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Old 07-26-2011
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Drug Mechanism of action of Class Ib antiarrhythmic drugs

Hey can somebody help me with class Ib antiarrythmics (lidocaine) ?
I really don't get its mode of action and why they use it post-MI
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Old 07-26-2011
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well Ib blocks the conductance of Na responsible for phase 0 of action potential curve of ventricular muscle...n this group specifically binds with ischemic tissue delaying the generation of next action potential n allowing the time for recovery this is done due to prolong diastole because the threshold for the next impulse is raised so dats y its used post MI
may b sme1 cn xplain it better
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Old 07-26-2011
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Quote:
Originally Posted by qurat21 View Post
well Ib blocks the conductance of Na responsible for phase 0 of action potential curve of ventricular muscle...n this group specifically binds with ischemic tissue delaying the generation of next action potential n allowing the time for recovery this is done due to prolong diastole because the threshold for the next impulse is raised so dats y its used post MI
may b sme1 cn xplain it better
thanks qurat21. that was helpful
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Old 07-27-2011
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Normally there are 3 configurations (shape) of Na channel. Resting, open and inactive or refractory

During resting stage The M gate which is outside the cell is closed and the H gate which is inside is open. After reaching Threshold potential the M gate opens and H gate start to close so for very brief time there is influx of Na. this is called Open state. Then the H gate closes and M gate opens, so now there is not Na influx and this is the Inactive state or refractory as the Na channel are now inactive.

So now tell me when does this H gate open?
It opens when the cells has re-polarized that means when the RMP is back to -85-90mv. Then Back to resting state. Rem these channels are made up of proteins.

Once the sodium h gate is in inactive state the cell cannot generate another AP what do you call it?
The cell is in refractory state, it is in resistance state. Which means once the cell is depolarized you need to wait for most of the Na channel to be in resting stage. And this stage is only achieved after the MP is back to 85-90mv.

Why most of the hypoxic tissues are in refractory state ie their H gate closed and M gate open?
After the cell has depolarized and repolarized, it is the job of Na/K ATPase pump is to reset the membrane potential so that another AP can be generated
Hypoxic tissues lack ATP to operate the Na/K ATPase pump. So without this pump the cell cannot reset the Membrane potential back to normal or does it very slowly compared to normal cells hence the hypoxic cells stay longer in the refractory state

What is the benefit of blocking channel that is in refractory or inactive state?
Rem we are blocking this channel in hypoxic/ischemic cardiac tissues. So by blocking the channel we are preventing it from returning to resting state. So the hypoxic tissue stays in refractory state. Thus preventing firing new AP. Hypoxic tissue has slow AP and healthy tissue has fast so this disparity in flow of current causes arrhythmia. Lidocaine preferentially binds to Na gate that is in inactive or refractory state
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Last edited by axax; 07-27-2011 at 12:10 AM.
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Quote:
Originally Posted by axax View Post
Normally there are 3 configurations (shape) of Na channel. Resting, open and inactive or refractory

During resting stage The M gate which is outside the cell is closed and the H gate which is inside is open. After reaching Threshold potential the M gate opens and H gate start to close so for very brief time there is influx of Na. this is called Open state. Then the H gate closes and M gate opens, so now there is not Na influx and this is the Inactive state or refractory as the Na channel are now inactive.

So now tell me when does this H gate open?
It opens when the cells has re-polarized that means when the RMP is back to -85-90mv. Then Back to resting state. Rem these channels are made up of proteins.

Once the sodium h gate is in inactive state the cell cannot generate another AP what do you call it?
The cell is in refractory state, it is in resistance state. Which means once the cell is depolarized you need to wait for most of the Na channel to be in resting stage. And this stage is only achieved after the MP is back to 85-90mv.

Why most of the hypoxic tissues are in refractory state ie their H gate closed and M gate open?
After the cell has depolarized and repolarized, it is the job of Na/K ATPase pump is to reset the membrane potential so that another AP can be generated
Hypoxic tissues lack ATP to operate the Na/K ATPase pump. So without this pump the cell cannot reset the Membrane potential back to normal or does it very slowly compared to normal cells hence the hypoxic cells stay longer in the refractory state

