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45 Cards in this Set
- Front
- Back
aortic valve anatomy
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3 cusps- leaflets
Non coronary cusp/LCC- LCA arises/RCC- RCA arises mercedes benz sign |
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aortic valve sclerosis
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aortic valve thickening without obstruction
25-30% >65, >80 about 1/2 have this on assessment of aortic valve disease marker for CVD structurally abn but hemodynamically not causing problems |
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Clinical findings
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short midsystolic ejection murmur, not loud,
localized to aortic area carotid pulse normal volume and contour s2 normal |
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echo features
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increased echogenicity of leaflets, without commusural thickening, no significant obstruction to outflow
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aortic valve sclerosis prognosis
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can progress to clinically significant stenosis in one of 8 and severe in 1/64
marker for widespread atherosclerotic disease |
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management of Ascelorosis
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control of Cardiac risk factors
follow up - to see if they progress |
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aortic valve stenosis
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restricted CO secondary to valve not opening adequately
some hemodynamic consequences |
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causes of AS
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congenitally abn valve, bicuspid valve
unicuspid or quad valve degeneric or calcific valve - from a sclerosis progressio Rheumatic valve disease rare causes: metabolic disease, collagen vascular- SLE, paget's disease, |
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bicuspid AV
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common 2% of population
3:1 male to female coexisting coarctation of aorta in 6%- decreased perfusion to periphery and leads to HTN associated to aortic root abn- leading to dilation and dissection biscupid is the most common |
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rheumatic aortic valve i
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involves more of the commissures not the cusps - thats why orifice is small
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incidence of differen etiology
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world wide rheumatic disease- most common
100% affects mitral- if no mitral valve involvement- not rheumatic in dev- degenerative and bicuspid bicuspid-more seen in younger degenerative- still could be bicuspid but usually older |
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pathyphys consequences of AS
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obstruction to aortic outflow- gradual
concentric LVH- to maintain wall stress- to pump blood through to maintain CO over time LV compliance will decrease- LVED pressure increases -systolic dysfunction - LV dilates, and significant LHF- CO drops even further |
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AS symptoms
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dyspnea on exertion and decreased exercise tolerance
dizziness, syncope angina |
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Dyspnea
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related to LVH, impaired relaxation, increased LV filling pressure, increased LA pressure, increased Pulmonary pressure - interstitial edema
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decreased exercise intolerance
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inability of LV to increase CO required with exercise due to fixed obstruction
exercising muscles need more blood |
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dizziness/syncope
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peripheral vasodilation to increase blood pressure to exercising muscle- so get vasodilation but no increase in CO - so get hypotensive
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ventricular arrhythmias
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calcifications can extend to conducting system
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angina
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supply demand mismatch- dont have CAD, still get angina- even with normal LV blood supply, hypertrophy is such that outstrips normal coronary blood supply
also compression on intramural cornary arteries due to prolonged contraction and impaired relaxation |
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physical exam AS
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decreased volume, slow upstroke central pulses, (parvus et tardus) low volume - low CO, dleayed upstroke- takes LV long time to overcome obstruction and reach peak pressure
check brachial and carotid pulses -for volume and contour large apex- LVH thrill in aortic area- significant AS- turbulent blood flow through small orifice S2 single - ventricle takes longer - A component is delayed and merged with P2- also softer b/c valve not very mobile S4- atria contracting into a stiffered ventricle systolic ejection murmur- loudest in the aortic area heard all over precordium - |
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how to tell severity of AS based on murmur
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way to tell severity- where it peaks in systole
early- ventricle doesnt have trouble overcoming obtruction late- ventricle having hard time overcoming obstruction |
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investigations AS
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ECG: LVH
CXR: AV calcification, LVH, dilated aortic root Echo: gold - visual appearance of valve- bicuspid? thickening commisural? leaflets? valve areas LV thickness size |
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grading AS
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valve areas:
