Hemodynamics class 3.pptx

1. Hemodynamic Disorders Dr Shallo Alemu 5/28/2023 hemodynamics 1

2. Hemostasis and thrombosis • Hemostasis is a precisely orchestrated process involving platelets, clotting factors, and endothelium that occurs at the site of vascular injury and culminates in the formation of a blood clot, which serves to prevent or limit the extent of bleeding 5/28/2023 hemodynamics 2

3. Hemostasis and thrombosis • Normal hemostasis – rapid and localized hemostatic plug formation at a site of vascular injury. • Thrombosis • Pathologic opposite to hemostasis. • Inappropriate activation of normal hemostatic process: • Clot (thrombus) in uninjured vessel • Thrombotic occlusion of a vessel after minor injury 5/28/2023 hemodynamics 3

4. • Both hemostasis and thrombosis depends on 3 components: • Endothelium • Platelet • Coagulation cascade 5/28/2023 hemodynamics 4

5. Normal hemostasis • Sequence of events at sites of vascular injury: I. Arteriolar vasoconstriction II. Primary hemostasis (platelet plug) III. Secondary hemostasis – fibrin deposition IV. Permanent plug • Polymerized fibrin and platelet aggregate V. Counter regulatory response • Restricts hemostatic plug at site of injury • Tissue plasminogen activator 5/28/2023 hemodynamics 5

6. 5/28/2023 hemodynamics 6

7. So when does the process of coagulation becomes pathologic? • If body is unable to mount coagulation,  bleeding diathesis • Platelets (number, functional abnormalities) • Clotting factor deficiencies • Hemophilia A,B and C • Vascular abnormalities • Vasculitis or amyloidosis 5/28/2023 hemodynamics 7

8. Hemophilia 5/28/2023 hemodynamics 8

9. Virchow's triads • If thrombosis is obstinate and excess 5/28/2023 hemodynamics 9

11. Endothelium • Prothrombic properties • vWF • Tissue factor • Tissue plasminogen activator inhibitor (t-PAI) • Antithrombotic properties • Heparin like molecules • Tissue factor pathway inhibitor • Thrombin receptor and Thrombomodulin • Prostacyclin, NO, ADPase, • t-PA 5/28/2023 hemodynamics 11

13. Endothelial injury • Most important factor in thrombus formation • Exposure to the highly thrombogenic sub endothelial ECM (collagen & tissue factors)  platelet adherence & contact activation 5/28/2023 hemodynamics 13

14. Stasis or turbulence blood flow • Normal blood flow is laminar. • Stasis & turbulence brings platelets to the surface and reduce PGI2, t-PA • Stasis is major factor in venous thrombi • Turbulence is pathogenesis mzm for arteries and cardiac thrombosis 5/28/2023 hemodynamics 14

15. Hypercoagulability • Any alteration of the coagulation pathway that predisposes to thrombosis • Primary hypercoagulable states • Mutations in factor V (Leiden factor) • Mutation in prothrombin gene • Antithrombin III deficiency • Protein C or S deficiency Secondary hypercoagulable states • High risk • Prolonged immobilization • Myocardial infarction • Tissue damage • Cancers • DIC • Low risk factors • Atrial fibrillation • Cardiomyopathy • Oral contraceptives • Smoking • Hyper estrogenic states E.g –pregnancy 5/28/2023 hemodynamics 15

16. Cont’d,… • Don’t forget these terms • Mural thrombi • Vegetation • The most common site of arterial thrombi in increasing order of frequency • Femoral arteries • Cerebral arteries • Coronary arteries • Common site venous thromboembolism • Leg veins • Vena cava • Dural venous sinuses 5/28/2023 hemodynamics 16

17. • Fates of thrombus • Propagation • Dissolution • Embolization • Organization & recanalization 5/28/2023 hemodynamics 17

18. Clinical significance • Thrombi are clinically significant because: • They can cause blood vessel obstruction (arterial thrombi causing myocardial infarction) or • Possible sources of emboli (venous thrombi causing pulmonary embolism, deadly complication) 5/28/2023 hemodynamics 18

19. Venous thrombosis (phlebothrombosis) • Affects the lower extremity veins~90% • Divided in to • superficial and • deep venous thrombosis • Superficial VT • Usually occurs in saphenous venous system • E.g in varicosities • Predisposes to infection after slight trauma  Varicous Ulcer • Rarely embolizes • Causes local edema ,pain ,tenderness(i.e symptomatic 5/28/2023 hemodynamics 19

