Working out the Clinical Kinks in Venous Congestion: A Discussion w/Rory & Korbin. #FOAMed, #FOAMcc, #FOAMus

It’s really exciting to be at the outer frontier, trying to figure out some new clinical areas. Now these have all been described, however the ability of clinicians to properly identify certain pathophysiological findings has been limited prior to POCUS. Following the trail being blazed by Dr. Andre Denault, we are also working on expanding the applications, particularly in resuscitation/deresuscitation and CHF/AKI. There are more questions than answers, but that’s exactly why it’s interesting.

So for those unfamiliar with the topic here is a small intro:

And for those following, here is the discussion:


Do expect more from us about this. Watch this space. It is practice changing.


Additional resources:

Here’s a link to the article referenced during the recording:

Andre and I discussing venous congestion

…if you dig around the blog in the past year there are a bunch more!


do share your thoughts!





Fluid Stop Points! More POCUS goodness from Korbin Haycock. #FOAMed, #FOAMcc

I am really enjoying this exchange, and I think it is in the true spirit of #FOAMed to foster these discussions, as we have the opportunity to combine and fine tune our understanding of a topic from several really bright people’s view and experience. 


Jon-Emile, excellent points and insight. I should clarify a couple of my comments. To be specific, by “renal vein flow” I am referring to intra-renal venous flow. Apologies for my imprecision! Thanks for pointing that out.

Yes, a lot of these renal and portal Doppler patterns are surrogates of CVP. But I don’t think any of us would use CVP in isolation these days to make any decision what-so-ever on whether fluids were indicated in our patient.

Also, to clarify, I am not using intra-renal venous flow or renal resistive index as measures of non-fluid responsiveness. Rather, I use these measures as a stop point for attempting to solve the patient’s hemodynamic dysfunction with crystalloid regardless of whether or not my straight leg test tells me the patient is still fluid responsive.

And that is a key re-iteration to me. It is important to set these stop points and not only look at whether the cardiac output can be maximized. This has been tried. And failed. Let’s remember that sepsis is not inherently a disease of low flow. It isn’t cardiogenic or hypovolemic shock at the core.

My rationale for the strategy of using intra-renal Doppler, E/e’, and Lung US (now, I can include portal vein pulsatility) as a stop point for IVF administration is that I think the patient is best served to avoid iatrogenic edema of the upstream organs, primarily the lungs and the kidneys. These are the two organs (maybe you could put the endothelium in this category as well–glycocalyx being a whole other can of worms!) most easily damaged by the chase for optimizing every bit of fluid responsiveness. We have good evidence that getting wet lungs and swollen, congested kidneys is a bad thing, and we have these tools to hopefully warn us when we are pushing things too far.

Absolutely. And the whole glycocalyx is something to keep in mind, even if only to me mindful to disrupt it as little as possible.

Of course renal resistive index, intra-renal venous flow, portal vein pulsativity, and whatever else you like will have limitations and confounders. As long as you understand what can cause abnormalities with these tools, you can make an educated guess as to what’s going on. If our creatinine is off and our RRI is high, but intra-renal venous flow and portal vein flow is normal, perhaps the RRI is caused by something other than renal congestion, like ATN. If the portal vein is pulsatile, but the Doppler patterns of the hepatic vein, kidney and the heart look ok, maybe something else is wrong with the liver. But, if all our modalities are in agreement and pointing to congestion, we should perhaps believe that it’s congestion and stop the fluids. 

That is an awesome approach to integrating RRI. I’ve been toying with it for the last couple of days, and much thanks to Korbin, I think that the limitations of RRI can be overcome by using the rest of our clinical and POCUS data.

It isn’t a hard technique, though in some patients getting a good signal can be tricky.

