Perhaps this slowed up (0.5x) A3C loop will help with that LVOT doppler!
Perhaps this slowed up (0.5x) A3C loop will help with that LVOT doppler!
So I recorded a chat with Domagoj (@domagojsono in the twitterverse), an anaasthetist-resuscitationist-intensivist from Freiburg a few months ago, but with H&R2019 and its aftermath, been slow in processing a lot of stuff I’ve got stocked… Apologies!
So in this one, DOmagoj and I discuss a bunch of resus topics, from eCPR to tissue oximetry. I’m really jealous of the fact that he does prehospital work with an ECMO van!!! …and with cool gear and of course, POCUS!
Here is the chat, hope it leads to thoughts, discussion and contribution!
And here are some links:
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.
Here are Korbin’s thoughts on this:
I’m very glad Dr. Eduardo Argaiz pointed this case out, as it brings up considerations apropos both chronic venous congestive cases as well as management of acute illness, particularly in sepsis, where we would expect patients to most likely be fluid responsive, but fluid tolerance is largely overlooked with current management strategies by the majority of clinicians.
Phil’s above audio commentary points out the difference is these two broad categories very nicely. If you didn’t listen to it–you should.
With respect to chronic venous congestive conditions, the knowledge and application of Doppler assessment to therapy will hopefully be the next advance in management at large. Already, I think there is more than adequate research available to show the value of Doppler POCUS (D’POCUS, D/POCUS, or DPOCUS?) in managing these patients. It’s only a matter of clinicians willing to commit to learning and integrate this technology into their skill set.
With respect to resuscitation of the acutely ill patient, there is by far less data, and we are probably into the realm of N=1 here, in terms of how to manage these patients. But, I personally believe–and I understand this is my opinion–that current trends in resuscitation (especially sepsis resuscitation), largely ignores the effect of over volume resuscitation and the potential downstream damage inflicted on our patients.
This theoretical damage of over aggressive fluid resuscitation is multifactorial, including glycocalyx shedding issues/endothelial dysfunction, positive fluid balance and EVLW causing increased mortality (which there is ample evidence for, I think), venous congestion leading to perfusion injuries to encapsulated organs, such as the kidney (AKI) and brain (congestive encephalopathy), and end organ edema leading to the perpetuation of a malignant inflammatory syndrome (portal HTN and gut edema).
In the case called out by Dr. Argaiz, (which can be reviewed by the previous post on this website) my patient had an IVC that whilst not plethoric, was not an IVC that one would expect to find in a patient with a typical distributive shock pattern (i.e. increased cardiac output, decreased SVR, and decreased RAP). Firstly, the complicating factor of atrial fibrillation with RVR was central to the patient’s shock state, however this was quickly addressed with rate control. However, in addition, this particular patient did exhibit additional signs of venous congestion. The portal vein was pulsatile and the intrarenal Doppler pattern was interrupted/bi-phasic in nature. Granted, a pulsatile PV Doppler could be interpreted as related to the hyper dynamic nature of septic shock (as the esteemed Dr. Denault correctly cautioned in his comments on the original post), however a less than flat IVC and the intrarenal findings gave weight to a venous congestive hypothesis as a cause the PV findings as well as a possible cause for his AKI evident on his initial labs.
With this particular case, given my personal global POCUS/FOCUS assessment of his increased LAP (high E/e’), RV dysfunction, RAP, PV, and intrarenal Doppler venous pattern, AND that fact that the RRI was insanely high with an AKI, I elected to treat my hypothetical construct of his renosarca with furosamide and his RRI with vasopressin (as the NE infusion did increase his MAP, BUT NOT decrease his RRI–which the vasopressin infusion did decrease, or so I presume as no other therapeutic interventions were given with respect to the time frame the RRI decreased).
In the end his kidneys had recovered by the next morning, which I’m sure that any intensivist will admit is the opposite of the norm, as the kidneys usually get, at least transiently worse initially-being the delicate sissies/whimps that they are. Whether this was because of the diuretic or the vasopressin, or something else, is debatable for sure, but it sure didn’t get better by 30 cc/kg of crystalloid mandated by CMS, because he got not a drop more than what was needed to push the diltiazem, the lasix, the antibiotics, and the vasopressors.
So to summarize, in the case of chronic cardiogenic venous congestion, clinician realization and adoption of Doppler assessment of this entity will likely be the next leap in improvement in the management of these patients. In the case of acute resuscitation, venous congestion may be a bit more nuanced, and a more comprehensive evaluation is in order in a case by case fashion. However, I think recognition of the issues of over aggressive volume administration will probably be the next frontier in sepsis resuscitation.
Love to hear your thoughts!
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.
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:
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:
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!
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!
oh yes and don’t forget The Hospitalist & The Resuscitationist 2019:
In Greek mythology, Prometheus (/prəˈmiːθiːəs/; Greek: Προμηθεύς, pronounced [promɛːtʰeús], meaning “forethought”) is a Titan, culture hero, and trickster figure who is credited with the creation of man from clay, and who defies the gods by stealing fire and giving it to humanity, an act that enabled progress and civilization. Prometheus is known for his intelligence and as a champion of mankind.
