presentation of right sided heart failure

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NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

StatPearls [Internet].

Right heart failure.

Stacy A. Mandras ; Sapna Desai .

Affiliations

Last Update: July 17, 2023 .

Continuing Education Activity

Heart failure is a condition in which the heart loses its ability to pump blood efficiently to the rest of the body. Right heart failure is most commonly a result of left ventricular failure via volume and pressure overload. Clinically, patients will present with signs and symptoms of chest discomfort, breathlessness, palpitations, and body swelling. This condition is evaluated using non-invasive techniques such as echocardiography, nuclear angiography, MRI, 64-slice CT, as well as invasive hemodynamic measurements. Management is aimed at increasing right ventricular contractility, reducing right ventricular afterload and optimizing volume status. This activity reviews the evaluation and management of right heart failure and highlights the role of the interprofessional team in improving care for affected patients.

Review the presentation of a patient with right heart failure.
Describe the workup of a patient with right heart failure.
Identify the treatment options for right heart failure.
Outline the importance of collaboration and communication among the interprofessional team members to recognize the clinical signs of heart failure and evaluate it using non-invasive and invasive measures which will enhance the delivery of care for the affected patients.
Introduction

When addressing heart failure, most commonly, the left ventricle (LV) is the topic of discussion, and the right heart overlooked. However, the right ventricle (RV) is unique in structure and function and is affected by a set of disease processes that rival that of the LV. This article will review the normal structure and function of the RV, describe the pathophysiology of RV failure (RVF), and detail the medical and surgical management of the various disease processes during which RVF occurs. [1] [2]

Right ventricular failure (RVF) is most commonly a result of left ventricular failure (LVF), via pressure and volume overload. [3]

In addition to LVF, there are other conditions of pressure overload that lead to RVF. These include transient processes such as:

Pulmonary embolism (PE)
Mechanical ventilation
Acute respiratory distress syndrome (ARDS)

Furthermore, chronic conditions of pressure overload may lead to RVF. These include:

Primary pulmonary arterial hypertension (PAH) and secondary pulmonary hypertension (PH) as seen in chronic-obstructive pulmonary disease (COPD) or pulmonary fibrosis)
Congenital heart disease (pulmonic stenosis, right ventricular outflow tract obstruction, or a systemic RV).

The following conditions result in volume overload causing RVF:

Valvular insufficiency (tricuspid or pulmonic)
Congenital heart disease with a shunt (atrial septal defect (ASD) or anomalous pulmonary venous return (APVR)).

Another important mechanism that leads to RVF is intrinsic RV myocardial disease. This includes:

RV ischemia or infarct
Infiltrative diseases such as amyloidosis or sarcoidosis
Arrhythmogenic right ventricular dysplasia (ARVD)
Cardiomyopathy
Microvascular disease.

Lastly, RVF may be caused by impaired filling which is seen in the following conditions:

Constrictive pericarditis
Tricuspid stenosis
Systemic vasodilatory shock
Cardiac tamponade
Superior vena cava syndrome
Hypovolemia.
Epidemiology

RVF is most often a result of LVF, and patients with biventricular failure have a 2-year survival of 23% versus 71% in patients with LVF alone. [4] [5]

In the CHARITEM registry, RVF accounted for 2.2% of heart failure admissions and was secondary to LVF in more than one-fifth of cases. In the Egyptian Heart Failure-LT registry, 4.5% of patients presenting with acutely decompensated heart failure had RVF versus 3% in other regions of the European Society of Cardiology. It has been proposed that this difference is due to the increased prevalence of rheumatic heart disease in this region.

Pathophysiology

During fetal development, the RV accounts for approximately 66% of the cardiac output, and via the ductus arteriosus and foramen ovale, shunts blood to the lower body and placenta. At birth, exposure to oxygen and nitric oxide, as well as lung expansion, leads to a rapid decrease in pulmonary vascular resistance (PVR). The lungs, which were bypassed in utero, become a low-pressure, highly distensible circuit. The thick-walled fetal RV becomes thinner. [6]

Anatomically the structures and resulting function of the RV and the LV are vastly different. For example:

The LV is elliptical and made of thick muscle fibers wrapped in two anti-parallel layers separated by a circumferential band. This results in a complex contraction that involves torsion, thickening, and shortening.
The RV, in contrast, takes a triangular and crescentic shape and is made up of both a superficial layer that runs circumferentially and parallels to the atrioventricular groove and a deeper layer that runs longitudinally from the base to the apex. Because of its structure, the contraction of the RV is limited to longitudinal shortening of the tricuspid annulus towards the apex. The RV free wall is displaced inward toward the septum and traction is created by the septum as it moves toward the LV in systole.
The RV is more heavily trabeculated and contains a circumferential moderator band at the apex.
The tricuspid valve (TV) is unique in that it has a large annulus and is tethered by greater than three papillary muscles which make it vulnerable to structural deformation under sustained increased pressure or volume loading.
Because the RV is substantially thinner than the LV with lower elastance, the RV is much more susceptible to increases in afterload. A modest change in PVR may result in a marked decrease in RV stroke volume. This is evident in patients with pulmonary arterial hypertension (PAH), pulmonary embolism (PE), mitral valve disease with secondary pulmonary hypertension (PH), and the adult respiratory distress syndrome (ARDS). The thinner RV is also more sensitive to the pericardial constraint.

Like the LV, contraction of the RV is preload dependent at normal physiologic filling pressures, and excessive RV filling can result in a shift of the septum towards the LV and ventricular interdependence causing impaired LV function.

Because of lower right-sided pressures and wall stress, the oxygen requirement of the RV is lower than that of the LV. Coronary blood flow to the RV is lower, as is oxygen extraction. For this reason, the RV is less susceptible to ischemic insults, and increases in oxygen demand are met via increases in coronary flow as is the case in PAH or increased oxygen extraction which occurs with exercise.

RV function is affected by atrial contraction, heart rate, and synchronicity. Each of these has important clinical implications, and RVF for any reason is a strong prognostic indicator.

The response of the RV to a pathologic load is complex. The nature, severity, chronicity, and timing (in utero, childhood or adulthood) each play a role in how the RV responds to an increased load. For example, in childhood, when confronted with congenital pulmonic stenosis, fetal right ventricular hypertrophy (RVH) persists and allows the RV to compensate for the increase in afterload.

In adulthood, however, the ability of RV to tolerate a chronic increase in afterload, such as that seen in PAH, is poor. In the early stages of PAH, the RV responds to elevated pulmonary arterial pressures (PAP) by increasing contractility, with little to no change in RV size. As PAP continue to rise, the RV myocardium begins to hypertrophy, and RV stroke volume (SV) is maintained. This, however, is not enough to normalize wall stress, and subsequently, dilatation occurs. This is accompanied by rising filling pressures, decreased contractility, loss of synchronicity as the RV becomes more spherical, and dilatation of the TV annulus resulting in poor coaptation of the valve leaflets and functional tricuspid regurgitation (TR). The TR worsens the RV volume overload, RV enlargement (RVE), wall stress, contractility and cardiac output.

This differs from the response of the RV to an acute increase in afterload, such as that seen with an acute PE. In this case, the RV responds with an increase in contractility and end-diastolic volume, but does not have time for the adaptations that are seen in chronic RVF to occur, and quickly fails when unable to generate enough pressure to maintain flow.

History and Physical

As with all disease states, the initial assessment of RVF begins with a thorough history and physical examination. The acuity, severity, and etiology should be determined so that an appropriate treatment plan may be put in place.

Clinically, patients present with the signs and symptoms of hypoxemia and systemic venous congestion. These include:

Breathlessness
Chest discomfort
Palpitations

Common findings on the exam include:

Jugular venous distension
Hepatojugular reflux
Peripheral edema
Hepatosplenomegaly/hepatic pulsation
Signs of concomitant LVF
Paradoxical pulse.

