Beta Blocker Overdose

According to NICE, beta blockers are the fourth most commonly prescribed drug in the UK, behind proton pump inhibitors, statins and paracetamol. These are highly accessible medications, which means the potential for us to come across a patient presenting with toxicity, whether intentional or not. It's quite high. Propanol, for example, is one of the top 10 most search drugs on the National Poisons Information Service, Toxbase. So that's why this month we're looking at beta blocker overdose. So, would it be stressful trying to remember what the treatment regime is for a toxic patient? Would you panic over what drug to give when you'd run out of atropin and does try to spot the signs of someone who's overdose on their beta blocker, send you into a frontic panic? Well, slow down. There's no pressure. [Music] So, hello and welcome to General Broadcast, my name's Josh. And I'm Simon. And welcome to another episode. I want to start by thanking geeky medics who continues to support this podcast in being free and open access to all of our listeners. And thanks to those of you at home who support us on coffee.com by donating and helping with websites and hosting these. That's thank you to people like Matt, self-reported, very tired, undergrad. Matt bought us both a coffee and left us a comment saying he's a long time listener. He says, "I definitely owe you both a coffee. The podcast helped me when making my decision to undertake a paramedic science degree. Since you've helped me with all my prep notes for uni and continue to now and I know it's helped others at uni. Here's a coffee. So Matt, thanks very much for your kind donation. We really do appreciate it. And if you like Matt, I've been a long time listener. Maybe you can inspire the essay or help to out in a NOSCII. Or even just to help with your sound like a brain box in that crew room discussion. And you'd like to buy us a coffee to say thanks. Well, you can find the details on how to do that in the show notes of this episode by going to coffee.com/generalbalkast. And Simon, before we get into these things, I think a celebration is in order. May a happy 50th. 50th? I was like, my birthday? I don't think I'm that old. No, you may look tired and haggard like. Yeah. I feel like I'm 50. No, the 50th episode, mate. General Wow. Is five years old. This is episode number 50. So awesome. Who does thought we made it that many in? I was surprised people are still listening to us waffle on. It's basically just me doing the proofs and my mum, but yeah, the last of the day. Here's to another 50. And to celebrate 50 episodes, we've partnered with GeekyMedics to run a little giveaway. So for all of you listening, for your chance to win one of their brand new textbooks, either their osky checklists book or their clinical examination book, you can find out how to do that on our social media. We're basically asking you to tag us either on a Twitter post or a Facebook post or another social media post and just share your favorite episode of General Borkast. It really helps us get the word out there about our podcast helps us get out there to other listeners. And it's a prime time with new people starting university, new students just about to embark on their journeys as student paramedics to be made aware of us and hopefully for you guys to win the chance to win one of those brilliant osky textbooks or clinical examination textbooks. So more about how to do that in the show notes or on our social media, but shall we get on with the episode? What are we talking about this month? Yeah, so I think we've got a good one this month. So we're going to be talking about Beatoblock or Overdose. So this one was your idea, Josh. And I think this has come from a particular job that you attended. So you've got a bit of a case study, I think, to kick us off, is that right? Yeah, absolutely. I will share the details of the case next. So as you said, this was the reason that we've chosen to talk about Beatoblock or Overdose this month is so obviously not including any identifiable information. The general overview of the case that I was involved with was this was a case from quite a while ago for a patient who had been seen or threw the window into their house by a neighbour and had called police to break in as a concern for welfare. And when police have got their days found patients, unresponsive with packets of propanolol around them suggested that they'd taken an overdose and a letter of intent. And so the police have scrambled us on our dispatcher who's picked up on the risks associated with this case and has dispatched us. And on-reached, Dave given us the updates that this is a patient who's taking a propanolol overdose is unresponsive and during our flight to see the update that the patient is now fitting. And shortly after landing we get the update that police are now doing CPR, this patient's in cardiac arrest. So by the time we get to the patient's side, it's estimated that this patient's been in cardiac arrest for about 15-20 minutes with CPR from police. And about five minutes before we arrived, the ambulance crews were right. And so we assess the patient together as they were getting them into the DCA. CPR wasn't ongoing at this point because they could feel the pulse. So we called this a time of loss. And our assessment in the back of the DCA, this patient had an OPA in situ. He was self ventilating low rate at about 12 a minute with a high end tidal CO2 noted. So it was a high end tidal CO2 of about 12. He was cold, periphery shut down, really weak, practically absent radial pulses and was markedly broadic cardiac within a regular rate somewhere between 35 and 45 feet a minute. And it looked like an idiot ventricular rhythm. So it wasn't nice in narrow, it was sort of broadish. And the patient had a reduced GCSO. It was a GCSO of seven that was eyes to voice one, mode to four. No obvious head injury and it should be normal. And with this patient we were ages from ED. We're talking sort of 40, 45 minutes from the nearest emergency department. And if he wasn't sort of post-rosk, so he was definitely peri-erest. So questionable whether or not he had arrested. But he was definitely, definitely still peri-erest. And so the question is then what do you do? There's clearly a lot to achieve. There's clearly a lot of obvious things that we can do. But what is the right care for this patient to help manage this complex dose of those 45 minutes from further help? So that's what we're going to look at. Yeah, I think the big key there is 40, 45 minutes from hospital. We can't just take the attitude of throwing the back and driving to definitive care as it were. We need to provide some interventions on the way. And I think actually there's a lot of stuff that we can achieve and do some really beneficial stuff of this patient. At a paramedic level and obviously critical care and more advanced paramedic practice level, even before we get to hospital. But I think in order to understand why we're doing those things, we probably should understand a little bit more about the kind of pharmacology of how beta blockers work. So Josh, you just want to go into a little bit of the pharmacology of beta blockers. To fully get beta blockers, we need to do a bit of a revision of the sympathetic nervous system. So as most people will know, the sympathetic nervous system is our fight or flight system. It ramps the body up for action and will bring about changes to optimize us for that. So you know, it's designed to increase blood flow to vital organs to muscles. It will dilate the iris to improve vision. It'll dilate airways to optimize oxygenation, etc, etc. You know, this is stuff that most people listening will be familiar with. But to help us understand beta blocker overdose, we need a little bit more detail than that. So how does this system activate? Well, when the hypothalamus in the brain detects a stimulus, warranting sympathetic response, it sends signals, which eventually end up that splank knick nerves in the spinal column. Now, splank knick nerves, if you remember, are 10 minute topic on autonomic dysreflexia, other autonomic nerves, which carry messages from the central nervous system to our visceral organs, like the heart, kidneys, guts, and the adrenal glands. The adrenal glands secrete adrenaline and noradrenaline directly into the bloodstream. And they're these hormones bind with adrenal