So I love the UVM EM Update at Stowe. It’s a great little conference, run by my good friend and all around awesome guy Peter Weimersheimer (VTEMsono) ED Pocusologist, and his super team including Kyle DeWitt (@emergpharm), Meghan Groth (ENpharmgirl) and Mark Bisanzo (@mbisanzo). It’s a smooth running show with some really amazing speakers where I always learn a bunch. Had the chance to finally meet Sergey Motov (@painfreeED) and learn from an awesome opioid lecture. And it’s always great to hang with Josh (@PulmCrit) and listen to the pearls!
So here is my fluid talk. The Keynote pdf is just below. Hope there’s a useful tidbit or two in there!
So anyone who knows Korbin (@khaycock2) realizes he is a true trailblazer in the ED, essentially doing cutting edge critical care from the get go in his shock patients. In my mind this should be the goal for any critically ill patients, that they get the highest level care right at entry and for however long they may be staying in the ED until they get to the ICU.
So today, I was really happy to corner Korbin lounging somewhere in sunny California (as 6 inches of snow come down hard in Montreal) to tell me how he is using this technology in his resus patients.
So this has got me interested in using this technology. I see it as an early warning signal that your patient may be less fluid tolerant than you may think, and that the signs of pulmonary fluid intolerance I use (oxygen requirement, appearance of B lines (FALLS Protocol-style), etc…) have yet to manifest.
So I’m looking forward to hearing Korbin explain this further (during H&R2020!) and in actual cases where the change in management is clear.
So here was a late-breaker talk at H&R2019. Portal vein pulsatility and hyponatremia by a nephrologist – intensivist. Love it. Sharad, a really great guy, also recently published a case report on this topic.
There is a lot of stuff on venous congestion in the woodwork, some of which we are involved in, but also some springing up from different places, and this is really exciting, because POCUS gives you a non-invasive tool to assess and differentiate pathological degrees of congestion that really nothing else can with as much breadth, and as part of a comprehensive exam.
Venous POCUS is worth learning, and keep your eye on this space for how it evolves as a clinical tool. Our VEXUS classification will soon have some real substance behind it.
So, venous congestion is the predominant physiopathology in CHF, with a number of ensuing problems including lung edema, effusions, hepatic congestion and cirrhosis, renal failure and even gut edema and failure, though less traditionally focused on.
Venous congestion is essentially a problem of salt and water, retained by a well-intentioned but (eventually) maladaptive neuro-endocrine process. The bottom line being: too much salt and water…
However, the vast emphasis in pharmacologic CHF management, if you look at guidelines and publications, is predominantly on various neuro-endocrine modulation strategies, and though these certainly have a role, it is logical that optimizing volume status must play a central role. So why is it not a recurrent theme of discussion? Well probably because our means to traditionally assess this is limited. What are the tools used by physicians worldwide to assess congestion? Weight, peripheral edema, JVD, crackles, CXR are pretty much it. Now even under the best of circumstances, these are hardly precise tools, and of intermediate specificity. But it is what is available, and taught, and in most cases, does the job fairly well. However, judging by the problem of recurrent admissions for CHF exacerbations, likely not good enough.
The Canadian HF Guidelines – as thorough as they are – are interesting in that the only time diuretics are addressed are in exacerbation, and a note to use the lowest dose possible to maintain stability… But little else in terms of guiding this assessment of stability or the dosage management. The usual “thorough history and physical” stuff, of course.
So what else could we do? Now my interest in POCUS is no secret, and it seems like the ideal tool for assessing both fluid collections and hemodynamics. So what do we know?
Lungs – at this point it’s beyond much debate, POCUS-enhanced physical examination is vastly superior to radiographs and traditional physical examination. Small effusions are easily seen as well as congestion in the form of B lines. In the case of sub-acute to chronic congestion, as we are not overly concerned with central lesions (not seen with ultrasound), the CXR is of no further benefit.
Peripheral edema – I’ll call this one a tie. Not that much benefit in measuring subcutaneous edema with a probe, except for exact reproducibility, at the cost of time. 😉
The Heart – another no-brainer. Ultrasound wins. With appropriate training, experience, and more important than either, the ability to recognize one’s own limitations.
