JOHN H. BUEHLER, M.D.; ARNOLD S. BERNS, M.D.; JAMES R. WEBSTER Jr., M.D., F.A.C.P.; WHITNEY W. ADDINGTON, M.D., F.A.C.P.; DAVID W. CUGELL, M.D., F.A.C.P.
Tissue hypoxia as a result of a wide variety of clinical situations has frequently been implicated as a cause of systemic acidosis due to the accumulation of lactic acid. Four patients suffering from smoke inhalation had lactic acidosis in association with carboxyhemoglobinemia. There was no evidence of decreased tissue perfusion, hypotension, arterial hypoxemia, or anemia. The following were tested in all patients: arterial pH (7.25 to 7.40), Pco2 (19 to 27 mm Hg), Po2 (63 to 116 mm Hg), HCO3- (11 to 19 meq/litre), carboxyhemoglobin (13% to 37%), and lactic acid (5.1 to 9.3 meq/litre). After therapy with oxygen and intravenous corticosteroids, there was prompt return of lactic acid levels, carboxyhemoglobin values, and arterial pH to normal. It is concluded that the cause of lactic acidosis in the presence of carboxyhemoglobinemia during smoke inhalation is tissue hypoxia. This tissue hypoxia is due to the reduction of the oxygen-carrying capacity of the blood and the concomitant shift of the oxyhemoglobin dissociation curve to the left, both known to result from carboxyhemoglobinemia.
BUEHLER JH, BERNS AS, WEBSTER JR, et al. Lactic Acidosis from Carboxyhemoglobinemia After Smoke Inhalation. Ann Intern Med. 1975;82:803–805. doi: https://doi.org/10.7326/0003-4819-82-6-803
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Published: Ann Intern Med. 1975;82(6):803-805.
Emergency Medicine, Endocrine and Metabolism.
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