receptors located on target organs to bring about changes. Now most people will be aware we have different types of adrenal receptors around the body that perform different functions. So we've got alpha-1, adrenal receptors that are found in blood vessels, responsible for vasoconstriction to increase blood pressure. So when we stimulate those alpha-1 adrenergic receptors, we see a vasoconstriction effect take place. And they're also found in the liver. So when they're stimulated glycogenylisys will occur and blood glucose will increase, again, all designed to optimize us for a phytoplyte situation. We've got alpha-2 adrenergic receptors. These are found in pre-synaptic neurons. That is responsible for a negative feedback loop. Because when these are stimulated, they inhibit further nor epinephrine release to hopefully get in control of the sympathetic response. So we don't need to focus too much on alpha-2 adrenergic receptors on this podcast. And then we come on to beta receptors, which is really where we need to focus on. Beta-1 adrenergic receptors are found in the heart. So when adrenerylin binds to the adrenergic receptors on cardiac amyocytes, it forces calcium gateways to let in the more calcium ions. This results in increased prototropy and increased heart rate, increased Inaetropy and increased contractility. And it also will result in increased dromotropy, which is the speed of conduction through the cardiac conduction system. So beta-1 adrenergic receptors focus on the heart, the easy way that I remember that is one beta. We've got one beta, that's our heart, is affected by beta-1. And beta-1 receptors are also found in the kidneys. And this activates the RAS system, the REN-IN angiotensin aldosterone system, which is the backbone of arbolacresia control. So really, really simply, adrenerylin results in REN-IN release, which results in angiotensin release. And that's a potent basal constrictor. Causing our blood pressure to rise. And then we move on to beta-2 adrenergic receptors. Now most people will be aware of these, found in the bronchial, they're responsible for poronco dilation to increase airflow. But they're also found in skeletal muscle, where vasodilation will take place in order to increase blood flow to muscles to prepare them for use in fight or flight. And then finally, there's also beta-3 adrenergic receptors. We don't need to worry too much about these, but just for awareness, they're found in adipose tissue and a responsible for lipolysis, increasing the available energy to cells. So in summary, we've got alpha-1 adrenergic receptors. These are found in the blood vessels, and typically responsible for vasoconstriction, also found in the liver, and will induce glycogenlysis. Alpha-2 adrenergic receptors, that's part of the negative feedback loop to stop the process. Beta-1 adrenergic receptors, they're found in the heart, and they increase heart rate, increase the strength of the beating, as well as found in the kidneys, which result in activation of the rough system to increase our blood pressure. And finally, beta-2 adrenergic receptors, that are found in the lungs, and that's responsible for poronco dilation. We do need to think a little bit about the different generations of beta-blockers, because there are certain agents and types of beta-blocker that are going to have different types of effect. Whether they are selective or non-selective, and there's three different generations of beta-blockers. So two that we're going to particularly talk about, Josh is propanolol, which is obviously what, this case is based around. And then we should mention, like, sotolol as well, because they've just got a few effects that you also need to consider, as opposed to some of the other beta-blockers. So first generation beta-blockers are propanolol, sotolol, and also include timolol, pindolol, and madolol. I mean, I've heard of propanolol and sotolol, but I haven't heard of the others. I don't see them used very often in clinical practice. But those first generation beta-blockers are non-selective, meaning that they will work on much more of the adrenergic receptors. So that's your alphas and all your betas. Whereas the second generation of beta-blockers are more beta-1 selective. So that's your a tenelol, bysoprolol, matoprolol, and ezmalol. And actually, all of those I do use in prescribing clinical practice. Obviously, bysoprolol, we give a lot for HLF, orally, people are a lot of people are on bysoprolol for blood pressure control, HLF control. With toprolol, we give to, as a IV beta-blocker to slow, you know, rates down. And ezmalol, actually, we can give in things like refractory cardiac arrest, which is a completely different topic. But it's something that, you know, is used occasionally for refractory VF arrests when you kind of get in out of your kind of standard A or less stuff. And the other thing about those, because they're beta-1 selective, and they are much more effects on the heart as opposed to the lump. They do affect the lump still in the beta-2, but they're less, they have less of effect on the lung. And therefore, like, you might find that some people say with asthma, who shouldn't really be prescribed beta-blockers, because it can be a bit dangerous. But because they're very beta-1 selective, in some patients, you can give things like bysoprolol, you know, to help and be more selective to the heart, rather than the lung. That's the kind of things that people think about when they're describing those. And then there's other beta-blockers that are third generation, some of which are non-selective, and some are beta-1 selective. So your non-selectives will be like a libettalol, and some of the new beta-1 selective ones like Nabivolol. But again, some people are on them, but don't see them that often in common practice. The common ones are a tenelol, bysoprolol, matoprolol, propanolol, and sotolol. I would say that's what I'd come across mostly, and the ones that some of those are, I'd prescribe. And I probably would just say, you know, the clinical relevance of that in this instance. The ones I remember are propanolol and sotolol being non-selective, because they're the ones from that sort of first generation group. Yeah, and that's important, isn't it? Because we're going to come on to why understanding those, the fact that they're non-selective, and they have other properties. I don't want to give away your bit later. For other properties, they can actually make the complications from an overdose significantly different or worse. So that's why it's worth knowing this. So if you know exactly what it is, you can prepare a little bit more. You know that there's a higher risk for some of them than others. Do you want to maybe talk a bit about how beta blockers in overdose work and what's actually happening? Yeah, so the main concern with the beta blocker overdose is cardiac instability. So propanol, as we've kind of mentioned, specifically has some concern in sodium channel blocking effects as well as its beta blocking effects. And Josh, you're going to discuss that kind of later, because that's kind of really relevant to this case. So we'll cover that in a bit. But generally with beta blockers, they competitively block beta one and beta two receptors, which in turn decrease production of intracellular, cyclic adenosine monophosphate or camp or CAMP. This has a blunting effect of like the circulating catacolamines, like adrenaline, noradrenaline. So in heart failure, for example, we've prescribed this is really beneficial because it reduces the demand on the myocardium by reducing heart rate, blood pressure, contractility. You know, the myocardium is already struggling. And if we can reduce that, it takes the workload off the heart. And it also prevents that ventricular remodeling that we see with heart failure patients. But obviously in overdose, that can then create a shock state because we're going to overdo that and we're going to get heart rate problems, blood pressure problems, contractility problems. So as a result, we see bradacardia, we see hypotension. And these are some of the most predominant symptoms. So Josh, you mentioned in your case study that, you know, the patient was, had a weak radial pulse, so that's kind of our hypotension. They were even potentially in cardiac arrest at one point when with the police, you know, possibly. And they were bradacardic. What was their heart rate? It