• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/93

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

93 Cards in this Set

  • Front
  • Back

----------------------------- A S ----------------------------------


1) What is the most common cause of AS?


1) BAV with superimposed calcification or calcification and rheumatic changes in tricuspid valves.




Note - BAV's account for 50% of the reason for an AVR

2) What needs to be described when assessing the anatomy of the AV with 2DE?

2) id # of leaflets, describe mobility, thickness and calcification of leaflets, determine level of obstruction

3) Describe BAV and the types of BAV. What is meant by the turn 'raphe'?


3) Most often = fusion of RCC and LCC = large anterior and small post cusp.


80% = both CAs arise from the anterior leaflet, 20% = RCC and NCC fusion


rare = LCC and NCC fusion


- only 2 commissures and only 2 cusps seen in systole


* Raphe = fusion line where 2 cusps join

4) Describe degenerative calcification of the AV and grades of AV calcification.


4) Calcification focused at the central part of each cusp.


*mild - few areas of dense echo with little acoustic shadowing


mod - more areas of dense echo + shadowing


sev - extensive thickening and increased echogenisity with prominent acoustic shadowing



5) Describe rheumatic AS. What is the difference between rheumatic AS and degenerative AS?


5) Characterised by commissural fusion, triangular orifice in sys, calcification along edges of leaflets, MV nearly always affected as well




* degen = middle of cusps affected


rheumatic = commissures and leaflet edges affected

6) Aortic stenosis can occur at points other then the valve. What are these points and briefly describe them.

6) The site of stenosis is base on the detection of increased velocities by CD or PW dop.


*Subvalvular - fixed discrete membrane of musc band = haemodyn's similar to obstruction at the leave of the valve


*dynamic - eg in HCM. Obstruction changes severity during vent ejection, prominent mid-late sys, obstruction varies with loading conditions


*supravalvular = rare, due to CHD's

7) Why is assessment of the AV so important ?

7) Especially with the advent of pericutaneous AV implant (TAVI etc...) anatomical assessment is increasingly important for patient selection and intervention planning
8) What are the 3 main ways to assess AS?

8) Jet velocity, Mean transaortic pressure gradient, valve area
9) What is meant by the term jet velocity? How is it measured and from which windows?


9) * Antergrade sys vel across the narrowed AoV


* measured with peadoff CW probe


* suprasternal, right parasternal, apical 4C, subcostal, right supraclavicular




Note - for calculations always take window with the highest velocity

10) What is CD useful for?




11) What is CW used not PW?


10) Useful in detection of jet direction and orientation and to avoid MR signal when placing Doppler line of site.




11) higher signal to noise ratio, more sensitive, no aliasing with high velocities, smaller footprint = can get better windows and angulation

12) List 3 things that are important to do to the spectral Doppler display in order to optimise it.




13) What part of the spectral trace should be measured for CW signal?

12) Optimise gain, 100mm/s sweep speed, increase wall filter, the vel curves should be smooth with dense outer edge and clear background




13) the modal velocity - outer edge with no fuzz



14) How can the shape of the spectral Doppler signal tell us?

14) Shape is helpful in distinguishing the level and severity of obstruction, the time course of vel signal = similar for fixed obstruction at any point.


*Severity of obstruct increased if the max vel occurs late in systole and the curve is more rounded


*mild obst - peak in early syst, triangular peak


*sev obst - rounded signal, mid sys = up gradient though out syst

15) What additional information can the shape of the signal tell us?


15) Also helpful in determining if the obst is fixed or dynamic.


*Dynamic = characteristic late peaking vel curve +/- often concave upward curve in early systole

16) What does the transaortic pressure gradient represent? How is it calculated?


16) *The difference in pressure between the LV and Ao in syst


*From velocity info - peak grad obtained from peak vel - calculation of mean and average vel in syst from this

16) How is the aortic pressure gradient and max gradient calculated?


16) *4V^2 (simplified Bernoullis)


* 4Vmax^2

17) How is the mean gradient calculated?

