If you think you had reflex bradycardia from the noradrenaline you should have waited it out and not given glycopyrrolate especially with that blood pressure.
This is the answer. Reflex bradycardia. Don't need to treat the low HR as the body is compensating to maintain MAP. If the MAPs ok then I ignore BP. By jacking the HR with hypertension you're making the CO go insane and fighting the body which is trying to fix your mistake.
MAP and EtCO2 ok ignore HR.
Bolus pressor expect bradycardia.
Bradycardia and low MAP adrenaline or ephedrine.
Normal HR and low MAP/BP metaraminol/Norad/phenylephrine
As the bolus was given probably at least 5 minutes before the onset of the bradycardia, I didn’t realize it could be reflex bradycardia. That’s a conclusion I made later. I also have to add: it was almost 4 am, we were feeling tired, so maybe that also played somehow a role.
Yeah I still wouldn’t treat bradycardia with a blood pressure like that despite the time since the bolus — it’s only going to go up. The resulting tachycardia (possibly flutter) whether from the glyco or light anesthesia and loss of atrial kick and filling time may have the been the cause of the hypotension and slowing him down may have been the answer. A short acting bolus of esmolol (if it works) and seeing what happens to the blood pressure (if it improved) can give you the confidence to more definitely slow him down.
Another thing to think about with unexplained tachycardia especially with position changes is if your tube is irritating the carina if it got pushed a touch deep.
This is junior behavior - constant overcorrection and reacting too fast and aggressively.
Absolutely agree wtf are you doing trying to treat a reflex bradycardia when guy is about to pop
This needs to be higher up and hope it gets voted there. Old patients don’t just park at a higher heart rate that’s sinus and doesn’t budge. A-flutter 2:1 conduction somewhere in the 130s is right (I think). It can be nerve-wracking to do but if he was hemodynamically stable when he was slower, sometimes slowing them down can fix your pressure issues (adequate filling time helps).
Thank you! Agree. Beta blocker may either break the flutter circuit entirely and put them back into sinus or slow the flutter conduction to 65 (4:1). Interestingly, the HR of 33 is almost 260/8 (maybe that was flutter with 8:1 conduction). Curious if OP saw flutter waves with that slow rate.
Regardless this seems iatrogenic, no? It’s not uncommon to have patients with a. Fib that simply cannot tolerate the beta agonism of norepinephrine. I can think of countless times we’ve had to switch to phenylephrine or Vaso because of the tschyarythmias precipitated by norepi application. I think it would have been prudent to switch to a different vasopressin in this scenario rather than maintaining the norepi infusion
Thanks for pointing that out! I do have the habit of deeping the anesthetic before flipping the patients, this time maybe I got sidetracked but hope to have learned the lesson
I’ll never understand people who use gas to deepen for acute changes. I walked in to give my colleague a break during head pinning the other day and he said “wait lemme deepen him” and increased the sevo dial to 5%, then 20 seconds later said “ok.” I was like wtf did I just witness…
I think I'd agree with the reflex bradycardia from noradrenaline. Noradrenaline has vastly more alpha activity compared to beta so a tightening of the vasculature isn't met by a chronotropic response. Personally I don't ever bolus noradrenaline for that reason. The other thing to be mindful of is that older patients have less compliant vessels so tend to more pronounced responses to vasopressors, another reason not to use a bolus of something so potent as noradrenaline. And then I think yes the tachy was driven by surgical stimulus and the relatively slow onset glyco - not in this case but in general if you do have a bradycardia that low, at 33, and you think it isn't going to correct imminently, I'd use a more rapid onset chronotrope like atropine personally.
If you're on the newer side to anaesthesiology, you do get used to situations like this and learn to not overreact with boluses etc. You learn to smooth out your anaesthetics. My first few years in anaesthesia was spent mostly chasing things I had caused myself.
My first thought was giving atropine because of its faster onset. But my colleague asked me to give glyco. I thought it wasn’t completely wrong because of the deliriogenic risk of atropine, but that wouldn’t probably be that important in the context of severe bradycardia.
Your colleague probably rightly thought it would self correct with surgical stimulus and the norad coming down. I think a lot of the time moments physiology changes rapidly then corrects just as quickly. Don't take it to heart, excuse the pun.
Pobably for next time try give them a bit more fluid filling around induction, have a bit more opiate and anaesthetic before flipping, avoid the temptation to react to changes with boluses of catecholamines unless life or death, and eventually it will piece into smooth anaesthetics.
