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51 Cards in this Set

  • Front
  • Back

1) What 2 valves can repairs be performed on?

2) What artefact to prosthetic valves result in?

1) TV and MV

2) Shadowing as the prosthetic (mech) valves = strong reflector of U/S

3) What is the main aim of developments in prosthetic valve development (mech and bioprosth)

3) to produce a valve which improves haemodynamics, with increased durability and decreased complications

4) What is the most frequently used bioprosthetic valve?

4) Stented xenograph - bovine or porcine

Note - stentless valves = increased EOA

5) What kind of clinical data should be obtained when assessing a prosthetic valve?

5) previous studies, operation info, details of symptoms and findings, type/size of replacement, HR and BP, Ht, Wt, BSA, ?PPM

6) What 2D/ m-mode info should be gathered when assessing a prosthetic valve?

6) Chamber size, LV wall thickness/ mass, LV function, Ao root measurements, Multiple and off axis views, asses the movement and seating of the valve, use TOE if unable to adequately assess

7) What Doppler echo info should be gathered when assessing a prosthetic valve?

7) Similar to assessment of a native stenotic valve; determination of gradients across the prosthesis, EOA, pressure recovery, patient prosthesis mismatch, regurgitation (peri and para prosthetic +/- physiological and abnormal)

8) What equation is used to assess the gradients across the MV?

8) Simplified Bernoullis or extended Bernoullis (when AVR+ increased CO or narrow LVOT = vel prox to prosthesis = increased)

9) What are the 2 equations used to calculate the EOA via the continuity equation?

9) SV.prosth valve = CSA. prox prosthesis x VTI. prosth valve

EOA = SV. pros valve / VTI. prosth valve

10) Where can pressure recovery occur?

10)* downstream from a valve - eg when the Ao is wider then the valve

*withing the valve (bileaflet or ball and cage) - due to the valve having a small central orifice and 2 larger lateral orifices

11) What is the equation to assess patient prosthesis mismatch (PPM)? What values must be proportionate to avoid PPM? What is PPM largely determined by? What are the grades of severity?

11) * gradient = Q^2 / (K x EOA^2)

*Q and EOA

* body size (not similar effect for obese patients - base body size on fat free mass)

* EOA = haemodynamically significant if:

>0.85cm^2/m^2 - mild

0.65-0.85 " " - moderate

<0.65 " " - severe

12) What is the main clinical outcome of PPM?

12) a decrease in long and short term survival and associated LV dysfunction

13) What values need to be recorded/ calculated for doppler assessment of an AVR, PVR, MVR/TVR?

13)*AVR - peak vel, mean gradient, VTI, DVI and EOA

*PVR - peak vel, derived mean press difference

*MVR/ TVR - peak vel, mean pressure gradient, VTI, P1/2T, HR

14) Why is the P1/2T not used to calculate the EOA in an MVR/ TVR?

14) Only used when there is mod-severe stenosis (<1.5cm^2). For large valve areas P1/2T reflects atrial and LV compliance characteristics and loading conditions

15) What are the 2 types of normal regurge seen in a prosthetic valve?

15)* closing vol - displacement of blood caused by the motion of the occluder

* true trivial or mild regurg - at hinges of occluder

Note - there can be a certain amount build in = " washing jets" to maintain a clean valve

16) What/ where is pathological prosth regurge seen?

16) *central - generally bioprosthetic

*paravalvular - around the sewing ring outside the valve = bad (trivial can be ok) - could indicate dishissence

17) What is the challenge when assessing prosthetic valves compared with native valves?

17)* Shadowing from the prosthesis - can use TOE to overcome this

*hard to quantify small jets

*can still used comparative flow measures of Reg vol and reg fraction

18) What is the purpose of echo during/ after valve replacement operation?

18) Check the placement of the valve to avoid later complications, TOE and TTE used, Colour to check for abnormal regurge, prior to a redo, to assess what the issues is - eg pannus or a clot causing the func issues - different treatments

19) What are 2 early complications of valve replacement and there causes?

19) * issues = related to tech difficulties in surgery and early infection

Eg - paravalular regurg, PPM, early thromboembolisum (rare), acute IE

20) What are 3 types of late complications and what causes them?

20) Varies with the ype of prosthesis and risk factors.

