Why do class II and IV arrhythmics prolong repolarization at the AV node?

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wanderingorion said:
Class II are B-blockers, which target AV nodal repolarization due to decreasing sympathetic activation.
Class IV are Ca-channel blockers, which inhibit L-Type Ca channels in the SA/AV nodes, increasing refractoriness of the heart.

Here's a good crash course: intro_to_antiarrhythmics [TUSOM | Pharmwiki]
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I know but FA says that they also prolong AV node repolarization, beta blockers will increase slope of nodal phase 4 and 0 i get that same with CCBs but idk why FA says they prolong AV node repolarization which is phase 3
 
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Ven0m said:
I know but FA says that they also prolong AV node repolarization, beta blockers will increase slope of nodal phase 4 and 0 i get that same with CCBs but idk why FA says they prolong AV node repolarization which is phase 3
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I found that B-stimulation in the AV node increases Ca++ and K+ currents, which decreases the refractory period of the node, so blocker would lengthen the PR interval. And it seems that CCBs effect the same thing.

Principles of Pharmacology

While an exact mechanism isn't mentioned, my spitballed theory is since repolarization is based on Ca/Na exchangers, coupled with Na/K exchangers, if the Ca influx is decreased by blockage of Ca channels (either directly by L-type blocks by CCB or indirectly through autonomic inhibition) then the exchange process would be hindered, therefore slowing down repolarization.
 
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According to "Pathophysiology of Heart Disease" it says that class II decrease slope of phase 4 in the SA node, while it prolongs refractoriness of the AV node.

Class IV focuses on SA and AV node since they are most dependent on Ca++ for firing. They decrease rate of rise of phase 0 depolarization and lengthen AV node refractory period. They also raise threshold potential of SA node.
 
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Necr0sis said:
According to "Pathophysiology of Heart Disease" it says that class II decrease slope of phase 4 in the SA node, while it prolongs refractoriness of the AV node.

Class IV focuses on SA and AV node since they are most dependent on Ca++ for firing. They decrease rate of rise of phase 0 depolarization and lengthen AV node refractory period. They also raise threshold potential of SA node.
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I get why B-blockers decrease the slope of nodal cell phases 0 and 4, because they cause less B1 stimulation -> lower cAMP levels -> less protein kinase A activity -> less phosphorylation (less opening) of inward Na+ channels (phase 4; causing decreased heart rate) and less phosphorylation (less opening) of L-type Ca2+ channels (phase 0; causing decreased conduction velocity and increased action potential duration + effective refractory period)...


however i still dont get how they slow the repolarization (phase 3) of AV node; wanderingorion's find is good enough i guess but i guess it doesn't matter much if the mechanism is so obscure; ill just wait for UW to teach me its relevance; thanks for taking time to help tho!
 
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