Systemic blood flow is a circuit : Systemic blood flow is a circuit
tarix 28.03.2017 ölçüsü 477 b. #12800
Systemic blood flow is a circuit : Systemic blood flow is a circuit : Heart →Arteries→ Arterioles→ Capillaries→ Venules→ Veins→ Heart Artery – any vessels that carries blood away from the heart.Tunica intima Tunica intima Endothelium and connective tissue Tunica media Smooth muscle and elastic tissue Tunica externa or tunica adventitia Connective and elastic tissue Large arteries are elastic (conducting) arteries – pressure reservoirs Large arteries are elastic (conducting) arteries – pressure reservoirs Medium arteries are muscular (distributing) arteries – more smooth muscle Contraction or relaxation of muscle changes the size of the lumen, and so controls the blood pressure in the vessel. Only a single layer of endothelium and a basement membrane Only a single layer of endothelium and a basement membrane Connect arterioles and venules Functional part of system True capillaries begin at a precapillary sphincter which controls blood flow through the capillary Relatively thin; less elastic Relatively thin; less elastic Larger in diameter than arteries Have valves to prevent backflow of blood Flow to heart is assisted by contraction of skeletal muscles Nervous control – innervated by sympathetic nervous system ONLY Nervous control – innervated by sympathetic nervous system ONLY Cardiac control center (primarily in medulla oblongata) Heart has both Sympathetic and Parasympathetic innervations. Baroreceptors and chemoreceptors: Baroreceptors and chemoreceptors: Monitor pressure Monitor blood levels of O2, CO2 and H+ Send information to cardiovascular center, which responds The increase in volume a vessel can accommodate for a given increase in pressure. The increase in volume a vessel can accommodate for a given increase in pressure. Depends on the ratio of elastic fibers to muscle fibers in the vessel wall. Elastic arteries more compliant than muscular arteries Veins more compliant than either artery (blood reservoirs) Decreased compliance suggests an increased stiffness of vessel wall. Determines the vessel’s response to changes in pressure. Mean arterial pressure is the average in pressure in the arteries throughout the cardiac cycle. Mean arterial pressure is the average in pressure in the arteries throughout the cardiac cycle. Depends on the compliance of the arteries and the amount of blood in the arterial system. A vascular system that runs “parallel” to the blood vascular system A vascular system that runs “parallel” to the blood vascular system Flow does not circulate – begins in tissue Returns to venous system at subclavian veins Fluid in vessels is lymph – mostly water and proteins Interstitial fluid→ lymphatic capillaries→ lymphatic vessels→ lymphatic trunks→ lymphatic ducts Lie along lymphatic vessels Lie along lymphatic vessels Contain lymphocytes that filter lymph and eliminate microbes/damaged cells/ toxins Biological filtration Thrombus- “clotting” in an unbroken vessel Thrombus- “clotting” in an unbroken vessel Maintains a point of attachment Organized differently than a clot usually due to damage to endothelium and exposure of collagen in the basement membrane Forms where blood is moving rapidly – see alternating lines of platelets and red cells trapped in fibrin Forms where blood is moving rapidly – see alternating lines of platelets and red cells trapped in fibrin Lines of Zahn Forms differently due to decreased blood flow Forms differently due to decreased blood flow Mixed region at site of attachmentMore blood clotting forms a downstream red cap Endothelial damage Endothelial damage Bacterial damage Damage to the myocardium Wear and tear – hemodynamic stress Hypertension increases this Arteriosclerosis Inflammation Tumors and irritation by their products Flow abnormalities Flow abnormalities Increases platelet contact with endothelium Reduction in flow: Arterial: Cardiac damage and decreased pumping action Increased blood viscosity Venous: Physical inactivity Varicose veins Turbulence: Turbulence: Damaged heart valves Congenital heart defects Compression of the vessel Weakened arterial wall - aneurysm Aging Aging Immobilization Injury to vessel endothelium Increased clotting response Effects: Decreased venous emptying Increased venous pressures Edema Pain 1 Resolution – 1 Resolution – Anticoagulation system Fibrolytic system Moderate exercise increases thrombus resolution 2 Organization 2 Organization The thrombus is digested by phagocytes and replaced by connective tissue – incorporating the thrombus into the vessel wall. May recanalize – small channels open up and restore blood flow 3 Propagation – 3 Propagation – Thrombus extends further down the vessel, usually a vein. Initial thrombus acts as a site for further platelet adherence. 