Venous Congestion from different Clinical Standpoints. #FOAMed, #FOAMcc, #FOAMus


So last week sometime we had an interesting twitter exchange which made me realize it is important to explain how some of us are using venous POCUS in different clinical scenarios, which is key, because the development of monosynaptic clinical reflexes with POCUS findings is a rabbit hole we should try not to go down. Instead, POCUS should be about asking the right question and taking that answer as a piece of the pathophysiologic puzzle facing us, which may mean intervening sometimes, and sometimes not, for the same given finding, but with different surroundings.

Here is the twitter exchange.

Thanks to those involved in that discussion – it is how we grow!

And here are some thoughts:

For those not up to speed on venous congestion POCUS I put up the chapter that Korbin Haycock, Rory Spiegel and I worked on in this earlier post.

Love to hear your thoughts and experiences!





Another interesting question from @JCHCheung! #FOAMed, #FOAMcc

So here’s another interesting question as a follow up to the previous discussions:

Most people would probably agree that florid congestive signs on POCUS means the RV is unable to pass any more extra volume to the left heart; whilst the absence of those signs mean that the patient may be able to cope with some additional volume without immediately engorging the vital organs.

And my question is: what about those in between? i.e. the patients who start to develop some mild congestive features on POCUS.

For those who are on the verge of congestion, diuresis would push the RV to the left (i.e. steep part) of Starling curve resulting in significant CO drop; conversely, extra volume pushes the RV to the right (i.e. flat part) leading to congestion or even D-shape LV, directly hindering CO as well. This margin becomes even smaller in patients whose RV starts to fail (i.e. entire Starling curve shifted downwards)

Great, great question. The crux of this, I think, is deciding which is the greater issue, congestion or poor perfusion. Obviously they are intertwined, so the decision will be on a case by case basis. Jonathan alludes here to a narrow “balance point” between congestion and preload dependancy. My feeling – and we’ll see if we can get some consensus – is that this indeed narrow in patients with marked pulmonary hypertension. When patients have pure pump failure congestion, my clinical experience is that you can decongest plenty without drop in systemic CO, in fact it often improves, likely related to ventricular interdependance. So let’s go on…

I’ll illustrate my point with the following scenario:

for previously healthy middle aged patients intubated and admitted to the ICU for ARDS from severe pneumonia, they quite often develop some acute cor pulmonale after mechanically ventilated for several days even if the PEEP/driving pressure isn’t exceptionally high; and they usually have resp failure and shock to start with.

Given that they don’t have pre-existing heart disease, the only signs suggesting the emergence of cor pulmonale could be subtle, without structural changes like dilated RV (RVEDD at most at upper normal range) nor abnormal septal movements. You may see TAPSE dropping to marginal level and portal vein PW signal may become a bit more pulsatile. IVC looks full and RVSP usually rises but not skyrocket. The MV inflow pattern & E/E’ suggest rather normal LA filling pressure, not surprising from a previously healthy heart.

In this case, it isn’t the LV diastolic dysfunction that overly afterloads the RV; and it isn’t the RV dilation that impairs the (D-shape) LV from ventricular interdependence. Therefore I’d consider the right heart circulation & left heart circulation running purely in series, whereby limiting the RV preload could reduce the LV CO.

Now, if this patient goes into shock, would you consider fluid challenge or diuretics? Everyone probably would also get other therapies on board, e.g pressor, inotrope, source control etc. But when the patient’s BP is 80/40mmHg, I am more prone to giving some fluid as I believe that reducing preload in a septic patient can precipitate arrest; and that RV only directly impairs LV CO once the IVS starts to shift, which should take more time and thereby easier to monitor.

Interesting case that happens commonly – if you do POCUS and look for it rather than blind-ish management. Here, you have congestion, likely due to pulmonary disease, fluids, on a normal-ish RV (which also means it is unable to mount a huge PAP).

So personally – and will full disclosure that this is not evidence-based (as if there was any evidence in our resuscitative practices!), I would consider this a relative contraindication to fluids, given the non-volume-tolerant state (ALI/pneumonia/ARDS and portal pulsatility) of the patient. With pulsatility and signs of organ dysfunction I would be diuresing or pulling fluid off. We’ll see if we can get Rory to comment, as he has been doing a fair bit of this.

