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!

 

cheers

 

Philippe

 

The rest of the chapters are here on iTunes!

…and a print version on Amazon in the next week or two.

 

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 https://emcrit.org/emnerd/em-nerd-the-case-of-the-deceitful-lantern/ and our discussion at https://thinkingcriticalcare.com/2019/02/19/the-andromeda-shock-study-a-physiological-breakdown-with-rory-spiegel-emnerd-foamed-foamcc-foamer/

cheers!

 

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!

 

Philippe

 

Is POCUS the new PAC??? A Chat with Jon-Emile Kenny (@heart_lung) #FOAMed, #FOAMcc

So here is what Jon tweeted a couple weeks ago:

Yikes! Does that spell doom for POCUS???

So clearly we had to get to the bottom of this statement…So a google hangout was in order.

 

Part 1 my intro:

and Part 2 our discussion:

 

So the bottom line is that we agree that there is a risk that POCUS may partly head the way of the PAC, or at least be challenged in a similar fashion. Hopefully the wiser physicians will see the inherently flawed logic that would push the field in that direction. Alternately, we could all get our minds and efforts together and try to do a triangulation of data to really pinpoint hemodynamics.

Love to hear comments!

For more of Jon’s physiology awesomeness, visit http://www.heart-lung.org.

Cheers

 

Philippe

 

 

PS for cutting-edge and bleeding edge discussions, including Jon-Emile and a lot more, don’t miss H&R2019 this may in Montreal…

Volume status, CHAISE study and other silly questions. #FOAMed, #FOAMcc, #FOAMer

So I just finished reading the CHAISE study, which compared Parm as a surrogate for Pmsf as a surrogate for “volume status.”

It is a really cool study for anyone who loves physiology, which I definitely do, and there may be some interesting elements that can be clinically used.

But let’s first set the record straight. I do not believe that “volume status” is a medical and especially not a scientific term. It is a vague reference to intravascular fluid and can be interpreted in a lot of different ways, making it essentially useless. There is such a thing as the status of your flight (on time, delayed, cancelled), your reservation (confirmed, cancelled), your postal delivery (returned, delivered, in-transit), etc.  But there are no such clear strata for “volume status.”

So what are the true scientific terms that can be measured? Blood volume. So if we had a bedside radiolabelled substance test that could give us our true blood volume, that could give us a real measure of “volume status.”

On the other hand, that would be of marginal use clinically, in all likelihood.

Why? Because there are only three questions that the savvy clinician is trying to answer, in order of importance:

1. Does my patient need fluid?

2. Is my patient volume tolerant?

3. Is my patient volume responsive?

The answer to the first question is mysterious, outside of the obvious extremes, and in my opinion, anyone who feels they can clearly answer correctly is deluding themselves.

The answer to the second question is complex and multi-factorial and includes echographic findings (venous congestion/hypertension, B lines, effusions, ascites) as well as physical examination findings (tight abdomen, edema) and clinical findings (respiratory failure, intracranial pathology) and more. But this is a critical one, because if the answer is no, then you need some really compelling evidence to even consider trying to answer the third question.

The answer to the third question is, outside of the extremes, a bit of a quagmire of assessments and technology with generally poor evidence, particularly in terms of duration of effect. The most fearsome aspect of this third question is that it is usually the first question asked instead of the last, and thus has the side effect of creating volume-responsiveness terminators who, 500cc shot after 500cc shot end up satisfied that they have blasted responsiveness into oblivion.

But that’s probably bad news for the patient, that they have now pushed into venous congestion or salt-water drowning. Unless, of course, they just look for volume-responsiveness in the same way that bird-watchers do, for the sake of scientific satisfaction, and do no more than look, or maybe snap a picture at most.

So sure, echocardiographic parameters for volume status should be under fire, as all other parameters should. The authors in this paper themselves state two critical assumptions in the Parm/msf logic:

(1) that the fluid stay intravascular in the 10 minutes (ok, I’ll buy that)

and

(2) that the compliance is linear (nope, I don’t buy that, especially not in sick patients on vasopressors – as opposed to the normal cardiopulmonary and hemodynamic patients this study was done on).

Essentially, what should be under fire is the obsession with a measurable variable to assess intravascular volume. Too many factors in play, and the answer is useless clinically anyway.

On the other hand, this study is fascinating in terms of what might be done using dynamic Parm… Maybe individualizing pressor response, unstressed volume recruit-ability?  I’ll let @iceman_ex tell us about that at H&R2019!

So what is important is stop points. And reverse points. And yes, these can be looked at using POCUS, and also CVP, and CVP tracings. And yes, there is good data that venous hypertension is a bad state. And this is what you should be looking at, to make sure you have not pushed your patient into a universally pathological state of non-volume-responsiveness.

