Wicked Clinical Case: POCUS & Prone save the day! #FOAMed, #FOAMcc, #FOAMer

So I get a call from a colleague in the ED at about 2am, telling me about a 39 yr old woman post-arrest. So I start putting on my boots and warming up the car (it’s January in Montreal folks).  Apparently she had presented earlier in severe acidosis, the diagnosis is unclear, but she apparently got 2 units for an Hb of 49, then went into respiratory failure and got intubated. She arrested about 30 minutes later, cause unknown.

I tell the ICU to prepare a bed but I want to see her in the ED first. Twenty minutes later I put probe to patient and see a full IVC with spontaneous echo contrast. On that I tell the nurse to hold the fluids – there was a bag and tubing and a pump with 100ml/hr on it – and turn into a subxiphoid view to see a normal RV and a hypokinetic LV with some WMAs. She has marked consolidations  in both posterior lung fields and B lines laterally, with small effusions and dynamic air bronchograms (indicating patent airways). At this point she has a HR of about 120, but there is neither perceptible BP (by NIBP) nor saturation. She’s on levophed at 20mcg. She’s about an hour post arrest which was witnessed and brief (<10min to ROSC).

The theories about the arrest are possible hyperkalemia: she was intubated with succinylcholine before the K of 6.1 was back from the lab, and her pre-intubation pH was 7.0, and post-intubation she was only ventilated at 400 x 18, possibly precipitating a drop in pH and a rise in K. Her EKG had some nonspecific signs at this point, but also a poor anterior R wave.

So we head to the ICU, as instrumentation was needed. Cerebral saturation (SctO2) is 42% and ETCO2 is 20mmhg, which reassures me that the BP is probably in the measurable range (normal SctO2 is >60% and varies, but 47% is certainly viable)…  A jugular CVC with continuous ScVo2 and a femoral arterial line goes in:


So with a BP of 59/44 (ignore the 100/46, not sure whose arm that was on!) I start epinephrine, as the POCUS is similar, as I want some added beta-agonism. ScVO2 matches SctO2 in the 40’s. We get the BP up the the 90-1oo range, the ETCO2 goes to 30, the SctO2 and ScVo2 go up into the high 40’s, which is very reassuring, because with this I know that my epi drip is improving perfusion and NOT over-vasoconstricting. Without looking at a real-time tissue perfusion index of some sort or other, it is nearly impossible to know rapidly whether your therapy is helping or harming (will discuss tissue saturation & resuscitation monitoring in more detail in another post sometime soon).


So now the sat finally starts to record in the low 60’s. We have a PEEP of 5, so start bringing it up. We hit 16 before the BP starts to drop, and that only gets us to the mid 70’s sat%. She actually squeezes my hand to command.


At this point I take a few seconds to recap in my mind. I’d spoken to the husband briefly and she had had recurrent episodes of feeling unwell with headache, nausea and diaphoresis, and that had been out for dinner earlier and she felt fine until later in the evening when this came on and eventually brought her to hospital. There was also a notion of hypertension at an ER visit a couple of weeks ago. Her history was otherwise not significant. Nonsmoker.

Pheo? Maybe, but shock?  I repeat the EKG, and now, in I and AVL, there is perhaps a 1mm ST elevation. She’s 39 and essentially dying. Lactate comes back >15, pH 6.9.  I give her a few more amps of NaHCO3. You can see the BP respond to each amp. I decide we need to go to the cath lab and get the cardiologist on call to get on the horn with the interventional team at a nearby hospital with a cath lab and ECMO, which is what I think she needs. Hb comes back at 116, making that initial 49 that prompted 2 PRBCs probably a technical or lab error…very unfortunate. There are no visible signs of significant bleeding.

But back to the patient, because this isn’t really a transferrable case.

Recap: a 39yr old woman in cardiogenic shock AND in severe congestive heart failure exacerbated by fluids and packed red cells, with a PO2 in the 40’s and sat in the 70’s.

So I decide to prone her.


Along with draining tamponades, this had to be one of the most rapid and rewarding maneuvers I’ve done. There was a scry drop of sat to the 40’s for a few seconds (may have been a technical thing), but then within a few minutes: BP to the 130’s, SctO2 to 59% and sat 100%!




We dropped the vasopressors, the FiO2, and all breathed a collective sigh of relief. Now for the novices out there, prone ventilation improves VQ mismatch by moving perfusion from diseased, posterior lung fields to now-dependant, relatively healthy, anterior lung fields.

