ECMO for Cardiac Arrest: a big CHEER! #FOAMed, #FOAMcc

So a couple of years ago after hearing Scott’s interview of Joe Bellezzo and Zack Shinar (http://emcrit.org/podcasts/ecmo/) I figured this was the future, and promptly got a hold of these guys and got them to present at CCUS 2013 (link to Zack’s lecture below), where their lectures were mind-blowing and instantly made any resuscitationist green with envy, me included.

So just last month, two articles came out in Resuscitation which are highly pertinent and add a lot of legitimacy to the concept of ECMO for CA, one being the CHEER study by Bernard et al (CHEER Study) and the other, a very interesting canadian retrospective observational study by Bednarczyk et al (ecmo arrest canadian).

 

CHEER!!!

First, the CHEER study. Very well done, designed to combine ECMO, mechanical CPR and hypothermia, N=26, so not massive, but given the magnitude of the treatment effect, IMHO highly significant. Very good criteria (18-65, VF) so basically working with patients having a reasonable prognosis (aside from the cardiac arrest…), and their starting point was after 30 minutes of unsuccessful ACLS.

Now, for experienced clinicians out there, it is fairly obvious that at around 30 minutes, we start to get a little discouraged. Maybe not ready to throw in the towel, but we know things are looking dim. And most of those who do get a late ROSC don’t tend to do very well on the long term…

So it takes the CHEER team about 56 minutes to ECMO runtime.  Now, by 56 minutes of no-ROSC, most arrests would have been called. I think that is a key point to underline – the study essentially begins here, at a point where prognosis is no longer that 8-26% “quoted” survival, but pretty close to 0%.

So what happens? 54% of these patients survive to hospital discharge with good neurological recovery. Lets put this in perspective again. They bring back half the people we probably would have given up on…and discharge them home!!!  That’s crazy impressive.

This pretty much correlates with the experience of Zack and Joe (www.edecmo.com), who recently told me the story of a 20 year old diabetic with a K of 9.0 and an arrest of over 45 minutes. Discharge home a week or so later. Completely fine. Back on facebook and skyping with Zack & Joe.

That’s a humbling thing, because in my ED, my ICU, my hands, she’s a goner. 

 

The Canadian Perspective

Ok, so the Bernardczyk article is also really interesting, because it shows that this can be accomplished in a community hospital, and not necessarily only a tertiary care center, and their numbers (albeit retrospectively) are in the same ballpark.

And here is an awesome point of view from their discussion which I completely agree with and ascribe to:

“This (…) challenges our understanding of cardiac arrest as a terminal manifestation of a dis-ease process with treatment options fraught with futility. Rather, for selected patients, cardiac arrest may be better considered anexacerbating symptom of underlying disease with a therapeutic window to effectively restore perfusing circulation while providing definitive therapy.”

 

Thoughts…

So one concern is with bringing back severely neurologically disabled patients. I think the CHEER, the canadian and the japanese data all pretty much refute this. ECMO, particularly paired with hypothermia (probably TTM style now), seems to have remarkable neuroprotective effects, despite prolonged low-flow states. I think we all rarely see patients with 40-50 minute range arrests showing CPC scores of 1…

So why might this occur?  Does the sudden flow reverse some of the vasoconstriction caused by the epinephrine?  I know from discussing with Joe that if they are thinking that the patient is going to ECMO, they will avoid epinephrine. Recent years have clearly shown that the improved ROSC of epinephrine comes at a cost of greater neurological damage, hence equivocal final result of intact neurological survival.

 

Bottom line?

If you’re a resuscitationist, get on board.  Its expensive, but no more than a bunch of other (sometimes dubious or dogmatic) things we do – and the data is there. I’ve been working on my (community) hospital and will not quit until we have it.

What do you need? A cooperating ER chief / ICU chief, and either a cath lab and a vascular surgeon in your institution or in a collaborating neighbourhood one.

…and some cojones.

 

Absolutely love to hear your thoughts, particularly from anyone with ECMO experience!

…this, of course, and more, at CCUS 2015!   http://ccusinstitute.org/Symposium7.html

 

cheers! (pun intended)

Philippe

 

…and here is Zack at CCUS 2013:

http://www.ccusinstitute.org/Video.asp?sVideo=Resuscitation%20Zach

 

Venous Hypertension: The Under-Appreciated Enemy…A Tale of Nephrologists, Neurosurgeons and Andre Denault…and a podcast. #FOAMed, #FOAMcc

So, some of you may have seen one of my earlier posts about the myth of low-flow renal failure in CHF (http://wp.me/p1avUV-2J), and be aware of my growing conviction that elevated venous pressures – too often sought after – are actually fairly nefarious.

