2. DMST 283 ECHO 2 > Aortic Stenosis > Flashcards

Aortic Stenosis Flashcards

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1
Q

Label the image

A
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2
Q

What is the valve ring?

A

Point of attachment of the cusps to the root wall

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3
Q

What is the sinus of valsalva?

A

Aorta cusps Rees’s into the sinus during systole

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4
Q

What is the sino-tubular junction?

A

Where the sinus of Valsalva becomes the tubular portion of the aorta

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5
Q

How do we get the measurement of the aortic root?

A

Measure from leading ledge to leading edge.

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6
Q

When is it common to see during aortic stenosis?

A

Post stenotic dilation

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7
Q

In terms of aortic commissaries, most age related calcification starts where? and how doe sit move?

A

At the the commissures and it works its way along the free edge to the valve orifice

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8
Q

Label the image

A
  1. Star: Aortic commissures
  2. Arrows: Free edge to the cusps
  3. Circle: Valve orifice
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9
Q

What is aortic stenosis?

A

Incomplete opening of the aortic valve during systole leading to a high velocity jet

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10
Q

What do we normally see during aortic stenosis in terms of the leaflets?

A

Thickened and tethered leaflets

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11
Q

What does the thickened and tethered leaflets cause?

A

Obstruction to flow from the LV to the Ao

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12
Q

What are signs/symptoms of AS?

A
  1. Mild- mod AS is rarely felt when it is isolated
  2. Symptoms are related to the pathophysiological responses to AS
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13
Q

In terms of AS what are symptoms related to the pathophysiological resonates to AS? 5

A
  1. exertional dyspnea/ SOB
  2. Fatigue
  3. Angina
  4. Signs of CHF
  5. Systolic thrill

ass ef

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14
Q

What is seen with a harsh ejection murmur? Where is it seen? 3

A
  1. Crescendo- decresendo
  2. RUSB
  3. May radiate to the carotid arteris
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15
Q

What is seen with auscultation? 4

A
  1. Harsh ejection murmur
  2. Systolic ejection click
  3. S4
  4. Ao regurgitation murmur
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16
Q

What are the manifestations of severe AS? (Signs) 3

A
  1. Angina
  2. Syncope
  3. CHF
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17
Q

What happens with Angina pectorals (chest pain/ CP)? 3

A
  1. Exacerbated by LVH (most muscle = more O2 demand)
  2. Compressions of intramyocardial arteries from high LV cavity pressure e
  3. Reduced coronary artery perfusion pressure withAS
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18
Q

What is syncope or presyncope (fainting)?

A

Reduced ability of the heart to maintain cerebral perfusion pressure through the stenotic valve

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19
Q

What does syncope or presyncope happen with?

A

Usually with exertion

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20
Q

What are CHF symptoms? 4

A
  1. Dyspnea
  2. Fatigue
  3. Cough
  4. Weight gain (fluid retention)
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21
Q

What is the role of echo is AS? 6

A
  1. Assess AV in 2D
  2. Determine etiology of the stenosis
  3. Exclude other sources of LVOT obstruction
  4. Assess LV size, systolic/ diastolic function
  5. Estimate severity of stenosis
  6. Identify associated valve lesions
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22
Q

In terms of Aortic valve assessment in 2D what do we look for? 5

A
  1. Equal opening/ coapt action of cusps
  2. Number of commissures when open
  3. Coronary implantation
  4. Degree of movement
  5. Morphological changes

cd men

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23
Q

What are some examples of morphological changes? 4

A
  1. Artheroslerosis
  2. Calcium (shadow)
  3. Commissures fusion
  4. Post stenosis dilation

accp

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24
Q

What are some 2D calcific changes we need to take note of when we scan the aortic valve? 3

