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[Should bicarbonates still be administered in lactic acidosis?]
J L Vincent1, S Blecic, J C Preiser
1Service des Soins Intensifs, Hôpital Erasme, Bruxelles.
Revue Medicale De Bruxelles
|May 1, 1993
Summary
Sodium bicarbonate treatment for lactic acidosis may worsen intracellular pH due to CO2 production. Alternative buffering agents like carbicarb, THAM, and dichloroacetate are explored for improved outcomes in circulatory failure.
Area of Science:
- Biochemistry
- Physiology
- Critical Care Medicine
Context:
- Lactic acidosis is a critical condition often linked with myocardial depression and intracellular acidosis.
- Bicarbonate administration is a traditional treatment, but its efficacy is debated in acute circulatory failure.
Purpose:
- To evaluate the physiological impact of bicarbonate administration during lactic acidosis.
- To discuss alternative buffering agents for managing intracellular pH disturbances.
Summary:
- Bicarbonate therapy for lactic acidosis may paradoxically worsen intracellular pH by increasing carbon dioxide (CO2) levels.
- This occurs due to the partial transformation of bicarbonate into CO2, exacerbating the veno-arterial CO2 gradient.
- The study reviews alternative treatments including carbicarb, THAM, and dichloroacetate.
Impact:
- Challenges the conventional use of sodium bicarbonate in lactic acidosis.
- Highlights the potential risks of CO2 accumulation with bicarbonate therapy.
- Suggests exploring alternative buffering agents for safer and more effective management of acid-base balance in critical illness.