Venous congestion – Now we’re getting to the interesting stuff. So even if for some, it may be the first time hearing about the clinical use of venous congestion markers in CHF, it isn’t new science. In the 90’s, several studies were published correlating portal vein pulsatility, congestion index, as well as hepatic vein doppler pattern with CVP, RV dysfunction, finding close correlation. In 2016, Iida et al published a great article on renal venous doppler and CHF which I highly recommend reading, and more recently, Andre Denault and William Beaubien-Souligny (@WBeaubien) have been doing tremendous work with portal vein pulsatility and post-op cardiac patients’ organ dysfunction. So the science correlating excessive venous congestion to organ dysfunction is there and is clear.
Why have we not yet widely studied this?
The answer is fairly simple. Prior to the growth of POCUS, there was no single clinician group holding the necessary set of clinical and echographic skills to make this clinical routine. Cardiologists are not all echo-capable, and even those that are would have had little or no experience dopplering abdominal organs and vessels. Radiologists – most of the literature coming from their field – are not pharmaco-clinicians and do not follow patients. Family physicians and internists, likely the bulk of the physicians looking after these patients, largely had not had access to or echo skills. Until now.
So a quick review: right-sided failure causes elevated RAP, so everything upstream gets congested. The first echo signal of this is the plethoric IVC (in both axes of course!!!), and an abnormal hepatic vein doppler (which is pretty much like a CVP tracing, just non-invasively) but is that the max? Nope. What is worse is when that pressure transmits thru backwards from hepatic veins to portal vein, transforming a normally monophasic flow with minimal variation into a progressively more pulsatile flow, to the eventual point of being intermittent. And when the IVC pressure transmits across a congested kidney such that the same thing occurs in the renal veins.
Those findings have been well studied and correlate with poor outcomes in CHF.
So when we find significant portal pulsatility, we diurese aggressively, creatinine notwithstanding. We almost always get an improvement in biochemical markers of renal function within 48-72 hours, with the only really tricky patients being those with severe pulmonary hypertension. More on that in another post.
Goonewardena et al had a really great observational study that showed that if CHF patients were discharged with a non-plethoric IVC and significant respiratory variation, they were less likely to be re-admitted. The figure below on the right shows the numbers:
So there is reasonable evidence to suggest a POCUS-guided approach, which we’ll go over in the next post, which should include our revised Advanced CHF Clinic guidelines.
I can already hear the thoughts… “is there any evidence for this?” But those asking that reflexively should first ask themselves “what is the evidence behind the way I assess congestion and manage CHF?”
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”?
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…
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.
(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.
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.
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)
All this from the perspective of a decongested venous system and a under-filled heart on US
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.
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.
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.
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…
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.
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
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.
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…
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.
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!
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):
So I was glad to see some great answers on twitter about this case, so let me fill you guys in on the management and the details.
So my diagnosis was of a (likely viral) myocarditis as a subacute process over the last weeks, with a superimposed pneumonia causing the acute deterioration and presentation to ED. I didn’t think that his elevated lactate represented shock, but rather a reflection of adrenergic activation and reduced hepatic clearance due to congestive hepatitis. He also had congestive renal failure. Of course, the LV had a 4 x 2 cm apical thrombus, which is likely secondary to the dilated cardiomyopathy.
So the management was diuretics, antibiotics, and anticoagulation, which resulted in a gradual improvement of the respiratory status and renal/hepatic dysfunction. He had a coronary angiogram the day following admission which showed two 50% stenoses deemed to be innocent bystanders.
I think the learning point in this case is that, without POCUS, this could easily have been treated as severe sepsis with multiple organ failure (potentially rationalizing away the BP of 140 as a “relatively low” BP due to untreated hypertension), and as such, may have received fluids… Especially south of the border where they are mandated to give 30 cc/kg to anything deemed “septic.” This would have been the polar opposite of the necessary treatment.
The scarier thought is that he may have then progressed to “ARDS,” been intubated and then the debate between keeping him dry and giving fluids for the kidneys may have ensued. Though a formal echo likely would have been done, it may not have happened in the first 24-48 hours… If MSOF progressed and he succumbed, the rational may have been that he was “so sick,” and died despite “best care…”
The reality is that he is not yet out of the woods today, with an EF of 15% and afib, but he is off O2 and sitting up in a chair. Fingers crossed he falls in the group of those with myocarditis who improve…
So I’d mentioned using NIRS to monitor and tailor therapy a few months ago, and promised a more in-depth discussion to come, so here we go.
