SUMMARY Effects of hemodialysis on extracellular fluid volume distribution, left ventricular volumes, and cardiac output were determined In patients with end-stage renal disease (n = 19). Distribution of extracellular fluid loss from hemodialysis differed widely among patients, so that weight change correlated weakly with contraction of total blood volume (index of determination 29%, p < 0.05). End-diastolic volume (EDV) decreased from 150 ± 49 ml (mean ± SD) to 118 ± 42 ml, p < 0.001; stroke volume (SV) decreased from 108 ± 36 to 86 ± 33 ml (p < 0.001) without change in ejection fraction (from 0.73 ± 0.09 to 0.74 ± 0.11).A significant correlation was found between total blood volume (TBV) and EDV before (r = 0.66, p < 0.005) and after dialysis (r = 0.61, p < 0.01). The correlation between TBV and SV was highly significant before (r = 0.78, p < 0.001) and after dialysis (r = 0.66, p < 0.005), but there was no correlation between change in TBV and change in EDV or in SV. The ratio of EDV to TBV (EDV/TBV X 100) was reduced significantly from 3.49 ± 0.92 to 3.06 ± 0.97, p < 0.001). There results suggest that, although intravascular volume was the major determinant of cardiac output in dialyzed patients, the postdialysis reduction in cardiac output might be related more to the relocation of blood volume than to the absolute degree of blood volume contraction. 8 These include determination of the relative participation from both intravascular and interstitial compartments to the total ECF loss during hemodialysis as well as the effect of hypovolemia on cardiac filling and possible influence of changed preload on cardiac output.

SUMMARY Blood pressure response to hemodialysis was investigated in IS patients with end-stage kidney disease; mean arterial pressure was unchanged in fire (Group 1) and reduced 10 mm Hg in 10 (Group 2). The two groups did not differ significantly with regard to either biochemical rallies or hemodynamic indices before dialysis, and both sustained comparable reduction in body weight, total blood volume, and cardiac output following dialysis. Heart rate remained unchanged In both. The only significant difference between the two was the response of total peripheral resistance (TPR) to fluid depletion. TPR rose adequately in Group 1 but was unchanged in Group 2 (7.5 ± 2.2 (SE) VS 0.7 ± 1.1 units, p < 0.02S) despite equal fall in cardiac output in both (881 ± 212 vs 890 ± 173 ral/m, p > 0.10). Thus, differences in arterial pressure response to fluid loss by hemodialysis could be due to impaired autonomic control of resistance vessels; this abnormality might not be revealed by tests of baroreceptor activity that depend only on heart rate responses to blood pressure variations. UREMIC patients frequently present difficulties in management during hemodialysis, particularly because of severe hypotension in some patients. This has been related either to the magnitude of fluid loss or to the autonomic neuropathy that has been reported in renal insufficiency.