Cipepofol

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What this tells me is if you **** around you're gonna find out. I'm honestly surprised no one died.

How did jama publish it. No pressor even running afaik?

"Anything is better than stupidity". Ppfst et al 25

I did a nice carotid recently with severe uncorrected AS. No tavi yet because "asymptomatic " despite recent good size stroke. Obviously some bean counter med person deems cva had nothing to do with ava 0.8. Smart idiots...


GA cause surgeons...

Anyways went real good with remi ppf roc tube induction but Obviously phenyl infusion.. why mess around with this... AS is totally fine if you treat them well... as long as sole AS no severe cad, hf ok. Add those things on top of 120 ppf induction you're boned

The protamine was fun too. She had relative heparin resistance...

Developed deficit on ssep with clamp too so I drove bp 190. Fixed it. No need of shunt... show AS might actually have been more significant in cva development than bean man thought...

Oh well. I just put the tubes in and agree. Smile. Just Do the goddam case



On phone. Cant typo ha geddit
 
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PpfSuxTube said:
Is this even ethical?
Or statistical usable?

88% of the propofol group had the primary outcome as anyone with even a hot minute of anesthesia would expect. I dont think I've ever seen that.
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Looks like they designed the study to allow some postinduction hypotension. Probably in order to show a difference. I would have omitted the alfenta myself. Anyway since they had norepi bolus and infusion ready, I don’t think it’s a big deal.
 
nimbus said:
Looks like they designed the study to allow some postinduction hypotension. Probably in order to show a difference. I would have omitted the alfenta myself. Anyway since they had norepi bolus and infusion ready, I don’t think it’s a big deal.
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Is alfenta even available in the US these days? I haven’t seen it in quite a while.
 
PpfSuxTube said:
What this tells me is if you **** around you're gonna find out. I'm honestly surprised no one died.

How did jama publish it. No pressor even running afaik?

"Anything is better than stupidity". Ppfst et al 25

I did a nice carotid recently with severe uncorrected AS. No tavi yet because "asymptomatic " despite recent good size stroke. Obviously some bean counter med person deems cva had nothing to do with ava 0.8. Smart idiots...


GA cause surgeons...

Anyways went real good with remi ppf roc tube induction but Obviously phenyl infusion.. why mess around with this... AS is totally fine if you treat them well... as long as sole AS no severe cad, hf ok. Add those things on top of 120 ppf induction you're boned

The protamine was fun too. She had relative heparin resistance...

Developed deficit on ssep with clamp too so I drove bp 190. Fixed it. No need of shunt... show AS might actually have been more significant in cva development than bean man thought...

Oh well. I just put the tubes in and agree. Smile. Just Do the goddam case



On phone. Cant typo ha geddit
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Primary endpoint was MAP<65 or MAP 20% lower than baseline. I don’t think it’s a big deal. And I’m speaking as someone who starts a low dose norepi infusion prior to induction on these patients.
 
nimbus said:
Primary endpoint was MAP<65 or MAP 20% lower than baseline. I don’t think it’s a big deal. And I’m speaking as someone who starts a low dose norepi infusion prior to induction on these patients.
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Agreed..no magic bullet or substitute for basic principles. Pre-induction volume and inopressor and a mindful induction...dealers choice.
 
Anyway the drug seems to have more potent CNS effects than propofol. Induction doses can be lower which may yield a better hemodynamic side effect profile at equipotent doses. Also less burning.
 
Teillard said:
Agreed..no magic bullet or substitute for basic principles. Pre-induction volume and inopressor and a mindful induction...dealers choice.
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Whats an inopressor?
And assuming it exists why would you want to give the ino part to someone with severe AS?

Dont basically...
Cards do it to induce severe gradient to diagnose lflg which should tell you enough to not electively use it...

Dob can't really be considered an inopressor. More likely inodilator. Although some do incr bp likely due to their relative posn on starling curve. But not for isolated severe as electively
 
PpfSuxTube said:
Whats an inopressor?
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I suppose he meant epi and norepi, maybe ephedrine, all of which have some beta effects.