For this not familiar with the technology or the concept, NIRS measures tissue saturation, predominantly venous. Hence physiologically it is akin to central/mixed venous gases, but localized. Cerebral NIRS found its foothold in the OR with carotid and cardiac surgery, but its use is now expanding. Given typical knowledge translation time of a decade, it should end up joining ETCO2 as a routine vital in monitored units, but probably not soon enough.
So in our unit at Santa Cabrini Hospital in Montreal, we’ve had this technology for about a year (the INVOS system), and have been studying its uses. In this time, three applications have stood out:
Finding the “Sweet Spot” for vasopressors.
Confirmation that therapeutic interventions are hemodynamically appropriate.
Cardiac arrest: CPR adequacy, prognostication and detecting ROSC.
Finding the “Sweet Spot” – I think (hope) that anyone reading this with professional interest understands that pressure does not necessarily equal perfusion. With that in mind, adjusting vasopressors to a pressure makes little sense, and represents at best a guesstimate of perfusion, which is what we really are after. We can all agree, however, that a certain minimum pressure is required, but whether that is 65, 55 or 45 MAP no one can say for sure. So the way I like to use it is to establish a baseline and watch the direction of the tissue saturation with vasopressor therapy. If the saturation begins to drop off, we may have reached a point at which excessive vasoconstriction is worsening tissue perfusion, and that inflexion point may represent the upper beneficial limit of the vasopressor – this may happen to be under 60 or 65 of MAP. However, it is key to understand that this inflexion point is reflective of the current state of hemodynamics, such that a change in volume status or cardiac output, in one direction or the other, would likely change the position of this physiological point. For example, a volume depleted patient may reach a decreasing tissue saturation point at 55 MAP, but, once volume replete, may reach a higher MAP of 65 or above before a drop in saturation is seen. Conversely, a patient whose best tissue saturations were around 65 MAP who suffers an MI and sudden drop in cardiac output may now see his perfusion compromised at that same MAP, which would now be achieved with a greater vasoconstriction, less cardiac output and consequently, poorer flow… I posted a case discussion which illustrates this.
Confirmation that therapeutic interventions are hemodynamically appropriate – I feel this is really important. When a patient’s life is literally on the line, and knowing that our interventions are seldom without potential nefarious side effects, it is poor medicine to be introducing a therapy without having some form of monitoring – preferably multiple – that we are headed in the right direction, or at least not making things worse. Of course, we already do this – with BP, sat, lactate, CCO, ultrasound, ETCO2 – but I think using a realtime measure of tissue saturation adds to this. It is also my firm opinion that integrated, multimodality monitoring is necessary – at least until someone develops some form of mitochondrial monitoring which tells us that the cytoenergetics are sufficient to survive. Until then we are stuck with surrogate markers and many of them (e.g. lactate) are the result of complex processes that preclude them being a simple indicator of perfusion adequacy. For instance, when giving a fluid bolus/infusion – after having determined that the patient is likely fluid responsive AND tolerant – one should expect to see an increase in ETCO2 (other parameters being constant), an increase in CO, an increase in NIRS values. The absence of such response should make one reconsider the intervention, because without benefit, we are left only with side effects.
Here is a patient’s cerebral (top) and and somatic (thigh – bottom) and CO values. This patient had an RV infarct and was in shock.
Following initiation of dobutamine, this is what occurred:
Given that we cannot always predict the response to an inotrope – depending on the amount of recruitable myocardium, it is reassuring to see an improving trend. This enabled us to decrease the vasopressor dose significantly.
Note that, so far, and unless some good evidence comes out, I don’t use a goal value, and so far, I have not identified a value that is predictive of prognosis. However, downward trends usually bode very poorly. For instance, I had a severe chronic cardiomyopathy patient whose cerebral saturation was 15%!!! But more surprisingly, she was awake, alert and hemodynamically stable. Adaptation.
Part 2 and the stuff on cardiac arrest coming soon!
Please, anyone using NIRS in shock, share your experience!
