1
Q
4 components of the aortic root
A
- valve ring = poin t of attachment of the cusps to the root wall
- cusps (NCC, RCC, LCC)
- sinus of valsalva = aortic cusps recess into the sinus during systole
- Sino-tubular junction = where the sinus valsalva becomes the tubular portion of the aorta
2
Q
aortic commissures
A
- most age related calcification starts at the commissures and work its way along the free edges to the orifice
3
Q
stenosis definiton
A
- formation of a high velocity jet through a narrowed orifice
4
Q
aortic stenosis
A
- incomplete opening of the aortic valve during systole leading to a high velocity jet
5
Q
effect of aortic stenosis
A
- causes and obstruction to flow from the LV to AO
6
Q
three levels of obstruction
A
- supravalvular = membrane, shelf in AO
- valvular - valvular AS
+ calcific, congenital, rheumatic
+ MOST COMMON - subvalvular - membrane or muscular IVS
+ hypertrophic cardiomyopathy
7
Q
afterlaod effect on the LV
A
outflow obstruction»_space; increasing after load» LV systolic pressure rises» TO keep SV normal»_space; increased force of contraction»_space; LVH develops (concentric) due to pressure overload
8
Q
clinical symptoms of aortic stenosis
A
- exertion dyspnea/ SOB
- fatigue
- chest pain
- dizziness/snycope
- arrhythmias
- signs CHF
9
Q
auscultation of aortic stenosis
A
- harsh éjection murmur
- systolic ejection click
- crescendo decrescendo murmur
- right upper sternal border
- may radiate to carotid arteries
- +/- aortic regurge murmur
10
Q
clinical manifestations of AS
A
- mild and moderate rarely felt
- symptoms are related to the pathophysiological response
- angina pectoris
+ mini heart attacks - syncope or presyncope
+ exertion not enough blood flow to brain - congestive heart failure
11
Q
etiology AS - in order of incidence
A
- calcific AS (degenerative) \+ thickening starts at the underside of the cusps \+ increased incidence with age \+ associated with bicuspid AV - congenital (bicuspid, uni.quad) - rheumatic \+ thickening starts at cusp edges
12
Q
calcific AS - epidemiology
A
- about 25% over 65 have some degree of aortic sclerosis
- 10-15% develop aortic stenosis
- progressive thickening over many years
- AV leaflets thicken then start to tether together at the edges
13
Q
calcific AS - pathology
A
- number cusps cannot be identified due to disintegration
- calcific aortic valve is seen as extension of the atherosclerotic process
- lipid deposition, inflammation and calcification cause leaflets to stick together
14
Q
pathogenesis of calcific AS
A
- endothelial damage»_space; endothelial cells lose ability to produce gasses that prevent clotting inflammation» foam cells infiltrate into tissue» macrophages engulf foam cells causing inflammation» necrosis, calcification and narrowing occurs
15
Q
6 jobs of echo in AS
A
- determine etiology of the lesion
- exclude other sources of LVOT obstruction
- assess LV size systolic, diastolic function
- assess degree of LVH
- estimate severity of stenosis
- identify associated valve lesion
16
Q
AV assessment - M Mode
A
- look for
+ diastolic closure line - normally at middle of aortic annulus
+ leaflet excursion 2.0cm - BOX
17
Q
AV assessment - 2D
A
- look for \+ equal opening/coaptation of cusps \+ cusp number \+ coronary implantation \+ degree of movement \+ morphology changes (atherosclerosis, calcium, commissural fusion, post stenotic dilatation)
18
Q
2D exam
A
- assess \+ walls \+ cavities \+ valve morphology - measure \+ IVS, LV, LVPW \+ LA, AoRoot, AscAo \+ LVOT - calculate \+ LV mass index \+ EF \+ LVOT area
19
Q
AV sclerosis
A
- some thickening and calcification(brightening)of cusps
- slight reduction of cusp excursion may be present
- CW doppler velocity through AV normal or slightly elevated
< 2.5m/s
20
Q
AV stenosis
A
- more obvious thickening and calcification of cusp
- obvious visual reduction of cusp excursion
- CW doppler velocity elevated through the AV >2.5m/s
21
Q
bicuspid AV is what shape when opened
A
- football shaped orifice when open
22
Q
bicuspid AV.
