Vaso vs. Norepi - NEJM

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bulgethetwine

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So what did you all think about the article in NEJM Feb 28, 2008, and the accompanying editorial from Dr. Parillo?

Vasopressin versus Norepinephrine Infusion in Patients with Septic Shock. NEJM Vol 358 No. 9 877-87 2008

My view: Yet another piece of proof that vasopresson potentiates the effects of catecholamine vasopressors. I thought it leaves the question in the title still, well, quite open for debate.

Wish we could have a large, multi-center, prospective, blinded trial comparing norepi vs. phenyl vs. dopa vs. vaso!

Oh, and some problems with the actual study in question:

1) Were the patients really that sick? Consider the (relatively) low mortality rate, and the baseline pressure of MAPs in the low 70s.

2) The treatment window was 12h. This needs to be shorter....

Any other comments?

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I don't think it has all that practical importance. With MAPS in the 70's, why would I be initiating another pressor? The question that needs to be answered is: Does vasopressin have a favorable outcome in patients with catecholamine refractory septic shock? To me, that is a much more clinically relevant question. Our ICU rarely adds a second pressor unless we're still struggling with hypotension despite escalating doses of the initial pressor. There's no evidence that adding vasopressin in order to decrease the dose of catecholamine has any benefit.
 
I don't think it has all that practical importance. With MAPS in the 70's, why would I be initiating another pressor? The question that needs to be answered is: Does vasopressin have a favorable outcome in patients with catecholamine refractory septic shock? To me, that is a much more clinically relevant question. Our ICU rarely adds a second pressor unless we're still struggling with hypotension despite escalating doses of the initial pressor. There's no evidence that adding vasopressin in order to decrease the dose of catecholamine has any benefit.

I think the article's authors were hypothesizing that while both Vasopressin and Cathecholamine can get the patient's pressure up to sufficient MAP (remember all the patients were in septic shock and by definition required pressors to maintain their blood pressure), the author's hoped that because vasopressin acts in different mechanisms from catecholamines it would decreased mortality via less side-effects i.e. from the article:

For example, norepinephrine, a potent and commonly used
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-adrenergic agent in cases of septic shock, may decrease cardiac output, oxygen delivery, and blood flow to vulnerable organs despite adequate perfusion pressureand the author's noted that there is a deficiency of endogenous vasopressin during shock. The study used low-dose vasopressin so that in theory they could "wean" patients off of cathecholamines. . .(This was the whole point of the study!) so that is why they initiated another pressor, i.e. "Catecholamines Bad!" "Vasopressin Good!" . . . it seems like there was a trend towards vasopressin being better long-term, albeit not significantly important . . . they also didn't measure endogenous levels of vasopressin, maybe if they have a machine that could measure endogenous vasopressin levels and dispense the proper amount of vasopressin, i.e. adjusted each half-hour, then they would see more benefit as pressumably this is more physiologic than supraphysiologic doses of cathecholamines.
 
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So what did you all think about the article in NEJM Feb 28, 2008, and the accompanying editorial from Dr. Parillo?

Vasopressin versus Norepinephrine Infusion in Patients with Septic Shock. NEJM Vol 358 No. 9 877-87 2008

My view: Yet another piece of proof that vasopresson potentiates the effects of catecholamine vasopressors. I thought it leaves the question in the title still, well, quite open for debate.

Wish we could have a large, multi-center, prospective, blinded trial comparing norepi vs. phenyl vs. dopa vs. vaso!

Oh, and some problems with the actual study in question:

1) Were the patients really that sick? Consider the (relatively) low mortality rate, and the baseline pressure of MAPs in the low 70s.

2) The treatment window was 12h. This needs to be shorter....

Any other comments?

I think the patients were very sick as they ALL had septic shock and required pressors to maintain that MAP in the low 70s . . . the people doing the study were basically weaning of one pressor for another because it was postulated that Vasopressin is less prone to causes damage for a number of reason . . .

Say I have a patient on levophed in the ICU, and say a moderate to high dose of levophed, and their blood pressure has a MAP of 72, is this patient sick? Very because without the pressor they would die. Seriously, if you don't understand this you need to review Septic shock.
 
I think the patients were very sick as they ALL had septic shock and required pressors to maintain that MAP in the low 70s . . . the people doing the study were basically weaning of one pressor for another because it was postulated that Vasopressin is less prone to causes damage for a number of reason . . .

Say I have a patient on levophed in the ICU, and say a moderate to high dose of levophed, and their blood pressure has a MAP of 72, is this patient sick? Very because without the pressor they would die. Seriously, if you don't understand this you need to review Septic shock.

I meant sick in a relative term. You're obviously not familiar with the sepsis literature vis-a-vis mortality rates, etc. I can provide you some references if it would help?
 
I think the patients were very sick as they ALL had septic shock and required pressors to maintain that MAP in the low 70s . . . the people doing the study were basically weaning of one pressor for another because it was postulated that Vasopressin is less prone to causes damage for a number of reason . . .

Say I have a patient on levophed in the ICU, and say a moderate to high dose of levophed, and their blood pressure has a MAP of 72, is this patient sick? Very because without the pressor they would die. Seriously, if you don't understand this you need to review Septic shock.


Being on a pressor does not indicate the SEVERITY of illness. The vast majority of GOOD sepsis literature uses APACHE and/or SOFA scores. (although APACHE is more common).

Here is a link: http://www.sfar.org/scores2/apache22.html

As you can see, scoring for sepsis severity is complex and is NOT based on pressor support alone. Without some type of ICU scoring, it is impossible to assess the severity of patients enrolled and the possibility of enrollment bias
 
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