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.

Fatigue, acid-base and electrolyte changes with exhaustive treadmill exercise in hemodialysis patients.

Aerobic conditioning exercises have been shown to be beneficial for maintenance hemodialysis patients, but biochemical changes during exhaustive exercise in these functionally anephric patients have been less thoroughly studied. We evaluated serum biochemical changes in 7 patients during and after treadmill exercise to patient exhaustion. Duration of exercise was limited by lower leg fatigue without claudication. At exhaustion, only mild changes from baseline rest values were noted in arterial pH (7.39 +/- 0.03-7.33 +/- 0.04) and lactate (0.94 +/- 0.3-5.73 +/- 2.68 mmol/l) despite normal exercise-induced intracellular fluid shifts as evidenced by albumin concentration increases (44.9 +/- 2.8-49.3 +/- 3.1 g/l). Increases in serum K+ concentrations are also modest (change in K from baseline = 0.87 +/- 0.22 mmol/l). An explanation for these minimal biochemical alterations at exhaustion is unclear, but could relate to exercise being limited well below estimated maximum cardiac output and muscle O2 extraction levels by early, unexplained muscle fatigue. Fatigue in hemodialysis patients does not appear to be due to muscle hypoxia.