- Fainting spells during activity.
- Chest discomfort, usually in the front of the chest.
- Chest pain.
- Swelling of the feet or ankles.
- Symptoms of lung disorders, such as wheezing or coughing or phlegm production.
- Bluish lips and fingers (cyanosis)
Which symptom is most commonly associated with right-sided heart failure?
The main sign of right-sided heart failure is fluid buildup. This buildup leads to swelling (edema) in your: Feet, ankles and legs.
What happens when you have right-sided heart failure?
Right-side vs. Left-side Heart Failure – When your heart is working normally, it pumps oxygen-rich blood through your lungs and to the rest of your body. The left ventricle, or left chamber, of the heart provides most of the heart’s pumping power. So when you have left-side heart failure, your heart can’t pump enough blood to your body.
The right ventricle, or right chamber, moves “used” blood from your heart back to your lungs to be resupplied with oxygen. So when you have right-side heart failure, the right chamber has lost its ability to pump. That means your heart can’t fill with enough blood, and the blood backs up into the veins.
If this happens, your legs, ankles, and belly often swell.
How do you detect right-sided heart failure?
Diagnosis – Diagnosis of right-sided heart failure typically requires a thorough physical examination by a cardiologist as well as medical history and any of a variety of tests. When reviewing health history, they will be especially suspicious of heart failure if you have had deep venous thrombosis or pulmonary embolus. Tests used to diagnose right-sided heart failure include:
- Electrocardiogram (ECG ) and echocardiogram studies, which can reveal elevated pulmonary artery pressure and may also reveal valvular heart disease or disease affecting the cardiac muscle
- Pulmonary function testing to confirm the presence and severity of COPD
- Blood tests to measure substances in the blood released in response to heart failure and to assess kidney, liver, and thyroid function
- Sleep study to determine if apnea is a factor
- Computerized tomography (CT) scans, which are 3-D X-rays of the heart
- Magnetic Resonance Imaging (MRI) which use radio waves, magnets, and a computer to create detailed pictures of the heart
- Cardiac catheterization, in which a catheter is inserted into a chamber or vessel of the heart to diagnose blockages and defects
- Coronary angiography, which involves injecting dye that can be seen on an X-ray into the heart chambers so the flow of blood through the heart can be visualized
- Chest X-rays to determine whether the heart is enlarged and/or the lungs are congested
- Cardiac stress testing, which assesses heart function during exercise under controlled conditions: Used along with an EKG, the test can show changes to the heart’s rate, rhythm, or electrical activity as well as blood pressure.
What is the number one cause of right-sided heart failure?
The most common cause of right-sided heart failure is actually left-sided heart failure. But other conditions, such as certain lung diseases, can cause the right ventricle to fail even when there is no problem with your left ventricle.
How quickly does heart failure progress?
Symptoms of heart failure – The main symptoms of heart failure are:
breathlessness after activity or at restfeeling tired most of the time and finding exercise exhaustingfeeling lightheaded or faintingswollen ankles and legs
Some people also experience other symptoms, such as a persistent cough, a fast heart rate and dizziness, Symptoms can develop quickly (acute heart failure) or gradually over weeks or months (chronic heart failure).
What can be done for right-sided heart failure?
Surgery and Other Procedures – If medications are not effective in managing right-sided heart failure, or if symptoms are severe, a ventricular-assist device implant or a heart transplant, may be necessary.
Ventricular assist device (VAD) surgery: This device can be implanted to help a weak heart pump more efficiently. Heart transplant surgery: This surgery is done when all other right-sided heart failure treatments have failed. The damaged heart is surgically removed and replaced with a healthy heart from a deceased donor.
What is the treatment for right heart failure?
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Abstract The prognostic significance of the right ventricle (RV) has recently been recognised in several conditions, primarily those involving the left ventricle, the lungs and their vascular bed, or the right-sided chambers. Recent advances in imaging techniques have created new opportunities to study RV anatomy, physiology and pathophysiology, and contemporary research efforts have opened the doors to new treatment possibilities.
- Nevertheless, the treatment of RV failure remains challenging.
- Optimal management should consider the anatomical and physiological particularities of the RV and include appropriate imaging techniques to understand the underlying pathophysiological mechanisms.
- Treatment should include rapid optimisation of volume status, restoration of perfusion pressure and improvement of myocardial contractility and rhythm, and, in case of refractory RV failure, mechanical circulatory support.
Disclosure: MA received lecture fees from Orion Pharma. SW received lecture fees from the European Society of Cardiology, and travel support from Bayer and Daichi Sankyo. All other authors have no conflicts of interest to declare. Received: 13 May 2019 Accepted: 05 July 2019 Published online: 04 November 2019 Correspondence Details: Mattia Arrigo, Acute Cardiology and Heart Failure Unit, Department of Cardiology – University Heart Center, University Hospital Zurich, Raemistrasse 100, 8091 Zurich, Switzerland.
