# Ketamine for RSI in hypertensive patients



## SandpitMedic (Nov 7, 2017)

I figure we have some good folks here who can comment on their experience with Ketamine in hypertensive patients. Generally, it is a relative contraindication in the traditional sense, but I have learned through various outlets that in recent studies that isn't necessarily true anymore. 

I'd like to hear what some of your opinions are, and any studies you could point to that either rationalize or dismantle that idea. @Remi @Summit @Chase @VentMonkey


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## VFlutter (Nov 7, 2017)

For me the question that I think of when considering Ketamine in a hypertensive patient is "Will an increase in SBP worsen the underlying pathology occurring?" In most cases, probably not. I think most studies have shown the increase ICP with Ketamine is minimal if at all. The mechanism behind the sympathetic response to Ketamine is not very well understood but probably is CNS mediated. So those whom are catecholamine depleted or have severe head injury probably will not have much of a response anyway. That is why many people recommend a low dose Ketamine dose for high shock index patients because the direct cardiac effects can outweigh the supposed sympathetic surge and cause worsening hypotension.

So unless you are dealing with a patient with a hemorrhagic stroke, ruptured aneurysm, etc that increased SBP is definitely harmful you probably are fine giving it with hypertension. The increase in pressure is usually minimal and transient anyway.

Also, lets say you have an ischemic stroke patient with a pressure of 180/100 (No tPA) that you need to intubate. What is going to be worse for that patient, a brief increased in pressure to 200/100 with Ketamine or a drop in pressure to 120/60 with Etomidate/Versed? 

https://www.openanesthesia.org/systemic_effects_of_ketamine/


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## EpiEMS (Nov 7, 2017)

Not an expert on the physiology, but my GoogleFu is strong.

There is some (fairly) recent moderate quality research out there indicating that the ICP response to ketamine is limited (or nonexistent), as @Chase said, for non-trauma patients and for traumatic injury. Obviously, based on the small _n's _and the not-ideal study design, more research is warranted.


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## VentMonkey (Nov 7, 2017)

Lidocaine anybody?


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## SandpitMedic (Nov 7, 2017)

VentMonkey said:


> Lidocaine anybody?


Not in the formulary for intubation anymore where I'm at.


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## VentMonkey (Nov 7, 2017)

SandpitMedic said:


> Not in the formulary for intubation anymore where I'm at.


We don’t have Ketamine in ours, so my experience is limited to literary knowledge only.

My personal opinion is that nearly every, if not every, drug we carry will have relative to direct contraindications for specific subsets of patient populations that we deal with. If we utilize Amidate on an already hemodynamically compromised patient who undoubtedly needs their airway protected and cannot achieve it without induction where do we weigh the risk vs. benefit? How would I immediately know how well the their kidneys are truly functioning to weigh out the risk vs. benefit with the induction sedative we carry? 

If you’re fortunate enough to carry both, well then at least you have those options. If I had them I would be more inclined to utilize the Amidate in the presence of a closed head injury, and Ketamine perhaps more along the lines of the refractory asthmatic who absolutely needs airway protection via induction.


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## Carlos Danger (Nov 7, 2017)

I personally would not use ketamine for induction in the OR for a very hypertensive patient, but if I were in the field and ketamine was my only option I would not hesitate to use it. It seems that the fears of ketamine causing significant increases in ICP are overblown.

When you think about ICP increases in people who you don't want to increase ICP in, laryngoscopy, especially sloppy or prolonged or multiple attempts is probably a much greater worry than the choice of drugs used.


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## EpiEMS (Nov 7, 2017)

Remi said:


> laryngoscopy, especially sloppy or prolonged or multiple attempts is probably a much greater worry than the choice of drugs used.



BLS the airway? Or perhaps go for an SGA? (I feel like this is kinda the theme of threads lately - ETI just doesn't make sense unless done well)


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## Carlos Danger (Nov 7, 2017)

EpiEMS said:


> BLS the airway? Or perhaps go for an SGA? (I feel like this is kinda the theme of threads lately - ETI just doesn't make sense unless done well)



Well BLS would certainly avoid the problems associated with laryngoscopy and drugs, and SGA's may as well, while still provide some measure of airway protection and ability to provide positive pressure ventilation.

