Transcript DEEPAK NANDAN ANATOMY Area-2.6-3.5 cm². Structure 3 cusps,3 commissures supported by fibrous annulus Arantius nodule 3 sinuses.

DEEPAK NANDAN
ANATOMY
Area-2.6-3.5 cm².
Structure
3 cusps,3 commissures supported
by fibrous annulus
Arantius nodule
3 sinuses
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Qualitative diagnosis
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Thin and delicate
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Plax-opening and closing
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Basal short axis view-Y-inverted Mercedes
Benz sign
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Maximum jet velocity
◦ BERNOULLI’s equation
◦ Multiple windows
◦ Parallel alignment
◦ Colour doppler
◦ Angle correction
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MIPG=4 xV²(maximal jet velocity)m/s
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MPG=4x(∑V1²+V2²+…Vn²)/n
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MPG=∆P(max)/1.45 +2
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MPG=2.4(Vmax)²
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Discrepancies
◦ Tech poor doppler recording
◦ Non parallel interrogation angle
◦ Pressure grad depends on flow rate & valve
narrowing –AR/LV dysfunction
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Continuity equation:-
SV (lvot)= SV (Ao)
SV=CSAxTVI
CSA (lvot) xTVI (lvot)=CSA (Ao) x TVI (Ao)
AVA=CSA x TVI (lvot) / TVI (Ao)
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Correlates well with invasive data (GORLINS)
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Adv compared to Berrnoulli
co-existing AR
Left ventricular dysfunction
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Rarely are all 3 leaflets imaged perpendicular
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Triangular shape- measurement error
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Deformities n irregularities- further exacerb
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AV- superior-inferior rapid moments
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0.25 cm2 margin
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Ao valve area≈Ao flow rate
Dist- true severe valvular stenosis (vs) mild
to mod stenosis with LV dysfn
Stepwise infusion of dobutamine(5—
30µg/kg/min)
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Flexible valves:- AVA ↑ when SV ↑
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True stenotis:- AVA↔ when SV ↑
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Flexible valves:-Vmax(lvot)/jet ↑
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True stenosis:-Vmax(lvot)/jet↔
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Safe& clinically useful, limitation- non
response to dobutamine
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Stress findings of severe stenosis
AVA<1cm²
jet velocity>40m/s
mean gradient>40mm of Hg
Lack of contractile reservefailure of LVEF to ↑ by 20% is a poor
prognostic sign
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Maximal aortic cusp separation (MACS)
Vertical distance between right CC and non CC
during systole
Stenotic AV → decreased MACS
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Limitations
Single dimension
Asymmetrical AV involvement
Calcification / thickness
↓ LV systolic function
↓ CO status
AVA
N
MACS
> 2cm2
< 0.75 cm2
> 1 cm2
gray area
N
> 15 mm
< 8 mm
> 12 mm
8 – 12 mm
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Ao valve resistanceflow independent measure of
stenosis severity
Resistance=(∆P/∆Q)mean x1333
Resistance=28√gradient( mean)/AVA
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Left ventricular stroke work loss(SWL)
SWL (%) = (100 ×∆ P mean) / (∆P mean +
SBP)
Principle-LV expends work during systole
to keep the AV open and to eject blood
into the aorta
Depends on the stiffness of AV
Less dependent on the flow
>25%--- poor outcome
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LVOT overestimated
LVOT TVI recorded
too close to valve
Hgh transAo flow
rate
mod-sev AR
Hgh output state
Large body size
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LVOT
underestimated
LVOT TVI-too far
frm val
Small body size
Lw transAo flw rate
low EF
small vent chamber
mod-sev MR
mod-sev MS
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Valve anatomy, etiology
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Exclude other LVOTO
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Stenosis severity – jet velocity
mean pressure gradient
AVA – continuity eq
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LV – dimensions/hypertrophy/EF/diastolic fn
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Aorta- aortic diameter/ assess COA
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AR – quantification if more than mild
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MR- mechanism & severity
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Pulmonary pressure
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Av ↑in MPG per yr = 0 to 10mm/yr
mean 7mm Hg
 AVA ↓ by 0.1 to ∓ 0.19cm²
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Jet vel < 3m/s – rate of symptom
onset needing MVR is 8 % /yr
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3-4m/s – 17%/yr
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>4m/s – 40% /yr
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Mitral annulus
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The leaflets
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Chordae tendinae-papillary muscle
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Underlying ventricular wall
Annulus
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Anterior- three scallops
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Posterior- three scallops
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Scallop 1-lateral most
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Scallop 3-medial most
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Antero lateral PM- chordae to AL half of
both leaflets
Dual blood supply
Postero medial PM- chordae to PM half
both leaflets
RCA blood supply
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Maximal excursion of leaflet tips
Tubular channel
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Commissural fusion⇒doming/bowing
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Chordal thickening ⇒ abnormal motion
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Progressive fibrosis⇒stiffening
⇒calcification
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Doming of the mitral valve (hockey stick
AML)
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Funnel shaped opening of mitral valves
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Focal thickening and beading of leaflets
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calcification
early diastolic doming motion of the AML, restriction of tip motion.
Pliable, little fibrosis, calcification, or thickening. Dilated LA
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2D short axis imaging of diastolic orifice
-planimetry
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Smallest orifice at the leaflet tips
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Inner edge of the black/white interface traced
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Correlates well with hemodynamic
assessment
1.
Funnel-shaped
Actual limiting orifice at the tip
2.
Instrumentation setting
‘’blooming” of the echoes due to
increased gain
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Increased echogenicity of leaflets
Decreased E-F slope
>80mm/s⇒MVA =4-6cm²
<15mm/s⇒MVA <1.3cm²
Paradoxical anterior motion of PML
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Trans mitral pressure gradient
single most imp factor in determining the
severity & relation to symptoms & functional
status
Depends on
Volume status
Heart rate
Peak pressure gradient
Early trans mitral flow volume
Cardiac output
High output states
Mitral reguritation
Mean pressure gradient
Average MVA
Cardiac output
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Measure of rate of decay of mitral valve
gradient
Time in ms at which initial instant pr
gradient declines to one half
Time interval from V max to the point
where velocity has fallen to Vmax/√2
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PHT=½ Peak=V½
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V½=Vmax/√2
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V½=V max/1.414
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V½=Vmax x .707
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MVA=220/PHT
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Post BMV- accuracy ↓
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Aortic regurgitation- over estimates MVA
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Severe LVH- ↓LV compliance
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Prosthetic mitral valve- not validated
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Independent of
Cardiac output
Mitral regurgitation
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Pressure half time=29% of Deceleration
time
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MVA=220 ÷ (0.29 × DT)
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MVA=759 ÷ DT
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Left atrial dilation
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Atrial fibrillation
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Spontaneous echo contrast
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LA thrombus
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Secondary pulm htn-TR
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Valve morphology
Exclude other causes of clinical presentation
MS severity
Mean transmitral pr gradient
2D valve area
PHT valve area
Assos MR
LA enlargement
Pulmonary art pressure
Co-existing TR severity
TEE for LA clot
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Individuals with score≤8 –excellent for BMV
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Those with score≧12-less satisfactory results
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