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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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Structure of blood vessels
Tunica intima
Endothelium and connective tissue
Tunica media
Smooth muscle and elastic tissue
Tunica externa or tunica adventitia
Connective 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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Control of Systemic Circulation
Nervous control innervated by sympathetic nervous system ONLY Cardiac control center (primarily in medulla oblongata) Heart has both Sympathetic and Parasympathetic innervations.
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Baroreceptors and chemoreceptors:
Monitor pressure Send information to cardiovascular center, which responds BARORECEPTORS located in the carotid sinuses and the wall of the L ventricle Monitors the level of arterial BP and counteracts rising pressure by VASODILATION through the stimulation of the vagus nerve.
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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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Diseases of Arteries and Veins
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
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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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FYI: Line of Zahn
visible and microscopic laminations produced by alternating pale layers of platelets mixed with fibrin and darker layer containing red blood cells. Their presence implies thrombosis at a site of rapid blood flow that happened before death. In veins or smaller arteries, where flow is not as constant, they are less apparent. They are named after German pathologist Friedrich Wilhelm Zahn (1845-1904).
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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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Factors that predispose to thrombosis
Endothelial damage Bacterial damage, autoimmunity Damage to the myocardium Wear and tear hemodynamic stress Hypertension increases this Arteriosclerosis
Inflammation
Tumors and irritation by their products Obesity
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Factors that predispose to thrombosis
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
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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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Other Causes (Venous)
Surgery longer than 30 minutes using GA, SA, or EA Hx of previous DVT, family Hx of blood clotting disorder Venous stasis r/t prolonged travel, bedrest, CVA Cardiac: Heart failure, MI, cardiomyopathy, malignancy Pregnancy, estrogen therapy, oral contraceptives Obesity
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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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Coiled Embolus in Pulmonary Artery
Pulmonary Emboli removed from Pulmonary Artery
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Embolus
Pulmonary infarct with hemorrhage
Lung
Lung Pulmonary Infarct
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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Greenfield Filter in Inferior Vena Cava with Trapped Emboli
Medical Management Of DVT
Bedrest with extremity elevated Anticoagulation
Heparin (unfractionated)
Given IV for 5-7 days Prevents conversion of prothrombin to thrombin and fibrinogen to fibrin Half-life approximately 2 hrs Monitor partial thromboplastin time (PTT) or anti Xa assay Protamine sulfate is antidote Must monitor platelets for Heparin Induced Thrombocytopenia (HIT)
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Additional Nrsng Considerations: HEPARIN
effect with aspirin, alcohol, and antibiotics effect with digoxin, antihistamines, nitroglycerin products risk of bleeding with chamomile, garlic, ginger, ginkgo, and ginseng therapy Monitor PTT (1.5-2.5 times control values) Initiate bleeding protocols (use electric razors, hold pressure for 5mins w/ venipunctures, soft toothbrushes)
Low molecular weight (LMW) heparin Lovenox, Fragmin
Given only SQ, daily or BID Dose is weight based Do not expel air bubble Lower risk of HIT and bleeding No need to monitor PTT
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L ow molecular weight O rthopedic surgeries dVt prophylaxis, immobility, stints, cardiac
surgereis indicators
LEave bubble in syringe
Never by IM, only SC give within 2hrs of preop
abdl surgery and 12hrs of knee surgery
NO rubbing after administered, NO aspiration, NO mixing with other drugs
X out for pork allergies, heparin allergies, PUD,
leukemia
Acova (argatroban) and Refludan (lepirudin)
Direct thrombin inhibitors Given continuously IV to patients allergic to Heparin or who experience HIT No know antidote Monitor PTT
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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
Plication of inferior vena cava
Filter inserted into vena cava to trap emboli
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Nursing Management Of Client With DVT
Administer and monitor anticoagulant therapy
Administer continuous IV Heparin via pump Administer LMW heparin SQ only do not expel air, aspirate, or massage site, and avoid scars and umbilicus Monitor PTT or anti Xa assay Monitor PT No IM medications or meds with ASA
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Monitor and manage complications
Bleeding expistaxis, hematuria, melena, bleeding gums, hematoma formation Thrombocytopenia platelets less than 100,000 or 25% decrease from previous level, increasing Heparin doses required Pulmonary embolus
