Congestive Heart Failure

Congestive heart failure (CHF), or heart failure, is a condition in which the heart can't pump enough blood to the body's other organs. This can result from narrowed arteries that supply blood to the heart muscle coronary artery disease past heart attack, or myocardial infarction, with scar tissue that interferes with the heart muscle's normal work high blood pressure heart valve disease due to past rheumatic fever or other causes primary disease of the heart muscle itself, called cardiomyopathy. heart defects present at birth congenital heart defects. infection of the heart valves and/or heart muscle itself endocarditis and/or myocarditis The "failing" heart keeps working but not as efficiently as it should. People with heart failure can't exert themselves because they become short of breath and tired. As blood flow out of the heart slows, blood returning to the heart through the veins backs up, causing congestion in the tissues. Often swelling (edema) results. Most often there's swelling in the legs and ankles, but it can happen in other parts of the body, too. Sometimes fluid collects in the lungs and interferes with breathing, causing shortness of breath, especially when a person is lying down. Heart failure also affects the kidneys' ability to dispose of sodium and water. The retained water increases the edema. How do you diagnose and treat congestive heart failure? Your doctor is the best person to make the diagnosis. The most common signs of congestive heart failure are swollen legs or ankles or difficulty breathing. Another symptom is weight gain when fluid builds up. CHF usually requires a treatment program of

rest proper diet modified daily activities drugs such as o ACE (angiotensin-converting enzyme) inhibitors o beta blockers o digitalis o diuretics o vasodilators

Various drugs are used to treat congestive heart failure. They perform different functions. ACE inhibitors and vasodilators expand blood vessels and decrease resistance. This allows blood to flow more easily and makes the heart's work easier or more efficient. Beta blockers can improve how well the heart's left lower chamber (left ventricle) pumps. Digitalis increases the pumping action of the heart, while diuretics help the body eliminate excess salt and water.

When a specific cause of congestive heart failure is discovered, it should be treated or, if possible, corrected. For example, some cases of congestive heart failure can be treated by treating high blood pressure. If the heart failure is caused by an abnormal heart valve, the valve can be surgically replaced. If the heart becomes so damaged that it can't be repaired, a more drastic approach should be considered. A heart transplant could be an option. Most people with mild and moderate congestive heart failure can be treated. Proper medical supervision can prevent them from becoming invalids. See the Related Items box above for links to the Cardiology Patient Pagein Circulation, Journal of the American Heart Association:

Take Heart With Heart Failure

Related AHA publications:

Heart and Stroke Facts Living With Con

Heart failure (HF) is generally defined as inability of the heart to supply sufficient blood flow to meet the body's needs.[1][2][3] It has various diagnostic criteria, and the term heart failure is often incorrectly used to describe other cardiac-related illnesses, such as myocardial infarction (heart attack) or cardiac arrest. Common causes of heart failure include myocardial infarction (heart attacks) and other forms of ischemic heart disease, hypertension, valvular heart disease, and cardiomyopathy.[4] Heart failure can cause a number of symptoms including shortness of breath (typically worse when lying flat, which is called orthopnea), coughing, chronic venous congestion, ankle swelling, and exercise intolerance. Heart failure is often undiagnosed due to a lack of a universally agreed definition and challenges in definitive diagnosis. Treatment commonly consists of lifestyle measures (such as decreased salt intake) and medications, and sometimes devices or even surgery. Heart failure is a common, costly, disabling, and potentially deadly condition. [4] In developing countries, around 2% of adults suffer from heart failure, but in those over the age of 65, this increases to 610%.[4][5] Mostly due to costs of hospitalization it is associated with a high health expenditure; costs have been estimated to amount to 2% of the total budget of the National Health Service in the United Kingdom, and more than $35 billion in the United States.[6][7] Heart failure is associated with significantly reduced physical and mental health, resulting in a markedly decreased quality of life.[8][9] With the exception of heart failure caused by reversible conditions, the condition usually worsens with time. Although some people survive many years, progressive disease is associated with an overall annual mortality rate of 10%.[10]

Contents
[hide]

1 Terminology 2 Classification 3 Signs and symptoms

o o
4 Causes

3.1 Symptoms 3.1.1 Left-sided failure 3.1.2 Right-sided failure 3.2 Signs 3.2.1 Left-sided failure 3.2.2 Right-sided failure 3.2.3 Biventricular failure

o o o o o o o o o o

4.1 Chronic heart failure 4.2 Acute decompensated heart failure 5 Pathophysiology 5.1 Systolic dysfunction 5.2 Diastolic dysfunction 6 Diagnosis 6.1 Imaging 6.2 Electrophysiology 6.3 Blood tests 6.4 Angiography 6.5 Monitoring 6.6 Algorithms 6.6.1 Framingham criteria 6.6.2 ESC algorithm 7 Management

o o o

7.1 Acute decompensation 7.2 Chronic management 7.3 Palliative care and hospice 8 Prognosis 9 Epidemiology

o o o

9.1 Gender 9.2 Race 9.3 Age 10 See also

11 References 12 External links

[edit]Terminology Heart failure is a global term for the physiological state in which cardiac output is insufficient for the body's needs. This occurs most commonly when the cardiac output is low (often termed "congestive heart failure" or CHF, because the body becomes congested with fluid). [11] It may also occur when the body's requirements for oxygen and nutrients are increased and demand outstrips what the heart can provide, (termed "high output cardiac failure")
[12]

. This

can occur from severe anemia, Gram negative septicaemia, beriberi (vitamin B1/thiamine deficiency), thyrotoxicosis, Paget's disease, arteriovenous fistulae, or arteriovenous malformations. Fluid overload is a common problem for people with heart failure but is not synonymous with it. Patients with treated heart failure will often be euvolaemic (a term for normal fluid status), or more rarely,dehydrated. Doctors use the words "acute" to mean of rapid onset and "chronic" of long duration. Chronic heart failure is therefore a long term situation, usually with stable treated symptomatology. Acute decompensated heart failure is a term used to describe exacerbated or decompensated heart failure, referring to episodes in which a patient can be characterized as having a change in heart failure signs and symptoms resulting in a need for urgent therapy or hospitalization.[13] 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 usually result in heart failure. Ischemic cardiomyopathy implies that the cause of muscle damage iscoronary 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. [edit]Classification

There are many different ways to categorize heart failure, including: the side of the heart involved, (left heart failure versus right heart failure) whether the abnormality is due to contraction or relaxation of the heart (systolic dysfunction vs. diastolic dysfunction) whether the problem is primarily increased venous back pressure (behind) the heart, or failure to supply adequate arterial perfusion (in front of) the heart (backward vs. forward failure) whether the abnormality is due to low cardiac output with high systemic vascular resistance or high cardiac output with low vascular resistance (low-output heart failure vs. high-output heart failure) the degree of functional impairment conferred by the abnormality (as in the NYHA functional classification) Functional classification generally relies on the New York Heart Association Functional Classification.[14] The classes (I-IV) are: Class I: no limitation is experienced in any activities; there are no symptoms from ordinary activities. Class II: slight, mild limitation of activity; the patient is comfortable at rest or with mild exertion. Class III: marked limitation of any activity; the patient is comfortable only at rest. Class IV: any physical activity brings on discomfort and symptoms occur at rest.

This score documents 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 doesn't reliably predict the walking distance or exercise tolerance on formal testing. [15] In its 2001 guidelines the American College of Cardiology/American Heart Association working group introduced four stages of heart failure: [16] Stage A: Patients at high risk for developing HF in the future but no functional or structural heart disorder; Stage B: a structural heart disorder but no symptoms at any stage; Stage C: previous or current symptoms of heart failure in the context of an underlying structural heart problem, but managed with medical treatment; Stage D: advanced disease requiring hospital-based support, a heart transplant or palliative care.

