AV Node Reentry Tachycardia (AVNRT)

As a non-invasive electrophysiologist, I have always had a problem understanding AVNRT. As a result, I set out to create a “Fun with ECGs” that explained the ingredients required to initiate and maintain the arrhythmia.

As its name implies, AVNRT is a reentrant junctional or supraventricular tachyarrhythmia which involves the fast and slow pathways within the AV node creating a self-perpetuating circus movement. It can be divided into typical (slow-fast) or atypical (fast-slow) as well as several rarer forms related to more than one slow or fast pathway with similar electrophysiological properties. On the ECG, they can be identified and differentiated by the positioning of the P wave in relation to the QRS complex, which in turn is related to the direction of the re-entrant AV nodal circuit. However, in about 60% of cases, the P wave is buried in the QRS/T and cannot be identified on the surface ECG.

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Typical AVNRT  (slow-fast) is by far the most common of the junctional tachyarrhythmias (>80%) and frequently occurs in young, otherwise healthy females. It starts abruptly, often provoked by dehydration, exertion, caffeine or alcohol. The tachycardia is frequently initiated by premature atrial ectopy which finds the fast pathway refractory and conducts anterograde via the slow pathway. With an echo beat, a reentry circuit may be created. The term slow-fast describes its movement in the AV node. The ventricular rate of these tachycardias is dependent on the electrical properties of these pathways and is usually in the range of 140 to 260 bpm.

On the ECG, the retrograde conduction to the atrium resulting in an inverted P wave is via the fast pathway (F) and hence the R-P timing is short. Consequently, the P wave may be embedded within or just beyond the QRS, creating a “pseudo” wave (P).

Apart from critical timing, to create AVNRT, the following AV nodal electrophysiologic properties are necessary:

• Dual AV nodal pathway physiology
• Retrograde conduction
• Echo beats

Let us discuss these in order.

Dual AV nodal pathway(s) physiology or simply dual AV nodal physiology results from two ill-defined extensions of the AV node creating different pathways for the propagating wave of depolarization, linking the atria and ventricles. These pathways are very familiar to the interventional electrophysiologist, but otherwise poorly understood by general cardiologists. Although, probably present in all human hearts, they are only occasionally recognised on the ECG as the cause of PR extension, retrograde VA conduction, echo beats and reentry tachyarrhythmias. One of these, the fast pathway lies within the anterior section of the triangle of Koch, whereas the other, the slow pathway lies adjacent to the coronary sinus and posterior tricuspid annulus.

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Their electrophysiology characteristics are as follows:

• Fast pathway: Faster conduction velocity but slower to recover, due to a longer refractory time.
• Slow pathway: Slower conduction velocity but quicker recover, due to a shorter refractory period. 

As the normal wave of atrial depolarization propagates from the sinus node in an inferior direction, it approaches the AV junction at multiple sites and enters both pathways. Because the fast pathway has a shorter conduction time, it reaches its distal connection and commences retrograde concealed depolarization of the terminal portion of the slow pathway, rendering it refractory. The result is the “normal” PR interval. 

In those patients whose ECGs are able to demonstrate slow pathway anterograde AV conduction, it is possible to create scenarios where the fast pathway blocks because of its longer refractory period allowing transfer of conduction to the slow pathway resulting in the abrupt appearance of a longer PR interval with a range of 350 ms to 550 ms. 

At night, the sinus rate is slower, and conduction is via the fast pathway with a 200 ms PR interval. During the day, the fast pathway may block as a result of the faster sinus rate and conduction is via the slow pathway with a 480 ms PR interval. 

Should the prolonged PR interval with slow pathway conduction be called first degree AV block as the changes are physiological? This change in PR interval may not be recognised as slow pathway conduction and it is thus important to observe the abrupt change in PR interval to confirm the transfer of conduction from one pathway to the other. Again are these changes autonomic nervous system influenced (extrinsic) or maybe pathology in the fast pathway (intrinsic)?  In most cases, where dual AV nodal pathways physiology is demonstrated, the fast pathway conduction is 200 ms or more suggesting some intrinsic disease may be required to trigger slow pathway conduction. 