PpfSuxTube said:
And assuming it exists why would you want to give the ino part to someone with severe AS?
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Epi is probably a poor choice but norepi is fine. There are times when the pure alpha of phenylephrine isn't exactly what the situation calls for.
 
PpfSuxTube said:
Whats an inopressor?
And assuming it exists why would you want to give the ino part to someone with severe AS?

Dont basically...
Cards do it to induce severe gradient to diagnose lflg which should tell you enough to not electively use it...

Dob can't really be considered an inopressor. More likely inodilator. Although some do incr bp likely due to their relative posn on starling curve. But not for isolated severe as electively
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I'll just say norepinephrine next time....
 
nimbus said:
Primary endpoint was MAP<65 or MAP 20% lower than baseline. I don’t think it’s a big deal. And I’m speaking as someone who starts a low dose norepi infusion prior to induction on these patients.
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Why norepi over neo? Why do you want beta agonism? Increasing HR and myocardial oxygen demand while reducing coronary perfusion time doesn’t seem ideal for most AS patients. Plus you’re increasing the risk (albeit low) of extravasation injury if using a peripheral IV.

I’m not saying there aren’t some circumstances where NE is reasonable, but it seems like an odd first line choice for all AS inductions.
 
DesiredMemberName? said:
Why norepi over neo? Why do you want beta agonism? Increasing HR and myocardial oxygen demand while reducing coronary perfusion time doesn’t seem ideal for most AS patients. Plus you’re increasing the risk (albeit low) of extravasation injury if using a peripheral IV.

I’m not saying there aren’t some circumstances where NE is reasonable, but it seems like an odd first line choice for all AS inductions.
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Moderation in all things. Just because someone has AS doesn't mean you must/should keep their HR as low as possible.

Frequently people with AS have impaired LV function too. It is sometimes useful to compensate for the negative inotropic effects of induction agents (and they all have some such effect) with some beta agonism.

When I induce people with AS, probably close to 100% get a norepi infusion started at the same time. So long as you're judicious with it and take other steps to keep the HR at a reasonable level, it's fine. Lots of these people have pacers/ICDs. What happens when you put a magnet on a pacer or reprogram an ICD to an asynchronous rate of 90 or 100? They do fine. Tachycardia is sometimes poorly tolerated in patients with severe AS, but you don't need to keep their HR at 55. Don't be afraid of the little bit of beta you get from norepi.

As for extravasation injuries by giving norepi peripherally ... the answer there is don't induce these patients with IVs you don't trust. Unless the patient is uncooperative, you can get access on 99% of everyone with ultrasound. Maybe that means a central line, or using a micropuncture kit to get into a deeper vein located with ultrasound. If you can't trust the IV with norepi, you shouldn't be trusting it to get the phenylephrine in to keep the patient's BP at an acceptable level.
 
pgg said:
Moderation in all things. Just because someone has AS doesn't mean you must/should keep their HR as low as possible.

Frequently people with AS have impaired LV function too. It is sometimes useful to compensate for the negative inotropic effects of induction agents (and they all have some such effect) with some beta agonism.

When I induce people with AS, probably close to 100% get a norepi infusion started at the same time. So long as you're judicious with it and take other steps to keep the HR at a reasonable level, it's fine. Lots of these people have pacers/ICDs. What happens when you put a magnet on a pacer or reprogram an ICD to an asynchronous rate of 90 or 100? They do fine. Tachycardia is sometimes poorly tolerated in patients with severe AS, but you don't need to keep their HR at 55. Don't be afraid of the little bit of beta you get from norepi.

As for extravasation injuries by giving norepi peripherally ... the answer there is don't induce these patients with IVs you don't trust. Unless the patient is uncooperative, you can get access on 99% of everyone with ultrasound. Maybe that means a central line, or using a micropuncture kit to get into a deeper vein located with ultrasound. If you can't trust the IV with norepi, you shouldn't be trusting it to get the phenylephrine in to keep the patient's BP at an acceptable level.
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Like I said:

DesiredMemberName? said:
I’m not saying there aren’t some circumstances where NE is reasonable, but it seems like an odd first line choice for all AS inductions.
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I’m not hearing a reason why it is superior to Neo for the vast majority of patients. Mostly it just sounds like something that might sometimes be useful and isn’t necessarily all that bad, and I agree.

