A 4-month-old African American boy presents with cough and wheezing of 1 week’s duration. His pediatrician had diagnosed bronchiolitis and prescribed nebulized albuterol, but the boy had no improvement. He gradually worsened and developed tachypnea, wheezing, and retractions, so his mother has brought him to the emergency department at a community hospital. He has no history of fever, rhinorrhea, diaphoresis, poor feeding, vomiting, or rash. A chest radiograph shows mild cardiomegaly but is otherwise normal. He is hospitalized and treated with intravenous methylprednisolone and nebulized albuterol.During his hospital stay, he develops tachycardia, which is believed to be due to albuterol. After discontinuing albuterol, clinicians administer nebulized levalbuterol, but there is no improvement in heart rate (HR). After several days of treatment, he continues to have tachycardia and tachypnea, prompting echocardiography, which shows severely reduced left ventricular (LV) function and dilatation. Ejection fraction (EF) is 40% (normal > 60%). He is transferred to the children’s hospital for cardiology consultation.On admission to the children’s hospital, his HR is 199 beats/min, temperature is normal, blood pressure is 77/66 mm Hg, and oxygen saturation is 99% in room air. Physical examination reveals subcostal retractions and coarse breath sounds without crackles (rales). There is no hepatomegaly. The rest of his physical examination findings are within normal limits. Complete blood cell count, electrolytes, and urinalysis yield normal results. Additional evaluation during his hospitalization leads to the diagnosis.Initial electrocardiography documents sinus tachycardia with biventricular hypertrophy (Fig 1). Repeat echocardiography confirms poor systolic function, severe LV dilatation, and EF of 30%. Clinicians administer digoxin, captopril, and furosemide for congestive cardiac failure (CCF). The following day, the boy has several bradycardic episodes, at which time rhythm strips reveal underlying atrial flutter (Fig 2). Direct current (DC) cardioversion is performed and sotalol is administered for antiarrhythmic control. After cardioversion, his HRs remain in the range of 120 to 140 beats/min. His clinical status rapidly improves, and the boy is discharged several days later. Follow-up echocardiography documents continued improvement, with one obtained 6 months after discharge showing normal LV function with mild mitral regurgitation. Borderline right ventricular hypertrophy is still present.Atrial flutter occurs when the electric current for muscle contraction in the heart passes through an accessory pathway, leading to a re-entry rhythm. Cases have been reported in the fetus and neonate following Coxsackievirus infection and maternal lithium ingestion. In older children without history of congenital heart disease or cardiac surgery, atrial flutter is exceedingly rare. It is diagnosed by documenting a sawtooth pattern on electrocardiography, most often with a 2:1 atrioventricular block. The pattern may be difficult to distinguish from supraventricular tachycardia due to atrioventricular block and rapid rate. In these cases, vasovagal maneuver or administration of adenosine may yield the diagnosis.Prolonged tachyarrhythmias may be complicated by tachycardia-induced dilated cardiomyopathy and subsequent heart failure. Infants and young children typically present with cough, wheezing, feeding intolerance, diaphoresis, and poor growth. In younger patients, diagnosis is often delayed until after CCF develops due to an inability to verbalize symptoms. If CCF is suspected based on the history and physical examination findings, the diagnosis should be confirmed by several tests. Chest radiography may show cardiomegaly or pulmonary congestion, electrocardiography may show sinus tachycardia and ST-segment and T-wave abnormalities, and echocardiography usually shows decreased ejection fraction. Laboratory studies may help evaluate the underlying cause.Treatment of tachycardia-induced cardiomyopathy is directed toward alleviating symptoms and decreasing morbidity. Commonly, triple therapy with digoxin, an angiotensin-converting enzyme (ACE) inhibitor, and diuretics is administered with or without a beta-blocker. Digoxin is commonly used in infants to lower HR and improve LV function. ACE inhibitors increase LV remodeling and, therefore, improve outcome. Diuretics are often used to decrease preload and provide symptomatic relief. Beta-blockers suppress tachycardia and are also believed to increase LV remodeling. If pharmacologic cardioversion is not achieved or more rapid cardioversion is necessary, as in cases of children who are hemodynamically unstable, DC cardioversion is a reasonable alternative. Digoxin should be continued for at least 6 months. Optimal nutrition is important for speedy recovery.
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