The First Steps Towards Physiological Resuscitation: A Team Effort. #FOAMed, #FOAMcc

(original figure from this old post)

So Rory (@EMnerd) hit us last week with an interesting question that was brought up by David Gordon, a resus fellow working with him, and thought some of us may be willing to belabour his point. A lengthy and really fascinating exchange ensued, which I felt was worth sharing with the #FOAMed community:

 

Rory (Spiegel @EMnerd) find him on emcrit.org

Korbin Haycock (please leave comments to encourage him to get on Twitter)

Segun (Olusanya @iceman_ex) find him on LITFL.com and The Bottom Line

Me (@ThinkingCC) also thinkingcriticalcare.com

David Gordon

My editorial comments!

 

Rory: 

David brought up an interesting question today. Why not do a straight leg raise and use TAPSE to assess the likelihood the pt will be “volume responsive”?

My answer was the following:
“I don’t think the RV increases TAPSE in response to fluid and so the only way TAPSE would be able to assess fluid responsiveness would be if it decreased in response to a a SLR. My contention is this would be a late marker of fluid intolerance and others signs of venous congestion (portal/renal vein doppler) would be seen far earlier. “
In addition I brought up that “volume responsiveness” is a flawed surrogate and we should rather be focusing on volume tolerance.
And that is, in my opinion, the critical concept. 
Anyway David seemed less than satisfied with my answers so I figured I would open the discussion to you physiology nerds…
Korbin: 
That’s an interesting thought, you have brought up.  To clarify, are you asserting that an increase in TAPSE from a volume challenge or SLR could be a indicator of volume responsiveness?  If I missed your meaning, please correct me.
I think Rory is right in his assessment that TAPSE would likely be a more valuable indicator of fluid tolerance (or more importantly , intolerance), rather than fluid responsiveness.  TAPSE, however,  may be (I don’t know) a more sensitive indicator of fluid tolerance than things like IVC collapsibility index, etc.  This might make sense as a decreasing TAPSE (or TAPSV, too for that matter) in response to a fluid challenge might be an earlier indicator that the RV won’t do much with more fluids before it would manifest in things like a non-collapsing, plethoric IVC, decreasing S’/D’ wave ratio on HVD, portal vein pulsitivity, or pulsatile intrarenal venous Doppler.
One problem I’ve had for a long time with fluid responsiveness from the standpoint of the circulation up to the pulmonary valve (IVC collapsibility index being the most common example), is that it doesn’t measure what you really want to know, and that is LV fluid responsiveness.  There is a whole lot going on hemodynamically from when blood leaves the RV to where it finally contributes to LV preload.  I think if you want to know if the patient is fluid responsive, there are quite a few ways to assess this directly, rather than looking at the RV, IVC, etc.
I stopped chasing every bit of volume responsiveness a long time ago, however it does have its place in managing the sick patient, I think.  Usually, my first question is about volume tolerance/intolerance, before I start to think about volume responsiveness.
To investigate the fluid tolerance/intolerance status, I’ll look into a lot of things, usually using a lot of ECHO/US information.  My sonographic considerations are: LV contractility, diastolic function and ventricular compliance, LVEDP, valve pathology, SVR, B-lines (and if B-lines are present, put that into the context of what the LVEDP is because if the pressures are low, but the lungs are wet, pulmonary vascular permeability is high and I’ll think very hard before giving fluids), pulmonary artery pressures, PVR, interventricular septal shifts, RV contractility, IVC, HVD, portal vein, and renal Doppler.
(has anyone ever seen an ED doc do this anywhere??? Wow!!!)
Also, I’m lucky to have some other tools at my place like transpulmonary thermodilution catheters and pulse wave analysis devices to assess things as well.  Sometimes these things make serial assessments more convenient than dragging the US machine over multiple times, and can also give additional information, like EVLW, PVPI, etc.
(I think in the case of Korbin’s hospital, it may be important to bring downstairs care upstairs!)
Secondarily, if I think the patient is volume tolerant and then I have determined that they are volume responsive, and would benefit from volume administration, the next question I ask myself is what’s the best way to do this.
