Functional Respiratory Imaging: A New Tool? A Chat with Jan De Backer.


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 (  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.

Here is the vid:


Here is the audio:


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…

Bedside Physiology in Septic AKI with Korbin Haycock. #FOAMed, #FOAMcc

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.

Video Link Here!


Audio Only:


Love to hear from anyone trying this!

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!





Resus Pet Peeves: The Hemoglobin in Hemorrhagic Shock. #FOAMed

For a little non-COVID #FOAMed, which we still need…

Here’s one that always gets me, that I always try to make sure the residents always understand before they leave our rotation!

I’m pretty sure if you have been fortunate enough to not come across someone doing this, you will – when you do, find a tactful way to share the knowledge!

Oh and don’t forget that H&R Reloaded is on!




H&R2020 Reloaded: The Virtual Experience now OnDemand!

If you missed it, and want to catch up on some fantastic cutting edge lectures, it is available OnDemand at the following link:

Now available here!


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.


H&R Reloaded Programme in PDF

June 15th update:

CME Accreditation just in, 12 Cat 1 AMA!


July 31st

Click here! Registration is open!

The H&R2020 Team

A Reader’s Question on Fluids! #FOAMed

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.

So here is my answer:


VExUS Rounds at The Ottawa Hospital! #FOAMed


It was great to e-meet a multi-disciplinary group of docs interested in POCUS yesterday, as I was invited by my friends Michael Woo and Ross Prager to talk about VExUS and venous congestion!

Great and very pertinent questions by the Ottawa group, so I’m hoping to see the use of venous doppler take off in their units!

Here is the talk:


love to hear your thoughts!



APRV & COVID Respiratory Failure with Spiegel & Farkas. #FOAMed, #FOAMcc

So at our last webinar (still to be edited due to an unfortunate trolling event), we briefly touched on modes of ventilation but really didn’t delve into it very deeply, so, being fortunate enough to know some really smart people, I figured I might gather up these two for a quick chat. They are both known for no-nonsense, out-of-the-box thinking, paired with solid physiological thinking, which in my mind is the only way to approach complex problems and system failure. Plus, with Rory (@EMnerd) and his powerful nihilistic approach, there would be no chance for a whimsical approach, it would have to have a base in physiology, evidence (bedside or literature) or both!

So just as a little brain teaser, I would like anyone reading to think about how many severe respiratory failure syndromes they are aware of that attack the lungs in a predictable volumetric fashion, where one can say, for instance, that consistently, X% of the parenchyma is affected. Kinda hard, huh? Yet, if asked how best to ventilate these patients, most of us who feel we have a good grasp of severe respiratory failure would answer without thinking twice: “lung protective ventilation: good peep and 4-6 ml/kg.” In a lear, confident tone, most likely as well.

Now I would say that only the first part is correct: lung protective ventilation. As to the second part, it would, to me, only hold true with uniform pathology and uniform patients. But I’ll let Rory rant about that himself, it’s far more entertaining!

So here is our chat.

Hope everyone gets something out of it!





COVID19 Ventilator Strategies, a #FOAMed Webinar.

So really glad to get some solid minds together here to discuss what is being done for ventilator approaches, and definitely looking forward to learning from everyone! Ventilating COVID19 patients isn’t easy and we need to make sure to minimize ventilator injury.

Some of the topics we plan to talk about:

  • ventilator modes, initial, rescue?
  • proning: right off the bat or as needed?
  • weaning: business as usual or a different approach?
  • tracheostomies: business as usual or delay?

Super excited to add Segun Olusanya (@iceman_ex) to the mix, (much thanks for staying up as it will be a middle of the night affair for him!) as well as newcomers – to the largely H&R crew – RebelEM‘s own Salim Rezaie (@srrezaie) as well as airway legend Rich Levitan (@airwaycam).

Register for the webinar here!

Please tweet questions for the webinar and follow @ross_prager for info!





Re-Thinking the Early Intubation Paradigm of COVID-19: Time to Change Gears? #FOAMed#CO

So we wrote this up last week, but the (relatively) slow process of submission made us decide to just go ahead and release it as pure #FOAMed literature, because while highly relevant and somewhat controversial 10 days ago, it is now almost already accepted!  What an incredible (in all senses of the word) time we are in…

So here are our thoughts:


I think it is important to clarify that none of us are saying that ventilators should NOT be used. HFNC or NIV approaches will not avoid intubation and mechanical ventilation for all patients, only for some, and for those it doesn’t, mechanical ventilation is an absolute life-saver. For many laypeople and perhaps non-critical care or acute care physicians, this may have been lost in much of the social media discussion…

For anyone interested in the development of the CAB-RSS score, do get in touch, we are in the process of an inter-observer validity study and eventually will integrate in a decision making algorithm.





