The ECG was recorded from a 37 year old woman with a long history of episodic palpitation.
ECG. Rhythm: There is a regular tachycardia present at a rate of 170 per minute. No atrial activity is visible.
Morphology: The QRS complexes are narrow (less than .10 seconds). There are non specific ST segment and T wave changes in the inferolateral leads.
Comment. The tachycardia is a narrow complex one and therefore must arise above the bifurcation of the bundle of His into the bundle branches ie it is of supraventricular origin. A supraventricular tachycardia may arise in the sinus node, atrial myocardium or the AV junctional tissue and the term junctional tachycardia is often reserved for the latter. The tachycardia may arise from enhanced automaticity of a group of cells in the region of the AV junction, or when a re-entry circuit becomes established. The former type is due to accelerated discharge from AV junctional tissue while the latter may involve a re-entry circuit entirely confined to the region of the AV junction (called an AV nodal re-entrant tachycardia or AVNRT) or be associated with an anomalous accessory pathway as in the Wolff Parkinson White syndrome (when it is known as an atrio-ventricular re-entrant tachycardia or AVRT). Irrespective of the mechanism the QRS morphology during the tachycardia will be the same as the QRS morphology in sinus rhythm unless a rate related conduction disturbance should occur during the tachycardia.
It is often impossible to deduce the type of tachycardia from the surface EGG. Clinical assessment may help – the tachycardia due to increased automaticity tends to start more gradually and is slower (rate 100 – 130) than the re-entrant types which usually start and stop abruptly and are faster – usually in the range of 150 – 250 per minute. The best clue to the probable origin will be obtained if P waves are visible and their relationship to the QRS complexes can be defined. The P wave morphology will be different during the tachycardia from that seen in sinus rhythm because atrial depolarization is initiated in the AV junction and atrial activation takes place by a different route from normal. Tachycardia of ‘low atrial’ origin is often classified with junctional tachycardia and in this case the P’ wave will usually precede the QRS complex. In the case of AVNRT, atrial and ventricular depolarization are initiated almost simultaneously from the AV junction and the P” wave is usually obscured by the QRS complex or is just visible in the terminal part of the complex, when the QRS complexes may resemble those seen in RBBE. In the case of AVRT where an accessory pathway is involved, the atria are activated some time after ventricular depolarization has commenced and in many cases the P’ wave can be seen following the QRS complex as a distortion of the ST segment or T wave. However, the timing of retrograde atrial activity will vary not only with the site of origin of atrial depolarization, but also with the relative refractory periods of the various pathways involved in the propagation of the tachycardia. For this reason none of the above rules are infallible and in most cases intracardiac studies are required if it is necessary to determine the exact type of tachycardia.
In the case illustrated no atrial activity is apparent in any lead so is is probably hidden in the QRS complex with the likelihood that this is an AV nodal re-entrant tachycardia.
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