Why not Levo?

  1. 0
    Hi, wanted to get some opinions on a recent very interesting patient that I had:Pt. was originally admitted to the floor with chest pain and RVR (both of which resolved in ER once nitro gtt was started). Apparently when he arrived on the floor, the charge there took one look at him and decided he didn't belong there, so I get him in ICU. When he arrives on our unit, he's looks to be about 15 mins from the wrong exit out of ICU (grey, sweatier than I've ever seen anybody, totally clamped down). SBP in the 70s, and of course, no IV access (the field start was infiltrated upon arrival). We quickly get a line in, start 3L NS boluses, and get a stat echo ordered. Echo shows sig right ventricular dilation and nearly no blood movement (which was new since the guys last echo, about 1mo ago). I start Neo which quickly gets up to 300mcg and vasopressin 0.04u/min per the intensivist who's hanging out in the room. We head for the newly ordered CT c contrast: guy has a massive PE. I'll mention here that this entire time, the guy is on 2L, sats 98ish, rate in the low 20s. So, we TPA him, and by 3am he's much improved. I didn't get a chance to ask the intensivist, or the cardiologist who was his first consult, why we didn't head for Levo. We use it all the time and it's usually our firstline pressor. Even when I was maxed out on Neo and vasopressin with MAPs in the 50s, it wasn't even brought up. I've done some research trying to look the reasoning up, but haven't been able to find anything. Any ideas? Pt has history of CAD, stent x2 in circ, HTN, no pulmonary disease to speak of, and chronic a-fib.
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  4. 0
    Quote from EyeSeeYuRN
    Hi, wanted to get some opinions on a recent very interesting patient that I had:Pt. was originally admitted to the floor with chest pain and RVR (both of which resolved in ER once nitro gtt was started). Apparently when he arrived on the floor, the charge there took one look at him and decided he didn't belong there, so I get him in ICU. When he arrives on our unit, he's looks to be about 15 mins from the wrong exit out of ICU (grey, sweatier than I've ever seen anybody, totally clamped down). SBP in the 70s, and of course, no IV access (the field start was infiltrated upon arrival). We quickly get a line in, start 3L NS boluses, and get a stat echo ordered. Echo shows sig right ventricular dilation and nearly no blood movement (which was new since the guys last echo, about 1mo ago). I start Neo which quickly gets up to 300mcg and vasopressin 0.04u/min per the intensivist who's hanging out in the room. We head for the newly ordered CT c contrast: guy has a massive PE. I'll mention here that this entire time, the guy is on 2L, sats 98ish, rate in the low 20s. So, we TPA him, and by 3am he's much improved. I didn't get a chance to ask the intensivist, or the cardiologist who was his first consult, why we didn't head for Levo. We use it all the time and it's usually our firstline pressor. Even when I was maxed out on Neo and vasopressin with MAPs in the 50s, it wasn't even brought up. I've done some research trying to look the reasoning up, but haven't been able to find anything. Any ideas? Pt has history of CAD, stent x2 in circ, HTN, no pulmonary disease to speak of, and chronic a-fib.
    Guess they may not have wanted the tachycardia that can come along with Levo, considering it's both an Alpha and Beta. Echo showing no blood movement due to the pe, don't want the heart to beat quicker/work harder espeically if the blood it does get isn't well oxygenated as it could cause some infarction in the heart itself. Neo just peripheral vasoconstrictor and reflexive bradycardia (not so bad) and of course vaso doesn't have any effects on the heart. Just my 5 cents...
  5. 0
    I appreciate the feedback... That makes sense.... My only thoughts were that it might have been used anyway as a last ditch effort. The other interesting thing about this case was that it presented as classic MI.. With a bit of cardio shock mixed in. We all couldn't believe that it was a PE because his resp distress wasn't too bad, considering what was actually going on.... Any thoughts on this?
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    Might have been that this wasn't a completely "acute" issue. Most likely developed over time and eventually got to the point where he had chest pain from his heart not getting the o2 it needed, got mad and went into RVR. Coronaries dilated with the Nitro supplying "more" o2 calming it down. just a temp fix though....but the PE kept on, most likely causing some muscles, organs, etc...to build up some acidosis due to hypoxia, hence another reason for the low bp and the reason why you gave some boluses too...Lungs usually the LAST to decompensate and thats most likely the reason why sats weren't as bad or RR effort not terrible.....RR rate was in the 20's to blow off the acidosis.....ABG/enzymes/ along with a CXR could've ruled out cardiac issues without even really doing an echo i would think....but given his cardiac hx I could see why one would think MI VS a million other things.....another thing that would've been interesting to see was if you had a CVP....
    Last edit by focker14 on Aug 30, '12
  7. 0
    Did you line him or just place a PIV?
  8. 0
    Focker, great ideas. If this guy would have had pre existing pulm issues, could the presence of collateral circulation be a culprit? Does that happen in the lungs like it does in a long hx CAD? Colorado, yes we got a fem CL shortly after echo, so we already knew results....hence not using cvp as a diagnostic.
  9. 0
    Honestly, i really don't believe that the lung builds "collateral" circulation for purposes of getting O2 to the heart especially because there is only two routes really to and from it PA/PV...the lungs proabably can develop some small type of collateral circulation within themeselves such as additional veins/arterioles around aveloi however typically speaking the lungs in response to low oxygenated areas really just "shunt" blood away from low perfused areas...ie....if no oxygenation taking place over yonder why are we expending the energy to get the blood there....your basic V/Q mismatch....the only the other thing you would have to keep in mind is that if there were collateral circulation (hypothetically) it is in place to compensate for the "ongoing" hypoxia.....when you add a PE into this situation I would imagine that even the best collateral circulation wouldn't be able to compensate for such a drastic change in oxygenation....
  10. 0
    just remember high dose neo kills the gut
  11. 2
    so does hypotension!!
    beckster_01 and EyeSeeYuRN like this.
  12. 1
    Last ditch efforts were definitely in play here!
    focker14 likes this.


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