H&R2019 Preliminary Programme!

 

So things are coming together really nicely. With a couple of attendees from last year becoming speakers, and the addition of some local talent, we’re back for another run. A bit bigger, yes, but not so big that the informal and inclusive atmosphere is lost. In order to really add some more in-depth, take-home skills, we have added the pre-congress courses (see here for more detail) which are truly awesome and will have participants leave with some very concrete and usable clinical skills.

Now there will be a few more additions to the programme, but this should give everyone a pretty good idea of what they are signing up for:

H&R2019 Preliminary Program

One of the things we are really striving to do is to tie things in together. For those of you who followed the posts on venous congestion, or on MAP and perfusion, everyone involved, Rory (@EMnerd), Josh (@Pulmcrit), Jon (@heart_lung), Segun (@iceman_ex), Korbin and the rest of us will be working to crystallize concepts and clinical applications in the huge grey zone that is acute resuscitation.  I am particularly interested in Felipe Teran’s (@FTeranMD) discussions on arrest physiology, because, as opposed to theory-based protocols and guidelines, guys like Felipe are using real-time physiology to guide resuscitation. As far as I’m concerned we all need to move towards this type of resuscitology as opposed to the blind recipe approach.

The workshops will be really cool. In the Castlefest-style, participants will be able to focus on the ones they really want to work on, or else give all of them a try. And there should be some pretty unique ones, such as portal and hepatic doppler, renovascular POCUS as well as a REBOA and ECMO workshops.

We should have registration up and running by november first. There is a 100 participant limit, so don’t wait too long, as we sold out last year!

Montrreal, May 22nd to 24th!

If you’ve got questions, please email hospresusconference@gmail.com or leave a comment!

cheers!

 

Philippe

The Resus Tracks 06: Farkas (@Pulmcrit) on Shock Perfusion and Infrared Tech! #FOAMed, #FOAMcc

So I had the chance to catch my friend Josh today, and, as always, he had some unique insights to contribute.

 

I really like the IR idea from the standpoint of objectivity and reproducibility. At first it sounded like a fancy (and fun, of course) way to check skin temperature as I routinely do, but the ability to objectify from doc to doc could be really interesting. Will get on that with my colleagues in my unit. We’ll see what we can come up with in the next months!

 

Love to hear from some others trying to tweak and optimize their resus!

 

cheers

 

Philippe

Shock Macro and Micro-circulation: Piecing things together. (Part 1) #FOAMed, #FOAMcc

 

So I have really, really enjoyed the discussions I had with these bright people on shock circulation:

Segun Olusanya (@iceman_ex) Resus Track 2

Rory Spiegel (@EMnerd) Resus Track 3

Korbin Haycock (tell him to get on twitter) Resus Track 4

Jon Emile (@heart-lung)  Resus Track 5

 

Some take home points so far:

I think that more questions than answers truthfully came out of this, and that is really the best part. But lets see what the common agreed upon thoughts were:

a. the relationship between the MAP and tissue perfusion it quite complex, and definitely not linear. So scrap that idea that more MAP is more perfusion. Could be more, same, or less…

b. you can definitely over-vasoconstrict with vasopressors such that a increasing MAP, at some point, can decrease tissue perfusion. Clinically, we have all seen this.

c. no matter what you are doing theorizing about physiology and resuscitation, THE MOST IMPORTANT IS TO CONTROL THE SOURCE!

 

Some of the interesting possibilities:

a. Korbin sometimes sees decreasing renal resistive indices with resuscitation, particularly with the addition of vasopressin.

b. the Pmsa – can this be used to assess our stressed volume and affect our fluid/vasopressor balance?

c. trending the end-diastolic velocity as a surrogate for the Pcc and trending the effect of hemodynamic interventions on tissue perfusion.

This stuff is fascinating, as we have essentially no bedside ability to track and measure perfusion at the tissue level. This is definitely a space to watch, and we’ll be digging further into this topic.

