POCUS, Mythology and Hemodynamic Awesomeness with Jon and Korbin! #FOAMed, #FOAMer, #FOAMus

In Greek mythologyPrometheus (/prəˈmθəs/GreekΠρομηθεύςpronounced [promɛːtʰeús], meaning “forethought”)[1] is a Titanculture 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.[2]

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.

Then Korbin Haycock chimes in and adds a level of understanding that I completely agree with but had difficulty in expressing, but which I think is key to understanding the current and future evolution of POCUS. Complex, operator-dependant medical leaps such as laparoscopic surgery suffered with similar growing pains. But I’ll let Korbin shed some light:
I think the issue of POCUS in resuscitation is somewhat analogous to Prometheus’s gift of fire to humanity.
Jon has quite aptly pointed out that if POCUS (particularly a single POCUS supplied data point such as IVC diameter), if used in isolation, without clinical context, and without comprehensive information, is not much better than using a single data point such as CVP to make complex clinical decisions. Multiple factors influence the behavior of the IVC, just as they do with the CVP. Being a dynamic entity, the IVC does have some advantages over a static number like the CVP. However, if considered by itself, the IVC POCUS evaluation will only result in the same pitfalls as using the CVP as a guide to fluid management. If POCUS is applied in such a blunt manner, we are doomed to repeat our previous folly of using the CVP as a guide to fluid resuscitation. I hope I am in the ball park of the core of Jon’s point here, if not as very eloquently stated by him.
Phil is advocating a more nuanced and sophisticated approach to POCUS than what the SHOC-ED trial investigators used to guide management in their study. Most shocked patients presenting to the ED (“Emerge!”) come with a phenotype of distributive shock. Indeed, these were the majority of the patients in the SHOC-ED trial. Any experienced clinician will recognize this syndrome virtually every time, with no more than an “eyeball and Gestalt” assessment from across the room and a set of vital signs. Current dogma is that this syndrome ought to be treated with 30 cc/kg of crystalloids and then to add a vasopressor if the patient’s blood pressure is still low. Given this, there couldn’t have been much difference as to how patients were managed in either group in this study. I however, disagree with this aggressive crystalloid administration approach, as I’m sure many readers of Phil’s blog do as well. What I gather Phil is saying here is, as he insightfully stated in the past, “IVC never lies, it’s just not telling you the whole story.” A complete POCUS gives us (OK, well almost) the whole story. The caveat here is you must know a whole lot about POCUS. Thus the Prometheus analogy. A little information is a child playing with fire.
Someone new to POCUS, with only a novice’s understanding of what an IVC POCUS evaluation means, will probably make the correct assessment of a patient’s fluid status about 60-70% of the time. This probably is only slightly better than an experienced clinician’s non-POCUS judgement. Hardly enough to translate into any meaningful clinical outcome in a trial without a ridiculously large sample size to find a pretty small benefit. But POCUS potentially offers so much more information. LV and RV systolic function, LV and RV diastolic function, SV, CO, SVR, PVR, RAP/CVP, sPAP/mPAP/dPAP, LVEDP/LAP/PAOP, valvular pathology, tamponade, fluid responsiveness (for what ever that’s worth!), RV/LV interactions (both in series and in parallel), EVLW, insight into pulmonary vascular permeability, renal resistive index/renal venous congestion, portal hypertension/congestion, gut flow resistance, and on and on. Most of this information can be more or less determined in less time that it takes to put in a central line in order to get the damned CVP (actually, I do like to know what my CVP is, for what it’s worth). The more data points you are able to collect with increased POCUS skills and experience, the more grasp you have as to what is going on with your patient and the right way to treat them. I would argue that given the information attainable with advanced POCUS skills, POCUS is a no-brainer that will enormously improve not only individual patient outcomes, but effect populations at large, if only the general hospital based practitioner can attain a more than introductory understanding of POCUS.
So, I guess the question is, “how much training is enough training?” I don’t know. Inevitably, POCUS knowledge will incur a bit of the Dunning-Kruger effect as pointed out by Jon’s example of an IVC POCUS fail. But reading Jon’s clinical case example, from the get go, I found myself asking questions that would change may management one way or another with additional information that I could get quickly and easily with additional POCUS interrogation of the patient. Jon pointed this out himself by revealing that the patient has pulmonary hypertension as manifested by the tricuspid regurgitation upon auscultation of the heart. With POCUS, I don’t need to guess what a heart murmur is or how bad it is or even if it is relevant to my patient in this case for that matter. POCUS can tell me it’s TR and it tells me what the sPAP/mPAP/dPAP and PVR is if I care to find out. So if this level of information can be gleaned, for me, no one can argue that POCUS has no merit. But, I’ve spent a lot of time striving to be good at this, just as probably a lot of people reading this have done as well. What about newbies?
Consider: At my main hospital, for a variety of sensible reasons I won’t get into, we decided to train a group of nurses in POCUS in order to evaluate septic patients. They achieve basic training in POCUS and are very competent sonographers with regard to IVC, gross LV and RV function, and pulmonary edema. They are a small group of very intelligent, skillful nurses that are excited to learn all they can. We had them evaluate every septic patient that presented to our hospital, do a POCUS exam, and discuss the findings with a physician. We established some very basic resuscitation endpoints largely based on POCUS findings applied to each individual patient and their POCUS exam. Our severe sepsis/septic shock mortality rates dropped from 35-38% to 8-10% with this program. Our hospital plans to publish this data officially soon for public analysis, but it did make a difference in our experience. That said, my nurses do frequently show me cases where I notice some small detail on their POCUS exam that propmts an additional investigation that alters the plan in management. Also, some of my very competent POCUS savvy residents make errors because they don’t have enough knowledge yet. I’m sure I can make these errors too at times as well, although hopefully less and less so with time.
Here’s my point: Heed Jon’s admonition to look at the big picture and not rely on isolated data points. Be inspired by Phil’s passion for the potential of a good POCUS evaluation. If you only get your toes wet with POCUS, you are playing with forbidden fire. But if you care to look into it further, POCUS opens up worlds to you. By all means, learn all you can about POCUS. Recognize that if you are new to POCUS techniques, there are improtant caveats to each finding, and physiology that needs to be considered with a comprehensive view, some of it may be strictly non-POCUS related information as well. Your patient is unique and only a careful comprehensive consideration of what’s going on with your patient will guide the best approach to your management of their illness. I don’t think SHOC-ED or any other trial for that matter can address the nuances of good individualized patient management. That is up to you.
‘Nuff said.
PS These are just the kind of discussions that can change both the way you approach medicine and manage your patients, and these are the ones you find behind the scenes and in the hallways of H&R2018. Don’t miss H&R2019 if you take care of sick patients. It’s the kind of small, chill conference where the faculty will be happy to take a few minutes and discuss cases and answer all your questions (if they can) about acute care.

