Push-Dose Pressors: RANT! and response.

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Amal M. -

Scott--nice response and thanks for addressing some of my concerns.

Robert H. -

Well posed arguements from both camps, I do enjoy a good rant!
My two cents are related to something (sadly) not academic.
Why do we treat numbers? Well the reasons are plentiful and though I am NOT a fan of this approach I find myself crawling back to it for one main reason. Sick patients sometimes die and their charts are often peer reviewed. Though your charts are likely reviewed by those who are saavy in the arts most of us are not so lucky and our peers may be out of date or not even EM or critical care trained. They are a great horse to ride by a reviewer, cranky consultant or worse: plaintiff's attorney and I think it demonstrates that you were attentive and "did everything you could". No evidence that it improves outcomes, no evidence that it harms pts, for me this kicks the coin over to giving it for now.

EMCrit -

Amal--It was a pleasure to have this discussion with you!

EMCrit -

Robert--If we are talking about a patient who drops from 120/80 to 90/60, I'm with you. No need to freak out when the pt looks great and they had a slight dip in their numbers. When the pressure drops to 60/40. not so much. You are not treating numbers at that point, you are treating a really bad situation that may lead to peri-intubation arrest.

Joseph B -

I believe money is in S.W's comments on coronary perfusion. The push dose is not meant to be a definitive vasopressor to maximize oxygen delivery to tissues, nor is it meant to be a fix-all solution to the crisis. It is a temporary measure to prevent a cardiac arrest while the underlying cause is corrected. The argument that an alpha agent causes harm by decreasing CO seems to be challenged by the results of the SOAP-II trial, although this is certainly extrapolating.

Dr.Mattu's cautions are also well received - the PDP should not be a substitute for critical thought in the crashing peri-intubation patient. Issues such as (volume status/autopeep/acs/ptx etc) all need consideration.

EMCrit -

Joseph-great comments. SOAP II was a comparison of two inopressors, not sure if it is ideal evidence for showing alpha is good for cardiac function. Phenylephrine vs. norepi or epi in volume replete patients with echo as end point would be a nice quick study to look at that. My contention is that in patients with v. low MAPs, both arms would have improved function. In pt's with reasonable MAPS, 50-65 heart function would improve on the norepi side and get worse on the phenyl side.

Joseph B -

Very interesting - my comment on SOAP-II is based on my understanding of norepi as primarily a potent alpha agent, with additional beta activity. Your comment regarding the effect on CO at varying MAPs is very thought provoking - (ie where is the line between a pure alpha agent causing harm and an inopressor providing benefit?). Doing a quick pubmed search there really isnt that much out there - unless youre a rodent or cat....

Thanks again for the great discussion.

Sam G -

One of the most interesting EMRAP sessions I've heard. Love listening to both of you.

Scott- I think your argument that push-dose pressors are essentially drips is a good one, since they are literally equivalent doses. However, the concentrations are not identical. I'm not sure what the standard dose of an epinephrine drip is, but the three concentrations I have seen are:

1mg in 250cc NS--->1: 250,000
1mg in 500cc NS--->1: 500,000
1mg in 1000cc NS--> 1:1,000,000

The concentration of the PDP epi dose:
1 mg in 10 cc NS----> 1:100,000

This is 2.5 to potentially 10 times the concentration of an infusion.

I’m not sure exactly how to weigh the ultimate impact of total volume vs concentration, but do you agree that you gotta wonder how this increased concentration (potency) would affect outcomes?

EMCrit -

Joseph, an EMCrit episode in a couple of weeks will go over this very topic.

Benjamin M. S., M.D. -

Amal, it was a rant to rank with the best of them. Great thinking points. Great emphasis of cautions we need to employ when jumping on bandwagons. And of course some great responses from Scott as well. Great learning experience, and great entertainment too.

Benjamin M. S., M.D. -

Also, as Scott mentioned, it depends on the situation whether pressors are the right response to post intubation hypotension. Our patients are far more likely to be volume depleted than elective surgery patients, and pressors can't be used to hide the need for good venous return to overcome positive pressure ventilation.

Amal M. -

Thanks for your comments.
I'd like to think that the purpose of education is not to tell people what to do, but to make people think about what they do. If this segment simply makes people think a bit more about causes, treatment, etc. of post-intubation or post-sedation hypotension, then it's mission accomplished.