When severe, presyncope or syncope may occur when the RV is unable to maintain cardiac output. This is accompanied on the exam by the following:

Hypotension
Tachycardia
Cool extremities
Delayed capillary refill
Central nervous system depression
Oliguria.

After the history and physical, the evaluation continues with an electrocardiogram, arterial blood gas, blood lactate, and chest x-ray. Blood work should include markers of end-organ function (renal and hepatic panel) to assess severity. A D-Dimer is useful in the diagnostic workup of suspected PE. There are no biomarkers specific for RVF, however B-type natriuretic peptide and cardiac troponin are highly sensitive for early detection of RVF and myocardial injury. When elevated, these are associated with poor prognosis in RVF due to PAH. [7] [8]

Noninvasive Measures

Echocardiography

The assessment of RV function can be challenging because of its location, shape and afterload dependence. Two-dimensional echocardiography (2DE) is the first-line and most commonly used non-invasive imaging modality to assess RV size, hemodynamics, and function. Images are acquired in multiple cross-sectional planes, and and the following measurements obtained:

Quantification of RV enlargement (RVE) and right atrial enlargement (RAE): Because of its shape, quantitative assessment of RV function is difficult and is often described qualitatively in comparison with LV function. A normal RV should not be more than two-thirds the size of the LV. RVE is a strong prognostic indicator.
TAPSE: Used to quantify the movement of tricuspid annulus toward the apex and estimates RV function. This has been a good predictor in patients with PAH and LVF, however, in patients with congenital heart disease or after cardiac surgery, it is less reliable.
Right ventricular strain: Another useful tool to assess RV function. The strain is a composite measurement of RV loading and dysfunction- abnormal strain patterns have been associated with disease progression, higher diuretic doses, and mortality in PAH. The strain has also been shown to predict RVF after implantation with a left ventricular assist device (LVAD) and predicts clinical outcomes in those referred for heart transplantation.
Fractional area of change (FAC): An important quantitative measurement of RV systolic function derived either by 2DE or magnetic resonance imaging (MRI). It has been shown to be an independent predictor of HF, sudden death, stroke and mortality in PE and in myocardial infarction.
Myocardial performance index (MPI): Estimates global ventricular function and is calculated by adding the isovolumic contraction and relaxation times divided by the ejection time. In RVF, MPI increases as the isovolumic times increase and contraction times decrease. MPI has been shown to predict PAH in connective tissue disease and is an independent prognostic indicator in PAH.
Eccentricity index: A useful measurement of RVE. Acquired in the short-axis view, at end-systole and end-diastole, the eccentricity index is a ratio of the length of two perpendicular minor-axis diameters, one of which bisects and is perpendicular to the interventricular septum. This allows for a quantitative measurement of septal-flattening and distinguishes between pressure and volume overload.
All of the hemodynamic variables measured during invasive right heart catheterization (RHC) may be estimated using echocardiography. For example, the diameter and collapsibility of the inferior vena cava (IVC) in the subcostal view may be used to estimate RA filling pressure. A normal IVC collapses more than 50% with inspiration and is associated with a RA pressure less than 10 mmHg. By measuring the maximum TR velocity and using a modified Bernoulli equation, the systolic PAP may be estimated. The diastolic PAP may be estimated by using the same equation on the pulmonic regurgitant jet or by transposing the pulmonary opening time on the tricuspid regurgitant velocity curve and calculating the pressure gradient between the RA and the RV.

Three-dimensional echocardiography has also been used more recently to quantify RV volumes and ejection fraction using a modified Simpson’s method (summation of disks). This has been validated to correlate well with the gold standard MRI, but is time-consuming and less feasible given the proximity of the RV to the sternum and its trabeculations.

Nuclear Angiography

First-pass radionuclide ventriculography was for a long time the gold standard to measure RV ejection fraction (RVEF). A bolus of the 99m-Tc tracer is injected, and a sequence of cardiac cycles is acquired as the bolus passes through the heart. A normal RVEF is 52% plus or minus 6% with 40% considered the lower limit of normal. Nuclear angiography is limited by its inability to measure RV volumes and sensitivity to cardiac arrhythmia.

Magnetic Resonance Imaging

Magnetic resonance imaging (MRI), as mentioned previously, is now the gold-standard for the measure of RV volumes and function. In addition to measuring RV mass, volumes and chamber dimensions, MRI can calculate and quantify regurgitant volumes, delayed enhancement, scar burden, strain, perfusion, and pulmonary pulsatility. Also, changes in the global function of the RV after medical therapy have been shown to have a direct correlation to the functional class and survival in patients with PAH.

MRI is limited by its temporal resolution, its contraindication in those with implantable cardiac devices, and the time required for data acquisition and analysis.

64-Slice Computed Tomography

Computed tomography (CT) may be used to measure RVEF and RV volumes. However, acquisition of RV parameters cannot be obtained simultaneously with LV parameters or CT angiography. This results in the need for additional radiation exposure which is not negligible, and therefore CT is not routinely used for this purpose.

Invasive Hemodynamic Measurement

Right heart catheterization (RHC) or pulmonary artery catheterization (PAC) is often very useful in making the diagnosis and tailoring management in RVF. Though it is an invasive procedure, RHC is considered safe with a low complication rate, especially in experienced centers. Current practice guidelines recommend the use of RHC for unexplained diagnostic or treatment-resistant cases, for the continuous and accurate measurement of right and left-sided filling pressures, cardiac output, and PVR.

The hemodynamic variables obtained in a RHC have important prognostic significance. A high RA pressure and low cardiac output have repeatedly been shown to be associated with poor outcomes in PAH. In addition, a PVR greater than three Woods units and pulmonary vascular compliance (SV/pulmonary pulse pressure) have both been associated with poor outcomes in LVF as well as PAH.

Treatment / Management

Management of Acute Right Ventricular Failure

Medical Management

Management of acute RVF starts with an assessment the severity of the patient’s condition and the decision to admit the patient to the intensive care unit (ICU) or intermediate care unit when appropriate. Rapid identification and management of triggering factors (i.e., sepsis, arrhythmias, drug withdrawal) are necessary. In the case of an RV infarct, rapid revascularization is essential, as is reperfusion therapy in a patient with a high-risk PE. As infection portends a very poor prognosis in acute RVF, preventative measures and prompt detection and treatment of infection are important. [9] [10]

The mainstay of treatment focuses on three tenants: optimizing volume status, increasing RV contractility, and reducing RV afterload.

Volume loading may be appropriate if the patient is hypotensive and has low or normal filling pressures. Placement of a PAC or central venous pressure monitoring is often helpful as while the RV is preload dependent. Volume loading may over distend the RV and result in a further decline in cardiac output. If volume overload is present, IV diuresis is indicated, or renal replacement therapy if volume removal cannot be accomplished with medication. In addition to improving symptoms, diuresis has the additional benefits of reducing TR, restoring synchronous RV contraction, and reducing ventricular interdependence. Sodium restriction, daily weights, and strict monitoring of fluid intake and urine output is advised to aid in maintaining euvolemia.

Efforts should also be made to restore sinus rhythm in patients with atrial arrhythmias given the contribution of atrial contraction to cardiac output in RVF. In addition, hemodynamically significant tachy- and bradyarrhythmias should be treated. Digoxin has been shown to be of some benefit in patients with severe PAH. However, care must be taken in the critically ill patient given its narrow therapeutic window and possible side effects.

When hemodynamic instability is present, vasopressors are indicated. Norepinephrine is the pressor of choice to improve systemic hypotension and restore cerebral, cardiac and end-organ perfusion. Inotropes, including dobutamine, levosimendan, and the phosphodiesterase-3 inhibitor milrinone are also helpful in that they improve contractility and cardiac output. Dobutamine is the inotrope of choice in RVF, as it leads to increased myocardial contractility via the beta receptor and vasodilatation/decreased afterload via the beta receptor. Caution should be taken however with dobutamine and milrinone as both may reduce systemic pressure. If this occurs, the addition of a vasopressor may be required.

