Cardiovascular Flashcards by Hannah Hutchison

MC underlying pathology of aortic dissection

chronic HTN –> separation of the intima and media and creation of a false lume

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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

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Stanford systemic classification of aortic dissection

Stanford type A dissections involve the ascending aorta, and Stanford type B dissections do not

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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

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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)

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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-

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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

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which type of aortic dissection requires immediate surgery

type A – requires open vascular repair

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which type of aortic dissection does not require surgery and can be treated with medical management

type B

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What are the three layers of the aorta?

Tunica intima
Tunica media
Tunic adventitia

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debakey classification for aortic dissection

type 1 (ascending aorta, descending aorta, arch)
type 2 (ascending aorta)
type 3 (descending aorta)

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Risk factors associated with aortic dissection

tobacco use
HTN
hyperlipidemia
atherosclerotic vascular disease
stimulant drug use

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what is a good test to dx aortic dissection in pts who are hemodynamically unstable

transport to operating room

bedside transesophageal echocardiogram

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Abdominal aortic aneurysm (AAA)

abnormal dilation of the aorta most commonly occurring between the renal arteries and the iliac bifurcation

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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

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PE for AAA

Pulsatile mass!!!!

may see grey turner sign or Cullen sign

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test of choice to evaluate AAA

Abdominal US

gold standard is angiography but is often only used before surgery

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screening for AAA

one time US for men 65-75 years who have ever smoked

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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

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Preferred anticoagulant for CA

LMWH
Edoxaban, Apixaban, Rivaroxaban

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preferred anticoagulant for liver disease and coagulopathy

LMWH

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preferred anticoagulant for kidney disease and renal impairment < 30 mg/mL

UFH followed by warfarin

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preferred anticoagulant for coronary artery disease

Warfarin
Apixaban
Edoxaban
Rivaroxaban

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Preferred anticoagulant for dyspepsia or GI bleed

Warfarin
Apixaban

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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

Cardiovascular Flashcards

(76 cards)