So a couple of recent and very interesting pieces to add to the puzzle. First, I listened to an awesome podcast about

ICP by Wilson (http://intensivecarenetwork.com/wilson-monro-kellie-2-0/) which is an absolute MUST LISTEN to anyone in acute care.  One of those moments where all of a sudden someone shines a light in a dark corner you’d never really paid much attention to. Really, really cool and game-changing, at least certainly in the physiology model I play with in my head every time I deal with a patient who is genuinely sick.  In a nutshell, just to make sure everyone actually goes to listen to it, Wilson explains how you can get venous hypertension simply from increased cerebral blood flow… And we happen to be faced with one of the most common causes of increased CBF almost every day: hypoxia.  So when you are dealing with neurological injury (CVA/SAH/post-arrest), the danger of hypoxia (remember the concept of avoiding secondary injury of hypoxia, hypotension and hyperthermia?) lies not only in the obvious cellular lack of oxygen, but also that it is the most potent stimulus for increased CBF, and the main issue being that our venous system is simply not designed to accommodate that kind of traffic, resulting in venous hypertension without (yet) truly elevated ICP.

I’m also faced with the recurrent problem of having to be somewhat “rude” when not following suggestions from nephrology consultants in some of  my ICU patients, when they advise fluids or holding diuretics in patients with renal failure AND elevated venous pressures (as assessed by a large, non-varying IVC – in the absence of reversible causes such as tamponade, tension pneumo, etc…).  It isn’t their fault. They aren’t looking at the venous system (not bedside sonographers yet – “looks dry” on exam/gestalt is as much as you’ll get), and they don’t hold venous hypertension in high (or any) regard (yet, hopefully).

So I was totally psyched when, during a really cool conference (#BMBTL) organized by @EGLS_JFandMax, my highly esteemed colleague and friend Andre Denault (not yet on twitter…working on him) gave a talk – here is a segment:

And here is the article he is referring to:

Fluid+balance+and+acute+kidney+injury

So it isn’t like this is unknown, it simply isn’t at the forefront of our clinical mind-set, for the most part. Congestive renal failure and congestive cerebral failure are simply not things we routinely diagnose, though they MUST be just as as prevalent as congestive heart failure, which we all clearly believe in…

So just another angle to keep in mind, both when resuscitating and when managing patients with organ dysfunction of almost any sort…

 

Love to hear your thoughts!

…and if you like this kind of stuff, if you are an acute care doc, you’ll want to come to CCUS2015! http://wp.me/p1avUV-bG

Philippe

 

Jon-Emile Kenny (of the awesome heart-lung.org fame) says:

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

 

dr.uthaler says:

hi, i am an anaesthesist / intensivist from austria. very interesting topic. at the esicm meeting last month in barcelona there was a very good session about hemodynamic monitoring focusing on the right heart and the venous system. the lectures about the guyton approach to fluid management were a big eye opener and certainly changed my approach to patients in the real life icu world. what i always do now is to correlate the cvp with the morphology of the right heart. lets say i have a cvp of 5 with a large right ventricle then i don’t hesitate to give diuretics. i really can’t understand how recent guidelines (surviving sepsis campaign) can still state a cvp of 10-12 as a target value ! new german s3 guidelines on fluid management at least advise not to use cvp for hemodynamic monitoring. guess who was against it? the german sepsis society, probably because they didn’t like to upset their friends from the surviving sepsis campaign group 🙂 let me send you a link to a very good article: Understanding venous return: Intensive Care Med. 2014 Oct;40(10):1564-6. doi: 10.1007/s00134-014-3379-4. Epub 2014 Jun 26. i went through some of the cited articles – awesome information! thanks for the interesting discussion and keep on posting !

Sounds like a good session!  I cannot understand why CVP remains in guidelines when there is clear, irrefutable evidence that it does not work to estimate either volume status or responsiveness.   As you say, other, more physiological information renders CVP irrelevant.  I have not used CVP in years. Thanks for the reference, will make sure to check it out!

thanks for reading!

Philippe

Pericardiocentesis for tamponade w/bedside ultrasound: Procedure Video. #FOAMed, #FOAMcc, #FOAMus

So this case was interesting on a couple of levels.

A 76 year old woman presented to the ER with a complaint of abdominal discomfort and was admitted with a diagnosis of pneumonia and lower abdominal cellulitis. She had a history of diabetes, obesity and remote oral cancer which had been treated 6 yrs ago.  The next morning, while still in the ER awaiting a ward bed, she had a hypotensive episode, and fortunately the ER doc on shift grabbed an ultrasound probe and took a look, calling me a few minutes later with a diagnosis of tamponade. She was absolutely correct. I saw and echo’d her shortly after:

The first two clips show the IVC, which is distended with minimal variation. This should prompt the bedside sonographer to anticipate downstream pathology (except for iatrogenic volume overload and renal failure…).

