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Onset of a regular narrow-complex tachycardia.


DIAGNOSIS: The first five P waves are sinus-initiated and are normally conducted to the ventricles. The sixth P wave is an atrial premature complex that is conducted to the ventricles with a long P-R interval and initiates atrioventricular (A-V) nodal reentrant tachycardia. Left ventricular hypertrophy with repolarization abnormality also is present.

A-V nodal reentrant tachycardia is a common arrhythmia that may develop in persons who have dual A-V nodal pathways. (1-3) One pathway conducts rapidly and has a relatively long refractory period. The other pathway conducts slowly and has a shorter refractory period. Normally A-V conduction is via the fast pathway as it was on the first five complexes of the electrocardiogram (ECG) in the Figure. When an atrial premature complex is sufficiently early, however, it finds the fast pathway refractory as the sixth P wave did. It may conduct down the slow pathway, which has a shorter refractory period, and reach the ventricles with a long P-R interval. If the fast pathway ceases to be refractory while the impulse is still traversing the slow A-V nodal pathway, the impulse may travel retrogradely over the fast pathway to reach the atria, thus producing an atrial echo beat. If the impulse again travels to the ventricles via the slow pathway, A-V nodal reentrant tachycardia has begun.

This perpetuation of down the slow pathway and up the fast pathway is manifested in this patient's surface electrocardiogram by a P wave occurring at the end of each QRS. In lead V1 this is seen as a notch and upward spike from the sixth QRS onward, whereas this deflection is not present in any of the first five QRSs. Likewise, a negative deflection is seen in leads II and aVF from the sixth QRS onward, but is not seen in the first five QRSs. Of interest is the eighth QRS from the end of the tracing. It is wider than the others and is the fusion of a ventricular premature complex with the QRS of the A-V nodal reentrant tachycardia. During this patient's many episodes of tachycardia, there were numerous ventricular premature complexes. Like the one shown here, none of them interrupted the tachycardia because none of them depolarized the A-V node. In the electrophysiology laboratory ventricular premature depolarizations can be introduced without disrupting A-V nodal reentrant tachycardia in virtually all patients. (4)

Could this be A-V reciprocating tachycardia utilizing a bypass tract? It is possible, but unlikely for four reasons. First, in none of the patient's numerous ECGs is there evidence of ventricular pre-excitation--but admittedly many accessory pathways only conduct retrogradely. (5) Second, the very short interval from the beginning of each QRS to the beginning of the retrograde P wave (0.07 seconds) and the retrograde P wave's having a pseudo r' deflection in lead [V.sub.1] and a pseudo S-wave configuration in the inferior leads strongly favor A-V nodal reentrant tachycardia over A-V reciprocating tachycardia utilizing a bypass tract. (5) Third, failure of frequent ventricular premature complexes to terminate the supraventricular tachycardia favors A-V nodal reentrant tachycardia over A-V reciprocating tachycardia utilizing a bypass tract. (4) Finally, and most importantly, the initiation of the tachycardia with a premature P wave with a very long P-R interval is classic for A-V nodal reentrant tachycardia. (4)

Dual A-V nodal pathways can be readily demonstrated in many patients by atrial pacing techniques but have never been shown histologically. Their dual electrophysiologic existence may be the result of the anisotropic properties of A-V nodal and transitional tissue, ie, electrical impulses conduct more rapidly parallel to muscle fibers than perpendicular to them, and the juxtaposition of the different rates of conduction predisposes to reentry. (4)


(1.) Moe GK, Preston JB, Burlington H. Physiologic evidence for a dual A-V transmission system. Circ Res 1956;4:357-375.

(2.) Denes P, Wu D, Dhingra RC, et al. Demonstration of dual A-V nodal pathways in patients with paroxysmal supraventricular tachycardia. Circulation 1973;48:549-555.

(3.) Rosen KM, Bauernfeind RA, Swiryn S, et al. Dual AV nodal pathways and AV nodal reentrant paroxysmal tachycardia. Am Heart J 1981;101:691-695.

(4.) Josephson ME. Supraventricular tachycardias. In: Josephson ME. Clinical Cardiac Electrophysiology: Techniques and Interpretations, 3rd edition. Philadelphia, Pa: Lippincott Williams & Wilkins; 2002:168-271.

(5.) Gonzalez-Torrecilla E, Almendral J, Arenal A, et al. Combined evaluation of bedside clinical variables and the electrocardiogram for the differential diagnosis of paroxysmal atrioventricular reciprocating tachycardias in patients without pre-excitation. J Am Coll Cardiol 2009;53:2353-2358.

D. Luke Glancy, MD Dr. Glancy is a professor in the Section of Cardiology in the Department of Medicine, Louisiana State University Health Sciences Center, New Orleans.
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Title Annotation:ECG of the Month
Author:Glancy, D. Luke
Publication:The Journal of the Louisiana State Medical Society
Article Type:Report
Geographic Code:1U7LA
Date:Mar 1, 2010
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