Understanding Alveolar Physiology & Ventilation in the COVID Era. #FOAMed #FOAMcc


First watch this:

Now that should be a good start point to realize that there is something most physicians, even those who routinely ventilate patients, overlook. The time constant required to recruit. One can easily picture the rapid derecruitment, then re-recruitment – known as atelectrauma for the novices- which will result not only in only temporary success with recruitment maneuvers (RMs), but likely also contribute to ongoing lung injury. Now in less severe cases of ALI, we “get away with it” and the patient gets better anyway. But when the rate of healing is less than the rate of VILI, we get in trouble. Only – just like aggressive fluid resuscitation – we can be blissfully unaware of the unwitting iatrogenic contribution and feel like “the patient succumbed despite everything we did.” Perhaps, but then again perhaps because as well.

In our shop, with conservative fluid management and aggressive de-resuscitation, ARDS has been seldom seen in the last 10-15 years (versus my first years of practice where I encouraged aggressive resuscitation in the ICU and to my ED colleagues), hence ventilation had become rather uninteresting… But with COVID now I’ve had to dust off my “fancier” ventilation strategies and have been using inverse ratio and APRV (not all our vents can do APRV). It would be fun if it wasn’t for the mortality…

So, what can that little rat lung video teach us?

First, the concepts of pressure-time integral (PTI) and alveolar surface area, things we do not routinely use as mental constructs. As we can see in the video, time is required for the pressure to move into the distal airways and recruit. That is why RMs often run in the 30-60 second range at anywhere from 30 to 40 cm/h2o. We all know that they work, but only transiently, and yes, a higher PEEP is usually used post RM, but this may not represent a sufficient PTI to prevent de-recruitment and continued atelectrauma.

Second, the visual example of heterogeneity. Though the Baby Lung analogy and lung protective concepts still hold, that heterogeneity highlights how a relatively low VT and respecting plateau pressure limits may not sufficiently protect certain more distended alveoli. Indeed, as compliance increases with recruitment, the stress is more evenly distributed across alveoli rather than preferentially in the ones that remain open. Hence a strategy that prevents de-recruitment becomes paramount.

This is where APRV comes in. I used it a bunch a few years ago when working in a center where we received commonly enough and had a bit more ADRS than commonly in my shop.  APRV stands for airway pressure release ventilation, and requires one to completely wipe the mind’s dry-erase board of ventilatory parameters and really just start thinking in terms of pressure-time integral.

APRV is essentially a bilevel ventilation mode over which a patient can take spontaneous breaths, analogous to a CPAP mode with occasional pressure release that allows for ventilation. Though APRV has been around for a long time, the work of APRV guru Nader Habashi and his APRV network have done tremendous work fine tuning their system of time-controlled adaptive ventilation (TCAV) which is a way of setting APRV appropriately to the patient’s physiology. I highly encourage reading their work and resources available – which includes mentoring. APRV isn’t a plug-and-play mode, it is paramount to understand the physiology behind it.

So we need to set P hi, P lo (it’s supposed to be 0 so an easy one), T hi and T lo – and yes FiO2 (at least one familiar one!). So basically you determine how much time the patient spends (this largely determines your respiratory rate) at a certain level of pressure, generally between 20-30 depending on severity of ALI and lung compliance, and how long an expiratory phase they get (really short).  That’s actually the one that needs understanding, because that’s the TCAV sweet spot, how you prevent as much VILI as possible.

You need to think of peak expiratory flow rates (PEFR – yup just like in outpatient asthma!), and adjust the T lo to 75% of the PEFR. This provides what Nader himself describes as the air cushion that remains in the lungs and prevents the alveoli from taking the brunt of the next positive pressure burst, particularly those at the most fragile end of the spectrum.

You need to remember the concept of functional residual capacity (FRC) as this is what we aim for to avoid recruitment-derecruitment.

So, caught your attention? If you have a physiologist’s soul (and if you’re resuscitating patients you really should!), and were not yet using TCAV-APRV, I hope you are thinking about it because it makes sense. And in these COVID patients we may not have the usual margin of safety to do our usual ventilation.

So, please register at the APRV Network, read all their free guideline documents which are great but I will not post as they require you to register (its free), and here are a couple of must-reads by Nader and his group:

dynamic alveolar physiology

history of APRV

And of course Scott has some awesome discussions with Dr. Habashi himself.

Oh yes and as per our Webinar last week, Josh Farkas has been using APRV on his COVID patients with success!


please share your COVID ventilation experience!

…and no offense, but please, though open, this is a blog intended for clinicians, not a forum for lay questions or comments. I simply do not have the time to answer them and will not, and I feel rude deleting them (but will do so) but clinical readers need concise information packaging, so please feel free to read or listen in e-silence. Again, I apologize for this recent necessity.