Right Heart

Special thanks for the supervision and contribution to this page from:

Dr Thanos Charalampopoulos

Consultant Cardiologist in Pulmonary Hypertension

Professor Robin Condliffe

Consultant Respiratory Physician
Sheffield Pulmonary Vascular Disease Unit

Dr Thanos Charalampopoulos - Consultant Cardiologist in Pulmonary Hypertension
Professor Robin Condliffe - Consultant Respiratory Physician
Sheffield Pulmonary Vascular Disease Unit

Written by Ben Stoney

Right Heart Assessment

Assessment of the right heart is important on the intensive care unit because there are a number of conditions common to critical care that cause acute or decompensated right heart failure.

Early recognition is essential as certain interventions may be indicated. It is also important to have an awareness that RV failure can spiral out of control leading to cardiogenic shock and death. 

Right ventricular assessment aims to look at the right ventricular size, function and pulmonary artery pressure estimation. It also assesses for signs of chronic changes related to raised pulmonary artery pressures. 

1. Causes of right heart failure on critical care

Causes of right heart failure on intensive care

The commonest causes of right heart failure on intensive care are:

  • Massive pulmonary embolus
  • Myocardial infarction
  • ARDS
  • Pulmonary arterial hypertension (PAH)
  • Chronic right heart failure
  • Sepsis
RV failure generally occurs due to:
  1. Increased afterload on the RV (pressure overload)
  2. Poor RV contractility 
  3. Increased preload (volume overload)

 The most common cause of RV failure on intensive care is due to an increased afterload which is tolerated poorly by the RV. 

Increased preload with volume overload is generally better tolerated by the RV and may show a dilated but well functioning RV. 


Pressure overload

  • Acute: PE, ARDS
  • Chronic: PAH (less commonly pulmonary artery or pulmonary valve stenosis 
  • Iatrogenic: Mechanical ventilation

Volume overload

  • Tricuspid regurgitation
  • Pulmonary regurgitation
  • Left-to-Right shunts
  • High output states e.g. anaemia, thyrotoxicosis, sepsis
  • Iatrogenic: excessive volume overload

RV myocardial pathology

  • RV myocardial infarction
  • Cardiomyopathy – septic, dilated, or Takotsubo’s
  • Myocarditis

2. Pathophysiology of RV failure

Anatomy and physiology of the right heart

Right ventricle anatomy:

The right ventricle is a thin walled structure that is triangular in the longitudinal plane and cresenteric in the short-axis plane.

The RV inlet drains blood from the RA into the RV via the tricuspid valve and the RV outlet drains blood to the pulmonary arteries via the pulmonary valve. 

The RV has three papillary muscles connected to the tricuspid valve. It also contains the moderator band and the apex is trabeculated.

RV contractility:

The right ventricle contracts in three ways:

  1. RV free wall contraction
  2. Longitudinal fibre contraction (apex to base) – contributes most to cardiac output
  3. LV traction during systole – contributing about 20-40%  of RV cardiac output.(1)

A4Ch image demonstrating RV contractility (predominantly longitudinal)

RV blood supply:

RV perfusion is by the right coronary artery and normally occurs in both systole and diastole, which is in contrast to the LV which is normally only perfused in diastole. 

In pathology as the RV dilates, the RV wall tension and oxygen consumption increases which leads to ischaemia of the RV. This is due to decreased coronary perfusion (because of the increased RV wall tension) and also due to the increased oxygen demand. 

Coronary blood flow throughout systole and diastole for the RV in contrast to mainly diastole for the LV

RV-PV coupling:

The RV pumps blood into the pulmonary vascular system. The RV is a low pressure, high capacitance system and the pulmonary vascular (PV) system is a low resistance, high compliance system. 

The RV and PV form a cardiopulmonary unit which is characterised by RV contractility and PV load (RV afterload). The RV-PV unit is normally ‘coupled’ allowing efficient transfer of load from the RV to PV. (2)

Pressure volume loops showing LV vs. RV. The RV is a low pressure system.