Most of the retrospective studies that are unsupportive of field RSI are looking primarily at TBI patients, probably because they make up a majority of the intubations done in the field.


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## TXmed (Nov 7, 2017)

My 2cents. 

I think for 90% of patients its fine. If im intubating in the hospital and have some time then maybe i can come up with a more comprehemsive RSI induction/sedation but in reality i dont worry too much about it.

What my concern is, and im still sifting through studies, isnt the sharp increase in catacholimines and BP. Its the rapid drop once the surge has stopped. 

Is it decreasing CPP for a period of time? Is it causing my trauma patients to speed up their time to decompensation?


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## Peak (Nov 9, 2017)

This is probably going to be the least popular opinion, but I think that this falls into a case of do you need it or not. RSI is far from a procedure without risk, and should not be performed in the field unless is is absolutely warranted. That being said if RSI is *needed* then the transient hypertension or hypotension associated with induction agents is not going to be the principal problem.

To me it's kind of like giving suc, my bailout is not the patient's respiratory drive because that is what we have decided needs to be managed (unless they are trismus, then they have suc and roc). Bailout is a LMA with a NG/OG to suction at a minimum.

Generally I would prefer ketamine for hemodynamically stable or hypotensive patients, and versed for hypertensive patients. Hypotension is generally easier to treat, especially given that we will have at least one liter hung and ready on a pressure bag whenever we RSI (anesthetic related hypotension is also easily treated with neo). If I was only allowed to have one I would prefer versed.

Etomidate without a barb or benzo will lower seizure threshold so it really shouldn't be used as the sole dissociate agent, especially in head trauma. Even if the patient does not have visible seizure behavior (for example because they received a paralytic) they may still be firing neurologically and increasing the oxygen/glucose consumption in their brain.


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## VFlutter (Nov 9, 2017)

Peak said:


> the transient hypertension or hypotension associated with induction agents is not going to be the principal problem.



Although that may be the case in many situations there are some patient populations that even brief episodes of hypertension/hypotension significantly worsen outcomes.


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## Peak (Nov 9, 2017)

Chase said:


> Although that may be the case in many situations there are some patient populations that even brief episodes of hypertension/hypotension significantly worsen outcomes.



More significantly than a deteriorating and unsecured airway?


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## Carlos Danger (Nov 9, 2017)

Etomidate is thought to lower the seizure threshold because giving it can result in epileptiform EEG activity, but that is not the same thing as a clinical seizure. I don't know that it has every been implicated as actually inducing seizures. Ketamine is said to not lower the seizure threshold, but is well known to actually induce seizures in epileptics. 

I don't think etomidate it is as good an option in most cases as the others (propofol, ketamine) plus appropriate adjuncts, which is why it's fallen out of favor. Certainly not in elective anesthesia because of the high rates of nausea associated with it. But in a truly emergent RSI, etomidate is still a good drug that just gets a bad rap. I would not hesitate for a moment to use it if I didn't have propofol or ketamine handy. It's almost as if people search for reasons to not like etomidate. Very much like succinylcholine.


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## Peak (Nov 10, 2017)

I have had cases where patients seized at sending facilities after being given etomidate for joint reduction, which is a whole different soap box but I digress. 

Suc gets a bad rap becasue it can potentiate malignant hyperthermia, and other than releasing trismus and rigid chest it doesn't really bring a whole lot to the party that Roc doesn't. While extremely rare reaction I have yet to see a crew that caries dantrolene, so its a pretty big roll of the dice.


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## Carlos Danger (Nov 10, 2017)

Peak said:


> I have had cases where patients seized at sending facilities after being given etomidate for joint reduction, which is a whole different soap box but I digress.
> 
> Suc gets a bad rap becasue it can potentiate malignant hyperthermia, and other than releasing trismus and rigid chest it doesn't really bring a whole lot to the party that Roc doesn't. While extremely rare reaction I have yet to see a crew that caries dantrolene, so its a pretty big roll of the dice.



