VEXUS Lite: Screening for Venous Congestion with Handheld POCUS. #FOAMed, #FOAMus

So recently a colleague asked me about one of my twitter posts where I had put a clip of doing venous congestion assessment using a handheld – which is without pulsed Doppler (PW).  Since VEXUS is predominantly based on Doppler findings, seems like 2D and colour might not cut it, but can it be done in a screening or “lite” fashion?

Definitely. Here is a mini-discussion about it, and some clips below to illustrate.

 

Pulsatile PV

Clearly Pulsatile PV likely near 100%

Ascites, plethoric IVC, pulsatile PV, markedly abnormal HV with “police siren” appearance due to substantial retrograde flow – likely VExUS 3 or C.

Normal looking HV

Markedly abnormal HV

 

Love to hear some questions or comments!

 

of course, lots of VExUS discussions with William Beaubien Souligny, Andre Denault, Rory Spiegel, Korbin Haycock and myself at H&R2020!

cheers

 

Philippe

 

The Resus Tracks: Trans-Pulmonary Dilution Catheters in the ED…myth or reality? #FOAMed, #FOAMer

So anyone who knows Korbin (@khaycock2) realizes he is a true trailblazer in the ED, essentially doing cutting edge critical care from the get go in his shock patients. In my mind this should be the goal for any critically ill patients, that they get the highest level care right at entry and for however long they may be staying in the ED until they get to the ICU.

So today, I was really happy to corner Korbin lounging somewhere in sunny California (as 6 inches of snow come down hard in Montreal) to tell me how he is using this technology in his resus patients.

 

 

So this has got me interested in using this technology. I see it as an early warning signal that your patient may be less fluid tolerant than you may think, and that the signs of pulmonary fluid intolerance I use (oxygen requirement, appearance of B lines (FALLS Protocol-style), etc…) have yet to manifest.

So I’m looking forward to hearing Korbin explain this further (during H&R2020!) and in actual cases where the change in management is clear.

 

cheers

 

Philippe

 

 

 

 

A few words on venous congestion, thresholds, and physiology. #FOAMed

 

So I’m really glad to see that recently, a lot of discussion has been taken place on the topic of right sided failure and venous congestion, which has huge clinical applications. Even more so, the fact that a lot of individual practitioners have taken this on and have been applying it clinically with physiological results is really amazing.

So a common question that has been popping up revolves around clinical thresholds of significance, and I thought it was worth clarifying that we need to stay away from a pure threshold approach, but rather try to embrace a holistic cardio pulmonary and whole body assessment.

So here’s my two cents:

Thank you, love to hear any comments!

Philippe

ps obviously, this type of discussion will be what H&R2020 will be chock full of!

 

Shock Macro and Micro-circulation: Piecing things together. (Part 1) #FOAMed, #FOAMcc

 

So I have really, really enjoyed the discussions I had with these bright people on shock circulation:

Segun Olusanya (@iceman_ex) Resus Track 2

Rory Spiegel (@EMnerd) Resus Track 3

Korbin Haycock (tell him to get on twitter) Resus Track 4

Jon Emile (@heart-lung)  Resus Track 5

 

Some take home points so far:

I think that more questions than answers truthfully came out of this, and that is really the best part. But lets see what the common agreed upon thoughts were:

a. the relationship between the MAP and tissue perfusion it quite complex, and definitely not linear. So scrap that idea that more MAP is more perfusion. Could be more, same, or less…

b. you can definitely over-vasoconstrict with vasopressors such that a increasing MAP, at some point, can decrease tissue perfusion. Clinically, we have all seen this.

c. no matter what you are doing theorizing about physiology and resuscitation, THE MOST IMPORTANT IS TO CONTROL THE SOURCE!

 

Some of the interesting possibilities:

a. Korbin sometimes sees decreasing renal resistive indices with resuscitation, particularly with the addition of vasopressin.

b. the Pmsa – can this be used to assess our stressed volume and affect our fluid/vasopressor balance?

c. trending the end-diastolic velocity as a surrogate for the Pcc and trending the effect of hemodynamic interventions on tissue perfusion.