RV decompensation:

Most commonly RV failure on intensive care is due to increased afterload (e.g. massive PE, ARDS, PAH). The RV poorly tolerates an increased afterload (compared with the LV). As the PVR increases the RV stroke volume decreases rapidly. The RV attempts to increase its contractility to maintain the SV. 

In chronic, slow rises in PVR, the right ventricle adapts by becoming hypertrophied to maintain RV-PV coupling and can therefore generate higher pressures than are seen in acute PVR rises. 

In acute rises of PVR, the RV-PV system becomes decoupled as the RV cannot accommodate an acute rise in pulmonary artery pressure (mPAP>40mmHg). There is rapid dilatation and dysfunction of the RV which leads to cardiogenic shock. 

Acute right heart failure

 In acute RV failure there is a chain reaction which leads to multiple detrimental effects on the RV. The main mechanisms affected are:

  • Increased PVR leading to RV dilatation, increased RV wall tension and oxygen demand.
  • Septal flattening leads to a decrease in LV preload and cardiac output, which reduces MAP and coronary perfusion pressure.
  • RV ischaemia leads to worsening contractility. There is increased RV myocardial oxygen demand and decreased oxygen supply due to worsening LV function (MAP & CO) and increased RV wall tension.
These effects on the RV can spiral out of control without intervention leading to cariogenic shock and even death. 

RV spiral of death from the ESC 2019 guidelines on PE

3. Right heart assessment 

Right Heart Assessment

Right heart assessment looks for signs of right heart decompensation and help identify the underlying cause. The main questions to try and answer are:

Right ventricular views

The RV can be assessed from the:

  • PSAX – RV size and septal shape and function
  • A4Ch – RV size & function
  • Subcostal – RV free wall hypertrophy
  • RVI, PSAX Av, A4Ch – assessment of tricuspid regurgitation maximum velocity (to estimate pulmonary artery pressure).

1. Is the RV dilated?

Assessment of RV size can take place visually in the PLAX & PSAX views, but the main assessment takes place in the A4Ch view.  

Further assessment of the RV size can by:

  • Measuring the RV dimensions
  • Assessing RV/LV ratio
  • Asking which is the apex-forming ventricle?

RV severely dilatation - A4Ch view showing RV basal diameter > LV basal diameter

RV dimensions

The RV is determined to be normal size when the RV basal width is no more than 2/3 that of the LV. The RV dimensions can also be measured for further assessment. 

These measurements are taken at end-diastole and involves measuring the basal RV diameter (RVD1), the mid-RV diameter (RVD2) and RV base to apex longitudinal diameter (RVD3).

 Formal measurement of the RV/LV basal ratio can also be taken where a ratio of >1.0 is significantly dilated.

RV dimensions measured and end-diastole, inside edge to inside edge and parallel with tricuspid annulus

RV severely dilatation - A4Ch view showing RV basal diameter > LV basal diameter

BSE reference ranges for normal RV dimensions

RV size












RV dimensions taken from the BSE reference range. Note RVD1 upper limit for males is 47mm whereas the American Society of Echocardiography upper limit is 41mm.

Abnormal basal RV diameter




RV focussed view measuring the basal diameter (RVD1) at end diastole. Measuring 52.89mm meaning the RV is dilated.

The 'apex-forming' ventricle?

The LV normally is the apex forming ventricle, but as the RV dilates it starts to take the place of the LV in the apex. 

If the RV is the apex forming ventricle then there is significant dilation of the RV. 

2. Is the RV impaired?

RV function has both radial and longitudinal components. As mentioned in the RV contractility section, the majority of RV stroke volume is due to the longitudinal function. 

It is important to visually assess the radial contraction of the RV free wall and the longitudinal contraction of the RV. 

