My friend, the IVC. #FOAMed, #FOAMer, #FOAMus, #FOAMcc

So I keep hearing and seeing people bash the IVC. Casually dismissing it with a shrug. “It’s not really good for volume responsiveness, you know…”

All that deserves is an eyeball-rolling emoji. That is, unfortunately, the reaction of docs who are trying to devise a threshold or recipe-based approach to POCUS management (which will be just as bad as any recipe-based medicine) as opposed to physiological understanding of what is going on with the patient.

There’s so much good information packed in scanning the IVC (properly, in both axes – for more, see a bunch of my previous posts), and frankly, volume responsiveness is the least of my concerns, that it is a shame to toss out the proverbial baby with the bathwater.

So I talked about this at Stowe EM – an awesome conference run by my friend Peter Weimersheimer (@VTEMsono), which I highly recommend to anyone for next year, great talks, people and spot:

Here are my slides:

IVC Stowe

And the audio:

 

Love to hear your thoughts!

Oh yes, and anyone looking to explore physiological, evidence-based, cutting- and bleeding-edge approaches to resus, don’t miss H&R2019 this May in Montreal!

cheers

 

Philippe

The Andromeda-SHOCK study. A physiological breakdown with Rory Spiegel (@EMnerd). #FOAMed, #FOAMcc, #FOAMer

So recently published was the Andromeda SHOCK trial (jama_hernndez_2019_oi_190001) in JAMA this month.

Definitely interesting stuff, and have to commend the authors on a complex resuscitation strategy that had some real-world flexibility built in in terms of later generalizability and applicability for real-world cases. However there are some fundamentals I have concerns about. Let’s see what Rory thinks:

Yeah. I think the bottom line of opening resuscitationists’ eyes to NOT apply monosynaptic reflexes of giving fluids to elevated lactate is good. In that sense, definitely a step forward.

However, the insistence on maximizing CO under the illusion of optimizing perfusion remains problematic and leads to a congested state unless only a small or perhaps moderate amount of fluid is required to achieve non-volume responsiveness. I think it’s important to realize that the most rapid correction of hemodynamics is a surrogate marker and has not been definitively associated with survival across the board (eg the FEAST study and others), and it’s only proven clinical impact may be on health care workers’ level of anxiety.

Tune in soon for some other smart docs’ take on this!

 

cheers

 

Philippe

 

oh yes and don’t forget The Hospitalist & The Resuscitationist 2019:

 

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…

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

The Subtleties of the SHOC-ED Trial: Don’t Just Read The Abstract! #FOAMed

So this was my comment to my friend Jon’s awesome discussion on the SHOC-ED Trial, which is certainly interesting.

Jon, great post as always! I do agree with most of it, but would have to caution readers about reading it with the filtered glasses that make people too often take home the message that they want to – usually the path of least resistance (or change). I think your main point and most critical one is that there is no protocol or recipe that should ever be applied to resuscitation, especially single-variable-based resuscitation (eg old school orders like CVP>12 lasix and <12 bolus), and substituting the IVC for CVP won’t help. And from a standpoint of volume-responsiveness, I totally agree, with the understanding that as the IVC gets more plethoric, the percentage of responsive patients will decrease, inevitably, but one cannot predict with certainty whether that one patient will or will not. However, the parallel change is that, as the IVC gets more plethoric, the volume tolerance is likely decreasing as well, so that your benefit to risk ratio is dropping. And of course you can’t recipe that just based on IVC, but should be looking at the site of pathology (eg lung, brain abcess, pancreatitis with ACS, etc…), physical exam, to determine your patient’s volume tolerance. Because we all know that most of that miraculous fluid will end up clogging the interstitium, with consequences ranging from cosmetic to fatal (though usually blamed on the patient being “so sick” in the first place, absolving the clinician from any wrongdoing). So comments like the one previous to mine, stating “give volume and see if the response occurs” are, in my mind, a poor approach. We know from studies that you cannot simply remove the fluid you gave and go back to the start with lasix (glycocalyx damage, etc), and we also know that much of the effect of said fluid administration dissipates in minutes to hours (I’m sure Jon can quote these studies off the top of his head!).

