supplied with venous blood becomes dyspnœic, although its lungs and body are receiving pure arterial blood. There is a regular sequence in the phenomena of dyspnœa leading up to the final stage termed “asphyxia.” If the trachea be suddenly blocked, so that no air can pass, the respiratory movements at once become deeper and more rapid. This condition is termed “hyperpnœa.” In a comparatively few seconds the system appears, as it were, to find out that inspiration is not needed. Expiratory efforts begin to preponderate. They increase in violence. All accessory muscles are brought into play. The cry for air is heard even by muscles which cannot help. Muscles of the limbs contract, although their contraction has no effect upon the capacity of the chest. Every expiratory effort is accompanied by convulsions of a flexor type. At the end of two minutes there is usually a sudden change. Attempts at expiration cease. Slow, deep, infrequent inspirations take their place, accompanied by convulsions of extensor muscles. Pupils are widely dilated, mouth open, head thrown back. The subject is absolutely insensitive to every kind of stimulus. The pulse shows a high arterial tension. The beating of the heart is slow and strong. In about four minutes from the time at which the windpipe was blocked respiratory movements cease. The arterial tension falls. The heart’s action grows rapidly weaker, although for two or three minutes longer it may still continue to flicker. Recovery is possible until it finally gives up. After death the right side of the heart is found gorged with blood, the left side empty, showing that the heart had been unable to force the blood through the capillaries of the lungs.