Cardiac arrest

February 7, 2019

The ECMO Project: Lend us a Hand!!!

So I’ve been quite passionate about adding ECPR to our shop for quite a while now, but bureaucratic hospital processes, particularly in Quebec these days, has us bogged down and makes progress slow and painful, despite good intentions. So we need a boost, not only to be able to offer this technology to our patients, but more importantly, to show that it can be done in a community hospital, that all you need is the desire to give your cardiac arrest patients the best chance at neurologically intact survival they can get.

Here’s a little explanation, particularly for the non-medical readers:

That, and of course a pre-determined corridor to a tertiary care center with a cath lab and a compatible ECMO system to yours.

We have the good fortune to be a couple blocks from the Montreal Heart Institute who are interested in collaborating, and we have the desire, skill and motivation to pull this this off.

It’s important for both MDs and non-MDs to understand that this approach would possibly save 50% of the patients that we normally have no hope to save. At the point when we initiate ECMO, these patients have almost no chance with the current means. That is an incredible impact.

But we do need your help. The government isn’t moving fast, and won’t until this is established practice (well Dr. Rola, where else is this being done locally? – same question/answer as when I asked for a 100,000$ ultrasound system for our ICU in 2004: nowhere around here!).

So I figured that if we can raise enough money, and with the help of our awesome Foundation – under the presidency of Mr. Arcobelli, no effort has been spared to raise funds and the quality of care that we offer at Santa Cabrini! So to help them out and to get the ball rolling, we’re setting up our project on chuffed.org, a crowdfunding site which is tied to the Santa Cabrini Hospital Foundation, and every dollar will be specifically earmarked for this and not used for anything else.

My hope is that by the end of 2019, we have an active ECMO unit able to be deployed for cardiac arrest cases in the east end of Montreal, and that in the years following, other community hospitals follow suit. We are a small community hospital, but with a big heart!

We need 250,000$. The device costs about 150,000$, each circuit about 7,000$ and we need to set up some training for the team. That should get us jumpstarted and cover the first 10 patients.

We’re more than happy to field any questions. As a start, the Critical Care & Ultrasound Institute be donating a minimum of 2,000$ (it’s a bit early to be able to commit to more, as we do have to feed the participants and bring the faculty…) from the H&R2019 conference,  , which takes place at Santa Cabrini Hospital from May 21-24, 2019.

I’d like to thank Joe Bellezzo, Zack Shinar and Scott Weingart from the @edecmo project who planted the seed and showed all of us that this could be done.

for those who want to know more:

CHEER Study

http://www.edecmo.org

ECPR 120 min case

I would also like to thank Santa Cabrini’s Team 6444  of operators, who are a major driving force behind this effort: Sandy Mormina, Rita Pisanelli and more!

PLEASE HELP AND DONATE AT: http://www.chuffed.org (not active yet, will be linked soon) and please forward this to friends and colleagues. You can also send a cheque labelled “ROLA ECMO Project” in the note part of the cheque (this will ensure that the money cannot be used for anything else) to the following address:

Santa Cabrini Hospital Foundation, 5655 Rue St-Zotique, Montreal, H1T1P7, QC, Canada.

Every dollar gets us a little bit closer!

 

cheers and thank you!

 

Dr. Philippe Rola

Chief of Service, Intensive Care Unit, Santa Cabrini Hospital

 

 

December 27, 2018

#POCUS IVC Pitfall Twitter Poll & Discussion. #FOAMed, #FOAMer, #FOAMcc

So I ran a couple of twitter polls sets the other day. Here is the first:

(if you want the twitter videos see here)

 

 

and part 2:

And to sum it up:

So I just wanted to illustrate something I keep bringing up, essentially that the entire IVC literature based on the AP diameter measurement is physiologically and mathematically flawed. I think the poll and images above clearly support this: given a short axis view, clinicians clearly have a different opinion (and possibly intervention!) than using only a long axis view.

My take, as I’ve said and will keep saying, is that there is a lot of info in IVC POCUS, and the one I am LEAST concerned with is volume responsiveness, which sadly seems to be everyone’s only focus nowadays when it comes to the IVC.

But here’s some food for thought, some of my clinical applications in 5 seconds of scanning:

initial shock patient: big fixed IVC -> no fluids, hurry and find the downstream problem and correct!

resp failure patient: small IVC -> it’s not a massive PE, keep looking for the cause don’t send for a STAT CT angio!

AKI patient: big IVC look at venous doppler and call for lasix, stop the fluids and albumin that were being mistakenly given!

AKI or shock patient & small IVC: sure , start with some fluids and reassess soon (that means hours not the next day)

 

etc..etc.. there’s more, and “fluid responsiveness” is only in extremes and fairly low on the list for me!