Also, there are IVs that seem ok and then infiltrate on induction or shortly thereafter. I would have to have a pretty good reason for why NE > Neo to justify even a small risk of catastrophic extravasation injury in every AS induction. Maybe such a justification exists, but I’m struggling to grasp it.
 
Can't think of too many of these patients that would not be on a beta blocker which mitigates a lot any meaningful increase in rate from NE. And I could think of more reasons than NE extravasation for having a bomb proof IV for these patients.
 
DesiredMemberName? said:
Like I said:



I’m not hearing a reason why it is superior to Neo for the vast majority of patients. Mostly it just sounds like something that might sometimes be useful and isn’t necessarily all that bad, and I agree.

Also, there are IVs that seem ok and then infiltrate on induction or shortly thereafter. I would have to have a pretty good reason for why NE &gt; Neo to justify even a small risk of catastrophic extravasation injury in every AS induction. Maybe such a justification exists, but I’m struggling to grasp it.
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Extravasation is so low on my list of concerns for a low dose norepinephrine infusion. Check it intermittently and you're fine.
 
DesiredMemberName? said:
Why norepi over neo? Why do you want beta agonism? Increasing HR and myocardial oxygen demand while reducing coronary perfusion time doesn’t seem ideal for most AS patients. Plus you’re increasing the risk (albeit low) of extravasation injury if using a peripheral IV.

I’m not saying there aren’t some circumstances where NE is reasonable, but it seems like an odd first line choice for all AS inductions.
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Alpha>>beta and a little beta is often useful during anesthesia induction and maintenance. No postinduction hypotension. I used to do phenylephrine too. Patients just seem more stable with norepi. Just try it. By low dose I mean 2-4mcg/min. I’ve never seen tachycardia from it.
 
Peripheral norepi is safe, and has data to support the practice. We only do phenylephrine here out of habit and convenience, there's no good data that shows phenylephrine to be superior to norepi in treating intraop transient hypotension.

Additionally, the low beta-agonist effect is minimal, and mostly just offsets the decreased HR from the alpha stimulation. Even at higher doses in the unit, I only very rarely see tachycardia from norepi. Even that is mostly restricted to the already kind of rapid a-fib patient with various electrolyte and metabolic derangements that are just itching to go into AF RVR.
 
DesiredMemberName? said:
Like I said:



I’m not hearing a reason why it is superior to Neo for the vast majority of patients. Mostly it just sounds like something that might sometimes be useful and isn’t necessarily all that bad, and I agree.

Also, there are IVs that seem ok and then infiltrate on induction or shortly thereafter. I would have to have a pretty good reason for why NE > Neo to justify even a small risk of catastrophic extravasation injury in every AS induction. Maybe such a justification exists, but I’m struggling to grasp it.
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There's nothing wrong with phenylephrine, beyond noting that in patients who need a LOT of vasopressor support, its ceiling is lower than that of norepi.

Your concern about HR in these patients is overstated. They will do fine with a sinus HR under 100, indeed they tend to be better at 85 than 45. As mentioned in another post, most of these patients are solidly beta blocked and just are not going to get tachycardic with 2-10 mcg/min of norepi running.

As for extravasation injuries - would I run 30 mcg/min through a dodgy 24g peripheral IV? No. I wouldn't run propofol through it either.


There's a trend in ICU care for early d/c of central lines, and avoiding them in the first place. Their comfort with running vasoactive drugs through peripheral IVs a lot higher now than it was years ago. There's r/b there and I confess some annoyance when I get to the ICU to pick up a sick patient and find they're on substantial doses but don't have a central line (or an a-line for that matter). But they're not really wrong in thinking that a good PIV is just fine for running vasopressors.

Again - if you don't feel good about a PIV then get better access. There's no reason not to. The days of semi-blindly trying to get an angiocath into someone with lousy veins should be over. Get the ultrasound and a micropuncture kit and put 10 cm of 4 Fr goodness into the upper arm. Or put something in the IJ. Or if it's not urgent and it's not really your problem yet, tell an RN to call the hospital IV team to do it.

