Another interesting question from @JCHCheung! #FOAMed, #FOAMcc

So here’s another interesting question as a follow up to the previous discussions:

Most people would probably agree that florid congestive signs on POCUS means the RV is unable to pass any more extra volume to the left heart; whilst the absence of those signs mean that the patient may be able to cope with some additional volume without immediately engorging the vital organs.

And my question is: what about those in between? i.e. the patients who start to develop some mild congestive features on POCUS.

For those who are on the verge of congestion, diuresis would push the RV to the left (i.e. steep part) of Starling curve resulting in significant CO drop; conversely, extra volume pushes the RV to the right (i.e. flat part) leading to congestion or even D-shape LV, directly hindering CO as well. This margin becomes even smaller in patients whose RV starts to fail (i.e. entire Starling curve shifted downwards)

Great, great question. The crux of this, I think, is deciding which is the greater issue, congestion or poor perfusion. Obviously they are intertwined, so the decision will be on a case by case basis. Jonathan alludes here to a narrow “balance point” between congestion and preload dependancy. My feeling – and we’ll see if we can get some consensus – is that this indeed narrow in patients with marked pulmonary hypertension. When patients have pure pump failure congestion, my clinical experience is that you can decongest plenty without drop in systemic CO, in fact it often improves, likely related to ventricular interdependance. So let’s go on…

I’ll illustrate my point with the following scenario:

for previously healthy middle aged patients intubated and admitted to the ICU for ARDS from severe pneumonia, they quite often develop some acute cor pulmonale after mechanically ventilated for several days even if the PEEP/driving pressure isn’t exceptionally high; and they usually have resp failure and shock to start with.

Given that they don’t have pre-existing heart disease, the only signs suggesting the emergence of cor pulmonale could be subtle, without structural changes like dilated RV (RVEDD at most at upper normal range) nor abnormal septal movements. You may see TAPSE dropping to marginal level and portal vein PW signal may become a bit more pulsatile. IVC looks full and RVSP usually rises but not skyrocket. The MV inflow pattern & E/E’ suggest rather normal LA filling pressure, not surprising from a previously healthy heart.

In this case, it isn’t the LV diastolic dysfunction that overly afterloads the RV; and it isn’t the RV dilation that impairs the (D-shape) LV from ventricular interdependence. Therefore I’d consider the right heart circulation & left heart circulation running purely in series, whereby limiting the RV preload could reduce the LV CO.

Now, if this patient goes into shock, would you consider fluid challenge or diuretics? Everyone probably would also get other therapies on board, e.g pressor, inotrope, source control etc. But when the patient’s BP is 80/40mmHg, I am more prone to giving some fluid as I believe that reducing preload in a septic patient can precipitate arrest; and that RV only directly impairs LV CO once the IVS starts to shift, which should take more time and thereby easier to monitor.

Interesting case that happens commonly – if you do POCUS and look for it rather than blind-ish management. Here, you have congestion, likely due to pulmonary disease, fluids, on a normal-ish RV (which also means it is unable to mount a huge PAP).

So personally – and will full disclosure that this is not evidence-based (as if there was any evidence in our resuscitative practices!), I would consider this a relative contraindication to fluids, given the non-volume-tolerant state (ALI/pneumonia/ARDS and portal pulsatility) of the patient. With pulsatility and signs of organ dysfunction I would be diuresing or pulling fluid off. We’ll see if we can get Rory to comment, as he has been doing a fair bit of this.

So in this patient it would be either no fluids, or diurese.

I don’t think one should have a general conception that reducing preload in a septic patient category is an issue. That may be so if you do not have the capability to look, and hence feel you should behave more cautiously. A septic patient with a tiny IVC may indeed be tipped over into low CO by removing fluids, but another with a full tank post resuscitation may benefit. So with the ability to assess hemodynamics, individualized approaches trump general ides and protocols. Much more to come on this in the next weeks as we break down a lot of interesting concepts in regards to vascular tone assessment and cardiac efficiency. 

I fully appreciate how ambiguous this situation is and that in reality the only way to find out the treatment that works is often by trial and error. Serial assessment by POCUS is definitely needed and one may even put the entire fluid thing aside and focus on other treatments. But just want to know your take and the reasons behind.

