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Blood Flow
Systemic blood flow is a circuit :
Heart Arteries Arterioles Capillaries Venules Veins Heart
Artery any vessels that carries blood away from the heart. Vein any vessels that carries blood toward the heart
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Tunica media
Smooth muscle and elastic tissue
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Arteries
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.
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Capillaries
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
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Veins
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
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Baroreceptors
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Chemoreceptors
Located in the medulla, carotid, and aortic body Monitor blood levels of O2, CO2 and H+
Chemoreceptors
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Compliance
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 vessels response to changes in pressure.
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Blood pressure
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.
MAP = [(2 DBP + SBP)] / 3 Normal: 70=110 mmHg MAP of 60mmHg is needed to supply blood to major organs
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Lymphatic 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
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Lymph nodes
Lie along lymphatic vessels Contain lymphocytes that filter lymph and eliminate microbes/damaged cells/ toxins Biological filtration
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Virchows Triad
Vascular wall injury Abnormal blood components Abnormal blood flow
Virchows Triad
Injury to the intimal lining creates site for clot formation Venous stasis due to reduced blood flow Hypercoagulability increased tendency to clot
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Arterial thrombus
Forms where blood is moving rapidly see alternating lines of platelets and red cells trapped in fibrin Lines of Zahn
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Venous thrombus
Forms differently due to decreased blood flow Mixed region at site of attachment More blood clotting forms a downstream red cap
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Inflammation
Tumors and irritation by their products Obesity
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Turbulence: Damaged heart valves Congenital heart defects Compression of the vessel Weakened arterial wall - aneurysm
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Other Causes
Aging (Venous: Over the age 40) Immobilization Injury to vessel endothelium Increased clotting response Effects: Decreased venous emptying Increased venous pressures Edema Pain
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Sequelae of Thrombosis
1 Resolution Anticoagulation system Fibrolytic system Moderate exercise increases thrombus resolution
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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
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Recanalization
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3 Propagation Thrombus extends further down the vessel, usually a vein. Initial thrombus acts as a site for further platelet adherence.
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Propagation
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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
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Embolism obstruction of vessel by matter circulating in blood stream Matter could be fat, air, infants cells, in addition to pieces of clot thromboemboli Thromboemoboli from the venous system tend to end up in the: lungs and liver
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Embolus
Lung
CASE OF RECURRENT PE
The next photograph is from an 86 year old male with chronic renal failure and bilateral deep vein thrombosis He was experiencing recurrent pulmonary emboli A filter was placed in the inferior vena cava to catch the emboli before they reached the lungs
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Arixtra (fondaparinux)
Inhibits factor Xa Given SQ at a fixed dose, once daily Excreted by kidneys Do not expel air bubble in syringe No known antidote
Coumadin (warfarin)
Given long term Inhibits hepatic synthesis of Vit K Half-life is 0.5-3 days Vit K is antidote Monitor Prothrombin time PT 1.5 - 2.5 times control International Normalized Ratio (INR) 2.0-3.0
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C heck VS, platelet count, PT O bserve for bleeding R eview bleeding protocol A void ASA, may use acetaminophen
FOODS effectiveness asparagus, cabbage, cauliflower, turnip greens, green leafy veggies DRUGS effectiveness GAS (glucocorticoids, alcohol, salicylate) DRUGS effectiveness ROPE (rifampin, oral contraceptives, phenytoin, estrogen)
Thrombolytic therapy
Lyse and dissolve clot Results in a 3 fold greater incidence of bleeding than Heparin Drugs Urokinase, Streptokinase, t-PA, Activase
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Provide bed rest with involved extremity elevated or FOB elevated Apply warm moist heat to affected extremity per order Measure thighs, calves and ankles daily Relieve discomfort
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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
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RISK FACTORS
Atherosclerosis Trauma Syphilis Congenital weakness Local infection Cigarette smoking
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Characteristics of Aneurysms
False aneurysm blood escapes into connective tissue, outside of arterial wall
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Dissecting aneurysm separation of arterial wall layers that fills with blood
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Assessment Findings
May be asymptomatic Chest pain Dyspnea, hoarseness or dysphagia pressure on trachea and bronchus Distended neck veins and edema of head and arms
PAIN: Constant, boring, neuralgia, intermittent low back, abdominal
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Radial pulses differ Tachycardia Hypotension following rupture leading to shock PULSATING MASS: abdominal, chest wall pulsation; audible bruit over aorta
thoracic aneurysm - edema of chest wall Abdominal aneurysm periumbilical
Skin has cyanosis, mottled below level of aneurysm Veins: dilated, superficial neck, chest, arms Cough: paroxysmal, brassy Diaphoresis, pallor, fainting following rupture Peripheral pulses:
Femoral present Pedal weak or absent
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Diagnostic Studies
Chest xray Transesophageal echocardiogram CT scan
NURSING DIAGNOSIS
Risk for injury R/T possible aneurysm rupture Pain R/T pressure on lumbar nerves Anxiety R/T risk of rupture
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Nursing Interventions
Similar to those with coronary artery bypass grafting or post cardiac cath
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The aortic abdominal aneurysm has an intramural thrombus, and its size is approximately 6.7 cm in diameter. The true lumen of the aorta is indicated by the arrowheads.