So transfer at this point was in the works. I planned to leave her prone until the last minute. The miraculous effect started to slowly wane within about 30 minutes, with sat and BP creeping down. At the time of transfer, we were back up to 80% FiO2.

So why is this?  Simple enough, this being simple pulmonary edema – rather than consolidated pneumonia – it migrated to dependent areas  relatively quickly. This was confirmed by a quick POCUS check:screen-shot-2017-01-05-at-10-48-06-pmscreen-shot-2017-01-05-at-10-48-26-pm

So in the still shots, you see a pristine “A” profile (normal, no edema) from the patient’s back, and a severe consolidation or “C” profile with ultrasound bronchograms in the antero-lateral (now dependant) chest. Impressive. (for those wanting some POCUS pearls see other posts and here). This is the reverse of her initial POCUS exam.

So we flipped her back and transported her – lights & sirens – the the cath lab, where they were waiting with ECMO cannulae. As an aside, it was quite refreshing to speak to the ICU fellow who spoke POCUS as well as french and english – it’s not usually the case, but I’m glad to see the change. I do believe it to be a direct effect of the influence of my friend and mentor, Dr. Andre Denault, one of the POCUS deities.

So she turned out to have a normal cath and a large adrenal mass. She did well on ECMO, being weaned off it today, and is now alpha-blocked and waiting for surgery, neurologically intact for all intents and purposes. A big thanks to the interventionists and the ICU team at the Montreal Heart Institute. Puts a smile on my face.


Take Home Points:

  1. don’t resuscitate without POCUS. I wouldn’t want anyone guessing with my life on the line, would you?
  2. keep pheo in mind as a cause of “acute MI” and shock
  3. if you’re not using some form of realtime monitor of perfusion (continuous CO, SctO2, ETCO2, ScvO2) then all you’ve got is looking at the skin and mentation, so you are essentially flying blind. Lactate and urine output are not realtime in real life.
  4. get ECMO in the house, it’ll come in handy. I’m working on it.


Love to hear some comments!





ps I’ll try to add more ultrasound clips from this case in the next few days.

Is medicine approaching a philosophical crossroads? Critically important meanderings by Dr. Lynn! #FOAMed, #FOAMcc

So I feel really honoured that some fantastically bright and forward-thinking people take precious time out of their days to read my rants, and even more so to leave some comments.  I sometimes feel that the message contained in these is actually more important than what I spewed out in the first place, so here is quite an essay by Dr. Lawrence Lynn:

Excellent. This may be the Critical Care Quote of 2014.

“The N=1 principle: remember that we are never treating hundreds of patients at once, and we do not have to decide what is best for most (which is what an RCT generally answers) but what is best for the one patient we are treating.”

In fact when RCTs use a simplistic unified guessed phenotype as a surrogate of a complex disease (e.g. sepsis) in a highly heterogeneous population of critically ill subjects, one cannot even say that the RCT tells what is best for “most” since the first question a scientist trying to understand the validity of the “true state” under test would say is “most of what”, Of course when a free (unboxed) scientist learns that the true state was defined by a guess the discussion is over.

This SCCM will be the 25th anniversary of the guessed sepsis and septic shock criteria. It marks 25 years of failed and non-reproducible sepsis trials using the guessed criteria as standards. The beribboned SCCM speakers will rise to the podium and speculate on and on about what all of these studies might mean. None of them will formally call for reform of the science. Thomas Kuhn shows us that they cannot call for reform any more than those holding the guessed geocentric model could call for reform. “Though they may lose faith.. they will not abandon the dogma which led them to crisis” .

So it is up to you, the young women and men to speak up and demand reform. 25 years if failure is enough. How long will you sit silently in the audience and listen to P values responsive to guesses from a few well meaning docs from another era.

Stand up as a group at this SCCM and demand reform. Let this anniversary ring in a new chapter in critical care research.

If you have not read this editorial below, read it before the SCCM. No one argues that this is not the true history of sepsis science but no one has the courage to stand up and demand reform.

Maybe the 25 year anniversary of failure as a function of using guesses as gold standards could provide the impetus. The world depends on you. There is no backup.



Here is the solution for a scientific revolution. First read this guide to Dr. Kuhn’s book “The Structure of Scientific Revolutions”. (especially chapter 4)


Then the young docs (and any of the old guard willing to break from the 25 year old dogma) should move together at the SCCM meeting, and plan to do so before the meeting in social media to collectedly call for reform of the science.

