2015 Ase Guideline - Lv Diastolic Function - Recommendations And Referrence Values

Front 1

1) What are 2 major indications that diastolic function / dysfunction are related to?

2) and you have normal syst func and diast dysfunc?

Back 1

1) SOB and or HF

2) yes

Front 2

3) What are the 4 pressures included under the umbrella term "LV filling pressures"? What are they closely related to?

Back 2

3) *mean pulm wedge pressure, mean LA pressure, LVEDP, pre A LVEDP

* Change in a predictable progression with myocardial disease such that LVEDP increases prior to the increase in LAP

Front 3

4) Optimal performance of the LV depends on its ability to cycle though 2 states. What are these 2 states? What are the 2 functions of the LV?

Back 3

4)*a) compliant chamber in diastole = filling of the LV from the LA. b) stiff chamber (rapid increase in pressure) in systole - ejection of SV at arterial pressure

* Systole and diastole

Note - the SV must increase with demand with out a huge rise in LAP

Front 4

5) When does diastole start? What 4 steps does it include?

Back 4

5) * at AV closure

* LV pressure fall, rapid filling, diastasis (at slower HRs), atrial contraction

Front 5

6) What is the main physiological consequence of diastolic dysfunction?

Back 5

6) Elevation of LV filling pressures....considered elevated when mean pulm wedge pressure > 12mmHg and LVEDP > 16mmHg

Note if exercised induced increase LVFP = limits exercise

Front 6

7) What are LV filling pressures determined by?

Back 6

7) *mainly -filling and passive properties of the LV wall

* + futher modulated by - incomplete relaxation and variation in diastolic tone

Front 7

8) What is relaxation? Is it active or passive?

Back 7

8) *process whereby the myocardium returns after contraction to its unstressed length and force. Normal hearts with a normal load = nearly complete at minimal pressure.

*contraction and relaxation = same molecular process - therefore is controlled by load, inactivation and asynchrony - ie is active

Front 8

9) How does increased afterload (pressure) or late systolic load (esp when combined with increased pre load) delay myocardial relaxation?

Back 8

9) by contributing to an increase in filling pressures

Front 9

10) Myocardial relaxation is an active process in which coupling and cross-bridge detachment of muscle fibre proteins. What is an essential molecule for this process? What is dys-synchrony due to?

Back 9

10)* calcium

* due to deleterious interactions between early re-extension in some segments and post systolic shortening of other segments --> delayed global LV relaxation and increased LV filling pressures

Front 10

11) What is the TAU?

Back 10

11) Widley accepted invasive measure of the rate of LV relaxation

Front 11

12) LV filling is determined by the interplay between LV filling pressure and filling properties. What are filling properties? Describe them.

Back 11

12) *Stiffness (change in pressure/ change in vol) = determined by myocard cell (eg titin) and interstitial matrix (fibrosis)

*compliance (change in vol/ change in press) = aka - end diastolic properties

Front 12

13) Name 2 extrinsic and 2 intrinsic properties that affect end diastolic properties.

Back 12

13) *extrinsic - pericardial restraint, ventricular interaction

*intrinsic - myocardial stiffness, myocardial tone, chamber geometry, wall thickness

Front 13

14) Name 4 structural or functional heart parameters that correlate with diastolic function (ie assess these because they give clues and extra information about what is going on)

Back 13

14) LVH, LA vol, LA func, PASP and PADP

Front 14

15) Why is it important to assess for LVH? What is a common cause of LVH? What happens to the LV myocardium that leads to diast dysf?

Back 14

15) *common and important reason for VLH

*HTN or decreased EF

*fibres get bulker and therefore are slower to stretch out and relax --> increased filling pressures

Front 15

16) Why is the LA volume so clinically important? What does it reflect? What is the indexed cut off volume?

Back 15

16) * Because of the significant relationship between LA remodelling and echo indecies of diastolic function.

* Dop vels and time intervals reflect filling pressures at the time of measurement, where as LA vol often reflects the cumulative effects of filling pressures overtime.

*>/= 34ml/m^2 = indep predictor of death, HF, AF and ischaemic stroke

Front 16

17) What is the function of the LA?

Back 16

17) *modulates LV filling though its reservoir, conduit and pump functions.

*act as reservoirs when AV valves are closed in systole and isovol relaxation time

*act as a pump which contributes to maintaining adequate LV vol actively emptying at the end of LV diastole (at onset P wave)

*actively and passively empties

Front 17

18) What is impaired LV relaxation associated with re LA?

