Pressors.

[RustedFox]

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Hey all,

Does anyone want to wax philosophical on which pressors they like to use in which situations ?

I dunno why, but I just can't seem to wrap my head around pressors.

 

[tkim]

not tachycardic - dopamine

tachycardic - phenylephrine

 

[jdh71]

Hey all,

Does anyone want to wax philosophical on which pressors they like to use in which situations ?

I dunno why, but I just can't seem to wrap my head around pressors.

Levophed vs Dopamine: basically equal, more arrhythmia with dopamine in the study (NEJM March 2010) - I think it's largely "lore" but most places let you start the dopamine in lower doses through a peripheral line because it's "safer". Bottom line, your knee-jerk pressor is Levophed. I like dopamine when I've got a CHFer in the 25-50% range and/or a patient that isn't tachy when he should be in sepsis (take a look at your oxygen delivery equation to find out why)

Levophed vs Vasopressin: Levophed wins (NEJM Feb 2008). I like vaso as a second line agent because it hits a different receptor. You can (some say "should") give it through a peripheral line. Can worsen gut ischemia.

Neo is just kind of a weak pressor. I'll use it when I want to avoid any ventricular irritation of any kind - usually patients with an ischemic cardiomyopathy that keeps going into v-tach on norepi (but sometimes you just need to use a stronger pressor and will have to abandon the norepi and run together with an antiarrhythmic and hope for the best)

Epi is obviously your pressor of choice in anaphylaxis. The surviving sepsis campaign recommends epi as second line, though I basically never see it used that way. Compared with levophed-dobutamine (Crit Care Med 2011) epi produces the same hemodynamic effects with regards to CI and oxygen derived parameters, however at the expense of more arrhythmias and decreased gut perfusion.

 

[turkeyjerky]

Why do you like dopamine in cardiogenic shock, despite the increased mortality observed in that subgroup in that study?

 

[jdh71]

Why do you like dopamine in cardiogenic shock, despite the increased mortality observed in that subgroup in that study?

I don't like dopamine in cardiogenic shock, not by itself.

 

[Hamhock]

Vasopressin: You can (some say "should") give it through a peripheral line..

Why do people recommend this? I am searching my small brain and can't come up with a hypothesis.

Please educate.

HH

 

[doctorFred]

i just gave a "pressors for dummies" lecture the other day, and as an expert *****, here's my summary page:


Septic shock
Start norepinephrine at 5mcg/min, titrate to 20-25mcg/min
Add vasopressin at 0.04units/min once the norepi is >10mcg/min
Consider dopamine at 5mcg/kg/min

Cardiogenic shock
Start dobutamine at 5-10mcg/kg/min
Consider an IABP or milrinone at 0.5/mcg/kg/min
Dobutamine and milrinone are technically not pressors and may require simultaneous dopamine or norepinephrine to prevent hypOtension

Post-op hypotension
Anesthesiologists love phenylephrine at 50mcg/min

Post-code hypotension
Start epinephrine at 5mcg/min

 

[xaelia]

Epinephrine and norepinephrine are probably equally efficacious, given the evidence available.

Once you're adding vasopressin to someone you're just prolonging the agony. Same with phenylephrine, unless you're treating a pure peripheral vasodilation such as neurogenic shock or transient post-operative effect.

Dopamine is bad and bad for you.

 

[RustedFox]

Wow.

Thanks all for the replies in such a short time. Keep it going.

 

[jdh71]

Why do people recommend this? I am searching my small brain and can't come up with a hypothesis.

Please educate.

HH

Some people think vasopressin can cause problems with coronaries when given by central line. The strength of evidence of this I'm not so sure about.

 

[jdh71]

Epinephrine and norepinephrine are probably equally efficacious, given the evidence available.

Once you're adding vasopressin to someone you're just prolonging the agony. Same with phenylephrine, unless you're treating a pure peripheral vasodilation such as neurogenic shock or transient post-operative effect.

Dopamine is bad and bad for you.

These are all pretty much wrong.

