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Hemodynamic disorders
Hemodynamics deals with the dynamics of blood flow through the circulatory system. It explains how physical laws govern blood flow and ensures transportation of nutrients, wastes, oxygen, and carbon dioxide throughout the body to maintain homeostasis. Disorders of hemodynamics can result in issues like edema, hyperemia, congestion, hemorrhage, thrombosis, embolism, and infarction. These disorders are caused by problems affecting blood vessels, blood flow, coagulation, or the balance of hydrostatic and oncotic pressures. Understanding hemodynamics is important for diagnosing and treating cardiovascular diseases and conditions.
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Hemodynamic disorders
- 1. Hemodynamic Disorders The studyof the blood flow is called hemodynamics. Thus hemodynamics deals with the dynamics of blood flow. The circulatory system is controlled by homeostatic mechanisms, much as hydraulic circuits and are controlled by control systems. Hemodynamic response continuously monitors and adjusts to conditions in the body and its environment. Thus hemodynamics explains the physical laws that govern the flow of blood in the blood vessels.
- 2. Blood flow ensuresthe transportation of nutrients, hormones, metabolic wastes, O2 and CO2 throughout the body to maintain cell- level metabolism, the regulation of the pH, osmotic pressure and temperature of the whole body, and the protection from microbial and mechanical harms. Edema (increased fluid in the ECF) Hyperemia (INCREASED flow) Congestion (INCREASED backup) Hemorrhage (extravasation) Hemostasis (keeping blood as a fluid) Thrombosis (clotting blood) Embolism (downstream travel of a clot) Infarction (death of tissues w/o blood) Shock (circulatory failure/collapse)
- 3. Containing Heart,artery, Vein General circulation Pulmonary circulation Functions Deliver oxygen and nutrients Carry away metabolic wastes A Healthy circulatory system ♠ Normal blood volumn ♠ Homeostasis
- 4. Normal homeostasis vessel wallintegrity intravascular pressure osmolarity normal hemostasis Edema Hyperemia & congestion Thrombosis & Embolism Infarction Hemorrhage Shock Three Major Causes of morbidity and mortality ♦ Myocardial infarction ♦ Pulmonary embolism ♦ Cerebral vascular accident
- 5. EDEMA Increased fluidin the interstitial tissue spaces General & local Pathogenesis Vascular hydrostatic pressure Plasma colloid osmotic pressure Lymphatic drainage
- 6. EDEMA Increasedhydrostatic pressure ( cardiac edema, etc.) Reduced plasma osmotic pressure (nephrotic, hepatic, malnutrient edema, etc. ) Lymphatic obstruction (filariasis infection — elephantiasis，breast surgery, etc ) Sodium and water retention (ARF, etc) Minimal Change Diseaseelephantiasis Pitting edema
- 7. EDEMA LM: Clearing and separationof the extracellular matrix elements Cell swelling Subcutaneous edema Pulmonary edema Edema of the brain • Morphology
- 8. Hydrothorax hydropericardium hydroperitoneum (ascites) Anasarca Clinical correlation from annoying to fatal indicate subtle disease benefit or harmful EDEMA Anasarca is a severe and generalized form of edema with widespread subcutaneous tissue swelling. It is usually caused by liver failure (cirrhosis of the liver), renal failure, right-sided heart failure, as well as severe malnutrition/protein deficiency.