E: [email protected] Open Access: This work is open access under the CC-BY-NC 4.0 License which allows users to copy, redistribute and make derivative works for non-commercial purposes, provided the original work is cited correctly. In 1616, Sir William Harvey was the first person to describe the importance of right ventricular function.1 However, the right ventricle (RV) has received little attention in the past, with cardiology dealing mostly with the diseases of the left ventricle (LV) and their potential treatment.
Since the early 1950s, however, the prognostic significance of RV function has been recognised in several conditions, primarily those involving the LV (e.g. chronic LV failure), the lungs and their vascular bed (e.g. pulmonary embolism, chronic pulmonary disease and pulmonary arterial hypertension) or the right-sided chambers (e.g.
- RV infarction, RV cardiomyopathies and congenital heart diseases).
- Recent advances in imaging techniques have created new opportunities to study RV anatomy, physiology and pathophysiology, and contemporary research efforts have opened the doors to new treatment possibilities.2,3 Nevertheless, the treatment of RV failure remains challenging.
This article aims to provide an overview of the pathophysiology, diagnosis and treatment of RV failure. Anatomical and Physiological Particularities of the Right Ventricle The RV is a unique chamber with distinct anatomy and physiology.4 It is coupled to systemic venous return and the pulmonary circulation.
- Since the pressure in the pulmonary circulation is generally much lower than it is in the systemic circulation, less muscle power is needed (a quarter of the LV stroke work).5 Therefore, the RV needs fewer muscle fibres and is much thinner than the LV, having about one-third of the thickness.
- Furthermore, venous return fluctuates, so the RV is much more compliant and is slightly larger (approximately 10–15%) than the LV, which allows it to accommodate large variations in venous return without altering end-diastolic pressure.
Each systolic contraction leads to a primarily longitudinal shortening, whereas LV contraction is more circumferential.6 Notably, both ventricles share the septum, and up to 40% of the RV systolic function is dependent on septal contraction.7 During exercise, a 30–50% decrease in predicted VO 2 max can be seen in healthy Fontan patients, which indirectly highlights the critical role of the RV for maintaining cardiac output.8 The RV consists of the inlet with the tricuspid valve, chordae tendineae, at least three papillary muscles, the trabeculated apex and the infundibulum (a muscular structure supporting the pulmonary valve leaflets).
- For imaging analysis, the RV is divided into four segments: the infundibulum, and the anterior, lateral and inferior wall.9 The right coronary artery, at least in most individuals, perfuses the RV free wall and the posterior third of the interventricular septum.
- The left anterior descending artery perfuses the apex and the anterior part of the septum.
Unlike the LV, RV perfusion occurs both in systole and diastole and the collateral vessels of the RV are denser than those of the LV. However, because of its thinner wall and higher dependence on coronary perfusion pressure, RV perfusion is more vulnerable to an increase in RV size (intramural pressure) and systemic hypotension.10 One of the main characteristics of the RV is its greater sensitivity to changes in afterload. Brisk increases in afterload are poorly tolerated and lead to RV dilatation to preserve stroke volume. One seminal work highlighted the response of the right and left ventricle to experimental increases in afterload.
While an increase on the left side leads to only a slight decrease in stroke volume, the same increase in the RV results in a marked fall in stroke volume ( Figure 1 ). A further important characteristic is ventricular interdependence. Excessive RV volume loading is constrained by the pericardium and therefore results in compression and D-shaping of the LV Volume overload in the RV therefore indirectly leads to a decrease in LV stroke volume.
The anatomical and functional particularities of the RV have been reviewed in detail elsewhere.4 Causes and Pathophysiology of Right Ventricular Failure The normal RV function is an interplay between preload, contractility, afterload, ventricular interdependence and heart rhythm.
Most cases of RV failure follow existing or new-onset cardiac or pulmonary diseases or a combination of both, which may increase RV afterload, reduce RV contractility, alter RV preload or ventricular interdependence or cause-related arrhythmias ( Table 1 and Figure 2 ). To understand RV failure, it is crucial to assess these five components.
Right Ventricular Failure in Cardiac Disease Increased afterload is the main pathophysiologic mechanism for RV failure of both pulmonary and cardiac origin. Indeed, the prevalence of left ventricular systolic or diastolic dysfunction and (post-capillary) pulmonary hypertension in patients with RV failure is particularly high, which corroborates the concept that the majority of RV failure is secondary to left-sided cardiac or pulmonary (vascular) diseases.11 Increased afterload is also a main cause of ventricular failure in patients with systemic RV (e.g.