So I posted about this a few weeks ago, and the discussion it brought up with Jon-Emile (www.heart-lung.org) turned out to be way better than the original post, and I just wanted to make sure everyone interested got to see it, so here we go (part 1 is here, for those who didn’t come across it:http://wp.me/p1avUV-bJ):
Jon-Emile: This is a great topic for review Philippe!
I have come across this problem, certainly on more than one occasion. I was first introduced to the idea of renal venous pressure and renal hemodynamics as a house-officer at Bellevue Hospital in New York. Dr. Jerome Lowenstein published work on this phenomenon as it pertained to ‘Minimal Change Syndrome.” He used to ‘wedge’ the renal vein and measure renal interstitial pressure in these patients and measured the response to diuresis. It was very enlightening and made me feel more comfortable given more diuretics in such patients. [Am J Med. 1981 Feb;70(2):227-33. Renal failure in minimal change nephrotic syndrome].
I am also glad that you bring up the cranial vault in this discussion, because I have often wondered if the encapsulated kidneys behave in a similar way. That is, as renal interstitial volume increases from edema, if there is some point on their compliance curve [like the cranium] where there is a very marked increase in renal interstitial pressure? I have found a few articles which loosely address this idea, but would be interested if anyone else knew of some. In such a situation, there would be a ‘vascular waterfall’ effect within the kidneys whereby the interstitial pressure supersedes the renal venous pressure [like West Zone II in the lungs]; then, renal blood flow would be driven by a gradient between MAP and renal interstitial pressure [not renal venous pressure]. I know of one paper that addresses this physiology in dogs, and finds the vascular ‘choke point’ to be in the renal venous system and not Bowman’s space.
What’s even more interesting, is that when renal interstitial pressure is elevated is that the kidney behaves in a sodium avid state [i.e. urine electrolytes will appear ‘pre-renal’] and this physiology has been known for at least a century!
Lancet. 1988 May 7;1(8593):1033-5. Raised venous pressure: a direct cause of renal sodium retention in oedema?
There is no good explanation as to why this occurs, but one I read is that the high renal interstitial pressure tends to collapse the afferent arteriole and the decrease in afferent arteriole trans-mural pressure which facilitates renin secretion [just like low blood pressure would]; but that would require a fairly high renal interstitial pressure unless the MAP was concomitantly low.
Again, what I must caution [and I’ve been personally wrong about this] is the reflex to give diuretics when seeing a ‘plump IVC’. When I was treating a woman with mild collagen-vascular-related pulmonary arterial hypertension, community-acquired pneumonia with a parapneumonic effusion and new acute renal failure, I assessed her IVC with ultrasound. It was plump an unvarying. I lobbied the nephrologist to try diruesis based on the aforementioned reasoning, but was very wrong. Her kidneys took a hit with lasix. What got her kidneys better was rehydration. In the end, what happened was her mild PAH raised her venous pressure and the hypoxemic vaso-constrction from her new pnuemonia only made that worse. Her right heart pressures, venous pressure and probably renal venous pressure were undoubtedly high. But I didn’t take into consideration her whole picture. She had a bad infection, had large insensible losses and had not been eating and drinking. She was hypovolemic, no doubt, despite her high right heart pressures. Fortunately, her pneumonia resolved and fluids brought her kidneys back to baseline.
Thanks again for another thought-provoking topic
Me: Great points as usual Jon, and your last one brings up a bit of a concern I have always had. To play devil’s advocate, one could argue that it may have been resolution of the pneumonia and its metabolic sequelae and possibly other treatment that resulted in improvement of her renal failure, rather than the fluid, no? Did her hypoxia resolution decrease PAP back to normal – with IVC dynamics restoring – and relief of renal congestion, and improvement “despite” fluid?
To me, fluid administration must – at least transiently – increase CO to have any effect on the perfusion side. To do so, my understanding is that it has to go from right to left. Because of the pericardium and interdependence, if RAP exceeds LVEDP, we will start to impair LV preload, which sets up the vicious cycle of a shrinking LV and growing RV. If we can’s increase our RT heart output, obviously our LV CO headed to the kidneys can’t increase either. Hence the assumption would have to be that somehow this additional fluid can – by increasing RV preload (without increasing RV size and further impinging LV?) – help overcome elevated PAP and increase right to left flow. To me, hard to believe without a pericardiectomy (on a short time frame, naturally). Hence I struggle with understanding how a really plump IVC with little variation (if significant pleural pressure variation is occurring) can really still need fluid.
