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.

 

cheers!

 

Philippe

 

My friend, the IVC. #FOAMed, #FOAMer, #FOAMus, #FOAMcc

So I keep hearing and seeing people bash the IVC. Casually dismissing it with a shrug. “It’s not really good for volume responsiveness, you know…”

All that deserves is an eyeball-rolling emoji. That is, unfortunately, the reaction of docs who are trying to devise a threshold or recipe-based approach to POCUS management (which will be just as bad as any recipe-based medicine) as opposed to physiological understanding of what is going on with the patient.

There’s so much good information packed in scanning the IVC (properly, in both axes – for more, see a bunch of my previous posts), and frankly, volume responsiveness is the least of my concerns, that it is a shame to toss out the proverbial baby with the bathwater.

So I talked about this at Stowe EM – an awesome conference run by my friend Peter Weimersheimer (@VTEMsono), which I highly recommend to anyone for next year, great talks, people and spot:

Here are my slides:

IVC Stowe

And the audio:

 

Love to hear your thoughts!

Oh yes, and anyone looking to explore physiological, evidence-based, cutting- and bleeding-edge approaches to resus, don’t miss H&R2019 this May in Montreal!

cheers

 

Philippe

The Andromeda-SHOCK study. A physiological breakdown with Rory Spiegel (@EMnerd). #FOAMed, #FOAMcc, #FOAMer

So recently published was the Andromeda SHOCK trial (jama_hernndez_2019_oi_190001) in JAMA this month.

Definitely interesting stuff, and have to commend the authors on a complex resuscitation strategy that had some real-world flexibility built in in terms of later generalizability and applicability for real-world cases. However there are some fundamentals I have concerns about. Let’s see what Rory thinks:

Yeah. I think the bottom line of opening resuscitationists’ eyes to NOT apply monosynaptic reflexes of giving fluids to elevated lactate is good. In that sense, definitely a step forward.

However, the insistence on maximizing CO under the illusion of optimizing perfusion remains problematic and leads to a congested state unless only a small or perhaps moderate amount of fluid is required to achieve non-volume responsiveness. I think it’s important to realize that the most rapid correction of hemodynamics is a surrogate marker and has not been definitively associated with survival across the board (eg the FEAST study and others), and it’s only proven clinical impact may be on health care workers’ level of anxiety.

Tune in soon for some other smart docs’ take on this!

 

cheers

 

Philippe

 

oh yes and don’t forget The Hospitalist & The Resuscitationist 2019:

 

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 http://www.heart-lung.org.

Cheers

 

Philippe

 

 

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

Volume status, CHAISE study and other silly questions. #FOAMed, #FOAMcc, #FOAMer

So I just finished reading the CHAISE study, which compared Parm as a surrogate for Pmsf as a surrogate for “volume status.”

It is a really cool study for anyone who loves physiology, which I definitely do, and there may be some interesting elements that can be clinically used.

But let’s first set the record straight. I do not believe that “volume status” is a medical and especially not a scientific term. It is a vague reference to intravascular fluid and can be interpreted in a lot of different ways, making it essentially useless. There is such a thing as the status of your flight (on time, delayed, cancelled), your reservation (confirmed, cancelled), your postal delivery (returned, delivered, in-transit), etc.  But there are no such clear strata for “volume status.”

So what are the true scientific terms that can be measured? Blood volume. So if we had a bedside radiolabelled substance test that could give us our true blood volume, that could give us a real measure of “volume status.”

On the other hand, that would be of marginal use clinically, in all likelihood.

Why? Because there are only three questions that the savvy clinician is trying to answer, in order of importance:

1. Does my patient need fluid?

2. Is my patient volume tolerant?

3. Is my patient volume responsive?

The answer to the first question is mysterious, outside of the obvious extremes, and in my opinion, anyone who feels they can clearly answer correctly is deluding themselves.

The answer to the second question is complex and multi-factorial and includes echographic findings (venous congestion/hypertension, B lines, effusions, ascites) as well as physical examination findings (tight abdomen, edema) and clinical findings (respiratory failure, intracranial pathology) and more. But this is a critical one, because if the answer is no, then you need some really compelling evidence to even consider trying to answer the third question.

The answer to the third question is, outside of the extremes, a bit of a quagmire of assessments and technology with generally poor evidence, particularly in terms of duration of effect. The most fearsome aspect of this third question is that it is usually the first question asked instead of the last, and thus has the side effect of creating volume-responsiveness terminators who, 500cc shot after 500cc shot end up satisfied that they have blasted responsiveness into oblivion.

But that’s probably bad news for the patient, that they have now pushed into venous congestion or salt-water drowning. Unless, of course, they just look for volume-responsiveness in the same way that bird-watchers do, for the sake of scientific satisfaction, and do no more than look, or maybe snap a picture at most.

So sure, echocardiographic parameters for volume status should be under fire, as all other parameters should. The authors in this paper themselves state two critical assumptions in the Parm/msf logic:

(1) that the fluid stay intravascular in the 10 minutes (ok, I’ll buy that)

and

(2) that the compliance is linear (nope, I don’t buy that, especially not in sick patients on vasopressors – as opposed to the normal cardiopulmonary and hemodynamic patients this study was done on).

Essentially, what should be under fire is the obsession with a measurable variable to assess intravascular volume. Too many factors in play, and the answer is useless clinically anyway.

On the other hand, this study is fascinating in terms of what might be done using dynamic Parm… Maybe individualizing pressor response, unstressed volume recruit-ability?  I’ll let @iceman_ex tell us about that at H&R2019!

So what is important is stop points. And reverse points. And yes, these can be looked at using POCUS, and also CVP, and CVP tracings. And yes, there is good data that venous hypertension is a bad state. And this is what you should be looking at, to make sure you have not pushed your patient into a universally pathological state of non-volume-responsiveness.

Cheers

Philippe

So Kylie (@kyliebaker888) had some comments and questions:

Hi Philippe, I just had to read the article after your blog. Most is a bit above my head (yeah right Kylie)– but I am perplexed by three things that I did understand -perhaps you can help me with….
1. Is P(arm) a useful measure? – it went up in 19 patients and down in 8 patients after a 500ml bolus yet they claim it went up (after statistical repeated measures or something)..if P(arm) is confounded by something else – I think they suggest sympathetic tone – shouldn’t we sort that before we start using P(arm) as a reference test.

I don’t think we can consider it to be a reference at all. I think it is an interesting physiological measure and that it might have some application in phenotyping vascular tone/compliance and possibly helping in vasopressor fine tuning. In my opinion for fluids it adds little to what we have.

2. What do you think of their IVC measure – 0.5cm below junction with RA?

As I do for all IVC diameter measures, I think it is inherently mathematically flawed to try to assess a volume using a diameter. Eyeball the whole IVC. A recent study finally looked at this. 3D IVC assessment and (of course) found it better.

3. What do you think of the fact that E changed, but e prime and E/e prime didn’t….That seems like there may not be enough precision in some of those measurements.

I agree.

I also have another savvy-clinician question to add to yours
Q4: Is my patient leaking?

Excellent!

Thanks!

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

 

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.

Here is the Final Programme:

H&R2019 Full Pamphlet

Wednesday May 22 – PreCongress course

  1. 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!

 

Register here!

FOR ANY QUESTIONS CONTACT HOSPRESUSCONFERENCE@GMAIL.COM.