The subsequent clips show subxiphoid views (and one clip of the associated left pleural effusion) showing a significant pericardial effusion and difficult to distinguish cardiac chambers.

Clinically, she was dyspneic, uncomfortable, HR 115, BP 130’s systolic (in ER in 80’s then got some fluid). Her heart sounds were not particularly quiet, and her JVP was difficult to assess due to obesity.

Here is the drainage video:

Her abdominal pain resolved very rapidly, her breathing improved and vitals stabilized.

Pathology is still pending, but bloody effusions commonly include malignancy, tuberculosis, but also simple viral paricarditis.

So I think this is a great case for the argument of integrating ultrasound into physical examination rather than as an ancillary test.  Because she didn’t present with a predominant hypotensive or respiratory component, the diagnosis wasn’t seriously entertaine, and obesity, body habitus and pleural effusion undoubtedly made physicians overlook the cardiomegaly. However, in my opinion and that of most bedside sonographers, abdominal pain warrants an abdominal us exam, and the distended IVC would have prompted at least a quick cardiac assessment, and the effusion would have been noted immediately.

In my CC/IM practice, hardly anyone escapes the probe, as cardiopulmonary and abdominal status is hardly ever irrelevant to me…

cheers!

 

Philippe

Bedside Ultrasound in Cardiac Arrest: A Quick Overview, ISURA 2014. #FOAMed, #FOAMcc, #FOAMus

Here’s a quick lecture I gave at Vincent Chan’s ISURA 2014 in Toronto.  It was a great event attracting anasthetists from all over the world, and it was an honor to work with Massimiliano Meineiri, Alberto Goffi, Adriaan Van Rensburg, Colin Royse and many more.

Unfortunately it was my first time using Prezi, which is pretty cool but doesnèt allow you to loop your videos, which really, really sucks!  So unfortunately the clips are very short…

Love to hear any comments!

Philippe

What’s this sign? Bedside Ultrasound Picture Quiz! #FOAMed, #FOAMcc, #FOAMus

Here is a one of the “classic” and physiologically important echocardiographic signs:

 

Screen Shot 2014-05-18 at 11.34.10 PM

 

What do you see in this parasternal short axis view, and what are the physiological implications?

Scroll below for the answer!

 

 

 

 

 

 

 

 

 

 

This is the “D” sign, aptly named for the D-shape taken by the LV (normally circular) when RV overload occurs and there is paradoxical septal motion and flattening, as early diastolic RV pressure exceeds early diastolic LV pressure.  This is NOT a good thing and points to a very strained hemodynamic pattern.

Note the RV is huge in this cut, bigger than the LV (remember that in all views, the RV should be about 60% of the LV size – this is simply due to the semi-lunar shape the RV takes as it “wraps” around the LV – they both have the same stroke volume). Also note the small posterior pericardial effusion.

So what is the diagnosis here?  Well there isn’t enough information to say with just this image.  This happens to be a case of worsening ARDS, but all you can tell is that there is acute right ventricular failure due to pressure overload, so that the diagnosis includes (a) PE, (b) acute pulmonary hypertension due to some kind of pulmonary disease – ARDS, pneumonia, etc…  Obviously, in the absence of significant parenchymal abnormalities on CXR or B lines/effusions/consolidations on lung ultrasound, PE should be strongly considered.

 

Happy scanning!

 

Philippe

Here is an excellent review on RV dysfunction and focused bedside ultrasound assessment:

RV bedside echo

or its link:

Click to access 38TOCCMJ.pdf

The Effort-Variation Index – a conceptual tool for IVC ultrasound. #FOAMed, #FOAMcc, #FOAMus

I recently had a colleague ask me to put on a graph the way I like to assess the IVC, at least conceptually.  I posted about this a few weeks ago (http://wp.me/p1avUV-8E), so I tried to come up with something useful for clinicians, correlating IVC variation with respiratory effort.

A useful concept to visualize this is the Effort-Variation Index (EVI). To obtain this, start by looking at a Frank-Starling curve, and broadly categorizing patients as being on the “empty” side, the “normal” or the “full” side.

Frank-Starling:Physiological

 

Next, if you look at how these groups would plot on a graph correlating IVC variation to respiratory effort, which, physiologically, would be the change in pleural pressure (delta Ppl), you should conceptually see something like this:

 

EVI

 

Note that this has not been validated, nor does it contain any values. It is simply, for now, a useful mental construct to understand the physiology behind the variability, and is useful when elaborating each patient’s physiological profile in the mind of the bedside clinician. Along any horizontal line, the IVC variation would be the same. You can therefore see that, given enough respiratory effort, a “full” patient could appear “normal” or even “empty.” Hence interpreting IVC variation without understanding this would lead to potential error.

