Right-sided heart failure is characterized by insufficient output by the right heart and increased systemic venous and pulmonary pressures. The most common cause is left-sided heart failure but various other conditions may be responsible as well. Principal symptoms include distal edema and profuse weakness and dyspnea. The diagnosis can be made by laboratory and imaging studies, while treatment is focused on the underlying cause together with supportive therapy.
The most prominent symptoms of right-sided heart failure are marked weakness, breathing difficulties, edema and ascites. Edema on the ankles (pedal edema), as well as ascites accompanied with hepatosplenomegaly are indicators of venous congestion, which is one of the main features of this condition [11]. Other symptoms may include abdominal pain, bloating, nausea and weight loss. In severe cases, where both left- and right-sided failure occurs, marked dyspnea and cyanosis may be observed. Clinical examination may reveal tachycardia, increased jugular venous pressure with sometimes visible distension, while a heart murmur may be observed during auscultation. To establish the severity of heart failure, the New York Heart Association (NYHA) classification system is used, and ranges from I (no limitations in daily or physical activity as a result of cardiac changes) to IV (symptoms occur at rest and any activity creates significant discomfort) [3].
A thorough clinical examination and a good patient history may provide vital clues that determine the course of workup in these patients. Initial studies should comprise ECG, chest X-ray and laboratory studies including CBC, liver and kidney function tests, serum electrolytes and brain natriuretic peptide (BNP). If the symptoms appeared abruptly, cardiospecific enzymes should be evaluated as well. Chest X-ray may reveal pulmonary edema or an increased cardiac silhouette, whereas ECG studies provide a good view into the cardiac conduction system. To make a definite diagnosis, echocardiography is the optimal imaging study, which provides an excellent view into the cardiac structures [12]. Additional techniques that may be of use to establish the overall condition of the patient are CT and MRI, while 3D echocardiography is showing promising results in replacing invasive methods for determination or right atrial pressure [13].
To effectively treat right-sided heart failure, resolution of the underlying cause is a must [1]. During the diagnostic workup, however, symptomatic therapy and correction of blood pressure and tissue oxygenation must be carried out, usually with the help of various pharmacologic agents. Digoxin, β-blockers, calcium-channel antagonists, diuretics, ACE inhibitors, aldosterone blockers and several other groups are all used under various circumstances [3]. Changes in dietary habits may be of particular importance, especially reduction in sodium intake, as it is shown to be a very important factor in the pathogenesis of atherosclerosis and other cardiovascular diseases, including MI. Directed therapy may be initiated in the case of endocarditis, where various antibiotic regimens exist, depending on the underlying pathogen, while congenital heart disease is usually treated surgically. Thrombolytic therapy is indicated in the setting of pulmonary embolism, whereas invasive cardiac surgery is required for patient with MI. Sometimes, despite after recommended treatment, heart failure may persist and require implantation of various devices. Defibrillators or pacemakers may be inserted and are used as a last resort in treating heart failure.
The outcome of patients with right-sided heart failure is not good, since its presence is shown to correlate with a poor prognosis [8]. A 50% overall mortality rate 4 years after making the diagnosis shows how dangerous heart failure is [6]. Mortality rates significantly depend on the underlying condition, however, since some diseases can be almost completely cured and pathophysiologic changes in the right heart can be almost fully reversed.
Causes of right-sided heart failure may be numerous, but the most common is left-sided heart failure, which puts immense pressure on the pulmonary vasculature and consequently on the right ventricle. Other causes include [5] [6]:
Various other factors, including iatrogenic, nutritional (obesity, selenium or thiamine deficiency), environmental (heavy alcohol consumption), infectious (Chagas disease), end-stage renal disease and several other have shown their properties in initiating heart failure [5].
