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- W1902045131 abstract "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." @default.
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- W1902045131 date "1984-01-01" @default.
- W1902045131 modified "2023-10-18" @default.
- W1902045131 title "Sodium and Water Excretion in Patients with Congestive Heart Failure and Cirrhosis" @default.
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- W1902045131 doi "https://doi.org/10.1007/978-1-4613-3897-0_11" @default.
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