Why Dopamine and not Levophed for head injury pts?

[jensfbay, BSN, DNP]

I recently received a pt. from OR who was already @ 400mcg/kg/min of Neo, but his systolic still went into the 60's after half an hour in the ICU. When he came, the neurosurgeon already said that it was a poor prognosis (although he wasn't brain dead yet), and all we were doing pretty much was to stabilize his vitals while his family makes the decision to either withdraw or wait till he is brain dead.My question is, why was Dopamine the next vasopressor of choice after Neo and Not Levophed? Thanks!

[CrufflerJJ, BSN, RN, EMT-P]

Hopefully the Neo dose was 400 mcg/min, not mcg/kg/min.

I am not sure about the answer to your question. Neo is a pure alpha agonist. Throwing dopamine into the mix would give you some beta stimulation at low doses (possibly boosting your pt's heart rate), and alpha only at high doses.

Consulting Dr. Google gives a couple interesting hits:

http://www.acnr.co.uk/pdfs/volume4issue5/v4i5management.pdf

That link says: "Norepinephrine appears to be more predictable and efficient at augmenting CPP when compared with dopamine."

Another link is:

Comparison of Dopamine and Norepinephrine after Traumatic Brain Injury and Hypoxic-Hypotensive Insult | Abstract

That abstract references a study in which norepinephrine and dopamine were compared for efficacy in boosting CPP following a hypoxic brain insult. A couple interesting statements from the abstract shown above:

"After severe brain trauma, blood-brain barrier disruption and alteration of cerebral arteriolar vasoreactive properties may modify the cerebral response to catecholamines."

...and...

"Both norepinephrine and dopamine failed to increase CPP, and ICP was significantly higher in TNE and TDA groups than in T group. Interestingly, norepinephrine was not able to alleviate the decrease in MAP. Neither norepinephrine or dopamine could induce an increase of MAP. LCBF decreased similarly in T, TNE and TDA groups. In conclusion, norepinephrine and dopamine are not able to restore values of CPP above 70 mm Hg in a model of severe brain trauma. Furthermore, their systemic vasopressor properties are altered."

It's interesting to me that following brain injury, pressors may no longer work the way we expect them to. In the past, I've seen vasopressin used in head trauma pts suffering from hypotension refractory to catecholamines. Different receptors, and all that jazz.

An interesting mention of vasopressin use in that situation is:

Vasopressin in Acute Brain Injury: A Note of Caution

Enjoy!

[Esme12, ASN, BSN, RN]

NIcely done.!

[hodgieRN]

I think dopamine was probably the next best thing in this scenario b/c many trauma pts experience some type of cardiogenic shock following a major accident. When I used to work in the ER, we hung dopamine on everyone with hypotension. Once they got to the unit, it was changed to levo or neo but you had to assume there would be some type of (cardio) shock upon arrival to the ER. As you know, dopamine is only used for symptomatic bradycardia/hypotension. On the neuro side of it, pts who are brain dead (or close to it) will herniate at some point and become bradycardic, so maybe that's why it was used after surgery. They probably figured why not cover everything until the family makes a decision.

But your pt sounded pretty much done and dopamine was probably used to buy time. I think using levo and then neo is still best practice for routine hypotension, like with sepsis. If the HR is fine, there's no need for dopamine (in my opinion).

Personally, I try to always stay away from vasopressin as treatment for blood pressure. Vasopressin is ADH, which will stop urine output. Brain injury pts often go into DI, and vasopressin can mask it. I try to only hang it if I see they are going into DI. Sometimes, I get pts from the floor and the nurse will have vasopressin hanging as the first-line pressor and I immediately take it down and switch to Levo. And report usually includes this..." The pt is septic and there no urine out, so I think they are going into renal failure." I think that happens b/c vasopressin gtts are not really titrated (unless you are on the unit treating DI), so it's more convenient. I would almost use dopamine over vasopessin for hypotention now that I think about it...

[Snowbird17]

Was he bradycardiac? Often happens with heads that are herniating. Otherwise, sounds like a personal preference by the MD.

Also, not shocking he dropped after an OR. They often give a bolus of Neo to has stabilize vitals to get them to unit and I see quite a few patients have sudden hypotension shortly after anesthesia leaves.

[CrufflerJJ, BSN, RN, EMT-P]

...They often give a bolus of Neo to has stabilize vitals to get them to unit and I see quite a few patients have sudden hypotension shortly after anesthesia leaves.

My sensitive, kind, non-judgmental phrase for that approach is "dump and run.":sarcastic:

I just love how you get a pt on a vent, only marginally sedated (with no orders entered for sedation upon arrival to the ICU). BP marginal when the pt shows up....then it tanks when the OR/anesthesia folks depart. This is generally followed by a pt coming almost awake, grabbing for the ET tube.

Fun times!

[cinja]

If your Pt's acidotic you can forget about dopamine working at improving SVR. I just beg to get Levo started once the "tank" is full.

[rebelccrn]

I would have to disagree with the statement that in all trauma pt's we should assume that they have cardiogenic shock. Unless with direct coronary injury, there should be no form of cardiogenic shock. Trauma patients experience distributive shock close in relation to septic shock with the overreaction of the immune response.

I agree with pretty much everything else that you said, though.