Back 17

18) = lower early diastolic AV gradient and a decrease in LA conduit volume, while the reservoir-pump complex = enhanced to maintain optimal LVEDV and SV

Front 18

19) The presence of what, in symptomatic patients, may infer increased LVFP in the absence of pulmonary disease?

20) what is the equation used to calculate PASP?

Back 18

19) increased PAP

20) PASP = 4 V.tr max vel ^2 + RAP

Front 19

21) What 2 factors can be used to derive the PADP? what is the equation?

22) How is the RAP derived?

Back 19

21) *end diastolic velocity of the pulm reg jet + RAP

* PADP = 4 V.end diast vel pulm jet^2 + RAP

22) by assessing the IVC diameter and collapsibility

Front 20

23) When is PADP higher then pulm wedge pressure?

Back 20

23) When PVR is > then 200 dynes.s.cm^2 or mean PAP > 40mmHg

Front 21

24) Name 3 ways to optimise the mitral inflow signal.

Back 21

24) Use CW doppler first to ensure the highest velocities are obtained, 1-3mm sample vol, sample vol at leaflet tips, colour to help align, optimise 2D gain etc..., 100m/s sweep speed to measure

Front 22

25) Where is the sample volume placed for the total mitral inflow VTI? What is it also known as?

26) What is mid-diastolic flow? Why is it important to realise?

Back 22

25) At the MV annulus, atrial filling fraction

26) Flow that occurs between the E and the A wave on the mitral inflow spectrum. Low levels are normal however >/= 20cm/s = marked delayed LV relaxation and elevated LVFP

Front 23

27) What happens to E, E/A, DT and A values with age?

Back 23

27) E and E/A = decrease

A and DT = increase

Note - age related changes my present as slowing of the myocardial relaxation = predisposes ageing to diastolic HF

Front 24

28) Name 4 variables that can affect mitral inflow.

Back 24

28) LV diastolic function, LV filling pressures, HR and rhythm, PR interval, CO, mitral annular size, LA function

Front 25

29) What are the main 2 factors use to identify mitral inflow patterns and haemodynamics?

30) What are the 4 classification of diastolic function?

Back 25

29) E/A ratio and DT

30) normal, impaired relaxation, pseudonormal filling, restrictive filling

Note - less common = triphasic

Note - most abnormals = elderly with severe long standing HTN or HCM

Front 26

31) What does the E wave represent?

Back 26

31) *Early diastolic filling of the LV

*Reflection of LA-->LV pressure gradient in early diastole

*Affected by - preload and alteration in LV relaxation

Front 27

32) What does the A wave represent?

Back 27

32) *Atrial contraction / late diastolic filling

* LA --> LV pressure gradient in late diastole

* Affected by - LV compliance and LA contractility

Front 28

33) What does the DT of the E wave represent?

Back 28

33) * The time from the peak E velocity to 0 flow at mid diasole

* Influenced by - LV relaxation, LV diastolic pressure following MV opening, LV compliance (relationship between LV pressure and vol)

Front 29

34) Alterations of _____ or _____, _______ recoil +/- LV _______ pressure directly affect mitral inflow velocities ( ______ + _____) and time intervals (________ and ________)

Back 29

LVESV, LVEDV, Elastic, diastolic, E, A, DT, IVRT

Front 30

35) For what cardiac disease do PW mitral inflow variables and filling patterns correlate better with ?

Back 30

35) DCM - correlated better with filling pressures, functional classifications and prognosis then LVEF

Front 31

36) What does a short IVRT and DT + increased E/A vel = ?

37) What does a psudo normal or restrictive pattern + MI indicate ?

Back 31

36) advanced diastolic dysfunction (if with increased LAP = worse function classification)

37) increase risk of; HF, unfavorable remodelling, cardiovascular mortality - despite LVEF

Front 32

38) When do mitral inflow values correlated poorly with haemodynamics?

39) A restrictive pattern + LA enlargement + normal EF is seen in what 3 conditions? What kind of prognosis does it have?

Back 32

38) CAD or HCM with LVEF >/= 50

39) * DCM, amyloidosis, heart transplant

* Poor

Front 33

40) Why have there been additional measures for assessing LV diastolic function developed?

Back 33

40) Because - LV filling pattern = same-ish in normal and abnormals - easy to distinguish when LV sys func is down (decreased LVEF) but harder when it is not. Other factors making mitral inflow values harder to interpret = sinus tachy, systemic disease, arrhythmias and first degree AV block

Front 34

41) Why doe FDAVB and sinus tachy make in the mitral inflow signal hard to interpret?

