Exam 3 Flashcards
Purpose looking at joint function? aterial system supplies O2, use muscle to make legs go up and down and muscles need O2
document pulses: 2+/3+, 4+ = bounding/too much pressure/fluid - assess bilaterally to see
ROM motions: STUDY - flexion/extension, external/internal rotation
cap refill: <3 seconds, painted nails = tip of finger
assessing
Disease process that affects the arteries
Begins early in adult hood and progresses slowly with age
Risk factors
Family history
20% > than 70
Obesity
Smoking (4X chance increase)
Stress
Preexisting health r/t destruction of vessels (DM12, clotting disorder, thromboemboli, trauma, vasospastic disorder) conditions
peripheral artery disease PAD
Dependent: hanging below Rubor: purple/blue red Cyanosis: blue Contralateral: opposite side Proximal (=close) vs distal (=far) Percutaneous: through the skin Autologous: self (autologous donation) Bruit: swish/turbulent blood flow - use bell side Excision: cut it out Angio- artery Veno- vein -graphy: picture -oscopy: view with camera through scope
vocab
Narrow lumen-> ischemia-> infarct
Obstructive lesions usually occur from aorta below the renal arteries to the popliteal arteries
Arteriosclerosis is the most common artery disease affecting muscle fibers and endothelial lining of the small arteries and arterioles (become thickened)
– affects fibers in vessel, stenosis (narrowing) of artery
Atherosclerosis-> arterial stenosis->obstruction by thrombus->aneurysm-> ulceration-> rupture of vessel
Vessel gets smaller, decreases O2 in blood, leads to ischemia/tissue death/infarction
Can occur where arteries go
Affect brain (AMB stroke) and heart (AMB MI), lungs and kidneys
patho of PAD
Structural changes from lack of oxygen & nutrients
Skin color changes: temp = cool, Color = pale/rubor, Elevate = harder for body in PAD, Drop = easier for PAD (*position = lay flat to decrease need on heart)
Pulse changes: Diminished = 1 occlusion in 1 leg
Sensation changes: nail buds = thick/cloudy/clubbed, ROM to check muscle use; no O2 to muscle = atrophy
- numbness/tingly (like SS DM12)
Ulceration/gangrene: PAD = pour wound healing r/t lack of O2 to blood; pain at rest = late stage
Edema: very rare with PAD
PAD assessment
Most have no symptoms
1- 5% have critical limb ischemia: pain at night waking them up. Progresses to gangrenous ulcers/poor wound healing
Acute limb ischemia: r/t embolus: immediate blocking (ex: cocaine)
- upper limbs are acute AMB more pain with hands above heal, like doing hair. Numbness/tingling is less common
Atherosclerosis- systemic disease that affects arteries of the brain, heart, kidneys, mesentery and limbs.
