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Heart failure is a pathophysiological state in which cardiac output is insufficient to meet the needs of the body and lungs.

Heart failure symptoms are traditionally and somewhat arbitrarily divided into "left" and "right" sided, recognizing that the left and right ventricles of the heart supply different portions of the circulation, however people commonly have both sets of signs and symptoms.

The left side of the heart receives oxygen-rich blood from the lungs and pumps it forward to the systemic circulation the rest of the body except for the pulmonary circulation.

Failure of the left side of the heart causes blood to back up be congested into the lungs, causing respiratory symptoms as well as fatigue due to insufficient supply of oxygenated blood.

Common respiratory signs are increased rate of breathing and increased work of breathing non-specific signs of respiratory distress.

Rales or crackles, heard initially in the lung bases, and when severe, throughout the lung fields suggest the development of pulmonary edema fluid in the alveoli.

Cyanosis which suggests severe low blood oxygen , is a late sign of extremely severe pulmonary edema. Additional signs indicating left ventricular failure include a laterally displaced apex beat which occurs if the heart is enlarged and a gallop rhythm additional heart sounds may be heard as a marker of increased blood flow or increased intra-cardiac pressure.

Heart murmurs may indicate the presence of valvular heart disease, either as a cause e. Backward failure of the left ventricle causes congestion of the lungs' blood vessels, and so the symptoms are predominantly respiratory in nature.

Backward failure can be subdivided into the failure of the left atrium, the left ventricle or both within the left circuit. The person will have dyspnea shortness of breath on exertion and in severe cases, dyspnea at rest.

Increasing breathlessness on lying flat, called orthopnea , occurs. It is often measured in the number of pillows required to lie comfortably, and in orthopnea, the person may resort to sleeping while sitting up.

Another symptom of heart failure is paroxysmal nocturnal dyspnea : a sudden nighttime attack of severe breathlessness, usually several hours after going to sleep.

Easy fatigability and exercise intolerance are also common complaints related to respiratory compromise. Compromise of left ventricular forward function may result in symptoms of poor systemic circulation such as dizziness , confusion and cool extremities at rest.

Right-sided heart failure is often caused by pulmonary heart disease cor pulmonale , which is typically caused by difficulties of the pulmonary circulation , such as pulmonary hypertension or pulmonic stenosis.

Physical examination may reveal pitting peripheral edema , ascites , liver enlargement , and spleen enlargement. Jugular venous pressure is frequently assessed as a marker of fluid status, which can be accentuated by eliciting hepatojugular reflux.

If the right ventricular pressure is increased, a parasternal heave may be present, signifying the compensatory increase in contraction strength.

Backward failure of the right ventricle leads to congestion of systemic capillaries. This generates excess fluid accumulation in the body.

This causes swelling under the skin termed peripheral edema or anasarca and usually affects the dependent parts of the body first causing foot and ankle swelling in people who are standing up, and sacral edema in people who are predominantly lying down.

Nocturia frequent nighttime urination may occur when fluid from the legs is returned to the bloodstream while lying down at night. In progressively severe cases, ascites fluid accumulation in the abdominal cavity causing swelling and liver enlargement may develop.

Significant liver congestion may result in impaired liver function congestive hepatopathy , and jaundice and even coagulopathy problems of decreased or increased blood clotting may occur.

Dullness of the lung fields to finger percussion and reduced breath sounds at the bases of the lung may suggest the development of a pleural effusion fluid collection between the lung and the chest wall.

Though it can occur in isolated left- or right-sided heart failure, it is more common in biventricular failure because pleural veins drain into both the systemic and pulmonary venous systems.

When unilateral, effusions are often right-sided. If a person with a failure of one ventricle lives long enough, it will tend to progress to failure of both ventricles.

For example, left ventricular failure allows pulmonary edema and pulmonary hypertension to occur, which increase stress on the right ventricle.

Right ventricular failure is not as deleterious to the other side, but neither is it harmless. Heart failure can be caused by a large number of cardiac diseases.

In addition to the causes mentioned above, viral infections of the heart can lead to inflammation of the muscular layer of the heart and subsequently contribute to the development of heart failure.

Genetic predisposition plays an important role. If more than one cause is present, progression is more likely and prognosis is worse. An uncommon cause is exposure to certain toxins such as lead and cobalt.

Additionally, infiltrative disorders such as amyloidosis and connective tissue diseases such as systemic lupus erythematosus have similar consequences.

Heart failure may also occur in situations of "high output" termed " high-output heart failure " , where the amount of blood pumped is more than typical and the heart is unable to keep up.