Epi and norepi can effectively give you the same MAP goals, in fact epi may be the better/stronger alpha agonist (perhaps too good in the splanchnic system) - the rest of the beta related effects are the problem. Last thing I want to deal with is v-tach or v-fib on top of my already shocky patient because I put him on a med that irritated the ventricle too much.

I've used a second pressor quite routinely and to good effect all the time. The patient's were sick but left the unit with expected return to baseline or close to. It's all about clinic context. In some patients add the second pressor is silly because you can tell they are dying and soon you'll be onto a third. Augmenting with a second pressor, more specially vasopressin is simply good critical care.

Dopamine is a great drug and pressor. You simply need to know how and when to use it.

 

[jdh71]

Post-op hypotension
Anesthesiologists love phenylephrine at 50mcg/min

One of the annoying things they'll also do is push a bolus of neo or ephedrine while leaving the PACU before hitting the ICU, and then bail before the hypotension shows up.

haha

owned

lawl

trolling in real life!

I'd rather have the patient some up on a gtts then the surprise hypotension. I tend to use norepi post op unless I have a reason not to. I'm not a surgical intensivist fellow, but we do see these post op patients often enough in the MICU these days.

 

[RustedFox]

jdh - very useful posts. Can you recommend any good 'broad reading' (besides the NJEM articles) that gives a summary on pressors ?

Same at you, doctorFred. ?

 

[tkim]

jdh - very useful posts. Can you recommend any good 'broad reading' (besides the NJEM articles) that gives a summary on pressors ?

Same at you, doctorFred. ?

do you have 'The ICU Book' by Marino?

 

[Jonathan13180]

This just happened last week with a post op pt with no central line, hypotensive and all that was done were neo pushes. Glad to see its not just our institution.

Has anyone read literature on levophed being superior to dobutamine in cardiogenic shock?

 

[jdh71]

jdh - very useful posts. Can you recommend any good 'broad reading' (besides the NJEM articles) that gives a summary on pressors ?

Same at you, doctorFred. ?

do you have 'The ICU Book' by Marino?

It's probably as good a resource as another, honestly. It's a bit old at this point, but the pathophys is pretty good. It would be a good a place as any to start with regards to pressors, though some of the recommendations in the book were controversial in '98, and anathema now - you can usually tell when he's beginning to editorialize. Though in his defense, it's really hard to get excellent EMB about anything in critical care because of the heterogeneity of the patient population. For instance, "shock" has many different etiologies, which we all know, but this makes it nuanced, also every patient comes into the situation +/- other comorbid and or chronic medical disease/problems. It will be a long time until an algorithm will be able to deliver critical care in a vacuum (but upcoming AI might be able to, and then we're all out of a job! ).

So . . . all of that is a lot words for the bottom line for me, which is, there is no one ultimate source of information. The clinician will need to make decisions based on 1) the patient, 2) the pathophys known (or assumed), 3) experience of the clinician, and often 4) situation gestalt and clinician intuition. Though in most situations you simply cannot go that* wrong with norepinephrine.

For me pressors were one of those things I just had to get used to by using them.

If you'd like a newer book, I might suggest Critical Care Medicine: The Essentials, by Marini. His background before going to medical school was as a mechanical engineer, so he breaks things down into physiology and physics in a way that makes a lot of sense. He's also a ventilator god, so that section you might find interesting as well for any SI or MI rotations you have to be on prior to finishing.

 

[jdh71]

This just happened last week with a post op pt with no central line, hypotensive and all that was done were neo pushes. Glad to see its not just our institution.

Has anyone read literature on levophed being superior to dobutamine in cardiogenic shock?

I'm not sure that's been done and a quick google scholar search doesn't pop up anything obvious. Dobutamine souldn't, IMHO, be thought of as a "pressor" but rather as an ionotrope - it will also often lower MAP, even if it increases SBP. Though sometimes because of ventricular irritation adding the dobutamine to the levophed just seems like a bad idea and you're stuck using the levophed by itself. In those situations it probably makes sense to push the nitro and lasix in an attempt to decrease preload.

