Ch 1 AoV Stenosis Flashcards
What are the 2 normal heart sounds?
S1 + S2
When is S1 + what causes the sound?
-End diastole
-Due to closure of MV + TV
(best heard at the lower left sternal border + apical region)
When is S2 + what causes the sound?
-End systole
-Due to closure of AoV + PV
(best heard at the 2nd-3rd intercostal space)
Explain S3 in children + young adults?
-Normal finding in children + young adults
-Ventricle capable of normal rapid expansion in early diastole
(best heard at the apex in LLD)
What is S3 known as?
Ventricular gallop
Explain S3 in middle aged + older adults?
-Sign of disease
-Indicates volume overload or increased transvalvular flow
-Due to congestive heart failure + MV or TV regurg
What is S4 known as?
Atrial gallop
When is S4 + what causes the sound?
-Late diastole (coincides with atrial contraction)
-Due to the right or left atria vigorously contracting against a stiffened ventricle
(best heard at the apex in LLD)
What does S4 indicate?
The presence of diastolic dysfunction
Explain the opening snap?
-Is a high pitched sound associated with MV or TV stenosis
-Occurs shortly after S2 + before S3
(best heard at the apex)
What are ejection clicks?
-Extra abnormal EARLY systolic heart sounds
-Occur shortly after S1
-Sounds have a sharp, high pitched sound best heard at the aortic + pulmonic areas (b/c it coincides with the opening of the AoV + PV)
Are S3 + S4 extra diastolic or systolic heart sounds?
Diastolic
What do ejection clicks indicate?
Presence of AoV or PV stenosis
or
Dilatation of the Ao or pulmonary artery
What are mid-late extra systolic heart sounds?
-Bulging of the leaflets into the atrium (MV or TV prolapse)
-Due to systolic prolapse of the MV or TV
-Leads to regurg
What are murmurs?
-Sound generated from turbulent blood flow
-Hemodynamic or structural changes causes laminar flow to become disturbed + produce audible noise
List 4 mechanisms that can cause murmurs?
-Flow across a partial obstruction (AS)
-Ejection into a dilated chamber (aortic systolic murmur associated with aortic aneurysm)
-Regurgitant flow across an incompetent valve (MR)
-Abnormal shunting of blood from 1 chamber into another low pressure chamber (VSD)
Murmurs can be described by what 4 things?
-Timing (diastole, systole, continuous)
-Intensity
-Configuration (shape)
-Location
How many grades of intensity are there to describe a murmur?
6 grades - refer to slide in notes
What are systolic ejection murmurs (SEM) caused by?
-Aortic or pulmonic stenosis
-Dilation of aortic or pulmonic root
(SL valves affected)
When do SEM’s begin + end?
-Begins after S1 + ends before S2
-Is a crescendo - decrescendo (meaning intensity rises than falls)
Where are SEM’s best heard?
AoV: 2nd-3rd intercostal space in RIGHT sternal border
PV: 2nd-3rd intercostal space in LEFT sternal border
What are pansystolic (holosystolic) murmurs caused by?
-MV + TV regurg
-VSDs
(AV valves affected)
When do pansystolic murmurs occur?
-B/w S1 + S2
-Is uniform in intensity
Where are pansystolic murmurs best heard?
Apex region
or
4th intercostal space at left sternal border
What is the m/c example of a late systolic murmur?
MV prolapse (redundant + elongated leaflets bowing into LA)
When do late systolic murmurs occur?
-Mid/late systole to S2
-Is preceded by a mid systolic click
-Is uniform in intensity
Where are late systolic murmurs best heard?
At the apex
What causes early diastolic murmurs?
Aortic or pulmonic regurg
(SL valves affected)
When do early diastolic murmurs occur?
-After S2
-Decrescendo in intensity
Where are early diastolic murmurs best heard?
2nd-3rd intercostal space at left sternal border
What causes mid-diastolic murmurs?
MV + TV stenosis
(AV valves affected)
When do mid-diastolic murmurs occur?
-B/w S1 + S2
-Decrescendo in intensity
-Has an opening snap
Where are mid-diastolic murmurs best heard?
At apex
Give an example of a continuous murmur?
A patent ductus arteriosus
-this is an abnormal congenital connection b/w the Ao + PA
-it has a crescendo - decrescendo in intensity
When are continuous murmurs best heard?
-Throughout the cardiac cycle
-There is a persistent pressure gradient b/w 2 structures during systole + diastole
What 3 things can cause AS?
-Congenital valve disease (bicuspid)
-Post inflammatory process (rheumatic disease)
-Age related calcification
How does AoV stenosis affect our CO?
