Ep 1 – Rocuronium For The FRCA Primary

Rocuronium – Gas Gas Gas Podcast for FRCA Primary

Introduction and Podcast Overview

00:00-00:34

Please listen carefully. Hello, and welcome to Gas, Gas, Gas, your one-stop podcast for the FRCA primary exam. This podcast will fill your brain with information. Listen to it, think about it, and check out the show notes on the website. There you will find the core diagrams you need to be able to draw and describe for the exam. This podcast can squeeze into your day – listen while you’re driving to work, cooking dinner, maybe when you’re on call, or in the gym. Eventually, the revision is going to end, but for now, expect facts, concepts, model answers, and the odd tangent. Remember to rate and follow the show to hear much, much, much more.

Topic Introduction: Rocuronium Overview

00:34-01:22

Hello, and welcome to the inaugural podcast of Gas, Gas, Gas. Thanks for being here. The title of today is rocuronium. We’re going to quickly talk about when and where, going to go through a model answer, and then we’re going to talk about those delightful core concepts which are going to inform your paralysing agent choices. So, without further faffing, here we go.

So, rocuronium is a non-depolarising muscle relaxant. It’s commonly used and it’s exceedingly convenient. It’s rapidly reversible with sugammadex, or, towards the end of a case when it’s wearing off, you can nudge it towards normality with cheaper drugs than sugammadex, i.e., glycopyrrolate and neostigmine. Generally speaking, it’s stable from a side-effect perspective, but it does trigger anaphylaxis, and this is something to be aware of at induction.

Complete Model Answer: Rocuronium

01:22-02:58

So, Doctor, tell us about your favourite muscle relaxant.

“Oh, well, I really like suxamethonium.”

“Hang on. Hello. We want you to talk about rocuronium.”

“Oh, okay.”

So rocuronium is a commonly used non-depolarising competitive muscle relaxant of the aminosteroid class. It is often presented as a clear colourless solution in ampoules with a concentration of ten milligrams per mil. The dose is one to one point two milligrams per kilo in RSI, or zero point six milligrams per kilo for a standard induction dose during anaesthesia requiring intubation.

It’s considered structurally similar to vecuronium, although its onset time is quicker. The effect site it works at is the nicotinic cholinergic receptor in the neuromuscular junction found in skeletal muscle. It’s considered to be quite water soluble, is thirty percent protein bound and has a very low volume of distribution at zero point two seven litres per kilo.

“Shall I keep talking?”

“Yes, how is it cleared?”

So, rocuronium is eliminated chiefly by the liver, with a small amount excreted by the kidney unchanged. Therefore it would accumulate and would be slow to clear in patients with liver or renal disease.

Side effects of note: It is considered a mild vagolytic, leading to a transient rise in heart rate and blood pressure. It causes minimal histamine release, and very rarely causes bronchospasm. It is a known cause of anaphylaxis, and also of note: on IV injection it can sting and cause irritation.

“You’ve said a lot there, but what does rocuronium actually do?”

Rocuronium causes muscle paralysis. This is utilised in anaesthesia to facilitate intubation through vocal cords, which would relax and separate when a patient is sufficiently paralysed, but it also facilitates operative intervention where a body cavity needs to be accessed which paralysis may facilitate, such as laparoscopic surgery.

Key Terminology and Mechanisms

02:58-04:39

So I used a few terms there. Non-depolarising: rocuronium achieves its paralysis whilst not causing any depolarisation of the muscle, i.e., contraction. You might want to think about this as rocuronium leads to the muscle consuming less oxygen compared to other drugs, whereas, for example, suxamethonium causes widespread discoordinated contraction of the muscle motor units before flaccidity, and may consume more oxygen to do so. However, how relevant that is, is another question.

Competitive: rocuronium is competitive, i.e., if you were to introduce another agent to the neuromuscular junction that had an affinity for the nicotinic acetylcholine receptor, and you had ten rocuroniums and ten of this other drug, if they had an equal affinity, you would have a broadly equal degree of receptor occupancy with both of those agents. If you were to put a hundred rocuroniums in, then they would likely outcompete the other unknown agent. This is a concept that’s utilised for reversal.

The last term that came up there is the neuromuscular junction. We’ll go into this in great detail in another podcast, but this is the interface between neuron and muscle motor unit. It’s a very small cleft whereby depolarising signal from the nerve has to be transmitted to the muscle.

Clinical Practice and Dosing Strategies

04:39-06:51

But then let’s think about what we’re doing actually in reality with rocuronium. It’s all well and good, reeling off numbers like we give 1 to 1.2 milligrams per kilo in RSI, 0.6 milligrams per kilo for routine intubations. I’m sure you’ve all given more and given less, depending on the situation.

So, just to think about RSIs first. A rocuronium RSI used to give me the heebie-jeebies because I thought, “Gosh, they’re going to be very paralysed, and then I’ve got to go get some sugammadex and I’m going to feel pretty embarrassed and there’s a lot to think about and what if I can’t intubate them.” Hopefully, generally speaking, that anxiety is going to wane with time as you train. It has for me.