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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Provide client teaching and discharge planning
Teach client measures to prevent recurrence Encourage rest periods with feet elevated Use of elastic stockings when ambulating
Teach client regarding Coumadin therapy
Stress importance of follow-up for PT Do not take OTC meds, vitamins, herbs Avoid alcohol Avoid large amounts of foods with Vit K Signs and symptoms to notify physician of Wear Medic Alert bracelet
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Other arterial problems
Aneurysms localized or diffuse
dilations/outpouching 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 thromo-emboli
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Asymptomatic until rupture
Embolism Death
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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Abdominal Aortic Aneurysm (AAA)
A sac or dilation formed at a weak point One or all three layers may be involved May rupture and lead to death
Characteristics of Aneurysms
False aneurysm blood escapes into connective tissue, outside of arterial wall
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Fusiform aneurysmsymmetric, spindleshaped expansion. Involves entire circumference
Saccular aneurysm out-pouching on one side only
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Dissecting aneurysm separation of arterial wall layers that fills with blood
Can you name the four types of aneurysm?
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Thoracic Aortic Aneurysm
Occurs most frequently in men, 50 70 yrs of age Etiology atherosclerosis, hypertension, infection 1/3 die from rupture
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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Medical Management of Thoracic Aneurysm
Control underlying hypertension Surgical repair
Resection of aneurysm and replacement with graft Repair with endovascular graft
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Nursing Interventions
Similar to those with coronary artery bypass grafting or post cardiac cath
Abdominal Aortic Aneurysm (AAA)
Occurs more frequently in caucasians, more in men and elderly clients Etiology atherosclerosis, hypertension, trauma, infection, congenital abnormalities in vessels, genetic predisposition Most are infrarenal
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Assessment Findings with AAA
Approximately 60% of clients are asymptomatic Pulsatile mass in the upper and middle abdomen Abdominal or low back pain Bruit may be heard Diminished femoral and distal pulses Patchy mottling of feet and toes
Diagnostic Tests with AAA
Abdominal ultrasound CT scan, MRI
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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Medical Management of AAA
If small, monitor every 6 months Keep BP down Surgery is treatment of choice if greater than 5cm or enlarging
Surgical resection and replacement with a graft Repair with endovascular graft
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Nursing Interventions for Client with AAA
Pre-operatively close monitoring for dissection or rupture of AAA and prepare for surgery
GOAL: Prevent complications
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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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
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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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Inflammatory Biomarkers and the Progression of Atherosclerosis
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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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Other risk factors
Smoking Nicotine is a vasoconstrictor Greater than 3 alcoholic drinks/ day 2-4 drinks / week lowers blood pressure
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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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Overactivity of renin / angiotensin/ aldosterone system
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Salt and water retention by kidneys
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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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The Journal of American Medical Association, 2003
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
Arteriospastic Disease: Raynauds Disease
Small arteries and arterioles of hands and feet constrict or vasospasm Cause unknown More frequent in women ages 16-40 yrs Induced by cold, stress, caffeine, nicotine Manifestations coldness, pain or numbness, pallor, cyanosis of fingers and toes, which progress to rubor (white-blue-red)
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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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Thromboangiitis Obliterans (Buergers Disease)
Inflammation or vasculitis of small and medium sized arteries and veins in the extremities Thrombus formation occurs and occludes vessels Cause is unknown More in men with history of heavy smoking
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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
Dx Duplex ultrasound, arteriogram and biopsy of vessels Tx
Improve circulation Relieve pain Protect from injury and infection Amputation if gangrene
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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
PULSES TEMPERATURE ULCERS
Normal Warm Moist, malleolar
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