Sodium and water balance in chronic congestive heart failure.

Abstract

As the characteristics of sodium and water balance in heart failure remain undefined, we evaluated the hemodynamic, metabolic, and hormonal effects of balanced sodium intake in 10 patients with chronic congestive heart failure. We discontinued diuretics to avoid their confounding influence, and all patients received 1 wk of 10 meq and 100 meq balanced sodium intake and controlled free water. Comparing sodium intake of 10 with 100 meq, the following observations were made. There was weight gain (2.0 kg) and increased sodium excretion (11±3 to 63±15 meq/24 h), unaccompanied by increase of blood volume. Both renin-angiotensin system and sympathetic nervous system activity were greater during the 10 meq diet, and suppressed with the 100 meq sodium diet. For both diets, plasma renin and urinary aldosterone excretion were correlated with urnary sodium excretion (r = -0.768, r = -0.726, respectively; P < 0.005). Systemic hemodynamics were minimally changed with increased sodium intake. However, reversal of vasoconstriction by captopril during the 10 meq diet, and its ineffectiveness during the 100 meq diet, indicated a renin-dependent mechanism in the former, and a renin-independent mechanism in the latter diet. There were two subgroups of response to the 100 meq diet: one group (a = 5) achieved neutral balance, while the second (a = 5) avidly retained sodium and water. Renin-angiotensin system activity was significantly higher in the latter group, and the mechanism for differences in sodium excretion for the subgroups could not be identified by blood volume or hemodynamic parameters. Orthostatic hypotension during tilt was greater during the 10 meq sodium diet, and in all cases, related to ineffective hemodynamic and hormonal compensatory responses.

Atrial natriuretic factor in normal subjects and heart failure patients. Plasma levels and renal, hormonal, and hemodynamic responses to peptide infusion.

“…In considering the mechanisms responsible for the attenuated response to ANF infusion in heart failure, it should be noted that, under basal conditions, many ofthe patients studied were retaining sodium while on a 100-meq sodium diet. This would be consistent with a previous study by our group (43) demonstrating that only 50% of such patients achieved sodium balance at this level of intake, while the remainder continued to avidly retain sodium. The responsible mechanism could not be identified, but this phenomenon was associated with different patterns of renin-angiotenin system activity.…”

A functional role for endogenous atrial natriuretic peptide in a canine model of early left ventricular dysfunction.

“…In these previous studies Low ANP Acute Heart Failure produced by acute inferior thoracic vena caval constriction was characterized by activation of PRA and aldosterone with sodium retention, responses not observed with Elevated ANP Acute Heart Failure produced by rapid ventricular pacing. In chronic severe CHF an escape from the RAAS-suppressing actions of ANP may result in sodium retention (26). Studies in humans and animal models of CHF have demonstrated a blunting of the second messenger cGMP response to endogenous and exogenous ANP in severe CHF, in contrast to a preservation of the second messenger response to acute and chronic endogenous elevation of ANP and exogenous administration of ANP in mild CHF (5,8,27).…”

Loop Diuretic Therapy in Heart Failure: The Need for Solid Evidence on a Fluid Issue

“…Salt restriction should be emphasized, knowing that an increase of daily dietary sodium intake of as little as 10 to 100 mEq results in a 2-kg weight gain and changes in RAAS and SNS activity. 35 350 Clin. Cardiol.…”