Cardiac dysrhythmias in children can be due to a structural abnormality or an intrinsic defect in the electrical conduction system of the heart. In a child with a structurally normal heart, the mechanisms for dysrhythmias are the same as in adults, although the incidence and prevalence are different. Supraventricular tachycardias (SVTs) originate above the ventricles. In children, the two peak ages of onset for SVT are from before birth through the first year of life, and from ages 6 to 8 years. In most cases, there is spontaneous clinical resolution within the first year. When treatment is necessary, it includes vagal maneuvers, pharmacotherapy, and ablation. Wolff-Parkinson-White syndrome is a type of reentrant SVT that involves an accessory pathway. Long QT syndrome is a prolongation of the QT interval due to a genetic channelopathy. Bradycardia and heart block can be due to maternal autoimmune antibodies or structural heart defects. Ventricular tachyarrhythmias can be due to underlying structural heart disease, cardiomyopathy, or a metabolic derangement and may lead to sudden cardiac death.
Case 3. ZW is a 2-month-old patient who is brought to your office by her parents for intermittent bouts of irritability and crying. Today, she is irritable but otherwise appears well. Her heart rate is moderately elevated at 250 beats/min.
In children, abnormal heart rhythms (dysrhythmias) can be due to structural abnormalities (eg, congenital heart disease, cardiomyopathy), but in children with structurally normal hearts, dysrhythmias are due to the same mechanisms as in adults, usually an intrinsic defect in the electrical conduction system of the heart.1 Evaluation of dysrhythmias should start with an electrocardiogram (ECG), and prolonged monitoring should be considered.2
Supraventricular Tachycardia
Supraventricular tachycardia (SVT) is any tachycardia that originates above the ventricles, but it is most often used to describe paroxysmal reentrant SVT. SVT is the most common dysrhythmia in the pediatric population, occurring in approximately 1 in 500 children.2 It has a bimodal incidence, with the first peak from the prenatal period through the first year of life, and the second peak from ages 6 to 8 years. Most affected infants will have spontaneous clinical resolution within the first year,3 but approximately 25% of those infants will have recurrence of symptoms later in childhood (from ages 6 to 8 years).4 Patients with SVT should be evaluated by a pediatric cardiologist before exercise.2,5
PERINATAL SVT
SVT can present prenatally with isolated tachycardia (fetal heart rate of 220 to 320 beats/min) or as hydrops fetalis secondary to tachycardia-induced cardiomyopathy.1,2 Fetal SVT is treated transplacentally with maternal drugs to convert or control the fetal tachycardia. The three most common oral drugs used for transplacental treatment of fetal tachycardia include digoxin, flecainide, and sotalol.1,6
In the neonatal period, signs of SVT include irritability, poor feeding, tachypnea, pallor, and sweating.2 These signs are nonspecific and difficult to differentiate from routine neonatal behaviors, often delaying the recognition or diagnosis of SVT. Consequently, tachycardia-induced cardiomyopathy may sometimes be the presenting sign.
PEDIATRIC SVT
Young children with SVT typically can report their symptoms and may describe their heart as racing, beeping, skipping, jumping up and down, or beating out of their chests.2 SVT can be triggered by activity and is characterized by abrupt onset, fast heart rate remaining after exercise, and an abrupt termination. Longer episodes of SVT can produce dizziness, lightheadedness, or chest tightness, but syncope is less common.1 Heart rate with SVT is typically (but not always) faster than the maximum heart rate. Maximum heart rate for a child can be estimated with the equation 220 beats/min minus the child’s age in years.7
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