So in this patient it would be either no fluids, or diurese.

I don’t think one should have a general conception that reducing preload in a septic patient category is an issue. That may be so if you do not have the capability to look, and hence feel you should behave more cautiously. A septic patient with a tiny IVC may indeed be tipped over into low CO by removing fluids, but another with a full tank post resuscitation may benefit. So with the ability to assess hemodynamics, individualized approaches trump general ides and protocols. Much more to come on this in the next weeks as we break down a lot of interesting concepts in regards to vascular tone assessment and cardiac efficiency. 

I fully appreciate how ambiguous this situation is and that in reality the only way to find out the treatment that works is often by trial and error. Serial assessment by POCUS is definitely needed and one may even put the entire fluid thing aside and focus on other treatments. But just want to know your take and the reasons behind.

Thanks again for all your work and these thought provoking posts; and my apologies for the supposedly quick question ending up being not so quick. It took me some effort to clearly delineate my question in mind.

Anyone interested in these topics should keep an eye out for the H&R2019 Tracks. A bunch of us are getting together before and during the conference and will be recording discussions on all these little cases and angles around hemodynamics and other fun resuscitationist topics.






POCUS & Venous Congestion: a #FOAMed Collaborative Chapter.


So given the importance of these topics, the number of questions and discussions we’ve had on the twitterverse, and most importantly in the spirit of #FOAMed, here is the chapter from the POCUS book which was co-authored by Rory Spiegel (@EMnerd), Korbin Haycock (@korbinhaycockmd) and myself.

Venous Congestion Chapter

We’re also in there introducing our VEXUS score, and if anyone wants to use/validate it clinically, please do!

Love to hear anyone’s thoughts!


PS we’ll all be at H&R2019 and running workshops on venous congestion:

The rest of the chapters are here on Amazon and the e-version here on iTunes!





TCD in the ED? A discussion with Jeff Scott. #FOAMed #FOAMer #FOAMcc

So a couple weeks ago I had the chance to sit in sunny Florida with Jeff Scott (@jsemccm), an ED-intensivist who runs the ED at Jackson South in Miami as well as rounding in the ICU at Jackson Memorial.

His group recently published an awesome article on TCD that pretty much made me realize I have to up my TCD game to the next level.

Here it is (unfortunately walled…)

And here is our discussion:

So there clearly is more to be done with TCD than I have been doing, and maybe it really has a place in the ED. I don’t work first line in the ED so initial stroke patients I only see if they deteriorate, but the idea of visualizing perfusion – or reperfusion – is really interesting.

So if you want to meet Jeff and have him teach you some POCUS TCD, don’t miss H&R2019 which is just around the corner. There aren’t many spots left! Jeff will be running a TCD workshop along with Rob Chen (@ottawaheartrob) which I’m really looking forward to!

Love to hear from anyone pushing the envelope of TCD (or any POCUS application). I believe we are only scratching the surface of what we can do with POCUS, and much study, based on front-line clinicians taking bold strides ahead to see what can be done.






My friend, the IVC. #FOAMed, #FOAMer, #FOAMus, #FOAMcc

So I keep hearing and seeing people bash the IVC. Casually dismissing it with a shrug. “It’s not really good for volume responsiveness, you know…”

All that deserves is an eyeball-rolling emoji. That is, unfortunately, the reaction of docs who are trying to devise a threshold or recipe-based approach to POCUS management (which will be just as bad as any recipe-based medicine) as opposed to physiological understanding of what is going on with the patient.

There’s so much good information packed in scanning the IVC (properly, in both axes – for more, see a bunch of my previous posts), and frankly, volume responsiveness is the least of my concerns, that it is a shame to toss out the proverbial baby with the bathwater.

So I talked about this at Stowe EM – an awesome conference run by my friend Peter Weimersheimer (@VTEMsono), which I highly recommend to anyone for next year, great talks, people and spot:

Here are my slides:

IVC Stowe

And the audio:


Love to hear your thoughts!

Oh yes, and anyone looking to explore physiological, evidence-based, cutting- and bleeding-edge approaches to resus, don’t miss H&R2019 this May in Montreal!




