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.
A PLR-induced increase in EtCO2 >5 % predicted a fluid induced increase in CI >15 % with sensitivity of 71 % (95 % confidence interval: 48–89 %) and specificity of 100 (82–100) %. (Intensive Care Med (2013) 39:93–100)
You clearly don't understand dynamic vs static indices. By defintion a CVP is static. No? By definition an ultrasound is not? No?
Look up PLR and ETCO2.l
Look up Paul Marik and John Myburgh.
You're intent on arguing, I get that. I'd love to take you to work with me sometime. You'd learn something about me.
That paper you cited sets up a straw man, in that it makes an untrue assertion (in the abstract anyway) that CVP is utilized for volume responsiveness "almost universally" and goes about stating the obvious about CVP. Everyone knows that stuff. No one uses CVP to assess volume responsiveness, except in Mogadishu maybe. Besides, Who uses just one indicator in isolation to guide any therapy let alone volume resus? Nobody.
Passive leg raise is a way to determine fluid responsiveness. Good tool. Again...people can be fluid responsive via SVV and PLR that don't need fluid. MAP and CVP used together (key word there, together) to tease that out. Moreover, using CVP with those other indices is how we decide when and if to start an inopressor in these types of patients.
As far as ETCO2 with PLR goes, do the authors control for pulmonary pathology? Fibrotic lung disease, acute lung injury, COPD, lung contusion, whatever? There are so many confounding factors that affect ETCO2 that the CCM journal your authors cite only say that it MAY predict it in SOME circumstances. Hardly reliable information. There are so many more accurate predictors, that's just looking for a solution to a problem that doesn't exist.
Finally, in the clinical area the terms "static" and "dynamic" with respect to indices are just not used. I use each indicator uniquely and in relationship to the other from TEE to urine output. Those words really don't have any meaning for me.
"Passive leg raise is a way to determine fluid responsiveness. Good tool. Again...people can be fluid responsive via SVV and PLR that don't need fluid. MAP and CVP used together (key word there, together) to tease that out. Moreover, using CVP with those other indices is how we decide when and if to start an inopressor in these types of patients."
Care to say that again? I'm not even sure what you are saying. Got a paper to prove it?
"As far as ETCO2 with PLR goes, do the authors control for pulmonary pathology? Fibrotic lung disease, acute lung injury, COPD, lung contusion, whatever? There are so many confounding factors that affect ETCO2 that the CCM journal your authors cite only say that it MAY predict it in SOME circumstances. Hardly reliable information. There are so many more accurate predictors, that's just looking for a solution to a problem that doesn't exist."
What proof are you providing? I've provided data and papers. You?
Here's an idea...if RAP isn't of any use to you or your patients, don't use it. I use it for the benefit of my patients, and it's one of the big reasons why I put central lines in in the first place. I understand what it means and what it doesn't mean. And I don't use indirect measurements of volume responsiveness. If there is an issue, I put in an arterial line and do a direct and reproduceable measurement.
jamst149
49 Posts
Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. - PubMed - NCBI
End all be all cvp