550 TRANSACTIONS OF SECTION I. 
Professor Waller considered that the fear of chloroform is excessive at the 
present day, but that the danger is very small if not more than 2 per cent. 
is administered. Idiosyncrasy is of some importance, but most cases of acci- 
dents arise from the giving of too much chloroform, and not from the use of 
too little. He demonstrated a portable chloroform apparatus which admirably 
fulfils the conditions desired. 
(i) Remarks by Dr. E. H. Empuey. 
The employment of the regulating inhaler is certainly a progressive step in 
the administration of chloroform. Anesthesia so induced is not attended by the 
great nervous excitation which so frequently accompanies the administration of 
chloroform by the drop method. This with the attendant exaggeration of 
respiratory intake, so raising the tension of the chloroform in the arterial blood 
for the time, constitutes an important contributing factor to the causation of 
primary syncope. Moreover, the uniformity of the resulting anesthesia by 
the regulating inhaler is quite remarkable. It is free from the oscillations in 
depth of narcosis so often observed in the drop method. 
Yet it has not been adopted in Melbourne. This appears to be due to the 
frequent necessity of transgressing the 2 per cent. boundary line of safety and 
of employing 2'5 or 3 per cent. concentration to induce anesthesia in reasonable 
time ; also because in the light degree of narcosis maintained, depressor reflexes 
appear to occur much more readily than in the deeper narcosis of the older 
method; but more especially has it been abandoned on the grounds of the 
toxicity of chloroform, however administered. Professor Waller has stated 
that the relative pharmacological potency of chloroform and ether is as 10 to 1. 
(I have found that 2°2 per cent. chloroform vapour is nine times as depressing 
to the myocardium as is 19°1 per cent. ether, and 40 times as depressing as is 
10 per cent. ether.) This is the relative toxicity, and the actual reason for the 
abandonment of chloroform. More especially is this the case since the adoption 
of the method of mixed ether narcosis, that is, the preliminary use of morphine 
and other alkaloids. One practically never hears of reflex, or the other form 
of syncope, in mixed ether narcosis. 
I cannot recall statistics of mortality from chloroform syncope, but I think 
Leonard Hill found, some years ago, that it represented about 90 per cent. of 
the total mortality. I have several experimental records of this form of death 
from chloroform. I find the mechanism of chloroform syncope to be the com- 
bined exaltation of the cardio-inhibitory and arterio-dilator nervous mechanisms 
—the heart is arrested and the arteries dilated. Whether the heart will free 
itself from the inhibition depends upon the degree of responsivity remaining in 
the heart when the inhibition occurred; also probably upon the extent of the 
compensatory rise of venous blood-pressure. If the vagus terminals give out 
early the heart frees itself. Venous pressure always rises in syncope. In 
chloroform syncope the rise is proportional to the degree of general intoxication. 
A high venous pressure in the cavities of the right side of the heart and in the 
great veins adjacent seems to exert a stimulus towards the restoration of the 
heart’s rhythm. Artificial respiration appears to exert a similar stimulus, it 
also exerts a stimulus towards restarting the respiratory rhythm. The rise of 
venous pressure in the right heart cavities may be augmented by gravity—that 
is, by turning the patient so that the head is on the fioor and the feet up, and 
by aspirating the splanchnic bed in doing artificial respiration. 
Deaths from excessive intoxication by chloroform, apart from cardiac inhibi- 
tion—that is, deaths from general paralysis of the cardio-vascular musculature 
and depression of the nervous mechanism of the circulation—must be very rare. 
Such cases are thought to occur during the course of anesthesia—that is, after 
the more dangerous period of induction. In most instances the respiration fails 
first, and then any further accession to the tension of chloroform in the blood is 
arrested. Artificial respiration then suffices to restore the blood-pressure. When 
such deaths do appear to occur the final stroke is probably always cardiac 
inhibition. The excitability of the vagi, which had become depressed by the 
chloroform after the initial period of excitation, is again exalted by the bulbar 
anemia consequent upon the low blood-pressure. It is extremely difficult to 