The ACC staging system is useful in that Stage A encompasses "pre-heart failure" - a stage where intervention with treatment can presumably prevent progression to overt symptoms. ACC stage A does not have a corresponding NYHA class. ACC Stage B would correspond to NYHA Class I. ACC Stage C corresponds to NYHA Class II and III, while ACC Stage D overlaps with NYHA Class IV. [edit]Signs

and symptoms

A man with congestive heart failure and marked jugular venous distension. External jugular vein marked by an arrow.

[edit]Symptoms 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, heart failure is not exclusively backward failure (in the part of the circulation which drains to the ventricle). There are several other exceptions to a simple left-right division of heart failure symptoms. Left sided forward failure overlaps with right sided backward failure. Additionally, the most common cause of right-sided heart failure is left-sided heart failure. The result is that patients commonly present with both sets of signs and symptoms. [edit]Left-sided failure
Wheezing

The sound of wheezing as heard with a stethoscope.

Problems listening to this file? See media help.

Backward failure of the left ventricle causes congestion of the pulmonary vasculature, and so the symptoms are predominantly respiratory in nature. Backward failure can be subdivided into failure of the left atrium, the left ventricle or both within the left circuit. The patient will have dyspnea (shortness of breath) on exertion (dyspne d'effort) 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 severe cases, the patient may resort to sleeping while sitting up. Another symptom of heart failure isparoxysmal nocturnal dyspnea a sudden nighttime attack of severe breathlessness, usually several hours after going to sleep. Easy fatigueability and exercise intolerance are also common complaints related to respiratory compromise. "Cardiac asthma" or wheezing may occur. Compromise of left ventricular forward function may result in symptoms of poor systemic circulation such as dizziness, confusion and cool extremities at rest. [edit]Right-sided failure 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 hepatomegaly (enlargement of the liver) may develop. Significant liver congestion may result in impaired liver function, and jaundice and even coagulopathy (problems of decreased blood clotting) may occur. [edit]Signs [edit]Left-sided failure Common respiratory signs are tachypnea (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 hypoxemia, 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.g. aortic stenosis) or as a result (e.g., mitral regurgitation) of the heart failure.

[edit]Right-sided failure Physical examination can reveal pitting peripheral edema, ascites, and hepatomegaly. Jugular venous pressure is frequently assessed as a marker of fluid status, which can be accentuated by thehepatojugular reflux. If the right ventriclar pressure is increased, a parasternal heave may be present, signifying the compensatory increase in contraction strength. [edit]Biventricular failure 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 in 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 both into the systemic and pulmonary venous system. When unilateral, effusions are often right-sided, presumably because of the larger surface area of the right lung. [edit]Causes [edit]Chronic

heart failure

The predominance of causes of heart failure are difficult to analyze due to challenges in diagnosis, differences in populations, and changing prevalence of causes with age. A 19 year study of 13000 healthy adults in the United States (the National Health and Nutrition Examination Survey (NHANES I) found the following causes ranked by Population Attributable Risk score:[17]

1. Ischaemic heart disease 62%

2. Cigarette smoking 16% 3. Hypertension (high blood pressure)10% 4. Obesity 8% 5. Diabetes 3%

6. Valvular heart disease 2% (much higher in older populations)

An Italian registry of over 6200 patients with heart failure showed the following underlying causes:[18] 1. Ischaemic heart disease 40% 2. Dilated cardiomyopathy 32% 3. Valvular heart disease 12% 4. Hypertension 11% 5. Other 5%

Rarer causes of heart failure include: Viral myocarditis (an infection of the heart muscle) Infiltrations of the muscle such as amyloidosis HIV cardiomyopathy (caused by human immunodeficiency virus) Connective tissue diseases such as systemic lupus erythematosus Abuse of drugs such as alcohol and cocaine Pharmaceutical drugs such as chemotherapeutic agents Arrhythmias

Obstructive sleep apnea a condition of sleep disordered breathing overlaps with obesity, hypertension, and diabetes and is regarded as an independent cause of heart failure. [edit]Acute

decompensated heart failure

Main article: Acute decompensated heart failure Chronic stable heart failure may easily decompensate. This most commonly results from an intercurrent illness (such as pneumonia), myocardial infarction (a heart attack), arrhythmias, uncontrolledhypertension, or a patient's failure to maintain a fluid restriction, diet, or medication.[19] Other well recognized precipitating factors include anaemia and hyperthyroidism which place additional strain on the heart muscle. Excessive fluid or salt intake, and medication that causes fluid retention such as NSAIDs and thiazolidinediones, may also precipitate decompensation.[20] [edit]Pathophysiology This section needs additional citations for verification.
Please help improve this article by adding reliable references. Unsourced material may be challenged and removed. (September 2010)

Heart failure is caused by any condition which reduces the efficiency of the myocardium, or heart muscle, through damage or overloading. As such, it can be caused by as diverse an array of conditions as myocardial infarction (in which the heart muscle is starved of oxygen and dies), hypertension (which increases the force of contraction needed to pump blood) and amyloidosis (in which protein is deposited in the heart muscle, causing it to stiffen). Over time these increases in workload will produce changes to the heart itself: Reduced contractility, or force of contraction, due to overloading of the ventricle. In health, increased filling of the ventricle results in increased contractility (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 crosslink actin and myosin filaments in over-stretched heart muscle.[21]

A reduced stroke volume, as a result of a failure of systole, diastole or both. Increased end systolic volume is usually caused by reduced contractility. Decreased end diastolic volume results from impaired ventricular filling as occurs when the compliance of the ventricle falls (i.e. when the walls stiffen). Reduced spare capacity. As the heart works harder to meet normal metabolic demands, the amount cardiac output can increase in times of increased oxygen demand (e.g. exercise) is reduced. This contributes to the exercise intolerance commonly seen in heart failure. This translates to the loss of one's cardiac reserve. The cardiac reserve refers to the ability of the heart to work harder during exercise or strenuous activity. Since the heart has to work harder to meet the normal metabolic demands, it is incapable of meeting the metabolic demands of the body during exercise. Increased heart rate, stimulated by increased sympathetic activity in order to maintain cardiac output. Initially, this helps compensate for heart failure by maintaining blood pressure and perfusion, but places further strain on the myocardium, increasing coronary perfusion requirements, which can lead to worsening of ischemic heart disease. Sympathetic activity may also cause potentially fatal arrhythmias. Hypertrophy (an increase in physical size) of the myocardium, caused by the terminally differentiated heart muscle fibres increasing in size in an attempt to improve contractility. This may contribute to the increased stiffness and decreased ability to relax during diastole. Enlargement of the ventricles, contributing to the enlargement and spherical shape of the failing heart. The increase in ventricular volume also causes a reduction in stroke volume due to mechanical and contractile inefficiency.[22]

The general effect is one of reduced cardiac output and increased strain on the heart. This increases the risk of cardiac arrest (specifically due to ventricular dysrhythmias), and reduces blood supply to the rest of the body. In chronic disease the reduced cardiac output causes a number of changes in the rest of the body, some of which are physiological compensations, some of which are part of the disease process: Arterial blood pressure falls. This destimulates baroreceptors in the carotid sinus and aortic arch which link to the nucleus tractus solitarius. This center in the brain increases sympathetic activity, releasing catecholamines into the blood stream. Binding to alpha-1 receptors results in systemic arterial vasoconstriction. This helps restore blood pressure but also increases the total peripheral resistance, increasing the workload of the heart. Binding to beta-1 receptors in the myocardium increases the heart rate and make contractions more forceful, in an attempt to increase cardiac output. This also, however, increases the amount of work the heart has to perform.