 

Love to hear some thoughts and comments!

 

Philippe

Another wicked ultrasound case! Can you see the culprit? Another reason to do bedside ultrasound… #FOAMed, #FOAMcc, #FOAMus

Reviewing some TEE cases with Max Meineiri of TGH yesterday (Max is an anaesthetist-intensivist-sonographer extraordinaire who has been kind enough to help me brush up my TEE skills recently), here is one that stood out for two reasons. Here is the story: An 84 year old woman is sent from a peripheral hospital to the cath lab for chest pain.  She arrests on the table after they found normal coronaries and the code blue is called. Max arrives on the scene, and due to CPR making TTE difficult (and also because Max walks around with a TEE probe in a hip holster by Dolce & Gabbana), in goes the TEE probe and right away they note a massively dilated and hypokinetic RV, and a small and under filled LV. Yup, sure looks like a PE in these circumstances. Not being satisfied with a presumptive diagnosis, Max gets to a short axis view of the aortic valve and pulls out the probe slightly, following the bifurcation of the main PA.  On the screen, the right PA is on the upper left field, and the left PA disappears towards the upper right (the left main stem bronchus makes it difficult to visualize).

Anything seem a little odd?   Yup, you can see the occlusive culprit a couple of centimetres into the right PA, moving with each beat.  Being in angio already, they threaded a PA cath and administered thrombolysis, but despite some visual fragmentation, she did not survive. So why is this case interesting? 1. the image is pretty cool. 2. More importantly, it highlights the importance of bedside ultrasound.  If a rapid, focused cardiac exam had been done at her presentation at the peripheral hospital, the first-line physicians most likely would have noted the severe RV dysfunction and questioned the diagnosis of coronary syndrome, possibly (hopefully) thrombolysing the patient, and very possibly averting the cardiac arrest. …I know, I know, we don’t have all the info, the ECGs, etc, and maybe this was really an ACS and she happened to have a DVT which embolized during transport, etc…do you buy that?  Ockham and his parsimonious razor don’t, and I would tend to side with them.   love to hear some thoughts!   Philippe

Bedside Ultrasound: Quite a Case! #FOAMed, #FOAMcc

So here is an awesome clip from an ICU colleague of mine, Lorraine Law.  She was managing a post arrest (elderly woman who collapsed at home and was resuscitated but remaining in profound shock) case using bedside ultrasound and came across this pathology:

video courtesy of Lorraine Law & Shirish Shantidatt

what do you think?

scroll below for my thoughts…

 

 

 

 

So the clip starts with a subxiphoid 4 chamber view that clearly shows a massively dilated RV with a hyperdynamic and underfilled LV.

[For the hemodynamic novices, remember that the ventricles are kind of like roommates who share a pericardium. Especially in acute scenarios, if one gets overloaded, the other will have to give way, until the pressure equilibrates. If the process is exceedingly slow, they can do some renovations and stretch the pericardium, but this takes likely weeks. In this case, the elevated PAP overloads the RV and the RVDP > LVDP, resulting in decreased diastolic filling, which in turn drops the stroke volume/cardiac output/MAP.]

We can see that the RV TAPSE (tricuspid valve excursion towards apex) is really minimal, supporting an acute or acute on chronic process.

The clip then shows a long axis view of the IVC with echogenic material, most likely thrombus, with a to and fro motion, going in and out of the RA. Wow. You don’t see this very often.  The only thing preventing further travel is actually the fact that the cardiac output is so low due to massive embolism so that the flow can in fact barely carry the clots forward anymore at this point, similar to the sluggish IVC clip I put up a few months ago (http://wp.me/p1avUV-5t).

The most likely diagnosis is pulmonary embolism, and thrombolysis is indicated. Unfortunately despite my colleague’s timely diagnosis, the clot burden was likely too much, and despite thrombolysis, the patient passed away of intractable shock.  One can imagine that the TPA actually has to make it to the lungs, and with such a degree of obstruction, it is likely that very little actually got to the pulmonary vasculature…

Unfortunate case, but quite impressive images.

A crazy thought, using hindsight and with the luxury of knowing the fatal prognosis: intracardiac (RV) TPA bolus? Small spinal needle?  Anyone bold enough? Food for thought if (when) I see one like this…

 

cheers!

