Cardiovascular Flashcards
MC underlying pathology of aortic dissection
chronic HTN –> separation of the intima and media and creation of a false lume
classic presentation of aortic dissection
> 60 years of age and presents with sudden onset of severe, sharp, and tearing chest or back pain
pulse or blood pressure asymmetry between limbs
Stanford systemic classification of aortic dissection
Stanford type A dissections involve the ascending aorta, and Stanford type B dissections do not
differences btwn type A and B dissections
Stanford type A dissections - occur proximal to the subclavian artery; more likely to present with chest pain radiating to the back or syncope; hypotension
Stanford type B dissections - occur distal to the subclavian artery; more likely to present with abdominal or back pain; HTN
Common chest XR findings for aortic dissection
widened mediastinum (> 8 cm at the aortic knob)
abnormal aortic or cardiac contour
displaced intimal calcification
widened right paratracheal stripe (≥ 5 mm)
tracheal deviation (usually rightward)
opacified aortopulmonary window
pleural effusion (usually left-sided)
what is the best diagnostic study for aortic dissection (esp if hemodynamically stable)
CT angiography
- keep in mind that MRI is gold standard but not normally done-
initial management of aortic dissection
aggressive reduction of blood pressure with beta-blockers (e.g., labetalol, esmolol) to a systolic blood pressure goal of 100–120 mm Hg
- patients with a history of asthma or bradycardia should be given esmolol to assess for tolerance because esmolol has a shorter half-life than labetalol
-Sodium nitroprusside can also be used to lower BP
morphine for pain
which type of aortic dissection requires immediate surgery
type A – requires open vascular repair
which type of aortic dissection does not require surgery and can be treated with medical management
type B
What are the three layers of the aorta?
Tunica intima
Tunica media
Tunic adventitia
debakey classification for aortic dissection
type 1 (ascending aorta, descending aorta, arch)
type 2 (ascending aorta)
type 3 (descending aorta)
Risk factors associated with aortic dissection
tobacco use
HTN
hyperlipidemia
atherosclerotic vascular disease
stimulant drug use
what is a good test to dx aortic dissection in pts who are hemodynamically unstable
transport to operating room
bedside transesophageal echocardiogram
Abdominal aortic aneurysm (AAA)
abnormal dilation of the aorta most commonly occurring between the renal arteries and the iliac bifurcation
sx AAA
most are asx
when sx - sense of abdominal fullness that may or may not be accompanied by pain. Abdominal pain - located at the hypogastrium and may radiate to the lower back - described as throbbing
triad of abdominal pain, hypotension, and a palpable pulsatile abdominal mass
PE for AAA
Pulsatile mass!!!!
may see grey turner sign or Cullen sign
test of choice to evaluate AAA
Abdominal US
gold standard is angiography but is often only used before surgery
screening for AAA
one time US for men 65-75 years who have ever smoked
surveillance for AAA Per the Society for Vascular Surgery
aneurysm is greater than 5.5 cm or the aneurysm has grown more than 0.5 cm in 5 months –> surgical repair (endovascular stent-graft placement)
aneurysm is 5.0-5.4 –> repeat US or CT q 6 months
aneurysm is 4.0-4.9 –> repeat US or CT q 12 months
aneurysm is 3.0-3.9 –> repeat US or CT q 3 years
Preferred anticoagulant for CA
LMWH
Edoxaban, Apixaban, Rivaroxaban
preferred anticoagulant for liver disease and coagulopathy
LMWH
preferred anticoagulant for kidney disease and renal impairment < 30 mg/mL
UFH followed by warfarin
preferred anticoagulant for coronary artery disease
Warfarin
Apixaban
Edoxaban
Rivaroxaban
Preferred anticoagulant for dyspepsia or GI bleed
Warfarin
Apixaban
preferred anticoagulant for pregnancy
LMWH
what is another name for primary upper extremity DVT
Paget-Schroetter syndrome
Signs and symptoms of upper extremity DVT
arm pain
swelling
cyanosis
heaviness
palpable venous cord
tx for upper extremity DVT
NSAIDs (pain)
Thrombolytics (alteplase)
Anticoagulants (heparin)
Venoplasty
Compression stocking
Limb elevation
early clinical signs of arterial occlusion
cold and pale extremity
pain out of proportion to exam
loss of sensation
loss of distal pulse
late clinical signs of arterial occlusion
poikilothermia (differences in temperature)
loss of motor function
what is the MC cause of morbidity from arterial occlusion
limb ischemia
what is commonly used to identify emboli in lower extremities
doppler US
embolic versus thrombotic occlusions
Embolic occlusions are more likely to present with atrial fibrillation and are associated with more severe complications of limb ischemia (e.g., limb loss, gangrene); abrupt onset
Thrombotic occlusions are more likely to present with diabetes mellitus, hypertension, and hyperlipidemia and are associated with a history of claudication; may take hours-days before sx are apparent