Clinical assessment combined with ECHO comes into play, as if the patient is genuinely volume depleted, volume repletion makes sense.  However, a lot of volume responsiveness is driven by syndromes of high CO and low SVR.  In these cases, I usually give very little volume and opt for a vasopressor to drive venous return instead.  This strategy tends to correct the CO/SVR derangement as well as take care of the volume responsiveness at the same time.  I feel much better if I know that my MAP is being generated by a balanced CO, SVR, and volume status rather than having a “normal” MAP.
I think that is a really, really important cognitive model. The common and traditional approach is to try to maximize CO with fluids and avoid the terrible vasopressors. In a disease where the primary derangement is vasodilatory, it doesn’t seem logical… However finding the right balance is difficult. And with the near-extinction of the PA catheter, we no longer have a low SVR value staring us in the face begging for some pressors.
Sorry to be so long winded, guys.  Hope I didn’t bore you with stuff I’m sure you already know.  These topics are really interesting to me though!  I’d be interested in all of your thoughts on the TAPSE question.
Segun:
I think the RV is more likely to dilate in response to Fluid than change TAPSE, as suggested by a paper or two on RVEDA changes as a predictor of Fluid responsiveness https://ccforum.biomedcentral.com/articles/10.1186/cc3503
(RV dilatation May result in a reduction in TAPSE too?) 
Potentially, yes. SV may not decrease but TAPSE may.
The end result should be a change in stroke volume, so one could argue that rather than TAPSE you could just measure RVOT VTI in response to a passive leg raise. (I don’t really see the difference between M mode and PW doppler, and RVOT VTI is simple enough to measure from a PSAX or RV outflow view)
TAPSE is an Uber-simplified method of looking at RV contractilty rather than volume (overloaded RVs can have excellent TAPSE, for instance). I think it would answer a very different question.
Me:
Interesting question indeed. I can’t agree more with Rory and Korbin. Korbin’s clinical run-through is, as far as I’m concerned, completely on point and, if i weren’t so lazy, and had all the hardware he is fortunate to have, would consider as gold a standard as possible, until  mitochondrial monitoring and trans-capillary flow monitor technology is made.
I think it requires a bit of a paradigm shift away from volume responsiveness, that has been all the rage in the last decade or since the end of the swan age, and instead towards focusing on tolerance. There is significant and building evidence that congestion is end-organ damaging, and evidence that chasing maximal CO is mortality-causing (80’s and 90’s literature supranormal o2 delivery and all that), hence on both fronts focusing on congestion makes more sense.
I think we have to follow the fluid path (venous congestion y/n, rv ok y/n, lungs ok y/n and finally lv ok y/n) and then do a global almost holistic ‘is fluid the best option’ reflection including brain, gut, kidneys, peripheral tissues, etc, with Korbin’s nice little twist on balance of CO, SVR for the BP/perfusion. I don’t think there’s any point of care monitoring tool to unequivocally ascertain the best level of each today.
Rory:
So here is my question, should we be asking “Is this pt likely to benefit from fluids?” rather than “Is this pt likely to augment their CO with fluids?” 
Stop for a moment and think of most of your septic patients (not all, yes, some have cardiomyopathy, some are profoundly hypovolemic), are they actually in a low CO state?  The near-obsession with CO is probably rooted in the common belief that the elevated lactate stems from hypoperfusion, a myth which has been debunked.

Lets say we use Korbin’s gold standard I think we still have to ask what is the benefits of giving this pt fluids? There are many patients I see who would meet all the criteria outlined by Korbin in whom I still don’t administer fluids because whatever increase in cardiac output I get will be transient at best. I am inclined to sit tight allow my antibiotics to take effect and let the pt correct their own vasoplegia. After an initial small aliquot of fluid in the ED I like to see obvious signs of hypovolemia before I give additional boluses. I do like the CLASSIC trials criteria:

(1) Lactate of at least 4 mmol/L
(2) MAP below 50 mmHg in spite of the infusion of norepinephrine
(3) Mottling beyond the edge of the kneecap (mottling score greater than 2)

