AoV assessment Flashcards
Causes of AI
o Degeneration → thickening
o Vegetative lesions → leaflet perforation/deformation
o Torn/flail cusps
o Congenital malformation of leaflets → inadequate coaptation
Bicuspid AoV, rheumatic valve, calcific valve dz
o Aortic disease → annular dilation
Marfan syndrome, cystic medial necrosis, familial Ao aneurysm, hypertension, systemic inflammatory dx
Echo features of AI
o LV volume overload
o Valvular lesions
o Diastolic flutter of MV and AoV
o ↑EPSS
2D/M-mode findings AI
valvular lesions
o Absence of lesion ≠ absence of dz
Echo not sensitive to show lesions/nodules <2mm
o Degenerative lesions: typically small, smooth, rounded
o Vegetative lesions: large hyperechoic masses
Floppy, prolapse in LVOT
- Diastolic fluttering of MV = most common M-mode finding (in Hu and dogs)
o 2nd to turbulence associated w regurgitant jet in LVOT during diastole while MV is open
o Jet do not have to be directed directly on MV but creates turbulent flow
o Reverse doming of septal leaflet toward LA - ↑EPSS: AI jet restrict MV motion
o Not correlate with AI severity - MV may close earlier because of ↑LV end diastolic pressures
- Jet lesion on septum or MV
LV size and fct w/ AI
- Acute AI = no LV dilation
- Chronic moderate to severe AI → volume overload
o Higher impact on LV fct vs MR (no flow in low pressure LA during systole)
o Hemodynamically insignificant AI will not cause LV dilation
o Myocardial failure suggested if no ↑FS and normal systolic dimension
EF <50-55% → poor px in Hu w AI
Color flow eval AI
Jet size
* Extent of regurgitation in LVOT
o Mild AI: just beyond AoV, dissipate quickly
o Moderate AI: extend at tip of MV
o Severe AI: beyond MV leaflets
* Jet height: proximal to AoV → end of jet
* Jet height/LVOT width ratio
o Mild AI <24%
o Moderate AI = 25-46%
o Severe AI > 47%
Vena contracta
* Smallest width of regurgitant jet on LAX parasternal view
o Mild AI <3mm highly specific
o Severe AI: >5mm highly sensitive, >7mm highly specific
* EROA can be calculated from vena contracta
o EROA >0.3cm2 = severe AI
Proximal isovelocity surface area - As discussed above
Effective orifice area calc
EROAAI = pi x (vena contracta/2)2
Doppler flow profile AI
Onset at AoV closure → rapid ↑ velocity to 3-5m/s → gradual decline during diastole → abrupt deceleration to baseline during IVCT → baseline at AoV opening
* Shape depend on time varying of PG → severity and chronicity
o Chronic severe AI: ↑Ao pulse pressure + low end diastolic AoP
Rapid ↓ in AoP = steeper diastolic slope
* Severe AI = T 1/2 <200ms
* Mild AI = T ½ >500ms
o Acute regurgitation: LV compliance not adapted → severe ↑ in LV end diastolic P
Triangular flow shape
Linear deceleration
Pressure 1/2 time AI
- Slope and pressure ½ time depend on how fast pressures btwn Ao and LV equilibrates = steep and short
o Rapid ↓ in Ao pressure
o Rapid ↑ LVP - Small regurgitant orifice = delay equilibration
o Plateau shape profile
o Long pressure ½ time - Hu:
o Pressure ½ time >500ms → hemodynamically insignificant AI
o Pressure ½ time <300ms → severe AI - Slope and ½ time depend on
o Size of regurgitant aperture
o LV compliance
o Ao diastolic pressure
Regurgitant volume calc AI
- In normal heart, Ao SV should = PA SV
- Not accurate if stenotic AoV
Regurgitant volume = PA SV – Ao SV
Ao diastolic flow reversal
- Flow in descending Ao: determine if significant reversal of flow in diastole
o Normally trivial
o Severe AI will cause flow reversal in proximal abdominal Ao
o Moderate AI will cause flow reversal in descending Ao - Analogous to PE finding of diastolic murmur in femoral arteries = Duroziez’s sign
types of AS
- Supravalvular: rare
o Reported in cats - Valvular
o Rarely single defect
o Seen in conjunction w subvalvular stenosis: >90% of dogs w AS - Subvalvular
o Narrowed LVOT 2nd to nodules/ridge of fibrous tissue
Ring may pull MV up to OT
Dynamic LVOTO → band may extend from MV
o ↓AoV area → fusion of Ao cusps
o LVCH
o ↑ blood flow velocity through stenotic area
SAS breeds
Most common in large breed dogs
* Golden Retrievers
* Rottweiler
* Boxer
* German Shepherd
* Newfoundland
AS: echo assessment
o MV morphology/motion
o AoV cusps anatomy/motion
o Visualized normal LCA
o Post stenotic dilation of ascending Ao
o Narrow OT and Ao
Progression of lesions
Progressive lesions as animal grow → 18 months
Lesion classes SAS
o Class 1: nodules
Tend to develop on ventricular side of AoV
o Class 2: fibrous ridge of tissue
Small and encircle OT w very little protusion into lumen
Extensive w small orifice for blood flow
o Class 3: tunnel type stenosis
Stiff MV forming posterior wall
IVS forms anterior wall
Common in Boxers and calves
Differentiate congenital fixed SAS from dynamic LVOTO in HCM
Absence of SAM in cats w SAS
What 2D measure can provide additional info
- Compare LVOT CSA vs Ao root CSA on R parasternal SAX→ provide additional info
o Help when flow velocity affected by other factors
