logic in selecting pressors?

[bulldog]

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Anyone have some common rules of thumb to select for pressors to use?

From MAP standpoint, seems like norepinephrine is 1st line for most cases. If that doesn't do job, then u'd add penylephrine. After that, you might add dopamine, or you might add vasopressin if they're in shock.

Any particular situation when u mjight use epinephrine or phenylephrine, or dobutamine as a first line tx?

 

[BADMD]

Anyone have some common rules of thumb to select for pressors to use?

From MAP standpoint, seems like norepinephrine is 1st line for most cases. If that doesn't do job, then u'd add penylephrine. After that, you might add dopamine, or you might add vasopressin if they're in shock.

Any particular situation when u mjight use epinephrine or phenylephrine, or dobutamine as a first line tx?

I'm going to throw out my 2 cents, for what it is worth.

First off, I'm going to assume that you aren't using any pressors on a patient who isn't in shock. My guess is that you mean septic shock when talking about vasopressin.

Secondly, no pressor is going to be effective if the patient is volume depleted. So some assessment of volume status is critical.

Now, lets think about how they all work.
Norepi - peripherial alpha agonist and some beta1
Phenylephrine - peripheral alpha, probably less potent than norepi
Epi - peripheral alpha and beta (I'll ignore the central effects for a moment)
Dopamine - "dopamine receptors at low doses (questionable)" then it is taken up into the nerve terminals and released as norepi and epi
Vaso - peripheral V1 receptor

Basically, the scheme you outline smacks the alpha receptors as the main mechanism of action. When one alpha doens't work, you add more. Given how potent most of these agents are, if you are "maxing" out one, I'm not sure why adding more of the same is really going to be effective (unless there is competative inhibition). Adding vasopressin may make some sense once everything is maxed as it works via completely different mechanism. By the same token you may get some benefit from dopamine, however most of what it does is get turned into epi and norepi.

Instead of just piling on more, that is when I'd start searching for problems beyond arteriolar vasodilation. Cardiac suppression? pH too acid for pressors to work? Adrenal insufficiency? Drug effect? This is when I really start looking for cardiac output measurements, do SVRs and more.

Personally, I like directing acting pressors, such as norepi, over indirect, such as dopmaine. However, the "best" choice is often related to the patient's heart rate. If it low, dopmaine may be more effective as it will likely cause a larger increase in the heart rate. If it is very high, phenyleprine will have the least effect.

In some overdoses, such as TCA or central alpha2 agonist, direct acting pressors are going to be more effect since dopamine may be blocked from working. By the same token, people who have sudden sniffer's death or arrest from chloral hydrate may benefit from a non-adrenergic pressor, since the catecholamines are what touched off the arrest in the first place.

I'm sure people will have other arguments for and against certain schema, but my thinking is this: If a lot of alpha isn't doing it, more won't help (generally). Find something else.

 

[Blade28]

That's a great post.

I just wanted to add the warning that, especially when first starting to work in an ICU, be careful about simply treating numbers. There's a tendency to do this, which isn't terribly surprising considering the amount of physiology discussed on rounds:

Vent settings - tinkered with after looking at the ABG
Pressors/vasoactive meds - titrated based on BP/MAP trends

Etc.

But as BADMD posted, the choice of pressor depends on the effect you want (besides just "raising the blood pressure"). It's important to know which receptors are affected by each medication, when to use fluid boluses, what the patient's fluid status is (which sometimes can only be determined by plotting a Frank-Starling curve), their renal function, etc.

 

[mikegoal]

In sepsis Norepi should be first. if on more then 5-10 then they should probably be on vasopressin as well(recent data suggest it is actually more helpful to be started even with lower doses of norepi)

after that it seems to be institution dependant

also dobutamine is not a pressor it is an inotrope

 

[elwademd]

I'm going to throw out my 2 cents, for what it is worth.

First off, I'm going to assume that you aren't using any pressors on a patient who isn't in shock. My guess is that you mean septic shock when talking about vasopressin.

