Levophed/Norepinephrine?

[WTEngel]

Ecgg, then we agree on the treatment (or should I say the link you posted agreed) just not the rationale. At this point I guess it really doesn't make too much of a difference.

 

[Ecgg]

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?

In the field is hard to assess. Hence why I asked if you running a pump and titrating it to MAP?

Usually if it's gravity drip in the hands of medics and nice bumps in transport, I am certain the pressure would be amazing upon arrival, but there would be profound vassoconstriction.

 

[Ecgg]

Ecgg, then we agree on the treatment (or should I say the link you posted agreed) just not the rationale. At this point I guess it really doesn't make too much of a difference.

You may be correct about the pathway, I need to review some of my lectures.

 

[Carlos Danger]

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?

The beta effects of dopamine are undesirable in most patients, though. The tachycardia associated with dopamine can increase Mv02 dramatically.

The easiest to use / safest pressor IMO is phenylephrine. Vasopressin works well in many patients, also.

 

[Summit]

Surviving Sepsis 2012 Update information here: http://www.survivingsepsis.org/Guidelines/Pages/default.aspx

Ecgg: I referred to what the patient might need thus the lack of response to a 1L bolus, not what they should definitely receive on the ambulance. It is unlikely such a large amount would be ordered on an ambulance without serial lactates and a metric to measure volume/preload status (CVP is usually used in sepsis although some question its reliability) particularly with a CHF history. I’ve certainly seen bigger patients in severe septic shock get 12L+ over the course of <2hrs and be on levophed and vaso.

LS5: CHF hx is not a contraindication to fluid resuscitation in the septic patient, but it is a good indicator for close attention.

 

[Dwindlin]

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.

Principle is sound, but in life most intensivists aren't going to consider pressors in sepsis after only 3 - 4 liters. The way I have been taught is actually fairly similar to Dr. Weingart's (from emcrit) preferred method. We don't like CVP, we use ultrasound. We give continuous fluids (large bore and with a pressure bag for the first several liters, but never on a pump) until BP improves or until there NO IVC COLLAPSE (notice we don't use that 13% collapse or what ever it is). Rarely will the patients end up with less than 8 - 10 liters before we start the pressor talk with patient/family.

As far as pressors go. We do some form of sympathomimetic (whether that is levo, epi, or dopa) and if we need a second we do a non-adrenergic (vaso generally). We don't stack adrenergic pressors here (thank god).

 

[Carlos Danger]

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.

Could have been sepsis, or possibly something else. There are a lot of conditions that will cause a transient (or not so transient, if not treated) hypotension on induction. Sepsis is certainly one of them.

What was the rest of the clinical picture? How much midazolam did you give? What drugs did you use to RSI?

 

[lightsandsirens5]

So just did follow up and found out he had a large hemorrhagic CVA. Go figure.

Now, as to me only using 1L of fluids, the main reason was not just the Hx of CHF, but the fact that he was already nearly drowning with Pulm. Edema.

Halo: 74 yom found unconscious by spouse at 0230 hours. Upon arrival GBG of 42. 25g of D50%W to no effect. Move to MICU, beginning of decline in resp. status. Corresponding decrease in saturation and increase in end tidal. Decide to RSI. Pre-induction vitals of: P:70. R: 8. BP: 130/80 (approx). SPO2: 88 (bagged up to 99 pre-induction). ETCO2: 50. GCS: 6 (1,1,4) Temp: 98.3F. Approx 75kg Male. For RSI, Drugs: Fent. 100mcg. Ketamine 125mg. Roc 75mg. Pass tube and confirm. Rapidly desaturated without PEEP. Needed 10 cmH2O to keep sat in mid 90s. Vitals of: P: 60. R. 14 (to keep end tidal at acceptable levels) BP: 100/70. SPO2: 96% (Without PEEP was 88%). ETCO2: 42. 15 minutes later begins to buck tube. 5 mg of midaz. That is when the floor fell out of his pressure. 50/20. 1L of fluid with zero effect. Horrible sounding edema. Turning PEEP up only dropped his MAP further. So I started Levo @ 4mcg/min. Brought his pressure to about 100/50. So I know I got CP with that. I hope I didn't vasoconstrict him so much I killed renal perfusion. Though with the size stroke he had, I doubt he will need it for long.

And yes the Levo was on a pump. I have to use the pump for all med drips. Which I would do anyhow.

 

[VFlutter]

Brought his pressure to about 100/50. So I know I got CP with that. I hope I didn't vasoconstrict him so much I killed renal perfusion. Though with the size stroke he had, I doubt he will need it for long.

Eh, I highly doubt you were actually getting cerebral perfusion. Even in the presence of normal ICP you are barley getting adequate CPP with that MAP. And most likely this guy's ICP was markedly elevated.

In the NICU it was not uncommon to max out multiple pressors to maintain crazy high MAPs in TBI/CVA patients.

If the patients ICP was 40 (Unconsciousness) then you would need a MAP of 110 just to maintain a minimum CPP of 70. Which is roughly 160/100....

