A ResusTEE case discussion with ED doc Serge Keverian. #FOAMed, #FOAMcc

So I’m really stoked about this story. Truly makes meducation worthwhile. While preparing H&R2019, I was chatting with Felipe Teran who suggested he could bring the ResuscitativeTEE course up, which I thought would be awesome. So we did, and got a bunch of local and international participants. Now to me this was part of exposing local ED docs to advanced resus, as we had recently started an Advanced Resus Committee at our shop, all in the line of upping the game and hopefully heading towards eCPR.

So some guys from another local community hospital also took the course and were pretty amped about it and wanted to pick our brains about the practical aspects of resusTEE, as we’ve got a bunch of cases under our belts at Santa Cabrini in the last couple of years.

Well, lo and behold, just days after the conference, these guys used resusTEE with awesome results!

Here is our discussion:

Resus TEE w Serge K

So we need to thank @FteranMD and the @resucitativeTEE team, Mae West, Laura Duggan, Tom Jelic and our own Philippe St-Arnaud for putting together a course solid enough that it had an immediate effect on the participants’ practice and on clinical outcomes.

It is also interesting because of all the political BS that takes place in a health care system, one of the common themes is the desire by some individuals and policies to “hog” the resources and want to centralize everything in so-called centres of excellence. There is, of course, some sense to this – concentrating the clinical experience (eg if you are only doing one central line or one heart transplant a year, you probably shouldn’t be doing any. This, to me, applies for many types of interventions or resources, especially those that are  not exceedingly time-sensitive, where the patients do have the time to get to the well-heeled service or doc that grows the elite expertise, no mater the field.

However, there are a lot of cases where the situation is critical and the patient lands in the closest ED, and the guys and gals in the trenches have to handle it. In my opinion, if these teams are motivated and willing to gain the skills, they need to be supported and equipped. This case is a great example of ED docs in a community hospital integrating an advanced resuscitation technique that is done in only a handful of centres, and in most cases, not yet being done in most tertiary/academic care centres, and doing so with great effect.

Same applies to techniques such as REBOA. We ran a workshop at H&R2019 using the REBOA simulator. It isn’t rocket science. If you’ve put in femoral art lines, let alone PA catheters, this is an exceedingly simple technique. It isn’t just the downtown academic centres that should be using resuscitative technology or procedures. Those patients living in the suburbs who arrest or get smashed may not have the time to make it to those EDs, and they pay the same taxes (in Canada) that keep the system going.

So if anyone reading this is involved even loosely in policy-making, whether institutional or broader, stop this childish nonsense. Let’s get everyone the care they need.

 

 

cheers

 

Philippe

A #5minutesofCC discussion with Josh Farkas: Fluids in the ICU! #FOAMed, #FOAMcc

 So for me, the best part of organizing a conference is all the behind the scenes, car, hallway, brunch, lunch and gym discussions that take place. Of course the talks are great, but often it’s in these discussions that the nitty gritty of clinical opinions on management come out.

So we did manage to record a few, and since Josh wrote up essentially the definitive review of fluid boluses:

 https://emcrit.org/pulmcrit/bolus/

I thought it made sense to put our discussion out to #FOAMed at the same time:

Love to hear your ideas!

Philippe

Venous Congestion from different Clinical Standpoints. #FOAMed, #FOAMcc, #FOAMus

 

So last week sometime we had an interesting twitter exchange which made me realize it is important to explain how some of us are using venous POCUS in different clinical scenarios, which is key, because the development of monosynaptic clinical reflexes with POCUS findings is a rabbit hole we should try not to go down. Instead, POCUS should be about asking the right question and taking that answer as a piece of the pathophysiologic puzzle facing us, which may mean intervening sometimes, and sometimes not, for the same given finding, but with different surroundings.

Here is the twitter exchange.

Thanks to those involved in that discussion – it is how we grow!

And here are some thoughts:

For those not up to speed on venous congestion POCUS I put up the chapter that Korbin Haycock, Rory Spiegel and I worked on in this earlier post.

Here are Korbin’s thoughts on this:

I’m very glad Dr. Eduardo Argaiz pointed this case out, as it brings up considerations apropos both chronic venous congestive cases as well as management of acute illness, particularly in sepsis, where we would expect patients to most likely be fluid responsive, but fluid tolerance is largely overlooked with current management strategies by the majority of clinicians.

Phil’s above audio commentary points out the difference is these two broad categories very nicely. If you didn’t listen to it–you should.

With respect to chronic venous congestive conditions, the knowledge and application of Doppler assessment to therapy will hopefully be the next advance in management at large. Already, I think there is more than adequate research available to show the value of Doppler POCUS (D’POCUS, D/POCUS, or DPOCUS?) in managing these patients. It’s only a matter of clinicians willing to commit to learning and integrate this technology into their skill set.

With respect to resuscitation of the acutely ill patient, there is by far less data, and we are probably into the realm of N=1 here, in terms of how to manage these patients. But, I personally believe–and I understand this is my opinion–that current trends in resuscitation (especially sepsis resuscitation), largely ignores the effect of over volume resuscitation and the potential downstream damage inflicted on our patients.

