Most anti-arrhythmic drugs, whatever their specific mechanisms, have two actions that reduce abnormal electrical activity, but cause tolerably small effects on normal myocardium.

Anti-arrhythmic drugs are divided into four classes, based on their mechanisms (Figure 51). However, most anti-arrhythmic drugs have properties of more than one class, often because drug metabolites have their own separate anti-arrhythmic effects or because the drugs exist as 50/50 mixtures of two stereoisomers with different actions. This classification system, introduced by Vaughan Williams and Singh, also excludes several drugs, and is not useful for matching specific drugs to particular arrhythmias. A more clinically relevant classification scheme is shown in Table 51.1.

Table 51.1 Site-based classification of anti-arrhythmic drugs.

Clinical trials have shown that class I agents do not enhance survival, and in fact are deleterious if used for some purposes (e.g. prevention of ventricular ectopic beats). Conversely, the class III agent amiodarone modestly increases survival, and class II agents (β-blockers) can suppress a wide spectrum of arrhythmias and increase survival in conditions such as chronic heart failure and ischaemic heart disease which frequently lead to lethal arrhythmias. However, because radiofrequency catheter ablation can effectively cure many superventricular tachyarrhythmias and implantable defibrillators are more effective than drugs in reducing the incidence of lethal ventricular arrhythmias, the emphasis of arrhythmia management is shifting towards device-based therapy.

Class I Drugs

Class I drugs act mainly by blocking Na⁺ channels, thus slowing and depressing impulse conduction. This suppresses re-entrant circuits which depend on an area of impaired conduction, as further Na⁺ channel blockade here may block conduction completely, which terminates the arrhythmia. Class I drugs can also suppress automaticity by raising the membrane potential threshold required for delayed afterpolarizations to trigger action potentials (APs).

Because they have a higher affinity for Na⁺ channels when they are open or inactivated, these drugs bind to Na⁺

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