Chf

Description: Congestive Heart Failure or CHF is a severe circulatory congestion due to decreased myocardial contractility, 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 by the 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 result of insufficient or defective cardiac filling and/or impaired contraction and emptying. Compensatory mechanisms increase blood volume, as well as the cardiac filling pressure, heart rate, and cardiac muscle mass, to maintain the pumping 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 the patient, the extent and rate at which cardiac performance becomes impaired, and which ventricle is initially involved in the disease process. A broad spectrum of severity of impairment of cardiac function is ordinarily included in the definition of HF. These impairments range from the mildest forms, which are manifest clinically only during stress, to the 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 status Signs that suggest CHF include the following:

• • • • • • • •

Tachycardia Third heart sound (S3) Increased jugular venous pressure Positive hepatojugular reflux Bilateral rales Peripheral edema not caused by venous insufficiency Laterally displaced apical impulse Weight gain In cardiogenic cases, clinical findings include cold and clammy peripheral structures, resulting from low cardiac output. Jugular venous pressure is elevated, and a ventricular gallop (S3) 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 is generally normal, the S3 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 to determine systolic and diastolic LV performance, the cardiac output (ejection fraction), and pulmonary artery and ventricular 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 examination demonstrates redistribution of blood flow to the nondependent portions of the lungs and the upper lobes. In grade II PVH, there is evidence of interstitial edema with ill-defined vessels and peribronchial cuffing, as well as interlobular septal thickening. 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 airspace edema 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 is more 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 heart and 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 usually normal.

Clinical manifestations a. It is clinically difficult to differentiate right from left ventricular failure. Failure of one chamber causes reciprocal changes in the opposite chamber. b. Weakness and fatigue c. Poor feeding, resulting in weight loss d. Developmental delays e. Irritability f. Pallor and Cyanosis g. Dyspnea, tachypnea, orthopnea, wheezing, cough, weak cry, grunting, mild cyanosis and coastal retractions h. Tachycardia and gallop rhythm i. Hepatomegaly j. Weight gain from edema, ascites and pleural effusion k. 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 5000 patients 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 patients with a previous myocardial infarction who were treated compared with those who were not treated. Control of other risk factors, 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 reverse the manifestations of congestive heart failure (CHF). In particular, blocking the renin-angiotensin system and the betaadrenergic 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.8 These benefits are also observed with several beta-blockers, including metoprolol and carvedilol.9 Patients often have difficulty tolerating either ACE inhibitors or beta-blockers. A number of additional drug regimens can be used in these cases. These drugs include loop and thiazide diuretics, as well as aldosterone antagonists. Diuretic therapy decreases 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 cardiac contractility. 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 been renewed.10 Finally, when patients' conditions are refractory to standard therapy, they often require hospitalization to receive intravenous diuretics, vasodilators, and inotropes.

Surgical Therapy Heart transplantation When progressive end-stage heart failure occurs despite maximal medical therapy, the criterion standard for therapy has been heart transplantation. Since Christiaan Barnard performed the first orthotopic heart transplantation in 1967, the world has 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 left ventricular (LV) function. However, the Veterans Affairs Cooperative Study of Surgery demonstrated a significantly increased survival rate in a subset of patients with left ventricular ejection fractions (LVEFs) of <50% after coronary bypass surgery compared with patients who were randomly selected to receive medical therapy. This survival benefit was particularly 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 the natural histories of both aortic stenosis and aortic regurgitation are well known, patients are often followed up conservatively 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 no inducible gradient is present (a finding that suggests some ventricular reserve), the outcome with standard AVR is poor. In this 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.

Mitral valve repair Mitral valve regurgitation can both cause and result from chronic heart failure. Its presence is an independent risk factor for cardiovascular morbidity and mortality.34 In addition to frank rupture of the papillary muscle in association with acute myocardial infarction, chronic ischemic cardiomyopathies result in migration of the papillary muscle as the ventricle dilates. This dilation causes tenting of the mitral leaflets, restricting their coaptation. Dilated cardiomyopathies can have similar issues, as well as annular dilatation. In addition to mitral regurgitation, the alteration in LV geometry contributes to volume overload, increases LV wall tension, and leaves patients susceptible to exacerbations of heart failure.35 Ventricular restoration After a transmural myocardial infarction occurs, the ventricle pathologically remodels from its normal elliptical shape to a spherical shape. This change in geometry is in part responsible for the constellation of symptoms associated with congestive heart failure and decreased survival

E. Nursing Management 1. Monitor for signs of respiratory distress a. Provide pulmonary hygiene as needed b. Administer oxygen as prescribed c. Keep the head of the bed elevated d. Monitor ABG values. 2. Monitor for signs of altered cardiac output, including a. Pulmonary edema b. Arrhythmias, including extreme tachycardia and bradycardia c. Characteristic ECG and heart sound changes 3. Evaluate fluid status a. Maintain strict fluid intake and output measurements b. Monitor daily weights c. Assess for edema and severe diaphoresis d. Monitor electrolyte values and hematocrit level e. Maintain strict fluid restrictions as prescribed 4. Administer prescribed medications which may include: a. Antiarrhythmias to increase cardiac performance b. Diuretics, to reduce venous and systemic congestion c. Iron and folic acid supplements to improve nutritional status.

5. Prevent Infection 6. Reduce cardiac demands a. Keep the child warm b. Schedule nursing interventions to allow for rest c. Do not allow an infant to feed for more than 45 minutes at a time d. Provide gavage feedings if the infant becomes fatigued before ingesting an adequate amount 7. Promote adequate nutrition. Maintain a high-calorie, low-sodium as prescribed. 8. Promote optimal growth and development 9. As appropriate, refer the family to a community health nurse for follow up care after discharge. Heart Failure, also known as Congestive Heart Failure, is a clinical syndrome that results from the progressive process of remodeling, in which mechanical and biochemical forces alter the size, shape, and function of the ventricle’s ability to pump enough oxygenated blood to meet the body’s metabolic requirements. Compensatory mechanisms of increased heart rate, vasoconstriction, and hypertrophy eventually fail, leading to the characteristic syndrome of heart failure: Elevated ventricular or atrial pressures, sodium and water retention, decreased cardiac output, and circulatory and pulmonary congestion. Systolic dysfunction occurs when the left ventricle is unable to relax and fill sufficiently to accommodate enough oxygenated blood returning from the pulmonary circuit. Systolic dysfunction leads to increased vascular resistance and increased afterload. Diastolic dysfunction leads to pulmonary vascular congestion.