This stuff is fascinating, as we have essentially no bedside ability to track and measure perfusion at the tissue level. This is definitely a space to watch, and we’ll be digging further into this topic.

 

Jon-Emile added a really good clinical breakdown:

I think one way to think of it is by an example. Imagine 3 patient’s MAPs are 55 mmHg. You start or increase the norepi dose. You could have three different responses as you interrogate the renal artery with quantitative Doppler:

patient 1: MAP increases to 65 mmHg, and renal artery end-diastolic velocity drops from 30 cm/s to 15 cm/s
patient 2: MAP increases to 65 mmHg and renal artery end-diastolic velocity remains unchanged.
patient 3: MAP increases to 65 mmHg and renal artery EDV rises from 10 cm/s to 25 cm/s

in the first situation, you are probably raising the critical closing pressure [i know i kept saying collapse in the recording] relative to the MAP. the pressure gradient falls and therefore velocity falls at end diastole. one would also expect flow to fall in this case, if you did VTI and calculated area of renal artery. in this situation you are raising arteriolar pressure, but primarily by constriction of downstream vessels and perfusion may be impaired. ***the effects on GFR are complicated and would depend on relative afferent versus efferent constriction***

in the second situation, you have raised MAP, and probably not changed the closing pressure because the velocity at the end of diastole is the same. if you look at figure 2 in the paper linked to above, you can see that increasing *flow* to the arterioles will increase MAP relative to the Pcc [closing pressure]. the increase in flow raises the volume of the arteriole which [as a function of arteriolar compliance] increases the pressure without changing the downstream resistance. increasing flow could be from beta-effects on the heart, or increased venous return from NE effects on the venous side activating the starling mechanism. another mechanism to increase flow and therefore arteriolar pressure relative to the closing pressure is the provision of IV fluids.

in the third situation, MAP rises, and EDV rises which suggests that the closing pressure has also fallen – thus the gradient from MAP to closing pressure rises throughout the cycle. how might this happen? its possible that raising the MAP decreases stimulus for renin release in afferent arteriole, less renin leads to less angiotensin and less efferent constriction. thus, paradoxically, the closing pressure falls with NE! another possibility is opening shunts between afferent and efferent arterioles [per Bellomo]. as above ***the effects on GFR are complicated and would depend on relative afferent versus efferent resistance changes***

 

This is really, really interesting stuff. So in theory, the MAP-Pcc gradient would be proportional to flow, so if we can estimate the direction of this gradient in response to our interventions, we may be able to decrease iatrogenism. I’ll have to discuss with Jon and Korbin which arterial level we should be ideally interrogating…

More to come, and next up will be Josh Farkas (@Pulmcrit), and I’m sure anyone following this discussion is looking forward to what he has to say. I know I am.

cheers!

 

Philippe

Resuscitation Tracks 02: Hemodynamics w/@iceman_ex #FOAMed, #FOAMcc

So I’m in the process of putting together my resus handbook, and the really good thing about writing something up is that it forces one to beef up the entire mental database and fill in blanks that may sometimes be filled by belief, habit, culture or leaps of faith. So part of my process will involve discussing stuff with the brightest guys I know. Who happen to be pretty bright. So I figured it might be stuff worth sharing!

Here, Segun and I discuss the possible uses of Pmsa, of resuscitation philosophy, and touch on the issue of blood pressure vs perfusion. (please skip to 0:30 – sorry can’t cut out!)

 

Love to hear some additions to our discussion!

Here is the paper I was referring to, with the graph on page 2:

MAP in sepsis review

cheers

 

Philippe

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: https://www.ncbi.nlm.nih.gov/pubmed/29573604

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!

cheers

 

Philippe

 

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. 

Korbin:

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!

Cheers

 

Philippe

 

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