Myocardial potassium exchange during respiratory acidosis: The interaction of carbon dioxide and sympathoadrenal discharge

The myocardial exchange of K + was studied under the following conditions: acute respiratory acidosis, respiratory acidosis when acidemia was prevented by an organic buffer, catecholamine administration, cardio-accelerator nerve stimulation and during respiratory acidosis following adrenergic blockade. Application of the Stibitz extension of the Fick equation allowed calculation of myocardial K + uptake in the unsteady state. During respiratory acidosis, the myocardium takes up K + as a result of the rise in P CO 2 , independent of direct change in extracellular [H +]. Catecholamines, both exogenously and endogenously, result in a sudden, short-lived uptake of K + by the heart. When sympatho-adrenal discharge is prevented during respiratory acidosis, there is a biphasic response consisting of an initial loss of myocardial K +, followed by a gain. These findings are discussed in terms of the Fenn hypothesis. The net effect of respiratory acidosis on myocardial K + exchange is interpreted as being the result of the interaction of increased P CO 2 and sympatho-adrenal discharge.