Published
Hey all, I had a patient who cardiac arrested and they thought he was in ARDS given his Pa02 compared to his FiO2 and we were increasing his PEEP upwards to around 14 until he finally started oxygenating in the 90's (he was in the 80's before on 100% FiO2). I heard the RT discussing that his blood pressure would probably be affected. I have three questions:
1. How can adding PEEP drop a patient's blood pressure? He was already acidotic (so on a bicarb gtt) and on multiple pressors but vary labile with his blood pressures. The RT assumed that him being on this additional PEEP could make this situation worse. I've been reading and I read that adding PEEP decreases the venous return to the heart, but if that is so, then why is the CVP elevated (isn't CVP an indicator of the venous return to the heart-aka preload)?
2. I don't quite understand the relationship between PEEP and urine output. When I've called providers about a patient's low UO and their intubated, they ask me how much PEEP they are on. Does the extra pressure compress blood flow to the kidneys???
3. Also a side question, why the patient was dropping his O2 sat, the provider also wanted to know his peak inspiratory pressure. Once she knew that, she went up on the PEEP, so does that mean the PIP was low or high to make such a decision.
I work in the operating room where the gold standard of resuscitation is practiced. Not bragging, that's just the fact. So here's a problem for you to solve with the ETCO2/PLR gimmick.
Say you have a guy in the OR having an ex lap for a ruptured bowel, is septic, coagulopathic and on inopressors via a midline. Educate me. How do you figure out what he needs?
jamst149
49 Posts
Thanks for not addressing anything i posted. Be it a paper or something i said.