Myoclonus is common after etomidate administration and is often confused for seizures. It's also occasionally seen with propofol and is generally harmless.

The incidence of MH after succinylcholine administration is extremely low. MH events usually happen when susceptible patients are exposed to multiple triggering agents (for example, sux plus a volatile anesthetic) and rarely on the first occurrence. An MH event following just succinylcholine administration for emergency airway management is practically unheard of. Probably significantly less likely than serious adverse reactions to other drugs that we use very frequently. Serotonin syndrome following fentanyl administration, for instance. I would go so far as to say that the risk of MH is not great enough to influence the use of sux, unless of course you are talking about a specific population in whom MH is more likely.


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## Peak (Nov 10, 2017)

While incidence of MH is low, survivability in EMS and the ED is virtually zero. I have no problem accepting risk when there is benefit but to do so without regard to patient is reckless and unprofessional.


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## Carlos Danger (Nov 10, 2017)

Peak said:


> While incidence of MH is low, survivability in EMS and the ED is virtually zero. I have no problem accepting risk when there is benefit but to do so without regard to patient is reckless and unprofessional.


The incidence isn't just low, it is practically non-existent. Can you share any data on the survivability of MH in emergency airway management? I'm not aware of any but admittedly I've never looked.


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## VentMonkey (Nov 10, 2017)

Peak said:


> I have no problem accepting risk when there is benefit but *to do so without regard to patient is reckless and unprofessional.*


I find this statement to be a bit egregious; Succs is our primary induction paralytic. We do have Roc, but don’t utilize it as our primary paralytic.

I don’t think that we’re necessarily reckless because of it, and it certainly doesn’t define our professionalism.


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## E tank (Nov 10, 2017)

Peak said:


> While incidence of MH is low, survivability in EMS and the ED is virtually zero. I have no problem accepting risk when there is benefit but to do so without regard to patient is reckless and unprofessional.



Immediate, profound paralysis providing optimal intubation conditions that resolves in a few minutes without any intervention at all is of no benefit?

 The odds of an individual anesthetist seeing an MH event is somewhere around 1 in 15000 anesthetics. Thats using triggering agents every day. The number for reported MH related deaths per year is 2-3 (two to three) out of 10's of millions of  MH trigger anesthetics per year. There are more anoxic brain injuries from failure to intubate/failure to ventilate events.


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## VFlutter (Nov 10, 2017)

Have you ever given Fentanyl to a patient without having Succ available? What happens if they get rigid chest syndrome and you can’t ventilate? 

Succ has it’s place in the tool box even if i do think Roc is preferable in most situations.  Risk of MH is probably 3rd on the list of my reasons not to use it. As Remi pointed out it’s hard to find much information as the actual incidence as the majority of cases are with concurrent volatile anethestic use but in any case it’s exceedingly rare. And if the very rare case does occur then manage as able, i.e hyperventilate, fluids, bicarbonate, and then divert to the closest facility with dantrelne.


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## E tank (Nov 10, 2017)

VentMonkey said:


> I don’t think that we’re necessarily reckless because of it, and it certainly doesn’t define our professionalism.



Argument from moral superiority...I use it when I have a weak argument.


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## VentMonkey (Nov 11, 2017)

E tank said:


> Argument from moral superiority...I use it when I have a weak argument.


Perhaps, but I don’t want to jump to any conclusions quite yet. 

Things get wonky trying to sift through everyone’s posts, even my own from time to time.


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## Carlos Danger (Nov 11, 2017)

E tank said:


> Immediate, profound paralysis providing optimal intubation conditions that resolves in a few minutes without any intervention at all is of no benefit?



