Mechanism

Excluding atrial fibrillation and atrial flutter, the most common SVT is AVNRT, accounting for approximately 60% of cases. AVNRT is characterized by the presence of two distinct pathways within the AV node that facilitate reentry by allowing an electrical impulse to cycle in one direction, creating a reentrant loop or circuit. The presence of two pathways is often referred to as dual AV nodal physiology. One pathway has a short conduction time but a long refractory period (fast pathway); the second has a long conduction time but a short refractory period (slow pathway). The differing conduction times and refractory periods of each pathway allow the electrical impulse to cycle in only one direction, using one pathway in the anterograde direction and one pathway in the retrograde direction. The pathways are joined into one final common pathway before impulses exiting the AV node to continue to the bundle of His (Figs. 27-1 and 27-2).

Figure 27-1 Representation of dual-pathway physiology.

Figure 27-2 Typical electrocardiographic recordings and anatomic representation of the common supraventricular tachycardias.

AV, atrioventricular.

From Delacretaz E. Clinical practice. Supraventricular tachycardia. N Engl J Med. 2006;354:1039–1051.

Typical or common AVNRT, which accounts for 95% of cases, employs the slow pathway in the anterograde direction and the fast pathway in the retrograde direction of the circuit. This is also termed slow-fast tachycardia. Conversely, in atypical or uncommon AVNRT, the anterograde limb of the circuit is rapidly conducting and the retrograde limb is slowly conducting, otherwise called fast-slow tachycardia.

Initiation of typical AVNRT is usually caused by a critically timed single premature atrial beat. Under normal circumstances, sinus beats are initially conducted down both the fast and slow pathways. The signal through the fast pathway reaches the final common pathway before the impulse in the slower conducted limb and proceeds to exit the AV node. When the conduction through the slow pathway ultimately reaches the final common pathway, it collides with the fast pathway, which is now refractory, unable to support any impulse. The collision essentially extinguishes the slowly conducted impulse.

In the case of a critically timed atrial premature beat, however, the circumstances may be present to initiate AVNRT. Following a normal sinus beat that was conducted over the fast pathway, the fast pathway remains refractory longer than the slow pathway (fast pathway: rapid conduction, long refractory period; slow pathway: slow conduction, short refractory period). When a premature atrial beat reaches the AV node and finds the fast pathway refractory, it is transmitted anterogradely down the slow pathway. Upon reaching the final common pathway, the fast pathway has now recovered and is able to accept the impulse. The fast pathway is activated, conducting the impulse retrogradely, depolarizing the atria and then reentering the slow pathway to conduct anterogradely again. This creates a sustained reentrant tachycardia.

In a similar fashion, remembering that the slow and fast pathways serve equal but opposite functions in atypical as compared with typical AVNRT, a ventricular premature beat may initiate the reentrant tachycardia by entering the slow pathway and conducting retrogradely. The circuit is then created in a manner similar to that described for common AVNRT.

ECG Recognition

Typical and atypical AVNRTs usually present as a narrow-complex tachycardia, although concomitant aberrancy/bundle branch block can rarely create a wide-complex tachycardia. Several differences in ECG characteristics may help distinguish between typical and atypical AVNRTs: P-wave morphology (width), P-wave location, and mechanism of initiation.

It should first be noted that the P-wave axis for both types is similar. In both, activation of the atria occurs in an inferior-to-superior direction (retrograde conduction of the fast pathway in typical or the slow pathway in atypical AVNRT). This produces a negative (inverted) P-wave axis in the inferior leads II, III, and aVF. The AV node is located posteriorly, creating posterior-to-anterior activation of the atria and therefore producing a positive (upright) P-wave axis in lead V₁. P-wave width, on the other hand, differs in the two forms. In typical AVNRT, the P wave tends to be narrow, whereas in atypical AVNRT, it is wider because of the differences in anatomic location of the fast and slow pathways that activate the atria.

Typical AVNRT can be distinguished from atypical AVNRT on an ECG by comparing the location of the P wave in relation to the QRS complex. In typical AVNRT, near-simultaneous conduction to the ventricles via the slow pathway anterogradely and to the atria via the fast pathway retrogradely may rarely make P wave visible on the ECG because they are inscribed in the QRS complex. When visualized, the P waves occur in close proximity to the QRS, creating a short RP interval (RP interval less than half the RR interval). This can sometimes manifest as a “pseudo-S wave” in the inferior leads II, III, and aVF, and a “pseudo-R wave” in lead V₁ (Fig. 27-3). Typical AVNRT, therefore, is an example of a “short-RP” tachycardia. In contrast, P waves are clearly visible in atypical AVNRT. Due to retrograde conduction through a slow pathway, the presence of the P wave occurs later than the QRS complex, resulting in an RP interval that is frequently longer than half the RR interval, called a long RP tachycardia (Fig. 27-4).

Figure 27-3 Atrioventricular nodal reentrant tachycardia.

Arrows show pseudo-S waves in II and pseudo-R waves in V₁.

Figure 27-4 Long RP tachycardia with inverted P waves highlighted by arrow.

Another ECG feature that may help to distinguish typical from atypical AVNRT is the mode of initiation of the reentrant circuit. Though obviously difficult to obtain on a standard 12-lead ECG, should a rhythm strip be available that demonstrates an initiating atrial premature beat, the diagnosis is more likely typical AVNRT. A ventricular premature beat is more likely to precipitate an atypical AVNRT (Table 27-1).

Table 27-1 Clinical Clues to the Differential Diagnosis of Supraventricular Tachycardia

Mechanisms

Approximately 30% of SVTs result from the presence of an accessory AV connection causing an AV reentrant circuit. Similar to the mechanisms described with AVNRT, AVRT requires the presence of two distinct pathways: the normal AV conduction system, which almost always serves as the anterograde limb of the circuit, and an AV accessory pathway (AP) that usually forms the retrograde limb. The presence of two circuits with different conduction velocities and different refractory periods sets up the milieu for the possibility of a reentrant rhythm when initiated by a critically timed atrial or ventricular premature beat.

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