So here’s another interesting question as a follow up to the previous discussions:
Most people would probably agree that florid congestive signs on POCUS means the RV is unable to pass any more extra volume to the left heart; whilst the absence of those signs mean that the patient may be able to cope with some additional volume without immediately engorging the vital organs.
And my question is: what about those in between? i.e. the patients who start to develop some mild congestive features on POCUS.
For those who are on the verge of congestion, diuresis would push the RV to the left (i.e. steep part) of Starling curve resulting in significant CO drop; conversely, extra volume pushes the RV to the right (i.e. flat part) leading to congestion or even D-shape LV, directly hindering CO as well. This margin becomes even smaller in patients whose RV starts to fail (i.e. entire Starling curve shifted downwards)
Great, great question. The crux of this, I think, is deciding which is the greater issue, congestion or poor perfusion. Obviously they are intertwined, so the decision will be on a case by case basis. Jonathan alludes here to a narrow “balance point” between congestion and preload dependancy. My feeling – and we’ll see if we can get some consensus – is that this indeed narrow in patients with marked pulmonary hypertension. When patients have pure pump failure congestion, my clinical experience is that you can decongest plenty without drop in systemic CO, in fact it often improves, likely related to ventricular interdependance. So let’s go on…
I’ll illustrate my point with the following scenario:
for previously healthy middle aged patients intubated and admitted to the ICU for ARDS from severe pneumonia, they quite often develop some acute cor pulmonale after mechanically ventilated for several days even if the PEEP/driving pressure isn’t exceptionally high; and they usually have resp failure and shock to start with.
Given that they don’t have pre-existing heart disease, the only signs suggesting the emergence of cor pulmonale could be subtle, without structural changes like dilated RV (RVEDD at most at upper normal range) nor abnormal septal movements. You may see TAPSE dropping to marginal level and portal vein PW signal may become a bit more pulsatile. IVC looks full and RVSP usually rises but not skyrocket. The MV inflow pattern & E/E’ suggest rather normal LA filling pressure, not surprising from a previously healthy heart.
In this case, it isn’t the LV diastolic dysfunction that overly afterloads the RV; and it isn’t the RV dilation that impairs the (D-shape) LV from ventricular interdependence. Therefore I’d consider the right heart circulation & left heart circulation running purely in series, whereby limiting the RV preload could reduce the LV CO.
Now, if this patient goes into shock, would you consider fluid challenge or diuretics? Everyone probably would also get other therapies on board, e.g pressor, inotrope, source control etc. But when the patient’s BP is 80/40mmHg, I am more prone to giving some fluid as I believe that reducing preload in a septic patient can precipitate arrest; and that RV only directly impairs LV CO once the IVS starts to shift, which should take more time and thereby easier to monitor.
Interesting case that happens commonly – if you do POCUS and look for it rather than blind-ish management. Here, you have congestion, likely due to pulmonary disease, fluids, on a normal-ish RV (which also means it is unable to mount a huge PAP).
So personally – and will full disclosure that this is not evidence-based (as if there was any evidence in our resuscitative practices!), I would consider this a relative contraindication to fluids, given the non-volume-tolerant state (ALI/pneumonia/ARDS and portal pulsatility) of the patient. With pulsatility and signs of organ dysfunction I would be diuresing or pulling fluid off. We’ll see if we can get Rory to comment, as he has been doing a fair bit of this.
So in this patient it would be either no fluids, or diurese.
I don’t think one should have a general conception that reducing preload in a septic patient category is an issue. That may be so if you do not have the capability to look, and hence feel you should behave more cautiously. A septic patient with a tiny IVC may indeed be tipped over into low CO by removing fluids, but another with a full tank post resuscitation may benefit. So with the ability to assess hemodynamics, individualized approaches trump general ides and protocols. Much more to come on this in the next weeks as we break down a lot of interesting concepts in regards to vascular tone assessment and cardiac efficiency.
I fully appreciate how ambiguous this situation is and that in reality the only way to find out the treatment that works is often by trial and error. Serial assessment by POCUS is definitely needed and one may even put the entire fluid thing aside and focus on other treatments. But just want to know your take and the reasons behind.
Thanks again for all your work and these thought provoking posts; and my apologies for the supposedly quick question ending up being not so quick. It took me some effort to clearly delineate my question in mind.
Anyone interested in these topics should keep an eye out for the H&R2019 Tracks. A bunch of us are getting together before and during the conference and will be recording discussions on all these little cases and angles around hemodynamics and other fun resuscitationist topics.
So I ran a couple of twitter polls sets the other day. Here is the first:
(if you want the twitter videos see here)
and part 2:
And to sum it up:
So I just wanted to illustrate something I keep bringing up, essentially that the entire IVC literature based on the AP diameter measurement is physiologically and mathematically flawed. I think the poll and images above clearly support this: given a short axis view, clinicians clearly have a different opinion (and possibly intervention!) than using only a long axis view.
My take, as I’ve said and will keep saying, is that there is a lot of info in IVC POCUS, and the one I am LEAST concerned with is volume responsiveness, which sadly seems to be everyone’s only focus nowadays when it comes to the IVC.