- 9. HYPEREMIA & CONGESTION Arterialhyperemia (hyperemia) An augmented blood flow inducing arteriolar and capillary dilation Venous hyperemia (congestion) Accumulation of Blood in Small Veins & capillaries result from drainage difficulty of veins A local increased volume of blood in a particular tissue
- 10. HYPEREMIA & CONGESTION Hyperemia: Activeprocess; Red, raised tempreture, increased volume ; Enhanced function; Congestion: passive process; general of local; Reddish blue color (cyanosis), low temperature, increased volume, edema; Decreased function
- 11. HYPEREMIA Types Physiological: Shy,exercise, taking Meal Pathological: Inflammatory, post-decompressed Significance －Benefits Plenty supply of O2, functional enhancement, nutrition substance － Hazards Headache , hemorrhage, stroke
- 12. CONGESTION An abnormal orexcessive accumulation of a body fluid. The term is used broadly in medicine. Examples include: nasal congestion (excess mucus and secretions in the air passages of the nose) seen with a common cold and congestion of blood in the lower extremities seen with some types of heart failure. Causes: Systemic: general or pulmonary Cardiac dysfunction (right or left) Local: local venous compression or obstruction External Compression --- Tumor, Bandage Occlusion of lumen --- Thrombosis, Embolism Thickening of venous wall Paralysis of neurogenic modulation --- Burn, frostbite
- 13. CONGESTION Chronic congestion Raisedvenous pressure Anoxia Metabolite accumulation Enlarged inter-endothelial gap Base membrane degeneration Parenchymal Interstitial fibrosis Atrophy Reticular fiber collapsed Increase permeability Degeneration Collagen increased Necrosis Fibroblast proliferation Microscopic scarring Edema Hemorrhage Congestive sclerosis
- 14. CONGESTION Morphology Grossly hemorrhagicand wet Microscopically rich of red blood cells in small vessels
- 15. CONGESTION Lung: Acute pulmonary congestion Gross:Plump swollen lung with shining pleura, edematous fluid flowing out while cutting the lung LM: Alveolar capillaries highly dilated (rosary- like appearance) and engorged with blood Alveolar cavity filled with eosinophilic edema fluid Manifestation Pink colored foamy sputum
- 16. CONGESTION Lung: Chronic pulmonary congestion Gross:Hard, with brown spots scattered —— Brown induration LM: Septa thickened and fibrosis Alveolar spaces containing ‘heart failure cells’— hemosiderin-laden macrophages Manifestation Rusty sputum, dyspnea, etc.
- 17. CONGESTION Liver: Acute hepatic congestion LM: —Dilation of central vein and sinusoids with blood — Atrophy, degeneration and necrosis of central hepatocytes
- 18. CONGESTION Liver: Chronic hepatic congestion Nutmegliver Gross: red-brown zones accentuated against the yellow surrounding zones LM: centrilobular necrosis and congestion, and perilobular fatty change; fibrosis Long-standing, severe hepatic congestion: hepatic fibrosis (cardiac cirrhosis)
- 19. Hemorrhage Causes • Rupture ofblood vessels Trauma Peptic ulcer, aneurism, atherosclerosis • Diapedesis Enlarged interendothelial gap (basement membrane injury). The intergrity of the vessels remains intact Injury to vascular wall: sever infection, anoxia, toxins Change in number and quality of platelets uremia, leukemia, idiopathic Disturbance of coagulation mechanism congenital disease, DIC , deficiency of Vit. K (Extravasation is when a chemotherapy medication or other drug leaks outside the vein onto or into the skin, causing a reaction. In chemotherapy, drugs are classified into two broad categories based on the effect they have on tissues when they extravasate—irritants and vesicants). The leakage of blood, lymph, or other fluid, such as an anticancer drug, from a blood vessel or tube into the tissue around it. It is also used to describe the movement of cells out of a blood vessel into tissue during inflammation or metastasis (the spread of cancer).
