The role of acetate in the etiology of symptomatic hypotension.
Acetate, although widely used as the source of buffer in hemodialysis, has been implicated in the development of symptomatic hypotension and hypoxemia during dialysis. Studies of acetate infusion clearly indicate a vasodilatory effect. Acetate also increases cardiac output. If the increase in cardiac output is not adequate to compensate for the decrease in peripheral resistance, hypotension can result. Acetate infusion studies indicate a significant increase in oxygen consumption. This may be the most plausible explanation for dialysis-induced hypoxemia. Correction of the hypoxemia with supplemental oxygen has been shown to reduce the incidence of hypotensive episodes and intradialytic symptoms. Studies comparing cardiovascular stability during acetate and bicarbonate dialysis indicate that bicarbonate dialysis is beneficial only when the fall in serum osmolality during dialysis is significant. If the fall in serum osmolality is blunted either with a high-sodium dialysate or mannitol infusions, there is little difference between acetate and bicarbonate. From a practical viewpoint, high-sodium dialysis is technically less complex and expensive than bicarbonate dialysis.
D000085:Acetates / Q000009:adverse effects*; D019342:Acetic Acid; D001639:Bicarbonates / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D006801:Humans; D007022:Hypotension / Q000209:etiology*; D009994:Osmolar Concentration; D006435:Renal Dialysis / Q000009:adverse effects*; D014655:Vascular Resistance / Q000187:drug effects
D000085:Acetates; D001639:Bicarbonates; D019342:Acetic Acid