The pathogenesis and treatment of hyponatremia in congestive heart failure

Abstract Acute intensification of chronic congestive failure in cardiac patients on low sodium diets may lead to continued water retention, with increasing edema and hyponatremia without external loss of sodium. This sequence is illustrated by the events following development of severe respiratory infections or escape from digitalization in such patients. Such a sequence may occur also, at times, in the presence of electrocardiographic changes suggestive of digitalis toxicity but actually due to potassium depletion. This clinical course is not favorably influenced by intravenous administration of either isotonic or concentrated sodium solutions. However, increasing cardiac output by adequate digitalization or decreasing bodily metabolic demand by treatment of the underlying infection may lead to increased excretion of water in excess of sodium, decreased body weight, and restoration of more normal serum electrolyte concentrations. This sequence of events is attributed to sustained production of antidiuretic hormone, invoked by some extraosmoreceptor mechanism, whenever the cardiac output becomes inadequate for the body's metabolic needs. The more protracted operation of this mechanism is illustrated by the progressive water retention and hyponatremia frequently observed in patients on a low sodium diet and unrestricted water intake during the terminal phase of congestive failure. A fatal outcome may be anticipated unless the cardiac output can be increased or the burden on the impaired circulation in some way diminished.