- Patients after atrial switch repair for complete transposition of the great arteries, with congenitally corrected transposition of the great arteries or after Fontan palliation) or with obstruction of the RV outflow tract.
- In patients with other forms of adult congenital heart disease (e.g.
- Atrial septal defect with relevant left-to-right shunt or severe pulmonary regurgitation in repaired Fallot’s tetralogy), chronic volume overload may induce RV dilation and failure.
Cardiac diseases involving the right heart may primarily reduce RV contractility or, through reduced cardiac output, reduce RV preload, contributing to RV failure. Virtually all myocardial diseases involving the left heart may affect the RV. These include myocardial ischaemia/infarction, myocarditis/septic cardiomyopathy, takotsubo cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, cardiac amyloidosis and Chagas disease.
Cardiomyopathies with primary involvement of the RV include arrhythmogenic RV cardiomyopathy (characterised by fibrofatty replacement of the RV myocardium), Uhl’s anomaly (which involves aplasia or hypoplasia of most of the RV myocardium), and Ebstein’s anomaly (defined as apical displacement of the septal and posterior tricuspid leaflets, which induces severe tricuspid regurgitation).
Pericardial diseases may alter RV preload and ventricular interdependence, while arrhythmia may aggravate RV dysfunction. Notably, iatrogenic RV failure through excessive volume loading or mechanical ventilation is frequently seen in critically ill patients, while ischaemic RV injury is sometimes seen after cardiac surgery.
- Finally, RV failure may be exacerbated in patients undergoing left ventricular assist device (LVAD) implantation, causing high morbidity and mortality and requiring temporary RV support.
- This topic has been reviewed extensively elsewhere.12 Right Ventricular Failure in Pulmonary Disease RV failure as a consequence of lung disease is commonly described as cor pulmonale.
These changes might occur dramatically – for example in fulminant pulmonary embolism – or might be due to longstanding respiratory disorders that result in chronic alterations of RV structure and function. In the context of acute respiratory insufficiency in a previously healthy individual, impending RV failure is almost exclusively seen with massive pulmonary embolism.
Of note, the elevation of pulmonary pressure following acute pulmonary embolism is observed only when more than half of the pulmonary vasculature is obstructed by thrombotic material.13 This is because distension and recruitment of additional pulmonary capillaries might decrease vascular resistance and compensate for circulatory changes.14 When thrombotic occlusion extends to more than 50% of the lung vessels and, in turn, pressure elevation occurs, the unconditioned RV can overcome a mean pulmonary arterial pressure of up to 40 mmHg.15 A higher afterload results in acute RV failure and obstructive shock.
Conversely, if there is acute pulmonary embolism and the RV is exposed to higher pressure values and can tolerate it, a pre-existing elevation of pulmonary pressure (i.e. the presence of pulmonary hypertension) with an antecedent adaption of the RV must be assumed.
- Many chronic lung diseases affect the pulmonary circulation and the right heart, but chronic obstructive pulmonary disease (COPD) is the most prevalent cause of respiratory insufficiency and cor pulmonale.
- COPD increases RV afterload by several mechanisms, including rarefaction of the vascular bed, hypercapnia and acidosis, pulmonary hyperinflation, airway resistance, endothelial dysfunction and hypoxia.16 Of these factors, hypoxia is arguably the most prominent driver of pulmonary hypertension and subsequent RV failure.
Hypoxic pulmonary vasoconstriction (the Euler-Liljestrand effect) results in pulmonary pressure elevation and, when persistent, vascular remodelling and fixed pulmonary hypertension.17 The presence of pulmonary hypertension has long been considered as the conditio sine qua non for the development of a cor pulmonale,18 Recent data have challenged this assumption and suggested that, in patients with lung disease, structural alterations in cardiac myocytes predate the development of clinically manifested pulmonary hypertension.19 As such, cor pulmonale and failing RV syndrome in lung disease may be part of a disease spectrum rather than being distinct entities.20 With its impact on RV function, pulmonary hypertension – more than airflow limitation – is the strongest predictor of an adverse outcome and mortality in patients with lung disease.
