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peripheral arterial disease
thickening/narrowing of artery walls
reduced blood flow
tissues aren’t as oxygenated
diabetes, HTN, hyperlipidemia, smokers are at higher risk
legs are most affected bc further away from the heart
clinical manifestation not present until 60-75% occlusion
athersclerosis
#1 cause of PAD
damage to endothelium or arteries
due to high BP to push blood thru
damage causes inflammation
inflammation will have platelets come over and plaque will form
occlusive thrombus → unstable plaque → could break off → dangerous
PAD modifiable risks
tobacco use
diabetes
HTN
obesity → build up of lipids and cholesterol
sedentary lifestyle
stress
PAD non-modifiable risks
age
gender
family history
ethnicity
ischemia clinical manifestations
intermittent claudication
leg muscle pain w activity
muscle isn’t getting enough blood flow and O2
worse w activity, better w rest
continuum of pain all the way to cell death
fontaine scale
I = asymptomatic
IIa = mild claudication
IIb = moderate - severe claudication
III = ischemic rest pain
IV = ulceration or gangrene
PAD assessment
perfusion
pulses → mark and document grade, use doppler to locate and mark w x
temperature → cooler than expected
cap refill → greater than 3 secs
paresthesia → numbness
pain → pain w activity
color → pallor
compare sides
chronic PAD assessment
no edema
thin, shiny skin, no hair
chronic loss of perfusion to hair cells → no hair growth
thick, brittle toenails
numbness, paresthesia, itching
dependent rubor
elevate foot → turns pale
lower foot → turns bright red
ankle-brachial index (ABI)
compare BP in ankle vs arm
ideally should be same or slightly higher than in arm
if BP in ankle is significantly lower → less blood flow there due to narrowed arteries
ABI = 1 is ideal
ABI < 1 is when to worry about problems with perfusion
equipment needed:
stethoscope & sphygomomanometer
doppler if pulse too faint
what to do:
lay pt supine
take BP in both arms and both ankles
use highest SBP measure from the arms & legs
calculate:
ABI = SBP ankle/SBP arm
chronic PAD
most commonly in pelvis and legs
if have occlusion @ artery → everything under that is at risk
cramps/pain with exercise
pain resolves with rest
intermittent claudication
with progression, can have pain @ rest
chronic PAD diagnostics
labs (cholesterol & glucose)
ABI
doppler flow studied
angiography
chronic PAD interventions
treat atherosclerosis
statins for cholesterol
antiplatelets → aspirin/clopidogrel
anticoagulation → prevent formation/breakdown of thrombus
peripheral vasodilators → incr diameter of artery for better flow
BP control → make sure hypotension doesn’t happen
exercise therapy → BP and BS control
stop smoking
surgery
angioplasty → insert catheter to blockage → stent to hold artery open → put pt on blood thinner/antiplatelet bc body will send platelets to new foreign object
stent
endarterectomy → remove pieces of plaque
arterial bypass → graft blood vessel and create new blood pathway to lower extremity
acute arterial occlusion (critical limb ischemia): assessment
emergency!!
6 P’s
pain
paresthesia
paralysis
poikilothermia
pulselessness
pallor
acute arterial occlusion: interventions
medications
thrombolytic → dissolve clots, ex) alteplase (tPA)
anticoagulant → prevent formation/growth of clot, ex) heparin
surgery
remove obstruction w angioplasty, stent, bypass
monitor circulation
6 P’s
keep warm
no direct heat → risk skin breakdown
warm blanket is good
cold will decr perfusion
protect skin
monitor for pressure ulcer
promote circulation
keep extremity flat/slightly dependent → help blood flow into artery
don’t cross legs
no restraints to affected extremity
monitor tx effects
arterial ulcers
may/may not have pain @ site
location/appearance
bony prominences on toes/feet
deep and caved
even edges
ulcer bed pale
little granulation tissue
cold feet
decreased/absent pulse
possible gangrene
treatment
restore circulation→ arterial bypass
prevent trauma and infection → good fitting shoes, avoid stepping on things, daily foot checks
DON’T ELEVATE → we need blood flow to go there
NO COMPRESSION
patient education: foot care
avoid getting nails done at salon not approved
interventions
prevent infection
protect site and promote healing w hyperbaric O2 and clean, dry dressings
surgery to improve circulation
could have to do amputation → but prob won’t heal well
foot care
goal #1: improve blood supply
dependent
exercise
no smoking
warmth
goal #2: prevent injury
inspect feet daily
clean feet
lamb’s wool → moisture wicking product
clip nails straight and even..
