Pathophysiology of intrahepatic sinusoidal portal hypertension and ascites formation in cirrhosis. Increases in the intrahepatic vascular resistance (IHVR) occur because of mechanical (fibrosis in the sinusoids, microthrombi in hepatic veins, and regenerative nodule formation) and dynamic (failure of sinusoidal relaxation) obstructive processes within the liver. At the same time, the splanchnic circulation undergoes progressive vasodilatation, leading to increases in portal blood flow (PBF) that further increase portal vein pressure. Systemic compensation for the splanchnic arterial vasodilation creates a hyperdynamic circulation marked by increased cardiac output (CO) and decreased peripheral vascular resistance (PVR). Progressive splanchnic vasodilatation, however, leads to eventual failure of this circulatory response and development of systemic vasodilatation and hypotension. This decrease in effective circulatory blood volume leads to activation of the renin‐angiotensin‐aldosterone‐sympathetic system (RAAS) and the nonosmotic release of antidiuretic hormone (ADH). This leads to avid renal sodium and water retention creating a volume overload and the development of ascites. | ATII, angiotensin II; CO, carbon monoxide; ET, endothelin; NE, norepinephrine; NO, nitric oxide. | Buob, S., Johnston, A. N., & Webster, C. R. L. (2011). Portal Hypertension: Pathophysiology, Diagnosis, and Treatment. Journal of Veterinary Internal Medicine, 25(2), 169–186. https://doi.org/10.1111/j.1939-1676.2011.00691.x

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