The Mechanism in the Development of Pulmonary Edema.

Abstract

In a paper recently published, Johnson 1 gives an account of 2 sets of experiments in which it was possible to prevent the development of pulmonary edema which otherwise would have occurred following the injection of adrenalin and caffein in rabbits. The first method consisted in the opening of the chest wall. In experiments independently carried out by both the writer in association with Dr. M. S. Fleisher, and by Dr. Johnson, the occurrence of pulmonary edema was prevented by this procedure. The second method consisted in the insufflation of air into the lung. Dr. Johnson attributes the prevention of pulmonary edema in these cases to increased pressure exerted on the walls of the capillaries of the lung acting in the direction from the alveoli towards the pleural surface. This increased pressure on the vessels tends to compress them and to counteract the increased pressure which obtains in the lumen of the vessel which latter is caused by the obstacle to the outflow of blood from the pulmonary veins produced by the spasm of the left ventricle and contraction of the peripheral arterioles. We believe that these considerations are of significance in the analysis of pulmonary edema and that the pressure exerted on the pulmonary vessels is an important factor in edema of the lung, but we suggest a modification in the definition of the manner through which the outside pressure acting on the pulmonary vessels influences the development of edema.

We believe that in the experiments of Dr. Johnson as well as in other cases of pulmonary edema the negative pressure which develops in the pleural cavity as well as in the alveoli of the lung during the phase of inspiration tends to suck out the fluid from the vessels concomitantly with the sucking of the air from the outside into the alveoli. The more intense the inspiratory movements are, the greater the tendency to withdraw fluid from the blood, provided other conditions make such a transudation possible.