Bedside Ultrasound Clip Quiz #4 – #FOAMed, #FOAMcc

So you’ve been doing ACLS for a few minutes in the ED on an elderly male who collapsed at a bus stop and shocked out of VF on the scene by EMS, and when you do a 3 second pause to assess the heart, just after an epi got flushed, this is what you see in the subxiphoid view:

 

Is this a case of tamponade?

Scroll below!

 

 

 

 

 

 

 

 

Nope!  There’s no pericardial effusion, and the atria are huge!  What you do see is microbubbles from the flushed IV medication in the RA and RV, and severe LV dysfunction.   The severe LA dilation suggests at least a component of chronic overload (also supported by significant leg edema in this case). Note that you can have severe LV dysfunction (post-resuscitation myocardial dysfunction or PRMD) after cardiac arrest of ANY etiology and does not necessarily imply pre-existing LV dysfunction or predict eventual LV function.

 

 

 

 

Is it still cool to cool in cardiac arrest? The new TTM Hypothermia trial! #FOAMed, #FOAMcc

So the other dayI read the TTM trial (http://www.nejm.org/doi/full/10.1056/NEJMoa1310519?query=featured_home#t=article) with great interest, as cardiac arrest and the post-resuscitation phase have always been among my pet topics.

First of all this is a big trial.  Bigger that the previous ones that established hypothermia as a standard of care. Does it obviate those previous results?  Absolutely not. Those trials were not 32/33 vs 36 but 32/33 vs “whatever happens.”

Hypothermia makes a lot of sense physiologically, but of course that doesn’t mean that it might not have some harmful side effects that have not yet been clearly delineated (besides the current known hemodynamic ones and relatively benign electrolyte and renal alterations).

However, it is pretty clear that, compared to 33 degrees, 36 does just as well, which leans towards saying that all we have to do is avoid fever, or stay in a very mild hypothermia.

Avoiding secondary injury in brain pathology is key (no desat, no hypotension, and no fever), and in anoxic encephalopathy, it is no different.  The key thing is that in this trial, the temperature was controlled – ie it would not be acceptable to do no cooling, and just chase the fever (which is very common) with acetaminophen, which would invariably result in significant time spent above 36 (oops, tylenol didn’t really work, ok lets put the blanket, etc …this is gonna be hours).

So is this the end of aggressive cooling?  Not necessarily.

For anyone interested in the topic, I suggest reviewing Peter Safar‘s data on dogs and cold aortic flushes – it is absolutely unbelievable to see dogs who  had an arrest, got the cold aortic flush (brain temp below 10 degrees), are left stone cold dead for 45 minutes, then resuscitated and are then able to go around a few days later and do doggie things like run and bark and eat…  So I don’t think that cooler isn’t necessarily better, but that we haven’t yet delineated what are the pros and cons of each temperature range or how to get there practically and safely.

So what should we do?  Well, it would seem reasonable to do either at this point, and accepting a temp between 32-36 (I have usually preferred 33-34 as they rarely drift down into the 20’s as I’ve seen the 32’s do) as being adequate. This may make hemodynamics a bit easier to manage in certain cases.
Also check out Scott’s take at:
 http://emcrit.org/podcasts/emcrit-wee-targeted-temperature-trial-changes-everything/#comment-58635
And the RAGE Podcast addresses this topic at about 25 minutes:
…and of course, keep abreast of further data and subgrouping that may become available on this, and further trials. But for now, its definitely still cool to cool, maybe just a little less…

A Paradigm shift: re-thinking sepsis, and maybe shock in general… #FOAMed, #FOAMcc

Thomas Kuhn, physicist and philosopher, in his groundbreaking and science changing text, The Structure of Scientific Revolutions, states that:

“Successive transition from one paradigm to another via revolution is the usual developmental pattern of a mature science.”

In other words, a science has growing pains and is bound to have a fair bit of debate and controversy, until a new paradigm becomes dominant.  I think that there is a current – in part prompted by the power of socio-professional media which has allowed minds to connect and knowledge to spread – that will see many of the things that are now “Standard of Care” out the door.

So first of all, the following are must-listens, the first a lecture by Paul Marik, whom I have had the chance to collaborate with in the last years and respect greatly, on knowledge, experience, and even more on his refusal to take anything for granted and being in a seemingly-constant quest for the improvement of medicine.

