Hypoxemia during
hemodialysis may result from several differing processes. We initially studied patients undergoing standard
acetate hemodialysis. At 15 minutes of dialysis,
leukopenia (primarily
neutropenia), a decline of platelet count, and
hypoxemia occurred, but without a significant change in mean minute ventilation. Complement activation (V/A ratios of C5a greater than 1.0) persisted throughout dialysis. Leukocyte count returned to baseline by one hour. To separate the effects of solute and/or gas fluxes from those of blood-membrane interaction we studied changes in Po2, WBC, C5a, TxB2, and PGI2 during a period of blood membrane interaction without dialysis, and during subsequent
acetate dialysis. Patients were studied with both
polyacrylonitrile (PAN) and
cuprophan membranes containing different priming solutions during membrane contact alone. Despite
leukopenia and complement activation,
hypoxemia failed to occur during membrane contact alone. At 15 minutes of subsequent
acetate dialysis, significant
hypoxemia occurred with both membranes. However, the degree of
hypoxemia was twice as great with a
cuprophan membrane primed with
acetate (18.6 +/- 3.3 mm Hg) compared with air or
bicarbonate (9.1 +/- 1.4 and 7.0 +/- 2.0 mm Hg, respectively), or compared with PAN (8 +/- 2.8 mm Hg). Changes in
thromboxane B2, PGI2, and C5a did not correlate with changes in Po2. We conclude that there are two major components to dialysis related
hypoxemia. One is membrane independent, and may relate to the metabolic effects of
acetate or to dialyzer CO2 loss. The remaining portion is membrane dependent, occurring with
cuprophan, but not with PAN, and is conditioned by an
acetate dependent interaction between blood and membrane.