A
- MOST COMMON TYPE OF AS IN PATIENTS UNDER 50 YEARS OLD
- occurs in 1-2% of the general pop
- affects more males than female
- familial inheritance 9%
- often occurs along with ascending aortic dilation which has 6% chance of rupture
23
Q
bicuspid AV structure
A
- multiple configurations possible
- bicuspid with raphe or without raphe
24
Q
raphe defintion
A
- seam that joins two cusps together
25
bicuspid AV - cusps fusion stats
- 85% RCC and LCC
| - 15% RCC and NCC
26
7 things to look for with bicuspid AV
- thickened leaflets
- eccentric closure
- normal valve excursion
- systolic doming of LARGER cusp
- concentric LVH
- LV dilation
- LA enlargement
27
what is best view to see bicuspid
- PSAX
28
anomalies associated with bicuspid AV
```
- congenital membranes
+ subvalvular/supravalvular
- supravalvular narrowing
+ ascending AO, AO arch or junction with descending A)
- sub aortic LVOT obstruction
+ associated with HCM (hypertrophic cardiomyopathy)
+ asymmetric septal hypertrophy
+ systolic anterior motion of AML
```
29
Rheumatic AS
- caused by scarring from rheumatic fever
- inflammatory condition
- caused by beta-hemolytic streptococci
30
acute phase of rheumatic fever
- endocardial vasculitis = swelling leads to valve damage
- myocardium
- pericardium
- synovial joints
- lungs and pleura
* * all of these have swelling which may or may not lead to swelling
31
rheumatic heart disease
```
- endocardial vasculitis
+ mitral MOST
+ aortic valve next
+ PV,TV
- may resolve of lead to progressive scarring
```
32
2D parameters of estimating AS severity
- AV planimetry
33
how is AV planimetry assessed
```
- using hemodynamic parameters like
+ peak velocity
+ mean pressure gradient
+ aortic valve area
+ indexed aortic valve area
+ dimensionless velocity ratio
```
34
2D AV planimetry
- identify number of cusps
- assess cusp mobility and commissural fusion
- assess valve calcification
- trace orifice in mid systole
35
continuity principle
- volume of low proximal to and in the narrowing most be equal
36
continuity equation stroke volume
stoke volume LVOT = stroke volume AV
37
continuity equation CSA and VTI
- CSAlvot x VTIlvot = CSAav x VTIac
38
continuity equation rearranged to determine Aortic valve area (AVA)
AVA = (o.785 x LVOTd^2) x VTIlovt / VTIav
39
three things needed for AVA continuity equation
- obtain LVOT diameter
- obtain VTI of LVOT in PW
- obtain VTI of aorta using CW
40
continuity equation relationship = velocity and area
- increase in velocity through stenotic valve is inversely proportional to the reduction in area of valve
41
where to go to get good AV alignment
- LATERAL
42
what 4 places should you asses AV velocity is over 2.5m/s
- apical
- right suprasternal or right supraclavicular
- right parasternal
- +/- subcostal
43
rationale behind sampling 4 please when AV velcoty high
- highest velocity could be found at any of these locations
- highest velocity and VTI are used for the calculation unless an arrhythmia is present then they are averaged over 5 beats
44
continuity equation peak velocity method
- uses single pint only from LVOT and AV
- less accurate than VTI
- unable to incorporate velocity over time
- will overestimate stenosis if waveform is narrow with high peak velocity
45
continuity equation VTI method
- uses velocity -time integral which incorporates all of the velocities throughout the ejection period
- incorporates the parabolic shape of a waveform
- does not overestimate the degree of stenosis
46
velocity ratio - relationship to degree of stenosis
VR = velocity LVOT / velocity AV
- inversely related to degree of stenosis
47
velocity ratio using VTI
VTIlvot / VTI av
48
AV sclerosis - severity values
- = 2.5m/s
49
mild aortic stenosis - severity values
```
av jet velocity = 2.5-2.9m/s
mean gradient = , 20mmHG
AVA cm^2 = > 1.5cm^2
indexed AVA to BSA = > 0.85
velocity ratio = > 0.50
```
50
moderate aortic stenosis - severity values
```
AV jet velocity = 3.0-4.0 m/s
mean gradient = 20-40mmHg
AVA cm^2 = 1.0-1.5cm^2
indexed AVA to BSA = 0.6-0.85
velocity ratio = 0.25 -0.5
```
51
severe aortic stenosis - severity values
```
AV jet velocity = >4.0m/s
mean gradient = > 40mmHg
AVA cm^2 = < 1 cm^2
indexed AVA to BSA = < 0.6
velocity ratio = < 0.25
```
52
subaortic stenosis wave form characteristics
- late peaking profile (dagger)
- asymmetric
- very high velocity
- will cover in CMO
53
severe aortic stenosis waveform characteristics
- acceleration time = deceleration time
| - symmetrical waveform
54
which starts later and ends earlier MR or AS
- AS
55
aortic stenosis with LOW EF
- low EF cannot generate enough force to push the blood out through the AV with high gradient/ velcoty
- gradients will be artificially low
+ IHD
+ CAD
+CMO
56
aortic stenosis with high EF
```
- increases force of contraction
+ fever
+ hypervolumia
+ pregnancy
+ LV overload due to moderate-severe AR
+ gradients artificially high
```
57
discrepancy of severity - severe velocity but not by area
- TECHNICAL ERRORS
+ LVOTd overestimated
+ LVOT VTI overestimated (measured to Cloe to AV)
= remeasure and recalculate AVA
58
discrepancy of severity - severe by area but not by velocity
- TECHNICAL ERRORS
+ LVOTd underestimated
+ LVOT VTI underestimated (measured to far from AV)
= remeasure and recalculate AVA
Echo 2
flashcards
Decks in class (18)
# Cards
-
Module 1 : Doppler Review39
-
Module 2 : Ventricular Systolic Function97
-
Module 3 : Diastolic Function70
-
Module 3.1 : Atrial Size and Function21
-
Module 4 : Aortic Stenosis58
-
Module 3.2 : Congestive Heart Failure57
-
Module 5 : Aortic Valve Regurgitation64
-
Module 6 : Mitral Stenosis81
-
Module 7 : Mitral Regurgitation79
-
Module 8 : Tricuspid and Pulmonary Stenosis84
-
Module 9 : Tricuspid and Pulmonary Regurgitation112
-
Module 10 : Systemic Hypertension71
-
Module 11 : Pulmonary Hypertension66
-
Module 13 : Ischemic Heart Disease84
-
Module 14 : Stress and Contrast Echo50
-
Module 15 : Dilated and Hypertrophic Cardiomyopathies59
-
Module 16 : Restrictive and Other Cardiomyopathies45
-
Module 17 : Pericardial Disease69
