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Understanding Hemodynamic Disorders & Edema: Overview and Mechanisms Explained

Explore the intricate world of hemodynamic disorders, thromboembolic disease, and shock. Learn about edema and its causes, such as increased hydrostatic pressure, reduced oncotic pressure, lymphatic obstruction, and sodium/water retention. Discover the role of water in the body and the various types of edema. Delve into the complexities of hyperemia, congestion, hemorrhage, hemostasis, thrombosis, embolism, infarction, and shock.

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Understanding Hemodynamic Disorders & Edema: Overview and Mechanisms Explained

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  1. HEMODYNAMIC DISORDERS Jv = ([Pc − Pi] − σ[πc − πi])

  2. Hemodynamic Disorders • Thromboembolic Disease • Shock

  3. Overview • Edema (increased fluid in the ECF) • Hyperemia (INCREASED flow) • Congestion (INCREASED backup) • Hemorrhage (extravasation) • Hemostasis (opposite of thrombosis) • Thrombosis (clotting blood) • Embolism (downstream travel of a clot) • Infarction (death of tissues w/o blood) • Shock (circulatory failure/collapse)

  4. EDEMA • ONLY 4 POSSIBILITIES!!! • Increased Hydrostatic Pressure • Reduced Oncotic Pressure • Lymphatic Obstruction • Sodium/Water Retention

  5. WATER • 60% of body • 2/3 of body water is INTRA-cellular • The rest is INTERSTITIAL • Only 5% is INTRA-vascular • EDEMA is SHIFT to the INTERSTITIAL SPACE • HYDRO- • -THORAX, -PERICARDIUM, -PERITONEAL • EFFUSIONS, ASCITES, ANASARCA

  6. INCREASED HYDROSTATIC PRESSURE • Impaired venous return • Congestive heart failure   • Constrictive pericarditis   • Ascites (liver cirrhosis)   • Venous obstruction or compression • Thrombosis     • External pressure (e.g., mass) • Lower extremity inactivity with prolonged dependency • Arteriolar dilation • Heat   • Neurohumoral dysregulation

  7. REDUCED PLASMA ONCOTICPRESSURE (HYPOPROTEINEMIA) • Protein-losing glomerulopathies (nephrotic syndrome) • Liver cirrhosis (ascites) • Malnutrition • Protein-losing gastroenteropathy

  8. LYMPHATIC OBSTRUCTION(LYMPHEDEMA) • Inflammatory • Neoplastic • Postsurgical • Postirradiation

  9. Na+ RETENTION • Excessive salt intake with renal insufficiency • Increased tubular reabsorption of sodium • Renal hypoperfusion Increased renin-angiotensin-aldosterone secretion

  10. INFLAMMATION • Acute inflammation • Chronic inflammation • Angiogenesis

  11. Jv = ([Pc − Pi] − σ[πc − πi])

  12. CHF EDEMA • INCREASED VENOUS PRESSURE DUE TO FAILURE • DECREASED RENAL PERFUSION, triggering of RENIN-ANGIOTENSION-ALDOSTERONE complex, resulting ultimately in SODIUM RETENTION

  13. HEPATIC ASCITES • PORTAL HYPERTENSION • HYPOALBUMINEMIA

  14. ASCITES

  15. RENAL EDEMA • SODIUM RETENTION • PROTEIN LOSING GLOMERULOPATHIES (NEPHROTIC SYNDROME)

  16. EDEMA • SUBCUTANEOUS (“PITTING”) • “DEPENDENT” • ANASARCA • LEFT vs RIGHT HEART • PERIORBITAL • PULMONARY • CEREBRAL (closed cavity, no expansion) • HERNIATION of cerebellar tonsils • HERNIATION of hippocampal uncus over tentorium • HERNIATION, subfalcine

  17. “Pitting” Edema

  18. Transudate vs Exudate • Transudate • results from disturbance of Starling forces • specific gravity < 1.012 • protein content < 3 g/dl, LDH LOW • Exudate • results from damage to the capillary wall • specific gravity > 1.012 • protein content > 3 g/dl, LDH HIGH