Increased sympathetic stimulation also causes the hypothalamus to secrete vasopressin (also known as antidiuretic hormone or ADH), which causes fluid retention at the kidneys. This increases the blood volume and blood pressure. Reduced perfusion (blood flow) to the kidneys stimulates the release of renin an enzyme which catalyses the production of the potent vasopressor angiotensin. Angiotensin and its metabolites cause further vasocontriction, and stimulate increased secretion of the steroid aldosterone from the adrenal glands. This promotes salt and fluid retention at the kidneys, also increasing the blood volume. The chronically high levels of circulating neuroendocrine hormones such as catecholamines, renin, angiotensin, and aldosterone affects the myocardium directly, causing structural remodelling of the heart over the long term. Many of these remodelling effects seem to be mediated by transforming growth factor beta (TGF-beta), which is a common downstream target of the signal transduction cascade initiated by catecholamines[23] and angiotensin II[24], and also by epidermal growth factor (EGF), which is a target of the signaling pathway activated by aldosterone [25] Reduced perfusion of skeletal muscle causes atrophy of the muscle fibres. This can result in weakness, increased fatigueability and decreased peak strength - all contributing to exercise intolerance.[26]

The increased peripheral resistance and greater blood volume place further strain on the heart and accelerates the process of damage to the myocardium. Vasoconstriction and fluid retention produce an increased hydrostatic pressure in the capillaries. This shifts the balance of forces in favour of interstitial fluid formation as the increased pressure forces additional fluid out of the blood, into the tissue. This results in edema (fluid build-up) in the tissues. In right-sided heart failure this commonly starts in the ankles where venous pressure is high due to the effects of gravity (although if the patient is bed-ridden, fluid accumulation may begin in the sacral region.) It may also occur in the abdominal cavity, where the fluid build-up is called ascites. In left-sided heart failure edema can occur in the lungs - this is called cardiogenic pulmonary edema. This reduces spare capacity for ventilation, causes stiffening of the lungs and reduces the efficiency of gas exchange by increasing the distance between the air and the blood. The consequences of this are shortness of breath, orthopnea and paroxysmal nocturnal dyspnea. The symptoms of heart failure are largely determined by which side of the heart fails. The left side pumps blood into the systemic circulation, whilst the right side pumps blood into the pulmonary circulation. Whilst left-sided heart failure will reduce cardiac output to the systemic circulation, the initial symptoms often manifest due to effects on the pulmonary circulation. In systolic dysfunction, the ejection fraction is decreased, leaving an abnormally elevated volume of blood in the left ventricle. In diastolic dysfunction, end-diastolic ventricular

pressure will be high. This increase in volume or pressure backs up to the left atrium and then to the pulmonary veins. Increased volume or pressure in the pulmonary veins impairs the normal drainage of the alveoli and favors the flow of fluid from the capillaries to the lung parenchyma, causing pulmonary edema. This impairs gas exchange. Thus, left-sided heart failure often presents with respiratory symptoms: shortness of breath, orthopnea and paroxysmal nocturnal dyspnea. In severe cardiomyopathy, the effects of decreased cardiac output and poor perfusion become more apparent, and patients will manifest with cold and clammy extremities, cyanosis, claudication, generalized weakness, dizziness, and syncope The resultant hypoxia caused by pulmonary edema causes vasoconstriction in the pulmonary circulation, which results in pulmonary hypertension. Since the right ventricle generates far lower pressures than the left ventricle (approximately 20 mmHg versus around 120 mmHg, respectively, in the healthy individual) but nonetheless generates cardiac output exactly equal to the left ventricle, this means that a small increase in pulmonary vascular resistance causes a large increase in amount of work the right ventricle must perform. However, the main mechanism by which left-sided heart failure causes right-sided heart failure is actually not well understood. Some theories invoke mechanisms that are mediated by neurohormonal activation. Mechanical effects may also contribute. As the left ventricle distends, the intraventricular septum bows into the right ventricle, decreasing the capacity of the right ventricle. [edit]Systolic

dysfunction

Heart failure caused by systolic dysfunction is more readily recognized. It can be simplistically described as failure of the pump function of the heart. It is characterized by a decreased ejection fraction (less than 45%). The strength of ventricular contraction is attenuated and inadequate for creating an adequate stroke volume, resulting in inadequate cardiac output. In general, this is caused by dysfunction or destruction of cardiac myocytes or their molecular components. In congenital diseases such as Duchenne muscular dystrophy, the molecular structure of individual myocytes is affected. Myocytes and their components can be damaged by inflammation (such as in myocarditis) or by infiltration (such as in amyloidosis). Toxins and pharmacological agents (such as ethanol, cocaine, andamphetamines) cause intracellular damage and oxidative stress. The most common mechanism of damage is ischemia causing infarction and scar formation. After myocardial infarction, dead myocytes are replaced by scar tissue, deleteriously affecting the function of the myocardium. On echocardiogram, this is manifest by abnormal or absent wall motion. Because the ventricle is inadequately emptied, ventricular end-diastolic pressure and volumes increase. This is transmitted to the atrium. On the left side of the heart, the increased pressure is transmitted to the pulmonary vasculature, and the resultant hydrostatic pressure

favors extravassation of fluid into the lung parenchyma, causing pulmonary edema. On the right side of the heart, the increased pressure is transmitted to the systemic venous circulation and systemic capillary beds, favoring extravassation of fluid into the tissues of target organs and extremities, resulting in dependent peripheral edema. [edit]Diastolic

dysfunction

Heart failure caused by diastolic dysfunction is generally described as the failure of the ventricle to adequately relax and typically denotes a stiffer ventricular wall. This causes inadequate filling of the ventricle, and therefore results in an inadequate stroke volume. The failure of ventricular relaxation also results in elevated end-diastolic pressures, and the end result is identical to the case of systolic dysfunction (pulmonary edema in left heart failure, peripheral edema in right heart failure.) Diastolic dysfunction can be caused by processes similar to those that cause systolic dysfunction, particularly causes that affect cardiac remodeling. Diastolic dysfunction may not manifest itself except in physiologic extremes if systolic function is preserved. The patient may be completely asymptomatic at rest. However, they are exquisitely sensitive to increases in heart rate, and sudden bouts of tachycardia (which can be caused simply by physiological responses to exertion, fever, or dehydration, or by pathological tachyarrhythmias such as atrial fibrillation with rapid ventricular response) may result in flash pulmonary edema. Adequate rate control (usually with a pharmacological agent that slows down AV conduction such as a calcium channel blocker or a beta-blocker) is therefore key to preventing decompensation. Left ventricular diastolic function can be determined through echocardiography by measurement of various parameters such as the E/A ratio (early-to-atrial left ventricular filling ratio), the E (early left ventricular filling) deceleration time, and the isovolumic relaxation time. [edit]Diagnosis

Acute pulmonary edema. Note enlarged heart size, apical vascular redistribution ( circle ), and small bilateral pleural effusions ( arrow ).

No system of diagnostic criteria has been agreed as the gold standard for heart failure. Commonly used systems are the "Framingham criteria"[27] (derived from the Framingham Heart Study), the "Boston criteria",[28] the "Duke criteria",[29] and (in the setting of acute myocardial infarction) the "Killip class".[30] [edit]Imaging 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. Normally, the EF should be between 50% and 70%; in systolic heart failure, it drops below 40%. 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 patient, 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. Chest X-rays are frequently used to aid in the diagnosis of CHF. In the compensated patient, 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. [edit]Electrophysiology An electrocardiogram (ECG/EKG) may be used to identify arrhythmias, ischemic heart disease, right and left ventricular hypertrophy, and presence of conduction delay or abnormalities (e.g. left bundle branch block). Although these findings are not specific to the diagnosis of heart failure a normal ECG virtually excludes left ventricular systolic dysfunction.
[31]

[edit]Blood

tests

Blood tests routinely performed include electrolytes (sodium, potassium), measures of renal function, liver function tests, thyroid function tests, a complete blood count, and often Creactive 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.

