Episode 66: Neuromuscular Blockers

In this episode, episode 66, I go through an overview of neuromuscular blockers including how they work, how to use them, and what their adverse effects are.  Happy New Year!

The dose of glycopyrrolate should be 0.01 to 0.015mg/kg, not 0.1 to 0.15.

Outline by Brian Park: Outline

References:

Miller’s Anesthesia 7th edition: Chapter 29: Pharmacology of Muscle Relaxants and Their Antagonists. Naguib M and Lien C.

Rocuronium vs succinylcholine for rapid sequence induction intubation. https://www.ncbi.nlm.nih.gov/pubmed/26512948

Neuromuscular blockade: what was, is and will be: https://www.ncbi.nlm.nih.gov/pubmed/25622380

Reversal of neuromuscular block: https://www.ncbi.nlm.nih.gov/pubmed/19468024

15 Replies to “Episode 66: Neuromuscular Blockers”

  1. This is a great episode that helped tie in previous droning lectures about neuromuscular blockade. You put out great content and I know many SRNAs who appreciate your podcasts. You’re making this mountain to climb doctorate just a little more attainable. Thank you.

  2. How about reversel after mivacurium. As far as I noticed, it wasn`t commented. I have heard that it is not necessary to reverse after 20 min (normal intubation dose). If true, is that bc of its short duration of action or its type of elimination? Any comments are highly appreciated 🙂

      1. We use mivacurium often for short cases that deemed to need a tube but in my fairly extensive experience you have perfectly adequate intubation conditions (remifentanyl / propofol induction) with half the recommended dose (I find that to be true of lower doses of Rocuronium as well) using lower dosage rarely have problems in a very high throughput environment where 90 done in general anesthesia (TOF (with accelerometer) and clinically), the need for routine reversal seems limited in my experience . One option that IMHO should not be forgotten is that intubation without relaxant is most of the time possible without risk to vocal cords in especially in the elderly.

        1. Thanks for the comments. I completely agree with you that it is often possible to intubate without blockade, especially with remi and propofol in adequate amounts.

  3. Great episode, as usual. I wanted to clarify my understanding of something: You mentioned that the ED95 of Succinylcholine was 0.5 mg/kg, and thus, we would normally give two times the ED95 for optimal intubating conditions, thereby giving us the 1 mg/kg dose we often use. However, when learning about this, I read from several sources that the ED95 is actually closer to 0.3 mg/kg, and we have to use more than twice the ED95 in the unique case of Succinylcholine for optimal intubating conditions, possibly due to the fact that Succinylcholine is actually being broken down by pseudocholinesterase before it even reaches the neuromuscular junction. Let me know if you’ve heard this logic before, and any thoughts that you can add will be greatly appreciated. Thanks in advance!

    1. Hi Anthony,

      Great point. According to Miller’s Anesthesia, 8th edition. the ED95 of Sux is 0.51-0.63mg/kg. However, the reason that you need that much to achieve 95% suppression of neuromuscular response (the definition of ED95) is because up to 90% of the administered dose can be hydrolyzed before reaching the neuromuscular junction. This effectively makes sux seem less potent than it really is. The estimate for it’s ED95 if it weren’t broken down on its way to the junction would be less than 0.3. But in reality what matters clinically is the dose you need to achieve a clinical effect and that ED95 is around 0.5.

      I hope that helps.

      Best,
      Jed

  4. Great post.
    You mentioned Cis-atracurium for RSI? Do you really do that? 2min is a long time until intubation.

    What about Sux and oxygen-consumption. Do you have a problem in giving it to patients who are in danger of sudden desaturation? (… I know, eventually all our patients are in danger of hypoxia)

    And one more thing, when you have abnormal pseudocholinesterase you can have a phase-II-block after sux and using neostigmine can act paradoxical and even prolong the blockade. Have you seen this in the past? What do you do when you have a unknown abnormal pseudocholinesterase as a differential? … probably just sedation and waiting to wean the patient from the ventilator.

    In my hospital we don’t have glycopyrrolate, we use atropine instead and normally in a ratio of 1:2 or 1:3 with neostigmine and the dosing of neostigmine depends on the TOF-Ratio (if you have accelerometer … the Dragees TOFscan is awesome … I have no financial disclosures). 😉
    Great podcast and great content.
    Thanks a lot and greetings from Germany.

    1. Hi Thomas. Good questions. I do not personally use cis-atracurium for RSI but in theory it could be done. I agree it’s an uncomfortable amount of time to wait, though with a big enough dose you can probably get relaxation in less than 2 minutes.

      In theory the muscle fasciculations from sux will cause a slight increase in o2 consumption for a brief period of time. I’ve never worried about it clinically however.

      Abnormal pseudocholinesterase can’t break down sux as well as the normal variant, so causes a prolonged block. In theory, neostigmine can further impair the action of pseudocholinesterase and so prolong the block even more. In the setting of a patient who is not regaining twitches after getting sux, the only option is to, as you say, sedate and support until they recover, which they will do eventually.

  5. I would like to point out that there isa typographical error in the Outline. In the second tablet her duration of Rocuronium should be 70-80 minutes and not 7-8. Thanks.

  6. When reading the outline (which is awesome) I noticed it says sux does not stimulate presynaptic nicotinic receptors. This concept took me a long time to wrap my head around (studying for a NMB exam this week) My understanding is sux does stimulate presynaptic nicotinic receptors, works like ACh, and continues to stimulate the neuron to prepare more ACh vesicles, like ACh would. Thus sux produces no fade because there is a continuous supply of ACh.

    My copy of Millers is 7th edition page 159 says “Presynaptic receptors, aided by calcium, facilitate replenishment of the motor nerve terminal, which can be stimulated by SCh and neostigmine and depressed by small doses of nondepolarizing NMBDs”

    1. Thanks Mike. What we meant is that succinylcholine does not block these receptors, and therefore does not cause fade in the way that nondepolarizers do. There may be some activation of these receptors, as you point out, but it is not significantly more than the activation from acetylcholine itself. And therefore the significant point is that succinylcholine does not block the action of these presynaptic receptors. Thanks!

  7. In both the audio and in the outline, you mention Glyco dose of 0.1-0.15 mg/kg. This would mean 7mg of Glyco for a 70kg patient. Shouldn’t this be 0.01-0.015 mg/kg or 0.1-0.15mg/mg of neostigmine? Thanks.

    1. Thanks for catching that. The dose should be 0.01-0.015. I have corrected this in the outline and noted it in the shownotes. Thanks!

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