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Vascular MCC NURSING DIANA BLUM MSN.  C reactive protein is a marker for cardiac inflammation  Increases mean: risk of damage  Homocysteine: protein.

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Presentation on theme: "Vascular MCC NURSING DIANA BLUM MSN.  C reactive protein is a marker for cardiac inflammation  Increases mean: risk of damage  Homocysteine: protein."— Presentation transcript:

1 Vascular MCC NURSING DIANA BLUM MSN

2  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

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

4  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 4 Manifestations :ARTERIAL (50% occulsion before symptoms)

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

6  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) 6 Most common affected areas from arteriosclerosis:

7  -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,  7 Pathophysiology of atherosclerosis

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

10 10

11  Indications for fem-pop bypass:  diabetes  hypertension  vasculitis  collagen disease  Bueger’s disease  Also, Embolectomy (surgical removal) 11 SURGERY

12 12 Fem-pop bypass

13 MEDICAL MANAGEMENT  ANTIPLATELET THERAPY  Aspirin, ticlid, plavix, pletal, trental  Beta blockers  ARBs  Statins  Radiation therapy  Angioplasty with stents

14 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

15  Monitor for the 5 P’s  pain, sudden  pallor  pulselessness  paresthesias  paralysis 15 Acute arterial stenosis

16 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

17 17

18  Autoimmune disease  Recurrent inflammation of small arteries and veins of the extremities resulting in thrombus formation and occlusion.  Unknown cause  Men 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

19  Enlargement of artery least 2X its normal  Aortic dissection  Medial & intimal layers separate  Risk Factors:  -hypertension  -cocaine use  - Marfan syndrome 19 Aneurysms of Central Arteries

20 20 Aortic Dissections: Type III most common type

21 Abdominal Aortic Aneurysm Size and Rupture Risk* AAA Diameter (cm)Rupture Risk (%/yr) < 40 4–4.91% 5–5.9*5–10% 6–6.910–20% 7–7.920–40% > 830–50% *Elective surgical repair should be considered for aneurysms > 5.0–5.5 cm.

22 22 Aortic dissection

23  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 23 Signs/symptoms of aortic dissection:

24  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 24 Treatment of hypertension for aortic dissection:

25  Mortality in 1 st 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 25 Surgery for distal dissections:

26 26

27 27 Dacron tube

28  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% 28 Abdominal Aortic Aneurysm (AAA)

29  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 29 Post-op nursing interventions for graft:

30  Elevation of head to 45° or less  Renal function lab  Respiratory status  Paralytic ileus (NG tube)  Assess for dysrhythmias post thoracic 30 Post-op nursing intervention (continued) Post graft

31  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 31 Venous manifestations:

32  Groin tenderness/pain  Unilateral sudden onset edema leg  Homan’s sign (appears in only 10% of pt  with DVT)  Ultrasonography 32 DVT :

33  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 33 DVT interventions:

34  Monitor for hemorrhage  Monitor PT/PTT  Heparin is therapeutic b/w 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 Nursing cares

35  - 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 35 Hypertension

36  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 36 Pathophysiologic processes for hypertension:

37  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 37 Possible Causes of PVR

38  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 38 Target Organ Disease from hypertension

39  Renal: acute=hematuria, azotemia  chronic=elevated creatinine  proteinuria  Retinopathy:  acute=papilledema, hemorrhages  chronic=hemorrhages,exudates,  39 Target organ disease from hypertension:

40  Lifestyle modification ABCD: ACE inhibitors; ARB B-blockers Calcium channel blockers Diuretics 40 Treatment of hypertension:

41  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 1 st 2 hours  = easily titratable  = monitor closely for hypotension  = shield this drip from light 41 Hypertensive Crisis: Treatment

42  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 42 STROKE: occlusion of cerebral vasculature

43  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

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45  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 45 Hemorrhagic stroke

46  Manage HTN  Avoid alcohol  Increase public awareness Prevention

47

48 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

49  Thrombolysis (who is not a candidate?)  Lower BP  Quit smoking  Decrease cholesterol  Antiplatelet (ASA) 49 Treatment for stroke: (Note similar to measures for myocardial ischemia/MI)

50  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 50 Stroke treatment (continued)

51  Carotid artery angioplasty  Arteriovenous Malformation (gamma radiation through Gamma knife)  Aneurysms (coils)  Craniotomy for clot removal 51 More stroke treatment:

52  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 52 Nursing Diagnosis

53  Rebleed  Vasospasm  Hydrocephalus  Hypoxia of brain Complications

54  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

55  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

56 QUESTIONS???


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