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Vascular

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Vascular

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  1. Vascular MCC NURSING DIANA BLUM MSN

  2. hormones • C reactive protein is a marker for cardiac inflammation • Increases mean: risk of damage • Homocysteine: protein that promotes coagulation by increasing factor 5 and factor 11 while depressing activation of protein C and increasing thrombus formation risk • Vitamin b6 and b12 and folate lowers homocysteine levels

  3. Arterial diseases: • Arteriosclerosis (atherosclerosis) • Aneurysm formation • Arteriosclerosis obliterans • Raynaud’s phenomenon • Arterial embolism • Thromboangiitis obliterans • Diabetic arteriosclerotic disease • hypertension

  4. Manifestations :ARTERIAL(50% occulsion before symptoms) • Prolonged capillary refill: • - 3 seconds or more • Ulcers: • - open lesions on feet from diminished distal perfusion • Ischemia (reduced oxygenation) • - leads to pain • Paresthesia (decreased sensation in • extremities = tingling/numbing) • Pain (in feet/leg muscles = burning, • throbbing, cramping) • -usually from exercise BUT also • with elevation of lower extremities

  5. Arteriosclerosis • -describes arterial disorders in which • degenerative changes result in • decreased blood flow • Atherosclerosis: • - most common form of arteriosclerosis, excessive accumulation of lipids

  6. Most common affected areas from arteriosclerosis: • Heart: coronary arteries (angina, MI, • death) • Brain (transient ischemic attacks =TIAs • CVA, death) • Kidneys (renal arterial stenosis lead to • chronic renal failure) • Extremities (gangrene of digits & • intermittent claudication)

  7. Pathophysiology of atherosclerosis • -inflammatory process, begins as fatty streaks that are deposited in the intima of the arterial wall • Genetics and environment play a factor in the progression • Elastic arteries: aorta, carotid, lg & med. sized muscular arteries (popliteals) most susceptible arteries. • Endothelial injury: may be initiated by smoking, hypertension, diabetes, hyperlipidemia, 

  8. Inflammatory cells(including macrophages) become attracted to the wall • Macrophages infiltrate wall and ingest lipid which turns them into foam cells • They then release biochemical substances that cause further damage and attract platelets which then causes clots to form

  9. Ankle-brachial index of blood pressure:Used to diagnose peripheral vascular disease • -compares the blood pressure at ankle with that of the arm. • -normally these should be the same (with a ratio of 1) • -lesser number than 1 shows decreased blood pressure at the ankle compared to upper extremity = = which indicates peripheral vascular disease to lower extremities

  10. SURGERY • Indications for fem-pop bypass: • diabetes • hypertension • vasculitis • collagen disease • Bueger’s disease • Also, Embolectomy (surgical removal)

  11. Fem-pop bypass

  12. MEDICAL MANAGEMENT • ANTIPLATELET THERAPY • Aspirin, ticlid, plavix, pletal, trental • Beta blockers • ARBs • Statins • Radiation therapy • Angioplasty with stents

  13. Nursing Interventions • Monitor BP for difference between arms • Could be indicative of aortic coarctation • Narrowing of aorta lumen • Monitor for carotid bruits • Assess cap refill, pulses,skin

  14. Acute arterial stenosis • Monitor for the 5 P’s • pain, sudden • pallor • pulselessness • paresthesias • paralysis

  15. Acute peripheral arterial occlusion • may result from rupture and thrombosis of an atherosclerotic plaque, an embolus from the heart or thoracic or abdominal aorta, an aortic dissection, or acute compartment syndrome • Symptoms and signs are sudden

  16. Buerger Disease • Autoimmune disease • Recurrent inflammation of small arteries and veins of the extremities resulting in thrombus formation and occlusion. • Unknown cause • Men 20-35 years old • All races • Link to heavy smoking/chewing tobacco • s/s: rubor (reddish blue) color to foot, no Pedal pulse, discolored legs when dangled, eventually gangrene sets in

  17. Aneurysms of Central Arteries • Enlargement of artery to @ least 2X its normal • Aortic dissection • Medial & intimal layers separate • Risk Factors: • -hypertension • -cocaine use • - Marfan syndrome

  18. Aortic Dissections: Type III most common type

  19. Aortic dissection

  20. Signs/symptoms of aortic dissection: • n/v, diaphoresis with pain • “tearing” pain • Sudden onset • not relieved with change of position • Dissection of ascending aorta: anterior CP with • radiation to neck, throat, jaw • Dissection of descending: interscapular back pain • radiation to lower back or abdomen

  21. Treatment of hypertension for aortic dissection: • IV propranolol • Nitropresside drip after beta blocker ( nitropresside by itself causes tachycardia AND  left vent. contractility that is why a beta-blocker should be given first, then start nitropresside drip) • Diagnosis: • CXR (but 10% normal) see medialstinal • widening • Contrast CT • MRI

  22. Surgery for distal dissections: • Mortality in 1st 48 hrs if unrepaired proximal aortic dissections is 40% • Usually distal dissections treated medically unless: • rapid expansion • saccular formation • persistent pain • hemodynamic compromised • blood leakage • impending rupture

  23. Dacron tube

  24. Abdominal Aortic Aneurysm (AAA) • 75% of all aneurysms Located between renal arteries & aortic bifurcation Symptoms from pressure exerted in surrounding structures. Many nonsymtomatic until ruptures Look for pulsating abdominal mass With rupture: hypovolemic shock & mortality around 90%

  25. Post-op nursing interventions for graft: • Vitals • Pulses distal to graft • Report: • changes in pulse • cool extremities distal to graft • white/blue to extremities distal to graft • severe pain • abd. distention • decreased UO

