Left Atrial Pressure

Left Atrial Pressure

Dr Steve Lobaz

Consultant Anaesthetist and Intensivist.
Barnsley Hospital

Left atrial pressure

Raised left atrial pressure (LAP) may be due to pre-existing systolic or diastolic dysfunction, mitral valve disease or aortic valve disease. During critical illness there can be acute rises of the LAP due to myocardial ischaemia, sepsis, volume overload, stress induced cardiomyopathy. (1) 

Ultrasound can be used as a non-invasive investigation to help differentiate between cardiac causes of pulmonary oedema (CPO) (due to a raised LAP) and non-cardiogenic causes of pulmonary oedema (NCPO) e.g. ARDS. It can also help assess fluid tolerance and aid weaning from mechanical ventilation. 

Assessment of left atrial pressure uses the same technique as assessing for diastolic dysfunction. Diastolic dysfunction has been shown to increase mortality in sepsis, increase weaning failure and affect outcomes post cardiac and non-cardiac surgery. (2)

It is worth noting that applicability of diastolic assessment in the critically ill patient is still uncertain, this is because most data and validation of methods has been performed on stable, spontaneously breathing patients in outpatient clinics. Diastolic dysfunction (or heart failure with preserved ejection fraction (HFpEF)) is due to impairment of relaxation of the left ventricle and as the severity increases the left atrial pressure rises.

In the critical care patient with unstable haemodynamics, critical illness and often mechanically ventilated the assessment is used to determine left atrial pressure. Recent studies comparing non-invasive echo LAP estimation vs invasive PAOP in the critically ill patient have shown ASE/EACVI algorithms predict elevated PAOP ≥18mmHg with a sensitivity and specificity of 74%. (3)(4)

The Intensive Care Society (ICS) FUSIC-HD group in 2021, developed a pragmatic algorithm for estimating LAP.

This algorithm combines lung ultrasound with a more detailed assessment of LAP, through measurement of early mitral valve (MV) inflow velocity (E & A waves).  A raised LAP risk profile can then be determined: low, intermediate, and high risk.  Normal LAP is 6-12mmHg, whereas high LAP is typical >25mmHg, causing pulmonary oedema.

Patients with an ‘Intermediate’ LAP risk profile, measurements of left atrial (LA) size, tricuspid regurgitation velocity maximum (TR Vmax) with pulsed-wave doppler (PWD) and tissue doppler imaging (TDI) to determine early LV diastolic lengthening (e’), may provide additional information that can stratify LAP risk further.

LAP assessment algorithm (FUSIC HD 2021)

Left atrial physiology

Step 1

B-lines

  • See FUSIC-Lung page for more detail on how to scan for B-lines.
  • Typical features of Cardiogenic Pulmonary Oedema (CPO): bilateral and symmetrical. Often gravitational, homogenous distribution.  Increased number of B-line with increasing severity.  Lung sliding is present.  Pleural effusions may be present in severe pulmonary oedema.
  • Typical factures of Non-Cardiogenic Pulmonary Oedema (NCPO): may be bilateral or unilateral B-lines, peripheral, patchy and often non-gravitational. Lung sliding usually present but may be diminished.  Pleural line may be irregular, thickened with subpleural consolidations evident.

Interventricular septal movement

  • In Apical 4ch and PSAX view, assess interventricular septal movement.
  • The presence of B-lines AND septal bowing into the right atrium (RA), indicate a high probability for raised LAP (High LAP) and presence of cardiogenic pulmonary oedema (CPO) causing dyspnoea.
  • If BOTH B-lines and Septal Bowing into the RA are NOT present, move down the algorithm to assess the MV inflow pattern.

INSERT video of fixed bowing IVS LA to RA

Step 2

Diastolic function

To understand the MV inflow pattern, it is important to revisit the cardiac cycle and to focus on changes in LV volume and LA/LV pressure during diastole (diastology). 

The LAP waveform is very similar to the RAP waveform; but the a and v waves are larger due to lower compliance within the LA.

Diastole is an active, rather than a passive, process requiring energy. In diastole the left ventricle relaxes and rapidly descends pulling in blood. 

Advancing age and critical illness may cause the ventricle to stiffen, causing relaxation to be impaired. Impaired relaxation causes an increased LAP and decreased LV filling.   Higher venous pressures are required to fill the atria and ventricle, resulting in increased risk of pulmonary oedema and hypoperfusion due to venous congestion and associated low stroke volume.

