The class I drugs all bind to sodium channels, but the different subsets of class I drugs bind to different states of the sodium channels with different affinities. Basically some drugs can act as blockers more in the depolarized state and others in the resting state. So if you have a more active heart, that's undergoing cycles of depolarization/repolarization more quickly, relatively speaking, it's spending more time in the depolarized state than it was at a slower heart rate. This facilitates drugs that preferentially bind and inhibit sodium channels in active state to a greater degree, and hence more drug action at faster heart rates.
That's how I understand it, hopefully that helps, and hopefully it's right. If you know anyone with the Kaplan pharm vids, aske them if you can watch the antiarrhythmics section since the guy does an excellent job of breaking it down.
Edit: just realized this thread was 2 weeks old... but whatever, hope it helps anyway.
