Right Heart Failure
Last updated 15th Jan 2022 - Tom Heaton
Right heart failure is:
The clinical syndrome when there are signs and symptoms caused by dysfunction of the right heart structures despite normal central venous pressures.
This is usually related to the right ventricle (RV) but can include the tricuspid valve or right atrium (RA).
The result is impaired perfusion of the lungs and reduced delivery of blood to the left side of the heart.
The right ventricle is an important part of the circulatory system that is often overlooked compared to the left side.
There are some key differences that are important to understand when managing problems.
The clinical syndrome when there are signs and symptoms caused by dysfunction of the right heart structures despite normal central venous pressures.
This is usually related to the right ventricle (RV) but can include the tricuspid valve or right atrium (RA).
The result is impaired perfusion of the lungs and reduced delivery of blood to the left side of the heart.
The right ventricle is an important part of the circulatory system that is often overlooked compared to the left side.
There are some key differences that are important to understand when managing problems.
Anatomy & Physiology
The RV is a different shape and construction compared to the left.
It is the most anterior part of the heart and can be almost considered as wrapping around the more muscular left ventricle.
As such, in cross-section it has a crescent shape whilst in side profile is more triangular.
The circulations of the left and right side are very different, despite both handling the same volume of cardiac output.
The key is that the pulmonary circulation is the destination of blood from the right ventricle and has pressures and resistance of about one fifth the systemic circulation.
The differences are well preserved even in exercise with the notably adaptability of lung vasculature recruitment keeping pulmonary vascular resistance low.
As such, the work required from the right ventricle is notably less (about ¼) and the ventricular musculature is correspondingly less.
The result is a ventricle that is well suited to manage variations in preload but less well able to handle changes in afterload.
The general pattern of contraction is also quite different, the right ventricle having just 2 layers of myocardial fibres rather than the 3 seen in the left.
The motion of contractility is that of longitudinal shortening (a bit more like peristalsis) compared with the concentric and twisting contraction of the left (a wringing motion).
The lower right sided pressures means that right sided coronary perfusion (in health) occurs throughout the cardiac cycle.
The actual supply will depend on the individual coronary set up but is from the right coronary artery in 80% of individuals.
It is the most anterior part of the heart and can be almost considered as wrapping around the more muscular left ventricle.
As such, in cross-section it has a crescent shape whilst in side profile is more triangular.
The circulations of the left and right side are very different, despite both handling the same volume of cardiac output.
The key is that the pulmonary circulation is the destination of blood from the right ventricle and has pressures and resistance of about one fifth the systemic circulation.
The differences are well preserved even in exercise with the notably adaptability of lung vasculature recruitment keeping pulmonary vascular resistance low.
As such, the work required from the right ventricle is notably less (about ¼) and the ventricular musculature is correspondingly less.
The result is a ventricle that is well suited to manage variations in preload but less well able to handle changes in afterload.
The general pattern of contraction is also quite different, the right ventricle having just 2 layers of myocardial fibres rather than the 3 seen in the left.
The motion of contractility is that of longitudinal shortening (a bit more like peristalsis) compared with the concentric and twisting contraction of the left (a wringing motion).
The lower right sided pressures means that right sided coronary perfusion (in health) occurs throughout the cardiac cycle.
The actual supply will depend on the individual coronary set up but is from the right coronary artery in 80% of individuals.
Pathophysiology
The RV is classically described as being preload tolerant because the thinner wall can distend better with increased filling.
However, this is only up to a point where the usual Frank-Starling decompensation will occur.
In addition, ongoing distension can dilate the tricuspid annulus leading to tricuspid regurgitation and a worsening of volume overload (as the regurgitated blood is ‘recycled’).
Also, the deranged shape can distort the shape of the LV, impairing its function.
This is known as ventricular interdependence, because the ventricles share the same non-distensible sac.
The lower muscle mass of the RV also makes it less able to respond to increased afterload.
This afterload is almost fully dependent on pulmonary vascular resistance.
In chronic states, remodelling can occur to adapt to this with hypertrophy and changed pressure-volume dynamics.
As with volume overload, the pressure overload can have a ventricular interdependence effect.
When RV pressures go higher than LV ones (only in diastole), there can be deviation of the septum to the LV (the D-shaped ventricle).
This understandably has a negative impact on LV filling and contractility.
The overall result of RV failure can then be LV dysfunction, as LV function itself suffers, coronary perfusion deteriorates and a vicious circle begins.
However, this is only up to a point where the usual Frank-Starling decompensation will occur.
In addition, ongoing distension can dilate the tricuspid annulus leading to tricuspid regurgitation and a worsening of volume overload (as the regurgitated blood is ‘recycled’).
Also, the deranged shape can distort the shape of the LV, impairing its function.
This is known as ventricular interdependence, because the ventricles share the same non-distensible sac.
The lower muscle mass of the RV also makes it less able to respond to increased afterload.
This afterload is almost fully dependent on pulmonary vascular resistance.
In chronic states, remodelling can occur to adapt to this with hypertrophy and changed pressure-volume dynamics.