Manifestations happen in the end organ supplied by arterial blood flow
Increased risk of mortality, MI, and CVD
clinical manifestations of PAD
Intermittent Claudication- very common
Muscle pain cramp caused by exercise or activity
Relieved by stopping muscle use
Arteries cannot provide blood flow with increased demand
Pain in muscles distal to diseased vessel
Exercise demands oxygen and nutrients->Tissues complete energy cycle without nutrients-> metabolites and lactic acid
-Treat: walking into pain = increasing blood flow to areas; lose weight, stop smoking, eat better
Rest Pain- Severe
Critical degree of arterial insufficiency
Pain worse at night
Interferes with sleep
pain with PAD
Hair loss: lower leg/ smooth/shiny skin Brittle nails: curve up Dry or scaling skin: lack of nutrients Atrophy: inability to do ROM Ulcerations Gangrene
chronic S/S of CAD
Palpation tips= Use finger tips Use light touch Symmetry in rate, rhythm, & quality Bilateral & at the same Bruits May be auscultated distal to an arterial stenosis
pulses in PAD
*Doppler: look at arterial signals; BP in limbs, vessels, size and compressibility
- look for thrombus/valve function
Exercise Testing: ankle BP while on tread mill. look for drop in ankle pressure which indicates claudication
Duplex Ultrasound: look for vascular obstruction, stenosis, vascular with reflux, image and audible sign
CTA: spiral looks for AA, graft rejections or occlusion, hemorrhage (computed tomorgraphy angiography)
MRA (magnetic resonance angiography): angiography-MRA scan with software to isolate blood vessels and give 3 d images - Looks for changes, aneurysms, DVT
Air Plethysmography: measurement of volume, ejection fraction, residual volume, venous reflex, calf muscle pump ejection
Venous Duplex
Angiography: look for occlusive artery disease with dye
Venography: use radiopaque contrast into venous system for image
Angioscopy
diagnostics for PAD
“Walk into Pain”
Cilostazola-vasodilator that interferes with platelet aggregation: dilate to get blood out, can’t use with low BP because you will pass out due to lack of perfusion everywhere else
Antiplatelet agents: aspirin, Plavix - make platelets slippery so clots are harder to form (this is prevention)
Thrombolysis: destroy
treatment of intermittent claudication for PAD
Revascularization or arterial bypass first-line intervention (most common) - cut vessel via autonomous donation and reroute blood to get same benefit of blood flow
Type of surgery depends on health of patient
Bypass grafts are done to reroute blood flow around occlusion
Doppler evaluation done on grafts post-op to ensure patency
Post op - worried about bleeding, pts BP goes up and pops open graft
- lots of care post op. pulses will be normal
surgical management of PAD
Angioplasty (percutaneous transluminal balloon angioplasty (PTA) w/ or w/o stent: into vascular system, find clot, squeeze out with balloon by force and leave stent. The sent is foreign object, so risk for clot. It will secrete anti-platelets meds to prevent that
Decreased hospital stay
Less trauma
Outpatient setting
– to get clot go through femoral artery, make hole and go in with camera.
— post op: monitor femoral artery, manual pressure, peusdoaneurism = swelling/hematoma/decrease BP/pain
Risks: Hematoma Embolization Dissection (rips open) Bleeding Stent migration
endovascular intervention for PAD
MAINTAIN ADEQUATE CIRCULATION: circulation issue, so prevent future/potential circulation risk
Activity level-get patient moving
Anticoagulation: increase clotting factors - lovenox to prevent clot
Monitor for compartment syndrome & renal failure
Monitor for local complications: bleeding, hemorrhage, swelling
Monitor for systemic complications (organ fails, kidney/heart/brain issue)
Pain management: opioids, narcotics, Tylenol
Maintain tissue integrity
- When sensation is lost, at risk for impaired tissue integrity (watch incision line and loss of sensation)
Postop teaching (take BP meds, notify for infection, stop smoking, no ice/heat, no tight clothing, no crossing legs
post op care for PADS
Inflammatory disorder->granulation formation->vessel destruction
Vasospasms that occurs with cold or stress