Thanks again for all your work and these thought provoking posts; and my apologies for the supposedly quick question ending up being not so quick. It took me some effort to clearly delineate my question in mind.

Anyone interested in these topics should keep an eye out for the H&R2019 Tracks. A bunch of us are getting together before and during the conference and will be recording discussions on all these little cases and angles around hemodynamics and other fun resuscitationist topics.






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 and our discussion at



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!




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






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

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!






The First Steps Towards Physiological Resuscitation: A Team Effort. #FOAMed, #FOAMcc

(original figure from this old post)

So Rory (@EMnerd) hit us last week with an interesting question that was brought up by David Gordon, a resus fellow working with him, and thought some of us may be willing to belabour his point. A lengthy and really fascinating exchange ensued, which I felt was worth sharing with the #FOAMed community:


Rory (Spiegel @EMnerd) find him on

Korbin Haycock (please leave comments to encourage him to get on Twitter)

Segun (Olusanya @iceman_ex) find him on and The Bottom Line

Me (@ThinkingCC) also

David Gordon

My editorial comments!



David brought up an interesting question today. Why not do a straight leg raise and use TAPSE to assess the likelihood the pt will be “volume responsive”?

My answer was the following:
“I don’t think the RV increases TAPSE in response to fluid and so the only way TAPSE would be able to assess fluid responsiveness would be if it decreased in response to a a SLR. My contention is this would be a late marker of fluid intolerance and others signs of venous congestion (portal/renal vein doppler) would be seen far earlier. “
In addition I brought up that “volume responsiveness” is a flawed surrogate and we should rather be focusing on volume tolerance.
And that is, in my opinion, the critical concept. 
Anyway David seemed less than satisfied with my answers so I figured I would open the discussion to you physiology nerds…
That’s an interesting thought, you have brought up.  To clarify, are you asserting that an increase in TAPSE from a volume challenge or SLR could be a indicator of volume responsiveness?  If I missed your meaning, please correct me.
I think Rory is right in his assessment that TAPSE would likely be a more valuable indicator of fluid tolerance (or more importantly , intolerance), rather than fluid responsiveness.  TAPSE, however,  may be (I don’t know) a more sensitive indicator of fluid tolerance than things like IVC collapsibility index, etc.  This might make sense as a decreasing TAPSE (or TAPSV, too for that matter) in response to a fluid challenge might be an earlier indicator that the RV won’t do much with more fluids before it would manifest in things like a non-collapsing, plethoric IVC, decreasing S’/D’ wave ratio on HVD, portal vein pulsitivity, or pulsatile intrarenal venous Doppler.
One problem I’ve had for a long time with fluid responsiveness from the standpoint of the circulation up to the pulmonary valve (IVC collapsibility index being the most common example), is that it doesn’t measure what you really want to know, and that is LV fluid responsiveness.  There is a whole lot going on hemodynamically from when blood leaves the RV to where it finally contributes to LV preload.  I think if you want to know if the patient is fluid responsive, there are quite a few ways to assess this directly, rather than looking at the RV, IVC, etc.
I stopped chasing every bit of volume responsiveness a long time ago, however it does have its place in managing the sick patient, I think.  Usually, my first question is about volume tolerance/intolerance, before I start to think about volume responsiveness.
To investigate the fluid tolerance/intolerance status, I’ll look into a lot of things, usually using a lot of ECHO/US information.  My sonographic considerations are: LV contractility, diastolic function and ventricular compliance, LVEDP, valve pathology, SVR, B-lines (and if B-lines are present, put that into the context of what the LVEDP is because if the pressures are low, but the lungs are wet, pulmonary vascular permeability is high and I’ll think very hard before giving fluids), pulmonary artery pressures, PVR, interventricular septal shifts, RV contractility, IVC, HVD, portal vein, and renal Doppler.
(has anyone ever seen an ED doc do this anywhere??? Wow!!!)
Also, I’m lucky to have some other tools at my place like transpulmonary thermodilution catheters and pulse wave analysis devices to assess things as well.  Sometimes these things make serial assessments more convenient than dragging the US machine over multiple times, and can also give additional information, like EVLW, PVPI, etc.
