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.
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:
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!
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:
- lactate is a marker of severity of insult/injury/inflammation but NOT something to specifically treat with an automatic fluid “chaser.”
- getting a global assessment of the patient’s perfusion – including things such as CRT is important.
- 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 https://emcrit.org/emnerd/em-nerd-the-case-of-the-deceitful-lantern/ and our discussion at https://thinkingcriticalcare.com/2019/02/19/the-andromeda-shock-study-a-physiological-breakdown-with-rory-spiegel-emnerd-foamed-foamcc-foamer/
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!
So recently published was the Andromeda SHOCK trial (jama_hernndez_2019_oi_190001) in JAMA this month.
Definitely interesting stuff, and have to commend the authors on a complex resuscitation strategy that had some real-world flexibility built in in terms of later generalizability and applicability for real-world cases. However there are some fundamentals I have concerns about. Let’s see what Rory thinks:
Yeah. I think the bottom line of opening resuscitationists’ eyes to NOT apply monosynaptic reflexes of giving fluids to elevated lactate is good. In that sense, definitely a step forward.
However, the insistence on maximizing CO under the illusion of optimizing perfusion remains problematic and leads to a congested state unless only a small or perhaps moderate amount of fluid is required to achieve non-volume responsiveness. I think it’s important to realize that the most rapid correction of hemodynamics is a surrogate marker and has not been definitively associated with survival across the board (eg the FEAST study and others), and it’s only proven clinical impact may be on health care workers’ level of anxiety.
Tune in soon for some other smart docs’ take on this!
oh yes and don’t forget The Hospitalist & The Resuscitationist 2019:
So here is what Jon tweeted a couple weeks ago:
Yikes! Does that spell doom for POCUS???
So clearly we had to get to the bottom of this statement…So a google hangout was in order.
Part 1 my intro:
and Part 2 our discussion:
So the bottom line is that we agree that there is a risk that POCUS may partly head the way of the PAC, or at least be challenged in a similar fashion. Hopefully the wiser physicians will see the inherently flawed logic that would push the field in that direction. Alternately, we could all get our minds and efforts together and try to do a triangulation of data to really pinpoint hemodynamics.
Love to hear comments!
For more of Jon’s physiology awesomeness, visit http://www.heart-lung.org.
PS for cutting-edge and bleeding edge discussions, including Jon-Emile and a lot more, don’t miss H&R2019 this may in Montreal…
So I’ve been quite passionate about adding ECPR to our shop for quite a while now, but bureaucratic hospital processes, particularly in Quebec these days, has us bogged down and makes progress slow and painful, despite good intentions. So we need a boost, not only to be able to offer this technology to our patients, but more importantly, to show that it can be done in a community hospital, that all you need is the desire to give your cardiac arrest patients the best chance at neurologically intact survival they can get.
Here’s a little explanation, particularly for the non-medical readers:
That, and of course a pre-determined corridor to a tertiary care center with a cath lab and a compatible ECMO system to yours.
We have the good fortune to be a couple blocks from the Montreal Heart Institute who are interested in collaborating, and we have the desire, skill and motivation to pull this this off.
It’s important for both MDs and non-MDs to understand that this approach would possibly save 50% of the patients that we normally have no hope to save. At the point when we initiate ECMO, these patients have almost no chance with the current means. That is an incredible impact.
But we do need your help. The government isn’t moving fast, and won’t until this is established practice (well Dr. Rola, where else is this being done locally? – same question/answer as when I asked for a 100,000$ ultrasound system for our ICU in 2004: nowhere around here!).
So I figured that if we can raise enough money, and with the help of our awesome Foundation – under the presidency of Mr. Arcobelli, no effort has been spared to raise funds and the quality of care that we offer at Santa Cabrini! So to help them out and to get the ball rolling, we’re setting up our project on chuffed.org, a crowdfunding site which is tied to the Santa Cabrini Hospital Foundation, and every dollar will be specifically earmarked for this and not used for anything else.
My hope is that by the end of 2019, we have an active ECMO unit able to be deployed for cardiac arrest cases in the east end of Montreal, and that in the years following, other community hospitals follow suit. We are a small community hospital, but with a big heart!
We need 250,000$. The device costs about 150,000$, each circuit about 7,000$ and we need to set up some training for the team. That should get us jumpstarted and cover the first 10 patients.
We’re more than happy to field any questions. As a start, the Critical Care & Ultrasound Institute be donating a minimum of 2,000$ (it’s a bit early to be able to commit to more, as we do have to feed the participants and bring the faculty…) from the H&R2019 conference, , which takes place at Santa Cabrini Hospital from May 21-24, 2019.
I’d like to thank Joe Bellezzo, Zack Shinar and Scott Weingart from the @edecmo project who planted the seed and showed all of us that this could be done.
for those who want to know more:
I would also like to thank Santa Cabrini’s Team 6444 of operators, who are a major driving force behind this effort: Sandy Mormina, Rita Pisanelli and more!
PLEASE HELP AND DONATE AT: http://www.chuffed.org (not active yet, will be linked soon) and please forward this to friends and colleagues. You can also send a cheque labelled “ROLA ECMO Project” in the note part of the cheque (this will ensure that the money cannot be used for anything else) to the following address:
Santa Cabrini Hospital Foundation, 5655 Rue St-Zotique, Montreal, H1T1P7, QC, Canada.
Every dollar gets us a little bit closer!
cheers and thank you!
Dr. Philippe Rola
Chief of Service, Intensive Care Unit, Santa Cabrini Hospital