Acetazolamide, a carbonic anhydrase inhibitor, is a diuretic drug which enhances renal excretion of water, sodium, potassium, and bicarbonate. Although increased excretion of water, sodium, and potassium are generally unwelcome in metabolic alkalosis, acetazolamide has been proposed as a treatment for alkalosis in patients with cardiac and respiratory failure. Its diuretic effect may be useful in edematous cardiac failure, provided that potassium losses can be matched effectively by an appropriate intake so that the potassium deficit can actually be reversed. It is more hazardous in respiratory failure, and particularly in hypercapnic patients. On the one hand, the effects of acetazolamide persist for 24 to 48 h, which may be a problem when the drug is found to decrease the pH and not the PaCO2. On the other hand, acetazolamide inhibits carbonic anhydrase and thus interferes with tissue CO 2 elimination. In patients with chronic obstructive pulmonary disease, it has been shown to cause a sustained and significant increase in the difference between tissue CO 2 tension and PaCO2. Thus the decrease in PaCO2 reported during acetazolamide therapy reflects, at least in part, altered tissue removal rather than improved pulmonary elimination of CO 2. Acetazolamide has also been reported to cause hematuria and renal failure. It should be avoided in renal and hepatic failure, and is ineffective in anuric patients.

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