The second link is Scott Weingart’s take on it, which I think is equally awesome.

I think Paul is pushing the envelope in an essential way, and Scott does a fantastic job of seeing or putting it in perspective. Enjoy:

http://emcrit.org/podcasts/paul-marik-fluids-sepsis/

http://emcrit.org/podcasts/fluids-severe-sepsis/

My (very) humble opinion on this is a rather simple, almost philosophical one:  why are we seemingly obsessed with treating a predominantly vasodilatory pathology with large amounts of volume?  I’ve said this in previous posts and podcasts, but this, in my opinion, is largely cultural and dogmatic. “Levophed – Leave’em dead” is something I heard as a student and resident, and came to take for granted that I should give lots of fluid in hopes of avoiding pressors… But there’s no evidence at all to support this.  The common behavior of waiting until someone has clearly failed volume resuscitation before starting pressors befuddles me (think how long it takes to get two liters of fluid in most ERs…).  If I was in that bed, I’d much rather spend an hour a bit “hypertensive” (eg with a MAP above 70) than a bit hypotensive while awaiting final confirmation that I do, in fact, need pressors.

I strongly suspect that it’s just a matter of improving vascular tone, giving some volume (which may be that 3 liter mark), and ensuring that the microcirculation/glycocalyx is as undisturbed as possible. Now when I say it may be the 3 liters, I firmly believe this will not apply to everyone, and that it will be 1 liter in some, and 4 in others, and that a recipe approach will be better than nothing, but likely harm some.

I think that blind (eg no echo assessment) of shock is absurd, and for anyone to propose an algorithm that does not include point-of-care ultrasound is only acceptable if they are in the process of acquiring the skill with the intention of modifying their approach in the very near future.

The whole microcirculation/glycocalyx is absolutely fascinating stuff, and undoubtedly will come under scrutiny in the next few years, and it is definitely something I will focus on in upcoming posts & podcasts. Our resuscitation has been macro-focused, and certainly it is time to take a look at the little guys, who might turn out to have most of the answers. For instance, there is some remarkable data on HDAC inhibitors (common valproic acid) and their salutatory effects in a number of acute conditions such as hemorrhagic shock (Dr. Alam) which have nothing to do with macro-resuscitation, and everything to do with cell signaling and apoptosis. Hmmm…

please share your thoughts!