A
  1. Bright echoes at cusp commissures
  2. How many cusps
  3. The more stenotic the AV is, the harder it is to tell # of cusps
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25
In terms of determining etiology of the stenosis what are the three categories we will look for? 3
1. Congenital 2. Degenerative 3. Rheumatic
26
What is the order of incidence for aortic stenosis etiology? 3
1. Calcific AS 2. Congenital (Bicuspid) 3. Rheumatic
27
For those under the age of 70 with the most common etiology for AS?
Bicuspid and it occurs 50% of the time with AS
28
For those over the age of 70, what is the most common etiology of AS?
Degenerative which occurs 48% of the time
29
What is the epidemiology of calcific/ degenerative etiology? How many of these will develop aortic stenosis?
1. Above 25% of all adults over 65 will have some degree of aortic sclerosis 2. 10-15%
30
M- mode often is ______ but handy when 2D is limited looking for AS
Overlooked
31
Label the M mod for 2 stenosis
1. Leaflet excursion ~2.0cm 2. Diastolic closure line - normally at middle of aortic annulus
32
What does this image demonstrate?
M- Mode with severe AS
33
What do we see with AV sclerosis? 4
1. **Some thickening and calcification** (brightening of the cusps) 2. Slight reduction of cusp excursion may be present 3. CW doppler velocity through AV normal or slightly elevated 4. **<2.5 m/s**
34
What do we see with AV stenosis? 4
1. Most **obvious thickening** and calcification of cusps 2. **Obvious visual reduction of cusp excursion** 3. CW doppler velocity elevated through the AV 4. **>2.5 m/s**
35
What is the ratio of Male to female having bicuspid AV?
3:1
36
What is a bicuspid AV? What does it look like? And how do we get it? 3
1. Only 2 leaflets, or fused leaflets 2. Football shaped 3. May be inherited
37
Bicuspid AV is most common type of AS in patients in what demographic?
Under 50 years old
38
How often do we see Bicuspid AV?
1-2% of the general population
39
What is the structure of the Bicuspid AV? 3
1. Multiple configurations possible 2. Bicuspid with raphe or with raphe 3. **raphe: seam that joins two cusps together**
40
What is the Cuspal fusion rates for the bicuspid valve? 2
1. 85% RCC and LCC 2. 15% RCC and NCC
41
What does this image demonstrate?
Raphe
42
What are some AV findings in a bicuspid AV? 4
1. **Thickened Leaflets** 2. **Eccentric closure** (M-mode) 3. Normal valve excursion 4. **Systolic doming of the larger cusps (PLAX)**
43
What view is best for viewing bicuspid AV?
PSAX
44
What are associated anomalies with Bicuspid valve? 3
1. **Post stenotic aortic root dilatation/ aneurysm/ Dissection** Typically asc dilatation 2. **LVH** 3. Congenital (**coarctation**, other supravalvular narrowing, VSD)
45
What is an eccentric closure line?
When there is a bicuspid AV valve and it pulls the leaflets down and it closes way closer to one side of the LVOT
46
Rheumatic AS is caused by what?
Scarring form rheumatic fever
47
In terms of excluding other sources of LVOT obstruction, what are the three things we look for? 3
1. Subvalvular 2. Supravalvular 3. HOCM
48
What is the possible location of supra- valvular? 2
1. Membrane shelf in Ao 2. Narrowing in ASC/Arch/ Desc Ao
49
What are possible valvular obstructions? 3
1. Calcific 2. Congenital 3. Rheumatic
50
Where are subvalvular obstructions found? 2
1. Membrane 2. Muscular IVS (Hypertrophic cardiomyopathy)
51
What does Subaortic- LVOT obstructions consist of? 3
1. Associated with Hypertrophic cardiomyopathy (HCM) 2. Asymmetric septal hypertrophy (ASH) 3. Systolic anterior motion (SAM) of AMVL *has*
52
When we assess LV size, systolic diastolic function what do we look for? 4
1. Walls 2. LV chamber 3. LV systolic function 4. LV diastolic function
53
When we do a LV assessment what do we look for in terms of the Wall? 3
1. Is there LVH due to high afterload? 2. Measure IVS/ LVPW 3. LV trace PSAX
54
In terms of LV assessment, what do we look for? 2
1. Dilated LV as disease progresses 2. Measure LVID
55