I’d really, really like to get your comments on this. I’ve had a number of conversations about this with people – some of them pretty bright – but none satisfying. Am hoping you can point out my flawed thinking.
Jon-Emile: Philippe, you ask very good questions. Your first point is quite valid. I think we have a bias of assigning meaning to a particular intervention because we think that particular intervention will work. For the patient I treated, we administered multiple drugs [oxygen, antibiotics, bronchodilators, we may have even given a dose of steroids] and yet I assign meaning to the fluids given. I think in all patients with complex hemodynamics that there are multiple co-varying interventions that all [hopefully] push the patient in the right direction – making it quite hard to grant significance to one in particular. Yet in the patient I treated, the timing with respect to creatinine change and urine output made it very hard to argue in favor of diuresis. We were checking her creatinine fairly regularly as she was in step-down and we were concerned about the trajectory of her illness. With lasix, her creatinine jumped abruptly on the following chemistry while with fluids, creatinine dropped and her urine output really picked up.
Which brings me to Ulrich’s point. It is well-taken and I hope to have a pulmccm post on this shortly. While the CVP does not have any correlation with volume status or volume responsiveness as you point out, the physiology of the CVP can help explain confusing echocardiographic findings.
All a plump, unvarying IVC with spontaneous inspiration means [if you believe the Guyton, or Magder approach] is that the IVC transmural pressure is remaining on the flat portion of its compliance curve during inspiration.
In other words, the IVC is at such high volume [on the flat portion] that lowering its transmural pressure [lowering the CVP, raising the intra-abdominal pressure or both] does not cause it to shrink in volume.
The question then becomes why is the IVC in this state? And a great analysis to this question is to consider the determinants of great vein volume [which really is a question of great vein/right atrial pressure or the CVP – which is related to volume by compliance].
There are two primary processes which will raise great vein volume and these flow from the Guyton Diagram 1. excessive venous return 2. poor cardiac function or a combination thereof [its really just inflow versus outflow]. Volume status plays one part of venous return, so certainly, if someone is hugely fluid overloaded, their venous return will be enhanced and this will favour a high great vein volume and high great vein pressure, BUT this will be mediated by cardiac function because if the heart can eject the large venous return it is receiving, then the great vein pressure and volume won’t change or may be low. Conversely, if cardiac function is poor, a patient could have a low venous return [e.g. be hypovolemic or euvolemic] and still have a high great vein volume and pressure – simply, because the heart can’t expel from the thorax what little venous return it receives. Importantly, poor cardiac function can mean almost anything [valve dysfunction, tachycardia with arrhythmia, high afterload, poor contractility, etc.].
To me, the above is the true value of thinking about Guyton and the CVP, so when I approach a patient, I try to think about what their venous return curve looks like [by a clinical exam] and I use a TTE to actually see what their heart function looks like [and to me this is the true power of ICU TTE]. The above also explains why CVP simply cannot be a marker of volume status.
In the patient I was treating, her history and physical really suggested poor venous return [she was clearly with a pneumonia, hadn’t been eating and was euvolemic to dry on examination] yet her great vein volume was high on TTE which meant that her cardiac function was most likely poor [on the Guyton Diagram her low venous return curve would be intersecting a very low, flattened cardiac function curve such that shifts with intra-thoracic pressure would not change right heart pressure at all].
But why was her heart function poor? Why could her right heart not eject what little inflow it was receiving? It was probably a combination of things. The pneumonia probably increased right heart afterload which caused some TR, she was tachycardic so wasn’t getting optimal filling time, she was septic with perhaps some underlying cardiomyopathy, perhaps her diastolic blood pressure was lower than normal [she was an elderly lady with likely stiff arteries] and she wasn’t perfusing her right coronary artery well and was suffering from relative ishcemia] it’s certainly is a lot of hand-waving, but all taken together perhaps plausible.
The antibiotics improved her lung function as did the bronchodilators which lowered pulmonary vascular resistance which improved right heart forward flow, maybe the inhaled beta-agonists increased her contractility, maybe the oxygen also lowered her pulmonary vascular resistance, maybe the steroids sensitized her to catechols and this raised her blood pressure and coronary perfusion pressure which improved her right heart function, but also maybe the fluids? Empirically, and in retrospect, venodilating her with lasix probably really lowered her venous return and this crashed what little cardiac reserve she had. It was improving her venous return with fluids that helped.