17) Calculated by averaging instant pressure over the ejection period - trace the outline of a spectral trace = VTI (vel time integral)
18) What is the clinical equation "simplified Bernoullis" derived from? What assumptions are made?


18) *Derived from the complex/ extended Bernoullis


* Assumptions = viscous losses and accel effects are negligible, uses an approx. for constant that relates to the mass dencity of blood (= a conversion factor for measurement units), assumes prox vel can be ignored (reasonable if prox vel <1)

19) When would you need to use the extended Bernoullis equation? What is this equation?


19)* When the prox vel >1.5m/s or the aortic vel <3.0m/s prox vel needs to be included in the equation




* Extended equation = 4 (Vmax^2 - Vprox.vel^2)




Note - generally only use max vel and gradient clinically as extended equation = mean + increased chance for error

20) Name 4 sources of error for pressure gradient calculations.


2) - malignant jet of U/S beam


- Recording MR jet


- neglection of increased proximal velocity


- Any underesti of aortic vel = even greater underesti in gradients due to squaring of the value in the equation

21) What are 2 concerns when comparing velocities obtained by Doppler to those obtained in the cath lab?


21) a) peak grad calcs are from max dop vel which therefore represents instantaneous pressure gradient across the valve NOT the difference between peak LV and Ao pressure


b) Phenomenon of pressure recovery

22) Briefly describe what pressure recovery is. What are favorable conditions for pressure recovery to occur?
22) conversion of potential energy to kinetic energy accross a narrowed cale = increased velocities and decreased pressure. Distal to the stenosed orifice = flow decel again and pressure increases (ie "pressure recovers")

* greatest in stenosed valves with a widening of the artery post the stenosis eg AS with AoRoot and asc Ao dilation

24) How can pressure recovery be calculated?




25) Pressure recovery is basically a ratio of what to what?

24) PR = 4V^2 x (2EOA/AoA) x (1-EOA/AoA)




25) EOA to AoA




Note - a relatively small AoA + EOA is required to create a relevant gradient favouring PR

26) When should pressure recovery be taken into consideration?

26) When assessing patient with Asc Ao <30mm or if the patient has congenital AS




Note - when asc Ao <30mm - initial pressure drop LV -> VC by dop measure may be significantly higher then pressure drop across the stenosis and therefore represent a pathophy relevant measure

27) Vel and pressure gradients are dependent on what? What happens for a given orifice area when flow rate increases or decreases?

27) *flow


*increases = increase in vel and gradient


*decreases = decreases in vel and gradient

28) When is AVA a helpful calc? What is the calc of AVA based on? What is the equation?

28) *AVA = helpful with flow rates are very high or very low


* Continuity equation - all blood going through the LVOT must got though the stenotic AV orifice so the SV must be the same on both sides




* AVA= [(CSA.lvot x VTI.lvot)/ VTI.av]

29) What is essential for accurate AVA calcs? How is this achieved?

29) Accurate LVOT diameter and VTI measurements. Very important that the VTI velocity is taken from the same point as the LVOT diameter is measured. LVOT becomes more elliptical further into the LV - calcs based on circular CSA.



30) Where and how is the LVOT diameter and LVOT VTI measured?

30) * LVOTd - inner edge ---> inner edge, mid systole, zoom, 3 beats to average, optimise picture, at same leave LVOT VTI taken


* LVOT VTI - PW, just prox to the AV, apical 5 C window, trace the model velocity

31) Why is miss measurement of LVOTd such an issue when calculating AVA with the continuity equation?




32) Why is measuring the LVOT Vel far from the valve an issue?

31) Because it gets squared in the equation which exaggerates the error (LVOTd = prone to interobserver error)




32) Because accuracy of the SV method assumes laminar flow with a spatially flat profile of flow, velocities get skewed the further from the valve you measure the vel

33) What are 2 theoretical concerns when using the continuity equation as a reliable parameter to predict clinical outcomes and make clinical decisions?

