Faculty Collaboration Database

Mechanisms producing hypoxemia during hemodialysis. Crit Care Med 1984 Apr;12(4):359-63

Date

04/01/1984

Pubmed ID

6705543

DOI

10.1097/00003246-198404000-00004

Scopus ID

2-s2.0-0021279072 (requires institutional sign-in at Scopus site)   15 Citations

Abstract

Arterial hypoxemia occurs frequently during hemodialysis. Proposed mechanisms for this phenomenon have included hypoventilation and embolism of granulocyte aggregates. We studied 18 patients with endstage renal failure who required chronic hemodialysis, and measured arterial blood gases, pulmonary gas exchange, and dialyzer gas exchange. During use of acetate as a dialysate buffer, PaO2 decreased to 80 +/- 6.8 torr, whereas during use of the bicarbonate buffer oxygen tension remained at 92 +/- 4.9 torr or greater. Hypoventilation and microembolism were not sufficient to explain the degree of hypoxemia during acetate dialysis. Hypoxemia occurred only after the 1st exposure to acetate; neither an instantaneous change to bicarbonate nor stopping dialysis restored oxygen tension to normal. We conclude that a pharmacologic action of acetate adversely affects lung function, aggravating the decreased alveolar oxygen tension (PAO2) due to hypoventilation. Hypoxemia was not present when bicarbonate was used. Acetate buffer should not be used for dialysis in patients with unstable cardiovascular or respiratory systems.

Author List

Quebbeman EJ, Maierhofer WJ, Piering WF

Author

Edward J. Quebbeman MD Emeritus Professor in the Surgery department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Acetates
Adult
Humans
Hypoventilation
Hypoxia
Kidney Failure, Chronic
Middle Aged
Oxygen
Pulmonary Gas Exchange
Renal Dialysis
Time Factors