(I think in the case of Korbin’s hospital, it may be important to bring downstairs care upstairs!)
Secondarily, if I think the patient is volume tolerant and then I have determined that they are volume responsive, and would benefit from volume administration, the next question I ask myself is what’s the best way to do this.
Clinical assessment combined with ECHO comes into play, as if the patient is genuinely volume depleted, volume repletion makes sense.  However, a lot of volume responsiveness is driven by syndromes of high CO and low SVR.  In these cases, I usually give very little volume and opt for a vasopressor to drive venous return instead.  This strategy tends to correct the CO/SVR derangement as well as take care of the volume responsiveness at the same time.  I feel much better if I know that my MAP is being generated by a balanced CO, SVR, and volume status rather than having a “normal” MAP.
I think that is a really, really important cognitive model. The common and traditional approach is to try to maximize CO with fluids and avoid the terrible vasopressors. In a disease where the primary derangement is vasodilatory, it doesn’t seem logical… However finding the right balance is difficult. And with the near-extinction of the PA catheter, we no longer have a low SVR value staring us in the face begging for some pressors.
Sorry to be so long winded, guys.  Hope I didn’t bore you with stuff I’m sure you already know.  These topics are really interesting to me though!  I’d be interested in all of your thoughts on the TAPSE question.
I think the RV is more likely to dilate in response to Fluid than change TAPSE, as suggested by a paper or two on RVEDA changes as a predictor of Fluid responsiveness
(RV dilatation May result in a reduction in TAPSE too?) 
Potentially, yes. SV may not decrease but TAPSE may.
The end result should be a change in stroke volume, so one could argue that rather than TAPSE you could just measure RVOT VTI in response to a passive leg raise. (I don’t really see the difference between M mode and PW doppler, and RVOT VTI is simple enough to measure from a PSAX or RV outflow view)
TAPSE is an Uber-simplified method of looking at RV contractilty rather than volume (overloaded RVs can have excellent TAPSE, for instance). I think it would answer a very different question.
Interesting question indeed. I can’t agree more with Rory and Korbin. Korbin’s clinical run-through is, as far as I’m concerned, completely on point and, if i weren’t so lazy, and had all the hardware he is fortunate to have, would consider as gold a standard as possible, until  mitochondrial monitoring and trans-capillary flow monitor technology is made.
I think it requires a bit of a paradigm shift away from volume responsiveness, that has been all the rage in the last decade or since the end of the swan age, and instead towards focusing on tolerance. There is significant and building evidence that congestion is end-organ damaging, and evidence that chasing maximal CO is mortality-causing (80’s and 90’s literature supranormal o2 delivery and all that), hence on both fronts focusing on congestion makes more sense.
I think we have to follow the fluid path (venous congestion y/n, rv ok y/n, lungs ok y/n and finally lv ok y/n) and then do a global almost holistic ‘is fluid the best option’ reflection including brain, gut, kidneys, peripheral tissues, etc, with Korbin’s nice little twist on balance of CO, SVR for the BP/perfusion. I don’t think there’s any point of care monitoring tool to unequivocally ascertain the best level of each today.
So here is my question, should we be asking “Is this pt likely to benefit from fluids?” rather than “Is this pt likely to augment their CO with fluids?” 
Stop for a moment and think of most of your septic patients (not all, yes, some have cardiomyopathy, some are profoundly hypovolemic), are they actually in a low CO state?  The near-obsession with CO is probably rooted in the common belief that the elevated lactate stems from hypoperfusion, a myth which has been debunked.

Lets say we use Korbin’s gold standard I think we still have to ask what is the benefits of giving this pt fluids? There are many patients I see who would meet all the criteria outlined by Korbin in whom I still don’t administer fluids because whatever increase in cardiac output I get will be transient at best. I am inclined to sit tight allow my antibiotics to take effect and let the pt correct their own vasoplegia. After an initial small aliquot of fluid in the ED I like to see obvious signs of hypovolemia before I give additional boluses. I do like the CLASSIC trials criteria:

(1) Lactate of at least 4 mmol/L
(2) MAP below 50 mmHg in spite of the infusion of norepinephrine
(3) Mottling beyond the edge of the kneecap (mottling score greater than 2)