 

cheers

 

Philippe

 

ps if you like physiology, and a physiologico-clinical approach, don’t miss H&R2019!

November 11, 2018

POCUS, Mythology and Hemodynamic Awesomeness with Jon and Korbin! #FOAMed, #FOAMer, #FOAMus

In Greek mythology, Prometheus (/prəˈmiːθiːəs/; Greek: Προμηθεύς, pronounced [promɛːtʰeús], meaning “forethought”)[1] is a Titan, culture hero, and trickster figure who is credited with the creation of man from clay, and who defies the gods by stealing fire and giving it to humanity, an act that enabled progress and civilization. Prometheus is known for his intelligence and as a champion of mankind.[2]

So, fresh from reading Jon’s post, I felt I had to add a bit of nuance in my previous post to what I feared some might extract as a take-home message, even if in fact, we are not that differing in opinion at all – which Jon expressed here:

i agree with ultrasound for finding the uncommon causes of shock. these examples seems to permeate twitter and make ultrasound very appealing. because ultrasound is non-invasive, it makes the risk-to-benefit ratio very low for these uncommon but highly-lethal and treatable causes.

but that needs to be compared to the risk-to-benefit ratio of ultrasound for the more common causes of shock – like ‘non-cardiogenic, septic’ etiologies as seen in SHOC-ED. here, “static’ ultrasound [as per the RUSH and ACES protocols] – per SHOC-ED – appears to be neither helpful nor harmful. your read of the discussion is perfect, but i was depressed because it read as if the authors only realized this ex post facto – study of previous monitoring utensils [e.g. PAC] should have pre-warned the authors …

i will take some mild issue with markers of volume responsiveness and tolerance. you are correct on both fronts – but what the data for the IVC reveals – perhaps paradoxically – is that true fluid responders can have a very wide-range of IVC sizes from small to large and unvarying … this was born out in most of the spontaneously breathing IVC papers [airpetian and more recent corl paper] the sensitivity was rather poor.

the same *could* be true for the opposite side of the coin. a large great vein may not mean a volume intolerant patient. i tried to exemplify how that could be so in the illustrative case in my post. an elderly man, with probable pulmonary hypertension and chronic TR who probably “lives” at high right-sided pressures. nevertheless, he likely has recurrent C. diff and is presenting 1. hypovolemic and 2. fluid responsive despite his high right-sided pressures. portal vein pulsatility *could* be quite high in this patient – but he still needed some volume.

the obvious underlying issue here – which I know you are well attuned to – is that a Bayesian approach is imperative. when you PoCUS your patients, you are inherently taking this into consideration – i know that you are a sophisticated sonographer. my hidden thesis of the post is that if ultrasound findings are followed in a clinical vacuum and followed without really understanding the physiology [which can explain clinico-sonographic dissociation – like the patient in my fictitious case]… disappointment awaits.

