Home > Flashcards > Print Preview
The flashcards below were created by user
on FreezingBlue Flashcards. What would you like to do?
**Atherosclerotic Arterial Disease
- Word meaning derived from Greek:
- Athere “fatty mush” & Skleros “hard”Soft deposits of fat harden with age; Known as “hardening of the arteries”
- Can occur in any artery throughout the body
- Related to coronary artery disease: the deposits that block blood flow to the heart BUT in the periphery INSTEAD of coronary arteries.
- =>Risk Factors
- Age: over 55 increases chance
- Gender: more common in men until 65, then it's equal in both sexes
- Ethnicity:greater in whites and blacks
- Family History
- Genetic factors: ;inherited defects in vessel walls
- Hyperlipidemia: genetic component
- Hypertension: modified with activity and smoking cessation
- Tobacco use: very irritating to the vessel walls, deposit start to build up which causes the plaque
- Physical inactivity
- Others: stress and heavy alcohol use.
**Pathophysiology of Atherosclerotic Arterial Disease (three stages)
- =>Fatty Streak formation
- can start in the 20's, it is reversible, lowering LDL (bad cholesterol can reverse this process)
- Serum lipoproteins are deposited in vessel intima lining
- then Foam cells are attracted to the site, form and make a yellowish tinge
- =>Fibrous plaque
- -start in 30's. Significant narrowing of the lumen which decreases blood flow
- characterized by Progressive lipid accumulation
- Smooth muscle cell proliferation
- Connective tissue matrix forms (fibrous cap)
- Growth of fibrous plaque causes increased lumen narrowingcalcium deposits cause decreased flexibility in vessels and hardening of arteries
- =>Complicated lesion
- This mass now ruptures..
- Inflammation can cause the fibrous plaque to rupture
- Plaque rupture can lead to acute occlusion, thrombus formation, or further extension of atheroma (accumulation of degenerative material/dead tissue in inner layer of arteries; consists of macrophages, cell debris, lipids like cholesterol, fatty acids, calcium and fibrous connective tissue)
- Accumulative material forms swelling in artery wall, protudes in the channel of the artery--restricting blood flow & narrows lumen
**Atherosclerosis VIDEO: How cholesterol clogs your arteries
Build up of fatty acids in walls of arteries, major cause of cardiovascular disease including stroke and Cholesterol: natural fat like substance, produced in liver, foundin saturated fat-foods. LDL-C is bad. Increase HDL's (goal)
- => Normal artery wall:
- 1: thin, smooth layer on inside
- 2. Muscular to push blood
- 3. Tough outer layer to protect artery
=> Smoking, high BP, diabetes and high cholesterol damages smooth layer, then LDL gets to wall of arteries.
- => 4 key stages:
- Macrophages consumes LDL-C. Become foam cells that are imbedded into vessel wall--Seen as fatty streaks which grows. Body tries to protect by surrounding them in a fibrous capsule --growth now called plaque. Expans into elastic wall--intrudes into innner opening of vessel. Reduces blood flow. Artery cannot expand anymore; during exercise. As plaque growsinto the artery opening, it squeezess the blood. The resulting increase in pressure in narrowing can damage the capsule covering the plaque which then may rupture --> blood clot that completely blocks artery.
- => Atherosclorisis
- in heart: angina-chest pain.
- In brain: Transient ischemia attacks (mini strokes).
- In legs: Intermittent claudication which can result in amputation in limb
=> Athero weakens artery wall, causing it to bulge (aneurysm); and if it ruptures--> hemmorage (fatal in brain!)
body compensation to keep up blood flowpressure that builds up above plaque eventually goes out to the siides to form colalteral circulationcirculation around plaque
**Peripheral Artery Disease (PAD)
Chronic, progressive narrowing and degeneration of arteries leading to reduction in distal blood flow
Primary cause is atherosclerosis
Smoking is most important risk factor (80-90%)
lower extremitiy PAD (intermittent claudication) is more common in african americans
Common locations: aortoilliac, femoral, popliteal, tibial, peroneal; Arteries below the knee in diabetics are usually affected.
