AVRT and Accessory Pathways

To understand the ECG in Wolff-Parkinson-White (WPW) syndrome, you simply have to picture a race.

When the sinus node fires, the impulse spreads through the atrium and arrives at two bridges simultaneously. It enters the AV node, and it enters the accessory pathway.

The AV node does its job. It detains the impulse, making it wait.

But the accessory pathway conducts instantly. The impulse flashes down the smuggler's path and begins to activate a small patch of the ventricle early. Because it enters working ventricular muscle (not the fast-conducting His-Purkinje system), it spreads slowly, cell-to-cell. On the ECG, this early, slow ventricular activation slurs the beginning of the QRS complex. We call this slur the Delta wave.

Meanwhile, the impulse that was detained in the AV node finally gets released. It races down the His-Purkinje highway, rapidly activating the rest of the ventricle. This finishes the QRS complex in its normal, sharp fashion.

The result is a fusion beat. A short PR interval (because the ventricle is hit early via the bypass tract) and a slurred, wide QRS (the Delta wave merging into the normal QRS). This is the hallmark of pre-excitation.

Pre-excitation alone just creates a weird-looking ECG. The real danger lies in the circuit. Just like AVNRT, having two pathways with different properties creates the perfect substrate for a continuous loop.

If a premature beat arrives at precisely the right moment—when the accessory pathway is refractory but the AV node is ready—the impulse will travel down the AV node normally. When it reaches the ventricle, it sweeps across the muscle and arrives at the bottom of the accessory pathway.

By now, the accessory pathway has recovered. The impulse shoots up the pathway backward (retrogradely) into the atrium. Once in the atrium, it finds its way back to the AV node. The loop is closed.

This is Orthodromic AVRT. It accounts for about 90% of AVRTs.

Because the impulse travels down the normal conduction system (the AV node and His bundle), the QRS complex is narrow and completely normal. The Delta wave vanishes entirely during the tachycardia. The impulse travels up the accessory pathway to activate the atrium, generating a retrograde P wave.

Crucially, this is a massive circuit. The impulse has to travel all the way down to the ventricles, across the muscle, up the pathway, and across the huge atrium. Because the circuit is so physically large, it takes time. Therefore, the retrograde P wave occurs well after the QRS complex. We see a long RP interval. The P wave separates from the QRS, sitting clearly in the ST segment or T wave.

In about 10% of cases, the circuit spins in the opposite direction. The impulse travels down the accessory pathway and up the AV node.

This is Antidromic AVRT.

Because the ventricles are being activated entirely through the accessory pathway, entering raw muscle outside the His-Purkinje system, ventricular depolarization is slow and bizarre. The QRS complex is maximally pre-excited. It is wide, ugly, and indistinguishable from Ventricular Tachycardia (VT) on a surface ECG.

In an unstable patient with a wide complex tachycardia, always treat it as VT. But if they have a known history of WPW, antidromic AVRT is the smuggler's path running in reverse.

Most reentrant tachycardias are uncomfortable, but rarely lethal. However, WPW harbors a deadly trap.

If a patient with WPW develops Atrial Fibrillation, the atrium begins firing chaotic impulses at 400 to 600 beats per minute. The AV node, doing its job as a tollbooth, decrements. It blocks most of these impulses, allowing perhaps 150 beats per minute to reach the ventricle.

But the accessory pathway has no decremental properties. It has no tollbooth. It simply conducts 1:1 up to its absolute refractory limit.

If the accessory pathway has a short refractory period, it might allow 250, 300, or even 350 beats per minute to slam directly into the ventricles. The ECG will show an incredibly fast, irregular, wide-complex rhythm (because the beats are pre-excited).

A ventricle pushed to 300 beats per minute cannot sustain cardiac output. It will rapidly degenerate into Ventricular Fibrillation. This is why giving an AV-nodal blocking agent (like adenosine, beta-blockers, or calcium channel blockers) in this scenario is a catastrophic error. Blocking the AV node only removes the tollbooth completely, forcing 100% of the atrial fibrillation down the smuggler's path.