Congestive Heart Failure
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This chapter provides an overview of the etiology and effects of congestive heart failure.
Congestive heart failure (CHF) occurs when the heart fails as a pump and is therefore unable to meet the circulatory and metabolic requirements of the body. Right-sided CHF occurs when blood is not efficiently pumped to the pulmonary vasculature, resulting in a systemic backup of blood. Left-sided CHF occurs when blood cannot be pumped to the systemic circulation, resulting in pulmonary vasculature congestion.
A congenital heart defect is the most common cause of CHF and, if severe, causes symptoms of CHF at birth, whereas milder defects cause symptoms by the time the infant is 6 months old. Inadequate cardiac output triggers both hemodynamic and neurohumoral responses meant to compensate for the failing heart. Although congenital heart defects account for most cases of pediatric CHF, other causes include infection, dysrhythmias, drugs, severe anemia, and tumors.
A congenital heart defect is the most common cause of CHF.In an attempt to reduce blood volume and cardiac workload, the heart chambers and blood vessels secrete natriuretic peptides, which promote diuresis. These peptides are classified as A-type natriuretic peptide (ANP), produced mainly by the atrial myocardium; B-type natriuretic peptide (BNP), produced by the ventricular myocardium; and C-type natriuretic peptide, produced by endothelial cells that line the blood vessels and also the kidneys. Peptide hormones are antagonists to the renin-aldosterone-angiotensin system and therefore limit aldosterone secretion and promote salt and water loss. They also lower blood pressure by promoting vasodilation by inhibiting the sympathetic nervous system and reducing circulating blood volume. Laboratory tests that measure these peptides are useful indicators of the success of treatment and/or level of cardiac decompensation.
Decreased cardiac output also triggers hemodynamic compensatory mechanisms. In response to low cardiac output the sympathetic nervous system is triggered, resulting in a rapid heart rate (to pump blood to the body quickly), stronger heart muscle contractions (to increase ejection fraction), increased stroke volume, and vasoconstriction (to return more blood to the heart). This compensatory mechanism makes the heart work harder by decreasing the amount of preload while increasing afterload and increasing cardiac muscle oxygen demands that cannot be met.
Stimulation of the renin-angiotensin-aldosterone system is the result of decreased blood flow to the kidneys and a decreased glomerular
filtration rate. As a consequence salt and water are retained, increasing intravascular volume. In the beginning the system has a positive effect by increasing preload and cardiac output. Eventually, however, the heart muscle becomes fatigued from pressure overload, the lung tissue becomes edematous, and symptoms of CHF worsen. Long-term untreated CHF results in cardiac muscle remodeling and ventricular hypertrophy.
filtration rate. As a consequence salt and water are retained, increasing intravascular volume. In the beginning the system has a positive effect by increasing preload and cardiac output. Eventually, however, the heart muscle becomes fatigued from pressure overload, the lung tissue becomes edematous, and symptoms of CHF worsen. Long-term untreated CHF results in cardiac muscle remodeling and ventricular hypertrophy.
Management of CHF is aimed at correcting the congenital defect causing the heart failure and/or reducing the workload of the heart by administering positive inotropic medications, diuretics, oxygen therapy, and vasodilators. Table 26-1 lists the signs and symptoms of the types of congestive heart failure.
ACQUIRED HEART DISEASERheumatic Heart Disease
Although treatment of strep throat with antibiotics has greatly reduced the number of rheumatic fever cases in the United States, Salt Lake City, Utah and Denver, Colorado, continue to have 30-50 pediatric cases of rheumatic fever yearly. The reason for this trend is unknown. In susceptible children an upper respiratory tract infection with group A β-hemolytic streptococci is the triggering event leading to rheumatic fever. Children and adolescents aged 5-15 years, females, and African-Americans are at highest risk for developing rheumatic fever within 1 to 5 weeks after an untreated strep throat. If more than one episode of strep throat is untreated, the child has an almost 50% chance of developing rheumatic fever.
