Hypoxia
During hemodialysis, PaO2Â 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 PaO2Â can be catastrophic.
Etiology
- 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 CO2Â 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 CO2Â 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
References:
- De Broe ME, De Backer WA. Pathophysiology of hemodialysis-associated hypoxemia. Adv Nephrol Necker Hosp 18:297-315, 1989
- 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
- Friedman EA. Hemodialysis as an artificial lung in sleep apnea. N Engl J Med 344:134-135, 2001