The ECG Blog

Filed under: Re-entry arrhythmias

AV Nodal Reentry Tachycardia (AVNRT)

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Patient: 55 y/o female with claudicatio intermittens. No cardiac history, but allegedly one similar episode 10 years ago when her heart “went crazy” for 20 minutes. When EMS arrives: Sudden onset of strong palpitations, dizziness, chest pain, paleness and mild diaphoresis. Blood pressure is 132/92 and the the patient has a rapid, regular pulse at around 180 mg. A 12 lead ECG is obtained.

ECG: The ECG shows a regular and fast narrow-complex tachycardia, probably of supraventricular origin. Inverted P waves are seen in V2 during the early phase of the T wave.

The patient arrives in the ER just a few minutes later and a new 12 lead is obtained

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ECG description:

Regular, narrow-complex tachycardia.
150 bpm
No visible P waves preceding QRS
Retrograde P waves with an RP interval of 120ms. Inverted in inferior leads II, III, aVF and upright in aVR and right precordial leads V1 and V2. Also called pseudo S-waves (inferior leads) or pseudo R-waves (right precordial).
Cardiac axis is normal at approx. 50°

Interpretation: A narrow-complex tachycardia is most likely to be supraventricular in origin, as this indicates normal His-Purkinje impulse propagation and simultaneous ventricular activation. However, there is no P wave preceding the QRS complex to indicate that a sinoatrial origin of the propagated impulse. The regularity rules out atrial fibrillation, and the fact that the P waves are not visible could of course just be due to the tachycardic rate. At a first glance we can only conclude that this is a supraventricular tachycardia. A natural next move would be to perform carotid pressure or other vagal manuevres to induce atrioventricular block in order to help us differentiate this rhythm. With the same intentions, and if carotid pressure doesn’t work, adenosine would be the drug of choice here.

A closer look

However, differentiation stop here, as the diagnosis lies right in front of us, clearly visible in both the ECGs. Although there is no sign of atrial activity preceding the QRS, take a look after the QRS complex. In all inferior leads, II, III and aVF, an inverted P wave with an RP interval of 120 ms followes each QRS complex. The same P wave with the same RP interval can be spotted in the right precordial leads V1 and V2, as well as in aVR. Logially, the P wave is upright in these leads. This means that the atrias are depolarized in a retrograde fashion, after ventricular systole.

Two tracts

The AV node normally has one conductive tract or approach leading the impulse to it. Some people however, have two. The two tracts are separated from each other and the rest of the myocardium by nonconductive tissues. When there are two tracts, these are named the anterosuperior or the fast “tract” and the posteroinferior or the “slow” tract. The two pathways, or tracts, are functionally different:

Anterosuperior / fast tract

very rapid impulse conduction
slow refractory time

Posterosuperior / slow tract

rapid impulse conduction
slow refractory time

Intranodal impulse conduction and establishment of the AV nodal reentry circuit

Consider a normal impulse coming from the sinoatrial node or the atria. When reaching the AV junction, it hits the two tracts simultaneously, and they will both start conducting the impulse at the same time. The fast tract however, will conduct the impulse faster. This way, the fast tract leads to AV node depolarization. The impulse travels further down His-Purkinje and causes ventricular contraction and a normal, narrow QRS. The electrical impulse will however spread in all directions, and some of it will also travel retrogradely and back up through the slow tract. Remember, this tract is much slower, and the impulse travelling retrogradely will meet the impulse still working its way down towards the AV node. The two impulses will collide and they essentially cancel each other out. Normally, this is what happens, and everything works out fine.

Now imagine that an ectopic site in the atria decides to fire prematurely. The premature impulse will reach the two tracts and and find the slow tract ready to accept it, because it has a shorter refractory period. The fast tract will be busy while it is still refractory from the previous impulse. The impulse is being conducted to the AV node through the slow tract, and when the AV node is depolarized, ventricular contraction and QRS occurs. It is the nature of electricity to spread in all directions possible, and the impulse will also this time try to spread retrogradely. Since it was conducted through the slow tract, the fast tract has had time to recover from its long refractory time and is now open for conduction again. The impulse spreads back up the fast tract. However, this time it will not be cancelled out by an impulse coming down simultaneously through the tract. When the retrograde impulse has been conducted back up again, it will now find the slow tract open for business again, because of the fast refractory time. And voilá, a reentry circuit is born. As you may understood, when the retrograde impulse reaches the atria again, atrial depolarization occurs. And as atrial activation happens after ventricular activation, the P wave follows the QRS complex. The P wave is inverted in leads II, III and aVF because it travels away from these leads.

Adenosine effect

This patient was given a 6mg rapid iv push of adenosine. Here is the electrocardiographic display of what happened. These complexes are extracted from the full rhythm strip presented further down.