Diastolic impairment may occur in patients with either a low or normal systolic function / ejection fraction.

4 stages of diastology

  1. Diastole starts when the AV closes. Isovolumic Relaxation occurs, which corresponds to the mid-end of the T-wave.  Here, the LV does not change in volume, but there is relaxation of myocytes, so intraventricular pressure falls.

  2. The 2nd phase of diastole is when blood flows rapidly from the LA to the LV, due to this pressure gradient – Rapid LV Filling.

  3. When the pressure inside the LV equalises the pressure in the LA, no flow occurs. This 3rd phase is called Diastasis.  This phase finishes when atrial contraction occurs.

  4. Atrial Contraction or Systole – this final 4th phase corresponds to the P-wave. Atrial contraction or kick causes a rise in LA pressure (LAP), increasing blood flow from the LA to the LV.  When pressure in the LV equalises the LA pressure, the MV then closes and diastole finishes: LV end-diastolic pressure (LVEDP).

Assessing diastolic function

E/A ratio

PWD can be used to measure the velocity of blood flow and therefore the volume of blood, through the MV into the LV during diastole.

The largest volume of blood and therefore velocity, passing between the LA and the LV, is during early diastole where there is rapid ventricular filling. This blood velocity produces a wave on PWD, which is called the E-wave. 

During diastasis, no flow occurs, therefore the MV flow velocity pattern falls close to zero.

Following Atrial Contraction, a further volume/velocity of blood travels through the MV. This atrial kick produces another wave on PWD called the A-wave.

Analysis of the MV inflow velocity pattern (E and A waves) can help determine if diastolic impairment is present and its severity.

Measuring MV inflow velocity

  • First, obtain the apical 4 chamber (A4Ch) view.
  • Position the PWD cursor at the level of the MV leaflets, as they open in diastole. Colour flow doppler (CFD) may be used to help determine the best cursor position.
  • Acquire the PWD image and save for analysis.

Analysis of MV inflow velocity

  • Use the ECG to help identify diastole.
  • The E-wave occurs between the T-wave and the QRS complex. The E-wave is always preceded by a negative deflection, the S-wave, where velocity of blood is in the opposite direction during systole (below the baseline).
  • The A-wave is often the easiest to find and is located just before or on the QRS. There is no A-wave present in patients with atrial fibrillation.
  • Measure and save the peak velocity of the E-wave and the A-wave.

Interpreting the measurements

Revisiting the LAP risk algorithm, if the E/A ratio is <0.8, then LAP is probably normal (low risk).  

If the E/A ratio is 0.8-2 (or >2 in a young patient or if LV hyperdynamic) they are intermediate risk for raised LAP and further assessment is needed.

If E/A >2 in a patient over 40 without a hyperdynamic LV then they are high risk for a raised LAP. 

Diastology explained

Diastolic function can be classified by the ASE (American Society of Echocardiography) into four categories:  Normal, Grade I Impaired Relaxation, Grade II Pseudonormal and Grade III Restrictive.  

Grade I Diastolic Dysfunction (Impaired Relaxation)

LV relaxation is impaired but NOT stiff.  Passive filling of the LV in early diastole is reduced, with a higher volume of blood left over for atrial systole.  At atrial contraction in late diastole, a greater volume/velocity of blood passes through the MV, producing a taller A-wave than the E-wave (E/A reversal).  Here E/A ≤0.8.  LAP is generally normal due the large A-wave, despite an increase in LV pressure.

Grade II Diastolic Dysfunction (Pseudonormal)

LV pressure is higher for the same level of volume, due to impaired LV relaxation and the LV becoming stiffer, less compliant.  For blood to flow between the LA and LV, LAP must now be higher to re-establish an early diastolic gradient.  Increased LAP results in pseudonormalisation of the E/A ratio, with a higher E-wave compared to the A-wave, giving an E/A >0.8 – <2.0.  The MV inflow pattern looks like the normal inflow pattern and is called a pseudonormal pattern. 

Pseudonormal MV inflow pattern and the Valsalva manoevre:

A Valsalva manoeuvre can sometimes be used, to help distinguish if a MV inflow pattern is truly normal or pseudonormal. 

During a Valsalva, intrathoracic pressure is increased, reducing venous return to the LA, decreasing LV filling and therefore LV pressure.  In a patient who has normal diastolic function, the decrease in preload, preserves the E>A pattern. 

