Hemodynamic studies in chronic uremia.

SUMMARY Hemodynamic functions and blood volume were observed in patients with chronic uremia. Thirty-one patients had clinical features of circulatory congestion and 37 did not. The degree of anemia and acidosis was comparable in both groups. However, cre-atinine clearance was significantly lower in patients with circulatory congestion. Both groups of patients had greater blood pressure, heart rate, plasma volume, and total peripheral resistance than normal. Resting cardiac output was abnormally decreased in 19% of the patients with circulatory congestion and in 14% of patients without features of circulatory congestion. There was no correlation between blood volume and blood pressure. Intravenous digitalization of seven of the patients with circulatory congestion produced clinical and hemodynamic improvement in only two. Hemodialysis effected an increase in cardiac output and a decrease in total peripheral resistance in six patients with congestion. In seven patients without circulatory congestion after dialysis there was a faIl in plasma and blood volume, associated with a slight decrease in cardiac output. It is suggested that congestion of the circulation in chronic uremia results from a variety of hemodynamic, myocardial, and metabolic alterations, rather than from any single abnormality. SYMPTOMS AND SIGNS of circulatory congestion including dyspnea, orthopnea, engorgement of neck veins, pulmonary basilar rales, and gallop rhythm are not unusual in Hemodialysis Blood volume severe renal insufficiency. In 1944 LaDuel observed a group of patients with acute glo-merulonephritis with symptoms and signs of circulatory congestion and suggested that right heart failure was the underlying disturbance. Subsequently, Davies2 reported normal cardiac output in acute glomerulonephritis complicated by circulatory congestion, and Eisenberg3 found that the blood volume was increased chiefly because of plasma volume expansion. This finding was in contrast to the increase in both red cell mass and plasma volume found in heart failure due to other causes.4 5 On reviewing an extensive series of cases of acute glomerulonephritis, Peters6 maintained that circulatory congestion was caused by cardiac decompensation. However, studies by De Fazio and associates7 revealed that in acute, oliguric glomerulonephritis cardiac output is frequently above normal, although the left ventricular filling pressure is elevated. Eichna and co-workers8 9 have emphasized that circulatory congestion associated with 87 acute glomerulonephritis does not imply myo-cardial failure but, rather, can be attributed to the water and salt retention caused by the renal disease. Interpretation of the underlying mechanism of circulatory congestion in chronic renal in-sufficiency is complicated by the fact that most patients …