A mechanism of hypoxemia during hemodialysis. Consumption of CO2 in metabolism of acetate.
The present study is an investigation of the role of acetate metabolism in dialysis-induced hypoxemia and of the relative roles of acetate metabolism, bicarbonate loss, and CO2 gas (g) loss in causation of hypoxemia. The loss of CO2 (g) measured in 23 patients during acetate dialysis was found to be negligible (0.21 +/- 0.01 mmol/min). The HCO-3 loss was substantial (3.4 +/- 0.5 mmol/min), but its predicted effect on dialysis hypoxemia was modest. The infusion of acetate at 4 mmol/min into 6 normal volunteers decreased the respiratory exchange ratio (R) from 0.83 +/- 0.06 to 0.71 +/- 0.06 with constant O2 consumption (VO2) and reduced net CO2 production (VCO2). In another experiment, the infusion of sodium acetate into 9 normal volunteers resulted in a similar reduction in R (from 0.82 +/- 0.04 to 0.71 +/- 0.04) and arterial pO2 (from 92.3 +/- 1.1 to 78.3 +/- 1.7 mm Hg). The results indicate that acetate metabolism can lead to reduction in R and hypoxemia and suggest that the same mechanism is responsible for hypoxemia during hemodialysis using acetate dialysate.
D000085:Acetates / Q000378:metabolism; D019342:Acetic Acid; D001639:Bicarbonates / Q000378:metabolism; D002245:Carbon Dioxide / Q000378:metabolism; D006801:Humans; D000860:Hypoxia / Q000209:etiology* / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D011659:Pulmonary Gas Exchange; D006435:Renal Dialysis / Q000009:adverse effects* / Q000379:methods
D000085:Acetates; D001639:Bicarbonates; D002245:Carbon Dioxide; D019342:Acetic Acid; D010100:Oxygen