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Right ventricular failure

Cardiologists have become “LV centric” though circulation is a closed system and the RV plays an integral part in it. A complex interventricular dependence between both ventricles is present. The RV fails when there is pressure or volume overload or myocardial disease such as RV infarction or cardiomyopathy. However, the commonest cause of RV failure is pulmonary hypertension. Epidemiologically, the most frequent pathology for pulmonary hypertension development is LV failure. Diagnosis of RV failure is a clinical exercise. ECG and markers such as lactate and BNP are helpful. Echo is very important in the diagnosis to exclude extrinsic causes and to quantify, in particular, PASP, IVC diameter and collapsibility index and TAPSE. CT and cardiac MRI have been useful to elucidate the underlying pathology.

Heart Failure (HF)


Introduction

Many a time the right ventricle (RV) is regarded as the “younger brother” of the left ventricle (LV) and is treated as a less important member of the contractile apparatus. This view stemmed from the concept that the RV functions rather as a passive conduit and its importance is not great as it pumps blood to only one organ, the lungs. However, the circulatory system is a closed one and both ventricles are interdependent, working together in an orchestrated complex pattern in health and disease. The failure of one ventricle deleteriously affects the performance of the other. This review will deal with the causes of right ventricular failure and its diagnosis, leaving the management to a second part of this series.

Background

Anatomically the RV is triangular in side section and crescent-like in cross-section. It is made up of superficial circular and deeper longitudinal fibres. The superficial fibres encircle the heart and are continuous with the subepicardial fibres of the LV. The deep longitudinal fibres run from the apex to the base of the heart. The RV contracts in three ways: the inward motion of the RV free wall, via shortening of longitudinal fibres pulling the apex towards the base of the heart, and traction by LV contraction. The contraction of longitudinal fibres contributes most to the systolic performance of the RV, whilst the LV traction component contributes about 20-40% of RV cardiac output.

The RV ejects the same stroke volume as the LV but against a much lower resistance of the pulmonary vasculature. This results in an RV stroke work which is almost one fourth that of the LV, hence the thinner RV wall. Because of the low resistance presented by the pulmonary circulation, the RV continues to eject through the early phase of systole. As such, there is no isovolumic relaxation phase on the right side.

There is important ventricular interdependence between the RV and the LV. The components of this are the sharing by both ventricles of the interventricular septum (IVS), the insertion of anterior and posterior ends of the RV free wall into the IVS, the encircling fibres and the pericardium. Acute dilatation of the RV, for example in RV infarction or significant pulmonary embolism, shifts the septum to the left. This shift raise impairs LV diastolic filling as well as its contractility. The constraining effect of the pericardial sac comes into play in diastole when a dilated ventricle restricts the filling of the other.

The RV cannot handle a pressure overload in the same way as a volume overload which it can withstand for years. However, to maintain cardiac output in the face of an acute rise of pulmonary pressure, e.g., in the context of large pulmonary embolus, the RV augments its force of contraction. Failure to adapt acutely results in rapid RV dilatation and dysfunction which is clinically manifest as hypotension and cardiogenic shock. On the other hand, when pulmonary arterial pressure (PAP) rises more gradually, the RV dilates using Starling’s law to preserve flow output. Usually, RV function is maintained until late stages of the disease. Eventually, the RV fails, becomes more spherical, tricuspid regurgitation ensues causing more right heart failure and a spiral process develops ending in venous system congestion.

It is important to elaborate on right heart failure (RHF) in the presence of left-sided failure as this is the most common scenario. Some of the mechanisms as to why RHF follows left-sided heart failure (HF) are: 1) they may both be affected by the same pathology whether it is ischaemia, inherited cardiomyopathy or myocarditis; 2) development of pulmonary hypertension in left ventricular failure (LVF) increases the afterload against which the RV has to pump; 3) severe LVF may result in decreased coronary perfusion for the right ventricle; 4) LV dilatation can impair RV diastolic function by increasing pericardial constraint. Nowadays, with the increasing use of ACE inhibitors and beta-blockers, more frequently patients with LVF survive to develop pulmonary hypertension and finally succumb with right ventricular failure. This is the reason why RV failure is considered “the common final pathway” [1]. Time and again it has been shown to be the most important indicator of poor prognosis in heart failure.