So, fresh from reading Jon’s post, I felt I had to add a bit of nuance in my previous post to what I feared some might extract as a take-home message, even if in fact, we are not that differing in opinion at all – which Jon expressed here:
i agree with ultrasound for finding the uncommon causes of shock. these examples seems to permeate twitter and make ultrasound very appealing. because ultrasound is non-invasive, it makes the risk-to-benefit ratio very low for these uncommon but highly-lethal and treatable causes.
but that needs to be compared to the risk-to-benefit ratio of ultrasound for the more common causes of shock – like ‘non-cardiogenic, septic’ etiologies as seen in SHOC-ED. here, “static’ ultrasound [as per the RUSH and ACES protocols] – per SHOC-ED – appears to be neither helpful nor harmful. your read of the discussion is perfect, but i was depressed because it read as if the authors only realized this ex post facto – study of previous monitoring utensils [e.g. PAC] should have pre-warned the authors …
i will take some mild issue with markers of volume responsiveness and tolerance. you are correct on both fronts – but what the data for the IVC reveals – perhaps paradoxically – is that true fluid responders can have a very wide-range of IVC sizes from small to large and unvarying … this was born out in most of the spontaneously breathing IVC papers [airpetian and more recent corl paper] the sensitivity was rather poor.
the same *could* be true for the opposite side of the coin. a large great vein may not mean a volume intolerant patient. i tried to exemplify how that could be so in the illustrative case in my post. an elderly man, with probable pulmonary hypertension and chronic TR who probably “lives” at high right-sided pressures. nevertheless, he likely has recurrent C. diff and is presenting 1. hypovolemic and 2. fluid responsive despite his high right-sided pressures. portal vein pulsatility *could* be quite high in this patient – but he still needed some volume.
the obvious underlying issue here – which I know you are well attuned to – is that a Bayesian approach is imperative. when you PoCUS your patients, you are inherently taking this into consideration – i know that you are a sophisticated sonographer. my hidden thesis of the post is that if ultrasound findings are followed in a clinical vacuum and followed without really understanding the physiology [which can explain clinico-sonographic dissociation – like the patient in my fictitious case]… disappointment awaits.
nice analogy – i think Korbin’s response is appropriate and i look forward to speaking alongside him in May. as i chew on the SHOC-ED a little and try to distill my concerns – i think what it boils down to is this: it’s less about playing with fire – i think – and more about how this fire is brought to the community as a whole. my post on pulmccm was more of a warning to the early adopters [like us] who are planning these trials. imagine 40 years ago:
-the flotation PAC is introduced, a small group of clinical physiologists use it thoughtfully, understand the caveats, the problems of data acquisition, interpretation, implementation, the problems with heart-lung interactions, intra-thoracic pressure, etc.
-these early adopters present their results to the community as a whole
-the physiology of the PAC is simplified
-the numbers from the PAC are introduced into algorithms and protocols and **widely** adopted into clinical practice
-the PAC is studied based on the above and found to make no difference in patient outcome.
-in 2010 a venerable intensivist suggests floating a PAC in a complicated patient and the fellow on rounds chuckles and states that their is ‘no evidence of benefit’
does this sound eerily familiar? is our present rhyming with the past? if the planners of POCUS trials are not careful, i promise you that the same will happen but insert any monitoring tool into the place of PAC. i can very easily visualize a fellow on rounds in the year 2030 scoffing at the idea of PoCUS because trials [SHOC-ED, and future trials x, y and z] showed no difference in patient outcome. is it because PoCUS is unhelpful or is it because the way it was introduced and studied was unhelpful? and the three of us will sound like the defenders of the PAC from 30 years ago: “PoCUS isn’t being used correctly, it’s over-simplified, it works in my hands, etc. etc.”
it’s not PoCUS that’s unhelpful, it’s how we’re implementing it – and i was most depressed when the authors of SHOC-ED appeared to stumble upon this only in the discussion of their paper – like you mentioned phil. imprecise protocols will result in equally imprecise data and the result will be nebulous trial outcomes. we should all be worried.
Excellent points Jon. The PAC example is very relevant, as on more than one occasion, I’ve had the argument put to me by some colleagues that essentially how I’m applying POCUS is really no different than the information gleaned from the PAC, and “that’s been shown to not be helpful to outcomes” etc. So, therefore, why do I bother?
Then again, I’ve seen a fair amount of phenylephrine being thrown at hypotensive cardiogenic shock patients after a 2 liter normal saline bolus didn’t do the trick.
You are absolutely spot on when you point out that seeing the big picture, knowing the physiology, and being aware of the pitfalls of isolated data points is important to making the right decisions in patient care.
Furthermore, I agree that when a clinical trial is done that doesn’t consider some of the nuances of all this, and “shows” that POCUS, or any other diagnostic modality for that matter, doesn’t contribute to better patient outcomes, it probably only serves to marginalize a potentially valuable diagnostic tool to an actually astute intelligent clinician.
I’m not meaning by saying this to bash the good intentions of the SHOC-ED trial. To be fair, it’s really hard to design a trial that can take into account all the permutations that are involved in any individual patient presents with, having their own unique clinical situations, hemodynamic profiles, co-morbidities (both known and undiagnosed), etc. POCUS, PAC, transpulmonary thermodilution, ECG, chest x-ray, CT scans, labs, physical exam–these are all merely tools that guide patient care. Albeit some are way more powerful than others. I can image various amounts of uproar if some of these traditional tools were subjected to clinical trials to prove their utility. The argument, if proven “useless” in a study for the oldest and well accepted tools would always be, “put it in the clinical context, and its value speaks for itself.” For me, I’d happily like to make clinical descisions based on information based on an advanced POCUS exam or PAC, rather than interpreting hepatojugular reflux or a supine chest x-ray.
Any diagnostic test requires that the clinician understand the limitations of that test, and understand that the whole clinical scenario must me taken into account. You’ve hit on that, I think, with your argument. This surely has implications when any technology or test is studied.
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