H&R2019 Lecture Series: Sharad Patel on Portal Vein Pulsatility and Hyponatremia!

 

 

So here was a late-breaker talk at H&R2019. Portal vein pulsatility and hyponatremia by a nephrologist – intensivist. Love it. Sharad, a really great guy, also recently published a case report on this topic.

There is a lot of stuff on venous congestion in the woodwork, some of which we are involved in, but also some springing up from different places, and this is really exciting, because POCUS gives you a non-invasive tool to assess and differentiate pathological degrees of congestion that really nothing else can with as much breadth, and as part of a comprehensive exam.

Venous POCUS is worth learning, and keep your eye on this space for how it evolves as a clinical tool. Our VEXUS classification will soon have some real substance behind it.

For those who want more H&R2019, the Essentials can be found here!

And here’s Sharad!

RV Doppler: Resistance vs. Back Pressure. Jon-Emile Kenny & Korbin Haycock! #FOAMed #FOAMer #FOAMcc #POCUS

So I’m still trying to digest the RVOT Doppler physiology and working my hand at generating the best views and Doppler angles I can (See previous post on RVOT Doppler here). Not sure yet how this will fit in to my clinical practice but I think it’s worth shining a light into this murky pseudo-science of resuscitation. These guys are helping define its potential use… Naturally, this is bleeding-edge stuff. Use it to try to understand what’s going on with your patient’s physiology, don’t use this on board exams! My comments in bold.

Now for the big guns…

 

Jon-Emile Kenny (@heart_lung), pulmccm.org, heart_lung.org

Hey Guys – great discussion as always!
One thing that I find confusing on this topic, and is helpful – i think – when scrutinizing the literature, is the difference between ‘impedance’ and ‘resistance.’ Elevated vascular ‘resistance’ is often used too broadly; for example, true/pure WHO II pulmonary venous hypertension [say from acute left atrial pressure hypertension, but before chronic, compensatory pulmonary arterial changes] is actually typified by a *decrease* in resistance, but an increase in *impedance.* To make things more confusing, acute left atrial hypertension will often display a high “resistance” mathematically … even though, the true resistance can be low. What am i saying? if you imagine an acute increase in the left atrial pressure, the pulmonary venous beds and pulmonary vascular beds “recruit and dilate” backwards [why we see cephalization on the CXR] typically from the bottom to the top of the lungs up the hydrostatic gradient. Recruitment and dilation actually *increases* the cross-sectional radius/area of the vascular beds — a true decrease in resistance [Poiseuille what?]! But, as these vascular beds are engorged, they reach that infamous, hockey-stick-shaped compliance curve point [go leafs go!], where the vessels become really stiff … that is, the compliance falls such that each ejection the RV throws into this dilated circulation, the pressure rises dramatically [especially the systolic pulmonary pressure] …

This I think is a key concept to understand and keep in mind when analyzing the venous system. The physical characteristics are more akin to a floppy plastic bag or balloon, with little rise in pressure until a certain point, then a sharp one – Jon’s “hockey stick.”  It was Jon who made me realize that, with exposure to chronically elevated right atrial pressures, one could have a very big IVC (say 25-30mm, but in fact a low CVP, whereas in normal IVCs exposed to normal CVPs, that sharp rise in pressure probably occurs somewhere around 20mm. Hence, the + value we use in the PAP calculation using TR Vmax for the RAP may be very inaccurate in chronically elevated PAP… Food for thought.

Thus, the calculated pressure gradient rises and and the calculated resistance falls, but what has actually happened is that compliance has fallen, not “resistance”. More broadly, the term “impedance” is composed of compliance, resistance and something called the characteristic impedance [the Windkessels!]. Typically what abnormal RV Doppler shows you is that *impedance* has risen. At the end, you are often still left with the why? Impedance can rise when “true resistance “falls, but compliance also falls [as above] – yet the calculated RVSP/regurgitant jet will also rise. The linked papers are fantastic, but they both excluded patients with left heart disease, so you can be more confident that the RVOT abnormalities seen are related to true ‘pre-capillary’ problems. I’d be willing to bet [and if there’s data, i’d be interested to read it] that patients with pure WHO II pulmonary venous hypertension have very similar abnormalities on the right side. The key means to distinguish – as Korbin talks about – is really looking at the left heart [E/e’] and clinical context to get a better sense of what’s going on.

What would also be interesting would be to look at acutely “decompensated” true left heart disease in volume overload and correlated with RVOT morphology and great vein Doppler velocimetry. My guess is that as you decongest the pulmonary veins [increase their compliance] that the RVOT envelope “pulsatility” goes away [the RV ejection envelope appears more rounded] as does the venous pulsatility in the great veins and intra-renal veins! It’s all about energy transfer … moving away from excessive potential energy trapped in distensible structures [i.e. congestion] to kinetic energy [normal, forward blood flow]

Jon.