There has been a strong movement over the past few years in the ED/EMS communities away from using succinylcholine. Ever since Weingart, et al started talking about how "Roc rocks, and Sux sucks" many paramedics and some ED docs have become convinced that succinylcholine is poison and should never be used. I've been involved in many discussions on this both online and in person, and my position is always that about 98% of the time it really doesn't matter what you use, but there is about 1% of the time that sux is a better choice and 1% of the time that roc is a better choice. More than once the response that I've gotten to that was, essentially, that I don't know what I'm talking about and anyone who uses succinylcholine doesn't know what they are doing because it has zero advantages and many disadvantages as compared to rocuronium.

Funny story to illustrate just how cultish this belief is: I was kicked off of the EMS Mentoring Society FB page - easily on the the more intelligent of all online EMS forums that I've participated in - because during a discussion on the topic of roc vs. sux, when one of the regulars (who happened to be one of the admins) was being particularly adamant that sux has no place anymore, my response to that was that while I couldn't care less what people prefer for RSI because you can make pretty much anything work, he and the others who share his very strong opinion probably don't have nearly enough experience using both drugs to be so throughly convinced that they know which one is always best.


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## E tank (Nov 11, 2017)

Remi said:


> ....he and the others who share his very strong opinion probably don't have nearly enough experience using both drugs to be so throughly convinced that they know which one is always best.




Funny...or not...I've personally given liters of SCh as have most of the guys I work with and our conversations on the topic have nothing to do with MH. Its a non issue. It's all about myalgias and fasciculations and having to go to the trouble of giving something else when the succs wears off. But even in the age of suggamadex (which I'm not sure even enters into the pre-hospital conversation) guys use SCh regularly for dicey airways or airways out of the  controlled environs of the OR.

Oh well...they don't know what they don't know....


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## Carlos Danger (Nov 11, 2017)

Yep, myalgia is the main thing I think about when I consider using sux.


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## Tigger (Nov 11, 2017)

Remi said:


> There has been a strong movement over the past few years in the ED/EMS communities away from using succinylcholine. Ever since Weingart, et al started talking about how "Roc rocks, and Sux sucks" many paramedics and some ED docs have become convinced that succinylcholine is poison and should never be used. I've been involved in many discussions on this both online and in person, and my position is always that about 98% of the time it really doesn't matter what you use, but there is about 1% of the time that sux is a better choice and 1% of the time that roc is a better choice. More than once the response that I've gotten to that was, essentially, that I don't know what I'm talking about and anyone who uses succinylcholine doesn't know what they are doing because it has zero advantages and many disadvantages as compared to rocuronium.
> 
> Funny story to illustrate just how cultish this belief is: I was kicked off of the EMS Mentoring Society FB page - easily on the the more intelligent of all online EMS forums that I've participated in - because during a discussion on the topic of roc vs. sux, when one of the regulars (who happened to be one of the admins) was being particularly adamant that sux has no place anymore, my response to that was that while I couldn't care less what people prefer for RSI because you can make pretty much anything work, he and the others who share his very strong opinion probably don't have nearly enough experience using both drugs to be so throughly convinced that they know which one is always best.


I am inclined to agree with you. One of my systems recently switched to Ketamine (most of the time) or Etomidate (when you think Ketamine is less advantageous), followed by Roc. I can't really say it makes much difference to me, though I think the primary fear of succs was more related to hyperK. Rather than carry succs and another paralytic, they wanted to get rid of that risk and lessen the formulary (more than a few other drugs got tossed, which again I have no issue with).


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## Carlos Danger (Nov 11, 2017)

Tigger said:


> I am inclined to agree with you. One of my systems recently switched to Ketamine (most of the time) or Etomidate (when you think Ketamine is less advantageous), followed by Roc. I can't really say it makes much difference to me, though I think the primary fear of succs was more related to hyperK. Rather than carry succs and another paralytic, they wanted to get rid of that risk and lessen the formulary (more than a few other drugs got tossed, which again I have no issue with).



If a system or an individual chooses to only use rocuronium, that's fine. I personally wouldn't do that and I don't think most other anesthesia providers would, but I understand the arguments and I kind of see why people make that choice.

What I take issue with is the people who argue passionately that roc is hands down the best choice in every case, and anyone who disagrees is an idiot - even people with much more experience in the area. For some reason, I've seen A LOT of that surrounding this issue.


