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:
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.
PS for cutting-edge and bleeding edge discussions, including Jon-Emile and a lot more, don’t miss H&R2019 this may in Montreal…
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)
(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.
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 also have another savvy-clinician question to add to yours
Q4: Is my patient leaking?
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!
ps if you like physiology, and a physiologico-clinical approach, don’t miss H&R2019!
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!
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.