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

Working out the Clinical Kinks in Venous Congestion: A Discussion w/Rory & Korbin. #FOAMed, #FOAMcc, #FOAMus

It’s really exciting to be at the outer frontier, trying to figure out some new clinical areas. Now these have all been described, however the ability of clinicians to properly identify certain pathophysiological findings has been limited prior to POCUS. Following the trail being blazed by Dr. Andre Denault, we are also working on expanding the applications, particularly in resuscitation/deresuscitation and CHF/AKI. There are more questions than answers, but that’s exactly why it’s interesting.

So for those unfamiliar with the topic here is a small intro:

And for those following, here is the discussion:

 

Do expect more from us about this. Watch this space. It is practice changing.

 

Additional resources:

Here’s a link to the article referenced during the recording: https://www.ncbi.nlm.nih.gov/pubmed/29573604

Andre and I discussing venous congestion

…if you dig around the blog in the past year there are a bunch more!

 

do share your thoughts!

cheers

 

Philippe

 

The Right Stuff: A New Series on Nutrition. #FOAMed

So here is a little video intro to a new series of posts and discussions I’ll be putting up on the blog in the next weeks and months. And yes, it will tie in to acutely ill patients too…

 

 

So please do leave comments and invite yourself into this discussion.

Remember, you are what you eat. It’s true.

 

cheers

 

Philippe

H&R2018 Keynote Lecture: Re-Defining Sepsis by Lawrence Lynn. #FOAMed, #FOAMcc

Lawrence’s work on sepsis analysis is truly groundbreaking. To put this in perspective, one has to recognize that sepsis is an exceedingly heterogeneous disease that, once upon a time, and for good reasons, an arbitrary definition was formulated. This, however, does not reflect sepsis adequately, and needs to change with observational data, as this has tremendous implications in therapeutics research.

Lawrence’s efforts have resulted in data systems revealing a number of different patterns of sepsis, with clear differences in physiologic effects or responses. This may explain why so many failed therapies for sepsis have occurred. It is entirely plausible that some of these therapies may have effects in some of these phenotypes of sepsis but get lost in the statistical mix.

Love to answer any questions anyone may have, and Lawrence will certainly chime in on the discussion!

cheers

Philippe