If pressure overload is the etiology of the RVF, as is the case in PAH, afterload reduction with pulmonary vasodilators is the primary therapy. These drugs target three therapeutic pathways, nitric oxide (NO), endothelin and prostacyclin. It has been demonstrated that regardless of the class of drug used; acute responsiveness has prognostic significance in acute RVF. In addition to lowering afterload, some of these agents, such as the endothelin receptor antagonist (ERA) bosentan and the phosphodiesterase-5 (PDE5) inhibitor sildenafil, have also been shown to directly increase RV contractility. The pulmonary vasodilators used to treat acute RVF include:

Inhaled nitric oxide (iNO) acts via the cyclic guanosine monophosphate (cGMP) pathway to cause pulmonary vasodilatation. It is rapidly inactivated by hemoglobin in the capillaries of the lung, thereby preventing systemic hypotension. The iNO acts only in ventilated areas of the lung, lowering PAP and PVR and improving oxygenation, without worsening hypoxia due to the ventilation-perfusion mismatch or shunting that can be seen with the systemic vasodilators. The iNO has been well studied in patients with acute RVF and has been shown in combination with dobutamine to improve CO, oxygenation, and PVR. Caution must be taken to avoid methemoglobinemia, and iNO must be withdrawn slowly to avoid hemodynamic decompensation from rebound PH.
The intravenous (IV) prostacyclins epoprostenol and treprostinil act via the cyclic adenosine monophosphate pathway to result in potent pulmonary vasodilatation, systemic vasodilatation, and inhibition of platelet aggregation. Epoprostenol is the prostacyclin of choice for critically ill patients with acute RVF given its 6-minute half-life. Epoprostenol is started at 1 ng/kg/min to -2 ng/kg/min and up-titrated as tolerated, with caution in patients with comorbidities, hypoxemia or hemodynamic instability. Like iNO, the prostacyclins decrease PAP and PVR and increase cardiac output, however dose-dependent side effects (hypotension, nausea/vomiting/diarrhea, and headache) often limit titration. Prospective data demonstrating treatment benefit of IV prostacyclins in acute RVF is limited.
Iloprost and treprostinil: inhaled prostacyclins. Both reduce PVR and improve cardiac output, with less systemic side effects. While treprostinil may also be given subcutaneously, it is inferior in critically ill, hemodynamically unstable patients due to its unpredictable absorption and longer half-life.
ERAs and PDE5-inhibitors: oral, pulmonary vasodilators that reduce PAP, reduce PVR, and improve cardiac output in patients with RVF. ERAs block the endothelin-A and endothelin-B receptors in endothelial and vascular smooth muscle cells, reducing the vasoconstrictive, proliferative and proinflammatory effects of endothelin. The use of ERAs in the ICU is limited by their longer half-life and hepatotoxicity (bosentan). PDE5-inhibitors block degradation of cGMP. In addition to the previously mentioned hemodynamic effects, PDE5i have been shown to reduce hypoxic pulmonary vasoconstriction (HPV) and the up-regulation of pro-inflammatory cytokines induced by HPV. The limited data for the use of PDE5-inhibitors in the ICU suggest a potential benefit in patients with RVF after mitral valve repair, coronary artery bypass grafting, or LVAD placement, and to reduce rebound PH in PAH patients weaning from iNO.

Caution must be taken with patients requiring mechanical ventilation, as excessive tidal volumes (V) and positive end-expiratory pressure (PEEP) increase PAP, RAP and RV afterload. Also, PEEP may worsen the picture by reducing venous return in the preload-dependent RV. While permissive hypercapnia leads to vasoconstriction, thereby increasing PAP and worsening RVF, hyperventilation acutely reduces PAP and acidosis-induced vasoconstriction. Care must be taken to avoid high V in this setting. The optimal ventilator setting for the patient with RVF is that which delivers adequate oxygenation and ventilation with the lowest V, plateau pressure, and PEEP.

Surgical Management and Interventional Therapies

For patients with reversible RVF refractory to medical therapy, surgical options are indicated either as a bridge to recovery or transplantation. Surgery may also be indicated for patients with RVF in the setting of valvular heart disease, congenital heart disease, and chronic thromboembolic pulmonary hypertension (CTEPH). Adequate preoperative diuresis is imperative, and the use of pulmonary vasodilators and inotropes peri-operatively may be needed. In addition, the irreversible end-organ damage is a contraindication for surgical management.

Veno-arterial (VA) extracorporeal membrane oxygenation (ECMO) may be indicated as salvage therapy in patients with massive PE and refractory cardiogenic shock following systemic thrombolysis. ECMO may also be used as a bridge to lung or heart-lung transplantation in patients with severe RVF due to end-staged PAH.

Mechanical support with a right ventricular-assist device (RVAD) may be an option for the patient with isolated RVF awaiting transplant. However, ECMO may be a better treatment option for unloading the RV in the setting of severely increased PVR as pumping blood into the PA may worsen PH and cause lung injury.

Patients with RVF due to LVF may benefit from LVAD implantation, with improved PAP before heart transplantation and possibly improved post-transplant survival. However, LVADs may worsen or lead to new RVF due to alterations in RV geometry and flow/pressure dynamics and biventricular support may be required.

Pulmonary thromboendarterectomy (PTE) is the treatment of choice for patients with CTEPH and is often curative. PTE has been shown to improve functional status, exercise tolerance, quality of life, gas exchange, hemodynamics, RV function, and survival, particularly in patients with proximal lesions and minimal small vessel disease. , PTE is not recommended for patients with massively elevated PVR (greater than 1000 dyn/cm to 1200 dyn/cm). Outcomes with PTE have been shown to directly correlate with the surgeon and center experience, concordance between the anatomic disease and PVR, preoperative PVR, the absence of comorbidities (particularly splenectomy and ventricular-atrial shunt) and post-operative PVR. Operative mortality in an experienced center is between 4% to 7%, and PTE should not be delayed in operative candidates in favor of treatment with pulmonary vasodilator therapy.

Surgical embolectomy or percutaneous embolectomy may be used for acute RVF in the setting of massive PE, but data comparing embolectomy with thrombolysis are limited.

Balloon atrial septostomy (BAS) is indicated for PAH patients with syncope or refractory RVF to decompress the RA and RV and improve CO via the creation of a right-to-left shunt. BAS may be used as a bridge to transplantation or as palliative therapy in advanced RVF/PAH and has a role in third world countries in which pulmonary vasodilators are not available. Mortality associated with BAS is low (approximately 5%), particularly in experienced centers, however spontaneous closure of the defect often necessitates repeating the procedure. Contraindications of BAS include high RAP (greater than 20 mmHg), oxygen saturation less than 90% on room air, severe RVF requiring cardiorespiratory support, PVRI greater than 55 U/m and LV end-diastolic pressure greater than 18 mmHg.

Cardiac resynchronization therapy (CRT) restores mechanical synchrony in the failing LV, leading to improved hemodynamics and reverse remodeling and improved morbidity and mortality in LVF. Animal studies and small case series suggest that RV pacing results in acute hemodynamic improvement in patients with RVF in the setting of PAH, however, no data show long-term clinical benefit in this population.

Ultimately, heart, lung, or combined heart-lung transplantation (HLT) is the treatment of last-resort for end-staged RVF. In patients with RVF due to PAH, RAP greater than 15 and CI less than 2.0 are poor prognostic indicators and referral for transplantation is indicated. It remains unclear at which point the RV is beyond recovery, however, in general, the RV is resilient, and most often lung transplant alone is sufficient with estimated 1-year-survival of 65% to 75% and 10-year survival of 45% to 66%.

Congenital patients with RVF in the setting of Eisenmenger syndrome may undergo lung transplantation with repair of simple shunts (ASDs) at the time of surgery or combined HLT, which has demonstrated a survival benefit in this population.