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.




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!





The Resus Tracks 04: Shock Circulation & Renal Perfusion with Korbin Haycock. #FOAMed, #FOAMer, #FOAMus


So I got to have a chat with ER doc extraordinaire Korbin Haycock today, reasserting my belief that tissue perfusion is not proportional to blood pressure.  I am again including the article discussed, and here is the graph in question:

Here is our talk:

And the paper – which is definitely worth a read, as it clearly supports individualizing therapy!

MAP in sepsis review


cheers and please jump into the discussion!



Resuscitation Tracks 02: Hemodynamics w/@iceman_ex #FOAMed, #FOAMcc

So I’m in the process of putting together my resus handbook, and the really good thing about writing something up is that it forces one to beef up the entire mental database and fill in blanks that may sometimes be filled by belief, habit, culture or leaps of faith. So part of my process will involve discussing stuff with the brightest guys I know. Who happen to be pretty bright. So I figured it might be stuff worth sharing!

Here, Segun and I discuss the possible uses of Pmsa, of resuscitation philosophy, and touch on the issue of blood pressure vs perfusion. (please skip to 0:30 – sorry can’t cut out!)


Love to hear some additions to our discussion!

Here is the paper I was referring to, with the graph on page 2:

MAP in sepsis review




Kylie & Korbin chime in to the Venous Congestion Issue. #FOAMed, #FOAMcc, #FOAMus

So I think much of the awesomeness of #FOAMed is sparking discussion and exchange, and the many little steps in clinical management besides the initial prescriptions. So I thought I would highlight and exploit a couple of really interesting reader comments:

So first, Kylie (@kyliebaker888):

Great to listen guys, thanks, and very timely. I had just read Tremblay’s paper after coming across a very pulsatile PV in a relatively well elderly patient with bad TR. Two questions – which PV are more likely pulsatile in the first place….Tremblay mentions RVF/TR and very thin folk. What is your experience?
Second Question – what did the GB wall/GB fossa look like after the initial very positive fluid balance? Does everyone blow out their GB wall with fluids, or only some?

It is always important to isolate the patients’ whose physiology may change the clinical signs (in this case PV pulsatility) and make their interpretation different. I agree that massive TR, especially chronic, would likely account for pulsatility. I am not certain about the physiology for the very thin patient, but I have heard the same thing from Andre.  So my personal take on a patient with severe TR and a pulsatile PV would be to look at the IVC variation, TR notwithstanding, if it is fixed and plethoric I would diurese – the organs don’t care what the cause of the congestion is.  

As for the GB, I have also seen edema, and then try to correlate with cholestatic enzyme changes that would be out of proportion to the hepatocellular enzymes if there is a primary GB process. This is certainly an imperfect science. In a critically ill septic patient, I have a low threshold to drain the GB if in doubt.

