Lactic acidosis from carboxyhemoglobinemia after smoke inhalation.

J. H. Buehler*, A. S. Berns, J. R. Webster, W. W. Addington, D. W. Cugell

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


Tissue hypoxia as a result of a wide variety of clinical situations had 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), Pco-2 (19 to 27 mm Hg), Po (63 to 116 mm Hg), HCO-2- (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.

Original languageEnglish (US)
Pages (from-to)803-805
Number of pages3
JournalAnnals of Internal Medicine
Issue number6
StatePublished - Jun 1 1975

ASJC Scopus subject areas

  • Medicine(all)


Dive into the research topics of 'Lactic acidosis from carboxyhemoglobinemia after smoke inhalation.'. Together they form a unique fingerprint.

Cite this