was like 35 to 40. It was a bit all over the place, but kind of hanging around that number, 35 yet. Yeah, so we're starting to understand why the pharmacology of these drugs causes those symptoms. You also said they had a reduced GCS, I believe it was seven. So some beta blockers, specifically ones that are highly lipophilic. So that means that they combine well with lipids. And as we know, the blood brain barrier is made of that phospholipid layer. And therefore, if they are, they combine well with lipids, they can move across that blood brain barrier easily. And that can result in CNS manifestations, such as seizures and reduced conscious level. What further affects our conscious level is the fact that the decreased contractility, the hypotension, the bradacardia, might cause reduced profusion. And cardiac output. And that results in cellular hypoxia, which makes this CNS toxicity even worse. And we all know that people that are hypoxic and if their brain doesn't get enough oxygen, they can have seizures and their conscious level is going to be reduced. Making it even worse is that Josh mentioned that beta blockers have an effect where they inhibit gluconeogenesis. And therefore, our blood glucose levels are affected. and we know also that if you have low blood glucose and hyperglycemia, that can cause seizures in reduced levels of consciousness. So we've got these all of these combined factors, you know, the going across the blood brain barrier easily, the decreased profusion in cardiac output and the hyperglycemia, all of which can lead to this reduced conscious level and the seizure activity. What's even more concerning is a lot of patients take polypharmacy overdoses. So if someone has co-ingested calcium channel blocker overdoses alongside their beta blocker, specifically agents like propanolol, then this can cause significantly profound hypertension and cardiotoxicity. So we need to be really cautious if people are on other kind of cardio selective medications in that overdose. Furthermore, propanolol has certain effects on sodium channel blockers. So just, this is where we're kind of coming in that propanolol specifically has more issues than some of the the other beta blockers. So tell us a little bit more about propanolol. So propanolol, when you read up about it, there's this great quote that is stuck in my mind with life in the past lane, which is propanolol is a sodium channel blocker masked as a beta blocker. And that's because in various studies, it's been demonstrated to have sodium channel blockade effects, which can be quite helpful if you're trying to manage a patient with a very unwell heart. But in overdose situations, not only do we have the beta blockade, so we've got the the bradycardia and hypertension that that's inducing ordinarily as its effect is a beta blocker. We've got the lipophilic elements of it is crossing the blood brain barrier and is inhibiting neurotransmission in the CNS. So we've got the CNS effects. We also get this enhanced cardio toxicity from its sodium channel blockade effects. So not only do you get the bradycardia, patients can also go on to develop an AV block. There's been examples where patients develop QRS prolongation or even QT effects, so QT prolongation. And this enhanced cardio toxicity means that cardio vascular collapse and propanolol overdose is all that much more likely and all that much more severe. There's also some studies that suggest propanolol might have calcium channel blockades. So you just get this triple effect on the heart to just really knock it for six and enhance the chances of a patient going into cardio vascular collapse. This is why it's important to establish if possible that the agent has been taken. Obviously they use beta rag and S like so, butymol to treat their asthma. And if they've taken a beta blocker overdose, this can induce bronchospasm because obviously we are blocking the beta two receptors, which is what would be stimulated if you had like a drug like subbutamol. So people may present with wee and bronchospasm and it may be really difficult to manage because you have blockade of these beta two receptors by the beta blocker overdose and meaning that the subbutamol doesn't work as well. So it's just some worthwhile considering that you know you might have challenging bronchospasm to manage. So we've kind of established that as part of our work up of the patients and the history tape. We want to know what specific agent the patient's taken if possible because of those extra effects. The other one that we should probably be aware of as I mentioned was Sotolol, which has anti-dysrhythmic properties similar to a type 3 anti-arhythmic. And this prolongs action potentials duration and then the refractory period of AV myocytes, which then causes a prolonged QT interval and that in itself can trigger the polymorphic ventricular tachycardias like torsarts and that can happen delayed after ingestion. So kind of up to 48 hours after ingestion, so just be aware of someone's taken a overdose the day before they may not be safe if it's you know things like Sotolol and risk of those polymorphic dysrhythmias. And we'll talk a little bit about managing those shortly because actually there's some some some new things appearing nationally that we might be able to do some interventions for these. I think one final thing on history take. Most people will be familiar with the things that we need to note down, which is the reagent, the amount if we can, in common overdose agents at also the timeline that that affects the overdose because the majority of patients will start to manifest symptoms within one to two hours, particularly with propanol. But as you said Simon, you talked about prolonged or delayed manifestations. It's probably worth bearing in mind that some of these medications may have a modified release component. So I think metoprolol has a modified release version and there may be others. So if the beta blocker has MR after it, just bear in mind that this may be a slower release and so seems as maybe delayed. Yeah, it's a great point actually because you know, toxin-based warns us about this and it's something we do in practice where a lot of drugs we kind of, they vary but most of the time it's between four and six hours of monitoring and the asymptomatic patient we can discharge and if they've got no symptoms, the modified release drugs tend to be a lot longer. So we might admit you feel like 12, 24 hours if you've had an MR version of a drug. So yeah, it's worth being aware of that. So if we kind of do an A to E then approach to our kind of like not an assessment but like management mainly of this, we can try to talk through the interventions we can give and then we'll talk a little bit about you know, cardiac arrest management as well. First of all then airway. So we've already talked about you get a reduced conscious level which means your airway is going to be a risk. So we need to manage our airway. And if conscious level has been maintained and we've got to the patient early in their ingestion, then we might want to consider kind of early activated charcoal within the first hour of a potentially toxic overdose. And obviously I use toxin-based to try and calculate you know, my toxic doses you can get like me know milligrams of micro-alcoholic kilogram doses on top space and that'll guide you to whether you know activated charcoal might be a good intervention. But yeah, within the first hour I think about activated charcoal obviously as long as the airway is maintained and the patient's fully conscious. And if they're not, then we need to manage our airway. I guess we've just talked about modified release but that our timeline that we often give for activated charcoal probably makes sense wouldn't it that that is extended if it's a modified release medication. So really interesting question about actually the answer to that. Because the medicines designed to hang around in the digestive tract. It's not long ago isn't it? Yes. So theoretically yeah, I think you're probably right. I've never seen anything over an hour. Personally, I'm not saying I'm right. I'm just saying I've never seen it. So you think about breathing then remember I said the bronchospasm can occur. So we need to treat this with salbutamol you know, regardless of the fact that we said that it may be challenging to respond to that. We can give our petropeum and we can also consider giving us that dose of steroids because that in the long term will reduce bronchospasm and that's guidance from from top space. If you are struggling to manage bronchospasm so we you know we've got hydrochlorosone, some trust have got prednisolone. So yeah we can consider steroids. So next time we're going to move on to circulation management and this obviously is probably the most important area it's going to be see as well. 