Also, I think it's important that we avoid taking anecdote or "it makes sense" concepts and being zealous in employing or advocating them without presenting some counter-arguments. Otherwise those things can quickly become considered standard of care, resulting in lawsuits against physicians based on dogma and popular thought. Such has happened with so many other therapies....steroids in spinal cord injury, amio in cardiac arrest, etc. etc. and now perhaps lytics in stroke (hate to open up another pandoras box, but we still need to question that therapy and not blindly go forth accepting it as SOC).

We're fortunate that EMRAP gives us at least one very popular medium through which to provide checks and balances on the things we hear and read.

EMCrit -


Concentrations are irrelevant in this circumstance (IV medication administration). Our hospital uses 4 mg in 250 ml of diluent for standard epi drips. Concentration is only important if you are trying to limit the amount of excess fluid the pt receives.

Andrew C. -

In Australia we use 6mg in 50ml or 6mg in 100ml concentrations.

Sam G -

Do you know of any literature showing any relationship between specifically the concentration of pressor used and effect/outcomes? This is probably tough to study, and volume would be a confounder, but it seems reasonable that a higher concentration of Epi could have a different (more deleterious) effect on target tissue(esp the heart) than a more diluted concentration.

EMCrit -


There is no relation. The only difference between concentrations of a med like this that matters, is how much excess fluid the pt gets from the diluent. Other than this it doesn't matter.

Ron R. -


I appreciate Amal's points, and I too hope there are not dead bodies piling up because I hadn't been using push dose pressors. That being said, Scott - You're the Man! That was a great response! Since I started listening to you on EM:Rap and EMCrit, I have learned so much. Ten years removed from residency, I was really feeling like I was losing touch with evidence based medicine, becoming stuck in the ways common to our shop. Largely through your podcasts, our entire group has been energized to try new things such as push dose pressors. You're coming to our hospital in May to do a grand rounds, and I hope to meet you there.

EMCrit -

Looking forward to it Ron.

Darren B., M.D. -

I enjoyed this debate too as I am regular user of bolus phenylephrine in the ED resus bay. This is just a tease, but we are compiling data right now on over 100 uses of push-dose phenylephrine in our ED. We won't be able to say anything about outcomes but hope to at least be able to speak to safety. Stay tuned!

Patrick W. -

Thank you for the interesting discussion. Here are my thoughts as an anesthesiologist in training. A domain that has been relatively well researched is that of the the "triple-low", which is basically the combination of a low BP, low BIS (bisspectral index, basically a summation EEG for measuring depth-of-anesthesia) and low end-tidal concentration of anesthetic (assuming use of gas). There have been multiple studies showing that triple lows are associated with increased short-term and long-term mortality. There is also some evidence that prompt correction of a triple low can have a positive effect on outcome. What remains to be sorted out is whether these are just sick patients who would have died anyway or whether the hypotension plays a causative role in their demise. To my knowledge there is no prospective data on this.

Obviously the term triple-low stems from (mostly elective) anesthesia, where the etiology of intraoperative hypotension is usually a different one than in the trauma room, however, keep in mind that all of our sedative agents will all cause hypotension (direct vaso/venodilation, inhibition of the baroreceptor reflex, etc.) in their own right. In this context pressors and inotropes can be a valuable in blunting the hypotensive response following induction. In my opinion, the preload-dependent patient is EXACTLY the patient you'd want to use them in, since they will predictably drop their pressure once you take away their sympathetic tone and transition them to positive pressure ventilation, even after adequate fluid resuscitation.

Amal's argument that phenylephrine may reduce cardiac output is correct, which is why at our hospital we use mostly norepinephrine (which still possesses some beta-agonism) and ephedrine. The only situations where we use phenylephrine are c-sections. Many places also use it when *pure* alpha-agonism is required (e.g. HOCM physiology). When I have a hypotensive patient running along at a HR of 50, I will often use ephedrine primarily. If the BP is worrying me (<75 SBP or a very rapid fall), I will often go directly to norepi and maybe add a bit of ephedrine if I'm concerned about bradycardia. My experience is that ephedrine's effect is quite short-lived, but often unpredictable. In some patients, even 20-30mg will not do *anything* and in others, 10mg lead to tachycardia with demand ischemia. We don't use a lot of epinephrine, but it's a logical option in a bradycardic/really hypotensive patient. When we have a really sick patient, we will volume resuscitate them whenever possible prior to induction and will start up some norepi PRIOR to pushing any induction meds - like this you can compensate for most of the drop post-induction and are not busy catching up. In the end, you need to use what you and your team feel comfortable with. Just my 2c.