But as Vene would say you can't just chase numbers.

 

[Carlos Danger]

Doesn't really sound like sepsis. Maybe the PEEP + fentanyl + midazolam caused the hypotension, especially if his EF was already low. Good job with the patient management.

I thought this was interesting: Medscape

Importantly, recognize that neurogenic pulmonary edema is an underdiagnosed condition. Patients with neurologic events often have multiple other comorbidities, which may obscure or mimic the diagnosis of neurogenic pulmonary edema. The lack of a standardized definition for neurogenic pulmonary edema also makes defining its epidemiology difficult.

As many as one third of patients with status epilepticus may have evidence of neurogenic pulmonary edema.[5] More than half the patients with severe, blunt, or penetrating head injury have associated neurogenic pulmonary edema. Approximately 71% of fatal cases of subarachnoid hemorrhage are complicated by neurogenic pulmonary edema. Neurogenic pulmonary edema may complicate subarachnoid and intercerebral hemorrhage in 30-70% of patients and may recur after initial resolution.[6, 7]

A series of 457 patients with subarachnoid hemorrhage reported a 6% prevalence of severe neurogenic pulmonary edema.[8] Solenski et al reported in 1995 that increased age and a worse clinical grade of subarachnoid hemorrhage were associated with neurogenic pulmonary edema.

 

[FLdoc2011]

You can also get direct cardiac dysfunction from severe neurological insults such as neurogenic stunned myocardium.

Have seen in quite a bit in severe strokes or intracranial hemorrhages where they have relapse of troponin and/or evidence of heart failure.

 

[Flight-LP]

The beta effects of dopamine are undesirable in most patients, though. The tachycardia associated with dopamine can increase Mv02 dramatically.

The easiest to use / safest pressor IMO is phenylephrine. Vasopressin works well in many patients, also.

I was reading thought the thread and wondering when someone was going to bring up this truth!

Neosynephrine is the way to go. It's safer, more effective on those acidic septic patients, and easier to administer than the typical multitude of pressor drips we commonly see. Plus I've rarely seen the need to add more pressors in comparison to hanging levophed. Just my personal experience though, individual results will vary.

I had the perfect example earlier this week. Septic patient, intubated, on Vanc and Cipro for Imperical coverage, on a bit of Cardizem, a little Insulin, Diprivan (?!?WTF over?!?), and THREE freaking pressors (Levo, Vaso, and Dopamine). Pressures were running in the 70's.

Yes this was what we term an inter facility rescue, although they did at least attempt to treat, lol.

After stopping the Diprivan (***cough***blood pressure***cough), killing all the pressors and starting neo, and then getting some fluid going, the pressure stabilized. Once at a decent perfusing level, we were able to reintroduce sedation and keep his pressure stabilized with only the neo.

I think the take home message is and should be that more is not always better. Over complicating the septic patient can be fatal or at least catastrophic. Of course so can under complicating, but I digress................

 

[Carlos Danger]

I was reading thought the thread and wondering when someone was going to bring up this truth!

Neosynephrine is the way to go. It's safer, more effective on those acidic septic patients, and easier to administer than the typical multitude of pressor drips we commonly see. Plus I've rarely seen the need to add more pressors in comparison to hanging levophed. Just my personal experience though, individual results will vary.

I had the perfect example earlier this week. Septic patient, intubated, on Vanc and Cipro for Imperical coverage, on a bit of Cardizem, a little Insulin, Diprivan (?!?WTF over?!?), and THREE freaking pressors (Levo, Vaso, and Dopamine). Pressures were running in the 70's.

Yes this was what we term an inter facility rescue, although they did at least attempt to treat, lol.

After stopping the Diprivan (***cough***blood pressure***cough), killing all the pressors and starting neo, and then getting some fluid going, the pressure stabilized. Once at a decent perfusing level, we were able to reintroduce sedation and keep his pressure stabilized with only the neo.

I think the take home message is and should be that more is not always better. Over complicating the septic patient can be fatal or at least catastrophic. Of course so can under complicating, but I digress................

Sounds like fun. I've been on more of those interfacility rescues than I could even begin to recall.

Let me guess.....they had dopamine on to counteract the myocardial depression of the propofol, and cardizem running to counteract the tachycardia and ectopy from the maxed out dopamine?

A practice that I developed for these situations was to significantly reduce or even DC everything that wasn't obviously necessary (i.e. here I probably would have left on the levo and vaso, as well as the ABX, and turned the rest off), re-evaluate the patient, and then systematically add things back in or turn more things (vaso) off as indicated. And of course these patients are almost always under-resuscitated with IVF.

A lot of times the bedside nurses or referring docs weren't happy about it, but much more often than not, I was able to safely transport the patient with a lot fewer infusions to worry about and a lot less polypharmacy to cloud things.

In my experience, propofol is not a good sedative by itself for transport anyway, and I have often replaced a propofol infusion with boluses of midazolam and fentanyl, even in patients who aren't hypotensive.