Sorry if this post is getting too long …
In terms of ventricular interdependence [an excellent, under-appreciated point in the ICU] I think that you have to be very careful extrapolating whether or not this effect is present from an IVC examination. In a classic paper [that caused much consternation at the time] Pinsky found that right atrial pressure was completely uncoupled from right ventricular end-diastolic volume [why the CVP is a poor indicator of volume responsiveness]. Her is a recent review of that paper by Pinsky himself.
The take home is that while right atrial volume and pressure [and by corollary great vein volume and pressure] can be high, this may not translate to a right ventricle near its elastic limit. Pinsky offers no good explanation as to why this is, but postulates that it may have to do with the complex RV geometry and how this changes during diastole. So until there is a widely accepted means of assessing RV filling with TTE [like an Ea ratio] which could pick up a restricted filling pattern, this is really hard to call on echo. As you are aware, you could look for a flattened septum or D sign during diastole, but I’m not sure how well that sign predicts a patient’s response to a fluid challenge – it certainly screams caution.
This Pinsky paper also highlights a potential disconnect between the physiology proximal to the tricuspid valve and the physiology below it which is also part of my general reluctance to use IVC volume change as a marker of fluid responsiveness, just as I have total reluctance to use CVP [or its change with respiration] as a marker of fluid responsiveness.
Unfortunately, a lot of the time it comes down to ‘guess and check’ – give fluids or give lasix and see what happens. This is why I firmly believe that determining volume status and volume responsiveness are the hands-down hardest party of ICU medicine.
If you’re still reading, I hope this helps.
One more point. I don’t think I gave a full explanation to one of your questions. Please bear with me as this is exceptionally hard to explain with words [indeed why I made heart-lung.org].
The venous return and cardiac function curves are essentially inverse of each other [that is lowering right atrial pressure increases venous inflow but decreases cardiac outflow] so they approximate the letter X [venous return is the \ and cardiac function is the / & the point at which the two lines intersect make up the CVP and defines cardiac output].
If you consider the patient I described, If we assume her venous return is low [because she is venodilated from sepsis and hypovolemic from low PO] then the venous return curve [\] is shifted leftwards. If we assume her cardiac function is poor the cardiac function curve slope [/] is shifted down and to the right.
When she takes a breath in, the lowering of intrathoracic pressure pulls the cardiac function curve leftwards [lowers its pressure relative to venous return] while the increase in in abdominal pressure with diaphragm decent tends to temporarily increase venous return by decreasing abdominal venous capacitance. This effect shifts the venous return curve in a rightward manner.
If the patient’s venous return curve initially intersects the ascending portion of the cardiac function curve [i.e. she is truly volume responsive] BUT, the intersection is very near the plateau of the cardiac function curve [i.e. the portion of the cardiac function curve that will render the patient non-volume responsive and also favour unvarying respiratory change in right atrial pressure/volume with inspiration], THEN with inspiration it is possible to see the intersection of the two curves on the flat portion of the cardiac function curve [as the cardiac function curve is pulled leftwards and the venous return curve is pushed rightwards], even though she does have some cardiac preload reserve. This would be an example of impaired specificity of IVC volume change with spontaneous inspiratory effort as a predictor of volume unresponsiveness [i.e. a false positive for a plump IVC predicting the lack of fluid responsiveness].
I address this physiology in chapter 6 parts C and D and chapter 8 part F.
Me: Very, very interesting. I think this discussion, as many, show how medicine is not a “hard science” but remains a “pseudo-science”, inherent to the fact that we are blending physics, chemistry, biology and cannot really apply simple principles of flow and pressures when dealing with elastic, muscular systems lined with microscopic coating whose compliance and resistance change from moment to moment and thru effect of neural and hormonal influence. There are simply too many unmeasurable variables to come up with single guidelines and rules.
I think, as you say, that there remains a need for some degree of trial and error, that we are hopefully narrowing with the appropriate application of technology and proper data integration.
I’ll percolate all this and see how I can tweak my mental model!
