USMLE ERP prolongation in class IC antiarrhythmics

[p53apoptosis]

Can someone explain why IC increases the ERP in the AV node and accessory bypass tracts, but not in the purkinje and ventricular tissue (pg 315 in FA)?

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[niku9]

IC have the slowest rate of dissociation among the class I AA. If i understand correctly, the slow rate of dissociation means IC AA preferentially affect myocardium with slow conduction velocities eg the AV node and bypass tracts. In the same way, IB AA have the fastest rate of dissociation so they preferentially block rapidly depolarizing tissue eg ventricles, which is why lidocaine and mexilitine are so useful for v-fib where the foci originate from the ventricles. Hope this makes sense

 

[Blind date18]

i dont think so, slow dissociation dissociation of drug has nothing to do with slow conduction and more over class 1 drugs are involved in blocking of fast sodium channels which are not seen in case of Av node

 

[bobjonesbob]

Can someone explain why IC increases the ERP in the AV node and accessory bypass tracts, but not in the purkinje and ventricular tissue (pg 315 in FA)?

apparently they also have some action on Ca2+ channels:

source: CV Pharmacology | Sodium-Channel Blockers (Class I Antiarrhythmics)

 

[p53apoptosis]

apparently they also have some action on Ca2+ channels:

View attachment 228977

source: CV Pharmacology | Sodium-Channel Blockers (Class I Antiarrhythmics)

Makes sense. Thanks for finding that!

 

[bobjonesbob]

Could someone explain why Class Ic is proarrhythmogenic particularly in damaged cardiac tissue? That part still doesn't make sense to me

 

[Cardiologyslave]

Could someone explain why Class Ic is proarrhythmogenic particularly in damaged cardiac tissue? That part still doesn't make sense to me

Ischemic cells are partially depolarized , and 1c will block fast na channels which will cause the partially depolarized cells to fire and cause arrhythmia ,