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.
D002245:Carbon Dioxide / Q000378:metabolism; D006801:Humans; D000860:Hypoxia / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D008567:Membranes, Artificial; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D006435:Renal Dialysis / Q000009:adverse effects*; D012119:Respiration
D008567:Membranes, Artificial; D002245:Carbon Dioxide; D010100:Oxygen