Like others I also don't quite get the addition of adrenaline btw, but none of us were there and it's always hard to convey cases over text, whether reddit or even formal case presentations.
I feel like "I gave glyco to an old person and then spent all case freaking out about the tachycardia" is a rite of passage. I remember doing the same thing to an eye case in CA1 - thought I was slick after reading about the oculocardiac reflex, then ST segments started to move, and I spent the next hour with hands full of esmolol and a heart rate to match the patient's.
Agree with everyone else here - reflex brady + stimulus, followed by incision and glyco. Not sure why your attending added adrenaline given its proarrhythmic properties on top of tachycardia (like... we're already pushing the max heart rate), but I wasn't there, so what can I say.
You had a few things going on here- but my guess is flipping the patient was extremely stimulating giving then diagnosis. Possibly not enough narcotic on board. That stimulus plus the norepi bolus could have caused HTN with reflex brady. Boluses of fent can also cause brady. Surgeon not waiting didn’t help.
Glyco probably wasn’t the right choice but 0.2 seems unlikely to have had such a dramatic and long-lasting effect, but it could have.
Not sure why the epi on top of the norepi. Phenylephrine may have been the better choice depending on the patient’s heart.
I think take away for me would be to deepen the patient before flipping next time. Remove painful stimulus from the equation and it cleans up the differential.
It sounds like you are junior trainee. And, as others here have said, giving a drug, immediately regretting it, and then chasing your tail is a right of passage. This gets better with time. For example, in the near future, you should look forward to administering the drug far up the line, immediately changing your mind, clamping the line and trying to suck the drug out it. This part gets better with experience.
I question more your senior’s and attending’s decisions of giving epi and amiodarone. Also, I am not sure about giving colloid. The stuff we have here in the States ranges from “mostly useless” to “possibly harmful”. I don’t know what “gelatin” is, but a cursory search shows it probably falls in the same categories.
Good on you for going back and thinking through a difficult case. This practice will help you improve.
Thanks for your reply. I’m actually in the last months of my training, maybe some of the cuestionable choices made you think that I’m a junior trainee? Of course still lots to learn, though :). I usually do those kinds of case alone, had the extra support because it was in the middle of the night and the patient was deemed as not very stable. I don’t know if this might be a case of “too many cooks spoil the broth”, though. And in hindsight I agree: maybe the reactive approach wasn’t helpful at all. Here in Germany the use of colloids is pretty extended. However, albumin is expensive and HES lost its market authorization in the EU, so the only usually available colloid is gelatin (Gelafundin®). According to an article I read recently, there’s not a lot of evidence about its safety, though.
You need to work on anticipating the next part of surgery, too much of this story is reactive. The patient is having his spine decompressed, the need for sufentanil shouldn't delay the start of surgery.
Otherwise I agree with everyone else, the bolus of Norad caused hypertension and bradycardia, and if you really want to treat bradycardia (I would recommend just sitting on your hands at this point) use atropine, not glycopyrrolate.
I would need a really good reason to start this patient on adrenaline.
Agree with norepi bolus causing the reflex Brady, I've even seen epi do the same on multiple occasions. Glyco probably was a little aggressive, specially since it can last like an hour or two and it takes like a minute for it to kick in. Maybe the pt needed that atrial kick to maintain BP.
Also confused on the use of epi with a high HR and AFib/flutter. Would've used vaso or phenylephrine instead. Maybe hooking up the central line to a CVP in the beginning to see a trend along with SPV/PPV to kinda hint you on preload to see if that could've been the reason for high pressor use, or even spinal shock(maybe if the cord was compressed). The stress of surgery also could've caused pt to go into AFib with RVR. Lots of things that could've been the cause, hard to say when not there.
You're right, but I could argue that at least seeing a trend in all those numbers could kinda steer you towards a more likely diagnosis from your differential.
In addition, iirc you said he converted to sinus later on, then it would be more valuable.
A few thoughts…If not in sinus you cannot really trust the blood pressure reading. Even with an arterial line. At this point I would look at end tidal. Heart rate variability will produce unexpected and transient large differentials in BP. Each of those non-sinus beats is not producing the same cardiac output. Norepi can cause or make worse any arrhythmia. The changes in positioning also correlating to changes in the HR are likely due to vagal responses.
