The Subtleties of the SHOC-ED Trial: Don’t Just Read The Abstract! #FOAMed

So this was my comment to my friend Jon’s awesome discussion on the SHOC-ED Trial, which is certainly interesting.

Jon, great post as always! I do agree with most of it, but would have to caution readers about reading it with the filtered glasses that make people too often take home the message that they want to – usually the path of least resistance (or change). I think your main point and most critical one is that there is no protocol or recipe that should ever be applied to resuscitation, especially single-variable-based resuscitation (eg old school orders like CVP>12 lasix and <12 bolus), and substituting the IVC for CVP won’t help. And from a standpoint of volume-responsiveness, I totally agree, with the understanding that as the IVC gets more plethoric, the percentage of responsive patients will decrease, inevitably, but one cannot predict with certainty whether that one patient will or will not. However, the parallel change is that, as the IVC gets more plethoric, the volume tolerance is likely decreasing as well, so that your benefit to risk ratio is dropping. And of course you can’t recipe that just based on IVC, but should be looking at the site of pathology (eg lung, brain abcess, pancreatitis with ACS, etc…), physical exam, to determine your patient’s volume tolerance. Because we all know that most of that miraculous fluid will end up clogging the interstitium, with consequences ranging from cosmetic to fatal (though usually blamed on the patient being “so sick” in the first place, absolving the clinician from any wrongdoing). So comments like the one previous to mine, stating “give volume and see if the response occurs” are, in my mind, a poor approach. We know from studies that you cannot simply remove the fluid you gave and go back to the start with lasix (glycocalyx damage, etc), and we also know that much of the effect of said fluid administration dissipates in minutes to hours (I’m sure Jon can quote these studies off the top of his head!).

As we have discussed in the past, I think POCUS is much underused as a fluid stop point – most of its use is on the ‘let’s find a cool reason to give.’  I would argue that you should hardly ever give fluid to a full IVC (especially if markers of pathological congestion are present – portal vein pulsatility and all), unless you are dealing with temporarily improving tamponade or tension pneumo, because even if you are volume responsive, you are likely not volume tolerant. This also goes to the point that a single, initial POCUS exam will potentially not have the same impact as a whole POCUS-based management which will use it to reassess congestion status, cardiac function, etc.

Having said all this, the most important part of the SHOC-ED article is, in my mind, their discussion, which is full of all the important reasons why the final conclusion is not `we don’t need to do POCUS in shock,’ which is what I see happening (similarly to the TTM reaction), as they outline the cognitive fallacy of putting on trial a diagnostic tool whilst the therapeutics are not yet clearly established. Those only reading the abstract or conclusion will actually miss the important points of this study which the authors clearly explain.

In particular, the ‘rare’ instances of tamponade or aortic aneurysm or PE in their series would be diluted out by the sepsis, but for those patients, it would matter. As the authors state:

‘one might argue that even a single unanticipated emergency procedure would justify the use of POCUS in critically ill patients.

I would have to wholeheartedly agree.




H&R2019! Final Programme. Register Now! Montreal, May 22-24, 2019! #HR2019


Click here to register!

So many apologies for all those who expressed interest in the last few days, but we are finally operational!  Registration is open and we have said goodbye to the snail mail process. Fortunately, we are a lot more cutting edge in medicine than in non-medical technology.

We are really excited about this programme, and a lot of it comes from the energy and passion coming from the faculty, who are all really passionate about every topic we have come up with.

Scientific Programme

Wednesday May 22 – PreCongress courses


Full day Resuscitative TEE Course 

Full day Keynotable

Half day Hospitalist POCUS (PM)

Half day Critical Care Procedures (AM)

Half day Brazilian Jiu-Jitsu for MDs (AM)

(for more details please see here)


Thursday May 23 – Day 1

0800-0820 – Respiratory failure on the wards – MALLEMAT

0820-0840 – Phenotyping Cardiac Arrest – SPIEGEL

0840-0900 – Help! my patient is bleeding! AJJAMADA

0900-0920 – Perioperative basics. KAUD

0920-0940 – Advanced POCUS-based management of CHF – ROLA

1020-1040 – Pharmacology Pearls – VINCENT

1040-1100 – Green Medicine: Can We Help Save the Planet? ZIGBY

1120-1140 – A Free Upgrade to your WBC: The NLR! FARKAS

Critical Care track

1240-1300 – pH-guided fluid resuscitation – FARKAS

1300-1320 – the Great EPI debate – SPIEGEL

1320-1340 – Revisiting CPR physiology: What do we know? – TERAN

1340-1400 – Cardiogenic Shock 2019 – OLUSANYA

1400-1420 – Late Breaker TBA – MALLEMAT

1420-1440 –  Intra-Arrest Hemodynamics: One Size Doesn’t Fit All – TERAN

Hospitalist track

1240-1310 EKG Pearls – MULLIE

1310-1330 Nutrition in the Hospitalized Patient – RUBINO

1330-1400 The Best Neuro Exam Ever! – TBA

1400-1420 Dermatology 101 – SKINNER

Workshops (1500-1700) 