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## SpecialK (Nov 12, 2017)

Bit late on this one, sorry chaps.  

My thinking is broadly I'm not overly concerned about it; the balance of risk is going to favour a secure airway and control of ventilation and oxygenation er any transient hypertension even in the case of Nana who we think has had a dirty big subarachnoid haemorrhage ... 

In the situation where ketamine was a bad idea ideally I'd be able to use e.g. etomidate or something else but I'm not sure etomidate has made it south of the equator too much just yet.


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## VentMonkey (Nov 12, 2017)

Having recently ran what my non-doctoral-degree self believes was most likely a potine bleed, myself and the hospital staff all seemed content with the Amidate/ Succs combo as well as the decision to withhold post-intubation long-acting paralysis.

While it certainly may not have been the “sexy” FOAM-ed preferred cocktail, it again worked just fine.


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## Docraven311 (Nov 28, 2017)

I personally do not mind using Ketamine in the hypertensive patient. Where I am currently, we have a CRNA that we run questions and scenarios by and he is also a firm believer in using it as well. The one drug that I have seen mentioned a lot in this thread that I absolutely hate is Sux. It is a horrible drug, especially if you are going to paralyze after tube confirmation. Roc should be used in my opinion, due the poor outcomes of using a shirt term paralytic and them a longer one. 

Plus, I am a firm believer in using video laryngoscopes to intubate. I believe that should be required on all trucks. Especially since the cost has come down. I know that we still need to know how to intubate the old way, but video scopes give us a much better chance at success and typically with less time in the mouth.


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## VentMonkey (Nov 28, 2017)

Docraven311 said:


> The one drug that I have seen mentioned a lot in this thread that I absolutely hate is Sux.* It is a horrible drug*, especially if you are going to paralyze after tube confirmation. Roc should be used in my opinion, due the poor outcomes of using a shirt term paralytic and them a longer one.


Why? What if you’re RSI-ing a suspected (non-traumatic) head bleed and you’re wanting to induce intially, but no longer paralyze post-sedation? It wears off fairly quickly, and allows for other post-intubation sedatives to manage the patient without the long-acting effects of, say, Roc or Vec.

Also, if we carried Amidate _and_ Ketamine, I would not subject suspected head injured patients to Ketamine even if it is a “what if” precaution. Each drug has their own pros and cons though I suppose. I don’t know of many (if any) that use it for long-acting induction. Succs is for pre-intubation paralysis.


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## VFlutter (Nov 28, 2017)

Docraven311 said:


> It is a horrible drug, especially if you are going to paralyze after tube confirmation. Roc should be used in my opinion, due the poor outcomes of using a shirt term paralytic and them a longer one.



Sux’s effectiveness as a post-intubation paralytic shouldn’t ever be an issue when discussing RSI since you should not be redosing it anyway.

And where does it show than patients have worse outcomes after short term then long term paralysis? And even in the transport environment i would argue that the vast majority of patients do not need post intubation paralysis anyway.


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## E tank (Nov 28, 2017)

Docraven311 said:


> Roc should be used in my opinion, due the poor outcomes of using a shirt term paralytic and them a longer one.



Agreed on the VL's but what poor outcomes paralyzing after succs?


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## Carlos Danger (Nov 28, 2017)

Docraven311 said:


> I personally do not mind using Ketamine in the hypertensive patient. Where I am currently, we have a CRNA that we run questions and scenarios by and he is also a firm believer in using it as well. The one drug that I have seen mentioned a lot in this thread that *I absolutely hate is Sux. It is a horrible drug, especially if you are going to paralyze after tube confirmation. Roc should be used in my opinion,* due the poor outcomes of using a shirt term paralytic and them a longer one.



Ugh this again. Really?


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## VFlutter (Nov 28, 2017)

Remi said:


> Ugh this again. Really?



You are just too inexperienced and naive to realize Succs Sucks!


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## VentMonkey (Nov 28, 2017)

...Roc rocks!


