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 a couple weeks ago I had the chance to sit in sunny Florida with Jeff Scott (@jsemccm), an ED-intensivist who runs the ED at Jackson South in Miami as well as rounding in the ICU at Jackson Memorial.
His group recently published an awesome article on TCD that pretty much made me realize I have to up my TCD game to the next level.
Here it is (unfortunately walled…)
And here is our discussion:
So there clearly is more to be done with TCD than I have been doing, and maybe it really has a place in the ED. I don’t work first line in the ED so initial stroke patients I only see if they deteriorate, but the idea of visualizing perfusion – or reperfusion – is really interesting.
So if you want to meet Jeff and have him teach you some POCUS TCD, don’t miss H&R2019 which is just around the corner. There aren’t many spots left! Jeff will be running a TCD workshop along with Rob Chen (@ottawaheartrob) which I’m really looking forward to!
Love to hear from anyone pushing the envelope of TCD (or any POCUS application). I believe we are only scratching the surface of what we can do with POCUS, and much study, based on front-line clinicians taking bold strides ahead to see what can be done.
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 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 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!
ps if you like physiology, and a physiologico-clinical approach, don’t miss H&R2019!
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!