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Figure 1 Antiarrhythmic drugs have diverse electrophysiologic effects on conduction, refractoriness, and automaticity in the heart. As an example we might consider the simplest form of atrial fibrillation (AF) due to re-entry around one or more obstacles (i.e., scars) that might be found in a patient with AF due to prior myocardial infarction. As a re-entry wave front circulates around an obstacle, it leaves in its wake a region of tissue that is refractory. In order for re-entry to be sustained around such an obstacle, the revolution time (RT) around the circuit must exceed the refractory period (RP) (i.e., RT > RP). Otherwise, the wave front would begin to encounter tissue that was still refractory, thereby preventing or extinguishing the re-entry. If RT < RP, re-entry is not possible, but when a (antiarrhythmic) drug slows conduction velocity more than it prolongs the RP, this drug could initiate re-entry (RT > RP), and the drug would be judged as proarrhythmic (arrow b). If a drug prolongs the RP to a greater degree than it slows conduction velocity, it will prevent re-entry and acts as antiarrhythmic (arrow a).