Then Korbin Haycock chimes in and adds a level of understanding that I completely agree with but had difficulty in expressing, but which I think is key to understanding the current and future evolution of POCUS. Complex, operator-dependant medical leaps such as laparoscopic surgery suffered with similar growing pains. But I’ll let Korbin shed some light:
I think the issue of POCUS in resuscitation is somewhat analogous to Prometheus’s gift of fire to humanity.
Jon has quite aptly pointed out that if POCUS (particularly a single POCUS supplied data point such as IVC diameter), if used in isolation, without clinical context, and without comprehensive information, is not much better than using a single data point such as CVP to make complex clinical decisions. Multiple factors influence the behavior of the IVC, just as they do with the CVP. Being a dynamic entity, the IVC does have some advantages over a static number like the CVP. However, if considered by itself, the IVC POCUS evaluation will only result in the same pitfalls as using the CVP as a guide to fluid management. If POCUS is applied in such a blunt manner, we are doomed to repeat our previous folly of using the CVP as a guide to fluid resuscitation. I hope I am in the ball park of the core of Jon’s point here, if not as very eloquently stated by him.
Phil is advocating a more nuanced and sophisticated approach to POCUS than what the SHOC-ED trial investigators used to guide management in their study. Most shocked patients presenting to the ED (“Emerge!”) come with a phenotype of distributive shock. Indeed, these were the majority of the patients in the SHOC-ED trial. Any experienced clinician will recognize this syndrome virtually every time, with no more than an “eyeball and Gestalt” assessment from across the room and a set of vital signs. Current dogma is that this syndrome ought to be treated with 30 cc/kg of crystalloids and then to add a vasopressor if the patient’s blood pressure is still low. Given this, there couldn’t have been much difference as to how patients were managed in either group in this study. I however, disagree with this aggressive crystalloid administration approach, as I’m sure many readers of Phil’s blog do as well. What I gather Phil is saying here is, as he insightfully stated in the past, “IVC never lies, it’s just not telling you the whole story.” A complete POCUS gives us (OK, well almost) the whole story. The caveat here is you must know a whole lot about POCUS. Thus the Prometheus analogy. A little information is a child playing with fire.
Someone new to POCUS, with only a novice’s understanding of what an IVC POCUS evaluation means, will probably make the correct assessment of a patient’s fluid status about 60-70% of the time. This probably is only slightly better than an experienced clinician’s non-POCUS judgement. Hardly enough to translate into any meaningful clinical outcome in a trial without a ridiculously large sample size to find a pretty small benefit. But POCUS potentially offers so much more information. LV and RV systolic function, LV and RV diastolic function, SV, CO, SVR, PVR, RAP/CVP, sPAP/mPAP/dPAP, LVEDP/LAP/PAOP, valvular pathology, tamponade, fluid responsiveness (for what ever that’s worth!), RV/LV interactions (both in series and in parallel), EVLW, insight into pulmonary vascular permeability, renal resistive index/renal venous congestion, portal hypertension/congestion, gut flow resistance, and on and on. Most of this information can be more or less determined in less time that it takes to put in a central line in order to get the damned CVP (actually, I do like to know what my CVP is, for what it’s worth). The more data points you are able to collect with increased POCUS skills and experience, the more grasp you have as to what is going on with your patient and the right way to treat them. I would argue that given the information attainable with advanced POCUS skills, POCUS is a no-brainer that will enormously improve not only individual patient outcomes, but effect populations at large, if only the general hospital based practitioner can attain a more than introductory understanding of POCUS.
So, I guess the question is, “how much training is enough training?” I don’t know. Inevitably, POCUS knowledge will incur a bit of the Dunning-Kruger effect as pointed out by Jon’s example of an IVC POCUS fail. But reading Jon’s clinical case example, from the get go, I found myself asking questions that would change may management one way or another with additional information that I could get quickly and easily with additional POCUS interrogation of the patient. Jon pointed this out himself by revealing that the patient has pulmonary hypertension as manifested by the tricuspid regurgitation upon auscultation of the heart. With POCUS, I don’t need to guess what a heart murmur is or how bad it is or even if it is relevant to my patient in this case for that matter. POCUS can tell me it’s TR and it tells me what the sPAP/mPAP/dPAP and PVR is if I care to find out. So if this level of information can be gleaned, for me, no one can argue that POCUS has no merit. But, I’ve spent a lot of time striving to be good at this, just as probably a lot of people reading this have done as well. What about newbies?
Consider: At my main hospital, for a variety of sensible reasons I won’t get into, we decided to train a group of nurses in POCUS in order to evaluate septic patients. They achieve basic training in POCUS and are very competent sonographers with regard to IVC, gross LV and RV function, and pulmonary edema. They are a small group of very intelligent, skillful nurses that are excited to learn all they can. We had them evaluate every septic patient that presented to our hospital, do a POCUS exam, and discuss the findings with a physician. We established some very basic resuscitation endpoints largely based on POCUS findings applied to each individual patient and their POCUS exam. Our severe sepsis/septic shock mortality rates dropped from 35-38% to 8-10% with this program. Our hospital plans to publish this data officially soon for public analysis, but it did make a difference in our experience. That said, my nurses do frequently show me cases where I notice some small detail on their POCUS exam that propmts an additional investigation that alters the plan in management. Also, some of my very competent POCUS savvy residents make errors because they don’t have enough knowledge yet. I’m sure I can make these errors too at times as well, although hopefully less and less so with time.
Here’s my point: Heed Jon’s admonition to look at the big picture and not rely on isolated data points. Be inspired by Phil’s passion for the potential of a good POCUS evaluation. If you only get your toes wet with POCUS, you are playing with forbidden fire. But if you care to look into it further, POCUS opens up worlds to you. By all means, learn all you can about POCUS. Recognize that if you are new to POCUS techniques, there are improtant caveats to each finding, and physiology that needs to be considered with a comprehensive view, some of it may be strictly non-POCUS related information as well. Your patient is unique and only a careful comprehensive consideration of what’s going on with your patient will guide the best approach to your management of their illness. I don’t think SHOC-ED or any other trial for that matter can address the nuances of good individualized patient management. That is up to you.Jon replies:

nice analogy – i think Korbin’s response is appropriate and i look forward to speaking alongside him in May. as i chew on the SHOC-ED a little and try to distill my concerns – i think what it boils down to is this: it’s less about playing with fire – i think – and more about how this fire is brought to the community as a whole. my post on pulmccm was more of a warning to the early adopters [like us] who are planning these trials. imagine 40 years ago:

