In a patient with cirrhosis and ascites, the 'forward failure' hypothesis attributes sodium retention to which primary mechanism?

• A Increased hepatic lymph production overloading the thoracic duct
• B Hypoalbuminaemia reducing plasma oncotic pressure causing capillary leak
• C Splanchnic vasodilatation reducing effective arterial blood volume, activating RAAS and ADH ✓
• D Portal hypertension directly stimulating renal tubular sodium reabsorption

Explanation

The 'peripheral arterial vasodilation' (forward failure) hypothesis proposes that splanchnic vasodilatation — mediated by NO, substance P and other vasodilators — reduces effective arterial blood volume. Baroreceptor unloading triggers compensatory RAAS activation, increased ADH secretion, and sympathetic activation, all promoting renal sodium and water retention. Hypoalbuminaemia contributes to ascites formation but is secondary; portal hypertension per se does not directly stimulate tubular transport.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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