Vascular MCC NURSING

DIANA BLUM MSN

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

hormones

Arteriosclerosis (atherosclerosis)Aneurysm formationArteriosclerosis obliteransRaynaud’s phenomenonArterial embolismThromboangiitis obliteransDiabetic arteriosclerotic diseasehypertension

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Arterial diseases:

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

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Manifestations :ARTERIAL(50% occulsion before symptoms)

-describes arterial disorders in which degenerative changes result in decreased blood flow Atherosclerosis: - most common form of arteriosclerosis, excessive

accumulation of lipids

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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)

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Most common affected areas from arteriosclerosis:

-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) mostsusceptible arteries.

Endothelial injury: may be initiated by smoking, hypertension, diabetes, hyperlipidemia,

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Pathophysiology of atherosclerosis

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

-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

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Ankle-brachial index of blood pressure:Used to diagnose peripheral vascular disease

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

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SURGERY

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Fem-pop bypass

MEDICAL MANAGEMENT

ANTIPLATELET THERAPYAspirin, ticlid, plavix, pletal, trental

Beta blockersARBs Statins Radiation therapyAngioplasty 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

Monitor for the 5 P’s pain, sudden pallor pulselessness paresthesias paralysis

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Acute arterial stenosis

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

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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

Buerger Disease

Enlargement of artery to @ least 2X its normal Aortic dissection

Medial & intimal layers separate Risk Factors: -hypertension -cocaine use - Marfan syndrome

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Aneurysms of Central Arteries

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Aortic Dissections: Type III most common type

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.

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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

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Signs/symptoms of aortic dissection:

IV propranololNitropresside 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

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Treatment of hypertension for aortic dissection:

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

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Surgery for distal dissections:

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Dacron tube

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%

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Abdominal Aortic Aneurysm (AAA)

VitalsPulses distal to graftReport: changes in pulse cool extremities distal to graft white/blue to extremities distal to graft

severe pain abd. distention decreased UO

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Post-op nursing interventions for graft:

Elevation of head to 45° or less Renal function lab Respiratory status Paralytic ileus (NG tube) Assess for dysrhythmias post thoracic

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Post-op nursing intervention (continued)Post graft

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

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Venous manifestations:

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

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DVT :

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

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DVT interventions:

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 medsNursing cares

- 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

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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

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Pathophysiologic processes for hypertension:

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 pumpAbility of blood vessel to stretch

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Possible Causes of PVR

Large vessels: aneurysmal dilation accelerated atherosclerosis aortic dissectionCardiac: acute= pulm edema, MI chronic= LVH

Cerebrovascular: acute= Intracranial bleed, coma, seizure mental status changes, TIA, stroke chronic=TIA, stroke

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Target Organ Disease from hypertension

Renal: acute=hematuria, azotemia chronic=elevated creatinine proteinuria Retinopathy: acute=papilledema, hemorrhages chronic=hemorrhages,exudates,

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Target organ disease from hypertension:

Lifestyle modification

ABCD:

ACE inhibitors; ARB

B-blockers

Calcium channel blockers

Diuretics

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Treatment of hypertension:

Parenteral agents for immediate redux of BP In ICU for monitoringArterial lineDrug 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

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Hypertensive Crisis:Treatment

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 activity42

STROKE: occlusion of cerebral vasculature

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

TIA

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

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Hemorrhagic stroke

Manage HTN Avoid alcohol Increase public awareness

Prevention

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

Thrombolysis (who is not a candidate?) Lower BP Quit smoking Decrease cholesterol Antiplatelet (ASA)

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Treatment for stroke:(Note similar to measures for myocardial ischemia/MI)

ASAHeparin (SQ or IV contin infusion)Low-molecular wt heparin (lovenox)Warfarin (coumadin)-------------------------------------------------------Obtain PT, PTT prior to therapyPT: monitor oral anticoag : goal=1.5 to 2 times pt baselinePTT: monitor heparin: goal=1.5 to 2 times pt baselineINR: monitor Warfarin: goal=2 to 3

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Stroke treatment (continued)

Carotid artery angioplasty Arteriovenous Malformation (gamma radiation through

Gamma knife) Aneurysms (coils) Craniotomy for clot removal

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More stroke treatment:

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

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Nursing Diagnosis

Rebleed Vasospasm Hydrocephalus Hypoxia of brain

Complications

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

Nursing interventions

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

Surgery and complications

QUESTIONS???