H&R2019 Lecture Series: Weimersheimer (@VTEMsono) on Massive Transfusion. #FOAMed, #FOAMer

Sorry for the delay, been bogged down in getting H&R2020 off the ground! But here is another goodie from H&R2019, my good friend Peter W. on an ever-important trauma topic.  Enjoy!

Weimersheimer on MT – H&R2019.

 

cheers

 

Philippe

ps for anyone interested, H&R2019 On Demand can be found here!

The Resus Tracks: A Chat with Domagoj Damjanovic! #FOAMed, #FOAMcc, #FOAMer

 

So I recorded a chat with Domagoj (@domagojsono in the twitterverse), an anaasthetist-resuscitationist-intensivist from Freiburg a few months ago, but with H&R2019 and its aftermath, been slow in processing a lot of stuff I’ve got stocked… Apologies!

So in this one, DOmagoj and I discuss a bunch of resus topics, from eCPR to tissue oximetry. I’m really jealous of the fact that he does prehospital work with an ECMO van!!! …and with cool gear and of course, POCUS!

Here is the chat, hope it leads to thoughts, discussion and contribution!

And here are some links:

low budget ultrasound simulation
and here’s the editorial in Resuscitation,

cheers

 

Philippe

 

Exploring the Pulmonary Vasculature with Korbin Haycock: RVOT Doppler. #FOAMed, #FOAMcc, #POCUS

So some recent twitter discussions, particularly involving my friend Korbin (@khaycock2) and Lars (@LMSaxhaug) – whom I am trying to get on the podcast soon – were really fascinating in regards to RV and pulmonary hypertension assessment. So time to dig into this a little.
The basic POCUS RV assessment is RV:LV ratio and TAPSE, along with RV free wall thickness (should be below 5mm) and the D sign in parasternal SAX. This is a solid start to screen for significant RV dysfunction.
The next level should be to measure PAP using TR Vmax, in order to assess the degree of pulmonary hypertension. Thats pretty much where I’ve been at for the last few years and wasn’t sure there was really a lot more that was necessary from an acute care standpoint where your immediate questions are fluids/pressors/inotropes and some inhalational pulmonary dilators. I wasn’t convinced I needed more.
But of course Korbin and Lars are on another level, and started to talk about doing RVOT doppler and looking at TR Vmax to RVOT VTI ratios to estimate pulmonary vascular resistance. Is there any difference there? Is my PAP not enough? Well, turns out there may be some useful information there, so I will let Korbin do the talking, and my apologies for my dumb questions during this discussion!
So I will be toying with RVOT doppler and trying to see if this is something that warrants a place in acute care management. I suspect it may be something that may tip towards earlier inhaled vasodilator therapy, or else make not using them a more confident choice. I do like the waveform analysis. I think we generally overlook a lot of good info by focusing on numbers over morphology!
So far, images using the PS SAX view have been quite good:
Additionally, RVOT notching could be suggestive of an acute PE – makes sense (study link here!)
Here are a couple of excellent references:
So thanks to Korbin and Lars for forcing me to up my doppler game some more!
cheers
Philippe
Formula Fun:
Tricuspid regurgitation pressure gradient for sPAP:
sPAP=4*(TRvelocity^2) + RAP or
sPAP=TRpg +RAP
mPAP=(sPAP)*0.61 + 1.9
Acceleration time equations for sPAP and mPAP:
sPAPlog= -0.004(AT) + 2.1
mPAP=90 – (0.62*AT)
Pulmonary Regurgitation pressure gradient:
mPAP=4*(Peak initial velocity^2) +RAP
dPAP=4*(End velocity^2) + RAP
dPAP-PCWP should be about <6mmHg or else PVR is likely, see PCWP equations below
PVR equation to screen for increased PVR, or if PVR < 3 WU:
PVR=10*(TRvelocity/RVOT VTI) + 0.16. TR velocity is in m/sec, if <2 WU, no increased PVR.  This equation is accurate up to 3 WU
PVR equations for increased PVR > 3 WU.  These equations less accurate if PVR < 3 WU:
PVR=5.19*(TRvelocity^2) – 0.4, or more simplified: 5 * (TRvelocity^2). Note that the 5 * (TRvelocity^2 is almost sPAP equation (4 * TRvelocity^2)=sPAP
PVR=sPAP/RVOT VTI if no RVOT notch present
PVR=(sPAP/RVOT VTI) + 3 if RVOT notch is present
PCWP equations (for detection of group 2 pHTN to elevated sPAP), as you know, this is a whole other area, and gets a quite a bit more complicated, but to summarize:
PCWP likely elevated if E/e’>15, unlikely if E/e'<8
In NSR, PCWP=1.24 * (E/lateral e’) + 1.9
In ST, PCWP=1.5 * (E/lateral e’) + 1.5
In atrial fibrillation averaged over 5 beats, PCWP=0.8 * (E/lateral e’) +6
Using color M-mode and propagation velocity: PCWP=5.27 * (E/Vp) + 4.6

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…