I am having trouble understanding two related concepts. First, why changes in ERP occur when there is the administration of certain antiarrhythmics (eg: Class IC). A neat explanation that I have developed to make it easier to remember is that IC has a stronger affinity to Na channels, as such, there is an increased block in Na current, which slows the upstroke. This ultimately delays the depolarization and thus the refractory period is delayed as well. I doubt this explanation has any merit in itself and would greatly love it if anybody could explain this concept to me.
The second thing that I am having trouble understanding is the mechanism of actions of antiarrhythmics as a whole. It seems paradoxical that I am asking this after the question above, and I do understand the mechanism of actions of all the classes (Class I= Na channel blocker; Class II= b blockers; Class III= K channel blockers; Class IV= Ca channel blockers), but I do not understand how blocking these and changing action potential durations can act as anti-arrhythmic.