- Joined
- Jan 14, 2006
- Messages
- 13,759
- Reaction score
- 24,218
Is this even ethical?
It's China.Is this even ethical?
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.
Is alfenta even available in the US these days? I haven’t seen it in quite a while.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.
Is alfenta even available in the US these days? I haven’t seen it in quite a while.
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
Agreed..no magic bullet or substitute for basic principles. Pre-induction volume and inopressor and a mindful induction...dealers choice.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.
Whats an inopressor?Agreed..no magic bullet or substitute for basic principles. Pre-induction volume and inopressor and a mindful induction...dealers choice.
I suppose he meant epi and norepi, maybe ephedrine, all of which have some beta effects.Whats an inopressor?
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.And assuming it exists why would you want to give the ino part to someone with severe AS?
I'll just say norepinephrine next time....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
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.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.
Moderation in all things. Just because someone has AS doesn't mean you must/should keep their HR as low as possible.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.
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.
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.
Extravasation is so low on my list of concerns for a low dose norepinephrine infusion. Check it intermittently and you're fine.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.
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.
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.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.
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..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.
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.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.
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.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.
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.
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.
How does phenyl cost more than norepi? It's 3 times cheaper for usIn 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.
How does phenyl cost more than norepi? It's 3 times cheaper for us
How does phenyl cost more than norepi? It's 3 times cheaper for us
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.I think @norski is on another continent.
Give over. That's just nonsense.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.
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.
This is nonsense.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.
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.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.
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.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.
This is bizarrely dogmatic and utterly divorced from reality for 99% of patients.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
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).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.
In the great majority of cases, they are functionally equivalent.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.
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.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.