If an IV is dodgy and you're worried enough about extravasation injury to not want to give NE through it, you shouldn't be trusting it for induction drugs either. The problem isn't NE vs phenylephrine. It's the IV.
 
pgg said:
There's nothing wrong with phenylephrine, beyond noting that in patients who need a LOT of vasopressor support, its ceiling is lower than that of norepi.

Your concern about HR in these patients is overstated. They will do fine with a sinus HR under 100, indeed they tend to be better at 85 than 45. As mentioned in another post, most of these patients are solidly beta blocked and just are not going to get tachycardic with 2-10 mcg/min of norepi running.

As for extravasation injuries - would I run 30 mcg/min through a dodgy 24g peripheral IV? No. I wouldn't run propofol through it either.


There's a trend in ICU care for early d/c of central lines, and avoiding them in the first place. Their comfort with running vasoactive drugs through peripheral IVs a lot higher now than it was years ago. There's r/b there and I confess some annoyance when I get to the ICU to pick up a sick patient and find they're on substantial doses but don't have a central line (or an a-line for that matter). But they're not really wrong in thinking that a good PIV is just fine for running vasopressors.

Again - if you don't feel good about a PIV then get better access. There's no reason not to. The days of semi-blindly trying to get an angiocath into someone with lousy veins should be over. Get the ultrasound and a micropuncture kit and put 10 cm of 4 Fr goodness into the upper arm. Or put something in the IJ. Or if it's not urgent and it's not really your problem yet, tell an RN to call the hospital IV team to do it.

If an IV is dodgy and you're worried enough about extravasation injury to not want to give NE through it, you shouldn't be trusting it for induction drugs either. The problem isn't NE vs phenylephrine. It's the IV.
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Agreed you will get sued just as fast for a skin burn from tissued iv for elective colonoscopy as you would even an intraop mi or death in severe AS..

That said my med surg icu are particularly lax about the quality of their ivs and it enrages me @ times... our csicu our lines are meticulous
 
pgg said:
There's nothing wrong with phenylephrine, beyond noting that in patients who need a LOT of vasopressor support, its ceiling is lower than that of norepi.

Your concern about HR in these patients is overstated. They will do fine with a sinus HR under 100, indeed they tend to be better at 85 than 45. As mentioned in another post, most of these patients are solidly beta blocked and just are not going to get tachycardic with 2-10 mcg/min of norepi running.

As for extravasation injuries - would I run 30 mcg/min through a dodgy 24g peripheral IV? No. I wouldn't run propofol through it either.


There's a trend in ICU care for early d/c of central lines, and avoiding them in the first place. Their comfort with running vasoactive drugs through peripheral IVs a lot higher now than it was years ago. There's r/b there and I confess some annoyance when I get to the ICU to pick up a sick patient and find they're on substantial doses but don't have a central line (or an a-line for that matter). But they're not really wrong in thinking that a good PIV is just fine for running vasopressors.

Again - if you don't feel good about a PIV then get better access. There's no reason not to. The days of semi-blindly trying to get an angiocath into someone with lousy veins should be over. Get the ultrasound and a micropuncture kit and put 10 cm of 4 Fr goodness into the upper arm. Or put something in the IJ. Or if it's not urgent and it's not really your problem yet, tell an RN to call the hospital IV team to do it.

If an IV is dodgy and you're worried enough about extravasation injury to not want to give NE through it, you shouldn't be trusting it for induction drugs either. The problem isn't NE vs phenylephrine. It's the IV.
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I’m not trying to condemn the practice of using NE as a first line pressor, and I acknowledge that the concerns I raised are largely theoretical. It’s just interesting to me to hear that this is such a common practice.

I do cardiac cases at a tertiary hospital in a major metro (lots of heart transplants, VADs, ecmo, aggressive/experimental Cath lab, etc.), and this isn’t something I’ve seen or heard from my partners, but I’ll ask around. I’ve never really had any problems inducing super sick AS patients with relatively low doses of Neo.