Workshops will have an open format where you can attend as many or as few as you would like, and spend as much time as you choose. This will enable you to focus on the areas you want to gain the most from:

Basic Hospitalist POCUS (IVC, lungs, heart, renovascular and GI, US-guided venous access),

Pharmacology Cases 

EKG Cases 

Nuts & Bolts: Troubleshooting Thoracic Drainage

Mid-Line Catheter Insertion  

KENNY’s Cardio-Pulmonary Physiology Workshop 

SPIEGEL’s The Art of the Bougie – Airway Workshop 


Meet the Faculty cocktail! 1900 – Location TBA


Friday May 24 – Day 2

0800-0820 Metabolic Resuscitation: is is for real? FARKAS

0820-0840 Acid-Base in 3 Parts – SPIEGEL

0840-0900 Late-Breaker TBA

0900-0920 Gut POCUS – BAKER

0920-0940 Diastology for Intensivists – CHEN

1020-1040 The Art of the Bougie – SPIEGEL

1040-1100 Renal Doppler in Acute Care. HAYCOCK

1100-1120  The IVC don’t Lie: Ask the Right Question! KENNY

1120-1140 Blood Pressure: a Closer Look. MAGDER

Trauma track

1240-1300 Permissive Hypotension: Permissive Death?  NEMETH

1300-1320 Thoracic Trauma – HAYCOCK

1320-1340 Massive transfusion – MALLEMAT

1340-1400 To REBOA or Not To REBOA – HAYCOCK

1400-1440 Traumatic Cardiac Arrest: How To Avoid Killing the Dead! NEMETH

Critical Care Track

1240-1300 Inhalation Therapy for acute RV Failure – DENAULT

1300-1320 Advanced Doppler for the Intensivist – KENNY

1320-1340 Pmsa: Is There a Clinical Use? OLUSANYA

1340-1400 Got ROSC! Now What? TERAN

1400-1420 – Insights on Delirium Using POCUS – DENAULT

Workshops (1500-1700)

Advanced POCUS (venous, shock, advanced CHF, GI, neuroPOCUS)

TERAN’s Intro to Resus TEE


Intro to ECMO


KENNY’s Advanced Physiology Workshop


Register here!

contact us at with any questions!

H&R2019 Pre-Conference Courses. May 22nd. Yup, it’s worth coming early!

So we are very, very excited about our pre-conference course lineup. It is simply awesome:

1. Full day Resuscitative TEE (Limited to 20 participants) 0830-1730


2. Full day Keynotable 0830-1730

3. Half day Hospitalist POCUS (Limited to 30 participants) afternoon 1330-1730

4. Half day Critical Care Procedures (Limited to 20 participants) morning 0830-1230

5 .Half day Brazilian Jiu-Jitsu for MDs (Limited to 30 participants) morning 0900-1200.


Note that sadly, you have to make some choices. No way to attend it all…


So here is some info to help you make your best pick:


1. Full day Resuscitative TEE: run by none other than Felipe Teran, and featuring Andre Denault as head instructor, this is a unique opportunity for a deep dive into everything about TEE in shock/arrest as well as extensive hands-on training on shock/arrest TEE using state-of-the-art simulators. Participants will obtain an Optional Competency Assessment,  providing a Workshop Certificate and a Focused TEE Competency Assessment Checklist certifying completion of 10 proctored examinations.

Limited to 20 participants. 795$USD. Note that conference registrants (minimum one day) will be prioritized for registration to this workshop, with proof of H&R2019 registration required. Remaining spots will be released to non-conference attendees on March 1st, 2019.




Keynotable Motreal Flyer

2. Full day Keynotable: the brainchild of educator extraordinaire Haney Mallemat, this course is intended for those who want to add some serious game to their presentations and didactic teaching. Sharing tips and pearls that have made him unquestionably one of the best docs to man the stage and podium, this is a rare opportunity not only to leave run-of-the-mill powerpoints behind, but also to enhance your future audience’s learning and become a master presenter.