normal 3- 4 cm2 mild 1.5-2 moderate 1-1.5 severe<1 |
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tx
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no medical tx
valve replacement only option: deciding when the valve needs to be replaced imp |
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indication for surgery
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any symptoms- indication that heart is not liking this
SOB, angina, dzziness, exercise intolerance in the absence of symptoms- LV pumping function decline- ie EF low <50 prophylaxis for endocarditis no longer recommended |
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surgical options
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percutaneous valve replacements- for those people that cant undergo surgery
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Aortic Regurgitation
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can be acute or chronic
same as insufficient caused by inadequate closure of leaflets- abn structure of dilation of aortic valve root or anullus |
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acute severe Regurg
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medical emerg- b/c LV unable to adapt to regurgitant flow- rapid heart failure and cardiogenic shock
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etiology severe acute regurg
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endocarditis- due to valve destruction
aortic dissection- Trauma- decelaration injuries |
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clinical features aortic dissection
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sudden collapse with preceding sudden knifelike mid capular back pain
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endocarditis
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fever, embolic events, sick with septic symptoms
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physical exam AR
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hypotensive
low pulse volume if dissection- inequality of upper limb pulses soft or absent S1- mitral valve closes early b/c inc LV diastolic pressure acute pulmonary HTN- loud P2 acute heart failure- S3 diastolic murmur is short or absent- very little difference between two areas - |
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definite diagnostic procedure
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echo can visualize abn valve - size
regurg and lV function size |
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tx of ASAR
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emergency Aortic valve replacement
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chronic AR etiology
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abnormal aortic valve :
RF, bicuspid or degenerative valve- same as AS also dilatation of aortic root bicuspid valve commonly associated with dilatation of the aorta connective tissue disorders- marfan- tends to dilate more than usual under increased pressure |
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pathyphys of AR
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increased LV SV - more blood is leaking back- by about 50%- increased LV volume, inc wall stress, LVH
CO inc due to inc LV stroke volume LV compensates by Dilating so LVEDP remains normal |
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chronic AR sx
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may be asymptomatic for decades
palpitation- decreased exercise capacity, HF symptoms dev of HF: dyspnea, orthopnea, PND angina uncommon- coronary arteries dilated- blood flow occurs during diastole |
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physical exam chronic AR
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high volume pulse with a sudden collapse - water hammer pulse
wide pulse pressure- big systolic pressure- very low diastolic pressure large and displaced apex due to LV dilatation and hypertrophy A2 soft and absent - due to AV leaflets not coapting diastolic decrescendo murmur- along left or R sternal border, high pitched blowing. longer the murmur, the more severe it is, except for Acute severe systolic ejection murmur due to high cardiac output austin flint murmur - |
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austin flint murmur
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AR regurg - goes to ward mitral valve- and produces a murmur close to one of mitral stenosis
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murmur in AR
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high pitched blowing decrescendo diastolic murmur at LSB
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unusual findings in chronic severe AR
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Demussett's - head bob when heart beats
mueller's sign- pulsation of uvula beckers' sign- pulsation of retinal arteries and pupils lighthouse sign- blanching and blushing of forehead |
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chronic AR echo
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identify valve pathology
assess aortic root and LV size and function assess severity of AR |
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natural hx of AR
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long latent period - decades
decomp: when LV systolic function fails progressive LV dilatation occurs initially reversible- but overtime irreversible |
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asymptomatic MR
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no support for medical tx
abx prophylaxis for endocarditis no longer reccommeded valve replacement EF<50 also presence of symptoms decline in LV function |
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symptomatic AR
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valve replace
ACE inhibitors, diuretics - short term |
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Mixed AV disease
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usually abnormal valve not root problems
sx same as AS and AR physical findings- some may cancel each otehr out- pulse volume and contour normal AR: inc CO AS reducing CO- moderate of both - may not indicate one or the other do echo indications for surgery - symptoms or decline in LV function |