It's a little tricky; the APD increase in theory should decrease heart rate, but the M-blocking activity may cause an increase in HR in some cases, mainly severe a-fib or flutter. With atrial tachycardia, so many impulses are being conducted to the AV node, the AV is somewhat refractory due to the swarm of impulses plus the activity of the vagus nerve (vagal activity and/or sympathetic activity is always present at some level in normal conditions). The result is that the ventricle doesn't see all the impulses has a slower rate of contraction compared to the atrium. If the a-fib is severe enough, the block can be large enough that the ventricle runs on its own pacemaker, which is slower than normal SA rhythm.
When quinidine is first administered, the abolishment of vagal activity rids the AV node of some of its refractory ability. This allows the impulses to get through and the atrial rhythm resumes, leading to tachyarrythmia, thus the IA drugs being categoried as possible pro-arrhytmics. The increased APD does help, but the swarm of atrial impulses is more significant. Hope this helps.