Registration 495$USD physicians, 375$USD trainees and other health care professionals. Register at or email

More details here.


3. Half-Day Hospitalist POCUS: Learn absolutely necessary skills for the day-to-day management of your hospitalized patients. It doesn’t matter how good a clinician you are, with ultrasound you will be a better one. Learn from a world-class clinician faculty how to assess the IVC for a number of clinical scenarios, how to assess lungs, do basic cardiac views, diagnose or rule out hydronephrosis, and safely tap ascites or pleural effusions.

Cutting edge today, standard of care tomorrow…

Faculty: Rola, Ajmo, Haycock, Baker, Olusanya

Practice on state-of-the-art simulators, normal volunteers and volunteer patients with true pathology.

Your patients need you to know this.

Limited to 30 participants so that your hands on and faculty experience is maximized. 300$CAN/250$USD


4. Half-Day Critical Care Procedures: If you are not already familiar with these key procedures any resuscitationist should have in their pocket, don’t miss this course. We’ll go over thoracic pigtail insertion, bedside percutaneous tracheostomy and emergency surgical airway, using manikins and natural simulators. Plenty of practice, until you’re comfortable with the techniques. By the end of this activity, participants should be able to independently insert pigtail catheters and perform an emergency surgical airway, and be able to perform a percutaneous tracheostomy with the backup and supervision of an experienced operator.

Faculty:  Ajmo, Farkas, Tremblay

Limited to only 20 participants, so don’t wait too long! 300$CAN / 250$USD




5. Brazilian Jiu-Jitsu for MDs: Nope, you didn’t accidentally click on a link. This is part of the pre-conference day. What does it have to do with medicine? A lot. With life? Everything. If you’re already got mad mat skills, come join us for a couple hours of fun. If not, treat yourself to an introduction into a martial art, a sport and even a lifestyle that cultivates physical and mental health like no others. The rest of the conference will change your practice, but this workshop might change your life.

Faculty: Spiegel, Rola, and some guest stars!

No experience necessary, only interest and enthusiasm.

It’s a bit too early to be sure who, but expect to have some interesting surprises as to who your instructors might be…

…oh, and acute care docs should find something in the words of Rickson Gracie, one of the legends of jiu-jitsu:

Limited to 30 participants, registration fee TBA, and will open on november 1st. You can reserve your spot in the meantime by emailing


So we are really looking forward to these courses. It’s a great opportunity to pick up some important skills and have plenty of time with some awesome instructors, all of whom are hoping to share as much clinical knowledge as possible.

Mark your calendars! Please email with any questions!

Hope to see you there!


The H&R Scientific Committee – St-Arnaud / Zambrana / Rola

Shock Macro and Micro-circulation: Piecing things together. (Part 1) #FOAMed, #FOAMcc


So I have really, really enjoyed the discussions I had with these bright people on shock circulation:

Segun Olusanya (@iceman_ex) Resus Track 2

Rory Spiegel (@EMnerd) Resus Track 3

Korbin Haycock (tell him to get on twitter) Resus Track 4

Jon Emile (@heart-lung)  Resus Track 5


Some take home points so far:

I think that more questions than answers truthfully came out of this, and that is really the best part. But lets see what the common agreed upon thoughts were:

a. the relationship between the MAP and tissue perfusion it quite complex, and definitely not linear. So scrap that idea that more MAP is more perfusion. Could be more, same, or less…

b. you can definitely over-vasoconstrict with vasopressors such that a increasing MAP, at some point, can decrease tissue perfusion. Clinically, we have all seen this.

c. no matter what you are doing theorizing about physiology and resuscitation, THE MOST IMPORTANT IS TO CONTROL THE SOURCE!


Some of the interesting possibilities:

a. Korbin sometimes sees decreasing renal resistive indices with resuscitation, particularly with the addition of vasopressin.

b. the Pmsa – can this be used to assess our stressed volume and affect our fluid/vasopressor balance?

c. trending the end-diastolic velocity as a surrogate for the Pcc and trending the effect of hemodynamic interventions on tissue perfusion.

This stuff is fascinating, as we have essentially no bedside ability to track and measure perfusion at the tissue level. This is definitely a space to watch, and we’ll be digging further into this topic.