Cheers

Philippe

So Kylie (@kyliebaker888) had some comments and questions:

Hi Philippe, I just had to read the article after your blog. Most is a bit above my head (yeah right Kylie)– but I am perplexed by three things that I did understand -perhaps you can help me with….
1. Is P(arm) a useful measure? – it went up in 19 patients and down in 8 patients after a 500ml bolus yet they claim it went up (after statistical repeated measures or something)..if P(arm) is confounded by something else – I think they suggest sympathetic tone – shouldn’t we sort that before we start using P(arm) as a reference test.

I don’t think we can consider it to be a reference at all. I think it is an interesting physiological measure and that it might have some application in phenotyping vascular tone/compliance and possibly helping in vasopressor fine tuning. In my opinion for fluids it adds little to what we have.

2. What do you think of their IVC measure – 0.5cm below junction with RA?

As I do for all IVC diameter measures, I think it is inherently mathematically flawed to try to assess a volume using a diameter. Eyeball the whole IVC. A recent study finally looked at this. 3D IVC assessment and (of course) found it better.

3. What do you think of the fact that E changed, but e prime and E/e prime didn’t….That seems like there may not be enough precision in some of those measurements.

I agree.

I also have another savvy-clinician question to add to yours
Q4: Is my patient leaking?

Excellent!

Thanks!

#POCUS IVC Pitfall Twitter Poll & Discussion. #FOAMed, #FOAMer, #FOAMcc

So I ran a couple of twitter polls sets the other day. Here is the first:

(if you want the twitter videos see here)

 

 

and part 2:

And to sum it up:

So I just wanted to illustrate something I keep bringing up, essentially that the entire IVC literature based on the AP diameter measurement is physiologically and mathematically flawed. I think the poll and images above clearly support this: given a short axis view, clinicians clearly have a different opinion (and possibly intervention!) than using only a long axis view.

My take, as I’ve said and will keep saying, is that there is a lot of info in IVC POCUS, and the one I am LEAST concerned with is volume responsiveness, which sadly seems to be everyone’s only focus nowadays when it comes to the IVC.

But here’s some food for thought, some of my clinical applications in 5 seconds of scanning:

initial shock patient: big fixed IVC -> no fluids, hurry and find the downstream problem and correct!

resp failure patient: small IVC -> it’s not a massive PE, keep looking for the cause don’t send for a STAT CT angio!

AKI patient: big IVC look at venous doppler and call for lasix, stop the fluids and albumin that were being mistakenly given!

AKI or shock patient & small IVC: sure , start with some fluids and reassess soon (that means hours not the next day)

 

etc..etc.. there’s more, and “fluid responsiveness” is only in extremes and fairly low on the list for me!

 

cheers

 

Philippe

 

ps if you like physiology, and a physiologico-clinical approach, don’t miss H&R2019!

Discussing “ARDS” (and of course fluid management and #POCUS) with @iceman_ex! #FOAMed, #FOAMcc

So sparked by some recent twitter discussions where we were talking about ARDS in a somewhat controversial fashion, I thought it may be worth expanding a bit on the topic.

Essentially my stand is that ARDS is largely an iatrogenic disease mediated by (1) overeager fluid resuscitation of various disease states that fundamentally do not require large amounts of fluids despite commonly held beliefs (sepsis, pancreatitis, etc…) and (2) the absence of frequently used “stop points” of fluid resuscitation with instead a misguided focus on detecting (and intervening upon) volume responsiveness.

In our ICU, true “ARDS” (eg not generated by salt water drowning) is a rarity. Maybe one or two a year, usually a massive primary pulmonary insult.

Anyhow, here, Segun and I discuss this:

 

Ognjen Gajic refers to this article in our discussion.

 

So it seems clear that there is much to discuss. We didn’t even really get into the juice of the stop points. Stay tuned!

 

oh yes… so if these controversial, cutting- and bleeding-edge topics, don’t neglect joining us at H&R2019. Segun and many others will be there!

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

 

 

cheers!

 

 

A Tale of Salt and Water: Venous Congestion and CHF (Part 1) #FOAMed, #FOAMim, #FOAMer

So, venous congestion is the predominant physiopathology in CHF, with a number of ensuing problems including lung edema, effusions, hepatic congestion and cirrhosis, renal failure and even gut edema and failure, though less traditionally focused on.