Includes - thromboembolisum (dep type of valve +/- AF etc...), pannus, degeneration, IE

Note - pannus and degen complications = less for AVR and greater for MVR or double replacement

Note - other complications for composites eg leaking from conduit attachment point

21) Why are prosthetic valves subject to IE? What occurs with IE?

21) *because they do not have there own blood supply and abnormal motion of blood over them = not protected from infection harbouring

* irregular vegetations grow and attach to the valve - stuff with valve function. Absesses and cavities can also form around the sewing ring --> dishissence

22) What is the difference between pannus and thrombus?

22) * Thrombus = blood clot = more common in mech valves due to increased damage to RBC's - large, soft echo-dencity, may significant interupt the valve

* pannus - smaller, dencer = myocardium growing over the sewing ring and occluding the valve, more common in the aortic position, long term - takes a while to grow / not acute

Note - can occur together

23) When is an SET/DOB used to assess a prosthetic valve? A rise of ____mmHg signifies what for an AVR?

23) *when the patient has extertional symptoms and no resting changes (pain, SOBOE...)

* 15, significant obstruction

Note - reproduction/ significant symptoms with no walls = abnormal valve dynamics

24) What can SOBOE post MVR be caused by? What pressure rise suggests obstruction of the MVR?

24) *primary valve failure, LV+/- RV dysfunc, PHTN, con-cardiac causes


25) Name 3 other techniques used for assessing valve replacements

25) Cinefluroscopy, CT, Cardiac cath

26) What are the 2 best views to asses AVRs from?

26) PLAX and Ap 5C

27) What is the normal velocity across an AVR like? What is this max vel?

28) What occurs with increasing stenosis?

27) *like a mildly stenotic native valve

* 2m/s

Note - >2m/s = suspect dysfunc

28) increased vel and duration of ejection and delayed peaking of velocity during systole

29) What causes an increased gradient in a normal prosthetic valve?

30) What other indicies should be used to assess AVR function and why?

29) small size, increased SV, PPM, valve obstruction

30) Don't rely on flow states alone - use shape of flow curve, EOA, DVI to assess as well

31) What parametres/ info can be gathered from the curve of the flow?

31) If the contour = rounded, mid jet peak, prolonged accel time(AT), prolonged ejection time(ET) and increased AT: ET ratio = AVR stenosis

Note - AT >100ms + AT:ET >0.4 = stenosis

32) How is the EOA of an AVR calculated?

32) EOA.avr = (CSA.avr x VTI.avr) / VTI.avr

Note - EOA depends on the size and type of the inserted valve, significant stenosis if <0.8cm^2. Crucial to measure LVOT correctly

33) What is the DVI? How is it calculated?

34) What is good about the DVI?

35) What is the value that suggest the increasing likelihood of obstruction?

33) * dimensionless ratio of the prox vel in the LVOT : flow velocity through the prosthesis

* DVI = V.lvot / V.avr

34)*less dependent on valve size, good when LVOT = hard to measure, not affected by flow conditions and AR

35) <0.25

36) What changes suggest AVR stenosis?

36) appearance of new murmur with new CHF changes, increased flow velocities >2m/s, pressure recovery changes, DVI <0.25, AT >100ms, DVI <0.3/0.25 + rounded jet = probable obstruction, make sure measurements are accurate

37) Why is it hard to assess AR of AVRs?

37) *jets can be eccentric, multiple jets, different sized jets, trivial = "physiologically normal", para and perivalvular, hard to measure VC, shadowing can obstruct

38)What methods have been used to attempt to assess AVR AR?

38) *Colour - jet area/ width : LVOT.diam

% of parav regurge to assess for dishissence (10% = mild, 20% = mod, >20% sev, >40% = dishis)

* Spec dop (CW and PW) - P1/2T (<200 = sev, >500 = mild), holosys flow in dec Ao = atleast mod, Reg flow = similar to native AR, LV overload present with AR (assess LV size/mass)

39) What is obscured by a prosthetic MV (esp mechanical) and what does this make it hard to evaluate?

40) What views are best to assess the MVR and why?

39) the LA, MR

40) *PLAX - can see more of LA + LVOT

* Apical - see leaflet excursion (can use artefact) detection of thrombus and pannus, paravalv leaks, dop though the valve for flows

41) Name 5 doppler parametres of MVR function that can be obtained.

41) Mitral E, mean Gradient, P1/2T, EOA, DVI

42) What are the cut offs for mitral E and mean gradient for MRV assessment?

