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Hemodynamic Disorders

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Hemodynamic Disorders

  1. 1. Chapter Three Hemodynamic Disorders
  2. 2. Normal fluid homeostasis <ul><li>vessel wall integrity </li></ul><ul><li>hemorrhage </li></ul><ul><li>Intravascular pressure or vascular volume </li></ul><ul><li>ischemia </li></ul><ul><li>hyperemia </li></ul><ul><li>edema </li></ul><ul><li>Maintenance of blood as a liquid </li></ul><ul><li>thrombosis </li></ul><ul><li>embolism </li></ul><ul><li>infarction </li></ul>
  3. 3. Hyperemia: Arterial hyperemia Venous hyperemia Section A
  4. 4. <ul><li>a local increased volume of blood in a particular tissue. </li></ul>Hyperemia Normal blood fluid Hyperemia Congestion
  5. 5. Physiological: exercise Pathological : Inflammatory Post-ischemic <ul><li>Arterial hyperemia: </li></ul><ul><li>Hyperemia is a local increased volume of blood in a particular tissue resulting from augmented blood flow due to arteriolar dilation. </li></ul>
  6. 7. <ul><li>Gross: </li></ul><ul><li>Larger; redder; increased temperature; cut surface is hemorrhage and wet. </li></ul><ul><li>LM: </li></ul><ul><li>Dilatation of arteriole and capillary. </li></ul>Morphology of hyperemia
  7. 8. <ul><li>Congestion </li></ul><ul><li>Congestion is a local increased volume of blood in capillaries and veinules resulting from impaired venous return from a tissue. </li></ul>Systemic —cardiac failure <ul><li>Etiology </li></ul>-L. heart failure -R. heart failure Pulmonary cong. Systemic cong. 1. External pressure 2. Internal occlusion Local
  8. 9. Pulmonary congestion Edema Hemorrhage Heart failure cells Brown induration
  9. 10. <ul><li>Gross: </li></ul><ul><li>Increased volume and weight of organs; blue-red color (cyanosis); reduced temp.; wetness and excessive blood on the cut surface. </li></ul>Morphology
  10. 11. Acute pulmonary congestion
  11. 12. Chronic pulmonary congestion
  12. 14. Liver congestion Atrophy Fatty change Nutmeg liver Centrilobular necrosis liver cirrhosis
  13. 15. <ul><li>Hepatic congestion </li></ul>Central veins and hepatic sinuses of the centrilobular regions are distended with blood.
  14. 17. <ul><li>Microscopically: nutmeg liver : </li></ul><ul><li>Degeneration, atrophy and/or necrosis of the liver cells in the centrilobular regions </li></ul><ul><li>Fatty degeneration of the liver cells in the peripheral part of the lobules </li></ul>
  15. 18. <ul><li>The central regions of the lobules become red-blue surrounded by a yellow-brown zone of uncongested liver substance. </li></ul>“ Nutmeg liver”
  16. 20. Cardiac cirrhosis of the liver in the longstanding cases
  17. 22. Thrombosis Thrombus Section B
  18. 23. <ul><li>Thrombosis is the process of formation of a clotted mass of blood within blood vessels or the heart in living body. </li></ul><ul><li>The resultant mass is called a thrombus. </li></ul>
  19. 24. Normal hemostatic process
  20. 28. <ul><li>Endothelium </li></ul><ul><li>Platelets </li></ul><ul><li>Coagulation cascade </li></ul>
  21. 29. <ul><li>Fig 5-6 </li></ul>Pro- and anticoagulant activities of endothelial cells
  22. 30. Platelet adhesion and aggregation
  23. 31. <ul><li>Fig 5-8 </li></ul>The coagulation cascade
  24. 32. Fibrinolytic system
  25. 33. THREE INFLUENCES OF THROMBOSIS <ul><li>Endothelial injury (most important). </li></ul><ul><li>Alone can induce thrombosis. </li></ul><ul><li>Alterations in normal flow. </li></ul><ul><li>Hypercoagulability. </li></ul><ul><li>When the last two are both present, </li></ul><ul><li>endothelial injury is not requisite. </li></ul>