What do we look for in terms of LV systolic function in terms of LV assessment? 2
1. Decreases EF as disease progresses 2. Measure Simpsons EF
56
What do we look for in terms of LV diastolic function in terms of LV assessment?
1. Measurement of diastolic functions
57
What is the AS afterload effect on LV? 4
1. Outflow obstruction >>>> increasing afterload 2. LV Systolic pressure rises 3. To keep SV normal >>>>> increase force of contraction 4. LVH develops (concentric) due to pressure overload
58
What are the hemodynamics parameters for AS severity? 5
1. Peak velocity 2. Mean pressure gradient 3. Aortic valve area 4. Indexed aortic valve area 5. Dimensionless velocity ratio
59
When would we use planimetry?
May be used if doppler parameters are difficult
60
What is a reason why we tend to look away from planimetry? 2
1. Not very accurate 2. Tends to overestimate AVA
61
What do we trace during planimetry?
The orifice in mid systole
62
What is hard to do with planimetry?
Trace calcified valves
63
What does planimetry helps us do?
Produces a valve area
64
What are AV spectral assessment locations? 5
1. **Apical** 2. RT suprasternal 3. SSN 4. **RT parasternal** 5. +/- subcoastal
65
When getting a AV spectral assessment what happens if AV velocity is >2.0 m/s? 5
Always use the Pedro probe (CW) to assess velocities of at least two of the list. 1. Apical 2. RT suprasternal 3. SSN 4. RT parasternal 5. +/- Subcoastal
66
What probe is a blind probe?
Pedoff probe
67
Why would we use a pedoff probe? 3
1. Higher signal to noise ratio 2. Better access to small intercostal spaces 3. Does not bias operator to 2D windows
68
Pedoff is all about getting what degree angle? If we want higher velocities what do we need to do? 2
1. 0 degree angle 2. To get higher, more accurate velocities
69
What is the best window for pedoff?
A5C
70
What is the process for Pedoff probe?
Find the idea view with normal probe, then switch to pedoff
71
When using a pedoff probe what window do we utilize?
A blind window
72
What are some of the blind windows for pedoff probes? Why are these better locations? 3
1. RT parasternal 2. RT clavicular 3. SSN *The highest velocities may be found from any of these locations*
73
When using the blind windows which valves do we use for calculations?
The highest velocities and VTI for calcs
74
In terms of AV spectral assessment locations, how many sample sites and what velocity are we looking for? 2
1. High velocity for multiple views on the same patient 2. Need to sample from multiple views on every AS patient
75
Where does AS and Mitral regurgitation appear on the baseline?
They both appear below the baseline in the approximate region in the apical view
76
Subaortic stenosis will be picked up in which what? How does it look?
1. Picked up in A5C CW 2. Much different spectral profile
77
What does a subarctic stenosis present like? (Velocity wise) 2
1. Late peaking profile 2. Very high velocity
78
What does a severe AS present like spectrally? 2
1. Acceleration = Deceleration time 2. Symmetrical waveform
79
What is the timing like in terms of AS? When is it seen? 4
1. No flow displayed during either isovolumic period 2. Only seen when AV is open 3. Starts later and ends earlier than MR 4. Typically a more pointed profile (V shape) than MR
80
What is the MR timing present like? When is it seen?3
1. Flow seen during both IVCT and IVRT 2. Only seen when MV is closed 3. Typically has a more rounded peak (parabolic) and higher velocity
81
What happens with AS with low EF?
Low EF cannot generate enough force to push the blood out through AV with high gradient/ velocity
82
Gradients will be artificially low with what diseases? 2
1. Ischemia heart disease 2. Coronary arterial disease
83
What does AS with high EF present like?
Higher than normal EF increases force of contraction
84
What are somethings we see with High EF? 5
1. Fever 2. Hyperbole is 3. Pregnancy 4. LV overload due to Mod-sev AI 5. Gradients will be artificially high
2. DMST 283 ECHO 2
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