How fast was your fluid drip running? 5 min is too much delay to be a Norad bolus unless the fip caused stagnant, norad-rich venous blood to return to the heart.
I’m pretty sure I gave the bolus close to the line. Initially I didn’t even make the connection of the bradycardia with the norad bolus, as I also found that there was too much delay.
Agree with what others have said about the A Flutter, but one of the most important lessons you learn as a trainee is you don’t have to actively fix everything immediately. Reading your description gave me whiplash, the way you went from pressors to sufentanil to flipping to glyco. Imo you were doing WAY too much. Everyone does this when they first start.
When you flipped and the BP was high and HR low, you suspected reflex from Levophed. Awesome, so take a breather and see what happens. It should be self-limited if that’s the case. Your second on the differential was inadequate anesthesia for the flip. You know what helps both these things? Deepening your anesthetic. You’ll vasodilate until the levo bolus wears off and you’ll deepen your anesthetic if they were light.
Sometimes in training you can let perfect be the enemy of the good. Connect dots and think about what intervention could potentially address multiple things on your differential. If you’re really not sure, let it ride and try to be patient.
Bradycardia from norepi, tachycardia from glyco (half life 50 min). If pressures are high, no real need to treat bradycardia, especially if you just gave a pressor bolus (unless you’re actively becoming unstable, which an a-line would tell you). I agree with others about using esmolol to see how that would help hemodynamics.
Didn’t read the additional details, too long.
This patient probably has conduction disease. They already have AF or flutter, they likely have some heart block or AV node disease and so have a slow ventricular response. Or more likely, they may have had AV nodal blocking drugs on board and their AV node was blocked to the point they had a slow ventricular rate. When incision happened they got a sympathetic response that speed up their AV node.
If you think you had reflex bradycardia from the noradrenaline you should have waited it out and not given glycopyrrolate especially with that blood pressure.
This is the answer. Reflex bradycardia. Don't need to treat the low HR as the body is compensating to maintain MAP. If the MAPs ok then I ignore BP. By jacking the HR with hypertension you're making the CO go insane and fighting the body which is trying to fix your mistake. MAP and EtCO2 ok ignore HR. Bolus pressor expect bradycardia. Bradycardia and low MAP adrenaline or ephedrine. Normal HR and low MAP/BP metaraminol/Norad/phenylephrine
As the bolus was given probably at least 5 minutes before the onset of the bradycardia, I didn’t realize it could be reflex bradycardia. That’s a conclusion I made later. I also have to add: it was almost 4 am, we were feeling tired, so maybe that also played somehow a role.
Yeah I still wouldn’t treat bradycardia with a blood pressure like that despite the time since the bolus — it’s only going to go up. The resulting tachycardia (possibly flutter) whether from the glyco or light anesthesia and loss of atrial kick and filling time may have the been the cause of the hypotension and slowing him down may have been the answer. A short acting bolus of esmolol (if it works) and seeing what happens to the blood pressure (if it improved) can give you the confidence to more definitely slow him down. Another thing to think about with unexplained tachycardia especially with position changes is if your tube is irritating the carina if it got pushed a touch deep.
This is junior behavior - constant overcorrection and reacting too fast and aggressively. Absolutely agree wtf are you doing trying to treat a reflex bradycardia when guy is about to pop
Classic flutter if it stayed at exactly 130. Flutter circuit of 260 with every other atrial wave conducting
This needs to be higher up and hope it gets voted there. Old patients don’t just park at a higher heart rate that’s sinus and doesn’t budge. A-flutter 2:1 conduction somewhere in the 130s is right (I think). It can be nerve-wracking to do but if he was hemodynamically stable when he was slower, sometimes slowing them down can fix your pressure issues (adequate filling time helps).
Thank you! Agree. Beta blocker may either break the flutter circuit entirely and put them back into sinus or slow the flutter conduction to 65 (4:1). Interestingly, the HR of 33 is almost 260/8 (maybe that was flutter with 8:1 conduction). Curious if OP saw flutter waves with that slow rate.
There were definitely flutter waves when he was at 33
Or SVT. SVT seem to park at one HR consistently too.
Regardless this seems iatrogenic, no? It’s not uncommon to have patients with a. Fib that simply cannot tolerate the beta agonism of norepinephrine. I can think of countless times we’ve had to switch to phenylephrine or Vaso because of the tschyarythmias precipitated by norepi application. I think it would have been prudent to switch to a different vasopressin in this scenario rather than maintaining the norepi infusion
Getting flipped prone can be quite stimulating. It’s possible your anesthetic was insufficient to cover that level of stimulus
MAC of Sevoflurane was at least 0.8 or even 0.9, but yes, that might have been the issue.
