vascular disease: disease of aorta, PVD Flashcards
normal artery from the inside out
- single layer of endothelial cells in subendothelial connective tissue
- separated from the media by the dense elastic membrane called the internal elastic lamina
- smooth muscle cells in layers of media lamina
- surrounded by its Lamina Adventitia
vascular lumen
channel for fluid transport
intima
thin columnar ring of active endothelial cells on a dense and “pliable” basement membrane the internal elastic lumen
media lamina
layers of smooth muscle cells in a metabolically active ECM composed of elastin, collagen and glycosoaminoglycans (where action happens)
adventitia
supportive fibrous tissue with nerves and blood vessels (vasovasorum)
Vasa vasorum
-in large and medium arteries
coursing into the outer one half to two thirds of media
large and medium arteries have
- Vasa vasorum
- well defined external elastic lamina,
- (external to media is) Adventitia: consisting of connective tissue with nerve fibers and vasa vasorum
veins
- low pressure systems
- have thin walls
large veins have
intimal
media
adventitial layers
medium sized veins
less adventitia
venules have
progressively less adventitia
post capillary venules
less adventitia (the least)
capillary compensition
endothelial cell encircling pericytes, but NO MEDIA thin walled slow flow function gas exchange (insufficient over great distances) nutrient exchange
highest density of capillaries
metabolically highly active tissues (like myocardium)
artery function
nutrients
oxygen
immuno-chemicals and cells for healing and growth
pharmacologic agents
all arterial diseases result from?
altered architecture
altered function
atherosclerosis
affects elastic and muscular arteries
-in large and medium sized arteries
HTN
affects small muscular arteries and arterioles
vasculitides
affects vessels of variable
tunica intima
- endothelial linning and connective tissue
- beneath connective tissue-> internal elastic lamina
tunica media
circumferential smooth muscle
external elastic lamina
tunica adventitia
connective tissue fibers
aortic dissection
- structural weakness of vessel wall
- loss of smooth muscle cells or insufficient extracellular matrix
- blood enters walls and separates the various layers
- causes rupture and/or obstruction of vessels branching off the aorta
aortic aneurysm
- dilations of blood vessels (abnormal bulge in vessel)
- involves entire thickness of wall
- causes rupture, thrombosis and embolization
- can predispose to dissection
- loss of smooth muscle cells or insufficient extracellular matrix
- causes: ischemia, genetic defect, defective matrix remodeling, trauma
LaPlace’s law
a principle of physics that the tension on the wall of a sphere is the product of:
- pressure times the radius of chamber
- and tension is inversely related to thickness of wall
common causes of aortic aneurysms
atherosclerosis (arch and abd) HTN cystic medial degeneration infectious such as TB, shyphilitic, staph, strep rheumatic aortitis trauma congenital defects marfan syndrome, ehler's danlos syndrome pregnancy (3rd trimester)
diagnosis of aortic aneurysm
- radiograph: widened mediastinum, shift of midline structures (like trachea)
- echo or TEE good for ascending or descending (not in arch)
presentation of ascending thoracic aortic aneurysm
- discovered accidentally
- usually asymptomatic
- occasional chest pain
- compression of local structures
- AR
complications from ascending thoracic aortic aneurysm
- chronic AR:
- LV dysfunction
- CHF - dissection
- . rupture
therapy of ascending thoracic aortic aneurysm
control HTN
beta-blockers
serial imaging to assess for progression
surgery
descending thoracic aortic aneurysms
usually associated with atherosclerosis
chronic aortic dissection
surgery
abdominal aortic aneurysm
- manifestation of atherosclerosis
- high risk of concurrent CAD
risk factors for abdominal aortic aneurysm
smoking is the strongest
family history aneurysm
HTN
dyslipidemia, diabetes, age, male sex
clinical manifestations of abdominal aortic aneurysm
often asymptomatic
back/flank or abdominal pain (expanding, inflamed, leaking)
LE claudication
distal embolization
complications abdominal aortic aneurysm
peripheral embolization of adherent thrombus
