Abstract
Eyster, 1 , 4 Villaret, Girons, Bosveil, 2 Clark, 3 Eyster and Middle-ton, 5 and Lemierre and Bernard 6 among others have noted the elevation of venous pressure in congestive heart failure, which they report is of serious prognostic significance when it persists. Eyster 1 , 4 concluded that an elevated venous pressure may point to impending cardiac decompensation, and that a sustained rise of general venous pressure is met only in this condition. More recent work has shown that other factors affect the level of venous pressure in man. Brandt 7 points out that the arteriolar pressure, the tonus of the veins, the visceral pressure in the abdomen and, most important of all, the circulating blood volume, also affect venous pressure. He found occasional coexistence of congestive heart failure and normal venous pressure, particularly in patients with auricular fibrillation or emphysema. Kroetz 8 believes that venous pressure may be affected by capillary and arterial pressure and by the venopressor mechanism described by Henderson. 9 Fleisch 10 suggests the possibility of a venomotor center in the brain. Brandt and Katz 11 found venous and arterial hypertension to coexist in the same patient, apparently due to an increased venous tonus. Arnoldi, 12 and Rotky and Klein 13 found many cases of essential hypertension without evidence of cardiac failure with elevated venous pressure. Connet 14 found that merely slowing the normal heart may elevate venous pressure. Von Gonczy and Kiss 15 frequently found the venous pressure elevated during the menopause.
This study was undertaken to investigate further the correlation of the various factors controlling venous pressure. Dogs were used, under morphine and sodium barbital anesthesia.
Get full access to this article
View all access options for this article.