Superb

You seem to suggest that sux increase ACh at the NMJ, isn't the MOA that sux binds to the ACh receptor, causes depolarisation and then does not disengage as quickly due to the lack of effect of AChE (rather is metabolised by pseudocholinesterase). I don't think it has effect on ACh concentration directly.

Very clear and covered a great extent, thank you!

Very conceptual and and easy thanks alot I wanted to learn this

Thx.easy to understand

Not all "roniums" aminosteroidals, roid, "ronium"; isoquinolones are the curare, "curiums"; I also agree with below, that you should include what fade is for NDNMB and what phase 1 and phase 2 is for depolarizing NMB; or take out the paralytics in the beginning and then you are not missing a reference between the TOF and paralytics.

Don't wanna be a hater but as a junior anaesthetist... this is a video littered with inaccuracy. eg Sux is a depolarising agent as it shares a structure similar to ACh thus is induces muscle contractions which vary in intensity. it is an ACh receptor agonist. you also need to explain that it is metabolised by pseudocholinesterase. moreover add that you get phase I muscle relaxation with Sux but a second dose can put someone into phase II relaxation as the ACh receptor undergoes a conformational change. depolarising agents act as competitive antagonists, ie they bind to the receptor quickly to the existing ACh just kinda stands around and cannot illicit depolarazation. then these should be split into their duration of action and include the fact that you have amino-steroids (rocuronium, vecuronium and pancuronium) which are the only ones which can respond to suggamadex and benzyl-isoquinolines (the rest). cis-atricurium and atricurium undergo Hoffman degradation. mivacurium is metabolized by pseudocholinesterase. then the rest ie vec, roc, and pan will respond to your neostigmine which in truth just increases the concentration of ACh to kick it off the receptor, the glycopyrrolate is an antimuscarinic to avoid the effects eg the increased secretions, bronchospasm, bradycardia etc. Honestly stopped watching at 05:36 since this isn't good as a quick revision of drugs or TOF.

Are These percentage are put assuming that the twitches are equal in intensity ?? so we have a TOF ratio of 1 in the first scenario and a TOF ratio of zero for the rest That being said, a ratio of zero doesn't really mean that you've reached a good paralysis state right??! Can make a video explaining the fade in TOF and what does it mean Thanks a lot for the post, really helpful

Correction: Can you make a video explaining the fade in TOF and what it means Thanks

Great video! 4:27 common mistake, but it's actually pronounced "buckle"

nice

Thanks !!!!!!!

where is explanation

The explanation of succinylcholine's Mechanism of Action is incorrect

The junior SHO anaesthetist & Registrar doing my anaesthesia during my very bungled op in the UK didn't understand what 'train of four' was & made so many serious errors = I woke up paralysed & suffocating in op theatre (& got brain damage) = HOW can anaesthetists be allowed to practice on patients if they aren't capable of the basics? SHO didn't seem to understand the blood pressure monitor either but the Registrar just let her bumble on. They also gouged out my throat (laryngoscope) & lied & covered up so my throat was left veey seriously damaged, untreated & undiagnosed: nobody believed me: all the docs & hospital believed the lying doctors/anaesthetists. I expect this happens in the USA/Canada too? But you wouldn't know because everyone keeps quiet & injured patients are discredited & silenced sadly = NO learning. 15 years alter my swallowing is still badly affected but my legal case failed.