According to a meta-analysis comparing BNP and N-terminal pro-BNP (NTproBNP) in the diagnosis of heart failure, BNP is a better indicator for heart failure and left ventricular systolic dysfunction. In groups of symptomatic patients, a diagnostic odds ratio of 27 for BNP compares with a sensitivity of 85% and specificity of 84% in detecting heart failure.[32] [edit]Angiography Heart failure may be the result of coronary artery disease, and its prognosis depends in part on the ability of the coronary arteries to supply blood to the myocardium (heart muscle). As a result,coronary catheterization may be used to identify possibilities for revascularisation through percutaneous coronary intervention or bypass surgery. [edit]Monitoring Various measures are often used to assess the progress of patients 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). [edit]Algorithms 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. [edit]Framingham criteria By the Framingham criteria, diagnosis of congestive heart failure (heart failure with impaired pumping capability)[11] 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: Major criteria:[33] Cardiomegaly on chest radiography S3 gallop (a third heart sound) Acute pulmonary edema Paroxysmal nocturnal dyspnea Crackles on lung auscultation Central venous pressure of more than 16 cm H2O at the right atrium Jugular vein distension Positive abdominojugular test Weight loss of more than 4.5 kg in 5 days in response to treatment (sometimes classified as a minor criterium[34])

Minor criteria:[33] Tachycardia of more than 120 beats per minute Nocturnal cough Dyspnea on ordinary exertion Pleural effusion Decrease in vital capacity by one third from maximum recorded Hepatomegaly Bilateral ankle edema

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.[33] The Framingham Heart Study criteria are 100% sensitive and 78% specific for identifying persons with definite congestive heart failure. [33] [edit]ESC algorithm The ESC algorithm weights the following parameters in establishing the diagnosis of heart failure:[35] Opposes if normal or absent

Influence

Supports if present

Parameter

+ - to some degree ++ - to intermediate degree +++ - to high degree

Compatible symptoms

++

++

Compatible signs

++

Cardiac dysfunction on echocardiography

+++

+++

Response of symptoms or signs to therapy

+++

++

ECG

Normal

++

Abnormal

++

Dysrhythmia

+++

Laboratory

BNP > 400 pg/mL and/or NT-proBNP > 2000 pg/mL

+++

BNP < 100 pg/mL and NT-proBNP < 400 pg/mL

+++

Hyponatraemia

Renal dysfunction

Mild elevations of troponin

Chest X-ray

Pulmonary congestion

+++

Reduced exercise capacity

+++

++

Abnormal pulmonary function tests +

Abnormal haemodynamics at rest [edit]Management

+++

++

Main article: Management 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.g. infection, alcohol ingestion, anemia,thyrotoxicosis, arrhythmia, hypertension). Treatments include lifestyle and pharmacological modalities. [edit]Acute

decompensation

Main article: Acute decompensated heart failure 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 circulationare adequate. Immediated treatments usually involve some combination of vasodilators such as nitroglycerin, diuretics such as furosemide, and possibly non invasive positive pressure ventilation(NIPPV). [edit]Chronic

management

The goal is to prevent the development of acute decompensated heart failure, to counteract the deleterious effects of cardiac remodeling, and to minimize the symptoms that the patient suffers. First-line therapy for all heart failure patients is angiotensin-converting enzyme (ACE) inhibition. ACE inhibitors (i.e., enalapril, captopril, lisinopril, ramipril) improve survival and quality of life in heart failure patients, and have been shown to reduce mortality in patients with left ventricular dysfunction in numerous randomized trials. [36][37] In addition to pharmacologic agents (oral loop diuretics, beta-blockers, ACE inhibitors or angiotensin receptor blockers, vasodilators, and in severe cardiomyopathy aldosterone receptor antagonists), behavioral modification should be pursued, specifically with regards to dietary guidelines regarding salt and fluid intake. Exercise should be encouraged as tolerated, as sufficient conditioning can significantly improve quality-of-life. In patients with severe cardiomyopathy, implantation of an automatic implantable cardioverter defibrillator(AICD) should be considered. A select population will also probably benefit from ventricular resynchronization. In select cases, cardiac transplantation can be considered. While this may resolve the problems associated with heart failure, the patient generally must remain on an immunosuppressive regimen to prevent rejection, which has its own significant downsides. [edit]Palliative

care and hospice

Without transplantation, heart failure caused by ischemic heart disease is not reversible, and cardiac function typically deteriorates with time. (In particular, diastolic function worsens as a function of age even in individuals without ischemic heart disease.) The growing number of patients with Stage D heart failure (intractable symptoms of fatigue, shortness of breath or chest pain at rest despite optimal medical therapy) should be considered for palliative care or hospice, according to American College of Cardiology/American Heart Association guidelines. [edit]Prognosis

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 prognosing acute heart failure, the 'EFFECT rule' slightly outperformed other rules in stratifying patients and identifying those at low risk of death during hospitalization or within 30 days.[38] Easy methods for identifying low risk patients are: ADHERE Tree rule indicates that patients with blood urea nitrogen < 43 mg/dl and systolic blood pressure at least 115 mm Hg have less than 10% chance of inpatient death or complications. BWH rule indicates that patients with systolic blood pressure over 90 mm Hg, respiratory rate of 30 or less breaths per minute, serum sodium over 135 mmol/L, no new ST-T wave changes have less than 10% chance of inpatient death or complications. A very important method for assessing prognosis in advanced heart failure patients is cardiopulmonary exercise testing (CPX testing). CPX testing is usually required prior to heart transplantation as an indicator of prognosis. Cardiopulmonary exercise testing involves measurement of exhaled oxygen and carbon dioxide during exercise. The peak oxygen consumption (VO2 max) is used as an indicator of prognosis. As a general rule, a VO2 max less than 12-14 cc/kg/min indicates a poor survival and suggests that the patient may be a candidate for a heart transplant. Patients with a VO2 max<10 cc/kg/min have clearly poorer prognosis. The most recent International Society for Heart and Lung Transplantation (ISHLT) guidelines[39] also suggest two other parameters that can be used for evaluation of prognosis in advanced heart failure, the heart failure survival score and the use of a criterion of VE/VCO2 slope > 35 from the CPX test. The heart failure survival score is a score calculated using a combination of clinical predictors and the VO2 max from the cardiopulmonary exercise test. [edit]Epidemiology
This section requires expansion.

Heart failure is the leading cause of hospitalization in people older than 65. [40] In developed countries, the mean age of patients with heart failure is 75 years old. In developing countries, two to three percent of the population suffers from heart failure, but in those 70 to 80 years old, it occurs in 2030 percent. Heart failure affects close to 5 million people in the USA and each year close to 500,000 new cases are diagnosed. What is of more concern is that more than 50% of patients seek readmission within 6 months after treatment and the average duration of hospital stay is 6 days.

In tropical countries, the most common cause of HF is valvular heart disease or some type of cardiomyopathy. Moreover as underdeveloped countries become more affluent, there has also been an increase in diabetes, hypertension and obesity which has resulted in heart failure. In USA, HF is much higher in African Americans, Hispanics, Native Americans and recent immigrants from the eastern bloc countries like Russia. This high prevalence in these ethnic populations has been linked to high incidence of diabetes and hypertension. In many new immigrants to the USA the high prevalence of heart failure has largely been attributed to lack of preventive health care or substandard treatment.[41] [edit]Gender Both men and women have similar incidence of HF. However, there are distinct differences between the two genders. Women generally develop heart failure after menopause. Women tend to become more depressed than men Women have similar symptoms but the intensity is more pronounced. Women usually survive a lot longer with heart failure than men.

[edit]Race New information suggests that elements of heart failure in African Americans and Caucasians may be different[42] and therapy for heart failure has different efficacies depending on racial, ethnic, and genetic backgrounds. [edit]Age Heart failure basically means that the heart muscles have become weak and do not function as normal.[43] Heart failure is a progressive medical disorder. As the heart gets weaker, symptoms and signs become prominent. Heart failure can affect the entire heart or only the right or left side. In the majority of cases, both sides of the heart are affected. [44] HF can occur at any age depending on the cause. In general heart failure does increase with age.

Congestive Heart Failure Overview

The heart is a pump that works together with the lungs. It pumps blood in 2 ways. It pumps blood from the heart to the lungs to pick up oxygen. The oxygenated blood returns to the heart.

