Blood loss in vaginal surgery.

Dog 1 developed ventricular asystole and apnoea thus followed a cardiac death. In the remaining 5 dogs apnoea preceded cardiac standstill. The blood gas values in all 6 animals made it unlikely that failure of the respiratory centre occurred because of primary pulmonary pathology. In animals 5, 8 and 9, cardiac output and related haemodynamic data suggest that apnoea resulted from inadequate blood flow to the vital centres. In animals 3 and 11, cardiac output and mean systemic arterial pressure were adequate: thus, by exclusion, apnoea was due to toxicity of the central nervous system. Death from oxygen toxicity was, therefore, cardiac in origin in 4 of the dogs, and central nervous system in origin in the remaining 2. Histological examination of the lungs revealed no remarkable changes. Much of the gross pulmonary pathological changes reported by previous workers may reflect mainly terminal or postmortem change. In the spontaneously breathing animal, changes in respiratory pattern indicating central nervous system involvement occur early, while changes in Pao., A-a O2 gradient and pulmonary shunt ratio are relatively late manifestations of oxygen toxicity. Death from oxygen toxicity, in the pressure range 1-2.5 ATA, seems more easily attributable to progressive disturbance of the central nervous system and of the myocardium than to primary pulmonary pathological changes.