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6. Echocardiographic principles > AoV assessment > Flashcards

AoV assessment Flashcards

1
Q

Causes of AI

A

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

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2
Q

Echo features of AI

A

o LV volume overload
o Valvular lesions
o Diastolic flutter of MV and AoV
o ↑EPSS

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3
Q

2D/M-mode findings AI

A

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
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4
Q

LV size and fct w/ AI

A
  • 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
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5
Q

Color flow eval AI

A

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

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6
Q

Effective orifice area calc

A

EROAAI = pi x (vena contracta/2)2

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7
Q

Doppler flow profile AI

A

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

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8
Q

Pressure 1/2 time AI

A
  • 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
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9
Q

Regurgitant volume calc AI

A
  • In normal heart, Ao SV should = PA SV
  • Not accurate if stenotic AoV

Regurgitant volume = PA SV – Ao SV

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10
Q

Ao diastolic flow reversal

A
  • 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
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11
Q

types of AS

A
  • 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
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12
Q

SAS breeds

A

Most common in large breed dogs
* Golden Retrievers
* Rottweiler
* Boxer
* German Shepherd
* Newfoundland

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13
Q

AS: echo assessment

A

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

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14
Q

Progression of lesions

A

Progressive lesions as animal grow → 18 months

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15
Q

Lesion classes SAS

A

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

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16
Q

Differentiate congenital fixed SAS from dynamic LVOTO in HCM

A

Absence of SAM in cats w SAS

17
Q

What 2D measure can provide additional info

A
  • 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
18
Q

Assessment for myocardial fibrosis

A

Focal areas w ↑ echogenicity
o Common on papillary muscles at base of IVS

19
Q

EOA AS

A
  • 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
20
Q

Continuity equation AoV

A

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

21
Q

M-Mode evaluation AS and changes

A
  • 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
22
Q

MR w/ SAS

A
  • 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
23
Q

Assessment of ventricular function in SAS

A
  • 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
24
Q

Color flow Doppler eval AS

A

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

25
Q

Spectral Doppler eval AS

A

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

26
Q

Optimal window to eval Ao flow

A

subcostal → parasternal windows not provide optimal alignment

27
Q

Underestimation of Ao flow factors

A

↓ forward flow from: myocardial failure, MR, sedation/anesthesia

28
Q

Ao obst flow profile

A
  • 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
29
Q

Differentiation of Ao flow from other flows

A

 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)

30
Q

Severity of SAS

A

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

31
Q

Normal Ao velocity range

A

o Normal Ao velocity range: 0.65-2.65m/s depending on study
 > 2.5m/s → SAS

32
Q

Causes of discrepancies in measurements of AS severity

A
  • 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
33
Q

Contrast continuity with Bernoulli in assessment of severity of valvular AS.

A

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

6. Echocardiographic principles (9 decks)

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