Jon-Emile added a really good clinical breakdown:

I think one way to think of it is by an example. Imagine 3 patient’s MAPs are 55 mmHg. You start or increase the norepi dose. You could have three different responses as you interrogate the renal artery with quantitative Doppler:

patient 1: MAP increases to 65 mmHg, and renal artery end-diastolic velocity drops from 30 cm/s to 15 cm/s
patient 2: MAP increases to 65 mmHg and renal artery end-diastolic velocity remains unchanged.
patient 3: MAP increases to 65 mmHg and renal artery EDV rises from 10 cm/s to 25 cm/s

in the first situation, you are probably raising the critical closing pressure [i know i kept saying collapse in the recording] relative to the MAP. the pressure gradient falls and therefore velocity falls at end diastole. one would also expect flow to fall in this case, if you did VTI and calculated area of renal artery. in this situation you are raising arteriolar pressure, but primarily by constriction of downstream vessels and perfusion may be impaired. ***the effects on GFR are complicated and would depend on relative afferent versus efferent constriction***

in the second situation, you have raised MAP, and probably not changed the closing pressure because the velocity at the end of diastole is the same. if you look at figure 2 in the paper linked to above, you can see that increasing *flow* to the arterioles will increase MAP relative to the Pcc [closing pressure]. the increase in flow raises the volume of the arteriole which [as a function of arteriolar compliance] increases the pressure without changing the downstream resistance. increasing flow could be from beta-effects on the heart, or increased venous return from NE effects on the venous side activating the starling mechanism. another mechanism to increase flow and therefore arteriolar pressure relative to the closing pressure is the provision of IV fluids.

in the third situation, MAP rises, and EDV rises which suggests that the closing pressure has also fallen – thus the gradient from MAP to closing pressure rises throughout the cycle. how might this happen? its possible that raising the MAP decreases stimulus for renin release in afferent arteriole, less renin leads to less angiotensin and less efferent constriction. thus, paradoxically, the closing pressure falls with NE! another possibility is opening shunts between afferent and efferent arterioles [per Bellomo]. as above ***the effects on GFR are complicated and would depend on relative afferent versus efferent resistance changes***


This is really, really interesting stuff. So in theory, the MAP-Pcc gradient would be proportional to flow, so if we can estimate the direction of this gradient in response to our interventions, we may be able to decrease iatrogenism. I’ll have to discuss with Jon and Korbin which arterial level we should be ideally interrogating…

More to come, and next up will be Josh Farkas (@Pulmcrit), and I’m sure anyone following this discussion is looking forward to what he has to say. I know I am.




The Resus Tracks 05: Kenny (@heart_lung) Tackles Shock Perfusion! #FOAMed, #FOAMcc, #FOAMus

So finally got around to corralling Physiology Jedi Master Jon-Emile Kenny for a chat, which is always a tremendous learning opportunity. And this time was no different. Jon breaks down some of the mysteries around arteriolo-capillary coupling and shock flow, and brings up some really interesting potential uses of the critical collapse pressure of small arterioles, and hints at how we may be able to use some POCUS techniques to clinically assess tissue perfusion.

Here you go:

Please leave comments and questions!

The article we refer in the beginning to is here:

MAP in sepsis review

And the article on critical closing pressure in the neurocirculation that Jon refers to is here:

CrCP Brain




The Resus Tracks 03 – Shock Circulation with @EMnerd! #FOAMed, #FOAMcc, #FOAMer

Here we go!


Discussing with Rory is always awesome, because he manages to distill things to the most important stuff. In this one he basically says sure Phil, it’s fun to think up all kinds of semi-theoretico-imaginary hemodynamic stuff, but you gotta make sure you control the source!



Love to hear comments and criticisms!




Here is the open access paper I was talking about, graph on page 2.

MAP in sepsis review


Kylie & Korbin chime in to the Venous Congestion Issue. #FOAMed, #FOAMcc, #FOAMus

So I think much of the awesomeness of #FOAMed is sparking discussion and exchange, and the many little steps in clinical management besides the initial prescriptions. So I thought I would highlight and exploit a couple of really interesting reader comments:

So first, Kylie (@kyliebaker888):

Great to listen guys, thanks, and very timely. I had just read Tremblay’s paper after coming across a very pulsatile PV in a relatively well elderly patient with bad TR. Two questions – which PV are more likely pulsatile in the first place….Tremblay mentions RVF/TR and very thin folk. What is your experience?
Second Question – what did the GB wall/GB fossa look like after the initial very positive fluid balance? Does everyone blow out their GB wall with fluids, or only some?

It is always important to isolate the patients’ whose physiology may change the clinical signs (in this case PV pulsatility) and make their interpretation different. I agree that massive TR, especially chronic, would likely account for pulsatility. I am not certain about the physiology for the very thin patient, but I have heard the same thing from Andre.  So my personal take on a patient with severe TR and a pulsatile PV would be to look at the IVC variation, TR notwithstanding, if it is fixed and plethoric I would diurese – the organs don’t care what the cause of the congestion is.  

