A directed history and physical examination can provide clues to the presence and possible etiologies of heart failure.
Abnormal vital signs with normal temperature may suggest cardiac disease.
Tachycardia of heart failure is often “monotonous” or incessant, and does not typically respond to treatment (i.e., volume, antipyretics, pain medications, etc.).
Tachypnea, failure to thrive, or diaphoresis with feeding, accompanied by abnormal lung sounds, tachycardia, gallop, and hepatomegaly suggest CHF in an infant.
New-onset heart failure may be less overtly symptomatic in older children. Symptoms of abdominal pain and nausea and anorexia can be present, sometimes diverting attention from the real cause.
Management is directed at the cause. Medications to consider include diuretics, vasodilators, inotropes, and neurohumoral modulators.
Heart failure is a clinical condition that results from impairment of the ventricle to fill with or eject blood. Heart failure is caused by ventricular pump dysfunction, or by overload of volume (preload) or pressure (afterload).1–3 Heart failure in children has many etiologies (Table 40-1). In the younger infant, congestive heart failure (CHF) is most likely related to structural heart disease, yet respiratory illnesses, anemia, and infection must be considered and appropriately managed. In an older child, the etiology may have a structural, metabolic, infectious, and/or environmental origin.1–3
Etiologic Basis of CHF in Children
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TABLE 40-1 Etiologic Basis of CHF in Children
Preserved Ventricular Pump Function
Ventricular Pump Dysfunction
Preload (Volume Overload)
Contractility (Reduced Contractility)
Ventricular septal defect (VSD)
Patent ductus arteriosus (PDA)
Atrioventricular canal defects
Aortic regurgitation (AR)
Mitral regurgitation (MR) (i.e., rheumatic fever)
Arrhythmogenic (complete heart block with bradycardia), SVT, or VT
Drug/Toxin: digoxin, Ca2+ channel/β-blocker, cocaine and other stimulants, anthracycline
Anemia: iron deficiency, sickle cell, thalassemia
Inflammatory: early Kawasaki, systemic lupus erythematous
Traumatic: cardiac tamponade, myocardial contusion
Afterload (Increased SVR/pressure overload)
Congenital: coarctation of the aorta, aortic stenosis, pulmonary stenosis
Metabolic: electrolyte abnormality, hypothyroidism
Other: Asphyxia, sepsis, renal failure
Cardiac output is determined by four factors: preload, afterload, contractility, and rate. Preload, or filling volume, is increased in left-to-right shunts. Afterload, or the resistance the ventricles face upon ejection of blood, has an important role in outlet obstruction or systemic hypertension. Contractility is altered in cardiomyopathy. Rate can either be too slow, resulting in inadequate output, or too fast, decreasing diastolic filling.2,3