(4) Oliguria 

All this from the perspective of a decongested venous system and a under-filled heart on US
Korbin:
To Rory’s point, I agree that just because there is a lack of fluid intolerance and the presence of fluid responsiveness, it doesn’t necessarily mean fluids are indicated.
If I have a clinical story that supports a likely lack of hydration plus I’m looking at a high SVR, low CO, and a low SV, I will usually give some fluids.  Mottling, especially if pressors are on board, to me is a clue that some sort of volume might be indicated.
That’s actually quite interesting.  The pathophysiology of mottling isn’t clear (click here for an interesting read), but definitely a space to earmark, when trying to find the optimal balance between vasopressors and CO augmentation.
As far as the lactate goes, as everyone here knows, there’s a whole lot of reasons to have a hyperlactatemia.  It’s drives me a little crazy when I see a lactate come back elevated and the first thing someone wants to do is give fluids, especially if they haven’t considered any of the stuff we’ve been talking about.
I think if you have a patient with a high lactate, the first thing to do is ask yourself why they have a high lactate, rather than trying to correct the number.
Rory:
Agreed, most of the time in a septic pt I view a rising lactate as a sign I don’t have source control rather than a signal to give additional fluids.
Philippe:
So in terms of fine tuning, here is one thing I like to do with tissue saturation – SctO2 (cerebral)  and peripheral:   if it drops with vasopressors I favor augmenting CO (fluids if not too congested, inotropes to consider) if it rises or stays flat with pressors i stay the course. This is definitely not evidence-based, but to me, if tissue saturation decreases while increasing vasopressor dose, it seems logical that the perfusion is dropping, and not a course worth pursuing. I like to think of it as an example of MBE (medicine-based evidence) in the patient in which it is occurring.
David:
It seems to me the feeling is that we shouldn’t be chasing any single indicator of fluid status/tolerance/response/optimization evaluation and the key is to ask the clinical questions and pair that with our sonographic assessment.   RV functional assessment may have a role in that discussion, but TAPSE may not be the best indicator as RVOT VTI may be a better answer to the initial question.
The study that Segun sent out seems to indicate that LVEDA may be a better predictor of SVI.  The septal interdependence plays a larger role than I initially thought and perhaps using M mode to look at changes in septal motion gives you more information about the ability of the heart as a whole to manage the fluids…
That’s an excellent point, because even if the RV can handle the fluid, if the LV cannot, it’s gonna end up in the lungs.
Philippe, what kind of time course do you allow for your lactate to change, other than just response to your initial resuscitation?
Lactate should improve over hours. As Rory says, if a day later it’s still hovering above 4, and you don’t have impaired hepatic clearance, you might be missing something…
Korbin:
That’s something that certainly something to consider, Rory.   I think a lactate that is suddenly rising is most likely driven by a catecholamine surge driven by something going the wrong way.  But not always.
The important thing is to stop and think about what’s going on.
Case in point:  Last week I had a patient that had cardiac arrest due to an asthma exacerbation.  I had put a TEE probe down during he resuscitation, and a little bit afterward based on what I was seeing on the TEE, I felt she needed a pressor.  I used epinephrine because the beta-2 agonism might help with bronchodilation.  Everything hemodynamically look pretty good, except the lactate came up.  The ICU resident saw the lactate and ordered a liter of LR.  I called them and explained that the epinephrine was likely the cause of the lactate and it probably wasn’t anything to worry about.
Rory:
Just the other day I was called to the floor to assess a pt because the treating team was concerned he was septic when his lactate came back at 6.5. I walked in the rm as they were hanging the 30cc/kg fluid bolus. A brief assessment revealed he was in florid CHF. Once I convinced them to stop giving fluids and instead use an aggressively dose of diuretics he did just fine and cleared his lactate without issue.

