Abstract
It is well known that interference with the flow in a vein will cause a rise in venous pressure within that vessel. Villaret, Saint-Girons and Justin-Besançon, 1 and others, have observed that mediastinal tumor or aortic aneurysm may lead to an elevation in venous pressure in one arm if its veins are obstructed. Runge 2 found a higher pressure in the saphenous vein than in the arm veins during pregnancy; a difference which disappeared after delivery. A similar difference was found by Villaret, Saint-Girons and Justin-Besançon 1 in cases of ascites or abdominal tumor. Brams, Katz and Kohn 3 noted a marked rise in pressure in the iliac veins with little or no change in the superior vena cava in experimentally induced abdominal distention in animals. Brams and Katz 4 observed that slowly increased compression of a vein in animals produced a gradual rise in venous pressure up to a certain level, after which little or no further change occurred.
In this investigation the effect of experimental compression was studied in man to determine: (a) whether or not the results are the same in persons with normal and failing hearts; and (b) what relation the maximum rise in venous pressure bore to the systolic and diastolic arterial blood pressures.
Six Subjects with normal hearts and normal blood pressures were selected as controls. Two patients with mediastinal tumor and 18 with varying degrees of cardiac failure comprised the group of abnormals. Cardiac failure in the latter was due to rheumatic fever, hypertension, cor pulmonale or arteriosclerosis. Venous pressure was measured by the direct method, using a hollow needle inserted into the median basilic vein after the patient rested under basal conditions for at least 15 minutes as described by Eyster. The needle was connected to a suitable mercury manometer since, in preliminary trials, it was found that compression of the vein produced a rise in venous pressure too great to be registered by an ordinary water manometer. The mercury manometer was found to be sufficiently sensitive for the needs of the present research.
Summary. 1. A series of 26 observations were made in man to study the effect of gradually increased compression on the venous pressure below the point of compression. This group consisted of 6 normal persons serving as controls and an abnormal group of 2 with mediastinal tumor and 18 with cardiac failure. 2. Venous pressure gradually rose as compression was increased, until the latter reached the level of the systolic arterial pressure. At that point or on slightly further compression the venous pressure fell from 2 to 80 mm. of mercury and remained unchanged at that lower level regardless of the degree of further compression. 3. The progressive rise and the drop at the systolic pressure level were found in all the groups of patients regardless of the actual level of the systolic blood pressure or the condition of the heart. No change in the slope of the venous pressure rise was seen when the compression force approximated the diastolic blood pressure.
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