AVRT and Accessory Pathways
When a congenital bridge bypasses the AV node's tollbooth, the stage is set for a massive macroreentrant circuit.
The AV node is supposed to be the only electrical bridge between the atria and the ventricles. It is the heart's natural tollbooth. It slows the impulse down, giving the ventricles time to fill, and protects them from erratic atrial storms.
But what happens when there is a smuggler's path?
In roughly 1 in 1000 people, the embryonic fibrous ring that separates the top and bottom chambers doesn't seal completely. A tiny, microscopic strand of working myocardium gets left behind, connecting the atrium directly to the ventricle. This is called an accessory pathway.
Unlike the AV node, this strand has no tollbooth. It does not delay conduction. It does not pause. It simply fires, handing the electrical spark straight into ventricular muscle. This anatomical quirk gives birth to pre-excitation and the dramatic tachycardia we call AVRT.
The Race to the Ventricle
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.
The Macroreentrant Circuit
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 larger circuit than AVNRT. The impulse has to travel all the way down to the ventricles, across the muscle, up the pathway, and across the atrium. Because the circuit is physically larger, it takes more time for the wave to return to the atrium. Therefore, the retrograde P wave separates visibly from the QRS, sitting in the ST segment or T wave. This is still a short RP tachycardia (RP < PR), but the RP interval is noticeably longer than in AVNRT, where the P wave is buried in or immediately after the QRS.
Down the AV node (narrow QRS), across the ventricle, up the accessory pathway, across the atrium. A larger loop than AVNRT, producing a short RP tachycardia with a visible retrograde P wave in the ST segment.
Antidromic AVRT
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 a wide-complex tachycardia of ventricular origin on a surface ECG (Chapter 9 tackles that differential).
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.
› Deep Dive: The Mahaim Fiber
Accessory pathways usually conduct fast, like normal working myocardium. Mahaim fibers are the exception. These are atriofascicular pathways that connect the right atrium (typically near the tricuspid annulus) to the right bundle branch or the distal RV myocardium. Unlike typical bypass tracts, Mahaim fibers exhibit decremental conduction: the faster you drive them, the slower they conduct. This property resembles AV nodal tissue more than normal myocardium.
During sinus rhythm, the Mahaim fiber conducts anterogradely but slowly, so pre-excitation is minimal or absent on the resting ECG. The tachycardia circuit runs anterograde down the Mahaim fiber and retrograde up the His-Purkinje system and AV node. Because ventricular activation begins in the RV via the pathway, the QRS has a characteristic LBBB morphology with a relatively narrow QRS (often 120-140 ms) and left axis deviation.
Adenosine often terminates Mahaim tachycardia because the pathway responds to autonomic modulation like AV nodal tissue. Ablation targets the atrial insertion of the pathway along the lateral tricuspid annulus. During ablation, a characteristic finding is the appearance of an accessory pathway potential, a discrete sharp signal between the atrial and ventricular electrograms, confirming catheter position on the fiber itself.
The Medical Emergency: AFib in WPW
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.
To cure WPW, we must find the microscopic strand of muscle and ablate it. We map it by looking for eccentric atrial activation.
Normally, if an impulse travels backward from the ventricle to the atrium, it goes up the His bundle and AV node. Therefore, the earliest atrial signal is recorded right in the middle of the heart, near the septum.
But during Orthodromic AVRT, the impulse travels up the accessory pathway. If the pathway is on the far left wall of the heart, the impulse enters the left atrium first. When we place a diagnostic catheter inside the Coronary Sinus (which wraps around the back of the left atrium), we see the earliest atrial signal way out laterally.
The atrial activation sequence is eccentric; it starts on the outside edge and moves inward. By moving our ablation catheter to the exact spot where the atrial signal is earliest, we find the atrial insertion of the pathway. One burn severs the bridge forever.
Key Takeaways
- Pre-excitation (WPW): The Delta wave is caused by early, slow ventricular activation via the accessory pathway, fusing with the normal QRS.
- Orthodromic AVRT: Down the AV node, up the accessory pathway. Narrow QRS, short RP tachycardia with a visible retrograde P wave (RP longer than AVNRT but still RP < PR).
- Antidromic AVRT: Down the accessory pathway, up the AV node. Wide, maximally pre-excited QRS. Looks identical to VT.
- AFib with WPW: A medical emergency. The pathway bypasses AV node protection. Avoid AV nodal blockers, which drive more impulses down the pathway.
- Mapping: Retrograde conduction up a left-sided pathway produces eccentric atrial activation (earliest signal in the lateral Coronary Sinus).