The document discusses various hemodynamic disorders including hyperemia, congestion, thrombosis, embolism, and infarction. Hyperemia is an increased blood volume in tissue from vasodilation. Congestion is increased blood volume from impaired venous return. Thrombosis is the formation of a blood clot within vessels. An embolism occurs when a piece of thrombus or other material blocks a vessel. Infarction is tissue death from blocked arteries or veins.

1. Chapter Three Hemodynamic Disorders

2. Normal fluid homeostasis vessel wall integrity hemorrhage Intravascular pressure or vascular volume ischemia hyperemia edema Maintenance of blood as a liquid thrombosis embolism infarction

3. Hyperemia: Arterial hyperemia Venous hyperemia Section A

4. a local increased volume of blood in a particular tissue. Hyperemia Normal blood fluid Hyperemia Congestion

5. Physiological: exercise Pathological : Inflammatory Post-ischemic Arterial hyperemia: Hyperemia is a local increased volume of blood in a particular tissue resulting from augmented blood flow due to arteriolar dilation.

7. Gross: Larger; redder; increased temperature; cut surface is hemorrhage and wet. LM: Dilatation of arteriole and capillary. Morphology of hyperemia

8. Congestion Congestion is a local increased volume of blood in capillaries and veinules resulting from impaired venous return from a tissue. Systemic —cardiac failure Etiology -L. heart failure -R. heart failure Pulmonary cong. Systemic cong. 1. External pressure 2. Internal occlusion Local

9. Pulmonary congestion Edema Hemorrhage Heart failure cells Brown induration

10. Gross: Increased volume and weight of organs; blue-red color (cyanosis); reduced temp.; wetness and excessive blood on the cut surface. Morphology

11. Acute pulmonary congestion

12. Chronic pulmonary congestion

14. Liver congestion Atrophy Fatty change Nutmeg liver Centrilobular necrosis liver cirrhosis

15. Hepatic congestion Central veins and hepatic sinuses of the centrilobular regions are distended with blood.

17. Microscopically: nutmeg liver ： Degeneration, atrophy and/or necrosis of the liver cells in the centrilobular regions Fatty degeneration of the liver cells in the peripheral part of the lobules

18. The central regions of the lobules become red-blue surrounded by a yellow-brown zone of uncongested liver substance. “ Nutmeg liver”

20. Cardiac cirrhosis of the liver in the longstanding cases

22. Thrombosis Thrombus Section B

23. Thrombosis is the process of formation of a clotted mass of blood within blood vessels or the heart in living body. The resultant mass is called a thrombus.

24. Normal hemostatic process

28. Endothelium Platelets Coagulation cascade

29. Fig 5-6 Pro- and anticoagulant activities of endothelial cells

30. Platelet adhesion and aggregation

31. Fig 5-8 The coagulation cascade

32. Fibrinolytic system

33. THREE INFLUENCES OF THROMBOSIS Endothelial injury (most important). Alone can induce thrombosis. Alterations in normal flow. Hypercoagulability. When the last two are both present, endothelial injury is not requisite.

34. Fig 5-6 Pro- and anticoagulant activities of endothelial cells

35. Endothelial injury Ulcerative atherosclerosis Transmural myocardial infarction Vasculitis Trauma Radiation Bacterial toxins

36. Alterations in normal blood flow Platelets activated by contact with endothelium. Slowed flow retards dilution of activated clotting factors and hepatic clearance. Stasis or turbulence retards the inflow of inhibitors. Turbulence may induce endothelial injury

37. Hypercoagulable states Primary (genetic): Antithrombin III deficiency Protein C deficiency Protein S deficiency Other combined deficiency

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.

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.

42. White thrombus Red thrombus Mixed thrombus Fibrin thrombus Types of thrombus

43. White thrombus Site: heart valve , artery Component: Platelet, fibrin

44. Mixed thrombus Site: heart chamber, vein Component: Platelet, fibrin,RBC

46. Mural thrombosis

47. Mural thrombosis

48. RED THROMBUS

49. Fibrinous thrombi are visible within parts of capi. of the glomerulus hyaline thrombi in a glomerulus

50. Absorption Organization Calcification Detachment Fate of thrombus

52. Organization and recanalization of thrombus During organization, the thrombus dissolved and blood could flow again.

54. Ischemia Congestion Heart valve disease DIC Embolism Effects of thrombosis

55. Embolism Embolus Section C

56. Embolism is a partial or complete obstruction of some part of the vascular system by any mass carried there in the circulation. The transported material is called an embolus. 99% thromboembolism.

57. Types of embolus Thromboembolism Fat embolism Air embolism Amniotic fluid embolism Other types

58. Etiology: Fractures of long bones Soft tissue trauma Burns Fat embolism

59. 90% of individuals with severe skeletal injuries 10% with clinical findings(1-3 days) Pulmonary insufficiency Neurologic symptoms Fat embolism

60. Fig 5-17

62. Etiology: Intravenous therapeutic procedures Obstetric procedures Chest wall injury Decompression sickness (nitrogen) Air embolism Gas bubbles within the circulation can obstruct vascular flow. A particular form of gas embolism called decompression sickness occurs when individuals are exposed to sudden changes in atmospheric pressure.

63. AMNIOTIC FLUID EMBOLISM Incidence: 1/50 000 deliveries Mortality rate: 80% Clinical onset: Sudden severe dyspnea, cyanosis, hypotensive shock, DIC

70. Embolus from left heart cavity or arterial system Embolus from right heart cavity or venous system Embolus from portal veins Paradoxical embolism Retrograde embolism Motional pathway of embolus:

72. Fig 5-16

74. THROMBOEMBOLISM Instantaneous death (>60%). Cardiovascular collapse. Right heart failure Pulmonary 1.Large emboli (5%):

76. 2.Small emboli (60-80%): Clinical silent in patients without cardiovascular failure. blood flow from bronchial arteries (collateral vascular supply)

77. 3. Between the extremes of large and small emboli (10-15%): Pulmonary hemorrhage. 4. Multiple small emboli: Pulmonary hypertension and vascular sclerosis.

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.

79. INFARCTION (INFARCT) Section D

80. infarct/infarction 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. The process whereby the infarct is developed is known as infarction.

81. Intrinsic occlusion for example, thrombosis, embolism expansion of atheroma Vasospasm Extrinsic compression for example, twisting of the vessels Etiology

82. INFARCTION Shape: Wedge-shaped Segmental Irregular Nature of necrosis Types: Red and white infarcts Morphology of infarct

87. LM: Ischemic coagulative necrosis Anemic infarct with few RBC Hemorrhagic infarct has engorgement and hemorrhage The pathology changes secondary to infarct such as hyperemia, hemorrhage, infla., organization and so on.

88. Myocardial infarct 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.

89. white infarct/anemic infarct arterial occlusions firm tissues

94. Venous occlusions Loose tissues Tissues with dual circulations Tissues previously congested Blood flow reestablished Red infarct/hemorrhagic infarct

95. The alteration of blood in pulmonary embolism

96. Hemorrhagic infarct of the lung

101. Hemorrhage Hemorrhage denotes an escape of blood from the cardiovascular system, usually is the result of the rupture of a blood vessel or the heart.