-the flotation PAC is introduced, a small group of clinical physiologists use it thoughtfully, understand the caveats, the problems of data acquisition, interpretation, implementation, the problems with heart-lung interactions, intra-thoracic pressure, etc.
-these early adopters present their results to the community as a whole
-the physiology of the PAC is simplified
-the numbers from the PAC are introduced into algorithms and protocols and **widely** adopted into clinical practice
-the PAC is studied based on the above and found to make no difference in patient outcome.
-in 2010 a venerable intensivist suggests floating a PAC in a complicated patient and the fellow on rounds chuckles and states that their is ‘no evidence of benefit’

does this sound eerily familiar? is our present rhyming with the past? if the planners of POCUS trials are not careful, i promise you that the same will happen but insert any monitoring tool into the place of PAC. i can very easily visualize a fellow on rounds in the year 2030 scoffing at the idea of PoCUS because trials [SHOC-ED, and future trials x, y and z] showed no difference in patient outcome. is it because PoCUS is unhelpful or is it because the way it was introduced and studied was unhelpful? and the three of us will sound like the defenders of the PAC from 30 years ago: “PoCUS isn’t being used correctly, it’s over-simplified, it works in my hands, etc. etc.”

it’s not PoCUS that’s unhelpful, it’s how we’re implementing it – and i was most depressed when the authors of SHOC-ED appeared to stumble upon this only in the discussion of their paper – like you mentioned phil. imprecise protocols will result in equally imprecise data and the result will be nebulous trial outcomes. we should all be worried.

Korbin adds:

Excellent points Jon. The PAC example is very relevant, as on more than one occasion, I’ve had the argument put to me by some colleagues that essentially how I’m applying POCUS is really no different than the information gleaned from the PAC, and “that’s been shown to not be helpful to outcomes” etc. So, therefore, why do I bother?

Then again, I’ve seen a fair amount of phenylephrine being thrown at hypotensive cardiogenic shock patients after a 2 liter normal saline bolus didn’t do the trick.

You are absolutely spot on when you point out that seeing the big picture, knowing the physiology, and being aware of the pitfalls of isolated data points is important to making the right decisions in patient care.

Furthermore, I agree that when a clinical trial is done that doesn’t consider some of the nuances of all this, and “shows” that POCUS, or any other diagnostic modality for that matter, doesn’t contribute to better patient outcomes, it probably only serves to marginalize a potentially valuable diagnostic tool to an actually astute intelligent clinician.

I’m not meaning by saying this to bash the good intentions of the SHOC-ED trial. To be fair, it’s really hard to design a trial that can take into account all the permutations that are involved in any individual patient presents with, having their own unique clinical situations, hemodynamic profiles, co-morbidities (both known and undiagnosed), etc. POCUS, PAC, transpulmonary thermodilution, ECG, chest x-ray, CT scans, labs, physical exam–these are all merely tools that guide patient care. Albeit some are way more powerful than others. I can image various amounts of uproar if some of these traditional tools were subjected to clinical trials to prove their utility. The argument, if proven “useless” in a study for the oldest and well accepted tools would always be, “put it in the clinical context, and its value speaks for itself.” For me, I’d happily like to make clinical descisions based on information based on an advanced POCUS exam or PAC, rather than interpreting hepatojugular reflux or a supine chest x-ray.

Any diagnostic test requires that the clinician understand the limitations of that test, and understand that the whole clinical scenario must me taken into account. You’ve hit on that, I think, with your argument. This surely has implications when any technology or test is studied.

‘Nuff said.
Philippe
PS These are just the kind of discussions that can change both the way you approach medicine and manage your patients, and these are the ones you find behind the scenes and in the hallways of H&R2018. Don’t miss H&R2019 if you take care of sick patients. It’s the kind of small, chill conference where the faculty will be happy to take a few minutes and discuss cases and answer all your questions (if they can) about acute care.
November 4, 2018

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

This event is past. It was awesome. If you really wish you’d been there, you can catch most of it here!

And don’t miss H&R2020!

Click here to register!

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.

The hidden gem in this conference is the 4 x 40 minutes of meet the faculty time that is open to all. Personally I’ve always felt that I learn so much from the 5 minute discussions with these really awesome thinkers and innovators, so wanted to make it a priority that every participant should get to come up to someone and say ‘hey, I had this case, what would you have done?’   Don’t miss it!

CME Accreditation for 14 hours of Category 1.

