What the simulator draws

The simulator plots one cardiac action potential on a voltage-versus-time axis and redraws it as parameters change. A ghost trace of the selected cell's untreated baseline sits behind the live curve, so every drug effect reads as a difference rather than an absolute. Phase shading labels each phase with its dominant current, from I_Na in phase 0 through I_Ca-L, I_Kr and I_K1, with I_f and I_Ca-T in pacemaker phase 4; the brief phase 1 notch is tinted but not labeled. Refractory period shading is on by default; a threshold line is optional. A measurement strip reports action potential duration, ERP, phase 0 dV/dt, and estimated QRS and QT; in pacemaker mode, heart rate, cycle length, APD, phase 4 slope, and maximum diastolic potential.

The four cell types

Four baselines are modeled. The ventricular myocyte rests near -85 mV with a phase 2 plateau of about 180 ms. The atrial myocyte rests near -80 mV with a shorter plateau and an action potential duration near 200 ms, part of why Class IC sodium blockade works well in atrial fibrillation. The Purkinje fiber rests near -90 mV and carries the longest action potential in the conduction system. The nodal cell has no stable resting potential: it drifts from a maximum diastolic potential of -65 mV up to a threshold of -40 mV, and its phase 0 is calcium-dependent.

Antiarrhythmic drugs by Vaughan-Williams class

Twenty-two agents can be switched on alone or combined: Class IA (quinidine, procainamide, disopyramide), Class IB (lidocaine, mexiletine, phenytoin), Class IC (flecainide, propafenone), Class II beta-blockers, Class III potassium blockers (amiodarone, sotalol, dofetilide, ibutilide, dronedarone), Class IV non-dihydropyridine calcium channel blockers, and adenosine, digoxin and magnesium. Each carries a short mechanism note, including use-dependent block for lidocaine, the CAST caution for flecainide, and inpatient initiation for sotalol and dofetilide. Agents with no meaningful nodal effect are disabled while the pacemaker cell is displayed.

Disease substrates and triggered activity

Four substrates, long QT, short QT, Brugada and ischemia, sit underneath any drug, so agents stack on a diseased baseline instead of replacing it. Adding sotalol to the long QT substrate carries the tool's QT estimate to 722 ms. The ischemia substrate sets resting potential to -65 mV, the depolarized state in which Class IB agents preferentially bind. Overlays add triggered activity: an early afterdepolarization during phase 3, whose amplitude grows as the action potential lengthens, and a delayed afterdepolarization in diastole after full repolarization.

Clinical scenarios and the surface ECG correlate

Eight one-click scenarios set cell type, drug and substrate together: lidocaine for VT, amiodarone for AF, flecainide pill-in-pocket, metoprolol for sinus tachycardia, adenosine for SVT, verapamil for AVNRT, plus two warning cases, sotalol driving torsades and quinidine syncope. Below the trace, a surface ECG panel redraws a single beat from the same parameters. In fast-response modes, QRS width tracks phase 0 upstroke velocity and QT tracks action potential duration; in pacemaker mode the strip holds a normal ventricular complex and only the cycle length changes.