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Carbon Dioxide Elimination after Acetazolamide in Patients with Chronic Obstructive Pulmonary Disease and Metabolic Alkalosis
Author(s) -
Krintel J. J.,
Haxholdt O. St.,
Berthelsen P.,
Brøckner J.
Publication year - 1983
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1983.tb01946.x
Subject(s) - medicine , acetazolamide , pulmonary disease , metabolic alkalosis , carbon dioxide , intensive care medicine , alkalosis , cardiology , anesthesia , acidosis , ecology , biology
Acetazolamide, an inhibitor of carbonic anhydrase, which catalyzes hydration/dehydration of carbon dioxide, has been used for correction of metabolic, alkalosis in patients with chronic obstructive pulmonary disease (COPD). Animal experiments have shown that the gradient between tissue and the alveolar CO 2 tension increases after inhibition of carbonic anhydrase, suggesting retention of CO 2 . In order to determine the true degree of carbon dioxide retention after total inhibition of carbonic anhydrase, 10 patients with COPD and pronounced metabolic alkalosis (base excess above 6) under controlled mechanical ventilation were studied. The study showed that there was a statistically significant increase in tissue Pco 2 and a temporary decrease in pulmonary carbon dioxide excretion. Furthermore, it was found that Pao 2 and Pvo 2 increased significantly after inhibition of carbonic anhydrase, which could, at least partly, explain the improvement seen in patients with COPD and metabolic alkalosis after treatment with acetazolamide.