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.
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!
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.
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:
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!
So a few months ago I got to talking with Korbin about POCUS, fluids and resuscitation, only to find out this guy is doing all sorts of awesome stuff in his ED in sunny California. Got to meet him at H&R2018 and he had even more tricks up his sleeve he was telling me about. He will definitely be back for H&R2019 on the faculty side of things.
In the meantime, let’s review renovascular ultrasound with him:
And here is our discussion that took place at TheRounds Backstage during #HR2018.
Interesting stuff. It isn’t always so easy to get a nice renal view in ICU patients, but with some perseverance you often can. I’ve been toying with it and tying it in with the hepatic and portal flow patterns, but I have to admit I had sort of dismissed renal resistive index based on what I could find in the literature, that is until I got to chat with Korbin, who made me see there are some interesting avenues, especially the example he states on seeing it improve with vasopressin use in shock patients, which correlates with some of the data out there suggesting decreased need for RRT and better outputs with vasopressin on board.
I have a feeling there is relevance to this in acute care, and that the next couple of years will reveal some usefulness. The glitch had always been in not knowing what the baseline RRI is, and that it can be abnormal in chronic RF. There are, however, many patients who were perfectly well previously and where the assumption that their baseline is normal is probably safe.