So I was really honoured to have been invited to talk about VExUS for the Mayo Clinic’s CC department. In the last year watching the spread of VExUS has been really rewarding because so far, everyone who has incorporated it into their clinical practice has seen the substantial impact it can have. And it is just the beginning, with exciting new studies in the pipeline and papers about to be published.
Anyhow, the invitation to speak “at” (Zoom of course given that this is COVID times) Mayo represents another step in the spread of precision medicine as applied to venous congestion.
Sorry to all for the delay, these last weeks have been busy! But as promised we are sharing some of the highlights of H&R Reloaded’s lectures, and here is one that should raise a few eyebrows. Andre Denault is one of the few clinicians whose research is groundbreaking, highly clinical and pertinent. Definitely not the kind of research that is done just to show research is being done.
So for all the amazing talks that were had at H&R Reloaded, by far the one that should change the landscape of acute care the most was Pendell’s, that had most participants’ and faculty members’ jaws drop. Not mine of course, because I had seen the pdf of the talk and had a chat with Pendell weeks before, which gave me time to pick it up off the floor.
I grew up in the Q vs Non-Q era, then came the STEMI vs NSTEMI.
It’s time to change.
There will be resistance. There will be inertia. But there’s virtually no way to prevent it. Might as well be ahead of the curve than among the last stragglers still insisting that the ST segment is infaillible.
So after chatting a few times, finally got to sit down and discuss Farid’s super interesting theories that certainly seem to tie in many elements of COVID pathology. Just to be clear, this is strictly exploratory and for the purpose of generating discussion and research, and should not form the basis of therapy today, though who knows if it may in the next weeks or days, as several studies are being done around this.
Jan de Backer is an aerospace engineer who, in concert with his respirologist father, designed an AI system that, from HRCT, can extract a ton of information about lung parenchymal, airway and vascular structure. With no contrast or anything. Just from a run-of-the-mill CT chest…
In full disclosure, I have (unfortunately!) no connection or interest in Fluidda (www.fluidda.com) outside of a clinical one.
So I’ve been meaning to speak with Jan whose tweets about functional respiratory imaging (FRI) and the FLUIDDA technology have been really piquing my interest, but its taken me unfortunately too long to do so, but here it is. I think this is fascinating technology, which is currently available to all freely (COVID times and all…), and in my opinion clearly deserves a trial run and some clinical experiences. If you are interested, drop me a line and I will link you up with Jan De Backer.
So if you are a fan of bedside physiology and personalized medicine, be sure not to miss H&R Reloaded, which will be packed with cutting and bleeding edge talks and faculty – a lot of the stuff we’ve been talking about is not what’s currently being done, or about and I think we just might have to add a talk on FRI…
So I’ve been meaning to fine tune this concept and really start applying and following more rigorously, so I wanted to see what the only clinician I know of doing it at the bedside was doing in a stepwise fashion.
AKI is one of those things that really, really bugs me. It’s common, it’s serious, impacts mortality in the ICU population, and yet to me, it is usually poorly managed by the vast majority of clinicians, usually by examination of surrogate indices and time-lagging imaging with poor specificity and sensitivity for the actual diagnoses you need to rule in or out, which are pre-renal failure and post-renal failure. With a probe in your hand and a decent understanding of physiology, you can rule both of these categories out in about 30 seconds, add a minute for VEXUS and in a grand total of 90 seconds you are left with either a diagnosis or else the intrinsic AKI category as the last one standing and it’s time to hunt for offenders.
But that’s not what we’re talking about today, but rather, the fine tuning of macro-hemodynamics in relation to your intra-renal micro-hemodynamics. Fascinating stuff.
So you can join us during H&R Reloaded’s Virtual Hangout Room and discuss this and a bunch of other skills or strategies involved in critical care and try to tease out the details from Korbin and the rest of our amazing faculty!
So after a lot of discussion, we decided to do this, a blend of the original H&R2020 with the current COVID-19 experience, essentially a look to the next year of critical care management as far as one can figure.
This will take place July 29-30-31 from 1800-2200.
Though WebConferencing can’t quite match the atmosphere of a boutique conference like H&R, we are setting up a virtual Hangout Room so that participants can exchange with the different faculty members in an open session.
So just got what I think is an excellent and common question from a reader, worth addressing with a mini-podcast:
Dr Rola, my name is Pedro Alvarado, i’m a Mexican critical care fellow (currently in the 2/2 training year). Been very interested in the last year on being able to answer the question: is my patient going to benefit form fluid administration? (particularly in the case of an objectively diagnosed distributive shock + ARDS, i think by the way, a very difficult to answer question in the majority of Mexican ICU´s).
To answer this question i thought, until recently, one should start by answering if the patient is fluid responsive. The concept of venous congestion and fluid tolerance seems to be the counterbalance that might complete the equaition of benefit/harm ratio of fluid administration on an already high-output state. As it is, i’ve been very interested in what you have recently been describing as the VexUs score. One question, you mention this US tool as a useful stop point for fluid administration in septic (distributive I assume) patients. I understand from your explanation that the further you document ultrasonographic sings of venous hypertension from the RA (hepatic -portal-renal vein), the worse the hypertension and possibly its consequences might be. Also you imply that the earliest you document signs of venous hypertension, the better, so that you can counterbalance benefit/harm ratio of fluid administration as soon as possible.
Understanding that the first, relatively easy measurable macrostructure to be affected by right-sided hypertension is the RA, what makes VExUS more valuable than a good,old CVP monitoring for this purpose? Far more expensive and time consuming, the US is. Also CVP absolute values and trends can be continuously measured.