 

[doctorFred]

Epinephrine and norepinephrine are probably equally efficacious, given the evidence available.

Once you're adding vasopressin to someone you're just prolonging the agony. Same with phenylephrine, unless you're treating a pure peripheral vasodilation such as neurogenic shock or transient post-operative effect.

Dopamine is bad and bad for you.

disagree with so much of this.

levophed has virtually no beta 2 activity, whereas epi has it in spades. they may be equally efficacious in their ability to raise a blood pressure, but levo does that without increasing myocardial oxygen demand.

as for vaso "prolonging the agony", i have no clue what you're talking about - adding vaso to hypotensive septic shock patients to augment levo's effectiveness is standard care in the MICU at our institution, and the half dozen of other MICUs in the northeast that i've rotated through. serum levels of vasopressin are inappropriately low in septic shock, and the ability of vaso to augment other vasoactive medications is well documented.

this is all straight out of the MGH Critical Care Handbook and Marino's ICU book as well.. again, virtually "standard of care."

now dopamine, on the other hand, may very well be "prolonging the agony", and again, i only use it as a third-line agent when vaso and levo are not keeping the pt.'s pressure up.

phenylephrine, as i mentioned, is primarily the tool of anesthesiologists.

 

[xaelia]

Since I'm getting ripped x2 in this thread, I'm going to have to ask people to support their positions with literature rather than "standard of care" and "tradition".

It's "standard of care" to do any number of things in medicine that provide no benefits (and likely harms).

Show me the literature where norepinephrine is superior to epinephrine except on a theoretical physiologic basis. And the literature supporting role of vasopressin. And dopamine.

In patient-oriented outcomes, not just "the numbers" or anecdotes. If we're going to have a discussion, it's going to have be based on citation of evidence and not personal practice.

 

[jdh71]

Since I'm getting ripped x2 in this thread, I'm going to have to ask people to support their positions with literature rather than "standard of care" and "tradition".

It's "standard of care" to do any number of things in medicine that provide no benefits (and likely harms).

Show me the literature where norepinephrine is superior to epinephrine except on a theoretical physiologic basis. And the literature supporting role of vasopressin. And dopamine.

In patient-oriented outcomes, not just "the numbers" or anecdotes. If we're going to have a discussion, it's going to have be based on citation of evidence and not personal practice.

There are no excellent randomized clinically controlled trials, so you may, if you like hide there. Which are difficult to design and control in the ICU for various reasons that have already been noted. So what do we do now, huh? You going to make the argument that your opinion is simply as valid then? Ok. The bottom line here, doctor, is that in the absence of the type of pedantic evidence you're asking for here, the rest of us are still trying to save a few lives, because that's what most of us signed up for. You might be doin' it for the lulz, or the bitches, or the money, but at the end of the day when all you have is your understanding of the physiology, experience, and clinical gestalt you do what needs doing to the best of your understanding. And based on that, your comments are not only ignorant and wrong, but kind of dangerous.

Besides, any doctor that can be replaced by some algorithm based only EBM (with all of the flaws that occur not only with the pee-review and publication process but with EMB itself) . . . should be.

Carry on then.

 

[deleted109597]

jdh,
Thanks for slumming it and stopping by the ED forum from your usual place to impart your wisdom. The attendings really like it when you use the

