Anatomy:

PLAX – A2 and P2

PSAX – A1-3 and P1-3. Measure with planimetry if good view.

A4C – A2/3 by septum and P1 laterally

A2C – P1/3 either side and A2 in the middle.

A3C – A2 and P2 (like PLAX)

Papillary muscles – anterolateral and postero-medial (inferoseptal wall).

Myxomatous degeneration – thickened annulus/leaflets with excessive movement.

Primary MR:

Abnormal valve – LV becomes chronically volume overloaded and EF increases.

Significant portion of EF may retrograde flow into LA:

  • ‘Normal EF’ may imply significant impairment

Over time LA and LV dilate, increasing wall stress, increasing chamber and annular dilation which worsens MR.

Most common causes:

  • Degeneration (myxomatous MR) – calcification/MVP.
  • Infective endocarditis
  • Rheumatic/inflammatory/iatrogenic

Secondary MR:

MR without leaflet abnormalities.

Functional/ischaemic

Posterolateral papillary muscle displacement and annular dilation.

Tethering of MV leaflets by displaced PM results in systolic restriction of MV leaflet motion and malcoaptation.

Acute MR:

Flail segment – ruptured papillary muscle of chordae tendinae, leaflet rupture or acute on chronic MR.

Lack of adaptation of LV/LA causes severe haemodynamic compromise, raised LAP and acute pulmonary oedema.


Assessment:

  1. Leaflet appearance – myxomatous degeneration, rheumatic, thickening, calcification.
  2. Leaflet mobility –
    • prolapse/flail
    • restriced systolic/diastolic mobility
    • tethering/tenting
  3. Structural integrity e.g. perforations.
  4. Coaptation
  5. Vegetations
  6. Chordae tendinae
  7. PM integrity
  8. Annular size
  9. Enlarged LA – chronicity Enlarged LV/RWMA/function
  10. Right heart assessment

Doppler:

Proximal isovelocity surface area (PISA)

Based on fluid dynamics principle – as flow approaches a finite circular orifice it forms concentric hemispheric shells with gradual increased surface area and increased velocity.

Forms proximal to MV leaflets.

  • Optimise image
  • Reduce Nyquist limit to 15-40cm/s – practically meaning reduce ‘baseline’ so lower colour limit 15-40, upper often goes up to 90ish.
  • Measure 1st aliasing shell at mid systolic (radius)
  • MR flow rate = product of the surface area and the shell’s aliasing velocity.
  • Surface area = 2πR^2 where R is radius measured.

Effective regurgitatant orifice area (EROA) = (PISA area x aliasing velocity)/MR peak velocity

  • EROA <0.2 is mild and >0.4 is severe.

Colour doppler jet area

How big is jet relative to LA

Nyquist 50-60cm/s

Multiple views to check:

  • jet direction – eccentricity of jet – after disease of contralateral leaflet
  • Mechanism – central, through leaflet, SAM
  • Number of jets

Potential problems:

  • Incorrect settings – lower sampling limit may overestimate severity (nyquist)
  • Eccentricity – may flatten out against wall leading to underestimation
  • Direction of flow jets
  • Entrainment of adjacent blood may overestimate

Vena contracta

Take multiple measurements if possible as it is a small measurement & therefore prone to error.

PW volumetric assessment

SV(MV) = CSA(MV) x VTI (MV)

SV(LVOT) = CSA(LVOT) x VTI(LVOT)

MR(vol) = SV (MV) – SV(LVOT)

MV annulus is measured in A4C.

MR regurgitant fraction:

RF = (MRvol/MVsv) x 100

For regurgitant volume – PW assessment at MV annulus (ie not at leaflet tips):

RV volume = SV(mv) – SV(lvot)

RF = RV/SV(mv) x 100

ROA = RV/VTI(mr)

Pain to measure and not frequently performed on critical care,.

Supporting features

Pulmonary venous inflow pattern

Varies with degree of MR.

Flow occurs during systolic and diastole with systolic wave (S) normally being much larger than diastolic (D)

With increased MR, S wave is dampened below D wave and may reverse.

CW doppler of MR velocity

Assessment of density and shape of doppler signal.

MV inflow

Even minor degree of stenosis/hyperdynamic circulation can increase this.

1.2m/s indicates severe regurgitation.

Dominant A-wave virtually rules out severe MR.

Implication for Critical Care

Dynamic variation can be seen on ITU.

Factors exacerbating MR – due to reduced overall LV work and increased LV afterload:

  1. Tachycardia/arrhythmias
  2. High SVR
  3. Maldistributation shock
  4. Transient myocardial ischaemia – reversible worsens LV geometry and function.
  5. Fluid loading
  6. Any increased myocardial oxygen demand e.g. drug OD/sepsis.

Factors reducing severity of MR – tend to reduce LV workload and afterload

  1. Vasodilation
  2. Haemofiltration
  3. Negatively inotropic sedative drugs
  4. Invasive ventilation/NIV – reduces ventricular loading by opposing RV outflow.

Assessment of severity in critical care is challenging and when sedated/I+V may have minimal MR which becomes severe when weaning/awake.

If failing to wean – repeat echo during spontaneous breathing trial.

Optimise circulation by:

  • Minimise fluid loading
  • Avoid tachycardia
  • Encourage sinus rhythm
  • Vasocilate
  • Avoid high SVR
  • NIV/invasive ventilation to off-load ventricle

In acute settings e.g. PM rupture these factors will be insufficient and surgery required utilising bypass.