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Just remember to tag us in the post to be in for your chance to win. Okay back to the podcast. So let's start off then with the high-potension. So we're going to manage high potension initially with increased stretch and contractility via the Frank style mechanism by giving some IV fluid to resuscitation. So that's our going to be our first intervention for high potension is giving fluids. So yes I would agree giving some fluids is not a bad idea. It's really quick, really simple isn't it. So hanging a bag of fluids and letting that go through is fine but it's probably worth bearing in mind that these patients aren't fluid, deplete and a lack of volume is not the reason for the high-potension in this patient. It's a rate and distributive issue. So yes, you may get some temporary improvement using the Frank Stalin mechanism by causing that, that stretches of cardiac muscle. However, what we need to be careful of is causing like a rebound type pulmonary edema because these patients will be at risk of a cardiac pulmonary edema because their heart is not pumping as normal, is it? So I wouldn't be looking to fill these patients with needless of needless and fluid. It's not a bad quick adjunct that pretty much any number of our ambulance team can enact while we're doing some of these other things. But it's important that we understand this is not the fix. Is that fair to say? Yeah, no, no, yeah, I would agree. And you know, the pulmonary edema is a great point actually, you know, not fluid overloading them. I think, you know, when we think about the, you know, our physiology and the fact that the contractility is decreasing an easy way to increase contractility is to increase stroke volume. So if we put more fluid into the ventricle, it's going to stretch more and we're there for increased cardiac output. So you are right. It's a temporizing measure, but it will just manage that hypertension just in the interim. But yeah, you are right. It's not the ideal management. We need something a little bit more, you know, a little bit more permanent. But yeah, it's just an easy start, I think, like you said, it's very quick. It's easy to do quick cannula and fluid's upgiven relatively quickly. But yeah, and you have a point and I suppose we need to double down on your point, especially in patients who have a background of heart failure. So the patients that might be on beta blockers themselves, you know, potentially could have heart failure. And, you know, actually smashing them full of fluids when this isn't a volume to pollution problem is not going to help. In fact, it's going to make it worse. So it's going to make the workload on that heart struggle even more. So yeah, so fluids, I think, to manage do have a place, as we said, if you think about the physiology, but they're not the permanent solution. So we kind of talked about then how else can we improve cardiac output? So if that's going to firstly work a little bit on our stroke volume, the other thing we need to look at is the other part of that equation is heart rate. So obviously it's heart rate stroke volume equals cardiac output. So if we're a bradycardic, then the first thing we're always going to do is think about a smatric bin. So five to 600 micro amdosis, which will obviously be repeated. And then if they're unresponsive, we need to think about other agents. So to me, I would be thinking about things like isoprenelin in recess or giving an adrenaline bonus, which is traditionally something that technically a paramedic can do, because of our paramedic drug exemptions, but it isn't in JRCalk, but Josh talked us about adrenaline and JRCalk. Yeah, well, so is in JRCalk now. Simple. Oh, yeah, I tried to really drum you up there. I wanted to drum roll moment where we were going to revolutionize it. Yeah, okay. Yeah, it's in JRCalk now. Good work. So as of July 2025 update, update 2.25 JRCalk has updated the bradycardi or algorithm to include adrenaline in the event that atropin is not successful. So this is for all bradycardias, not just beta blocker induced, but obviously it does apply here. On the, as you said, Simon, you can repeat atropin a number of times and having seen a few beta blocker overdoses, I would suggest that you're going to be giving it all over the care episode that you present with this patient. Theoretically, it shouldn't make a huge amount of difference because it's not a vaguely mediated bradycardia. But one of the things as my career goes on and I get more experience that I'm learning about atropin is it just seems to work for some reason. It's always worth a try. Yeah, it's like said degree heart blocks shouldn't work often does in this instance shouldn't work, but it does or seems to. So with these patients, we're throwing absolutely everything we can at them to get their heart rate up. So I would suggest that you draw all your atropin up and you just be giving a meal every now and then because it may have some benefit if there is any vaguely mediated suppression on the heart. But we're talking about adrenaline. So as you say, yeah, legally, paramedics have been able to give this without it being in the JARC, our update is in a huge amount of guidelines. So without this update, I would have absolutely felt supported to do it because it's in a load of national guidelines, but it is helpful that it's now in a national ambulance guideline. So JARC would suggest if the patient's unresponsive to a dose of atropin, then trial a 50 microgram aliquot of adrenaline. So that is 0.5 mills of a one-in-tenth thousand millegette and you again JARC would support you, trialing that every three to five minutes, we've no upper dose. Now that is a reasonable whack of adrenaline to be there, but these patients will need high levels in order to out-compete the beat blocker. So you know, as an example, in my case, I had the syringe driver available, we were upping and upping and upping. This patient by the time we dropped them off, hospital was on 800 micrograms an hour of adrenaline infusion, which again is a reasonable whack of adrenaline. But yeah, trying them on a 50 microgram aliquot definitely seems reasonable. You can then dilute that if you want to titrate that even further. So you could dilute that to one in a hundred thousand concentration. Personally, I'd make that up into 20 mills. So that's two mills for one in ten thousand millegette in a 20 mill syringe and then dilute that sodium chloride that gives you a ten microgram per mill concentration, which is a standard post-rosque concentration. And then you could try getting that to the patients, a mill a minute or a couple of mills a minute, which would not be unreasonable. Like I say, these patients, when they are as unwell as the patient I had in my case study, we are throwing absolutely everything we can to get their heart rate and their blood pressure up. And they will use a huge amount of adrenaline over your per episode. I mean, I know they were in cardiac arrest, but they are still peri-arrests, aren't they? The patient you have, you're moving this day, peri-arrests. And actually, that adrenaline is going to, I know we can get into the real nitty gritty of pharmacology and talk about the different doses of adrenaline, you know, high dose, low dose, and how one affects blood pressure, more one affects heart rate, more, but actually it will help both heart rate and blood pressure response, which is what we want in these patients. Yeah, absolutely. So you are getting alpha-1 receptor activity and you're getting, well, you're getting all the adrenal receptor activity on you, but what we really care about here is the alpha-1 and the beta-1 activity. If you're struggling with the weas of the natumatic as well, the beta-2 would be helpful. The issue is that in a non-competitive beta blocker, all of these receptors are blocked. So we're not going to have the response to a dose of adrenaline that we would normally expect as a post-roscopation. So