Further quantitative assessment of the RV function can be done with the following:

  • TDI of lateral tricuspid valve
  • RV Fractional Area Change (FAC)

A4Ch image demonstrating RV contractility (predominantly longitudinal)


RV systole is predominantly in the longitudinal plane with some inward motion of the RV free wall. This makes the tricuspid annular plane systolic excursion (TAPSE) reflects longitudinal function and correlates with RV ejection fraction. It’s weakness is that it is not a measure of global RV function but only the longitudinal displacement of the basal RV free wall. TAPSE can be normal with an otherwise significantly reduced RV function if the contractility of the apical and mid-free wall of the RV is poor. 

To measure the TAPSE get an optimal view in the A4Ch and place the M-mode line through the lateral annulus of the tricuspid valve. Press M-mode again and freeze the image after a few cardiac cycles. Measure using callipers the distance from the highest to the lowest point of lateral annulus of the tricuspid valve.

Tips for TAPSE:

  • Angle and load dependent
  • Align M-mode parallel to longitudinal motion of TV annulus
  • Sweep speed 100 mm/s
  • Distance not slope
  • Decrease gain to avoid noise artefact
  • Correlate with visual assessment 

BSE reference values for TAPSE:

  • TAPSE ≥17 is normal
  • TAPSE <10mm is severely impaired.

Aligning the cursor for TAPSE

TAPSE assessment using M-mode with a measurement of 2.61cm from the lowest to the highest point of the lateral annulus of the tricuspid valve. This is a normal TAPSE.

TAPSE assessment using M-mode with a measurement of 0.94cm from the lowest to the highest point of the lateral annulus of the tricuspid valve. This indicates the RV is severely impaired.

TDI of lateral tricuspid valve

Tissue doppler imaging (TDI) of the tricuspid valve is similar to TAPSE in that it assesses the longitudinal function of the lateral tricuspid annulus. The difference is that TAPSE assesses distance travelled by the lateral tricuspid annulus using M-mode, whereas, TDI uses the doppler principle to measure the velocity of the lateral tricuspid annulus. 

Blood flow is high velocity, low amplitude, whereas, tissue motion is low velocity, high amplitude. TDI mode removes the high pass filter that usually filters out lower velocities and reduces gain amplification meaning it filters out the low amplitude signals produced by blood flow (essentially applying a low pass filter). 

Measure the systolic wave also known as S’ (S prime). 


Tips for TDI:

  • Cursor over lateral TV annulus
  • Decrease gain to avoid noise artefact
  • Ignore first systolic deflection if present (isovolumetric contraction)
  • Correlate with TAPSE
  • Abnormal <9.5 cm/s
  • Does not reflect global RV function

Colour tissue doppler imaging. PW doppler is then placed on the lateral tricuspid valve to obtain the velocities.

TDI of lateral tricuspid valve with PW doppler. Velocity measured at 7cm/s = abnormal

Fractional Area Change of the RV

A trace of the endocardial border of the right ventricle is taken at end systole and end diastole. This obtains a measurement in cm².

FAC (%) = [(End diastolic area – end systolic area)/end diastolic area] x100

  • Requires adequate endocardial definition (including apex)
  • Avoid trabeculations
  • Does not take into account RVOT
  • Not great reproducibility 











RV focussed view showing area trace for end-systole equalling 24.61cm².
RV area for end-diastole was previously calculated as 30.76cm². FAC has been calculated by the machine as 20%

3. Is there pressure overload?

Pressure overload conditions

  • Acute: PE, ARDS
  • Chronic: PH (less commonly pulmonary artery or pulmonary valve stenosis 
  • Iatrogenic: Mechanical ventilation

Pressure overload echo findings

  • RV dilated
  • IVS flattening in systole
  • PASP increased TR Vmax ≥ 2.9m/s
  • Decreased pulmonary acceleration time (<105ms) +/- notching
  • RVSD – reduced TAPSE, TDI lateral tricuspid valve, or FAC – late sign
  • Chronic pressure overload = right ventricular hypertrophy >0.5cm 

Pulmonary artery systolic pressure estimation

Pulmonary artery pressures (PAP) and pulmonary vascular resistance (PVR) are not the same thing but they are related. The equation:

Δ Pulmonary pressure = CO x PVR

Where, Δ Pulmonary pressure = mPAP – PCWP.
So an increase in pulmonary artery pressures can be due to an increase in PVR or the CO. 

