334 PROFESSOR E. A. SCHAFER AND DR H. J. SCHARLIEB ON THE 
stopped and the blood-pressure fell to zero. Artificial respiration (by the pump) was now started, and main- 
tained for five minutes, and two injections of 4 ¢.c. adrenalin chloride (1 per mille) were meanwhile made 
into the pleural cavity without the least result being apparent, the heart remaining quiescent and the blood- 
pressure at zero the whole time. Intermittent compression of the thorax was now substituted for perflation, 
and the heart responded to this by a pulsation with each compression, although in the intervals the blood- 
pressure returned to zero, After continuing the compression for a little over a minute, the heart commenced 
beating spontaneously and the average blood-pressure rose to 50 mm. Hg. It required, however, another 
three minutes of artificial respiration before the diaphragm began to act and the intermittent compression 
could be desisted from for a time; but even then (although no more chloroform had been inhaled) the 
respirations again gradually failed and ceased after ten minutes. A second spell of intermittent compression, 
lasting two minutes, now, however, effected complete restoration. When this was established and the lid 
reflex had become brisk, the blood-pressure being 110 mm. Hg., chloroform was again administered in 
strong form. The blood-pressure gradually fell. In two minutes the lid reflex had disappeared, and in 
another minute respirations had ceased, followed in twenty seconds by complete cessation of heart 
beat. Five minutes was now allowed to elapse, during which the animal was to all appearance dead, 
Artificial respiration by chest compression was then recommenced, and two more doses of 3 c¢.c, adrenalin — 
chloride solution were successively injected. Five minutes after the artificial respiration was commenced. 
and immediately after the final dose of adrenalin, the heart began to beat spontaneously, and the blood- 
pressure, at first very low, gradually rose in about four or five minutes, during which artificial respiration 
was maintained, to about 100 mm. Hg. Natural respiration was, however, not again resumed, the medulla 
oblongata having to all appearance been deprived for too long a time in this instance of blood. 
In the second dog a lethal dose of chloroform vapour was administered twice. The first time both heart 
and respiration (the latter ten seconds before the heart) had stopped after three and a half minutes’ adminis- 
tration. Half a minute later the chloroform was removed, and 4 c.c. of 1 per 1000 adrenalin chloride solution 
was injected into the pleural cavity. This produced no apparent effect. Three minutes after cessation of 
heart and respiration, chest compression was begun. Each compression produced a heart response, and the 
blood-pressure rose from zero to a few millimetres. After four minutes’ chest compression another similar 
dose of adrenalin was injected into the pleural cavity, chest compression being continued. The blood- 
pressure then began to recover, the heart now beating slightly more rapidly than the chest compression, but 
natural respiration (diaphragm) was not resumed until another six minutes had elapsed. As in the last 
case, however, the natural respirations gradually became shallower and slower again, although no more 
chloroform was given, and fifteen minutes later ceased altogether, the heart and blood-pressure also becoming 
weak and low; the administration at this stage of a decoction of pituitary, and later of another dose of 
adrenalin, with the idea of restoring the heart’s action, produced no visible effect. After two minutes’ 
cessation of respiration (the heart still beating feebly), recourse was again had to chest compression and then 
to artificial respiration by the pump. This was very soon followed by recovery of heart and blood-pressure, 
and a few minutes later natural respirations were resumed and maintained, and artificial respiration was 
discontinued ; recovery was, in fact, complete. 
(3) In late stages of administration the heart is paralysed by the direct effect of the 
drug, acting either upon its muscular tissue (as is usually assumed), or (as we believe) 
by exciting the neuro-muscular inhibitory end-apparatus, and through this rendering 
the muscular tissue non-excitable. This effect can probably only occur with a consider- 
able dosage of chloroform in the blood, and the respiratory centre is invariably first 
paralysed, so that the respirations become slow and shallow and cease before the heart; 
the time difference between the cessation of heart and respiration being considerably 
longer than when the cessation occurs early in the administration. This final effect 
upon the heart is not antagonised by atropine. The heart is found to be entirely 
inexcitable, and no treatment is of any avail short of removal of the poisoned blood 
from the coronary vessels and the substitution of blood free from chloroform. It is 
conceivable that this substitution might be done by heart massage, or even by com- 
