This shows 
that the refractory condition is due to the influence of the drug upon the heart, and 
it is commonly assumed by writers upon the subject that chloroform enters into 
combination with the contractile substance of the cardiac muscle and thereby deprives 
it of irritability. That this assumption is not justified is clear from the fact that no 
such effect—in doses which are more than sufficient to paralyse the heart—is produced 
upon either skeletal or upon plain muscular tissue. It is impossible to believe that the 
chemical constitution of these forms of contractile tissue is so different from that of 
heart muscle, that the one combines with chloroform and is thereby rendered devoid 
of irritability, whilst the others show no tendency to combine with or to be materially 
affected by the drug. It is much more probable that the effect produced is one of 
excitation of the terminations of the inhibitory nerves, the heart being thereby 
rendered irresponsive to stimuli. The argument that may be urged against this 
hypothesis, that if this were so the effect of chloroform in paralysing the heart would 
be prevented by atropine, is met by the statement that, although atropine blocks the 
* An instance of the last-named complication is illustrated in fig. 20. In this animal the breathing was laboured, 
owing to obstruction of the air-tubes by mucus.’ There was marked dyspnea, and the heart-heats were very slow 
and even arrested whenever the dyspncéa became intense. The violent respiratory efforts succeeded from time to time 
in clearing the air-passages, and this was followed by partial recovery. This pronounced inhibition was due to 
asphyxia, which, if more marked than in the instance given, may lead to entire arrest of the heart. Such inhibition 
from asphyxia does not occur with cut vagi. The condition is one which is not unfamiliar to anesthetists, who are 
cognisaut of its cause and danger. It is not liable to occur if a prior dose of atropine be administered, partly on 
account of the effect of this on the vagi and also because atropine tends to prevent the secretion of the mucus which 
causes the obstruction to respiration. This reason for the administration of atropine will apply equally to ether as 
to chloroform anesthesia. 
+ SHERRINGTON and SowrTon (op. cit.), in the isolated and perfused cat’s heart arrested by chloroform, obtained 
a renewal of the contractions on stimulation of accelerator nerves. But it is doubtful if this could be obtained with 
a strong dose of chloroform. 
{ SHERRINGTON and Sowron. 