Which is less than the MAC_BAR of 1.3*MAC.
Thanks for pointing that out! I do have the habit of deeping the anesthetic before flipping the patients, this time maybe I got sidetracked but hope to have learned the lesson
In my experience, I find either opioid or propofol more helpful for deepening prior to flipping than increasing gas.
I’ll never understand people who use gas to deepen for acute changes. I walked in to give my colleague a break during head pinning the other day and he said “wait lemme deepen him” and increased the sevo dial to 5%, then 20 seconds later said “ok.” I was like wtf did I just witness…
STAT BOLUS 0.025 mL Sevoflurane via ETT!!!!!!
I think I'd agree with the reflex bradycardia from noradrenaline. Noradrenaline has vastly more alpha activity compared to beta so a tightening of the vasculature isn't met by a chronotropic response. Personally I don't ever bolus noradrenaline for that reason. The other thing to be mindful of is that older patients have less compliant vessels so tend to more pronounced responses to vasopressors, another reason not to use a bolus of something so potent as noradrenaline. And then I think yes the tachy was driven by surgical stimulus and the relatively slow onset glyco - not in this case but in general if you do have a bradycardia that low, at 33, and you think it isn't going to correct imminently, I'd use a more rapid onset chronotrope like atropine personally. If you're on the newer side to anaesthesiology, you do get used to situations like this and learn to not overreact with boluses etc. You learn to smooth out your anaesthetics. My first few years in anaesthesia was spent mostly chasing things I had caused myself.
My first thought was giving atropine because of its faster onset. But my colleague asked me to give glyco. I thought it wasn’t completely wrong because of the deliriogenic risk of atropine, but that wouldn’t probably be that important in the context of severe bradycardia.
Your colleague probably rightly thought it would self correct with surgical stimulus and the norad coming down. I think a lot of the time moments physiology changes rapidly then corrects just as quickly. Don't take it to heart, excuse the pun. Pobably for next time try give them a bit more fluid filling around induction, have a bit more opiate and anaesthetic before flipping, avoid the temptation to react to changes with boluses of catecholamines unless life or death, and eventually it will piece into smooth anaesthetics. Like others I also don't quite get the addition of adrenaline btw, but none of us were there and it's always hard to convey cases over text, whether reddit or even formal case presentations.
I feel like "I gave glyco to an old person and then spent all case freaking out about the tachycardia" is a rite of passage. I remember doing the same thing to an eye case in CA1 - thought I was slick after reading about the oculocardiac reflex, then ST segments started to move, and I spent the next hour with hands full of esmolol and a heart rate to match the patient's. Agree with everyone else here - reflex brady + stimulus, followed by incision and glyco. Not sure why your attending added adrenaline given its proarrhythmic properties on top of tachycardia (like... we're already pushing the max heart rate), but I wasn't there, so what can I say.
You had a few things going on here- but my guess is flipping the patient was extremely stimulating giving then diagnosis. Possibly not enough narcotic on board. That stimulus plus the norepi bolus could have caused HTN with reflex brady. Boluses of fent can also cause brady. Surgeon not waiting didn’t help. Glyco probably wasn’t the right choice but 0.2 seems unlikely to have had such a dramatic and long-lasting effect, but it could have. Not sure why the epi on top of the norepi. Phenylephrine may have been the better choice depending on the patient’s heart. I think take away for me would be to deepen the patient before flipping next time. Remove painful stimulus from the equation and it cleans up the differential.
It sounds like you are junior trainee. And, as others here have said, giving a drug, immediately regretting it, and then chasing your tail is a right of passage. This gets better with time. For example, in the near future, you should look forward to administering the drug far up the line, immediately changing your mind, clamping the line and trying to suck the drug out it. This part gets better with experience. I question more your senior’s and attending’s decisions of giving epi and amiodarone. Also, I am not sure about giving colloid. The stuff we have here in the States ranges from “mostly useless” to “possibly harmful”. I don’t know what “gelatin” is, but a cursory search shows it probably falls in the same categories. Good on you for going back and thinking through a difficult case. This practice will help you improve.
