ICU clinical question

Tenesma · Sep 20, 2003

i am sorry - but this situation doesn't make much sense... what is the rationale in maintaining a SBP>120 for perfusion to a foot??!!!... that same rationale would dictate that we should have every ischemic foot on the vascular service on pressors...

it is a stupid order that has no support in the critical care literature.... beyond that, let's say they did some vascular surgery to assist w/ reperfusion to the foot (who knows what vascular structure was injured w/ the tib/fib), then the last thing you would want is a vasoconstrictor!!!!!

i think you should ask the surgeons why they need a higher perfusion pressure to the foot - the only explanation i can think of is that they are planning a staged vascular repair to that leg, and this is an interim effort??? but this is exceedingly rare as the vascular repair should have been done the first time around...

You don't need a PA line - especially as there is a very poor link between SVR (systemic vasc. resistance) and peripheral perfusion

and levophed is a far better drug than dopamine - your argument for dobutamine is a good one, but if this is a young relatively healthy trauma patient there is no need for it - especially since most trauma patients have a huge catecholamine surge to begin with, and therefore already have a Cardiac Output of 8-12L/min

my 2 cents

AmiK25 · Sep 20, 2003

Tenesma,

Thank you for your input. This was not my patient, so I was not aware of the entire picture regarding what surgery had been done or was being planned. All I knew was that vascular surgery had asked the ICU resident to maintain a SBP of 120 for perfusion. I know that levo is a better drug than dopamine in most cases, but I thought in this instance it should not be used b/c of its vasoconstrictive action. I attempted to ask the resident why he wanted levo but he could not give me a straight answer. As it was not my patient, I did not want to get too involved in the discussion or try to take over my colleague's patient.

Tenesma · Sep 20, 2003

well this brings up an interesting issue: which is more vasoconstrictive - dopamine or levophed? i feel as far as peripheral vasoconstriction goes - they are about equivalent since you are often titrating them to a specific blood pressure parameter - the big difference lies in mesenteric/splanchnic circulation vasoconstriction/dilation....

New CCU RN · Sep 20, 2003

Wouldn't the vasoconstrictive affects also be dependant on the amount of Dopamine being used, meaning if it is in the range of 5mcg/kg/min vs 20mcg/kg/min?

AmiK25 · Sep 20, 2003

That is what I was think CCURN. The patient was on about 6-8 mcg/kg/min, which should not cause much alpha effect, right? When the resident brought up levo, I said what about vasoconstriction and he said that was already happening with the dopamine. However, I was always taught that you do not get the vasoconstrictive effects until you get up over 10 mcg.

Tenesma · Sep 20, 2003

while it is true that the higher the dose of dopamine the more vasoconstriction you get - just as you get more vasoconstriction with a higher dose of levophed....

we have to start moving away from the old concept that dopamine does something at a certain mcg/kg/min as we already know that weight has little to do w/ vasoconstriction.... you titrate your vasoactive drugs based on effect not based on weight....

when you say that 6-8mcg/kg/min should not cause much alpha - you have to be careful, as it causes much more alpha than a lower dose and less alpha than a higher dose, and in a patient it is very difficult to know exactly which dose is the magic borderline between primarily dopaminergic activity vs. beta-adrenergic vs. alpha-adrenergic...

so even at small doses of dopamine you will see vasoconstriction - here is an example that you might have been exposed to:

let's say you are weaning somebody off dopamine, you can't just turn it off at 3-5mgc/kg/min (i am using your weight based system) as you will see a drop in blood pressure - hence even at low doses you have vasoconstriction...

so try to unlearn what you have been taught about dopamine - there are no magic numbers involved

New CCU RN · Sep 20, 2003

Tenesma,

First of all wondering how you dose your Dopa if it isn't using mcg/kg/min. Isn't that just a standard way to dose it?

We always turn Dopa off at 3-5mcg/kg/min. That is where we start when we hang the gtt and we also turn it off there. If the patient is at the point where we can wean the gtt off, that is our cutoff point unless they are one of those exceptions that are extremely sensitive to the Dopamine. However, just because my unit does that, I am not claiming it to be the only way to do things, but I will say in my personal experience, I have never had a problem with turning it off at 3-5mcg.