In my mind lactate in and of itself uninterruptible. In a pt who is otherwise improving and the lactate is not clearing as fast as I would like I tend to just stop checking it. The one I find troublesome is in the post resus pt who doesn’t look great, I don’t have an obvious source, their pressor requirements are slowly rising and the lactate is hovering in the 4-5 range. That’s the pt that tends to do poorly if you don’t identify and establish source control

Korbin:
Agree with that Rory.
If I have those patient with a persistent lactate elevation, and they look like they could be malnourished, I’ll give them some thiamine, too.
Segun:
My two cents- there’s data soon to be released that compared echocardiographic dimensions (RV/LVEDA, IVC etc) to mean systemic pressure- showing no correlation with ANY echocardiographic parameters.
It would seem that going purely by dimensions, you cannot predict volume state on echo… so at the moment we can detect hypERvolaemia with lung, portal vein, and renal vein POCUS (and to a degree IVC), and profound hypOvolaemia by looking at doppler patterns (although the patient is more likely to tell you).
The other side of things, which has been clearly elucidated by everyone in this thread, is the concept of “permissive responsiveness”. Ruthlessly thrashing every heart to its maximum myocardial stretch doesn’t necessarily seem to be the best idea, to my mind.
I agree with everyone’s thoughts. Beyond the initial LLS/Shocked AF stage, you need a very good reason to give a fluid bolus!
And don’t get me started on lactate…
Korbin
I would only comment that the magic of Doppler probably is far more valuable than cardiac dimensions when dealing with hemodynamics.  Dimensions give anatomic values that can be extrapolated to hemodynamics, but PW and CW Doppler interrogation infers pressure differentials, which can directly be applied to things like flow and resistance.  Tissue Doppler has the added informative value of cardiac compliance, so that a comprehensive picture can be painted in light of filling pressures and the relationship to preloading.
When I look at all this together, I really feel that in most cases, a quite accurate picture of what’s going on is within grasp.
To emphasize again, something like B-lines with a compliant, low LVEDP LV, tells me valuable information about pulmonary vascular permeability.  Tread carefully about fluids here.
David:

How does the RV respond to a fluid bolus?

To answer this question first we must understand the role of the right heart in the circulatory system. Often the right ventricle (RV) is compared to the left ventricle, in reality it serves an entirely different function. The left ventricle generates the necessary pressures required to maintain systemic perfusion. The right ventricle’s job is to enable venous return, which is generated by the gradient between the mean systemic filling pressure and the right atrial pressure (RAP). The role of the RV is to maximize that gradient by keeping the RAP as low possible. 

With this in mind let us examine the RV’s response to a fluid bolus. As the RV becomes filled, conformational changes occur within the RV that allow it to increase its stroke volume without increasing the distending pressure.Under normal circumstances, the RV end diastolic distending pressure does not increase in response to fluid loading. Therefore, if the RV is functioning appropriately, RAP does not accurately reflect RV preload. But in pathological states, when the RV is hypertrophied, diseased, or overdistended there is an inverse relationship between RVEDV and RV stroke volume. Any fluid, or increased RV pressure beyond this point results in an increase in RAP, decreasing venous return.1

1. Pinsky MR. The right ventricle: interaction with the pulmonary circulation. Critical care (London, England). 2016;20:266.

So that was the discussion. I certainly thought it was very interesting. Following this, we decided we’d band together and try to hammer out what we think should be the optimal management of shock, trying to tie in physiology, the scant evidence that is out there about resuscitation, and the pitfalls of venous congestion. Finding the sweet spot in the balance between vasopressors, inotropes and fluids is a very real challenge that all resuscitationists face regularly, and it is very unlikely that, given the complexity of such a protocol, looking at tolerance, responsiveness and perfusion, that an RCT would be done anytime soon.

We’ll be sure to share when we come to a consensus, but certainly the broad strokes can be seen here, and I’d love to hear anyone’s take on this!

And of course, we’ll definitely be discussing this further with smarter people at H&R2019 – think Jon-Emile Kenny (@heart_lung), Andre Denault and Sheldon Magder!

Cheers

Philippe

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!

