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Echo 2 > C6: AV stenosis > Flashcards

C6: AV stenosis Flashcards

1
Q

where is the sinotubular junction

A

where the sinus of valsalva becomes the AO

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2
Q

is it common to see post stenotic dilation of the AO from AS

A

yes

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3
Q

where are the Aortic commissures

A

where the leaflets attach to the annulus

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4
Q

where do most age related calcifications of the AV start

A

AO commissures and works its way along the free edge to the center of the valve

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5
Q

define stenosis

A

formation of a high velocity jet through a narrowed orifice

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6
Q

define AO stenosis

A

incompetent opening of the AV during systole leading to a high velocity jet… leaflets will be tethered and thickened

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7
Q

do value leaflets calcify, or tether, first?

A

calcify

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8
Q

3 levels of obstruction of AS

A

1 supravalvular - membrane of shelf in AO.. usually congenital

2 valvular - calcific, congenital, rheumatic

3 subvalvular - membrane or muscular IVS (hypertrophic cardiomyopathy)

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9
Q

what is the most common cause of AS

A

valvular

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10
Q

do the LVOT and AV velocities usually peak at the same time

A

no, LVOT peaks first

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11
Q

what does the instantaneous peak measure

A

the pressure gradient at one point in time, the LVOT and AV pressure wont both be at their peak at one point in time so the difference b/w them will be greater

this is what we measure on echo

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12
Q

what does the peak to peak method of measuring press different than instantaneous peak

A

it measures the press gradient b/w the peak press of the LVOT and AV, its more accurate than instantaneous peak

Done in the cath lab

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13
Q

describe the effect of afterload on the LV

A

LV systolic pressure will rise, to keep SV norm, theres an increase in inotropy which causes concentric LVH due to the pressure overload

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14
Q

symptoms of AS

A 
SOB
fatigue
chest pain/palpitations
syncope
arrthythmias
signs of CHF
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15
Q

would a patient have symptoms w/ mild-moderate AS

A

not usually

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16
Q

w/ AS, what will you hear w/ auscultation

when and where

A

when:
harsh ejection murmur during systole
systolic ejection click and a crescendo-decrescendo murmur

where:
right upper sternal border that may radiate to CCAs

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17
Q

if you have a murmur from AS is it likely you will also hear a regurg murmur?

A

yes, if the valve doesn’t open well, then its likely it doesnt close well either

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18
Q

3 primary manifestations of severe AS

A

angina pectoris:
made worse by LVH, also caused by poor profusion of CA and the compress of coronary arteries from high cavity press, prolonged contraction and impaired relaxation

syncope or presyncope:
usually w/ exertion…. heart has reduced ability to maintain cerebral perfusion press w/ AS

CHF

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19
Q

what is presyncope

A

symptoms you feel before passing out

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20
Q

3 etiologies of AS

A 
calcified AS (degenerative):
also called age related AS, thickening starts at the underside of the cusps, can be associated w/ bicuspid AV

congenital:
bicuspid (more common type of congenital), uni, or quad

rheumatic:
thickening starts at cusp edges

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21
Q

which etiology of AS is the most common

A

calcific/degenerative

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22
Q

What % of adults over 65 will have some degree of AO sclerosis

A

25%

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23
Q

What is the precursor to AO stenosis

A

Sclerosis

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24
Q

W/ AO sclerosis will there be an increase in blood velocity?

Why or why not

A

No, its not yet restrictive

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25
Q

What % of patients w/ AO sclerosis will develop AS

A

10-15%

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26
Q

Describe the pathology of calcification AS

It’s an extension of what pathology

A

There are lipid deposits, inflammation and calcifications that cause the leaflets to stick together

atherosclerosis

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27
Q

what is the pathogenesis of calcific AS

A

endothelial damage causes the endothelial cells to lose the ability to produce gasses that prevent clotting and inflammation…. in time this leads to necrosis, calcifications and narrowing

