What's up What's up if you can answer me What is the relation of an Indian in the middle of the forest Amazon and our patient in the operating room Because this is what we are going to see in today's video class, release the vignette o Hello crew of the ship all right in this video lesson of the Anesthesia course o basics we're going to talk a little bit about neuromuscular blockers the first professionals to use neuromuscular blockers were the South American Indians hundreds of years ago hunting and fishing professionals the shamans and some tribes were aware of making a certain paste with a mixture of herbs that they put in Ponta das Flechas to hunt animals that potion he extremely useful because animals affected died in minutes and that even gave a certain status to the people who leave that knowledge and and in the 19th century Spanish expeditionaries who were out there in the Amazon rainforest had contact with this situation and they realized that the animals did not die immediately the heart kept beating. Soon they realized that that poison was actually a potent paralytic they called this poison Heal in an attempt to reproduce the speech of the Indians in relation to the poison the Indians spoke the Hari fly I like something that means poison a interesting feature that they realized is that this poison does not it worked when they ate something that had a poison only when it was administered intramuscularly and relax there and then I explain why By the 1930s, the Pharmaceutical Industry was able to separate a molecule of this substance and called tubocurarine they started to use in Patience who had multiple sclerosis and tetanus but soon they started using it as an adjunct in general anesthesia to improve my relaxation since then several neuromuscular blockers have been synthesized each one with its characteristic but with a purpose in common to promote reversible muscle paralysis blockers neuromuscular disorders also known as peripheral action muscle relaxants are widely used in medicine as well as being useful in thoracic surgery ophthalmic they are also very interesting to facilitate intubation of the patient and also ICU patients who are on mechanical ventilation in the veterinary use of neuromuscular blockers is much more restricted first because we can intubate veterinary patients with much more ease and what unfortunately the maintenance of veterinary patients on mechanical ventilation for a long period is practically unviable So what we use is basically to facilitate the mechanical ventilation in case of anesthesia in osteosynthesis surgeries that the muscles are very tight and also eye surgery But even so not every procedure will need the use of the blocker neuromuscular and for us to understand the mechanism of action of neuromuscular blockers at we have to understand what happens on the motor plate in this animation very simple interesting we can see that the junction of the motor plate presents nicotinic receptors we can see that these receptors have five go up units being two Alpha which are the subunits that acetylcholine will act the influx of calcium promotes release of acetylcholine to crack then two acetylcholine molecules will act on the nicotinic receptor there in the subunits Alpha promoting muscle contraction this occurs when 70 80 percent of receptors are stimulated but this slit also has a very enzyme important that acetylcholinesterase acetylcholinesterase it breaks down EA acetylcholine felt and strain and it is very important because it removes acetylcholine of the nicotinic receptor promoting muscle pay in neuromuscular blockers yesterday to exactly in Alpha units of nicotinic receptors How about acetylcholine But depending on of how they act they are considered agonists or antagonists we will start first by talking about neuromuscular blockers depolarizing agents that are represented by succinylcholine and suxamethonium These drugs will bind to the nicotinic receptor E as acetylcholine will promote the activation of the receptor favoring the influx of sodium and the efflux of potassium in that case there will be muscle contraction The difference is that acetylcholinesterase cannot break down these drugs, that is, they stay there connected a receiver a much longer time not allowing repolarization then first muscle contraction occurs mainly in the face muscles of the extremities and then muscle paralysis the Hill thread with suxamethonium they were very used in the past because they promoted excellent my relaxation of short duration The problem is that they do not act only nicotinic receptors of motor plate And then the problem begins because of the initial muscle contraction patients returning from anesthesia often complained about energy obviously this was due to the mechanism of action that first had to the contraction happens and then the muscle paralysis this contraction muscle also happens in the muscles of the eyeball increasing the pressure intraocular promoting pain they also act on muscarinic receptors that control the sino-atrial node promoting bradycardia they also promote mast cell degranulation releasing stamina promoting hypotension and finally how long they stay attached to nicotinic motor plate receptors they favor the potassium efflux promoting hyperkalemia that reaches up to there is a billion equivalent per good liter in view of that we can already see that this group is not that interesting but we have to talk mainly because they are the basis of neuromuscular blockers and also for us understand how non-depolarizing neuromuscular blockers non-depolarizing neuromuscular blockers act will also act in the Alpha subunit of nicotinic receptors But different from the previous ones those here have not done agonist so do not open the sodium channels and consequently not the Initial muscle contraction then with that mechanism of action we no longer have those undesirable effects of another group of depolarizing blockers so we're not going to have post-anesthetic myalgia of the orocular bradycardia and hyperkalemia, however These drugs in the groups of neuromuscular blockers do not depolarizing They do not act only on nicotinic receptors it the muscarinic receptor atoms So we have some action problems antagonist at the muscarinic receptors of the sino-atrial node promote an effect vagolytic so we can have tachycardia we can not forget that muscarinic receptors are also there at the big junction Leonardo the sympathetic nervous system So depending on the dose we can have blocking muscarinic receptors in the sympathetic system and then in