Working out the Clinical Kinks in Venous Congestion: A Discussion w/Rory & Korbin. #FOAMed, #FOAMcc, #FOAMus

It’s really exciting to be at the outer frontier, trying to figure out some new clinical areas. Now these have all been described, however the ability of clinicians to properly identify certain pathophysiological findings has been limited prior to POCUS. Following the trail being blazed by Dr. Andre Denault, we are also working on expanding the applications, particularly in resuscitation/deresuscitation and CHF/AKI. There are more questions than answers, but that’s exactly why it’s interesting.

So for those unfamiliar with the topic here is a small intro:

And for those following, here is the discussion:

 

Do expect more from us about this. Watch this space. It is practice changing.

 

Additional resources:

Here’s a link to the article referenced during the recording: https://www.ncbi.nlm.nih.gov/pubmed/29573604

Andre and I discussing venous congestion

…if you dig around the blog in the past year there are a bunch more!

 

do share your thoughts!

cheers

 

Philippe

 

Renovascular #POCUS: Technique with Korbin Haycock. #FOAMed, #FOAMcc, #FOAMus

Korbin Haycock, ER doc extraordinaire.

 

So a few months ago I got to talking with Korbin about POCUS, fluids and resuscitation, only to find out this guy is doing all sorts of awesome stuff in his ED in sunny California.  Got to meet him at H&R2018 and he had even more tricks up his sleeve he was telling me about. He will definitely be back for H&R2019 on the faculty side of things.

In the meantime, let’s review renovascular ultrasound with him:

And here is our discussion that took place at TheRounds Backstage during #HR2018.

Interesting stuff. It isn’t always so easy to get a nice renal view in ICU patients, but with some perseverance you often can. I’ve been toying with it and tying it in with the hepatic and portal flow patterns, but I have to admit I had sort of dismissed renal resistive index based on what I could find in the literature, that is until I got to chat with Korbin, who made me see there are some interesting avenues, especially the example he states on seeing it improve with vasopressin use in shock patients, which correlates with some of the data out there suggesting decreased need for RRT and better outputs with vasopressin on board.

I have a feeling there is relevance to this in acute care, and that the next couple of years will reveal some usefulness. The glitch had always been in not knowing what the baseline RRI is, and that it can be abnormal in chronic RF. There are, however, many patients who were perfectly well previously and where the assumption that their baseline is normal is probably safe.

Love to hear comments from anyone using this!

 

cheers

 

Philippe

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  !!!

Jon-Emile (@heart_lung) chimes in on the whole portal vein POCUS! #FOAMcc, #FOAMed

When it comes to physiology, there`s no doubt that Jon is the man, so I was really curious about his take on all this, which, no surprise, is definitely worth sharing, just in case everyone doesn`t go read the comments.

 

Jon:

Wow; there is a lot to unpack here.

My first comment is that intra-renal venous flow [*not renal vein flow], hepatic vein flow, portal vein flow, etc, etc, etc [as well as IVC size and respiratory variation] are all ultrasonographic transductions of the central venous pressure …so I’ll give my boxed disclaimer that volume status and volume responsiveness cannot definitively and reliably obtained from this marker because the CVP is too complicated to make these physiological leaps.

Indeed. It is important to realize that, as Jon states below, that the angle for looking at the PV in this case is to assess congestion, rather than responsiveness or the ever-so-nebulous ‘status.’

Wait for it … volume tolerance and the CVP, is a bit more nuanced, i think.  with a high CVP, you really have to ask yourself – **why** is the CVP elevated and go from there.  if the CVP is elevated because of tamponade, its very different management from a high CVP from a massive PE or air-trapping versus a high CVP from volume overload.

Absolutely. Diuresing a pre- or full-fledged tamponade, PE or air-trapping could have disastrous consequences, i.e. PEA arrest!

There seems to be some confusion about *the renal vein* versus *intra-renal vein*.  the lida trial is clear that it is intra-renal vein flow.  i am not terribly familiar with *the renal vein flow, however, my hunch is that renal vein flow should always be biphasic [just as the jugular venous flow, SVC flow, IVC flow and hepatic vein flow are always biphasic] – that is a normal pattern close to the right atrium.  normally the systolic inflow velocity is greater than the diastolic inflow velocity and there is fairly good data correlating reversal of systolic to diastolic venous flow ration to right atrial pressure [in the IVC and SVC].