However, in patients who have a raised LAP in the presence of impaired LV relaxation, the decrease in preload caused by the Valsalva, lowers LAP and blood flow, which then unmasks elevated LV pressures and underlying impaired LV relaxation, reversing the E>A pattern to A>E.  (Dokainish H, 2015. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4374097/)

The MV inflow at peak Valsalva in a patient with normal diastolic function the E/A <0.5 and E>A normal pattern remains.  However, if there is diastolic dysfunction the E/A >0.5 and A-wave is greater than the E-wave (A>E).

Grade III Diastolic Dysfunction (Restrictive)

The LV filling pressure is high due to a very stiff LV. High LAP forces the MV to open early.  However, despite this, there is rapid equilibration between the LA and LV, with the high resting LV diastolic pressure resulting in a rapid deceleration time of E, and very high E>>A restrictive filling pattern with E/A >2.0.

If the E/A >2.0 and the patient is >40yrs old and their LV not hyperdynamic, there is a very high probability for the presence of high LAP being present (High Risk).

In the presence of restrictive diastolic dysfunction, a Valsalva manoeuvre may help distinguish between an irreversible and reversible restrictive filling.   The Valsalva will decrease preload, therefore in an irreversible restrictive filling pattern, E>>A will not change, whereas in a reversible restrictive filling pattern, a pseudonormal or impaired relaxation pattern will be seen, due to the increased intrathoracic pressure decreasing LAP.

Step 3

Intermediate LAP risk and further assessment

When E/A is 0.8 – 0.2, or the E/A >2.0 and the patient is <40yrs old or their LV is hyperdynamic (Intermediate Risk), further assessment is required to determine raised LAP risk.

Intermediate Risk can be evaluated further by assessing:

  • LA size
  • TR Vmax
  • E/e1. 

LA dilatation and elevated TR Vmax provide evidence of longstanding dysfunction and would not be expected acutely.  2 or 3 low risk features are suggestive of low LAP risk, whereas 2 or 3 High risk features are suggestive of high LAP risk.

Left atrial (LA) size

LA enlargement occurs due to elevated LAP or an increase in blood flow.

The degree of LA enlargement depends on LA wall compliance and presence of atrial fibrillation (AF). AF causes scarring of the LA wall which can lead to and/or exacerbate dilatation.

Disproportionate enlargement of the LA in relation to the LV in athletes, may be suspicious of underlying myocardial disease.

Left atrial size assessment

Visual assessment or ‘Eye-balling’ of the LA can be done. In the PLAX view the LA, aortic root and the right ventricular outflow tract are normally all a similar size – if the LA appears larger than the other 2 then it is likely dilated.

In the PSAX or A4Ch the inter-atrial septum can be assessed for bowing towards the RA.  

LA Diameter is considered dilated in the PLAX view, if >45mm in women and >50mm in men and is high risk for raised LAP.

Measure when the LA is at its largest, ideally in end-systole (end of the T wave).  Measure at the level of the midpoint of the sinus of Valsalva, perpendicular to the plane of the LA.  Ensure image not affected by artefact. 

LA Area is considered to be dilated if >22cm2 in the A4Ch view.

The ASE recommends that formal LA size (LA Volume) should be reported as an indexed LA Volume/BSA and measured using the biplane disc summation technique. This is beyond a more advanced echo technique and probably not necessary in the acute ICU setting.

Tricuspid regurgitation maximal velocity (TR Vmax)

Please visit the FUSIC-SY section on ‘Right Heat’ for more information on how and why to obtain TR Vmax measurements. https://fusic-sy.co.uk/right-heart/

The FUSIC-HD algorithm considers TR Vmax >2.8m/s high risk for high LAP and ≤2.8m/s low risk on Continuous Wave Doppler (CWD) measurement.

Continuous wave doppler through the tricuspid regurgitation jet. Velocity is below the baseline as the flow is away from the echo probe. The maximal velocity of the regurgitant jet contour is measured.
Measured a 4.6m/s in the above image

Caveats and tips for TR peak velocity

  • Angle and flow dependent.
  • TR signals taken from several windows and use the signal with highest velocity.
  • In AF take an average of 5 measurements in the view with the highest velocities.
  • Sweep speed 100mm/s.
  • ONLY well-defined, spade-shaped, dense spectral profile is measured.
  • Comment on the quality of the doppler envelope.
  • Challenging to get accurate estimation when no or very severe TR.

Limitations of TR peak velocity in severe TR

  • In severe TR there is a rapid RV-RA pressure equalisation leading to triangular or unclear doppler trace.
  • If TR is triangular then peak TR velocity most likely underestimated

Severe TR jet filling most of LA and incomplete TR doppler envelope below.

