The influence of short periods of induced acute anoxia upon pulmonary artery pressures in man.

The effects of acute anoxia on pulmonary artery blood pressure, induced by breathing low oxygen (10 per cent 02 in N2) for short periods of time, have not been reported in man. Since acute anoxia is used extensively as a cardiac test and is frequently encountered in anesthesia, changes resulting in the pulmonary artery blood pressure should be of interest. METHODS. The influence of breathing 10 per cent oxygen in nitrogen has been studied on 5 unanesthetized, conscious white males in a resting basal condition. Their age ranged from 23 to 47 years. Four of the subjects had essentially normal cardiac function wit#hout pulmonary involvement. In the fifth subject a diagnosis of aortic insufficiency had been made; his brachial artery blood pressure values were within normal limits except for a slight lowering of the diastolic pressure. In table 1 appear data on the average blood pressure values, including systolic, diastolic and mean pressures, in the brachial artery, pulmonary artery and right ventricle of the five subjects. All individual measurements were within normal limits. Right heart pressures and cardiac output were determined by using the right heart catheterization technique (1, 2, 3, 4). Arterial, pulmonary artery and right ventricle blood pressures were measured using the Hamilton manometer (5). In two cases pulmonary artery and right ventricle pressures were taken simultaneously using a double lumen catheter (6); the arterial blood was obtained from the brachial artery and the mixed venous blood from the pulmonary artery. A demand t,vpe valve ” (Army Air Forces A-16) was used to supply the compressed air or t’he 10 per cent oxygen mixture to the subject. The expired gas was collected in a calibrated Tissot spirometer. Measurements of cardiac output and blood pressures were determined first while breathing ambient air (21 per cent oxygen). Then the subjects breathed the 10 per cent oxygen mixture for a pericd of approximately 10 minutes, at the end of which the cardiac output was measured and tlhe blood pressures recorded from the brachial artery, pulmonary artery and right ventricle. A second series of control measurements, while breathing ambient air, was taken 30 minutes after the end of the period of low oxygen breathing. RESULTS. The average data obtained on the 5 subjects appear in table 1.