–Cold/stress trigger spasm/inflammatory response, so avoid cold/stress
Raynaud’s phenomenon is common with patients who have lupus or scleroderma (those with a weak immune system)
Etiology-unknown
Affects women age 16-40 years old who live in cold climates
Causes skin and muscle atrophy
Raynauds Disease
Skin color cyanotic (vasospasm) Then vasodilation causes redness (rubor) Numbness Tingling Burning pain -progresses/cuts circulation - leads to atrophy, chronic lack of O2 to tissues
Symptoms of Reynaud’s Disease
Avoid stimuli that causes vasoconstriction (Usually cold or smoking)
Calcium channel blocker (pain) (best treatment)
acute conditions: corticosteriods
Sympathectomy
wear special gloves to keep warm, smoking cessation and increase activity
Treatment of Raynaud’s Disease
Is a localized out-pouching sac or dilation formed at a weak point in the artery wall
-disruption is loss of elastic fibers/collagen (ex: HTN increases pressure/creates pouch)–> degeneration of medial layer of vessel wall thought to be an inflammatory response (wall becomes thin/ulceration forms)
Types:
Abdominal aortic aneurysm
Thoracic aortic aneurysm
Peripheral aneurysms
Dissecting aneurysms
Aneurysms: can occur anywhere
Most common type (it’s below renal arteries (kidneys) and above iliac)
80% morality due to rupture and hemorrhage
Caused by:
Congenital weakness - vessel formed incorrectly –> trauma –> weakness of vessel or genetics
Trauma
Disease: Chronic increase in BP, atherosclerosis
Treatment: for rupture, only treatment is surgery to clamp vessel
abdominal aortic aneurism (AAA)
Risk factors/causes:
If symptoms occur
-Heart beating in abdomen when lying flat
-Abdominal mass
-If associated with thrombus, may cause cyanosis in the toes
Prior to rupture
-Severe back or abdominal pain r/t pressure on spinal cord
– increase heart rate, diaphoresis, back pain indicate rupture aneurysm
-NO deep palpation in abdomen
Best diagnostic indication of AAA- pulsatile mass in abdomen - if skinny
-Palpable if not obese
-Bruit: swoosh heard with bell
-CT to determine the size
– 3 cm wide: not high risk, no surgery, picture q 6 months
– > 5.5 cm: fix it r/t increased risk for dissection/rupture
abdominal aortic aneurism (AAA)
Ultrasound Q 6 months
- Stop smoking,
Antihypertensives: control BP withany one
- diuretics,
- Beta blockers
- Ace inhibitors
- Ca channel blockers
Surgical Treatment
> 5.5 cm (or enlarging)
Endovascular grafting
1. Open procedure for rupture: cut out vessel & close them up
–Major issue: weaken area, susceptible to blow out/hemorrhage, traumatic
–The vessel feeds everything, kidney, liver, heart, brain, spinal cord
–Clamping stops blood flow to all the organs
–Longer surgery/longer clamped = increased risk
2. Prior to dissection/endovascular grafting: don’ cut, leave in diseased part, put polyester pant in
–risks: clotting, platelet aggregation on stents so give antiplatelet meds (Plavix to reduce clotting), body doesn’t like polyester stent = fever/decrease in WBC/lysis of WBC, give NSAID/steroids and resolves in a week, stent migration, polyester stent leaks (occurs when BP is high, fluid in aneurysm = failed graft)
Treatment of AAA
TEGRITY THIS SLIDE 23
Caused by atherosclerosis
Symptoms
Boring pain when supine
Dyspnea- pressure on airway (esophagus/trachea) from mass)
Cough (pressure on airway (esophagus/trachea) from mass)
Hoarseness (pressure on airway (esophagus/trachea) from mass)
Stridor: harsh high pitch sound in upper airway r/t thoracic issues
Dilated veins in chest, neck and arms r/t increased pressure
Unequal pupils r/t pressure dilating
Diagnosed by chest xray, TEE (Trans-esophageal echocardiogram: look at back of heart with camera to find clots/aneurysm) , and CT (most common)
thoracic aortic aneurysm
high in chest
more deadly r/t lack of S/S
*BP control - 1st thing Pain control Close monitoring Open surgical repair - ICU post op w/ vent until body/organs compensate - vessel is clamped during surgery, no O2 blood, do coagulation tests after Endovascular graft -Less invasive Post-op assessment Mentation: slow to arouse but arousal Vision: PERRLA Speech Strength: could come out paraplegic: test by squeezing hands/pushing foot - see if spinal cord was affected Abd pain/ flank pain: S/S of rupture and still leaking; can go through retroparitenium to look for bruising-manifests as back pain Vomiting & bloody diarrhea r/t clamped vessel effecting mesentery/renal circulation and blood supply to spinal cord (ischemic colitis AMB bloody diarrhea) Paraplegia Organ failure