Back 34

41) = partial or complete E and A wave fusion + DT not measurable

Note - if mitral inflow vel at the start of the A wave >20cm/s, A wave vel may be high and = decreased E/A ratio. IVRT not affected when waves fused

Front 35

42) What does atrial flutter do to the mitral inflow signal? What is the best indicator of PAP in this case?

Back 35

42) *= rapid atrial contractions = no E, A, E/A or DT. Multiple A waves to 1 E wave

* TR velocities (if no lung disease)

Front 36

43) What is the valsalva maneuver? What does it do?

44) What can the maneuver help distinguish?

Back 36

43)* forced expiration against a closed glottis.

* Complex haemodynamic process involving 4 phases = decreased LV preload

44) normal from pseudo normal diastolic filling

Front 37

45) What is pseudonromal diastolic filling profile caused by? How does the valsalva maneuver help assess it?

Back 37

45) * caused by mild- mod increase in LAP in the setting of delayed myocardial relaxation

* valsalva = decreases preload --> mitral inflow changes to impaired or normal pattern

Front 38

46) How does the psudonorm filling profile change with valsalva if the underlying pattern is normal or impaired ?

Back 38

46) *normal = both E and A decrease proportionally = no change in E/A ratio

*Impaired = decrease E vel with long DT, A = untouched or increased --> decreased E/A (decrease of >/=50% = specific for increased LVFP)

Front 39

47) What is one major limitation of the valsalva maneuver?

Back 39

47) not everyone can perform an adequate one - a decrease of 20cm/s in peak mitral E = usually considered adequate effort in patients without restrictive filling. LAck of reversibility with valsalva = imperfect as an indicator of diastolic filling pattern

Front 40

48) Name 4 things that must be done to optimise pulmonary venous flow doppler signal.

Back 40

48) use RUPV, 2-3mm sample vol, > 0.5 cm into the RUPV, decrease filter settings, 100 m/s sweep speed, end expiration

Front 41

49) What measures are taken from the PV trace?

Back 41

49) * S = peak sys vel (above baseline)

*D = peak diastolic vel (above baseline)

*S/D ratio

*Peak A reversal velocity (below the baseline, late diastole)

*A reversal duration

*A.reversal - A duration

*DT of D wave

Front 42

50) When is there 2 S waves? Which one is used to compute S/D ratio?

Back 42

50)* When the PR interval = prolonged

*S1 = atrial relaxation - influ by changes in LAP, LA contraction and LA relaxation

*S2 = used to compute the S/D ratio - related to SV and pulse wave propagation in PA tree

Front 43

51) What is the D velocity influenced by?

Back 43

51) Change in LV filling and compliance

Note - changes in parallel with mitral E vel

Front 44

52) What is the A reversal duration influenced by?

Back 44

52) Late diastolic pressure, atrial preload and LV contractility

Front 45

53) A decrease in LA compliance and an increase in LAP = ________ in S vel, ________ in D vel, a S/D ratio < _____, systolic filling fraction < ______% and what of the DT?

Back 45

53) decrease, increase, 1, 40, shortening (usually <150ms)

Front 46

54) What does an increase in LVEDP cause?

55) What does AF do the the PV signal?

Back 46

54) Increased A reversal vel, increased A reversal duration, Increase A reversal - mitral A duration

55) Blunting of S wave and absents of A reversal vel/ duration

Front 47

56) Which waveform of the PV signal is dominant in normal you people ? What increases with ages?

57) What is a normal A reversal value and what does an increase A reversal value indicate?

Back 47

56) D, S/D ratio

57) = 35cm/s, > 35 = increased LVEDP

Front 48

58) What causes a decrease in S velocity of the PV signal?

59) What limits the accuracy of PV flow profile?

Back 48

58) decreased LA compliance and increased mLAP

59) EF > 50%, AF, MV disease, HCM

Front 49

60) The A reversal - A wave (mitral) duration = the only indicator of what?

61) What is the first haemodynamic abnormality seen with diastolic dysfunction?

62) an A reversal - A duration value > then ____ indicates an increased LVEDP

Back 49

60) age-inderpendent indicator of LV A wave pressure increase

61) increase in LVEDP

62) 30m/s

Front 50

63) What 2 rhythms make it hard to assess PV flow profile?

