Dialysis-Associated Hypoxemia: Insights into Pathophysiology and Prevention

It is clear that much research continues in an attempt to better understand DAH. A reasonable synthesis scenario based on current knowledge is as follows. Within the first 5–10 minutes of dialysis with a cellulosic membrane, blood contact leads to complement activation, generation of anaphylatoxins, leukoagglutination, and pulmonary microleukoaggregates. In addition, release of thromboxane in the lung occurs and causes pulmonary hypertension. This series of events causes mild hypoxemia and is preventable when noncellulosic membranes are used. As dialysis proceeds subsequent hypoxemia is dependent on the dialysate composition. With acetate dialysate, outward CO₂ dialysance occurs concomitant with inward acetate dialysance. This leads to reflex hypoventilation, increased oxygen consumption (which lowers RQ), and possibly direct central respiratory suppression. These changes account for the late hypoxemia seen. With bicarbonate dialysate, the above events do not occur. If rapid alkalinization ensues, however, because of a high dialysate bicarbonate concentration, hypoventilation and hypoxemia may be seen.
A clear understanding of these pathophysiologic mechanisms provides a framework from which the preventative measures outlined can be understood and applied. Future research should focus on a better understanding of the sequence of events following blood-membrane interaction, particularly in regard to activation of prostenoids. In addition, a more precise method is needed to determine the appropriate bath bicarbonate concentration for individual patients to avoid rapid alkalinization and hypoxemia. Finally, methods of identification of patients at risk of serious consequences from DAH need to be developed as well as noninvasive means of monitoring such individuals during dialysis. Much progress has been made in these areas in the past 10 years, but there is still more to learn.