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45 Cards in this Set

  • Front
  • Back
aortic valve anatomy
3 cusps- leaflets
Non coronary cusp/LCC- LCA arises/RCC- RCA arises
mercedes benz sign
aortic valve sclerosis
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
Clinical findings
short midsystolic ejection murmur, not loud,
localized to aortic area
carotid pulse normal volume and contour
s2 normal
echo features
increased echogenicity of leaflets, without commusural thickening, no significant obstruction to outflow
aortic valve sclerosis prognosis
can progress to clinically significant stenosis in one of 8 and severe in 1/64
marker for widespread atherosclerotic disease
management of Ascelorosis
control of Cardiac risk factors
follow up - to see if they progress
aortic valve stenosis
restricted CO secondary to valve not opening adequately
some hemodynamic consequences
causes of AS
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,
bicuspid AV
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
rheumatic aortic valve i
involves more of the commissures not the cusps - thats why orifice is small
incidence of differen etiology
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
pathyphys consequences of AS
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
AS symptoms
dyspnea on exertion and decreased exercise tolerance
dizziness, syncope
angina
Dyspnea
related to LVH, impaired relaxation, increased LV filling pressure, increased LA pressure, increased Pulmonary pressure - interstitial edema
decreased exercise intolerance
inability of LV to increase CO required with exercise due to fixed obstruction
exercising muscles need more blood
dizziness/syncope
peripheral vasodilation to increase blood pressure to exercising muscle- so get vasodilation but no increase in CO - so get hypotensive
ventricular arrhythmias
calcifications can extend to conducting system
angina
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
physical exam AS
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 -
how to tell severity of AS based on murmur
way to tell severity- where it peaks in systole
early- ventricle doesnt have trouble overcoming obtruction
late- ventricle having hard time overcoming obstruction
investigations AS
ECG: LVH
CXR: AV calcification, LVH, dilated aortic root
Echo: gold -
visual appearance of valve- bicuspid? thickening commisural? leaflets?
valve areas
LV thickness size
grading AS
valve areas:
normal 3- 4 cm2
mild 1.5-2
moderate 1-1.5
severe<1
tx
no medical tx
valve replacement only option:
deciding when the valve needs to be replaced imp
indication for surgery
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
surgical options
percutaneous valve replacements- for those people that cant undergo surgery
Aortic Regurgitation
can be acute or chronic
same as insufficient
caused by inadequate closure of leaflets- abn structure of dilation of aortic valve root or anullus
acute severe Regurg
medical emerg- b/c LV unable to adapt to regurgitant flow- rapid heart failure and cardiogenic shock
etiology severe acute regurg
endocarditis- due to valve destruction
aortic dissection-
Trauma- decelaration injuries
clinical features aortic dissection
sudden collapse with preceding sudden knifelike mid capular back pain
endocarditis
fever, embolic events, sick with septic symptoms
physical exam AR
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 -
definite diagnostic procedure
echo can visualize abn valve - size
regurg
and lV function size
tx of ASAR
emergency Aortic valve replacement
chronic AR etiology
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
pathyphys of AR
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
chronic AR sx
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
physical exam chronic AR
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 -
austin flint murmur
AR regurg - goes to ward mitral valve- and produces a murmur close to one of mitral stenosis
murmur in AR
high pitched blowing decrescendo diastolic murmur at LSB
unusual findings in chronic severe AR
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
chronic AR echo
identify valve pathology
assess aortic root and LV size and function
assess severity of AR
natural hx of AR
long latent period - decades
decomp: when LV systolic function fails
progressive LV dilatation occurs

initially reversible- but overtime irreversible
asymptomatic MR
no support for medical tx
abx prophylaxis for endocarditis no longer reccommeded
valve replacement EF<50
also presence of symptoms
decline in LV function
symptomatic AR
valve replace
ACE inhibitors, diuretics - short term
Mixed AV disease
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