But here’s some food for thought, some of my clinical applications in 5 seconds of scanning:
initial shock patient: big fixed IVC -> no fluids, hurry and find the downstream problem and correct!
resp failure patient: small IVC -> it’s not a massive PE, keep looking for the cause don’t send for a STAT CT angio!
AKI patient: big IVC look at venous doppler and call for lasix, stop the fluids and albumin that were being mistakenly given!
AKI or shock patient & small IVC: sure , start with some fluids and reassess soon (that means hours not the next day)
etc..etc.. there’s more, and “fluid responsiveness” is only in extremes and fairly low on the list for me!
ps if you like physiology, and a physiologico-clinical approach, don’t miss H&R2019!
(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
My editorial comments!
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”?
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)
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
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!
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
- Full day Resuscitative TEE course
FOR DETAILS SEE HERE
2. Full day Keynotable
3. Half day Hospitalist POCUS (PM)
4. Half day Critical Care Procedures (AM)
5. Half day Brazilian Jiu-Jitsu for MDs (AM)
for more details on these pre-conference courses please see here.
Main Conference Programme: H&R2019 Full Pamphlet
Thursday May 23rd Meet the Faculty cocktail! 1900 – Location TBA – BOOKMARK THIS PAGE!
NOTE: THIS WAS THE H&R2018 PAGE, SO IF YOU ARE LOOKING FOR H&R2019, CLICK HERE!
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.
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:
If you’re crazy busy, or have any questions, feel free to email firstname.lastname@example.org or tweet (@ThinkingCC) to reserve a spot!
Download the brochure here:
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.
So Rory (@EMnerd) is in the process of working on a fluid resus protocol for Shock-Trauma, and asked me if we could have a chat about it, which I feel very honored for – and had a brief impostor syndrome crisis – but it’s always great to chat with people who are really bright, really physiological and after the same goal, to make patients better. Always a pleasure to chat with Rory, so here it is.
I really can’t wait to see their protocol, because I think this is a huge and complex endeavor, but has to be done. I will try to put pen to paper (probably really pixels to a screen but that doesn’t sound as good) and put what I try to do for fluid resus on a diagram of sorts.
Love to hear comments and questions.
PS please skip the first 30 seconds which are a technical blank… Ièm not tech saavy so can’t trim it!
A great comment by Dr. Korbin Haycock
One issue to consider is the degree of pulmonary vascular leakage. If, as in the case of sepsis, the pulmonary vasculature is more prone to the development of lung interstitial edema, lower LVEDP’s possibly will still result in as much lung wetness as higher LVEDP’s. Therefore, reliance of E/e’ ratios may not be the best measure of a fluid resuscitative endpoint in sepsis (and aren’t we really talking about sepsis resuscitation here?). I believe that it’s relatively clear that EVLW will adversely affect outcomes, but pushing for every bit of increased stroke volume/fluid responsiveness is less clear to be beneficial, even if it makes sense from a DO2/VO2 perspective (which may not be the real issue in sepsis anyway, as mitochondrial utilization of the DO2 provided may be the real problem, rather than DO2/VO2 balance). If the assumption is that the kidneys and lungs are the most delicate organs and most at risk to over aggressive fluid administration, and will impact mortality/LOS in the ICU, perhaps a combined strategy of attention to E/e’ ratios, development of B-lines, or the renal resistive index increasing would be a signal for a different strategy rather than fluids to increase venous return (i.e. switching from crystalloids to norepinephrine or vasopressin if the CO is elevated and will tolerate a minor ding from the increase in SVR). If any of those three variables indicate a problem, stop the fluids, switch to a vasopressor. If the issue is the CO rather than the SVR, use an inotrope instead. Of course RV/LV interactions as mentioned in the comments above must be considered. No point in giving fluids to an empty LV if the RV is failing–you’ll just congest the kidneys.
So a few years ago I had a patient in the ICU, post op for some abdominal surgery, and, using POCUS, I detected a hyper echoic area in the liver, in a wedge shape. I scanned the patient and, lo and behold, there was a matching area of air-filled hepatic venous sinuses on CT scan. Well, my surgical colleague and I were very concerned and proceeded to inform the patient he would be needing exploratory surgery for what was likely ischémie bowel. He essentially – though in more polite words – told us we were idiots and that his belly felt fine and he didn’t think surgery would be needed at all.
His belly did feel fine. So were his labs. So we worried, but, given this whole thing about free will and consent, etc, couldn’t very well force him into what we felt was necessary surgery.
The next day he was fine. On POCUS, the area of air had shrunk. The next day, it was gone altogether.
We thanked him for his keen clinical acumen and for teaching us a good lesson.