thanks

Philippe

Enough with the “Normal” Saline!!!!! #FOAMed, #FOAMcc

Enough with the “Normal” Saline!
So its been about a year since a JAMA article (http://jama.jamanetwork.com/article.aspx?articleid=1383234) finally showed that the downside of 0.9% saline isn’t just theoretical, but has some associated clinical morbidity (bad for the kidneys!).  Sadly enough, it still seems to be the routine fluid used for boluses. Whether the ER, hospitalist or intensivist, residents, students…it seems people are reluctant to let go.
Today, rounding in the ICU, I was changing an order for a bolus from another doc from NS to RL, and a nurse asked me why.  I gave her a capsule summary and she was in disbelief.  “Come on Phil, they wouldn’t call it normal saline if it wasn’t!”
I’m an internist by training, so naturally I grew up using NS, since that’s what all the attendings and residents used around me.  Ringer‘s was the stuff the surgeons used, so well, I guess it had to be wrong…no?
So forward to 2001 and John Kellum‘s lecture on acid-base I’ve previously mentioned, and my exploring Stewart’s Physicochemical Approach, and wait, I look at the back of a bag of NS, and find out, much to my dismay, that the stuff I’ve been using like holy water has a pH of 5.6.  And who have I been giving liters and liters of this stuff to?  Yup, mostly patients with acidosis. Hmmm. Interesting. So although I don’t necessarily advocate correcting metabolic acidosis for the sake of doing so (see my previous post on bicarb), I’m not a proponent of worsening acidosis either, even if by another mechanism.
I think there are a number of factors that have resulted in this situation.  For starters, there is the issue of false advertising – the “normal saline” monicker has been influencing subliminal thought for decades (think Malcolm Gladwell thin-slicing), making physicians feel they are giving and inherently “good” substance.  Then there’s the whole tribalism thing with the surgeons vs non-surgeons making all the non-surgeons polarize away from RL (not that RL is perfect, just a bit better, and certainly closer to “normal”). Finally, there’s this sad, sad factor that makes people, even (or maybe even more) smart people reluctant to accept that they have been doing something wrong (or, for those who are offended right now, not ideal) for a long time (I sure was) and prefer to fight it and rationalize it for a few more years until, eventually, the evidence becomes overwhelming or the changing of the guard has fully taken place.
I think what we should be hanging on to is not a drug or a fluid but rather what we learned in the first couple of years of med school: physiology.  Now mind you, at that point we (or most of us) didn’t have a clue how to use it for anything more that answering multiple choice questions, but at some point, we have to go back to it and realize that is what we should be basing our assessment of our therapeutic acts and decisions.
So…if I have a situation where I am low on chloride, I might want to use NS. But otherwise, let try to give something whose composition is a bit closer to our own than NS is.  So, for my students and residents, don’t let me see you prescribing boluses of NS.  If you really, really need to, wait until your next rotation please.
thanks!
Philippe
ps for a great review of the original aritcle, please see Matt’s on PulmCCM at :
Reply:  by Marco Vergano
Totally agree!
I have been struggling for years with the bad habit of some of my colleagues prescribing NS as the most harmless and physiologic replacement fluid. Here in Italy we don’t have such a clear separation between internists and surgeons about NS/RL choice: the bad habit of easily prescribing NS is ubiquitous.
Given the results you mentioned about the increased incidence of renal failure with NS, I am wondering if the ban on ALL starch solutions would have been necessary after the introduction of new balanced starch/electrolyte solutions.
What I really don’t like about RL is that it’s not only hypotonic, but also low in sodium. In our ICU we often have many ‘neuro’ patients (trauma or vascular) and sodium variations become a major issue. Also I prefer Ringer’s acetate over lactate on most of the patients who struggle to ‘manage’ their own lactate.
So my favorite solution remains our good old “Elettrolitica reidratante III” (very similar to Plasma-lyte).

Bedside Ultrasound: The Sluggish IVC – something to look for… #FOAMed, #FOAMcc

So take a look at this:

I’m sure most experienced bedside sonographers come across this all the time.  For those who are starting out, and until now have just been looking at size and variation, take a second to look at the flow.  You can actually see the flow stop and start, which tells you your cardiac output is bad.  It could be bad because of the RV, the LV, the pericardium, the tension pneumothorax, anything, but it’s bad.  So just in case you were only gonna look at the IVC, keep looking! You will find something abnormal downstream, perhaps that you can do something about (not fluids, though).

I have seen this disappear and clear up with – when possible – correction of the problem, back to the normally anechoic IVC we usually see.

thanks!

Philippe

ps note there is also a mirror artifact in the right lower portion of the field, making it look as though there are two beating hearts.

Beta-blockers in Sepsis? Interesting… #FOAMed, #FOAMcc

Very interesting article in JAMA: http://jama.jamanetwork.com/article.aspx?articleID=1752246

I’m curious as to whether this has been generating interest in the cc community.  I think it is one of those articles that – at least conceptually – shines light in an area we don’t spend much time reflecting on.

I know that as an IM resident, and a CC fellow, my understanding of vasopressor therapy was pretty basic: squeeze the vessels to bring up the pressure, and hope you don’t squeeze so hard the fingers and toes fall off. In truth, no one ever really pointed out that to some degree or other, the same process killing off the fingers is probably happening to a varying degree in all organs. But maybe I just nodded off and missed it.

Since then, however, I’ve had some time to  re-examine things, and my practice has slowly been evolving.  For one thing, bedside ultrasound allows a really good assessment of inotropy, so I started to ask myself why I was giving b-agonists to patients who clearly didn’t need any help with contractility (e.g. normal, and even more so, hyperdynamic RVs and LVs).  After all, I’m putting them at risk for arrhythmias, or at least tachycardia. So whereas levophed (norepinephrine) remains my reflex pressor, I routinely shift to phenylephrine when faced with arrhythmias (most commonly fast atrial fibrillation) or tachycardia (beyond 110-120) once adequate volume resuscitation has been done.  Why 110-120?  Its an absolute guess. Somewhat educated – or I try to convince myself of that – in figuring that at some point, the increased CO via HR will be offset by decreased filling time, and with the weak but recurring data showing an association between tachycardia over 90-100 and poor outcome.

