326 PROFESSOR E. A. SCHAFER AND DR H. J..SCHARLIEB ON THE 
with an independent (slower) rhythm. In all such cases as these recovery may be 
effected if artificial respiration be started soon (fig. 15), before the respiratory centre 
has been allowed to remain too long under the influence of the.chloroform plus anzemia ; 
or if the anzesthetisation be not very deep, there may be spontaneous recovery (fig. 12). 
In other cases the ventricle does not escape spontaneously (fig. 14); but it may be 
caused to contract by rhythmic compression through the chest wall (fig. 15). The 
arrest of the heart (and, secondarily, of the respiration) is due therefore to an excitation 
by chloroform of the cardio-inhibitory centre.* ARLoING showed that it does not occur 
with cut vagi, and this is also emphasised by EmMBLEy ; moreover, it does not occur if 
a small dose of atropine has been previously given (see below, p. 328), and it may also 
fail to be apparent after prolonged anzesthetisation with chloroform in moderate dosage. 
It fails to occur also in certain individuals, which seem to be less susceptible than 
others to the cardio-inhibitory effects of the drug. Instances are shown in fig. 22, A, and 
nnn 
“rr 
OTT 
ni 
Fic, 15.—Tracing showing (secondary) inhibition of heart from strong chloroform inhalation, with simultaneous cessation of 
respiration. Recovery, after 30 seconds’ arrest, by means of artificial respiration effected by chest compression. 
a, vespiration ; 0, arterial pressure ; c, time in 10 seconds; d, signal line (2 mm. above abscissa of blood-pressure). 
also in fig. 16; the latter from a dog in which the inhalation of air strongly charged with 
chloroform vapour was pushed until respirations had ceased, the heart continuing to 
beat with great regularity five minutes longer, but during the last three minutes at a 
slower rate (probably the result of independent ventricular action). 
In connection with this subject, we have investigated the effect of vagal excitation 
upon the heart in different stages of chloroform anzesthesia, and the effect of small 
doses of atropine upon the result of vagal excitation. In light anesthesia, an 
adequate stimulation of the vagus produces, as in absence of anesthesia, complete 
arrest of cardiac movements with a fall of blood-pressure to zero. But even if the 
excitation be continued, this condition does not last, for although the auricles may 
* The above tracings make it abundantly evident that the assertion of Lawrie (Lancet, 1890, vol. i. p. 1393), 
founded on the report of the Hyderabad Commission, “that sudden death from stoppage of the heart is not a risk 
of chloroform itself,” is completely erroneous. 