Prevalence

Right heart failure as the primary presentation of acute decompensated HF and cause of hospitalisation accounted for 2.2% of HF admissions in the CHARITEM registry [2]; however, it was present as secondary to acute LV failure in more than one fifth of the cases.

In our Egyptian Heart Failure-LT registry, 4.5% of patients with acute heart failure presented with RHF as opposed to 3% in other ESC regions [3]. This could be attributed to the even higher incidence of rheumatic heart disease. In support of this, Hassanein et al reported that the incidence of valvular heart disease was more than double the other ESC regions (17.5% of our cohort versus 8%) in the same registry [3]. Rheumatic fever affects the mitral valve mainly in the form of stenosis, but also mitral regurgitation or a combination of both. Neglected mitral valve disease results in pulmonary hypertension, severe functional tricuspid regurgitation and right-sided heart failure. In addition, rheumatic heart disease not infrequently causes organic tricuspid valve disease (stenosis, regurgitation or a combination of both). Decades ago, infection by S. Mansoni caused pulmonary hypertension in Upper Egypt, but the eradication programmes for schistosomiasis have resulted in this problem now being a rare occurrence. It is still endemic in sub-Saharan Africa.      

Causes of right heart failure

The causes of RHF can be divided broadly into three categories: secondary to pulmonary hypertension, RV and tricuspid valve pathology, and diseases of the pericardium.

Pulmonary hypertension (PH) is the most common cause of RHF (Table 1). The commonest cause of pulmonary hypertension is left-sided heart failure. LVF, whether due to systolic HF or HF with preserved LV systolic function or severe mitral valve disease, results in PH and, if left untreated, leads to RHF. This is termed PH type 2 according to the WHO classification and is a post-capillary PH as it is associated with high wedge pressure [4].

 

Table 1. Classification of pulmonary hypertension

1. Pulmonary arterial hypertension (PAH)

1.1. Idiopathic (IPAH)

1.2. Heritable

1.3. Drugs and toxins

1.4. Associated with:

1.4.1. Connective tissue disease

1.4.2. HIV infection

1.4.3. Portal hypertension

1.4.4. Congenital systemic-to-pulmonary shunts

1.4.5. Schistosomiasis

1’. Pulmonary veno-occlusive disease

1” Persistent pulmonary hypertension of the newborn

2. Pulmonary hypertension secondary to left heart disease

2.1. Left ventricular systolic dysfunction

2.2. Left ventricular diastolic dysfunction

2.3. Left-sided valvular heart disease

3. Pulmonary hypertension associated with lung diseases and/or hypoxaemia

3.1. Chronic obstructive pulmonary disease

3.2. Interstitial lung disease

3.3. Sleep-disordered breathing

3.4. Alveolar hypoventilation disorders

3.5. Chronic exposure to high altitude

3.6. Developmental abnormalities

4. Chronic thromboembolic pulmonary hypertension (CTEPH)

5. Miscellaneous

5.1. Haematological

Chronic haemolytic anaemias, sickle cell, thalassaemia

Myeloproliferative disorders

Post-splenectomy

5.2. Systemic disorders

e.g., sarcoidosis

5.3. Metabolic disorders

a. thyroid disorders

b. glycogen storage diseases

c. Gaucher’s disease

5.4. Others

e.g., chronic renal failure, fibrosing mediastinitis 

PH types 1, 3, 4 and most of 5 in the WHO classification are pre-capillary; all are characterised by low or normal wedge pressure. The second most common cause of PH is secondary to lung disease. The commonest lung diseases are obstructive airway disease followed by lung fibrosis. Another important cause which is frequently overlooked is obstructive sleep apnoea (OSA). PH is present in 17-53% of individuals with OSA [5]. Lung diseases cause pulmonary hypertension via hypoxia which causes polycythaemia, vasoconstriction and vascular remodelling, in addition to damage of lung parenchyma with loss of vascular bed.

