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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
What % of patients w/ AO sclerosis will develop AS
10-15%
26
Describe the pathology of calcification AS It’s an extension of what pathology
There are lipid deposits, inflammation and calcifications that cause the leaflets to stick together atherosclerosis
27
what is the pathogenesis of calcific AS
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
28
causes of endothelial damage
force from high velocity blood flow, high BP, age
29
6 roles of echo in AS
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
30
where should the diastolic closure line of the AV be found on M mode
middle of the AO annulus
31
how might AS appear of M mode
- 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
32
can it be hard to see the valves on M mode w/ calcific AS
yes
33
what can cause morphology changes on the AV
atherosclerosis calcium commissural fusion post-stenotic dilation
34
is the AV is very stenotic, can it be hard to tell how many cusps it has
yes
35
describe the changes seen w/ AV sclerosis
- 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
36
describe the changes seen w/ AV stenosis
- 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
37
what is AV sclerosis
atherosclerosis on the AV
38
will you always have sclerosis before stenosis
yes
39
when a bicuspid AV is open, what shape does it make
football
40
does a bicuspid AV usually occur with a dilated AO root and ascending AO
yes
41
what type of AS is most common in patients under 50
congenital, bicuspid AV
42
does bicuspid AV effect one gender more than the other
yes, males
43
familial inheritance rate for bicuspid AV What % of the general population has a bicuspid AV
9% 1-2%
44
describe the structure of a bicuspid AV
- multiple configurations possible | - bicuspid w/ or w/ raphe
45
where is cuspal fusion most likely to occur w/ a bicuspid AV
85% RCC and LCC | 15% RCC and NCC
46
what is a raphe
seam that joins 2 cusps together
47
2D assessments w/ a bicuspid AV
eccentric closure line/non central coaptation systolic doming of the larger cusp norm leaflet excursion concentric LVH LV dilation LA dilation thickened leaflets
48
can you see a raphe if the AV is closed
no
49
another term for raphe
rudimentary cusp
50
what view in a bicuspid AV best seen how can we diagnose a raphe
PSAX you need to show the football shaped opening in systole in PSAX to diagnose this
51
anomalies associated w/ bicuspid AV
``` congenital membranes (sub or supravalvular) supravalvular narrowing subAO LVOT obstruction ```
52
where should you look for a supravalvular narrowing
ascending/descending AO | AO arch or junction
53
subAO LVOT obstruction is associated w/ which condition
HCM- hypertrophic cardiomyopathy
54
describe rheumatic AS, 2 types how does it cause AS
inflammatory condition caused by beta-hemolytic steptococci acute chronic causes scarring and leads to rheumatic AS
55
w/ rheumatic AS, where does the thickening of the AV start
leaflet tips
56
what is involved in the acute phase of rheumatic AS
-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
endocardial vasculitis most often affects which valves
Mitral - most common- 75-80% AV - 20-25% PV, TV - 5%
58
2 possible outcomes of endocardial vasculitis
resolve completely | or lead to progressive scarring
59
which type of rheumatic HD do we most commonly see
chronic
60
what is a 2D parameter that can be used to assess AS
AV planimetry
61
AV planimetry in done in which views what are we looking for
PLAX, PSAX... trace the orific in mid-systole of cusps mobility and commissural fusion valve calcification
62
what parameters are usually used to assess AS why
hemodynamic parameters AV planimetry is not as accurate, especially w/ calcific valves
63
what is the continuity rule
the volume of flow prox and distal to a narrowing must be equal, so blood flow speeds up in the narrowing
64
how does the continuity rule apply to SV formula
SV of the LVOT = SV of the AV LVOT (pie (r^4) x VTI) = AV (pie (r^4) x VTI)
65
3 items you need for AVA continuity equation
LVOT diameter LVOT VTI w/ PW AV VTI w/ CW Use the highest AV VTI (or velocity) from all views
66
where should the LVOT PW be taken
same spot at the LVTO diameter
67
how are area and velocity of a stenotic valve related
inversely eg, area reduction of 3 times, will cause velocity through that area to be tripled
68
is alignment to the AV usually more lateral than the apex
yes
69
is the mean or peak gradient more important for AS
mean
70
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
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
when would you get a good AV velocity from a subcostal view
if the jet is eccentric
72
why do we assess many locations if the AV velocity is >2.5m/s
highest velocity can be found at any of the 4 locations
73
how does the peak velocity method assess AS cons of this method
-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
which method is more accurate for AS, peak velocity or VTI
VTI
75
how does the VTI method assess AS pros of this method
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
which is more stenotic, a parabolic waveform, or a narrow waveform w/ high velocity
parabolic
77
what is the velocity ratio formula for AV
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
how are the degree of a stenosis and velocity related
directly
79
AV jet velocity for mild AS severely abnorm value
2.5 - 2.9 m/s >4 m/s
80
AV mean gradient (CW) value for mild AS severe AS
Mild: <20 mmHg severe: >40 mmHg
81
AV area value for mild AS severe AS
mild: >1.5 cm^2 severe: < 1 cm^2
82
indexed AVA to BSA value for mild AS severe AS
mild: > 0.85 severe: <0.6
83
LVOT/AV velocity ratio value for mild AS severe AS
mild: >0.5 severe: <0.25
84
what does a velocity ratio of <0.25 indicate
the velocity of the blood increases 4 fold when moving from the LVOT through the AV
85
describe the spectral waveform of subAO stenosis compared to severe AS
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
example of a subAO stenosis
SAM - systolic anterior motion of the MV leaflet
87
compare the timing and duration of the AS and MR
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
if the AV velocity indicates severe AS but the area does not, what might be causing this? how can you fix this
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
how can you overestimated the LVOT VTI
measuring the velocity too close to the AV when the blood is starting to pick up speed
90
if the AV velocity is normal but the area indicates severe AS, what might be causing this? how can you fix this
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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