One hundred and twenty experiments to ascertain the part played by vagus inhibition in chloroform poisoning. In 54 eases yagus inhibition embarrassed the circulation to a inore or less dan gerous extent, and in 33 experiments was the immediate cause of death. To sum up: 1. A heart which has been poisoned by inhalations of chloroform of a strength of 2 per cent. and upward can always be permanently inhibited by stimulation of the vagi with the faradic current when the blood-pressure has fallen to about 40 to 50 millimetres of mercury pressure. 2. Chloroform raises the excitability of the vagus mechanism, particularly in the early part of the ad ministration. 3. The increased excita bility of the vagus mechanism is due to the action of chloroform on the vag,us centres, and the inhibitory action is more intense from being exercised upon a heart whose spontaneous excitability is diminished by the action of the chloro form upon it. 4. Chloroform adminis tered to morphinized dogs in air contain ing,. not more than 1.5 per cent. of the vapor, after a period of mild excitation slowly depresses vagus excitability. The excitability may again be raised with more or less readiness according to the duration of the administration and the endurance of the vagi by increasing the percentage strength of the chloroform or by asphyxia. 5. Vagus inhibition is, in clogs, the great factor in the causa tion of sudden death from chloroform. 6. Dangerous inhibition is liable to occur whenever the strength of chloroform in the air inhaled rises above 2 per cent. E. li. Embley (13rit. Med. Jour., April 12, 1902).
Raul has traced chloroform deaths to reflex paralys.is of the tongue and neigh boring parts, while Vallas considers pri mary syncope, due to laryngeal reflex, as one of the usual modes of death when chloroform is employed.
We have, in the production of asthma through intranasal pressure, distinct col lateral evidence of the nervous relation. ship existing between the upper and lower respiratory tract, and, in the re current branch of the pneurnogastric, an evident indirect association between the larynx and the heart, to say nothing of the sympathetic system, which plays the most important role in all reflex mani festations.
Symptoms of Collapse.—According to Guthrie, the symptoms are alike in all cases, and. are as follow: Sudden and complete blanching of the face takes place, leaving it of a ghastly-gray hue. The term "pallor" conveys no idea of the actual appearance. The eyelids fall open, the eyeballs are fixed in the up ward position, with pupils fully dilated as under extreme atropinism. At the same time the cornea becomes glazed and sticky, giving an appearance which, once seen, is never forgotten. It can only be described in a somewhat fanciful manner by saying that the light seems to fade from the eye as does the color from the cheek and lips. Probably it is
due to flaccidity of the cornea from de crease of intra-ocular tension, noticed by Dubois (Soc. de Biologie, '84). It is the undoubted look of death.
The appearance of a person in a dead faint, or just after a severe accident, is no more than the shade of that which obtains in cases of chloroform collapse.
The pulse and cardiac impulse are at these times no longer to be felt. Respira 12071 C077???207ay ceases at the moment when the blanching and stoppage of the pulse occur, but at times a few feeble and irregular inspiratory gasps are subse quently drawn. The patient is, to all appearances, dead. Whether the heart actually ceases to beat at such times will probably never be ascertained, for the moments are too valuable to be spent in delicate investigations on this point. Neither is it possible to affirm from clin ical observation that the heart becomes dilated, as in the experiments of Mac William and Johnson on animali. Time cannot be wasted in mapping out the area of the heart's dullness in a patient who is in imminent danger of death.
In some cases lividity, accompanied by turgescence of the veins of neck and face, immediately precedes the blanch ing and look of death, and is coincident with the stoppage of respiration. Pos sibly dilatation of the heart has actually taken place, and the condition is that of the true cardiac syncope described by Snow.
It might be objected that, were dilata tion present, the cyanosis should con tinue, and not give place to pallor; but, possibly', as the heart fails regurgitation tak-es place into the inferior cava, and allows the blood from the distended veins of neck and head to enter the right heart.
In children, cyanosis, except where actual mechanical asphyxia has been pro duced, is less apparent than pallor. -Un der treatment, children almost invariably recover from these alarming conditions, whereas in adults the reverse is unfort unately the case.
Athetosis of the fingers is a prernoni lh tory sign of impending asphyxia in chloroform nareosis. Koblank (Centralb. f. Cynilk., No. 1, 1900).
As a rule, the preliminary signs of collapse are sufficiently well marked, and if observed in time many a catastrophe may be averted.
These signs are circulatory and respi ratory.
The circulatory sign is the presence of increasing pallor, not amounting to absolute blanching.
Failure of respiration is marked by a peculiar type of breathing, in which ex piration is extremely short and inefficient, while inspiration is sudden, forcible, and gasping, often accompanied by falling of the lower jaw, and spasmodic clonic con traction of the chin-depressers and mus cles of the neck. The inspiratory gasps are irregular and broken, and occur with increasing slowness until the condition of sudden collapse ensues.