Last week I posted a lecture an incredible by Paul Marik on Fluid Management in severe sepsis. The lecture is the equivalent of a bucket of ice water poured over your head. Now let's give you a towel and discuss.

Want to add a journal club to this flipped classroom?

Then read these pieces in Critical Care:

* Bellomo on Norepinephrine and the Kidney

* Rethinking Resus Goals by Dunser

* Response: Rethinking Resus Goals by Marik and Bellomo

* Pharmacodynamic Analysis of a Fluid Challenge (Crit Care Med 2016;44:880)

The Low-Fluid Volume Early Pressor Experiment has Already Been Tried

It was called standard care 15-20 years ago--patients did not do all that well.

Should we Increase DO2?

We know from that shooting for supranormal DO2 is actually harmful. The original goal-directed therapy trials did not pan out and this may be why.

There is definitely a group of Severe Sepsis patients that are receiving inadequate oxygen delivery. I have treated these patients; I have documented ScvO2s in the 50's and 60's on initial check in a EGDT-type algorithm.

Far more commonly, patients are in pure vasodilatory shock (Jones' trial patients). The latter fact doesn't disprove the former. Using the studies demonstrating the deleterious effects of shooting for above normal delivery doesn't say anything about normalizing patients with low delivery.

Marik's Goals

* Achieve adequate perfusion pressure

* Improve microcirculatory flow

* Limit Tissue Edema

All right on point; how do we get there is the question.

Rivers Trial as a Waterfall?

This is not actually what that trial showed. And the way CVP was used was not actually debunked by the 7 mares article (Note: I'm not advocating you use CVP, I'm just pointing this out! We have better ways to accomplish assessing fluid responsiveness so CVP should be sent to the junk bin)

I will make the utterly blasphemous statement that Dr. Rivers and Dr. Marik are actually in near-complete agreement if you followed both of their protocols explicitly in the ED.

MAP and Association to Survival

Not sure what this is proving: both groups (the flow-optimizers and the desert-inducers) believe in shooting for MAP goals. Patients in whom it is impossible to get the MAP up will die more frequently.

But is it Flow or Pressure that Matters?

I must say, I am still in the tissue flow camp

On to the Glycocalyx

Now this is where stuff gets really interesting. Every day, there is increasing research and more publications on the fundamental role of the vascular glycocalyx. But how do we integrate this clinically?

Chris Nickson tweeted this amazing lecture from Rob Wise. It will explain the Glycocalyx in 5 minutes. It lives on Life in the Fast Lane.

 

Now as to its relation to fluids in sepsis, we are being told hypervolemia is bad. But if the fluids are leaking from the vascular space are we ever seeing hypervolemia in the vasculature or is the problem whole body volume overload--not if we believe BNP/ANP are the root of the problem, they only respond to vasculature fluids. If we are doing a fluid responsiveness strategy, we should not be seeing the vascular overload.

Do balanced vs.