Because of significant advances in medical care that have enabled a longer life expectancy, incidence and prevalence rates of heart failure have risen in the past few decades [5]. Rough estimates suggest that the prevalence rate of heart failure in general is between 1-2% in countries of the Western world, while an incidence rate is established to be approximately 5-10 per 1000 individuals [7]. Prevalence rates are shown to rise abruptly after 70 years, showing that between 10-20% of individuals over 70 years develop heart failure, indicating that advanced age is a significant factor [6]. In the United States, approximately 5 million individuals are affected by this condition and incidence rates indicate that more than 500,000 cases occur every year [3]. Exact prevalence rates of right-sided heart failure are not formed yet, but it is one of the most important predictors of mortality in heart failure [8]. Namely, heart failure that is caused by MI and several other causes has substantially different outcomes depending on the presence or absence of right-sided heart failure [8].
The pathogenesis of right-sided heart failure is complex and various pathological events occur simultaneously. Through the inferior vena cava and the portal vein, the venous circulation drains into the right atrium. During diastole, blood is pooled into the right ventricle and then forced into the pulmonary circulation during systole. Depending on the underlying condition that affects the right heart, various mechanisms contribute to eventual failure. In the case of MI, sudden cessation of blood flow leads to hypoxia, myocardial necrosis and fibrosis, thus reducing the viability of myocardial cells to perform their function. In endocarditis, stenosis of pulmonary or tricuspid valve necessitates a greater contractile force to combat higher resistance. Pulmonary hypertension, however, is one of the most significant factors in the development of right-sided heart failure, which occurs in the setting of left-sided heart failure and various lung diseases [9]. The right heart is unable to overcome increased resistance in the pulmonary vasculature and the end-result, regardless of the cause, is inadequate tissue oxygenation and diffuse hypoxia. In order to restore adequate oxygen supply to tissues, various compensatory mechanisms are activated. Cardiac remodeling, increased oxygen extraction from tissue, changes in systemic circulation and hormonal stimulation are some of the most important [3]. Right ventricular hypertrophy and dilation occurs to maximize output, while upregulation of sympathetic tone results in increase heart rate. The renal system triggers the renin-angiotensin-aldosterone system that contributes by retention of salt and water. However, all of these effects can cause significant damage to the heart if the condition that led to activation of these mechanisms is not resolved. More importantly, the right heart is not able to sustain such powerful stimulation for longer periods [10]. Over time, progressive deterioration of right heart function, leading to irreversible fibrosis of myocytes with both systolic and diastolic dysfunction.
Various steps can be made to prevent the onset of heart failure. Firstly, proper management of various conditions that may precipitate heart failure is vital, while dietary habits that include low sodium intake may significantly reduce the risk for developing cardiovascular diseases in general. The diagnosis of heart failure in early stages is proven to significantly prolong survival, which is why a thorough workup by the physician may ultimately save a patient's life.
Right-sided heart failure is a clinical entity that occurs as a result of various conditions that impair right heart function, resulting in reduced output and volume overload [1]. Left-sided heart failure is the most common cause, most likely as a result of pulmonary edema, eventually leading to an acute right heart failure known as cor pulmonale. Myocardial infarction, endocarditis affecting either tricuspid or pulmonary valves, congenital heart disease (right-to-left shunts), Ebstein malformation, as well as various forms of cardiomyopathy have all been described as precipitating factors of right-sided heart failure [2]. Under physiological circumstances, the entire venous system is drained into the right atrium, from where it travels into the right ventricle and eventually into the pulmonary circulation. Abnormalities in pulmonary circulation (such as hypertension as a result of left-heart failure), deficient right ventricle contractility (cardiomyopathy, endocarditis) and impaired either systolic and/or diastolic function of the right heart leads to reduced cardiac output and tissue oxygenation [3]. Because hypoxia of various organs may occur, several compensatory mechanisms are activated, including dilation and hypertrophy of the right ventricle, activation of the sympathetic system that results in increased contractility and heart rate acceleration, salt and water retention from the kidneys and blood flow changes [4]. However, as the cause is either not resolved or the onset of heart failure is acute and sudden, these compensatory mechanisms cause more harm than benefit, which may lead to irreversible changes in cardiac myocytes, mainly apoptosis, collagen deposition and fibrosis of the cardiac muscle. In the case of