Echocardiography can be used to estimate pulmonary artery systolic pressure (PASP), but it requires the presence of tricuspid regurgitation.

During systole the RV pressure (RVSP) equals the PASP (unless pulmonary stenosis or RVOT obstruction is present) and any regurgitant flow through the tricuspid valve into the RA can be assessed with CW doppler to obtain a velocity. This velocity reflects the pressure gradient between the RVSP and RAP. (8)

The modified Bernoulli equation can be used to then estimate the PASP.

RVSP – RAP = 4V²

RVSP = PASP = 4V² + RAP (mmHg)

Right atrial pressure estimation is controversial due to potential inaccuracies of measurement. It is especially difficult in the ventilated patient as intra-thoracic pressures are altered compared with spontaneous breathing. It is better to use CVP if available. 

The ESC/ERS Pulmonary Hypertension guidelines 2022 recommend using the peak TR velocity for assigning echocardiographic probability of PH. (3) 

Peak TR velocity ≥ 2.9m/s is raised

Other signs of raised PASP that can be easily assessed:

  • Right ventricular dilatation
  • Reduced right ventricular function
  • Flattened inter-ventricular septum
  •  IVC dilated >2.1cm with reduced variability

Views to assess TR maximal velocity

The 3 windows to assess the TR maximal velocity from are:

  • RV inflow view
  • PSAX AV level
  • A4Ch

RV inflow view: in this clip RV appears large and hypertrophied.

Modified A4Ch to help align CW doppler with TR jet.

Tricuspid regurgitation maximal velocity

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

Estimating Right Atrial Pressure

IVC diameter and collapsibility

  • Measured in 2D or M-mode and end-expiration
  • 1-2cm from caval atrial junction 
  • Assess collapse with a sniff in non-ventilated patients

Estimating RA pressure

Signs of a high RAP:

  • Hepatic vein Vd>Vs
  • Dilated RA
  • Intra-atrial septal bulge into LA

Estimating RAP:

  • IVC≤2.1cm & >50% collapse (sniff) = 0-5mmHg
  • IVC>2.1cm & <50% collapse (sniff) = 10-20mmHg
  • All other cases = 5-10mmHg

IVC fully collapses with spontaneous respiration - estimated RAP = 0-5mmHg

Estimated RAP = 10-20mmHg
IVC >2.1cm with <50% collapse on sniff

IVC diameter and distensibility

For mechanically ventilated patients the IVC diameter increases in inspiration due to increased intra-thoracic pressure decreasing venous return. 

  • Measured in 2D or M-mode and end-expiration
  • 1-2cm from caval atrial junction
  • Assess distensibility in ventilated patients as a marker of fluid responsiveness 
  • It is better to use CVP as estimate for RAP in ventilated patients
Distensibility index in ventilated patients is calculated as:
DI IVC= (Dmax – Dmin)/Dmin
  • DI >18% predicts fluid responsiveness

IVC diameter variability (DV IVC) in ventilated patients is calculated:

DV IVC = 100 x [(Dmax – Dmin)/Dmean]

  • DV >12% predicts fluid responsiveness (7)

Mechanically ventilated patient with visual minimal respiratory variation/distensibility of the IVC

Other signs of pressure overload

Other signs of pressure overload include:

  • IVS flattening in systole
  • Pulmonary ejection acceleration time reduced +/- notching
  • RV dilation 
  • RV function impaired
    • Acute: Apical contractility preserved, with reduction in mid-free wall and TAPSE (McConnell’s sign)
    • Chronic: In general apical contractility reduced first, then mid-free wall, then TAPSE reduced last

Interventricular septum

In both severe pressure and volume overload RV dilatation is seen with a flattened inter-ventricular septum on the PSAX view (the LV becomes D-shaped). In normal circumstances the LV is circular with the inter-ventricular septum curved towards the RV. In conditions of pressure or volume overload the IVS can start to flatten and become D-shaped.