Definitely the intra-renal vein should be the target here – not always easy in some patients, because the renal vein itself, especially the right (no crossover) really has an IVC pattern and won`t necessarily reflect the effect of intra-renal hypertension.

The pulsatility that evolves in the intra-renal vein as the CVP rises is beyond me, but the authors postulate that it has to do with the compliance of the vein at higher CVP and intra-renal interstitial pressure which makes some sense.  But it is important to note that the compliance curves of an intra-renal vein and *the* renal vein are probably quite different.

Secondly, the pulsatility of the PV is a neat idea because of its relative ease of assessment.  However, the pulsatility, presumably, is due to the PV encroaching the limits of its compliance curve – the PV, like the CVP – has an inflow and outflow pressure.  It is highly likely that a pulsatile PV in a post-operative cardiac patient relates to an angry RV – but is this always true?  What about the cirrhotic?  What about differential partitioning of fluid into the splanchnic bed versus the lower body?  What about differential expression of adreno-receptors between splanchnic arteries [beta and alpha] and splanchnic veins [mostly alpha].  My point is that there could be *other* inflow and outflow differentials that are affecting PV volume, compliance and therefore pulsatility that are not yet recognized.  A cirrhotic on bomb dose phenylephrine/vasopressin may have their splanchnic venous volume recruited with blood expelled towards the liver, an engorged PV that is pulsatile – but is that RV failure?  Is that a patient who needs to be decongested?  I don’t know.

Thirdly, there are complex cardiac contributions to venous flow phase and vein pulsatility such as arrythmia – atrial compliance, etc.  As the comment above notes – how might afib contribute to SVC or IVC venous inflow?  It’s hard to know, but my hunch would be that afib itself would tend to reverse the normal S wave: D wave supremacy … that is, decrease the normal systolic inflow velocity relative to the diastolic inflow velocity.  if the atrium is not emptied fully then its pressure with rise.  if atrial pressure rises, when the atrium is pulled downward during ventricular systole, the S wave will be diminished.  additionally, the more chronically dilated and poorly compliant the right atrium, the greater its pressure will be with the loss of atrial kick.

Fantastic points. Again, looking at POCUS metrics CANNOT BE DONE IN ISOLATION, from the rest of the POCUS and clinical data.

Lastly, the venous inflow pattern analysis approach to CVP estimation – i think – is better than IVC size and collapse because of how IVC size and collapse can also be affected by IAP, ITP/PEEP, etc.  Because ITP affects systolic and diastolic inflow patterns similarly, that confound should be lessened.  Nevertheless, as Dr. Denault mentions in the cases above – you have to treat the patient!  This means integrating what the data is telling you in the patient in front of you.  If in a certain clinical context the test results do not make sense, it’s probably a false positive or false negative test.

I dug up this gem from 30+ years ago. Excellent paper [https://www.ncbi.nlm.nih.gov/pubmed/3907280 – “Ultrasonic assessment of abdominal venous return. I. Effect of cardiac action and respiration on mean velocity pattern, cross-sectional area and flow in the inferior vena cava and portal vein”].

Ok that’s on my short reading list for the next 48h!

They show the venous inflow waveform for the IVC [presumably very similar to *the renal vein]; Afib *does* cause the S wave to become attenuated – so it would change the normal biphasic form to more of a monophasic form. In theory, giving a calcium channel blocker and slowing the patient down should improve this somewhat. They even have a brief discussion on portal vein pulsatility.

This venous inflow stuff is very interesting and potentially very applicable. @iceman tweeted out wave velocity patterns in the MCA during high ICP – indeed – an increase in ICP renders the flow more pulsatile and then there is loss of diastolic flow. Probably similar physiology for an intra-renal vein as intra-renal capsular pressure rises. A good sign that the kidney is under pressure!

Thank you Jon for some really excellent physiological points and the reminder that, in POCUS just as in clinical medicine, we cannot rely on one assessment, and that measure must be considered in the context of the factors affecting it. Otherwise, we are not truly tailoring our therapy to the patient, but only pretending to.