right-sided heart failure, the end-result is reduced movement of venous circulation that leads to congestion, portal hypertension, development of ascites and hepatosplenomegaly. Consequently, one of the main clinical presentations of patients with right-sided heart failure is peripheral edema, especially of the extremities and ankles (known as pedal edema), usually accompanied with diffuse weakness and dyspnea. Because of venous congestion in the gastrointestinal system, abdominal discomfort, bloating and weight loss may be reported as well. Clinical examination may reveal tachycardia (and in case of endocarditis, a heart murmur may be noted on auscultation), lower oxygen saturation, enlarged liver and spleen and elevated jugular venous pressure. Workup should include laboratory studies such as complete blood count (CBC), liver transaminases, cardiospecific enzymes (in case symptoms appeared abruptly), urine function tests (blood urea nitrogen and creatinine), serum electrolytes, brain natriuretic peptide levels and albumin count. Plain radiography is a simple and easy diagnostic method that may identify signs of heart failure, while electrocardiography (EKG), echocardiography, computed tomography (CT) and magnetic resonance imaging (MRI) are useful techniques to identify the underlying cause responsible for heart failure. Treatment is aimed at resolving the condition that caused heart failure, but it is not always possible. Symptomatic therapy, dietary changes and in some cases, device implantation is necessary. Heart failure has a poor prognosis if the disease that caused it is not treated. For these reasons, finding the cause is imperative in achieving good outcomes.
Right-sided heart failure is a clinical syndrome that describes failure of either the right atrium and/or right ventricle as a result of various diseases. It may occur as a separate condition, where marked changes in structure of these heart chambers are observed, or it may occur together with left-sided heart failure. In fact, left-heart failure is the most common cause of right-sided heart failure, while congenital heart disease, infection of heart valves (endocarditis), vascular diseases such as hypertension, myocardial infarction (heart attack) and numerous other conditions may trigger this pathological event. Right-sided heart failure often develops as a result of increased pressures in the blood vessels of the lungs (known as pulmonary hypertension), where the right heart should pump blood that arrived from all the veins in the body. Additionally, various conditions within the right heart can significantly harden its function. The end-result is a need for increased effort of the right heart to pump the blood into the lungs, which is achieved by activating several compensatory mechanisms. The heart enlarges its chambers and increases muscle size and strength, neural networks that increase the velocity and the strength of the heart are stimulated and the kidneys attempt to decrease blood flow through them while savoring water and salts to compensate for blood pressure changes. These actions are effective in short-term circumstances, but since heart failure is considered to be the end-stage disease of the heart, these mechanisms persist for a prolonged period of time and eventually start to actually harm the individual and cause further deterioration.
Once right-sided heart failure occurs, the main feature is reduced velocity of blood flow through the venous system, manifesting as swelling of the extremities, particularly ankles, liver and spleen enlargement, together with extreme fatigue that occurs due to insufficient oxygen delivery by the damaged heart. To make the diagnosis, various imaging and laboratory studies need to be carried out. Chest X-ray, electrocardiography and often echocardiography are required, while various blood tests including serum electrolytes, liver and kidney function tests, as well as levels of proteins in blood are necessary to evaluate the status of various organs. It is important to find the underlying disease that is responsible for right-sided heart failure, as treatment success solely depends on managing the cause.
Depending on the condition responsible, various therapeutic approaches exist. Usually, symptomatic management is necessary in initial stages before the cause is determined, after which directed treatment may be initiated. Various drugs, surgical procedures and implantation of devices that assist in normal cardiac functioning serve as appropriate treatment modalities. It is estimated that more than 5 million people in the United States suffer from heart failure and more than 500 000 new cases occur every year. Moreover, it was observed that approximately 2-3% of people in the Western world have this condition, with the majority being over 75 years of age. When taking into consideration the fact that the survival rate 4 years after the diagnosis of heart failure is 50%, the significance of this condition must not be undermined. In fact, an early diagnosis of the underlying condition may be lifesaving for the patient, but much can be done in terms of prevention. Reduced sodium intake through diet, cessation of heavy alcohol consumption and smoking (well-known factors for atherosclerosis) and ensuring long-term patient care can reduce the burden of this condition in a significant manner worldwide.