the rest of us are still trying to save a few lives

Because honestly, we aren't. I'm only in it for the first million, then I'm going to be an investment banker. Xaelia is going to break it big with medical informatics. I guess maybe that's why he is so into the stats/data.
However, you and Fred are still practicing anecdote based medicine, and worse still, hiding behind the "physiology" argument. I guess this means you give renal dose dopamine, steroids, Xigris, and xopenex too. I mean, there's a physiologic argument for those. Stone heart, anesthetics with epi in digits, we could play this game all day.
While it may be difficult to make a double blind trial, it isn't impossible, as they've already compared dopamine and levophed in the ICU. They've compared PA catheters to non-invasive monitoring. They've compared Edwards catheters to lactate clearance. But people still like to argue that they "need" what they've been doing because "it just makes sense." While we aren't talking groundbreaking, wash your hands before delivering babies type changes from SOP, we should always strive towards patient centered outcomes. And it's impossible to argue a n=1, as there's only one side. That is, unless you always give one pressor first, give it an hour (without changing anything else), and then switch to a different one.
Many people much smarter than me (and maybe you, you never know) have looked into it and haven't been able to get much of a difference between epi and norepi, even though they hit different receptors.
You yourself said the Marino book is pushing its age, and truthfully, our understanding of healthy physiology is poor, much less the disease state.

 

[xaelia]

There are no excellent randomized clinically controlled trials, so you may, if you like hide there.
...
You going to make the argument that your opinion is simply as valid then?
...
The bottom line here, doctor, is that in the absence of the type of pedantic evidence you're asking for here, the rest of us are still trying to save a few lives, because that's what most of us signed up for.
...
You might be doin' it for the lulz, or the bitches, or the money....
...
And based on that, your comments are not only ignorant and wrong, but kind of dangerous.

I see our opportunity for healthy, intelligent, discussion has concluded.

 

[jdh71]

jdh,
Thanks for slumming it and stopping by the ED forum from your usual place to impart your wisdom. The attendings really like it when you use the. Because honestly, we aren't. I'm only in it for the first million, then I'm going to be an investment banker.

Ahh. I see the "attendings" are unable to appreciate a little rhetoric. Too over your head? I've noted this and it won't happen again.

Xaelia is going to break it big with medical informatics. I guess maybe that's why he is so into the stats/data. However, you and Fred are still practicing anecdote based medicine

And so are you, every . . . single . . . day. Hell, show me the randomized placebo controlled trial demonstrating the effectiveness of vasopressors in the first place. Why do we even use pressors in the first place, huh? Oh?! You mean because we all anecdotally found that patients in many shock states lived when they had higher blood pressures? Whoa. Blows my freakin' mind.

and worse still, hiding behind the "physiology" argument.

Actually, no, I'm no hiding behind that argument. I first made the point that there is no excellent randomized trials here, and because of that appealed to physiology and first principles. Perhaps an "attending" can go back and re-rea what was said?

I guess this means you give renal dose dopamine, steroids, Xigris, and xopenex too

Renal dose dopamine was debunked with evidence years ago, steroids are still used in stress doses for patients that actually need them, activated protein C is now off the market and I couldn't use it if I wanted to, but no, it was not used even in patient's with APACHEII's >25 outside of the rare attending that wouldn't pull the plug without having said they did "everything". The data on xopenex is pretty clear.

Congratulations, an "attending" brought up a nice straw man or two, all of which actually illustrated my point and to what end? Hell, as long as we are coming up with wild accusations, you like smelling farts!! Amirite?!

While it may be difficult to make a double blind trial, it isn't impossible, as they've already compared dopamine and levophed in the ICU. They've compared PA catheters to non-invasive monitoring. They've compared Edwards catheters to lactate clearance.

It's not just difficult but may be damn near impossible the way we need it to be to get the kind of information we are looking for. The patient population is simply too heterogenous with respect to what brought them in, why they are in shock, and what else they have wrong with them chronically at baseline. If you had 10 years and multiple sites you probably could get enough septic shock patients from GNRs with the only chronic medical issues of DM2 and HTN to make a definitive case for, against, or equivalence of one pressor vs another but . . . then . . . only for THAT patient population infected with those bugs. The evidence can only say what it can say even with the best randomized trials. So we're left with trials like the recent norepi vs dopamine, which attempts to be so big that it can make a statement about "all comers", and when you look at "all comers" the difference in their primary end point, 28 day mortality, was no different, but when you look at the sub-group analysis for cardiogenic shock, these patients did worse. Wait. So what's going on here? Can we or can we not extrapolate this study like brainless, non-thinkink idiots or not? While the study was not designed, nor powered, to look at cardiogenic shock, there it is, this pesky sub-group analysis . . . yay . . . interrupting the simplicity that I was trying to add to my patient acre with EBM . . .