**Clinical Manifestations of PAD
- => Intermittent claudication is “classic” symptom
- Ischemic muscle pain precipitated by activity BUT Relieved by rest <10 minutes
- Only 10% of patients (not a very good indicator...)
- -muscle pain is due to waste products like lactic acid b/c decreased circulation
- nerve tissue ischemia
- loss in pressure or pain sensation: neuropathy--> leads to injury
- =>Rest pain w/ advanced PAD
- Aggravated by limb elevation
- Worse at night:: because they're lying down when blood flow is insufficent to meet the basic metabolic needs of distal tissues, pt report danging legs on side of bed to relieve pain; when they're laying in bed with feet up, decreasesd circulation (rest pain) so danging helps increase circulation so paingoes away
- -Thin, shiny, taut, hairless skin
- -Thickened, brittle nails
- -Cool skin temperature: lack of arterial circulation
- -Calf muscle atrophy: no nutrients to buiild muscles
- -Diminished or absent pulses
- -Increased cap refill
- -Elevation pallor: blanching when feet up
- -Dependent rubor: turn red when feet are dangling
- -Erectile dysfunction in males
- -“Rest” pain =Severe sign
**Arterial (ischemic) Leg Ulcers
Over bony prominences: ankles, tip of toes
Margins are smooth, round, look “punched-out”
Skin is thin, shiny, dry, and hairless
collateral circ may help prevent and heal, but with lack of blood circulation.. minor injuries do occur and gangrene/tissue necrosis occurs
**Necrotic Toe-Other complication: arterial occlusion, MI, strokes
**Acute Arterial Occlusion
Acute arterial ischemia can occur with emboli, thrombosis, vasospasm, and/or trauma
common scenario: thrombus that forms in lower arteries and moves to heart.
Patients with chronic PAD more susceptibleSix P’s of arterial occlusion: pain, pallor (white blanching), paralysis, pulselessness, paresthesia, and poikilothermia ( cool to the touch) ; mottled pale loose skin and loss of movement in toes
Can progress quickly to tissue necrosis and gangrene
Requires surgical intervention and/or thrombolytic therapy like heparin drip
ex: pt's right foot: dark, bluish, mottled vs. left normal leg
** Acute Arterial OcclusionDiagnostics
=> Ankle-brachial index (ABI):
take the BP above ankle and take BP at the arm, then systolic of ankle BP over the highest Brachial Systolic to get a ratio!
=> Duplex ultrasound:
- -formula: Ankle systolic BP/highest brachial systolic BP
- Normal 0.91- 1.30 (around 1)
- Mild 0.71-0.90
- Moderate 0.41-0.70
- Severe <0.40-no acute systems
Maps blood flow in a visual format; differential b/w arterial and venous
=> Doppler Probe:
Detects blood flow in auditory form; Used to find pulse like for pedal pulses.
- =>Segmental blood pressure
- BP at thigh and then below knee with patient lying supine. Taking BP down leg and seeing if it drops
- Drop >30mmHg suggests PAD
noninvasive scans with injected dyes. Usually done for surgery.
EKG, Urine Analysis: increased protein/blood...checking for abnormalities in general
**PAD: Goals of Collaborative Care
- Reduce the risk of CV disease
- Improve functioning
- Manage pain
- Prevent progression/complications of disease:
- ==Collaborative Care==
- =>Risk factor modification
- Smoking cessation is #1!
- Aggressive management of HTN, hyperlipidemia, diabetes
- Foot care and injury prevention: daily skin checks for neuropathies of lower extremities.