While there is no magic that occurs between say 9 and 10 mcg of Dopa, there is still quite difference between Levo which is primarily alpha and Dopa which is a mix. I can see AmiK's wondering why the doc would want something that is known to vasoconstrict, thus increase the risk of a decrease perfusion

A blood pressure does not necessarily mean end organ perfusion, it simply makes us feel better!!

Also, I disagree that turning off the drip and seeing hypotension is conclusive that there is vasoconstriction... it depends on the whole patient scenario and the reason behind the shock state in the first place....

I am wondering if you could to refer me to the literature that disagrees with Dopamine have the various affects dependant upon dosaging.. .that is new news to me.

Tenesma · Sep 20, 2003

new CCU RN:

dopamine is dosed as mcg/min - I don't include weight in its management... in adults I start off at about 100-200mcg/min and titrate up as needed.... however because of its chronotropy I pretty much always choose levophed as my first choice drug... the only time i use dopamine is if 1) it is the only pressor available 2) i am doing a cardiac case - and then only intra-operatively for specific reasons....

while you are right about blood pressure not reflecting end-organ perfusion - in somebody who is asleep, not peeing, etc it quickly becomes our best clue about perfusion...

now when you say: "i disagree that turning off the drip and seeing hypotension is conclusive that there is vasoconstriction" that doesn't make much sense to me, as blood pressure is based on vascular resistance - in adults Cardiac Output is based primarily on filling pressures/venous return, and if you have loss of vascular resistance you have loss of venous return thus you have a lower blood pressure (unlike in pediatrics where the cardiac ouput is primarily dependent on heart rate) - so if you turn off a pressor and see hypotension you can thus conclude that the pressor is providing vasoconstriction to improve venous return.

as far as dopamine having different effects depending on dosage has been delineated, we all know that at lower doses it is primarily dopaminergic, and as you increase the doses you lose dopaminergic effects in favor of alpha behavior... so i didn't say anything that goes against the literature, but here are a few references that may provide some surprising insight into dopamine (on a sidenote, it always amuses me when somebody tries to argue regarding dopamine versus levophed, especially since dopamine works in the body by releasing norepinephrine at the synapses :)

1) dopamine causes pulmonary vasoconstriction therefore invalidating interpretations of wedge pressures as dopamine will be falsely elevating your wedge pressure in an unpredictable way (Cope, DK Pulmonary Capillary pressure: a review. Crit. Care Med. 1992, 20:1043-1056)

2) Ischemic limb necrosis occurs more frequently w/ dopamine than any other vasoconstrictor available (unless of course you are in a terminally ill ICU patient on high-dose epinephrine) (Sundram P. Am J. Cardiology 1990 119:891-898

3) there is less vasoconstriction, and improved organ perfusion when compared to phenylephrine (aka. neosynephrine) or dopamine (dasta, JF. Ann Pharmacother 1990 24:153-156 and Desairs P. Crit Care Med 1989 17:426-429)

another issue w/ dopamine is that if it is run for a longer period of time (>24 hours) you start seeing tachyphylaxis (just as you see w/ nitroglycerin) and therefore if you are going to use it properly you need to provide "holidays"...

so i think in this patient levophed is still a better drug to increase SBP --- however what i am still wondering about is why do they need to artificially raise the blood pressure to maintain a palpable pulse - and how is a palpable pulse different in outcome from a dopplerable pulse??? sounds like random voodoo management of this poor trauma patient's foot...

i am very curious as to how things play out for this guy

Surgical Hrt RN · Sep 20, 2003

Ok, here is my 2 cents. I have seen patients that were Levo dependent lose fingers and toes due to the massive amount of vasoconstriction. Neosynpehrine is less constrictive, but I have never in all my years of nursing, some of which I might add was spent doing trauma ICU, heard of using DOPAMINE for perfusion to a FOOT!!!!! That is just absurd. It will perfuse kidneys and heart, but it is constrictive also. That order was NUTS!!!!!!! :eek:

gaspassah · Sep 21, 2003

i would also say that if the order said to titrate to keep pedal pulses.....does that mean increase the dose...what if the loss of pulse was due to vasc. diff higher in the leg? the nurse ups the dose = more vasoconstriction and increase chance for loss of limb. very confusing, ive never seen anything like it. should have been fixed in surg.

Maximus · Sep 23, 2003

Craziness! Vasocontriction. Why? I would have asked for a rational and if not a good one would have refused to start it. If they wanted perfusion pressure higher could try fluid and inotropes.