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DMST 283 ECHO 2 > Aortic Stenosis > Flashcards

Aortic Stenosis Flashcards

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
Q

In terms of determining etiology of the stenosis what are the three categories we will look for? 3

A
  1. Congenital
  2. Degenerative
  3. Rheumatic
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26
Q

What is the order of incidence for aortic stenosis etiology? 3

A
  1. Calcific AS
  2. Congenital (Bicuspid)
  3. Rheumatic
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27
Q

For those under the age of 70 with the most common etiology for AS?

A

Bicuspid and it occurs 50% of the time with AS

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28
Q

For those over the age of 70, what is the most common etiology of AS?

A

Degenerative which occurs 48% of the time

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29
Q

What is the epidemiology of calcific/ degenerative etiology? How many of these will develop aortic stenosis?

A
  1. Above 25% of all adults over 65 will have some degree of aortic sclerosis
  2. 10-15%
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30
Q

M- mode often is ______ but handy when 2D is limited looking for AS

A

Overlooked

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31
Q

Label the M mod for 2 stenosis

A
  1. Leaflet excursion ~2.0cm
  2. Diastolic closure line - normally at middle of aortic annulus
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32
Q

What does this image demonstrate?

A

M- Mode with severe AS

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33
Q

What do we see with AV sclerosis? 4

A
  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
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34
Q

What do we see with AV stenosis? 4

A
  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
Q

What is the ratio of Male to female having bicuspid AV?

A

3:1

36
Q

What is a bicuspid AV? What does it look like? And how do we get it? 3

A
  1. Only 2 leaflets, or fused leaflets
  2. Football shaped
  3. May be inherited
37
Q

Bicuspid AV is most common type of AS in patients in what demographic?

A

Under 50 years old

38
Q

How often do we see Bicuspid AV?

A

1-2% of the general population

39
Q

What is the structure of the Bicuspid AV? 3

A
  1. Multiple configurations possible
  2. Bicuspid with raphe or with raphe
  3. raphe: seam that joins two cusps together
40
Q

What is the Cuspal fusion rates for the bicuspid valve? 2

A
  1. 85% RCC and LCC
  2. 15% RCC and NCC
41
Q

What does this image demonstrate?

A

Raphe

42
Q

What are some AV findings in a bicuspid AV? 4

A
  1. Thickened Leaflets
  2. Eccentric closure (M-mode)
  3. Normal valve excursion
  4. Systolic doming of the larger cusps (PLAX)
43
Q

What view is best for viewing bicuspid AV?

A

PSAX

44
Q

What are associated anomalies with Bicuspid valve? 3

A
  1. Post stenotic aortic root dilatation/ aneurysm/ Dissection Typically asc dilatation
  2. LVH
  3. Congenital (coarctation, other supravalvular narrowing, VSD)
45
Q

What is an eccentric closure line?

A

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
Q

Rheumatic AS is caused by what?

A

Scarring form rheumatic fever

47
Q

In terms of excluding other sources of LVOT obstruction, what are the three things we look for? 3

A
  1. Subvalvular
  2. Supravalvular
  3. HOCM
48
Q

What is the possible location of supra- valvular? 2

A
  1. Membrane shelf in Ao
  2. Narrowing in ASC/Arch/ Desc Ao
49
Q

What are possible valvular obstructions? 3

A
  1. Calcific
  2. Congenital
  3. Rheumatic
50
Q

Where are subvalvular obstructions found? 2

A
  1. Membrane
  2. Muscular IVS (Hypertrophic cardiomyopathy)
51
Q

What does Subaortic- LVOT obstructions consist of? 3

A
  1. Associated with Hypertrophic cardiomyopathy (HCM)
  2. Asymmetric septal hypertrophy (ASH)
  3. Systolic anterior motion (SAM) of AMVL

has

52
Q

When we assess LV size, systolic diastolic function what do we look for? 4

A
  1. Walls
  2. LV chamber
  3. LV systolic function
  4. LV diastolic function
53
Q

When we do a LV assessment what do we look for in terms of the Wall? 3

A
  1. Is there LVH due to high afterload?
  2. Measure IVS/ LVPW
  3. LV trace PSAX
54
Q

In terms of LV assessment, what do we look for? 2

A
  1. Dilated LV as disease progresses
  2. Measure LVID
55
Q

What do we look for in terms of LV systolic function in terms of LV assessment? 2

A
  1. Decreases EF as disease progresses
  2. Measure Simpsons EF
56
Q

What do we look for in terms of LV diastolic function in terms of LV assessment?