that situation we can have bradycardia and hypotension the good news is that for us to achieve this effect of bradycardia and hypotension we have to use doses very high and non-depolarizing neuromuscular blockers used today are quite safe Speaking of which the blockers non-depolarizing neuromuscular cells are divided into two groups the first synthesized non-depolarizing neuromuscular blocker was the pancuronium It is very interesting because it is little biotransformed is basically excreted in the kidney route for this reason It is not indicated for nephropathic patients that vagolytic effect that I mentioned for you it is also quite intense. So in this case pancuronium promotes tachycardia today we have other drugs in this group that are very safer they do not promote these cardiovascular effects in doses clinics and they have a very short period of action like vecuronium rocuronio IP coronary the other group is formed by atracurium and cisatracurium doxacurium and mivacurium they are very interesting because they are broken down by esterases plasmatic and are very stable so the action period is very short they are interesting to do in for example by continuous infusion and those effects cardiovascular diseases are basically non-existent in clinical doses table shows the main neuromuscular blockers used in the with doses and time of action we have what they should be done intravenously to promote effect suitable and immediate and neuromuscular block doesn’t happen evenly all at once happens in stages this can be interesting some situations first we have paralysis of the muscles of the face and fingers, because the groups muscles are smaller after this blockage reaches the center of the patient taking the large muscle groups until he finally reached the diaphragm a blockage return is likewise first diaphragm then the large muscle groups of the abdomen thorax musculature and extremities this it can be interesting because for example we can increase the dose of neuromuscular blockers in ophthalmic surgery and continue keeping the patient on spontaneous ventilation we can see in this work here that we use much lower doses of atracurium and we we managed to block the eyeball for a reasonable time to do several in Palmas but we have to understand that we can in this patient also have respiratory depression due to weakness of the chest muscles So I only recommend doing this if you have access to the capnograph or a gas analyzer to go there may be the CO2 of the ok patient and even though the period of action of the new neuromuscular blockers that be well educated around 20 30 minutes we must do the reversal of neuromuscular block we have several monitoring techniques of muscle contractility But in practice what we do is to reverse the patient and be evaluating there How is the ventilation of this animal evaluating the CO2 to see if that animal already has conditions and to ventilate alone as a mechanism of action of neuromuscular blockers occurs by competition and it's very easy for us to solve this, we just need to increase the demand for acetylcholine At Fenda we do this by administering neostigmine, which is a acetylcholinesterase enzyme blocker with that we will not have degradation of acetylcholine and will increase the concentration in the Slit it will displace the neuromuscular blocker going back to muscle contractility the whole problem is that this acetylcholinesterase is not blocked only at the mu junction but it is also in the whole body and then there is stimulation of the system parasympathetic due to excess acetylcholine so it is very common when we are doing the block reversal the animal has bradycardia and salivation so in practice we use the right Zig mines and atropine the right dose the Zig mine is from 0.
05 to 0 1mg that preferably via intravenous and atropine 0 0 3 to 0 0 4mg that if the reversal is in large animals we exchange atropine for eosin to lessen the impact on digestive motility In this case the dose of the workshop is 0. 01 0. 02 MG kg-1 other possibility of reversion is the use of sugammadex sugammadex is excellent because it is specific to reverse the neuromuscular block of rocuronium and the vecuronium it can encompass this molecule And then this and asks for the effect so it doesn't work by increasing the concentration of acetylcholine but blocking the neuromuscular blocker The problem is that this medicine is extremely expensive even for medicine so it is not as used so a very important thing is that we monitor this patient after the reversal I suggest you monitor at least for a time I have a very interesting case in relation to this I once took a emergency an animal that we needed to do neuromuscular block and I used pancuronium a long time ago but it’s worth talking to this patient returned to breathe alone but after 15 minutes which was the period of action of the Daniel Zig Minas and atropine, that animal was blocked again because this animal was a kidney disease and we hadn’t done the exam because it was emergency this animal kept coming and going from the block because we kept repeating the southern ring of Minas and atropines from time to time during more or less What time do we have to have absolute certainty that this patient has ventilatory autonomy and that he will not get blocked again as the conclusion of this video lesson we have to neuromuscular blockers are used to facilitate ventilation mechanics promote and give me total relaxation and thereby facilitate surgeries orthopedic and ophthalmic non-depolarizing neuromuscular blockers are the most used because they promote few adverse effects is very important reverse neuromuscular block using Leo signina and anticholinergics to avoid hypoventilation problems good staff even though neuromuscular blockers do not promote changes in the nervous system they make up a group of important when we talk about general anesthesia whether injectable or inhaled this video lesson was done mainly with the suggestion of several who have watched our videos classes so keep communicating with us there commenting criticizing praising suggesting themes this keeps the channel running smoothly Ok see you in the next video lesson big hug and see you soon It won't go away no, you forgot to talk about the Indian business that can eat the meat of the animal I didn't forget not my old man I just wanted to know if I was going to watch until the end here is like the Marvel movie if you don’t see until the end you lose old thing I think that it is good what the Indian can eat the meat of the animal that he cassol.
