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Vascular Problems, Stroke, Aneurysms, and HTN Crisis By Diana Blum MSN MCC NURS 2140 Vascular Disorders • Common disorders in America: • hypertension • atherosclerosis • arterial occlusive disease • abdominal aortic aneurysms (AAA) • deep vein thrombosis (DVT) • venous insufficiency 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 PAD Arterial diseases: • • • • • • • • Arteriosclerosis (atherosclerosis) Aneurysm formation Arteriosclerosis obliterans Raynaud’s phenomenon Arterial embolism Thromboangiitis obliterans Diabetic arteriosclerotic disease hypertension 5 Manifestations :ARTERIAL (50% occulsion before symptoms) • 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 6 (continued): • Hallmark sign: Intermittent claudication (pain in • exercising muscles – usually in calf • - directly related to decreased • blood supply during activity & • recedes with rest • Temperature: (COLD) • Skin color changes: skin pale on • elevation but red dependent 7 (continued) • Reactive hyperemia: (reduced blood flow to extremity results in arteriolar dilation so when the blood supply is restored, the affected area becomes warm/red from congestion • Pulse changes: Peripheral diminished or absent 8 (continued) • Prolonged capillary refill: • - 3 seconds or more • Ulcers: • - open lesions on feet from diminished distal perfusion 9 • • • • • Arteriosclerosis -describes arterial disorders in which degenerative changes result in decreased blood flow Atherosclerosis: - most common form of arteriosclerosis, excessive accumulation of lipids 10 Major risk factors of arteriosclerosis: • • • • • • • Hypertension (MOST SIGNIFICANT) Cigarette smoking (nicotine has DIRECT vasoconstricting effect) Elevated serum cholesterol (fat causes obstructive plaques) Obesity (increased work to heart) Diabetes (hyperglycemia causes damage to vessel wall) • Other: increase age, inactivity, family hx 11 • • • • • • • • 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) 12 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, 13 • 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 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 15 16 SURGERY • Indications for fem-pop bypass: • diabetes • hypertension • vasculitis • collagen disease • Bueger’s disease • Also, Embolectomy (surgical removal) 17 Fem-pop bypass 18 MEDICAL MANAGEMENT • ANTIPLATELET THERAPY – Aspirin, ticlid, plavix, pletal, trental • Beta blockers • ARBs • Statins • Radiation therapy • Angioplasty with stents 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 Acute arterial stenosis • Monitor for the 5 P’s • pain, sudden • pallor • pulselessness • paresthesias • paralysis 21 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 23 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 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 25 Thoracic Aortic Aneurysm • • • • 85% are caused by atherosclerosis More frequent in men b/w 40-70 years old Most common site for dissection 1/3 of pts with this die from rupture • • • • • • • S/S Asymptomatic Pain is primary symptom—constant Dyspnea Cough Hoarseness Stridor Aphonia (weakness or complete loss of voice) • Unequal pupils Diagnostics • Chest x-ray • TEE • CT Aortic dissection 29 Aortic Dissections: Type III most common type 30 Abdominal Aortic Aneurysm Size and Rupture Risk* AAA Diameter (cm) Rupture Risk (%/yr) <4 0 4–4.9 1% 5–5.9* 5–10% 6–6.9 10–20% 7–7.9 20–40% >8 30–50% *Elective surgical repair should be considered for aneurysms > 5.0–5.5 cm. 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 32 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 33 • GOAL: to keep blood pressure to lowest • possible but yet allows tissue perfusion – Per physican recommendations 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 35 36 Dacron tube 37 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% 38 Nonsurgical management of AAA • Monitor growth: freq. CT scans • Antihypertensives • SURGICAL: • graft 39 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 40 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 41 Venous diseases: • Venous thrombosis (thrombophlebitis) • known as DVT • Varicose veins • Venous stasis ulcers 42 Venous manifestations: • 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 43 • • • • • • • • 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 44 • DVT risk for pulmonary embolism • - legs • - seen post hip surgery, knee replacement pregnancy, ulcerative colitis, hrt failure, immobility 45 DVT : • • • • • Groin tenderness/pain Unilateral