Diagnosis of Right Ventricular Failure Clinical Signs The clinical signs of RV failure are mainly determined by backward failure causing systemic congestion. In severe forms, the right heart dilates and, through interventricular dependence, can compromise LV filling, reducing LV performance and causing forward failure (i.e.
hypotension and hypoperfusion). Backward failure presents as elevated central venous pressure with distension of the jugular veins and may lead to organ dysfunction and peripheral oedema.21 The association between systemic congestion and renal, hepatic and gastrointestinal function in heart failure has been extensively studied.22 Elevated central venous pressure is the main determinant of impaired kidney function in acute heart failure.23,24 Hepatic dysfunction is also highly prevalent in acute heart failure; systemic congestion frequently presents with a cholestatic pattern, while hypoperfusion typically induces a sharp increase in circulating transaminases.25 Finally, systemic congestion may alter abdominal function, including reduced intestinal absorption and impaired intestinal barrier.26 ECG The ECG in chronic RV failure often shows right axis deviation as a consequence of RV hypertrophy.
- Other ECG criteria are RS-ratio in lead V5 or V6 ≤1, SV5 or V 6≥7 mm, P-pulmonale or a combination of these.
- While the sensitivity of those criteria is quite low (18–43%), the specificity ranges from 83% to 95%.27 RV strain is sometimes seen in massive pulmonary embolism as an initial S deflection in I, an initial Q-deflection in III and T-Inversions in III (high specificity, low sensitivity), as well as in V1–V4.28 Moreover, RV failure is often accompanied by atrial flutter or AF.
Imaging The primary working tool for imaging the (failing) RV is echocardiography. It should be emphasised that a comprehensive assessment of the anatomy and function of the right heart should include left heart function, pulmonary haemodynamics, the tricuspid valve and the right atrium. However, because of the RV’s complex shape, echocardiography can only partially visualise it. Careful attention should be paid in obtaining an RV focused view from the apical four-chamber view with rotation of the transducer to obtain the maximal plane.8 Other views, such as the short axis and RVOT view, add anatomical and functional information. Guidelines recommend a comprehensive approach and using a combination of these measurements to assess RV function as none of them alone can adequately describe RV function in different scenarios.29 Moreover, these measurements are all somewhat load dependent and therefore subject to physiologic variation. Newer imaging techniques, such as 3D-echocardiography and strain imaging, have proven to be useful and accurate imaging modalities but have limitations because they depend on good image quality and lack validation in larger cohorts.31,32 Cardiac MRI has become the standard reference method for right heart acquisition as it is capable of visualising anatomy, quantifying function and calculating flow. In addition, it is useful in cases where image quality by echocardiography is limited. Moreover, it can provide advanced imaging with tissue characterisation, which is useful in different cardiomyopathies, such as arrhythmogenic RV cardiomyopathy, storage disease and cardiac tumours. Limitations are mainly due to the thinness of the RV wall, which can make it challenging to differentiate it from surrounding tissues.9 In addition, pacemakers or pacemaker leads may interfere with image acquisition during MRI and lead to artefacts that impair visualisation of the RV walls. Cardiac CT and nuclear imaging play a minor role although cardiac CT can help to visualise anatomy when MRI is not feasible. There are concerns regarding radiation exposure from both nuclear imaging and dynamic imaging by CT angiography. Medical Treatment of Acute Right Ventricular Failure The Heart Failure Association and the Working Group on Pulmonary Circulation and Right Ventricular Function of the European Society of Cardiology recently published a comprehensive statement on the management of acute RV failure.33 The triage and initial evaluation of patients presenting with acute RV failure aim to assess clinical severity and identify the cause(s) of RV failure, with a focus on those requiring specific treatment. Management of acute RV failure requires not only an understanding of the anatomical and physiological particularities of the RV but also rapid identification and treatment of the underlying causes and related pathophysiological disorders (see above). In this context, echocardiography and other imaging modalities are frequently essential to identify the cause of RV failure and guide treatment. In patients presenting with severe RV failure, rapid initiation of treatment to restore haemodynamic stability is essential to prevent significant, potentially irreversible end-organ damage. Acute treatment consists of four elements: volume optimisation; restoration of perfusion pressure; improvement of myocardial contractility; and advanced options ( Figure 3 ). Volume Optimisation A common misconception is that RV failure should consistently be treated with volume supplementation. Conversely, while the RV might physiologically be able to accommodate large variations in preload and some patients with RV failure are preload dependent, a large proportion of RV failure is caused, associated with or aggravated by RV volume overload. In such cases, volume loading has the potential to overdistend the RV and thereby increase wall tension, decrease contractility, aggravate tricuspid regurgitation, increase