 

Comments:

Marco says:

Really quite impressive images. A couple of weeks ago I admitted a pretty young patient after a successful resuscitation due to massive pulmonary embolism. Immediately after ROSC in emergency department, he was transported to the cath-lab where TPA bolus was administered directly through a PA cathether. In ICU we continued the infusion. In less than 24 hours we obtained a relative hemodynamic stability and discontinued all the vasopressors, but the case remains unfortunate because despite therapeutic hypothermia the post-anoxic damage was so severe that led to cerebral death declaration two days later.

 

Thanks Marco, very interesting.  There is a recent study on catheter directed thrombolysis in PE reviewed at PulmCCM:(http://pulmccm.org/main/2014/randomized-controlled-trials/catheter-directed-thrombolysis-submassive-pe-better-heparin-rct/)

A physiological point about PE resuscitation is the relative inefficiency of CPR, as both venous return and LV filling is severely limited, so systemic perfusion is even worse than the usually poor output during chest compressions…

Thanks for reading!

Marco replies:

Thanks, Philippe!
The point about the possible inefficiency of CPR is crucial in my opinion. The patient I brought as example had a witnessed cardiac arrest (he called EMS when in respiratory distress) and CPR without interruption from the beginning, nevertheless he resulted in brain death declaration.
I remember very clearly a 43-year-old woman that 3 years ago had a massive PE in the OR shortly after a long lumbar vertebral stabilization. We admitted her to ICU after more than 80 minutes of CPR, a bolus of rTPA and with severe hemodynamic instability. RV was extremely dilated. When she eventually regained stability I had little hope about her neurological recovery, but surprisingly she was extubated the following day and last year she returned to our 12-months post-ICU follow-up showing perfect recovery.
I think that systemic and cerebral perfusion during “obstructive” cardiac arrests such as massive PE is very difficult to asses with current technology. A couple of times I was tempted to check it with trans cranial doppler, but usually there’s too much confusion during CPR.
When I was a resident I witnessed to a iatrogenic cardiac arrest in a patient with advanced monitoring that led to an interesting publication: http://www.researchgate.net/publication/10832333_Cerebral_perfusion_pressure_and_cerebral_tissue_oxygen_tension_in_a_patient_during_cardiopulmonary_resuscitation

 

Wow, very interesting cases.  What fortune to have been able to record that data, as obviously getting that in during CPR would be almost impossible.  TCD, at least after ROSC, could be contributory… Another option is using NIRS, which I’ll be working with this summer.

thanks again!

Philippe

An Update on Pulmonary Embolism: NEJM’s PIETHO Study…what’s the verdict? #FOAMed, #FOAMcc

As has been discussed in a previous post (http://wp.me/p1avUV-7T), patients with sub-massive PE (hypoxic, tachycardic, some troponin rise, etc…but no hypotension) remain in a grey zone, which is, to me , a dubious situation at best – their mortality can be up to 15%, morbidity likely more.  Everyone agrees the low-risk patients don’t need thrombolysis, and everyone pretty much agrees that the patient in shock needs it.  There is data out there suggesting that some patients clearly benefit from thrombolysis despite not being in shock, in good part relating to avoiding chronic pulmonary hypertension and its consequences.

The issue for many clinicians is that they have a “stable” patient in front of them, and they are considering giving them a drug that can potentially give them a bleed in the head and leave them dead or crippled. Many shy away from this. Part of this is cultural, because the same docs probably wouldn’t hesitate giving the drug to a lateral or posterior MI, which is not likely to kill you, or even leave you a cardiac cripple (just to be clear, I’m not advocating against thrombolysis in these cases, just trying to find a parallel), but since the AHA guidelines say to do it and everyone else does it, there’s no trepidation. It is the standard of care.  For most of us acute care clinicians who do not do outpatient medicine, if the patient survives and gets discharged home, chalk one up in the win column. But, as has become clear in recent years with the post-critical illness syndromes, morbidity can be just as important as mortality, especially in the younger patients. Kline et al (Chest, 2009) showed how almost 50% of “submassive PE” patients treated with anticoagulation alone had dyspnea or exercise intolerance at 6 months. They only had a 15% improvement in their pulmonary artery pressures (mean 45 mmhg).

What are the real risks? Pooling the data together gives a value around 2% with a spread between 0.8% and 8%, more or less. This represents each patient’s inherent risk of bleeding, as well as some of the inconsistencies with post-thrombolysis anticoagulation (safest to aim for 1.5-2 x PTT baseline in the first 48h).

