Heart<unk>  is a complex syndrome whereby there is inadequate output of the heart to meet the metabolic demands of the body. Abnormal function of different anatomic parts of the heart cause heart<unk>  including the pericardium, the myocardium, the endocardium, the heart valves and the great vessels. Symptoms of heart<unk>  are due to a lack of both forward blood flow to the body, and backward flow into the lungs. Heart<unk>  is a clinical syndrome characterized by symptoms of dyspnea, edema and fatigue and signs such as rales on physical examination. Heart<unk>  may be classified based on ejection fraction into heart<unk>  with preserved ejection fraction (HFpEF) and heart<unk>  with reduced ejection fraction (HFrEF). LV remodeling is the basic concept for HFpEF pathophysiolgy. Two models are emerging in HFpEF pathophysiology, the traditional model discussed about ventricular diastolic dysfunction , LV hypertrophy, impaired relaxation, endothelial dysfunction, arterial and ventricular stiffness and their effect on cardiac function. The emerged model discussed role of systemic microvascular endothelial inflammation due to existing comorbidities such as, diabetes, hypertension, obesity, smoking and ischemia in cardiac remodeling and dysfunction. The pathogenesis of HFrEF is related largely to cellular proliferation and metabolism. Pathological processes that result in progression of HF and are common to both HFrEF and HFpEF are altered excitation-contraction coupling, epigenetic modifications, changes in sarcomeric coupling proteins, increased adrenergic drive, increased activity of renin-angiotensin aldosterone axis, nitric oxide insensitivity, adensoine triphosphate (ATP) depletion, reactive oxygen species production and an elevated cell death rate. The causes of heart<unk>  can be broadly divided into cardiac and non-cardiac. Cardiac causes include aortic regurgitation, aortic stenosis, arrhythmias, arrhythmogenic right ventricular dysplasia, arteriovenous fistula, atrial fibrillation, atrial septal defect, cardiac amyloidosis, cardiac aneurysm, congenital heart disease, constrictive pericarditis, dilated cardiomyopathy, Eisenmenger syndrome, endocarditis, hypertension, hypertrophic cardiomyopathy, hypoplastic left heart syndrome, interferon gamma, ischemic heart disease, malignant hypertension, mitral regurgitation, mitral stenosis, myocardial infarction, oxaprozin, patent ductus arteriosus, pericardial effusion, pericardial tamponade, pericarditis, peripartum cardiomyopathy, pertuzumab, restrictive cardiomyopathy, rheumatic carditis, rupture of the papillary muscles, Takotsubo cardiomyopathy, tricuspid insufficiency, valvular heart disease, ventricular aneurysm, ventricular septal defect.<unk>  should be distinguished from other conditions that cause dyspnea, fatigue and edema. Heart<unk>  affects close to 5 million people in the the United States of America and each year close to 500,000 new cases are diagnosed.<unk>  is responsible for a significant portion of the healthcare budget, and more than 50% of patients seek re-admission within 6 months after treatment and the average duration of hospital stay is 6 days.  In 2005 the prevalence among adults aged 20 and older in the United States was 5,300,000 (about 2,650,000 males, and 2,650,000 females). Heart<unk>  is associated with significantly reduced physical and mental health, resulting in a markedly decreased quality of life.<unk>  is also associated with a poor prognosis. If left untreated, heart<unk>  may result in death due to complications associated with the condition. Heart<unk>  resulting from atherosclerotic coronary artery disease has been shown to be associated with higher incidence of fatal events compared to heart<unk>  that results from other cardiac diseases. Heart<unk>  is a progressive disease with a major impact on the patient's quality of life. With the exception of heart<unk>  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%. In the Framingham experience, 80% of men and 70% of women with heart<unk>  who were under 65 years of age had died within 8 years of the diagnosis. There are several diagnostic criteria / algorithms that are used to diagnose heart<unk>  including an algorithm from the ESC, Framingham study, and Boston. The classic symptoms of heart<unk>  include dyspnea, fatigue, and fluid retention. Patients with heart<unk>  present in different ways. Some patients present with exercise intolerance but show little evidence of congestion or edema. Other patients present with mild symptoms of edema and pulmonary congestion. The ejection fraction is usually below 35% in patients who are symptomatic with systolic heart<unk> . BNP levels may be useful in the initial establishment of the diagnosis of heart<unk>  in the patient with dyspnea of unclear etiology. Chest x-ray in a patient with heart<unk>  shows cardiomegaly (cardiac enlargement and pulmonary congestion (Kerley B lines, and in some cases pleural effusion). CMR may be used for assessment of LV and RV size and morphology, systolic and diastolic function, and for characterizing myocardial tissue for the purpose of understanding the etiology of LV systolic or diastolic dysfunction. Echocardiography is commonly used to diagnose and monitor the progression of heart<unk> . 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 divided by the EDV, a value known as the ejection fraction (EF). In pediatrics, the shortening fraction is the preferred measure of systolic function. Coronary angiography is perfomred in patients with heart<unk>  in whom there is a suspicion of underlying atherosclerosis as the basis for the heart<unk> . Patients who are troponin or CK-MB positive, who have dynamic EKG changes or other signs and symptoms of an acute coronary syndrome who are revascularization candidates should undergo coronary angiography. Acute heart<unk>  can occur in the setting of a new onset heart<unk>  or worsening of an existing chronic heart<unk>  (also known as acute decompensated heart<unk> , flash pulmonary edema, ADHF). ADHF presents with acute shortness of breath due to the development of pulmonary edema (the rapid accumulation of fluid in the lung). Other signs and symptoms of ADHF include hypotension with impaired and organ perfusion manifested by worsening renal function, altered mentation and cold clammy extremities. ADHF associated with a poor prognosis if not treated aggressively. Like chronic heart<unk>  therapy, the goal is to improve symptoms but unlike chronic therapy the other goals are to improve oxygenation and hemodynamic stability. The mainstays of the acute medical treatment in acute decompensated<unk>  include oxygen to improve hypoxia, diuresis to reduce both preload and intravascular volume and vasodilators to reduce afterload. Some of the mainstays of chronic heart<unk>  therapy are not initiated acutely (ACE inhibtors,beta blockers and digoxin). End of life care in the patient with<unk>  is focused on making the patient comfortable. Invasive procedures should be minimized, and patients may elect to have their defibrillators inactivated. The growing number of patients with Stage IV heart<unk>  (intractable symptoms of fatigue, shortness of breath or chest pain at rest despite optimal medical therapy) should be considered for palliative care or hospice.
Congestive heart failure
Lung cancer
Asthma
Pulmonary amyloidosis
High output failure
Cirrhosis
Right heart failure
Heart failure