- 20. hemorrhage Petechiae Purpuras Ecchymoses Hematoma Hemothorax Hemopericardium Hemoperitoneum hemoarthrosis The clinical significance depends on the volume, the rate of loss and the site. Hemorrhagic shock Stroke
- 21. Hemostasis & thrombosis Normalhemostasis Maintain blood in a fluid, clot-free state Localized hemostatic plug <>Thrombosis Blood clot (thrombus) formation in cardiovascular system of a living body
- 22. Hemostasis Three components Vascular wall Platelets Coagulationcascade Events in hemostasis vasoconstriction primary hemostasis secondary hemostasis antithrombotic counter- regulation
- 23. Hemostasis & thrombosis Endothelium Antithrombotic Antiplatelet Anticoagulant fibrinolytic Prothrombotic
- 24. Hemostasis & thrombosis Platelet Adhesion Secretion Aggregation Coagulation cascade
- 25. thrombosis Pathogenesis Endothelial injury Turbulence of blood flow Hypercoagulability
- 26. thrombosis Morphology Arterial thrombi Originate from injury sites Venous thrombi (phlebothrombi) Originate from the sites of stasis both extends to the heart pale platelet and fibrin layers Lines of Zahn dark erythrocyte-rich layers
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- 28. thrombosis LM: Platelets Trabeculae+ Neutrophil fibrin + red cells
- 29. thrombosis Types Mural thrombus Occlusive thrombus Globularthrombus Vegetation Bacterial thrombus Tumor thrombus Pale thrombus Mixed thrombus Red thrombus Hyaline thrombus
- 30. thrombosis Mural thrombus VegetationHyaline thrombus
- 31. thrombosis Differentiation between thrombusfrom postmortem clot Thrombus Postmortum clots Dry wet and gelatinous “chicken fat” supernatant Rough surface Smooth surface Hard Soft Friable Gelatinous Lines of Zahn Homogenous Firmly attached No attachment Slit due to contraction, fragmentation, generate embolus No slit
- 32. thrombosis Fate Propagation and obstruction Dissolution Embolization Organization and recanalization Calcification
- 33. thrombosis Clinical correlations Venousthrombosis (phlebothrombosis) Varicosities, embolism (sometimes fatal), DVT, trauma, surgery, post partum Cancer associated thrombosis Cardiac and arterial thrombosis Mural thrombus cardiac infarction, rheumatic heart disease Embolize peripherally, brain, kidney, spleen, etc
- 34. thrombosis DIC (Disseminated intravascularcoagulation) Usually happens in many severe disorders severe bacterial or viral infection, allergic disease, anoxia, trauma, shock, malignancy ,etc. Coagulation System is Activated Microthrombi are Formed in Capillaries of Many Organs Platelets + Fibrin ( lung ,brain ,kidney,liver,GI tract,adrenal gland,etc.) Consumption of coagulation substance and activation of fibrinolytic system hemorrhage diathesis, multiorgan dysfunction consumption coagulopathy / defibrination syndrome
- 35. Embolism Occlusion of cardiovascularsystem by some insoluble mass. The mass is termed “Embolus Solid, liquid, gaseous mass Thromboembolism 99% Fat, air, amniotic fluid, tumor fragments, bits of bone marrow, etc
- 36. Embolism Route of emboli Arterial emboli —— systemic embolism Venous emboli —— pulmonary embolism Portal vein emboli —— hepatic embolism Paradoxical emboli Emboli from veins of the general circulation pass through an atrial or ventricular septal defect, entering arteries of the general circulation. Retrograde emboli
- 37. Embolism Incidence: 20-25/100,000 hospitalized patients Source:>95% from DVT above the knee Pulmonary Thrombo-embolism
- 38. Embolism Results: (depends onthe size, number and the clinical setting) Few Emboli with Small Size : asymptomatic → infarction (pain and dyspnea) Numerous Small Emboli : decrease the volume of pulmonary circulation sharply, pulmonary hypertension and right ventricular failure Medium Sized Emboli: hemorrhage, infarction Large Emboli: sudden death, saddle embolus
- 39. Embolism Source: 80%from intra-cardiac mural thrombi; aortic aneurysms, ulcerated AS plaques, vegetations Target sites: lower extremities, brain, intestines, kidney, spleen Consequences: infarction Systemic Thrombo-embolism
- 40. Embolism Fat Embolism Source: Fracturesof long bones Soft tissue trauma Results: ф > 20μm, pulmonary embolism ф < 20 μm, cerebral embolism or other organ embolism Special staining (Sudan III )
- 41. Embolism Pathogenesis obstruction &toxic effect of free fatty acid Symptoms Tachypnea, dyspnea, tachycardia; irritability, restlessness, delirium or coma; anemia and thrombocytopenia Fat Embolism
