So this morning I shared a case that I’m looking after on Twitter and got asked a really interesting question. But a bit too much for the 140 characters of Twitter. So here’s the answer!
Thanks!
#POCUS IVC Pitfall Twitter Poll & Discussion. #FOAMed, #FOAMer, #FOAMcc
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!
cheers
Philippe
ps if you like physiology, and a physiologico-clinical approach, don’t miss H&R2019!
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!
cheers!
A Tale of Salt and Water: Venous Congestion and CHF (Part 1) #FOAMed, #FOAMim, #FOAMer
So, venous congestion is the predominant physiopathology in CHF, with a number of ensuing problems including lung edema, effusions, hepatic congestion and cirrhosis, renal failure and even gut edema and failure, though less traditionally focused on.
Venous congestion is essentially a problem of salt and water, retained by a well-intentioned but (eventually) maladaptive neuro-endocrine process. The bottom line being: too much salt and water…
However, the vast emphasis in pharmacologic CHF management, if you look at guidelines and publications, is predominantly on various neuro-endocrine modulation strategies, and though these certainly have a role, it is logical that optimizing volume status must play a central role. So why is it not a recurrent theme of discussion? Well probably because our means to traditionally assess this is limited. What are the tools used by physicians worldwide to assess congestion? Weight, peripheral edema, JVD, crackles, CXR are pretty much it. Now even under the best of circumstances, these are hardly precise tools, and of intermediate specificity. But it is what is available, and taught, and in most cases, does the job fairly well. However, judging by the problem of recurrent admissions for CHF exacerbations, likely not good enough.
The Canadian HF Guidelines – as thorough as they are – are interesting in that the only time diuretics are addressed are in exacerbation, and a note to use the lowest dose possible to maintain stability… But little else in terms of guiding this assessment of stability or the dosage management. The usual “thorough history and physical” stuff, of course.
So what else could we do? Now my interest in POCUS is no secret, and it seems like the ideal tool for assessing both fluid collections and hemodynamics. So what do we know?
Lungs – at this point it’s beyond much debate, POCUS-enhanced physical examination is vastly superior to radiographs and traditional physical examination. Small effusions are easily seen as well as congestion in the form of B lines. In the case of sub-acute to chronic congestion, as we are not overly concerned with central lesions (not seen with ultrasound), the CXR is of no further benefit.
Peripheral edema – I’ll call this one a tie. Not that much benefit in measuring subcutaneous edema with a probe, except for exact reproducibility, at the cost of time. 😉
The Heart – another no-brainer. Ultrasound wins. With appropriate training, experience, and more important than either, the ability to recognize one’s own limitations.
Venous congestion – Now we’re getting to the interesting stuff. So even if for some, it may be the first time hearing about the clinical use of venous congestion markers in CHF, it isn’t new science. In the 90’s, several studies were published correlating portal vein pulsatility, congestion index, as well as hepatic vein doppler pattern with CVP, RV dysfunction, finding close correlation. In 2016, Iida et al published a great article on renal venous doppler and CHF which I highly recommend reading, and more recently, Andre Denault and William Beaubien-Souligny (@WBeaubien) have been doing tremendous work with portal vein pulsatility and post-op cardiac patients’ organ dysfunction. So the science correlating excessive venous congestion to organ dysfunction is there and is clear.
Why have we not yet widely studied this?
The answer is fairly simple. Prior to the growth of POCUS, there was no single clinician group holding the necessary set of clinical and echographic skills to make this clinical routine. Cardiologists are not all echo-capable, and even those that are would have had little or no experience dopplering abdominal organs and vessels. Radiologists – most of the literature coming from their field – are not pharmaco-clinicians and do not follow patients. Family physicians and internists, likely the bulk of the physicians looking after these patients, largely had not had access to or echo skills. Until now.
So a quick review: right-sided failure causes elevated RAP, so everything upstream gets congested. The first echo signal of this is the plethoric IVC (in both axes of course!!!), and an abnormal hepatic vein doppler (which is pretty much like a CVP tracing, just non-invasively) but is that the max? Nope. What is worse is when that pressure transmits thru backwards from hepatic veins to portal vein, transforming a normally monophasic flow with minimal variation into a progressively more pulsatile flow, to the eventual point of being intermittent. And when the IVC pressure transmits across a congested kidney such that the same thing occurs in the renal veins.