It then pumps blood out into the circulatory system of blood vessels that carry blood through the body. The heart consists of 4 chambers.

The upper chambers are called atria, and the lower chambers are calledventricles. The right atrium and ventricle receive blood from the body through the veins and then pump the blood to the lungs. The left atrium and ventricle receive blood back from the lungs and pump it out the aorta into the arteries, feeding all organs and tissues of the body. Because the left ventricle has to pump blood through the entire body, it is a stronger pump than the right ventricle. Heart failure sounds frightening because it sounds like the heart just stops working. Do not be discouraged by the term heart failure-the heart has not stopped beating or pumping. Heart failure means the tissues of the body are temporarily not receiving enough blood and oxygen. With advancements in diagnosis and therapy for heart failure, patients are feeling better and living longer.

Although heart failure is a serious medical condition, the heart does not just stop abruptly. Heart failure may develop gradually over several years, or move quickly after aheart attack or a disease of the heart muscle. Heart failure is an illness in which the pumping action of the heart becomes less and less powerful. That is, the heart does not pump blood as well as it should. When this happens, blood does not move efficiently through the circulatory system and starts to back up, increasing the pressure in the blood vessels and forcing fluid from the blood vessels into body tissues.

When the left side of the heart starts to fail, fluid collects in the lungs (pulmonary edema). This extra fluid in the lungs (congestion) makes it more difficult for the airways to expand as you inhale. Breathing becomes more difficult, and you may feel short of breath, particularly with activity or lying down. When the right side of the heart starts to fail, fluid collects in the feet and lower legs. As the heart failure becomes worse, the upper legs swell and eventually the abdomen collects fluid (ascites). Weight gain accompanies the fluid retention and is an excellent measure of how much fluid is being retained. Puffy swelling (edema) is a sign of right heart failure, especially if the edema ispitting edema. With pitting edema, a finger pressed on the swollen leg leaves a finger imprint. Nonpitting edema is not caused by heart failure. Congestive heart failure (CHF) is generally classified as systolic or diastolic heart failure and becomes progressively more common with increasing age. Systolic heart failure: The pumping action of the heart is reduced or weakened. A common clinical measurement is the ejection fraction (EF). The ejection fraction is a calculation of how much blood is ejected out of the left ventricle (stroke volume), divided by the maximum volume remaining in the left ventricle at the end of diastoleor relaxation phase. A normal

ejection fraction is greater than 50%. Systolic heart failure has a decreased ejection fraction of less than 50%. Diastolic heart failure: The heart can contract normally but is stiff, or less compliant, when it is relaxing and filling with blood. This impedes blood filling into the heart and produces backup into the lungs and CHF symptoms. Diastolic heart failure is more common in patients older than 75 years, especially in women withhigh blood pressure. In diastolic heart failure, the ejection fraction is normal. Heart failure affects 1% of people aged 50 years, about 5% of those aged 75 years or older, and 25% of those aged 85 years or older. Heart failure is the most common reason for Medicare patients to be admitted to the hospital. As the number of elderly people continues to rise, the number of people diagnosed with this condition will continue to increase. In the United States, nearly 5 million people have heart failure. Each year about 550,000 new cases are diagnosed. The condition is more common among African Americans than whites. The rate of death from heart failure is about 10% after 1 year. About half of those with CHF die within 5 years after their diagnosis. These statistics vary widely by a patient's exact diagnosis and therapy. Advances in research are providing more options and improving outcomes for people with CHF

Congestive Heart Failure Causes

Congestive heart failure (CHF) is a syndrome, not a disease, that can be brought about by several causes. CHF is a weakening of the heart brought on by an underlying heart or blood vessel problem, often a combination of several different problems, including the following: Weakened heart muscle Damaged heart valves Blocked blood vessels supplying the heart muscle (coronary arteries), leading to a heart attack Toxic exposures, like alcohol or cocaine Infections High blood pressure that results in thickening of the heart muscle (left ventricular hypertrophy) Pericardial disease, such as pericardial effusion (a large collection of fluid around the heart in the space between the heart muscle and the thick layer of pericardiumsurrounding the heart) and/or a thickened pericardium, which does not allow the heart to fill properly Congenital heart diseases Prolonged, serious arrhythmias While these conditions often combine to produce CHF, sometimes the causes of diseased heart muscles are not known; this is called idiopathic cardiomyopathy or heart muscle disease of unknown cause.

CHF is often a result of the following lifestyle habits: Unhealthy habits, such as smoking and excessive use of alcohol, are often to blame. Obesity and lack of activity may contribute to CHF, either directly or indirectly through accompanying high blood pressure, diabetes, and coronary artery disease. Years of uncontrolled high blood pressure damages both heart and blood vessels. Along with lifestyle risk factors, a number of diseases (for example, diabetes, heart attack [myocardial infarction], and congenital heart disease) can damage the heart and lead to congestive heart failure. Over a hundred other, less common, causes of CHF include a variety of infections, exposures, complications of other diseases, toxic effects, and genetic predisposition. Whether through disease or lifestyle choices, the pumping action of the heart can be impaired by several mechanisms: Heart muscle damage (cardiomyopathy): The heart muscle can become weak because of damage or disease and thus does not contract or squeeze as forcefully as it should. This damage to the muscle can occur from coronaryheart disease (coronary artery disease) leading to a heart attack, or long-standing high blood pressure, viral infection, alcohol abuse, diabetes, or many other less common causes. Sometimes, the cause is not known.

Heart attack (myocardial infarction): A heart attack commonly causes severe pain in the chest, shortness of breath, nausea, sweating, and/or a feeling of impending doom. Heart attack may rapidly lead to either cardiac arrest (no heartbeat) or permanent damage of the left ventricle. If this damage is bad enough, that part of the heart will not work properly, which leads to heart failure. High blood pressure (hypertension): Abnormally high blood pressure increases the amount of work the left ventricle has to do to pump blood out into the circulatory system. Over time, this greater workload can damage and weaken the heart. This can lead to heart failure if this damage is allowed to go on unchecked. Proper treatment of high blood pressure can prevent left ventricular hypertrophy and heart failure. Heart valve problems: The valves of the heart normally keep the blood flowing in the right direction through the heart. Abnormal heart valves impede this forward flow in 1 of 2 ways. o An incompetent valve is a valve that does not close properly when it should and allows blood to flow backward in the heart, "against the current." When blood flows the wrong way across a valve, the heart has to work harder to keep up its output. Eventually, this backed up blood accumulates in the lungs and the body. o A stenotic valve is a valve that does not open properly when it should. Blood flow through the narrowed opening is blocked, creating an increased workload on the heart. Abnormal rhythm or irregular heartbeat: Abnormal heart rhythms lower the heart's effectiveness as a pump. The rhythm may be too slow or too fast, or irregular. The heart has to pump harder to overcome these rhythm disorders. If this excessively slow or fast heartbeat is sustained over hours, days, or weeks, the heart can weaken, which can cause heart failure.

Other conditions may have injured the heart such as thyroid disorders (too much or too little thyroid hormone) or treatments for cancer (radiation or certain chemotherapy drugs).