Differential Diagnosis
Community-Acquired pneumonia (CAP)
Goodpasture syndrome
Idiopathic pulmonary fibrosis (IPF)
Interstitial (Nonidiopathic) Pulmonary fibrosis
Myocardial infarction
Nephrotic syndrome
Neurogenic pulmonary edema
Pneumothorax imaging
Respiratory failure
Venous insufficiency
Viral pneumonia
Enhancing Healthcare Team Outcomes

Right heart failure is a systemic disorder that can affect many organs and hence is best managed by an interprofessional team. The outcomes of patients with RVF is worse than those with LVF, but it does depend on the cause and other comorbidities. Patients with persistently elevated pulmonary artery pressures have the worst outcomes. Many of these patients require repeat admissions and also have prolonged stays. Despite the various therapies for RVF, the outcomes have not greatly improved over the past two decades. While heart transplant is the ideal treatment for patients with no lung pathology, the shortage of donors is a limiting factor. [11] (Level V)

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Disclosure: Stacy Mandras declares no relevant financial relationships with ineligible companies.

Disclosure: Sapna Desai declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Cite this Page Mandras SA, Desai S. Right Heart Failure. [Updated 2023 Jul 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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Right Ventricular Failure

Chris Nickson and James Pearlman
Mar 22, 2023
Find and treat the cause (e.g. PE, ARDS, MV failure, fluid overload, pulmonary HTN)
Management focuses on: volume and preload optimisation / RV contractility / RV afterload reduction
Patients with HFrEF / HFpEF with Left Heart Failure (LHF) have worse prognosis if they have concomitant RHF
Afterload is the primary determinant of normal RV function and RVEF is inversely proportional to PAP
RV is better suited to changes in volume than pressure due to compliance and the thin free wall but when the RV afterload increases for whatever reason –> the RV dilates
As RV dilates –> promotes TR –> worsens RV dilation –> vicious cycle of ‘auto-aggravation’ (shift to descending portion of the Frank-Starling curve)
Termed: Ventricular interdependent filling
Elevated right heart pressures –> coronary sinus congestion –> reduction of coronary blood flow –> can provoke RV ischaemia
Venous congestion also affects: liver / renal function / fluid retention –> Which may also worsen RHF
volume/pressure overload: LVF, PE, ARDS, amniotic fluid embolism
mechanical: MV
cardiac: cardiomyopathies, ARVD, TV rupture, tricuspid or pulmonary regurgitation
respiratory: cor pulmonale, OSA, COPD
muscular disease
neuromuscular; poliomyelitis, amyotrophic lateral sclerosis, muscular dystrophy
connective tissue: SLE, CREST, RA, hepatic porto-pulmonary syndrome
cardiac: LVF, intra-cardiac shunt, cardiomyopathies

CLINICAL FEATURES

raised JVP with a prominent V wave from TR
low cardiac output and hypotension –> cardiogenic shock
hepatic enlargement (depending on chronicity), ascites
peripheral oedema (may or may not have this)
Precordial heave
If secondary to pulmonary hypertension –> loud P2
An increase in the amplitude of the systolic murmur during inspiration (Carvallo sign) may distinguish TR from MR

INVESTIGATIONS

Bloods: NT-proBNP (may be difficult to interpret as is not specific to right heart), elevated troponins (useful in prognostication), LFTs (cholestatic picture in chronic failure with synthetic function impairment, transaminitis in acute), EUCs
Cardiac silhouette may appear globular
Loss of retrosternal airspace on lateral –> RV enlargement
Rightward displacement of the cardiac silhouette well beyond the spin –> RA enlargement
If PH: main PA enlarged
May see cause of PH — i.e. COPD
ECG: Right axis deviation, sinus tachycardia, atrial arrhythmias (common), SI/QIII/TIII (high specificity / low sensitivity), RV Strain pattern. E.g: PE ECGs , RVH ECGs
RV dilation (can grossly compare w/ LV size on AP4C)
Diastolic interventricular septal flattening (left-ward shift) = volume overloaded state
Systolic interventricular flattening (left-ward shift) = pressure overloaded state
RV hypokinesis (mild, moderate, severe)
Look at TAPSE and RVFAC (TAPSE <17mm, RFAC <35% are abnormal)
Right heart catheterisation: elevated pressures
cMRI: Gold standard of quantitative non-invasive measurement of RV volume, mass and EF

Focuses on:

Fixing the underlying cause (if you’re able to)

Management of volume and preload

RV contractility
RV afterload
Aim for CVP 8-12mmHg
May require judicious fluid boluses –> If not volume responsive stop
Fluid and salt restriction
Aggressive diuretic therapy (mainstay: loop diuretics. Consider addition of thiazides, and aldosterone antagonist)
Renal Replacement Therapy (RRT) should be reserved for those who are refractory to diuresis ( UNILOAD and CARRESS-HF Trials)
sequential TTE/TOE, PAC, or right heart catheterisation may be helpful in fluid titration

RV Contractility with Inotropes and Vasopressors

If CO / BP inadequate –> Commence inotropes
no selective right heart inotrope exists
beta-agonists, calcium sensitisers and phosphodiesterase inhibitors (PDEIs)
must decrease afterload or else increased contractility with increased myocardial O2 consumption will take place
levosimendan : shown to reduce PVR and improve RV function
milrinone : increased contractility via a non-beta-adrenergic mechanisim –> does not increase myocardial oxygen demand
Adrenaline , noradrenaline , phenylephrine and vasopressin: increase MAP and thus coronary perfusion but if not appropriately used will increase myocardial O2 consumption by increasing afterload too much
Vasopressin may be preferentially used given it has less effect on PVR as well as its renal effect via selective efferent arteriole constriction
Digoxin: Unknown if beneficial, although may improve CO

Afterload Reduction

Minimise PVR: avoid hypoxia, acidaemia, alveolar distension
Consider GTN / SNiP –> may be at the cost of reduced coronary perfusion
Consider role of: RAASi, B-blockers, hydralazine
prostaglandins (INH, IV, SC): increased NO release
NO : pulmonary vasodilator, oxygenation and PVR improve but no mortality benefit, rebound pulmonary hypertension observed
sildenafil and tadalafil (PDE-III inhibitor): oral medication, phosphodiesterase enzyme
milrinone (Mostly a PDE-III inhibitor, does also have some PDE-V inhibition): decreases PVR, can be given IV or nebulised
Endothelin receptor antagonists: Early trials are promising –> Bosentan
recombinant BNP: neseritide, reduces preload and afterload -> improved Q without inotropy (increased mortality + renal failure)

Mechanical Ventilation and PEEP

distending alveolar pressure transmitted through pulmonary capillary bed –> determines the opening pressure of pulmonary valve
PEEP contributes to augmentation of preload because of transmitted pressure to RV
Avoid gas trapping (watch PEEP!)

Surgical Intervention and RV Support

TV surgery (for TR or TS)
Would be unusual for PV lesion, however should be considered
MV repair / replacement
Biventricular pacing for resynchronisation
RVAD (LVAD if LVF is the cause of RVF)
Palliative procedure such as balloon atria septostomy (BAS)

Figure 11. Management of acute right-sided heart failure. All management must be undertaken with an awareness of the patient’s hemodynamic status. If this status is not clear clinically, then invasive assessment/monitoring should be undertaken. Hemodynamic targets provide rough guidelines for tailored therapy. AV indicates atrial-ventricular; CI, cardiac index; CVP, central venous pressure; CVVHF, continuous venovenous hemofiltration; DCCV, direct current cardioversion; IV, intravenous; LV, left ventricular; MAP, mean arterial pressure; NS, normal saline; PAH, pulmonary arterial hypertension; PCWP, pulmonary capillary wedge pressure; PM, pacemaker; RAP, right atrial pressure; RHC, right-sided heart catheterization; RV, right ventricular; UF, ultrafiltration; and UOP, urine output.

