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chf

chf

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07/10/2013

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Description:
Congestive Heart Failure
or
CHF
is a severe circulatory congestion due to decreased myocardialcontractility, which results in the heart’s inability to pump sufficient blood to meet the body’s needs.
 
Background
Congestive heart failure (CHF) is a clinical syndrome in which the heart fails to pump blood at the rate required bythe metabolizing tissues or in which the heart can do so only with an elevation in filling pressure.The heart's inability to pump a sufficient amount of blood to meet the needs of the body's tissues may be a resultof insufficient or defective cardiac filling and/or impaired contraction and emptying. Compensatory mechanismsincrease blood volume, as well as the cardiac filling pressure, heart rate, and cardiac muscle mass, to maintain thepumping function of the heart and to cause a redistribution of blood flow. Despite these compensatory mechanisms,the ability of the heart to contract and relax declines progressively, and heart failure (HF) worsens.The clinical manifestations of HF vary enormously and depend on a variety of factors, including the age of thepatient, the extent and rate at which cardiac performance becomes impaired, and which ventricle is initially involvedin the disease process. A broad spectrum of severity of impairment of cardiac function is ordinarily included in thedefinition of HF. These impairments range from the mildest forms, which are manifest clinically only during stress, tothe most advanced forms, in which cardiac pump function is unable to sustain life without external support
Symptoms and signs
 Symptoms that suggest congestive heart failure include the following:
Dyspnea on exertion
Dyspnea at rest
Orthopnea
Paroxysmal nocturnal dyspnea
Fatigue
Decreased exercise tolerance
Unexplained cough, especially at night
Acute confusional state, delirium
Abdominal symptoms (nausea, abdominal pain or distention)
Decreased food intake
Decline in functional statusSigns that suggest CHF include the following:
Tachycardia
Third heart sound (S
3
)
Increased jugular venous pressure
Positive hepatojugular reflux
Bilateral rales
Peripheral edema not caused by venous insufficiency
Laterally displaced apical impulse
Weight gainIn cardiogenic cases, clinical findings include cold and clammy peripheral structures, resulting from low cardiac output.Jugular venous pressure is elevated, and a ventricular gallop (S
3
) is present. Lung examination reveals crackles.In noncardiogenic cases, the periphery is usually warm as a result of a high-flow state. Jugular venous pressure isgenerally normal, the S
3
gallop is absent, and the lungs are usually clear to auscultation.
 
Examination
Echocardiography
 Echocardiography is the preferred examination. Two-dimensional and Doppler echocardiography may be used todetermine systolic and diastolic LV performance, the cardiac output (ejection fraction), and pulmonary artery andventricular filling pressures. Echocardiography also may be used to identify clinically important valvular disease.
Radiography
In cardiogenic cases, radiographs may show cardiomegaly, pulmonary venous hypertension, and pleural effusions.Pulmonary venous hypertension (PVH) may be divided into 3 grades. In grade I PVH, an upright examinationdemonstrates redistribution of blood flow to the nondependent portions of the lungs and the upper lobes. In grade IIPVH, there is evidence of interstitial edema with ill-defined vessels and peribronchial cuffing, as well as interlobular septalthickening. In grade III PVH, perihilar and lower-lobe airspace filling is evident, with features typical of consolidation (eg,confluent opacities, air bronchogram and the inability to see pulmonary vessels in the area of abnormality). The airspaceedema tends to spare the periphery in the mid and upper lung.In noncardiogenic cases, cardiomegaly and pleural effusions are usually absent. The edema may be interstitial but ismore often consolidative. No cephalization of flow is noted, though there may be shift of blood flow to less affected areas.The edema is diffuse and does not spare the periphery of the mid or upper lungs.In cases of large, acute MI and infarction of the mitral valve, support apparatus may produce atypical patterns of pulmonary edema that may mimic noncardiogenic edema in patients who in fact have cardiogenic edema.In cases that are clinically troublesome, multidetector-row gated CT scanning may provide excellent analysis of the heartand reveal the nature of the pulmonary edema.
Electrocardiography
In cardiogenic cases, the ECG may show evidence of MI or ischemia. In noncardiogenic cases, the ECG is usuallynormal.
 