rupture risk strongly related to size and rate of expansion
indications for surgery
-diameter >5.5 cm
-expansion rate: >1 cm year
-symptoms
treat vascular risk factors and assess for underlying CAD
aortic dissection risk factors
- long standing arterial HTN
- smoking, dyslipidemia, cocaine/crack
- connective tissue disorders
- hereditary vascular conditions: Marfans, Ehler’s-Danlos, bicuspid aortic valve, coarctation of aorta
- vascular inflammation: giant cell arteritis, takayasu, Behcet;s disease, syphilis
- deceleration trauma
- iatrogenic factors: catheters/instrument intervention, valvular/aortic surgery, graft anastomosis, side of cross-clamping the aorta
pathophysiology of aortic dissection
- intimal tear leads to penetration of blood within the aortic wall
- false lumen forms separating layers of aortic wall
aortic dissection: De Bakey, type I
originates in ascending aorta, propagating at least to the aortic arch and often beyond it distally
aortic dissection: De Bakey, type II
originates in and as confident to the ascending aorta
aortic dissection: De Bakey, type III
originates in descending aorta and extends distally down the aorta, (rarely retrograde)
aortic dissection: standford type A
always involves the proximal aorta
-all dissection involving the ascending aorta
aortic dissection: standford type B
NO proximal involvement at all
- descending aorta dissection only
- all dissection not involving the ascending aorta
Type A common presenting symptoms
- none
- pain, numbness, TIA, stroke
- symptoms: related compression of adjacent tissue such as chest pain, dyspnea, hoarseness, dysphagia, CHF (ascending aorta), aortic insufficiency, head and neck swelling
complications of type A dissection
- aortic rupture
- cerebral ischemia
- pericardial tamponade
- acute aortic regurg. leading to pulmonary edema and cardiogenic shock
- coronary insufficiency
complications from acute type A dissection
- rupture of pericardium, pleura, peritoneal cavity
- disruption of aortic annulus
- extension into great arteries of neck or the coronaries, causing vascular obstruction and ischemic consequences like MI or stroke or spinal vascular disruption
clinical presentation: aortic dissection
- abrupt onset of severe pain in chest or back
- ripping, tearing or migrating pain
- focal neurologic deficits if dissection extends into cerebral vessels
- syncope
physical exam of aortic dissection
- unequal upper extremity BP’s
- tachycardia
- pulse deficits
- focal neurologic deficits
- aortic insufficiency (acute)
- evidence of pericardial tamponade
imaging for aortic dissection
CT scanning
TEE
MRI
aortography
therapy for acute aortic dissection
establish beta-blockers CCB vasodilators adequate analgesia low threshold for intubation if unstable
type A dissection initial treatment
- surgery
- aortic rupture, pericardial tamponade, cardiogenic shock, cerebral/coronary insufficiency
- valve sparing surgery if NO pathological changes to aortic cusps (if normal size aortic root)
- stabilization with IV access and monitoring and anti-hypertensives therapy
- mortality is very high patient presents with hemorrhage or evidence of distal ischemia (CVA)
- immediate ICU admission
type B dissection: unstable
- impending rupture
- propagation with compromise of downstream vasculature
- unrelieved pain
- treatment: same as Type A
type B dissection: is stable and uncomplicated
- control blood pressure and cardiac contractility
- beta blockers
- ACE-I, ARB’s, CCB
- monitor every 6-12 months
acute aortic dissection therapy for Type B
beta blockers
surgery
IRAD
chronic aortic occlusion
-progressive narrowing of distal aorta
-ASPVD
-in renals or iliac
Sx: claudication of low back, butt and impotence (or none)
PE: absent pulse obstruction, bruit, skin/hair changes, redness on dependency
acute aortic occlusion
-distal aorta-> MEDICAL EMERGENCY
-pre-existing narrowing with plaque and rupture
-acute ischemia of lower extremities
-pain with rest
-pallor
-absent pulse
-DX: aortography
TX: stabilize for surgery or thrombectomy or revascularization
aortitis
- can cause or aneurysms and dissection
- complications depend on locations and severity of underlying mechanism of the disease process
rheumatic causes of aortitis
-endarteritis of vasovasorum
