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Thirty previously edematous cardiac patients were examined for evidence of increased osmotic inactivation of sodium through isotope dilutional studies of body composition. The basic assumptions were that increased osmotic inactivation of exchangeable sodium would result in the following changes: (a) an increase of the residual sodium, that is, the amount of total exchangeable sodium which is not accounted for as total extracellular sodium, as derived from a corrected 82bromide space, and (b) a departure from the established close correlation between the serum sodium level and the total exchangeable cation concentration (total exchangeable sodium+ potassium/total body water), resulting in a rise of the exchangeable cation concentration out of proportion to serum sodium.In 10 males and 10 females with previous cardiac edema the total exchangeable sodium, the 82bromide space, and the derived totalextracellular sodium were slightly, but not significantly, higher than in control groups of similar age and body weight. The residual sodium, assumed to include the osmotically inactive sodium, was close to the same in the groups compared.In 10 previously edematous cardiac patients the total exchangeable sodium, the total exchangeable cation, and total body water were significantly lower than in 10 edematous cardiac patients of similar age and sex. Nevertheless, the total exchangeable cation concentrations were close to the same in the two groups. The serum sodium levels were equal, and the relationship between serum sodium and exchangeable cation concentrations were within normal limits.The assumptions basic for the study are discussed, and it is concluded that increased osmotic inactivation of sodium could not be demonstrated.

Total Exchangeable Sodium in Previously Edematous Cardiac Patients: Is There Evidence for Osmotic Inactivation of Sodium?