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.
Causes of right heart failure on intensive care
The commonest causes of right heart failure on intensive care are:
The most common cause of RV failure on intensive care is due to an increased afterload which is tolerated poorly by the RV.
RV myocardial pathology
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.
The right ventricle contracts in three ways:
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
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.
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:
RV spiral of death from the ESC 2019 guidelines on PE
Right heart assessment looks for signs of right heart decompensation and help identify the underlying cause. The main questions to try and answer are:
The RV can be assessed from the:
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:
RV severely dilatation - A4Ch view showing RV basal diameter > LV basal diameter
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 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.
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:
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:
BSE reference values for TAPSE:
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:
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
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%
Pressure overload conditions
Pressure overload echo findings
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:
Views to assess TR maximal velocity
The 3 windows to assess the TR maximal velocity from are:
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
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
Signs of a high RAP:
IVC fully collapses with spontaneous respiration - estimated RAP = 0-5mmHg
Estimated RAP = 10-20mmHg
IVC >2.1cm with <50% collapse on sniff
For mechanically ventilated patients the IVC diameter increases in inspiration due to increased intra-thoracic pressure decreasing venous return.
IVC diameter variability (DV IVC) in ventilated patients is calculated:
DV IVC = 100 x [(Dmax – Dmin)/Dmean]
Mechanically ventilated patient with visual minimal respiratory variation/distensibility of the IVC
Other signs of pressure overload include:
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.
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
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.
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.
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.
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.
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.
Acute pulmonary embolism may present to intensive care due to:
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:
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.
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%).
The choice between thrombolysis and heparin alone is based on haemodynamic instability, recently defined in the ESC PE 2019 guidlines as:
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.
Volume overload conditions
Volume overload echo findings
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)
Common causes RV myocardial pathology
Myocardial pathology echo findings
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.
RV failure management (6) should focus on:
If unresponsive to these therapies then consideration of:
Content created by Ben Stoney
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