I think that the kidney, being an encapsulated organ, and the fact that much of our crystalloid ends up as interstitial edema, the kidney will develop sub-optimal flow patterns before CVP would cause congestion. The same is true regarding the lung, except that it’s just related to increased pulmonary permeability due to inflammation. Regardless, the idea is to save organs, and the earlier you can detect the problem, the sonner you can stop battering the more delicate organs with fluid.

As I think we have all mentioned, you really have to look at the whole picture, and put it together to tell the story of what is wrong, so we can logically and thoughtfully treat our patients.

I really appreciate this discussion. Thanks!



Thanks to Andre, Jon and Korbin for making this very educative for all!





ps don’t miss the POCUS Workshops on venous assessment at  !!!

Jon-Emile (@heart_lung) chimes in on the whole portal vein POCUS! #FOAMcc, #FOAMed

When it comes to physiology, there`s no doubt that Jon is the man, so I was really curious about his take on all this, which, no surprise, is definitely worth sharing, just in case everyone doesn`t go read the comments.



Wow; there is a lot to unpack here.

My first comment is that intra-renal venous flow [*not renal vein flow], hepatic vein flow, portal vein flow, etc, etc, etc [as well as IVC size and respiratory variation] are all ultrasonographic transductions of the central venous pressure …so I’ll give my boxed disclaimer that volume status and volume responsiveness cannot definitively and reliably obtained from this marker because the CVP is too complicated to make these physiological leaps.

Indeed. It is important to realize that, as Jon states below, that the angle for looking at the PV in this case is to assess congestion, rather than responsiveness or the ever-so-nebulous ‘status.’

Wait for it … volume tolerance and the CVP, is a bit more nuanced, i think.  with a high CVP, you really have to ask yourself – **why** is the CVP elevated and go from there.  if the CVP is elevated because of tamponade, its very different management from a high CVP from a massive PE or air-trapping versus a high CVP from volume overload.

Absolutely. Diuresing a pre- or full-fledged tamponade, PE or air-trapping could have disastrous consequences, i.e. PEA arrest!

There seems to be some confusion about *the renal vein* versus *intra-renal vein*.  the lida trial is clear that it is intra-renal vein flow.  i am not terribly familiar with *the renal vein flow, however, my hunch is that renal vein flow should always be biphasic [just as the jugular venous flow, SVC flow, IVC flow and hepatic vein flow are always biphasic] – that is a normal pattern close to the right atrium.  normally the systolic inflow velocity is greater than the diastolic inflow velocity and there is fairly good data correlating reversal of systolic to diastolic venous flow ration to right atrial pressure [in the IVC and SVC].

Definitely the intra-renal vein should be the target here – not always easy in some patients, because the renal vein itself, especially the right (no crossover) really has an IVC pattern and won`t necessarily reflect the effect of intra-renal hypertension.

The pulsatility that evolves in the intra-renal vein as the CVP rises is beyond me, but the authors postulate that it has to do with the compliance of the vein at higher CVP and intra-renal interstitial pressure which makes some sense.  But it is important to note that the compliance curves of an intra-renal vein and *the* renal vein are probably quite different.

Secondly, the pulsatility of the PV is a neat idea because of its relative ease of assessment.  However, the pulsatility, presumably, is due to the PV encroaching the limits of its compliance curve – the PV, like the CVP – has an inflow and outflow pressure.  It is highly likely that a pulsatile PV in a post-operative cardiac patient relates to an angry RV – but is this always true?  What about the cirrhotic?  What about differential partitioning of fluid into the splanchnic bed versus the lower body?  What about differential expression of adreno-receptors between splanchnic arteries [beta and alpha] and splanchnic veins [mostly alpha].  My point is that there could be *other* inflow and outflow differentials that are affecting PV volume, compliance and therefore pulsatility that are not yet recognized.  A cirrhotic on bomb dose phenylephrine/vasopressin may have their splanchnic venous volume recruited with blood expelled towards the liver, an engorged PV that is pulsatile – but is that RV failure?  Is that a patient who needs to be decongested?  I don’t know.