As for the GB, I have also seen edema, and then try to correlate with cholestatic enzyme changes that would be out of proportion to the hepatocellular enzymes if there is a primary GB process. This is certainly an imperfect science. In a critically ill septic patient, I have a low threshold to drain the GB if in doubt.

Then Korbin gives his two cents, and then some! 

Great case, loved it. Thoughtful management, brilliant!

I couldn’t help thinking as I listened, that it is so important to avoid over-resuscitation with fluids in the first place. We all know that the majority of crystalloids given will end up as interstitial edema, so any benefit from the increase in stroke volume is temporary at best (consider carefully what you gain and at what cost). Wet lungs=increased mortality, days on the vent, and ICU stays. Wet kidneys=AKI 2-3 days after initial resuscitation and potential RRT. Congested liver=gut edema and continuation of inflammatory cytokines/sepsis syndrome. Too much fluids–>BNP levels rise, high BNP levels in the presence of LPS=glycocalyx shedding, and more interstitial edema everywhere.

Cannot agree more.

I think there is some decent evidence that an early fluid liberal approach combined with a late fluid restrictive approach can potentially benefit a patient in septic shock, but its clear that an overall positive fluid balance does harm. Perhaps, even the early fluid liberal strategy (in sepsis specifically) should be tempered by a careful consideration of what is really going on.

My take here is that, by using POCUS, there is no need for a “general approach.” POCUS takes essentially no time. In about 5 seconds you can confirm a small IVC that can (initially) take fluid, a medium one (that you need to watch) or a full one (yes, it happens – that gets no fluid). So to me there is no need to have a pre-determined approach…

Sepsis is an entity characterized by venous return being limited by a decrease in mean systemic pressure (MSP) due to an increase in venous capacitance, rather than a decrease in fluids that generates the stressed volume (MSP=fluid filling/venous capacitance). The body compensates with an adrenergic response that maintains (or attempts to maintain) MAP by an increase in a catecholamine driven augmentation in cardiac output/contractility. This adrenergic response likely has more to do with the increase in lactate production observed in sepsis, rather than actual tissue hypo-perfusion and anaerobic metabolism mechanism. Increases in CVP inhibit venous return and congest the kidneys and GI tract (the left atrial pressures are the equivalent problem for the lungs, combined with the fact that pulmonary vascular permeability is increased in sepsis as well). Given this, I think in distributive shock, we should fix the lack of MSP by an earlier vasopressor therapy approach, both to supplement and decrease the crystalloid load to the patient, which is un-natural and contrary to their deranged septic physiology.


Also, could the type of crystalloid given be important? NS gives a considerable sodium load compared to LR, and this likely promotes/sustains fluid retention that is difficult to remove during de-resuscitation. The high chloride levels of NS will promote an increase afferent arteriolar vasoconstriction and thus decrease GFR, making it more difficult to diuresis the patient later on, and contribute to AKI beyond the iatrogenic interstitial kidney edema caused by the crystalloids we gave.

Absolutely. NS is given by medical peeps only by cultural habit. Most do not know the pH (zero SID due to chloride) of  a solution they give by the buckets. RL is the best option I have available.

If you are involved in the early phase of resuscitation of a shocked patient, consider the downstream consequences of your fluid strategy that you give your patient that may give you a temporary comfort because they will look better in the short term.

Dr. Maitland and the FEAST study corroborates exactly this.

This is not to say that an aggressive and upfront resuscitation is not critical–it surely is. I’m saying resuscitate smarter, not wetter. Look for stop points for crystalloids–E/e’ ratios, consider PVPI, RV dilation/TAPSE, hepatic vein doppler, IVC dynamics, portal vein pulsatility, intra-renal venous Doppler patterns and renal resistive index. Fix the hemodynamics from an approach of the root of their problem, rather than pushing fluids for every hypotensive patient (whether you are taking care of them early, or late in the time frame of their illness). Fluids do have their place, but be careful and cognizant of their real down side. Look at your patient, think it through, and make the best actions for them.

Ok, now I don’t even get to have a punchline. Thanks Korbin!

So if this interests you, tune in to The Great Fluid Debate at H&R2018, and I look forward to meeting both Kylie and Korbin who will be in attendance and, I’m sure, putting us all on the spot!

And yes, there will be a POCUS workshop on portal and hepatic vein POCUS.

click here if you want to take part: H&R2018