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    Default ARDS, acidosis, hypotension... question from an ICU RN

    I'm a new RN. working ICU in a level i trauma center.. have been lurking your amazing forum since nursing school and always found the clinical insights to be so educational. i think it's amazing that you guys are so willing to share with each other, and the CRNA-hopefuls... I had this patient a couple of weeks ago that I've thinking about ever since, and have been trying to fully understand the clinical picture. I'm hoping you guys can help me out..

    ---------------------

    19yo male s/p unrestrained rollover, multiple fx (no head injury), acute renal failure, DIC, ARDS
    was weaned from oscillator on icu day 6. pCO2/pO2 have since been within normal limits. hco3 has been 18-20, pH 7.2-7.3, anion gap 14
    currently icu day 12, still on rotorest, drips: argatroban, lorazepam 6mg/hr, no pressors

    when i got report at 0700, vent settings were biLevel 12/19, f=23, PS 12, fio2 0.55, IE 1:2.
    HR 120, BP 170/60. spo2 94%, tachypneic in the 40s, tidal volumes were between 50-150 (minute ventilation ~4L)
    night nurse said "That's how he's been all night.. his HR and BP actually went up a little a couple hours ago, but that was after his fentanyl PCA ran out....."

    started to feel nervous... gave a prn dose of fent to rule out pain (no effect.) i thought we should increase the PIP and get an ABG... was about to call the 1st year (teaching hospital) when BP plummeted to 70/30 before my eyes.. spo2 82%..

    ABG was 6.98 / 90.7 / 174(bagging) / 20.4, lactate 1.2
    the attending came to bedside. we did a recruitment maneuver, then changed to biLevel 10/25, f=30, PS 18. gave two amps bicarb, fluids, norepi, started nimbex.. within two hours norepi was off and abg was within normal limits... patient stayed in ICU another month but made consistent forward progress after this point.

    -----------------------

    i've been trying to figure out the exact patho of his tanked hemodynamics, and have had a surprisingly hard time finding a straightforward answer in my usual go-to texts/online resources. ended up having to dig through free journal articles.. forgive me if i'm naive/just completely wrong:

    poor minute ventilation lead to co2 trapping --> respiratory acidosis on top of the existing metabolic acidosis (from the renal failure?) --> pushed the pH so low that the enzymes activated by catecholamines became inactivated (despite the fact that endogenous catecholamine production was probably up.. evidenced by earlier slight increase in HR/BP?) --> decreased SVR?

    other questions:
    - was this a form of distributive shock? i can't imagine it was cardiogenic even though i have read that LV contractility can be impaired by respiratory acidosis... is the effect enough to tank BP, and wouldn't the decreased afterload counter this? on the other hand, i can't find anything about distributive shock not related to sepsis, anaphylaxis, and neurogenic....... but this seems to fit the definition anyhow.
    - why give bicarb; was it risky when pCO2 was so high already? (i don't understand when exactly it is indicated to use bicarb)


    i feel like i'm about to bridge a "big picture" gap in understanding, but need some non-anectodal guidance.... i tried to ask the MICU senior resident the other day, and he said "we don't care so much about the biochemistry after school..." any help would really be appreciated. thanks for taking the time to read this long post!
    Last edited by baggins; 09-18-2012 at 08:40 AM.

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