Thirdly, there are complex cardiac contributions to venous flow phase and vein pulsatility such as arrythmia – atrial compliance, etc.  As the comment above notes – how might afib contribute to SVC or IVC venous inflow?  It’s hard to know, but my hunch would be that afib itself would tend to reverse the normal S wave: D wave supremacy … that is, decrease the normal systolic inflow velocity relative to the diastolic inflow velocity.  if the atrium is not emptied fully then its pressure with rise.  if atrial pressure rises, when the atrium is pulled downward during ventricular systole, the S wave will be diminished.  additionally, the more chronically dilated and poorly compliant the right atrium, the greater its pressure will be with the loss of atrial kick.

Fantastic points. Again, looking at POCUS metrics CANNOT BE DONE IN ISOLATION, from the rest of the POCUS and clinical data.

Lastly, the venous inflow pattern analysis approach to CVP estimation – i think – is better than IVC size and collapse because of how IVC size and collapse can also be affected by IAP, ITP/PEEP, etc.  Because ITP affects systolic and diastolic inflow patterns similarly, that confound should be lessened.  Nevertheless, as Dr. Denault mentions in the cases above – you have to treat the patient!  This means integrating what the data is telling you in the patient in front of you.  If in a certain clinical context the test results do not make sense, it’s probably a false positive or false negative test.

I dug up this gem from 30+ years ago. Excellent paper [ – “Ultrasonic assessment of abdominal venous return. I. Effect of cardiac action and respiration on mean velocity pattern, cross-sectional area and flow in the inferior vena cava and portal vein”].

Ok that’s on my short reading list for the next 48h!

They show the venous inflow waveform for the IVC [presumably very similar to *the renal vein]; Afib *does* cause the S wave to become attenuated – so it would change the normal biphasic form to more of a monophasic form. In theory, giving a calcium channel blocker and slowing the patient down should improve this somewhat. They even have a brief discussion on portal vein pulsatility.

This venous inflow stuff is very interesting and potentially very applicable. @iceman tweeted out wave velocity patterns in the MCA during high ICP – indeed – an increase in ICP renders the flow more pulsatile and then there is loss of diastolic flow. Probably similar physiology for an intra-renal vein as intra-renal capsular pressure rises. A good sign that the kidney is under pressure!

Thank you Jon for some really excellent physiological points and the reminder that, in POCUS just as in clinical medicine, we cannot rely on one assessment, and that measure must be considered in the context of the factors affecting it. Otherwise, we are not truly tailoring our therapy to the patient, but only pretending to.

Don’t miss Jon and the POCUS workshops at  next april!

The Resuscitation Tracks 1: Portal Vein POCUS with Dr. Andre Denault. #FOAMed, #FOAMcc, #FOAMus

So this is one of the key discussions I wanted to have in my process of synthesizing my resuscitation algorithm. Dr. Denault is the one guy I’d call a mentor, and I think one of the rare and true clinician-scholar, who is just as comfortable being the anaesthetist/intensivist at the bedside of the crashing patient as he is being the keynote speaker in major conferences, or writing the textbooks that lead the field in acute care/perioperative TEE and critical care POCUS.

So to put some perspective to this discussion, back in 2014 I organized a resuscitation afternoon for internists with Andre and another awesome guy you probably all know, Haney Mallemat (@criticalcarenow). In a quick 15 minute discussion between talks, he shared with me the most recent of his discoveries, portal vein POCUS as a marker of right-sided failure/volume overload in his post-op cardiac patients, and how aggressively managing these resulted in much improved post-operative courses in terms of weaning, vasopressors and even delirium.

Interesting stuff.

So here you are:

So I’ll let you all ponder that and I would really like to hear comments and ideas. Sometime in the next few weeks I’ll be finalizing my resus algorithm – which will not be a recipe approach, as you might suspect if you have been following this blog, and will rely heavily on POCUS and the clinical exam.

cheers and thanks for reading and listening!

