BASIC ACTIONS: According to Vaughan Williams antiarrhythmic agents are divided into four classes of action (Table 1). A given agent may display actions of several classes. In general, except for class II drugs there is no causal relationship between the class of action and the mechanism precipitating the arrhythmia. MECHANISM OF ACTION OF CLASS I DRUGS: The effect of class I antiarrhythmic drugs is primarily based on prolongation of the refractory period. It is assumed that the sodium channel can be in one of at least three functional conditions (Figure 1), resting, activated or inactivated. Conductance is achieved only in the state of activation, during the initial phase of the action potential which is caused by rapid sodium influx. The transition from inactivation to resting condition, which is prerequisite for renewed activation, takes place during repolarization and is responsible for the refractory period of the action potential (Figure 1). Class I antiarrhythmic drugs block the sodium channels such that they remain in a nonconductive state. As a function of the number of inoperative sodium channels, sodium influx is reduced and the rate of rise of the action potential is diminished. In order to enable sufficient sodium channels to make the transition from inactivated to resting condition, repolarization of the action potential has to continue and, concomitantly, the absolute refractory period is increased. Since the attenuation of the rapid sodium influx also causes a decrease in the conduction velocity in myocardium and in the intraventricular conduction system, reentry arrhythmias can be precipitated. DIFFERENCES IN THE ACTION OF CLASS I DRUGS: Due to different rate-dependency of the various class I drugs and the effect on the duration of the action potential as well as on specified ECG parameters, subclasses a, b and c were designated (Table 2). Access of the drug to the sodium channel receptor is facilitated during activation and inactivation but not in the resting condition. Accordingly, the effect increases in proportion to the frequency with which the sodium channel is opened. With the beginning of the cardiac cycle, there is an exponential increase in the number of blocked sodium channels and, with transition to the resting condition, an exponential decrease (Figure 2). The velocity of the increase or decrease is dependent on the properties of the given agent. Substance with rapid binding kinetics, that is time constants of 0.2 to 2.0 s are assigned to group Ib, those with time constants of 8 to 14 s to group Ic (Table 3). Group Ia is intermediate. A similar grouping is yielded on assignment according to the temporal course of deblocking. EXPLANATION FOR THE DIFFERENCES IN EFFECTS: With antiarrhythmic agents of class Ib, due to their rapid binding kinetics, at a rate of approximately 1 Hz (60/min) steady-state is achieved with no accumulation of block. Each incoming impulse with a normal interval can activate the unblocked membrane (Figure 2). Premature impulses occurring with shorter intervals are inhibited more the earlier their incidence. Consequently, class Ib antiarrhythmic drugs are particularly effective for premature beats and frequent tachycardias while, during normal sinus rhythm, in some instances, no effect such as PQ or QRS prolongation can be observed (Table 2).(ABSTRACT TRUNCATED AT 400 WORDS)