-location affected: ascending thoracic aorta most common
-associated with:
rheumatoid arthritis
AS
psoriatic
reiter’s syndrome
relapsing polychondrits
IBS
takayasu’s arteritis
- young asian women
- inflammatory process
- often the arch and ascending aorta
- can cause obstruction
- acute and chronic phase
- no therapy
tertiary syphilus
- 15-30 years past primary disease
- proximal aorta and root to arch, saccular or fusiform shape
- calcified ascending aortic aneurysm is classic
- PCN, excision and repair treatment
giant cell arteritis
- older woman more than men
- large medium size vessels
- aortitis with aortic insufficiency and associated with PMR and obstruction of medium size vessels of the body
Buerger’s disease
- young male smoker
- no TX except stop smoking
aortic coarctation
- strong associaton with bicuspid aortic valve
- aortic aneurysm and dissection, VSD, berry aneurysm of circle wills, premature CAD
- pressure gradient across obstruction (>15-20 mmHg, considered significant)
clinical manifestations of aortic coarctation
asymptomatic HTN arm, leg, pulse differential leg fatigue bicuspid aortic valve cerebral hemorrhage
diagnosis of aortic coarctation
physical exam ECG with evidence of LVH chest radiograph echo cardiac MRI contrast aortography with invasive hemodynamics
TX aortic coarctation
surgery
percutaneous stenting
acute PAD results from
Embolic sources:
- atrial fib.
- MI
- ventricular aneurysm
- cardiomyopathy
- infectious sources
- prosthetic heart valves
- atrial myxoma
acute PAD is
a medical emergency
important to identify PAD
-surrogate marker for coronary artery disease
chronic PAD of LE
- occlusive arterial disease
- atherosclerosis
- risks rise from AODM, dyslipidemia, HTN, smokers
- high association with cerebral vascular and heart disease
chronic PAD sites
- stenotic or occlusive segmental lesions
- large and medium sized arteries
- plaques, calcification, thinning media, destruction of muscle and elastic fibers, fragmentation of internal elastic lamina and thrombi of platelets and fibrin
- sites-> femoral and popliteal, tibial and perineal, abdominal and iliac
hallmarks of LE PAD disease
- claudication
- reproducible sx-> effort, location, examination
spectrum of LE arterial disease
asymptomatic claudication rest pain numbness, tingling, lack sensation ulceration and gangrene
claudication
- Sx occur one joint level distal to the point of obstruction
- cramping, pain or weakness in a muscle group that occurs after a reproducible amount of effort
signs of chronic PAD
- decreased or absent pulses distal to obstruction
- bruits heard over narrowed artery
- muscle atrophy and weakness with exercise
- skin texture(thin and shiny) and color changes (cool, pale, blue) and hair loss
ankle to brachial index (ABI)
- Pros: quick stethoscope and BP cuff
- Cons: gives no info on disease level (ABI artificially elevated in calcified vessels in diabetes)
how to ABI
- patient must be lying down
- measure systolic and diastolic BP on right and left arms
- higher systolic reading of left and right arm is used in the assessment
- pressure in each foot posterior tibial artery and dorsalis pedis artery are measured with higher of the two values used as the ABI for that leg
- ABI is calculated by dividing the systolic blood pressure at the ankle by systolic blood pressure in arm
- average each of systolic BP
management of PAD therapy
- supportive measures: care of feet, compression hose, protective shoes
- non-operative intervention: life style changes, exercise, no smoking, diet management
- pharmacologic: control BP, treat AODM, cholesterol
- no help with most vasodilators, heparin or alpha-blockers or CCB
- trental may help
- surgery and possibly thrombolytics for acute disease
Consequences of DVT
PE
Death
Chronic venous stasis: leg swelling, heat, redness, pain, cyanosis due to stasis, ulcers
Calf pain with weight bearing
Consequences of SVT
Heaviness of limb Pain Severe swelling Ulcerations Cosmetic dis figuration
Diagnosis of PVD: deep vein type
History and physical exam
D-dimmer (sensitive)
Duplex venous ultrasound and direct visualization with non-compression of the vein
Treatments
Thrombolytics Avoid weight bearing Anticoagulants Support hose Treat underlying condition (if one)