A
  1. Measurement of diastolic functions
57
Q

What is the AS afterload effect on LV? 4

A
  1. Outflow obstruction&raquo_space;» increasing afterload
  2. LV Systolic pressure rises
  3. To keep SV normal&raquo_space;»> increase force of contraction
  4. LVH develops (concentric) due to pressure overload
58
Q

What are the hemodynamics parameters for AS severity? 5

A
  1. Peak velocity
  2. Mean pressure gradient
  3. Aortic valve area
  4. Indexed aortic valve area
  5. Dimensionless velocity ratio
59
Q

When would we use planimetry?

A

May be used if doppler parameters are difficult

60
Q

What is a reason why we tend to look away from planimetry? 2

A
  1. Not very accurate
  2. Tends to overestimate AVA
61
Q

What do we trace during planimetry?

A

The orifice in mid systole

62
Q

What is hard to do with planimetry?

A

Trace calcified valves

63
Q

What does planimetry helps us do?

A

Produces a valve area

64
Q

What are AV spectral assessment locations? 5

A
  1. Apical
  2. RT suprasternal
  3. SSN
  4. RT parasternal
  5. +/- subcoastal
65
Q

When getting a AV spectral assessment what happens if AV velocity is >2.0 m/s? 5

A

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
Q

What probe is a blind probe?

A

Pedoff probe

67
Q

Why would we use a pedoff probe? 3

A
  1. Higher signal to noise ratio
  2. Better access to small intercostal spaces
  3. Does not bias operator to 2D windows
68
Q

Pedoff is all about getting what degree angle? If we want higher velocities what do we need to do? 2

A
  1. 0 degree angle
  2. To get higher, more accurate velocities
69
Q

What is the best window for pedoff?

A

A5C

70
Q

What is the process for Pedoff probe?

A

Find the idea view with normal probe, then switch to pedoff

71
Q

When using a pedoff probe what window do we utilize?

A

A blind window

72
Q

What are some of the blind windows for pedoff probes? Why are these better locations? 3

A
  1. RT parasternal
  2. RT clavicular
  3. SSN

The highest velocities may be found from any of these locations

73
Q

When using the blind windows which valves do we use for calculations?

A

The highest velocities and VTI for calcs

74
Q

In terms of AV spectral assessment locations, how many sample sites and what velocity are we looking for? 2

A
  1. High velocity for multiple views on the same patient
  2. Need to sample from multiple views on every AS patient
75
Q

Where does AS and Mitral regurgitation appear on the baseline?

A

They both appear below the baseline in the approximate region in the apical view

76
Q

Subaortic stenosis will be picked up in which what? How does it look?

A
  1. Picked up in A5C CW
  2. Much different spectral profile
77
Q

What does a subarctic stenosis present like? (Velocity wise) 2

A
  1. Late peaking profile
  2. Very high velocity
78
Q

What does a severe AS present like spectrally? 2

A
  1. Acceleration = Deceleration time
  2. Symmetrical waveform
79
Q

What is the timing like in terms of AS? When is it seen? 4

A
  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
Q

What is the MR timing present like? When is it seen?3

A
  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
Q

What happens with AS with low EF?

A

Low EF cannot generate enough force to push the blood out through AV with high gradient/ velocity

82
Q

Gradients will be artificially low with what diseases? 2

A
  1. Ischemia heart disease
  2. Coronary arterial disease
83
Q

What does AS with high EF present like?

A

Higher than normal EF increases force of contraction

84
Q

What are somethings we see with High EF? 5

A
  1. Fever
  2. Hyperbole is
  3. Pregnancy
  4. LV overload due to Mod-sev AI
  5. Gradients will be artificially high

DMST 283 ECHO 2 (14 decks)

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