Management of acute right-sided heart failure 2

SUMMARY OF TREATMENT OPTIONS

Treat the cause!
Oxygenation
Mechanical ventilation — aggressively treat hypercarbia, acidosis (all increase PVR)
Target CVP 8-12 if able
vasodilators + inotropes
milrinone (50mcg/kg bolus -> 0.2-0.8mcg/kg/min) [caution with bolus administration]
sildenafil 50-100mg PO preoperatively
inhaled nitric oxide 20-40ppm (good in bypass, doesn’t cause systemic hypotension as inactivated when bound to Hb)
inhaled prostacyclin (increases cAMP) – 50mcg in saline nebulised every hour OR 50ng/kg/min nebulised into inspiratory limb
IV prostacyclin (if inhaled not available) – 4-10ng/kg/min
pacing to improve A-V synchrony / biventricular device

References and Links

Wiesbauer F. Medical Treatment of Heart Failure . Medmastery
Lahm T, McCaslin CA, Wozniak TC, Ghumman W, Fadl YY, Obeidat OS, Schwab K, Meldrum DR. Medical and surgical treatment of acute right ventricular failure. J Am Coll Cardiol. 2010 Oct 26;56(18):1435-46. doi: 10.1016/j.jacc.2010.05.046. Review. PubMed PMID: 20951319 . [ Free Full Text ]
Walker LA, Buttrick PM. The right ventricle: biologic insights and response to disease: updated. Curr Cardiol Rev. 2013 Feb 1;9(1):73-81. Review. PubMed PMID: 23092273 ; PubMed Central PMCID: PMC3584309 .
Konstam MA, Kiernan MS, Bernstein D, Bozkurt B, Jacob M, Kapur NK, Kociol RD, Lewis EF, Mehra MR, Pagani FD, Raval AN, Ward C; American Heart Association Council on Clinical Cardiology; Council on Cardiovascular Disease in the Young; and Council on Cardiovascular Surgery and Anesthesia. Evaluation and Management of Right-Sided Heart Failure: A Scientific Statement From the American Heart Association. Circulation. 2018 May 15;137(20):e578-e622. doi: 10.1161/CIR.0000000000000560. Epub 2018 Apr 12. PMID: 29650544 . [ Free Full Text ]
Costanzo MR, Guglin ME, Saltzberg MT, Jessup ML, Bart BA, Teerlink JR, Jaski BE, Fang JC, Feller ED, Haas GJ, Anderson AS, Schollmeyer MP, Sobotka PA; UNLOAD Trial Investigators. Ultrafiltration versus intravenous diuretics for patients hospitalized for acute decompensated heart failure. J Am Coll Cardiol. 2007 Feb 13;49(6):675-83. doi: 10.1016/j.jacc.2006.07.073. Epub 2007 Jan 26. Erratum in: J Am Coll Cardiol. 2007 Mar 13;49(10):1136. PMID: 17291932 .
Bart BA, Goldsmith SR, Lee KL, Givertz MM, O’Connor CM, Bull DA, Redfield MM, Deswal A, Rouleau JL, LeWinter MM, Ofili EO, Stevenson LW, Semigran MJ, Felker GM, Chen HH, Hernandez AF, Anstrom KJ, McNulty SE, Velazquez EJ, Ibarra JC, Mascette AM, Braunwald E; Heart Failure Clinical Research Network. Ultrafiltration in decompensated heart failure with cardiorenal syndrome. N Engl J Med. 2012 Dec 13;367(24):2296-304. doi: 10.1056/NEJMoa1210357. Epub 2012 Nov 6. PMID: 23131078 ; PMCID: PMC3690472.

Critical Care

Chris Nickson

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University . He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine . He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE . He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com , the RAGE podcast , the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump .

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ICU Advanced Trainee BMedSci [UoN], BMed [UoN], MMed(CritCare) [USyd] from a broadacre farm who found himself in a quaternary metropolitan ICU. Always trying to make medical education more interesting and appropriately targeted; pre-hospital and retrieval curious; passionate about equitable access to healthcare; looking forward to a future life in regional Australia. Student of LITFL.

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Heart failure occurs when the heart muscle doesn't pump blood as well as it should. Blood often backs up and causes fluid to build up in the lungs and in the legs. The fluid buildup can cause shortness of breath and swelling of the legs and feet. Poor blood flow may cause the skin to appear blue or gray. Depending on your skin color, these color changes may be harder or easier to see. Some types of heart failure can lead to an enlarged heart.

If you have heart failure, your heart can't supply enough blood to meet your body's needs.

Symptoms may develop slowly. Sometimes, heart failure symptoms start suddenly. Heart failure symptoms may include:

Shortness of breath with activity or when lying down.
Fatigue and weakness.
Swelling in the legs, ankles and feet.
Rapid or irregular heartbeat.
Reduced ability to exercise.
A cough that doesn't go away or a cough that brings up white or pink mucus with spots of blood.
Swelling of the belly area.
Very rapid weight gain from fluid buildup.
Nausea and lack of appetite.
Difficulty concentrating or decreased alertness.
Chest pain if heart failure is caused by a heart attack.

When to see a doctor

See your health care provider if you think you might have symptoms of heart failure. Call 911 or emergency medical help if you have any of the following:

Chest pain.
Fainting or severe weakness.
Rapid or irregular heartbeat with shortness of breath, chest pain or fainting.
Sudden, severe shortness of breath and coughing up white or pink, foamy mucus.

These symptoms may be due to heart failure. But there are many other possible causes. Don't try to diagnose yourself.

At the emergency room, health care providers do tests to learn if your symptoms are due to heart failure or something else.

Call your health care provider right away if you have heart failure and:

Your symptoms suddenly become worse.
You develop a new symptom.
You gain 5 pounds (2.3 kilograms) or more within a few days.

Such changes could mean that existing heart failure is getting worse or that treatment isn't working.

More Information

Heart failure care at Mayo Clinic

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Chambers and valves of the heart

A typical heart has two upper and two lower chambers. The upper chambers, the right and left atria, receive incoming blood. The lower chambers, the more muscular right and left ventricles, pump blood out of the heart. The heart valves help keep blood flowing in the right direction.

Enlarged heart, in heart failure

If the heart weakens, as it can with heart failure, it begins to enlarge. This forces the heart to work harder to pump blood to the rest of the body.

Heart failure can be caused by a weakened, damaged or stiff heart.

If the heart is damaged or weakened, the heart chambers may stretch and get bigger. The heart can't pump out the needed amount of blood.
If the main pumping chambers of the heart, called the ventricles, are stiff, they can't fill with enough blood between beats.

The heart muscle can be damaged by certain infections, heavy alcohol use, illegal drug use and some chemotherapy medicines. Your genes also can play a role.

Any of the following conditions also can damage or weaken the heart and cause heart failure.

Coronary artery disease and heart attack. Coronary artery disease is the most common cause of heart failure. The disease results from the buildup of fatty deposits in the arteries. The deposits narrow the arteries. This reduces blood flow and can lead to heart attack.

A heart attack occurs suddenly when an artery feeding the heart becomes completely blocked. Damage to the heart muscle from a heart attack may mean that the heart can no longer pump as well as it should.

High blood pressure. Also called hypertension, this condition forces the heart to work harder than it should to pump blood through the body. Over time, the extra work can make the heart muscle too stiff or too weak to properly pump blood.
Heart valve disease. The valves of the heart keep blood flowing the right way. If a valve isn't working properly, the heart must work harder to pump blood. This can weaken the heart over time. Treating some types of heart valve problems may reverse heart failure.
Inflammation of the heart muscle, also called myocarditis. Myocarditis is most commonly caused by a virus, including the COVID-19 virus, and can lead to left-sided heart failure.
A heart problem that you're born with, also called a congenital heart defect. If the heart and its chambers or valves haven't formed correctly, the other parts of the heart have to work harder to pump blood. This may lead to heart failure.
Irregular heart rhythms, called arrhythmias. Irregular heart rhythms may cause the heart to beat too fast, creating extra work for the heart. A slow heartbeat also may lead to heart failure. Treating an irregular heart rhythm may reverse heart failure in some people.
Other diseases. Some long-term diseases may contribute to chronic heart failure. Examples are diabetes, HIV infection, an overactive or underactive thyroid, or a buildup of iron or protein.