(4) Oliguria 

All this from the perspective of a decongested venous system and a under-filled heart on US
To Rory’s point, I agree that just because there is a lack of fluid intolerance and the presence of fluid responsiveness, it doesn’t necessarily mean fluids are indicated.
If I have a clinical story that supports a likely lack of hydration plus I’m looking at a high SVR, low CO, and a low SV, I will usually give some fluids.  Mottling, especially if pressors are on board, to me is a clue that some sort of volume might be indicated.
That’s actually quite interesting.  The pathophysiology of mottling isn’t clear (click here for an interesting read), but definitely a space to earmark, when trying to find the optimal balance between vasopressors and CO augmentation.
As far as the lactate goes, as everyone here knows, there’s a whole lot of reasons to have a hyperlactatemia.  It’s drives me a little crazy when I see a lactate come back elevated and the first thing someone wants to do is give fluids, especially if they haven’t considered any of the stuff we’ve been talking about.
I think if you have a patient with a high lactate, the first thing to do is ask yourself why they have a high lactate, rather than trying to correct the number.
Agreed, most of the time in a septic pt I view a rising lactate as a sign I don’t have source control rather than a signal to give additional fluids.
So in terms of fine tuning, here is one thing I like to do with tissue saturation – SctO2 (cerebral)  and peripheral:   if it drops with vasopressors I favor augmenting CO (fluids if not too congested, inotropes to consider) if it rises or stays flat with pressors i stay the course. This is definitely not evidence-based, but to me, if tissue saturation decreases while increasing vasopressor dose, it seems logical that the perfusion is dropping, and not a course worth pursuing. I like to think of it as an example of MBE (medicine-based evidence) in the patient in which it is occurring.
It seems to me the feeling is that we shouldn’t be chasing any single indicator of fluid status/tolerance/response/optimization evaluation and the key is to ask the clinical questions and pair that with our sonographic assessment.   RV functional assessment may have a role in that discussion, but TAPSE may not be the best indicator as RVOT VTI may be a better answer to the initial question.
The study that Segun sent out seems to indicate that LVEDA may be a better predictor of SVI.  The septal interdependence plays a larger role than I initially thought and perhaps using M mode to look at changes in septal motion gives you more information about the ability of the heart as a whole to manage the fluids…
That’s an excellent point, because even if the RV can handle the fluid, if the LV cannot, it’s gonna end up in the lungs.
Philippe, what kind of time course do you allow for your lactate to change, other than just response to your initial resuscitation?
Lactate should improve over hours. As Rory says, if a day later it’s still hovering above 4, and you don’t have impaired hepatic clearance, you might be missing something…
That’s something that certainly something to consider, Rory.   I think a lactate that is suddenly rising is most likely driven by a catecholamine surge driven by something going the wrong way.  But not always.
The important thing is to stop and think about what’s going on.
Case in point:  Last week I had a patient that had cardiac arrest due to an asthma exacerbation.  I had put a TEE probe down during he resuscitation, and a little bit afterward based on what I was seeing on the TEE, I felt she needed a pressor.  I used epinephrine because the beta-2 agonism might help with bronchodilation.  Everything hemodynamically look pretty good, except the lactate came up.  The ICU resident saw the lactate and ordered a liter of LR.  I called them and explained that the epinephrine was likely the cause of the lactate and it probably wasn’t anything to worry about.
Just the other day I was called to the floor to assess a pt because the treating team was concerned he was septic when his lactate came back at 6.5. I walked in the rm as they were hanging the 30cc/kg fluid bolus. A brief assessment revealed he was in florid CHF. Once I convinced them to stop giving fluids and instead use an aggressively dose of diuretics he did just fine and cleared his lactate without issue.