ventricular interdependence, impair LV filling and, ultimately, reduce systemic cardiac output and exacerbate organ dysfunction.24,33,34 In patients with RV failure and signs of venous congestion, diuretics are often the first option to optimise volume status. Notably, in patients with massive renal congestion due to severe RV dysfunction and/or severe tricuspid regurgitation, sufficient renal perfusion pressure (i.e. mean arterial pressure minus central venous pressure) and an adequate diuretics plasma concentration are crucial to achieving the desired effect. Furthermore, since most of the effect of IV loop diuretics occurs within the first hours – with sodium excretion returning to baseline within 6–8 hours – 3–4 daily doses or continuous infusion are required to maintain the decongestive effect.35 In the context of RV failure, early evaluation of the diuretic response (by measuring urine output or post-diuretic spot urinary sodium content) to identify patients with an inadequate diuretic response is even more important than it is in other forms of acute heart failure. If decongestion is insufficient, rapid intensification of loop diuretic dose, starting a sequential nephron blockade (combining diuretics with a different mode of action) or the use of renal replacement therapy/ultrafiltration should be considered. In the absence of elevated filling pressure, cautious volume loading guided by central venous pressure monitoring may be appropriate.33 Restoration of Perfusion Pressure Vasopressors are primarily indicated to restore arterial blood pressure and improve organ perfusion. Noradrenaline can restore systemic haemodynamics without increasing RV afterload (i.e. there is no effect on pulmonary vascular resistance).36 Restoration of coronary perfusion pressure by vasopressors is a mainstay of therapy since the failing RV dealing with volume and/or pressure overload is particularly susceptible to ischaemic injury. Furthermore, vasopressors restore cerebral, renal and hepato-splanchnic perfusion pressures. Clinical data suggest that targeting a mean arterial pressure (MAP) of 65 mmHg may be reasonable. However, MAP alone should not be used as a surrogate measure of organ perfusion pressure, especially in patients with RV failure and severe tricuspid regurgitation with massively elevated central venous pressure. Organ-specific perfusion pressure targets include 50–70 mmHg for the brain, 65 mmHg for renal perfusion and >50 mmHg for hepato-splanchnic flow.37 Therefore, the MAP targets should be personalised based on the measures of organ function and tissue perfusion. Improvement of Myocardial Contractility Dobutamine, levosimendan and phosphodiesterase III inhibitors improve contractility and increase cardiac output and are indicated in patients with severe RV failure causing cardiogenic shock despite treatment with vasopressors.33 Levosimendan and phosphodiesterase III inhibitors may favourably affect the ventricular-arterial coupling by combining RV inotropy and pulmonary vasodilation and might be preferentially indicated in patients with pulmonary hypertension caused by left heart disease.24,38 The use of epinephrine is not recommended.39–41 Advanced Options In patients with pre-capillary pulmonary hypertension, therapy should be driven by treatment of the underlying disease. Long-term oxygen therapy in hypoxic patients might stabilise pulmonary hypertension despite continued progression of lung disease, whereas supplementary oxygen in patients without hypoxia or moderate desaturation is not beneficial.42,43 The role of pulmonary vasodilators is highly controversial. Intravenous prostacyclin analogues effectively reduce RV afterload, but may aggravate systemic hypotension. Alternatively, inhaled nitric oxide or inhaled prostacyclin may be considered.33 These agents should be used only in an appropriate setting (specialised units) and in selected patients because of the risk of an increase in ventilation/perfusion mismatch and subsequent clinical deterioration. Notably, long-term therapy with phosphodiesterase-5 inhibitors, endothelin receptor antagonists, guanylate cyclase stimulators, prostacyclin analogues and prostacyclin receptor agonists are not recommended for the treatment of pulmonary hypertension due to left heart disease, which is the most prevalent cause of RV dysfunction. In patients with refractory RV failure despite treatment with vasopressors and inotropes, advanced therapeutic options including fibrinolysis for pulmonary embolism or mechanical circulatory support should be considered (see below). In the absence of long-term therapeutic options, palliation and supportive care should be offered to patients and relatives.44 Mechanical Circulatory Support for Advanced Right Ventricular Failure Mechanical circulatory support with RV assist devices (RVADs) should be considered when RV failure persists despite treatment with vasopressors and inotropes ( Figure 3 ). Because reversibility of severe RV failure is more likely to be possible and more rapid than LV failure of similar magnitudes, temporary RVADs (t-RVADs) can be a valuable therapeutic option for many patients.45 The often-reported poor survival rates of RVAD recipients should not discourage the appropriate use of t-RVADs, because patient mortality depends mainly on the primary cause of RV failure, the severity of end-organ dysfunction and the timing of RVAD implantation, and much less on adverse events and complications related to RVAD implantation, mechanical support or removal (selection bias).12 The most important determinants of success are optimal patient selection (according to