Those findings have been well studied and correlate with poor outcomes in CHF.
So what could we do?
What we are doing now is systematically assessing CHF patients in terms of their venous side. What we see so far is that some have full, plethoric IVCs, maybe B lines and effusions, maybe some peripheral edema, but may or may not have those worse markers of abnormal doppler flows, and those who don’t generally don’t have significant organ dysfunction such as renal failure (I discussed this a few years ago in my pre-doppler era in terms of re-thinking common approaches).
So when we find significant portal pulsatility, we diurese aggressively, creatinine notwithstanding. We almost always get an improvement in biochemical markers of renal function within 48-72 hours, with the only really tricky patients being those with severe pulmonary hypertension. More on that in another post.
Goonewardena et al had a really great observational study that showed that if CHF patients were discharged with a non-plethoric IVC and significant respiratory variation, they were less likely to be re-admitted. The figure below on the right shows the numbers:
So there is reasonable evidence to suggest a POCUS-guided approach, which we’ll go over in the next post, which should include our revised Advanced CHF Clinic guidelines.
I can already hear the thoughts… “is there any evidence for this?” But those asking that reflexively should first ask themselves “what is the evidence behind the way I assess congestion and manage CHF?”
cheers
Philippe
Refs
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 emcrit.org
Korbin Haycock (please leave comments to encourage him to get on Twitter)
Segun (Olusanya @iceman_ex) find him on LITFL.com and The Bottom Line
Me (@ThinkingCC) also thinkingcriticalcare.com
David Gordon
My editorial comments!
Rory:
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…
Korbin:
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.
Segun:
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 https://ccforum.biomedcentral.com/articles/10.1186/cc3503
(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.
Me:
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.
Rory:
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
Korbin:
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.
Rory:
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.
Philippe:
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.
David:
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…
Korbin:
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.
Rory:
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
Korbin:
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.
Segun:
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…
Korbin
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.
David:
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!
Cheers
Philippe
POCUS, Mythology and Hemodynamic Awesomeness with Jon and Korbin! #FOAMed, #FOAMer, #FOAMus
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.
Philippe
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.
cheers
Philippe
H&R2019! Final Programme. Register Now! Montreal, May 22-24, 2019! #HR2019
This event is past. It was awesome. If you really wish you’d been there, you can catch most of it here!
And don’t miss H&R2020!
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):
Cook
Fisher-Paykel Healthcare
GE Healthcare
Maquet-Gettinge
Masimo
Medquest
MD Management
Medtronic
Novartis
Teleflex
The Accreditation is as follows:
Here is the Final Programme:
Wednesday May 22 – PreCongress course
- Full day Resuscitative TEE course
FOR DETAILS SEE HERE
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!
FOR ANY QUESTIONS CONTACT HOSPRESUSCONFERENCE@GMAIL.COM.
H&R2019 Pre-Conference Courses. May 22nd. Yup, it’s worth coming early!
So we are very, very excited about our pre-conference course lineup. It is simply awesome:
1. Full day Resuscitative TEE (Limited to 20 participants) 0830-1730
H&R2019 REGISTRANTS SHOULD RECEIVE A CODE ENABLING REGISTRATION. FOR ANY QUESTIONS CONTACT HOSPRESUSCONFERENCE@GMAIL.COM.
2. Full day Keynotable 0830-1730
3. Half day Hospitalist POCUS (Limited to 30 participants) afternoon 1330-1730
4. Half day Critical Care Procedures (Limited to 20 participants) morning 0830-1230
5 .Half day Brazilian Jiu-Jitsu for MDs (Limited to 30 participants) morning 0900-1200.