no heating pads
no bare feet
venous ulcers
caused by inadequate tissue O2 and nutrient exchange
veins in legs are not moving blod to heart well
blood pools in legs instead of flowing back to heart
poor healing in extremities w/o blood flow
moderate ulcer discomfort
location/appearance
ankle
superficial
pink ulcer bed
uneven edges
granulation tissue present
ankle edema (swollen)
pulses present
brown pigment esp @ ankle
scaring from previous ulcers
wet wound…serous drainage
treatment
long-term wound care (unna boot, moist dressing)
elevate extremity
compression hose → we want blood to return back to heart
elevation
infection prevention
moist dressing to promote healing
healthy diet
aneurysms
bulging or ballooning of vessels (usually arteries)
caused by weakening of artery wall - could be from HTN, smoking, plaque buildup
most common is in anterior communicating artery and middle cerebral artery
aneurysm risks
age
male
HTN
CAD
family hx
smoking
hypercholesterolemia
lower extremity PAD
carotid artery disease
obesity
aneurysm locations
cerebral
aortic
abdominal aorta (AAA - 75% of aortic aneurysms)
thoracic aorta (TAA) - above the heart
most occur below renal arteries
popliteal peripheral
aneurysm clinical manifestations
TAA and AA are often asymptomatic until they are pretty large
thoracic aortic aneurysm (TAA): deep, diffuse pain that may extend to shoulder
ascending aortic aneurysm (AAA): angia, chest pain, cough, SOB, hoarseness, decreased venous return, may mimic abdominal/back disorders, pulsatile mass left of midline in periumbilical area may be present
aneurysm complications
lots of ppl live w them bc repair could be too risky
rupture
if AAA or TAA → massive hemorrhage
if cerebral → s/sx of stroke
dissection
false lumen created between layers of artery → blood fills area
bleeding but not a rupture → filling pouch of blood
if in ascending aortic arch, sx required; otherwise, manage conservatively
aneurysm diagnostics
often found while imaging for other problems, not a death sentence
x-ray
echocardiogram
CT → primary way found
MRI
ultrasound
aneurysm interventions
prevent rupture & dissection → these will be emergency
wellness & education (DM, HTN, obesity, lipid management, exercise)
routine monitoring if < 5.5 cm
surgical care if > 5.5 cm
OAR (open repair)
endovascular grafts → cover aneurysm with mesh so it doesn’t rupture
raynaud phenomenon
episodic, vasospastic disorder of small arteries
involves fingers and toes
vasoconstriction
young women (15-40 yrs old)
auto-immune connection?
aggravated by cold/stress
vasospasm - vasoconstriction
blanching → turns white
cynosis → turns purple or blue
hyperemia → rubor when blood returns - turns bright red
“vasospastic phenomenon where cold/stress causes temporary color changes (white/blue/red) without long-term tissue damage”
raynaud phenomenon interventions
patient teaching
goal is to prevent episodes
avoid cold, tobacco, drugs
stress reduction
when spasms → use warm water to promote vasodilation
treatment
calcium channel blockers → promote vasodilation
sympathectomy → cut thru nerves that activate vasoconstriction and vasodilation → have to be severe case to do this
buerger’s disease
thromboangitis obliteratans
inflammatory, occlusive, thrombotic arterial disease
“a rare inflammatory disease caused directly by smoking, leading to thrombosis and gangrene”
cause is recurrent inflammation
distal extremities - upper/lower extremities
occurs in:
more men than women
ppl under 40 yrs old
smokers
hx of periodontal disease
assessment
same as PAD
color/temp change
thrombosis
cold sensitivity
interventions
stop smoking
can lead to amputation
circulatory system review
right side of heart → deoxy blood
left side of heart → oxy blood
flow of O2 blood: left ventricle → aorta → arteries → arterioles → capillaries
flow of deoxy blood: capillaries → venules → veins → superior/inferior vena cava → right atrium
blood moves back to heart with original force of LV, muscular contraction, and valves to keep blood flowing in one direction
arteries
moves blood AWAY from heart
moves oxygenated blood
