Recurrent ventricular fibrillation treated by multiple countershocks.

Dichlorphenamide was administered to 13 patients with chronic respiratory failure, and the effects on gas exchange at rest and during exercise and on the acid-base state of CSF were observed. The ventilation for a given level of CO₂ production was increased both at rest and during exercise, resulting in an increased arterial Po₂ and decreased Pco₂.The ventilatory stimulation paralleled the development of a metabolic acidosis but was not associated with tissue CO₂ accumulation. Indeed, CSF Pco₂ and the oxygenated mixed venous (rebreathing) Pco₂ fell by the same amount as arterial Pco₂. The level of CO₂ elimination after two minutes of exercise was as great for a given work load after dichlorphenamide as before. These findings do not support the view that the drug impairs CO₂ transport from tissues either at rest or during exercise. They are most consistent with the view that the primary locus of action of dichlorphenamide in therapeutic doses is the kidney. The metabolic acidosis which results is likely the basis of the respiratory stimulatin, perhaps by its effects on the CSF H₂CO₃-HCO₃ - system. Inhibition of carbonic anhydrase in the red cell and choroid plexus are probably unimportant effects.