Don’t miss Jon and the POCUS workshops at  next april!

Portal Vein POCUS: A Reader’s Case and a Follow-Up to the Denault Discussion

So I’ve been meaning to post a follow up and discussion about portal vein POCUS and how I am integrating it so far, and a few days ago I got a really interesting comment from Dr. Korbin Haycock, and I think it’s got some awesome elements to discuss.

Before we get into it, I would invite anyone reading this to go listen to the original Denault Track here, without which this discussion would be missing some elements.

What we are looking at here is the physiological assessment of venous congestion, and how doppler interrogation of the portal vein may help us. So here is Korbin’s case, and I will interject (in bold) where I think a point can be made, or at least my thoughts on it.

“Awesome post. Awesome website. I had never heard about portal vein pulsatility until reading your blog. I have previously been looking at the renal resistive index and renal vein Doppler pattern in my hypotensive/shock patients (along with doing a bedside ECHO and POCUS pulmonary exam) to guide when to stop fluid resuscitiation.

Very impressive. I have only ever heard of a handful of resuscitationists looking at this (including Andre, and consequently myself) so I’m gonna have to have a chat with this fellow soon! For those who have not tried or are not familiar, some basic info can be found here. I’ll have to review this, but I think one issue with RI is that there is an associated ddx, so that without knowledge of baseline, I would not be certain how to use it. Renal vein doppler seems very interesting to me, as that venous path is the one of the cardiorenal syndrome (forget about all that “low flow” nonsense in CHF – not in shock – patients), and there is clearly bad prognosis associated with abnormal (discontinuous) flow patterns. Here is a really good study (Iida et al)  and its editorial (Tang).

Iida Doppler_CHF Heart Failure JACCHF 2016

Tang Editorial JACCHF 2016

I had a case last night that I think illustrates that fluid administration can be the wrong thing to do in some septic shock patients. Plus, I got to try something new and look at the portal vein for pulsatility.

My case was a gentleman in his late 60’s with a history of HTN, atrial fibrillation and HFrEF who presented with three days for a productive cough and fever. POC lactate was 2.7. His HR was 130-140’s, in atrial fibrillation, febrile, MAP was 50, and he looked a bit shocky and was diaphoretic. The resident had started antibiotics and a fluid bolus of LR, of which not much had gone in (maybe 200cc) when I came to start a night shift and evaluated the patient. I asked that the fluids be stopped until we could have a look at him.

His IVC was about 1.5-2 cm with >50% collapsibility.

So I’m gonna hit the pause button right there for a couple of comments. That’s not a hypovolemic IVC. The RAP may be raised by some of the  It may very well be volume responsive, but I think the first thing to go for is correcting that tachycardia. The antibiotics are definitely the right call, but the fluids should, in my opinion, be held until assessment for volume tolerance is done.

His LV looked to have some mildly decreased EF and was going very fast. RV looked normal. His average SV was 45, CO was 6.1, E/e’ ratio indicated a slightly elevated left atrial pressure. His estimated/calculated SVR by the ECHO numbers was about 550. Lungs were dry anteriorly, without B-lines, but PLAPS view was c/w bilateral lower lobe PNA. Renal vein Doppler was biphasic and the resistive index was very high. I looked at his portal vein and it was pulsatile.

Excellent. So there is pulmonary pathology, which makes fluid tolerance already of concern. The CO is certainly adequate and SVR is low, suggesting a vasodilatory shock etiology. 

In the past, based on the IVC and the way the RV looked, I would have done a straight leg raise or given a given some crystalloid to see if his SV and BP improved, and if it did, give some IVF. Instead, I told the staff to given no more fluids and I gave him 20 mg of diltiazem.

His heart rate decreased from 130-140’s to 90. His averaged SV increased to 65 (probably due to increased LV filling time and better diastolic perfusion time), CO was 5.9, estimated SVR was 570. The renal and portal vein Doppler were unchanged. The MAP didn’t bulge and stayed low at 50-55. At this point I ordered furosemide and but him on a norepinephrine infusion to increase the SVR, first at 5 mcg/min, then 7 mcg/min.

