- Congestive heart failure (CHF) is a clinical syndrome and a directed history and physical examination can provide valuable clues to the presence and possible etiologies of heart failure.
- Abnormal vital signs such as unexplained tachycardia or tachypnea 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 an abnormal lung examination, tachycardia, hyperactive precordium, gallop, and hepatomegaly suggest CHF in an infant.
- New-onset heart failure may be less overtly symptomatic in older children. Malaise, decrease in the level of daily activity, and weight loss may be the only complaint. Symptoms of abdominal pain and nausea and anorexia can be present, sometimes diverting attention from the real cause.
- New biomarker, B-type natriuretic peptide (BNP) may help with the diagnosis of suspected CHF in some cases.
- Management is directed at the cause. Medications to consider include diuretics, vasodilators, inotropes, and neurohumoral modulators.
Heart failure is a “clinical syndrome in which heart disease reduces cardiac output, increases venous pressures, and is accompanied by molecular abnormalities that cause progressive deterioration of the failing heart and premature myocardial cell death.”1 It is a failure of the cardiovascular system to meet metabolic demands. Heart failure results from the interplay of hemodynamic, neurohumoral, cellular, and developmental factors. Function is no longer dependent on supply and demand of the heart but on improving hemodynamics, improving symptoms, and providing myocardial preservation, and remodeling at the same time. CHF has many etiologies (Table 48–1). In the younger infant, 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, and/or environmental origin.2–4
Table 48-1. Etiologic Basis of CHF |Favorite Table|Download (.pdf)
Table 48-1. Etiologic Basis of CHF
Preload (Volume Overload)
Left-to-right shunt: VSD, PDA, AV fistula, atrioventricular canal defects, Epstein's anomaly
Inflammatory: infectious (myocarditis), cardiomyopathy
Anemia: iron deficiency, sickle cell, thalassemia
Rheumatic: rheumatic fever, early Kawasaki, SLE
Toxin: digoxin, Ca2+ channel/β-blocker, cocaine and other stimulants
Afterload (increased SVR)
Traumatic: cardiac tamponade, myocardial contusion
Congenital: coarctation of the aorta, aortic stenosis, pulmonary stenosis
Metabolic: electrolyte abnormality, hypothyroidism
Other: Asphyxia, hypoglycemia, hypocalcemia, sepsis
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, is important 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
In acute CHF, end-organ hypoperfusion explains most clinical ...