This theoretical damage of over aggressive fluid resuscitation is multifactorial, including glycocalyx shedding issues/endothelial dysfunction, positive fluid balance and EVLW causing increased mortality (which there is ample evidence for, I think), venous congestion leading to perfusion injuries to encapsulated organs, such as the kidney (AKI) and brain (congestive encephalopathy), and end organ edema leading to the perpetuation of a malignant inflammatory syndrome (portal HTN and gut edema).

In the case called out by Dr. Argaiz, (which can be reviewed by the previous post on this website) my patient had an IVC that whilst not plethoric, was not an IVC that one would expect to find in a patient with a typical distributive shock pattern (i.e. increased cardiac output, decreased SVR, and decreased RAP). Firstly, the complicating factor of atrial fibrillation with RVR was central to the patient’s shock state, however this was quickly addressed with rate control. However, in addition, this particular patient did exhibit additional signs of venous congestion. The portal vein was pulsatile and the intrarenal Doppler pattern was interrupted/bi-phasic in nature. Granted, a pulsatile PV Doppler could be interpreted as related to the hyper dynamic nature of septic shock (as the esteemed Dr. Denault correctly cautioned in his comments on the original post), however a less than flat IVC and the intrarenal findings gave weight to a venous congestive hypothesis as a cause the PV findings as well as a possible cause for his AKI evident on his initial labs.

With this particular case, given my personal global POCUS/FOCUS assessment of his increased LAP (high E/e’), RV dysfunction, RAP, PV, and intrarenal Doppler venous pattern, AND that fact that the RRI was insanely high with an AKI, I elected to treat my hypothetical construct of his renosarca with furosamide and his RRI with vasopressin (as the NE infusion did increase his MAP, BUT NOT decrease his RRI–which the vasopressin infusion did decrease, or so I presume as no other therapeutic interventions were given with respect to the time frame the RRI decreased).

In the end his kidneys had recovered by the next morning, which I’m sure that any intensivist will admit is the opposite of the norm, as the kidneys usually get, at least transiently worse initially-being the delicate sissies/whimps that they are. Whether this was because of the diuretic or the vasopressin, or something else, is debatable for sure, but it sure didn’t get better by 30 cc/kg of crystalloid mandated by CMS, because he got not a drop more than what was needed to push the diltiazem, the lasix, the antibiotics, and the vasopressors.

So to summarize, in the case of chronic cardiogenic venous congestion, clinician realization and adoption of Doppler assessment of this entity will likely be the next leap in improvement in the management of these patients. In the case of acute resuscitation, venous congestion may be a bit more nuanced, and a more comprehensive evaluation is in order in a case by case fashion. However, I think recognition of the issues of over aggressive volume administration will probably be the next frontier in sepsis resuscitation.

 

Love to hear your thoughts!

Cheers

 

Philippe

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

 

The Hospitalist POCUS Course Participant Info.

 

So here is a little intro for those taking part in the course, or for those considering, though I don’t think there are many spots left.

 

The Hospitalist POCUS Course

Participants should receive course e-notes in the week prior, if you do not, please email hospresusconference@gmail.com to let the team know.

If you are thinking of registering the link is here.

cheers and see you there!

 

Philippe

Venous Congestion: A Reader’s Questions. #FOAMed, #FOAMcc, #FOAMus

I’m always glad for questions, because I think that it’s what forces everyone’s thinking to progress. So yesterday a couple of really good ones from Jonathan Cheung:

My 1st question: I am just curious if it is possible for a collapsible IVC and PW findings suggestive of venous congestion to coexist, say, for example, if the congestion actually leads to increased IAP (perhaps not to the extent of intra-abdominal hypertension) or even 3rd spacing to form ascites in a leaky patient.
This is a question that has come up a couple of times. My physiological answer would be that, in primary systemic congestion, the start point is the increased CVP, which leads to IVC distension, then hepatic vein distension, whose pressure transmits thru the hepatic to the portal circulation, and then pulsatility develops. So in these cases a plethoric IVC is an inherent part.
On the other hand, local phenomena, such as cirrhosis, organ-specific edema (ischemic bowel, renal capsular hematoma, etc) can lead to edema and congestive signs in the local circulation without central venous congestion.
This is an important delineation, because the therapy for localized inflammation and edema is not likely the same as for central venous hypertension.
My 2nd question is: does the physiological changes by pronation (e.g. variable change in transpulmonary pressure, slight “off loading” of the abdomen etc.) cause an observable change to the spectral findings? I often have this question in mind when I want to assess fluid status in a prone patient on whom doing an echo isn’t always possible.
First I would argue that the only trouble with prone and POCUS is for cardiac views – hence TEE. But for venous doppler, the kidneys are perfect, the PV and IVC are totally accessible laterally and the IVC even posteriorly.
Secondly, I think it’s important to remember that physiologically, venous congestion is venous congestion, no matter the cause, and that end organs can suffer similar consequences. At least initially, proning should drop the PAP and unload the RV, but this will likely change over a variable amount of time. Very tough to properly assess the physiology in my opinion.
I’ll try to get Korbin, Rory and Jon-Emile to chime in!
Cheers
Philippe
Click here to come meet this interesting bunch of docs!