Another POCUS HPVG case… Critical…or not? #FOAMed, #FOAMcc

So a couple years ago I posted a discussion about HPVG around an interesting case, noting how, although traditionally felt to give a poor prognosis, this was extrapolated from early data when it was being detected by conventional radiographs. This simple fact, due to the relatively low sensitivity of radiographs for air in the portal system, meant that these cases had a lot of air, implying a worse underlying process that that detected by POCUS, which is exquisitely sensitive to the detection of air bubbles.

Had another interesting case today which I tweeted. This is an elderly patient, POD#3 for a subtotal colectomy for an obstruction, in the ICU with severe AKI. When scanning his RUQ for fluid tolerance assessment, here is what I see:

Impressive. Frank bubbles coming up the PV, and the liver parenchyma with extensive HPVG. He had some abdominal pain, but he was not in shock (at least not pressor or lactic acidosis shock). My first reflex, since he was in AKI (non pre-renal and non obstructive, and with new evidence of loss of integrity of the bowel mucosa, was to get the surgeons to go take a look.

We agreed to scan first and take it from there. Their view was that, given the absence of frank shock, they were not keen to go back in. I have to say I would have preferred that they did go take a look straightaway, but, as they pointed out, opening someone up is not entirely without drawbacks.

So the scan was equivocal, with some air noted in the mesenteric vessels and possible in the mucosa of a bowel loop. Clinically he had not deteriorated. In the meantime, we had stopped his early enteral feeds and put his NGT on suction.

So I took another POCUS look, figuring that if things looked worse, I might take another charge at the surgical team:

Lo and behold, things had resolved… Biochemically, not much change either, and hemodynamics still fine.

So clearly, at least today, the decision to not operate was the right one. Kudos to the surgical team. And it was a more risky decision than that to operate, since the consequences of missing something correctable are worse than those of an unnecessary “white” exploratory laparotomy…

So what did happen? In all likelihood, the post-op ileus on an ill bowel resulted in some dilation and “mucosal leak.”  The NG suction likely decompressed the bowel and allowed the circulation to clear the HPVG.

So the lesson for all POCUS users is that we are using a highly sensitive tool for HPVG, such that this finding is certainly more common than commonly thought, and should be concerning but not necessarily ominous or requiring surgical intervention. Certainly close monitoring and repeat assessments, clinical, POCUS and biochemical are important.

The challenge will be discerning the cases that do need intervention, which is not simple, since waiting for shock or hemodynamic instability would represent a late intervention, likely with poorer outcomes – surgery on vasopressors is a bit suboptimal.

Love to hear comments and others’ experience!





The Andromeda-SHOCK trial with Korbin Haycock and the Nuclear Bomb Approach to Sepsis. #FOAMed, #FOAMer, #FOAMcc

So managed to pin another really bright guy down today and get his thoughts. Of course we digress some, but I think in all the topics that are truly important to sepsis resuscitation.



So I think all the resuscitationists I have spoken to tend to hover around the same common points:

  1. lactate is a marker of severity of insult/injury/inflammation but NOT something to specifically treat with an automatic fluid “chaser.”
  2. getting a global assessment of the patient’s perfusion – including things such as CRT is important.
  3. a strategy that seeks to exterminate fluid responsiveness is non-sensical and pathological.

The nice thing for our southern neighbours is that this study may give you a solid excuse to shake off that lactate mandate.

And I think that Korbin’s ending remarks are important, and it is something I try to teach residents, that there is little value in rapidly normalizing hemodynamic values – which treats the medical team very well – if there is an aftermath that is not beneficial for the patient. Kathryn Maitland’s FEAST study is the real groundbreaker for that concept. So probably a coordinated and careful ground assault is better than dropping the nuke.

 For more discussion on this trial check out Rory Spiegel’s breakdown at and our discussion at



a couple points:

First, much thanks to Scott Weingart whose technical pointers are improving my audio quality! Still a ways to go but on the path!

Second, if you’re not registered for H&R2019, there’s only about 20 spots left. And only a handful for the much-anticipated Resuscitative TEE course. Don’t miss out. If you enjoy these discussions, there will be plenty of that, especially in the protected meet-the-faculty times.

And finally, though he doesn’t yet have a blog, you can now follow Korbin on twitter @khaycock2!