The most widely used scheme for the classification of antiarrhythmic drug actions recognizes four classes: 1. Class 1 action is sodium channel blockade. Subclasses of this action reflect effects on the action potential duration (APD) and the kinetics of sodium channel blockade. Drugs with class 1A action prolong the APD and dissociate from the channel with intermediate kinetics; drugs with class 1B action shorten the APD in some tissues of the heart and dissociate from the channel with rapid kinetics; and drugs with class 1C action have minimal effects on the APD and dissociate from the channel with slow kinetics.
2.
Class 2 action is sympatholytic. Drugs with this action reduce β-adrenergic activity in the heart.
3.
Class 3 action manifests as prolongation of the APD. Most drugs with this action block the rapid component of the delayed rectifier potassium current, IKr.
4.
Class 4 action is blockade of the cardiac calcium current. This action slows conduction in regions where the action potential upstroke is calcium dependent, eg, the SA and AV nodes.
A given drug may have multiple classes of action as indicated by its membrane and ECG effects (Tables 14–2 and 14–3). For example, amiodarone shares all four classes of action. Drugs are usually discussed according to the predominant class of action. Certain antiarrhythmic agents, eg, adenosine and magnesium, do not fit readily into this scheme and are described separately.
Drugs with local anesthetic action block sodium channels and reduce the sodium current, INa. They are the oldest group of anti-arrhythmic drugs and are still widely used.
By blocking sodium channels, procainamide slows the upstroke of the action potential, slows conduction, and prolongs the QRS duration of the ECG. The drug also prolongs the APD (a class 3 action) by nonspecific blockade of potassium channels. The drug