Here are some key references:

Sessler DI, Sigl JC, Kelley SD, Chamoun NG, al E. Hospital stay and mortality are increased in patients having a “triple low” of low blood pressure, low bispectral index, and low minimum alveolar concentration of volatile anesthesia. Anesthesiology 2012;116.

Monk TG, Saini V, Weldon BC, Sigl JC. Anesthetic Management and One-Year Mortality After Noncardiac Surgery. Anesthesia & Analgesia 2005.

Saager L, Greenwald SD, Kelley SD, Schubert A, Sessler D. Vasopressors May Reduce Mortality Associated with a “Triple Low” of Low Blood Pressure, BIS, and MAC. 2009;354.

Alfred S. -

I agree with Amal on this one. If a patient begins with relatively normal vitals and drops after an induction agent like propofol or remifentanil, then there is no need to add immediate pressors just to elevate the BP. It will come back on it's own. Amal is right on, we have no data that the use of pressors just to make the numbers look good will have any effect on patient out come.

It is interesting we see this same effect when we use induction agents for procedural sedation. We don't go adding pressors when we give propofol to cardiovert someone and they have a transient drop in BP. We just wait and recognize it will return to normal.

There are lots of anecdotes by the doc's commenting on Amal's rant on their experiences using push dose pressors with good results. I have lots of cases of not using it with good results. Problem is the plural of anecdote is not data.

If we are discussing a critically ill patient, then they should not be receiving negative inotropes for induction in the first place. And if they do require pressors, it will be in the form of an infusion to treat the underlying problem and not the side effects of the induction.

Amal is also right that the history of medicine is full of therapies that just made sense, but on closer inspection turned out to be useless or even harmful. Until we have good data to the contrary, I am afraid this might be another example of treating ourselves and not the patient.

Great discussion though.

Michael S., -

Sam G:
"The concentration of the PDP epi dose:
1 mg in 10 cc NS----> 1:100,000"

If I'm not mistaken, Sam, 1 mg in 10 cc would be 1:10,000 (ie. Crash cart Epi). To get 1:100,000 you would want 0.1 mg in 10 ml.

Prehospital we are now using Epi 1:100,000 slow IV push for anaphylaxis refractory to IM Epi 1:1000, whereas before we were using 1:10,000 slow IVP for refractory anaphylaxis.

I would like to see Epi added as a push dose pressor for post ROSC care. Typically with the current "choreographed" or pit-crew approaches to field resuscitation, an IO is placed as our first-line access. We may get ROSC and then have pressures fall and the pt re-arrest prior to being able to establish IV access for a drip. Gravity drips typically don't work well with IO's, but push dose pressors would be fantastic for IO's.

Mel H. -


1:1,000 1mg/mL 0.1%
1:10,000 0.1mg/mL 0.01%
1:100,000 0.01mg/mL 0.001%
1:200,000 0.005mg/mL 0.0005%

Sam G -

That is supposed to read 0.1mg in 10cc NS. The 0.1 mg (or 100 microgms) is what Scott's formula calls for.
0.1mg in 10cc NS is in fact a 1:100,000 concentration, as noted from the Chart above (thanks Mel!)

That's amazing that your prehospital protocol calls for iv Epi- I have not heard of iv epi being used prehospital. Also, theoretically I totally agree with you about push-dose pressors in ROSC as well.

Mike W. -


I am the medical director a flight program and many of our crew members listen to you podcasts. Your work is often quoted at our staff meetings. Im curious about your thoughts on using push dose pressors in the field v. using pressor infusions. My personal thoughts have been that this should be reserved the docs in the department and used only in the peri-procedure setting... not as a treatment for following vitals in the unstable patient. Thanks.

EMCrit -


Most of the flight services have been using push-dose epi for years on the Australian services. I think the same indications apply. Temporary hypotension --push dose, prolonged--infusion.

Juliana Lefebre, D.O. -

Dr. Mattu and Dr. Weingart,

Is there any other literature support of the use of push-dose pressors other than papers submitted by anesthesiology in C-section scenarios? I am currently looking at this concept with the flight medical team at my hospital in conjunction with the medical director. As valuable its use, we would love to have literature support of push-dose pressors so we can start implementing this into our flight medic and ED protocols.


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