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A Role for Acetazolamide in Chronic Obstructive Pulmonary Disease

Paul D. Miller, MD; Arnold S. Berns, MD

JAMA. 1977;238(22):2400-2401.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

METABOLIC alkalosis leads to hypercarbia (increased Pco₂). The increase in the blood Pco₂ owing to alveolar hypoventilation is the respiratory compensation for metabolic alkalosis as the ventilatory drive is blunted by the elevated Hco₃^- levels.¹ Hypercarbia induced by a metabolic alkalosis is of no clinical consequence in most normal persons, since the rise in Pco₂ rarely exceeds 10 mm Hg, but it can lead to severe carbon dioxide narcosis in those with chronic obstructive pulmonary disease (COPD) who already are severely hypoxic and hypercarbic. Metabolic alkalosis owing to diureticinduced intravascular volume, chloride, or potassium depletion² usually requires more than 24 hours to be generated.^2,3 Because of this, metabolic alkalosis as the cause for persistent hypercarbia in subjects with COPD is generally not considered in the first few hours after hospitalization. In patients with decompensated COPD with hypercarbia and congestive heart failure (CHF), rapid . . . [Full Text PDF of this Article]

Author Affiliations
From the Department of Medicine, University of Colorado Medical Center, Denver.

Footnotes
Reprint requests to Department of Medicine, Box C281, University of Colorado Medical Center, 4200 E Ninth Ave, Denver, CO 80220 (Dr Miller).

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