age, comorbidities, RV dysfunction aetiology and reversibility potential) and optimal timing of implantation to avoid significant, potentially irreversible end-organ injury. For that reason, these patients require close haemodynamic and laboratory monitoring, with particular attention to liver and kidney function, and early transfer to a centre with experience in RVAD implantation in case of persistent haemodynamic instability. Choosing the most appropriate device also maximises the success of mechanical circulatory support. First, the strategy (e.g. bridge to recovery, bridge to bridge – i.e. LVAD/biventricular VAD/total artificial heart – or bridge to transplant) should be defined. Second, the need for an oxygenator should be anticipated because it may influence device selection. Third, the function of both the LV and RV should be carefully assessed to predict the need for isolated RV support or biventricular support (either durable or temporary). In addition to device characteristics, it is crucial to consider local expertise and availability. For short-term support, several t-RVADs, both percutaneous and surgical devices, are available. Percutaneous t-RVADs allow early initiation of support without the need for surgery. They are approved for a shorter period of time, and can sustain a lower flow than surgical devices. They are categorised according to their mechanism of action as either ‘ direct RV bypass’, such as the Impella RP (Abiomed) and TandemHeart RVADs (TandemLife) or ‘ indirect RV bypass’ systems, such as venous-arterial ECMO (VA ECMO).46 Impella RP is a microaxial flow 22 Fr catheter, approved for 14 days’ use, that delivers blood (at a rate of up to 4 l/min) from the RA into the pulmonary artery (PA).47 The TandemHeart RVAD uses an extracorporeal centrifugal flow pump and two venous cannulas or a single cannula with two lumens (Protek Duo cannula) to deliver blood from the RA to the PA with the additional possibility of oxygenating the blood.48 Directly bypassing the RV function reduces RA pressure, raises mean PA pressure and increases left ventricular preload, while the left ventricular afterload remains unchanged. The VA ECMO is the less expensive device. It bypasses the RV indirectly, displacing venous blood from the RA across an oxygenator into the peripheral arterial circulation. It induces a decrease in RA and PA pressure and LV preload but increases LV afterload if not cannulated centrally via surgical access.49 Surgical t-RVADs require an open sternotomy or thoracotomy for direct RA and PA cannulation and their connection to an extracorporeal centrifugal flow pump. They allow more extended and greater support in terms of flow at the cost of an invasive implantation and removal. However, more recently developed surgically implantable short-term extracorporeal CF-RVADs can be removed without reoperation; that is, the CentriMag system (Chalice Medical), which allows 30 days of support with up to 10 l/min blood flow).50 For more durable, long-term support, isolated pulsatile RVADs, surgically deployed rotary-flow RVADs and biventricular support with pulsatile VADs or total artificial heart replacement are potential options; however, the majority of patients using these are required to remain in the hospital under close surveillance. This is one reason why the use of durable isolated right ventricular assist devices (e.g. LVADs in the RV position) to support isolated RV or biventricular failure has been evaluated.51–54 A significant limitation of this approach is that LVADs are designed to operate in the systemic circulation with higher resistance and, where pulmonary resistance is low, they are more prone to complications, such as repetitive suction events. Because of the many technical limitations of durable RV support and because RV function may not recover, cardiac transplantation remains the only successful long-term treatment. Arrhythmic Aspects of Right Ventricular Failure Cardiac rhythm plays an important yet often underestimated role in RV function. One one hand, the failing RV, specifically if experiencing an increased afterload, such as in pulmonary hypertension, is highly dependent on a regular heart rate to function adequately, as its contractile reserve is very limited.55 The need for a constant sympathetic drive to maintain cardiac output may be one reason why beta-blocker therapy is not effective in right heart failure.56 On the other hand, RV pressure overload, an integral part in the pathophysiology of RV failure, is often associated with supraventricular arrhythmias, such as atrial fibrillation, atrial flutter or (multi-)focal atrial tachycardia, all of which negatively affect RV filling and thereby contribute to the vicious cycle of aggravating RV failure, eventually culminating in cardiogenic shock. Therefore, in addition to careful volume management to optimise RV preload and RV wall stress, prompt rhythm control of supraventricular tachyarrhythmias is central. Importantly, diastolic filling of the failing RV depends on atrial contraction (‘atrial kick’) and atrioventricular synchrony.57,58 Therefore, rate control alone is generally insufficient to restore haemodynamic stability.59 In the acute setting, prompt electrical cardioversion (ECV) is the treatment of choice to restore sinus rhythm, although ECV efficacy in restoring and maintaining sinus rhythm may be reduced in critically ill patients.58,60,61 Retrospective analyses in patients with pulmonary hypertension indicate that maintaining sinus rhythm is associated with a reduction in clinical deterioration.62 Since beta-blockers and calcium channel antagonists may hamper RV