Mechanism of Delta Waves: Depolarization Fusion

When you look at a delta wave on the ECG, you’re seeing more than just “pre-excitation.” You’re watching two separate depolarization fronts collide in real time. The classic slurred upstroke of the QRS is simply the surface expression of a fusion beat—one that happens on every single beat in patients with manifest accessory pathways.

Two Conduction Systems, Two Speeds

Under normal physiology, atrial impulses funnel through the AV node, where conduction slows dramatically before being delivered to the His–Purkinje system. When an accessory pathway bypasses this AV nodal delay, part of the ventricle begins depolarizing early through slow, myocyte-to-myocyte conduction.

This creates two very different vectors:

• A slow, early wavefront from the accessory pathway (AP), spreading across adjacent ventricular myocardium.

• A fast, later wavefront originating from the His–Purkinje system after the AV nodal delay.

Fusion of Wavefronts = Delta Wave

These two depolarization fronts meet and merge within the ventricular myocardium. Because the AP-mediated depolarization arrives first, the earliest portion of the QRS represents this sluggish, non–Purkinje activation. On the ECG, that early low-slope vector translates into the delta wave—a slow initial rise of the QRS.

The remainder of the QRS is shaped by the rapidly spreading His–Purkinje activation, which overtakes and dominates the majority of ventricular depolarization. The final QRS morphology therefore reflects a weighted combination of:

• How early the AP activates the ventricle

• How much myocardium the AP wavefront can recruit before Purkinje activation arrives

• The relative vector orientation of the AP’s early depolarization

What Controls Delta Wave Prominence?

Several anatomic and electrophysiologic factors influence how “visible” the delta wave becomes:

• Accessory pathway location: Septal pathways often generate smaller delta waves because the Purkinje system quickly overwhelms early activation. Free wall pathways have more time and space to pre-excite myocardium.

• AV nodal conduction time: Faster AV nodal conduction narrows the pre-excitation window, reducing delta prominence; slower AV nodal conduction exaggerates it.

• Accessory pathway conduction velocity: Decremental or diseased pathways produce subtle or intermittent delta waves (e.g., Mahaim fibers, intermittent pre-excitation).

• Atrial cycle length: Shorter R-R intervals bring AP and AV nodal conduction characteristics into closer competition, altering the degree of fusion beat-to-beat.

Why It Matters Clinically

Understanding the delta wave as a fusion phenomenon clarifies several practical points:

• QRS morphology in WPW is not a pure AP vector—it’s a composite of AP + Purkinje activation.

• Intermittent delta waves do not mean the pathway is gone, only that the balance between these two pathways has shifted temporarily.

• The degree of pre-excitation is dynamic, explaining why the QRS changes with rate, autonomic tone, medications, and atrial arrhythmias.

This fusion concept also explains why antidromic AVRT produces a very wide QRS—here, the accessory pathway completely drives ventricular activation, eliminating the fusion component entirely.