But if I was doing an RSI, I would generally give everyone one hundred milligrams because the situation at hand is they’re sick. You want to gain control. Paralysed patients are easier to ventilate if you needed to. And getting the tube in the hole is always a good thing because then you can focus on the hundred other tasks you need to deal with with a critically ill patient.

A hundred milligrams covers everyone. It even covers the morbidly obese. SOBA, which is the Society for Obesity and Bariatric Anaesthesia, recommend rocuronium targeted at lean body weight of an individual. So, therefore, everyone will end up sufficiently paralysed with a hundred milligrams, pretty much, unless you’re talking very, very, very muscular individual, in which case you might need to think twice and give them a bit more.

The things to remember when you’re thinking about this dose is it’s got very low volume of distribution, it’s very water soluble, so it doesn’t really get into the fat, so it doesn’t matter so much if they’re morbidly obese.

When you’re going down the route of in-theatre elective cases, some people prefer atracurium, some people like rocuronium, some people like rocuronium because you can bail out at the end and not think too hard about the dose if you just use sugammadex, which appears to be a tendency that’s slowly increasing as sugammadex is now cheaper.

Most people would probably give less rocuronium than 0.6 milligrams per kilo, and accept that they’ll have to wait longer to intubate. At the classic intubating dose, it’s one point five minute wait, whereas with atracurium at zero point five milligrams per kilo, you’re looking at about a three minute wait. So you might as well pick one you like or just mix and match as you see fit.

Critical Safety Considerations: Anaphylaxis

06:51-08:14

The important thing to never truly forget when it comes to rocuronium is it does cause anaphylaxis, and it causes anaphylaxis at entirely the wrong time, because you might think you’ve knocked their SATS probe off. You might think maybe I’ve intubated their oesophagus when I was rather sure that I was intubating the lungs. And sometimes when you’re getting someone off to sleep you get distracted. That three minute wait for paralysis to fully work with your atracurium or your one and a half with your rocuronium. You might start daydreaming or talking to the ODP. Bad news, don’t do that.

My experience was the SATS trace had disappeared and we were fiddling around with the SATS probe wondering why it wasn’t working before maybe about twenty seconds later we thought, “Oh, hang on, the SATS probe’s fine, and it’s just because there’s no pulsatile flow in their finger anymore because they’ve gone into florid anaphylaxis.”

Do you treat anaphylaxis with sugammadex? The jury’s out. No one’s officially said yes or no. There’s case reports that suggest that it works really well. I would argue that if you’ve got an anaphylactogenic drug floating around in your plasma, it’s going to keep triggering any mast cells that weren’t triggered or are partially triggered until your liver clears it. Mopping that up probably is only a good thing. And I would, nine times out of ten, I think, give it, and I have given it for rocuronium anaphylaxis in the single event.

Pharmacological Principles: Bowman Principle

08:14-08:47

Rocuronium is less potent than vecuronium. I mentioned vecuronium earlier. This is to illustrate a principle called Bowman principle. Bowman principle suggests that if you are using a less potent agent, you have to give more of it in order to have the same effect. However, because you’re adding more and it’s a competitive molecule, you actually paradoxically achieve a faster onset time than you would otherwise expect with a supposedly weaker drug.

The other thing to note with vecuronium as another aminosteroid is sugammadex works for vecuronium too.

Examination Context and Future Topics

08:47-10:28

In summary, rocuronium is a really commonly used drug that you certainly need to be familiar with, and you’re going to get examined on, at least in part, about the agent itself, before the examiner then wants to explore such concepts as the neuromuscular junction, the interplay between acetylcholine, rocuronium and reversal approaches, or how to go about understanding the depth of paralysis your patient is currently experiencing.

We’re talking train of four monitoring being that objective or subjective monitoring. They may ask about objective approaches to measuring the train of four, be that accelerometers or electromyography of the muscle itself, to understand how deeply anaesthetised your patient is and/or how reversible they are, as well as the sequelae of incomplete reversal in patients, which you could accidentally have a paralysed patient in recovery and you’re going to feel very sheepish when that happens if you’ve not done it properly and thought hard about it.

Always be reversing. Some of the bosses might not bother. Always be reversing, unless there’s a contraindication to the…

Future podcasts. We’re going to talk in great detail about acetylcholine. We’re going to talk about how you trigger that saltatory conduction down your nerve sheath to get to your neuromuscular junction in the first place, going to explore the delights of how excitation-contraction coupling comes about, what other drugs, agents, and toxins can influence your muscle power and whereby they act, and naturally we’re going to talk about suxamethonium, atracurium, sugammadex, neostigmine, and glycopyrrolate. But we’re getting carried away.

Conclusion and Call to Action

10:28-10:59

See you next time. If you found it useful or awful, please like and subscribe and rate the show. Definitely check out the show notes for those diagrams and the detail of this content. It is a bucket of content to get to grips with. Keep working at it, and you will get better, faster, and stronger. It is vital to keep your interest alive for the science that we’re covering and not overcook yourself. You will be amazed by what you know come exam day. Don’t freak out, keep studying.