Back 50

63) AF and FDAVB

Front 51

64) How is colour m-mode of flow propagation velocity achieved? What measurements are taken from the trace?

Back 51

64) *m-mode placed though the center of the MV in 4C view, colour box over the LV, shift colour baseline up until spectrum = blue ~ >50cm/s Nyquist limit)

* measure the slope of the first aliasing velocity during the early diastolic filling phase

Front 52

65) What markedly changes the early diastolic filling wave of the colour m-mode trace?

Back 52

65) a decrease in LV relaxation or LV failure

Note - normally the early filling E wave propagates rapidly towards the apex and is driven by a pressure gradient between the LV base ---> apex = suction force attributed to the LV restoring forces and LV relaxation

Note - MI and HF = slowing/ decrease suction forces

Front 53

66) What is Mitral E/ Vp velocity proportional to?

67) What gives a false normal Vp?

68) what is a normal Vp velocity?

Back 53

66) LAP

Note - therefore used to predict LV filling pressures with IVRT

67) Patients with normal EF +/- normal LV volumes but abnormal filling

68) > 50cm/s

Front 54

69) Where is the Vp measured from?

Back 54

69) from the plane of the MV --> 4 cm distally into the LV

Front 55

70) How is DTI for diastolic functional assessment imaged?

71) what are the main measurements take?

Back 55

70) apical 4 C view, cardiac crux and late MV annulus, optimise scale, optimal dop cursor alignment, sweep speed 100m/s

71) crux - e' (early diastolic) and a' (late diastolic)

lateral - lat e'

Note - can also get e' accel, DT intervals, accel and decel rates, time interval between QRS complex and onset of e' (prolonged in imp LV relax)

Front 56

72) What are the 2 most common ratios these values are used for?

73) What affects e'?

Back 56

72) * e'/a'

*E/e' - important role in estimation of LVFPs

73) LV relaxation, Preload, syst func, LV minimal pressure

Front 57

74) What is e' used to correct for in patients with cardiac disease?

75) What are the main haemodynamic determinants of a'?

Back 57

74) for the effect of LV relaxation on mitral E vels. E/e' = used to predict LVFPs

75) LA sys func and LVEDP - therefore increased LA contractility = increase a', increased LVEDP = decreases a'

Front 58

76) Irrespective of ____ - e' velocity is decreased and delayed occurring at the ___-___ pressure cross over point.

77) What occur earlier with psudonormal or restrictive filing?

Back 58

76) LAP, LA-LV

77) mitral E vels

Front 59

78) What is the influence of increasing age on the DTI values?

79) The E/e' ratio is used to draw inferences about LV relaxation and LV filling pressures. What are the cut offs for normal, intermediate and increased LVFP by E/e'?

Back 59

78) *decrease - e'

*increased - a' and E/e'

79) *normal - <8

*intermed - 8-15 - use additional measures

*increased - > 15

Front 60

80) List 2 instances where annular velocities and E/e' should not be used

Back 60

80) *normal subjects

*significant annular calcification, surgical rings, MS or MVR = decreased e'

*where there is mod-severe first degree MR + normal LV relaxation due to increased flow acceleration though the reg valve = increase e'

*constrictive pericarditis = annulus paradoxus - septal e' higher then lateral e'

Front 61

81) When is systolic strain expressed as % shortening or % radial thickening?

82) What is meant by the term strain rate?

Back 61

81) shortening - when done in log axis, radial thickening when done is SAX

82) the speed or myocardial shortening/ thickening

Front 62

82) What do + and what do - strain valves indicate?

83) What 2 methods are used to obtain strain measurements?

Back 62

82) + = lengthening/ thickening

- = shortening/ thinning

83) DTI and speckle tracking (better as less angle dependent)

Front 63

84) What information about diastolic function does strain provide?

Back 63

84) Regional diastolic strain rate to evaluated diastolic stiffness during stunning and infarction. Timing of transition from myocardial contraction to relaxation = id of ischaemic segments

Front 64

85) What causes LV torsion/ twisting?

Back 64

85) * due to obliquely orientated muscel fibers in the subepicardium which course towards the apex in a counter- clockwise direction. Sub endo fibers spiral anticlockwise

Front 65

86) When does twisting and untwisting occur? and what causes each?

Back 65

86) * Diast untwisting = late systole (mainly in IVRT) - finishes at MV opening. Caused by elastic recoil of fibres = LV suction effect = filling. A decrease = diast dysfunc (not the only cause of diast dysfunc)

*Syst twisting = wringing affect pushes all blood out into Ao from apex to base

Front 66

87) What is responsible for prolonging the IVRT?