Don’t miss Andre running a POCUS workshop on PV/HV at  next april!



Bedside Ultrasound Quiz Part 2: A 50 yr old man with dyspnea, acidosis, hepatitis and leg edema. #FOAMed, #FOAMer, #FOAMus

So I was glad to see some great answers on twitter about this case, so let me fill you guys in on the management and the details.

So my diagnosis was of a (likely viral) myocarditis as a subacute process over the last weeks, with a superimposed pneumonia causing the acute deterioration and presentation to ED.  I didn’t think that his elevated lactate represented shock, but rather a reflection of adrenergic activation and reduced hepatic clearance due to congestive hepatitis.  He also had congestive renal failure. Of course, the LV had a 4 x 2 cm apical thrombus, which is likely secondary to the dilated cardiomyopathy.

So the management was diuretics, antibiotics, and anticoagulation, which resulted in a gradual improvement of the respiratory status and renal/hepatic dysfunction. He had a coronary angiogram the day following admission which showed two 50% stenoses deemed to be innocent bystanders.

Bottom Line:

I think the learning point in this case is that, without POCUS, this could easily have been treated as severe sepsis with multiple organ failure (potentially rationalizing away the BP of 140 as a “relatively low” BP due to untreated hypertension), and as such, may have received fluids… Especially south of the border where they are mandated to give 30 cc/kg to anything deemed “septic.”  This would have been the polar opposite of the necessary treatment.

The scarier thought is that he may have then progressed to “ARDS,” been intubated and then the debate between keeping him dry and giving fluids for the kidneys may have ensued.  Though a formal echo likely would have been done, it may not have happened in the first 24-48 hours… If MSOF progressed and he succumbed, the rational may have been that he was “so sick,” and died despite “best care…”

The reality is that he is not yet out of the woods today, with an EF of 15% and afib, but he is off O2 and sitting up in a chair. Fingers crossed he falls in the group of those with myocarditis who improve…

Love to hear anyone’s thoughts!




Hepatic Portal Venous Gas (HPVG): a Less Ominous Sign than We Thought? A Case of HPVG associated with massive PE… #FOAMed, #FOAMcc

So a few years ago I had a patient in the ICU, post op for some abdominal surgery, and, using POCUS, I detected a hyper echoic area in the liver, in a wedge shape.  I scanned the patient and, lo and behold, there was a matching area of air-filled hepatic venous sinuses on CT scan. Well, my surgical colleague and I were very concerned and proceeded to inform the patient he would be needing exploratory surgery for what was likely ischémie bowel. He essentially – though in more polite words – told us we were idiots and that his belly felt fine and he didn’t think surgery would be needed at all.

His belly did feel fine. So were his labs. So we worried, but, given this whole thing about free will and consent, etc, couldn’t very well force him into what we felt was necessary surgery.

The next day he was fine. On POCUS, the area of air had shrunk. The next day, it was gone altogether.

We thanked him for his keen clinical acumen and for teaching us a good lesson.

However, we were a bit perplexed, because traditional teaching equated portal venous air with a severe bowel disorder, usually ischemic or inflammatory, with exceedingly high mortality. At least that is what we had been fed. We are both grads of 1999. Hmmm…

So over the next few years we saw a few of these cases, sometimes bad, sometimes not, and a review of the literature (see below)  showed an interesting evolution of the disease. Described in the 1950’s on plain films, hepatic air was a bad omen indeed, with mortality in the 75-90% range. In the CT era, the mortality started to “drop” to the 35-60% range. Now you can find quite a few reports of “surprisingly” good outcomes with conservative management. So this evolution doesn’t represent a change in severity so much as the technological capability to detect smaller and smaller amounts of air in the venous system – just increased sensitivity. And now, with POCUS – ultrasound is the most sensitive detector of air in a vascular tree – the associated mortality is likely to take another drop, not only because of our ability to detect very small amounts of air, but also because we are actually looking at the area, and also in a wider range of patient’ pathologies that those commonly associated with HPVG.