 

Jon-Emile added a really good clinical breakdown:

I think one way to think of it is by an example. Imagine 3 patient’s MAPs are 55 mmHg. You start or increase the norepi dose. You could have three different responses as you interrogate the renal artery with quantitative Doppler:

patient 1: MAP increases to 65 mmHg, and renal artery end-diastolic velocity drops from 30 cm/s to 15 cm/s
patient 2: MAP increases to 65 mmHg and renal artery end-diastolic velocity remains unchanged.
patient 3: MAP increases to 65 mmHg and renal artery EDV rises from 10 cm/s to 25 cm/s

in the first situation, you are probably raising the critical closing pressure [i know i kept saying collapse in the recording] relative to the MAP. the pressure gradient falls and therefore velocity falls at end diastole. one would also expect flow to fall in this case, if you did VTI and calculated area of renal artery. in this situation you are raising arteriolar pressure, but primarily by constriction of downstream vessels and perfusion may be impaired. ***the effects on GFR are complicated and would depend on relative afferent versus efferent constriction***

in the second situation, you have raised MAP, and probably not changed the closing pressure because the velocity at the end of diastole is the same. if you look at figure 2 in the paper linked to above, you can see that increasing *flow* to the arterioles will increase MAP relative to the Pcc [closing pressure]. the increase in flow raises the volume of the arteriole which [as a function of arteriolar compliance] increases the pressure without changing the downstream resistance. increasing flow could be from beta-effects on the heart, or increased venous return from NE effects on the venous side activating the starling mechanism. another mechanism to increase flow and therefore arteriolar pressure relative to the closing pressure is the provision of IV fluids.

in the third situation, MAP rises, and EDV rises which suggests that the closing pressure has also fallen – thus the gradient from MAP to closing pressure rises throughout the cycle. how might this happen? its possible that raising the MAP decreases stimulus for renin release in afferent arteriole, less renin leads to less angiotensin and less efferent constriction. thus, paradoxically, the closing pressure falls with NE! another possibility is opening shunts between afferent and efferent arterioles [per Bellomo]. as above ***the effects on GFR are complicated and would depend on relative afferent versus efferent resistance changes***

 

This is really, really interesting stuff. So in theory, the MAP-Pcc gradient would be proportional to flow, so if we can estimate the direction of this gradient in response to our interventions, we may be able to decrease iatrogenism. I’ll have to discuss with Jon and Korbin which arterial level we should be ideally interrogating…

More to come, and next up will be Josh Farkas (@Pulmcrit), and I’m sure anyone following this discussion is looking forward to what he has to say. I know I am.

cheers!

 

Philippe

The Resus Tracks 05: Kenny (@heart_lung) Tackles Shock Perfusion! #FOAMed, #FOAMcc, #FOAMus

So finally got around to corralling Physiology Jedi Master Jon-Emile Kenny for a chat, which is always a tremendous learning opportunity. And this time was no different. Jon breaks down some of the mysteries around arteriolo-capillary coupling and shock flow, and brings up some really interesting potential uses of the critical collapse pressure of small arterioles, and hints at how we may be able to use some POCUS techniques to clinically assess tissue perfusion.

Here you go:

Please leave comments and questions!

The article we refer in the beginning to is here:

MAP in sepsis review

And the article on critical closing pressure in the neurocirculation that Jon refers to is here:

CrCP Brain

cheers!

 

Philippe

The Resus Tracks 04: Shock Circulation & Renal Perfusion with Korbin Haycock. #FOAMed, #FOAMer, #FOAMus

 

So I got to have a chat with ER doc extraordinaire Korbin Haycock today, reasserting my belief that tissue perfusion is not proportional to blood pressure.  I am again including the article discussed, and here is the graph in question:

Here is our talk:

And the paper – which is definitely worth a read, as it clearly supports individualizing therapy!

MAP in sepsis review

 

cheers and please jump into the discussion!

 

Philippe

The Resus Tracks 03 – Shock Circulation with @EMnerd! #FOAMed, #FOAMcc, #FOAMer

Here we go!

 

Discussing with Rory is always awesome, because he manages to distill things to the most important stuff. In this one he basically says sure Phil, it’s fun to think up all kinds of semi-theoretico-imaginary hemodynamic stuff, but you gotta make sure you control the source!

Thanks!

 

Love to hear comments and criticisms!

 

Philippe

 

Here is the open access paper I was talking about, graph on page 2.

MAP in sepsis review

 

POCUS & Venous Congestion – A Clinical Case Discussion with Rory Spiegel (@EMnerd_), #FOAMed, #FOAMus, #FOAMcc

Hi, so as a follow up to our earlier discussion, which can be found here, Rory and I discuss a recent case he had, which I think exemplifies well many of the clinical conundrums that are seen in fluid resuscitation, one being the general resistance of many to diurese patients who are still in shock on vasopressors, instead preferring to (hopefully) wait until shock resolution to de-resuscitate. But sometimes, it is exactly what they need, as some of this congestion may be, in fact, a cause of shock…

Here you go:

Love to hear opinions, so feel free to reach out.

 

For those who may be interested at learning some of these POCUS skills, check out H&R2018 (#Hres2018)!

 

cheers!

 

Philippe