If more than one episode of strep throat is untreated, the child has an almost 50% chance of developing rheumatic fever.The inflammatory process of rheumatic fever is set up by the sensitization of B lymphocytes by streptococcal antigens. Antistreptococcal antibodies then develop, leading to immune complexes that cross-react with antigens in cardiac tissue. A multiorgan inflammatory process involves connective tissue, the heart, joints, central nervous system, and subcutaneous tissue. Residual heart valve damage may follow a single episode of rheumatic fever and result in CHF.
Table 26-1 Signs and Symptoms of Congestive Heart Failure | ||||||||
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The main signs and symptoms of rheumatic fever include carditis, multijoint pain, Sydenham chorea (St. Vitus’ dance), rash on the trunk and extremities, and subcutaneous nodules over the joints, scalp, and spinal column. Streptococcal antibody titers are higher in children with rheumatic fever than they are in children with strep throat alone. Sydenham
chorea is self-limiting but may not be manifested for months to years after the acute infection. Signs and symptoms include emotional instability and involuntary movements leading to ataxia, slurred speech, and muscle weakness.
chorea is self-limiting but may not be manifested for months to years after the acute infection. Signs and symptoms include emotional instability and involuntary movements leading to ataxia, slurred speech, and muscle weakness.
Streptococcal antibody titers are higher in children with rheumatic fever than they are in children with strep throat alone.Mitral valve insufficiency is the most common valve disorder associated with rheumatic fever. Mitral valve stenosis, aortic valve insufficiency, and aortic stenosis may also occur.
Mitral valve insufficiency is the most common valve disorder associated with rheumatic fever.
CARDIOMYOPATHYCardiomyopathy, a condition in which the heart muscle stretches and becomes weak, results in CHF. There are three main types of cardiomyopathy: dilated, hypertrophic, and restrictive.
Dilated Cardiomyopathy
Idiopathic dilated cardiomyopathy occurs most frequently, although long-term tachyarrhythmias, chronic heart inflammation, Duchenne muscular dystrophy, alcoholism, and inborn errors of metabolism (fatty acid oxidation) account for some cases of dilated cardiomyopathy. As dilated cardiomyopathy progresses the child develops classic signs of CHF, with an ejection fraction of around 40% (normal, 65-70%). Treatment begins by correcting the cause, such as medication to control arrhythmias, treatment of symptoms, and cardiac heart transplantation if other measures fail.
Hypertrophic Cardiomyopathy
Hypertrophic cardiomyopathy results in ventricular hypertrophy and ventricular septum hypertrophy, which causes an outflow obstruction. One in 500 individuals has a generic link for this disease and will develop familial hypertrophic cardiomyopathy. Signs and symptoms usually begin
in older children and adolescents. Metabolic disorders such as glycogen storage disease (Pompe’s disease) also cause hypertrophic cardiomyopathy. Because of an enzyme deficiency, glycogen cannot be metabolized correctly and is deposited in the myocardium. The infant with this disorder usually does not live past 12 months of age.
in older children and adolescents. Metabolic disorders such as glycogen storage disease (Pompe’s disease) also cause hypertrophic cardiomyopathy. Because of an enzyme deficiency, glycogen cannot be metabolized correctly and is deposited in the myocardium. The infant with this disorder usually does not live past 12 months of age.
One in 500 individuals has a generic link for this disease and will develop familial hypertrophic cardiomyopathy.Although signs and symptoms of poor cardiac muscle perfusion, including exercise intolerance and angina, may occur, sudden cardiac death during a sports activity may be the first indication of the condition. Exercise stress testing can help diagnose the disorder. Treatment options include implantable cardiac defibrillators, beta-blockers, dual-chamber pacemakers, surgical myectomy (removal of part of the septum), and, for the adult, ethanol ablation of part of the septum that reduces outflow obstruction.
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