In liver cirrhosis, does the patient develop systemic hypotension or portal hypertension?

Cirrhosis and Blood Pressure Changes

In liver cirrhosis, patients develop both systemic hypotension and portal hypertension simultaneously—these are not mutually exclusive but rather two distinct manifestations of the same pathophysiological process. 1

Portal Hypertension (Increased Pressure in Portal Circulation)

Portal hypertension is the hallmark vascular complication of cirrhosis and develops through two mechanisms 1:

• Increased intrahepatic resistance (70% structural component from fibrosis and regenerative nodules, 30% functional component from endothelial dysfunction) 1
• Increased portal venous inflow from splanchnic vasodilation 1
• Portal hypertension is defined as hepatic venous pressure gradient (HVPG) >5 mmHg, with clinically significant portal hypertension occurring at HVPG ≥10 mmHg 2, 3
• This elevated portal pressure is essential for ascites development—fluid accumulation does not occur below 8 mmHg portal pressure gradient 1

Systemic Hypotension (Decreased Arterial Blood Pressure)

Systemic arterial hypotension develops as a direct consequence of the same pathophysiology causing portal hypertension 1, 4:

• Splanchnic and peripheral arterial vasodilation occurs due to overproduction of nitric oxide and other vasodilators that bypass hepatic degradation through portosystemic collaterals 1, 4, 5
• This vasodilation leads to decreased systemic vascular resistance and low arterial blood pressure 4, 6
• The resulting "effective hypovolemia" (despite actual hypervolemia) activates compensatory mechanisms including the sympathetic nervous system and renin-angiotensin-aldosterone system 1
• Patients develop a hyperdynamic circulatory state characterized by increased cardiac output, elevated heart rate, and reduced systemic vascular resistance with low blood pressure 4, 6, 7

The Paradox Explained

The key pathophysiological sequence is 1, 4:

1. Increased intrahepatic resistance → elevated portal pressure (portal hypertension)
2. Portosystemic collateral formation → vasodilators bypass hepatic clearance
3. Splanchnic vasodilation → increased portal inflow (worsening portal hypertension) AND systemic vasodilation (causing hypotension)
4. Compensatory mechanisms → sodium/water retention, increased blood volume, elevated cardiac output (attempting to maintain blood pressure but failing due to severe vasodilation)

Clinical Significance

• Portal hypertension leads to varices, ascites, hepatorenal syndrome, and splenomegaly 1, 8
• Systemic hypotension contributes to renal dysfunction, hepatorenal syndrome, and limits use of certain medications (vasodilators cannot be used alone as they worsen hypotension) 1
• HVPG ≥16 mmHg is strongly associated with increased mortality 2, 8
• The hyperdynamic state persists even after liver transplantation 7

Critical caveat: Vasodilators targeting the functional component of increased intrahepatic resistance should not be used alone because they also cause systemic vasodilation, decrease arterial blood pressure, and may worsen sodium retention 1