I can say we will need and use large amounts of adrenaline with these patients. And the absolute gold standard would be to put lots of syringe driver if you've gotten enhanced compared to even there of high dose adrenaline. It's kind of similar to what we were saying about the cell beauty, more or less, not going to be as effective as you're going to need more more dose. And it's weird because I am old enough to know and you probably not in terms of professional career that actually this is not the first time that we've given adrenaline for this reason. So when I was a student paramedic many, many moons ago, there was a little line at the bottom of the productart here algorithm that said, if there is risk of acistually adrenaline bonuses can be given. But it didn't tell us what those bonuses were, how to do it, how to draw up, how to do anything, but it did allow us to do it. And then after they updated from 2006, God knows, I mean, that's how long ago we're talking the 2006 Jowlc out to the 2012 pocketbook. I think it was the next one. It just that line disappeared, which was interesting for those of us that were always doing it a union as part of our kind of Sims or part of our patient care. But suddenly that was then considered to be not part of the guidelines, which was hard. So I'm glad it's back in. I think it's sensible. We do need some sort of management for like shock and high-potention pre-hospitalia. So this is good. And just to clarify that something that a row paramedic can do, obviously they have to satisfy themselves with their competence and stuff, go and read up on your pharmacology of adrenaline, adrenaline as to a patient with pulses. It's more risky. We have to face that then, the cardiac arrest or given it I am. But we have to make sure we give the right dose and not the wrong medication. You don't want to give you one in one thousand IV dilute because that's going to cause you problems badly. So yeah, so just obviously just go and have a read up on that for to mineralise yourself with the new JLQC update, but at least it gives some ammunition for row paramedics to do another level of intervention to treat these patients. - Let's move on then. As we're talking about adrenaline and cardiac arrestal parriarist patients, we could probably talk about amoeodraine if the patient was on cardiac arrest. How would you manage amoeodraine in sign-in if this patient was in a shockable cardiac arrest? - So to be honest, probably from my knowledge of amoeodraine in this specific case, I would just be giving you standard doses in cardiac arrest if they were in VF. If they were in a polymorphic fatigue and perriarist, I might give another drug, but I think you want to talk more about amoeodraine before I go on to that. - Yeah, so this is a difficult one because we now are out of accepted guidelines. So this is not in a talk space as far as I could see. This isn't in the RCUK, less algorithm. This is just research and what's in a variety of other sources looking at this circumstance. So I gave a radio call to the ops officer that was on scene prior to me arriving. When we got the update that this patient was in cardiac arrest and basically asked them if they were in a shockable rhythm, not to give amoeodraine. And my rationale for that was, we know amoeodraine is a class three anti-aridmic, which means it has mainly potassium blocking effects, but it also has sodium channel blocking, beta blocking, and calcium blocking effects. My rationale for that was if we've got a patient that's overdosed on a beta blocker with large sodium channel blocking effects, probably what we don't need is more of that. As I say, wouldn't necessarily advocate that with other people and I can see you smiling on the camera there. - I completely, well, I mean, when you think about the pharmacology, it completely makes sense. It's never crossed my mind, completely makes sense. So I'm gonna have to go and look at it. - So many research. - I'm gonna have to look at it. - It's just looking at, I made a pharmacology of the drug, I think, - We've seen it in my science lane and stuff. - Now you've said it, it kind of completely makes sense. And actually, it's stuff you don't think of. You kind of go into this pattern. And it does kind of prove that we need good thinking when we know it's not just protocol-driven practice when we're managing these critically sick patients. We do need to think about why and what we're doing. There's lots of stuff that seems, oh, let's improve their physiology, but actually, if you improve the physiology wrongly, you can cause more harm. So actually, that's a really good one for me to go away and do my own reflection on. - Also, it's like we often say isn't it? That the ALS algorithm is the lowest standard. It's not the standard. And guidelines guide, and they're great for the majority of patients, but they're not great to fit every patient. Like I say, this isn't me suggesting this is necessarily the right care that everybody goes out and does because this is rare, low-tier evidence. But in my mind, that was my clinical decision at the time. Turns out the patient wasn't in a shockable with them and again, realistically, other than the perhaps very, very early stages of cardiac arrest, these patients are unlikely to be in a refractory, shockable rhythm. It's more likely to be a low-slow PEA or a low-slow state. So that was my rationale for the clinical decision at the time. - Yeah, and that low-flow PEA state and going into access to the makes sense from when we think about the pharmacology, doesn't it? Apart from when I mentioned Sotelol, which obviously can cause because of that change to the actual potential, can cause that, and you know, polymorphic ventricular tachycardia. And the drug I was on about was, I'd give IV magnesium for that because that's obviously a standard treatment for the Tulsard type arrhythmias, which is appearing and potentially going to be appearing in J.O.K. I don't know if it'll be for that reason. But obviously it's one of the drugs that are currently being discussed nationally for to be added to the new exemptions. I think it's probably going to be for other things, like asthma and probably a clamped exegers, but it's going to be an exempted drug. So it's another thing we could think about on managing Tulsard arrhythmias. But again, going off topic a little bit, it's quite a specialist case. So let's move on then to consider other drugs. So we've talked about we talked about activated charcoals, talked about actually, and we talked about adrenaline, we talked a bit about cardiac arrest management. But this patient still wasn't responsive to any of that heart rates, the same blood pressure as the same, and GCS is still pretty much the same. What else is there for us to consider in helping this patient who is in cardiovascular collapse? - So probably the next thing would be to think about some transcutaneous pacing, which can obviously be done pre-hospital, if you've had the training to do it, pretty basic procedure, with the patient in your case study, that GCS is probably low enough that you could pace them. And, but obviously if they're conscious, then probably may not need to pace them, because if they're refusing, well enough, they're probably not compromised enough to knee-pacing, but if they are then little bits of sedation theoretically, but I think pacing is an option, and obviously there's transvenous pacing as well, if you've got specialist center. Transportants is specialist places. I mean, I work in small DGH, and I don't have this to avail to me, and it would be a long secondary transfer. So, but some places, if you work like London, also like you might be able to take them to a center that does VA ECMO, and then obviously we can then support the profusiness of the rest of the body by kind of taking over that circulation. - Finally, and I find no way aggregate in this, but it's just something that I've heard recently mentioned in another unnamed podcast that's quite popular, and also I know there's a trial going on about looking at the using Roboa to medically manage cardiac arrest, and I think the theory of that is about using arterial lines and improving diastolic resuscitation. So, if we can manage to improve diastolic readings in a rest, this perfuses the coronaries better, and we have a much more likelihood chance of getting rosk is what the research is looking at is