Depending on which phase of the cardiac cycle the IVS appears D-shaped will determine whether it is pressure or volume overload or a combination of the both.

  • Pressure overload – the IVS is D-shaped in systole
  • Volume overload – IVS is D-shaped in diastole, paradoxical septal motion may be present where hyperdynamic ventricles appear to move the septum anteriorly during systole.
  • Both pressure and volume overload – IVS appears D-shaped throughout both systole and diastole.

PSAX view of a D-shaped septum in both systole and diastole - indicating both pressure and volume overload

PSAX view of a D-shaped septum in systole - indicating pressure overload

Diastolic septal flattening (flattening when mitral valve open and ECG helpful to determine systole/diastole) - indicating volume overload

Pulmonary ejection acceleration time

It is important to be aware that pulmonary ejection acceleration time is not part of the FUSIC HD curriculum but is involved in the 60/60 sign which is in the literature in the assessment for PE; which is why it is included here. 

In raised pulmonary artery pressures the doppler trace in the RVOT changes. Due to increased resistance to flow the acceleration time decreases (note it will also decrease in tachycardia). The doppler envelope also changes from a smooth and rounded trace to become notched in mid-systole when the pulmonary artery pressures are raised. 

In pulmonary hypertension the acceleration time of <105ms and the presence of the mid-systolic ‘notch’ is used as a sign of pre-capillary pulmonary hypertension. 

In the 60/60 sign for PE, where there is an acute rise in pulmonary artery pressures, the pulmonary acceleration time of <60ms and the presence of the mid-systolic notch is used to help inform diagnosis. This is combined with the TR pressure gradient of <60mmHg. In chronically raised pulmonary artery pressures it would be rare for the pulmonary artery acceleration time to be so reduced without the TR pressure gradient being >60mmHg. In acute pulmonary artery pressure rises it is hard for the non-compensated (hypertrophied) RV to generate a pressure gradient of >60mmHg. 

  • Measured in the PSAX view at the AV level or RV outflow view. 
  • PW doppler is placed in the RVOT at the pulmonary valve level and aligned with the direction of flow.
  • Obtain doppler trace 
  • Measure from onset of pulmonary flow and peak pressure

RV outflow view - RVOT with pulmonary valve and pulmonary artery seen. PW doppler aligned with direction of blood flow at pulmonary valve.

Pulmonary ejection acceleration time measured from onset of flow to peak flow (red arrows). Note acceleration time 47msec.
Yellow arrow indicated mid-systolic notching.

Limitations of pulmonary ejection acceleration time

The limitations of the pulmonary ejection acceleration time are that it requires a good accurate doppler trace with the start of systole and the peak of systolic flow clearly identified. As the measurement is in milliseconds (msec) then small variations in measurements can easily over or under estimate the acceleration time. 

4. Is this acute or chronic?

RV free wall hypertrophy

If the onset of increased pulmonary vascular resistance is slow the RV has time to compensate. The RV is usually thin walled with low resistance to flow, but as the resistance to flow increases, the RV myocardial work increases and the muscle hypertrophies. So a hypertrophied RV indicates that the raised pulmonary artery pressures are chronic. 

This can be assessed from the subcostal view. The RV free wall is measured and a value >5mm indicates that the RV is hypertrophied. 

Tips for measuring RVH

  • US beam perpendicular to RV free wall
  • Focus and decrease depth 
  • Exclude epicardial fat, trabeculations and papillary muscle (note in image above the bright white pericardial layer is not measured).
  • 2D or M-mode
  • Measure at end-diastole
  • Hypertrophy > 0.5cm

Subcostal view:

Subcostal view of dilated and impaired RV. Not visually hypertrophied.

