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Mechanisms producing hypoxemia during hemodialysis
Critical Care Medicine
|April 1, 1984
Summary
Acetate buffer during hemodialysis can cause arterial hypoxemia (low blood oxygen) by affecting lung function. Bicarbonate buffer does not cause this adverse effect, making it a safer option for dialysis patients.
Area of Science:
- Nephrology
- Pulmonary Physiology
- Biochemistry
Background:
- Arterial hypoxemia is a common complication during hemodialysis.
- Potential causes include hypoventilation and granulocyte aggregate embolism.
- The role of dialysate buffer composition requires further investigation.
Purpose of the Study:
- To investigate the impact of acetate versus bicarbonate dialysate buffer on arterial oxygen tension during hemodialysis.
- To determine the underlying mechanisms of hypoxemia during hemodialysis with acetate buffer.
Main Methods:
- Studied 18 patients with end-stage renal failure undergoing chronic hemodialysis.
- Measured arterial blood gases (PaO2), pulmonary gas exchange, and dialyzer gas exchange.
- Compared oxygen tension during acetate and bicarbonate buffer use.
Main Results:
- Acetate buffer use led to a significant decrease in PaO2 (80 +/- 6.8 torr) compared to bicarbonate buffer (>= 92 +/- 4.9 torr).
- Hypoxemia was observed only after initial acetate exposure and did not resolve immediately upon switching buffers or stopping dialysis.
- Hypoventilation and microembolism did not fully account for the observed hypoxemia.
Conclusions:
- Acetate exerts a pharmacologic effect that impairs lung function, worsening hypoxemia.
- Bicarbonate buffer does not induce hypoxemia during hemodialysis.
- Acetate buffer is contraindicated in hemodialysis patients with cardiovascular or respiratory instability.