So, as most of you had figured out, the fever and white count turned out to be fairly insignificant. I started diuretics on him and stopped IV fluids (in truth, he spent a few hours still receiving IV NS at 100cc/hr as it sadly slipped by me – I know… NS to add insult to injury). I also stopped antibiotics to the alarm of some, but keep in mind we have a lot of c.difficile in our institution, and I did not believe the had CHF AND a significant pneumonia (that would go against Occam’s razor…). He was not septic, and another discrepancy that led me away from the diagnosis of pneumonia is that a patient with significant bilateral infiltrates due to pneumonia is sick: toxic, dyspneic, fulfills Scott’s LLS score of 1 (Looks Like Shit – range 0 to 1).
Within a few hours and perhaps a negative balance of a liter or so, he feels much better. Here is his IVC at that point:
36 hours later, his CXR is clear and he is off O2.
Angiogram turns out normal – as anticipated – EKG only ever had some vague non-specific ST abnormalities. He likely had a viral cardiomyopathy – some ancillary tests still pending (HIV, etc), but is to be discharged soon.
For those who voted pneumonia, certainly initially it could not be ruled out, only the clinical evolution made it highly unlikely as a significant player.
For those who felt this represented pulmonary embolism, remember that the primary hemodynamic mechanism will be right heart failure, hence the RV would most likely be as large, and potentially larger depending on the severity of the embolism. Again, this cannot be ruled out by bedside ultrasound, it can only be ruled out as a main cause of respiratory failure. Also note that the chest xray is generally normal, or may show the peripheral wedge shaped infarct (Hampton’s hump). Bilateral infiltrates would not be the rule. But it’s always a good thing to keep it in mind!
I think this case illustrates well the limitations of physical examination, and although more commonly, pneumonias (especially in the elderly) get digressed because they “had crackles,” sometimes, patients we might not expect may have CHF.
From the moment one notes a large, plethoric IVC, one should anticipate downstream pathology of some kind (overzealous iatrogenic fluid overload being the exception), whether tamponade, pulmonary embolism, LV failure, pulmonary hypertension, but something.
Hence, in this case, bedside ultrasound proved invaluable. After all, he was recieving less-than-optimal therapy for CHF: fluids and antibiotics… This may be a case that would have proceeded to “ARDS”, and although I don’t doubt that at some point along the line, an echo would have been done, the delay may have had consequences. In our center, no one gets into the ICU without at the very least a cardiopulmonary bedside ultrasound. It is done routinely, not only for specific indications – the real indication is having a patient in front of you.
Please don’t forget, if this is up your alley, don’t miss CCUS 2015: Way Beyond EGDT and ACLS!!! #CCUS2015
Jon Emile says:
Great case, great windows and images. I agree with your management totally. I do recall once, however, having a patient admitted for heart failure following a bedside TTE performed by a great resident, unfortunately [and in retrospect] the patient likely had a septic cardiomyopathy. The patient felt great with diuresis, but then his BP crashed as the sepsis took hold.
Recall the classic paper by Parrillo NEJM 1993 who looked at the left ventricle during the acute phase of septic shock and found LVEDV to LVESV values of 225 ml to 150 mL. The EF was in the low 30s. During the recovery phase, LVEDV to LVESV was 150 to 75 mL and EF of 50%. He noted that dilation of the left ventricle seemed to confer a mortality benefit, & that this may be a compensatory response to maintain stroke volume. This may be more striking in young patients as yours. When I first read your case a mycoplasma peri-myocarditis came to mind [I treated a case of this as a resident in the Manhattan VA]. The classic finding in this disease being bullous myringitis.
Thanks for the awesome echo videos!
Great point Jon! Septic cardiomyopathy – which is very common – is definitely something to keep in mind. Indeed the LV dilation noted by Parillo would be a sensical adaptation to limited contractility. I remember seeing a particularly impressive case in a young woman with significant dilation and an EF in the 15-20% range, with incredibly rapid recovery to the 40’s and 50’s by a day later. I’ve yet to see septic cardiomyopathy happen, however, in a patient who isn’t that sick, i.e. no pressors, no acidosis, etc…
Great point about mycoplasma, which was brought up by our ID consultant at first, but who also agreed he wasn’t that sick and agreed to stop once noting the CXR had cleared with diuresis.