The MOPETT trial which, as a #FOAMite you have certainly come across, showed that a half-dose of TPA was highly effective, and they felt it might be possible to go lower. The physiological beauty in that is that, unlike other sites we thrombolyse with full dose TPA, the lungs get 100% of the TPA (coronary artery gets maybe 5%, brain gets 15%).  Mind you, of course, the culprit clot/artery obviously doesn’t get 100%, but much, much more (if we figure that you need about 50% vascular area occlusion to cause RV dysfunction) TPA per “clot” than other pathologies. One can argue that anatomically, there is a greater clot burden than coronary or arterial thrombolysis, which may offset this somewhat. However, the date was quite clear in this trial that the therapy was effective, and the bleeding was none.

Ok, so let’s get to the PIETHO. 1000 patients, TPA+heparin vs heparin alone in normotensive but intermediate risk patients. So, first question is how was that risk defined?  Patients needed to have echocardiographic/CT signs of RV dysfunction AND a positive troponin. Interestingly enough, onset of symptoms was up to 15 days before randomization…not exactly early treatment, and unfortunately there is no information about the actual time to thrombolysis or subgrouping.  The results were as one could imagine. The combined endpoint of death or hemodynamic decompensation was 2.6% in the thrombolytic group vs 5.6% in the anticoagulation.  I’m not a fan of combined endpoints. Hemorrhagic stroke was 2.0% vs 0.2%. Their conclusion? Exercise caution. Hmmm…not much of a step forward. Basically tells us what we know. It helps the hemodynamics, but you can bleed. They do re-affirm that bleeding is more likely in the over-75.

 

What do we REALLY need to figure out? 

1. echographic risk stratification – at least into moderate and severe RV dysfunction.

2. longer term outcomes (hopefully PIETHO has a follow-up study in the pipeline, since they had good numbers).

3. a point-of-care study – time is of the essence, and may have an impact on dosage. IMHO thrombolysis should be done within a few hours of presentation at most.

4. further dosage data – 1/2? 1/3? 1/4? small boluses q1h until RV function improves?

I wish I could do it, but community hospitals don’t have the ideal setup, nor do I have a research team that can handle something of this scale. But surely someone can!

 

Bottom line?

It won’t change my practice. I will continue to offer thrombolysis in select cases, especially the younger patients, who obviously have a lower risk of bleeding, and stand to benefit the most, as pulmonary hypertension  can be crippling. I know I’d take the risk of bleeding when I see 50% dyspnea/exercise intolerance two years down the road…

Finally, bedside ultrasound to anyone with dyspnea/hypoxia should be a standard of care for every acute care physician. No ifs, ands or buts, no exception. Waiting for a CT angio or formal (read daytime hours) echocardiogram is, to me, unacceptable. If you, a friend or family member were in that ER bed, would you trust a physical examination and a CXR to rule out the need for an immediate intervention? I wouldn’t, not my own, and not even Dr. Bates’, Dr. DeGowin’s or Dr. Sapira’s, or all three combined.

cheers!

 

 

 

Kline JA, Steuerwald MT, Marchick MR, Hernandez-Nino J, Rose GA. Prospective evaluation of right ventricular function and functional status 6 months after acute submassive pulmonary embolism: frequency of persistent or subsequent elevation in estimated pulmonary artery pressure. Chest 2009;136:1202e1210.

Guy Meyer, M.D., Eric Vicaut, M.D., Thierry Danays, M.D., Giancarlo Agnelli, M.D., Cecilia Becattini, M.D., Jan Beyer-Westendorf, M.D., Erich Bluhmki, M.D., Ph.D., Helene Bouvaist, M.D., Benjamin Brenner, M.D., Francis Couturaud, M.D., Ph.D., Claudia Dellas, M.D., Klaus Empen, M.D., Ana Franca, M.D., Nazzareno Galiè, M.D., Annette Geibel, M.D., Samuel Z. Goldhaber, M.D., David Jimenez, M.D., Ph.D., Matija Kozak, M.D., Christian Kupatt, M.D., Nils Kucher, M.D., Irene M. Lang, M.D., Mareike Lankeit, M.D., Nicolas Meneveau, M.D., Ph.D., Gerard Pacouret, M.D., Massimiliano Palazzini, M.D., Antoniu Petris, M.D., Ph.D., Piotr Pruszczyk, M.D., Matteo Rugolotto, M.D., Aldo Salvi, M.D., Sebastian Schellong, M.D., Mustapha Sebbane, M.D., Bozena Sobkowicz, M.D., Branislav S. Stefanovic, M.D., Ph.D., Holger Thiele, M.D., Adam Torbicki, M.D., Franck Verschuren, M.D., Ph.D., and Stavros V. Konstantinides, M.D., for the PEITHO Investigators*, Fibrinolysis for Patients with Intermediate- Risk Pulmonary Embolism, N Engl J Med 2014;370:1402-11.

