Why the PR Interval Shortens in WPW Syndrome

A shortened PR interval in Wolff–Parkinson–White (WPW) syndrome is a direct consequence of ventricular preexcitation through an accessory pathway that bypasses the AV node. The key mechanism is not simply “faster conduction”—it is anatomical bypass of the AV nodal delay.

1. The AV Node Normally Creates the Bulk of the PR Interval

Under normal physiology:

• Atrial tissue conducts rapidly via fast Na⁺-channel–dependent propagation.

• The AV node, using slow L-type Ca²⁺ channels, introduces a controlled delay.

• This AV nodal delay is responsible for ~80–90% of the PR interval.

Thus, the PR interval primarily reflects nodal refractoriness, not atrial or Purkinje conduction.

2. WPW Introduces an Alternative Pathway Without Nodal Delay

In WPW, the myocardium contains an atrioventricular accessory pathway (Kent bundle) that:

• Conducts rapidly (Na⁺-channel–dependent)

• Does not exhibit decremental conduction

• Bypasses the AV node entirely

When an impulse travels down this pathway, it reaches the ventricular myocardium before the impulse traversing the AV node can arrive.

This early arrival of ventricular activation is preexcitation.

3. The PR Interval Shortens Because Early Ventricular Depolarization Defines Its End Point

The PR interval ends at the first moment of ventricular depolarization.
In WPW, this moment is determined by:

• Accessory pathway conduction, which reaches the ventricles earlier than AV nodal conduction.

Because this early ventricular depolarization triggers the onset of the delta wave, the PR interval appears short (<120 ms).

It is not that the AV node is conducting faster—the AV node often still conducts normally. The accessory pathway simply beats it to the ventricle, cutting the PR interval short.

4. Delta Wave Confirms Early Ventricular Activation

The slurred upstroke (delta wave) represents:

• Fusion between early ventricular activation (via accessory pathway)

• And later activation through the His–Purkinje system

The presence of a delta wave confirms that ventricular myocardium is being depolarized outside the His–Purkinje network, and its timing is what shortens the PR interval.