During hemodialysis, PaO2 falls about 10-20 mmHg. This decrease has no clinical consequences in patients with normal oxygen tension, but in seriously ill patients with predialysis hypoxemia, the drop in PaO2 can be catastrophic.


  • Acetate dialysate (now obsolete).  Can also be seen with use of bicarbonate dialysate
  • Acetate causes hypoxemia by at least two mechanisms:
    • Increased oxygen consumption in the metabolism of acetate to bicarbonate
    • Intradialytic loss of CO2
  • Rapid correction of chronic metabolic acidosis
  • Bioincompatible membranes
    • Activate complement1
  • Hypocapnea due to intradialytic loss of CO2 and adaptation to chronic metabolic acidosis predisposes to periodic breathing and sleep apnea syndrome (SAS)1
  • SAS is also a cause of hypoxia in HD patients2
    • High prevalence in HD patients (54-80%) and has both obstructive and central components
    • Can alter autonomic responses and cause arrhythmias, pulmonary hypertension, and systemic hypertension

Treatment and Prevention

  • Dialysis-induced hypoxemia can be attenuated by interventions that increase the CO2 content of the dialysate either by direct administration or by using bicarbonate buffered dialysate
  • Use of biocompatible membranes might be helpful
  • In critically ill patients who may already have some degree of predialytic hypoxia, it is necessary to increase the ventilated volumes and/or the percentage of FiO2
  • Improvement in SAS has been reported with the use of prolonged dialysis such as nocturnal and daily hemodialysis2,3


  1. De Broe ME, De Backer WA. Pathophysiology of hemodialysis-associated hypoxemia. Adv Nephrol Necker Hosp 18:297-315, 1989
  2. Hanly PJ, Pierratos A. Improvement of sleep apnea in patients with chronic renal failure who undergo nocturnal hemodialysis. N Engl J Med  344:102-107, 2001
  3. Friedman EA. Hemodialysis as an artificial lung in sleep apnea. N Engl J Med 344:134-135, 2001