treatment of thoracic aortic aneurysm
Location- Renal artery - most common Femoral artery - most common Popliteal artery - most common Caused from atherosclerosis
Symptoms-
Pulsating mass and lack of circulation distal to aneurysm - may hear bruit directly below
Pain & Swelling
Peripheral aneurysms
Aorta diseased by arteriosclerosis will tear resulting in dissection
Causes:
HTN: want a low BP
Blunt force trauma: fast way to push open
Cocaine use: constricts/vasodilator & make it more narrow
most common in aortic arch
may be confused with MI
Symptoms Sudden onset: goes from intermittent back pain to severe; abdominal swells, increase BP/heart rate/ dyspnea, tachypnea, diaphoresis --If BP has >15 mm difference, that's a sign Severe pain Pale Sweating Tachycardia Increased BP Change in BP in contralateral arm
dissecting aneurysm
Vitals: check often heart rate and BP
I/O: don’t want fluid overload –> increase pressure in venous system that can raise BP
Bilateral upper arm BP
Bilateral peripheral pulses (Take ALL pulses - could have PAD everywhere)
Sensory function (spinal cord injury)
Temp of extremity
Color changes (hematomas), cap refill
Signs of embolization
Monitor access site (Endo)*
Lie flat (Endo)* - 0 degree to prevent changes in pressure in femoral artery
Monitor temp - blood flow/perfusion to extremities/infection - vascular reaction to graft within 1 week
Call MD w/ persistent coughing, vomiting, sneezing, BP greater than 180 - increase interthoracic pressure in femoral artery
Running IV fluids if not adequate po intake
Monitor for complications: MI, ARDS, acute renal failure, GI complications
post op nursing care for aneurysm
Venous blood flow reduced by thrombus or embolus, incompetent valves, or reduction of circulation to surrounding muscles
Decreased venous blood flow-> Increased venous pressure-> increased capillary pressure-> filtration of fluid into the interstitial space-> tissue edema
Edematous tissue gets lack of nutrients-> breakdown, injury, infection
-Tissue is mostly fluid - gets stretched and can break - increased risk of ulceration
venous disorders
Thrombosis, deep vein thrombosis (DVT), thrombophlebitis, and phlebothrombosis
Cause (DVT is combo of causes)
Virchow’s Triad
-Stasis blood: blood not moving
-Vessel wall injury (or external factor of clotting - body responds by clotting factors)
-Altered coagulation r/t alteration in hormones
– Heparin works on those disorders
Venous Thrombosis
Swelling, pain, and warmth in area with clot
+ Homans sign
Pulmonary Embolism (PE)
Assessment of hx
+ of d-dimer
if unsure: compare to contralateral side and/or measure it
if untreated: body will break down the clot in know
known DCT: treat with heparin (short 1/2 life so wears off fast - too sliperry with no clotting can lead to hemorrhage)
NO SCD’S
DVT symptoms
SCD’s
Ted hose
Medication
Heparin: measure PTT; antidote = protamine sulfate
- start on heparin for 2-3 days until therapeutic (INR = 2-3)
-complication: heparin induced thrombocytopenia: massive clotting/bleeding
Lovenox: type of heparin; give subq; longer 1/2 life
Coumadin: measure PTT/INR; antidote = vitamin K
prevention of DVTs
use SCDs to prevent not treat
Monitor Drug Therapy -aPTT (PTT) -PT (prothrombin time) -INR -ACT (Activated Coagulation Therapy) School of thought on DVTs: Reposition patient frequently (elevation): elevate from venous stasis return Bedrest vs early ambulation Watch for bleeding complications Comfort (warm packs): careful in PAD r/t decreased sensation Apply compression devices
nursing management of DVT
Thrombolytic therapy: inject to dissolve -Dissolves clots If given within 3 days after acute thrombosis: poor candidates are elder, high pulse pressure, low weight, recent stroke/operation, CHF Long term damage less likely Coumadin PO INR monitored Given before heparin discontinued due to 3-5 day delay Vena cava filter
treatment of DVT