Mohsen Sharifi, MDa,b,*, Curt Bay, PhDb, Laura Skrocki, DOa, Farnoosh Rahimi, MDa, and Mahshid Mehdipour, DMDa,b, “MOPETT” Investigators, Moderate Pulmonary Embolism Treated With Thrombolysis (from the “MOPETT” Trial), Am J Cardiol 2012

The IVC Assessment by bedside ultrasound: Let’s apply some common sense! #FOAMed, #FOAMcc

So I have a huge issue the IVC and its ultrasound assessment. For the most part, neither the yay-sayers or the nay-sayers are applying much sound physical principles, as far as I’m concerned.

To assess a patient’s volume status, it may be practical to begin with the sub-xiphoid view of the IVC, since the decision to give fluids or not – especially in emergency situations – can then be taken within the first few seconds of examining the patient. The physiological rationale behind assessing the IVC as a marker for volume responsiveness is simple and solid. As the venous compartment fills, the size of the IVC will gradually increase until it reaches a maximal size of about 20-25mm or even 30mm, depending on physical size and chronicity.

Concomitantly, the phasic respiratory variation will decrease as the venous pressure increases and the effect of varying intrathoracic pressure is no longer felt. At this point, the flat part of the Starling curve of the right ventricle is approaching, and there is little response to volume, and little physiological rationale to support giving more.

Currently, many use a variation of about 20% or more to suggest a volume responsive state in ventilated patients or an inspiratory collapse “sniff test” of 50% or more in spontaneously breathing patients.

There remains controversy around using IVC assessment for volume responsiveness, and with good reason! There are a few important reasons why:

a. technique – First of all, there is the manner in which IVC measurement has been taught: the M-mode measurement of the antero-posterior (AP) diameter during breathing (usually of ventilated patients) about 3 cm below the diaphragm. Although highly practical and reproducible, it has many shortcomings. If we look at the physiology, what changes with cycles of respiration is the volume of blood entering the chest/right atrium. Hence the key variable we are trying to assess is the transient variation in IVC size – which is a volume, not a linear dimension (I’m getting painful flashbacks of using pressure  to determine volume!)Hence the use of a single linear measure on one point along the length of the IVC to assess this is inherently flawed. For instance, the figure to the left shows how, if this IVC were to be measured in its AP diameter, the variability may not be that great. In the short axis, however, one can clearly see the significant change in surface area, and hence volume between phases of mechanical ventilation. Also, the IVC is rarely perfectly circular, but often ovoid, and occasionally with the greatest diameter in an anteroposterior axis, making that single AP measurement even less relevant.

b. intrathoracic pressure – Secondly, the variation in intrathoracic or intrapleural pressure (Pip) must be measured, as, for instance, a young and fit patient can generate large changes, which would result in more significant IVC variation, as compared to a frail elderly patient, even if they are on the same point of their Starling curve, invalidating the IVC measurement. All “sniffs” are not created equal.

c. intra-abdominal pressure – Finally, the intra-abdominal pressure (IAP) must also be assessed, since an elevated pressure would decrease the size of the IVC and make that measure no less accurate, but less relevant in terms of representing venous filling.

So what should we do?

Instead, a more global assessment of the IVC volume, measuring short axis area measurements and variation at several points along the IVC would give a much more accurate estimate of IVC volume variation. This is currently being studied by our group.

“Eyeballing the IVC” Attempting to link evidence and physiology, some bedside sonographers’ approach is to take a global look at the IVC in both long and short axis during respiration, while clinically assessing the respiratory effort and the abdominal pressure. This approach is analogous to the “eyeballing” of LV function – versus more formal measurements such as Simpson’s disk method, etc – which has been proven just as accurate with sufficient clinical experience.

The figure below shows an IVC that is about 10-12mm along most of its intrahepatic segment on expiration, and collapses almost completely on inspiration. If this belongs to a patient breathing with little effort and with a soft abdomen to palpation, it is physiologically quite clear that this patient would be fluid responsive. It also shows how impressive the collapse is in the short axis.

IVC insp dual

For instance, let’s say Patient A is in respiratory distress and using accessory muscles and presents to the ER with a respiratory rate of 35 and a systolic BP of 80. His IVC measures approximately 21 mm in diameter at several points along its axis, and has a brief collapse to about 10 mm with strong inspiratory efforts. His abdomen is soft during inspiration but firm during a prolonged expiratory phase.

Patient B is brought to the ER somnolent with a respiratory rate of 10 and a systolic BP of 80. His IVC measures 15 mm with minimal respiratory variation. His respirations are shallow and his abdomen soft. These two patients show how the IVC assessment needs to be taken in clinical context.

