Refractory period in Class IC anti arrythmics

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voicesinmyhead

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First aid says refractory period of the AV node is prolonged by IC drugs like propafenone.

But Uworld says refractory period is not changed at all.

Also as these drugs are proarrythmogenic, shouldnt the refractory period be anything but prolonged?

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I am pretty sure they are prolonged, I remember reading that IC drugs are the worst for you out of all 3 classes of the sodium channel blockers.

Something to do with 90%, it blocks 90% of the channels or something like that? Can't remember, anybody can chime in if they know what I am referring to.
 
Class 1C antiarrhythmics prolong the phase 0 depolarization without appreciably altering the overall length of the AP/ERP. Class 1A lengthens the ERP while 1B shortens it. These different changes in overall ERP duration are the basis of the whole 1A/B/C nomenclature system.
 
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Class 1C antiarrhythmics prolong the phase 0 depolarization without appreciably altering the overall length of the AP/ERP. Class 1A lengthens the ERP while 1B shortens it. These different changes in overall ERP duration are the basis of the whole 1A/B/C nomenclature system.

Thanks! i didnt know they were the same. But why does FA say IC prolongs refractory period in AV node?
 
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Bump!

Does anybody know the anwser to this question?

"But why does FA say IC prolongs refractory period in AV node?"

May it have anything to do with blocking Ca2+ channels (reference: goodman), prolonging AP duration and eventually refractory period?
 
You are right.
Propafenone also has β-blocking activity in addition to Ca++ channel blocking activity.
 
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