what is the gold standard test to different btwn thrombotic and embolic occlusions
CT angiogram
Arterial occlusion most commonly occurs from
in situ thrombosis from the superficial femoral artery or popliteal artery in the setting of preexisting PAD
classic presentation of limb ischemia
the six Ps: pallor, pain, paresthesia, paralysis, pulselessness, and poikilothermia
How do you know when tissue is viable for thrombotic/embolic occlusion
mild pain
capillary refill < 3 seconds
normal motor function and sensation
audible arterial and venous doppler flow
how do you know when tissue is nonviable for thrombotic/embolic occlusion
absent capillary refill
profound paralysis or sensory deficits
inaudible arterial or venous Doppler pulses
tx embolic occlusion
surgical consultation and hourly neurovascular checks are indicated
IV fluids
analgesics
UFH
revascularization via thrombectomy or catheter-directed thrombolysis
tx nonviable tissue embolic occlusion
amputation
Syncope
transient period of loss of consciousness (LOC) caused by inadequate cerebral blood flow that typically lasts 8 to 10 seconds and is self-limited, resolving spontaneously
what is the MC cause of syncope
reflex syncope
what is reflex syncope
cerebral hypoperfusion secondary to vasodilation or bradycardia
what is the MC cause of reflex syncope
vasovagal reactions
classic sx of reflex syncope
there is a classical prodrome of symptoms, including nausea, sweating, or feeling hot or cold
sx of syncope related to cardiopulmonary dz
sudden onset without prodromal symptoms
Orthostatic hypotension
a drop in systolic blood pressure > 20 mm Hg or diastolic blood pressure > 10 mm Hg measured with the patient supine, then after standing for 1 to 2 minutes, and again at 4 to 5 minutes
what extremities are MC affected in peripheral arterial disease
lower extremities
common sx peripheral arterial dz
intermittent claudication, arterial ulcers, tissue ischemia, decreased or absent peripheral pulses, dry, shiny, hairless, atrophic skin, and cool distal extremities
pain that worsens with limb elevation
if advanced –> pain at rest
diagnose peripheral arterial dz
ankle brachial index – levels < 0.9 are abnormal
at what levels on ABI does claudication normally start to occur
Claudication typically occurs with an ankle-brachial index between 0.4 and 0.9
at what levels on ABI does rest pain normally start to occur
between 0.2 and 0.4
at what levels on ABI does tissue loss start to occur
0 - 0.4
wet vs dry gangrene
dry - clear demarcation; usually starts on fingers and toes; hard, dry texture
wet - moist, gross swelling, blistering (usually there is bacterial invasion)
tx gangrene
dry - surgical revascularization
wet - surgical debridement followed by revascularization
if no response to revascularization –> amputation
describe arterial ulcers
extremely painful
deep, “punched out” appearance
Granulation tissue is pale in color or necrotic
Weak or absent pulses
Little to no drainage
describe venous ulcers
Larger and less painful
worse with extended periods of standing/sitting, better with LE elevation or walking
presence of drainage
pink/red granulation tissue
normal pulses
MC cause PAD
atherosclerosis
Chronic venous insufficiency
condition in which incompetent valves, particularly in the LE cause venous HTN, edema, fibrosis, and hyperpigmentation
The most common presenting symptom of chronic venous insufficiency
progressive pitting edema of the LE
mainstay of tx for chronic venous insufficiency
graduation compression stockings
if there is occlusion to the distal superficial femoral artery, where would you feel pain
calf
varicose veins is caused by
venous insufficiency
which vein is most commonly affected in varicose veins
saphenous vein
who is more commonly affected by varicose veins: men or women
women
remember that sx for varicose veins are the same for chronic venous insufficiency
how large are varicose veins
at least 3 mm in diameter
why do we get hyperpigmentation in varicose veins and venous insufficiency
deposits of hemosiderin
gold standard diagnosis of venous disease
duplex US of saphenous vein
duplex US of saphenous vein for dx of venous disease
Normal retrograde flow occurs in 0.5 seconds or less
Flow that is greater than 0.5 seconds is indicative of valvular incompetence and venous insufficiency
what is the MC valvular disorder in the US
mitral valve regurgitation
what is the MC cause of mitral valve regurgitation
mitral valve prolapse
murmur associated with mitral regurgitation (what does it sound like)
holosystolic murmur best heard at the apex and radiating to the axilla
blowing and high pitched
what test is used to confirm mitral valve regurgitation
transthoracic echocardiogram (TTE)
if insufficient –> ransesophageal echocardiogram (TEE), stress test, or cardiac cath
what is the most commonly used preoperative prophylactic measure for atrial fibrillation
beta blockers