- =>Nutritional Therapy
- Diet high in fruit, vegetables, whole grains
- Low in saturated fat, cholesterol, sodium
- Target BMI
- =>Exercise Therapy
- Walking is most effective exercise: improveds oxygen extraction into legs and skeletal muscle metabolism and endothelial function
- Supervised rehabilitation program or home exercise program
- taught to walk to point of pain and then rest until pain subsides then walk again
- 30-40 mins, 3-5x week
81-325 mg PO-325: more for acute episodes
- 2. Clopidogrel (Plavix ) 75 mg PO: can be prescribed with ASA; given w/ high risk pts: stents, previous thrombous
- -bleeding complication for both platelets: goal over 100
=>Treatment of intermittent claudication
: Study showed improved walking ability and quality of life (off-label). Ace-Inhibitor. Prefered for HTN.
- Phosphodiesterase inhibitors: Pentoxifylline (Trental)
- Cilostazol (Pletal)
- -Only drugs currently approved for PAD and intermitted claudication.
Phosphodiesterase inhibitors' Treatment of intermittent claudication
First drug in category; Decreases blood viscosity and improves RBC flexibility
No longer widely used
Phosphodiesterase inhibitors;Treatment of intermittent claudication
Inhibits platelet aggregation and smooth muscle proliferation, promotes vasodilation, increases HDL (used more than trental!)
normal: 100mg PO BID on empty stomach
SE/Contraindications: Headaches, GI sideffects that go away on their own, increaed risk of sudden cardiac death--use with caution
tPA (tissue plasminogen activator)
Given IV ONLY by doctor.
Acute situation: stroke ischemic as long as no prior history of bleeding and not taking any blood thinners.
must be given within two hours of start of symptoms!
activates enzymes from that dissolve clot in hour or two, may be used if ischemic clot is stable.
Heparin drip: usually administered after TPA, prevents clot formation and prevent the current clot from moving--stabilizes clot. Prevents enlargement of thrombus.
-labs: PTT (check Q6H and readjust the values)
-HIT: hep induced thrombocytopenia: decreased platelets.
So then they give: Argatroban dripArgatroban drip: used if you're allergic to heparin
=> Anti-platelet agents- inhibit platelet aggregation
**PAD Collaborative Care (con't)
=> Radiological intervention
- 1. Percutaneous transluminal balloon angioplasty w/ stent placement--lifetiime plavix or aspirin
- -put in stents, conscious sedation-twilight sleep; put in device through femoral artieries-balloon angioplasty (put cath in middle of lumen and inflate balloon to open up the lumen against the plaque. Usually need to put in a stent (flexible tube to prevent artery from collapsing on itself; they're covered in plt/antithrombin medication b/c body is going to attack it as a foreign object)
- Performed in cath lab
- Restenosis even is pretty high
via laser, drill.
go in and get the clot out, Cryoplasty (freeze the tissue)
- =>Surgical intervention
- Peripheral Artery Bypass w/ autogenous or synthetic graft. Usually saphenous vein w/o branching from legs.
: surgically go in and take out the clot or the plaque
Patch graft angioplasty:
open artery, remove plaque and sew patch into place (use vein, artery or synthetic material)
-last resort: for severe or advance limb ischemia, failed surgery, ulcers that aren't healing.. /:
**Nursing Responsibilities: Post Procedure
Monitor for bleeding
- Frequent circulatory assessment
- Pain management
- Monitor surgical wounds for complications
- => Discharge teaching
- Risk modification strategies
- Exercise therapy
- Foot/ulcer care
- S/S that necessitate RTC
Peripheral Artery Disease : Surgical Care post-op:
- => Limb assessment
- Pulse checks
- Skin color: color, motion, sensitivity
- Cap refill: ted hose to increase circulation Sensation and movement
- monitor surgical wounds: bleeding or hematoma
- -> Discharge: risk modificaation strategies, exercise, foot ulcer care and s/s of return.
- -dramatic increase in pain or loss of previous felt pulses, or decreasing AVI--communicated to doctor b/c signifies occlusion.
=>after surgery: limb assessment: pulse, sensation, movement, temp, color, cap refill
- =>If pt had a Bypass: Bypass graft patency (make sure that the graft/vein is working and blood is flowing through it)
- -Ususally Q15 for first hr, Q1H for 4 hours then Q2H then Q4!
