Definition Congestive heart failure (CHF) is a clinical syndrome in which the heart fails to pump blood at the rate required by the metabolizing tissues or in which the heart can do so only with an elevation in filling pressure. Epidemiology According to the American Heart Association, heart failure affects nearly 5.7 million Americans of all ages
Heart failure statistics for the United States are as
follows: Heart failure is the fastest-growing clinical cardiac disease entity in the United States, affecting 2% of the population Heart failure accounts for 34% of cardiovascular-related deaths Approximately 670,000 new cases of heart failure are diagnosed each year About 277,000 deaths are caused by heart failure each year Heart failure is the most frequent cause of hospitalization in patients older than 65 years, with an annual incidence of 10 per 1,000 The prevalence of heart failure increases with age. The prevalence is 1-2% of the population younger than 55 years and increases to a rate of 10% for persons older than 75 years. Nonetheless, heart failure can occur at any age, Etiology From a clinical standpoint, classifying the causes of heart failure into the following 4 broad categories is useful: Underlying causes: Underlying causes of heart failure include structural abnormalities (congenital or acquired) that affect the peripheral and coronary arterial circulation, pericardium, myocardium, or cardiac valves, thus leading to increased hemodynamic burden or myocardial or coronary insufficiency Fundamental causes: Fundamental causes include the biochemical and physiologic mechanisms, through which either an increased hemodynamic burden or a reduction in oxygen delivery to the myocardium results in impairment of myocardial contraction Precipitating causes: Overt heart failure may be precipitated by progression of the underlying heart disease (eg, further narrowing of a stenotic aortic valve or mitral valve) or various conditions (fever, anemia, infection) or medications (chemotherapy, NSAIDs) that alter the homeostasis of heart failure patients Genetics of cardiomyopathy: Dilated, arrhythmic right ventricular and restrictive cardiomyopathies are known genetic Underlying causes Underlying causes of Specific underlying factors systolic heart failure cause various forms of include the following: heart failure, such as Coronary artery disease systolic heart failure (most Diabetes mellitus commonly, left ventricular Hypertension systolic dysfunction), heart Valvular heart disease failure with preserved LVEF, (stenosis or regurgitant acute heart failure, high- lesions) output heart failure, and right heart failure. Arrhythmia (supraventricular or ventricular) Infections and inflammation (myocarditis) Peripartum cardiomyopathy Congenital heart disease Drugs (either recreational, such as alcohol and cocaine, or therapeutic drugs with cardiac side Underlying causes of Underlying causes of high- diastolic heart failure include output heart failure the following: include the following: Coronary artery disease Anemia Diabetes mellitus Systemic arteriovenous Hypertension fistulas Valvular heart disease (aortic Hyperthyroidism stenosis) Beriberi heart disease Hypertrophic cardiomyopathy Paget disease of bone Restrictive cardiomyopathy Albright syndrome (fibrous (amyloidosis, sarcoidosis) dysplasia) Constrictive pericarditis Multiple myeloma Underlying causes of acute heart failure include the Pregnancy following: Glomerulonephritis Acute valvular (mitral or aortic) Polycythemia vera regurgitation Carcinoid syndrome Myocardial infarction Myocarditis Arrhythmia Underlying causes of right heart failure include the following: Left ventricular failure Coronary artery disease (ischemia) Pulmonary hypertension Pulmonary valve stenosis Pulmonary embolism Chronic pulmonary disease Neuromuscular disease Pathophysiology The Frank-Starling mechanism, in which an increased preload helps to sustain cardiac performance Alterations in myocyte regeneration and death Myocardial hypertrophy with or without cardiac chamber dilatation, in which the mass of contractile tissue is augmented Activation of neurohumoral systems The release of norepinephrine by adrenergic cardiac nerves augments myocardial contractility and includes activation of the renin-angiotensin-aldosterone system [RAAS], the sympathetic nervous system [SNS], and other neurohumoral adjustments that act to maintain arterial pressure and perfusion of vital organs. In acute heart failure the finite adaptive mechanisms that may be adequate to maintain the overall contractile performance of the heart at relatively normal levels become maladaptive when trying to sustain adequate cardiac performance. The primary myocardial response to chronic increased wall stress is myocyte hypertrophy, death/apoptosis, and regeneration eventually leads to remodeling, usually the eccentric type Eccentric remodeling further worsens the loading conditions on the remaining myocytes and perpetuates the deleterious cycle. The idea of lowering wall stress to slow the process of remodeling has long been exploited in treating heart failure patients. The reduction of cardiac output following myocardial injury sets into motion a cascade of hemodynamic and neurohormonal derangements that provoke activation of neuroendocrine