- 42. Embolism Gas Embolism Source: Exogenic:transfusion, operation or trauma in the neck or chest, artificial pneumothorax, pneumoperitoneum Endogenic: caisson disease or decompression sickness Results: Small amount of gas may be absorbed Occupies the heart ventricle, interrupted the blood flow cause death Gas embolism in multiple organs (brain, pulmonary)
- 43. Embolism Amniotic Fluid Embolism LowIncidence (1/10,0000~80, 000) with high mortality rate (70%~80%) Amniotic fluid may enter vascular system through Sinusoids which placenta attached Torn cervical vessels Emboli consists squamous epithelial cells, lanugo hair, fat, fetal feces, mucin and TXA2 Cause of death multiple embolism; reflex vasoconstriction, pulmonary embolism; allergic shock ; DIC
- 44. INFARCTION The formation ofa localizad area of ischemic necrosis within a tissue or organ due to impaired arterial supply or the venous drainage The necrosis area is called “infarct”. An extremely important cause of clinical illness: myocardiac infarction cerebral infarction
- 45. INFARCTION Causes Occlusion ofarterial supply or venous drainage Thrombosis, embolism, athermanous plaques, external compression Functional spasm of arteriole Types White infarcts (anemic infarcts) Red infarcts (hemorrhagic infarcts) Septic infarcts
- 46. INFARCTION White infarction Arterialocclusion Solid, compact organs Few collateral circulation (spleen, kidney, heart, brain, etc.) Morphology Gross • Dull pale, dry, wedge-shaped necrotic lesion • A hemorrhagic zone surrounding
- 47. INFARCTION LM Ischemic coagulative necrosis Hemorrhagiczone : inflammatory and granulation tissue. Most undergo organization and scarring in the end.
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- 51. INFARCTION Red infarction ♦ Arterialocclusion ♦ Venous occlusion ♦ Loose tissue ♦ Dual circulations: lung , small intestine Previously congested Re-established blood flow to a site of previous arterial occlusion and necrosis
- 52. INFARCTION Hemorrhagic infarction of thelung Gross Roughly wedged shaped Dark red, solid area Base beneath the pleura Fibrin exudation LM Coagulative necrosis Large amounts of RBC filled in alveolar space Obscure structure
- 53. INFARCTION Hemorrhagic infarction ofthe intestine
- 54. INFARCTION Septic Infarction Bacteriacontaining emboli May form abscess and pus
- 55. INFARCTION Fate of Infarct ♦Enzymatic lysis, liquefaction and absorption ♦ Organization with scar formation ♦ Encapsulation and Calcification
- 56. INFARCTION Factors that influencedevelopment of an infarct Nature of the vascular supply Rate of development of occlusion Vulnerability to hypoxia Oxygen content of blood
- 57. SHOCK a sudden upsettingor surprising event or experience. an acute medical condition associated with a fall in blood pressure, caused by such events as loss of blood, severe burns, allergic reaction, or sudden emotional stress, and marked by cold, pallid skin, irregular breathing, rapid pulse, and dilated pupils. "he died of shock due to massive abdominal haemorrhage" synonyms:trauma, a state of shock, traumatism, prostration, stupor, stupefaction, collapse, breakdown" she was taken to hospital suffering from shock after the accident" The typical signs of shock are low blood pressure, rapid heart rate, signs of poor end-organ perfusion (e.g., low urine output, confusion, or loss of consciousness), and weak pulses. ... Circulatory shock is not related to the emotional state of shock
- 58. Shock is alife-threatening condition in which delivery of oxygen to the organs is low, causing organ damage and sometimes death. Blood pressure is usually low. Shock has several causes: Low blood volume, inadequate pumping action of the heart, or excessive widening (dilation) ofblood vessels. Flowchart of initial management of traumatic hemorrhagic shock. In the acute phase of traumatic hemorrhagic shock, the therapeutic priority is to stop the bleeding. As long as this bleeding is not controlled, the physician must manage fluid resuscitation, vasopressors, and blood transfusion to prevent or treat acute coagulopathy of trauma.
- 59. Resuscitative strategies intraumatic hemorrhagic shock AP, arterial pressure; SAP, systolic arterial pressure; TBI, trauma brain injury; Hb, hemoglobin; PT, prothrombin time; APTT, activated partial thromboplastin time.