To Propofol or Not to Propofol?

[CWATT]

I did my Paramedic training in an area where Propofol was a Critrical Care only drug, so while I was familiar with its purpose but I did not receive any specific training on its use.

I have now transferred to a different region where Propofol is within my scope, however despite completing the ‘gap training’ which primarially involved independent reading, there was no specific discussion on when Propofol would be indicated over other general anaesthetics such as Ketamine.

I do have experience using Ketamine so I am struggling to derive any scenario other than Continuity of Care (keeping an IFT patient on the same med as the sending facility for no other reason than ease/simplicity provided vitals are stable) to use Propofol over Ketamine.

Re: a Stroke — I know Propofol is said to dec. ICP and CMRO2 through myocardial depression and vasodilation, but those mechanisms also decrease CPP. I would not feel confident using Propofol in a hypertensive stroke patient because I would most likely be transporting this patient en route to CT, so I would have to treat any stroke as hemorrhagic and my goals of therapy would be MAP > 80 or SBP >140. Furthermore, Ketamine is said to have neuroprotective effects and in certain settings not increase ICP while improving CPP. Lastly, I wouldn’t be able to titrate sedation independent of BP with Propofol, where as if I was using Ketamine I could manage hypertension with Labetalol.

TBI — the goals of therapy are the same as a hemorhagic stroke (MAP >80), so Ketamine would seem like a better agent here as well.

Status Epilepticus — I’ll admit this one might seem like a no-brainer, but Ketamine is considered an anticonvulsant and is indicated when conventional drugs are ineffective. However, in Status we would be approaching the patient with airway management as our priority concern and can always add IV Midazolam (or Lorazepam if available) for recurrent seizure activity. Moreover, my protocols do not allow for Propofol as an inductin agent so I’m reaching for Ketamine already (not to say I wouldn’t switch to Propofol if I thought it was in the best interest of the patient, but I think the anticonvulsant benefits don’t outweigh the risks of balancing sedation when titrating from Ketamine over to Propofol).


So my questions are:

- when should I reach for Profol over Ketamine?

- Being a GABAa agonist, does Propofol experience the same wide-range of efficacy across patient populations like Benzos?


Thanks,
- C

 

[Akulahawk]

Where I work (in an ED), we use Propofol mostly as a post-RSI sedative. We use other agents for induction and then we go to Propofol to maintain sedation. I try to keep the patient reasonably well sedated but my goal is usually to get the patient out of the ED and over to the ICU before long. We're not that good at maintaining sedation in the ED as we don't do it all that often, or at least in my ED nor in any ED I've worked in. My experience with Propofol is that as long as you're not actively jostling the patient, Propofol works reasonably well but if you move 'em around a bit, they'll wake up for a bit and then it's not as easy to get 'em back down until you've stopped jostling them and good luck with that in the transport environment. From what I've seen thus far, Propofol works reasonably well but it's best when used in a combination.

 

[VFlutter]

For practicality sake unless it is a seizure or therapeutic hypothermia patient I will usually discontinue it and use push dose analgesia and sedation. Propofol has some advantages listed above however it is finicky with our transport pumps and tends to require decently increased doses to maintain the same level of sedation in transport.

 

[CWATT]

For practicality sake unless it is a seizure or therapeutic hypothermia patient...

What’s the benefit/association/etc of Propofol with therapeutic hypothermia?

 

[wanderingmedic]

When I worked CCT I really preferred Ketamine, or Fentanyl + Versed. One thing to keep in mind is that sedation does not equal pain control. Having a tube down one's throat and receiving PPV causes discomfort. Additionally, the underlying pathology that required intubation may also be causing the pt pain. Sedating the patient does not remove their ability to sense pain, so a good approach to anesthesia is always pain control + sedation. Even with propofol I like to make sure we are adding something for pain control, especially if the patient is (probably) in pain.