In my mind lactate in and of itself uninterruptible. In a pt who is otherwise improving and the lactate is not clearing as fast as I would like I tend to just stop checking it. The one I find troublesome is in the post resus pt who doesn’t look great, I don’t have an obvious source, their pressor requirements are slowly rising and the lactate is hovering in the 4-5 range. That’s the pt that tends to do poorly if you don’t identify and establish source control

Agree with that Rory.
If I have those patient with a persistent lactate elevation, and they look like they could be malnourished, I’ll give them some thiamine, too.
My two cents- there’s data soon to be released that compared echocardiographic dimensions (RV/LVEDA, IVC etc) to mean systemic pressure- showing no correlation with ANY echocardiographic parameters.
It would seem that going purely by dimensions, you cannot predict volume state on echo… so at the moment we can detect hypERvolaemia with lung, portal vein, and renal vein POCUS (and to a degree IVC), and profound hypOvolaemia by looking at doppler patterns (although the patient is more likely to tell you).
The other side of things, which has been clearly elucidated by everyone in this thread, is the concept of “permissive responsiveness”. Ruthlessly thrashing every heart to its maximum myocardial stretch doesn’t necessarily seem to be the best idea, to my mind.
I agree with everyone’s thoughts. Beyond the initial LLS/Shocked AF stage, you need a very good reason to give a fluid bolus!
And don’t get me started on lactate…
I would only comment that the magic of Doppler probably is far more valuable than cardiac dimensions when dealing with hemodynamics.  Dimensions give anatomic values that can be extrapolated to hemodynamics, but PW and CW Doppler interrogation infers pressure differentials, which can directly be applied to things like flow and resistance.  Tissue Doppler has the added informative value of cardiac compliance, so that a comprehensive picture can be painted in light of filling pressures and the relationship to preloading.
When I look at all this together, I really feel that in most cases, a quite accurate picture of what’s going on is within grasp.
To emphasize again, something like B-lines with a compliant, low LVEDP LV, tells me valuable information about pulmonary vascular permeability.  Tread carefully about fluids here.

How does the RV respond to a fluid bolus?

To answer this question first we must understand the role of the right heart in the circulatory system. Often the right ventricle (RV) is compared to the left ventricle, in reality it serves an entirely different function. The left ventricle generates the necessary pressures required to maintain systemic perfusion. The right ventricle’s job is to enable venous return, which is generated by the gradient between the mean systemic filling pressure and the right atrial pressure (RAP). The role of the RV is to maximize that gradient by keeping the RAP as low possible. 

With this in mind let us examine the RV’s response to a fluid bolus. As the RV becomes filled, conformational changes occur within the RV that allow it to increase its stroke volume without increasing the distending pressure.Under normal circumstances, the RV end diastolic distending pressure does not increase in response to fluid loading. Therefore, if the RV is functioning appropriately, RAP does not accurately reflect RV preload. But in pathological states, when the RV is hypertrophied, diseased, or overdistended there is an inverse relationship between RVEDV and RV stroke volume. Any fluid, or increased RV pressure beyond this point results in an increase in RAP, decreasing venous return.1

1. Pinsky MR. The right ventricle: interaction with the pulmonary circulation. Critical care (London, England). 2016;20:266.

So that was the discussion. I certainly thought it was very interesting. Following this, we decided we’d band together and try to hammer out what we think should be the optimal management of shock, trying to tie in physiology, the scant evidence that is out there about resuscitation, and the pitfalls of venous congestion. Finding the sweet spot in the balance between vasopressors, inotropes and fluids is a very real challenge that all resuscitationists face regularly, and it is very unlikely that, given the complexity of such a protocol, looking at tolerance, responsiveness and perfusion, that an RCT would be done anytime soon.

We’ll be sure to share when we come to a consensus, but certainly the broad strokes can be seen here, and I’d love to hear anyone’s take on this!

And of course, we’ll definitely be discussing this further with smarter people at H&R2019 – think Jon-Emile Kenny (@heart_lung), Andre Denault and Sheldon Magder!



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.Jon replies:

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.

Korbin adds:

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.

‘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.

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.

This programme has benefitted from an unrestricted educational grant from the following sponsors (listed alphabetically):


Fisher-Paykel Healthcare

GE Healthcare




MD Management





The Accreditation is as follows:


Here is the Final Programme:

Final Programme

Wednesday May 22 – PreCongress course

  1. Full day Resuscitative TEE course



    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 here.


Main Conference Programme: H&R2019 Full Pamphlet

Social Events:

Thursday May 23rd Meet the Faculty cocktail! 1900 – Location TBA – BOOKMARK THIS PAGE!


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