Water and electrolyte balance during recovery from severe congestive failure on a 50 milligram sodium diet.

Abstract The clinical and metabolic effects of a diet furnishing 50 mg. of sodium, 1.32 Gm. of chloride, 4.33 Gm. of potassium and adequate water, protein, and total calories were determined in seven patients with severe congestive failure. The major lesion was rheumatic mitral stenosis in four patients and hypertensive and/or arteriosclerotic heart disease in the other three patients. Prior to the institution of the special diet, the congestive failure had proved refractory to a standard regimen consisting of bed rest, low-sodium diet, digitalization, and frequent mercurial diuretics, carried out for a nine to forty-nine-day control period of hospitalization in four patients and for several weeks under medical supervision at home in two patients. Progressive decompensation developed in the remaining patient despite digitalization at home. The cardiac failure was manifested by marked passive congestion and edema of both circuits in four patients, and by marked pulmonary congestion but little or no peripheral edema in three patients. The extracellular volume decreased by an average of 8.28 L. in the four patients with marked peripheral edema and by 1.44 L. in the three with little or no clinically detectable edema. Chloride and water were lost from the extracellular space in isotonic proportions in the two patients with initially normal plasma levels, whereas relatively less chloride was lost in the five patients with initial hypochloremia, permitting a rise in plasma level. Plasma sodium concentrations were initially elevated in four patients and normal in three and maintained a plateau during recovery from congestive failure, indicating parallelism in losses of extracellular sodium and water, even in the presence of hypernatremia. Plasma potassium concentrations were initially normal in all patients and were also maintained at a plateau through proportionate reduction of total extracellular potassium and water. In six patients there was a net cellular gain of 3.7 to 33.9 Gm. of nitrogen available for protein synthesis, and in one patient there was a loss of 21.6 Gm., attributable to a marked proteinuria. During recovery from congestive failure on the special diet, the intracellular compartment lost from 230 to 2,890 ml. of water (average 1,325 ml.), but it gained from 115 to 385 meq. of sodium (average 234 meq.) in six of the seven patients and gained significant amounts of potassium in all patients. The cellular uptake of potassium for purposes other than protein synthesis ranged from 62 to 454 meq. (average 259.9) in the four patients with marked peripheral edema and from 97 to 338 meq. (average 222.2) in the three patients with marked pulmonary congestion but little or no peripheral edema. The positive intracellular balances of potassium and sodium observed during recovery probably represented replenishment of a deficit incurred during the development of congestive failure. The findings in this study are in accord with the hypothesis that the development of congestive failure is accompanied by an alteration of cellular metabolism, manifested by liberation of ionized base from osmotically inactive constituents of the protoplasm, followed by shifts of potassium and sodium out of the cells and water in the opposite direction to maintain osmotic equilibrium with the extracellular compartment. Recovery from congestive failure is accompanied by cellular release of water and uptake of potassium and sodium, with coincident osmotic inactivation of cell base.