Many people much smarter than me (and maybe you, you never know) have looked into it and haven't been able to get much of a difference between epi and norepi, even though they hit different receptors.

No difference in what? Compared where? I find them compared in one place "recently" and well with similar MAP goals, but more arrhythmias in the epi group. The bottom line for this was that epi can be generally used safely, and it was well received because most of the rest of the world either cannot afford or has no access to some of the newer and more expensive agents. Though, we are not having a discussion about which pressor is better in the jungles of africa - at least I wasn't, and maybe I should have clarified that better; I tend to assume on this message board at least we're talking about western hospital medicine as it's practiced in the united states - and if that is the context for the discussion, why would you start a pressor with higher rates of arrhythmias when you simply don't have to? Especially in light of the medicolegal liability environment we all work in.

The bottom line, again, as I've pointed out more than once here is that you need to apply your brain, education, and training to the evidence available and to that not available and come up with the best treatments possible for your patient. This should not come as a surprise to anyone posting on this board.

 

[jdh71]

I see our opportunity for healthy, intelligent, discussion has concluded.

Don't make eye contact as you slowly back out 😉

 

[tkim]

not tachycardic - dopamine

tachycardic - phenylephrine

 

[jdh71]

^^^ I like it

 

[tkim]

^^^ I like it

I like to KISS in the ED. Very binary - sort of like:

 

[jdh71]

I like to KISS in the ED. Very binary - sort of like:

So there IS a method to the madness. I knew there had to be.

 

[tkim]

phenylephrine, as i mentioned, is primarily the tool of anesthesiologists.

Had a guy come in with afib/RVR @ 210 hypotensive @ 70/p. Narrow complex, did not look like WPW. EMS lit him up once without effect. Guy got adenocard x2, cards on board, recommended dilt gtt without bolus because of hypotension. Lit him up two more times without change. Plenty of fluids running.

Had drawn up a stick of neo to give the patient to bring his pressure up, and if it did, to bolus with dilt to see if that would change things. Before I could do that his rate came down to the 130's, and his pressure came up slightly to 80/p with a decent map, so bolused with 10 of dilt instead. With the slower rate it looked as if he had some ST elevation, so we transfered to the tertiary.

Had he persisted in the higher rate and lower BP, I would have given him the neo stick and given him the full 20 of dilt.

Next time I might throw amio, ca, and a two gram slam of mag in the mix.

Point being, we can and should use neo as well. Have started neo gtts of tachycardic hypotensive pts. Works well. Would have been my first time using neo boluses.

 

[tkim]

So there IS a method to the madness. I knew there had to be.

Whoa now hoss, it's not like flipping a coin - more like a roll of the dice - each face representing a different specialty that you can consult.

If you work at a tertiary, it becomes more like a 20-sided die, like the kind you use in Dungeons and Dragons.

Vorpal Foley of Gomere: +2 to successfully insert past enlarged prostate

 

[jdh71]

Had a guy come in with afib/RVR @ 210 hypotensive @ 70/p. Narrow complex, did not look like WPW. EMS lit him up once without effect. Guy got adenocard x2, cards on board, recommended dilt gtt without bolus because of hypotension. Lit him up two more times without change. Plenty of fluids running.

Had drawn up a stick of neo to give the patient to bring his pressure up, and if it did, to bolus with dilt to see if that would change things. Before I could do that his rate came down to the 130's, and his pressure came up slightly to 80/p with a decent map, so bolused with 10 of dilt instead. With the slower rate it looked as if he had some ST elevation, so we transfered to the tertiary.

Had he persisted in the higher rate and lower BP, I would have given him the neo stick and given him the full 20 of dilt.

Next time I might throw amio, ca, and a two gram slam of mag in the mix.

