272 Z. Fejfar 



reflects a temporary improvement of the impaired water 

 balance. It runs its course within a few hours. It was there- 

 fore possible to follow the sequence of events and investigate 

 the relationship between central venous pressure, systemic 

 and renal haemodynamic changes, and renal function. 



Cardiac output, right auricular pressure, water content of 

 plasma, and renal function (renal blood flow, glomerular 

 filtration rate and excretion of electrolytes) were studied 

 from the early hours of the afternoon until the following 

 morning in ten normal subjects and 25 patients with heart 

 disease of different origin, 19 of them having congestive failure 

 of varying degree (Brod and Fejfar, 1949, 1950; Fejfar and 

 Brod, 1950a,b,d). 



Cardiac output was measured by a direct Fick method and 

 right auricular pressure by a water manometer attached to 

 the cardiac catheter ; changes of water content in plasma were 

 assessed from the percentage change in plasma proteins, 

 haematocrit and the disappearance curve of Evans blue. 

 Renal plasma flow was estimated by the clearance of PAH 

 (j9-aminohippuric acid), glomerular filtration rate by the clear- 

 ance of inulin, and chlorides by the Van Slyke and Hiller 

 (1947) modification of Sendroy's method. 



A nocturnal diuresis was observed in 11 patients with con- 

 gestive failure. In none of them was it preceded by a decrease 

 in right auricular pressure. On the other hand the increase in 

 urine output at night started in all these patients with an 

 elevation in renal blood flow. The decrease in urine flow at 

 night occurred in seven decompensated cardiacs; in all of 

 them it was associated with a diminution in renal blood flow 

 (Fig. 1). The increase in renal blood flow was not related to a 

 similar change in cardiac output, which increased simultane- 

 ously in only half of the investigated subjects. 



There is thus evidence in dynamic observations that the 

 increase in central venous pressure in congestive failure is not 

 the primary cause of cardiac oedema, the main factor being 

 impaired renal function. 



A low renal blood flow with a diminished glomerular 