contractility because of their negative inotropic effect, amiodarone should be used if antiarrhythmic medical therapy to maintain sinus rhythm is warranted. Class Ic antiarrhythmics, as well as sotalol and dronedarone, should not be used in structural heart disease. If medical therapy fails, AV synchronous pacing, with either the patient’s indwelling device or transvenous pacing wires may be considered.2 The interplay of the right and left ventricles, sharing their interventricular septum and competing for the limited space within the pericardium, leads to ventricular interdependence.33 Consequently, the loss of synchronous ventricular contraction is associated with a significant deterioration of RV contractile force. Notably, cardiac resynchronisation therapy (CRT) is standard care in patients with heart failure with reduced LV ejection fraction (HFrEF) and a wide QRS complex (>130 ms), and serves to resynchronise LV contraction. Many patients with HFrEF also have reduced RV function, either as a consequence of increased RV afterload (post-capillary pulmonary hypertension) or secondary to a cardiomyopathy affecting both ventricles.33 Because of anatomical and technical obstacles (difficult reliable assessment of RV function and the absence of an epicardial RV venous system for safe lead placement) and as RV function has gained attention only in recent years, very limited data on isolated right cardiac resynchronisation exist. However, though scarce, there are data on the interplay of LV resynchronisation and RV function. Indeed, reverse LV remodelling is associated with reduced RV afterload.63 Not surprisingly, several observational studies have demonstrated significant improvement in RV function after CRT.64 Similarly, CRT was associated with significant improvement of RV fractional area change in a post-hoc analysis of the Multicenter Automatic Defibrillator Implantation Trial With Cardiac Resynchronization Therapy trial (MADIT-CRT).65 However, no such effect was observed in a post-hoc analyses of the REsyncronization reVErses Remodeling in Systolic left vEntricular dysfunction (REVERSE) and Cardiac Resynchronization-Heart Failure (CARE-HF) trials, which used TAPSE to assess RV function.66,67 Of note, TAPSE is mainly influenced by longitudinal movement of the RV free wall and may underestimate the contribution of the interventricular septum and outflow tract. Importantly, both observational studies and post-hoc analyses of randomised clinical trials may serve only to generate hypotheses and do not allow reliable conclusions. The value of left cardiac resynchronisation in isolated RV failure is unknown. Similarly, data on the prevalence of sudden cardiac death (SCD) in isolated RV failure are scarce, at best. It is therefore not surprising that current guidelines do not recommend ICD therapy for primary prevention of SCD in patients with isolated RV failure.68 An exemption is patients with arrhythmogenic RV cardiomyopathy, in whom, if certain risk factors for SCD are present, an ICD for primary prevention of SCD may be considered (IIb; level of evidence C). In cases of secondary prevention, on the other hand, after documented haemodynamically relevant ventricular tachycardia or following survived SCD, and after secondary causes have been excluded, ICD therapy is recommended, regardless of right or left ventricular function. Conclusion The assessment of RV failure should consider the anatomical and physiological particularities of the RV and include appropriate imaging techniques to understand the underlying pathophysiological mechanisms. Treatment should include rapid optimisation of volume status, restoration of perfusion pressure, and improvement of myocardial contractility and rhythm and, in case of refractory RV failure, mechanical circulatory support. References
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Which side of the heart is first affected in heart failure?
– Heart failure develops when your heart isn’t able to pump enough blood to adequately supply your tissues with oxygen. Most of the time, heart failure develops on the left side of your heart. Right-sided heart failure most commonly develops due to left-sided failure, but some lung or heart problems can also lead to right-sided failure.
What are the signs heart failure is getting worse?
Signs That Chronic Heart Failure Is Getting Worse By Maya Guglin, MD, as told to Mary Jo DiLonardo Your heart’s job is to pump blood around your body to supply all your organs with the oxygen they need to work well. When your heart doesn’t pump as strong and as efficiently as it’s supposed to, you have heart failure.
As your heart struggles to pump blood, fluid levels build up in your body. This excessive fluid causes almost all symptoms of heart failure. Typically, people with heart failure complain of shortness of breath and fatigue. They might also gain some weight. There are two pumping chambers in the heart: the left and right ventricles.
The left side of the heart collects oxygen-rich blood from the lungs. So, if the left ventricle is more affected by heart failure, the fluid builds up in the lungs, and the main symptom is shortness of breath. At first it happens only when you try to do something really physically challenging like running.
- But as the disease progresses, it becomes difficult to walk up the steps.
- Then it becomes harder to walk fast, then harder to walk at all.
- You have to stop often and catch your breath.
- Eventually, you start waking up at night because your lungs fill with “unpumped” fluid.
- You have to sit up, then the gravity pulls the fluid down, and your lungs can breathe again.