Where I work (in an ED), we use Propofol mostly as a post-RSI sedative. We use other agents for induction and then we go to Propofol to maintain sedation. I try to keep the patient reasonably well sedated but my goal is usually to get the patient out of the ED and over to the ICU before long. We're not that good at maintaining sedation in the ED as we don't do it all that often, or at least in my ED nor in any ED I've worked in. My experience with Propofol is that as long as you're not actively jostling the patient, Propofol works reasonably well but if you move 'em around a bit, they'll wake up for a bit and then it's not as easy to get 'em back down until you've stopped jostling them and good luck with that in the transport environment. From what I've seen thus far, Propofol works reasonably well but it's best when used in a combination.

I've had the same experience with propofol in the ED and on the road. However, I have found that the aforementioned affects of movement and jostling can be mitigated by a little fentanyl or morphine.

Another thing to keep in mind is that the ambulance is oftentimes a much more stimulating environment than the ED/ICU. Most of the time I have found that patients who were well sedated on the unit, require more once they are on the road.

 

[Carlos Danger]

Propofol is an excellent anesthetic that is really good at a lot of different things. I don't recommend using it for RSI or any procedural sedation because it can get away from you really quickly if you don't have plenty of experience with it, and the ramifications of that happening in a sick patient can be very serious. It isn't a hard drug to use, using it that way safely just takes experience that is hard to come by outside of anesthesia practice.

The reason it seems to not work well as an infusion in the transport setting has to do with both the fairly steep dose-response curve of the drug and it's rapid elimination from the site of action, which are it's biggest advantages over other IV anesthetics. It takes effect very quickly and wears of very quickly. This means it can be easily titrated, which makes it a good choice for sedation in the hospital where you want to use the lowest dose of sedation possible. It makes sense that if a patient is not over-sedated, increasing stimulation will require a corresponding increase in sedation. So it follows that moving from a nice quiet ICU bed to a much more stimulating transport environment will require a much larger dose of drug. This is not a limitation of propofol; it is a positive feature of it. The only reason you don't see such a pronounced increase in sedation requirements with other drugs is because those drugs are inferior in their ability to be titrated, and those patients were effectually over-sedated before transport.

When I worked CCT I really preferred Ketamine, or Fentanyl + Versed. One thing to keep in mind is that sedation does not equal pain control. Having a tube down one's throat and receiving PPV causes discomfort. Additionally, the underlying pathology that required intubation may also be causing the pt pain. Sedating the patient does not remove their ability to sense pain, so a good approach to anesthesia is always pain control + sedation. Even with propofol I like to make sure we are adding something for pain control, especially if the patient is (probably) in pain.

Not to drag this topic off into the weeds, but I try to address this very pervasive misunderstanding every time I see it. There are good reasons to use analgesics in combination with sedatives, rather than just higher doses of sedatives. But those reasons have nothing to do with patient comfort.

A well-sedated patient does not experience pain. Once a large enough number of those GABA receptors are activated, the conscious part of the brain is completely turned off, and you don't experience anything at all, no matter how noxious or painful the stimulus is. You still have physiological responses (typically sympathetic) to stimuli of course, but that all happens in your lower CNS and doesn't in any way indicate that you are experiencing anything.

We do painful surgeries all the time on propofol infusions. Yes, we almost always use analgesics or nerve blocks in conjunction with the propofol, but that has to do with controlling hemodynamics and preventing physiological changes in the neurological system that relate to the processes of nociception and pain interpretation, and ensuring that the patient wakes up comfortably. It has nothing at all to do with keeping the patient comfortable during the surgery.

 

[CWATT]

@Remi — how does this apply to Ketamine which does not interact with GABA receptors? My understanding is Ketamine offers mild analgesia but it is strongly recommended -and I always did- add Fentanyl for patient comfort.

 

[Peak]

@CWATT Are you carrying propofol or are you only allowed to maintain it during transfers?

Your first question is a bit more difficult and is far more in depth than can simply be answered in a few posts.