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28
Q

causes of endothelial damage

A

force from high velocity blood flow, high BP, age

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29
Q

6 roles of echo in AS

A
  1. determine the etiology of the lesion (congenital, degenerative, rheumatic)
  2. exclude other sources of LVOT obstruction
  3. assess LV size, systolic and diastolic function
  4. assess degree of LVH
  5. estimate severity of stenosis
  6. identify associated valve lesions
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30
Q

where should the diastolic closure line of the AV be found on M mode

A

middle of the AO annulus

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31
Q

how might AS appear of M mode

A
  • Ao closure line not in the middle of the AO annulus
  • ‘extra lines’ seen where the AO root is located due to calcium deposites
  • AV won’t open fully
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32
Q

can it be hard to see the valves on M mode w/ calcific AS

A

yes

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33
Q

what can cause morphology changes on the AV

A

atherosclerosis
calcium
commissural fusion
post-stenotic dilation

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34
Q

is the AV is very stenotic, can it be hard to tell how many cusps it has

A

yes

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35
Q

describe the changes seen w/ AV sclerosis

A
  • some thickening and calcifications of the cusps
  • slight reduction of cusp excursion
  • CW doppler velocity of AV norm or slightly elevated

CW velocity of AV <2.5 m/s

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36
Q

describe the changes seen w/ AV stenosis

A
  • obvious thickening and calcifications of the cusps
  • obvious reduction of cusp excursion
  • CW doppler velocity elevated through AV

CW velocity of AV >2.5 m/s

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37
Q

what is AV sclerosis

A

atherosclerosis on the AV

38
Q

will you always have sclerosis before stenosis

A

yes

39
Q

when a bicuspid AV is open, what shape does it make

A

football

40
Q

does a bicuspid AV usually occur with a dilated AO root and ascending AO

A

yes

41
Q

what type of AS is most common in patients under 50

A

congenital, bicuspid AV

42
Q

does bicuspid AV effect one gender more than the other

A

yes, males

43
Q

familial inheritance rate for bicuspid AV

What % of the general population has a bicuspid AV

A

9%

1-2%

44
Q

describe the structure of a bicuspid AV

A
  • multiple configurations possible

- bicuspid w/ or w/ raphe

45
Q

where is cuspal fusion most likely to occur w/ a bicuspid AV

A

85% RCC and LCC

15% RCC and NCC

46
Q

what is a raphe

A

seam that joins 2 cusps together

47
Q

2D assessments w/ a bicuspid AV

A

eccentric closure line/non central coaptation
systolic doming of the larger cusp
norm leaflet excursion
concentric LVH

LV dilation
LA dilation
thickened leaflets

48
Q

can you see a raphe if the AV is closed

A

no

49
Q

another term for raphe

A

rudimentary cusp

50
Q

what view in a bicuspid AV best seen

how can we diagnose a raphe

A

PSAX

you need to show the football shaped opening in systole in PSAX to diagnose this

51
Q

anomalies associated w/ bicuspid AV

A 
congenital membranes (sub or supravalvular)
supravalvular narrowing
subAO LVOT obstruction
52
Q

where should you look for a supravalvular narrowing

A

ascending/descending AO

AO arch or junction

53
Q

subAO LVOT obstruction is associated w/ which condition

A

HCM- hypertrophic cardiomyopathy

54
Q

describe rheumatic AS, 2 types

how does it cause AS

A

inflammatory condition caused by beta-hemolytic steptococci

acute
chronic

causes scarring and leads to rheumatic AS

55
Q

w/ rheumatic AS, where does the thickening of the AV start

A

leaflet tips

56
Q

what is involved in the acute phase of rheumatic AS

A

-endocardial vasculitis (inflammation of the endocardium, most important) - swelling that leads to valve damage

-inflammation of the myocardium, pericardium, synovial joints, lungs and pleura
(these may or may not lead to scarring)

57
Q

endocardial vasculitis most often affects which valves

A

Mitral - most common- 75-80%
AV - 20-25%
PV, TV - 5%

58
Q

2 possible outcomes of endocardial vasculitis

A

resolve completely

or lead to progressive scarring

59
Q

which type of rheumatic HD do we most commonly see

A

chronic

60
Q

what is a 2D parameter that can be used to assess AS

A

AV planimetry

61
Q

AV planimetry in done in which views

what are we looking for

A

PLAX, PSAX… trace the orific in mid-systole

of cusps
mobility and commissural fusion
valve calcification

62
Q

what parameters are usually used to assess AS

why

A

hemodynamic parameters

AV planimetry is not as accurate, especially w/ calcific valves

63
Q

what is the continuity rule

A

the volume of flow prox and distal to a narrowing must be equal, so blood flow speeds up in the narrowing

