Push Dose Pressors

[Carlos Danger]

I have a decent amount of experience with different kinds of dosing with ketamine for induction but none with etomidate (ive only used 0.3mg/kg), i guess with the popularity of ketamine the education on etomidate and different ways you can use the drug for induction have dwindled.

Etomidate is not not nearly as versatile a drug as ketamine. But it's what I did my first couple hundred RSI's with, so I'm used to it. It's very reliable, it gives a very dense anesthesia / amnesia, and it's fairly cardiac stable.

 

[TXmed]

at dosing ranges LESS than 0.2-0.3mg/kg does it provide good enough anesthia ?

 

[E tank]

at dosing ranges LESS than 0.2-0.3mg/kg does it provide good enough anesthia ?

Anecdotal experience being what it is, I've used 2/kg lidocaine for ICU intubation. Point being, the patient will determine what's enough in those situations.

As for inopressor pushes, there are those times where even whack after whack of epic is useless and the difference between collapse or not is a unit or two of vasopressin. Been there often enough to bring a vial with me to the unit for tubes.

 

[Carlos Danger]

at dosing ranges LESS than 0.2-0.3mg/kg does it provide good enough anesthia ?

In a sick, hypotensive patient, yes. You can halve that, easily.

Think about what you are trying to accomplish with your induction agent.

In a hypertensive TBI who is already obtunded anyway, you primarily just want to blunt the spike in ICP that follows laryngoscopy and ETI, so you need to use a beta blocker or a large dose of an induction agent or plenty of fentanyl to do that. In reality, in most of those cases you could just give some lidocaine and some esmolol and be just fine.

If, however, your primary goal is prevent a depression of hemodynamics, then your goals are the exact opposite.......you want to use a much smaller doses of any depressant meds.

It doesn't take much of an induction agent to provide some anxiolysis and amnesia. Sure, in a perfect world, our patients would be completely comfortable and unaware of anything. But when it comes to sick patients in the field, the world is far from perfect, and preserving hemodynamics takes priority over everything else.

 

[Brandon O]

Very broadly speaking, I think the worst thing you can do for a sick heart is to make it beat any faster than necessary. Tachycardia does much more to tip Mv02 balance in an undesirable direction than does increasing wall tension / afterload.

Mostly I agree. Although one could also argue that with a sick heart -- i.e. a decompensating patient where pump failure is a significant contributor -- they likely need more, not less cardiac support. But now we're getting into nitpicking between the patient with coronary artery disease and the one with cardiomyopathy and really at the end of the day I don't disagree with you.

I suppose my only real point was that there are folks in whom pushing a pure vasoconstrictor (neo) is probably not hemodynamically optimal. Epi may or may not be the best solution to this, but it's usually around in the ICU setting (and in the field). It MAY be the "best" choice for a last-ditch, patient-is-dying push, but calling anything "best" in that case is a bit rich.

We could probably really kick this discussion up a notch by bringing in the AS or PAH patients. But then I'll just get all sweaty.

 

[Carlos Danger]

I suppose my only real point was that there are folks in whom pushing a pure vasoconstrictor (neo) is probably not hemodynamically optimal. Epi may or may not be the best solution to this, but it's usually around in the ICU setting (and in the field). It MAY be the "best" choice for a last-ditch, patient-is-dying push, but calling anything "best" in that case is a bit rich.

We could probably really kick this discussion up a notch by bringing in the AS or PAH patients. But then I'll just get all sweaty.

I would, too, lol.

I'd be happy to talk about that, though. I'd love to hear about the ICU perspective of managing an AS or PAH patient from an ICU perspective. I know what we do in the OR, but if you have a septic patient in the ICU with severe AS, how does that affect your management?

 

[Brandon O]

I would, too, lol.

I'd be happy to talk about that, though. I'd love to hear about the ICU perspective of managing an AS or PAH patient from an ICU perspective. I know what we do in the OR, but if you have a septic patient in the ICU with severe AS, how does that effect your management?

Not sure how much I can say that would be especially clever. I would more heavily push preload and try to avoid aggressive afterload increases (although in the end you need what you need). Maybe someone can do a balloon valvuloplasty or something. Mostly, and this goes double for the PAH folks, it's the Goldilocks principle -- maintain euboxia. These are not the people to get laissez faire about their pressure, oxygenation, ventilation, etc, or you may fall down a spiral you can't get out from.

But in reality this is getting pretty far into the specialty realm where the right thing to reach for is a telephone. I can talk about floating a Swan in the severe PAH patient or starting pulmonary vasodilators, but if they're not already in a shop with things like mechanical support/bypass and cardiac surgery and a real CCU (not my current place), they probably ought to be. I expect you feel similarly.

 

[VFlutter]

I would, too, lol.

I'd be happy to talk about that, though. I'd love to hear about the ICU perspective of managing an AS or PAH patient from an ICU perspective. I know what we do in the OR, but if you have a septic patient in the ICU with severe AS, how does that affect your management?

If we are talking push dose pressors I would not be too concerned by the transient increase in afterload from 200-300mcg of Neo even in an severe AS patient. But like anything else it's risk vs benefit. What will kill them first, the profound hypotension or the potential for cardiac decompensation. I suppose using Epi with beta and alpha may be more desirable in that situation.

 

[E tank]

We could probably really kick this discussion up a notch by bringing in the AS or PAH patients. But then I'll just get all sweaty.

I'm in too... let's throw in severe mitral insufficiency...OR is second to second management. How do you guys in the unit prioritize your management goals?

 

[E tank]

If we are talking push dose pressors I would not be too concerned by the transient increase in afterload from 200-300mcg of Neo even in an severe AS patient. But like anything else it's risk vs benefit. What will kill them first, the profound hypotension or the potential for cardiac decompensation. I suppose using Epi with beta and alpha may be more desirable in that situation.

Yep... you got it, but without the increase in HR... so raise the arterial resistance and the contractility and you've really got it.

 

[Brandon O]

I'm in too... let's throw in severe mitral insufficiency...OR is second to second management. How do you guys in the unit prioritize your management goals?

I'd say etiology matters. Acute MR from a pap muscle rupture or ischemia really just needs surgical management. More chronic may be better tolerated. But basically reduce/limit afterload (nitroprusside?), keep up the rate and squeeze (epi?), sinus rhythm (amio?), euvolemic to dry, maybe a balloon pump. Manage like HFrEF.

Far from an expert.

 

[E tank]

I'd say etiology matters. Acute MR from a pap muscle rupture or ischemia really just needs surgical management. More chronic may be better tolerated. But basically reduce/limit afterload (nitroprusside?), keep up the rate and squeeze (epi?), sinus rhythm (amio?), euvolemic to dry, maybe a balloon pump. Manage like HFrEF.

Far from an expert.

Nice... don't know what HRrEF is but you're on the right track... issues...phtn, a fib, arterial resistance, diastolic failure for starters...ef may be preserved or not. Goals... venous return to LV (by mitigating effects of phtn on the RV), optimize arterial resistance for LV out flow (I HATE SNP, prefer nicardipine), HR 80-95 or so, milrinone maybe with some vaso...or just epi, but it can drive PA pressures...

Getting technical here, but the principles are what are important... lots of ways to skin a cat...