Titrating Multiple Pressors

Specialties MICU

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Tonight I had a patient on Norpinephrine, Epinephrine, Phenylephrine, Dopamine and Vasopressin with orders to titrate all of them to MAP> 60. My question is, does anyone have any advice when titrating this many pressors? I'm good with titrating two or three, but totally lost when dealing with this number. Granted in this patient's case she was maxed so titration really wasn't an issue, but in the future any advice? Thanks!

Specializes in Transitional Care, Home Care.

Thank you, Muno!

Specializes in ER trauma, ICU - trauma, neuro surgical.

One thing I like to do is get rid of vasopresson asap. Vasopressin is also anti-diuertic hormone and the urine output will come to a stand still. Urine output is so important in the critical care setting and it can be an indicator for so many other things. The vasopressin basically cuts this out. I always get vasopressin down. We only like to use vasopressin for diabetes insipidus or last-line vasopressor.

Dopamine has a max of 20 mcg, but much won't happen after 15 mcg or so.

I like to use Neo and Levo to max before dopamine. High rate dopamine causes tackycardia, so I will put the Neo up 300 mcg or the levo up to 30 mcg before I use dopemine.

Epi gtts are great vasopressors and I think they are under used. However, they can cause many issues like tachycardia, ischemia, etc, but it a great pressor. Great for post-codes too.

Neo has a higher range of dosing, so I find it more predictable since you can go up by 20's. Titrating Neo can give you that nice cherry on top if you need a dash of pressor. Levo works if you go up by 2-4, but Neo has that nice range. We tend to use Levo more often.

If you are titrating that many drips, there is nothing wrong with taking one down and going way up on another. If you have Dopamine at 20, levo at 30, Neo at 150, and vasopressin at 0.4, take the vasopressin down and crank the Neo up 250. If you have a pt on Neo 100, and Levo 10, take the Neo down go up to 16-20 on the levo or vice versa. Less gtts are easier to work with and more predictable.

Don't forget to never underestimate the power of fluid boluses, blood, and albumin. Albumin being the big one. If the blood levels are ok, and the fluid is topped off, Albumin is a great way in increase the oncotic pressure in the vascular system. Sometimes, the 500 bottle of albumin can (sometimes) greatly reduce the dosage of pressors.

I agree that more volume (dry?) and maybe blood (low hct?) might be good options when you are on multiple pressors. Steroids might help also. Lots of people think bicarb helps, but after reading lots of books I'm not sure its a good idea. I have given it to really sick people but I'm not sure if it helped as I was throwing all kinds of stuff at them. Calcium seems to help usually. Treating the underlying cause is always a good idea if you know what's wrong.

I see patients in my unit on levophed and neosynephrine occasonally. I don't get it. Typically Levophed is the first-line pressor. It has some Beta but mostly Alpha activity. So why choose a pure Alpha agent (Neo) as the second pressor? All that does is increase afterload further. I mean if the patient is tachycardic and you have a good h/h and plenty of volume in, sure you don't want Beta stimulation. But why do you want 2 alpha agents? Thats why vasopressin makes sense once you max out on levophed, it acts via a different pathway. Maybe add epi or vasopressin as the 2nd/3rd ones.

Yes, more volume is always a good idea! Some septic patients just can't seem to live without Levo for a day or two, usually at a wussy dose like 5-10 mcg, but in most circumstances you should always be giving volume with your pressors.

Bicarb isn't always a good idea, that's why it's not an ACLS drug. I had an ACLS instructor who made her student (a cardiologist) do her mega-code over because she called for bicarb lol. Anyways, it has its place. If your last ABG had a pH of 6.8-7.2, it's usually merited. Pressors do not work in an acidotic environment, at least not well. If you've never seen someone with a MAP of 50 maxed out on Levo skyrocket up to a MAP of 120 after getting a bicarb bolus, it's quite the site to behold. It does and will work, but if you have no rationale for it, it's useless. There's also the role it plays in ion exchange with hyperkalemia.

Calcium gluconate/chloride is nice for dealing with the hyperkalemia associated with acidosis. I usually don't see calcium come out until we're debating throwing in a dialysis catheter while watching sine waves march across their ECG monitor.

Levo and Neo are our top two pressors. Levo initially, and if it fails to work or we're dealing with arrythmias/severe tachycardia, then we go to Neo. You'll always find those two wherever you go. MICU loves Levo, SICU loves Neo. It's all in the physician training. MICU they get septic patients who have some cardiac depressant effects which might be helped by the beta effects of Levo, while SICU they're looking at volume depleted patients that need Neo to get 'em through a rough patch. A generalization? Sure, but that's what I've come to figure out in my years of dealing with doctors from both sides of the fence.

We usually won't run Neo/Levo side by side unless the patient is crunking hard and needs it. In septic shock your SVR is nearly nonexistent once you're in the later stages, and sometimes two pressors are required to get an adequate SVR. We could run Vaso, sure, but it's just not as popular on my unit, and Epi is unheard of.

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