Is this something that you got from training or did you switch to NE because you had patients crashing on induction with Neo?

Again, not throwing shade. I’m genuinely curious to learn about different ways people practice, and this one is new to me.
 
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I already have norepi spiked for post-bypass. If, for some reason, I feel that I need a pressor pre-bypass, then I'll start it, rather than spike a bag of phenylephrine. Some of my colleagues, though, will do phenylephrine infusion pre-bypass and norepi infusion post for...*frantic hand wave motion* reasons. If it's just a few boluses, sure, phenylephrine is fine, and pharmacy gives us pre-made sticks, so I'll just use that, outside of severe RV dysfunction.
 
DesiredMemberName? said:
I’m not trying to condemn the practice of using NE as a first line pressor, and I acknowledge that the concerns I raised are largely theoretical. It’s just interesting to me to hear that this is such a common practice.

I do cardiac cases at a tertiary hospital in a major metro (lots of heart transplants, VADs, ecmo, aggressive/experimental Cath lab, etc.), and this isn’t something I’ve seen or heard from my partners, but I’ll ask around. I’ve never really had any problems inducing super sick AS patients with relatively low doses of Neo.

Is this something that you got from training or did you switch to NE because you had patients crashing on induction with Neo?

Again, not throwing shade. I’m genuinely curious to learn about different ways people practice, and this one is new to me.
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I have norepi at the ready for every cardiac case and most "big" cases where I anticipate hypotension. I had one faculty in training who started strongly favoring Norepi based on newest literature, then the ACCRAC podcast strongly endorsed it, then another podcast talked a lot about the literature behind its effectiveness and safety profile. All of that combined has led to me favoring it over phenylephrine in bigger cases or with sicker more complex patients. I definitely use NE when inducing my severe AS patients that are coming for SAVR.
 
DesiredMemberName? said:
I’m not trying to condemn the practice of using NE as a first line pressor, and I acknowledge that the concerns I raised are largely theoretical. It’s just interesting to me to hear that this is such a common practice.

I do cardiac cases at a tertiary hospital in a major metro (lots of heart transplants, VADs, ecmo, aggressive/experimental Cath lab, etc.), and this isn’t something I’ve seen or heard from my partners, but I’ll ask around. I’ve never really had any problems inducing super sick AS patients with relatively low doses of Neo.

Is this something that you got from training or did you switch to NE because you had patients crashing on induction with Neo?

Again, not throwing shade. I’m genuinely curious to learn about different ways people practice, and this one is new to me.
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abolt18 said:
I have norepi at the ready for every cardiac case and most "big" cases where I anticipate hypotension. I had one faculty in training who started strongly favoring Norepi based on newest literature, then the ACCRAC podcast strongly endorsed it, then another podcast talked a lot about the literature behind its effectiveness and safety profile. All of that combined has led to me favoring it over phenylephrine in bigger cases or with sicker more complex patients. I definitely use NE when inducing my severe AS patients that are coming for SAVR.
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I’m at a quaternary center (we send nobody out, fix other people’s disasters, etc.). I use NE for nearly all cardiac cases, even for critical AS. Only use phenylephrine for non-cardiac cases and only because the premade sticks are conveniently available. Plenty of evidence showing comparable safety when run peripherally through a reliable IV (i.e., one you placed yourself), and most pump cases you’ll want some form of beta-1, especially after cardioplegia/bypass. I’d rather run a NE/vaso combo for vasoplegia than phenylephrine anything, but that’s just my preference. Only use phenylephrine for one specific/nuanced cardiac case with it in the protocol (which is likely outdated now).
 
In our place, we only use phenylephrine for bolus, nearly banned the use of infusions due to cost, and use noradrenalin(NE if you prefer) as first line when we think it's useful. 20mcg/ml solution, peripheral veins. Also mostly remi+prop tivas. All in the same line. Works great.
 
norski said:
In our place, we only use phenylephrine for bolus, nearly banned the use of infusions due to cost, and use noradrenalin(NE if you prefer) as first line when we think it's useful. 20mcg/ml solution, peripheral veins. Also mostly remi+prop tivas. All in the same line. Works great.
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How does phenyl cost more than norepi? It's 3 times cheaper for us
 
PpfSuxTube said:
How does phenyl cost more than norepi? It's 3 times cheaper for us
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That does sound odd.

