SUPRAVENTRICULAR TACHYCARDIA - ECG DIAGNOSIS AND ANATOMY

This paper reviews the anatomical substrates responsible for the induc tion and maintenance of supraventricular tachycardia and discusses the ECG findings associated with these tachycardias. The normal anatomy o f the supraventricular conducting system: particularly within the atri a, is complex with conduction proceeding along preferential pathways, which are in turn determined in part by the anisotropic properties of the atrial myocardium. There appear to be at least dual inputs to the atrioventricular node, a posteriorly situated slow pathway and an ante rior fast pathway. It is sometimes possible to relate ECG findings dir ectly to anatomical substrates; for example, in some cases of atrial t achycardia the site of the atrial focus (left or right, superior or in ferior) can be determined by the polarity of the P wave. The anatomica l substrates responsible for intra-atrial re-entry, atrial flutter and atrial fibrillation relate to anatomical barriers to impulse propagat ion and areas of slow conduction. In atrial flutter the crista termina lis, Eustachian valve, inferior vena cava, coronary sinus os, and tric uspid annulus have been identified as anatomical barriers to conductio n around which a macro re-entrant circuit within the right atrium may conduct, usually in a counter-clockwise direction. Clockwise direction of conduction, and other mechanisms of tachycardia, occur in some of the less typical forms of atrial fluter. Atrial fibrillation is caused by multiple wavelets which randomly conduct through the atrial myocar dium and are responsible for the irregular 'fibrillation waves' on the EGG. Supraventricular tachycardia presents as a narrow complex tachyc ardia unless pre-existing or rate-related bundle branch block is prese nt. Less common causes for a broad complex tachycardia occurring in su praventricular tachycardia include an accessary atrioventricular or at riofascicular pathway conducting antegradely during tachycardia, or ac cessory pathway participation as a bystander during supraventricular t achycardia. ECG features which can help to distinguish between atriove ntricular nodal re-entrant tachycardia and atrioventricular re-entrant tachycardia include: (i) the presence of a delta wave during sinus rh ythm which is highly suggestive of atrioventricular re-entrant tachyca rdia as the mechanism of supraventricular tachycardia; (2) the finding of a pseudo s (lead II) or pseudo r' (lead V-1) during tachycardia in atrioventricular nodal re-entrant tachycardia; (3) lengthening of the tachycardia cycle length in cases of atrioventricular re-entrant tach ycardia when bundle branch block occurs ipsilateral to the accessory p athway and (4) the finding of QRS alternans during tachycardia which i s suggestive of atrioventricular re-entrant tachycardia.'Long RP' tach ycardia may be caused by an atrial tachycardia due to an inferiorly si tuated area of abnormal automaticity, atypical atrioventricular nodal re-entrant tachycardia with slow retrograde conduction, or atrioventri cular re-entrant tachycardia with an accessory pathway conducting slow ly from ventricle to atrium during tachycardia.