Arterial oxygenation is unchanged during hemodialysis in patients mechanically ventilated in assist-control mode.

Dialysis-induced hypoxemia can occur in spontaneously breathing renal failure patients but whether it occurs during bicarbonate hemodialysis in critically ill patients receiving mechanical ventilation in assist-control mode is not clear. Twenty-one patients admitted to the medical intensive care unit who required mechanical ventilation and hemodialysis with the use of a cuprammonium dialyzer were enrolled and 25 sessions of hemodialysis were performed. Arterial blood gas, white blood cell count, minute ventilation, respiratory rate, and blood pressure were measured before dialysis (time 0) and at 15, 30, 60, 120, 180, and 240 minutes thereafter. The white blood cell count dropped immediately and reached the nadir 15 minutes after hemodialysis began. Thereafter, it recovered and overshot the predialysis value at the end of dialysis. The serum HCO3- concentration increased progressively after dialysis began and resulted in significant metabolic alkalosis. The P (A-a)O2 was not aggravated and minute ventilation was not depressed by rapid metabolic alkalosis under mechanical ventilatory support. The PaO2 remained stable throughout hemodialysis. No significant hypoxemia occurred in groups of varying predialysis cardiopulmonary dysfunction. These findings suggest that in renal failure patients ventilated in assist-control mode, l) hypoventilation and accompanying hypoxemia did not occur during bicarbonate (35 mEq/L) dialysis, despite significant metabolic alkalosis; and 2) patients with higher Acute Physiologic and Chronic Health Evaluation (APACHE) III scores and P(A-a)O2 levels were not more prone to dialysis-induced hypoxemia.