42) * earl peak mitral E (E vel) - normal = 1-2.7 m/s, normal mech bileaflet - <1.9m/s, >/= 1.9 = normal with high flow vels*mean grad = normal =< 5-6m/s, dep on type of valve, haemodyn state, PPM, stenosis

43) What are the cutoffs for P1/2T, EOA and DVI assessment?

43) *P1/2T - makred prolonged (>200ms) = clue to obstruction (rarely >130ms)

*EOA (by continuity only) - only bioprosth and single tilting discs are bileaf mech = single small central orifice + 2 large = funnny numbers/ hard to assess

*DVI - VTI.mvr : VTI.lvot ratio, mech <2.2 = norm

44) What are 3 indirect signs that can be used to assess for MVR MR (as imaging is limited by reberb artefact in LA)?

44) hyperdynamic LV with decrease sys output, increased mitral E vel, DVI >2.2, dence CW signal with early sys max vel (>/= 1.9m/s, mean grad >6mmHg), parge PISA, increased PASP

45) What 3 parametres suggest significant MR?

45) well preserved EF (>60%), normal or enlarged LV, relative decrease in LVOT or RVOT SV, jet area <4cm^2 = mild or >/= 8 = mod->sev, VC width (mild 1mm, mod 2mm, large 3-6, >/=6mm), PV reversal, PISA >/= 0.5cm^2

46) Why is the PV/PVR hard to visualise?

47) What are the best views to assess RVOT/ PVR?

48) What compromises EOA calcs/ stenosis assessment?

46) because of its location - anteriorly and superioly

47) PLAX and SAX of RVOT

48) RVOT = funnel shaped, often PA branch stenosis with PV issues therefore conduit done too - connections can be stenotic too

49) How is function evaluated? What are some auxiliary findings that suggest PV dysfunction?

49) *There is lack of standardised values therefore mainly on anatomical assessment (leaflet mobility and structure)

* cusp or leaflet thickening/ immobility, narrowed forward flow colour map, peak vel though PVR >3m/s (>2m/s though homograft), increasing peak vels on serial studies, impared RV func or increased RVSP, RV syst HTN

50) What is seen in severe PR? How is it normally assessed?

50)* vol overlaod of the RV and flattening of the IVS in diastole and paradoxical IVS motion

* Colour assessement (VC, reg jet width), jet width (<25% = mild, >50% = sev), flow reversal in distal main PA, rapid decel by CW or PW, signal dencity

51) What dop parametres are measured for TVR? How can the EOA be calculated?

51) *peak tricusp E, peak tricusp A, P1/2T, mean gradient, VTI

*EOA = SV.lvot / VTI. tvr

52) How is obstruction of the TVR assessed?

52) visualisation of decreased opening of the leaflets and narrow colour signal, E vel >1.7m/s, mean grad >6mmHg, P1/2T >230m/s, enlraged RA and IVC + HV size and flow pattern (= indirect indicators)

53) What are some indirect indicators of TR? What must be considered when using these?

52) * RV and RA dilation, diastolic IVS flattening (vol overload), dilation of IVC and hep vein

*These changes might have occured before TVR

54) What limits assesement of TVR and TR?

55) What parametres of the CW signal are useful indicators?

54) Attenuation caused by reflection of the U/s off the valve (esp is mechanical) - shadowing over the RA

55) signal density and V cut off = significant regurg

56) What is the advantage of TOE over TTE when assessing MVR and TVR?

56) Angle of bean approach re to the valve is reversed therefore direction of shadowing caused by valve is reversed therefore now can see the LA and RA and MR and TR!!

57) Why are prosthetic valves largely avoided in children?

57) because of PPM as the child grows, rapid degeneration and calcification with tissue valves, long term use of anticoags with mech = issues

Note - large use of Ross proceeder (pulm autograft)

58) What can limit prosth valve assessment in peads?

58) multiple surgeries leading to chest wall deformities, often multiple issues - CHD = assessing one thing = hard, must consider the patients size/ body in context of the assessemnt

59) What is likely to occur in pead valve replacements?

60) What are potential pitfalls in calc EOA in peads?

59) pannus and PPM

60) shunts (ASD = decreased flow across MV and AV or PDA - increased flow across MV and AV)

61) What corresponding structures should also be evaluated?

61) Atrial and ventricular size