Perhaps this slowed up (0.5x) A3C loop will help with that LVOT doppler!
Perhaps this slowed up (0.5x) A3C loop will help with that LVOT doppler!
As with all continuing medical education events, this one will make you a better physician. But we know who you are: It’s 2am. Your pager is blowing up. You go to the floor with 3 simultaneously crashing patients. We’ve all been there. As a result, we’ve collectively designed this educational event to bring together an ultimate think-tank on how to improve your clinical management of all those things that make us scared at night, and even in the day… If it’s an organ that can fail, we’ve got you covered for a solid, easy, memorable approach to how to support it.
Mixed throughout the day will be cases to solidify your newly acquired clinical pearls & hands on stations with all the toys you need to stabilize your patients.
Hosted by The IBCC (Internet Book of Critical Care) co-creators Adam Thomas and Josh Farkas – also the man behind PulmCrit – this is going to be jam-packed with physiology, clinical pearls, interactive and case-based. If you take care of patients on the wards, this is one not to miss.
Co-directors: Adam Thomas & Josh Farkas.
Hypotension on the wards – Adam Thomas reviews the physiology of shock, the use of invasive & non-invasive monitoring, POCUS & “how your radiologist can help”, initial stabilization (hint, it is not just giving fluid), the hunt for & elimination of hypovolemic, cardiogenic, obstructive shock & distributive shock, as well reviewing the role of hormones and regulatory cytokines as well as how this can potentially be modulated.
Recognizing Illness at a Glance – in this interesting talk, Daniel Kaud shares his data-linkage and pattern recognition skills on common but important pathologies, to help clinicians develop rapid muscle memory and make elusive diagnoses.
Initial stabilization of respiratory failure – this can be one of the most harrowing and time-critical clinical scenarios facing the hospitalist, before the critical care team can take over or the patient can be transferred. Adam Thomas takes participants thru the identification of respiratory failure, the rule of 2s in type & treatment of respiratory failure and the right tools for the job on the wards.
Managing the Congestive Heart Failure Patient – here, Philippe Rola introduces a physiologic and POCUS-based approach to the management of the admitted CHF patient, particularly with the management of effusions and venous congestion.
Physiologic approach to Renal Failure – nephro-intensivist Sharad Patel drags the management of this common disease into this century and will share a rapid approach based on evidence, physiology and the efficiency that POCUS brings to bedside diagnosis and clinical decision-making.
The Biliary patient – whether neoplasia or lithiasis, these patients are often real puzzles. Echo? ERCP? MRCP? Drain? Stent? Fever? Jaundiced? Let’s lay down a solid base for approaching these before calling for the GI SWAT team.
Cirrhosis for the Hospitalist – in this one, hepatologist Ahn Le reviews the most pertinent pearls related to the care of patients with cirrhosis, such as managing encephalopathy, ascites, coagulopathy and more.
ID pearls – microbiologist extraordinaire Silvana Trifiro runs us through some interesting cases to make sure we don’t overlook sometimes subtle symptoms and signs of unexpected infectious diseases.
Neuro pearls – Jeff Scott shares some interesting cases highlighting key elements of the examination and management of neurological emergencies.
Wound Management – microbiologist Marc Laroche sheds some light into what is for most of us a nebulous topic, and provides a thorough, but simple and practical approach to the dressings and management of the various wounds that hospitalists come across.
Lytes, a Pot-Pourri – Josh Farkas, inventor of the “Nephron Bomb,” brings his unique, hard-hitting physiological approach to electrolyte management. This is the thinking doc’s approach, not a check-the-box one.
Clinical Cases – tying everything together, Sharad Patel, Adam Thomas, Silvana Trifiro and Josh Farkas will discuss several cases bringing together several of the key concepts and skills explored during the day.
We reserve the right to make the programme even more awesome by adding to or modifying the above, and promise you’ll come out of this one with a few extra notches on your belt!
But wait…only 30 spots. So don’t wait till the last minute!
Hope to see you there!
…and of course, if you stumbled on this, do make sure to check out the main event, H&R2020!
Adam, Josh, Philippe & The H&R2020 Team.
So managed to pin another really bright guy down today and get his thoughts. Of course we digress some, but I think in all the topics that are truly important to sepsis resuscitation.
So I think all the resuscitationists I have spoken to tend to hover around the same common points:
The nice thing for our southern neighbours is that this study may give you a solid excuse to shake off that lactate mandate.
And I think that Korbin’s ending remarks are important, and it is something I try to teach residents, that there is little value in rapidly normalizing hemodynamic values – which treats the medical team very well – if there is an aftermath that is not beneficial for the patient. Kathryn Maitland’s FEAST study is the real groundbreaker for that concept. So probably a coordinated and careful ground assault is better than dropping the nuke.
For more discussion on this trial check out Rory Spiegel’s breakdown at https://emcrit.org/emnerd/em-nerd-the-case-of-the-deceitful-lantern/ and our discussion at https://thinkingcriticalcare.com/2019/02/19/the-andromeda-shock-study-a-physiological-breakdown-with-rory-spiegel-emnerd-foamed-foamcc-foamer/
a couple points:
First, much thanks to Scott Weingart whose technical pointers are improving my audio quality! Still a ways to go but on the path!
Second, if you’re not registered for H&R2019, there’s only about 20 spots left. And only a handful for the much-anticipated Resuscitative TEE course. Don’t miss out. If you enjoy these discussions, there will be plenty of that, especially in the protected meet-the-faculty times.
