Abstract
A FALL in partial pressure of arterial oxygen, or oxygen tension (Pao2), occurring during hemodialysis is a well described phenomenon.1 , 2 The published data, however, are disparate over its cause and clinical implications. Bischel, Scoles and Mohler3 described a small but statistically significant fall in Pao2 at the end of dialysis and concluded that pulmonary arterial microembolization from the dialysis membrane was its cause. Other authors1 , 2 , 4 have described a decline in Pao2 of greater magnitude during the course of dialysis. Craddock and his associates4 believed that the underlying mechanism was related to complement-mediated leukostasis in pulmonary capillaries. . . .
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