Effects of cooler temperature dialysate on hemodynamic stability in “problem” dialysis patients

Effects of cooler temperature dialysate on hemodynamic stability in “problem” dialysis patients. Symptomatic hypotension is a common and disabling complication of hemodialysis treatments. The incidence of symptomatic hypotensive episodes is particularly high in patients who have normal or low blood pressure at the initiation of dialysis and in patients who have large interdialytic weight gains. The aim of this study was to determine whether cooling the dialysate temperature from 37°C to 35°C improved tolerance to dialysis in a group of 12 of these “problem” patients. A double-blinded protocol was performed in six hypotension-prone and six large weight gainers who were subjected to two identical hemodialyses except for the dialysate temperature of 37°C or 35°C. Changes in biochemical parameters and weight were comparable during the two maneuvers. Recumbent blood pressure declined significantly (P < 0.01) during 37°C dialysis but not 35°C dialysis; blood pressure was significantly lower at 1, 2, and 3 hours of 37°C dialysis compared to 35°C dialysis (P < 0.05). Further, both supine and upright blood pressure was significantly lower following 37°C dialysis (P < 0.02). This lower blood pressure was present in both subgroups of patients. All 18 episodes of symptomatic hypotension noted during the study occurred during 37°C dialysis. A significantly greater increase in peripheral vascular resistance (calf blood flow was measured directly by venous occlusion plethysmography) occurred upon exposure to the 35°C dialysate in both subgroups of patients (P < 0.01); supine and upright post-dialysis plasma norepinephrine values were also significantly greater (P < 0.001) after 35° dialysis. Thus, 35°C dialysate significantly improves the hemodynamic tolerance to hemodialysis in hypotension-prone and large weight gainer patient groups and also reduces the incidence of symptomatic hypotension. This improvement is partly the result of a greater increase in peripheral vascular resistance, possibly mediated via the efferent sympathetic nervous system