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Sinus arrhythmia is normal in children and ado-lescents. Other arrhythmias are rare in childhood and may be transient or permanent. Congenital arrhythmias may occur in structurally normal or abnormal hearts. They may be secondary to myocardial disease (e.g. rheu-matic fever, myocarditis) or follow exposure to toxins, drugs or surgery to the heart. Children with suspected arrhythmia require a detailed history and examination. The arrhythmia should be identified and characterized by ECG. Intermittent arrhythmias may be detected by 24hr ECG. Underlying congenital heart disease should be excluded by echocardiography.
The most common abnormal arrhythmia in childhood. Re-entry within the A–V node is the most common mechanism of SVT.
Sudden onset (and cessation) lasting from seconds to hours; heart rate 250–300beats/min. SVT is well-tolerated in older children, but heart failure may occur in the young infant. Often precipitated by febrile illness.
Pre-excitation syndrome predisposing to SVT. This is due to an abnormal re-entry circuit of the AV node and an accessory conduction pathway con-necting atrium to ventricle on the right or left lateral cardiac border, or within the ventricular septum. It may be associated with Ebstein anomaly, post-surgical repair, and cardiomyopathy. ECG shows short PR interval and delta wave (slow upstroke of QRS complex).
· Medical: adenosine (emergency) β-blocking medication, flecainide, amiodarone.
· Interventional: electrophysiological studies and intracardiac ablation when a teenager.
Long QT syndrome may be associated with sudden loss of conscious-ness during exercise, stress or emotion, usually in late childhood. If un-recognized, sudden death from VT may occur. Inheritance is autosomal dominant; there are several phenotypes. Prolongation of the QT interval on ECG is associated with many drugs, electrolyte disorders, and head injury.
Long QT syndrome is a channelopathy caused by specific gene muta-tions with gain or loss of function. There is a range of effect from Long QT, Short QT, Brugada syndrome and cardiomyopathy. Anyone with a family history of sudden unexplained death, or syncope on exertion must be assessed for these.
Rare. Mothers of affected children are usually positive for serum anti-Ro or anti-La antibodies and have underlying connective tissue disorder.
·Foetal hydrops and intrauterine death.
·Neonate: heart failure.
·Childhood: asymptomatic; syncope.
·Management Endocardial/epicardial pacemaker.
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