33) * The continuity equation measures the effective valve area (EVA) ie the area that the flow stream passes though NOT the anatomical area (EVA = smaller)


* Observed changes in AVA change with changes in flow rate eg decreased EVA with LV dysfunction as decreased driving pressure to open cusps

34) What is it important to do when performing a serial study assessing AVA?

34) Ensure that measurments are taken from the same spot and if anything has changed find out why. Make note of heart rate and rhythm as well as BP (ie flow rate changing changes AVA)

35) What are 3 alternative measures that can be used to measure AS severity?

35) Simplified Bernoullis, Velocity ratio, Planimerty

36) Explain the simplified Bernoullis measure.

36) Based on the concept that in a native AV stenosis the shape of the vel curve in the LVOT and the AoV = similar therefore equation =




AVA = [(CSA.lovt x V.lvot) / V.av]




Note - less well accepted

37) What are the units for the Vel ratio? What is the equation for the ratio? What are the valves fro a totally normal valve and a severely stenosed valve?

37) * It is dimensionless


* Vel ratio = [V.lvot / Vav]


* severe <0.25 (ie 25% normal valve area)


* no stenosis = 1 (100% normal valve area)

38) What is planimetry? What are some major limitations? What view is it performed in?

38) * Direct visualisation and measurement of the valve orifice


* inaccurate when valve heavily calcified due to shadowing... + high inter observer variability


*SAX AoV level

39) Name 8 states that can co-exist with AS that can affect the assessment of AS

39) LV systolic dysfunction, Stress echo, LVH, HTN, AR, MV disease, increased CO, Asc Ao dimensions/ dilation

40) What is mean by "low flow, low gradient AS"? What is a Dob stress echo useful for in this case?

40) = EOA <1cm^2, LVEF <40%, mean press gradient <30-40mmHg - because LV cant generate pressure enough to open cusps therefore = stenotic.


*DSE helps differentiate between severe AS + LV sys dysfunc and Mod AS with another cause of LV dysfunc

41) In sev AS + sys dysfun of LV what is the LV dysfunc due to and will replacing the valve fix the issue?


41) due to an increase in afterload caused by the stenotic AV --> LV failure and decreased EF


* Replace the valve = fix the LV dysfunc




Note - not the same for mod AS + other cause of LV sys dysfunc. - EOA is small coz LV = stuffed eg from MI = RMWAs

42) A person with a decreased EF but AS vel of 4.0m/s and a mean gradient of 40mmHg does not have what?

42) poor LV func - the vent = demonstrating normal response to increased afterload/ sev AS - vent func will improve if the stenosis is fixed


43) What are reliable findings when using DSE to assess "low flow, low gradient AS"?



43) - Increased AVA to a final area of >1cm^2 = not severe stenosis


- Sev stenosis if >4.0 (AS jet) or >40mmHg + AVA = 1.0cm^2 at any flow rate


- absents of contractile reserve




Note - SET = samething/ type of assessment

44) Why are the vel and mean gradient lower then expected for a give AVA (even when there is sev AS) for people with LVH?

44) LVH = small LV cavity and diastolic dysfunction. LHV due to AS or chronic HTN.

45) in ___ to ___% of cases AS is accompanied by ____. An increase in the pressure load of the LV = changes in _____ and _____. What should therefore always be recorded?

45) 35, 45, HTN, Flow, EF, BP at time of testing



46) AR is present in ____% of adults with AS. Generally the AR is only ___ to ___ and therefore does not affect measurement of AS. What happens if AS is severe?

46) 80, mild, moderate.


* IF severe = increased trans aortic flow rate = max vel and mean gradient will be higher then expected for a given valve area

47) What can MV disease be due to in the presents of AS? What is it important to distinguish between re MV disease? What what three parameters should be estimated from TR jet velocity and RAP?




48) What 2 confounding factors affect the assessment of AS re MV disease?


47) *consequence of LV overload or concurrent MV disease (ie Rhumatic valve disease)


* weather it is primary or seconday


* LV size, LVH, LV syst and diast func




48) * severe MR - will make transaortic flow low = low gradient even with AS present


* increased vel MR jet may be mistaken for AS jet

49) What does an increased CO cause? What condition can lead to miss diagnosis? What can help id severity in this case?