20. Deep Vein Thrombosis (DVT) • May embolize, hence serious • Occurs in deep veins of calf muscles • May cause pain or edema • Asymptomatic in ~50%, because of collateral bypass channels. Might be noted after causing pulmonary embolism. • Higher incidence in middle aged & elderly people ,due to increased platelet aggregation & decreased PGI2 by endothelium 5/28/2023 hemodynamics 20

21. Predisposing factors to DVT • Trauma, surgery, prolonged bed rest • Reduced physical activity • Injury to vessels • Procoagulant release from tissues • Reduced t-PA activity (fibrinolysis) • Pregnancy & puerperal states • Increase coagulation factors & decrease synthesis of antithrombic substances • Myocardial infarction & heart failure  stasis in the left side 5/28/2023 hemodynamics 21

22. • Malnutrition, debilitating conditions (cancer)  marantic thrombosis • Inflammation of veins (thrombophlebitis) • Migratory thrombophlebitis- unknown etiology • sometimes associated with cancer, especially pancreatic cancer  Trosseau syndrome 5/28/2023 hemodynamics 22

23. Arterial thrombosis • Following abnormal vessel wall & turbulence is commonest predisposing factor • Myocardial infarction causing dyskinetic contraction & endocardial damage. • May narrow or occlude the lumen of arteries such as coronary &cerebral arteries  myocardial & cerebral infarctions respectively 5/28/2023 hemodynamics 23

24. Embolism 5/28/2023 hemodynamics 24 Embolus –detached intravascular solid, liquid or gaseous mass that is carried by blood to sites distant from its point of origin.

25. Causes of embolism • Thrombus (90% cases)  thromboembolic • Unless specified embolism  thromboembolism • Platelet aggregates • fragment of a tumor • Less commonly, emboli are composed of fat droplets, bubbles of air or nitrogen, atherosclerotic debris (cholesterol emboli), tumor fragments, bits of bone marrow, or amniotic fluid 5/28/2023 hemodynamics 25

26. • Thromboembolism, based on the site of origin & impaction, is divided in to: • Pulmonary thromboembolism (PTE) • Systemic thromboembolism • Crossed embolism(paradoxical embolism) 5/28/2023 hemodynamics 26

27. Consequences • Systemic embolization • Ischemic necrosis (infarction) of downstream tissues, whereas • Embolization in the pulmonary circulation • Hypoxia, hypotension, and right-sided heart failure 5/28/2023 hemodynamics 27

28. Pulmonary thromboembolism • Embolus in the pulmonary arteries & their branches • Derived from thrombus in the systemic veins or right side of the heart. • ~95% arise from deep leg veins and follows venous return, pass through heart and arrest pulmonary arteries a. If large thrombus  block right ventricle out flow or bifurcation of the main pulmonary trunk (saddle embolus) or both of its branches  sudden circulatory arrest and death b. It may result in cor- pulmonale or CVA collapse if 60% of blood volume is obstructed 5/28/2023 hemodynamics 28

29. Very small embolus (60-80% of cases) • Clinically silent, obstruction of medium sized arteries these embolus may cause pulmonary hemorrhage but not infarction, because collaterals from bronchial circulation. • But in poor cardiorespiratory condition, medium arteries obstruction  pulmonary infarction • Small end-arterial vessel obstruction causes infarction. • Recurrent thromboembolism  pulmonary hypertension in the long run 5/28/2023 hemodynamics 29

30. Systemic thromboembolism • 80% arise from intracardiac mural thrombi • 2/3 of intramural thrombi associated with left ventricular wall infarcts & 25% with dilated left atria (rheumatic heart diseases) • Remainder originate from aortic aneurysms, thrombi overlying ulcerated atherosclerotic plaques, fragmented valvular vegetations, or the venous system (paradoxical emboli); • 10% to 15% of systemic emboli are of unknown origin. • Major sites of embolization: lower extremities(75%), brain(10%), intestines, kidneys, spleen 5/28/2023 hemodynamics 30

32. Fat Embolism • Fat globules in the circulation • Commonly - fractures of long bones or, • Rarely - soft tissue trauma and burns. • the fat enters the circulation by rupture of the marrow vascular sinusoids or rupture of venules. • 90% of individuals with severe skeletal injuries • fewer than 10% of such patients show any clinical findings. 5/28/2023 hemodynamics 32

33. • Fat embolism syndrome • pulmonary insufficiency, • neurologic symptoms, • anemia, and • thrombocytopenia and • fatal in about 10% of cases. • Typically, the symptoms appear 1 to 3 days after injury, • sudden onset of tachypnea, dyspnea, and tachycardia. • Neurologic symptoms - irritability and restlessness, with progression to delirium or coma. • The pathogenesis of this syndrome involves both mechanical obstruction and chemical injury. 5/28/2023 hemodynamics 33