However, we were a bit perplexed, because traditional teaching equated portal venous air with a severe bowel disorder, usually ischemic or inflammatory, with exceedingly high mortality. At least that is what we had been fed. We are both grads of 1999. Hmmm…
So over the next few years we saw a few of these cases, sometimes bad, sometimes not, and a review of the literature (see below) showed an interesting evolution of the disease. Described in the 1950’s on plain films, hepatic air was a bad omen indeed, with mortality in the 75-90% range. In the CT era, the mortality started to “drop” to the 35-60% range. Now you can find quite a few reports of “surprisingly” good outcomes with conservative management. So this evolution doesn’t represent a change in severity so much as the technological capability to detect smaller and smaller amounts of air in the venous system – just increased sensitivity. And now, with POCUS – ultrasound is the most sensitive detector of air in a vascular tree – the associated mortality is likely to take another drop, not only because of our ability to detect very small amounts of air, but also because we are actually looking at the area, and also in a wider range of patient’ pathologies that those commonly associated with HPVG.
Clinical Case: HPVG and PE!
So a couple weeks ago I saw a patient in the ED who’d recently broken an ankle, had her foot put in a boot and managed conservatively and came back dyspneic and tachycardic. Here are a couple of clips:
As always, I start with the IVC:
Big & fixed.
So here the source of the problem is pretty clear, a large common femoral DVT.
She wasn’t very echogenic so I don’t have great clips of the heart but she had a dilated and hypocontractile RV with a McConnell’s sign (preserved apical contraction), small and hyper dynamic LV with septal flattening.
Now here is where it gets interesting, the portal vein:
You can clearly see bubbles traveling up the portal vein. Ominous, or not?
So clinically, her abdomen was normal, she had no abdominal symptomatology at all…
So the severe RV obstruction resulted in significant venous congestion. Additionally, the decreased cardiac output – as manifested by a lactate of 4 and mild tachycardia/hypotension (110 HR, BP sys 90’s) was clear.
The etiology of HPVG in the literature isn’t clear – mucosal disruption, bacterial gas are all mentioned but as far as I could find, no definitive answer.
Is it possible that there is a “normal” inward leak of mucosal gas that is normally fully dissolved in the venous bloodstream, but that, in cases of low flow and/or venous congestion, the dissolution capacity (per unit time) decreases, and that gas comes out of solution? Alternately, those who have increased intraluminal pressure (gastric distension, etc), the increased transmembrane gas driving pressure may overload an adequate blood flow…
This would explain the benign course of many patients, particularily those with gastric dilation.
Based on hemodynamics, tachypnea and, to some degree, venous congestion, I decided to thrombolyse her using 1/2 dose lytics. Within a couple of hours her HR decreased to the 90’s and BP rose to 110 systolic. Echographically, however, the IVC/RV findings remained similar, but the HPVG decreased. By the next day, HPVG was altogether gone, lactate had resolved and dyspnea was significantly better.
Take Home Message:
HPVG, although not quite as poor a prognostic sign as once thought, nonetheless warrants concern and investigation, even if the abdominal exam is entirely normal and without symptomatology, as correction of an underlying cause of “benign” HPVG (whether low-flow or bowel distension) would still need to be addressed.
In the meantime, I suspect that, reported or not, this has been noted by other POCUS enthusiasts, since we are now looking more frequently at this area, and are dealing with patients with low-flow states, congestion, bowel obstruction/ileus or more than one of these.
Hopefully some investigators will take a look at this phenomenon and delineate the pathophysiological mechanism!
Love to hear of your experience with this.
For those interested in POCUS, see here for a quick read primer on clinical applications of POCUS.
HPVG Review article 2009:
So today, a 33F presented following syncope. She was mildly tachypneic wiyh a HR of 135 and BP of 130/80. I’m inserting the clip of my bedside ultrasound evaluation, as this takes place essentially simultaneously with my history-taking:
So this clip runs thru a few views, starting with an IVC long axis, showing a relatively plethoric IVC with minimal variation. This is not normal. Tells me to expect something abnormal downstream, unless someone has flooded the patient with IV fluids. The next view is the parasternal long, then short axis, showing an increased RV to LV ratio, and a small, hypercontractile LV, with septal flattening consistent with RV pressure overload, the “D” sign. The apical 4 chamber follows with little else to add (difficult to measure TAPSE well in that segment).
So this is sure looking like pulmonary embolism, and I’m already toying with a half dose TPA, MOPETT-style, until the reveals that the cause of her starting oral contraceptives two months ago was to control heavy menses associated with large uterine fibroids… So I figure I’ll buy myself some decision time anyhow by ordering the CT angio – unless in pre-arrest, I don’t thrombolyse without formal confirmation – but I did start IV heparin on the echo findings. Here is the CT:
So this indeed confirms submissive embolism, particularly to the left PA.
Next? I work in a community hospital, and although I’m totally comfortable thrombolysing PE, in this case, I was concerned about bleeding related to the fibroids, and I haven’t yet figured out a way to embolize bleeding vessels at the bedside, so I felt that the safest thing was to transfer her to a tertiary care center with a solid interventional radiology program. So off she went. I’ll update if anything funky was done like a catheter suction and I can get some clips.
So in terms of POCUS, I think this illustrates how speedily a diagnosis can be made, and although in this case the pre-test probability and index of suspicion was pretty high, it isn’t always!
For more POCUS tips, see here!
A 60 year old woman, known for COPD, shows up short of breath and hypotensive.
The clip goes thru a series of views of the IVC and the heart.
What do you see?
Answer and further case data coming soon!