**Nursing Diagnoses: PAD
Ineffective Peripheral Tissue Perfusion r/t decreased arterial blood flow
Activity intolerance r/t imbalance between oxygen supply and demand
Risk for Impaired Skin Integrity and Risk for Injury r/t decreased peripheral circulation and sensation
Ineffective Self-Health Management r/t lack of knowledge
Acute or Chronic Pain
**Thromboangiitis Obliterans: (Buerger’s Disease)
- NOT CAUSED BY PLAQUE, there can be thrombus (non-atherosclerotic--difference from PAD); AFFECTS ONLY SMOKERS.
- -no lipid accumulation in the vessels.
- -Unlike PAD, it doesn't affect major organs, only focuses on the extremites
Nonatherosclerotic, inflammatory disease of small to medium peripheral arteries and veins of upper/lower extremities
Inflammation damages arterial wall and thrombosis/fibrosis can occur leading to tissue ischemia
- =>Risk factors
- Male <40
- TOBACCO USE
- =>Clinical Manifestations
- Intermittent claudication
- Acute, severe pain in hands/feet
- Rest pain: pain when extremities are elevated
- Ischemic ulcerations and gangrerne (mottled--poor circulation)
- Color/temperature changes of limbs
**Thromboangiitis Obliterans Collaborative Care
Smoking cessation- only effective treatment (MUST STOP. Any source of nicotine will keep the disease going. You can't even cut down.. Cold turkey.)
Avoid second hand smoke. Don't use nictoine replacement: increased sensitivity to nicotine
Management of complications
Drug therapy has not proven successful; steroids aren't helpful even though this disease is inflammatory. nor do anticoagulants.
Surgery (sympathectomy) may help control pain. Surgical cutting of sympathetic nerve/ganglion to decrease pain stimulation and arterial spasm
Vascularization is not option b/c diffuse manifestation of this disease--usually happens somewhere else.
Episodic, vasospastic disorder of small cutaneous arteries in fingers/toes
Non inflammatory, no thrombus. Just vasospasms-> ischemai
Occurs bilaterally, usually not painful but can be when severe
- =>Etiology unknown
- Exaggerated response to SNS simulation
- Occupational trauma
- -Occurs primarily in young women
- -When associated w/ autoimmune disorders disorder (rheumatoid arthritis and Lupus) is called secondary Raynaud’s phenomenon
- => Triggers:
- Sudden vasoconstriction precipitated by
- Exposure to cold (even just going into freezer)
- Emotional upset
- Caffeine: vasoconstrictor
- Tobacco vasoconstrictor
- Occupational trauma: pianists, cashiers (ppl that use hands a lot)
** Raynaud’s Phenomenon Clinical Manifestations
- =>Patriotic Fingers
- Exposure to stimuli causes vasoconstriction resulting in pallor (white)
- Deoxygenated blood pools during vasospasm resulting in cyanosis (blue)
- Vasodilation as it kind of results, and exaggerated hyperemia resulting in rubor (red)
- -can be numbness/tingling when circulation comes back (pins and needles)
- -one episode can last usually a minute, but also several hours possible
- -Complications: small pinpoint lesions, ulcers, gangrene ulcers in advanced stages-if symptoms persist for several years in abscence of underlying disorders, then raynaud's is diagnosed.
- -usually fingers, diameters of vessels are small there.
- =>Limit episodes
- Avoid smoking and caffeine
- Avoid medications that have vasoconstrictive effects: migraine meds, pseudophedrine, cocaine, meth
- Avoid temperature extremes (gloves whehn handing cold object and layer clothes)
- Stress management
- Acupuncture: some success...
- =>Interventions for severe disease
- Calcium channel blockers PO (only treatment)--Extended Release ProCardia
- Topic NTG (nitroglycerin)
- Digital sympathectomy: cutting symp nerves to reduce condition