very, very early on, but it's something I'm following the interest is some good trials going on across the country with some of the air amplitudes looking at, using kind of like a medical Roboa type approach or a diastolic resuscitation with intra arterial blood pressure monitoring intra-rest, which is kind of where I'm focusing my learning on other moments, because I'm just really interested in this. And it could turn out to be another one of them things that we think how it works, it doesn't work, and some people are fans of it, some people are not fans of it, like DST, but it's kind of, I just think it's kind of a nice little future avenue, but Josh is kind of sternly looking at me down the camera, so I think he wants to tell me that I'm talking rubbish and it's not gonna work, it's not gonna add any benefit. - No, no, I think it's all very interesting. I think talking about that, and VA-ACMO and stuff like that, that's again, highly specialist, it's probably one of those things that's a little bit down the road, both in accessibility to the majority of people, and there's far more things that we can be trying prior to getting to that point, that we're gonna talk about in a second. - Oh yeah, as I said, in my center, I've got nowhere near an ECMO, so I'm never gonna get an ECMO, so, you know, it's not gonna be. It's interesting things to think about for the future, and you know, the final last, you know, ditch things to think about. You mentioned about pacing, so I think that's interesting, and that's something that I tried with this patient. Having looked at the evidence since, it turns out that it's quite a poorly evidence than beta blockade, it's unlikely to work. There was one case example I found from, I think the '80s, where it was demonstrated to have worked, but broadly, it doesn't seem to be efficacious, and in fact, it didn't work in my case, and debrishing it with colleagues up and told that a potential reason for this might be the acidosis that these patients very quickly spike into profoundly acodotic patients can have quite high thresholds for pacing capture, so it might be something to revisit later on in the patient care episodes, once we have tried some other things that we're about to come into talk about, isn't what I tried, I tried it, once it didn't work, and we've done. - So, whilst we're on the subject, then, of, I'm sure there's people screaming and saying, we haven't talked about the elephant in the room, in relation to beta blockade, we were talking about things that might work, might not work, the evidence is questionable, but if some of it we've always done, glucagon, you give Ivy glucagon right to your beta blockade basis, because we all do. - Oh, yeah, and this is something that definitely came up that our governance session prompted some and some interesting discussion, so shall I talk about glucagon something? - Yeah, tell me that, tell me that, my administration of glucagon is, it's gonna save this patient's life, and it's a key treatment that I have to give. - Good. - I'm happy to have that please. - The cameras are argument-friemed, locked and loaded, ready to go. - No, no, not at all. I just know that, I, I, it's something that again, we've always done, isn't it? But actually, I think it's not that effective. - Oh, right. So, go on. - Glucagon, when you look at any of the guidelines, you, you will see Glucagon as a treatment for beta blocker overdose with cardiovascular collapse. And you might be sitting there going, what, why on earth do we want to increase this patient's blood sugars to try and help their heart rate? Well, what we're after isn't actually the Glucagon. What we're after is the insulin response, because insulin is known to have an ionotropic effect. And it does this through a fairly complicated mechanism, essentially bypassing the adrenal receptor mechanism in cardiac myocytes to promote calcium influx into cardiac cell. So, Glucagon results in a serum glucose increase because of glycogenesis. And this results in the pancreatic cells releasing insulin to lower this. And the insulin is what is helpful here. So, you'd be right in thinking, this is not in JR-Calc, but JR-Calc is a guideline. It isn't the legal framework through which UK paramedics can administer medications. Glucagans sit under schedule 19, and the indication for that is for emergency situations. And I would suggest a patient who is pranachardic, high-contentive, periarest, unresponsive to treatment thus far is definitely an emergency situation. The challenge for us is achieving a high dose, because if you look at the guidelines, so guidelines like, talk space, any kind of poison control, little link to stuff from emergency medicine cases, life in the fast lane, which I think is a pretty trustworthy reference source. And even Simon, the UK resusc council, would suggest giving Glucagon, if beta blockers or calcium channel blockers, are a potential cause of the pranachardia. And talk space, for example, would suggest giving an intravenous dose of between five and 10 milligrams in adults administered over a one to two minute period. And for reference, the Glucagon that's carried in a standard ambulance bag is one milligram. So what we're trying to achieve here is at least five drugs bags to see to give one dose, which, as I'm sure most people listening, are giggling at the notion of getting five ambulances to any scene these days. What did I do on scene? Well, I was fortunate enough to be able to source four milligrams of Glucagon. So there was an ops officer, there was two DCAs. And there was some ARV on response helice officers, which have an auto injector of Glucagon in their kit. So we managed to give four milligrams as a step-dose to this patient. That was reconstituted as an IV solution with the small vials of glucose that come in those kits. But if you're all thinking of doing this, you can't reconstitute it with water for injection or sodium chloride because that will cause the Glucagon to precipitate. So it should be reconstituted with the small vial of glucose comes in the kit. And it must be used immediately because again, the Glucagon can precipitate. So once you've got the dose ready to go, you should give it IV. So make sure that you've got your intravenous access before this. Of course you will have because this is not our first line treatment attempt for this brand of cardio. So go on. So I suppose my issues with it are that there's no real evidence that it works. And I think that a lot of the studies that do show that it works were done on like an old version of Glucagon. And the old version of Glucagon was a pancreatic extract which contained insulin. So you get those really beneficial effects. And they've never studied it with kind of that recombinant Glucagon that we use nowadays. It's really expensive. You need a lot of it. And as you said, you may not have enough stocks. It can induce vomiting when given IV. So then you might have your airway risk. And the primary purpose of why we're getting it is exactly what you said was to do with insulin. So why don't you just give insulin? And that's my thing. So why don't we just give us high dose insulin? OK, it gets eventually. Yeah, so yeah, in fact, yeah, you didn't have any insulin. But you know, come play with us big boys in hospital. And yeah, we're just going to give some high dose insulin therapy because it's known to have some ionotropic effects. So that's going to be beneficial for our cardiac response. And it does this by passes a Dreno receptor mechanisms and promotes calcium influx into myocytes. So we're not dependent upon the kind of response of catacolamines and the adrenergic system in order to get that response. So in those patients with severe impairment of myocardial contractivity, the insulin and dextrace infusion has been shown to improve that systemic perfusion. It's also particularly useful in the presence of astrosis. And yeah, it kind of optimizes the use of carbohydrates by cardiac myocytes and modulates that interact cellular calcium. So we use that as our kind of effectively to stabilize the cardiac response and as an ionotropic. But is insulin and dextrace something that you think we could give pre-hospital? So I think the challenge, I mean, I don't know how long it takes to set up a uglicemic insulin process. Neither do I. I perspore it and the nurses do it for me and they're much, much better. Like, and they, I would like a