Subcostal view - RV free wall measuring 0.91cm indicating hypertrophy. Note on ECG that measurement is taken at end diastole.

4. Acute pressure overload conditions

Pulmonary Embolism

Acute pulmonary embolism may present to intensive care due to:

  • Cardiac arrest
  • Haemodynamic instability 
  • Oxygen or ventilatory support
  • Mechanical circulatory/oxygenation support 

A PE should also be considered in undifferentiated haemodynamic instability or shock. 

Echocardiography plays a key role in diagnosing PE in the haemodynamically unstable patient, but it is also important to be aware of its limitations in this context.


Echo findings in PE. Taken from ESC PE guidelines 2019.

Echo and PE: The evidence from ESC guidelines 2019

A negative echo cannot rule out PE (NPV 40-50%)

RV dilation or dysfunction may be present when there isn’t a PE (due to other cardiorespiratory disease).

RV dilation is found in >25% with PE.

60/60 sign & McConnell’s sign – high positive predictive value – but only present in 12-20% of PE patients.

Mobile right heart thrombi essentially confirms the diagnosis of PE and is associated with high mortality. It may be detected in up to 18% of PE patients in the ITU setting. 

Echo is important for haemodynamically unstable patients with suspected high risk PE, because a normal echo excludes PE as the cause of haemodynamic instability. 

Haemodynamically unstable patients with suspected PE and unequivocal signs of RV pressure overload, McConnell sign, 60/60 sign or right heart thrombi justify emergency reperfusion therapy. As long as immediate CTPA not feasible, high clinical suspicion for PE and no other obvious cause of RV pressure overload. 

In some patients with suspected PE there may be increased RV wall thickness or tricuspid regurgitation maximal velocity beyond values normally compatible with acute RV pressure overload (>3.8m/s or estimated PASP >60mmHg). In these cases CTEPH or other causes for PH should be considered.

Mobile right heart thrombus

Echo findings for PE

Echo findings for PE are the same as those for acute pressure overload, leading to right heart strain, such as:

  • Dilated RV
  • IVS septal flattening in systole
  • Impaired RV – decreased TAPSE, decreased S’, decreased FAC
  • Dilated IVC
  • Raised pulmonary artery pressure estimation
  • McConnell’s sign 
  • 60/60 sign 

McConnell's sign

This is the presence of acute RV dysfunction on echo with akinesia of the mid free RV wall with preservation of RV apical contractility. This is a sign of acute RV pressure overload that is highly specific for PE, but can also be seen in other conditions that lead to acute rises in pulmonary artery pressures – such as acute cor pulmonale secondary to ARDS.

For an critical care focussed discussion on these dilemmas visit this link: https://criticalcarenow.com/acute-cor-pulmonale-in-ards-the-conjunction-fallacy/

In chronic RV dysfunction the impairment of the RV contractility usually affects the RV apex first, then the RV mid-free wall and the longitudinal function (TAPSE) is the last to be affected. 

McConnell's sign - note preserved apical contractility with reduced RV mid free wall contractility.

60/60 sign

This sign is the co-existence of an acceleration time of pulmonary ejection of <60ms with a mid-systolic “notch”. Combined with a peak systolic tricuspid valve gradient of <60mmHg. (TR Vmax </= 3.8m/s).

It is worth noting that an acceleration time of pulmonary ejection of <105ms with mid-systolic “notching” is seen in pulmonary hypertension. So it is important to look for other signs of chronic pressure overload.  

It is rare in acute RV pressure overload for the peak systolic pulmonary artery pressure to be >60mmHg. This is due to the RV not being able to generate higher pulmonary artery pressures unless there is an element of hypertrophy which happens in chronic pressure overload. 

Pulmonary ejection time in the RVOT of 47msec (<60msec). Note the presence of the mid-systolic notch.