Chronic stable heart failure may easily decompensate. This most commonly results from a concurrent illness such as myocardial infarction a heart attack or pneumonia , abnormal heart rhythms , uncontrolled hypertension , or a person's failure to maintain a fluid restriction, diet, or medication.

A number of medications may cause or worsen the disease. This includes NSAIDS, COX-2 inhibitors , a number of anesthetic agents such as ketamine , thiazolidinediones, some cancer medications , several antiarrhythmic medications , pregabalin , alpha-2 adrenergic receptor agonists , minoxidil , itraconazole , cilostazol , anagrelide , stimulants e.

By inhibiting the formation of prostaglandins , NSAIDs may exacerbate heart failure through several mechanisms including promotion of fluid retention, increasing blood pressure , and decreasing a person's response to diuretic medications.

Certain alternative medicines carry a risk of exacerbating existing heart failure, and are not recommended. Heart failure is caused by any condition which reduces the efficiency of the heart muscle, through damage or overloading.

Over time these increases in workload, which are mediated by long-term activation of neurohormonal systems such as the renin—angiotensin system , leads to fibrosis , dilation, and structural changes in the shape of the left ventricle from elliptical to spherical.

The heart of a person with heart failure may have a reduced force of contraction due to overloading of the ventricle. In a normal heart, increased filling of the ventricle results in increased contraction force by the Frank—Starling law of the heart , and thus a rise in cardiac output.

In heart failure, this mechanism fails, as the ventricle is loaded with blood to the point where heart muscle contraction becomes less efficient. This is due to reduced ability to cross-link actin and myosin filaments in over-stretched heart muscle.

No system of diagnostic criteria has been agreed on as the gold standard for heart failure. The National Institute for Health and Care Excellence recommends measuring brain natriuretic peptide BNP followed by an ultrasound of the heart if positive.

One historical method of categorizing heart failure is by the side of the heart involved left heart failure versus right heart failure. Right heart failure was thought to compromise blood flow to the lungs compared to left heart failure compromising blood flow to the aorta and consequently to the brain and the remainder of the body's systemic circulation.

However, mixed presentations are common and left heart failure is a common cause of right heart failure.

More accurate classification of heart failure type is made by measuring ejection fraction , or the proportion of blood pumped out of the heart during a single contraction.

Synonyms no longer recommended are "heart failure due to left ventricular systolic dysfunction" and "systolic heart failure".

Synonyms no longer recommended include "diastolic heart failure" and "heart failure with normal ejection fraction.

Heart failure may also be classified as acute or chronic. Chronic heart failure is a long-term condition, usually kept stable by the treatment of symptoms.

Acute decompensated heart failure is a worsening of chronic heart failure symptoms which can result in acute respiratory distress. There are several terms which are closely related to heart failure and may be the cause of heart failure, but should not be confused with it.

Cardiac arrest and asystole refer to situations in which there is no cardiac output at all. Without urgent treatment, these result in sudden death.

Myocardial infarction "Heart attack" refers to heart muscle damage due to insufficient blood supply, usually as a result of a blocked coronary artery.

Cardiomyopathy refers specifically to problems within the heart muscle, and these problems can result in heart failure.

Ischemic cardiomyopathy implies that the cause of muscle damage is coronary artery disease. Dilated cardiomyopathy implies that the muscle damage has resulted in enlargement of the heart.

Hypertrophic cardiomyopathy involves enlargement and thickening of the heart muscle. Echocardiography is commonly used to support a clinical diagnosis of heart failure.

This modality uses ultrasound to determine the stroke volume SV, the amount of blood in the heart that exits the ventricles with each beat , the end-diastolic volume EDV, the total amount of blood at the end of diastole , and the SV in proportion to the EDV, a value known as the ejection fraction EF.

In pediatrics, the shortening fraction is the preferred measure of systolic function. Echocardiography can also identify valvular heart disease and assess the state of the pericardium the connective tissue sac surrounding the heart.

Echocardiography may also aid in deciding what treatments will help the person, such as medication, insertion of an implantable cardioverter-defibrillator or cardiac resynchronization therapy.

Echocardiography can also help determine if acute myocardial ischemia is the precipitating cause, and may manifest as regional wall motion abnormalities on echo.

Ultrasound showing severe systolic heart failure [40]. Ultrasound of the lungs showing edema due to severe systolic heart failure [40].

Chest X-rays are frequently used to aid in the diagnosis of CHF. In a person who is compensated, this may show cardiomegaly visible enlargement of the heart , quantified as the cardiothoracic ratio proportion of the heart size to the chest.

In left ventricular failure, there may be evidence of vascular redistribution "upper lobe blood diversion" or "cephalization" , Kerley lines , cuffing of the areas around the bronchi , and interstitial edema.

