Each patch of tissue is a node of the Mitchell–Schaeffer minimal ionic model — a two-variable simplification of cardiac excitation used to study reentry (Mitchell & Schaeffer, 2003). Voltage v and a gate variable h evolve as:
dv/dt = h·v²(1-v)/τ_in − v/τ_out + D·∇²v
dh/dt = (1-h)/τ_open if v < v_gate (recovering)
= −h/τ_close if v ≥ v_gate (inactivating)
The D·∇²v term is diffusive electrotonic coupling between neighboring cells — the same cable-equation mechanism that carries the wavefront across real atrial muscle, here setting the effective conduction velocity.
- S1 fires a planar wave from the left edge, like a normal sinus beat sweeping the atrium.
- S2 fires a second, spatially limited beat. If timed while part of the S1 wave's wake is still refractory, the S2 wavefront can only propagate one direction — a unidirectional block — curling around the refractory tail into a self-perpetuating spiral: a reentrant circuit (rotor). This is the classic S1-S2 induction protocol used in electrophysiology labs.
- τ_close sets the refractory period (tissue "wavelength" = conduction velocity × APD). Shorter τ_close shrinks the wavelength, making the tissue far more likely to sustain a rotor once one starts — the mechanism linking short atrial refractoriness to fibrillation persistence.
- Fibrosis scatters non-conducting patches through the tissue. Diffuse fibrosis fragments a single rotor into multiple meandering wavelets — the multiple-wavelet hypothesis of atrial fibrillation.
The color map runs resting (blue) → depolarized (white/red); height also rises with local voltage so the wavefront reads as a moving ridge, and a true rotor appears as a spiral that never dies out on its own.