Causes of sudden heart failure also include:

Allergic reactions.
Any illness that affects the whole body.
Blood clots in the lungs.
Severe infections.
Use of certain medicines.
Viruses that attack the heart muscle.

Heart failure usually begins with the lower left heart chamber, called the left ventricle. This is the heart's main pumping chamber. But heart failure also can affect the right side. The lower right heart chamber is called the right ventricle. Sometimes heart failure affects both sides of the heart.

Risk factors

Diseases and conditions that increase the risk of heart failure include:

Coronary artery disease. Narrowed arteries may limit the heart's supply of oxygen-rich blood, resulting in weakened heart muscle.
Heart attack. A heart attack is a form of coronary artery disease that occurs suddenly. Damage to the heart muscle from a heart attack may mean the heart can no longer pump as well as it should.
Heart valve disease. Having a heart valve that doesn't work properly raises the risk of heart failure.
High blood pressure. The heart works harder than it has to when blood pressure is high.
Irregular heartbeats. Irregular heartbeats, especially if they are very frequent and fast, can weaken the heart muscle and cause heart failure.
Congenital heart disease. Some people who develop heart failure were born with problems that affect the structure or function of their heart.
Diabetes. Having diabetes increases the risk of high blood pressure and coronary artery disease.
Sleep apnea. This inability to breathe properly during sleep results in low blood-oxygen levels and an increased risk of irregular heartbeats. Both of these problems can weaken the heart.
Obesity. People who have obesity have a higher risk of developing heart failure.
Viral infections. Some viral infections can damage to the heart muscle.

Medicines that may increase the risk of heart failure include:

Some diabetes medicines. The diabetes drugs rosiglitazone (Avandia) and pioglitazone (Actos) have been found to increase the risk of heart failure in some people. Don't stop taking these medicines without first talking to your health care provider.
Some other medicines. Other medicines that may lead to heart failure or heart problems include nonsteroidal anti-inflammatory drugs (NSAIDs) and some medicines used to treat high blood pressure, cancer, blood conditions, irregular heartbeats, nervous system diseases, mental health conditions, lung and urinary problems, and infections.

Other risk factors for heart failure include:

Aging. The heart's ability to work decreases with age, even in healthy people.
Alcohol use. Drinking too much alcohol may weaken the heart muscle and lead to heart failure.
Smoking or using tobacco. If you smoke, quit. Using tobacco increases the risk of heart disease and heart failure.

Complications

If you have health failure, it's important to have regular health checkups, even if symptoms improve. Your health care provider can examine you and run tests to check for complications.

Complications of heart failure depend on your age, overall health and the severity of heart disease. They may include:

Kidney damage or failure. Heart failure can reduce the blood flow to the kidneys. Untreated, this can cause kidney failure. Kidney damage from heart failure can require dialysis for treatment.
Other heart problems. Heart failure can cause changes in the heart's size and function. These changes may damage heart valves and cause irregular heartbeats.
Liver damage. Heart failure can cause fluid buildup that puts too much pressure on the liver. This fluid backup can lead to scarring, which makes it more difficult for the liver to work properly.
Sudden cardiac death. If the heart is weak, there is a risk of dying suddenly due to a dangerous irregular heart rhythm.

One way to prevent heart failure is to treat and control the conditions that can cause it. These conditions include coronary artery disease, high blood pressure, diabetes and obesity.

Some of the same lifestyle changes used to manage heart failure also may help prevent it. Try these heart-healthy tips:

Don't smoke.
Get plenty of exercise.
Eat healthy foods.
Maintain a healthy weight.
Reduce and manage stress.
Take medicines as directed.
Heart failure. National Heart, Lung, and Blood Institute. https://www.nhlbi.nih.gov/health-topics/heart-failure. Accessed Nov. 30, 2022.
Ferri FF. Heart failure. In: Ferri's Clinical Advisor 2023. Elsevier; 2023. https://www.clinicalkey.com. Accessed Nov. 30, 2022.
Colucci WS. Determining the etiology and severity of heart failure or cardiomyopathy. https://www.uptodate.com/contents/search. Accessed Nov. 30, 2022.
Colucci WS. Evaluation of the patient with suspected heart failure. https://www.uptodate.com/contents/search. Accessed Nov. 30, 2022.
Heart failure (HF). Merck Manual Professional Version. https://www.merckmanuals.com/professional/cardiovascular-disorders/heart-failure/heart-failure-hf. Accessed Nov. 28, 2022.
Vasan RS, et al. Epidemiology and causes of heart failure. https://www.uptodate.com/contents/search. Accessed Nov. 28, 2022.
Goldman L, et al., eds. Goldman-Cecil Medicine. 26th ed. Elsevier; 2020. https://www.clinicalkey.com. Accessed Nov. 28, 2022.
AskMayoExpert. Heart failure with reduced ejection fraction (HFrEF) (adult). Mayo Clinic; 2022.
Rakel D, ed. Heart failure. In: Integrative Medicine. 4th ed. Elsevier; 2018. https://www.clinicalkey.com. Accessed Nov. 28, 2022.
AskMayoExpert. Heart failure with preserved ejection fraction (HFpEF) (adult). Mayo Clinic; 2022.
Allen L. Palliative care for patients with advanced heart failure: Decision support, symptom management, and psychosocial assistance. https://www.uptodate.com/contents/search. Accessed Nov. 28, 2022.
The dying patient. Merck Manual Professional Version. http://www.merckmanuals.com/professional/special-subjects/the-dying-patient/the-dying-patient. Accessed Nov. 28, 2022.
Ami TR. Allscripts EPSi. Mayo Clinic. Oct. 4, 2022.
Mancini D. Heart transplantation in adults: Indications and contraindications. https://www.uptodate.com/contents/search. Accessed Nov. 28, 2022.
Sawalha K, et al. Systematic review of COVID-19 related myocarditis: Insights on management and outcome. Cardiovascular Revascularization Medicine. 2021; doi:10.1016/j.carrev.2020.08.028.
Armstrong PW, et al. Vericiguat in patients with heart failure and reduced ejection fraction. The New England Journal of Medicine. 2020; doi:10.1056/NEJMoa1915928.
Armstrong PW, et al. A multicenter, randomized, double-blind, placebo-controlled trial of the efficacy and safety of the oral soluble guanylate cyclase stimulator. Journal of the American College of Cardiology: Heart Failure. 2018; doi:10.1016/j.jchf.2017.08.013.
Verquvo (approval letter). New Drug Application 214377. U.S. Food and Drug Administration. https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=214377. Accessed Nov. 28, 2022.
Heidenreich PA, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure: A report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022; doi:10.1161/CIR.0000000000001063.
Clarke JD, et al. Effect of inotropes on patient-reported health status in end-stage heart failure: A review of published clinical trials. Circulation: Heart Failure. 2021; doi:10.1161/CIRCHEARTFAILURE.120.007759.
Lopez-Jimenez F (expert opinion). Mayo Clinic. Dec. 2, 2021.
Types of heart failure. American Heart Association. https://www.heart.org/en/health-topics/heart-failure/what-is-heart-failure/types-of-heart-failure. Accessed Nov. 28, 2022.
Zannad F, et al. SGLT2 inhibitors in patients with heart failure with reduced ejection fraction: a meta-analysis of the EMPEROR-Reduced and DAPA-HF trials. Lancet. 2020; doi:10.1016/S0140-6736(20)31824-9.
Sodium-glucose cotransporter-2 (SGLT2) inhibitors. U.S. Food and Drug Administration. https://www.fda.gov/drugs/postmarket-drug-safety-information-patients-and-providers/sodium-glucose-cotransporter-2-sglt2-inhibitors. Accessed Jan. 10, 2022.
Lee MCH, et al. Clinical efficacy of SGLT2 inhibitors with different SGLT1/SGLT2 selectivity in cardiovascular outcomes among patients with and without heart failure: A systematic review and meta-analysis of randomized trials. Medicine (Baltimore). 2022; doi:10.1097/MD.0000000000032489.
Mankad R (expert opinion). Mayo Clinic. Jan. 12, 2023.
ACC, AHA, HFSA issue heart failure guideline. American Heart Association. https://newsroom.heart.org/news/acc-aha-hfsa-issue-heart-failure-guideline. Accessed Jan. 31, 2023.
Heart failure action plan
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Echocardiogram
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Palliative care
Stress test
Ventricular assist device

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Signs of Right-Sided Heart Failure

Frequent symptoms, rare symptoms, complications, when to see a doctor.

