Haemodynamic Disorders

Transcription

1 Haemodynamic Disorders ZHANG WEI 张伟 Ph.D., A.P. Institute of Pathology & Forensic Medicine Department of Pathology & Patho-physiology Zhejiang University School of Medicine

2 Thrombosis 血栓形成 Def. Process of formation of a solid mass (thrombus 血栓 ) from the constituents of the blood within the heart or the vascular system in a living organism.

3 Factors and mechanism of thrombosis Virchow Triad 魏尔啸三要素 : three primary influences predispose to thrombus formation. Endothelial injury 心血管内皮损伤 Alterations in normal blood flow (Stasis or turbulence of blood flow) 血流状态改变 Blood hypercoagulability 血液凝固性增高

4 (1)Endothelial injury endothelial cells possess antiplatelet, anticoagulant, and fibrinolytic properties. Exposure of subendothelial collagen Adherence of platelets Release of tissue factor Depletion of PGI 2 & PA (plasminogen activators )

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6 Damage to vascular endothelium is the dominant influence thrombogenesis, and the only one which, by and of itself, may lead to thrombus formation. It may occur in the following situations: ulcerated atherosclerotic plaques; vascular traumatic or inflammatory injury; endocardium in the site of myocardial infarction or myocarditis; cardiac surgery.

7 (2)Alteration of blood flow (stasis 停滞 and turbulence 涡流 ) In normal laminar blood flow, all of the formed elements are separated from the endothelial surface by a clear plasmatic zone.

8 axial flow axial flow

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10 Turbulence and stasis lead to thrombosis clinical settings: -ulcerated atherosclerotic plaques -aneurysms -myocardial infarction -healed rheumatic mitral stenosis -atrial fibrillation and arrhythmias -sickle cell anaemia

11 (3)Hypercoagulability 血液高凝状态 Genetic (primary) Acquired (secondary)

12 Hypercoagulable states Primary (Genetic) Common Mutation in factor V gene (factor V Leiden) Mutation in prothrombin gene Mutation in methyltetrahydrofolate gene Rare Antithrombin III deficiency Protein C deficiency Protein S deficiency Very rare Fibrinolysis defects Secondary (Acquired) High risk for thrombosis Prolonged bedrest or immobilization Myocardial infarction Atrial fibrillation Tissue damage Cancer Prosthetic cardiac valves DIC Heparin-induced thrombocytopenia Antiphospholipid antibody syndrome Lower risk for thrombosis Cardiomyopathy Nephrotic syndrome Hyperestrogenic states (pregnancy) Oral contraceptive use Sickle cell anemia Smoking

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14 1. Process of Thrombosis 1 Endothelial injury platelets adhesion and aggregation. Platelets activation release reaction (ADP, TXA 2, 5-HT) platelet aggregation.

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18 2. Types of thrombus Pale Thrombus Vegetations Mixed Thrombus (body of thrombus) Red Thrombus (tail of thrombus) Hyaline Thrombus or Microthrombus

19 left atrium vegetations mitral valve left ventricle Vegetations on the mitral valve in rheumatic endocarditis. Note the small pink vegetations along the line of closure. These thrombi are made of platelets.

20 Microthrombus (Fibrin thrombus) Constitution: fibrin Location: micro-circulation in DIC. Especially in capillaries of kidney, lung, brain and liver

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23 Sites of Thrombosis Arterial Thrombosis Cardiac Thrombosis Venous Thrombosis

24 Mural thrombus Occlusive thrombus

25 mural thrombus

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27 Mural Thrombus

28 Result of thrombus 1. Softening, liquefaction, absorption. 2. Organization, recanalization. 3. Calcification. 4. Detachment of thrombus followed by thromboembolism.

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32 Effects of Thrombus Prevention of excessive bleeding Obstruction of arteries and veins Possible sources of emboli

33 Embolism 栓塞 Def. Occlusion or obstruction of some part of the cardiovascular system by an abnormal mass (solid, liquid, or gaseous) transported from a different site by the circulation. The transported mass is called as embolus.

34 1. Routes of embolus transportation The same direction as the blood (1) Arterial emboli induce embolism in brain, kiney, spleen and lower limbs. (2) Venous emboli usually lodge in the lung. (3) Portal vein system: liver.

35 (4) Crossed or Paradoxical embolism 交叉性栓塞 反常性栓塞 : In case of congenital septum defect of the heart, venous emboli may enter from the right into the left heart chambers. (5) Retrograde embolism 逆行性栓塞 : Emboli occasionally may travel against the direction of blood flow.