Point being, we can and should use neo as well. Have started neo gtts of tachycardic hypotensive pts. Works well. Would have been my first time using neo boluses.

Agreed. This is the perfect neo patient, which I alluded to in my first post here. I also like amio in these patients much more that dilt. There isn't a lot of great evidence that amio is actually worse on BP, or worse in controlling afib RVR. And my experience (here we go again), I've had many more problems with dilt and blood pressure than amio.

 

[jdh71]

Whoa now hoss, it's not like flipping a coin - more like a roll of the dice - each face representing a different specialty that you can consult.

If you work at a tertiary, it becomes more like a 20-sided die, like the kind you use in Dungeons and Dragons.

Vorpal Foley of Gomere: +2 to successfully insert past enlarged prostate

Yeah but if that patient is sitting there with a high prostatic THAC0, you may have to cast summon urologist in order to successfully attack.

 

[tkim]

Yeah but if that patient is sitting there with a high prostatic THAC0, you may have to cast summon urologist in order to successfully attack.

Let's not get crazy now. All of my campaigns allow summons uro or nsurg only once during game play. And like all summoned creatures, you have to roll seperately to see if they attack you once they appear.

D&D - good times. I can almost feel all the face zits coming back.

 

[ohiovolffemtp]

Does anyone have any perspective or data on the use of vasopressin vs. epi in cardiac arrest management. I've been unable to find any EBM that really shows a benefit, but in my hospital the head of ACLS - an anesthesiolgy prof - has had great experience with it on pre-arrest patients. He's published articles showing vaso's value in pre-arrest situations on pt's on ACEI's, ARB's, and alpha blockers.

Any thoughts?

 

[jdh71]

Let's not get crazy now. All of my campaigns allow summons uro or nsurg only once during game play. And like all summoned creatures, you have to roll seperately to see if they attack you once they appear.

D&D - good times. I can almost feel all the face zits coming back.

That's true, and you'd still have to roll to see if they would appear at all.

 

[jdh71]

Does anyone have any perspective or data on the use of vasopressin vs. epi in cardiac arrest management. I've been unable to find any EBM that really shows a benefit, but in my hospital the head of ACLS - an anesthesiolgy prof - has had great experience with it on pre-arrest patients. He's published articles showing vaso's value in pre-arrest situations on pt's on ACEI's, ARB's, and alpha blockers.

Any thoughts?

From 2001, no survival benefit after arrest, when used during arrest
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(01)05328-4/fulltext

Here's nice rather recent review:
http://downloads.hindawi.com/journals/emi/2012/815857.pdf

No real evidence for or against it. Might be better when used together.

 

[turkeyjerky]

Does anyone have any perspective or data on the use of vasopressin vs. epi in cardiac arrest management. I've been unable to find any EBM that really shows a benefit, but in my hospital the head of ACLS - an anesthesiolgy prof - has had great experience with it on pre-arrest patients. He's published articles showing vaso's value in pre-arrest situations on pt's on ACEI's, ARB's, and alpha blockers.

Any thoughts?

I think the two situations you're describing are very different animals.

 

[Rendar5]

Ahh. I see the "attendings" are unable to appreciate a little rhetoric. Too over your head? I've noted this and it won't happen again.

jdh, I'm reading these posts and see you were a dick to a non-dickish response. Thus the sarcastic response which you didn't seem to understand the purpose of. It wasn't to create a college-style debate complete with discussion of logic fallacies. The rest of your posts were a nice discussion tho.

 

[jdh71]

jdh, I'm reading these posts and see you were a dick to a non-dickish response. Thus the sarcastic response which you didn't seem to understand the purpose of. It wasn't to create a college-style debate complete with discussion of logic fallacies. The rest of your posts were a nice discussion tho.