Our pharmacy prepares 100 mL bags and 10 mL syringes of phenylephrine and stocks the OR fridges with it. Maybe there's less waste that way than there would be putting 10 mg / 1 mL vials in every OR, with the side benefit of eliminating the risk of dilution errors by the end users.

I always thought it was a dirt cheap drug, and that the most expensive part of it was the packaging.

Just looked at henryschein.com

10 mg / 1 mL vials - $60.99 for a box of 25

So yeah, dirt cheap. And I'm sure our hospital gets a much better bulk deal than I can get for small quantities.
 
nimbus said:
I think @norski is on another continent.
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Quite right. We pay the same for 0,5mg/5ml of phenylephrine as we do for 1mg/1ml NE, and we can't really get larger ampoules of phenylephrine either.

In the same vein(hah), it's cheaper to dilute epi 1mg/1ml to 10mcg/ml in a 100ml bag than using ephedrine, but the durations are obviously on different levels, so not something we do often.
 
T-burglar said:
Phenylephrine has one indication - unstable a fib RVR where controlling the HR has already been demonstrated to improve the BP … and even then only until you can cardiovert .

Use NE otherwise.
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Give over. That's just nonsense.

I do every case under the sun except heart transplant and they get the phenyl that my pharmacy draws up as well as levo infusions and more as needed. Phenyl is just fine for most cases.
 
Everywhere I’ve practiced phenylephrine has always been more readily available (premade sticks and infusion bags). Norepi is there if needed but it’s slightly more work to ask for it and dilute it.

I suppose we could push to make it more readily available and maybe that would change practice patterns, but there just doesn’t seem to be any need or desire to do so.

Thanks for sharing your experiences.
 
DesiredMemberName? said:
Everywhere I’ve practiced phenylephrine has always been more readily available (premade sticks and infusion bags). Norepi is there if needed but it’s slightly more work to ask for it and dilute it.

I suppose we could push to make it more readily available and maybe that would change practice patterns, but there just doesn’t seem to be any need or desire to do so.

Thanks for sharing your experiences.
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We have phenylephrine 100mcg/ml sticks on our carts. In our hallway omnicell, we have premade phenylephrine 50/250 and norepinephrine 4/250 bags.
 
T-burglar said:
Phenylephrine has one indication - unstable a fib RVR where controlling the HR has already been demonstrated to improve the BP … and even then only until you can cardiovert .

Use NE otherwise.
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This is nonsense.
 
T-burglar said:
Phenylephrine has one indication - unstable a fib RVR where controlling the HR has already been demonstrated to improve the BP … and even then only until you can cardiovert .

Use NE otherwise.
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I remember when I was a resident, doing a guest rotation at the Univ of VA in 2007, that a widespread opinion there was that NE was superior to phenylephrine for hypotension due to induction agents or neuraxial blocks. IIRC they'd just published some study measuring surrogate endpoints or other handwaving p-value chasing nonsense or something ... they pushed it for first line routine use in all comers.

It struck me as weird local culture. The idea that using NE over phenylephrine as a first line agent in routine anesthetics somehow made any difference at all in outcomes was ridiculous. A CT surgery fellow told me that phenylephrine and its pure alpha was poison. Poison.

As a resident I just did what I was told, of course.

Ain't nothing wrong with phenylephrine.
 
pgg said:
I remember when I was a resident, doing a guest rotation at the Univ of VA in 2007, that a widespread opinion there was that NE was superior to phenylephrine for hypotension due to induction agents or neuraxial blocks. IIRC they'd just published some study measuring surrogate endpoints or other handwaving p-value chasing nonsense or something ... they pushed it for first line routine use in all comers.

It struck me as weird local culture. The idea that using NE over phenylephrine as a first line agent in routine anesthetics somehow made any difference at all in outcomes was ridiculous. A CT surgery fellow told me that phenylephrine and its pure alpha was poison. Poison.