As with volume overload, the pressure overload can have a ventricular interdependence effect.
When RV pressures go higher than LV ones (only in diastole), there can be deviation of the septum to the LV (the D-shaped ventricle).
This understandably has a negative impact on LV filling and contractility.
The overall result of RV failure can then be LV dysfunction, as LV function itself suffers, coronary perfusion deteriorates and a vicious circle begins.
Aetiology
There are different classifications possible.
An acute vs chronic differentiation is quite useful.
Thinking about it as a primary cardiac problem vs a secondary problem is also something that I find useful.
Acute
Primary
Chronic
Primary
An acute vs chronic differentiation is quite useful.
Thinking about it as a primary cardiac problem vs a secondary problem is also something that I find useful.
Acute
Primary
- MI
- Myocarditis
- Tamponade
- LVAD associated
- Pulmonary embolism
- Severe respiratory disease
- High output failure
Chronic
Primary
- Ischaemic heart disease
- Valvular heart disease
- LV dysfunction
- Cardiomyopathies
- Constrictive pericarditis
- Pulmonary hypertension
- Note this may include cardiac causes
Assessment
Clinical features
- Raised JVP
- Elevated CVP
- Trend may be useful
- Dominant V wave could reflect TR
- Trend may be useful
- Hepatic distension
- Shock - variable total CVS compromise
Investigations
Bloods
ECG
CXR
Echo
- FBC
- U&E
- LFTs
- Blood gas
- Troponin
- BNP
- TFTs
ECG
- May be normal
- Abnormalities may include
- Right axis deviation
- RBBB
- S1Q3T3 pattern (RV strain)
- Right axis deviation
CXR
- May help assess contributing causes e.g. covid
- May show cardiomegaly, but the RV component of heart shadow is fairly small in normal films.
Echo
- Essential part of assessment
- TTE is usually adequate
- Can be challenging to assess RV function (due to its shape)
- Key information
- RV size
- RV systolic function
- RV systolic pressures
- Septal position
- RV size
- A more detailed account of echo assessment of the RV is described elsewhere.
Management
The focus of this will be on the management of patients with acute failure rather than chronic.
Optimal supportive care is (as always) a key part of management.
Resp
CVS
Maintaining adequate coronary perfusion is an important part of the supportive care to avoid a negative downward spiral.
There is no selective RV agent so the CVS parameters and therapies need balancing.
The postulated negative effects of noradrenaline and adrenaline on pulmonary vasculature resistance do not seem well justified and thus these remain suitable initial supportive therapies.
Levosimendan induces inotropy and reduces PVR which looks to be an attractive combination.
Milrinone has a similar profile.
Pulmonary vasodilators:
Specific therapies will be needed for certain aetiologies e.g. PE.
Additional options may be considered in certain circumstances when medical therapy is failing, although these include specialist centre involvement:
Optimal supportive care is (as always) a key part of management.
Resp
- Optimise gas exchange as needed
- Normoxia to minimise hypoxic vasoconstriction
- Normocapnia (and by extension avoid acidaemia)
- Normoxia to minimise hypoxic vasoconstriction
- High PEEP may worsen RV afterload but has a clear role in oxygenation.
- Impact on preload too - a balance may be needed.
- Impact on preload too - a balance may be needed.
CVS
- Ensure optimal preload
- Diuresis in cases of volume overload
- Avoid volume depletion, especially with increased afterload
- Diuresis in cases of volume overload
- Maintain RV perfusion pressure with vasopressor agents
- Consider balloon pump or inotropic support
- RV afterload reduction agent
- Avoid hypothermia (worsens PVR)
Maintaining adequate coronary perfusion is an important part of the supportive care to avoid a negative downward spiral.
There is no selective RV agent so the CVS parameters and therapies need balancing.
The postulated negative effects of noradrenaline and adrenaline on pulmonary vasculature resistance do not seem well justified and thus these remain suitable initial supportive therapies.
Levosimendan induces inotropy and reduces PVR which looks to be an attractive combination.
Milrinone has a similar profile.
Pulmonary vasodilators:
- Nitric oxide - no mortality benefit and rebound pulmonary hypertension seen
- Sildenafil
- Prostaglandins - can be given inhaled or IV
Specific therapies will be needed for certain aetiologies e.g. PE.
Additional options may be considered in certain circumstances when medical therapy is failing, although these include specialist centre involvement:
- ECMO
- RVAD
- Transplant consideration
Links & References
- Nickson, C. Right ventricular failure. LITFL. 2020. https://litfl.com/right-ventricular-failure/
- Murphy, E. Shelley, B. The right ventricle-structural and functional importance for anaesthesia and intensive care. BJA Education. 2018. 18(8):239-245. https://www.bjaed.org/article/S2058-5349(18)30058-1/fulltext
- Bersten, A. Soni, N. Oh’s Intensive Care Manual (6th ed). 2009. Butterworth Heinemann Elsevier.
- Borlaug, B. Right heart failure: causes and management. UpToDate. 2020.