thicker and more elastic vessels
higher pressure
no valves
ex) aorta, carotid artery
capillaries
connects arteries and vein
site of O2 exchange
no valves
one cell thick
very low pressure
ex) lung and tissue capillaries
veins
moves blood TOWARD the heart
deoxygenated blood
low pressure
has valves for one way flow
thin wall, less muscular
ex) vena cava, jugular vein
peripheral venous disease
venous thrombosis: deep and superficial (DVT and SVT)
superficial thrombosis is closer to skin and outside of body
deep thrombosis is deeper inside the body and are more troublesome, involving the iliac and femoral deep veins
virchow’s triad: vessel wall injury, venous stasis, hypercoagulable state
all these will contribute to formation of thrombus
risk for DVT
venous stasis
see in younger men w muscles that compress veins
age
CHF
obesity
orthopedic surgery
pregnancy → fetus grows and compresses inferior vena cava
prolonged immobility
varicose veins → damaged valves in veins cause swollen/twisted/enlarged veins
vessel wall injury
surgery
IV therapy
IV meds or drug use
metabolic syndrome
DM
HTN
smoking
trauma
hypercoaguable state
prolonged immobility
meds
clotting disorders
high altitudes
hormone replacement therapy
prengnacy
maligancies
tobacco
polycythemia vera → exessive RBCs
why is smoking bad for PVD?
nicotine-induced vasoconstriction
increased hyper-coagulability
endothelial damage
reduced O2-carrying capacity
body responds by incr RBCs → cause further endothelial damage
impairs venous valve function
increases inflammation
reduced physical activity
alteration of fibrinolytic system
synergistic effect with other risk factors
DVT clinical manifestations
edema
UNILATERAL SWELLING
redness
pain
tenderness
temp > 100.4
sense of fullness in extremity
DVT diagnostic tests
clinical assessment
d-dimer > 0.5 mg/L
elevated d-dimer means body is breaking down clot
doesn’t necessarily mean DVT is present, just that the body is breaking a clot down
ultrasound - most common
MRI
venography
inject dye into veins and look
DVT interventions
do not mobilize an existing clot
avoid valsalvas
no massage
prevent new thrombus from forming
administer anticoagulants
elevate limb
use SCDs to stimulate muscular contraction, but not over clot site
administer analgesics for comfort
monitor for complications - pulmonary embolism is big prob!
DVT intervention - direct oral anti-coagulants
factor Xa inhibitors
apixaban
rivaroxaban
thrombin inhibitors
dabigatran
vitamin K anagonist
warfarin
DVT anticoagulant therapy
give meds like apixaban, rivaroxaban, dabigatran, warfarin
watch for bleeding
bleeding precautions
report signs of bleeding → black stools, nose bleeds, excessive bruising, AMS
avoid aspirin, NSAIDs, certain supplements
wear an alert bracelet
carry pharmacy card
DVT intervention - low molecular weight heparin
lovenox
inactivates factor Xa
baseline coagulation studies before administering
SQ (can give bolus IV dose to start)
antidote is protamine sulfate
once daily vs BID for heparin
requires less monitoring than heparin
comes in prefilled syringe for easier self administration
40 mg dose is DVT pph
DVT: general-post op prevention
active
active ROM
TCDB
early ambulation
body alignment
feet supported if sitting
passive
passive ROM
intermittent pneumatic compression
compression stockings
adequate hydration
leg elevation, raise foot of bed
DVT/VTE surgical management
goal: prevent PE
thromboectomy
greenfield filter
ligation or external clips
varicose veins - etiology
hereditary
prolonged standing
pregnancy
tumors
chronic disease: heart disease, cirrhosis
obesity
varicose veins - assessment
raised vessels: dark, tortous
feelings of heaviness, aching
LE edema
varicose veins - diagnosis
doppler flow studies
venography
plethysmography
varicose veins - prevention
walking/exercise
weight reduction
compression socks or tights
no clothing that binds (garters, leggings that bind/roll, spanx)
no crossing legs, prolonged standing or sitting
varicose veins - treatment
sclerotherapy: irritating chemical injection into the vein
laser ablation
surgery: vein ligation and stripping