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.




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




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!



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!



Love to hear comments and criticisms!




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

MAP in sepsis review


H&R2019. A bit Bigger. A LOT Better! #HR2019

First of all thanks to all of last April’s participants and faculty who made this an awesome event. For those of you who missed the inaugural event, no worries, this edition will be even better. Building on the feedback, we’re cooking up a really nice little program that will keep H&R small, packed with clinically useful talks and both cutting and bleeding edge lectures (don’t expect guideline rehash!), and even more faculty interaction.

We will have some parallel tracks to make sure the ED people get some more ER-specific stuff, that the CC people get some esoteric tweaks about obscure ICU topics, and the hospitalists and pick and choose.

We’ve added a pre-conference course day packed with great stuff. The real problem will be choosing:

Felipe Teran (@FTeranMD) brings us a full day, resuscitative TEE workshop including basic certification – first time in Canada!

For educators and anyone wanting to up their presentation game, my good friend Haney Mallemat (@CriticalCareNow) brings his unique Keynotable workshop. If you’ve ever heard Haney talk, you know he is the leader of the pack when it comes to delivery, so not-to-miss opportunity to learn form the master.

Hospitalist POCUS? Check. Hospitalist procedures? Check. Percutaneous tracheostomy and emergency surgical airway? Check. Advanced POCUS like renovascular and transcranial doppler? Check. And a lot more…

Basic info:

May 22nd – pre-conference courses

May 23rd – The Hospitalist

May 24th – The Resuscitationist

Preliminary programme available October 1st here.


So mark your calendars. Bring the fam, check out Montreal, and pack in a bunch of solid, ready-to-use clinical knowledge but also some paradigm-shifting approaches and viewpoints!








Resuscitation Tracks 02: Hemodynamics w/@iceman_ex #FOAMed, #FOAMcc

So I’m in the process of putting together my resus handbook, and the really good thing about writing something up is that it forces one to beef up the entire mental database and fill in blanks that may sometimes be filled by belief, habit, culture or leaps of faith. So part of my process will involve discussing stuff with the brightest guys I know. Who happen to be pretty bright. So I figured it might be stuff worth sharing!

Here, Segun and I discuss the possible uses of Pmsa, of resuscitation philosophy, and touch on the issue of blood pressure vs perfusion. (please skip to 0:30 – sorry can’t cut out!)


Love to hear some additions to our discussion!

Here is the paper I was referring to, with the graph on page 2:

MAP in sepsis review




The Right Stuff: An Outline. #FOAMed

So, lets get an idea of what we’ll be going over and some basic ideas and principles. And to put things in perspective, I am tackling this from an MD’s point of view. I am not in the business of making people lose weight, I’m not a personal trainer, I don’t have a healthy recipe book to sell, and I don’t run a lucrative organic farm (not sure those exist). I am doing this because I think it is important to look at medicine and health care from the ground up, and make sure we are doing things right. The steady rise in chronic disease and the epidemic of obesity tells us that clearly, we are not doing so.

The principles that apply to sick humans should also apply to those who are well and wanting to remain so. The idea of optimal nutrition ties in to healing injuries and optimal performance as well.

This is an exceedingly complex field, I do not pretend to have completely understood it, but I have seen a lot of consistent signals in media, literature and among trusted friends and colleagues  in the last years, and mostly in the last months when I have focused a fair bit of my reading of medical literature on the topic. There is something there that is largely being ignored both by the general public and the health care professionals.

So let’s get started…with some ideas, some starting points:

  1. Nutrition as is generally discussed in the developed world, including most medical practice, has very little true scientific basis. It is more historic and cultural-based. It is time to review this.
  2. Certain paradigms need to be challenged and re-thought. In the ICU and in acute care, in the outpatient world and in that of the healthy humans. We are all healthy until we get sick.
  3. In chronic disease, the importance of nutrition and the therapeutic impact is much, much undervalued and under-appreciated, and the truth is that most professionals in the health care system – doctors included – have no more than a rudimentary understanding of nutrition, and the little that was taught to them was, as stated above, shoddy from a scientific standpoint.
  4. Our digestive system and body is so much more complex than we think and know. It isn’t just what goes in and what is used, but the individual’s particular genetic traits, current state of health, his or her microbiome (the billions of microbes in our intestines), and the time and frequency of what goes in.
  5. Physiology is controlled by hormones and neurotransmitters.


So first, ditch the whole calorie concept. It is utter nonsense. Indeed, as Jason Fung says, we do not have calorie receptors. Calories are a measure of thermodynamic energy, which we are utterly unable to handle, store, collect, etc. The human body simply does not work that way. There are a lot of calories in wood, but we are unable to extract anything from it at all. We absorb glucose, fructose, fatty acids, amino acids, water, vitamins and minerals. So the calories in-calories out is irrelevant from a physiology standpoint. Can it work for people trying to lose weight? To some degree, as it will likely bring on a state of being more mindful of what one eats. But if you truly want to understand nutrition, you have to look elsewhere.

In the case of metabolic syndrome, which has become the scourge of developed countries, the real evildoer is insulin.

Wait, but isn’t insulin something important? Required to control blood glucose, etc? If you don’t have any or enough, aren’t you diabetic? Yup. All true. For those who develop the metabolic syndrome, a strong driving force is insulin. How? Chronically elevated insulin levels required to control blood glucose levels will have two main effects over time:

  1. increased adipose tissue – insulin is a storage/growth hormone. Turned on by excess glucose, it shifts metabolism towards the synthesis of glycogen (short term energy stores), and when this is maximized, the liver makes fatty acids, in turn taken in by adipocytes (fat cells) and used to synthesize triglycerides. The breakdown of fats is also inhibited by insulin.
  2. a progressive development of insulin resistance. Why is this important? Because over time, this will cause increased serum insulin levels, as the body will need to make more insulin for the same level of blood glucose control.

We can see how this sets up a vicious cycle that ends up in weight gain and, more importantly, the metabolic syndrome… And we all know the far-reaching and myriad of clinical consequences this will have.


Love to hear comments and ideas!







Next post: understanding the hormonal modes involved in nutrition, and some podcats discussions!




Some interesting stuff by some actually smart people:

Jason Fung’s The Obesity Code and The Complete Guide to Fasting

Tim Ferriss’s The Four Hour Body

Jason Fung on youtube