TR Vmax 3.82m/s and TRmax PG 58.5 mmHg (<60mmHg). Combined with the pulmonary acceleration time <60msec this is the 60/60 sign.

DVT scanning and suspected PE: The evidence from ESC guidelines 2019

The majority of PE’s originate from lower limb DVTs and rarely from the upper limb. 

Compression ultrasonography for DVT diagnosis has a sensitivity >90% and specificity ~95% for proximal symptomatic DVT. It shows a DVT in 30-50% of patients with PE. 

For patients with suspected PE a 4-point (bilateral groin and popliteal fossa) compression DVT scan can be performed. A positive proximal DVT scan has a high positive predictive value for PE.

The only validated diagnostic criterion for DVT is incomplete compressibility of the vein – this indicated the presence of thrombus. Flow measurements can generally be unreliable. 

For haemodynamically unstable patients with suspicion of PE a combination of echocardiography and point-of-care 4-point DVT scan may further increase specificity. 

An echo without signs of RV dysfunction and a normal DVT scan exclude PE with a high negative predictive value (96%).

Treatment decisions

The choice between thrombolysis and heparin alone is based on haemodynamic instability, recently defined in the ESC PE 2019 guidlines as:

  • Cardiac arrest; or
  • Obstructive shock; or
    • SBP <90, or SBP ≥90 needing vasopressors
    • End organ hypoperfusion
  • Persistent hypotension
    • SBP<90 or drop of ≥40mmHg that persists >15mins
    • Not caused by arrhythmias, hypovolaemia, sepsis
Thrombolysis is the treatment of choice for PE when there is haemodynamic instability as above. 

Classification of PE severity and the risk of early (in-hospital or 30 day) mortality

Haemodynamic instability as defined above
PESI/sPESI - PE severity index/simplified PESI
*Yes/No - One or none positive out of RV dysfunction and elevated cardiac troponins section
ESC PE 2019 guidelines table

For high risk PEs without haemodynamic instability there is often concern when there are features of RV dysfunction on echo and raised troponin. These PEs are classified as intermediate-high risk and are at risk of deterioration within the first few hours to days, so they need close monitoring. The treatment is with low molecular weight heparin but if haemodynamic deterioration occurs they should be treated with systemic thrombolysis, unless contraindications. If contraindications for systemic thrombolysis are present then alternatives such as percutaneous catheter directed treatment (clot aspiration or in-situ low dose thrombolysis) or surgical embolectomy can be considered. 

The reason for LMWH in the intermediate-high risk group is that the risks of life-threatening bleeding due to thrombolysis outweigh the expected benefits. 
It has been found that thrombolysis leads to rapid improvement of pulmonary artery pressures when compared with heparin alone, but at 1 week post thrombolysis or heparin alone there is no difference in echocardiographic features between the two groups. This supports the decision to reserve thrombolysis for only PEs with haemodynamic instability. (5)
The role of reperfusion in intermediate-high risk PE patients is still being studied with ongoing RCTs comparing both catheter directed therapy and half dose systemic thrombolysis with anticoagulation alone, and standard practice may change in the future. 

5. Volume overload

Volume overload

Volume overload conditions

  • Tricuspid regurgitation
  • Pulmonary regurgitation
  • Left-to-Right shunts
  • High output states e.g. anaemia, thyrotoxicosis, sepsis
  • Iatrogenic: excessive volume overload

Volume overload echo findings

  • IVS flattening in diastole
  • Hyperdynamic RV with TAPSE increased (but RV may be impaired)
  • No RV hypertrophy but may have apical trabeculations (unless pressure and volume overload)
  • Peak TR velocity normal

RV dilated and impaired. Not hypertrophied. Prominent apical trabeculation.

