Left-to-right cardiac shunts (VSD) Hemangioma (arteriovenous malformation) Anomalous left coronary artery Metabolic cardiomyopathy Acute hypertension (hemolytic uremic syndrome) Supraventricular tachycardia Kawasaki disease Postoperative repair of congenital heart disease
Rheumatic fever Acute hypertension (glomerulonephritis) Viral myocarditis Thyrotoxicosis Hemochromatosis/hemosiderosis Cancer therapy (radiation, doxorubicin) Sickle cell anemia Endocarditis Cor pulmonale (cystic fibrosis) Arrhythmias Chronic upper airway obstruction (cor pulmonale) Unrepaired or palliated congenital heart disease Cardiomyopathy
BPD, Bronchopulmonary dysplasia; PDA, patent ductus arteriosus; VSD, ventricular septal defect.
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Heart failure presents in infants as poor feeding, failure to thrive, tachypnea, and diaphoresis with feeding. Older children may present with shortness of breath, easy fatigability, and edema. The physical examination findings depend on whether pulmonary venous congestion, systemic venous congestion, or both are present. Tachycardia, a gallop rhythm, and thready pulses may be present with either cause. If left-sided
Oxygen Improves oxygenation in presence of pulmonary edema
Sodium, fluid Decreases vascular congestion; decreases restrictions preload
Furosemide Salt excretion by way of ascending loop of Henle; reduces preload; afterload reduced with control of hypertension; may also cause venodilation
Combination of Greater sodium excretion distal tubule and loop diuretics
Digitalis Inhibits membrane Na+, K+-ATPase and increases intracellular Ca2+, improves cardiac contractility, increases myocardial oxygen consumption
Dopamine Releases myocardial norepinephrine plus direct effect on β-receptor, may increase systemic blood pressure; at low infusion rates, dilates renal artery, facilitating diuresis
Dobutamine β1-Receptor agent; often combined with dopamine
Amrinone/ Nonsympathomimetic, noncardiac glycosides milrinone with inotropic effects; may cause vasodilation
Captopril/enalapril Inhibition of angiotensin-converting enzyme; reduces angiotensin II production
Mechanical Improves coronary flow, afterload counterpulsation failure is predominant, tachypnea, orthopnea, wheezing, and pulmonary edema are seen. Hepatomegaly, edema, and distended neck veins are signs of right-sided failure.
The absence of cardiomegaly on a chest x-ray usually rules out the diagnosis of heart failure. An echocardiogram assesses the heart chamber sizes, measures myocardial function, and diagnoses congenital heart defects when present.
Initial treatment is directed at improving myocardial function and optimizing preload and afterload. Diuretics, inotropic support, and, often, afterload reduction are employed (Table 145-3). Long-term therapy usually consists of diuretics and afterload reduction is added. Long-term therapy withβblockers also may be beneficial, although this remainssomewhat controversial in pediatric patients. Spironolactoneis usually added to the medical regimen because of its effecton cardiac remodeling.
Although uncommon in the United States, acute rheumatic fever remains an important preventable cause of cardiac disease. It is most common in children 6 to 15 years of age. It is due to an immunologic reaction that is a delayed sequela of group A beta-hemolytic streptococcal infections of the pharynx. A family history of rheumatic fever and lower socioeconomic status are additional factors.
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