liver pathophysiology and manifestations of portal hypertension n.
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Liver Pathophysiology and Manifestations of Portal Hypertension. Evan Pivalizza November 2008. Physiology blood supply. 25% CO HA: 25% HBF, 45-50% O 2 PV: 75% HBF, 50-55% O 2 Flow ∞ pre-portal arterioles Flow + Resistance thru liver = portal pressure

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Liver Pathophysiology and Manifestations of Portal Hypertension


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    1. Liver Pathophysiology and Manifestations of Portal Hypertension Evan Pivalizza November 2008

    2. Physiology blood supply • 25% CO • HA: 25% HBF, 45-50% O2 • PV: 75% HBF, 50-55% O2 • Flow ∞ pre-portal arterioles • Flow + Resistance thru liver = portal pressure • PV: Presinusoidal(pre-capillary) + post-sinusoidal → venous resistance via SNS stimulation

    3. Portal hypertension • ↑ blood flow into system • Resistance portal system or portacaval collaterals • → ↓ PV flow (partial compensation ↑ HA flow) • O2 supply may be maintained • Total HBF ↓

    4. Pharmacokinetics Hepatic extraction  • HBF • Protein binding ( albumin – acidic drugs, alpha1 acid Gp often ↑ - basic drugs) • Intrinsic ability hepatic enzymes clear drug

    5. Highly extracted –  HBF • Morphine, lidocaine, midazolam (Cl fent/sufent , alfent ) • Poorly extracted drugs – Cl independent HBF • Highly protein bound • Diazepam, lorazepam, coumadin, phenytoin • Less protein binding • STP

    6. Hypoxemia in Liver Disease • Causes • Infection • Pleural effusion/ascites/hydrothorax (V/Q mismatch) • Hepato-Pulmonary Syndrome • Intrapulmonary VD • Vascular alterations lung tissue • Preop hypoxemia (indication for transplant) • ↑ mortality if PaO2 < 50 • Orthodeoxia (worse with standing)

    7. Diagnosis HPS • 4 - 25% incidence • ↑ A-a gradient (RA PaO2 < 70) • Intrapulmonary vascular dilations • Contrast TTE/TEE • Delayed contrast-enhanced echo (3-6 cycles vs. direct shunt – 1-2) - bubbles normally trapped alveoli → LA > 3 cardiac cycles • Technetium labeled albumin

    8. Treatment • Pressure controlled or limited TV • PEEP (maintain CO to sustain HBF) – NOT over PEEP • Consider prone

    9. Porto-Pulmonary Hypertension • Def: MPAP > 25 (rest), 30 (exercise), PCWP < 15, PVR > 240 (125) • Mild (<35), moderate (<45), severe (> 45 -periop mortality > 50%) • Volume overload • High CO • Cardiomyopathy

    10. MPAP < 35, PVR < 240, good cardiac function = proceed • MPAP > 35, attempt VD Rx • MPAP > 40, PVR > 240 = delay

    11. Rx: Plt aggregation/VC/endothelial proliferation • Oral • Endothelin antagonists (Bosentan) • Sildenafil • Simvastatin • Inhaled – NO, prostacycline • IV – Epoprosetenol + usual aids RV function (PDE inhibitors etc)

    12. HepatoRenal Syndrome • Predisposed renal failure • Radiocontrast imaging • NSAIDs • Hypovolemia variceal hemorrhage • HRS

    13. 17% pts admitted with ascites • 50% pts - die liver failure • Reversible renal VC + mild systemic hypotension • Kidney structurally normal (imbalance VC/VD mediators)

    14. Type 1 • Acute, progressive, 80% mortality • Type 2 • Diuretic resistant ascites, slow progression

    15. Rx: • Volume (albumin, esp. with paracentesis) • Systemic VC (terlipressin, vasopressin) • Transplant (liver + kidney)

    16. Coagulation • ↓ fibrinogen, II, V, VII, IX, X • Also, ↓coag inhibitors (ATIII, protein C,S) • Thrombocytopenia (hypersplenism) • Platelet function defect • ↑ fibrinolysis • ↑ FDPs → ↓ plt function (Ib binding) • ↓ Plasminogen activator inhibitor • Primary (vs. secondary – to activated thrombosis)