Well. I think I did understand the purpose. And I think it's important to point out when people are arguing nonsense. I have an argument style that is known as "agressively right" and it can occasionally get out of hand. I simple have a bit of a knee jerk response to people when they start getting all pedantic about EBM with all of it's flaws. EBM isn't bad, it's good, but it's only good as far as it goes and only within logical contexts. To say dopamine is "bad" is simply stupid. It's often not the best pressor given the clinical context. However to make that statement and then hide behind the EBM is chicken****. EBM is not the end all be all of patient care. MOST of what any of us do in medicine is not backed by level 1A evidence pure and simple and it's even worse in critical care. Take a look at the level of evidence as listed in the surviving sepsis guidelines for instance. Or, alternatively, look at how every bit of EGDT has been torn to shreds. CVP? Continuous SvO2? Lolwut?! Etc. We're doctors and the day we can be replaced by a computer running EBM in an algorithm, we should be.

 

[ohiovolffemtp]

Jdh71 - thank you - that was helpful.

 

[zinjanthropus]

Pressors are a great example of how pathophysiology often does not translate to clinical outcomes or experiences. I can't think of many examples where I wouldn't go for levophed first. Can't think of any scenario where I would use dopamine at this point.

 

[RustedFox]

Pressors are a great example of how pathophysiology often does not translate to clinical outcomes or experiences. I can't think of many examples where I wouldn't go for levophed first. Can't think of any scenario where I would use dopamine at this point.

ACLS bradycardia algorithm is the only thing I can think of offhand. However, I've seen isoproterenol used more commonly by the attendings 'round here for that purpose.

 

[Apollyon]

ACLS bradycardia algorithm is the only thing I can think of offhand. However, I've seen isoproterenol used more commonly by the attendings 'round here for that purpose.

Isuprel? Seriously? Honestly, that is SO 1980s!

(It's all beta, and was known for worsening cardiac ischemia.)

 

[RustedFox]

Isuprel? Seriously? Honestly, that is SO 1980s!

(It's all beta, and was known for worsening cardiac ischemia.)

For realz ?

Huh. Seemed to do the trick. Go figger.

 

[Apollyon]

For realz ?

Huh. Seemed to do the trick. Go figger.

Right on! What works is what works. Isoproterenol is structurally very similar to epi, but the alpha effect is so minimal as to be called inconsequential. Isuprel got dropped from ACLS one or two iterations before I took it the first time (1995).

 

[RustedFox]

Right on! What works is what works. Isoproterenol is structurally very similar to epi, but the alpha effect is so minimal as to be called inconsequential. Isuprel got dropped from ACLS one or two iterations before I took it the first time (1995).

Son of a gun. - And here I thought I was all clever when I amended the bradycardia mnemonic from "Pacing Always Ends Danger" (Prepare pacers/Atropine/Epi/Dopamine) to "Pacing Always Ends Imminent Danger" (same, add Isuprel).

Just goes to show; the old dogs know a thing or two.

 

[Hamhock]

I think this is a great discussion, for the most part.

It has highlighted the lack of evidence for pressor choice.

However, I remain a dopamine hater (no GOOD evidence to support this, I admit).

Based on experience, anecdote, or theory, can anyone describe a situation when dopamine - the most promiscuous, destabilizing, and unknown of pressors - is their first choice?

JDH? You above implied it's indicated in specific situations. Can you provide an example?

And, yes: I know the AHA likes it - but the AHA likes all kinds of nonsense and my opinion of ACLS has been expressed elsewhere. Without citing the AHA, can anyone explain why they think dopa is a good idea for the unstable bradycardia patient? ....vs epi, pacing, correcting the underlying etiology?

HH

 

[emergiQ]

Some great posts here!

I'm not going to wade too much into which pressor to use in which circumstance. But my residents that work with me in the ED and ICU know me in particular for one or two quotes:

Never say "never" or "always" in medicine... and the closely related "The only thing to be dogmatic about is: to not be dogmatic!".

The point is, while I think one can wax poetic about which pressor is ideal for a given circumstance, I think the exercise to choose a pressor based on pressor and patient physiology, the vitals, presumed diagnosis, etc. is a very good one for choosing the first pressor, but after that all bets are off. Patients, on an individualized basis, have so much variability in receptor genotype and phenotype that of course they don't all react the same to the patient you had "yesterday" on the same drips, and more important than choosing the right pressor is to monitor your decisions very closely and be able to check your ego at the door if you need to rapidly make a change.