At this stage, you may even have wheezing like in asthma and you may even start coughing. The cough follows the same pattern as shortness of breath: It’s worse when you are lying down and better when you sit up. But if it gets this far, it’s time to go to the emergency room or call an ambulance.
- This is serious.
- The right side of your heart collects the blood from your whole body.
- If your right ventricle fails, extra fluid accumulates in your liver, kidneys, gut, and legs.
- At first, you might notice that your ankles and feet swell by the end of the day.
- It’s not unusual at all for this to happen to people who spend a lot of time on their feet, so this symptom is easily overlooked.
Next, the swelling can continue to creep up your body and move into the shins, thighs, and pelvis. If you put your fingertip on your leg and press lightly, the pit where your fingertip was stays and slowly goes away over the next minute. The medical term for that is “pitting edema.” Eventually blisters may form, skin may break, and the clear fluid inside can start to seep out.
- When the tissues are in that condition, it’s easy to catch an infection called cellulitis, and legs become purple and angry.
- Don’t let that happen! See a doctor before it gets that bad.
- It’s more common to have the left ventricular failure first.
- For example, a large heart attack almost always involves the left ventricle.
But if you allow the fluid accumulation in the lungs to persist, this will spread to the rest of the body. It’s important to be aware that heart failure is not the only condition that causes feet and legs to swell. Dilated veins called varices can cause very similar symptoms.
- That’s why you should always let your doctor know about any symptoms you’re having.
- Let the specialists sort this out.
- Sometimes you might eat just a little, yet suddenly feel very full.
- But even though you are barely eating, you notice that you’re somehow gaining weight.
- That’s also from all the fluid that you’re collecting in your body.
When the liver gets swollen from it (your doctor may call it “distended”), it may cause stomach pain on the upper right side. Some people think they might have an inflamed gallbladder. It’s actually an enlarged liver. The easiest way to know that heart failure is getting worse is you’re able to do less and less.
People start pacing themselves. They stop doing hobbies that involve any physical activity. They used to go fishing, but not anymore. They used to play 18 holes – now they are down to nine. They avoid stairs whenever they can. They choose to only walk short distances, and they do it very slowly. They don’t use the bedroom upstairs and instead sleep on the couch in the living room.
Then they decide to sleep in a recliner. Then they can’t sleep at all. If you notice that the disease makes you change your habits, it’s time to visit a doctor. They will almost always be able to help. There are medications that can treat heart failure, including diuretics – or water pills – that work the fastest.
Photo Credit: StockByte / ThinkstockSOURCE:Maya Guglin, MD.
: Signs That Chronic Heart Failure Is Getting Worse
What stage of heart failure is shortness of breath?
Stage 2 of Congestive Heart Failure – Stage two of congestive heart failure will produce symptoms such as fatigue, shortness of breath, or heart palpitations after you participate in physical activity. As with stage one, lifestyle changes and certain medication can help improve your quality of life. will discuss treatment with you and help you on your healthcare journey while living with CHF.
Is right-sided heart failure serious?
– Heart failure is a widespread disease, especially as a person ages. However, specific steps and lifestyle changes may help prevent heart failure from occurring or minimize the symptoms if it does happen, such as not smoking, managing high blood pressure, and exercising regularly.
What is the most common cause of right-sided heart failure Mcq?
What is the most common cause of right-sided heart failure? Question 17 Explanation: Left-sided heart failure (LHF) is the most common cause of right-sided heart failure (RHF).
What is the difference in signs symptoms of right and left-sided heart failure?
Does Left-Sided Heart Failure Lead To Right-Sided Heart Failure? – Left-sided heart failure occurs when the left ventricle of the heart is weakened and cannot as efficiently pump blood into the body. As a result of the diminished ejection fraction, fluid can flow back into the lungs and put additional stress on the right side of the heart.
Coronary artery disease Heart attack Heart valve disease High blood pressure Irregular heart beat Congenital heart disease Diabetes Some diabetes medications Alcohol use Sleep apnea Smoking or tobacco use Obesity Viral infections
In addition to the symptoms noted above, left-sided and right-sided heart failure can cause:
Rapid weight gain A persistent cough Fatigue Heart palpitations Protruding neck veins Irregular pulse
Doctors typically use a physical exam and a procedure called an echocardiogram to diagnose heart failure. The echocardiogram produces detailed images of the heart that the doctor reviews to assess the damage to the heart.
Which symptom is most commonly associated with the left-sided heart failure?
Left-sided Heart Failure Symptoms – The symptoms of left-sided heart failure are the generally the same for heart failure broadly and include:
Shortness of breathDifficulty breathing when lying downWeight gain with swelling in the feet, legs, anklesFluid collection in the abdomenFatigue or a general feeling of weakness