There is no general agreement concerning the action of specific electrolyte disorders and acid-base balance upon concentrations by determining their intracellular/extracellular relationships. Crismon and associates8 could not relate the intracellular potassium concentration to typical electrocardiographic events in hyperkalemia. Bellet, too, could not establish a definite relationship of the electrocardiographic changes to skeletal muscle potassium content.9 He considered, among other possibilities, that differences in the metabolic activity of heart and skeletal muscle were the cause of this lack of correlation. His comparison of intracellular to extracellular potassium concentrations with the electrocardiogram gave no better results than serum potassium concentration alone. Ktihns,10 on the other hand, noted such a relationship in animal experiments. In relating intracellular/extracellular potassium concentrations he used a value termed "cardiac potassium quotient" with a normal range of 25 to 32. Reduction of this quotient was associated with typical hyperkalemic changes, and elevation with typical hypokalemic changes in the electrocardiogram. There was, however, no consistency between the electrocardiographic alterations and absolute potassium or sodium concentrations, intracellular or extracellular. Changes in the autonomic nerve tone and pharmacologic actions of epinephrine, insulin, veratrine, and in particular quinidine, have been noted to simulate electrocardiographic patterns of hypokalemia.9 [11][12][13] It is also well known that pre-existent or concomitant alterations of the ST-T segment caused by heart Circulation, Volume XIV, November 1956 by guest on May 9, 2018 http://circ.ahajournals.org/ Downloaded from