49) * causes increased flow gradients in mild- mod stenosis


* LVOTO


* shape of spectral CW signal (early peaking = severe)

50) Why is it important to assess the asc Ao size?

50) timing of intervention, pressure recovery considerations

51) What is a normal AVA in adults? What is a severely stenosed AVA in adults?




52) What is indexing AVA for BAS controversial?


51) 3-4 cm, =1.0 cm (25% of normal area)




52) Because valve area does not increase with excess body weight

53) A max jet velocity of 4m/s = a mean gradient of ~____mmHg = ____ AS, and a max jet velocity of 3m/s = max gradient of ~ _____mmHg = ____ AS


53) 40, sev, 20, mod




Note - the relationship between peak and mean gradient deps on shape of vel curve which varies with stenosis severity and flow rate

54) What is the likely cause of an AS vel > 4m/s and an AVA >1.0?

53) increased output state, mod-sev AR, large body size (double check measurments eg LVOTd...)
55) What is the likely cause for AS vel = 4m/s and AVA = 1.0cm?


55) Decreases CO state, small body size, severe MR


(check measurements, evaluate for decreased trans-aortic flow gradient (inc MR severity), assess LV syst func/ EF, DES if EF <55%)

------------------------------- M S --------------------------------




1) What is MS the most frequent complication of? What is the mech of this disease in causing MS?

1) *Rheumatic fever


* mainly = commissural fusion


*Other = chordal shortening and fusion, leaflet thickening, superimposed calcification --> restricted leaflet motion of the leaflet tips

2) Describe degenerative MS. What is if frequently associated with?


2) Mainly annular calcification, Generally no haemodynamic consequences (can have some MR if leaflets are involved or restricted), bases of leaflets involved


* Age, HTN, atherosclerosis and AS

3) Name 3 other causes of MS

3) Congenital (malformation of the supravalv apparatus), inflammation (SLE), influtrative, carcinoid, drug induced leaflet thickening and restriction

4) Name the 5 indicies for assessing MS severity

4) Pressure gradients, MVA planimetry, P1/2T, Continuity equation, PISA
5) What is the diastolic pressure gradient derived from? What method is used to obtain the max velocity?


5) * From the transmitral flow velocity flow curve using the simplified Bernoullis (4V^2)


*CW Doppler + PW at the level of the leaflets and at the level of the valve = VTI - ap 4C window

6) What is colour used for in detection of MS severity by pressure gradient method?




7) What 2 factors influence the max gradient?




8) Name 3 factors that affect transmitral flow.


6) location of the jet and orientation of the jet (? eccentric or not?)




7) LA compliance and LV diastolic function




8) HR, CO, MR



9) What is the advantage of MVA planimetry? What does it best correlate with? When should it be measured? What can make this an un reliable measure?

9) * Is a direct measure of the MVA - no assumptions


*Anatomical orifice


* mid diastole in SAX view


* poor technique, heavy calcification of the leaflets = hard to define orifice

10) What is the P1/2T? What is the P1/2T inversely proportional to? How is it obtained?


10) * the time interval in milliseconds between the max mitral gradient (early diastole) and timepoint where the gradient = 1/2 the max initial value


*MVA ie; MVA = [220/(P1/2T)]


*tracing the decal slope of the E vace of the dog spec CW signal used to get MS gradient

11) In patients with decreased LA compliance and NO MS - what can happen to the P1/2T?

11) shorten/ decrease like in MS - frequently occurs with the elderly so take into consideration when assessing MS
12) What is the continuity equation based on? What is the equation?

12) * The conservation of mass theory


* MVA = [pi (D.lvot^2/4) (VTI.ao/ VTI.mv)]




Note - there is increased error with this method as there is multiple measurements that need to be done

13) What is the PISA method based on? What is the equation?