When your heart is healthy, it evenly moves your blood throughout your body. But, if your heart muscles begin to weaken, they can’t pump enough blood through your body.

Heart failure can affect just one side of your heart or both sides. This article covers the signs of right-sided heart failure and when you should seek medical attention for your symptoms.

Jose Luis Pelaez Inc / Getty Images

When your heart is healthy, blood moves from your veins into the right side of your heart. From there, it goes into the lungs to pick up oxygen, then moves through the left side of your heart and is pumped through the rest of your body.

If you have right-sided heart failure, the right side of your heart can’t handle all the blood being returned to it by your veins. Consequently, blood begins to back up in your veins.

Here are some of the common signs of right-sided heart failure:

Swelling in legs and feet (known as edema ): When your blood backs up in your veins, some of the fluid can escape from your veins into the surrounding tissues. Swelling and fluid retention is one of the most common symptoms of heart failure.
Shortness of breath : Feeling short of breath after doing everyday activities is one of the early signs of heart failure because you aren’t getting enough oxygen from your blood. As your heart grows weaker, you may notice trouble catching your breath after simpler activities like getting dressed.
Coughing : As your heart grows weaker, you may feel the need to cough more regularly.
Swelling in the abdomen : Fluid may accumulate in your abdominal cavity from heart failure. This is also known as ascites .
Dizziness and difficulty concentrating : A weaker heart could lower the amount of oxygen getting to your brain. This may lead to trouble focusing, confusion, and dizziness.
Chest discomfort : Swelling and fluid in your chest can leave you feeling pressure or pain in your chest.
Increased need to urinate : Needing to go more frequently, especially at night, could be a sign of heart failure.
Fatigue : Feeling low on energy often could be a sign of heart failure. You may feel like it is more difficult to sleep from trouble breathing while lying flat and increased need to use the bathroom at night.
Poor appetite and nausea : Fluid buildup in your abdomen puts pressure on your stomach. This may make you feel full quickly, suppress your appetite, and leave you feeling sick or nauseous.
Gaining weight quickly : A sudden increase in weight (5 pounds or more within a few days) could be a sign you are retaining fluid.

Less common symptoms of right-sided heart failure can be indicators of worsening heart function, and some symptoms can be life threatening.

Rare symptoms include:

Bulging veins in your neck : Swelling in the veins in your neck can be a sign of heart failure.
Pulmonary edema : Fluid buildup in your lungs happens more often as heart failure progresses and is usually a sign that the left side of the heart is also affected. Pulmonary edema causes difficulty breathing, especially when laying flat, and can become life threatening without treatment.
Heart palpitations and irregular heartbeat : Feeling like your heart is racing, fluttering, or skipping a beat isn’t always a sign of heart problems, but these can be symptoms of right-sided heart failure.
Fainting or passing out : If you pass out or lose consciousness, it could be a sign of a medical emergency. It’s recommended to call your doctor or seek medical attention if you or a loved one experiences this.
Coughing up pink or bloody mucus : If you are coughing up blood-tinged mucus, this could be a sign of worsening pulmonary edema. Contact your doctor or seek medical attention if you notice pink, blood-tinged phlegm.
Low blood pressure : Low blood pressure, also called hypotension, occurs in about 10% to 15% of people with heart failure. It’s usually a later symptom of heart failure and often indicates a low ejection fraction (the percent of blood moving out of the heart with each pump).

If you have heart failure, it can take a toll on other areas of your body. Complications of right-sided heart failure can include:

Liver damage : If fluid builds up in your abdomen, it can put pressure on the blood vessels around your liver. Over time, this can lead to scarring and tissue damage in your liver which interferes with healthy liver function.
Kidney damage : The fluid and blood flow changes from heart failure can lead to chronic kidney disease or renal failure. If left untreated, renal failure can require long-term dialysis .
Malnutrition : Heart failure can lower your appetite and energy levels, making it difficult to eat the amount of food your body needs. Low food intake can lead to severe muscle and fat loss, as well as vitamin and mineral deficiencies.
Heart valve dysfunction : The valves in your heart keep blood flowing in the right direction. Weakened muscles and backed-up blood can interfere with these valves. Weak heart valves may lead to blood leaking back through the valve instead of moving forward.
Cardiac arrest : Heart failure increases the risk for sudden cardiac arrest (heart attack).

It’s a good idea to speak with your doctor to check your heart health if you:

Notice swelling in your legs
Become winded easily with normal activities

There is no cure for heart failure. Still, with treatment, you can slow the progression of it and stay feeling better for longer.

You should seek immediate medical attention or call 911 if you or a loved one is experiencing:

Sudden shortness of breath, irregular heartbeat, or chest pain
Trouble breathing and blood-tinged phlegm
Fainting or loss of consciousness

A Word From Verywell

Experiencing problems with your heart can be frightening, leading some people to ignore the symptoms. You likely won’t experience all of the signs of right-sided heart failure right away. It’s important to share symptoms that seem minor and any changes in your health with your doctor.

While there is no treatment to reverse heart failure, medications and lifestyle changes can help keep your heart muscles strong and slow the progression of heart failure.

American Heart Association. Types of heart failure .

Cautela J, Tartiere J-M, Cohen-Solal A, et al. Management of low blood pressure in ambulatory heart failure with reduced ejection fraction patients . European Journal of Heart Failure . 2020;22(8):1357-1365. doi:10.1002/ejhf.1835

National Heart, Lung, and Blood Institute. Heart failure .

By Ashley Braun, MPH, RD Ashley Braun, MPH, RD, is a registered dietitian and public health professional with over 5 years of experience educating people on health-related topics using evidence-based information. Her experience includes educating on a wide range of conditions, including diabetes, heart disease, HIV, neurological conditions, and more.

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European Society of Cardiology
e-Journal of Cardiology Practice
E-Journal of Cardiology Practice - Volume 14

Right ventricular failure

Dr. Bassem Sobhi Ibrahim

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.

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 stems 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.

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 through 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 via 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; and 4) LV dilatation can impair RV diastolic function by increasing pericardial constraint. Nowadays, with the increasing use of ACE inhibitors and beta-blockers, patients with LVF more frequently 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.

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 than in 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].

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 30–50% 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's 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 and 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.

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.