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37 2. Types of emboli Thromboembolism >99% Fat embolism Air embolism Amniotic fluid embolism Others

38 Thromboembolism 血栓栓塞 Pulmonary Thromoembolism Systemic Thromboembolism

39 Pulmonary Thromoembolism 肺动脉血栓栓塞 Sites of Origin the large deep veins of the lower leg Over 95% of pulmonary thrombi come from the deep leg vein above the level of the knee Prognosis the size of the occluded vessel the status of the patient s cardiovascular system.

40 Effects of Emboli Small emboli ---clinical silent Medium-sized emboli ---infarction, if left cardiac failure massive emboli ---sudden death

41 Clinical effect Majority clinically silent (60-80%), undergo organization If > 60% of pulmonary circulation is obstructed SUDDEN DEATH, right heart failure (RHF) Main pulmonary trunk Saddle emboli 骑跨性栓子 Smaller branches Small multiple emboli

42 Large embolus: fatal Mechanical obstruction + severe strain on the right side of the heart (acute cor pulmonale) + reflexive vascular and bronchial spasm.

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45 Systemic Thromoembolism Sites of Origin: Left cardiac thrombi(80%), arterial thrombi Effects the size the lodged vessel the collateral blood supply in the tissue the vulnerability of the tissue to ischemia

46 Morphology: They produce occlusion of blood stream most frequently in the spleen, the kidneys, the brain, and lower extremities, often with resultant infarcts in the organs and gangrene in the limbs.

47 Fat embolism Etiology: Morphology: Fracture of long bones Significant soft tissue trauma Pancreatitis

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50 Pulmonary fat embolism: Sequences: the quantity and site of embolism. 9~20g fat 75% pulmonary arteries are occluded asphyxia, right sided heart failure.

51 Gas embolism 1Air embolism 空气栓塞 Etiology: As a complication of trauma (chest), cardio-thoracic surgery, various diagnostic or therapeutic procedures, or rupture of veins during delivery.

52 Sequences: Small volume: absorbed >100ml: acute distress, fatal.

53 2Decompression sickness 减压病 Etiology and mechanism: Decompressed rapidly from high atmospheric pressure to a normal level of pressure (in deep sea divers, in underwater construction workers) or from normal atmospheric pressure to a low pressure (in aviators) Gas comes out of solution in the blood and tissue fluid in the form of minute bubbles which are composed of O 2, CO 2 and nitrogen. The nitrogen is of low solubility and persists as minute bubbles.

54 Amniotic fluid embolism 羊水栓塞 Etiology and mechanism: After rupture of membranes, some of the amniotic fluid may be forced by vigorous uterine contractions and then up to the placenta margin to enter the uterine sinusoids.

55 Morphology: The classic findings in the pulmonary arteries and capillaries at autopsy are epithelial squames from fetal skin, lanugo hairs 胎毛, fat from vernix caseosa, and mucin, presumed to be from the fetal GIT.

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57 Infarction 梗死 Def. Ischemic necrosis of tissue or organ caused by occlusion of either its arterial supply or its venous drainage is referred to infarct, the process of infarct formation is called as infarction.

58 1. Causes of infarct: (1) thrombosis: (2) arterial embolus: (3) arterial spasms: (4) blood vessel by pressure:

59 2. Factors: (1) nature of vascular supply: 1 effective anastomosis 吻合 2 double blood supply (liver, lung etc.) (2) vulnerability of the organ or tissue to hypoxia (nerve cells, myocardium > fibroblasts)

60 3. Types classified on the basis of their color (reflecting the amount of hemorrhage) and the presence or absence of microbial infection. white (anemic) infarct red (hemorrhagic) infarct septic infarct

61 (1)White infarct: Result of arterial occlusion, commonly seen in compact, solid organs with less collateral circulation, such as the kidneys, spleen and heart.

62 (2) Red infarct: occur: 1) with venous occlusions (such as in ovarian torsion); 2) in loose tissues (such as lung), which allow blood to collect in the infarcted zone; 3) in tissues with dual circulations (e.g., lung and small intestine; 4) in tissues that were previously congested;

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64 morphology Most infarcts tend to be wedge-shaped, with the occluded vessel at the apex and the periphery of the organ forming the base. margins : better defined by a narrow rim of hyperemia attributable to inflammation at the edge of the lesion.

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72 Organs of soft, loose tissue with double supply, infarcts tend to remain hemorrhagic (Red infarct)

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75 (3) Septic infarct: When an infarct is produced by a septic embolus, the infarct is converted to an abscess.

76 4. Fate of infarct (1) Small infarct: softened, absorbed (2) Large infarct: organization and scar formation (3) Septic infarct: abscess formation (4) Infarction of brain, myocardium or lung: sometimes may cause sudden death.

77 Thanks!