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Signs of dissection - severe back or abdominal pain, elevated BP, decreased pedal pulses Signs of rupture constant, intense back pain; falling BP, shock, death
Post-operatively
Hemodynamic monitoring Frequent VS checks Neuro checks Assess heart and lungs
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Encourage turning, coughing and deep breathing Assess for and prevent thrombophlebitis Assess for paralytic ileus Assess renal function Maintain patient flat in bed without sharp flexion of hips/knees which places pressure on femoral and popliteal arteries
Discharge teaching
Avoid heavy lifting/straining for 4-6 weeks Gradually increase activities Avoid prolonged sitting or standing and smoking Observe for changes in color and temperature of extremities; check pedal pulses Prophylactic antibiotics before invasive procedures
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Arterial Occlusions
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
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Atherosclerosis
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
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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
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Clinical manifestations
Signs and symptoms of inadequate perfusion TIAs, often associated with exercise or stress When lesion becomes complicated, can result in tissue infarction Coronary artery disease myocardial ischemia In brain major cause of stroke
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The reddish-black appearance of the small bowel seen here at autopsy is due to bowel ischemia with infarction. Given that the blood supply to the small intestine has many anastomoses, the amount of infarction shown here requires extensive vascular disease (arterial thrombosis or embolism, or much less commonly venous thrombosis) or severe cardiogenic shock. This patient had severe mesenteric atherosclerosis with diabetes mellitus.
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Treatment
Exercise Smoking cessation Control of hypertension and/ or diabetes Reduce LDL cholesterol by diet or medication or both
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Systemic Hypertension
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
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Causes one in eight deaths worldwide Third leading cause of death in the world Affects 50 million Americans
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Primary 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
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Suspected causes
Interaction of genetics and environment Overactivity of sympathetic nervous system Overactivity of renin / angiotensin/ aldosterone system Salt and water retention by kidneys And others
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Secondary hypertension
Caused by a systemic disease process that raises peripheral resistance or cardiac output = 5 - 10 % of cases. Renal vascular disease Hyperaldosteronism Cushings syndrome, DM, hyperthyroidism PHEOCHROMOCYTOMA tumor that releases catecholamines and causes hypertensive emergencies) Drugs ( oral contraceptives, corticosteroids, antihistamines)
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Complicated hypertension
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).
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White-coat Phenomenon
Client is NORMOTENSIVE except when the blood pressure is measured by a health professional.
Clinical manifestations
None in early stages other than elevated BP Some individuals never have symptoms; others become very ill and die
Diagnosis should be made after three or more consistent BP readings are taken after a 5-minute period of rest because BP can vary from day to day, within different periods of the same time.
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Treatment
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
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Venous Disorders
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
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ETIOLOGY
Primary varicose veins familial Secondary varicose veins trauma, DVT, inflammation/damaged valves
PATHOPHYSIOLOGY
Incompetent valves Chronic venous insufficiency
Reduction in the venous return Increase in the venous pressure Venous stasis
Excessive dilation of the vein spreading of the valve cusps Valvular incompetency = reflux of blood from the superficial veins to enter the deep veins by the muscular pump
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Manifestations
Distended veins that may be bluish in color and bulging Pain in the feet and ankles; heaviness or feeling of heat in the legs Swelling of the extremities Stasis ulcers Itching over the affected area
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Nursing Assessment
Inspection of the LE
Edema, discoloration, tenderness or discomfort, (+) Homans sign, signs of PE (anxiety, dyspnea, tachypnea, air hunger, tachycardia, diaphoresis, chest pain)
POSITIVE TRENDELENBURG TEST (done to evaluate valve incompetence Client is placed in a supine position with elevated legs As the client sits up, the veins would normally fill from the distal end. If there are varicosities, the veins fill from the proximal end.
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Treatment
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 (palliative only; not curative) Surgical removal - but only when deep vein are open.
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VEIN LIGATION SURGERY involves ligation (tying off) of the entire vein (usually the saphenous) and dissection and removal of the incompetent tributaries.
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Nursing Management
Encourage not to stand in one position for a long period of time Take a walk each day for 30-60 mins. Rest if intermittent claudication occurs Suggest light warm clothing is essential to prevent vasoconstriction Do not cross legs or ankles when sitting Elevate legs when in a supine position
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Raynauds Syndrome
If the symptoms are persistent for 3 years with intermittent attacks
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Dx noninvasive blood flow studies before and after cold application Medical tx
Calcium channel blockers Norvasc (amlodipine), Procardia (nifedipine) Alpha adrenergic receptor blockers prazosin (Minipress), doxazosin (Cardura) Nitrates transdermal or long acting oral nitrates Avoid smoking, cold, stress and ETOH, limit caffeine and chocolate
Nursing management
Teach client relaxation techniques, biofeedback Teach client to minimize exposure to stimuli Teach client to wiggle and massage digits May apply warmth to extremities intermittently
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Clinical manifestations
Claudication with exercise in arches of feet Digital pain which may be constant Intense rubor or cyanosis of feet when dependent Absent or decreased pedal or radial pulses Ulcerations and gangrene commonly occur
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ASSESSMENT
COLOR EDEMA NAILS PAIN
ARTERIAL DISEASE
Pale None or minimal Thick and brittle Worse with elevation and exercise, may be sudden or severe, rest pain; claudication Decreased, weak, or absent Cool Dry and necrotic
VENOUS DISEASE
Ruddy, cyanotic if dependent Usually present Normal Better with elevation, positive Homans sign, dullness or heaviness
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