Ultrasound of the lung may also be able to detect Kerley lines. Although these findings are not specific to the diagnosis of heart failure a normal ECG virtually excludes left ventricular systolic dysfunction.

Blood tests routinely performed include electrolytes sodium , potassium , measures of kidney function , liver function tests , thyroid function tests , a complete blood count , and often C-reactive protein if infection is suspected.

An elevated B-type natriuretic peptide BNP is a specific test indicative of heart failure. Additionally, BNP can be used to differentiate between causes of dyspnea due to heart failure from other causes of dyspnea.

If myocardial infarction is suspected, various cardiac markers may be used. Hyponatremia low serum sodium concentration is common in heart failure.

Vasopressin levels are usually increased, along with renin, angiotensin II, and catecholamines in order to compensate for reduced circulating volume due to inadequate cardiac output.

This leads to increased fluid and sodium retention in the body; the rate of fluid retention is higher than the rate of sodium retention in the body, this phenomenon causes "hypervolemic hyponatremia" low sodium concentration due to high body fluid retention.

This phenomenon is more common in older women with low body mass. Severe hyponatremia can result in accumulation of fluid in the brain, causing cerebral edema and intracranial hemorrhage.

Angiography is the X-ray imaging of blood vessels which is done by injecting contrast agents into the bloodstream through a thin plastic tube catheter which is placed directly in the blood vessel.

X-ray images are called angiograms. As a result, coronary catheterization may be used to identify possibilities for revascularisation through percutaneous coronary intervention or bypass surgery.

There are various algorithms for the diagnosis of heart failure. For example, the algorithm used by the Framingham Heart Study adds together criteria mainly from physical examination.

In contrast, the more extensive algorithm by the European Society of Cardiology ESC weights the difference between supporting and opposing parameters from the medical history , physical examination , further medical tests as well as response to therapy.

By the Framingham criteria, diagnosis of congestive heart failure heart failure with impaired pumping capability [46] requires the simultaneous presence of at least 2 of the following major criteria or 1 major criterion in conjunction with 2 of the following minor criteria.

Minor criteria are acceptable only if they can not be attributed to another medical condition such as pulmonary hypertension , chronic lung disease , cirrhosis , ascites , or the nephrotic syndrome.

The ESC algorithm weights the following parameters in establishing the diagnosis of heart failure: [23]. Heart failure is commonly stratified by the degree of functional impairment conferred by the severity of the heart failure as reflected in the New York Heart Association NYHA Functional Classification.

People with NYHA class II heart failure have slight, mild limitation with everyday activities; the person is comfortable at rest or with mild exertion.

A person with NYHA class IV heart failure is symptomatic at rest and becomes quite uncomfortable with any physical activity.

This score documents the severity of symptoms and can be used to assess response to treatment. While its use is widespread, the NYHA score is not very reproducible and does not reliably predict the walking distance or exercise tolerance on formal testing.

The ACC staging system is useful since Stage A encompasses "pre-heart failure" — a stage where intervention with treatment can presumably prevent progression to overt symptoms.

Histopathology can diagnose heart failure in autopsies. The presence of siderophages indicates chronic left-sided heart failure, but is not specific for it.

A person's risk of developing heart failure is inversely related to their level of physical activity. Maintaining a healthy weight as well as decreasing sodium , alcohol, and sugar intake may help.

Additionally, avoiding tobacco use has been shown to lower the risk of heart failure. Treatment focuses on improving the symptoms and preventing the progression of the disease.

Reversible causes of the heart failure also need to be addressed e. Treatments include lifestyle and pharmacological modalities, and occasionally various forms of device therapy and rarely cardiac transplantation.

In acute decompensated heart failure ADHF , the immediate goal is to re-establish adequate perfusion and oxygen delivery to end organs.

This entails ensuring that airway, breathing, and circulation are adequate. Immediate treatments usually involve some combination of vasodilators such as nitroglycerin , diuretics such as furosemide , and possibly noninvasive positive pressure ventilation NIPPV.

The goals of treatment for people with chronic heart failure are the prolongation of life, the prevention of acute decompensation and the reduction of symptoms, allowing for greater activity.

Heart failure can result from a variety of conditions. In considering therapeutic options, it is important to first exclude reversible causes, including thyroid disease , anemia , chronic tachycardia , alcohol abuse , hypertension and dysfunction of one or more heart valves.

Treatment of the underlying cause is usually the first approach to treating heart failure. However, in the majority of cases, either no primary cause is found or treatment of the primary cause does not restore normal heart function.

In these cases, behavioral , medical and device treatment strategies exist which can provide a significant improvement in outcomes, including the relief of symptoms, exercise tolerance, and a decrease in the likelihood of hospitalization or death.

