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What causes AI?
- -Congenital valve abnormality (bicuspid)
- -Calcification/sclerosis with age
- -Inflammatory disease: Rheumatic, lupus, ankylosing spondylitis
- -Myxomatous degeneration
- -Endocarditis
- -Idiopathic Aortic Root/annulus dilation
- -Aortic Root abnormalities eg: aortic aneurysm, dissection, coarctation
- -Other: syphyllis, Phen-fen, infiltrative disease (amyloid or glycogen storage), sarcoidosis, hemodosis
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What is Myxomatous valve disease?
- Connective tissue disorder >
- -cusps become thickened, elongated, and redundant
- -sagging cusp in short axis can appear as a cylindrical mass
- -flail cusp may flutter in LVOT during diastole or appear as flutter on m-mode closure line
- -primarily associated with MVP
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What is the most common cause of acute AI?
Endocarditis
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What is Endocarditis?
- Infection of endocardium leading to vegetation on leaflets or perforation of valvular tissue
- most commonly occurs with staff infections, IV drug users, prosthetic valves
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What is the most common cause of chronic AI?
Idiopathic AoR dilation and annulus dilation
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What is coarctation?
congenital stenosis of aorta >> narrows near insertion of ductus arteriosus (pre or post ductal)
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What other conditions can cause AoR abnormalities?
- -Chronic hypertension
- -Marfans
- =inherited connective tissue disorder, affects eyes, skeleton, CV system >> valve dilation, dissection
- -Cystic medial necrosis
- =disorder of large arteries >> focal degeneration of elastic tissue and muscle in the media, associated with aneurysm, dissection, and Marfans
- -syphyllis >> uncommon extensive calcification of dilated root
- -Phen-phen >> thickened MV/AV and insufficiency
- -Infiltrative diseases >> amyloid or glycogen storage, sarcoidosis, hemodosis
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What are the common Echo findings of AI?
- -Diastolic jet in LVOT
- -incomplete closure of cusps
- -anatomic abnormality of valve or root
- -initial hyperkinesis of LV walls due to volume overload (may see early diastolic dip of IVS)
- -progressive dilation of LV due to volume overload >> increased LVEDP
- -eventual decrease in LV systolic function
- -fine fluttering and damping of AMVL
- -premature closure of MV and opening of AV on m-mode seen in acute/severe AI
- -raised fibrotic lesion on septum or AMVL may be seen with chronic AI
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What are the signs/sx of AI?
- -DOE
- -fatigue
- -palpitations (LV dilation, irritible wall > arrythmias)
- -angina
- -dizziness
- -syncope (uncommon)
- -signs of CHF = syncope, cough, SOB, crackles, paroxysmal nocturnal dyspnea
- -signs of RHF = JVD, ascites, hepatomegaly, peripheral edema
- -wide pulse pressure (decreased DBP < 50% SBP)
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How is AI treated?
- -CHF treatment = afterload reduction therapy
- -valve replacement when indicated
- >>LVID > 5.5cm and FS < 25%, or significant change in LV size/function
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What kind of murmur/s may be heard with AI?
- -Diastolic high pitched blowing decrescendo murmur at LSB
- -severe AI >> Austin Flint murmur = low pitch diastolic rumble at apex
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What are possible EKG finding with AI?
- -LVH due to increased mass (dilation)
- -LAE
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What does the cath pressure tracing show in AI?
significantly decreased aortic pressure with increased LV pressure in diastole, loss of dicrotic notch
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What kind of pulse might be felt in cases of significant/severe AI?
pulsus bisferiens/biphasic = two strong systolic peaks, caused by midsystolic pressure dip (decrease in the lateral wall pressure of the ascending aorta)
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How can AI severity be measured/calculated using 2D color flow, and what are the criteria?
- 1. Jet area/LVOT area * 100
- > 25-64% = moderate AI (ASE)
- trace LVOT and ROA (regurgitant orifice area) in PSSAX
- OR trace ROA and calculate LVOT (.785 * LVOTd2 )
- 2. Jet (vena contracta) diameter/LVOT diameter
- > 25-64% = moderate AI
- 3. Vena Contracta (neck of jet) width
- > .3-.6 cm = moderate AI (OTTO)
4. Presence of a PISA = moderate to severe AI
*Color flow often eyeballed, not specifically measured (jet <1/4 LVOT = mild)
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How is AI evaluated in CW Doppler?
-Intensity of signal
-slope of signal or PHT* (.29*decel time)
- >500msec = mild
- 200-500 = moderate
- <200 = severe
*correlates poorly to jet area (poor R-value)
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How is AI evaluated in PW Doppler?
1. Calculate regurgitant fraction:
- RV= Aortic SV - Mitral SV (total SV - forward SV)
- > 30-59cc/ml = moderate AI
- RF = Aortic SV - Mitral SV/Aortic SV *100
- > 30-49% = moderate AI
- EROAcm2 = RV/VTIRJ> .10-.29 = moderate AI
* remember SV = CSA * VTI
2. PW of MV inflow shows reduced decel time or steep slope in significant AI due to increased LVEDP
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How can AI be distinguished from MS when using a Pedoff probe?
AI starts with AV closure, MS starts with MV opening
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Color and PW Doppler may reveal flow reversal where/when?
with severe AI:
1. Holodiastolic flow reversal in descending aorta (2D SSN)
2. flow reversal in abdominal aorta
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Evaluation of valvular regurgitation involve assessment of what specific factors?
- -valve anatomy
- -severity of the regurgitation
- -chamber enlargement due to volume overload
- -ventricular function
- -degree of pulmonary hypertension
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