  26. Post-op nursing intervention (continued)Post graft • Elevation of head to 45° or less • Renal function lab • Respiratory status • Paralytic ileus (NG tube) • Assess for dysrhythmias post thoracic

  27. Venous manifestations: • Skin color changes: reddened or • cyanotic • Edema: pooling of fluid results in edema • Venous stasis ulcers: skin breakdown • due to increased pressure from • chronic pooling of blood • Decreased mobility: may result from • the edema • Pain: • - in feet/ leg muscles; aching/throbbing • - results from venous stasis & increases • as day progresses (esp with sitting • or standing) • Temperature changes: • - warm to touch since blood can enter • but cannot leave affected parts

  28. DVT : • Groin tenderness/pain • Unilateral sudden onset edema leg • Homan’s sign (appears in only 10% of pt • with DVT) • Ultrasonography

  29. DVT interventions: • Rest (do NOT massage area) • Low-molecular weight heparin • Coumadin • TPA • ****Contraindications to anticoagulant therapy • Pt compliance, bleeding, aneurysms, trauma, alcohol, recent surgery, liver or kidney disease, hazard jobs, pregnancy

  30. Nursing cares • Monitor for hemorrhage • Monitor PT/PTT • Heparin is therapeutic b/w 60-92 on ptt • Coumadin is therapeutic b/w 2-3 on PT/INR • Monitor for Thrombocytopenia • Monitor Platelets • s/s; purpura, bruising, hematomas • Provide bedrest • Ted Hose or ace wraps for prevention of DVT • SCDs for prevention of DVT • Pain meds

  31. Hypertension • - excessive tension exerted on arterial walls which places pts at increased risk for target organ damage • -asymptomatic until complications develop • - elevation may be systolic or diastolic or both • - normal <120 mmHg systolic • <80 mmHg diastolic

  32. Pathophysiologic processes for hypertension: • BP=CO X peripheral resistance • Elevated BP is direct result of increased • peripheral resistance, increased CO or • both • Renin-angiotensin-aldosterone system • Aldosterone: increased water/Na+ retention thus increasing ECF volume which leads to increased CO with subsequent increase BP

  33. Possible Causes of PVR • Narrowing of blood vessels, PVD, CAD, kidney disease: > renin/angiotensin =vasoconstriction • Release of catecholamine (epinephrine and adrenalin) = vasoconstriction • > blood volume= more work to pump • > Blood viscosity=harder to pump • Ability of blood vessel to stretch

  34. Target Organ Disease from hypertension • Large vessels: aneurysmal dilation • accelerated atherosclerosis • aortic dissection • Cardiac: • acute= pulm edema, MI • chronic= LVH • Cerebrovascular: • acute= Intracranial bleed, coma, seizure • mental status changes, TIA, stroke • chronic=TIA, stroke

  35. Target organ disease from hypertension: • Renal: acute=hematuria, azotemia • chronic=elevated creatinine • proteinuria • Retinopathy: • acute=papilledema, hemorrhages • chronic=hemorrhages,exudates,

  36. Treatment of hypertension: • Lifestyle modification ABCD: ACE inhibitors; ARB B-blockers Calcium channel blockers Diuretics

  37. Hypertensive Crisis:Treatment • Parenteral agents for immediate redux of BP • In ICU for monitoring • Arterial line • Drug of choice: sodium nitroprusside • =direct acting arterial & venous vasodilator • = reduces BP rapidly but lower mean arterial pressure no more than 25% over 1st 2 hours • = easily titratable • = monitor closely for hypotension • = shield this drip from light

  38. STROKE: occlusion of cerebral vasculature • DUE TO: • 1. emboli that lodges in cerebral vasculature • (from a-fib, vegetations on an infect valve) • 2. atherosclerotic plaque (occludes carotid arteries) • 3. venous occlusion (secondary to thrombosis) • 4. arterial dissection (in carotid or vertebrobasilar system) • 5. severe hypotension ( infarct in cerebral areas) • 6. hemorrhage :occurs during activity

  39. TIA • Sudden loss of function resulting from disrupted blood supply to area in brain • 5 types: • Large artery • Caused by atherosclerosis • Small penetrating artery • Most common • Also called lacunar strokes because it creates a cavity • Cardiogenic emboli • Usually from afib • Cryptogenic • No known cause • Other • Caused from Drug use, migraines,spontaneous

  40. Hemorrhagic stroke • Bleeding into brain tissue or ventricles, subdural, or subarachnoid spaces due to ruptured aneurysm or from severe hypertension • VASOSPASM (after a bleed) • 4-14 days post hemorrhage • Management is difficult

  41. Prevention • Manage HTN • Avoid alcohol • Increase public awareness

  42. Assessment Tools • Neurological assessment upon admission or change in client status, including: • Level of consciousness • Orientation • Motor ability • Pupils • Speech/language • Vital signs • Blood glucose

  43. Treatment for stroke:(Note similar to measures for myocardial ischemia/MI) • Thrombolysis (who is not a candidate?) • Lower BP • Quit smoking • Decrease cholesterol • Antiplatelet (ASA)

  44. Stroke treatment (continued) • ASA • Heparin (SQ or IV contin infusion) • Low-molecular wt heparin (lovenox) • Warfarin (coumadin) ------------------------------------------------------- Obtain PT, PTT prior to therapy PT: monitor oral anticoag : goal=1.5 to 2 times pt baseline PTT: monitor heparin: goal=1.5 to 2 times pt baseline INR: monitor Warfarin: goal=2 to 3