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[Changes in acid-base equilibrium and CO2 output induced by bicarbonate infusion]
F Cavaliere1, M A Pennisi, F La Mura
1Istituto di Anestesiologia e Rianimazione, Università Cattolica del Sacro Cuore, Roma.
Minerva Anestesiologica
|November 9, 2000
Summary
Bicarbonate therapy for metabolic acidosis can cause tissue hypercapnia. This study shows CO2 retention is initially confined to blood, suggesting hyperventilation may prevent tissue issues.
Area of Science:
- Critical Care Medicine
- Physiology
- Biochemistry
Background:
- Bicarbonate therapy for metabolic acidosis can lead to tissue hypercapnia.
- The study investigates the distribution of CO2 retention following bicarbonate administration.
Purpose of the Study:
- To test the hypothesis that CO2 retention is initially confined to blood.
- To determine if tissue hypercapnia is a consequence of blood hypercapnia.
Main Methods:
- A prospective study was conducted in a general Intensive Care Unit.
- Ten mechanically ventilated patients received escalating doses of sodium bicarbonate.
- Hemodynamic parameters, arterial and venous blood gases, and CO2 output were monitored.
Main Results:
- PetCO2 increased in all patients, while hemodynamic parameters remained stable.
- Arterial PCO2 and TCO2 increased, while venous PCO2 was unchanged, indicating CO2 remained within the vascular compartment initially.
- CO2 output through the lungs increased after a latency period, with a dose-dependent response.
Conclusions:
- CO2 and bicarbonate did not significantly diffuse out of the vascular compartment during the study.
- Continued bicarbonate infusion leads to CO2 release via the lungs.
- Improving CO2 release through hyperventilation may prevent tissue hypercapnia during bicarbonate therapy.