  26. 34. <ul><li>Fig 5-6 </li></ul>Pro- and anticoagulant activities of endothelial cells
  27. 35. Endothelial injury <ul><li>Ulcerative atherosclerosis </li></ul><ul><li>Transmural myocardial infarction </li></ul><ul><li>Vasculitis </li></ul><ul><li>Trauma </li></ul><ul><li>Radiation </li></ul><ul><li>Bacterial toxins </li></ul>
  28. 36. Alterations in normal blood flow <ul><li>Platelets activated by contact with </li></ul><ul><li>endothelium. </li></ul><ul><li>Slowed flow retards dilution of activated </li></ul><ul><li>clotting factors and hepatic clearance. </li></ul><ul><li>Stasis or turbulence retards the inflow of </li></ul><ul><li>inhibitors. </li></ul><ul><li>Turbulence may induce endothelial injury </li></ul>
  29. 37. Hypercoagulable states Primary (genetic): Antithrombin III deficiency Protein C deficiency Protein S deficiency Other combined deficiency
  30. 38. Hypercoagulable states Secondary (acquired): High risk: Prolonged bed rest or immobilization. Myocardial infarction. Tissue damage (surgery, fractures, burns). Cardiac failure. Cancer. Acute leukemia. DIC. Thrombotic thrombocytopenia.
  31. 39. Hypercoagulable states Secondary (acquired): Low risk: Atrial fibrillation. Cardiomyopathy. Nephrotic syndrome. Hyperlipidemia. Late pregnancy/postdelivery. Oral contraceptives. Lupus anticoagulant. Sickle cell anemia. Smoking. Thrombocytosis.
  32. 42. <ul><li>White thrombus </li></ul><ul><li>Red thrombus </li></ul><ul><li>Mixed thrombus </li></ul><ul><li>Fibrin thrombus </li></ul>Types of thrombus
  33. 43. White thrombus Site: heart valve , artery Component: Platelet, fibrin
  34. 44. Mixed thrombus Site: heart chamber, vein Component: Platelet, fibrin,RBC
  35. 46. Mural thrombosis
  36. 47. Mural thrombosis
  37. 48. RED THROMBUS
  38. 49. Fibrinous thrombi are visible within parts of capi. of the glomerulus <ul><li>hyaline thrombi in a glomerulus </li></ul>
  39. 50. <ul><li>Absorption </li></ul><ul><li>Organization </li></ul><ul><li>Calcification </li></ul><ul><li>Detachment </li></ul>Fate of thrombus
  40. 52. Organization and recanalization of thrombus During organization, the thrombus dissolved and blood could flow again.
  41. 54. <ul><li>Ischemia </li></ul><ul><li>Congestion </li></ul><ul><li>Heart valve disease </li></ul><ul><li>DIC </li></ul><ul><li>Embolism </li></ul>Effects of thrombosis
  42. 55. <ul><li>Embolism </li></ul><ul><li>Embolus </li></ul>Section C
  43. 56. <ul><li>Embolism is a partial or complete obstruction of some part of the vascular system by any mass carried there in the circulation. </li></ul><ul><li>The transported material is called an embolus. </li></ul><ul><li>99% thromboembolism. </li></ul>
  44. 57. Types of embolus <ul><li>Thromboembolism </li></ul><ul><li>Fat embolism </li></ul><ul><li>Air embolism </li></ul><ul><li>Amniotic fluid embolism </li></ul><ul><li>Other types </li></ul>
  45. 58. <ul><li>Etiology: </li></ul><ul><li>Fractures of long bones </li></ul><ul><li>Soft tissue trauma </li></ul><ul><li>Burns </li></ul>Fat embolism
  46. 59. <ul><li>90% of individuals with severe skeletal injuries </li></ul><ul><li>10% with clinical findings(1-3 days) </li></ul><ul><li>Pulmonary insufficiency </li></ul><ul><li>Neurologic symptoms </li></ul>Fat embolism
  47. 60. <ul><li>Fig 5-17 </li></ul>
  48. 62. Etiology: Intravenous therapeutic procedures Obstetric procedures Chest wall injury Decompression sickness (nitrogen) Air embolism <ul><li>Gas bubbles within the circulation can obstruct vascular flow. </li></ul><ul><li>A particular form of gas embolism called decompression sickness occurs when individuals are exposed to sudden changes in atmospheric pressure. </li></ul>
