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Supraventricular arrhythmias (SVAs), with the exception of atrial fibrillation, are a group of rapid, regular tachycardias that use the atria and/or the atrioventricular (AV) node as part of their arrhythmia mechanism. This chapter examines the different electrophysiological mechanisms behind the most common SVAs. Atrial flutter is the result of macrore-entry, confined to the atria. Atrial tachycardia is focal in origin, commonly from muscle sleeves within the pulmonary veins. AV nodal reciprocating tachycardia is the most common form of junctional re-entrant tachycardia. Accessory pathways give rise to the other form of junctional re-entrant tachycardia, AV reciprocating tachycardias. When associated with ventricular preexcitation it gives rise to Wolff-Parkinson-White syndrome. Risk stratification for individuals with ventricular preexcitation may be attempted using non-invasive criteria. The different 12-lead ECG characteristics of each arrhythmia are described together with examples. The acute treatment of SVAs typically involves intravenous adenosine, which should terminate all arrhythmias that depend on the AV node (AVNRT and AVRT) and transiently unmark those that are confined to the atrium (atrial flutter and atrial tachycardia). Alternative acute and long-term pharmacological therapy is also discussed. Curative treatment with radiofrequency ablation is a realistic option for most SVAs. The procedure, outcomes and risks are explained. © 2006 Elsevier Ltd. All rights reserved.

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Journal article



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259 - 267