Abstract

Standard hemodialysis (dialysate temperature >or=37 degrees C) induces an increase in body temperature capable of eliciting circulatory adjustments dictated by the maintenance of thermal homeostasis. These adjustments oppose, and can overcome, those elicited by the hypovolemia caused by the ultrafiltration process, and thus predispose patients to develop hypotensive crises during the treatment. Hemodynamic studies in hypotension-prone patients treated with standard hemodialysis showed that during the hypotensive crisis the peripheral vascular resistances decrease, while the stroke volume decreases proportionally more than the blood volume, suggesting cardiac underfilling due to blood volume redistribution. On the other hand, removal of the body heat surplus by cool dialysis helped the same patients to sustain their peripheral vasoconstriction and cardiac filling. To prevent the increase in body temperature, dialysate temperature should be regulated in such a way as to remove through the dialyzer the heat surplus accumulated in the body as a result of the ultrafiltration process. The amount of heat removal should be tailored to each patient because there are wide interindividual and intraindividual variations in baseline body temperature and ultrafiltration requirements. This can be accomplished by the use of a device that can adjust the dialysate temperature automatically in order to keep the body temperature of the patient unchanged (isothermic hemodialysis). Isothermic hemodialysis reduced from 50% to 25% the incidence of treatments complicated by episodes of symptomatic hypotension in a large randomized clinical trial involving 95 high-risk patients. The thermoregulated treatment results in better patient tolerance because the cold stress inherent in this procedure is lower than that inflicted by the use of a fixed low temperature as was done in the past. Overall, the available evidence supports the Gotch hypothesis that the increase in body temperature during hemodialysis is due to the ultrafiltration process eliciting peripheral vasoconstriction and heat accumulation in the body. Heat accumulation brings into play the thermal homeostatic mechanisms endangering cardiovascular tolerance to ultrafiltration.

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