Clinical manifestations
a. It is clinically difficult to differentiate right fromleft ventricular failure. Failure of one chamber causes reciprocalchanges in the opposite chamber.b. Weakness and fatiguec. Poor feeding, resulting in weight lossd. Developmental delayse. Irritabilityf. Pallor and Cyanosisg. Dyspnea, tachypnea, orthopnea, wheezing, cough, weak cry, grunting, mild cyanosis and coastal retractionsh. Tachycardia and gallop rhythmi. Hepatomegaly j. Weight gain from edema, ascites and pleural effusionk. Distended neck and peripheral veins.l. Sweating
 
Medical Therapy
Medical therapy, including preventive measures, is the first-line strategy for treating patients with heart failure.In 1997, the Systolic Hypertension in the Elderly Program (SHEP) Cooperative Research Group observed nearly 5000patients with isolated systolic hypertension.7 Heart failure occurred more than twice as often in a group given placebo than in a group treated with antihypertensive agents. In addition, the risk of heart failure was reduced by 80% among patientswith a previous myocardial infarction who were treated compared with those who were not treated. Control of other riskfactors, including diabetes, coronary artery disease, and structural valve disease, similarly prevents pathologic ventricular remodeling and the development of heart failure.Once the diagnosis of heart failure is established, a number of pharmacologic strategies are available to limit and reversethe manifestations of congestive heart failure (CHF). In particular, blocking the renin-angiotensin system and the beta-adrenergic system improves mortality rates among patients with heart failure. Use of angiotensin-converting enzyme (ACE)inhibitors, as well as angiotensin receptor blockers, increase survival and decrease repeat hospitalizations.8These benefits are also observed with several beta-blockers, including metoprolol and carvedilol.
Patients often have difficulty tolerating either ACE inhibitors or beta-blockers. A number of additional drug regimens can beused in these cases. These drugs include loop and thiazide diuretics, as well as aldosterone antagonists. Diuretic therapydecreases ventricular diastolic pressure, reducing ventricular wall stress and maximizing subendocardial perfusion.Digoxin, a cardiac glycoside, is used to improve symptoms associated with congestive heart failure by enhancing cardiaccontractility. Although digoxin does not confer a survival benefit, it has reduced the number of hospitalizations because of worsening heart failure.Enthusiasm for vasodilator therapy with a combination of hydralazine and isosorbide dinitrate has recently beenrenewed.10  Finally, when patients' conditions are refractory to standard therapy, they often require hospitalization to receiveintravenous diuretics, vasodilators, and inotropes.
Surgical Therapy
Heart transplantation
When progressive end-stage heart failure occurs despite maximal medical therapy, the criterion standard for therapy hasbeen heart transplantation. Since Christiaan Barnard performed the first orthotopic heart transplantation in 1967, the worldhas seen tremendous advancement in the field of cardiac transplantation.
Coronary artery bypass grafting
Studies of medical versus surgical therapy for coronary artery disease have historically focused on patients with normal leftventricular (LV) function. However, the Veterans Affairs Cooperative Study of Surgery demonstrated a significantlyincreased survival rate in a subset of patients with left ventricular ejection fractions (LVEFs) of <50% after coronary bypasssurgery compared with patients who were randomly selected to receive medical therapy. This survival benefit wasparticularly evident at the 11-year follow-up point (50% vs 38%).
Aortic valve replacement
Diseases of the aortic valve can frequently lead to the onset and progression of congestive heart failure. Although thenatural histories of both aortic stenosis and aortic regurgitation are well known, patients are often followed upconservatively after they present with clinically significant heart failure. Congestive heart failure is a common indication for aortic valve replacement (AVR), but one must be cautious in patients with low EFs and possible aortic stenosis. If noinducible gradient is present (a finding that suggests some ventricular reserve), the outcome with standard AVR is poor. Inthis situation, transplantation might be the only option, although the use of percutaneous valves, an apical aortic conduit, or a left ventricular assist device (LVAD) might offer an intermediate solution.

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