Secondly, no pressor is going to be effective if the patient is volume depleted. So some assessment of volume status is critical.

Now, lets think about how they all work.
Norepi - peripherial alpha agonist and some beta1
Phenylephrine - peripheral alpha, probably less potent than norepi
Epi - peripheral alpha and beta (I'll ignore the central effects for a moment)
Dopamine - "dopamine receptors at low doses (questionable)" then it is taken up into the nerve terminals and released as norepi and epi
Vaso - peripheral V1 receptor

Basically, the scheme you outline smacks the alpha receptors as the main mechanism of action. When one alpha doens't work, you add more. Given how potent most of these agents are, if you are "maxing" out one, I'm not sure why adding more of the same is really going to be effective (unless there is competative inhibition). Adding vasopressin may make some sense once everything is maxed as it works via completely different mechanism. By the same token you may get some benefit from dopamine, however most of what it does is get turned into epi and norepi.

Instead of just piling on more, that is when I'd start searching for problems beyond arteriolar vasodilation. Cardiac suppression? pH too acid for pressors to work? Adrenal insufficiency? Drug effect? This is when I really start looking for cardiac output measurements, do SVRs and more.

Personally, I like directing acting pressors, such as norepi, over indirect, such as dopmaine. However, the "best" choice is often related to the patient's heart rate. If it low, dopmaine may be more effective as it will likely cause a larger increase in the heart rate. If it is very high, phenyleprine will have the least effect.

In some overdoses, such as TCA or central alpha2 agonist, direct acting pressors are going to be more effect since dopamine may be blocked from working. By the same token, people who have sudden sniffer's death or arrest from chloral hydrate may benefit from a non-adrenergic pressor, since the catecholamines are what touched off the arrest in the first place.

I'm sure people will have other arguments for and against certain schema, but my thinking is this: If a lot of alpha isn't doing it, more won't help (generally). Find something else.

That's a great post.

I just wanted to add the warning that, especially when first starting to work in an ICU, be careful about simply treating numbers. There's a tendency to do this, which isn't terribly surprising considering the amount of physiology discussed on rounds:

Vent settings - tinkered with after looking at the ABG
Pressors/vasoactive meds - titrated based on BP/MAP trends

Etc.

But as BADMD posted, the choice of pressor depends on the effect you want (besides just "raising the blood pressure"). It's important to know which receptors are affected by each medication, when to use fluid boluses, what the patient's fluid status is (which sometimes can only be determined by plotting a Frank-Starling curve), their renal function, etc.

In sepsis Norepi should be first. if on more then 5-10 then they should probably be on vasopressin as well(recent data suggest it is actually more helpful to be started even with lower doses of norepi)

after that it seems to be institution dependant

also dobutamine is not a pressor it is an inotrope

all well said!

also, you've got to throw in situation dependent too. if the er calls about someone hypotensive with a fever and a white count, and the patient's already on dopamine... you've got to "work it out"- i.e. assess the patient, figure out the volume status, get the fluids going if they're not already, add another pressor and get the other off, continue the antibiotic or switch it... or whatever else the situation may call for.

to add to blade28's post, if you're in the neuro surg icu, the map and icp are important, as the difference is the cerebral perfusion pressure.

 

[Blade28]

I forgot to add that determining the patient's type of shock is important too - very different treatment goals/meds when treating septic shock vs. cardiogenic shock, for example.

 

[carrigallen]

nothing better than ordering a full-dose beta blocker on a patient together with starting dobutamine.

 

[Blade28]

This is also a good topic to discuss with your residents/upper-levels.

I wouldn't be single-handedly throwing pressors at low MAP numbers 3 months into my intern year.

 

[Idiopathic]

whatever you do, start an arterial line with your pressure.

ive unfortunately run into some MICU attendings/fellows/residents that are vehemently opposed to arterial lines and have people on replacement doses of VP and 24 mics of levophen WITHOUT AN A-LINE!

Ludicrosity.

 

[Blade28]

Oh, and hold the tube feeds when using pressors. Trust me.