Case 2: Wide-Complex Tachycardia in a Newborn

Twelve hours after birth, an otherwise healthy newborn infant is noted to have an irregular pulse during routine examination in the well-child unit. The infant was born at term after an uncomplicated pregnancy and vaginal delivery.An electrocardiogram (ECG) reveals frequent single premature wide complexes corresponding to the pulse irregularity. The infant has good perfusion, easily palpable pulses in all 4 limbs, and no murmur. He is afebrile and has been feeding and voiding normally. He is transferred to the intensive care unit for monitoring and further evaluation.In the following hours, the infant exhibits frequent wide-complex couplets, progressing to runs of wide-complex beats lasting up to 45 seconds at a time (Figure). Periods of wide-complex arrhythmia are unrelated to activity level, and the infant continues to demonstrate good perfusion. An arterial line is placed and reveals that while in sinus rhythm at a heart rate of 146 beats per minute, the blood pressure is 75/40 mm Hg. The heart rate is 161 beats per minute and the blood pressure is 65/35 mm Hg during the wide-complex rhythm.Further analysis of the patient’s ECG during periods of sinus activity reveals a normal corrected QT interval, and no features suggestive of supraventricular tachycardia (SVT). The infant also has an entirely normal electrolyte panel and echocardiogram.Given the runs of intermittent monomorphic wide-complex beats at a rate slightly above the background sinus rate in an otherwise well-appearing infant, a benign accelerated idioventricular rhythm was suspected. The patient was monitored in the hospital and no treatment was initiated.On his second day, the infant remained stable and the arrhythmia burden clearly improved. A 24-hour Holter monitor at this time revealed that 20% of the QRS complexes were ventricular in origin. The longest run was 20 seconds in duration, at a rate of 181 beats per minute, which was an improvement from the previous day when runs lasted up to 45 seconds. By the third day, only isolated premature ventricular contractions (PVCs) were noted, and the patient was discharged from the hospital. Follow-up Holter studies at 1 week and 1 month revealed no further ventricular ectopy.Ventricular arrhythmias are uncommon in pediatrics, but when encountered, they require immediate evaluation. When interpreting pediatric ECGs, QRS intervals should always be compared with age-appropriate reference values; this is especially important for neonates in whom subtle QRS widening may be easily overlooked, because they are often less than adult cutoff values. Hemodynamically unstable patients should be treated according to the latest Pediatric Advanced Life Support algorithms, whereas stable patients may be monitored and further investigated.Several immediately life-threatening conditions warrant consideration. Channelopathies such as long-QT syndrome may be recognized by accurate calculation of the corrected QT interval. Electrolyte disturbances such as hyperkalemia should be identified and corrected if found. Echocardiography should also be performed to assess for evidence of myocardial pathology, such as myocarditis.Distinguishing between ventricular arrhythmia and SVT with aberrant conduction may be challenging. The presence of preexcitation or bundle branch conduction patterns during periods of sinus activity suggest SVT; however, SVT may occur with normal baseline morphology. Capture beats and fusion beats (such as those demonstrated on the Holter monitor of our patient) are helpful in identifying arrhythmias originating from the ventricles. A capture beat occurs when the sinoatrial node transiently captures the ventricles in the midst of ventriculoatrial dissociation to produce a QRS of normal duration. A fusion beat occurs when sinus and ventricular beats coincide to produce a hybrid-appearing complex, often at the initiation of a run of ventricular beats.Once a ventricular arrhythmia is suspected, certain features may assist in distinguishing those that tend to be benign from those that are more concerning. Polymorphic ventricular tachycardia commonly represents an acutely unstable myocardial conduction and repolarization pattern. As a result, it is often associated with concurrent or impending hemodynamic instability (eg, torsades de pointes, catecholaminergic polymorphic ventricular tachycardia). In contrast, monomorphic ventricular arrhythmias frequently arise from a focus of enhanced automaticity or reentrant circuits in the ventricular myocardium and are more often able to maintain cardiac output. The other important characteristic is the arrhythmia rate. Ventricular arrhythmias with rates within 10% to 15% of the background sinus rate are characteristic of benign idiopathic ventricular arrhythmias, and are also generally hemodynamically stable. Ventricular arrhythmias with rates in excess of 200 beats per minute, however, are more suggestive of a condition at risk for destabilization.Although recent advances in cardiac electrophysiology have increased our understanding of benign idiopathic ventricular arrhythmias, they continue to be a diagnosis of exclusion. They present along a spectrum, ranging from frequent isolated PVCs to sustained ventricular tachycardia. Although 20% to 30% of healthy children may exhibit infrequent PVCs and even the rare couplet, ventricular ectopy is considered significant when at least 10% of the QRS complexes in a 24-hour period are ventricular in origin.Once pathologic causes of wide-complex tachycardia are ruled out, monomorphic idioventricular rhythms in pediatric patients have an excellent prognosis. Infants with idioventricular arrhythmias are often asymptomatic and identified incidentally. The ectopy in these infants usually spontaneously resolves within the first few years after birth. Given the typically benign and self-limited natural history, pharmacologic treatment is generally reserved for cases exhibiting incessant ventricular tachycardia, hemodynamic instability, or impaired cardiac function.

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