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 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

CCUS Institute POCUS & Resuscitationist Mini-Fellowship: Evolution.

 

So over the last couple of years, the POCUS Mini-Fellowships have been slowly but steadily morphing into POCUS-Resus training.  With POCUS essentially critical in all aspects in resus, including venous congestion assessment, ventilation, diagnostics, it is a natural extension to blend the exchange into many of the other tools that we use, including discussions around fluids choices, pressor choices, monitoring using NIRS tissue oximetry, ETCO2, and overall resuscitation strategies.

Some structured workshops will include percutaneous pigtail insertion, vascular access phantom practice and both surgical and percutaneous surgical airway manikin practice, depending on participants’ choice.

We have recently expanded with the addition of Dr. Philippe St-Arnaud, ER and CC doc and EDE (Emergency Department Echography) Instructor extraordinaire, who will increase our availability – which had been fairly limited – apologies to those whom we could not accommodate due to scheduling reasons.

This is an excellent complement to an RLA (I’m part of that faculty) or ULA fellowship, to bring a real clinical experience into the mix.

Of course, if you are a canadian resident you can get a whole month of this for free by doing an ICU elective at Santa Cabrini Hospital (well, americans are also welcome but more hoops to jump thru!).

For more details and registration information see here.

And here is some of the most recent feedback from the fellows:

Anyway, I wanted to say thank you again. You have inspired our group to continue to move POCUS into our clinical practice; we have started a fluid management algorithm in our observation unit, and hoping that the soon-to-be-added ButterflyIQ to the unit will improve its utilization. Over the last few years, we have caught a few myocarditis cases and new CHF cases initially placed in observation as “influenza,” managed hundreds of CHF cases, and had a handful of +FAST exams in our ED that we were not quite expecting (in fact, having one that was just texted to me from a co-worker is what prompted this email!).   Our POCUS program is still in its infancy, but I think the horse is out of the barn at this point. On behalf of all of our patients that we will see, thank you.

Additionally, I have gone on to co-direct a sono-wars type event at our national physician assistant conference (AAPA), for PA students. At the inaugural event, we had free workshops and a competition that included 200 student learners, representing about 30% of PA programs from all over the country. We opened a huge door for PA programs to start implementing POCUS longitudinally within their curriculum. We received amazing feedback on the program, and are hoping to publish results soon (currently with journal editors)… 

I am excited to pay forward my debts to those that have helped me.  You not only helped me, but generations of PA’s for years to come. Thank you so much for your time and commitment to excellence. What you do matters; please keep running the mini-fellowship! Patrick Bafuma EM PA @EMinFocus, Hudson Valley, NY, USA.

 

        This review is for the CCUS Institute Bedside Ultrasound (US) Mini-Fellowship. I was fortunate to do the mini-fellowship after the Hospitalist & Resuscitationist conference, and I was able to put into practice various techniques that we learned. Dr. Rola was a pleasure to work with and was well-versed with the latest US and free online access meducation (FOAM). The atmosphere was conducive to learning, and we picked up an ultrasound almost immediately and used it extensively through each day. We used various US machines and were able to get a good feel for all of them. My US experience before the mini-fellowship had been a two-day introductory course with healthy medical students as volunteers. At the mini-fellowship, being able to learn on actual critically ill patients was illuminating and helped cement what I had learned. We also went over relatively new bedside techniques such as point-of-care trans-cranial doppler (TCD) and optic nerve US (ONSD). Overall, the experience was well worth the 2800 mile trip, and I would enthusiastically recommend it to anyone that is interested in learning practical applications of US. – Dr. Pranay Parikh, Los Angeles, USA.

 

So join us for a few days of intense, real clinical learning.

cheers,

 

Philippe

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

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

So first, Kylie (@kyliebaker888):

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

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

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

Then Korbin gives his two cents, and then some! 

Great case, loved it. Thoughtful management, brilliant!

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

Cannot agree more.

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

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

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

Agree.

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

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

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

Dr. Maitland and the FEAST study corroborates exactly this.

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

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

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

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

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

cheers!

Philippe

 

H&R2018: Final Program! Only a few spots left!

Do you take care of sick patients?  If so, you’ll be liking these two days.

Jon-Emile Kenny, Rory Spiegel, Josh Farkas and Andre Denault in the same, small auditorium. It’s a treat.

So here is the schedule for both days, including the workshops, which at this point are almost filled. We’re quite excited as it has really come along well, and all the speakers are amped to teach and learn, which is the point of this whole thing.

 

Due to fire code, space is limited so register now! And honestly, the workshops are almost full, but if there is sufficient demand, we might add one or two, so don’t be shy. Someone even asked for a Neuro-POCUS workshop. A couple more inquiries and we’ll do it!

Download the brochure and registration form here: H&R2018 – Brochure-Participants

 

Thanks and see you in Montreal in April!

 

The Scientific & Organizing Committee

The Hospitalist & The Resuscitationist. Montreal, April 18th & 19th, 2018. #Hres2018

So for this winter, we’ve put together a little gem of a conference which will be a mix of hospitalist and critical care medicine, both with a dash of POCUS for good measure. Our focus here will be short, to the point, highly relevant and highly physiological talks on key topics, in short, 15 minute talks.

What are we going to talk about?

Day 1: The Hospitalist

 

Day 2: The Resuscitationist

 

 

You can figure there will also be late-breakers, “ask the crowd” talks and more.

Workshops? Sure:

Yup. You can ask for a workshop. Enough similar requests will probably make it happen. A few have already asked for Neuro-POCUS, so that is a likely addition.

