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

In Greek mythologyPrometheus (/prəˈmθəs/GreekΠρομηθεύςpronounced [promɛːtʰeús], meaning “forethought”)[1] is a Titanculture 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.

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

 

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!

Scientific Programme

Wednesday May 22 – PreCongress courses

NOTE DUE TO LIMITED SPACE AND UNTIL JANUARY 1ST REGISTRATION FOR THESE IS RESERVED FOR H&R2019 ATTENDEES, FOLLOWING WHICH REMAINING SPOTS WILL BE OPENED TO ALL-COMERS. H&R2019 REGISTRANTS SHOULD RECIEVE A CODE ENABLING REGISTRATION. FOR ANY QUESTIONS CONTACT HOSPRESUSCONFERENCE@GMAIL.COM.

Full day Resuscitative TEE Course THIS COURSE IS CURRENTLY FULL. DUE TO DEMAND WE MAY ADD A SECOND TEE DAY. EMAIL US (above) TO BE PUT ON THE WAITING LIST.

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 on these pre-conference courses 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

0940-1020 – MEET THE FACULTY OPEN DISCUSSION

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

1420-1500 MEET THE FACULTY OPEN DISCUSSION

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

0940-1020 MEET THE FACULTY OPEN DISCUSSION

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

1420-1500 – MEET THE FACULTY OPEN DISCUSSION

Workshops (1500-1700)

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

TERAN’s Intro to Resus TEE

HAYCOCK’s Intro to REBOA

Intro to ECMO

POCUS-SIM

KENNY’s Advanced Physiology Workshop

 

Register here!

contact us at hospresusconference@gmail.com 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

H&R2019 REGISTRANTS SHOULD RECIEVE 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 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 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!

Hope to see you there!

 

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

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

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

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

cheers!

 

Philippe

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