How the model works
A rule-based response selects a later rhythm while disease and drug burden remain.
Electrical and antiarrhythmic actions have explicit rhythm-dependent outcomes. A successful conversion is a selected teaching endpoint, not a calculated probability of success, a guarantee of return of spontaneous circulation or a resuscitation protocol.
The model remembers an eligible underlying recovery rhythm where appropriate. Ending VT need not erase pre-existing AF or conduction disease. Drug-related myocardial and vascular effects can remain even after a rhythm changes.
Temporary ventricular pacing supports selected slow rhythms at a chosen pacing rate and adds ventricular stimuli/capture. It does not restore AV conduction or necessarily synchronize atrial contraction. Atrial-sensed ventricular pacing and atrial-paced ventricular-paced rhythms have separate atrial and ventricular timing.
CRT represents a responsive dyssynchrony example in selected myocardial disease. Pacemaker-mediated tachycardia represents a device tracking loop; routine shock/drug choices do not reprogram the device. Battery, lead threshold, sensing noise and detailed programmable device logic are not modeled.
Synchronized cardioversion has selected successful endpoints for AF/flutter and eligible organized tachycardias. MAT, compensatory sinus tachycardia, escape rhythms and AV block are not routine conversion targets. VF/polymorphic VT do not provide a reliable synchronization target.
Defibrillation can terminate VF/polymorphic VT in the selected successful example. Using an unsynchronized shock on an organized rhythm intentionally demonstrates a possible VF complication; the model is not estimating its probability. Zero-rate asystolic states are not made shockable.
Amiodarone/procainamide/lidocaine responses depend on the arrhythmia, starting pressure, myocardial phenotype, other drugs and pacing. Lidocaine does not convert atrial arrhythmias and can leave nonischemic monomorphic VT unchanged in the chosen refractory example. AF in substantial atrial/valve disease may slow without converting.
Danger examples include pre-excited AF with inappropriate drugs, additive conduction suppression, proarrhythmia with combined antiarrhythmics and hypotension in fragile pump states. Drugs do not independently terminate VF in place of defibrillation. Rate/pressure effects are later response snapshots, not time-to-conversion or toxicity kinetics.
Atropine can improve the modeled cardioinhibitory component and selected vagal pauses/AV block. The vasodepressor component can persist, so restoring rate does not guarantee normal BP. A non-vagal complete block is not assumed to recover simply because atropine is present.