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## Peak (Nov 28, 2017)

Yeah! We shouldn't change what we are doing to be more evidence based. I'm gonna keep doing the same thing I was a decade ago because it worked okay for me.


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## Carlos Danger (Nov 28, 2017)

Peak said:


> Yeah! We shouldn't change what we are doing to be more evidence based. I'm gonna keep doing the same thing I was a decade ago because it worked okay for me.


Exactly what evidence has been provided in this thread?


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## Peak (Nov 28, 2017)

Remi said:


> Exactly what evidence has been provided in this thread?



That's the part were you do more continuing education than just to renew you state license.


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## Carlos Danger (Nov 28, 2017)

Peak said:


> That's the part were you do more continuing education than just to renew you state license.


Ok so you don’t have any. Gotcha.


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## Peak (Nov 28, 2017)

Remi said:


> Ok so you don’t have any. Gotcha.



If I posted evidence based studies would you actually change your mind? I seriously doubt it. This comes from the person who posted that etomidate presents epileptiform eeg tracings and mycolonic activity, but that it doesn't cause seizures.


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## VFlutter (Nov 28, 2017)

Peak said:


> If I posted evidence based studies would you actually change your mind? I seriously doubt it. This comes from the person who posted that etomidate presents epileptiform eeg tracings and mycolonic activity, but that it doesn't cause seizures.



I do not think Remi was imply that epileptiform eeg activity with concurrent myoclonic jerks are not seizures however they are commonly independent of each other. There are many reasons for myoclonus other that epileptic seizures and there are patients with epileptiform eeg activity without clinical seizure activity. So a patient whom has myoclonus after etomidate is not necessarily seizing even if it may he interpreted as such.

And i get the the rationale to avoid Etomidate in the head injury or epileptic patient however your statement that it should never be used without a barbiturate or Benzo is a little extreme. Lowering the seizure threshold is not going to induce spontaneous seizures in patients except of those mentioned.


“Etomidate is a hypnotic nonbarbiturate, ultra–short-acting anesthetic agent associated with involuntary muscle movements in 10–70% of patients. These movements can be violent and mimic seizure activity. Etomidate is often administered because of its cardiovascular stabilizing effect. In patients without epilepsy, surface electrode recordings during the myoclonic movements are not associated with epileptiform activity.54

In epilepsy patients, etomidate (0.2 mg/kg) can activate seizure foci within 30 seconds55 and has been used intraoperatively for this purpose.

Despite the lack of evidence that etomidate causes seizures in nonepileptic patients, epileptiform activity occurred in 6 of 30 nonepileptic patients who were induced with etomidate for heart valve replacement.” 

https://www.epilepsy.com/learn/prof...ilepsy-patients/general-anesthetics/etomidate


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## TXmed (Nov 28, 2017)

No medication is good or bad, sucks or rocks. But it is how the clinician chooses to use them for the patient at hand, that makes the difference. 

@Peak without data, you're just a fool with an opinion.


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## E tank (Nov 28, 2017)

TXmed said:


> No medication is good or bad, sucks or rocks. But it is how the clinician chooses to use them for the patient at hand, that makes the difference.
> 
> @Peak without data, you're just a fool with an opinion.



And just for the record..."data" is a loaded term....


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## VentMonkey (Nov 28, 2017)

Peak said:


> Yeah! We shouldn't change what we are doing to be more evidence based. I'm gonna keep doing the same thing I was a decade ago because it worked okay for me.


An _extremely_ ironic post in a thread chocked full of the heavy-hitters on this forum with regards to EBM. You don’t know what you don’t know.


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## Carlos Danger (Nov 29, 2017)

Peak said:


> If I posted evidence based studies would you actually change your mind? I seriously doubt it.



I gotta be honest, I don't even know what you are talking about. Why don't you stop being so cryptic and just say what it is that you think I'm wrong about? And if you have evidence to support why you think I'm wrong, post it. Just saying "but, but, your wrong and there's evidence" and then failing to produce the evidence makes it look like you really can't support your position. Anyone can claim that there is evidence to support any opinion. Claims of proof without providing the proof are meaningless. Put up or shut up.