Congestive Heart Failure Symptoms

People with congestive heart failure (CHF) sometimes do not suspect a problem with their heart. The early symptoms are often shortness of breath, cough, or a feeling of not being able to get a deep breath. If you have a known breathing problem, such as asthma, chronic obstructive pulmonary disease (COPD), oremphysema, you may think you are having an "attack" or worsening of that condition. If you usually do not have breathing problems, you may think you have a cold,flu, or bronchitis. To make matters worse, any or several of these conditions may coexist along with congestive heart failure. Congestive heart failure has the following 3 major symptoms: o Exercise intolerance A person may be unable to tolerate exercise or even mild physical exertion that he or she may have been able to do in the past. The body needs oxygen and other nutrients during physical activity. A failing heart cannot pump enough blood to provide these nutrients to the body. The ability to exercise, even to walk at a normal pace, may be limited by feeling tired (fatigue) and having shortness of breath. Ordinary activities, such as sweeping, vacuuming, pushing a lawnmower, or even walking about the house, may be difficult or impossible.

o o

The shortness of breath that accompanies these activities usually gets better with rest. o o o o o Shortness of breath If a person has CHF, he or she may have difficulty breathing (dyspnea), especially when he or she is active. When CHF worsens, fluid backs up into the lungs and interferes with oxygen getting into the blood, causing dyspnea at rest and at night (orthopnea). If a person has CHF, he or she may awaken at night short of breath and have to sit or stand up to get relief. This is called paroxysmal nocturnal dyspnea. Several pillows may help with a more comfortable sleep. A person may also prefer sleeping in a recliner rather than in a bed. As the buildup of fluid in the lungs becomes very severe, a frothy, pink liquid may be coughed up. Fluid retention and swelling Puffy swelling (edema) in the legs, the feet, and the ankles may occur, particularly at the end of the day or after prolonged sitting or standing.

o o

o o

Often, the swelling is more noticeable in the ankles or on the lower leg in the front where the bone is close to the skin. Press down on the skin in the puffy areas; the indentation where the finger pressed may be visible for a few minutes. This is called pitting edema. Nonpitting edema is not caused by heart failure. Pitting edema is not synonymous with heart failure; it can have other causes, includingliver and kidney failure. Swelling may be so severe as to reach up to the hips, scrotum, abdominal wall, and eventually the abdominal cavity (ascites). Daily weight checks are mandatory in persons with heart failure because the amount of fluid retention is usually reflected by the amount of increasing shortness of breath and weight gain. Persons with heart failure should know what their dry weight is or what they weigh when they feel good with no pitting edema.

Congestive heart failure usually does not cause chest pain. Remember, though, that other serious conditions that do cause chest pain, such as angina and myocardial infarction, can coexist with heart failure.

When to Seek Medical Care

Often cardiologists who specialize in heart failure can work together with primary caredoctors and other health care providers. Certain symptoms need to be checked by a doctor. If you have any of these symptoms, call your health care provider for an appointment. If the symptoms are severe or of sudden onset, seek immediate emergency care. You have shortness of breath that seems to be getting worse or causes difficulty sleeping. You fall asleep in bed but wake up at night with shortness of breath. You sleep better in a semi-upright position in a chair or recliner than flat in bed. Your shortness of breath develops with mild exertion and is worse than usual. You have unusual fatigue that is not relieved with rest. You have a dry cough that will not go away or seems otherwise unusual. You have swelling in your ankles, feet, or legs that does not go away. Other, more subtle symptoms of heart failure warrant a visit to your health care provider, especially if linked to any of the symptoms already listed. Abdominal bloating or discomfort Persistently pale skin Poor appetite Other than childbirth, congestive heart failure is the most common reason for hospital admission in the United States, especially for people older than 65 years. This highlights the fact that many people with heart failure will have to go to the hospital, either at the beginning of their illness or from time to time because of it. Always take chest pain seriously. Although failure of the heart does not cause pain, several important conditions associated with congestive heart failure do. If these symptoms develop quickly or worsen rapidly, seek emergency treatment. Shortness of breath

Severe, unrelieved chest pain Swelling in the legs that becomes painful, even in one leg, especially if associated with signs of an infection (redness, warmth to the touch, fever) Fainting

Congestive Heart Failure (cont.)

Heart Disease (Coronary Artery Disease) Slideshow Pictures Cholesterol Drugs Slideshow Pictures Heart-Healthy Foods Slideshow Pictures
IN THIS ARTICLE

Congestive Heart Failure Overview Congestive Heart Failure Causes Congestive Heart Failure Symptoms When to Seek Medical Care Exams and Tests Congestive Heart Failure Treatment Self-Care at Home Medical Treatment Medications Surgery Other Therapy Next Steps Follow-up Prevention Outlook Support Groups and Counseling For More Information Web Links Multimedia Synonyms and Keywords Authors and Editors Viewer Comments:Congestive Heart Failure - Symptoms Experienced

Exams and Tests

Congestive heart failure (CHF) can be confused with other illnesses that cause breathing difficulties, such as bronchitis, pneumonia, emphysema, and asthma. Talking to a medical professional, along with a physical exam and tests available only at a medical office or hospital, is necessary to make an exact diagnosis. Chest x-ray film: This is very helpful in identifying the buildup of fluid in the lungs. Also, the heart usually enlarges in CHF, and this may be visible on the x-ray film. Electrocardiogram (ECG): This painless test measures the electrical activity (rhythm) of the heart.

It can reveal several different heart problems that can cause heart failure, including heart attacks, rhythm disorders, long-standing strain on the heart from high blood pressure, and certain valve problems. The ECG gives clues as to the underlying cause of heart failure. For this test, which takes just a few minutes, you lie on a table with electrodes fastened to the skin of your chest, arms, and legs. The ECG result may, however, be normal in heart failure. Blood tests: You may have blood drawn for lab tests.

Blood cell counts: Low blood cell counts (anemia) may cause symptoms much like CHF or contribute to the condition.

Sodium, potassium, and other electrolyte levels, especially if the person has been treated with diuretics and/or has kidney disease Tests of kidney function B-type natriuretic peptide (BNP) o This is a hormone produced at higher levels by the failing heart muscle. This is a good screening test; the levels of this hormone generally increase as the severity of heart failure worsens. o Interestingly, BNP has been produced by recombinant DNA technologyand can be used as a treatment for heart failure in the hospital (seeMedications). Echocardiogram: This is a type of ultrasound that shows the beating of the heart and the various cardiac structures. An echocardiogram can be useful in determining the cause of heart failure (such as muscle, valves, or pericardium), and it provides an accurate measurement of ejection fraction. This very safe, painless technique is similar to that used to look at a fetusduring pregnancy. MUGA scan: This stands for multiple-gated acquisition scanning. heart. As the heart pumps the blood with the dye in it, pictures are taken. The pumping performance of the left and right ventricles can be determined. People with an allergy to iodine or shellfish have special considerations and may not be able to have this test because the dye contains iodine. Stress test: A treadmill or medication (nonwalking) stress test is used to help evaluate the cause or causes of heart failure, in particular, regarding coronary artery disease. This test is frequently combined with nuclear imaging orechocardiography to improve accuracy. A small amount of a mildly radioactive dye is injected into a vein and travels to the

Congestive Heart Failure Treatment

The treatment of heart failure depends on the exact cause, but it can usually be treated effectively. The overall goals of treatment are to correct underlying causes, to relieve symptoms, and to prevent worsening of the condition. Symptoms are relieved by removing excess fluid from the body, improving blood flow, improving heart muscle function, and increasing delivery of oxygen to the body tissues.

Self-Care at Home
Congestive heart failure is a serious medical condition that requires professional medical help. Once diagnosed and under the care of a qualified medical professional, you can and should do several things at home to increase your comfort and reduce the chance of your condition getting worse. In fact, the more active role you take in managing your heart failure, the more likely you are to do well. Making the lifestyle changes described here will make a real difference. Not only will you feel better, but you will be increasing your chances of a longer, healthier life. Treat swelling with the following measures: Elevate the feet and legs if they are swollen. Eat a reduced-salt diet. Weigh in every morning before breakfast and record it in a diary that can be shown to a health care provider. Avoid the following: Not taking prescribed medications Smoking (in all forms) Alcohol (up to 1 drink per day is usually fine, unless prone to excessive intake/alcoholism) Keep walking or join a cardiac rehabilitationprogram (this program can monitor increasing or decreasing exercise capacity) Excessive emotional stress and/or depression (Moderate-to-severe mental depression has been shown to double mortality risk.) High altitude (Breathing is more difficult because of the lower level of oxygen in the atmosphere; pressurized cabin air travel is usually fine.) Herbal or other complementary medicine without first consulting a doctor to see if they are safe Know the following: People with diabetes must control their blood sugar level every day. Know the HbA1C level. It should be less than 7.0, preferably less than 6.5. People with high blood pressure should measure it regularly, and make sure they know the value, (systolic pressure should be below 140 mm Hg in everyone and even below 130 if the person has diabetes).