-The AoV area decreases + LV can not empty as well now (decreases CO)
-LVH develops to maintain CO across stenotic AoV
-LV is less compliant, LVEDP and LV size increases to maintain CO
-LA hypertrophy + increased size occurs to fill stiff LV
List 3 changes to the heart structures when AoV stenosis is present?
-LVH
-LA dilation
-Irreversible changes to upstream cardiac chambers
List 3 symptoms with AS?
-Angina pectoris (chest pain due to CAD)
-Syncope (fainting)
-Congestive heart failure (b/c heart can’t pump enough blood out to meet the demands of the body)
List 2 main fluid dynamics of AS?
-High velocity jet
-Distal flow disturbance
What is vena contracta?
Narrowest region in valve area
The diagnostic features of rheumatic stenosis are ___ + ___?
Commissural fusion + MV involvement
___ is the m/c indication for valve replacement surgery + the 2nd m/c indication for surgery in older adults?
AoV stenosis
SF of AoV stenosis?
-Echogenic leaflets
-Reduced systolic opening
(calcific shadowing + reverb can occur)
Which view do we identify a bicuspid AoV?
2D PSAX AoV level
How does a bicuspid AoV appear in PLAX + PSAX?
PLAX:
-systolic bowing of leaflets into Ao, causing “domelike” appearance
-systolic doming + diastole sagging of leaflets
PSAX:
-will see only 2 open leaflets in systole
-2 leaflets seen with commissures at 4 o’clock + 10 o’clock
The m/c bicuspid valve phenotype is fusion of the ____?
Right + left coronary cusps (70-80%)
(a raphe is seen in the larger leaflet, appears tri-leaflet in diastole)
Accurate identification of AoV leaflets is done in what part of cardiac cycle?
Systole
The l/c bicuspid valve phenotype is fusion of the ____?
RCC + NCC
AS is often associated with dilation of the ___ + ___?
Ao sinuses + Asc Ao
Risk of Ao dissection + rupture occurs if Asc Ao measure > ___mm?
> 45mm
List the most important complications associated with bicuspid AoV?
-Dilation of Ao sinuses + Asc Ao
-Ao dissection + rupture if >45mm
-AoV stenosis (most frequent!)
-Ao regurg
-Infective endocarditis
What kind of surveillance do pt’s with bicuspid AoVs undergo?
Annual imaging, even if no symptoms
Ao rheumatic valve disease is never isolated, what is almost always associated with it?
Rheumatic MV disease
2D findings of rheumatic AS?
-Echogenic leaflets
-Commissural fusion
-Systolic doming of AoV leaflets
List 3 differential diagnosis for LVOT obstructions?
-Fixed subvalvular obstruction
-Dynamic subaortic obstruction
-Supravalvular stenosis
List 3 quantification methods for AS severity?
-Peak Ao jet velocity (best one)
-Mean Ao pressure gradient
-AVA
What is the strongest predictor of the clinical outcome of AS?
The max Ao jet velocity (most reliable + reproducible)
The max Ao jet velocity is the key element in decision making about timing of ___ ___?
Valve replacement
How to obtain Ao velocity?
-CW through AP5 + AP3
-Use pedoff probe in apicals, SSN + right parasternal views
(use pedoff b/c we get higher doppler recordings)
Any doppler angle other than 0 degrees will lead to an over or under estimation of the true velocity?
Underestimation
(do not use angle correct)
What can be mistaken for AS?
-MR
-Subaortic obstruction
How to differentiate AS from MR?
MR:
-Occurs at longer periods during cardiac cycle (during IVCT + IVRT)
-More rounded + less steep
-Higher velocity waveform
AS:
-Occurs at shorter period during cardiac cycle (after IVCT + ends before IVRT)
-Well defined peak with a steeper velocity
-Lower velocity waveform
Pressure gradients can be calculated with what equation?
Bernoulii’s
The AVA continuity equation is based on what?
The conservation of mass
(what flows in, must flow out)
AVA formula?
A1 x V1 / V2
A1 = LVOT from PLAX
V1 = LVOT VTI (Ap5 with PW)
V2 = AoV VTI (Ap5, Ap3, SSN, RPS with CW)
List a main pitfall when evaluating AS?
Getting severe AS by velocity or by pressure gradient, but not by AVA
Due to:
-LVOT diameter being overestimated
-LVOT velocity being recorded too close to valve
Which measurement in the AVA is more prone to pitfalls?
LVOT in PLAX
80% of pt’s with AS also have what?
AR (this results in increased transaortic pressure gradient)
When does LV diastolic + systolic dysfunction occur when AS is present?
Diastolic: early in disease
Systolic: late in disease
What is concentric hypertrophy?
Increase in LV mass due to increased wall thickness w/o chamber dilation