  49. 63. AMNIOTIC FLUID EMBOLISM Incidence: 1/50 000 deliveries Mortality rate: 80% Clinical onset: Sudden severe dyspnea, cyanosis, hypotensive shock, DIC
  50. 70. <ul><li>Embolus from left heart cavity or </li></ul><ul><li>arterial system </li></ul><ul><li>Embolus from right heart cavity or </li></ul><ul><li>venous system </li></ul><ul><li>Embolus from portal veins </li></ul><ul><li>Paradoxical embolism </li></ul><ul><li>Retrograde embolism </li></ul>Motional pathway of embolus:
  51. 72. <ul><li>Fig 5-16 </li></ul>
  52. 74. THROMBOEMBOLISM <ul><li>Instantaneous death (>60%). </li></ul><ul><li>Cardiovascular collapse. </li></ul><ul><li>Right heart failure </li></ul>Pulmonary 1.Large emboli (5%):
  53. 76. 2.Small emboli (60-80%): <ul><li>Clinical silent in patients without </li></ul><ul><li>cardiovascular failure. </li></ul><ul><li>blood flow from bronchial arteries </li></ul><ul><li>(collateral vascular supply) </li></ul>
  54. 77. 3. Between the extremes of large and small emboli (10-15%): Pulmonary hemorrhage. 4. Multiple small emboli: Pulmonary hypertension and vascular sclerosis.
  55. 78. Systemic embolism I . 80-85% from heart, secondary to myocardial infarction. II . 5-10% from auricular thrombi associated with rheumatic heart disease and atrial fibrillation. III . 5% from the dilated cardiac chamber of myocarditis / cardiomyopathy. VI . Less common sources: Debris from ulcerative atheromata, or thrombi in aneurysms, infectious endocarditis, prosthetic valves, paradoxical emboli. V . Unknown.
  56. 79. <ul><li>INFARCTION </li></ul><ul><li>(INFARCT) </li></ul>Section D
  57. 80. infarct/infarction <ul><li>An infarct is a localized area of ischemic necrosis in a tissue or organ produced by occlusion of either its arterial supply or its venous drainage. </li></ul><ul><li>The process whereby the infarct is developed is known as infarction. </li></ul>
  58. 81. Intrinsic occlusion for example, thrombosis, embolism expansion of atheroma Vasospasm Extrinsic compression for example, twisting of the vessels Etiology
  59. 82. INFARCTION <ul><li>Shape: Wedge-shaped </li></ul><ul><li>Segmental </li></ul><ul><li>Irregular </li></ul><ul><li>Nature of necrosis </li></ul><ul><li>Types: Red and white infarcts </li></ul>Morphology of infarct
  60. 87. <ul><li>LM: </li></ul><ul><li>Ischemic coagulative necrosis </li></ul><ul><li>Anemic infarct with few RBC </li></ul><ul><li>Hemorrhagic infarct has engorgement and hemorrhage </li></ul><ul><li>The pathology changes secondary to infarct such as hyperemia, hemorrhage, infla., organization and so on. </li></ul>
  61. 88. <ul><li>Myocardial infarct </li></ul>The myocardial cells shows coagulative necrosis with the outline of the myocardium. In the margin of the infarct there are numerous inflammatory exudation and connective tissue.
  62. 89. white infarct/anemic infarct <ul><li>arterial occlusions </li></ul><ul><li>firm tissues </li></ul>
  63. 94. Venous occlusions Loose tissues Tissues with dual circulations Tissues previously congested Blood flow reestablished Red infarct/hemorrhagic infarct
  64. 95. The alteration of blood in pulmonary embolism
  65. 96. <ul><li>Hemorrhagic infarct of the lung </li></ul>
  66. 101. Hemorrhage <ul><li>Hemorrhage denotes an escape of blood from the cardiovascular system, usually is the result of the rupture of a blood vessel or the heart. </li></ul>

Editor's Notes

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