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 formation
Arteriosclerosis obliterans
Raynaud’s phenomenon
Arterial embolism
Thromboangiitis obliterans
Diabetic arteriosclerotic disease
hypertension
Arterial diseases:
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Manifestations :ARTERIAL
(50% occulsion before symptoms)
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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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 -describes arterial disorders in which
 degenerative changes result in
 decreased blood flow
 Atherosclerosis:
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- most common form of arteriosclerosis, excessive
accumulation of lipids
Arteriosclerosis
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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)
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 -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, 
Pathophysiology of atherosclerosis
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 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
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 Indications for fem-pop bypass:
 diabetes
 hypertension
 vasculitis
 collagen disease
 Bueger’s disease
 Also, Embolectomy (surgical removal)
SURGERY
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Fem-pop bypass
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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
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pain, sudden
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pallor
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pulselessness
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paresthesias
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paralysis
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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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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
 Enlargement of artery to @ least 2X its normal
 Aortic dissection
 Medial & intimal layers separate
 Risk Factors:
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-hypertension
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-cocaine use
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- Marfan syndrome
Aneurysms of Central Arteries
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Aortic Dissections: Type III most
common type
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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.
Aortic dissection
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 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
Signs/symptoms of aortic dissection:
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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:
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CXR (but 10% normal) see medialstinal
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widening
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Contrast CT
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MRI
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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
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Dacron tube
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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%
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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
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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
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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
Venous manifestations:
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DVT :
 Groin tenderness/pain
 Unilateral sudden onset edema leg
 Homan’s sign (appears in only 10% of pt
 with DVT)
 Ultrasonography
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 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
DVT interventions:
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 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
Nursing 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
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<80 mmHg diastolic
Hypertension
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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
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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
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 Large vessels: aneurysmal dilation
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accelerated atherosclerosis
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aortic dissection
 Cardiac:
 acute= pulm edema, MI
 chronic= LVH
 Cerebrovascular:
 acute= Intracranial bleed, coma, seizure
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mental status changes, TIA, stroke
 chronic=TIA, stroke
Target Organ Disease from
hypertension
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 Renal: acute=hematuria, azotemia
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chronic=elevated creatinine
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proteinuria
 Retinopathy:
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acute=papilledema, hemorrhages
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chronic=hemorrhages,exudates,
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Target organ disease from
hypertension:
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Treatment of hypertension:
Lifestyle modification
ABCD:
ACE inhibitors; ARB
B-blockers
Calcium channel blockers
Diuretics
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Hypertensive Crisis:
Treatment
Parenteral agents for immediate redux of BP
In ICU for monitoring
Arterial line
Drug of choice: sodium nitroprusside
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=direct acting arterial & venous vasodilator
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= reduces BP rapidly but lower mean arterial
pressure no more than 25% over 1st 2 hours
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= easily titratable
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= monitor closely for hypotension
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= shield this drip from light
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STROKE: occlusion of cerebral vasculature
DUE TO:
 1. emboli that lodges in cerebral vasculature
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(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
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 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
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
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Prevention
 Manage HTN
 Avoid alcohol
 Increase public awareness
Assessment Tools
 Neurological assessment upon admission or change in client status,
including:
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Level of consciousness
Orientation
Motor ability
Pupils
Speech/language
Vital signs
Blood glucose
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)
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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
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More stroke treatment:
 Carotid artery angioplasty
 Arteriovenous Malformation (gamma radiation through
Gamma knife)
 Aneurysms (coils)
 Craniotomy for clot removal
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 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
Nursing Diagnosis
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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
 Evacuation of blood via craniotomy
 Goal of surgery is to prevent further rupture/bleed
 Post op complications
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Disoriented
Amnesia
Korsaff’s syndrome (psychosis caused by lack of thiamine)
Personality changes
Intraop emboli
Electrolyte disturbances
GI bleed
Surgery and complications
QUESTIONS???