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disorganised, when the distended stomach presses on the diaphragm, and inspiratory movements are slightly impeded, and the lung-circulation embarrassed, the feeble heart encounters a struggle for which it has no resources, and an apnoeal paroxysm is the result. I believe, indeed, that flatulency, acting in the way suggested, is beyond all others the most frequent exciting cause of cardiac apnoea in cases of cardiac disorganisation; and although, from being a cause temporary in its nature and removable, it is not necessarily a fatal excitant, yet occasionally it is even fatal when the degeneration has reduced the cardiac power to its minimum.

There are again cases, as we have seen, in which cardiac apnoea may occur without any predisposing organic change; but in these instances some poison has been introduced into the blood, and has acted so suddenly and powerfully that the predisposition is not requisite, the exciting cause being immediately brought into action with all-sufficient potency. Poisons which produce these effects act one and all on the same general plan; that is to say, they arrest the action of the heart primarily through the blood. They include a large group of poisons: some of the alkaloids, as strychnine, brucine, and nicotina: the ammonias, the cyanides, and certain of the volatile poisons, such as nitrite of amyl and amylene.

Turning now to the consideration of the symptoms presented during an attack of acute cardiac apnœa, we find them reducible, physiologically, to one leading state-spasm of the muscular system, with its

attendant details of pain and reduction of temperature. The recent progress of physiological science has led us closely to a correct understanding of the reason why this spasm should occur. It has shown us that this spasmodic state need have no organic lesion of the nervous centres for its cause, but that it is a product of a derangement existing between blood and muscle. Let me explain this as tersely as I can.

For the sustainment of the perfect balance of the muscular force, three conditions are absolutely required. First, it is necessary that the muscle should have a full supply of blood. Secondly, it is requisite that the blood thus supplied should

possess the power of giving to the muscular structure a permanent temperature, which must not vary materially from 98°. Thirdly, it is essential that the nervous connection betwixt the muscle and nerve-centre be everywhere intact. We can prove these positions by a variety of experiments.

We lay bare the heart of an animal and keep up artificial respiration. If the experiment be neatly done, and the animal operated on be kept gently anæsthetised, the heart may be observed, if the pericardium be unopened, beating rhythmically and with sufficient power to sustain both the pulmonic and systemic circuits for a long period of time. We watch the animal thus placed, and we observe that so long as the circulation is steady there is no convulsion, no spasm. But we interfere with this steady circuit of blood; we compress the great aorta,

for instance, at its origin, and cut off the supply of blood in this way from the systemic circulation; and the results are, first, tremulousness, then convulsion, and finally tonic spasm.

Or, in lieu of mechanically arresting the blood through the aorta, we check it on the venous side, by compressing the superior and inferior cavæ; and now we see the heart cease action and its left side close in permanent systole: upon this the muscles of the systemic circuit become rapidly convulsed, and, as the blood which they retained is applied, spasmodically contracted.

If again, instead of mechanically obstructing the flow of blood, we inject through the pericardium upon the heart a stream of water reduced in temperature nearly to freezing point, we observe the heart make a rigid contraction; whereupon, the central organ ceasing its play and the muscles generally losing their vascular supply, there follow general tremor, convulsion, and spasm.

Once more, we modify the operation by injecting into the heart, through the external jugular, some one of the poisons I have named-ammonia, tobacco, hydrocyanic acid, strychnine; and, as the poison finds its way into the coronary system, we see first in the heart disturbance of action, palpitation, spasmodic contraction, cessation of motion, and afterwards a continuance of these changes carried on to the muscular system at large.

We may vary these experiments in a variety of ways. Instead of laying bare the heart, we may stop

its action by introducing through the thoracic wall a finely pointed pair of forceps, and by compressing the vessels at the base by one firm grip; the results will be the same-general muscular tremor, convulsion, spasm, cessation of motion in spasm.

Or we may reduce the temperature of the blood by making the animal breathe an air intensely chilled; the results will be identical in fact, although the time in which such results will be presented may be considerably lengthened.

Lastly, we may modify this line of research by transferring it from the muscular system at large to some particular muscle. We may inject into the structure of such muscle one or other of the agents to which I have referred, or we may reduce the temperature, or we may cut off its blood-supply; and we shall find as results tremor, convulsion, contraction, more or less persistent.

Between the effects produced by all the agents just described and those effects which are excited on muscle by galvanism, there is moreover a great similarity there are the same contractions and the same pain; and not only so, but symptoms closely analogous to those of cardiac apnoea may be produced by directing a powerful intermittent shock through the chest from the sternum to the lower division of the vertebral column.

The lessons to be gathered from these observations are very important in regard to cardiac apnoea. They show that, inasmuch as the arrest of blood to a muscle produces spasm, so cardiac apnœa invariably

is excited by any cause that shall rob the heart of the power to feed itself by its coronary vessels, or by any cause that shall so modify the blood as to render it incompetent on entering the coronary system to support the muscle. They show further that the cause of the spasmodic constriction of the chest is the same; that, the heart failing in power, and failing therefore to supply the general muscular system, the involuntary muscles quickly use up their received blood and take on permanent contraction. They explain also why in extreme cases, for the same reasons, the voluntary muscles become similarly implicated.

The question may naturally be asked, why, in all cases of sudden arrest of the heart, the whole voluntary system of muscles is not equally affected with the involuntary during the paroxysm? The answer to this question is exceedingly simple. In all cases of the kind, the arterial system is left charged with blood, and the muscles therefore are, for a certain time, prepared to withstand the arrest. The involuntary muscles, however, go on acting independently and, consequently, use up their blood-supply, and having used it up assume the contractile state; but the voluntary muscles, having no necessity for action, undergo less rapid change and remain longer in a state of relaxation, feeding passively, as it were, on the supply of blood which they had previously received. We see this same fact beautifully illustrated in death from hæmorrhage; as the current of blood is fatally flowing, the heart first ceases, then the muscles of respiration; lastly the voluntary muscles

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