Abstract

T HE association of hyponatremia, edema and sodium retention in certain disease states is an apparent paradox. Particular attention has been drawn to the presence of low serum sodium concentrations in certain patients with severe congestive heart failure [ 7,2]. Earlier reports ascribed this abnormality to sodium depletion induced by dietary restriction and the administration of mercurial diuretics, and advocated correction of the serum hypotonicity by the infusion of hypertonic sodium chloride solution [.MJ. It has since been clearly demonstrated that the body sodium stores are increased in the hyponatremic, edematous cardiac patient [6,7], and that treatment with hypertonic saline solution is generally unavailing and often harmful [1,2,8]. In contrast, correction of the hyponatremia and clinical improvement have been observed to result from successful mercurial diuresis [9], thus shifting the therapeutic emphasis from attention to the hyponatremia per se to the treatment of the underlying heart failure. While understanding of the clinical significance and the management of the hyponatremic cardiac patient has advanced, knowledge of the disturbances in body fluid and electrolyte metabolism associated with development of or recovery from this syndrome has remained scant. The present report deals with studies in a group of patients with advanced cardiac disease and congestive failure. Detailed metabolic observations have been made during the development of hyponatremia and during the restoration of a normal serum sodium concentration. The results emphasize the complexity of this Rochester, New York

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