Several excellent reviews of dialysis-associated hypoxemia (DAH) have been published (1-4). The causes, clinical manifestations, and prevention of this entity, however, are still the subjects of continuing investigation. The hypoxemia is a major concern in some patients, occumng within 15 minutes of initiation of dialysis in up to 90% of patients, decreasing the arterial oxygen tension (Pa02) from 5 to 35 mm Hg and resolving within 60-120 minutes after discontinuation of dialysis (5, 6). In addition, studies of DAH have led to new and important thoughts about blood-membrane interaction. Although many etiologies have been proposed to explain DAH, the effects of both the dialyzer membrane and the dialysate bath have received particular attention. Briefly, cellulosic dialyzer membranes (particularly Cuprophane) activate the alternative complement pathway and within minutes after contact with the blood induce Ieukoagglutination and profound neutropenia. Subsequent lung sequestration of white blood cell microaggregates causes intrapulmonary diffusion abnormalities which widen the alveolar to arterial oxygen gradient (AaDOz), causing early (5-15 minutes), modest hypoxemia. In addition, with acetate dialysate baths, more severe hypoxemia occumng somewhat later in dialysis ( 15-60 minutes) is due to compensatory hypoventilation induced by extracorporeal loss of COZY altered metabolism causing increased oxygen consumption, and possibly depression of the central respiratory center. This commentary will explore the relative pathophysiologic and clinical importance of these and other proposed mechanisms.
Clinical SignificanceThe clinical manifestations of DAH are variable and to a large degree depend on the patient's underlying cardiopulmonary status. Reports of the benign effects of modest decreases in the Pa02 cannot be applied to patients with already compromised cardiac or pulmonary status who require different (albeit often more costly) dialysis strategies.