Breathlessness rehabilitation for chronic obstructive pulmonary disease COPD and heart failure has been proposed with exercise training as a core component.

Rehabilitation should also include other interventions to address shortness of breath including psychological and education needs of people and needs of carers.

Various measures are often used to assess the progress of people being treated for heart failure. These include fluid balance calculation of fluid intake and excretion , monitoring body weight which in the shorter term reflects fluid shifts.

Behavior modification is a primary consideration in chronic heart failure management program, with dietary guidelines regarding fluid and salt intake.

Exercise should be encouraged and tailored to suit individual capabilities. The inclusion of regular physical conditioning as part of a cardiac rehabilitation program can significantly improve quality of life and reduce the risk of hospital admission for worsening symptoms; however, there is no evidence for a reduction in mortality rates as a result of exercise.

Furthermore, it is not clear whether this evidence can be extended to people with heart failure with preserved ejection fraction HFpEF or to those whose exercise regimen takes place entirely at home.

Home visits and regular monitoring at heart failure clinics reduce the need for hospitalization and improve life expectancy. First-line therapy for people with heart failure due to reduced systolic function should include angiotensin-converting enzyme ACE inhibitors ACE-I or angiotensin receptor blockers ARBs if the person develops a long term cough as a side effect of the ACE-I.

In people who are intolerant of ACE-I and ARBs or who have significant kidney dysfunction, the use of combined hydralazine and a long-acting nitrate, such as isosorbide dinitrate , is an effective alternate strategy.

This regimen has been shown to reduce mortality in people with moderate heart failure. Second-line medications for CHF do not confer a mortality benefit.

Digoxin is one such medication. Its narrow therapeutic window, a high degree of toxicity, and the failure of multiple trials to show a mortality benefit have reduced its role in clinical practice.

Diuretics have been a mainstay of treatment for treatment of fluid accumulation, and include diuretics classes such as loop diuretics, thiazide-like diuretics , and potassium-sparing diuretics.

Although widely used, evidence on their efficacy and safety is limited, with the exception of mineralocorticoid antagonists such as spironolactone.

Anemia is an independent factor in mortality in people with chronic heart failure. The treatment of anemia significantly improves quality of life for those with heart failure, often with a reduction in severity of the NYHA classification, and also improves mortality rates.

Vasopressin receptor antagonists can also be used to treat heart failure. Conivaptan is the first medication approved by US Food and Drug Administration for the treatment of euvolemic hyponatremia in those with heart failure.

The AICD does not improve symptoms or reduce the incidence of malignant arrhythmias but does reduce mortality from those arrhythmias, often in conjunction with antiarrhythmic medications.

Cardiac contractility modulation CCM is a treatment for people with moderate to severe left ventricular systolic heart failure NYHA class II—IV which enhances both the strength of ventricular contraction and the heart's pumping capacity.

The CCM mechanism is based on stimulation of the cardiac muscle by non-excitatory electrical signals NES , which are delivered by a pacemaker -like device.

CCM is particularly suitable for the treatment of heart failure with normal QRS complex duration ms or less and has been demonstrated to improve the symptoms, quality of life and exercise tolerance.

This is especially problematic in people with left bundle branch block blockage of one of the two primary conducting fiber bundles that originate at the base of the heart and carries depolarizing impulses to the left ventricle.

Using a special pacing algorithm, biventricular cardiac resynchronization therapy CRT can initiate a normal sequence of ventricular depolarization.

People with the most severe heart failure may be candidates for ventricular assist devices VAD. VADs have commonly been used as a bridge to heart transplantation, but have been used more recently as a destination treatment for advanced heart failure.

In select cases, heart transplantation can be considered. While this may resolve the problems associated with heart failure, the person must generally remain on an immunosuppressive regimen to prevent rejection, which has its own significant downsides.

People with heart failure often have significant symptoms, such as shortness of breath and chest pain. Palliative care should be initiated early in the HF trajectory, and should not be an option of last resort.

Without transplantation, heart failure may not be reversible and heart function typically deteriorates with time.

Prognosis in heart failure can be assessed in multiple ways including clinical prediction rules and cardiopulmonary exercise testing.

Clinical prediction rules use a composite of clinical factors such as lab tests and blood pressure to estimate prognosis. Among several clinical prediction rules for prognosticating acute heart failure, the 'EFFECT rule' slightly outperformed other rules in stratifying people and identifying those at low risk of death during hospitalization or within 30 days.

A very important method for assessing prognosis in people with advanced heart failure is cardiopulmonary exercise testing CPX testing. CPX testing is usually required prior to heart transplantation as an indicator of prognosis.

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