Portal HTN Flashcards
2 general causes of portal HTN
- increase in resistance to portal flow
- increase in portal venous flow
- P = R x F
main mechanism that leads to increased intrahepatic resistance
- deposition of fibrous tissue and the formation of nodules disrupts the architecture of the liver leading to an increased resistance to flow and to portal HTN
most common cause of portal HTN and site of increased resistance
- cirrhosis
- site of increased resistance is sinusoidal
examples of increased resistance in pre-hepatic
- portal or splenic vein thrombosis
examples of increased resistance in pre-sinusoidal
- schistosomiasis
- at the level of the portal triad
examples of increased resistance in post-sinusoidal
- veno-occlusive disease where fibrosis occurs in the central veins
examples of increased resistance in post-hepatic
- Budd-Chiari
- right sided heart failure
- hepatic vein thrombosis
increased intrahepatic resistance in cirrhosis is both structural and functional
- structural: sinusoidal fibrosis and regenerative nodules
- functional: active vasoconstriction
levels of vasodilators and vasoconstrictors in during cirrhosis
- NO activity is reduced
- endothelin-1(vasoconstrictor) activity is increased
3 main mechanisms of portal HTN in cirrhosis
- increased intrahepatic resistance: structural (fibrosis) and functional (decreased NO)
- increased splanchnic inflow (increased NO)
- increased collateral resistance
paradox of portal HTN
- in the intrahepatic vasculature there is a deficiency of NO leading to vasoconstriction but in the extrahepatic vasculature there is an overproduction leading to vasodilation
definition and cause of hyperdynamic circulatory state (HCS)
- consequence of portal HTN that plays an important role in the development and/or worsening of the complications of cirrhosis
- HCS results from systemic vasodilation, sodium retention, and blood volume expansion
splanchnic vasodilation as a consequence of HCS
- subsequent increase in portal venous inflow maintains portal hypertension and leads to increase in blood flow through collaterals that lead to variceal growth and their eventual rupture
peripheral vasodilation as a consequence of HCS
- leads to a decrease in effective blood volume that in turn leads to sodium retention which can lead to ascites
- with further vasodilation there is renal vasoconstriction which can lead to hepatorenal syndrome
late result of HCS
- high output heart failure with decreased peripheral utilization of O2
vasodilation in the pulmonary circulation as a consequence of HCS
- leads to arterial hypoxemia and hepatopulmonary syndrome
cerebral vasodilation as a consequence of HCS, especially in acute liver failure
- leads to brain edema and hepatic encephalopathy
factors associated with variceal growth
- Child-Pugh B/C cirrhosis, alcoholic etiology, presence of red wale marks on initial endoscopy
threshold portal pressure for variceal growth
- 11-12 mmHg
- the threshold HVPG level is necessary but not sufficient for the development of gastroesophageal varices
- factors other than pressure, such as volume of blood flow and local anatomic factors may contribute to the formation of varices
definitive method to diagnose portal HTN
- portal pressure measurements
portal pressure measurement equation
- HVPG = WHVP - FHVP
- hepatic venous pressure gradient (HVPG)
- wedged venous hepatic pressure (WHVP)
- free venous hepatic pressure (FHVP)
- normal HVPG ranges from 3-6 mmHg
when is HVPG normal
- pre-hepatic and presinusoidal portal HTN
- post-hepatic HTN - WHVP and FVHP are both elevated making HVPG normal
when is HVPG elevated
- sinusoidal HTN secondary to blockage of intersinusoidal communications by fibrous tissue
- post-sinusoidal HTN
predictors of variceal hemorrhage
- variceal size (larger ones are more likely to bleed)
- cherry red signs
- Child-Pugh B/C
- variceal wall tension (increased pressure leads to increased radius and the wall becomes thinner)
MOA of vasoconstrictors in treating HTN and varices
- increase splanchnic arteriolar resistance thereby reducing portal venous inflow
MOA of venodilators in treating HTN and varices
- reduces mean arterial pressure and subsequent reduction of portal inflow
MOA of TIPS/shunt surgery in treating HTN and varices
- shunt that bypasses the site of increased resistance, normalizing pressure
- however there is an increased incidence of hepatic encephalopathy and liver failure
MOA of variceal band ligation/sclerotherapy
- attempts to obliterate the variceal
- does not modify splanchnic flow or intrahepatic resistance so variceal recurrences is the rule
prevention of varices
- non-selective beta blockers DO NOT prevent the development of varices
prevention of variceal hemorrhaging
- non-selective beta blockers PREVENT first variceal hemorrhage
- if beta blockers are contraindicated (asthma, COPD) then use band ligation therapy
treatment of acute variceal hemorrhage
- safe vasoactive drug (somatostatin, OCTREOTIDE, vapreotide), endoscopy, antibiotic prophylaxis
- 2nd line: TIPS/shunt therapy
most common AE of TIPS
- hepatic encephalopathy
treatment of recurrent hemorrhage
- best treatment is beta blockers with band ligation
90% of gastric varices can be controlled by
- endoscopic cyanoacrylate injection
- TIPS
treatment of hypertensive gastropathy
- non-selective beta blockers