look at it. No idea. I'd just give this dose for me. And they know exactly what to do. I think the challenge, as with all of this stuff, is the shelf life cost of achieving this. So you mentioned magnesium earlier Simon. And I know this discussions within, within very sambulant services about if magnesium is introduced as an exemption, is that going to be put on every ambulance because realistically, how often is it going to be used? A lot. Magnesium is the emergency medicine wonder drug that saves everyone from every problem. I mean, I mean, you like, yeah, you want to talk about everything in the face mate, then be prepared to. Yeah. I've got more against magnesium than you do against glucose. Adding, adding, adding, totally, I love magnesium. But I am one of the fond camp. But I am aware that there's a lot of people that, and they're probably right, we do give it for a lot of stuff and it's evidence-based is questionable. I think the thing is, is if you give something to enough people, you're likely to accidentally help on it. So, you know, just give everybody magnesium the minute they come through the hospital and it door and it might help. That's basically what you guys do anyway and resources, isn't it? So, yeah, I think realistically, that's not going to happen pre-hospital because they're a huge amount of wastage for a very small number of patients that it would lead benefit to. And, you know, I get the, with some slight tongue in cheek about glucogone, I really get the point that the evidence base is limited. There's a reasonable degree of arguments against it. The metagenic effect of high levels of IV, the glucogone, is a really valid critique of it as a therapy, particularly in the patient that I described, who has a reduced GCS anyway. What you really don't want to do is add airway and breathing issues into this big circulation issue, isn't it? So, that's a really valid critique. I, I, I, I just, but actually a lot of stuff we do in emergency care doesn't have a really strong evidence base all the time, you know, we can't trial everything or haven't, haven't, haven't, tried everything yet. And that's why we change practice, because things work. Sometimes they don't, and we do trials, we find that they don't work. You know, I mean, I, like, I always use the same example, but I always used to give TXA to GI bleeds. And now I don't, because of the evidence base. Yeah, so. Yeah, and, and I'll link to a quote on the topic of glucogone. We'll put some evidence, what evidence there is up there on the, on the topic that notes an evidence base is often lacking and one therefore needs to rely on the combination of practical experience case reports and the assessment of biological plausibility. There's a sound theoretical basis for the use of glucogone in the cardiovascular and compromised patient who's taken a beat blocker over those. And that's row collar, albeit in a 2003 response to best best paper. Is it the absolute best thing that this patient needs? No, you're right. You glistening against your own therapy is probably what they need is practical to do that in a lead-eed department. It's probably not practical to do that in an ambulance. Whether critical care teams carry that, my one doesn't to my knowledge, the majority don't. But possibly, you know, something that may happen. We did have glucogone available. And as one of my heart colleagues really help fully pointed out, actually, that heart teams typically will carry up to six doses in their response bags because of the way that they respond to the patient. as a team to a scene. So if heart are readily available to you, then you may be able to get six doses to seem relatively quickly. Of course, the argument against that would be, if you're close to a heart team, I would suggest you're probably close to a hospital. So it doesn't necessarily play out, unfortunately. But if we're talking about treatment options, Simon, with their variable evidence base behind them, should we go on to talk about sodium bike up? - Yeah, I feel this is turning to like a slaggy batch for sort of like, I like these treatments, and you like these. So between them. - And in between them. - Back up our plan. - No, actually, yeah. - So yeah, sodium bike carbonate then. Sodium bike carbonate has kind of gone quite a lot out of favor with a lot of things, particularly the management of acetosis. But in terms of beta blocker overdose, it's still well and truly recommended by Toxbase. So yeah, if cardiac arrest occurs because you'd beta blocker overdose, then obviously as you're part of your ALS process, and you're giving your other drugs, your adrenaline and withholding your amyodron, Josh, withholding your amyodron, potentially. - Maybe. - Maybe, yeah. If you do have like either arrest or cure arrest prolongation on your ECG, then you can give a sodium bike carbonate, 0.5% bolus. It might be like an ACP or critical care supporting. I don't use sodium bike carbonate because I'm not a massive fan of it, but in this particular case, I think it's worth giving and it is recommended by Toxbase. - And that's generally when we see it being given, isn't it? Those are the classic one would be a tri-cyclic overdose because we know there's huge sodium channel blockades with that, you know, why does it work? Well, you've already kind of touched on that. Sodium bike carbon is often used to narrow cure arrest widening that's induced by varying Toxic overdoses. The mechanism, well, it could be that by raising the serum sodium concentration, you overwhelm the sodium channel blockade, so kind of the similar mechanism to what we've been describing with high dose adrenaline. There's also some thought process that that doesn't fully explain it. It might be the increasing of the pH. So aiming to reverse that acidosis that might reduce the free drug levels in the serum that are alterating the polarization of the cell or it's more than likely a combination of both mechanisms. So it isn't deeply well evidenced in propanol overdose, but like you said, side of those good evidence and sodium channel blockade, such as what we take from tri-cyclic overdose and it is still recommended in Toxbase management. And interestingly, you mentioned about cardiac arrest and QRS prolongation being an indication for it, but there is also a note in there in the case of propanol overdose that your patient has fitted or is fitting that would also be an indication for sodium bicarb, because it's an indication of how toxic that patient is. And if I remember the guideline rightly, it's a reduced conscious level without the CG changes we just thought to have isn't enough, but fitting is enough, because it's that's that's really happening. Yeah. Because that's sodium bicarb then. And then finally, calcium or the chloride or glutamate has cardiac membrane stabilization effects. You know, as we said, it does, it has been reported to have some calcium channel blockade effect. So there may be some benefits to giving a serum increase in calcium. I'll link to an evidence source that supports that. So it says treatment with calcium salts may provide benefits for hypertensive patients who are overdose on beta blockades. There's some US sources that would support that, but currently in UK guidelines, it isn't in toxin, it isn't in reputable UK guidance. Again, for a lot of these overdose patients, there isn't the evidence base to support them. Necessarily, and a lot of it is using the theory of Havons' medicines, behave counteract it and case examples and experience. This isn't particularly common, but my experience with this patient, I felt that the glucogon has an example appeared to have some effect. Was it the glucogon? Was it the atropin? Was it the adrenaline? Was it chance? Was it a combination of all other things that you were throwing at this patient? You'll never know, will you? You'll never know in a scientific method type fashion. And I suppose the other issue with toxicology evidence-based treatments is how often the people take single ingestion, overdoses and not polypharmacy. So it's really hard to study two evidence to do. And a lot of it is based upon the theory of how the drugs work, encounter act in those drugs and there is things. So, one final thing all those, if you, things like glucogon, sodium bicarb and calcium, I don't think they can all go through the same line. Or certainly need a big flush afterwards because of the risk of