So this study – counterintuitive as it may sound to some – is really about blunting the potentially unwanted effects of b-agonists.  They randomised 336 patients to IV esmolol to a HR <95 vs a control group of standard care. They found a reduced mortality of 60%… Obviously the massive benefit should be taken with a healthy dose of skepticism, but even just the fact that they didn’t make patients worse is very, very significant.

Read the paper. They do a great job of reviewing the concept and it’s worth going over their protocol.

Physiologically, we know that catecholamines can cause stress cardiomyopathy.  The question is, when cardiomyopathy is noted, how often do we think this is related to therapy?  More often, we figure it’s the disease process – septic cardiomyopathy. At the bedside, this is impossible to differentiate.

The concept of lusitropy – active relaxation – and its contribution to cardiac output – is often overlooked, and can be affected by catecholamines. In fact it can be the most important factor related to preload, despite getting much less attention than volume loading. Remember that preload is not a pressure (especially not a CVP!!!), but a volume, and physiologically it is the degree of myocardial stretch. The ventricle is not passive, and its compliance is highly related to the active relaxation phase. Fluids will not affect this.

In addition, the decreased filling time by tachycardia can also decrease output.

Fantastic study, even if only to open the door.  I would have liked (in typical N=1 fashion and as a bedside sonographer) to see a quick echo prior to initiation, and seeing if there would have been an association with baseline RV/LV function and response/outcome to esmolol. Intuitively and physiologically, it would seem that the hyperdynamic RVs and LVs would have benefitted most, since they didn’t need beta agonism to start with – but I can also entertain that those would be unaffected and that the worse ventricles could have been worsened by stress cardiomyopathy… So a critical question in my opinion.

So…bottom line?  Is this practice-changing? It might be.  For me, I might start looking at RV/LV and opting for a quicker conversion to neosynephrine if I see a hyperdynamic state or lowering my HR threshold to do so…100? 105? – maybe just a shift rather than a change in practice. I’m not sure I’ll start esmolol infusions yet, but it will be at the back of my mind and I might, given the right set of circumstances. What I would like to see is reproducibility, and if it does happen, I would be happy to get HR’s under 95.

Love to hear what anyone else has to say!

 

 

Philippe

 

Epidemiology: Legends & Facts – The Publication Bias – #FOAMed, #FOAMcc

So until a few years ago I reluctantly admit I was one of those who read the title, abstract, intro and quite diagonally went thru methods and results before starting to pay attention at the discussion.  On one hand I got to read a lot more articles per unit time, but my analysis was rudimentary at best…

That was until a colleague, good friend, judoka and microbiologist extraordinaire Peter Barriga started to shine some light into my epidemiological darkness while teaching me some judo.  So while waiting for his textbook to come out, here are a few principles that I’ve found very interesting, revealing, but also somewhat frightening: in part, they explain the lack of strength and consistency found in much of the medical literature

So let’s look at the publication bias.  This refers to the likelihood that a study will be published in a major medical journal.  Not surprisingly, journals are generally more interested in positive studies than negative ones.  After all, who would be interested in reading a journal where more than half the studies concluded with “well, this didn’t work…”   It would feel like a waste of reading time.

Now, let’s look at our whole p value, a number (0.05) which we are culturally in love with. What does it really mean?  It means that there is a 1 in 20 or less likelihood of the result being purely chance. So let’s say a popular drug for sepsis is studies by 20 teams,  the same study done 20 times could yield 1 positive and 19 negative results – by chance alone.

The question then becomes, which study is picked by a big journal to be published… One of the 19 negative studies or…the positive one?

Fortunately nowadays due to the information age, a study registry exists where all studies – including negative ones – can be found, so that anyone interested enough in a particular topic can dig up all the data and have an accurate assessment, but is that the case for most physicians?  Or do most pick up the big titles of the big journals…?

Hmmm… So I think it is incumbent on all of us to examine the main things we do in our practice, and make sure we have carefully looked at the available data surrounding it, and not just blindly applied guidelines, recipes or whatever our seniors and mentors are doing or have shown us.

more to come on how to make our practice GEBM (good evidence based medicine) rather than just EBM…

 

Philippe