Clinical Case: HPVG and PE!

So a couple weeks ago I saw a patient in the ED who’d recently broken an ankle, had her foot put in a boot and managed conservatively and came back dyspneic and tachycardic. Here are a couple of clips:

As always, I start with the IVC:

Big & fixed.

Hepatic veins:

Biphasic flow.

Femoral veins:

So here the source of the problem is pretty clear, a large common femoral DVT.

She wasn’t very echogenic so I don’t have great clips of the heart but she had a dilated and hypocontractile RV with a McConnell’s sign (preserved apical contraction), small and hyper dynamic LV with septal flattening.

Now here is where it gets interesting, the portal vein:

You can clearly see bubbles traveling up the portal vein. Ominous, or not?

So clinically, her abdomen was normal, she had no abdominal symptomatology at all…


Pathophysiological musings:

So the severe RV obstruction resulted in significant venous congestion. Additionally, the decreased cardiac output – as manifested by a lactate of 4 and mild tachycardia/hypotension (110 HR, BP sys 90’s) was clear.

The etiology of HPVG in the literature isn’t clear – mucosal disruption, bacterial gas are all mentioned but as far as I could find, no definitive answer.

Is it possible that there is a “normal” inward leak of mucosal gas that is normally fully dissolved in the venous bloodstream, but that, in cases of low flow and/or venous congestion, the dissolution capacity (per unit time) decreases, and that gas comes out of solution?  Alternately, those who have increased intraluminal pressure (gastric distension, etc), the increased transmembrane gas driving pressure may overload an adequate blood flow…

This would explain the benign course of many patients, particularily those with gastric dilation.


Clinical course:

Based on hemodynamics, tachypnea and, to some degree, venous congestion, I decided to thrombolyse her using 1/2 dose lytics. Within a couple of hours her HR decreased to the 90’s and BP rose to 110 systolic.  Echographically, however, the IVC/RV findings remained similar, but the HPVG decreased. By the next day, HPVG was altogether gone, lactate had resolved and dyspnea was significantly better.


Take Home Message:

HPVG, although not quite as poor a prognostic sign as once thought, nonetheless warrants concern and investigation, even if the abdominal exam is entirely normal and without symptomatology, as correction of an underlying cause of “benign” HPVG (whether low-flow or bowel distension) would still need to be addressed.

In the meantime, I suspect that, reported or not, this has been noted by other POCUS enthusiasts, since we are now looking more frequently at this area, and are dealing with patients with low-flow states, congestion, bowel obstruction/ileus or more than one of these.

Hopefully some investigators will take a look at this phenomenon and delineate the pathophysiological mechanism!

Love to hear of your experience with this.




For those interested in POCUS, see here for a quick read primer on clinical applications of POCUS.


HPVG Review article 2009:



The NYC Tracks with Jon-Emile part 2: a discussion on congestion, pulmonary and otherwise. #FOAMed, #FOAMcc, #FOAMus

So here is our second discussion, where we delve a bit into diuretic physiology, the issue of organ congestion, the myth of the “low-flow” acute renal failure associated with CHF (see earlier post), and a couple other things including a great way to determine if a patient isn’t respecting the low salt diet prescription!

I meant to, but forgot to discuss with Jon what I think is an important end-point in CHF management: the IVC. Yes, it is useful not just to make the diagnosis of congestion, but also target normalization of IVC physiology prior to discharge. It just makes common sense. If you decongest a patient just enough to get them off O2 and send them home, they bounce back a lot quicker than if you make sure you’re given them some intravascular leeway.  How do you determine this? Simple enough, make sure your IVC is down at least to below 20mm, and has recovered the classic acxvy and respiratory variation. I personally try to get into the 8-12 mm range, but that’s arbitrary. Here is some good data for 20mm:


Without further due, here is the NYS Track 2:


Please share your thoughts!