precipitation. So that's just something to bear in mind when we're giving those salts kind of drugs. So I think after that long talk we've covered circulation, cardiac arrest management in one of the so just briefly then disability. Obviously we've talked about this patient is reduced level consciousness so we're going to need to kind of manage a railway. Maybe some ventilator support. We also might need to provide some oxygenation if they are fitting. And obviously fitting is a, and seizures is another complication that we've talked quite a lot about to managing that. So we want to manage hyperglycemia with glucose if we find hyperglycemia because of what we talked about earlier. And then obviously standard stuff like benzo-diazapines for seizure control as per standard practices. And that's most of what we can do from an A to E and management perspective. So finally then we should probably have a quick chat about pre-learning this patient. Standard at-mistrealert doesn't take a lot of knowledge to know that that's where this patient's going and that they're going to get to recess. Couple of little pointers that I would definitely advocate that we do is to give an early pre-learning to state the suspected or concerned toxins that the patient's overdosed on. So concerning that this is a propanolol overdose. And it might be reasonable, you know, depending on the time of day this is in the middle of the night. So accepting that night everybody's top of their game. If you're in this situation it might be reasonable to pre-learning the hospital that this is a patient that would require sodium bot carb. If you haven't been able to give it this is a patient that would require uglisemic insulin therapy as an ionostrophic effect. And definitely somebody that's going to want anesthetics or prepare down there. If they've got to, there's definitely somebody who's going to want anesthetics or critical care outreach down there with them because like he said, Simon was patient with a reduced GCS, may require an anesthetic on their a bit more stabilized in order to control their airway and take further control of their cardiovascular status. So just bluntly saying those things, one I think it makes you sound really professional and two, it just closes that potential loop of missed things that just add delays to your patient care all the time you get them to hospital. Yeah, it's going to be a pretty physiologically challenging airway, I feel. So, or airway management and fear or RSI. So I think, yeah, I agree, I think get your expertise in the room. Josh, do you just want to summarise the case and kind of briefly go over your management from what we've just talked about, what bits you of that you did and how the case kind of went and prognosis? Following on then from where we left the case, it started this podcast, so we were in the back of the ambulance reassessing the patient. We initially felt the patient was parioresc, so we gave larger doses of adrenaline in order to prevent that. So I gave sort of 100 microgram of boluses, initially to prevent an emergent re-erest. We gave some atropin to the patient, we were giving multiple doses of atropin all throughout the patient care episode. I think we probably maxed out on the atropin that we had in our drug bag, available, probably giving doses every five, 10 minutes when we were able to, because like it's elucidated, so I mean this is all right, you've alluded to, so I mean this was a busy period in the back of this truck. We started the patient on an adrenaline infusion, but the time we arrived at hospital, he was on an 80-million-hour infusion, that's 800 micrograms per hour infusion, had some fluids running to try and get some of that Frank-style in mechanism going, but we didn't give over a litre over the 40 minutes of the patient because again we didn't want to push any fluid onto the patient's chest, and a lot of the time we were using that for a flush, so the large amount of drugs that we were giving. This patient actually required a little bit of sedation because of some agitation and the middle ground of GCS that they were with, so they had some sedation as well, and then as I said, we gave that glute gum in a sort of throwing everything out of the patient we could in order to try and maintain heart rate. and blood pressure, as well as the time for critical transfer to hospital. I didn't give any calcium and I have to be honest, I'm not sure whether I would, if I was to see this patient again, I think at this point there's probably not enough evidence out there to support that as standard, but if I cried everything and there was no change, it might be a decision that I share, with somebody to see if it seems reasonable. I didn't have sodium bicarb available to me at the time, but where I see the patient again would have, so they would have also received some sodium bicarb because of the fitting and the cardiac arrest that had been witnessed because the patient did rearrest on route several times but responded to immediate adrenaline and voluses after that. So all in all it was about a 40-15 minute transfer to hospital. We got that pre-alert in stating the needs for ulyssemic insulin therapy and for bicarb as we walked in and handed over some hospital team. I think if I'm honest, I left the care episode thinking that this was a patient was sadly going to go on to die because of how unstable they were, the period of downtime beforehand, just how toxic they appeared. Actually, I was pleasantly surprised to find out a few days later that they were awake and talking and stable on ITU. So I take away from this and this is what all of the guidelines say is that these are highly reversible patients, even if the timelines don't seem favorable, even if the gasses seem accrocious and the ECGs and stuff are massively deranged. They all say these are salvageable patients that you should throw everything at before you reach the decision of futility. This is an absolute example of somebody that writing this case down, I would not have thought of the sea tile, but hopefully he's gone on to make a good recovery. It's a great example isn't it, why? Joke Hothton says statements that make sense when you think about them, but at first glance, they don't always explain why. It's a good example of why drug overdoses are kind of reason for not calling cardiac arrests pretty hostley without senior support because that's a fantastic case that shows the recovery. I've been in situations where we've been running patients to hospital and it's the un-spoken elephant in the room, everybody's thinking the timeline is a trumptious here. What are we doing? But these patients can be really, really salvageable, particularly if they've had really good pre-hospital care and that chain of surviving been in place. So if you can get them to an antidote just because it seems quite far down the line doesn't necessarily mean that all is lost. We've talked about the pharmacology in beta blocker overdose, discussed how these patients can present on a spectrum of severity, but the certain groups of beta blockers, namely first generation non-selective drugs, may cause our patients more problems, particularly drugs like propanol that have additional complicating factors such as their ability to cross the blood brain barrier and suppress GCS, potentially cause fitting, and their sodium channel blocking effects, adding to their cardiotoxicity. We've talked about our graduated approach to managing these patients following an ABC format and we can start with a fluid bolus to support our blood pressure whilst readying our atropin. But following that, we're going to work down to Braddock, Ardior algorithm. We can use regular doses of atropin and draw up low dose adrenaline, attempting up to 50 micrograms alacrots every few minutes, and considering other elements that can help us that might be available from specialist care agencies such as pacing, sodium bicarb and other cardiac stabilising medications. Ultimately, these patients need a clear pre-alert and are rapid transfer to hospital for further treatment. But that's all for this month. Thanks again to our sponsors GeekyMedix who helped keep this podcast free and open access and to those of you that support us at home. If you'd like to buy us a coffee, you can do so following the link down in the show notes at coffee.com/generalrawcast and we hope you'll join us for the next month's episode.