o Normal LVOT:Ao ratio
Mild >0.5
Moderate 0.3-0.5
Severe >0.5
Assessment for myocardial fibrosis
Focal areas w ↑ echogenicity
o Common on papillary muscles at base of IVS
EOA AS
- Effective orifice area: calculated in Hu
o Useful if stenosis is valvular
o Not possible to measure if subvalvular (cannot record OT and Ao velocity separately)
RVOT not always match LVOT volume calculation
EOA: cannot differentiate mild stenosis and normal LVOT
Continuity equation AoV
o Used to calculate stenotic valve area
o All other measures derived from echo
o Can be normalized to body size (/BSA)
VTIRVOT x PA = normal SV
CSALVOT = ((〖CSA〗_PV x 〖VTI〗_PV))/〖VTI〗_LVOT
SVLVOT = SVAo
SV = CSA x VTI
CSALVOT x VTILVOT = CSAAo x VTIAo
M-Mode evaluation AS and changes
- Chronic pressure overload → concentric hypertrophy
o Tend to normalize LV wall stress
o Relative wall thickness = wall thickness/radius → measure LVH
o LV mass: calculated from tracing endo/epicardial borders at end diastole - Degree of hypertrophy
o Boxers: correlates w severity of stenosis/pressure gradient
o Not documented u=in other breeds
o Cannot be used as indicator of severity - Normal ratio IVS:LVIDd = 0.22 to 0.34
MR w/ SAS
- MR present in many dogs
o Some from SAM → invariable MR
Degree/duration of SAM → indicative of PG severity
Longer apposition to IVS = ↑ severity of obstruction
Assessment of ventricular function in SAS
- Systolic function: ↑FS%, Vcf, normal LVET
o Preserved until later in dz - Diastolic function: from compensatory LVH
o Pseudonormal transmitral flow
o Cause of c/s in Hu: exercise intolerance, lethargy, dyspnea
Color flow Doppler eval AS
o MR
Common w AS from calcification
Can cause underestimation of stenosis (low volume flow → ↓ transAo PG)
o AI: 50-75% of dogs
Diastolic flutter of septal MV leaflet
Endocarditis: 5% of dogs w SAS (1 study)
o CHF may develop 2nd to MR or AI
Spectral Doppler eval AS
o Use PW Doppler to determine level of obstruction/ site of ↑ velocity
DDX for LVOTO: fixed subvalvular obstruction, dynamic LVOTO, supravalvular stenosis
Presence of closing click = sample volume is immediately adjacent to valve
o High velocity flow through LVOT/Ao → obstruction to outflow
Correlates with PG from KT
* Not correlate to peak to peak in KT: peak Ao and peak LV NOT occur simultaneously
* Correlate to KT max and mean
Velocity must ↑ as flow moves through narrowed area
* L apical views: may underestimate by 26%
Velocity ratio LVOT:Ao
* Little obstruction → ratio near 1
* Valve area ½ normal → ratio = 0.5
* Valve area ¼ normal → ratio = 0.35
Optimal window to eval Ao flow
subcostal → parasternal windows not provide optimal alignment
Underestimation of Ao flow factors
↓ forward flow from: myocardial failure, MR, sedation/anesthesia
Ao obst flow profile
- Fixed obstructions: symmetric, with peak in m id systole
o Smooth velocity curve, well defined peak velocity, spectral darkening along outer edge
o Highest velocity signal = most // angle (5% error with < 15 degree angle) - Dynamic obstruction: dagger shaped during acceleration
o Late peak velocity: progressive ↓ in OT as IVS contract or SAM
Differentiation of Ao flow from other flows
MR: start early in systole, flow start at onset of QRS, last longer to end of T wave
* LVOT/Ao flow: later in systole, end of QRS
* MR pressure gradient can be used to confirm stenosis PG
TR, VSD, PA stenosis, peripheral vascular stenosis (ie subclavian artery)
Severity of SAS
pressure gradient
Mild <50mmHg, moderate 50-80mmHg, severe >80mmHg
Will be influenced by:
* Low output → myocardial failure
* ↑SV → AI, PDA, stress
* ↓SV → sedation/anesthesia, MR
Normal Ao velocity range
o Normal Ao velocity range: 0.65-2.65m/s depending on study
> 2.5m/s → SAS
Causes of discrepancies in measurements of AS severity
- Severe AS by velocity/PG but not valve area
o Overestimation of LVOT
o LVOT velocity recorded too close to valve
o ↑SV: AI, high output state, large body size - Severe AS by valve area but not velocity/PG
o Underestimation of LVOT
o LVOT velocity recorded too far from valve
o Small body size
o ↓SV: ↓EF%, small ventricular chamber, MR, mitral stenosis
Contrast continuity with Bernoulli in assessment of severity of valvular AS.
Bernoulli equation:
* Mean gradient: from velocity curve throughout systole
* Accuracy is flow dependent
Continuity equation
* Volume proximal and w/I stenotic orifice is equal
o Product of flow velocity x CSA maintained constant across a stenotic zone
Acceleration of flow: generated by hypertrophied ventricle = ↑ ventricular systolic pressure → ↑ kinetic energy of RBCs
Distal to obstruction:
* Peak flow velocity α PG across stenosis → Bernoulli
* Marked flow disturbance: loss of kinetic E from heat and friction
* Measures effective orifice area
* Flow independent
o Not affected by the presence of AI (which ↑SV)
o Not affected by LV systolic dysfct (which ↓SV)
* Requires LVOT diameter + flow velocity → prone w error
