Cardiac tissue is an excitable medium: a resting cell fires an action potential once a diffusing depolarization wave pushes it past threshold, then stays refractory before it can fire again. This panel integrates the Barkley model, a standard two-variable reduction of that behaviour used to study reentrant arrhythmias:
∂u/∂t = D∇²u + (1/ε)·u(1−u)(u−(v+b)/a)
∂v/∂t = u − v
u is the fast "voltage" variable (depolarization), v is the slow recovery variable, and D∇²u is diffusive current spreading through the tissue sheet — the height and colour of each block above track u in real time.
- Seed Rotor — breaks an activation front to create a single spiral wave, the reaction-diffusion analogue of a reentrant circuit (e.g. monomorphic VT).
- Excitability (a) and time-scale (ε) control the wavefront's curvature sensitivity and excitation duration. Raising ε or lowering a shortens and narrows the excitable wake behind the front — past a critical point the spiral core meanders and the arm tears into independent daughter wavelets. This spontaneous spiral wave breakup is a leading model for how a single reentrant rotor degenerates into the spatially chaotic activity of ventricular fibrillation.
- Diffusive coupling (D) sets how fast excitation spreads between neighbouring cells (conduction velocity); lowering it also destabilizes wavefronts and promotes breakup, mirroring how fibrotic or ischemic tissue with reduced coupling is pro-fibrillatory.
- Ectopic Beat fires a random premature stimulus into the sheet — timed into vulnerable, partially refractory tissue it can itself seed a new rotor, just as a premature ventricular contraction can trigger reentry clinically.
Time and space here are the model's own dimensionless units (standard for reaction–diffusion excitable-medium models), not calibrated milliseconds — the qualitative route to breakup is what this simulation reproduces faithfully, not absolute cardiac timing.