Sodium and Water Excretion in Patients with Congestive Heart Failure and Cirrhosis

  • Daniel Bichet
  • R. W. Schrier
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 35)


Possible pathophysiologic mechanisms producing sodium and water excretion in patients with congestive heart failure and cirrhosis are reviewed. Sodium retention in cirrhosis seems to be mediated by a decreased central blood volume (afferent mechanism) and increased sympathetic activity, as well as stimulation of the renin aldosterone system (efferent mechanism). An increase in renal sympathetic activity appears to 1) diminish renal hemodynamics, 2) decrease distal fluid delivery, and 3) impair “escape” from aldosterone. Sodium retention in cardiac failure appears to be due to similar multifactorial mechanisms. Impairment in water excretion in association with congestive heart failure and cirrhosis seems to be mediated by a persistent non-osmotic release of AVP. In addition, the diminished fluid delivery to the distal diluting segment can contribute to the abnormal water excretion in cirrhosis and cardiac failure.


Sodium Retention Water Excretion Urinary Sodium Excretion Central Blood Volume Ascites Formation 
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© Martinus Nijhoff Publishing, Boston/The Hague/Dordrecht/Lancaster 1984

Authors and Affiliations

  • Daniel Bichet
  • R. W. Schrier

There are no affiliations available

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