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November 28, 1977

Acute Metabolic Alkalosis Perpetuating Hypercarbia: A Role for Acetazolamide in Chronic Obstructive Pulmonary Disease

Author Affiliations

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

JAMA. 1977;238(22):2400-2401. doi:10.1001/jama.1977.03280230064027

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

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