EDEMA 185 



tenance of a difference in potential, or a gradient in osmotic pressura A 

 gradient has been attributed by Starling to the blood proteins. He 

 assumes that a difference in osmotic pressure between the blood and tissue 

 fluids, due to the fact that the capillary walls are impermeable to the 

 blood proteins, balances a difference in hydrostatic pressure, so that the 

 direction of the movement of fluid depends on disturbances in this balance. 

 That is to say, under ordinary circumstances the hydrostatic pressure in 

 the capillaries is greater than that outside 6f the capillaries by an amount 

 corresponding to the difference in osmotic pressure ; the osmotic pressure 

 of the blood plasma being also greater than that of the tissue fluids. A 

 continued disturbance of the equilibrium, leading to the flow of fluid from 

 the blood vessels to the tissues, would depend on the outpouring of mole- 

 cules from the tissue cells, though the nature of the molecules responsible 

 for such disturbances has not yet been determined. 



If edema is dependent on osmotic phenomena there must be a source of 

 energy sufficient to disturb the lymph balance so that the volume of the 

 tissues is increased beyond normal limits. Such a source, if it exists, may 

 be looked for in the metabolism of the cell. This source, according to 

 Loeb, is the altered metabolism due to diminution of the oxygen supply. 

 Araki had already shown that a diminution in the oxygen supply resulted 

 in the formation of lactic acid by the tissues. Loeb showed that this 

 condition was accompanied by swelling, which he attributed to increased 

 osmotic pressure. 



There is known to be production of lactic acid in the tissues in at 

 least some cases of heart failure. Peabody, Meyer, and DuBois, and Pea- 

 body, Wentworth, and Barker have shown, however, that there is a normal 

 or increased consumption of oxygen in severe cases of heart failure, and 

 that there is a normal respiratory quotient, indicating that there is no 

 profound change in intermediary metabolism. In addition, the studies 

 of Lundsgaard show that though there is increase in the degree of oxygen 

 unsaturation of the venous blood in heart failure, edema may persist in 

 spite of the fact that the venous blood contains approximately one-half 

 of the oxygen content of the arterial blood ; that is to say, even when the 

 degree of oxygen unsaturation in the venous blood is within normal limits. 

 It may not be correct, therefore, to speak of lack of available oxygen in 

 heart disease, though there may be some inability to utilize oxygen prop- 

 erly, and a lowering of the maximal oxygen tension in the tissues. The 

 occurrence of polycythemia in cases of chronic heart failure suggests 

 disturbance in oxygen supply to the tissues. 



A further possible source of disturbance to osmotic equilibrium, 

 especially in heart disease, depends on alteration in the heterogeneous 

 acid-base equilibrium, due to the increase of free carbonic acid and bicar- 

 bonates in the tissues and in the blood, and to the decrease in oxygen in 

 combination with hemoglobin. Various electrolytes are involved in this 