To recognize the transition on the ECG, it is important to understand the factors that allow slow pathway activation (onset) or reversion back to fast pathway conduction (offset).

Slow pathway conduction onset:

The transition from fast pathway to slow pathway assumes fatigue in the fast pathway usually due to increase in the heart rate and shortening of the  P-P interval or atrial ectopy.  Sometimes there are no obvious triggers.

• No discernible change in the sinus rate. 

• Atrial ectopic.

• Ventricular interpolation.

• Wenckebach AV block

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Slow pathway conduction offset: 

The return to fast (normal) AV conduction requires a slowing or pause in the sinus rate. 

• Nocturnal heightened vagal tone.

• Sinus pause (yellow highlight). 

• Junctional ectopic (red highlight).

• Ventricular ectopic compensatory pause.

• Interpolated ventricular ectopic (yellow highlight).

• Wenckebach AV block pause.

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Retrograde conduction implies conduction from an ectopic site to the atrium via the AV node or accessory pathway. II results in a P wave configuration which differs from an anterograde P wave, and in most ECG leads is inverted. The site from where the impulse originates can be the AV node, Bundle of His, distal conducting system or the body of the ventricles including ventricular pacing. On the ECG, the QRS complex usually precedes the inverted retrograde P wave but on occasion may follow it. 

 There is controversy as to whether anterograde and retrograde conduction use the same AV pathways. Although dual AV nodal pathways may play a role, some authorities believe that within a pathway, there are separate anterograde and retrograde channels. This might explain why bidirectional AV conduction may not have the same timing. When  AV nodal disease is present, it becomes more complicated. For instance, with complete AV block, there is no anterograde conduction but in about 10% of cases, retrograde conduction is possible.

The two main sites for the ectopic focus that results in retrograde conduction are the ventricles and AV junction. 

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Ventricular ectopy

With ventricular ectopy and VA conduction, the inverted P wave lies in the ST segment or T wave of the ectopic with the timing of the conduction being from the onset of the QRS to the commencement of the P wave or where it is best recognised. The timing is referred to as the RP interval. It is not always easy to recognise these P waves, which are frequently mistaken for non-conducted sinus P wave. 

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When retrograde conduction is delayed, there is a long RP interval  (first degree VA block) and the inverted P wave may emerge from the ectopic T wave and easily identified.

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Ventricular arrhythmias

Retrograde conduction can be recognised with ventricular arrhythmias. Because VA conduction is often fragile, 1:1 conduction usually only occurs with slow ventricular rhythms.   

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Unlike AV conduction which is robust, VA conduction is fragile and as the ventricular rate increases, VA blocks such as 2:1 occur (section 11.7).

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Junctional ectopic/rhythm

With junctional rhythm, there are two scenarios of retrograde P waves.

The inverted P wave follows the QRS.  The ectopic focus lies low in the AV junction, allowing the anterograde wave to depolarize the ventricles well before the retrograde wave slowly traverses the AV junction to depolarize the atria (red arrows).  

The inverted P waves follow the QRS and lies in the ST segment/T wave.

The inverted P wave precedes the QRS.  The ectopic focus lies high in the AV junction allowing the retrograde wave to rapidly depolarize the atria first, then slowly traverses the AV junction anterograde to depolarize the ventricle (red arrows).

Inverted P waves with short PR intervals. 

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Echo beats  or reciprocal beats are propagating electrical complexes that return and reactivate their site of origin. For teaching, it is easier to remember or say echo beats, although reciprocal beats are a more precise description. They are great mimickers and can be very hard to diagnose even when the footprints are recognised. For this reason, echo beats are frequently missed or more likely misdiagnosed. An echo beat will occur if the critical timing of a retrograde P wave allows it to propagate anterograde to the ventricle.  As with retrograde conduction, the most common initiating focus is a junctional ectopic or rhythm although atrial ectopics,  ectopic atrial rhythms, ventricular ectopics, ventricular pacing and sinus rhythm with a prolonged PR interval may all generate echo beats with appropriate timing. 