  19. HYPEREMIA/(CONGESTION)

  20. HYPEREMIA Active Process CONGESTION Passive Process Acute or Chronic

  21. CONGESTION • LUNG • ACUTE • CHRONIC • LIVER • ACUTE • CHRONIC • CEREBRAL

  22. ACUTE PASSIVE HYPEREMIA/CONGESTION, LUNG

  23. Kerley B Air Bronch-ogram

  24. CHRONIC PASSIVE HYPEREMIA/CONGESTION, LUNG

  25. Acute Passive Congestion, Liver

  26. Acute Passive Congestion, Liver

  27. CHRONIC PASSIVE HYPEREMIA/CONGESTION, LIVER

  28. HEMORRHAGE • EXTRAVASATION beyond vessel • “HEMORRHAGIC DIATHESIS” • HEMATOMA (implies MASS effect) • “DISSECTION” • PETECHIAE (1-2mm) (PLATELETS) • PURPURA <1cm • ECCHYMOSES >1cm (BRUISE) • HEMO-: -thorax, -pericardium, -peritoneum, HEMARTHROSIS • ACUTE, CHRONIC

  29. EVOLUTION of HEMORRHAGE • ACUTE CHRONIC • PURPLE GREEN BROWN • HGB BILIRUBIN HEMOSIDERIN

  30. HEMATOMAvs.“CLOT”

  31. HEMOSTASIS • OPPOSITE of THROMBOSIS • PRESERVE LIQUIDITY OF BLOOD • “PLUG” sites of vascular injury • THREE COMPONENTS • VASCULAR WALL, i.e., endoth/ECM • PLATELETS • COAGULATION CASCADE

  32. SEQUENCE of EVENTSfollowing VASCULAR INJURY • ARTERIOLAR VASOCONSTRICTION • Reflex Neurogenic • Endothelin, from endothelial cells • THROMBOGENIC ECM at injury site • Adhere and activate platelets • Platelet aggregation (1˚ HEMOSTASIS) • TISSUE FACTOR released by endothelium, plats. • Activates coagulation cascadethrombinfibrin (2˚ HEMOSTASIS) • FIBRIN polymerizes, TPA limits plug

  33. PLAYERS • ENDOTHELIUM • PLATELETS • COAGULATION “CASCADE”

  34. ENDOTHELIUM • NORMALLY • ANTIPLATELET PROPERTIES • ANTICOAGULANT PROPERTIES • FIBRINOLYTIC PROPERTIES • IN INJURY • PRO-COAGULANT PROPERTIES

  35. ENDOTHELIUM • ANTI-Platelet PROPERTIES • Protection from the subendothelial ECM • Degrades ADP (inhib. Aggregation) • ANTI-Coagulant PROPERTIES • Membrane HEPARIN-like molecules • Makes THROMBOMODULIN Protein-C • TISSUE FACTOR PATHWAY INHIBITOR • FIBRINOLYTIC PROPERTIES (TPA)

  36. ENDOTHELIUM • PROTHROMBOTIC PROPERTIES • Makes vWF, which binds PlatsColl • Makes TISSUE FACTOR (with plats) • Makes Plasminogen inhibitors

  37. ENDOTHELIUM • ACTIVATED by INFECTIOUSAGENTS • ACTIVATED by HEMODYNAMICS • ACTIVATED by PLASMA • ACTIVATED by ANYTHING which disrupts it

  38. PLATELETS • ALPHA GRANULES • Fibrinogen • Fibronectin • Factor-V, Factor-VIII • Platelet factor 4, TGF-beta • DELTA GRANULES (DENSE BODIES) • ADP/ATP, Ca+, Histamine, Serotonin, Epineph. • With endothelium, form TISSUE FACTOR

  39. NORMAL platelet on LEFT, “DEGRANULATING” ALPHA GRANULE ON RIGHT AT OPEN WHITE ARROW

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