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Old 03-06-2016
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Default About 1b class Na blockers

Hello everyone

This class of drugs really confuses me , so I'm really looking for more explanations


How this class decrease AP and it doesn't cause tachycardia?

How come it also decreases the refractory period and extends the time for recovery ?


And does it work by blocking the h gate of Na channels ? And also how is it really effective for ischemic tissues because it blocks the inactivated channels while the ischemic tissues already has a Long Effective refractory period ?

Thank you guys and I'd really appreciate your help
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Old 03-07-2016
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Originally Posted by Mayar View Post
Hello everyone

This class of drugs really confuses me , so I'm really looking for more explanations


How this class decrease AP and it doesn't cause tachycardia?

How come it also decreases the refractory period and extends the time for recovery ?


And does it work by blocking the h gate of Na channels ? And also how is it really effective for ischemic tissues because it blocks the inactivated channels while the ischemic tissues already has a Long Effective refractory period ?

Thank you guys and I'd really appreciate your help
It decreases AP duration because it presumably blocks the window current. Plateau phase of the action potential is not just calcium and potassium, other ions are contributing as well. IB drugs block sodium contribution to the plateau phase shortening it. It does not cause tachycardia because it does not work on the nodal tissue. Rate control under normal circumstances comes from the SA node, IB works on the contractile portion of the heart.

I do not know about ERP and recovery time.

IB drugs preferentially work on inactivated channels. Ischemic tissue has low ATP, low ATP means that Na+/K+ pump does not work and sodium builds up intracellularly. That means the membrane potential is less negative than under normal circumstances. When the membrane potential rises sodium channels are inactivated. I do not remember the M and H gate nomenclature but the inactivation gates are closed. The same logic why nodal cells do not have functional fast sodium channels, the membrane potential is less negative and the channels are inactivated.
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