Atrioventricular Nodal Re-entrant Tachycardia (AVNRT) is the most common cause of paroxysmal supraventricular tachycardia, and is characterised by:

  • Absent P waves, or inverted P waves after the QRS complex
  • Narrow (<120 ms) QRS complex
  • Heart rate 140-250 bpm, with a regular rhythm
  • Can occur in the young and healthy
  • Three quarters of patients are female

AVNRT should not be confused with atrioventricular re-entrant tachycardia (AVRT) seen, for example, in Wolff-Parkinson-White syndrome. In AVNRT, the AV node becomes the pacemaker, firing action potentials in a retrograde direction to the atria (as well as in the normal manner to the ventricles). In AVRT, there is an accessory pathway which carries action potentials from the ventricles back to the atria.

Common AVNRT (slow-fast AVNRT)

AVNRT can occur in patients who have two pathways in (or around) their AV node (Figure 1). We know that these pathways exist because if the slower one is surgically ablated, AVNRT can be prevented from occurring. The normal pathway conducts action potentials slightly more quickly than the slower, alternate route. Because of this, action potentials following the slow pathway reach the fast pathway again slightly later, after the action potential has already passed through and when it is temporarily refractory to stimulation. So, ordinarily, the existence of the slow pathway is of little clinical significance. However, a perfectly timed premature atrial contraction (PAC) can throw a spanner in the works and all hell breaks loose.

common avnrt

Figure 1: : Normal conduction of the cardiac action potential from the sinoatrial node, around the atrium down to the atrioventricular node. In patients susceptible to AVNRT, there are two pathways through the AV node (or around it, depending on who you ask). The normal pathway conducts action potentials rapidly, and has a long refractory period. The other pathway conducts more slowly, but has a shorter refractory period. The cardiac action potential travels down both pathways, but by the time the action potential on the slower pathways reaches the faster one, the fast pathway is already refractory, its action potential having already passed through. So, ordinarily, nothing much comes of the slow pathway. The exception to this rule is a perfectly timed ectopic beat (premature atrial contraction, or PAC) - arising elsewhere in the atrium - arriving at the SA node while the fast pathway is refractory. Under these circumstances, the slow pathway (which becomes excitable more rapidly than the fast pathway) carries the action potential to the fast pathway, just in time for the fast pathway to become excitable again.

The slow pathway doesn’t remain refractory for as long as the faster pathway, so premature atrial contraction (PAC) arising from outside the SA node can excite the slow pathway while the faster one is still refractory. In the time it takes for the action potential on the slow route to reach the normal faster route, the latter may have stopped being refractory just in time to be depolarised by the arriving action potential. Cardiomyocytes act as simple electrical cables, so the AP spreads in either direction from here: backwards to depolarise the atria, and forwards to depolarise the ventricles (Figure 2). Because the slow pathway activates the fast one, this fairly common AVNRT is known as “slow-fast AVNRT”.


Figure 2: Initiation and propagation of AVNRT. (a) A chance, premature atrial contraction (PAC) occurs while the fast pathway is still refractory, but the slow pathway has become excitable. If the timing is right, the slow conduction of the action potential means that it arrives at the fast pathway when it too has become excitable again. (b) From here, the action potential is conducted to the ventricles, as normal, but also in a retrograde manner to the atria. Because the slow pathway is refractory for a shorter time, it is excitable when the action potential reaches it (c), and so the cycle begins to perpetuate. The AV node has become the dominant, high speed pacemaker causing contractions of both the ventricles and the atria at roughly the same time.

This process isn’t a single, aberrant event. Once a PAC has initiated a retrograde action potential, a self-perpetuating cycle (AKA circus motion) evolves. When the action potential travels in a retrograde manner up towards the atria, it reaches the start of the slow pathway (which is no longer refractory) and depolarises it, starting the process over again. In this way, the AV node becomes the new pacemaker, constantly firing action potentials to the atria and ventricles at much the same time. This is why the P wave is often absent: it is usually hidden in the QRS complex produced by the almost simultaneous depolarisation of the ventricles. In some cases the atria depolarise slightly after the ventricles, causing the P wave to appear at the end of the QRS complex. When present, the P wave will be upside down because it is travelling in the opposite direction, towards the electrode it normally moves away from.

Uncommon AVNRT (Fast-slow AVNRT)

Most (about 80%) cases of AVNRT occur as described above and are termed “slow-fast AVNRT” because it is the slow pathway that activates the fast one to initiate the process. However, there is a fast-slow variant (or “uncommon AVNRT”). The reason that most AVNRT are slow-fast is that the slow pathway has the shorter refractory period, so spends more time in an excitable state. However, it is possible for a PAC to activate the fast pathway during the shorter period when it is not refractory, it’s just less likely. Once activated, the fast pathway activates the slow one generating a clockwise circus motion (Figure 3).

uncommon avnrt

Figure 3: Uncommon (AKA fast-slow) AVNRT involves the circus motion moving clockwise after the faster pathway is activated by a premature atrial contraction (PAC). This is less likely to occur than the more typical slow-fast AVNRT simply because the longer refractory period of the faster pathway renders it less likely to be depolarised by a PAC. What’s the difference? Because the slow pathway conducts depolarisation to the atria, atrial contraction is more delayed than in typical AVNRT. For this reason, there is an increased likelihood of the inverted P wave following the QRS complex, rather than being buried within it.

AVNRT and the ECG

The absence of the P wave is the typical characteristic of either form of AVNRT and narrow complex tachycardia. There is often some ST depression, but it is generally not flattened and does not reflect ischaemia.

Figure 4: Representations of typical normal and AVNRT ECG recordings (lead II). In AVNRT the P wave is generally absent, but may appear inverted (because it is travelling backwards to the atria) after the QRS complex in some cases. This is more likely in uncommon AVNRT, and it would be most obvious in leads V1-V3 rather than the rhythm traces above.

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