Most common Western valvular heart disease.
Long latent period from sclerosis to severe LV outflow obstruction.
- Degeneration/calcification of normal trileaflet valve
- Bicuspid aortic valve – responsible for 60% of AVR in <70s.
- Rheumatic – rare in developed world.
Average increase in transvalvular peak velocity of 0.1-0.3m/s per year with reduction in AVA by 0.1cm^2 per year.
Increased LV pressure:
- Reduced compliance causing diastolic dysfunction
- Secondary PHT
- Above leads to increased myocardial oxygen demand and ischaemia – compounded is coronary artery disease preesnt.
- Finally – LV dilation and failure.
Mortality from symptomatic AS = 50% at 2y.
Aim to identify:
- Cause e.g. calcification
- Number of leaflets
- LV function/LVH
- Other valvular pathology
Right and non-coronary cusps visible.
Colour to assess for turbulant flow
M-mode to see movement of leaflets.
Careful measurement of LVOT diameter as LVOT area used in continuity equation.
Identify aortic pathology as it is associated with congenital AV pathology e.g. bicuspid AV.
5% of bicuspid AVs associated with coarctation.
Look for fusion of cusps:
- Left-right cusp fusion
- Right-non cusp fusion
Colour to assess for associated AR.
Optimise image & alignment
Colour flow over entire LVOT
PW in LVOT
CW through AV.
Repeat A5C measurements with A3C to assess/improve accuracy.
Subcostal SAX – if poor PSAX views.
Blind doppler – hunt for maximal velocity. Required for departmental studies. Not required for ACCE.
Used to calculate AVA.
AV area x AV VTI = LVOT area x LVOT VTI
= AV area = LVOT area x LVOT VTI / AV VTI
Relatively flow independent measure.
LVOT VTI / AV VTI
Flow dependent measure.
Assessment of severity:
Can be challenging particularly in presence of reduced LV function as reduces velocity of flow across valve & therefore underestimates severity.
IF AV thickened with Vmax <2.5m/s and normal LVEF – can report as ‘aortic valve thickening with no stenosis’
If Vmax >2.5m/s then following table:
If vmax suggests severe but AVA moderate:
- Due to high flow (pregnancy/AR/anaemia/anxiety etc.
- Measurement errors: PW too far into AV/LVOT too big
- Check measurements
- Further interrogate valve appearance
- Waveform shape – dagger/arched
- Correct for BSA
If Vmax moderate but AVA severe:
- Low flow causes reduced vmax despite severe AS
- Measurement erros
- Need to correct for BSA
- Again – check measurements, interrogate valve appearance, waveform etc.
Low gradient, low flow AS.
- If LVEF is low
- If severe LVH – may have normal LVEF but cavity size is so small that SV and flow are low.
- Severe MS
- Mean gradient <40mmHg
- AVA <1.0cm^2
- one of the following:
- LVEF <40%
- SVI <35ml/m^2
- Flow <200m/s
Dobutamine stress echo is useful in low flow states.
- If true severe stenosis LV function should improve but AS is fixed and severe. Valve gradient will increase but AVA with remain the same or reduce.
- In non-severe cases – AVA will increase as SV increases.
Implication for Critical Care:
In true AS – fixed lesion that can only be altered by surgery.
Maintaining output relies on ‘status quo’ between cardiac work and SVR.
Increasing cardiac work with inotropes leads to increased gradients and therefore reduced cardiac output/systemic perfusion.
Over-vasoconstriction leads to tachycardia, reduced coronary filling time causing ischaemia and reduced cardiac output by reducing ventricular filling time.
Avoid moderate-high doses of inotropes/vasopressors
Low dose vasopressor can maintain constant SVR when using sedatives.
Maintain adequate oxygenation, Hb (e.g. target >100) and fluid volumes.
If over-resuscitated and high ventricular filling pressures – careful offloading may improve CO.
Take over high work of breathing
Avoid sedatives with significant haemodynamic impact.
Aggressive treatment of arrhthmias
Rarely – AVR/valvuloplasty may be required prior to weaning from ventilation.