Over half of patients presenting to ED with cardiogenic pulmonary oedema have normal systolic function.

Diastolic dysfunction may have independent mortality effect in critical illness.

Four phases:

  • Isovolumetric relaxation – energy dependent prior to opening of mitral valve. ATP breaks actin-myosin cross-bridges. Intracardiac pressure drops to lowest point at the end of this phase – minimal LV diastolic pressure.
  • Early filling – second phase accounts for 80% of ventricular filling. Low resting pressure in LV cavity allows easy flow of blood.
  • Diastasis – equalisation of LA and LV pressure. V short/non existent at high rates.
  • Atrial systole – fourth phase as atria contract to fill ventricle. Final 10-20%. Absent during AF.

Assessment:

Qualitative:

Presence of LVH makes diastolic dysfunction highly likely due to impaired relaxation leading to reduced early passive filling.

LA volume reflects effect of raised LV filling pressure.. In absence of left sided valve disease/ASD an enlarged LA volume suggests raised LVEDP from systolic/diastolic dysfunction.

IAS bulging towards right atrium rather than gentle to and fro motion.

Raised PA pressures common – estimating RVSP in patients with TR, mean/diastolic PA pressure in patients with PR and pulmonary acceleration time..

Quantitative:

Transmitral doppler patterns:

1-3mm sample volume PW doppler placed at MV tips in A4C.

Ensure alignment.

First wave (E wave) represents passive movement of blood accross MV into LV during phase 2 of diastolic cycle.

Second wave (A wave) represents active atrial contraction – phase IV of diastolic cycle.

Measure:

  • Peak E wave velocity.
  • Peak A wave velocity.
  • E/A ratio.
  • Time taken for passive filling to decelerate from peak to zero – deceleration time.

Initial sweep speed 25-50mms to look for flow variation with respiratory.

Then increase to 100mm/s to take measurements. Take at end-expiration. Should average over three consecutive cycles.

Grading:

  • Normal
  • Grade 1 diastolic dysfunction: impaired relaxation.
  • Grade 2 diastolic dysfunction: pseudonormalisation – E/A returns to normal as a result of a compensatory increase in LA pressure.
  • Grade 3 diastolic dysfunction: restrictive filling.

Cannot create a full picture as cannot differentiate between normal and pseudonormal. Need to combine with other features.

Pulmonary venous flow

Flow normally forwards in both systole and diastole with short retrograde period of flow during atrial contraction.

Place PW doppler around 0.5cm inside entrance of pulmonary veins. Any vein can be used but RUPV most commonly visualised in A4C.

Measure in end-expiration with sweep speed of 50-100ms averaged over three consecutive cycles..

  • S wave – blood flow into pulmonary veins during RV systole.
  • D wave – blood flow during passive period of LV diastole.
  • a wave – occurs during atrial contraction.

From this can measure:

  • S/D ratio – normally systolic wave is dominant. As LV filling pressure rises this flattens and diastolic waves become dominant.
  • Peak a velocity – usually low and increases with rising LVEDP.
  • a wave duration – lengthens with increasing LVEDP.

Pulmonary venous flow begins to flow significantly towards grade 2 diastolic function and therefore is most useful when pseudonormalisation suspected.

Caveats:

  • Reduced EF – increase in LA pressure likely due to systolic dysfunction.
  • a-A duration is time between duration of a wave and duration of mitral inflow A wave – reliable age and EF independent predictor of increased LVEDP.

Tissue doppler annular velocities (TDi)

Looks specifically at low-velocity movements of ventricular walls adding information about active relaxation.

Enables differentiation between normal function and pseudonormal function. Also can be used in AF where there is no A wave.

Early diastolic velocity known as e’ (e-prime) and represents active relaxation of ventricle.

Occurs 20ms earlier than E wave providing a suction effects for E wave.

In diastolic dysfunction it occurs at the same time/later than E wave.

Studies shown that e’ is a load-independent marker of LV relaxation.

Average of lat/med annular velocities should be used.

As resting LVEDP rises, e’ wave shortens.

Late diastolic velocity is a’, represents myocardial velocity associated with atrial contraction.

Practicality:

  • e’ is compliance of LV in load independent manner.
  • E/A ratio <8 is associated with normal LV filling pressures.
  • E/A ratio >13 is associated with increased filling pressures.
  • Between these values – combine with other features.

Implication for critical care:

Not a steady physiological state as in outpatient clinic.

Snapshot of current loading/afterload influenced by pathology/fluid balance/organ support/drug therapy.

Diagnosis of diastolic dysfunction should only be made 6-8 weeks following resolution of critical illness.

For critical care, independent assessment of:

  • LV relaxation – TDi has been validated as relatively preload/afterload independent measure of LV relaxation. Normal values – 8cm/s at septal & 10cm/s at lateral annulus.. Values below this – impaired LV relaxation.
  • LV filling pressures – can be estimated using E/e’ ratio. Average E/e’ ratio <8 is normal, and E/e’ >13 indicates raised LVEDP. In grey area, ancillary measures can be used.

These two factors are not directly related in this physiological state.

Management is challenging:

  • Avoid precipitating factors.
  • Treatment of any underlying causes.
  • Treatment of physiological sequelae.
  • Identify acute illnesses associated with diastolic dysfunction e.g. hypoxia, MI, hypertension, tachyarrhythmias.
  • Rationalise ITU therapies associated with diastolic dysfunction e.g. mechanical ventilation & vasopressors.
  • Cautious use of fluids – treat overload with vasodilators, diuretics or CVVH. Raised LV filling pressures can be treated with NIV.

Weaning from mechanical ventilation:

Observe patient’s cardiovascular response to a spontaneous breathing trial looking for features predictive of weaning failure such as:

  • tachycardia
  • hyper/hypotension
  • pulmonary oedema.

Withdrawal of PPV causes:

  • Increased venous return.
  • Increased LV afterload.
  • Decreased LV compliance.
  • Propensity to coronary ischaemia.

Can look at LV compliance and filling pressures prior to and during a SBT. Those who successfully wean have:

  • Higher rate of LV relaxation (e’) on baseline TTE.
  • Significant increase in rate of relaxation during SBT.
  • Lower LV filling pressures.

LV filling pressures rise, usually from a higher starting point, in those who fail.

80% prevalence of impaired LV ventricular relaxation in those who fail to wean.

Effect is seen even in the absence of LV systolic dysfunction.

Evidence suggests that an E/e’ ratio measured 10 min into SBT of >14.5 predicts weaning failure with sensitivity of 75% and specificity of 95.8%