If only one calls for reform, of course grants, promotions, etc can dry up for that person. That is of course what those on academic tenure tracks are afraid of. Young academics are taught to rub elbows with the thought leaders, not to formally and publically question the leaders fundamental dogma. Sure you can go your own way a little off the path, for example, questioning whether or not a given threshold is the right one. However this freedom is a façade, as one cannot question whether there actually is a unified phenotype of “sepsis” definable by simple thresholds without risking much.

However, as Dr. Kuhn teaches, with any reform movement in science, once critical mass is reached there will be no repercussions because the old guard will actually join and move with the paradigm shift. They will even try to lead the shift as they see that leading with the old dogma is not possible and they desire to remain thought leaders and certainly do not wish to be among the last clinging to the old dogma.

The crisis Dr. Kun describes in chapter 4 is upon us. Look around. Do you see that the public cannot help save themselves. It is up to us to begin this revolution. Don’t let this crisis go to waste. Again, it is up to us. There is no back up.

I feel sorry for the Arise team. How much time was wasted? How many man hours? How much time, resources, and good data, which could have been acquired to determine the many actual phenotypes of sepsis was lost. Yet, it was known by some that the unified phenotype of sepsis/septic shock was guessed. Why didn’t anyone tell the ARISE team their “true state” was a guess. Wouldn’t ARISE have been performed differently if that was know to the statisticians.

Why didn’t anyone tell those in Zambia before they treated infected HIV patients with EGDT? Did anyone who came through the supra normal values era really think that Rivers treatment group was representative of the broad population of severely infected patients? One size fits all in sepsis? Really? That doesn’t even work for socks …phenotypes of feet differ.

You men and women are very smart. This blog.. Ollie’s, Scott’s. These are awesome for an old trench warrior – who spent his life at the critical care beside – to read. You understand the complexity. One day you will see that I am one of your greatest allies. You will see that you have been working in a well meaning paternal science and Dr. Kuhn warns of the loss derived from well meaning paternal science. .

I know I cannot expect all of you to rise up and call for reform. Dr. Kuhn says you cannot. He says that cannot happen until another fundamental pathway upon which the science can rest is found. That will not happen until the science moves to identify the varied phenotypes of sepsis.

Once I thought (many years ago) that armed with his teachings we might not be doomed to make the same mistakes. I have learned over the past decades that, while science changes…scientists do not.

One thing I lament is the loss of a good tool like SVcO2. I wrote about the complexity of SVO2 and how to consider these complexities when using SVO2 as a physiologic marker (a tool) in 1985s, This is long before anyone thought one could select a SVO2 value and write a protocol. No one thought in those simple terms in those days. Now, in the era of threshold science, it’s “guess the threshold, come to a consensus on the guess, apply for a grant and…. study it in a RCT (without telling the statistician that the “true state” is a guess)..

All I can say is, don’t let them study bedside ultrasound with the simplistic thresholds and a guessed unified (one size fits all) phenotype or that tool like the SVcO2 might be quickly discredited also..

If you let leaders define their own guessed protocols and control them from a central authority you will wind up using only the tools which they think, as a function of their simplistic “true state” threshold world, are proven..


Lawrence Lynn


Now that’s certainly food for thought at a deeper level!

Lawrence, we will certainly have to discuss SCVO2 at some point – I also agree that, well integrated with other modalities, it can provide insight into hemodynamic optimization.




L’Échographie au chevet pour l’Interniste: ASMIQ/CCUS 2014, #FOAMed, #FOAMcc, #FOAMus

Belle journée aujourd’hui à a deuxième collaboration éducative entre l’ASMIQ (Association des Spécialistes en Médecine Interne du Quebec) et le CCUS, lorsque une trentaine d’internistes ont approfondi leur habiletés échographiques.

Tel que promis, et dans l’esprit de #FOAMed, voici les présentations et videos:

Dr. Ian Ajmo nous fait une revue de l’évaluation de la volémie, en particulier l’échographie de la veine cave inférieure (VCI):

présentation PDF gestion-voleěmie – copie

vidéo https://vimeo.com/96308958,

Dr. Anne-Patricia Prévost révise l’échographie pulmonaire et cardiaque ciblée:

presentations PDF ASMIQ 2014 coeur ASMIQ 2014 poumons


https://vimeo.com/96315383,         https://vimeo.com/96315382,


Merci aussi à Dr. Simon Benoit et Dr. Nicolas Buissières qui ont fait un travail excellent dans les ateliers pratiques!




What’s this sign? Bedside Ultrasound Picture Quiz! #FOAMed, #FOAMcc, #FOAMus

Here is a one of the “classic” and physiologically important echocardiographic signs:


Screen Shot 2014-05-18 at 11.34.10 PM


What do you see in this parasternal short axis view, and what are the physiological implications?