A particular type of PH results from acute pulmonary embolism, and can result in acute right heart failure as the RV fails to maintain blood flow past an obstructing large embolus. Recurrent showers of smaller pulmonary emboli can end in chronic thromboembolic pulmonary hypertension (CTEPH). Here emboli do not completely resolve, but they partially recanalise and are endothelialised, resulting in pulmonary artery obstruction.

All congenital heart diseases with increased pulmonary blood flow, mainly left-to-right shunts, can lead to PH. The development of PH depends on the duration of exposure and its magnitude, i.e., ventricular septal defect and patent ductus arteriosus (post-tricuspid defects) patients tend to develop PH earlier than atrial septal defect patients (pre-tricuspid).

Pulmonary hypertension type 1 is idiopathic or secondary to connective tissue. Idiopathic PAH affects mostly females. It is thought to be caused by an imbalance of vasodilator NO pathway and vasoconstriction endothelin-1 pathway. It is characterised by increased pulmonary vascular resistance due to remodelling and occlusion of the pulmonary arterioles.

Less commonly, RV failure could result from direct affection of myocardial disease by myocarditis, cardiomyopathy, ischaemia, or arrhythmia. Right ventricular infarction complicates 30 to 50% of inferior myocardial infarction and it is usually caused by occlusion of the proximal right coronary artery. Compared with the left ventricle, the right ventricle is more resilient in the face of ischaemia. This is due to less myocardial oxygen demand, coronary perfusion occurring throughout the cardiac cycle, and a dual blood supply - the left anterior descending artery supplies the anterior two thirds of the septum. So, in the majority of cases, the RV recovers within a few days. However, during the initial presentation profound hypotension and shock may be present.

The tricuspid valve is organically affected in rheumatic heart disease, in infective endocarditis in IV drug addicts, or by trauma caused by pacemaker electrodes during implantation or retrieval. Ebstein’s anomaly frequently presents as right heart failure in children or in early adulthood.

Gradual accumulation of fluid in the pericardial sac can compress the thin-walled RV and prevent its filling, presenting as RHF. Constrictive pericarditis is one of these diagnoses which can be easily missed. It is caused by fibrosis and calcification of the encasing pericardium restricting diastolic filling of the ventricles. The commonest cause used to be prior tuberculosis infection, but nowadays it is mostly secondary to chest radiotherapy or previous cardiac surgery.

Clinical diagnosis

Symptoms of right heart failure are mainly due to systemic venous congestion and/or low cardiac output. This includes exertional dyspnoea, fatigue, dizziness, ankle swelling, epigastric fullness and right upper abdominal discomfort or pain.

In taking past medical history it is very important to inquire about the presence of coronary artery disease, emphysema/chronic bronchitis, history of deep venous thrombosis, recurrent abortions, autoimmune diseases especially scleroderma and systemic lupus erythematosus (SLE), and infections, e.g., HIV, tuberculosis and schistosomiasis. Family history of PAH can be present as some cases of PAH can have a familial occurrence.

Signs: raised jugular venous pulse (JVP), left parasternal lift, an accentuated second pulmonary sound, right ventricular gallop, usually a pansystolic murmur over the tricuspid area which increases with inspiration, and sometimes diastolic murmur of pulmonary insufficiency; also, an enlarged tender liver, ascites frequently present as well as ankle oedema.

It is worth mentioning a few points to highlight the importance of raised JVP as a clinical sign. It is a specific sign of right heart failure and reflects raised right atrial pressure. It correlates well with raised left heart filling pressure in LV failure. Raised JVP is a prognostic marker. Analysis of the SOLVD study has shown that it correlates with mortality and a risk of heart failure hospitalisation in LVF [6]. Kussmaul sign, which is an increase of JVP on inspiration, can help in pointing to the cause of RHF. It is caused by impaired RV diastolic compliance with increased venous return, as seen in constrictive pericarditis and RV infarction.    

