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Computer analysis of hypoxemia during hemodialysis.

作者信息

Thews O

机构信息

Institut für Physiologie und Pathophysiologie, Johannes Gutenberg-Universität Mainz, F.R.G.

出版信息

Artif Organs. 1991 Dec;15(6):454-61.

PMID:1763967
Abstract

Arterial oxygen partial pressure decreases during hemodialysis if acetate as buffer is used or if certain types of bioincompatible dialyzer membranes are used. Several hypotheses considering the main cause of this hypoxemia have been proposed. To gain more insight into the mechanisms leading to this hypoxemia, a mathematical model for the computerized simulation of exchange processes during hemodialysis has been used. To simulate the ventilation-perfusion ratio (VA/Q), a simplified two-compartment model of the lung has been applied. The simulation results reveal that hypoxemia during hemodialysis has two reasons. In acetate hemodialysis, the main cause is a shift of the CO2-bicarbonate equilibrium caused by "consumption" of hydrogen ions during acetate metabolization resulting in hypoventilation due to a decrease in CO2 partial pressure. During hemodialysis with bioincompatible dialyzer membranes, the hypoxemia may be explained by an increase in inhomogeneity of the VA/Q ratio in the lung. The loss of CO2 and bicarbonate into the dialysate during acetate hemodialysis has only a minor effect on arterial PO2 and cannot explain the observed hypoxemia. The decrease of O2 diffusing capacity during hemodialysis with bioincompatible membranes has only a negligible effect on the arterial PO2. The simulation results show also that the venous PO2 in the brain may fall below a critical level of less than 25 mm Hg, thereby possibly causing oxygen deficiency in the cortex.

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