Voelkl N. F., Quaife R. A., Leinwand L. A., Barst R. J., McGoon M. D., Meldrum D. R., Dupuis J., Long C. S., Rubin L. J., Smart F. W., Suzuki Y. J., Gladwin M., Denholm E. M., & Gail D. B. National Heart, Lung, and Blood Institute Working Group on Cellular and Molecular Mechanisms of Right Heart Failure. Right ventricular function and failure. Report of the National Heart, Lung, and Blood Institute working group on cellular and molecular mechanisms of right heart failure. Circulation. 2006 Oct. 24 114 (17): 1883-91.
Mockel M., Searle J., Muller R., Slagman A., Storchmann H., Oestereich P., Wyrwich W., Ale-Abaei A., Vollert J. O., Koch M., & Somasundaram R. Chief complaints in medical emergencies: do they relate to underlying disease and outcome? The Charité Emergency Medicine Study (CHARITEM). Eur J Emerg Med. 2013 April 20 (2): 103-8.
Hassanein M., Abdelhamid M., Ibrahim B., Elshazly A., Aboleineen M. W., Sobhy H., Nasr G., Elmesseiry F., Abdelmoniem A., Ashmawy M., Farag N., Youssef A., Elbahry A., Elrakshy Y., Sobhy M., Abdel Dayem T. M., Ebeid H., Reda A., Boshra H., Saleh A., & Maggioni A. P. Clinical characteristics and management of hospitalized and ambulatory patients with heart failure--results from ESC heart failure long-term registry--Egyptian cohort. ESC Heart Failure. 2015 2: 159-67.
Galie N., Humbert M., Vachiery J. L., Gibbs S., Lang I., Torbicki A., Simonneau G., Peacock A., Vonk Noordegraaf A., Beghetti M., Ghofrani A., Gomez Sanchez M. A., Hansmann G., Klepetko W., Lancellotti P., Matucci M., McDonagh T., Pierard L. A., Trindade P. T., Zompatori M., Hoeper M., Aboyans V., Vaz Carneiro A., Achenbach S., Agewall S., Allanore Y., Asteggiano R., Paolo Badano L., Albert Barberà J., Bouvaist H., Bueno H., Byrne R. A., Carerj S., Castro G., Erol Ç., Falk V., Funck-Brentano C., Gorenflo M., Granton J., Iung B', Kiely D. G., Kirchhof P., Kjellstrom B., Landmesser U., Lekakis J., Lionis C., Lip G. Y., Orfanos S. E., Park M. H., Piepoli M. F., Ponikowski P., Revel M. P., Rigau D., Rosenkranz S., Völler H., & Luis Zamorano J. 2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension: The Joint Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS). Endorsed by the Association for European Paediatric and Congenital Cardiology (AEPC), International Society for Heart and Lung Transplantation (ISHLT). Eur Heart J. 2016 Jan. 37 (1): 67-119.
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Dazner M. H., Rame E., Stevenson L. W., & Dries D. L. Prognostic importance of elevated jugular venous pressure and a third heart sound in patients with heart failure. N Engl J Med. 2001 Aug. 23 345: 574-81.
Bleeker G. B., Steendijk P., Holman E. R., Yu C. M., Breithardt O. A., Kaandorp T. A., Schalij M. J., van der Wall E. E., Bax J. J., & Nihoyannopoulos P. Acquired right ventricular dysfunction. Heart. 2006 April 92 Suppl I: i14-8.
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Krüger S., Graf J., Merx M. W., Koch K. C., Kunz D., Hanrath P., & Janssens U. Brain natriuretic peptide predicts right heart failure in patients with acute pulmonary embolism. Am Heart J. 2004 Jan. 14 7(1): 60-5.
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Notes to editor

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:

Consultant Cardiology

Cardiology Department

Nevill Hall Hospital, Abergavenny, NP7 7EG

Email: [email protected]

Author disclosures:

The author has no conflicts of interest to declare.

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Right Heart Failure
When addressing heart failure, most commonly, the left ventricle (LV) is the topic of discussion, and the right heart overlooked. However, the right ventricle (RV) is unique in structure and function and is affected by a set of disease processes that rival that of the LV. This article will review the normal structure and function of the RV, describe the pathophysiology of RV failure (RVF), and ...
Right heart failure: Clinical manifestations and diagnosis
INTRODUCTION. Right heart failure (RHF) is a clinical syndrome in which symptoms and signs are caused by dysfunction of the right heart structures (predominantly the right ventricle [RV] but also the tricuspid valve apparatus and right atrium) or pericardium, resulting in impaired ability of the right heart to perfuse the lungs at normal ...
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In right-sided heart failure, the heart's right ventricle is too weak to pump enough blood to the lungs. As blood builds up in the veins, fluid gets pushed out into the tissues in the body. Right-sided heart failure symptoms include swelling and shortness of breath. Treatment focuses on stopping progression of the disease and improving symptoms.
Right heart failure: Causes and management
INTRODUCTION. Right heart failure (RHF) is a clinical syndrome in which symptoms and signs are caused by dysfunction of the right heart structures (predominantly the right ventricle [RV], but also the tricuspid valve apparatus and right atrium) or impaired vena cava flow, resulting in impaired ability of the right heart to perfuse the lungs at ...
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The authors discuss the mechanisms, clinical presentation, and evaluation of right ventricular failure, ... Bernstein D, et al. Evaluation and management of right-sided heart failure: a scientific ...
Evaluation and Management of Right-Sided Heart Failure: A Scientific
Background and Purpose: The diverse causes of right-sided heart failure (RHF) include, among others, primary cardiomyopathies with right ventricular (RV) involvement, RV ischemia and infarction, volume loading caused by cardiac lesions associated with congenital heart disease and valvular pathologies, and pressure loading resulting from pulmonic stenosis or pulmonary hypertension from a ...
Right sided heart failure: Symptoms, outlook, treatment
Left sided heart failure is the primary cause of right sided heart failure. When the left ventricle is not working as effectively, fluid pressure increases and ends up moving back through the lungs.
Right-Sided Heart Failure: Symptoms, Causes, Treatment
Some other causes of right-side heart failure include: Coronary artery disease. This is the most common form of heart disease and cause of heart failure. When you have coronary artery disease ...
Heart Failure Clinical Presentation
In older children, left-sided venous congestion causes tachypnea, respiratory distress, and wheezing (cardiac asthma). Right-sided congestion may result in hepatosplenomegaly, jugular venous distention, edema, ascites, and/or pleural effusions. Uncompensated heart failure in older children may cause fatigue or lower-than-usual energy levels.
Right Ventricular Failure • LITFL • CCC Cardiology
Management of acute right-sided heart failure. All management must be undertaken with an awareness of the patient's hemodynamic status. If this status is not clear clinically, then invasive assessment/monitoring should be undertaken. Hemodynamic targets provide rough guidelines for tailored therapy.
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Heart failure usually begins with the lower left heart chamber, called the left ventricle. This is the heart's main pumping chamber. But heart failure also can affect the right side. The lower right heart chamber is called the right ventricle. Sometimes heart failure affects both sides of the heart.
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Right-sided heart failure (RHF) and tricuspid regurgitation (TR) ... Clinical presentation and course. Right HF and TR are debilitating conditions strongly affecting quality of life, hospitalization rates and survival. 38 They can be considered as parts of a multi-organ syndrome involving cardiac ...
Evaluation and Management of Right-Sided Heart Failure
heart failure (HF), after cardiac surgery, acute myocardial infarction (MI), congenital heart disease (CHD), and PH. To distinguish right-sided HF (RHF) from structural RVD, we define RHF as a clinical syndrome with signs and symp-toms of HF resulting from RVD.1 RHF is caused by the inability of the RV to support optimal circulation in the
Right-Sided Heart Failure: Symptoms and Complications
Here are some of the common signs of right-sided heart failure: Swelling in legs and feet (known as edema ): When your blood backs up in your veins, some of the fluid can escape from your veins into the surrounding tissues. Swelling and fluid retention is one of the most common symptoms of heart failure. Shortness of breath: Feeling short of ...
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Guideline-directed medical therapy (GDMT) for heart failure (HF) with reduced ejection fraction (HFrEF) now includes 4 medication classes that include sodium-glucose cotransporter-2 inhibitors (SGLT2i). Patients with advanced HF who wish to prolong survival should be referred to a team specializing ...
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Right-sided or right ventricular heart failure usually occurs as a result of left-sided failure. When the left ventricle fails and can't pump enough blood out, increased fluid pressure is transferred back through the lungs. This damages the heart's right side. When the right side loses pumping power, blood backs up in the body's veins.
Right ventricular failure
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.
Left vs. right sided heart failure: Symptoms, treatment, and more
Left sided heart failure is more common, and right sided heart failure usually occurs as a result of left sided heart failure. Certain conditions, such as CAD and high blood pressure, have close ...