Right ventricular infarction should be suspected in the context of inferior MI by the triad of raised JVP, hypotension and clear lung fields.

Technical clues to diagnosis

Manifest heart failure is not difficult to diagnose if careful attention is paid to clinical signs. However, the underlying aetiology behind RHF can sometimes be elusive. On the one hand, if there is a long history of ischaemic cardiomyopathy or chronic obstructive airway disease, usually history plus simple investigations can easily determine the diagnosis. However, reaching the diagnoses of other less common causes such as PAH, CTEPH or constrictive pericarditis can be a challenge.

Electrocardiography in patients with pulmonary hypertension shows signs of RV hypertrophy in the form of right axis deviation, dominant R in V1 and dominant S in V5 or 6 + P pulmonale. An elevated ST in V3R and V4R denoting RV infarction is present in 50% of inferior MI.

Echocardiography can give a rapid estimate of the RV size, shape and shift of the IVS. An RV/LV basal diameter of more than 1 plus loss of sphericity of the LV (the D sign) are taken as evidence of a rise in PAP [7]. Flattening of the septum occurs in diastole in volume overload, e.g., in the shunts and in systole in pressure overload and in both systole and diastole as the pressure rises more as in all advanced pulmonary hypertension including Eisenmenger’s syndrome.

Because of the RV geometry and the complex 3D shape, measurement of RV function is a challenge. Tricuspid annular plane systolic excursion (TAPSE) is a rapid and reproducible parameter as it is a surrogate of the longitudinal fibres’ function. It measures the tucking effect of the apex on the tricuspid annulus. It is not affected much by loading condition. It is angle-dependent. Longitudinal displacement of 17 mm or less is indicative of poor RV function and poor prognosis [8].

Estimation of pulmonary hypertension is an integral part of evaluation of a patient with suspected RVF. PASP can be estimated non-invasively in the absence of pulmonary stenosis by measuring the velocity of tricuspid regurgitation and applying the simplified Bernoulli equation+JVP. In symptomatic patients, a peak tricuspid regurgitation velocity >2.8 m/s is consistent with the presence of significant pulmonary hypertension.

Special attention should be paid to IVC diameter and distensibility in relation to respiration when examined in the subcostal view. A distended IVC >21 mm with decreased inspiratory collapse points to the presence of pulmonary hypertension and denotes raised right atrial pressure [9].

Examination of the PA and the flow across it gives a further clue for PH. As RV pressure increases, peak systolic velocity will occur earlier in systole, resulting in a more triangular shape of the pulmonary flow envelope instead of the normal dome shape. Thus, a value of less than 100 ms of PA acceleration time is regarded as indicative of PH. Also, a dilated PA >25 mm, especially if it is associated with early diastolic pulmonary regurgitation >2.2 m/s, is another echocardiographic feature.

In constrictive pericarditis, because of the dissociation of intrathoracic and intracardiac pressures, there is a respiratory variation in the peak flow velocity across the mitral valve. Thus, there is a drop of pressure in the pulmonary veins during inspiration but not in the left atrium, resulting in a decrease of the normal gradient pressure responsible for LV filling. Consequently, during inspiration, there is a decrease in the initial E velocity on the transmitral flow velocity curve. During expiration, as the intrathoracic pressure increases, the gradient of the pulmonary veins/left atrium is restored and is seen on echo as a pronounced increase in the initial E velocity. In severe cases a septal bounce can be visualised.

Contrast echo is useful in the detection of intracardiac shunts.

A lung function test is needed when the diagnosis of cor pulmonale is contemplated to confirm the presence and severity of obstructive airway disease. High-resolution CT of the chest is helpful when underlying lung fibrosis is a possible diagnosis. Overnight oximetry is useful when sleep-breathing disorders are suspected to demonstrate repeated episodes of desaturation from 10 to almost 40 sec with an anoxia/hypoxia index (AHI) of at least 15/hour, consistent with the diagnosis.