What is the benefit of blocking channel that is in refractory or inactive state?
Rem we are blocking this channel in hypoxic/ischemic cardiac tissues. So by blocking the channel we are preventing it from returning to resting state. So the hypoxic tissue stays in refractory state. Thus preventing firing new AP. Hypoxic tissue has slow AP and healthy tissue has fast so this disparity in flow of current causes arrhythmia. Lidocaine preferentially binds to Na gate that is in inactive or refractory state
Thanks axax .. but what i dont understand is .. if the ischemic tissues are already in a refractory state(h gate closed because of lack of ATP) how r they at a risk of having an arrythmia?? and why do we have to give antiarrythmics if they r already in s refractory state?
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good explanation. in an ischaemic tissue there is no atp to run the NA-K pump, that means we cannot throw the 3 na out and bring in 2 k instead, that means we cannot restore the cell to its original -90. instead the 3na inside make the cell more positive. making the cell more positive is depolarization, if it reaches the firing potential -action potential is generated. since this is not a coordinated activity and this entire process is due ischaemic, the different cells will depolarize and eventually fire = arrythmias.
i'm not sure about this second part, but i think the idea of giving the class Ib which has higher affinity for this inactive Na channel is to prevent further firing of the cell, and hence prevent the formation of a prolonged arrythmic state.

The Na channel talked about before is not ATP dependant, that is voltage dependant.
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the ischemic tissue is in partially depolarised state so the threshold for the action potential is lower so tht means an action potential can b easily generated in ischemic tissue but at the same time the conduction in ischemic tissue is slower than normal tissue is this responsible for arrythmia ??? n then we give lidocaine because it blocks inactive Na channels n raises the threshold for generation of impulse
need more xplanations!!!
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I see where you are getting confused.
What i ment was

The voltage gated Na channels in hypoxic/ischemic cardiac tissues stay in refractory state slightly longer (rem they do not not say in refractory forever unless the cell is dead) than the normal cardiac tissues. Normally All voltage gated Na channels should open when threshold potential is reached and then close and then cycle back to resting state. Ready for next AP. When next AP occur the rest of normal cardiac tissue is depolarizing but the ischemic tissues won't depolarize with the rest as it is in refractory, it will depolarize later when others have finish depolarized. This disparity of flow of electrical current leads to arrhythmia.
So to prevent this we want to keep the ischemic tissues in refractory period, so that it can't generate its own AP and disrupt the normal cardiac electrical activity .
I hope this clears the confusion.
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Quote:
Originally Posted by axax View Post
I see where you are getting confused.
What i ment was

The voltage gated Na channels in hypoxic/ischemic cardiac tissues stay in refractory state slightly longer (rem they do not not say in refractory forever unless the cell is dead) than the normal cardiac tissues. Normally All voltage gated Na channels should open when threshold potential is reached and then close and then cycle back to resting state. Ready for next AP. When next AP occur the rest of normal cardiac tissue is depolarizing but the ischemic tissues won't depolarize with the rest as it is in refractory, it will depolarize later when others have finish depolarized. This disparity of flow of electrical current leads to arrhythmia.
So to prevent this we want to keep the ischemic tissues in refractory period, so that it can't generate its own AP and disrupt the normal cardiac electrical activity .
I hope this clears the confusion.
thanks axax i get it now ..
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Old 05-23-2016
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Quote:
Originally Posted by axax View Post
Normally there are 3 configurations (shape) of Na channel. Resting, open and inactive or refractory

During resting stage The M gate which is outside the cell is closed and the H gate which is inside is open. After reaching Threshold potential the M gate opens and H gate start to close so for very brief time there is influx of Na. this is called Open state. Then the H gate closes and M gate opens, so now there is not Na influx and this is the Inactive state or refractory as the Na channel are now inactive.

So now tell me when does this H gate open?
It opens when the cells has re-polarized that means when the RMP is back to -85-90mv. Then Back to resting state. Rem these channels are made up of proteins.

Once the sodium h gate is in inactive state the cell cannot generate another AP what do you call it?
The cell is in refractory state, it is in resistance state. Which means once the cell is depolarized you need to wait for most of the Na channel to be in resting stage. And this stage is only achieved after the MP is back to 85-90mv.

Why most of the hypoxic tissues are in refractory state ie their H gate closed and M gate open?
After the cell has depolarized and repolarized, it is the job of Na/K ATPase pump is to reset the membrane potential so that another AP can be generated
Hypoxic tissues lack ATP to operate the Na/K ATPase pump. So without this pump the cell cannot reset the Membrane potential back to normal or does it very slowly compared to normal cells hence the hypoxic cells stay longer in the refractory state

What is the benefit of blocking channel that is in refractory or inactive state?
Rem we are blocking this channel in hypoxic/ischemic cardiac tissues. So by blocking the channel we are preventing it from returning to resting state. So the hypoxic tissue stays in refractory state. Thus preventing firing new AP. Hypoxic tissue has slow AP and healthy tissue has fast so this disparity in flow of current causes arrhythmia. Lidocaine preferentially binds to Na gate that is in inactive or refractory state
Hi,can sumone help me clarify this point?If Class 1B anti-arrythmics like Lidocaine block the inactive Sodium channels & keep the cells in the refractory state,how do they decrease the AP duration...?
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