Peak said:


> This comes from the person who posted that etomidate presents epileptiform eeg tracings and mycolonic activity, but that it doesn't cause seizures.



OK, so part of the problem here seems to be that you are confused about some basic neurophysiology. Let me break it down for you:

1. Just like PAC's or PVC's or a first-degree conduction block on an EKG often has no clinical meaning, an "epileptiform" EEG pattern does not mean that the patient is having a seizure.

2. The myoclonus that propofol and etomidate causes is completely distinct from seizure activity. Myoclonus of this type is caused by disinhibition of the extrapyramidal medullary tracts, which influence balance and coordination and fine motor control. Most types of seizure activity are caused by ectopic neural discharge in the cortex. Completely different parts of the brain, completely different physiology.

3. Etomidate and ketamine both lower the seizure threshold. This does not mean they cause seizures. The brain of an epileptic is always on the verge of a seizure and as soon as you nudge it in that direction, it will. Quite a few drugs and stimuli do that, not just these two drugs. This does not happen in non-epileptics.  

4. What happens with etomidate is someone will read that it lowers the seizure threshold, and then they use it maybe ten times, and 4 or 5 out of those ten times they'll see pretty pronounced myoclonus, and they go tell people "etomidate causes seizures, and I've seen it" when no, they did not.

To summarize: etomidate does not cause seizures. It does lower the seizure threshold, but that only results in seizures in epileptics. And guess what? Your beloved ketamine does the exact same thing.


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## CWATT (Nov 29, 2017)

I was going to post yesterday but after browsing this thread I realized I’d better not bring a knife to a gun-fight...

So I have evidence! (sort of)

‘The Walls Manual of Emergency Airway Management — Fifth Edition’ has the following to say...

“In 2009, Jabre et al. Published the largest clinical trial to date involving ketamine 2mg per kg for RSI in adults, and comparing it to etomidate 0.3mg per kg, both with succinylcholine as the NMB agent.  There were *no significant hemodynamic differences* between the two groups.  The study concluded ketamine is a safe alternative to etomidate for endotracheal intubation in critically ill patients... This study has been followed by others supporting the same conclusion” p. 257

If Etomidate is the gold-standard of hemodyamically stable induction agents and these studies are finding ‘no significant differences’, I don’t see any reason why you wouldn’t use it in hypertensive patients.


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## Peak (Dec 2, 2017)

Remi said:


> Why don't you stop being so cryptic and just say what it is that you think I'm wrong about?



I don't think you are wrong, but that like most medics (including myself several years ago) tend to think of RSI as a field procedure without really thinking about the effects when they are in the ED or ICU. Things like the after effects of drugs and which hospital EMS goes to can make a huge determination in patient outcome, these are things that are not well taught in P school. I have also learned that most medics don't really care that much what the patient outcomes are once they are out of their care.


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## Carlos Danger (Dec 3, 2017)

Peak said:


> I don't think you are wrong, but that like most medics (including myself several years ago) tend to think of RSI as a field procedure without really thinking about the effects when they are in the ED or ICU. Things like the after effects of drugs and which hospital EMS goes to can make a huge determination in patient outcome, these are things that are not well taught in P school. I have also learned that most medics don't really care that much what the patient outcomes are once they are out of their care.



What you'll generally find on this forum is folks who do think about outcomes and do want to learn and integrate the best practices into what they do, to the greatest extent that they are able to.

I'll discuss airway management and the related pharmacology all day long, and I welcome differing opinions. I learn plenty from the discussions on here. Show some good quality evidence that contradicts what I think is true, and I''l definitely re-evaluate. I welcome opportunities to learn and improve.

But it is unhelpful when people spout off about how others are wrong because their favorite podcaster or blogger has a different opinion on how things should be done. Just because an internet personality - or 5 of them - says something doesn't make it fact. Just because something appears in a published article doesn't mean it is high quality evidence that should change practice. Even if high-quality evidence does arise that supports something, it still doesn't mean that something is always the best option in every scenario. Medicine is complex and can't be boiled down to rigid protocols.


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