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.
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.
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.
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.
Severe respiratory disease
High output failure
Ischaemic heart disease
Valvular heart disease
Note this may include cardiac causes
Trend may be useful
Dominant V wave could reflect TR
Shock - variable total CVS compromise
May be normal
Abnormalities may include
Right axis deviation
S1Q3T3 pattern (RV strain)
May help assess contributing causes e.g. covid
May show cardiomegaly, but the RV component of heart shadow is fairly small in normal films.
Essential part of assessment
TTE is usually adequate
Can be challenging to assess RV function (due to its shape)
RV systolic function
RV systolic pressures
A more detailed account of echo assessment of the RV is described elsewhere.
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.
Optimise gas exchange as needed
Normoxia to minimise hypoxic vasoconstriction
Normocapnia (and by extension avoid acidaemia)
High PEEP may worsen RV afterload but has a clear role in oxygenation.
Impact on preload too - a balance may be needed.
Ensure optimal preload
Diuresis in cases of volume overload
Avoid volume depletion, especially with increased afterload
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.
Nitric oxide - no mortality benefit and rebound pulmonary hypertension seen
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: