A critical examination of dialysis-induced hypotension.

Abstract

Dialysis-induced hypotension has received considerable attention recently because of its high incidence of occurrence. Several factors have been proposed as etiologic mechanisms. They include hypovolemia, autonomic dysfunction, decreasing serum osmolality, vasodilation (or the inhibition of compensatory vasoconstriction), efficiency of diffusive solute transport, depletion of vasoactive substances and blood gas and acid-base changes. The primary determinants of blood pressure being cardiac output and total peripheral resistance, the magnitude and direction of change of these two parameters determines the blood pressure response. If the rate of ultrafiltration exceeds the rate of vascular refilling, hypovolemia results. Intracellular fluid shifts secondary to preferential solute removal from the extracellular space may compromise vascular refilling and contribute to hypovolemia. If the hypovolemia is not compensated for by increases in heart rate or stroke volume, the cardiac output falls. Autonomic dysfunction, a previous history of myocardial infarction or impaired tissue oxygenation secondary to hypoxia may limit compensatory increases in heart rate and stroke volume. Even if the cardiac output falls, if compensatory vasoconstriction is elicited, blood pressure can be maintained. The experimental evidence suggests that the diffusive aspect of dialysis therapy plays an important role in inhibiting compensatory vasoconstriction. Such inhibition is not observed with hemofiltration, a therapy based on convective rather than diffusive solute removal. While autonomic dysfunction and the diffusive removal of vasoactive substances may play a role in inhibiting the vasoconstrictive response, the use of acetate as a buffer source and the decreasing serum osmolality seem to be of greater importance. Acetate produces vasodilation. It also has a positive inotropic effect. Studies suggest that the vasodilation produced by acetate is compensated for by a proportionate increase in cardiac output except during the early stages of the therapy when the fall in total peripheral resistance may overwhelm the increase in cardiac output. The substitution of bicarbonate for acetate results in a decrease in the incidence of symptomatic hypotension in some patients. This alleviation of symptoms appears to be significant only when the dialystate sodium concentration is relatively low (130–135 m M ). At higher dialysate sodium concentrations (140–145 m M ), the blunting of the fall in serum osmolality seems to be of greater importance than the nature of the buffer source in reducing the incidence of symptomatic hypotension. It is not clear if blunting the fall in serum osmolality has a greater beneficial influence on the cardiac output or on the total peripheral resistance. While the etiology of dialysis-induced hypotension is complex, controversial, and multifactorial, amelioration of symptomatic hypotension with a higher dialysate sodium concentration offers a practical solution. The substitution of bicarbonate for acetate is a technically more complex and expensive alternative.