For adults we use a ton of propofol. Propofol is easly to titrate and very effective in a variety of cases. It has the added benefit of being very easy to string up a bottle or put a 60mL syringe on a pump very quickly. Propofol also has some downsides. I think on of the more common and profound issues we run into is hypotension. Appropriate fluid bolusing and a bit of neo or levo; this is of course for routine anesthetic related hypotension and not from profound overdoses of propofol. We frequently use propofol in neuro cases.

Ketamine has been discussed at lengths in various other topics. My personal opinion is that generally I don't like it as a sole agent for (non-procedural) sedation. When administered with an appropriate benzo or narc I find it much easier to gain the desired effect. Ketamine certainly has a much wider therapeutic index than propofol and is probably much safer to be given by the vast majority of casual EMS/ED/low-acuity or low volume critical care providers. I find ketamine to generally be more beneficial in those who respiratory driven, and in those who are more cooperative/less anxious with the procedure.

Propofol is used for refractory status epilepticus, so I wouldn't discount it's use in the emergency setting. There are some variable arguments about how seizure patients wake up from propofol and some eeg activity in the first few minutes of propofol infusion, but I wouldn't worry about this as much in the critical patient. Without whipping up some literature ketamines effects on seizures are pretty mild and I've seen arguments that it both prevents and precipitates seizures.

I'd personally rather bolus a patient with versed or ativan and +/- fentanyl on top of their sedation in the vast majority of cases rather than crank their maintenance sedation up for procedures or transport.

As to the effects across populations, I've seen anesthesia use it as their primary induction and maintenance agent in just about everyone from infants to geriatrics.
Propofol has a much narrower therapeutic index than the vast majority of benzos or barbiturates, and a lot of care must be taken with giving it. It is a drug I would never give without full monitoring, far above what I would consider the minimum for most of the other drugs we give. There is a good reason why a lot of states very strongly limit which clinicians can give propofol and in what settings, and the threshold for consulting anesthesia when using propofol should be very low

Alcoholics among a few other populations can metabolize propofol like crazy, although this phenomenon isn't exclusive to it. We will crank up propofol up to 100mcg/kg/min for short periods of time but this comes with many other risks beyond typical dosing. We are typically looking at other options for these patients including ketamine, precedex, versed drips, phenobarbital, and other drugs depending on the individual presentation.

 

[Brandon O]

@CWATTKetamine certainly has a much wider therapeutic index than propofol and is probably much safer to be given by the vast majority of casual EMS/ED/low-acuity or low volume critical care providers.

I would sort of quibble with this. I agree that it has a wider range of safe dosing that will not cause hypotension, respiratory depression, etc. But it lacks the clear dose-response relationship of something like propofol. If a patient is agitated on low dose (subdissociative) ketamine, turning it up is not always the answer, as it may lead to partial dissociation which is not helpful. Likewise if desiring to titrate down from full dissociation.

Achieving actual sedation with ketamine is a bit all-or-nothing unless you want to start pushing your luck. In the ICU I don't order it to be nurse-titrated. Flat rate only. Hence unless we're trying to basically put them under general anesthesia it tends to be more of an adjunct.

 

[E tank]

For IFT, if something like propofol is required, paralysis would be very helpful in that propofol titration to a certain goal (coughing on the tube, other movement) by folks that may not have a lot of experience with it is simplified as long as a minimum rate for sedation is maintained.

ICU sedation OTOH, without paralysis, is made far easier when propofol is combined with something else as someone else already mentioned. My personal choice is precedex and works great to limit the dose of each drug and makes waking up and eventual extubation much easier. Propofol as the primary sedative is a nice way to go, but limiting the dose by using a modest adjunct should be part of the conversation.

 

[Peak]

I would sort of quibble with this. I agree that it has a wider range of safe dosing that will not cause hypotension, respiratory depression, etc. But it lacks the clear dose-response relationship of something like propofol. If a patient is agitated on low dose (subdissociative) ketamine, turning it up is not always the answer, as it may lead to partial dissociation which is not helpful. Likewise if desiring to titrate down from full dissociation.

