The salt-avid state of congestive heart failure revisited

Congestive heart failure (CHF), a clinical syndrome, comprises a constellation of signs and symptoms whose origins are rooted in a salt-avid state mediated largely by effector hormones of the renin-angiotensin-aldosterone system (RAAS). Stimuli that normally lead to an activation of this circulating neurohormonal system include reduced dietary sodium, upright posture with or without exercise, and thermal stress. These stimuli remain operative in patients with heart failure; however, here renal perfusion is reduced, leading to excessive RAAS activation. This can contribute to an inability to adequately excrete dietary sodium (salt sensitivity). Active Na+ and water retention (salt avidity) account for an initial expansion of intravascular volume and subsequent rise in extravascular volume. Neurohormonal regulation of Na+ excretion therefore is the pathophysiologic basis for clinical decompensation and the appearance of CHF. By contrast, and despite comparable levels of heart failure, expressed as diastolic or systolic ventricular dysfunction, patients in whom circulating RAAS hormones remain normal are clinically compensated without CHF. Interventions, such as regulated dietary Na+, prolonged bed rest, intermittent periods of semirecumbency (with legs up), water immersion, thermal neutrality, and pharmacologic interference with the generation and activity of RAAS hormones, can be used to attenuate the salt avidity found in patients with CHF.