Liver disease is progressive in response to chronic liver injury. This progression results in irreversible scarring and nodularity of the liver. This change in liver parenchyma interferes with blood flow through the liver, disrupting its biochemical function.There is also active intrahepatic vasoconstriction accounting for 20% to 30% of total increased intrahepatic resistance. Additionally, there is an increase in portal venous inflow that results from splanchnic arteriolar vasodilatation and insufficient portal decompression through collaterals. This increase in flow exacerbates portal hypertension. End-stage liver disease results in a hyperdynamic circulation characterized by a decrease in systemic vascular resistance, a decrease in arterial BP, and an increase in cardiac output and heart rate. This is likely related to splanchnic and peripheral vasodilatation, leading to a reduction in the effective arterial blood volume. This results in diminished renal blood flow and stimulation of the renin-angiotensin-aldosterone system, sympathetic nervous system, and antidiuretic hormone, leading to renal artery vasoconstriction, sodium retention, and volume expansion.