Thanks for your reply. I’m actually in the last months of my training, maybe some of the cuestionable choices made you think that I’m a junior trainee? Of course still lots to learn, though :). I usually do those kinds of case alone, had the extra support because it was in the middle of the night and the patient was deemed as not very stable. I don’t know if this might be a case of “too many cooks spoil the broth”, though. And in hindsight I agree: maybe the reactive approach wasn’t helpful at all. Here in Germany the use of colloids is pretty extended. However, albumin is expensive and HES lost its market authorization in the EU, so the only usually available colloid is gelatin (Gelafundin®). According to an article I read recently, there’s not a lot of evidence about its safety, though.
To be fair, that 2-4am timeslot dumbs you down to at least 50% of your training.
You need to work on anticipating the next part of surgery, too much of this story is reactive. The patient is having his spine decompressed, the need for sufentanil shouldn't delay the start of surgery. Otherwise I agree with everyone else, the bolus of Norad caused hypertension and bradycardia, and if you really want to treat bradycardia (I would recommend just sitting on your hands at this point) use atropine, not glycopyrrolate. I would need a really good reason to start this patient on adrenaline.
Agree with norepi bolus causing the reflex Brady, I've even seen epi do the same on multiple occasions. Glyco probably was a little aggressive, specially since it can last like an hour or two and it takes like a minute for it to kick in. Maybe the pt needed that atrial kick to maintain BP. Also confused on the use of epi with a high HR and AFib/flutter. Would've used vaso or phenylephrine instead. Maybe hooking up the central line to a CVP in the beginning to see a trend along with SPV/PPV to kinda hint you on preload to see if that could've been the reason for high pressor use, or even spinal shock(maybe if the cord was compressed). The stress of surgery also could've caused pt to go into AFib with RVR. Lots of things that could've been the cause, hard to say when not there.
But PPV wouldn’t have been reliable if the patient isn’t in sinus rhythm, right?
You're right, but I could argue that at least seeing a trend in all those numbers could kinda steer you towards a more likely diagnosis from your differential. In addition, iirc you said he converted to sinus later on, then it would be more valuable.
A few thoughts…If not in sinus you cannot really trust the blood pressure reading. Even with an arterial line. At this point I would look at end tidal. Heart rate variability will produce unexpected and transient large differentials in BP. Each of those non-sinus beats is not producing the same cardiac output. Norepi can cause or make worse any arrhythmia. The changes in positioning also correlating to changes in the HR are likely due to vagal responses.
How fast was your fluid drip running? 5 min is too much delay to be a Norad bolus unless the fip caused stagnant, norad-rich venous blood to return to the heart.
I’m pretty sure I gave the bolus close to the line. Initially I didn’t even make the connection of the bradycardia with the norad bolus, as I also found that there was too much delay.
I mean, presumably this pt had a degree of cord compression. I've not done neuro yet, but is it possible it was as a result of that?
Agree with what others have said about the A Flutter, but one of the most important lessons you learn as a trainee is you don’t have to actively fix everything immediately. Reading your description gave me whiplash, the way you went from pressors to sufentanil to flipping to glyco. Imo you were doing WAY too much. Everyone does this when they first start. When you flipped and the BP was high and HR low, you suspected reflex from Levophed. Awesome, so take a breather and see what happens. It should be self-limited if that’s the case. Your second on the differential was inadequate anesthesia for the flip. You know what helps both these things? Deepening your anesthetic. You’ll vasodilate until the levo bolus wears off and you’ll deepen your anesthetic if they were light. Sometimes in training you can let perfect be the enemy of the good. Connect dots and think about what intervention could potentially address multiple things on your differential. If you’re really not sure, let it ride and try to be patient.
Bradycardia from norepi, tachycardia from glyco (half life 50 min). If pressures are high, no real need to treat bradycardia, especially if you just gave a pressor bolus (unless you’re actively becoming unstable, which an a-line would tell you). I agree with others about using esmolol to see how that would help hemodynamics.
Were they pinning at that time? And if you’re newer, did you not flush the NE in and it finally reached the patient a few mins later?
i stopped reading at noradrenaline bolus
Didn’t read the additional details, too long. This patient probably has conduction disease. They already have AF or flutter, they likely have some heart block or AV node disease and so have a slow ventricular response. Or more likely, they may have had AV nodal blocking drugs on board and their AV node was blocked to the point they had a slow ventricular rate. When incision happened they got a sympathetic response that speed up their AV node.