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!

 

Cheers

 

Philippe

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.

 

cheers!

 

Philippe

 

The Hospitalist POCUS Course Participant Info.

 

So here is a little intro for those taking part in the course, or for those considering, though I don’t think there are many spots left.

 

The Hospitalist POCUS Course

Participants should receive course e-notes in the week prior, if you do not, please email hospresusconference@gmail.com to let the team know.

If you are thinking of registering the link is here.

cheers and see you there!

 

Philippe

Venous Congestion: A Reader’s Questions. #FOAMed, #FOAMcc, #FOAMus

I’m always glad for questions, because I think that it’s what forces everyone’s thinking to progress. So yesterday a couple of really good ones from Jonathan Cheung:

My 1st question: I am just curious if it is possible for a collapsible IVC and PW findings suggestive of venous congestion to coexist, say, for example, if the congestion actually leads to increased IAP (perhaps not to the extent of intra-abdominal hypertension) or even 3rd spacing to form ascites in a leaky patient.
This is a question that has come up a couple of times. My physiological answer would be that, in primary systemic congestion, the start point is the increased CVP, which leads to IVC distension, then hepatic vein distension, whose pressure transmits thru the hepatic to the portal circulation, and then pulsatility develops. So in these cases a plethoric IVC is an inherent part.
On the other hand, local phenomena, such as cirrhosis, organ-specific edema (ischemic bowel, renal capsular hematoma, etc) can lead to edema and congestive signs in the local circulation without central venous congestion.
This is an important delineation, because the therapy for localized inflammation and edema is not likely the same as for central venous hypertension.
My 2nd question is: does the physiological changes by pronation (e.g. variable change in transpulmonary pressure, slight “off loading” of the abdomen etc.) cause an observable change to the spectral findings? I often have this question in mind when I want to assess fluid status in a prone patient on whom doing an echo isn’t always possible.
First I would argue that the only trouble with prone and POCUS is for cardiac views – hence TEE. But for venous doppler, the kidneys are perfect, the PV and IVC are totally accessible laterally and the IVC even posteriorly.
Secondly, I think it’s important to remember that physiologically, venous congestion is venous congestion, no matter the cause, and that end organs can suffer similar consequences. At least initially, proning should drop the PAP and unload the RV, but this will likely change over a variable amount of time. Very tough to properly assess the physiology in my opinion.
I’ll try to get Korbin, Rory and Jon-Emile to chime in!
Cheers
Philippe
Click here to come meet this interesting bunch of docs!

Relational Time Patterns: An EKG for Sepsis? A deeper look into the StormTracker with @patientstormdoc! #FOAMed, #FOAMcc, #FOAMim

So if anyone has been following the sepsis debates on the Twitterverse, one of the recurrent issues has been around threshold science. Let’s not forget that sepsis did not define itself. Rather, a bunch of saavy and experienced docs have sat around a table at various times and defined sepsis. Indeed, did not describe it, but defined it.

Now sepsis is a highly heterogeneous syndrome rather than a specific disease, a complex interplay between any number of infectious agents and different host sites and hosts, both sides with different immunological histories.

So Lawrence, a veteran ICU doc, has been focusing most of the last decade on developing an extensive clinical data gathering system that delineates relational time patterns of various clinical categories (eg myeloid, hemostatic, respiratory, cardiac). In a sense, this creates a visual matrix that changes over time:

So here is our discussion:

Now what such a tool can be used for I think falls into two categories, the clinical, and more importantly, research, particularly in sepsis.

Clinically, this can be used as a visual tool to monitor and detect failure of therapy (antibiotic resistance) or the development of a second septic source (eg staph pneumonia in influenza). Now one can say that looking at all these data points is what the experienced clinician does, but it isn’t possible to do so, for example, for all my 10 ICU patients in the first second I walk in. On the other hand, a quick look at each patient’s graph, compared to the previous day’s, would immediately flag those who are worsening, and perhaps focus clinical attention and time management in a better fashion. It may even make us catch some we might otherwise have missed, if only by not noticing a platelet drop from 340 to 167 – I could see something like that going under my radar from time to time.

Research-wise, I think this really opens a whole new world, where different phenotypes of sepsis can be potentially described (work we are currently undertaking), and describing the phenotypes (as opposed to arbitrary cutoff definitions) may lead to better categorization and more importantly therapeutic research that may be better tailored to the phenotype.

At some point, AI will be able to learn these patterns, and it will be important that clinicians – much as we double check the machine’s EKG interpretation – understand the patterns themselves.

Lawrence will be at H&R2019 and running workshops on this technology.

Love to hear some comments!

 

cheers

 

Philippe

 

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:

https://www.google.ca/amp/s/thinkingcriticalcare.com/2018/11/04/hr2019-final-programme-register-now-montreal-may-22-24-2019-hr2019/amp/

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

 

cheers

 

Philippe

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.

 

cheers

 

Philippe