Suxamethonium, being a depolarising neuromuscular blocker, it acts as agonist on M2 receptors at the heart resulting in the bradycardia. Here in this video, by mistake it was shown as it is inhibiting M2 receptors which is corrected. So it stimulates M2 receptors. On the other hand non-depolarising NMB act as antagonists and they produce tachycardia.
In phase 1 block the cells membrane potential is entirely depolarised and it takes a (relatively) long time to fully repolarise. Until it has repolarised it cannot transmit an action potential. The receptors themselves are as sensitive as they normally are, but triggering them does nothing. In phase 2 block the receptors have been triggered so much that they become less sensitive to further stimulation and you get something more like a non-depolarising block.
Doesn’t suxamethonium produce tachycardia if it antagonize the M2 receptors. Because when ACh binds to M2 receptors it causes bradycardia. I think succinylcholine initially agonize the M2 receptors like acetylcholine does
Yes intially it will antagonise but later on it will desensitize those receptors. Although there would be initial activation of those receptors but it will be for a less time that if we look at overall result it will render M2 receptors desensitized and cause bradycardia. Note: This is just a side effect of the drug we do not clinically use it in tachycardia to lower the heart rate.
Thanks ,I've got a question; as you said this drug deactivates the T-tubule .so how on Earth are we going to have the activation of Rayanodine receptors on the SR to cause over influx of calcium ion resulting in hyperthermia??.You must have meant to say HYPOTHERMIA
Depolarising neuromuscular blockers initially increase calcium release from SR which results in initial muscle fasciculations. So this leads to raise in the temperature producing hyperthermia.
Suxamethonium, being a depolarising neuromuscular blocker, it acts as agonist on M2 receptors at the heart resulting in the bradycardia. Here in this video, by mistake it was shown as it is inhibiting M2 receptors which is corrected. So it stimulates M2 receptors. On the other hand non-depolarising NMB act as antagonists and they produce tachycardia.
Phase II is the desensitization of nicotinic Acetylcholine receptors due to depolarising action of succinylcholine. In phase II, even muscle is repolarised and ready for contraction but still receptors are not ready for activation. So when ACh is released by exocytosis, still it can't produce any response as the receptors are not working.
Sir , What will be the consequences if we give depolarising muscle relaxants after non deploarising muscle relaxants. For eg , we give vecuronium first for intubation and give scoline afterwards for maintenance .
OMG finally. In a way I can understand. AND you even went into chemical structures. THANK YOU!!!
Just perfect!!! Thank you ,sir.
You are welcome!
I was expecting u to teach phase 1 n phase 2 block also since ach esterase inhibitors worsen phase 1 block but they can treat phase 2 block 😒
Excellent presentation 👍
It would have been better if you had taught about phase 1 and phase 2 block also
Very helpful video.. thanks
12:18how does due to constant opening of sodium channels causes k ion to move out of the cell..Does it is a part of repolarization or something else..
Potassium channels are also opened. It is a feature of depolarisation
Hello sir ,
Is there any need of skeletal muscle contraction when body is in rest condition ( parasympathetic condition )?
Thank you.
Thank you so much
Plz clarify since m2 receptor is only cholinergic which causes bradycardia but how it causes bradycardia on its blockade instead of tachycardia...!?
Suxamethonium, being a depolarising neuromuscular blocker, it acts as agonist on M2 receptors at the heart resulting in the bradycardia. Here in this video, by mistake it was shown as it is inhibiting M2 receptors which is corrected. So it stimulates M2 receptors. On the other hand non-depolarising NMB act as antagonists and they produce tachycardia.
@@egpat thank u sir
Best video... concept cleared
THANKS
Very Nicely Explained 👍👍❤
Thanks mate!
Amazing.
Thank you soooooooo much
Glad it is useful. Thanks for watching !
Why prolong time depolarization of nicotinic receptor cause desensitisation??
I dont get the answer, I need it, plz.
In phase 1 block the cells membrane potential is entirely depolarised and it takes a (relatively) long time to fully repolarise. Until it has repolarised it cannot transmit an action potential.
The receptors themselves are as sensitive as they normally are, but triggering them does nothing.
In phase 2 block the receptors have been triggered so much that they become less sensitive to further stimulation and you get something more like a non-depolarising block.
Best ❤️❤️
💡
Doesn’t suxamethonium produce tachycardia if it antagonize the M2 receptors. Because when ACh binds to M2 receptors it causes bradycardia. I think succinylcholine initially agonize the M2 receptors like acetylcholine does
Yes intially it will antagonise but later on it will desensitize those receptors. Although there would be initial activation of those receptors but it will be for a less time that if we look at overall result it will render M2 receptors desensitized and cause bradycardia.
Note: This is just a side effect of the drug we do not clinically use it in tachycardia to lower the heart rate.
Thanks a lot sir
Brillent sir thank u.
Thanks ,I've got a question; as you said this drug deactivates the T-tubule .so how on Earth are we going to have the activation of Rayanodine receptors on the SR to cause over influx of calcium ion resulting in hyperthermia??.You must have meant to say HYPOTHERMIA
Depolarising neuromuscular blockers initially increase calcium release from SR which results in initial muscle fasciculations. So this leads to raise in the temperature producing hyperthermia.
Can phase ll block be reversed ?
If m2 is blocked then how it cause bradycardia ?
It act at the Muscarinic receptor that control SA node firing, reduce SA node firing causing bradycardia particularly in children
Suxamethonium, being a depolarising neuromuscular blocker, it acts as agonist on M2 receptors at the heart resulting in the bradycardia. Here in this video, by mistake it was shown as it is inhibiting M2 receptors which is corrected. So it stimulates M2 receptors. On the other hand non-depolarising NMB act as antagonists and they produce tachycardia.
I want to know the phase II block. Can you explain the mechanism? Please~~~
Phase II is the desensitization of nicotinic Acetylcholine receptors due to depolarising action of succinylcholine. In phase II, even muscle is repolarised and ready for contraction but still receptors are not ready for activation. So when ACh is released by exocytosis, still it can't produce any response as the receptors are not working.
Sir ,
What will be the consequences if we give depolarising muscle relaxants after non deploarising muscle relaxants.
For eg , we give vecuronium first for intubation and give scoline afterwards for maintenance .
@@ashutoshgautam9449 it will prevent twitching and fasciculations
@@ashutoshgautam9449it will not work. The vecuronium will block it's action and it will be broken down.
Fade phenomenon explain nahi kiya
Pls explain fade phenomenon
Sure, I will describe it another video. Thanks for your interest.