Patient A has some 50% inspiratory collapse of a large IVC in the context of large variations in Pip, whereas Patient B has little variation of a mid-sized IVC in the context of very small variations in Pip. In all likelihood, Patient A is not very volume responsive, while Patient B probably is.

Volume Responsiveness vs. Volume Tolerance – it is critically important to distinguish the difference between these two concepts as they are often misused interchangeably: Volume responsiveness refers to an increase in cardiac output (CO) to a fluid challenge. This is a purely hemodynamic concept. Volume Tolerance refers to whether or not a patient can tolerate volume without clinically significant side effects. This is a complex clinical assessment that should include: -the patient’s plasma oncotic pressure (serum albumin) and level of capillary leak, if present, -the patient’s pathology – is there risk of capillary leak in critical tissues such as lung, brain, abdomen? -the type of fluid being considered (isotonic crystalloid vs hypertonics or colloids/blood products). It is important to distinguish that not all patients who are volume responsive are necessarily volume tolerant.

Volume assessment summary – this issue remains a difficult one, even with the use of bedside ultrasound, because the optimal point for any one patient to be on his or her Starling curve at any one time in different clinical conditions remains elusive. Despite considerable study and several proposed management algorithms, there is no means by which to determine exactly how much of any given fluid is enough, without being too much.

In my opinion… – no direct evidence – keeping an IVC below 20mm and probably below 15mm with significant respiratory variation, if hemodynamics allow, is probably ideal. However, bedside ultrasound allows to clearly identify the cases where fluid is clearly needed and those where fluid is unlikely to benefit. Both of these scenarios are easily and routinely missed by traditional examination. Additionally, when the IVC assessment is done in conjunction with lung ultrasound, it becomes possible to detect early development of pulmonary edema and halt aggressive fluid resuscitation (FALLS Protocol, Daniel Lichtenstein).

 

Technical Pearl: the part of the IVC we generally assess being the intrahepatic segment, it is possible to find it almost by scanning through any part of the liver, which happens to provide a great acoustic window. This may be particularly useful when the epigastric area is difficult to access (incision/bandage, drains, in the OR, etc…) or when there is bowel gas in the epigastrium. The figures below show the same IVC, first in a “traditional” epigastric view, then in a view approximately along the plane of the red arrow on the CT scan.

2 views IVC std:liver

CT liver IVC views

 

Bottom line?

When assessing volume status, it is absolutely essential to keep the clinical question in mind. It is a great minority of patients who are volume responsive who actually need volume. Normal, healthy humans are very much fluid responsive and fluid tolerant but certainly not in need of any. Much of the current studies and literature focus on assessing volume responsiveness in the setting of shock, which, although arguably the most important, is not the only type of information that can be obtained from the IVC. For instance, as will be discussed in the chapter on congestive heart failure, knowing that your patient is very “full” should prompt further diuresis. If you are dealing with managing severe anasarca, knowing that a patient’s intravascular volume is low may prompt the use of albumin or hypertonics prior to further diuresis to help resorb some of the interstitial fluid. Another critical question to which there is currently no answer is just how much fluid to give to patients in shock. There are many opinions but no certainty. It is common practice to fill a patient in shock until they are no longer fluid responsive, in an effort to avoid or minimize the use or dose of vasopressor medications. There is no study to date that compares a “moderate fluid/early vasopressors” vs “aggressive fluid/avoid-vasopressors-if-possible” approach.

Hopefully this will be answered soon. In light of the clear evidence linking positive fluid balance and mortality, it would seem wise to fill to a “moderate fullness” where some respiratory variation remains, rather than to the point of no longer being fluid responsive. After all, physiologically, the only time humans are really full (>20mm IVC with little or no variation) is in pathological states of congestive heart failure or obstructive shock. So again, when assessing an IVC, keep in mind what your clinical question is and interpret the sonographic data accordingly.

 

cheers!

 

Comments:

Marco says:

Thanks Philippe, very interesting post.
Using your great categorization, I think that the worst scenario is represented by a patient who is volume responsive but poorly volume tolerant. In that case, it is important to have clear in mind which is our target: cerebral perfusion, oxygenation and lung extravascular fluid, ventilatory weaning, renal function, avoiding vasopressors or mechanical ventilation, etc…
Very often, maintaining a brain dead heart beating donor, every organ would require a different volemic status, and if all of them are suitable for transplantation you have to compromise.
Just a last thought: as well as “all sniffs are not created equal”, also tidal volumes are very variable. Assessing respiratory variations during protective (low TV) ventilation requires a thoughtful interpretation of the results.

 

Absolutely. Interpretation of the findings in each individual case is key. 

Philippe