sudden onset edema leg Homan’s sign (appears in only 10% of pt with DVT) Ultrasonography 46 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 47 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 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 49 S/S • • • • • Often none Occipital headache more severe on rising Lightheadedness Epistaxis Known as the ‘Silent Killer’ 50 Factors that determine arterial pressure • Cardiac output which is the volume of blood pumped by the heart in 1 minute • Peripheral vascular resistance which is the force in the peripheral blood vessels that the left ventricular must overcome to eject blood out of the heart 51 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 52 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 53 • 95% of cases of hypertension are 1st degree (essential) • 2nd degree hypertension: CHAPS • Cushing’s syndome • Hyperaldosteronism • Aortic coarctation • Pheochromocytoma • Stenosis of renal arteries 54 Complications • Damage to blood vessels of the eyes, heart, kidney, brain resulting in: • Stroke • CHF • AMI • Renal failure • Blindness 55 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 56 Target organ disease from hypertension: • Renal: acute=hematuria, azotemia • chronic=elevated creatinine • proteinuria • Retinopathy: • acute=papilledema, hemorrhages • chronic=hemorrhages,exudates, • 57 Treatment of hypertension: • Lifestyle modification ABCD: ACE inhibitors; ARB B-blockers Calcium channel blockers Diuretics 58 HTN CRISIS • Sometimes rare sometimes fatal • Diastolic BP 120-130 – Causes vascular damage • Can be caused by renal failure, HTN, Med withdrawal 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 60 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 61 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 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 66 manifestations • • • • • Severe headache LOC Tinnitus Dizziness Hemiparesis Prognosis: variable diagnostics • CT • Lumbar puncture • Angiography Prevention • Manage HTN • Avoid alcohol • Increase public awareness 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 • Risk assessment for complications including fall, pressure ulcer, painful hemiparetic shoulder, spasticity/contractures, and deep vein thrombosis • • • • Pain assessment Administration and interpretation of dysphagia screen Nutrition and hydration screening Screening for alterations in cognition, perception, and language using validated tools • Assessment of activities of daily living (ADL) using validated tools • Assessment of bowel and bladder function • Depression screening using a validated tool • Assessment/screening of caregiver burden using a validated tool • Screening of stroke clients and their partners for sexual concerns • Assessment of stroke client and their caregivers' learning needs, abilities, learning preferences and readiness to learn • Referral for further assessment and management, as indicated • Documentation of all assessments and screenings 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) 75 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 76 More stroke treatment: • Carotid artery angioplasty • Arteriovenous Malformation (gamma radiation through Gamma knife) • Aneurysms (coils) • Craniotomy for clot removal 77 Nursing assessment with anticoagulant therapy: • Observe for bleeding • Also, antiplatelet meds (Plavix, Persantine) cause • bruising, hemorrhage, liver disease (need liver function tests) • GIVE clopidogrel (Plavix) with food 78 Nursing Diagnosis • • • • • • • • • Impaired physical mobility: -flaccid, spasticity Disturbed sensory perception: -vision, proprioception, sensation Unilateral neglect: - use both sides of body (dress affected side first) Impaired verbal communication:: -expressive, receptive, both Impaired swallowing: – must be evaluated, must prevent aspiration !!! But yet meet caloric needs • Urinary and/or bowel incontinence 79 Complications • • • • Rebleed Vasospasm Hydrocephalus Hypoxia of brain Nursing interventions • • • • • • • • • • Administer oxygen Provide adequate hydration Evaluate swallow function Frequent neuro checks Strict I/O Seizure precautions Monitor ICP Monitor BP closely Teach stress reduction techniques Manage agitation Surgery and complications • Evacuation of blood via craniotomy • Goal of surgery is to prevent further rupture/bleed • Post op complications – Disoriented – Amnesia – Korsaff’s syndrome (psychosis caused by lack of thiamine) – Personality changes – Intraop emboli – Electrolyte disturbances – GI bleed QUESTIONS???