As we have discussed in the past, I think POCUS is much underused as a fluid stop point – most of its use is on the ‘let’s find a cool reason to give.’  I would argue that you should hardly ever give fluid to a full IVC (especially if markers of pathological congestion are present – portal vein pulsatility and all), unless you are dealing with temporarily improving tamponade or tension pneumo, because even if you are volume responsive, you are likely not volume tolerant. This also goes to the point that a single, initial POCUS exam will potentially not have the same impact as a whole POCUS-based management which will use it to reassess congestion status, cardiac function, etc.

Having said all this, the most important part of the SHOC-ED article is, in my mind, their discussion, which is full of all the important reasons why the final conclusion is not `we don’t need to do POCUS in shock,’ which is what I see happening (similarly to the TTM reaction), as they outline the cognitive fallacy of putting on trial a diagnostic tool whilst the therapeutics are not yet clearly established. Those only reading the abstract or conclusion will actually miss the important points of this study which the authors clearly explain.

In particular, the ‘rare’ instances of tamponade or aortic aneurysm or PE in their series would be diluted out by the sepsis, but for those patients, it would matter. As the authors state:

‘one might argue that even a single unanticipated emergency procedure would justify the use of POCUS in critically ill patients.

I would have to wholeheartedly agree.

cheers

 

Philippe

H&R2019! Final Programme. Register Now! Montreal, May 22-24, 2019! #HR2019

 

Click here to register!

Registration is open and we have said goodbye to the snail mail process. Fortunately, we are a lot more cutting edge in medicine than in non-medical technology.

We are really excited about this programme, and a lot of it comes from the energy and passion coming from the faculty, who are all really passionate about every topic we have come up with.

The hidden gem in this conference is the 4 x 40 minutes of meet the faculty time that is open to all. Personally I’ve always felt that I learn so much from the 5 minute discussions with these really awesome thinkers and innovators, so wanted to make it a priority that every participant should get to come up to someone and say ‘hey, I had this case, what would you have done?’   Don’t miss it!

CME Accreditation for 14 hours of Category 1.

H&R2019 Final Programme

Wednesday May 22 – PreCongress course

  1. Full day Resuscitative TEE course

DUE TO OUTSTANDING DEMAND FOR THIS COURSE, A SECOND RESUSCITATIVE TEE DAY HAS BEEN ADDED, WHICH WILL BE TUESDAY MAY 21ST. THERE ARE ONLY 20 SPOTS AVAILABLE, NOTE THAT THESE ARE OPEN TO H&R2019 REGISTRANTS ONLY, SO REGISTER FOR THE CONFERENCE FIRST TO SECURE YOUR SPOT.

FOR DETAILS SEE HERE, AND FOR NOW ADD YOURSELF TO THE WAITLIST.

FOR ANY QUESTIONS CONTACT HOSPRESUSCONFERENCE@GMAIL.COM.

    2. Full day Keynotable

    3. Half day Hospitalist POCUS (PM)

    4. Half day Critical Care Procedures (AM)

    5. Half day Brazilian Jiu-Jitsu for MDs (AM)

for more details on these pre-conference courses please see: 

 

Main Conference Programme:

Thursday May 23 – Day 1

Meet the Faculty cocktail! 1900 – Location TBA

 

Friday May 24 – Day 2 

Don’t miss it, spots are limited!

 

 

 

 

 

Register here!

contact us at hospresusconference@gmail.com with any questions!

The Resus Tracks 06: Farkas (@Pulmcrit) on Shock Perfusion and Infrared Tech! #FOAMed, #FOAMcc

So I had the chance to catch my friend Josh today, and, as always, he had some unique insights to contribute.

 

I really like the IR idea from the standpoint of objectivity and reproducibility. At first it sounded like a fancy (and fun, of course) way to check skin temperature as I routinely do, but the ability to objectify from doc to doc could be really interesting. Will get on that with my colleagues in my unit. We’ll see what we can come up with in the next months!

 

Love to hear from some others trying to tweak and optimize their resus!

 

cheers

 

Philippe