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December 1960

Electroencephalographic and Biochemical Changes in Acute Hypoxia and Hypercapnia

Author Affiliations

Durham, N.C.; Galveston, Texas
From the Departments of Medicine and Psychiatry, Duke University School of Medicine and Veterans Administration Hospital.
Dr. Wilson is presently of the Department of Neuropsychiatry, University of Texas Medical Branch, Galveston, Texas.

Arch Neurol. 1960;3(6):704-710. doi:10.1001/archneur.1960.00450060092010

Introduction  Serum potassium alterations have been demonstrated in hyper- and hypocapnic states.1-6 It has been postulated that these changes, in part, may represent physiologic buffering mechanisms,6 but their relationship to the maintenance of normal cerebral function has not been investigated with controlled experiments. In chronic pulmonary failure a significant increase of serum potassium has been observed in patients who were both chronically hypoxic and hypercapnic.7 It was suggested that the elevation of serum potassium might serve as a buffering mechanism whereby normal cerebral function was maintained in spite of markedly elevated arterial blood carbon dioxide levels. If this theory were correct, prevention of increase in serum potassium by glucose infusion as previously used in the studies of the early hyperkalemia of hyperventilation8 should result in increased sensitivity of cerebral electroactivity to carbon dioxide. However, it is possible that the increase in serum potassium seen in the

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