 

So, who will be talking?  The lineup already includes Andre Denault, Josh Farkas (@Pulmcrit), Jon-Emile Kenny (@heart_lung), Rory Spiegel (@EMnerd), Hussein Fadlallah, Peter Barriga, Daniel Kaud, Davide Maggio, Michael Palumbo, William Beaubien-Souligny, and a few more to confirm. And who knows who might do an impromptu drop-in…

 

The short answer is yes. Of course, it does depend on what you do. If you are a hospitalist, involved in critical care or acute care of any kinds, you will find something here for you. Totally awesome for IM residents/FM residents planning on doing some hospital medicine or ICU coverage. Who will get the most bang for his or her buck here? Real docs training or working in the trenches. This isn’t a cutting edge research conference, but a cutting edge clinical application conference.

 

Oh yes, and the CME, of course:

 

This will be a small, fun conference. Space is purposely limited, for an intimate feel and to encourage discussion between peers. No need for these exclusive “meet-the-professor lunch” or anything like that: that’s what the whole event is like!

 

Registration is open! Print, fill, write a cheque and send the form below:

RegistrationV2

If you’re crazy busy, or have any questions, feel free to email hospresusconference@gmail.com or tweet (@ThinkingCC) to reserve a spot! 

Download the brochure here:

H&R2018 Brochure – Participants

 

cheers!

 

The H&R 2018 Scientific & Organizing Committee:

Dr. Philippe St-Arnaud – ER and Critical Care doc, POCUS instructor and constantly pushing the clinical envelope.

Dr. Carola Zambrana – our Hospitalist on the panel, constantly seeking excellence in care and working on bringing POCUS to the wards.

Dr. Mario Rizzi – our friendly neighborhood respirologist and educator.

Dr. Philippe Rola – Critical Care doc, long time POCUS aficionado and instructor, working at bringing POCUS into the everyday physical exam.

 

Fluid Stop Points! More POCUS goodness from Korbin Haycock. #FOAMed, #FOAMcc

I am really enjoying this exchange, and I think it is in the true spirit of #FOAMed to foster these discussions, as we have the opportunity to combine and fine tune our understanding of a topic from several really bright people’s view and experience. 

Korbin:

Jon-Emile, excellent points and insight. I should clarify a couple of my comments. To be specific, by “renal vein flow” I am referring to intra-renal venous flow. Apologies for my imprecision! Thanks for pointing that out.

Yes, a lot of these renal and portal Doppler patterns are surrogates of CVP. But I don’t think any of us would use CVP in isolation these days to make any decision what-so-ever on whether fluids were indicated in our patient.

Also, to clarify, I am not using intra-renal venous flow or renal resistive index as measures of non-fluid responsiveness. Rather, I use these measures as a stop point for attempting to solve the patient’s hemodynamic dysfunction with crystalloid regardless of whether or not my straight leg test tells me the patient is still fluid responsive.

And that is a key re-iteration to me. It is important to set these stop points and not only look at whether the cardiac output can be maximized. This has been tried. And failed. Let’s remember that sepsis is not inherently a disease of low flow. It isn’t cardiogenic or hypovolemic shock at the core.

My rationale for the strategy of using intra-renal Doppler, E/e’, and Lung US (now, I can include portal vein pulsatility) as a stop point for IVF administration is that I think the patient is best served to avoid iatrogenic edema of the upstream organs, primarily the lungs and the kidneys. These are the two organs (maybe you could put the endothelium in this category as well–glycocalyx being a whole other can of worms!) most easily damaged by the chase for optimizing every bit of fluid responsiveness. We have good evidence that getting wet lungs and swollen, congested kidneys is a bad thing, and we have these tools to hopefully warn us when we are pushing things too far.

Absolutely. And the whole glycocalyx is something to keep in mind, even if only to me mindful to disrupt it as little as possible.

Of course renal resistive index, intra-renal venous flow, portal vein pulsativity, and whatever else you like will have limitations and confounders. As long as you understand what can cause abnormalities with these tools, you can make an educated guess as to what’s going on. If our creatinine is off and our RRI is high, but intra-renal venous flow and portal vein flow is normal, perhaps the RRI is caused by something other than renal congestion, like ATN. If the portal vein is pulsatile, but the Doppler patterns of the hepatic vein, kidney and the heart look ok, maybe something else is wrong with the liver. But, if all our modalities are in agreement and pointing to congestion, we should perhaps believe that it’s congestion and stop the fluids. 

That is an awesome approach to integrating RRI. I’ve been toying with it for the last couple of days, and much thanks to Korbin, I think that the limitations of RRI can be overcome by using the rest of our clinical and POCUS data.

It isn’t a hard technique, though in some patients getting a good signal can be tricky.

I think that the kidney, being an encapsulated organ, and the fact that much of our crystalloid ends up as interstitial edema, the kidney will develop sub-optimal flow patterns before CVP would cause congestion. The same is true regarding the lung, except that it’s just related to increased pulmonary permeability due to inflammation. Regardless, the idea is to save organs, and the earlier you can detect the problem, the sonner you can stop battering the more delicate organs with fluid.

As I think we have all mentioned, you really have to look at the whole picture, and put it together to tell the story of what is wrong, so we can logically and thoughtfully treat our patients.

I really appreciate this discussion. Thanks!

 

 

Thanks to Andre, Jon and Korbin for making this very educative for all!

Cheers

 

Philippe

 

ps don’t miss the POCUS Workshops on venous assessment at  !!!