Then Korbin gives his two cents, and then some! 

Great case, loved it. Thoughtful management, brilliant!

I couldn’t help thinking as I listened, that it is so important to avoid over-resuscitation with fluids in the first place. We all know that the majority of crystalloids given will end up as interstitial edema, so any benefit from the increase in stroke volume is temporary at best (consider carefully what you gain and at what cost). Wet lungs=increased mortality, days on the vent, and ICU stays. Wet kidneys=AKI 2-3 days after initial resuscitation and potential RRT. Congested liver=gut edema and continuation of inflammatory cytokines/sepsis syndrome. Too much fluids–>BNP levels rise, high BNP levels in the presence of LPS=glycocalyx shedding, and more interstitial edema everywhere.

Cannot agree more.

I think there is some decent evidence that an early fluid liberal approach combined with a late fluid restrictive approach can potentially benefit a patient in septic shock, but its clear that an overall positive fluid balance does harm. Perhaps, even the early fluid liberal strategy (in sepsis specifically) should be tempered by a careful consideration of what is really going on.

My take here is that, by using POCUS, there is no need for a “general approach.” POCUS takes essentially no time. In about 5 seconds you can confirm a small IVC that can (initially) take fluid, a medium one (that you need to watch) or a full one (yes, it happens – that gets no fluid). So to me there is no need to have a pre-determined approach…

Sepsis is an entity characterized by venous return being limited by a decrease in mean systemic pressure (MSP) due to an increase in venous capacitance, rather than a decrease in fluids that generates the stressed volume (MSP=fluid filling/venous capacitance). The body compensates with an adrenergic response that maintains (or attempts to maintain) MAP by an increase in a catecholamine driven augmentation in cardiac output/contractility. This adrenergic response likely has more to do with the increase in lactate production observed in sepsis, rather than actual tissue hypo-perfusion and anaerobic metabolism mechanism. Increases in CVP inhibit venous return and congest the kidneys and GI tract (the left atrial pressures are the equivalent problem for the lungs, combined with the fact that pulmonary vascular permeability is increased in sepsis as well). Given this, I think in distributive shock, we should fix the lack of MSP by an earlier vasopressor therapy approach, both to supplement and decrease the crystalloid load to the patient, which is un-natural and contrary to their deranged septic physiology.


Also, could the type of crystalloid given be important? NS gives a considerable sodium load compared to LR, and this likely promotes/sustains fluid retention that is difficult to remove during de-resuscitation. The high chloride levels of NS will promote an increase afferent arteriolar vasoconstriction and thus decrease GFR, making it more difficult to diuresis the patient later on, and contribute to AKI beyond the iatrogenic interstitial kidney edema caused by the crystalloids we gave.

Absolutely. NS is given by medical peeps only by cultural habit. Most do not know the pH (zero SID due to chloride) of  a solution they give by the buckets. RL is the best option I have available.

If you are involved in the early phase of resuscitation of a shocked patient, consider the downstream consequences of your fluid strategy that you give your patient that may give you a temporary comfort because they will look better in the short term.

Dr. Maitland and the FEAST study corroborates exactly this.

This is not to say that an aggressive and upfront resuscitation is not critical–it surely is. I’m saying resuscitate smarter, not wetter. Look for stop points for crystalloids–E/e’ ratios, consider PVPI, RV dilation/TAPSE, hepatic vein doppler, IVC dynamics, portal vein pulsatility, intra-renal venous Doppler patterns and renal resistive index. Fix the hemodynamics from an approach of the root of their problem, rather than pushing fluids for every hypotensive patient (whether you are taking care of them early, or late in the time frame of their illness). Fluids do have their place, but be careful and cognizant of their real down side. Look at your patient, think it through, and make the best actions for them.

Ok, now I don’t even get to have a punchline. Thanks Korbin!

So if this interests you, tune in to The Great Fluid Debate at H&R2018, and I look forward to meeting both Kylie and Korbin who will be in attendance and, I’m sure, putting us all on the spot!

And yes, there will be a POCUS workshop on portal and hepatic vein POCUS.

click here if you want to take part: H&R2018




POCUS & Venous Congestion – A Clinical Case Discussion with Rory Spiegel (@EMnerd_), #FOAMed, #FOAMus, #FOAMcc

Hi, so as a follow up to our earlier discussion, which can be found here, Rory and I discuss a recent case he had, which I think exemplifies well many of the clinical conundrums that are seen in fluid resuscitation, one being the general resistance of many to diurese patients who are still in shock on vasopressors, instead preferring to (hopefully) wait until shock resolution to de-resuscitate. But sometimes, it is exactly what they need, as some of this congestion may be, in fact, a cause of shock…

Here you go:

Love to hear opinions, so feel free to reach out.


For those who may be interested at learning some of these POCUS skills, check out H&R2018 (#Hres2018)!