And finally, though he doesn’t yet have a blog, you can now follow Korbin on twitter @khaycock2!
So, venous congestion is the predominant physiopathology in CHF, with a number of ensuing problems including lung edema, effusions, hepatic congestion and cirrhosis, renal failure and even gut edema and failure, though less traditionally focused on.
Venous congestion is essentially a problem of salt and water, retained by a well-intentioned but (eventually) maladaptive neuro-endocrine process. The bottom line being: too much salt and water…
However, the vast emphasis in pharmacologic CHF management, if you look at guidelines and publications, is predominantly on various neuro-endocrine modulation strategies, and though these certainly have a role, it is logical that optimizing volume status must play a central role. So why is it not a recurrent theme of discussion? Well probably because our means to traditionally assess this is limited. What are the tools used by physicians worldwide to assess congestion? Weight, peripheral edema, JVD, crackles, CXR are pretty much it. Now even under the best of circumstances, these are hardly precise tools, and of intermediate specificity. But it is what is available, and taught, and in most cases, does the job fairly well. However, judging by the problem of recurrent admissions for CHF exacerbations, likely not good enough.
The Canadian HF Guidelines – as thorough as they are – are interesting in that the only time diuretics are addressed are in exacerbation, and a note to use the lowest dose possible to maintain stability… But little else in terms of guiding this assessment of stability or the dosage management. The usual “thorough history and physical” stuff, of course.
So what else could we do? Now my interest in POCUS is no secret, and it seems like the ideal tool for assessing both fluid collections and hemodynamics. So what do we know?
Lungs – at this point it’s beyond much debate, POCUS-enhanced physical examination is vastly superior to radiographs and traditional physical examination. Small effusions are easily seen as well as congestion in the form of B lines. In the case of sub-acute to chronic congestion, as we are not overly concerned with central lesions (not seen with ultrasound), the CXR is of no further benefit.
Peripheral edema – I’ll call this one a tie. Not that much benefit in measuring subcutaneous edema with a probe, except for exact reproducibility, at the cost of time. 😉
The Heart – another no-brainer. Ultrasound wins. With appropriate training, experience, and more important than either, the ability to recognize one’s own limitations.
Venous congestion – Now we’re getting to the interesting stuff. So even if for some, it may be the first time hearing about the clinical use of venous congestion markers in CHF, it isn’t new science. In the 90’s, several studies were published correlating portal vein pulsatility, congestion index, as well as hepatic vein doppler pattern with CVP, RV dysfunction, finding close correlation. In 2016, Iida et al published a great article on renal venous doppler and CHF which I highly recommend reading, and more recently, Andre Denault and William Beaubien-Souligny (@WBeaubien) have been doing tremendous work with portal vein pulsatility and post-op cardiac patients’ organ dysfunction. So the science correlating excessive venous congestion to organ dysfunction is there and is clear.
Why have we not yet widely studied this?
The answer is fairly simple. Prior to the growth of POCUS, there was no single clinician group holding the necessary set of clinical and echographic skills to make this clinical routine. Cardiologists are not all echo-capable, and even those that are would have had little or no experience dopplering abdominal organs and vessels. Radiologists – most of the literature coming from their field – are not pharmaco-clinicians and do not follow patients. Family physicians and internists, likely the bulk of the physicians looking after these patients, largely had not had access to or echo skills. Until now.
So a quick review: right-sided failure causes elevated RAP, so everything upstream gets congested. The first echo signal of this is the plethoric IVC (in both axes of course!!!), and an abnormal hepatic vein doppler (which is pretty much like a CVP tracing, just non-invasively) but is that the max? Nope. What is worse is when that pressure transmits thru backwards from hepatic veins to portal vein, transforming a normally monophasic flow with minimal variation into a progressively more pulsatile flow, to the eventual point of being intermittent. And when the IVC pressure transmits across a congested kidney such that the same thing occurs in the renal veins.
Those findings have been well studied and correlate with poor outcomes in CHF.
So what could we do?
What we are doing now is systematically assessing CHF patients in terms of their venous side. What we see so far is that some have full, plethoric IVCs, maybe B lines and effusions, maybe some peripheral edema, but may or may not have those worse markers of abnormal doppler flows, and those who don’t generally don’t have significant organ dysfunction such as renal failure (I discussed this a few years ago in my pre-doppler era in terms of re-thinking common approaches).
So when we find significant portal pulsatility, we diurese aggressively, creatinine notwithstanding. We almost always get an improvement in biochemical markers of renal function within 48-72 hours, with the only really tricky patients being those with severe pulmonary hypertension. More on that in another post.
Goonewardena et al had a really great observational study that showed that if CHF patients were discharged with a non-plethoric IVC and significant respiratory variation, they were less likely to be re-admitted. The figure below on the right shows the numbers:
So there is reasonable evidence to suggest a POCUS-guided approach, which we’ll go over in the next post, which should include our revised Advanced CHF Clinic guidelines.
I can already hear the thoughts… “is there any evidence for this?” But those asking that reflexively should first ask themselves “what is the evidence behind the way I assess congestion and manage CHF?”
In Greek mythology, Prometheus (/prəˈmiːθiːəs/; Greek: Προμηθεύς, pronounced [promɛːtʰeús], meaning “forethought”) 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.
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.
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.
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.
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!
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):
The Accreditation is as follows:
Here is the Final Programme:
Wednesday May 22 – PreCongress 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
Thursday May 23rd Meet the Faculty cocktail! 1900 – Location TBA – BOOKMARK THIS PAGE!
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 best is yet to come.
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