As a resident I just did what I was told, of course.

Ain't nothing wrong with phenylephrine.
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That is one of the annoying things about inbred academic institutions. Everyone thinks that they have the One True Way, and perpetuates that idea to trainees that anything different is malpractice.

Hilariously tangentially related, as an outside resident rotating through a certain very well known program for a month, I had to laugh at the number of attendings that told me, "This is the [program name redacted] way to do things!" However, they all did it differently, and didn't realize it.
 
I’ll tell you what’s wrong with PE - it frequently doesn’t work.

The physiology of the two is nearly the same except NE preserves the heart rate related contribution to cardiac output which is almost always desirable (even if it’s not terribly important) but most importantly it rarely rarely fails to increase blood pressure

Who wants to **** around with incrementally increasing the dose of pheneylephrine before throwing up their hands and just starting a pressor that does the same thing but always works
 
There’s literally no use case for phenylephrine except when you want to exert as much downward pressure on the heart rate from as many different therapeutics as possible
 
T-burglar said:
There’s literally no use case for phenylephrine except when you want to exert as much downward pressure on the heart rate from as many different therapeutics as possible
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This is bizarrely dogmatic and utterly divorced from reality for 99% of patients.
 
DesiredMemberName? said:
Why norepi over neo? Why do you want beta agonism? Increasing HR and myocardial oxygen demand while reducing coronary perfusion time doesn’t seem ideal for most AS patients. Plus you’re increasing the risk (albeit low) of extravasation injury if using a peripheral IV.

I’m not saying there aren’t some circumstances where NE is reasonable, but it seems like an odd first line choice for all AS inductions.
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A screengrab from a recent Chest article. Most now recommend that norepinephrine can safely be used in peripheral IVs in moderation. The added benefit is decreased need for central line placement with its comparatively higher risk of complications (CLABSI and placement risks).

1750165833391.png

1750165747745.png
 
It’s not dogmatic it’s a reasoned rationale for when to use phenylephrine over norepinephrine when you’re interested in utilizing its ancillary effects instead of just “getting the blood pressure up”

And it’s grounded in reality and practicality , based on our best current understanding of the physiologies of these drugs in various disease states, rather than divorced from it.
 
T-burglar said:
It’s not dogmatic it’s a reasoned rationale for when to use phenylephrine over norepinephrine when you’re interested in utilizing its ancillary effects instead of just “getting the blood pressure up”

And it’s grounded in reality and practicality , based on our best current understanding of the physiologies of these drugs in various disease states, rather than divorced from it.
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In the great majority of cases, they are functionally equivalent.

The 35 year old chunky woman getting a cysto for a stone, whose SBP wants to sag to the 80s after induction, isn't going to do better with norepinephrine than phenylephrine. I'll grant you that NE has a higher ceiling, and that there are patients who need it. Mostly in the realm of cardiac & major vascular surgery, or patients who are vasoplegic for other reasons (e.g. sepsis).

Hypotensive patients who get phenylephrine don't get significant (detrimental) reflex bradycardia unless you overshoot normotension and make them hypertensive.

It's absolute nonsense to suggest there's a meaningful difference in the effects of NE vs PE in most cases, even "big" cases. I say that in the spirit of respectful debate; I know from your post history that you're good at this anesthesia thing. This is a weird hill to die on, though.
 
T-burglar said:
It’s not dogmatic it’s a reasoned rationale for when to use phenylephrine over norepinephrine when you’re interested in utilizing its ancillary effects instead of just “getting the blood pressure up”

And it’s grounded in reality and practicality , based on our best current understanding of the physiologies of these drugs in various disease states, rather than divorced from it.
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It's not like it's used in normal vascular tone states. It's restoring tone to 'normal' and it works 99% of time. Never saw cardiac function on an echo suddenly get worse because of it.
 
Let me try stating my position another way.

I use NE because it does essentially the same thing as PE but it is more reliable (it always works) and I never have to deal with PE insensitivity wasting my time.

I use PE only when I want its distinct ancillary effect that NE does not provide.
 
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