Scroll below for the answer!











This is the “D” sign, aptly named for the D-shape taken by the LV (normally circular) when RV overload occurs and there is paradoxical septal motion and flattening, as early diastolic RV pressure exceeds early diastolic LV pressure.  This is NOT a good thing and points to a very strained hemodynamic pattern.

Note the RV is huge in this cut, bigger than the LV (remember that in all views, the RV should be about 60% of the LV size – this is simply due to the semi-lunar shape the RV takes as it “wraps” around the LV – they both have the same stroke volume). Also note the small posterior pericardial effusion.

So what is the diagnosis here?  Well there isn’t enough information to say with just this image.  This happens to be a case of worsening ARDS, but all you can tell is that there is acute right ventricular failure due to pressure overload, so that the diagnosis includes (a) PE, (b) acute pulmonary hypertension due to some kind of pulmonary disease – ARDS, pneumonia, etc…  Obviously, in the absence of significant parenchymal abnormalities on CXR or B lines/effusions/consolidations on lung ultrasound, PE should be strongly considered.


Happy scanning!



Here is an excellent review on RV dysfunction and focused bedside ultrasound assessment:

RV bedside echo

or its link:


The Effort-Variation Index – a conceptual tool for IVC ultrasound. #FOAMed, #FOAMcc, #FOAMus

I recently had a colleague ask me to put on a graph the way I like to assess the IVC, at least conceptually.  I posted about this a few weeks ago (http://wp.me/p1avUV-8E), so I tried to come up with something useful for clinicians, correlating IVC variation with respiratory effort.

A useful concept to visualize this is the Effort-Variation Index (EVI). To obtain this, start by looking at a Frank-Starling curve, and broadly categorizing patients as being on the “empty” side, the “normal” or the “full” side.



Next, if you look at how these groups would plot on a graph correlating IVC variation to respiratory effort, which, physiologically, would be the change in pleural pressure (delta Ppl), you should conceptually see something like this:




Note that this has not been validated, nor does it contain any values. It is simply, for now, a useful mental construct to understand the physiology behind the variability, and is useful when elaborating each patient’s physiological profile in the mind of the bedside clinician. Along any horizontal line, the IVC variation would be the same. You can therefore see that, given enough respiratory effort, a “full” patient could appear “normal” or even “empty.” Hence interpreting IVC variation without understanding this would lead to potential error.


Love to hear some thoughts and comments!



Another wicked ultrasound case! Can you see the culprit? Another reason to do bedside ultrasound… #FOAMed, #FOAMcc, #FOAMus

Reviewing some TEE cases with Max Meineiri of TGH yesterday (Max is an anaesthetist-intensivist-sonographer extraordinaire who has been kind enough to help me brush up my TEE skills recently), here is one that stood out for two reasons. Here is the story: An 84 year old woman is sent from a peripheral hospital to the cath lab for chest pain.  She arrests on the table after they found normal coronaries and the code blue is called. Max arrives on the scene, and due to CPR making TTE difficult (and also because Max walks around with a TEE probe in a hip holster by Dolce & Gabbana), in goes the TEE probe and right away they note a massively dilated and hypokinetic RV, and a small and under filled LV. Yup, sure looks like a PE in these circumstances. Not being satisfied with a presumptive diagnosis, Max gets to a short axis view of the aortic valve and pulls out the probe slightly, following the bifurcation of the main PA.  On the screen, the right PA is on the upper left field, and the left PA disappears towards the upper right (the left main stem bronchus makes it difficult to visualize). Anything seem a little odd?   Yup, you can see the occlusive culprit a couple of centimetres into the right PA, moving with each beat.  Being in angio already, they threaded a PA cath and administered thrombolysis, but despite some visual fragmentation, she did not survive. So why is this case interesting? 1. the image is pretty cool. 2. More importantly, it highlights the importance of bedside ultrasound.  If a rapid, focused cardiac exam had been done at her presentation at the peripheral hospital, the first-line physicians most likely would have noted the severe RV dysfunction and questioned the diagnosis of coronary syndrome, possibly (hopefully) thrombolysing the patient, and very possibly averting the cardiac arrest. …I know, I know, we don’t have all the info, the ECGs, etc, and maybe this was really an ACS and she happened to have a DVT which embolized during transport, etc…do you buy that?  Ockham and his parsimonious razor don’t, and I would tend to side with them.   love to hear some thoughts!   Philippe

Bedside Ultrasound: Quite a Case! #FOAMed, #FOAMcc

So here is an awesome clip from an ICU colleague of mine, Lorraine Law.  She was managing a post arrest (elderly woman who collapsed at home and was resuscitated but remaining in profound shock) case using bedside ultrasound and came across this pathology:

video courtesy of Lorraine Law & Shirish Shantidatt

what do you think?

scroll below for my thoughts…





So the clip starts with a subxiphoid 4 chamber view that clearly shows a massively dilated RV with a hyperdynamic and underfilled LV.