Note that sadly, you have to make some choices. No way to attend it all…
So here is some info to help you make your best pick:
1. Full day Resuscitative TEE: run by none other than Felipe Teran, and featuring Andre Denault as head instructor, this is a unique opportunity for a deep dive into everything about TEE in shock/arrest as well as extensive hands-on training on shock/arrest TEE using state-of-the-art simulators. Participants will obtain an Optional Competency Assessment, providing a Workshop Certificate and a Focused TEE Competency Assessment Checklist certifying completion of 10 proctored examinations.
Limited to 20 participants. 795$USD. Note that conference registrants (minimum one day) will be prioritized for registration to this workshop, with proof of H&R2019 registration required. Remaining spots will be released to non-conference attendees on March 1st, 2019.
2. Full day Keynotable: the brainchild of educator extraordinaire Haney Mallemat, this course is intended for those who want to add some serious game to their presentations and didactic teaching. Sharing tips and pearls that have made him unquestionably one of the best docs to man the stage and podium, this is a rare opportunity not only to leave run-of-the-mill powerpoints behind, but also to enhance your future audience’s learning and become a master presenter.
Registration 495$USD physicians, 375$USD trainees and other health care professionals. Register at http://www.keynotable.net or email info@keynotable.net.
More details here.
3. Half-Day Hospitalist POCUS: Learn absolutely necessary skills for the day-to-day management of your hospitalized patients. It doesn’t matter how good a clinician you are, with ultrasound you will be a better one. Learn from a world-class clinician faculty how to assess the IVC for a number of clinical scenarios, how to assess lungs, do basic cardiac views, diagnose or rule out hydronephrosis, and safely tap ascites or pleural effusions.
Cutting edge today, standard of care tomorrow…
Faculty: Rola, Ajmo, Haycock, Baker, Olusanya
Practice on state-of-the-art simulators, normal volunteers and volunteer patients with true pathology.
Your patients need you to know this.
Limited to 30 participants so that your hands on and faculty experience is maximized. 300$CAN/250$USD
4. Half-Day Critical Care Procedures: If you are not already familiar with these key procedures any resuscitationist should have in their pocket, don’t miss this course. We’ll go over thoracic pigtail insertion, bedside percutaneous tracheostomy and emergency surgical airway, using manikins and natural simulators. Plenty of practice, until you’re comfortable with the techniques. By the end of this activity, participants should be able to independently insert pigtail catheters and perform an emergency surgical airway, and be able to perform a percutaneous tracheostomy with the backup and supervision of an experienced operator.
Faculty: Ajmo, Farkas, Tremblay
Limited to only 20 participants, so don’t wait too long! 300$CAN / 250$USD
5. Brazilian Jiu-Jitsu for MDs: Nope, you didn’t accidentally click on a link. This is part of the pre-conference day. What does it have to do with medicine? A lot. With life? Everything. If you’re already got mad mat skills, come join us for a couple hours of fun. If not, treat yourself to an introduction into a martial art, a sport and even a lifestyle that cultivates physical and mental health like no others. The rest of the conference will change your practice, but this workshop might change your life.
Faculty: Spiegel, Rola, and some guest stars!
No experience necessary, only interest and enthusiasm.
It’s a bit too early to be sure who, but expect to have some interesting surprises as to who your instructors might be…
…oh, and acute care docs should find something in the words of Rickson Gracie, one of the legends of jiu-jitsu:
Limited to 30 participants, registration fee TBA, and will open on november 1st. You can reserve your spot in the meantime by emailing hospresusconference@gmail.com.
So we are really looking forward to these courses. It’s a great opportunity to pick up some important skills and have plenty of time with some awesome instructors, all of whom are hoping to share as much clinical knowledge as possible.
Mark your calendars! Please email hospresusconference@gmail.com with any questions!
The H&R Scientific Committee – St-Arnaud / Zambrana / Rola
A Primer on Pigtail insertion. #FOAMed, #FOAMcc
So I recorded this for our incoming residents to Santa Cabrini ICU, whom we expect to become well versed in this procedure by the end of their rotation with us. The difference between a smooth and simple insertion – best for both patient and operator, is in the little details.
Figured I might as well put it up on #FOAMed in case anyone else may benefit!
Here is the podcast:
And here is a video displaying the technique.
cheers
Philippe
thinking critical care 
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.