I will say that pressors I almost never used as a fellow, I have come to incorporate into my toolbox over 3 years as an intensivist. Partly because I work in a busy mixed SICU with CT surgery, full transplant, trauma, general and sub-specialty surgery, and even bone marrow transplant.... so I've seen lots of different persepctives (the nice was of saying 'other people's dogma'). Even isoproterenol, mentioned above, is, one astute poster mentioned, "so yesterday!" but has been the choice "today" a number of times for me in the past year (usually after they failed one my first line agents).

Also, no one has mentioned methylene blue yet, a "pressor" that works by inhibiting guanylate cyclase. I have used it in cardiac patients post bypass who are vasoplegic when phenyl and vaso have failed. There was a recent case report in annals about using it in the setting of amlodipine OD and there are some other articles (one listed below) but they are more from the perspective of explaining the physiology, not as definitive proof of its efficacy (a common theme for pressor articles!). When I use methylene blue, I dose it as a bolus over 20 minutes of 2 mg/kg, then run it at 1mg/kg/hour.

1. Methylene Blue for Treatment of Refractory Shock. Ann Emerg Med 58🙁6) December 2011 565-567
2. Kwok and Howes. Use of methylne blue in sepsis: a systematic review: J Int Care Med 2006: 21: 359-63

By the way, if anyone is interested and going to the 10th Annual Western States Winter Conference on Emergency Medicine (WSWCEM) in Park City Jan 29 - Feb 2nd, I'll be giving a pressor talk. Welcome to come out, have some fun, and educate me about any new pearls you've got for pressor use!

 

[jdh71]

I think this is a great discussion, for the most part.

It has highlighted the lack of evidence for pressor choice.

However, I remain a dopamine hater (no GOOD evidence to support this, I admit).

Based on experience, anecdote, or theory, can anyone describe a situation when dopamine - the most promiscuous, destabilizing, and unknown of pressors - is their first choice?

JDH? You above implied it's indicated in specific situations. Can you provide an example?

And, yes: I know the AHA likes it - but the AHA likes all kinds of nonsense and my opinion of ACLS has been expressed elsewhere. Without citing the AHA, can anyone explain why they think dopa is a good idea for the unstable bradycardia patient? ....vs epi, pacing, correcting the underlying etiology?

HH

Eh. "Indicated" might be a bit of a strong word. I'll use it in cardiogenic shock with dobutamine if I think that's what's needed, and in septic patients who are not mounting an appropriate tachy response (you can also use epi, or norepi/dobutamine similarly). I'll consider it in septic patients who are not in cardiogenic shock, but do run around with EF's in the 25-50% range.

 

[jdh71]

Also, no one has mentioned methylene blue yet, a "pressor" that works by inhibiting guanylate cyclase. I have used it in cardiac patients post bypass who are vasoplegic when phenyl and vaso have failed. There was a recent case report in annals about using it in the setting of amlodipine OD and there are some other articles (one listed below) but they are more from the perspective of explaining the physiology, not as definitive proof of its efficacy (a common theme for pressor articles!). When I use methylene blue, I dose it as a bolus over 20 minutes of 2 mg/kg, then run it at 1mg/kg/hour.

1. Methylene Blue for Treatment of Refractory Shock. Ann Emerg Med 58🙁6) December 2011 565-567
2. Kwok and Howes. Use of methylne blue in sepsis: a systematic review: J Int Care Med 2006: 21: 359-63

By the way, if anyone is interested and going to the 10th Annual Western States Winter Conference on Emergency Medicine (WSWCEM) in Park City Jan 29 - Feb 2nd, I'll be giving a pressor talk. Welcome to come out, have some fun, and educate me about any new pearls you've got for pressor use!

Mind blown.

I've used insulin as a pressor twice. Never even heard of this methylene blue business. Super, super cool.