 

Korbin (@khaycock2)

Thanks for the reply Jon-Emile, as usual you bring an incredible amount of intelligent well thought out points.

As you mentioned, afterload is much better described in terms of the 3-element Windkessel model as resistance is only one component of said model (the other factors being vascular compliance and characteristic impedance). Please correct me if I’m wrong, but I believe that the most practical and easiest way to non-invasively determine arterial load is to calculate the Ea (formula: (SBP*0.9)/SV). This would include all of the factors that determine afterloading conditions instead of simply using resistance as it is only one of those factors.

Clinically speaking, I think it is important to address why afterloading conditions are abnormal when we come across undifferentiated pulmonary HTN in the acute setting. Practically in my mind, this is simply finding if the pHTN is due to post-capillary “back pressure” from elevated left atrial pressures or due to elevated pre-capillary pulmonary vascular resistance (or could be some combination of both of course). Both of these conditions can cause elevated pulmonary artery pressures, as you have pointed out, and there are a few other contributors to the afterload as well that we are ignoring (or else we’d blissfully nerd out all day and forget to take care of the patients).

I agree with this concept. This is what may direct me to use pulmonary vasodilators, whether inhaled or even the choice of milrinone or vasopressin (not a vasodilator per se but a non-pulmonary vasoconstrictor). If all the pulmonary hypertension is post-capillary, there would be little or no benefit. This important decision point is what prompts me to look into this whole right-sided Doppler thing… Let’s see what else Korbin has to add! 

So how can find out the cause(s) of the elevated PAP? Is it resistance or back pressure from the left atrium? This is essentially the topic of the post. Because PVR=(mPAP-LAP)/CO, it has been suggested that the TR gradient can be a surrogate for the mPAP-LAP and RVOT VTI be a surrogate for CO. Thus if the ratio is high, we can assume that a significant component of the pHTN is due to resistance in addition to or to the exclusion of the contribution of LAP. You have rightly questioned and very well explained why you wonder if these are valid assumptions that translate to the finding the clinical causes of pHTN.

You pointed out that the cited papers in the post excluded patients with LV failure, thus bringing into question if the TR/VTI ratio methods and their permutations are actually detecting PVR as the primary etiology of the pHTN or are corrupted by elevations in LAP. Here are 3 papers that included a significant number of patients with pHTN and elevated PCWPs as measured by RHC that show that the TR/VTI methods do seem to work to detect PVR elevations themselves even if the LAP are high:

1) Am J Cardiol. 2013 September 15; 112(6): 873–882. doi:10.1016/j.amjcard.2013.05.016.
2) J Am Soc Echocardiogr 2013;26:1170-7.
3) J Am Coll Cardiol 2003;41:1021–7.

Somewhere in my files I have a study that shows that the mid systolic notch is fairly specific for high PVR and independent of LAP as well. but apologies, I’d have to look for it.

As I might have mentioned in the audio portion of the post (I can’t remember), there is a second method to flesh out PVR from LAP causes of pHTN. First, you need to find a good estimation of the LAP. ECHO has multiple ways of various accuracies to get a number. The formulas are listed above. I don’t believe any of them are validated in acutely sick patients though. Once you have a LAP number, turn your attention to the pulmonary valve regurgitant jet which will almost always be there if there’s pHTN. The wave form is sort of down-sloping trapezoidal lasting through diastole. The velocity at end-diastole can be squared, multiplied by 4, then added to the RAP to give you the end-diastolic PAP. This is normally < 6 mmHg higher than the LAP pressure measurement, if it is a bit more higher, there likely is increased PVR. This is the same principle used in a RHC, where the inflation of the balloon stops flow and therefore eliminates resistance so that the PCWP can be measured and differentiated from the dPAP. The problem with this method is that it doesn’t work as well as the TR/VTI methods

I really enjoyed your thoughts about how Doppler waveform patterns may be affected once compliance limits have been reached, and I’m sure there is something to this that is real as well no doubt! I thought it might be helpful to provide you with the additional studies that included the patients with high LAP, and do a bit of re-explaining/restating your points to anyone new to this stuff.

Thanks again Jon!

Jon replies:

Hey Korbin – thanks for the references – I’ll dig into them. My main concern is that the mPAP-LAP will disproportionately rise (mostly because the sPAP disproportionately rises) when the left atrial pressure is high … that is when it’s actually not a “resistance” problem but rather a back pressure problem, the mathematical resistance is high. As you mention, this is why there’s a push to move away from “PVR” with RHC and more towards the dPAP-PCWP gradient which should be less than 6 mmHg. I made a cartoon describing this in an old post (https://pulmccm.org/critical-care-review/icu-physiology-1000-words-folly-pulmonary-vascular-resistance/). Thanks for these references, I’ll read them and see if they make sense from the framework I’ve adopted – which is entirely stolen from this great article

Naeije, R., et al., The transpulmonary pressure gradient for the diagnosis of pulmonary vascular disease. Eur Respir J, 2013. 41(1): p. 217-23.

