Levophed/Norepinephrine?

lightsandsirens5

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Do you use it? I am kind of curious to see who does? I used it for the first time last night and the nurse could not believe I brought someone in from the field on a Levo drip.

I was truly impressed by it and am very grateful that I had it at my disposal. I no like BP of plus or minus 50/20, especially in a pt completely refractory to 1000 ccs of NS who's MAP continued to decrease.
 

chaz90

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I haven't been anywhere that had Levo in the field. I know of some places that used to use it, but they've gone to Dopamine as the only EMS pressor now. Do you have a choice of Levophed vs. others?

Was your patient septic by the way? That's the time I'd most like to have a more alpha specific agonist.
 
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MagicTyler

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I've heard a rumor that Levo is being added to Arizona drug list, and is preferred over dopamine for hypotention not related to hypovalemia
 
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lightsandsirens5

lightsandsirens5

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For pressor drips I can hang Levo, Dopamine and Epi.

I'm thinking he was septic. That is the only thing that makes sense.

What really sucked, and the reason I had to hang Levo, was we had to RSI him cause I was loosing the airway. And the only way to keep him down was with Versed. And the only way to keep his sats out of the toilet was with 10 of peep. So it KILLED his pressures. And a liter of saline did squat, so I went with the Levo. It worked like a charm though.
 

chaz90

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Yeah, I can see Versed plus 10 of PEEP being bad news in an already septic patient. Sounds like good work and a cool call though!
 

mrg86

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We just started using it in my county, it is first line for septic/neurogenic shock that is refractory to fluids. 8-12 mcg/min titrated to effect and then backed down if BP allows.
 

STXmedic

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We've got it as a pressor option, along with dopa (no epi). Our doc also wants it initiated on all ROSC patients. I've given it once with seemingly good success at a previous employer (septic patient after a liter and a half).
 

Ecgg

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Well is certainly works, it's why they called it Levophed or leave 'em dead. Although "raising the bp" is not a measure of success, without knowing end organ perfusion status and urine output.

You guys use IV pumps, or gravity drips?
 
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Dwindlin

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Not sure I get get the warm and fuzzies from pre-hospital use of levo. There are concerns of putting through a peripheral line, dopa is much safer in this aspect. Not to mention if you really think the patient was septic then I wouldn't expect much from one liter. These patients tend to get massive amounts of fluid resuscitation before we admit defeat and start pressors.

Personally I feel about pressors the way I feel about vents. Use as infrequently as humanly possible, in as small amount as absolutely necessary, for as short amount of time as humanly possible.
 

Summit

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Peripheral levo is a bit scary. Central levo can have some nasty side effects too, but it is great in the septic pt among others.

The reason that 1L NS did nothing in a septic patient is because they probably needed 6L or 12L or more. Med control ought to approve more fluid.
 

Ecgg

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Peripheral levo is a bit scary. Central levo can have some nasty side effects too, but it is great in the septic pt among others.

The reason that 1L NS did nothing in a septic patient is because they probably needed 6L or 12L or more. Med control ought to approve more fluid.

12L more? Probably after 2nd bolus of 20ml/kg with that BP would be good idea to think about a pressor, unless the patient is 600lbs.
 
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WTEngel

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We would use norepinephrine for our sepsis protocol back when I was doing CC transport.

I am reaching back to biochem class here...I seem to remember that norepinephrine has the lowest pKa of the four pressors we commonly use (epi, norepi, dopamine, dobutamine.) this in and of itself doesn't mean anything spectacular, other than the fact that the higher the pKa of the drug, the less effective it will be in an acidic environment. Most septic patients we are dealing with are acidic.

Also, dopamine is a precursor of epi and norepi. In acidic conditions, the pathway it takes to convert to norepi and epi will not proceed as effectively as it would when conditions are a homeostatic 7.4. Remember, pH is logarithmic, so even a slight move has magnitudes of effect on h+ concentration.

All this is to say, in my experience, norepi was a better drug in profound sepsis, and I believe it has to do with the acidosis we find many septic patients in. This is why in many protocols, norepi is first line for SERIOUS sepsis, but can be preceded by dopamine in early stage or even moderate sepsis.

The last thing ill add (in this post anyway) is that septic patients are a balancing act, and I rarely managed them with only a single pressor. Generally it was a combination of pressors, while keeping an eye on end organ perfusion, pH, lactate, pyruvate, etc.
 

Ecgg

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We would use norepinephrine for our sepsis protocol back when I was doing CC transport.

I am reaching back to biochem class here...I seem to remember that norepinephrine has the lowest pKa of the four pressors we commonly use (epi, norepi, dopamine, dobutamine.) this in and of itself doesn't mean anything spectacular, other than the fact that the higher the pKa of the drug, the less effective it will be in an acidic environment. Most septic patients we are dealing with are acidic.

Also, dopamine is a precursor of epi and norepi. In acidic conditions, the pathway it takes to convert to norepi and epi will not proceed as effectively as it would when conditions are a homeostatic 7.4. Remember, pH is logarithmic, so even a slight move has magnitudes of effect on h+ concentration.

