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!





Renovascular #POCUS: Technique with Korbin Haycock. #FOAMed, #FOAMcc, #FOAMus

Korbin Haycock, ER doc extraordinaire.


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.

Love to hear comments from anyone using this!





CHF-associated Renal Failure: Low-Flow…or not??? #FOAMed, #FOAMcc

So here’s a common enough clinical scenario:  An elderly patient with CHF presents in exacerbation, requiring significant oxygen and eventual NIPPV. He is admitted to a critical care bed.  The next day, it’s noted that his creatinine has almost doubled. He remains on NIPPV. The intensivist is hesitant about how aggressively to pursue diuresis: he’s worried about worsening the “low-flow state” and the renal function.

I know I grew up hearing that as a resident, and never questioned it. On the surface, it makes plenty of sense. Someone with CHF has a “bad heart”, pre-renal failure is a definite entity, so why not?

So let’s examine those assumptions. First of all, not all patients who present with CHF actually have a bad ventricle, some may have valvular heart disease, hypertension with elevated filling pressures, etc… Secondly, few of our CHF patients are really in a severe “low-flow state”, since that would essentially be cardiogenic shock, a very different entity, even if along the same spectrum. More importantly, however, the renal autoregulation curve is actually broader that most of the rest of our tissues and organs. That makes it unlikely that, in someone normotensive (as most patients in CHF tend to be), worsening renal failure is attributable to a “low-flow state”.  The ARF attributable to a low-flow state – which we see often enough – is the organ failure resulting from shock: shock liver, shock kidneys, etc…

So…what could it be?  Let’s continue to apply basic physiological principles. What is the pathognomonic feature of CHF?

Congestion: pedal edema, ascites, effusions, anasarca, etc…

What if we had…congestive renal failure?

I have to credit a bright colleague of mine, Dr. Jason Fung (, for putting me on that track. As a bedside sonographer, what I could see in most of these patients is that their IVCs were still really full, and that most didn’t have other clinical signs of poor flow such as cool extremities and decreased mentation. And given that they were still in significant respiratory failure, I felt they needed diuresis. Also, the full IVCs suggest that these patients are on the flat part of the Starling curve (after all, that’s what the fluid retention causing CHF is trying to do!) and that they should not suffer a drastic drop in cardiac output with ongoing diuresis.

Well, Jason was the first to point out to me that the elevated IVC pressure (CVP) is directly downstream from the kidney! And directly by a couple of inches, the length of the renal veins! I have to say that was an embarrassing lightbulb moment, but a lightbulb moment nonetheless.

So let’s review renal blood supply and flow physiology. As is the case for any organ, the following applies:

Q = (P art – P ven) / R

where Q is renal blood flow (RBF), P art is MAP and P ven is CVP, and R is the renal vascular resistance.

Let’s keep that in mind.

Uniquely, the kidney has two set of arterioles which modulate the GFR and allow for the celebrated autoregulation curve. The resistance of each is controlled by the number of factors, hormones and drugs.

The reason P ven is CVP is that the renal vein drains directly into the IVC, which drains in turn into the RA, the pressure is the same. Now some of you may have read my rants against CVP in some of my posts (see, but that is in reference to its use as a marker of preload and volume responsiveness. When the answer one is seeking is the downstream venous pressure, barring some pathological venous obstruction, CVP is it.

Hence, the higher the CVP, the lower the RBF.

This makes complete sense, but how often has anyone heard this mentioned in the management of renal dysfunction in CHF patients?  As in the case for many things in medicine, we often forget (or are not taught to) link basic physiology (all that medical school stuff…) with clinical pathophysiology (…the “real” world).

Well, it turns out that fortunately, a bunch of smart people have been looking into this matter, and the best study in my opinion is by Mullens et al (JACC vol 53, n 7, 2009), which reveals a clear increase in prevalence of worsening renal failure with increasing CVP, but more interestingly, the lack of significant association between cardiac index and worsening renal failure, which is the “low-flow” traditional hypothesis.  The most clinically important finding in this study, however, is their finding that failing to reduce the CVP to below 8 resulted in a 51% incidence of renal failure (vs 18% for those patients who were reduced to a CVP < 8mmhg).

An excellent review for this was recently published by Gnanaraj et al (Kidney International 83, 384-391, mar 2013), which reveals a fairly strong association between an elevated CVP and renal dysfunction.

So it seems fair to conclude that congestive renal failure is an under-recognized clinical entity that is commonly untreated (or even improperly treated) due to unfounded and unphysiological concerns.

Now something our group will be focusing on is a study on the use of IVC sonography in the assessment of CHF-associated renal failure. We believe that IVC ultrasound will provide a better, simpler and less invasive method to assess renal congestion.

The use of IVC ultrasound in CHF would not be new:  Goonewardena et al (JACC Cardiovasc Imaging 2008; 1, 595-601, or found that IVC size at discharge was the best predictor of readmission. In other words, if someone didn’t get your IVC down below 20 mm, you were much more likely to be readmitted.

As an ICU physician, I rarely discharge patients home.  But I do make sure I get IVCs into a normal range (below 15mm generally) before my CHF patients leave my unit, and, especially recently, I do make sure to continue diuresis when faced with a distended IVC with little variation and worsening renal failure.

This is certainly a topic that merits further study, but I think there is enough good evidence and physiological rationale to hang up those old beliefs in a dark closet and start treating congestive renal failure.

Please let me know what you think, what your practice experience is, and if you have anything else to add!

thank you,

Philippe Rola