If an adequate supply of oxygen be withheld and its percentage in the blood is reduced to a certain point, the death of the animal follows in three to five minutes, accompanied by a series of phenomena commonly included under the term asphyxia. This may be divided into four stages. 1. Dyspnoea. 2. Convulsion. 3. Exhaustion. 4. Inspiratory spasm. As asphyxia is a mode of death the symptoms of which the physician can be called upon to treat, he should be able to recognize its different phases.
If the air passages be closed completely the respirations become deep, labored and rapid. The respiratory efforts are more and more energetic, and the various supplementary muscles are called into play one after the other, until gradually the second stage is reached in about one minute.
As the struggles for air become more severe, the inspiratory muscles lose their power, and the expiratory efforts become more and more marked, until finally the entire body is thrown into a general convulsion, in which the traces of a rhythm are hardly apparent. This stage of convulsion is short, the expiratory muscles becoming suddenly relaxed by exhaustion.
Then the longest stage arrives, in which the animal lies almost motionless, making some quiet inspiratory attempts. These become gradually deeper and slower, until they are nothing more than deep gasps separated by long irregular intervals.
The pupils of the eyes become widely dilated, the pulse can hardly be felt, and the animal lies apparently dead, when often, after a surprisingly long interval, one or more respiratory gasps follow, and with a gentle tremor the animal stretches itself in a kind of tonic inspiratory spasm, after which it is no longer capable of resuscitation. This last pulseless stage, to which the term asphyxia is more properly confined, is the most irregular in duration, but always the longest.
The blood of an animal which has died of asphyxia is nearly destitute of oxygen, the haemoglobin being in a much more reduced condition than is found in venous blood. The first and most obvious effect produced by the circulation of blood so deficient in oxygen is excessive stimulation of the respiratory centre, which causes the extreme and varied actions just described. In the first stage of asphyxia, the venous blood, reaching the systemic arterioles, affects their muscular walls, exciting the vaso-con-strictor mechanism, so as to cause a rapid and considerable rise in blood pressure and consequent distention of the left ventricle. The general constriction of the small arteries may be brought about by the venous blood acting as a stimulus to the cells of the medullary and spinal vasomotor centres, or more probably it acts as a direct stimulant to the muscle cells of the arterioles themselves. The centres in the medulla which govern the inhibitory fibres of the pneumogastric are also stimulated, and consequently the heart beats more slowly. The increase in arterial tension and the slow beat give rise to distention of the ventricle, which, when a certain point is reached, impedes the working of the heart, and its muscle begins to beat more and more feebly, so that in the third stage the pulse can hardly be felt. The muscular arterioles then become exhausted and relax, the blood pressure falls rapidly, and with the death of the animal it reaches the level of atmospheric pressure. Both sides of the heart and great veins are engorged with blood in the last stage of asphyxia; the cardiac muscle being exhausted, from want of oxygen, is unable to pump the blood out of the veins or empty its cavities. Owing to the force of the rigor mortis of the left ventricle, and the greater capacity of the systemic veins, the left side is found comparatively empty some time after death, and at post-mortem examination the right side alone is found over-filled.