• Excessive workload (volume and/or pressure) secondary to congenital heart disease (CHD) or acquired heart disease in the presence of normal myocardial function
• Normal workload in the presence of myocardial dysfunction

• Arrythmias: supraventricular or ventricular tachycardia, complete heart block (CHB)
• Volume overload: atrioventricular (AV) valve regurgitation or arteriovenous malformations (AVM)
• Primary myocardial disease: cardiomyopathy, myocarditis
• Anemia: Rh disease, fetomaternal and twin-twin transfusion
• Premature closure of foramen ovale or ductus arteriosus

• Myocardial dysfunction: asphyxia, sepsis, myocarditis, hypoglycemia
• Pressure overload: left-sided obstructive lesions (e.g., aortic stenosis, coarctation of the aorta, hypoplastic left-heart syndrome)
• Volume overload: patent ductus arteriosus, truncus arteriosus, aortopulmonary window, total anomalous pulmonary venous return, AVM
• Arrythmias: supraventricular or ventricular arrythmias, CHB

• Volume overload: left-to-right shunt physiology (e.g., patent ductus arteriosus, truncus arteriosus, aortopulmonary window, ventricular septal defect, common AV canal defect, total anomalous pulmonary venous return)
• Myocardial dysfunction: endocardial fibroelastosis, glycogen storage disease, myocarditis, Kawasaki syndrome, anomalous left coronary artery from pulmonary artery
• Secondary causes: renal disease, hypertension, hypothyroidism, sepsis
• Arrhythmias: supraventicular
  • Ventricular tachycardia, complete heart block
• Pressure overload: coarctation of the aorta, residual aortic stenosis, subaortic membrane

• Unrepaired CHD with volume and/or pressure overload
• Repaired CHD with residual defects that result in volume and/or pressure overload
• Acquired heart disease: pericarditis, myocarditis, endocarditis, acute rheumatic fever
• Secondary causes: hypertension, thyrotoxicosis, chemotherapy (doxorubicin, radiation), sickle cell anemia, cor pulmonale, neuromuscular disease (e.g., Duchenne muscular dystrophy)

• Respiratory disease
• Hypoalbuminemia
• Anemia
• Hypothyroidism
• Poisoning: parathione, salicylates
• Arrythmias
• Viral myocarditis
• Syndromes: Marfan, Hurler, Noonan
• Sepsis

• Prolonged feedings associated with tachypnea, retractions, and excessive perspiration
• Emesis, inadequate caloric intake, and failure to thrive
• Irritability with feeding and frequent respiratory infections

• Exercise intolerance with exertional dyspnea
• Chronic cough, wheezing, orthopnea, fatigue, weakness, anorexia, nausea, and edema
• Weight loss secondary to anorexia and nausea
• Weight gain secondary to fluid retention

• Tachycardia
• Gallop
• Tachypnea
• Wheezing
• Crackles
• Retractions
• Nasal flaring
• Grunting
• Hepatomegaly
• Splenomegaly
• Edema (periorbital)
• Cool and/or mottled extremities
• Poor capillary refill
• Weak pulses

• Tachycardia
• Gallop
• Tachypnea
• Cool and pale extremities, with cyanosis and poor capillary refill
• Jugular venous distension
• Wheezing (“cardiac asthma”)
• Hepatomegaly
• Splenomegaly
• Edema (periorbital or peripheral)
• Pulsus alternans
• Pulsus paradoxus

• Abnormal P-waves and nonspecific ST-T wave changes
• May help in the diagnosis of a cardiac anomaly (e.g., anomalous left coronary, pericarditis, arrhythmia)

• Rule out CHD
• Assessment of cardiac function

• Delineation of cardiac hemodynamics and anatomy (used only in selected cases)
• Cardiac biopsy may be helpful in the diagnosis of myocarditis or cardiomyopathy
• Electrophysiologic study to delineate arrhythmia

• Abnormalities in the pH, PaO₂, and PaCO₂ may be seen.
• Hyponatremia, hypokalemia, and/or hypochloremia (2⁰ to chronic diuretic therapy)
• Anemia, leukocytosis, or leukopenia (e.g., viral myocarditis)
• Elevation of ESR (e.g., rheumatic fever or Kawasaki syndrome)
• Proteinuria, high urine specific gravity, microscopic hematuria

• Surgical palliation or correction of structural abnormality
• Radiofrequency ablation of arrythmia
• Interventional cardiac catheterization (e.g., balloon dilation of aortic or pulmonary stenosis, coil embolization of patent ductus arteriosus, device closure of atrial septal defect)
• Medical treatment of endocarditis, myocarditis, anemia, or hypertension

• General measures: restriction of physical activity, oxygen, tube feedings, increase in caloric content of feedings, limit of salt intake
• Pharmaceutical management
  • Inotropic agents (digoxin, dopamine, dobutamine)
  • Diuretics (loop diuretics: e.g., furosemide )
  • Afterload reducing agents (angiotensin converting enzyme inhibitors: e.g., captopril and enalapril)

• Intravenous immunoglobulin (IVIG) for myocarditis
• Limited use of cardiac anthracycline drugs
• SBE prophylaxis to prevent infective endocarditis
• Controlling arrhythmias with pharmacotherapy, or
• Treatment of tachyarrythmias with radiofrequency ablation and bradyarrythmias (CHB) with pacing

• In patients with CHF, on the basis of left-to-right shunting, spontaneous clinical improvement of CHF may indicate the development of pulmonary vascular disease.
• Patients with a VSD can develop a right ventricular muscle bundle even if the VSD spontaneously closes. Some patients may also develop a subaortic membrane or prolapse of a coronary cusp with subsequent aortic insufficiency.
• In ductal dependent lesions, an increase in PaO₂ with metabolic acidosis may be 2⁰ to increased pulmonary blood flow with decreased systemic blood flow.

Q: My child has a large ventricular septal defect and is on digoxin and Lasix. Should I take salt out of his diet?
A: No. Excessive salt restriction is not necessary. A no-added-salt diet is sufficient.

Q: What is the importance of tachycardia and bradycardia in heart failure?
A: Tachycardia limits diastolic filling time and may result in a decreased output. However, bradycardia may be poorly tolerated in patients with heart failure and a relatively fixed stroke volume who are dependent on heart rate to maintain an appropriate output.

Emmanoulides GC, Riemenscheider TA, Allen HD, Gutgesell HP, eds. In: Moss and Adams. Heart disease in infants, children, and adolescents, including the fetus and the young adult, 5th ed. Baltimore: Williams & Wilkins, 1995.

Fyler DC, ed. Nadas’ pediatric cardiology. Philadelphia: Hanley & Belfus, 1992.