Back 66

87) decreased myocardial relaxation --> decreased LVP during IVR phase = longer time before LVP drops below LAP = delay MV opening = prolonged IVRT

Front 67

88) What 2 other measures can be used to directly estimate LV relaxation?

89) What are 3 surrogate measures of LV relaxation?

Back 67

88) *AR CW signal - short P1/2T,

*MR CW signal- V cut off of MR signal = increased LAP and rounded slow accent and decent of MR signal below baseling = LV sys dysfunc and inpaired relax

89) mitral inflow vels, DTI annular signals, Vp via colour m-mode

Front 68

90) a lat e' < ____ and/ or a septal e' < _____ = impaired myocardial relaxation

Back 68

90) 8.5, 8

Front 69

91) What is a direct method for calculating LV chamber stiffness? What are 2 surrogate measures of LV stiffness?

Back 69

91)* diastolic pressure curves

* DT of mitral E vel - increased stiffness = shorter DT

*A wave transition time = generated by atrial contraction - press vel wave enters LV -> moves though LV inflow tract -> reflects off apex -> Ao. Relates to LVEDP

Front 70

92) Whey does exercise increase diastolic dysfunction and symptoms?

93) What happens to E/e' ratio in normal and dystol dysfunc patients with ex? + DT?

Back 70

92) Because increase in filling pressures needed to maintain adequate LV filling and SV

93) *normal = proportional increase = E/e' unchanged. DT slight decrease

*dysfunc = e' increases = increased E/e' = increased LVFPs. DT shortens >50ms

Front 71

94) When is it important to exclude pericardial disease?

95) What happens to filling pressures in constrictive pericarditis?

Back 71

94) When assessing for ? HF

95) Mitral inflow pattern = pseudonorm/ restrictive, E/A >1, Short DT, Mitral E vel >/= 25% with expiration + HV = prominent diast flow reversal in expiration+ annulus paradoxos

Front 72

96) What velocities increase in patients with pulmonary diseased during inspiration?

97) What helps distinguish constrictive pericarditis from restrictive CM?

Back 72

96) SVC and IVC velocities

97) preservation of vertical excursion - septal e' >/= 7

Note - limited if there is significant annular calcification

Front 73

98) What does MS affect?

99) What changes does primary MR cause?

Back 73

98) Transmitral flow gradients

99) LA and LV enlargment, increased compliance of both LV and LA --> attenuation of LAP

Front 74

100) What changes are seen in the mitral inflow parametres in the presents of mod/ sev MR?

101) An increase/normal or decreased EF has a good correlation with E/e' representing filling pressures

Back 74

100) increase peak E and decreased sys flow wave (PV flow) and S/D ratio

Note - MR can = mitral and pulm flow changes that mimic advanced diastolic dysfunc

101) decreased EF

Front 75

102) What measures can be used when a patient has MR and normal EF?

Back 75

102) A reversal to mitral A time interval, IVRT, IVRT:T.E-e'

Front 76

103) Where is there impaired mitral filling with PHTN?

Back 76

103) Because of decrease LV filling NOT diast dysfunc

Front 77

104) What is the difference between the mitral inflow parametres in a person with PTHN and diast dysfunc 2ndary to PHTN?

Back 77

104) *PHTN = normal lat e', normal E/E' (<8)

*2ndary = increase E/e' - mitral E increased due to increased LAP, lat e' decreased because of myoc diseaase

Note - successful decrease in PVR = increased CO = LV filling reverts to normal = increased E/e'

Front 78

105) What happens to the mitral A vel in MS?

Back 78

105) Increases >1.5m/s

Front 79

106) When does diastolic dysfunction normal develop in cardiac disease? What kind of prognostic marker is it? What parameter is a strong indicator of significant cardiovascular events?

Back 79

106)*early

* good one

* E/e'

Front 80

107) What are the main indicators of abnormal relaxation?

108) What are the main indicators of decreased operating compliance?

Back 80

107) IVRT and Isovol or early diastolic annular motion or LV strain rate

108) Mitral E DT, A wave transition time, LVEDP: LVEDV, surrogates of increased LVEDP (mitral A wave duration, decreased a', prolonged Ar duration in PV flow)

Front 81

109) What are indicators of early diastolic LV and LA pressures?

Back 81

109) E/e' ratio, DT of mitral E in decreased EFs, LA enlargement (reflects chronic not acute pressure changes)