Diastolic septal flattening - in keeping with volume overload

Significant tricuspid regurgitation

Normal TR Vmax 2.44 m/s (<2.9m/s)

6. Myocardial pathology

Myocardial pathology

Common causes RV myocardial pathology

  • RV myocardial infarction – commonly from RCA occlusion 
  • Cardiomyopathy – septic, dilated, Takotsubo’s or arrhythmogenic right ventricular cardiomyopathy (ARVC)
  • Myocarditis

Myocardial pathology echo findings

  • RV not dilated (may be dilated in cardiomyopathy)
  • RV impaired
  • Peak TR velocity normal
  • RWMA may be present, evidence of thinning/scaring may be present

RV severely impaired. Cardiac MRI showed RV infarct (occluded RCA).

Focused RV view - poor longitudinal, mid-free wall and apical contractility

Disproportionately impaired RV compared to LV

TR Vmax = 2.8m/s which is normal (<2.9m/s).

Dilated and impaired RV - is it always pulmonary hypertension?

As shown in the volume overload and myocardial pathology section, a dilated and impaired RV is not always due to acute or chronic pulmonary hypertension. 

Volume overload or myocardial pathology must also be considered in the differential diagnosis. The assessment of pulmonary artery pressure along with other echo signs can help identify the underlying cause. 

7. Management of right heart failure on critical care

Management principles

RV failure management (6) should focus on:

  • Treating the underlying cause (e.g. PE, ARDS, PAH, MI, sepsis)
  • Optimising:
    • Preload
    • Afterload 
    • RV contractility
  • Considering advanced options

Preload optimisation

  • In hypovolaemia, RV infarct, or acute PE a cautious fluid challenge of 250-500ml IV fluid can be considered. If unresponsive don’t continue and don’t give if flattened IVS on echo. 
  • In hypervolaemia, treat the overloaded RV with diuretics. Renal replacement therapy can be considered if unresponsive despite this. 

Afterload optimisation

  • Mechnical ventilation should be optimised with lung protective ventilation, minimise PEEP.
  • Avoid hypoxia, hypercarbia and acidosis as these increase PVR.
  • Consider pulmonary vasodilators: inhaled NO or prostacyclins.

RV contractility

  • Maintain sinus rhythm
  • Consider inotropes – e.g. milirone, dobutamine 
  • Consider vasopressors to improve RV perfusion pressure – e.g. vasopressin or noradrenaline

If unresponsive to these therapies then consideration of:

  • Mechanical circulatory support: RVAD or ECMO
  • Transplantation


  1. Right Ventricular Failure. Dr. Bassem Sobhi Ibrahim. ESC, Vol. 14, N° 32 – 12 Dec 2016. https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-14/Right-ventricular-failure
  2. Assessment of right ventricular function – a state of the art. Hameed, Abdul et al. Current Heart Failure Reports, 5th June 2023, 20pages 194–207 (2023).
  3. 2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. Humbert et al. European Heart Journal, Volume 43, Issue 38, 7 October 2022, Pages 3618–3731
  4. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS): The Task Force for the diagnosis and management of acute pulmonary embolism of the European Society of Cardiology (ESC). Konstantinides, S. et al. European Heart Journal, Volume 41, Issue 4, 21 January 2020, Pages 543–603
  5.  Comparison of alteplase versus heparin for resolution of major pulmonary embolism. Konstantinides, S. et al. Am J Cardiol. 1998 Oct 15;82(8):966-70
  6. Treatment of right heart failure: is there a solution to a problem? Mehmood, M. et al. ESC, Vol. 14, N° 33 – 19 Dec 2016
  7. Predicting and measuring fluid responsivesness with echocardiography. Miller, A. Mandeville, J. Echo Research and Practice. ID: 16-0008; June 2016. https://echo.biomedcentral.com/articles/10.1530/ERP-16-0008
  8. Acute and Critical Care Echocardiography. Coleburn, C. & Newton, J. Oxford Clinical Imaging Guides. Oxford University Press. 2017. 

Content created by Ben Stoney
Design by Max Broadbent