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.

What the numbers are, and what they are not

Each drug carries a set of multipliers on the cellular model: a fraction of phase 0 sodium current removed, a multiplier on action potential duration, a shift in the refractory fraction. Sodium and calcium block compose multiplicatively, so stacking two blockers reduces what is left rather than subtracting past zero, and a combination that leaves less than about 13% of phase 0 is refused rather than printed. The QRS estimate follows cable theory, where conduction velocity scales with the square root of upstroke velocity, so QRS scales as one over the square root of the phase 0 multiplier. These are illustrative magnitudes for teaching the shape of each class effect; they are not a dose-response model, no agent carries a sourced per-dose change in QRS or QTc, and there is no pacing rate, so use-dependent and reverse use-dependent block are described in the mechanism notes rather than produced by the model. Printed estimates that cross a guideline threshold are flagged with the guideline that names them.

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 ventricular mode, QRS width tracks phase 0 upstroke velocity and QT tracks action potential duration. In Purkinje mode the strip is a ventricular reference whose QRS widens with the Purkinje upstroke while the QT holds, and in atrial mode it is a fixed ventricular reference throughout, because an atrial action potential contributes only the P wave. In pacemaker mode the strip holds a normal ventricular complex and only the cycle length changes.