Causes:

Highest incidence still Rheumatic fever.

Others:

  • Calcification
  • Congenital abnormalities
  • Inflammatory conditions e.g. RA, post MV surgery, abnormal serotonin metabolism (e.g. carcinoid).

General:

Normal MV area = 4-6cm2 with no measurable gradient.

Haemodynamic consequences:

  • Pressure gradient between LA and LV
  • LA becomes grossly enlarged, pulmonary hypertension common.
  • RVH, TR, raised RAP & R heart failure.

Assessment:

Appearance:

PLAX & PSAX views

Leaflet mobility and shape in diastole.

Thickening/calcification

Subvalvular involvement.

Associated features & consequences

MV area:

PSAX – find max excursion.

Inner area traced & valve area measured.

May be unreliable as relies on geometric alignment – 3D echo may help.

Pressure 1/2 time:

Time taken for transmitral pressure to halve from its peak value.

Measured in A4C view with CW – try to align flow with colour doppler.

If there are two peaks, trace the flatter of the two.

In AF, take multiple measurements as in diastolic assessment.

Relationship between MVA and P1/2t is:

MVA(cm^2) = 220 / p1/2t (m/s)

Mean gradient (mmHg):

Same image as above but trace around signal.

Underlying formula:

Pressure gradient = 4 x velocity^2

Limitations:

P1/2t affected by abnormal LA/LV compliance.

High resting LV pressure e.g. LVH/AR with shorten P1/2t and overestimate valve area.

ASD shortens P1/2t and offloads blood, overestimating valve area.

Presentation & reasons for decompensation:

Symptoms of fatigue/breathlessness normally start at MVA <1.5cm^2

Fixed CO state therefore patients have minimal reserve in situations where CO is augmented by volume or a change in cardiac rate/rhythm e.g. sepsis/pregnancy.

Presentations:

  • Haemoptysis due to PHT/vascular congestion/sudden haemorrhage due to rupture of thin walled dilated bronchial veins.
  • Thromboembolism – often cerebral due to AF, low or reduced CO and dilated LA/appendage.
  • Infective endocarditis.
  • Right sided heart failure – may also be precipitated by intubation & ventilation.

Implications for Critical Care:

Avoid tachycardia – reduced LV filling time/raised RA pressure, increasing RH strain and precipitating pulmonary oedema.

Active phase of diastolic filling is essential for maintaining CO – therefore AF may lead to acute decompensation.

Rate control with B-blockade/Ca channel blockers essential.

Rhythm control important but may be difficult due to severe LA enlargement.

Balloon mitral valvotomy or surgical MVR is only definitive therapy.