Question regarding fluids and hemodynamics/case

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Absolutely I agree that maxing norepinephrine before adding another agent is usually suboptimal care. In my experience people needing 3 or more agents without something acute and immediately fixable however generally do very poorly no matter what kind of care they get.
Not disagreeing with add another agent, but there is no ceiling effect for vasopressors (imo) so max dose is not a word I'd throw around.

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No ceiling effect but for whatever reason in our shop when we get to around 0.3 norepi were looking hard at other things. Around 0.4 norepi with 4 vaso were usually throwing the kitchen sink at them with epi, steroids, cyanokit or blue depending obviously on the specifics of the patient...
At that stage and that level of support i would say 1 week mortality is over 50%

So im surprised this 80 yo rallied so well.
Fluids are voodoo. No one agrees. And we dont understand fluid balance enough.

Without tee or some measure of intravascular volume theres no way we can comment further on your pt.
But 8litres is very far outside the norm in our place anyway
 
Without tee or some measure of intravascular volume theres no way we can comment further on your pt.

No such thing as measurement of volume status - I'm rather cynical about this. Just some fancy monitors of varying utility. I like to flip coins personally and rely on heuristics and then When the (lidco, cheetah, tee, sg, ppv, flotrac, etc.) Agree with me then they are useful.
 
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No such thing as measurement of volume status -
I'd say yes and no. I share your skepticism of all the non and minimally invasive monitors out there, and I also question whether the word "volume status" really has the utility that we think it does.

Ultimately, what we are all interested in is adequate oxygen delivery. If I have a tee with decent enough windows to calculate a reasonably accurate LVEDV and LVESV, and if I know the pt's HR, sat, and hgb, then I can tell you if that pt has met some arbitrary threshold for adequate DO2 at a cardiac index of 2.2 etc. (of course keeping in mind that the pt may have some underlying disease process like sepsis where mitochondrial dysfunction/tissue hypoxia can occur despite adequate macro level DO2). However, with that information, I can pretty confidently say that the pt does not need another 4L of crystalloid to reach "euvolemia." I think you could also reasonably do the same thing with a CCO/SVO2 swan, which is the gold standard to which all those other devices you mentioned are compared.
 
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