Unclear doppler envelope due to severe TR making PASP estimate inaccurate. The TR Vmax can be seen to be close to 4m/s so still raised.

Severe TR doppler envelope - triangular trace

Mitral valve inflow E-wave divided by mitral annular tissue e' (E/e')

Measuring e'

Tissue Doppler Imaging (TDI) can be used to measure how rapidly the LV muscle moves down to allow LV filling. TDI can be assessed at either the lateral (e’ lateral) or medial aspect (e’ septal) of the MV annulus.  The lateral annulus is most commonly used.  However, both measurements can be made and values averaged.

Obtain the same Apical 4Ch View and angle used for PWD. Select tissue Doppler imaging (TDI).  Place the cursor through the thickest part of the lateral annulus or medial aspect of the MV.  Obtain the TDI waveform and save the image.

Analysis of e' and E/e'

TDI studies the movement / velocity of LV myocardial tissue during diastole. TDI at the MV insertion site (septal, lateral wall) results in a wave pattern similar to the PWD flow pattern, but in reverse.  Movement towards the probe is in red, and blue away. 

In diastole, during the early phase of LV relaxation, the myocardium moves away from the probe, rapid descent of the ventricle, causing a negative deflection. This wave is called e’ or “e prime”.  Normally, e’ >10cm/sec.  In young hyperdynamic hearts, this may be >15-20cm/sec.

During diastasis, there is no movement of the LV.

Atrial systole then occurs which produces the a’ wave. Normally, e’ > a’.

The e’ wave is preceded by the systolic S’ prime wave, as movement of the myocardium is towards the probe, which is seen as a positive deflection above the baseline.

  • Normally, E/e’ is <8 (septal) or <10 (lateral). If E/e’ is <8 the patient is deemed to have Low LAP risk.

  • If e’ is <10cm/sec, diastolic dysfunction is present. If E/e’ >14 the patient is deemed to have High LAP risk.

  • Grade I Diastolic Dysfunction (Impaired Relaxation): due to slow decent of the LV, e’ <10cm/sec.  Often e’ < a’ .  LAP is normal with LV filling from ventricular decent. E/e’ <10. 
  • Grade II Diastolic Dysfunction (Pseudonormal): e’ <10cm/sec with slow decent of the LV.  Often e’ = a’.  E/e’ 10-14.  LV filling is from increased LAP as LV becomes less compliant.

  • Grade III Diastolic Dysfunction (Restrictive): e’<10cm/sec, usually less than 6.  Often e’ = a’ or e’ < a’.   E/e’ >14 due to high LAP.  Rapid inflow is from increased LA pressure and not rapid decent of the LV.

The ratio of E/e’:  e’ gets smaller the higher the degree of LAP.  Therefore, E/e’ increases as the LAP increases.  The higher the E/e’ the higher the LAP risk (<8 low risk, >14 high risk).

Pitfalls

  • It is important to save images from the same view and angle and to do measurements (E, A and e’) after both PWD and TDI measurements have been obtained.
  • Measurements are not valid if there is significant MV pathology (moderate mitral annular calcification, any mitral stenosis or regurgitation of more than moderate severity, mitral valve repair or prosthetic mitral valve). Measurements also not valid in patients with LV assist devices, LBBB or ventricular paced rhythms.
  • Sometimes the E and A wave may fuse together in tachycardic patients, making it difficult to differentiate. Carotid massage may be useful in slowing the heart rate and increasing E/A wave separation.
  • The E/A ratio is not reliable in atrial fibrillation (AF) as there is no active LV filling (no A-wave or a’) and is affected by volume status. E/e’ is a more reliable metric in patients with AF, when the E/e1 is averaged over 3 representative beats.  A short E-wave deceleration time <160ms indicates raised LAP post electrical cardioversion.

Summary: Diastolic dysfunction, E/A & E/e'

References

  1. https://ccforum.biomedcentral.com/articles/10.1186/s13054-022-04115-9
  2. ACCE book 
  3. https://ccforum.biomedcentral.com/articles/10.1186/s13054-022-04115-9#Tab3
  4. Brault C, Marc J, Mercado P, Diouf M, Tribouilloy C, Zerbib Y, et al. Estimation of pulmonary artery occlusion pressure using doppler echocardiography in mechanically ventilated patients. Crit Care Med. 2020;(Dd):E943–50.

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