All this is to say, in my experience, norepi was a better drug in profound sepsis, and I believe it has to do with the acidosis we find many septic patients in. This is why in many protocols, norepi is first line for SERIOUS sepsis, but can be preceded by dopamine in early stage or even moderate sepsis.

The last thing ill add (in this post anyway) is that septic patients are a balancing act, and I rarely managed them with only a single pressor. Generally it was a combination of pressors, while keeping an eye on end organ perfusion, pH, lactate, pyruvate, etc.

I think it's much more simpler. Septic shock is a distributive shock (AKA warm shock in adults mostly ~70% gram negative LPS) due to massive release of nitric oxide severe dasodialtion occurs through the body, I would imagine alpha drug would be a better choice at the stage OP patient was.
 
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WTEngel

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I understand that sepsis is a distributive form of shock and I realize the patho behind its onset.

I think you're missing my point... Norepinephrine is synthesized from dopamine anyway...so one would reasonably believe that dopamine should be just as good in sepsis, because it will ultimately increase endogenous norepinephrine, right?

This is not the case however, as that pathway will not proceed reliably in acidic conditions. So we give norepinephrine straight away, because endogenous norepinephrine biosynthesis has been largely stalled.

We both agree that norepi is a good drug of first choice for sepsis.
 

Arovetli

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12L more? Probably after 2nd bolus of 20ml/kg with that BP would be good idea to think about a pressor, unless the patient is 600lbs.

Pressors are typically 2nd line behind fluid resuscitation...perhaps only to be used after adequate resuscitation attempts, often of multiple liters of fluid, have failed or pulmonary edema develops. EGDT suggests about 5 liters, and early abx/fluids over pressors if possible.
 

Handsome Robb

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No levo here, only dope (standing) and Epi (for bradycardia and hypoTN refractory to TCP and dope after MD contact...never ever heard of someone hanging one).

As far as fluids go, 1L isn't a lot, we have to give 2L before we can go to a pressor unless we really have a good reason.

Dope isn't a great choice for most of the patients that I see that need a pressor, it'd be awesome to have levophed but I don't see it happening anytime soon.
 

STXmedic

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I've heard of the poor effects of levo through a peripheral line. However, I've asked many EM docs and a couple intensivists, and all have given me the same answer: in the short term, it is not a concern.
 
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lightsandsirens5

lightsandsirens5

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Man, I am still baffled, because the pre RSI pressure was 13x/8x. So it wasn't like I was thinking Sepsis at that point.

The other issue was he had a Hx of CHF, and his breath sounds were already horrible. So I really didn't feel like dumping 6000 CCs into him.

What kind of complications are we talking with peripheral Levo? Severe vasoconstriction? We start it at 2 mikes/min, which I am assuming isn't too bad?

Ecgg: I wasn't too concerned with urine output in the field, but MAP/BP is all we have to really look at to make an educated guess as to if end organ perfusion is actually occurring? Or am I missing something?
 

Ecgg

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I understand that sepsis is a distributive form of shock and I realize the patho behind its onset.

I think you're missing my point... Norepinephrine is synthesized from dopamine anyway...so one would reasonably believe that dopamine should be just as good in sepsis, because it will ultimately increase endogenous norepinephrine, right?

This is not the case however, as that pathway will not proceed reliably in acidic conditions. So we give norepinephrine straight away, because endogenous norepinephrine biosynthesis has been largely stalled.

We both agree that norepi is a good drug of first choice for sepsis.

Pressors are typically 2nd line behind fluid resuscitation...perhaps only to be used after adequate resuscitation attempts, often of multiple liters of fluid, have failed or pulmonary edema develops. EGDT suggests about 5 liters, and early abx/fluids over pressors if possible.



http://www.sccm.org/Documents/SSC-Guidelines.pdf

(1C); initial fluid challenge in patients with sepsis-induced
tissue hypoperfusion and suspicion of hypovolemia to achieve a
minimum of 30 mL/kg of crystalloids (more rapid administration
and greater amounts of fluid may be needed in some patients)
(1C); fluid challenge technique continued as long as hemodynamic
improvement, as based on either dynamic or static variables
(UG); norepinephrine as the first-choice vasopressor to
maintain mean arterial pressure ≥ 65 mm Hg (1B); epinephrine
when an additional agent is needed to maintain adequate blood
pressure (2B); vasopressin (0.03 U/min) can be added to norepinephrine
to either raise mean arterial pressure to target or
to decrease norepinephrine dose but should not be used as
the initial vasopressor (UG); dopamine is not recommended
except in highly selected circumstances



So OP patient is refractory to fluid bolus, granted 1L is low, but it should not be 12L by any means.

say 90kg patient i'd give 2 (20ml/kg that is 3.6L total) bolus if refractory still, I may do 1 more if no pul edema and then go for the presssor.
 

WTEngel

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MAP is a decent indicator of perfusion (better than straight BP) but the primary concern in patients we start pressors on is renal perfusion. In some cases we end up in a "rob Peter to pay Paul" situation, stealing perfusion from the kidneys by way of vasoconstriction, in order to maintain cerebral and cardiac perfusion.

In the short term, you have to do what you have to do, in the long term, you'll end up chasing renal function and metabolic derangements for days if not weeks.
 

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