64
Q

how does the continuity rule apply to SV

formula

A

SV of the LVOT = SV of the AV

LVOT (pie (r^4) x VTI) = AV (pie (r^4) x VTI)

65
Q

3 items you need for AVA continuity equation

A

LVOT diameter
LVOT VTI w/ PW
AV VTI w/ CW

Use the highest AV VTI (or velocity) from all views

66
Q

where should the LVOT PW be taken

A

same spot at the LVTO diameter

67
Q

how are area and velocity of a stenotic valve related

A

inversely

eg, area reduction of 3 times, will cause velocity through that area to be tripled

68
Q

is alignment to the AV usually more lateral than the apex

A

yes

69
Q

is the mean or peak gradient more important for AS

A

mean

70
Q

when the AV CW velocity is over 2.5 m/s, which 4 views should you assess velocities from

Which velocity and VTI is used to calculate

A

apical
R suprasternal or R supraclavicular (pedoff probe)
R parasternal
subcostal

Highest numbers are used, unless patient has arrthyhmias, then average values over the 5 beats

71
Q

when would you get a good AV velocity from a subcostal view

A

if the jet is eccentric

72
Q

why do we assess many locations if the AV velocity is >2.5m/s

A

highest velocity can be found at any of the 4 locations

73
Q

how does the peak velocity method assess AS

cons of this method

A

-it gives you an AVA uses only a single point from both the LVOT and AV

  • unable to incorporate velocity over time
  • will over estimate stenosis if the waveform is narrow w/ a high peak velocity
74
Q

which method is more accurate for AS, peak velocity or VTI

A

VTI

75
Q

how does the VTI method assess AS

pros of this method

A

Gives you an AVA using velocity time integral which incorporates all of the velocities in the ejection period

  • incorporated the parabolic shape of the waveform
  • doesn’t over estimate degree of stenosis
76
Q

which is more stenotic, a parabolic waveform, or a narrow waveform w/ high velocity

A

parabolic

77
Q

what is the velocity ratio

formula for AV

A

a different way to quantify the degree of stenosis of a valve… the ratio can also be done using VTI

VR = velocity of LVOT/velocity of AV
or
VTI = VTI LVOT/VTI AV

78
Q

how are the degree of a stenosis and velocity related

A

directly

79
Q

AV jet velocity for mild AS

severely abnorm value

A

2.5 - 2.9 m/s

> 4 m/s

80
Q

AV mean gradient (CW) value for mild AS

severe AS

A

Mild: <20 mmHg

severe: >40 mmHg

81
Q

AV area value for mild AS

severe AS

A

mild: >1.5 cm^2
severe: < 1 cm^2

82
Q

indexed AVA to BSA value for mild AS

severe AS

A

mild: > 0.85
severe: <0.6

83
Q

LVOT/AV velocity ratio value for mild AS

severe AS

A

mild: >0.5
severe: <0.25

84
Q

what does a velocity ratio of <0.25 indicate

A

the velocity of the blood increases 4 fold when moving from the LVOT through the AV

85
Q

describe the spectral waveform of subAO stenosis compared to severe AS

A

subAO stenosis: late peaking profile and fast DT - dagger sign…. very high velocity

severe AS: acceleration time and DT are the same so you have a symmetrical waveform

86
Q

example of a subAO stenosis

A

SAM - systolic anterior motion of the MV leaflet

87
Q

compare the timing and duration of the AS and MR

A

AS: starts later and ends sooner than MR - stenosis never occurs during the isovolumic periods

MR: occurs during the isovolumic period (no gap b/w outflow and inflow)

88
Q

if the AV velocity indicates severe AS but the area does not, what might be causing this?

how can you fix this

A

technical errors - LVOTd or LVOT VTI overestimated (re measure)

large body size - calculate indexed AVA

high transAO flow - significant AR, pregnancy, tachycardia, fever, etc )used AVA for severity)

89
Q

how can you overestimated the LVOT VTI

A

measuring the velocity too close to the AV when the blood is starting to pick up speed

90
Q

if the AV velocity is normal but the area indicates severe AS, what might be causing this?

how can you fix this

A

technical errors - LVOTd or LVOT VTI underestimated (re measure)

small body size - calculate indexed AVA

low transAO flow

low EF: dobutamine stress echo
norm EF: patient may have significant MR or low indexed SV… use AVA for severity in both cases

Echo 2 (15 decks)

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