34. Air Embolism • Gas bubbles within the circulation can obstruct vascular flow (and cause distal ischemic injury) almost as readily as thrombotic masses. • Air may enter the circulation during obstetric procedures or as a consequence of chest wall injury. • in excess of 100 mL of air is required to produce a clinical effect; • bubbles -> physical obstructions and may coalesce to form frothy masses sufficiently large to occlude major vessels. 5/28/2023 hemodynamics 34

35. Amniotic Fluid Embolism • is a grave but uncommon complication of labor and the immediate postpartum period (1 in 50,000 deliveries). • mortality rate in excess of 80%. 5/28/2023 hemodynamics 35

36. • Onset – • sudden severe dyspnea, • cyanosis, and • hypotensive shock, • seizures and coma. • If the patient survives, • pulmonary edema , • DIC - release of thrombogenic substances from amniotic fluid. 5/28/2023 hemodynamics 36

37. Amniotic Fluid Embolism 5/28/2023 hemodynamics 37

38. Infarction • Potential consequence of thromboembolic events  Ischemic necrosis  Infarction • Infarct – is an area of ischemic necrosis caused by occlusion of either the arterial supply or venous drainage in a particular tissue • ~99% of all infarction result from thrombotic or embolic events 5/28/2023 hemodynamics 38

39. • Other mechanisms (mostly arterial) • Local spasm • Atheroma expansion due to hemorrhage in to atheromatous plaque. • External compression of vessels, e.g. trauma (compartment syndrome) • Entrapment of vessels at hernial sacs etc…. 5/28/2023 hemodynamics 39

40. Development and Types of infarcts • Development and size of infarcts • Nature of vascular supply, collaterals • Rate of development of occlusion • Susceptibility of the tissue for hypoxia • Oxygen content of the blood • Duration and severity of ischemia • Types • The basis of their color (reflecting the amount of hemorrhage) in to: • hemorrhagic (red) infarcts • Anemic (white) infarcts • Presence or absence of microbial infection • Septic infarcts • Bland infarcts 5/28/2023 hemodynamics 40

42. Types • Red infarcts occur in: • Ovarian torsion-venous occlusion • In loose tissues (lung) • Allow blood to collect in infarct zone • Tissue with dual circulation • In previously congested tissues • Areas where blood flow reestablished(arterial occlusion & necrosis) • White infarcts occur in: • Arterial occlusion - in single artery sites • Solid organs - heart, spleen, kidney • Why is this so? Show off your hands 5/28/2023 hemodynamics 42

43. Clinical examples of infarction • Myocardial infarction(MI) • Following occlusion of coronary arteries by thrombus formed on ulcerating atheroma • Is white infarct (why?) • Can cause sudden death, cardiac failure etc… • Cerebral infarcts • May appear as pale or hemorrhagic • Can result in increased intracranial pressure • Is one type of cerebrovascular accidents or stroke • Lung infarcts • Are typically dark red &conical (wedge shaped, why?) • Can result in hemoptysis, piercing type chest pain 5/28/2023 hemodynamics 43

44. Disseminated Intravascular Coagulation (DIC) • Acute or chronic thrombohemorrhagic disorder occurring as a result of progressive activation of coagulation pathway beyond physiologic set point due to disease resulting in failure of all components of hemostasis • Hence the name consumptive coagulopathy 5/28/2023 hemodynamics 44

45. Etiology and Pathogenesis • DIC is not a primary disease • Pathologic activation of coagulation system • Massive or prolonged release of soluble tissue factors &/or endothelial derived thromboplastin in to the circulation with generalized • Two mechanisms to cause DIC • Release of tissue factor or thromboplastin substance • Wide spread injury to endothelial cells 5/28/2023 hemodynamics 45

46. • Tissue thromboplastin is derived from trauma, burns, surgery, obstetrics procedures like placenta, dead fetus or amniotic fluid; cancers like acute promylocytic leukemia, adenocarcinoma of the lung • In our set up commonly from gram negative sepsis, i.e. bacterial endotoxin 5/28/2023 hemodynamics 46

47. • Endothelial injury result from:- • Ab-Ag complex deposition in lupus erythematosis • Extreme temperature • Hypoxia, acidosis, shock 5/28/2023 hemodynamics 47

48. END THANK YOU! 5/28/2023 hemodynamics 48

Hemodynamics class 3.pptx

Hemodynamics class 3.pptx

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