Pulmonary Oedema
LV Diastolic dysfunction
See diastolic dysfunction and TTE exam for more info.
The LV will either be stiff or dilated or both or its relaxation will be reduced (sepsis, drugs).
It is an important cause of cardiogenic pulmonary oedema even with reasonable systolic function.
Causes
Systolic dysfunction (will always be accompanied by diastolic dysfunction).
IHD
Hypertrophy
- Hypertension
- AS
- Hypertrophic cardiomyopathy
Sepsis (sepsis induced cardiomyopathy)
Inotropes (adrenaline). PDE inhibitors (lusitropes) preserve diastolic function better.
Diastolic dysfunction is diagnosed by estimation of LVEDP. In some circumstances diastolic dysfunction can exist without elevated L heart pressures (hypovolaemia, sepsis).
If LV compliance is reduced the LVED PV relationship shifted up and left so:
- LV can be under filled despite high filling pressures.
- Optimum filling range narrow (under or over filled easily)
Therefore a hypovolaemic LV with diastolic dysfunction will have elevated filling pressures, may respond well to fluid, but will easily be overloaded with pulmonary oedema resulting.
See diastolic dysfunction for more info.
Elevated left heart pressures
In critically ill patients the question you should be asking is not ‘what is this patients diastolic function?’ but rather ‘does this patient have a high LV filling pressure or not, how does this relate to pulmonary oedema and how does it respond to interventions?’. This is just as well as doppler profiles of diastolic filling are determined by:
LV relaxation and compliance
LV preload and afterload
LV interactions (RV, pericardium, lungs)
LV filling pressure
Heart rate
Age
Evaluation of pulmonary oedema
Introduction
Pulmonary oedema is common in critically ill patients.
Echo is useful in distinguishing between cardiogenic (hydrostatic) oedema from elevated pulmonary vascular pressures, and non-cardiogenic pulmonary oedema (ARDS) from capillary-alveolar leak.
Elevated left heart and pulmonary vascular pressures are an important cause of weaning failure.
Echo is therefore very useful in both acute respiratory failure and in weaning failure.
Diastolic dysfunction will always accompany systolic dysfunction.
Hydrostatic pulmonary oedema can exist with normal LV function - AV or MV regurg, volume overload, diastolic dysfunction, mitral stenosis.
ARDS can exist alongside LV systolic dysfunction.
Hydrostatic pulmonary oedema has to be diagnosed by measurement of significantly elevated LV filling pressures whatever the systolic function.
Echo, as well as distinguishing between an ARDS and hydrostatic pulmonary oedema, will often also reveal the underlying cause (RV systolic overload in ARDS and poorly contracting, dilated, LV or severe valvulopathy or LVOT obstruction in hydrostatic oedema).
Direct measurement of LV pressures, while the gold standard, is very invasive. The surrogate of PAOP is often used but TTE provides a simple non-invasive measure.
Doppler
Many doppler indices have been validated in estimating LV filling pressures and show good correlation with directly measured PAOP.
The doppler trace is influenced by other factors such as age, HR and ventricular interactions. Treatment interventions which alter LV loading can also alter the doppler trace (eg initiating IPPV or venodilation can improve LV inflow by preload reduction in a failing heart).
IVRT, E deceleration time and duration of the mitral valve and pulmonary vein A waves are less reproducible than other measures (inter-observer variability).
Em and Vp both reflect the rate of early LV relaxation.
The Em reflects early diastolic relaxation so is more preload independent. Lateral Em is more accurate than septal Em and is more reproducible than Vp (Vp harder to measure accurately). Diagnosis of left ventricular diastolic dysfunction in the setting of acute changes in loading conditions. 2007 Crit Care 11:R43
This means lateral Em is the best measure of intrinsic diastolic function (as it is less effected by other things).
Em normally >15 laterally and <8 with diastolic dysfunction. E/Em <10 normally and >10 with raised LV pressures (although an E/Em of >8 may be more appropriate for elevated LAP in ventilated patients).
The Em velocity is in effect the amount of blood entering the LV while the E is also determined by the driving pressure. Therefore the E/Em ratio can be thought of as how much pressure is needed to move the blood.
While Em reflects early relaxation, the E wave is determined by both relaxation and LV filling pressure.
Calculating the E/Em ratio corrects for the effects of early relaxation to give the most accurate determination of LV filling pressures.
E/Em lateral has been shown in ventilated ICU patients to have a sensitivity of around 85% and a specificity of around 90% for predicting elevated PAOP (threshold value >8).
Simple doppler parameters have also shown good performance in Afib (in spontaneously breathing patients). Several measurements should be taken and averaged.
In conclusion:
Lateral Em is the best measure for assessing underlying diastolic function.
E/Em is the best measure for assessing LV filling pressure.
Treatment
Serial echos are useful. Treatment of hydrostatic oedema will rapidly improve both symptoms and mitral inflow parameters (in severe diastolic dysfunction, where the LV pressure volume curve is steep, it only takes a small increase in preload to overload the LV).
This helps distinguish between ARDS and hydrostatic oedema.
It should also be borne in mind that if the 1st echo is after treatment the doppler profile may not look too bad. This is why it is important to use TDI of the lateral MV annulus (Em) as this is the least load dependent parameter and will remain impaired after other MV inflow parameters have improved.
Suggested algorithm for diagnosing the cause of pulmonary oedema (adapted from Haemodynamic monitoring using echocardiography in the critically ill):
Pulmonary oedema
E/Em <10 Yes ARDS - assess RV
E/Em >10
Impaired LV function yes CCF
No
Significant Valve disease yes valve disease
No
Em <8 yes diastolic dysfunction
No
Volume overload