Why the study?
What are the determinants of arterial hypoxemia during hemodialysis using an acetate dialysate in spontaneously breathing patients?
What are the determinants of arterial hypoxemia during hemodialysis using an acetate dialysate in spontaneously breathing patients?
Arterial hypoxemia during acetate hemodialysis is primarily driven by a decrease in ventilation secondary to CO2 removal by the dialyzer.
Identifies ventilation reduction as key driver of hypoxemia in acetate dialysis; leaves open relevance to modern bicarbonate regimens.
With measured values of arterial blood gas tensions, of expired respiratory gas fractions, and volume of the expired ventilation, the determinants of alveolar oxygen tension (PAO2) were used to evaluate their influence on the development of the arterial hypoxemia that occurs in spontaneously breathing patients undergoing hemodialysis using an acetate dialysate. Dialysis produced no significant changes in the alveolar-arterial O2 tension gradient (AaDO2). The extracorporeal dialyzer removed an average of 30 ml.m-2.min-1 of CO2. Accordingly the pulmonary gas exchange ratio (R) dropped from a mean predialysis value of 0.81 to 0.62 (P less than 0.001). The arterial CO2 tension remained constant throughout, whereas the minute ventilation, both total (P less than 0.01) and alveolar (P less than 0.01), decreased during dialysis. This decrease in ventilation accounts for more than 80% of the fall in PAO2. During dialysis there was a decrease (P less than 0.001) in arterial oxygen tension (PaO2), which varied among the individuals from 9 to 23% of control. During the postdialysis hour PaO2 returns to control values concomitant with increase in ventilation. The quantitative gas exchange relationships among R, alveolar ventilation, and AaDO2 predict the PaO2 values actually measured.
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Patterson et al. (1981) studied this question.
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