To generate echo beats, the impulse must be propagated retrograde to the atrium and then anterograde to the ventricle. To do this, dual AV nodal pathway physiology may be required. A single reentrant conducted atrial complex is seen as an echo beat, whereas a continual circus movement is a reentrant rhythm or tachycardia. Because of the timing, they may demonstrate aberrant ventricular conduction, usually with a right bundle branch block configuration.

How are echo beats created?

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Junctional ectopic or slow junctional rhythm

• Slow junctional rhythm without retrograde conduction (red highlight).
• The next complex (green highlight) has both anterograde conduction to the ventricle and retrograde conduction to the atrium (pink arrows).
• The atrial impulse can now conduct anterograde to the ventricle via the previously blocked and now non-refractory AV pathway (blue arrow, blue highlight), resulting in an echo beat (blue highlight).

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If the echo P wave is very premature, it may conduct to the ventricle with aberrant ventricular conduction.

A similar example of a junctional rhythm with echo beats mistakenly called ectopics.

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Atrial ectopic

To generate an echo beat, the ectopic should be premature and the atria non-refractory to the retrograde conduction. The mechanism involves dual AV nodal pathways. It may be impossible to differentiate echo beats from either atrial couplets or atrial interpolated beats and the diagnosis depends on differing P waves, which is usually very subtle

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If the atrial ectopic is very premature then it may be conducted with aberration.

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If dual AV nodal pathways are required for echo beats, could a combination of an AV nodal and pre-excitation pathways do the same thing?

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Ventricular ectopic

With appropriate timing, a ventricular ectopic with retrograde conduction can result in an echo beat. Again it is likely that dual AV nodal physiology is involved and a junctional beat precedes the ventricular ectopic, rendering the fast pathway refractory.

Another example of an atrial or junctional ectopic (blue arrow), prior to a ventricular ectopic (red highlight) and an echo beat (pink arrow).

Echo beats from a ventricular focus can be difficult to differentiate from couplets.

The report was a ventricular couplet (green highlight) with pre-excitation. There is a narrow QRS ventricular ectopic (red highlight) with fast pathway retrograde conduction (pink arrow) and anterograde slow pathway conduction with aberrant ventricular conduction. 

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Interpolated ventricular ectopics and echo beats may occur in the same tracing.

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Can slow pathway conduction create an echo beat?

Sinus rhythm (red arrows) with a prolonged PR interval (400 ms) due to slow pathway conduction (S). With recovery of the fast pathway, there is retrograde conduction (pink arrow, F) and an echo beat via the slow pathway (red highlight). With a pause in fast pathway conduction, there is a return to a shorter PR interval, albeit still slow  (300 ms).  

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The genesis of AVNRT

With appropriate timing, echo beats can replicate, creating a reentry circuit.

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With degenerative disease in the AV junction, a “slowly” conducting reentry pathway can be created on the ECG. Because of delayed conduction, Wenckebach block and refractoriness results in short runs. Such ECGs provide a window into the mechanisms by which the circus movements of the faster AVNRT are established.

Here is an example.

Get out your callipers. Put in your coloured arrows and highlight and see if you can create the reentry circuit.

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My interpretation follows.

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Sinus bradycardia (red arrows) with first degree AV block (240 ms) and a bundle branch block.

Short run of a tachycardia (yellow highlight) with inverted P waves (pink arrows)

Retrograde conduction with the first inverted P wave (pink arrow) 420 ms  after the onset of the sinus generated QRS. 

The retrograde P wave conducts to the ventricle along the slow pathway ( S1, 320 ms) as an echo beat . 

Once again there is anterograde conduction this time via the fast pathway (red highlight, F1) resulting in an inverted P wave (broad purple arrow) 

Anterograde conduction (red highlight, S2) follows.

The cycle is repeated with F2, S2, F3 (red highlight, broad purple arrows).

After S4, there is no retrograde conduction (red highlight, purple shadowed stippled P wave) and the reentry rhythm is abruptly terminated. This results from an increasing AV nodal Wenckebach block in the slow pathway (S1 320 ms to  S4 440 ms).

Now imagine this with fast AV/VA conduction and you have AVNRT.

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Harry Mond