Venous congestion is essentially a problem of salt and water, retained by a well-intentioned but (eventually) maladaptive neuro-endocrine process. The bottom line being: too much salt and water…

However, the vast emphasis in pharmacologic CHF management, if you look at guidelines and publications, is predominantly on various neuro-endocrine modulation strategies, and though these certainly have a role, it is logical that optimizing volume status must play a central role. So why is it not a recurrent theme of discussion?  Well probably because our means to traditionally assess this is limited. What are the tools used by physicians worldwide to assess congestion?  Weight, peripheral edema, JVD, crackles, CXR are pretty much it. Now even under the best of circumstances, these are hardly precise tools, and of intermediate specificity. But it is what is available, and taught, and in most cases, does the job fairly well.  However, judging by the problem of recurrent admissions for CHF exacerbations, likely not good enough.

The Canadian HF Guidelines – as thorough as they are – are interesting in that the only time diuretics are addressed are in exacerbation, and a note to use the lowest dose possible to maintain stability… But little else in terms of guiding this assessment of stability or the dosage management. The usual “thorough history and physical” stuff, of course.

So what else could we do?  Now my interest in POCUS is no secret, and it seems like the ideal tool for assessing both fluid collections and hemodynamics. So what do we know?

Lungs – at this point it’s beyond much debate, POCUS-enhanced physical examination is vastly superior to radiographs and traditional physical examination. Small effusions are easily seen as well as congestion in the form of B lines. In the case of sub-acute to chronic congestion, as we are not overly concerned with central lesions (not seen with ultrasound), the CXR is of no further benefit.

Peripheral edema – I’ll call this one a tie. Not that much benefit in measuring subcutaneous edema with a probe, except for exact reproducibility, at the cost of time.  😉

The Heart – another no-brainer. Ultrasound wins. With appropriate training, experience, and more important than either, the ability to recognize one’s own limitations.

Venous congestion – Now we’re getting to the interesting stuff. So even if for some, it may be the first time hearing about the clinical use of venous congestion markers in CHF, it isn’t new science. In the 90’s, several studies were published correlating portal vein pulsatility, congestion index, as well as hepatic vein doppler pattern with CVP, RV dysfunction, finding close correlation.  In 2016, Iida et al published a great article on renal venous doppler and CHF which I highly recommend reading, and more recently, Andre Denault and William Beaubien-Souligny (@WBeaubien) have been doing tremendous work with portal vein pulsatility and post-op cardiac patients’ organ dysfunction. So the science correlating excessive venous congestion to organ dysfunction is there and is clear.

Why have we not yet widely studied this?

The answer is fairly simple. Prior to the growth of POCUS, there was no single clinician group holding the necessary set of clinical and echographic skills to make this clinical routine. Cardiologists are not all echo-capable, and even those that are would have had little or no experience dopplering abdominal organs and vessels. Radiologists – most of the literature coming from their field – are not pharmaco-clinicians and do not follow patients. Family physicians and internists, likely the bulk of the physicians looking after these patients, largely had not had access to or echo skills. Until now.

So a quick review:  right-sided failure causes elevated RAP, so everything upstream gets congested. The first echo signal of this is the plethoric IVC (in both axes of course!!!), and an abnormal hepatic vein doppler (which is pretty much like a CVP tracing, just non-invasively) but is that the max? Nope. What is worse is when that pressure transmits thru backwards from hepatic veins to portal vein, transforming a normally monophasic flow with minimal variation into a progressively more pulsatile flow, to the eventual point of being intermittent. And when the IVC pressure transmits across a congested kidney such that the same thing occurs in the renal veins.

Those findings have been well studied and correlate with poor outcomes in CHF.

 

So what could we do?

What we are doing now is systematically assessing CHF patients in terms of their venous side. What we see so far is that some have full, plethoric IVCs, maybe B lines and effusions, maybe some peripheral edema, but may or may not have those worse markers of abnormal doppler flows, and those who don’t generally don’t have significant organ dysfunction such as renal failure (I discussed this a few years ago in my pre-doppler era in terms of re-thinking common approaches).

So when we find significant portal pulsatility, we diurese aggressively, creatinine notwithstanding. We almost always get an improvement in biochemical markers of renal function within 48-72 hours, with the only really tricky patients being those with severe pulmonary hypertension. More on that in another post.

Goonewardena et al had a really great observational study that showed that if CHF patients were discharged with a non-plethoric IVC and significant respiratory variation, they were less likely to be re-admitted. The figure below on the right shows the numbers:

So there is reasonable evidence to suggest a POCUS-guided approach, which we’ll go over in the next post, which should include our revised Advanced CHF Clinic guidelines.

I can already hear the thoughts… “is there any evidence for this?” But those asking that reflexively should first ask themselves “what is the evidence behind the way I assess congestion and manage CHF?”

 

cheers

 

Philippe

 

Refs

Portal vein pulsatility and CHF

Iida et al. article

Beaubien-Souligny and Andre Denault open access article