People with elevated lipid levels (cholesterol and triglycerides) can take medications to get the bad cholesterol, or LDL, below 100, and the triglycerides below 150.

Medical Treatment
If no underlying correctible cause of heart failure is established, medical treatment is composed of lifestyle changes and medications. Lifestyle changes recommended by your health care provider can help relieve symptoms, slow the progression of heart failure, and improve one's quality of life. Lifestyle changes that may be helpful in preventing or relieving heart failure include those recommended by the American Heart Association and other organizations as part of a heart-healthy lifestyle. See Self-Care at Home for more information. Medications help control both the underlying causes of heart failure and the symptoms. Medications are the most critical part of therapy for heart failure. Usually, several types of medications are required to address as many of thephysiologic imbalances as possible. Procedures Other treatment or procedures, such asangioplasty or a pacemaker, may be offered, depending on the underlying cause of the heart failure. Angioplasty: This is an alternative to coronary bypass surgery for some people whose heart failure is caused by coronary artery disease and is compounded by heart damage/heart attack. Angioplasty is used to treat narrowing or blockage of a coronary artery that supplies the left ventricle with blood. A long, thin tube called a catheter is inserted through the skin, into a blood vessel, and threaded into the affected artery. This procedure is performed while the person is under local anesthesia. At the point of the atherosclerotic narrowing or blockage, a tiny balloon and/or an expandable metal stent, attached to the end of the catheter, is inflated/deployed. The inflated catheter pushes aside the cholesterol deposits (plaque) that are blocking the artery so that blood can flow through in a more normal manner. Pacemaker: This device controls the rhythm of the heartbeats. A pacemaker is an electrode on the tip of a wire, usually implanted inside the heart by an electrophysiologist or specialized cardiologist in the cardiac cath lab. This wire goes to the right ventricle, frequently with a second wire to the right atrium (dual chamber pacemaker). A pacemaker can stimulate a heart that is beating too slowly to beat faster, or it can control an irregular heartbeat (sometimes, this requires medications in addition to the pacemaker). In certain circumstances, a device called an intracardiac defibrillator (ICD) may be implanted as part of a pacemaker device. This defibrillator can detect and electrically shock a life-threateningarrhythmia back to normal. The pacemaker may also be used to synchronize the pumping action of the left and right ventricles (cardiac resynchronization therapy). This approach requires an extra lead

placed behind the heart in a coronary vein overlying the left ventricle. Synchronization improves the effectiveness of the heart as a pump.

Medications
People with heart failure usually take several different medications that work in different ways to lessen heart failure symptoms, to prevent worsening of the underlying disease, and to prolong life. Diuretics (water pills): The buildup of fluid is usually treated with a diuretic. Diuretics cause the kidneys to remove excess salt and accompanying water from the bloodstream, thereby reducing the amount of blood volume in circulation. With a lower volume of blood, your heart does not have to work so hard. The number of red and white blood cells is not changed. The end result is an improvement of the ability to breathe (clear out water in the lungs) and a lessening of the swelling in the lower body. Most of these drugs tend to remove potassium from the body, but some drugs, such as diuretics containing triamterene orspironolactone, can increase potassium levels, so potassium levels have to be watched carefully. Diuretics commonly used in heart failure include furosemide (Lasix), bumetanide(Bumex), hydrochlorothiazide(HydroDIURIL), spiro nolactone (Aldactone),eplerenone (Inspra), triamterene (Dyrenium), torsemide (Demadex), ormetolazone (Zaroxolyn), or a combination agent (for example, Dyazide). Spironolactone and eplerenone are not only mild diuretics when used with stronger diuretics like furosemide (Lasix), but when used in small doses, (not diuretic doses), they have been shown to prolong life when used in combination with angiotensinconverting enzyme (ACE) inhibitors. This suggests they have additional effects on the myocardium to prevent progression of myocardial scarring and enlargement. Inotropes: IV inotropes are stimulants, such as dobutamine and milrinone, that increase the pumping ability of the heart. These are used as a temporary support of a very weak left ventricle that is not responding to standard CHF therapy. Digoxin (Lanoxin): This drug improves the pumping ability of the heart, causing it to pump more forcefully, a so-called positive inotrope. However, digoxin is a very weak inotrope and is now only an add-on therapy to ACE inhibitors and beta-blockers. Although commonly used, not all people receive digoxin because it is less effective than several of the other classes of medications discussed in this article. Digoxin helps relieve symptoms after vasodilators and diuretics have been tried, but it does not prolong life. Digoxin is an old medicine, used for more than 200 years, that is derived from the foxglove plant. This medication can also be used to control the rhythm of the heart (in atrial fibrillation). Excessive digoxin can build up in the blood and cause potentially dangerous abnormal heart rhythms (arrhythmias). The risk of developing arrhythmias is enhanced if the dose is excessive, the kidneys are impaired and do not excrete digoxin from the

body properly, or the potassium in the body is too low (low potassium may result from taking diuretics). Vasodilators: These medications enlarge the small arteries or arterioles, which relieve the systolic workload of the left ventricle. The heart has to work less to pump blood through the arteries. This also generally lowers blood pressure. ACE inhibitors are the most widely used vasodilators for CHF. They block the production of angiotensin II, which is abnormally high in congestive heart failure. Angiotensin II causes vasoconstriction with increased workload on the left ventricle, and it is directly toxic to the left ventricle at excessive levels. ACE inhibitors are important because they not only improve symptoms, but they also have been proven to significantly prolong the lives of people with heart failure. They do this by slowing progression of the heart damage and in some cases improving heart muscle function. Some common examples of ACE inhibitors are captopril (Capoten),enalapril (Vasotec), lisinopril (Zestril/Prinivil), benazepril (Lotens in),quinapril (Accupril), fosinopril (Monopril), and ramipril (Altace). Angiotensin II receptor blockers (ARBs) work by preventing the effect of angiotensin II at the tissue level. Examples of ARB medications includecandesartan (Atacand), irbesartan (Avapro), olmesartan (Benicar), losartan(Cozaar ), valsartan (Diovan), telmisartan (Micardis), and eprosartan (Teveten). These medications are usually prescribed for people who cannot take ACE inhibitors because of side effects. Both are effective, but ACE inhibitors have been used longer with a greater number of clinical trial data and patient information. ACE inhibitors and ARBs may cause the body to retain potassium, but this is generally only a problem in people with significant kidney disease, or in people who are also taking a potassium-sparing diuretic, such as triamterene or spironolactone. Calcium channel blockers are arterial vasodilators that are not used for treatment of heart failure per se because clinical trials have proven no benefit for prolongation of life. Calcium channel blockers are useful for lowering blood pressure if the cause of the CHF is high blood pressure and the patient is not responding to ACE inhibitors or ARBs. Isosorbide dinitrate and hydralazine (BiDil) is a fixed dose combination of isosorbide dinitrate (20 mg/tablet) and hydralazine (37.5 mg/tablet). This drug is indicated for heart failure in black individuals based in part on results of the African American Heart Failure Trial. Two previous trials in the general population of people with severe heart failure found no benefit but suggested a benefit in black patients. Compared with a placebo, this drug showed a 43% reduction in mortality rate, a 39% decrease in hospitalization rate, and a decrease in symptoms from heart failure in black patients. Nitrates are venous vasodilators that include isosorbide mononitrate (Imdur) and isosorbide dinitrate (Isordil). They are weaker than the ACE inhibitors and ARBs and are primarily used in combination with an arterial vasodilator, such as hydralazine. Hydralazine (Apresoline) is a pure smooth muscle arterial vasodilator that may be used for CHF. Recent trial data have shown hydralazine to be especially effective in African Americans, but it does not replace ACE inhibitors or ARBs. Hydralazine is especially valuable in patients who have poor kidney function and/or are intolerant to ACE inhibitors and ARBs.

