The carbon dioxide content of blood and alveolar air in obstructed expiration

Abstract

In the course of a study of the effects of respiration on the circulation and more especially the modification of these effects in asthma and emphysema, we noted (1) low pulse pressure in those cases uncomplicated by atherosclerosis, probably due to a diminished systolic volume; (2) the loud pulmonic second sound pointing towards increased resistance in the lesser circulation; (3) polycythemia, possibly a teleologic phenomenon designed to compensate for a lessened minute volume output from the left ventricle; (4) enlarged veins in the neck and cyanosis suggesting a certain amount of venous stasis. These observations led us to believe that there was considerable circulatory disturbance in conditions associated with obstructed expiration.

Due to the lack of adequate clinical material, we decided to study this subject in the experimental animal.

Dogs were used. A saturated solution of chloretone and morphine was employed for inducing anesthesia. A T-tube was inserted into the trachea. (There was no increase in the dead space.) The CO2 in the blood was determined by the method of Barcroft and Haldane; that in the alveolar air according to Henderson's method. (Inspiratory samples were taken.) The minute volume was determined by means of a Dreser tube for collecting expired air. We first did a series of controls and found that the C02 content of the blood and of the alveolar air varied with the minute volume, thus corroborating the work of Haldane and Priestley. Anesthesia produced effects varying only with the ventilation. In another series we inserted a valve which worked only one way and produced obstruction to expiration for varying lengths of time.