1 / 17

Liver Pathophysiology and Manifestations of Portal Hypertension

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

eitan
Download Presentation

Liver Pathophysiology and Manifestations of Portal Hypertension

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  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)

More Related