4 Infarction – 4 Infarction – an infarct is an area of necrosis caused by ischemia and hypoxia. More common in arteries than veins due to blood flow patterns Collateral circulation and anastomosis prevent infarction Embolism – obstruction of vessel by matter circulating in blood stream Matter could be fat, air, infant’s cells, in addition to pieces of clot – thromboemboli Thromboemoboli from the venous system tend to end up in the: lungs and liver Anticoagulants Anticoagulants Fibrinolytics – t-Pas Prophylactic aspirin therapy Arteriosclerosis – abnormal thickening and hardening of the arterial walls Arteriosclerosis – abnormal thickening and hardening of the arterial walls Smooth muscle cells and collagen fibers migrate into the tunica intima, causing stiffening and thickening, narrowing the lumen Can exacerbate high blood pressure, and cause weakening and outpouching of vessel walls A form of arteriosclerosis where soft deposits of intra-arterial fat and fibrin harden over time – atheroma A form of arteriosclerosis where soft deposits of intra-arterial fat and fibrin harden over time – atheroma May see build up in skin – Xanthoma or arcus in cornea. In general, patients suffer few symptoms unless > 60 % of blood supply is blocked Progressive over years Progressive over years Starts with some injury to endothelium Smoking, hypertension , hyperlipidemia, diabetes, autoimmune disease, and infection Inflammation, release of enzymes by macrophages causes oxidation of LDL, which is then consumed by macrophages – foam cells – accumulate to form fatty streaks Fatty streaks of lipid material appear first as yellow streaks and spots Smooth muscle cells proliferate, and migrate over the streak forming a fibrous plaque Fibrous plaque results in necrosis of underlying tissue and narrowing of lumen Fibrous plaque results in necrosis of underlying tissue and narrowing of lumen Inflammation can result in ulceration and rupture of the plaque, resulting in platelet adherence to the lesion = complicated lesion Can result in rapid thrombus formation with complete vessel occlusion → tissue ischemia and infarction Signs and symptoms of inadequate perfusion – TIAs, often associated with exercise or stress Signs and symptoms of inadequate perfusion – TIAs, often associated with exercise or stress When lesion becomes complicated, can result in tissue infarction Exercise Exercise Smoking cessation Control of hypertension and/ or diabetes Reduce LDL cholesterol by diet or medication or both Aneurism – dilation in the arterial wall Aneurism – dilation in the arterial wall Most arise in aorta or major branches as a result of atherosclerotic wall damage Males over 50 at greatest risk for aortic aneurysms Disturbs blood flow, predisposing to thrombus formation - can release thromoemboli Asymptomatic until rupture Asymptomatic until rupture Treatment by surgical repair Aortic Dissection –bleeding into vessel wall, separating vessel layers Men in 40-60 y.o. age group with hypertension Younger persons with connective tissue disease or congenital defects Presents with pain – life threatening A consistent increase in arterial blood pressure caused by increased Cardiac output or increased peripheral resistance or both A consistent increase in arterial blood pressure caused by increased Cardiac output or increased peripheral resistance or both Leads to damage of vessel walls If arteries constrict over a long time with increased pressure in vessel, the wall becomes thicker to withstand the stress. Results in narrowing of arterial lumen Leads to inflammatory response Causes one in eight deaths worldwide Causes one in eight deaths worldwide Third leading cause of death in the world Affects 50 million Americans Also called essential or idiopathic hypertension Also called essential or idiopathic hypertension 92- 95 % of all cases No specific cause identified Can happen with retention of sodium and water → increased blood volume. Also low dietary potassium, calcium and magnesium intakes Smoking Smoking Nicotine is a vasoconstrictor Greater than 3 alcoholic drinks/ day Interaction of genetics and environment Interaction of genetics and environment Overactivity of sympathetic nervous system Overactivity of renin / angiotensin/ aldosterone system Salt and water retention by kidneys And others Caused by a systemic disease process that raises peripheral resistance or cardiac output = 5 - 10 % of cases. Caused by a systemic disease process that raises peripheral resistance or cardiac output = 5 - 10 % of cases. Renal vascular disease Adrenocortical tumors Adrenomedullary tumors Drugs ( oral contraceptives, corticosteroids, antihistamines) Sustained primary hypertension that damages the structure and function of the vessels themselves. Sustained primary hypertension that damages the structure and function of the vessels themselves. Commonly affects heart, aorta, kidneys, eyes, brain, and lower extremities (target-organ damage). None in early stages other than elevated BP None in early stages other than elevated BP Some individuals never have symptoms; others become very ill and die Modification of life style Modification of life style Drugs Diuretics, beta-blockers, angiotensin converting enzyme inhibitor Compliance is often difficult – patients stop taking medication when they feel better – can get rebound effects Varicose veins – dilations, can lead to valvular insufficiency Varicose veins – dilations, can lead to valvular insufficiency Can occur in superficial veins (saphenous) or deep veins Causes of secondary varicose veins: Deep vein thrombosis Congenital defects and pressure on abdominal veins Prevention – little can be done after valves become incompetent Prevention – little can be done after valves become incompetent Avoid stressors, such as standing for long periods Elastic support stockings Sclerotherapy – injections of drugs to induce fibrosis of vessel Surgical removal - but only when deep vein are open. 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