[For the hemodynamic novices, remember that the ventricles are kind of like roommates who share a pericardium. Especially in acute scenarios, if one gets overloaded, the other will have to give way, until the pressure equilibrates. If the process is exceedingly slow, they can do some renovations and stretch the pericardium, but this takes likely weeks. In this case, the elevated PAP overloads the RV and the RVDP > LVDP, resulting in decreased diastolic filling, which in turn drops the stroke volume/cardiac output/MAP.]

We can see that the RV TAPSE (tricuspid valve excursion towards apex) is really minimal, supporting an acute or acute on chronic process.

The clip then shows a long axis view of the IVC with echogenic material, most likely thrombus, with a to and fro motion, going in and out of the RA. Wow. You don’t see this very often.  The only thing preventing further travel is actually the fact that the cardiac output is so low due to massive embolism so that the flow can in fact barely carry the clots forward anymore at this point, similar to the sluggish IVC clip I put up a few months ago (http://wp.me/p1avUV-5t).

The most likely diagnosis is pulmonary embolism, and thrombolysis is indicated. Unfortunately despite my colleague’s timely diagnosis, the clot burden was likely too much, and despite thrombolysis, the patient passed away of intractable shock.  One can imagine that the TPA actually has to make it to the lungs, and with such a degree of obstruction, it is likely that very little actually got to the pulmonary vasculature…

Unfortunate case, but quite impressive images.

A crazy thought, using hindsight and with the luxury of knowing the fatal prognosis: intracardiac (RV) TPA bolus? Small spinal needle?  Anyone bold enough? Food for thought if (when) I see one like this…





Marco says:

Really quite impressive images. A couple of weeks ago I admitted a pretty young patient after a successful resuscitation due to massive pulmonary embolism. Immediately after ROSC in emergency department, he was transported to the cath-lab where TPA bolus was administered directly through a PA cathether. In ICU we continued the infusion. In less than 24 hours we obtained a relative hemodynamic stability and discontinued all the vasopressors, but the case remains unfortunate because despite therapeutic hypothermia the post-anoxic damage was so severe that led to cerebral death declaration two days later.


Thanks Marco, very interesting.  There is a recent study on catheter directed thrombolysis in PE reviewed at PulmCCM:(http://pulmccm.org/main/2014/randomized-controlled-trials/catheter-directed-thrombolysis-submassive-pe-better-heparin-rct/)

A physiological point about PE resuscitation is the relative inefficiency of CPR, as both venous return and LV filling is severely limited, so systemic perfusion is even worse than the usually poor output during chest compressions…

Thanks for reading!

Marco replies:

Thanks, Philippe!
The point about the possible inefficiency of CPR is crucial in my opinion. The patient I brought as example had a witnessed cardiac arrest (he called EMS when in respiratory distress) and CPR without interruption from the beginning, nevertheless he resulted in brain death declaration.
I remember very clearly a 43-year-old woman that 3 years ago had a massive PE in the OR shortly after a long lumbar vertebral stabilization. We admitted her to ICU after more than 80 minutes of CPR, a bolus of rTPA and with severe hemodynamic instability. RV was extremely dilated. When she eventually regained stability I had little hope about her neurological recovery, but surprisingly she was extubated the following day and last year she returned to our 12-months post-ICU follow-up showing perfect recovery.
I think that systemic and cerebral perfusion during “obstructive” cardiac arrests such as massive PE is very difficult to asses with current technology. A couple of times I was tempted to check it with trans cranial doppler, but usually there’s too much confusion during CPR.
When I was a resident I witnessed to a iatrogenic cardiac arrest in a patient with advanced monitoring that led to an interesting publication: http://www.researchgate.net/publication/10832333_Cerebral_perfusion_pressure_and_cerebral_tissue_oxygen_tension_in_a_patient_during_cardiopulmonary_resuscitation


Wow, very interesting cases.  What fortune to have been able to record that data, as obviously getting that in during CPR would be almost impossible.  TCD, at least after ROSC, could be contributory… Another option is using NIRS, which I’ll be working with this summer.

thanks again!