Antiarrhythmics

Mechanisms by class

Antiarrhythmic drugs act via distinct ion channel or receptor mechanisms (classically the Vaughan Williams classification: sodium channel blockade, beta-blockade, potassium channel blockade, calcium channel blockade) - mechanism determines both which arrhythmia an agent treats and its characteristic pro-arrhythmic risk profile
Class I (sodium channel blockers) slow conduction velocity; Class II (beta-blockers) reduce sympathetically-driven automaticity and AV nodal conduction; Class III (potassium channel blockers, e.g. amiodarone, sotalol) prolong repolarisation/refractory period - directly increasing QT interval and torsades de pointes risk, the class's defining pro-arrhythmic trade-off; Class IV (non-dihydropyridine calcium channel blockers) slow AV nodal conduction

Widely used across arrhythmia management, though several classes carry meaningful pro-arrhythmic risk requiring careful patient selection and monitoring

ECG monitoring (QT interval particularly for Class III agents, PR/QRS for Class I) is essential both before initiation and during treatment given the mechanism-based pro-arrhythmic risk inherent to several classes
Baseline and periodic organ function assessment (e.g. thyroid and liver function for amiodaration given its extensive extracardiac toxicity) is required for specific agents with recognised non-cardiac adverse effect profiles

Agent selection matched to the specific arrhythmia mechanism and patient comorbidity (e.g. avoiding Class IC agents in structural heart disease given proarrhythmic risk demonstrated in trial evidence)
Regular ECG monitoring throughout treatment, particularly at initiation and dose changes, given the class-inherent pro-arrhythmic risk

Amiodarone's extensive extracardiac toxicity (thyroid, pulmonary, hepatic, corneal deposits), Class IC pro-arrhythmic risk in structural heart disease (CAST trial), QT prolongation and torsades de pointes with Class III agents
Antiarrhythmic drugs, almost paradoxically, all carry some degree of pro-arrhythmic risk - the mechanism that suppresses one arrhythmia (altering conduction/repolarisation) can itself provoke a different, sometimes more dangerous arrhythmia, which is why ECG monitoring is integral to safe use across this entire drug class, not an optional precaution

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