systems, most notably the above- mentioned adrenergic systems and RAAS. The release of epinephrine and norepinephrine, along with the vasoactive substances endothelin-1 (ET-1) and vasopressin, causes vasoconstriction, which increases calcium afterload and, via an increase in cyclic adenosine monophosphate (cAMP), causes an increase in cytosolic calcium entry The increased calcium entry into the myocytes augments myocardial contractility and impairs myocardial relaxation (lusitropy). The calcium overload may induce arrhythmias and lead to sudden death. The increase in afterload and myocardial contractility (known as inotropy) and the impairment in myocardial lusitropy lead to an increase in myocardial energy expenditure and a further decrease in cardiac output. The increase in myocardial energy expenditure leads to myocardial cell death/apoptosis, which results in heart failure and further reduction in cardiac output, perpetuating a cycle of further increased neurohumoral stimulation and further adverse hemodynamic and myocardial responses. Clinical Presentation Exertional dyspnea and/or Exophthalmos and/or visible dyspnea at rest pulsation of eyes Orthopnea Distention of neck veins Acute pulmonary edema Weak, rapid, and thready pulse Rales, wheezing Chest pain/pressure and palpitations S3 gallop and/or pulsus alternans Tachycardia Increased intensity of P2 heart Fatigue and weakness sound Nocturia and oliguria Hepatojugular reflux Anorexia, weight loss, Ascites, hepatomegaly, and/or nausea anasarca Central or peripheral cyanosis, pallor Diagnosis The Framingham criteria for the diagnosis of heart failure consists of the concurrent presence of either 2 major criteria or 1 major and 2 minor criteria.
Major criteria include the Minor criteria are as
following: follows: Paroxysmal nocturnal dyspnea Nocturnal cough Weight loss of 4.5 kg in 5 days Dyspnea on ordinary in response to treatment exertion Neck vein distention Rales A decrease in vital capacity Acute pulmonary edema by one third the maximal value recorded Hepatojugular reflux S 3 gallop Pleural effusion Central venous pressure Tachycardia (rate of 120 greater than 16 cm water bpm) Circulation time of 25 seconds Bilateral ankle edema Radiographic cardiomegaly Pulmonary edema, visceral congestion, or cardiomegaly at autopsy The New York Heart Association (NYHA) classification system categorizes heart failure on a scale of I to IV, [as follows: Class I: No limitation of physical activity Class II: Slight limitation of physical activity Class III: Marked limitation of physical activity Class IV: Symptoms occur even at rest; discomfort with any physical activity The American College of Cardiology/American Heart Association (ACC/AHA) staging system is defined by the following 4 stages : Stage A: High risk of heart failure but no structural heart disease or symptoms of heart failure Stage B: Structural heart disease but no symptoms of heart failure Stage C: Structural heart disease and symptoms of heart failure Stage D: Refractory heart failure requiring specialized interventions Management Treatment includes the following: Nonpharmacologic therapy: Oxygen and noninvasive positive pressure ventilation, dietary sodium and fluid restriction, physical activity as appropriate, and attention to weight gain Pharmacotherapy: Diuretics, vasodilators, inotropic agents, anticoagulants, beta blockers, and digoxin Surgical options Electrophysiologic intervention Revascularization procedures Valve replacement/repair Ventricular restoration Extracorporeal membrane oxygenation Ventricular assist devices Heart transplantation Total artificial heart Prognosis In general, the mortality following hospitalization for patients with heart failure is 10.4% at 30 days, 22% at 1 year, and 42.3% at 5 years, despite marked improvement in medical and device therapy. Each rehospitalization increases mortality by about 20-22%.
Mortality is greater than 50% for patients with NYHA class
IV, ACC/AHA stage D heart failure. Heart failure associated with acute MI has an inpatient mortality of 20-40%; mortality approaches 80% in patients who are also hypotensive (eg, cardiogenic shock). Heart failure related to systolic dysfunction has an associated mortality of 50% after 5 years. References Framingham Classification: Ho KK, Pinsky JL, Kannel WB, Levy D. The epidemiology of heart failure: the Framingham Study. J Am Coll Cardiol. 1993 Oct. 22(4 Suppl A):6A-13A. [Medline]. American Heart Association. Classes of heart failure. Available at http://www.heart.org/HEARTORG/Conditions/HeartFailure/AboutHeartFailure/Classes- of-Heart-Failure_UCM_306328_Article.jsp . Accessed: September 6, 2011. [Guideline] Hunt SA, Abraham WT, Chin MH, et al, and the American College of Cardiology Foundation; American Heart Association. 2009 Focused update incorporated into the ACC/AHA 2005 guidelines for the diagnosis and management of heart failure in adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines developed in collaboration with the International Society for Heart and Lung Transplantation. J Am Coll Cardiol. 2009 Apr 14. 53(15):e1-e90. [Medline]. [Guideline] Hunt SA, for the Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure). ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2005 Sep 20. 46(6):e1-82. [Medline].