13) * Based on the hemispheric shape of converging diastolic mitral flow on the atrial side of the MV


* MVA = [(pi r^2/ Vn) / V.max mitral]



Note - can then x by opening angle of the MV leaflets and / by 180 to angle correct ---> method no recommended due to increased error due to multiple measurements and angle correction


14) Name 2 other factors that must be considered when assessing MS.


14) * Valvular anatomy + supra valvular apparatus anatomy eg - chordal shortening, commissural fusion...


* Associated lesions eg - LA enlargement, associated MR, other valvular disease (eg with rheumatic fever)

15) What is SET useful for in patients with MS?
15) For patients who's symptoms are equivocal or discordant with severe MS
16)What are the best methods for grading MS? When are PISA and the continuity method used?


16)*mean gradient and valve area using Planim and P1/2T


*only when the above are no good

17) How do you assess a combined MS and TR lesion? When is intervention recommended for a combined lesion?


17) *rest and ex tolerance + mean grad velocities


* When there is Mod MR and MS symptoms

18) What is a normal MVA? MS tends to be symptomless with an MVA greater then what?


18) * 4-5 cm


* > 1.5 cm



19) What would be the main reason for considering significant MS with an MVA <1.5?




20) What happens when MS is referenced to BSA?

19) CO becomes subnormal at rest and fails to rise with exercise




20) Severity of MS is overestimated in obese people

21) What is a specific sign of Rheumatic valvular disease of the MV?

21) commissural fusion and "hocky sticking of the anterior leaflet of the MV
22) What is a balloon commissurotomy?

22) Cath balloon used to un-fuse/ tear the MV commissure back apart

------------------------------- T S ---------------------------------




1) Name 4 causes of TS. What is almost always present? What does this lead to and why?

1) *TS = rarest stenotic lesion - can be caused by carcinoid, Rheumatic fever, CHD, endocarditis (assc with pacemaker or valve), pacemaker induced adhesion, lupis valvulitis, mech obstruction by tumor.


*TR


* increased RAP due to increased transvalvular gradient

2) What 4 things are you looking for when assessing the anatomy of the TV?

2) Thickening/ calcification of the leaflets, restricted mobility and doming, decreased leaflet separation at peak opening, RA enlargement, valvular obstruction

3) What is the use of colour in TS?

3) assessing presents, direction and qualitative assessment of TS.

4) In regards to the doppler assessment of a stenotic valve what are the hallmark doppler changes?

4) *Increase in transvalvular velocity by CW doppler,


*peak inflow though the valve = normal = rarely >0.7m/s - in TS = >1.0m/s and may approach >2m/s in inspiration


*increase in tricups inflow with inspiration = normal,

5) What is the mean pressure gradient range for TS derived from the simplified Bernoullis equation? What is it lower then?

5) * 2-10mmHg (higher if combined with significant TR)


* MS

6) what are the 2 primary consequences of TS?

6) 1 - elevation of RAP


2 - Dvl of right sided congestion

7) What is clinically more relevant for assessment severity and decision making?




8) Can P1/2T be used for assessment of TR/ TS?

7) TR assessment




8) Yes but not validated.


Generally - longer the P1/2T = greater the TS severity, >190 frequently associated with critical stenosis

9) Can the continuity equation be used to assess TS? What are its limitations?




10) A valve area of = ____m/s = severe TS despite/ irregardless of TR

9) Yes, theoretically. SV and tricuspid inflow velocity VTI can be recorded by CW. In absence of TR can obtain SV from R or LVOT.

*Main limitations = TV annular diameter measurement, obtaining accurate measurements of the inflow vol passing though the TV


10) 1


Note - as severity of TR increases = less accurate/ underesti of TS

11) Is there much standardised data on TS assessment?

11) No - therefore important to use multiple measures and assess from all angles/ assess anatomy

------------------------------ P R ---------------------------------




1) What is the common site at which PS occurs? What is a common axillary finding?

1)* Valve (can also occur (less commonly) at the RVOT due to RVH or above the valve/ PA ST junction).


