76 



Scientific Proceedings (72). 



Yet we all know that most emphysematous patients show 

 rather well marked cyanosis without any evidence of hepatic 

 congestion, edema, etc. He concluded from his studies "that the 

 real difficulty of ventilation in asthma and emphysema lies in a 

 distention of the infundibula and this fails to allow an equal dif- 

 fusion of C0 2 throughout the alveolar air." Yet he adds, "when 

 we consider that an infundibulum has a diameter of not more than 



1 mm. and that in hyperdistention the infundibula cannot be 

 enlarged more than 2 to 3 mm., it seems astonishing that when 



2 liters of air distributed in such small chambers are diluted 

 with the addition of 3.5 liters the diffusion of gases is not uniform 

 throughout the entire mass." To which we would add that 

 one must remember that C0 2 has a coefficient of diffusion twenty 

 times that of oxygen. 



In view of these facts, and our own studies, we are inclined to 

 believe that the circulatory factor, contrary to Hoover, is the 

 important one. The cough in asthmatics, with its rises in intra- 

 bronchial pressure, would certainly embarrass the lesser circulation, 

 and the voluntary attempts to aid expiration would act in the same 

 manner. There is here a long-drawn-out expiration with a rise 

 in intrabronchial pressure, as a result of which resistance to the 

 flow through the pulmonary capillaries is great. During this 

 phase there is little opportunity for gaseous exchange. Then there 

 follows only a short inspiration during which the C0 2 is released 

 as the blood is taken up by the depleted pulmonary sponge. The 

 absence of a permanent fall in blood pressure in our animal may be 

 explained by a compensatory vasomotor contraction of the sys- 

 temic arterioles, and the rise in intra-abdominal pressure. From 

 our studies we therefore conclude that the high CO2 content of the 

 alveolar air in asthma, and obstructed expiration in general is 

 due to a circulatory cause. The rise in intrabronchial pressure 

 during the long-drawn-out expiration interferes with the free flow 

 through the pulmonary circuit, thus causing a damming back of the 

 blood to the venous side. There is a consequent accumulation of 

 C0 2 in the blood with the liberation of the alveolar air C0 2 chiefly 

 during the short inspiratory phase of asthmatic breathing. 1 



1 We might add that a pathologic study was made of the lungs of our valve dogs 

 by Dr. Alexander Fraser, of the Department of Pathology of University and Bellevue 