Achieving actual sedation with ketamine is a bit all-or-nothing unless you want to start pushing your luck. In the ICU I don't order it to be nurse-titrated. Flat rate only. Hence unless we're trying to basically put them under general anesthesia it tends to be more of an adjunct.

I respectfully disagree. We use ketamine on a very large number of patients in our PICU and our nurses titrate without a problem. We use it in the adult ICUs as well but with less frequency. We give it sub dissociative, for partial dissociation (mostly for conscious intubations), and for sedation. If your nurses can't figure out how to titrate ketamine then they need more training, and perhaps shouldn't be working in an ICU.

 

[E tank]

I respectfully disagree. We use ketamine on a very large number of patients in our PICU and our nurses titrate without a problem. We use it in the adult ICUs as well but with less frequency. We give it sub dissociative, for partial dissociation (mostly for conscious intubations), and for sedation. If your nurses can't figure out how to titrate ketamine then they need more training, and perhaps shouldn't be working in an ICU.

So...PICU...how often do you paralyze mechanically ventilated patients there?

 

[Peak]

So...PICU...how often do you paralyze mechanically ventilated patients there?

Typically multiple at a time, but it certainly varies based on the time of the year. We have the largest level IV NICU in the region so we tend to get quite a bit from that as well as our congenital heart program.

 

[E tank]

Typically multiple at a time, but it certainly varies based on the time of the year. We have the largest level IV NICU in the region so we tend to get quite a bit from that as well as our congenital heart program.

So you paralyze or you don't? I'm guessing you do... and titrating sedation, in that circumstance...is reduced to MAP and HR....way easier than allowing a patient to breathe on his own with support...and not at all a metric of whether someone should be an ICU nurse or not...

 

[Brandon O]

If your nurses can't figure out how to titrate ketamine then they need more training, and perhaps shouldn't be working in an ICU.

Thanks, I'll pass it along.

It is not a matter of training. Ketamine does not have a direct dose-response relationship, so "titrating" it at the bedside doesn't make sense. With the possible exception you mentioned, I don't think anybody should be sitting in the ICU partially dissociated.

The one exception might be titration within a sub-dissociative range (e.g. .1-.3 mg/kg) in response to pain. But that's not a sedative.

 

[Peak]

So you paralyze or you don't? I'm guessing you do... and titrating sedation, in that circumstance...is reduced to MAP and HR....way easier than allowing a patient to breathe on his own with support...and not at all a metric of whether someone should be an ICU nurse or not...

It depends on their clinical presentation. We don't add vec or roc unless we need to or are doing certain procedures. And titration for dissociation is not based on hemodynamics.

 

[Peak]

Thanks, I'll pass it along.

It is not a matter of training. Ketamine does not have a direct dose-response relationship, so "titrating" it at the bedside doesn't make sense. With the possible exception you mentioned, I don't think anybody should be sitting in the ICU partially dissociated.

The one exception might be titration within a sub-dissociative range (e.g. .1-.3 mg/kg) in response to pain. But that's not a sedative.

That's a bit like saying you can't titrate milrinone or vaso.

 

[Brandon O]

That's a bit like saying you can't titrate milrinone or vaso.

In many circumstances I think that is correct.

 

[Peak]

In many circumstances I think that is correct.

Many, but certainly not all. Definitely not in the last glenn I took care of.

 

[Brandon O]

Many, but certainly not all. Definitely not in the last glenn I took care of.

Inotropes should be titrated to markers of perfusion, which (unless there is a Swann or non-invasive cardiac output monitor) is usually a thoughtful gestalt of the clinical exam, echo, labs, etc. While I recognize that nurses are capable of being thoughtful, it's a different matter from just responding to an isolated bedside variable like the blood pressure.

Titrating vasopressin is controversial. I don't usually do it, although I wouldn't argue if someone wanted to. In any case it's not exactly a model of fine-tuning; usually people just move between .04 and 0 in two or three clicks at most.