This programme has benefitted from an unrestricted educational grant from the following sponsors (listed alphabetically):

Cook

Fisher-Paykel Healthcare

GE Healthcare

Maquet-Gettinge

Masimo

Medquest

MD Management

Medtronic

Novartis

Teleflex

 

The Accreditation is as follows:

 

Here is the Final Programme:

Final Programme

Wednesday May 22 – PreCongress course

  1. Full day Resuscitative TEE course

FOR DETAILS SEE HERE

 

    2. Full day Keynotable

    3. Half day Hospitalist POCUS (PM)

    4. Half day Critical Care Procedures (AM)

    5. Half day Brazilian Jiu-Jitsu for MDs (AM)

for more details on these pre-conference courses please see here.

 

Main Conference Programme: H&R2019 Full Pamphlet

Social Events:

Thursday May 23rd Meet the Faculty cocktail! 1900 – Location TBA – BOOKMARK THIS PAGE!

 

Register here!

FOR ANY QUESTIONS CONTACT HOSPRESUSCONFERENCE@GMAIL.COM.

 

September 27, 2018

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

H&R2019 REGISTRANTS SHOULD RECEIVE A CODE ENABLING REGISTRATION. FOR ANY QUESTIONS CONTACT HOSPRESUSCONFERENCE@GMAIL.COM.

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.

TEE Day PROGRAM

Flyer

 

Keynotable Montreal 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 http://www.keynotable.net or email info@keynotable.net.

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 hospresusconference@gmail.com.

 

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 hospresusconference@gmail.com with any questions!

Register here!

 

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

September 6, 2018

The Resus Tracks 06: Farkas (@Pulmcrit) on Shock Perfusion and Infrared Tech! #FOAMed, #FOAMcc

So I had the chance to catch my friend Josh today, and, as always, he had some unique insights to contribute.

 

I really like the IR idea from the standpoint of objectivity and reproducibility. At first it sounded like a fancy (and fun, of course) way to check skin temperature as I routinely do, but the ability to objectify from doc to doc could be really interesting. Will get on that with my colleagues in my unit. We’ll see what we can come up with in the next months!

 

Love to hear from some others trying to tweak and optimize their resus!

 

cheers

 

Philippe

September 4, 2018

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.

cheers!

 

Philippe

August 28, 2018

The Resus Tracks 04: Shock Circulation & Renal Perfusion with Korbin Haycock. #FOAMed, #FOAMer, #FOAMus

 

So I got to have a chat with ER doc extraordinaire Korbin Haycock today, reasserting my belief that tissue perfusion is not proportional to blood pressure.  I am again including the article discussed, and here is the graph in question:

Here is our talk:

And the paper – which is definitely worth a read, as it clearly supports individualizing therapy!

MAP in sepsis review

 

cheers and please jump into the discussion!

 

Philippe

August 21, 2018

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!

Thanks!

 

Love to hear comments and criticisms!

 

Philippe

 

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

MAP in sepsis review

 

August 18, 2018

H&R2019. A bit Bigger. A LOT Better! #HR2019

First of all thanks to all of last April’s participants and faculty who made this an awesome event. For those of you who missed the inaugural event, no worries, this edition will be even better. Building on the feedback, we’re cooking up a really nice little program that will keep H&R small, packed with clinically useful talks and both cutting and bleeding edge lectures (don’t expect guideline rehash!), and even more faculty interaction.

We will have some parallel tracks to make sure the ED people get some more ER-specific stuff, that the CC people get some esoteric tweaks about obscure ICU topics, and the hospitalists and pick and choose.

We’ve added a pre-conference course day packed with great stuff. The real problem will be choosing:

Felipe Teran (@FTeranMD) brings us a full day, resuscitative TEE workshop including basic certification – first time in Canada!

For educators and anyone wanting to up their presentation game, my good friend Haney Mallemat (@CriticalCareNow) brings his unique Keynotable workshop. If you’ve ever heard Haney talk, you know he is the leader of the pack when it comes to delivery, so not-to-miss opportunity to learn form the master.

Hospitalist POCUS? Check. Hospitalist procedures? Check. Percutaneous tracheostomy and emergency surgical airway? Check. Advanced POCUS like renovascular and transcranial doppler? Check. And a lot more…

Basic info:

May 22nd – pre-conference courses

May 23rd – The Hospitalist

May 24th – The Resuscitationist

Preliminary programme available October 1st here.

 

So mark your calendars. Bring the fam, check out Montreal, and pack in a bunch of solid, ready-to-use clinical knowledge but also some paradigm-shifting approaches and viewpoints!

 

cheers!

 

Philippe