Cardiac MRI is the gold standard nowadays for measurement of RV volumes and function. MRI has the advantage of tissue characterisation which is useful in such conditions as arrythmogenic right ventricular dysplasia or myocarditis. It is also useful in the diagnosis of congenital heart diseases. Cardiac MRI, as well as CT, can detect pericardial thickening of more than 2 mm, which is useful when constrictive pericarditis is considered.

CT pulmonary angiography is essential if CTEPH is suspected. Typical CT features in CTEPH patients include: asymmetric enlargement of central pulmonary arteries, in contrast to other causes of pulmonary hypertension, plus a variation of size in segmental arteries and a mosaic pattern of lung parenchyma (areas of hyperattenuation and low attenuation) [10].

Right heart catheterisation (RHC) is needed for the diagnosis of PAH and may also be needed in constrictive pericarditis. PAH (pre-capillary) is defined by a high PAP above 25 mmHg with normal wedge pressure <15 mmHg and increased pulmonary vascular resistance (>3 Wood units). In constrictive pericarditis, there is an increase and equalisation of end pressure in all four chambers plus a dynamic respiratory variation in LV and RV pressure tracings.

Biochemical markers

Systemic venous congestion affects the liver and kidney and results in derangement of their function. Raised transaminases and bilirubin plus prolonged prothrombin time are common in right HF and reflect poor prognosis [11]. Raised renal chemistry is frequently noted and may improve with diuretics.

There are no specific biomarkers for right heart failure, but raised BNP and troponins reflect stress and injury in different RHF scenarios. Their rise reflects the severity of the condition and portends poor prognosis. For example, Krüger [12] has noted that BNP is elevated in acute pulmonary embolism complicated by RV dysfunction but is within normal range when RV function is preserved. Patients with pulmonary embolism and plasma lactate level >2 mmol/L are at high risk of death and adverse outcome [13].

Diagnostic algorithm [4]

A useful working algorithm in right heart failure is to establish the presence of PH or another cause, mainly primary myocardial disease or pericardial disease. If a careful history taking, with a chest X-ray to reveal symptoms and signs, and an ECG, raise suspicion of PH or RHF, then the next step is to perform transthoracic echo. Echo is useful in investigating LV and RV systolic/diastolic function and valvular structure and will confirm the presence of PH. At this stage, LVF as the commonest cause can be proven or refuted. If PH is present and there is no significant LV dysfunction, then proceed to exclude the second commonest - lung diseases. This includes lung function test, transfer factor and high-resolution CT, and overnight oximetry if interstitial lung disease or OSA still needs to be excluded. If tests are negative/inconclusive thus far, then a ventilation perfusion scan is the next step for CTEPH exclusion. A positive V/Q scan necessitates CT pulmonary angiography for confirmation, while a negative scan increases the probability of PAH type 1. RHC is needed in addition to connective tissue disease screening, including antiphospholipid antibodies, HIV and a test for schistosomiasis if relevant.

Conclusion

Even though right ventricular failure does not take centre stage in the field of heart failure research and clinical trials, it is actually the final pathway of left-sided heart failure. Pulmonary hypertension is the commonest cause of right heart failure. Other causes are RV myocarditis, genetic cardiomyopathy, ischaemia as well as pericardial disease. Due to the unusual anatomy of RV, assessment of its function is a challenge. However, technical advances, especially in echocardiography and cardiac MRI, are helping to evaluate RV function and volumes as well as measurement of pulmonary artery pressure. Careful history taking, clinical examination and the targeted use of investigations can elucidate the underlying pathology.

References


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Notes to editor


Author:

Dr Bassem Sobhi Ibrahim, FRCP, FACC

Director of Heart Failure Unit, National Heart Institute, also board member of the HF Working Group of EgSC Cairo, Egypt

 

Address for correspondence:

Dr. Bassem Sobhi Ibrahim, FRCP, FACC

Consultant Cardiology

Cardiology Department

Nevill Hall Hospital, Abergavenny, NP7 7EG

UK

Email: bassemi2002@yahoo.co.uk

 

Author disclosures:

The author has no conflicts of interest to declare.

 

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.