* RVH



2) What is the most common cause of PS? Name 2 less common causes of PS.

2) *PS = almost always congenital - PV leaflet abnormalities eg Bi or Uni cuspid valves.


*Can also, less commonly, be caused by - rheumatic fever, carcinoid disease, tumor compressing RVOT

3) Name 3 congenital conditions that PS can be associated with.

3) TOF, complete AV canal, double outlet RV, univentricular heart.




Note - peripheral PS may co-exist with PR in noonans and williams syndrome

4) PS can occur proximal to the PV (below the PV). What can prox PS result from?

4) *Can be congenital or acquired.


*Congenital - re to a VSD +/- RVOTO secondary to dvl of mid cavity obstruction or infundibular musc band/ double chamber RV


*Other + acquired - RVH, Iatrogenic (post surgery...), HCM, infiltrative processes (glycogen storage disorder), compression from tumor or vasc structure



5) Where can distal (above valve) PS occur?

5) Mainly in the pulm trunk at the bifurcation or more distally in the branch vessels. Rarely membrane just above the valve.




Note - generally isolated findings

6) Name the 4 way/ methods use to assess PS severity.

6) Transpulmonic pressure gradient, valvular anatomy, assessment of assc lesions, alternative indicies of severity

7) What is the transpulm pressure gradient derived from? What views can the relevant doppler signal be obtained from?

7)* CW doppler signal + simplified Bernoullis equation


* SAX or PLAX +/- subcostal view

8) in what situations would the modified Bernoullis equation not be appropriate for calculating the pressure gradient?

8) When there is supravalv or infundibular stenosis or when there is pulmonary stenosis as a part of a congenital disorder or as a result of RVH

9) Is it possible to detect the site of stenosis if there are multiple in series? What technique could be used?

9) *Not really (???there may be significant PR with increased doppler gradient compared with the net pressure decrease across both stenoses)


*PW could be handy

10) What is useful when separating dynamic from fixed PV obstruction?

10) The signal shape = late syst peaking with "dagger shaped" jet for dynamic stenosis


*fixed = peak vel develops in early systole

11) Why is pressure across the valve the method of choice for assessing PS? What is the peak jet vel and peak gradient for a) mild, b) mod and c) severe PS?

11) * Because the PV area = very hard to obtain




*mild - a) < 3 m/s


b) < 36 mmHg


*mod - a) 3-4


b) 36-64


*sev - a) >4


b) >64

12) What are some other indicies that can be used to assess PS?

12) *Determination of RVSP from TR vel and esti RAP,


*PASP should = RVSP - PV pressure gradient


*When there are multiple stenoses in RVOT/ pulm tree the measured PV gradient fails to account for much of RVSP = clue

13) What is the normal morphology of the PV leaflets?

13) Thin, mobile and dome-shaped

14) What are the most common result of PS regarding changes in chamber anatomy?




15) What is the normal and abnormal wall thickness of the RV?

14) * severe PS --> RVH --> RV enlargement --> RA enlargement


*Dilation of the PA beyond the valve




15) Normal = 2-3mm


abnormal = >5mm

-------------------------- Ref. values ---------------------------




1) What is the a) Ao jet vel, b) mean grad, c) AVA, d) AVA indexed to BSA, and e) vel ratio for aortic selerosis, mild, mod and severe AS?

1) *Ao sclerosis - a) </= 2.5, b) - , c) - , d) normal = 3-4cm, e) -


*mild - a) 2.6-2.9, b) <20, c) >1.5, d) >0.85, e) >0.5


*mod - a) 3-4, b) 20-40, c) 1-1.5, d) 0.6-0.85, e) 0.25-0.5


*sev - a)>40, b)>40, c)<1, d)<0.6, e) <0.25

2) What are the findings indicative of significant TS?

2) * mean press grad - >/= 5mmHg


* inflow VTI - >60 cm


*P1/2T - >/= 190ms


*valve area by continuity - </= 1cm^2


* enlarged RA >/= mod


* dilated IVC