Ketamine for RSI in hypertensive patients

SandpitMedic

SandpitMedic

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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
 
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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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.
 
Lidocaine anybody?
 
SandpitMedic said:
Not in the formulary for intubation anymore where I'm at.
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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.
 
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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Remi said:
laryngoscopy, especially sloppy or prolonged or multiple attempts is probably a much greater worry than the choice of drugs used.
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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)
 
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)
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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.
 
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?
 
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.
 
Peak said:
the transient hypertension or hypotension associated with induction agents is not going to be the principal problem.
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Although that may be the case in many situations there are some patient populations that even brief episodes of hypertension/hypotension significantly worsen outcomes.
 
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.
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More significantly than a deteriorating and unsecured airway?
 
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.
 
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.
 
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.
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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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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.
 
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.
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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.
 
Peak said:
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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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.
 
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.
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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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