Electroencephalographic and Biochemical Changes in Acute Hypoxia and Hypercapnia

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