Fluids and Sepsis Twitter Case #foamed

So this morning I shared a case that I’m looking after on Twitter and got asked a really interesting question. But a bit too much for the 140 characters of Twitter. So here’s the answer!



2 thoughts on “Fluids and Sepsis Twitter Case #foamed

  1. ipswichultrasound

    Hi Philippe,
    Very interesting. I can understand Rajiv’s query and I am wondering if there were also some subliminal biases affecting you. Was it lung tissue damage that made you fear easy precipitation to ARDS? Did she already have B line in other areas? Or are you simply illustrating that we can manage patients quite well on minimal fluids? I am also pondering what effect ADH has and whether everyone has the same post-stress response, and how it would interact with our fluid resusuitation. Would Lawrence know?

  2. This is a nice illustration of correcting the physiologic problem at its root rather than giving a therapy that will temporarily improve cardiac performance, but at the expense of probably iatrogenic extravascular lung water, and possibly causing more wide spread vascular dysfunction as well (glycocalyx interactions with shearing forces, naturetic peptide, LPS, etc.).

    The hemodynamic profile of the patient was likely an elevated CO, decreased SVR, and a decreased CVP. An important point is that the CVP is not reduced due to volume depletetion, but rather a lack of venous tone combined with the increased CO sucking the blood out of the venous system. The fact that the IVC is “normal looking” when she was hypotensive, may be a clue that she isn’t so volume tolerant after all, as most people would have a very flat IVC under these circumstances.

    We presumably don’t know her LAP, as you didn’t mention if you did LV diastology investigation, but she likely has at least a relaxation abnormality. With PNA, we know her lungs are prone to get wet even with normal LAPs.

    Giving a vasopressor raises the SVR, the CO will likely dip a bit twoards normal or could increase as the venous squeeze increases preload to the ventricles. Giving the vasopressor makes the MAP normal by making the variables that generate the MAP normal, rather than by making one variable increase whilst the original derangement persists.

    One final point is that a rise in CVP has the possibility of decreasing organ perfusion via congestive mechanisms. The tempting strategy to raise the CO by giving fluids, may make us think we are helping organ perfusion, and we are reassured because the MAP increases, but remember that the perfusion also depends on the relationship of MAP-CVP. So, if the CVP increases more relative to the increase I the MAP, have we really done anything to help perfuse the patient?

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