Hypoxemia during hemodialysis: a critical review of the facts.

The literature describing the fall in PaO2 during dialysis is intensively and critically reviewed. This phenomenon is related to both the type of membrane used (cellulosic v noncellulosic membrane), and to the composition of the dialysate (acetate v bicarbonate). It appears that a ventilation/perfusion mismatch due to pulmonary leukostasis can, in part, explain hypoxemia in patients dialyzed with cellulosic membranes. This phenomenon is especially apparent in patients with preexisting pulmonary abnormalities. However, hypoventilation remains the major cause of hypoxemia. This hypoventilation is mainly due to CO2 consumption during acetate metabolism (acetate dialysis), or alkalinization of the blood (bicarbonate dialysis). The metabolic consequences of acetate metabolism, and of bicarbonate and CO2 losses through the dialyzer are critically analyzed. The cause for the increment in oxygen consumption during acetate dialysis is examined. Finally, the respective role of these combined factors are described and used to explain the changes in VCO2, VO2, respiratory quotient (RQ), and PaO2 reported in the literature during dialysis against acetate and/or bicarbonate.

The acid-base status does not influence the rate of acetate metabolism in hemodialyzed patients.

The present study was undertaken to evaluate whether the acid-base status influences the rate of acetate metabolism in patients chronically hemodialyzed against acetate. Ten patients (5 "intolerant" and 5 "tolerant" to acetate) received in a randomized order and for three consecutive dialyses each of the six following infusions in the venous line of the dialyzer: NaHCO3 (22, 44 or 88 mEq/h), NaCl (22 or 44 mEq/h) or Dextrose 5% in water (30 mmol/h). Plasma acetate was measured at the end of the dialysis. Bicarbonate infusions increased significantly blood pH and plasma bicarbonate but did not change the plasma acetate concentration at the end of dialysis. We conclude that the rate of acetate metabolism is not modified by changes in the acid-base status within the range usually observed in hemodialyzed patients. A significant hypoxemia per dialysis was noted only in AT patients with lower plasma acetate and rapid acetate metabolism. We conclude that acetate metabolism (and not plasma acetate concentration) plays a significant role in dialysis-induced hypoxemia.