Beta-blockers: These drugs slow down the heart rate, lower blood pressure, and have a direct affect on the heart muscle to lessen the workload of the heart. Specific beta-blockers, such as carvedilol (Coreg) and long-acting metoprolol(Toprol XL), have been shown to decrease symptoms, hospitalization due to CHF, and deaths. Beta-receptors are in the heart muscle and in the walls of arteries. Thesympathetic nervous system produces a chemical called norepinephrine that is toxic to the heart muscle in prolonged, high doses. Beta-blockers work by blocking the action of norepinephrine on the heart muscle. In the past, doctors treating heart failure thought that blocking norepinephrine was bad and would make the heart worse because norepinephrine is a stimulant that makes the heartbeat stronger. However, clinical trials have proven that beta-blockers gradually improve the systolic function of the left ventricle, thereby improving symptoms and prolonging life. The foundation of modern therapy of systolic heart failure is a combination of ACE inhibitors and beta-blockers. If at all possible, every patient should be on both drugs for improvement of left ventricular function and prolongation of life. Natriuretic peptides: Nesiritide (Natrecor), or B-type natriuretic peptide (BNP), is a new medication produced by recombinant DNA technology. BNP is normally produced by the heart muscle. When the left and/or right ventricle are under excessive workload, excess BNP is excreted into the bloodstream. Because the natural BNP is already increased with heart failure, why additional BNP works is not totally understood. However, giving additional BNP intravenously lowers the pressure in the lungs and is a mild diuretic, so lung water is removed and excreted through the kidneys, resulting in relief ofpulmonary congestion. Nesiritide is given into the vein (intravenously [IV]) to help stabilize people whose heart failure is suddenly worse. Commonly used in the emergency department, nesiritide is used to more rapidly stabilize the patient. Some people may not need to be admitted to the hospital. Getting the most out of your medications involves the following: Other medications may be prescribed, depending on the underlying cause of the heart failure or on the medical condition. Keep a diary of daily weight, and bring it to the doctor every follow-up visit. Since people with heart failure are often on many drugs, the likelihood of drug interactions increases. The medications taken for other medical problems may affect what drugs are prescribed for heart failure. Because of this, people are advised to always bring a current list of medications and any other supplements or nonprescription drugs with them every time they visit a doctor. Note that many of these medications come in combination pills under different marketing names. Take your medication as directed by your health care provider. If he or she does not tell you how to take your medication, ask. Follow the recommendations of your health care provider about diet, exercise, and other lifestyle issues. Be sure you are informed about the side effects of your medications.

Develop an action plan with your doctor so you and your family know what to do promptly if your symptoms worsen

Surgery
Surgery can repair some underlying causes of heart failure, such as blockage of the coronary arteries, a valve problem, a congenital heart defect, or too thick of a pericardium. However, once the heart's ability to pump blood is severely, permanently, and irreversibly impaired, no surgery can repair the damage. The only alternative is a heart transplant. This option is for patients who are not elderly and who do not have other medical conditions that would make it unlikely for a heart transplant to be successful. Heart transplant evaluations are done in specialized centers. Intra-aortic balloon pump is used as a temporary support of left ventricle function, such as in a large heart attack, waiting for the heart to recover.

Left ventricle assist device (LVAD) is surgically implanted to mechanicallybypass the left ventricle. A clinical trial showed that complications are too high and the device did not significantly prolong life if used on a long-term basis. This device is used as a temporary left ventricle support to get the patient awaiting a heart transplant out of bed. Left ventricle volume reduction surgery, which removes a piece of dead heart muscle, is considered experimental at this time. Totally implantable artificial hearts are being developed for patients with severe, endstage heart failure. o These devices are most commonly used as a temporary bridge to heart transplantation. o This technique is constantly improving but is still limited to specialized centers and is considered experimental at this time.

Other Therapy
A rapidly growing newer therapy is called cardiac resynchronization therapy and involves a biventricular pacemaker. One pacer is placed in a coronary vein on the back side of the heart, overlying the left ventricle. The other pacer is placed in the usual right ventricle position. This improves the coordination of contraction between the left and right ventricle, especially if the patient has left bundle branch block. Biventricular pacing has been shown to improve exercise capacity, and, in a recent clinical trial, it has been found to prolong life. Cardiac resynchronization therapy is frequently combined with an ICD to shock a person out of life-threatening arrhythmias, such as ventricular tachycardia orventricular fibrillation. The worse the left ventricle, the higher the risk for sudden death secondary to these arrhythmias. Whether biventricular pacing will work so well as to prevent deterioration of the left ventricle and the need for heart transplantation is unknown

Next Steps Follow-up

If you have congestive heart failure, you will need frequent, regular medical attention to adjust your medications and watch for side effects. Schedule regular visits with your health care provider as he or she recommends because congestive heart failure is a serious medical condition that requires constant monitoring. Educate yourself as much as possible about this life-threatening condition. Establish a daily routine for taking medication properly and on schedule. Weigh in daily. Every morning, record the weight in a diary, and take it to the health care provider every visit. An accurate bathroom scale is helpful in monitoring weight gain or loss from day to day. This will help to see fluid retention. Keep a list of all medications, with the exact name and dose, and know why each one is taken. Bring them to each follow-up visit so the doctor can double check to make sure you are on the correct medication and dose. Reminder boxes for medications are helpful. Be sure to keep all these medications away from small children who may accidentally swallow them. Many of the drugs prescribed for congestive heart failure are more dangerous in overdose than other medications.

The heart is the muscular organ of the circulatory system that constantly pumps blood throughout the body. Approximately the size of a clenched fist, the heart is composed of cardiac muscle tissue that is very strong and able to contract and relax rhythmically throughout a person's lifetime. The heart has four separate compartments or chambers. The upper chamber on each side of the heart, which is called an atrium, receives and collects the blood coming to the heart. The atrium then delivers blood to the powerful lower chamber, called a ventricle, which pumps blood away from the heart through powerful, rhythmic contractions. The human heart is actually two pumps in one. The right side receives oxygen-poor blood from the various regions of the body and delivers it to the lungs. In the lungs, oxygen is absorbed in the blood. The left side of the heartreceives the oxygen-rich blood from the lungs and delivers it to the rest of the body.

Systole
The contraction of the cardiac muscle tissue in the ventricles is called systole. When the ventricles contract, they force the blood from their chambers into the arteries leaving the heart. The left ventricle empties into the aorta and the right ventricle into the pulmonary artery. The increased pressure due to the contraction of the ventricles is called systolic pressure.

Diastole
The relaxation of the cardiac muscle tissue in the ventricles is called diastole. When the ventricles relax, they make room to accept the blood from the atria. The decreased pressure due to the relaxation of the ventricles is called diastolic pressure.

Electrical Conduction System

The heart is composed primarily of muscle tissue. A network of nerve fibers coordinates the contraction and relaxation of the cardiac muscle tissue to obtain an efficient, wave-like pumping action of the heart.

The Sinoatrial Node (often called the SA node or sinus node) serves as the natural pacemaker for the heart. Nestled in the upper area of the right atrium, it sends the electrical impulse that triggers each heartbeat. The impulse spreads through the atria, prompting the cardiac muscle tissue to contract in a coordinated wave-like manner. The impulse that originates from the sinoatrial node strikes the Atrioventricular node (or AV node) which is situated in the lower portion of the right atrium. The atrioventricular node in turn sends an impulse through the nerve network to the ventricles, initiating the same wave-like contraction of the ventricles. The electrical network serving the ventricles leaves the atrioventricular node through the Right and Left Bundle Branches. These nerve fibers send impulses that cause the cardiac muscle tissue to contract.

1. Sinoatrial node (SA node) 2. Atrioventricular node (AV node) 3. Common AV Bundle 4. Right & Left Bundle Branches