Maybe Phil should do a point-counterpoint podcast where Rory comes in at the end and shakes his head because nothing really matters in the end.

“Nihilism rules…”

Jon

Korbin:

Thanks Jon, I would like to see what you think. Thanks back at you for the reference you mentioned in your reply. And you’re hilarious!

Jon replies:

I had a read of the references that you provided, thank you. I think my concerns still apply, however. My main concern is what is being used as the gold standard for ‘pulmonary vascular resistance.’ An elevated calculated pulmonary vascular resistance (e.g. in WU) doesn’t actually tell you where the pathology is. the assumption is that an elevated calculated pulmonary vascular resistance is caused by a high pre-capillary resistance in the pulmonary circulation, but this isn’t necessarily true. as i showed in that post that i linked to (https://pulmccm.org/critical-care-review/icu-physiology-1000-words-folly-pulmonary-vascular-resistance/) … if one were to acutely cross-clamp the descending aorta, below the diaphragm, the calculated pulmonary vascular resistance would rise, even though the pathology is totally outside of the thorax!! i have no doubt that the TRV / RVOT-VTI would also rise in that very same patient with the cross-clamped descending aorta such that the good correlation between the calculated ‘pulmonary vascular resistance’ and the TRV / RVOT-VTI is maintained – but the pathology is in the abdomen – not the pulmonary vascular tree! So many exclamation marks; but i’m not yelling. In a hypothetical patient with a cross-clamped descending aorta, one might be tricked into giving a pulmonary vasodilator — but that would be the absolute wrong thing to do, even though the calculated pulmonary vascular resistance is high. The treatment is to afterload reduce the struggling LV (remove the cross clamp) — which would then lower the calculated “pulmonary” vascular resistance and the TRV / RVOT-VTI.

the problem in reasoning lies in what happens with the left atrial pressure rises (as would happen if one acutely cross-clamped the descending aorta). it is assumed that as the LAP rises that the mPAP – LAP gradient stays the same or rises in proportion. but what happens when the LAP rises is that the mPAP rises disproportionately because of pulmonary vascular engorgement/stiffening (in fact, the pulmonary vascular resistance has fallen because of recruitment and dilation of the pulmonary tree). what *does* rise in proportion is the dPAP – LAP gradient [should stay below 7 mmHg]. i strongly suspect that the ability of the TTE to detect/calculate the dPAP – LAP gradient is not yet refined enough because there is a lot of supposition and inference when making dPAP and LAP measurements with pulsed wave Doppler.

alas, with either an elevated TRV / RVOT-VTI (or calculated pulmonary vascular resistance from a RHC), one still doesn’t know if it’s purely a left-sided problem (e.g. purely elevated LV afterload) – which could seriously alter management. to know that, i think that a full interrogation of the left heart and pulmonary veins must be done before knowing exactly what an elevated TRV / RVOT-VTI specifically identifies. in addition to that vascular resistance post above, i dug into some more of this in a discussion on the SIOVAC trial a while back (https://pulmccm.org/randomized-controlled-trials/choose-wisely-avoid-sildenafil-pulmonary-hypertension-corrected-left-heart-valvular-disease-siovac-trial/) – which, in my opinion, should never have passed ethics.

Jon

So this is really fascinating stuff. I must admit both Korbin and Jon make excellent points, and for now am not sure if and how to use RV Doppler in clinical decision-making, but until then will be sure to polish up these skills so that they are ready for prime time, and use them in observation of physiology in my shock patients. We’ll see what conclusions I draw.

cheers

 

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

 

POCUS & Venous Congestion: a #FOAMed Collaborative Chapter.

 

So given the importance of these topics, the number of questions and discussions we’ve had on the twitterverse, and most importantly in the spirit of #FOAMed, here is the chapter from the POCUS book which was co-authored by Rory Spiegel (@EMnerd), Korbin Haycock (@korbinhaycockmd) and myself.

Venous Congestion Chapter

We’re also in there introducing our VEXUS score, and if anyone wants to use/validate it clinically, please do!

Love to hear anyone’s thoughts!

 

PS we’ll all be at H&R2019 and running workshops on venous congestion:

https://www.google.ca/amp/s/thinkingcriticalcare.com/2018/11/04/hr2019-final-programme-register-now-montreal-may-22-24-2019-hr2019/amp/

The rest of the chapters are here on Amazon and the e-version here on iTunes!

 

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: