Carbon dioxide elimination after acetazolamide in patients with chronic obstructive pulmonary disease and metabolic alkalosis.
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 CO2 tension increases after inhibition of carbonic anhydrase, suggesting retention of CO2. 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 PCO2 and a temporary decrease in pulmonary carbon dioxide excretion. Furthermore, it was found that PaO2 and PVO2 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.
D000086:Acetazolamide / Q000494:pharmacology*; D000328:Adult; D000368:Aged; D000471:Alkalosis / Q000209:etiology / Q000378:metabolism*; D002245:Carbon Dioxide / Q000378:metabolism*; D005260:Female; D006801:Humans; D008173:Lung Diseases, Obstructive / Q000150:complications / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000032:analysis; D012121:Respiration, Artificial
D002245:Carbon Dioxide; D000086:Acetazolamide; D010100:Oxygen