Totally awesome to see. It isn’t unusual for me to diurese patients in vasopressor-dependant shock, as more and more data is emerging on how venous congestion has deleterious effects on the gut and may even contribute to the SIRS-type state. And once a patient is in a euvolemic to hypervolemic state, the only fluid they get from me is the one containing norepinephrine. Maintenance fluid is not for critically ill patients IMO.

The NE gtt increased his MAP to 75 mmHg. His SV was 80, CO 7.1 (I was a little surprised it didn’t go down a bit), estimated SVR was 700. I had his labs back at this point and his creatinine was 1.8 and the last creatinine we had was 1.1 a few months ago. His renal vein pattern was still biphasic and his renal resistive index was also still quite high at 0.89, which would probably predict a significant kidney injury in 2-3 days.

Even though his MAP and hemodynamics looked great, I was worried about the renal resistive index. I ordered a little more furosemide and started him on a little bit of a vasopressin infusion. After things settled down, MAP was 75-80, his average SV was 80, CO 7.3, estimated SVR was about 800, and his renal resistive index (RRI) was 0.75. He looked much better too. The second lactate was 1.3.

Very interesting to see the drop in RRI.  Great case to show how you don’t need to chase lactate with fluids. That is an antiquated knee-jerk reflex hinging on the concept that hyperlactatemia is primarily due to tissue hypoperfusion, which we have learned is not the main cause. 

This morning his creatinine had improved to 1.3 and he is doing well.

South of your border, CMS considers me a bad doctor for not giving 30 cc/kg crystalloid as a knee jerk reaction and instead giving a diuretic and early vasopressors as we did in this patient. Just looking at his IVC would indicate that IVF would be a reasonable strategy. If I had done a SLR or fluid challenge and found him fluid responsive, in the past, I would be temped to chase every bit of fluid response with pushing more fluids, but the renal and portal vein Doppler made me stop fluids in this patient this time. I think this example illustrates the importance of looking at each of your patients on a case by case basis and looking at the whole picture (heart, lungs, kidneys, now portal system too for me!), rather than following protocols.

Kudos. 

 

So then, Andre decides to chime in as well:

Very interesting but be careful about the interpretation of portal pulsatility because it can be falsely positive particularly in hyperdynamic young patient, which was may be not the case. We published an algorithm in order to identify the true portal pulsatility associated with right heart failure and fluid overload and a normal portal vein with pulsatility:

Tremblay Portal pulsatility Flolan Mil AACR 2017

(Tremblay 2017 A&A care report) A & A Case Reports. 9(8):219–223, OCT 2017 DOI: 10.1213/XAA.0000000000000572 , PMID: 28604468)

The latter will be associated with normal RV even hyperdynamic, normal hepatic venous and renal flow, normal IVC. We still need to explore the significance of portal hypertension outside the area of cardiac surgery where we are finalizing our studies.

Always tell my residents and fellow, treat the patient and not the number or the image. That being said, the patient got better so cannot argue with success.

So I think this is a really important point, that it can become dangerous in POCUS to look for a simple, single-factor “recipe” with which to manage the patient, when in fact you can have many factors which, integrated, can give you a much better understanding about your patient’s pathophysiology.

My take on portal vein POCUS so far is that it is a marker of critical venous congestion, beyond simply a plethoric IVC. I think it is wise to stop fluids before the plethoric IVC, but a plethoric IVC with a pulsatile PV should bring fluids to a screeching halt and some decongestive therapy started. The data for this?  Andre is cooking it up, but in the meantime, there is plenty of evidence that congestion is plenty bad, and NO evidence that maximizing CO works at all, so I am very comfortable in witholding fluids and diuresing these patients. 

For fun, here is a little figure from Tang et al about the doppler patterns discussed.

Love to hear everyone’s thoughts!

and for those interested, there will be a workshop run by Andre and myself on this at :

more to come on this soon…

cheers

 

Philippe