A cautionary tale for budding bedside sonographers… #FOAMed, #FOAMcc

First of all, congratulations to all who are picking up a probe and working to add it to their diagnostic and therapeutic armamentarium. It will serve you – but more importantly, your patients – for the rest of your career.

I would like to caution you, however, in remembering that this, unlike knowledge, is a skill.  More than half the challenge is in image acquisition, and this requires practice. Practice, practice, practice. You can’t just reach for the probe in that one patient during your shift in whom you really want to have an idea of his or her cardiac function or volume status, then try to remember how to do it.  That’s a road to early discouragement and worse, never developing the skill or the necessary confidence.

Especially early on, scan everyone you can, including yourself.  You make a very patient patient.

If you’re not a fortunate medical student whose school is one of the pioneering ones with an undergraduate programme, take every course you can.  Make friends with ultrasound tech and spend some lunch hours watching some of their exams.  Pin (4 point restraints preferably) a colleague to a gurney when a machine is available.

Once you can reliably acquire images, start making clinical calls on the extremes: the tiny or the huge IVC, the hyperdynamic and the minimally moving ventricle, etc… and as your skills and experience grow, work your way towards the middle.

The last thing we need, as a bedside sonographer community, is to have the current trainees, which really represent the first generation (as most of the educators out there today are largely self-taught, or at least devised their own unique programs), misuse this amazing tool. We are under scrutiny, as it is a novel application (of an old technology), and cannot afford mistakes, lest roadblocks re-appear.

So practice, practice, practice, and if you’re not sure, get another opinion or another diagnostic modality!

happy scanning!



Bedside Ultrasound Picture Quiz #6 – #FOAMed, #FOAMcc

So your intubated patient has developed abdominal distension and residuals are 250. You scan the LUQ:


Screen Shot 2013-10-28 at 11.32.45 PM



what do you see?  what should you do?

scroll below…













dilated stomach2


You have gastric distension with at least a liter of fluid in there.   Put in an OG, hold feeds, assess the rest of the abdomen to r/o bowel obstruction, consider motility agents and look for a reason behind the ileus or obstruction.




Steroids for cardiac arrest…really? My take on the VSE study – #FOAMed, #FOAMcc

So I’ve been asked a few times for my opinion about the VSE study in the last couple of months, so here we go.

JAMA2013;310(3):270-279. doi:10.1001/jama.2013.7832.

First of all, lets look at it from a theoretical perspective.  How would steroids contribute to ROSC (return of spontaneous circulation)?  Hard to believe they possibly could, given the ultra-short timeframe to ROSC – minutes mostly – and the much longer action of steroids.  However, it is quite possible – and in view of this study perhaps likely – that there is an effect on shock and RONF (return of neurological function).

Why?  Post arrest shock results in MSOF due to a cascade of inflammation resulting from the hypoxic insult. Remember that we are not designed to survive these events. Being designed to fight off moderate trauma and infection (eg being bitten by an animal or clubbed by another caveman) our physiological reaction often overshoots the mark resulting in more damage than good, as it does in sepsis (variably depending on our different geno/phenotypes).  So whether liver, kidney or brain damage, some component is not only related to pure hypoxia but also to an inflammatory cascade that has a prolonged effect. This is the same thing we are targeting with cooling, on top of a simple metabolic supply/demand issue, so in terms of biological plausibility, it makes some sense.

In the post-ROSC phase, there is always the possibility of relative adrenal insufficiency – after all, the adrenals have taken a hit as all the other organs did – so again there is biological plausibility.

There’s quite a bit of debate out there as to whether or not to apply this.  I’m pragmatic, not a purist, and my beliefs lie in evidence, biological plausibility and the risk/benefit ratio.  In this case, I think the decision is actually quite simple.  The way I see it, the steroids are harmless and probably helpful, so I have been giving solumedrol in the last few months.

If anything, I’m more concerned about the harm I may be doing with epinephrine/vasopressin, especially in terms of RONF.  I do hope an epi (various doses) vs placebo study is done, because it is difficult to withhold, knowing that there is greater immediate effect on ROSC… Hard decision as the clinician at the bedside, and hopefully this will become clearer in the near future.

For those unclear about the whole epi debate, the physiological issue is that the relationship between pressure and perfusion is represented by an inverted U curve – at very high pressures (from vasoconstriction) perfusion is decreased (think of the extremities on high dose pressers with a decent BP).  So although we may help coronary perfusion pressure and thus ROSC, end-organ damage is greater…and nothing matters much without a brain.


So bottom line:  I’d go ahead with the steroids, and for now the V and E, but I wouldn’t be surprised to drop or decrease those soon.

More to come on resuscitation and its future (the present for some of us…) in posts and podcasts!

Hope this helps!




CCUS Annual Symposium 2014 – The Ultrasound-Assisted Physical Exam! stay tuned!

This year, we’re putting together a really, really interesting event.  Bedside ultrasound being a hot topic and at the brink of revolutionizing clinical examination and practice, we figured that this year, we’d go back to basics to some degree with a general ultrasound approach, but also a step further in looking at it from an integration perspective, meaning how to approach clinical problems with ultrasound as an added tool.

Talks will be clinical problem-based – e.g. the patient with dyspnea, the patient with renal failure, etc, essentially showing participants how to integrate their growing ultrasound skills into routine use.  There will be a ton of faculty led workshops to review all the basic ultrasound skills (lung, cardiac, abdominal, vascular) on live models and on advanced CAE simulators, both adult and pediatric.

Our faculty will be fantastic, including Andre Denault, Haney Mallemat (@criticalcarenow), JF and Max (@EGLS_JFandMax), Edgar Hockmann, Catherine Nix, Alberto Goffi, Massimiliano Meineri, Matt Hoffmann (www.pulmccm.org), Jeff Burzynski, Jason Fisher, Alyssa Abo and many more…

The two day core event will take place in Montreal, on may 10th and 11th, and, equally interesting will be a pre-congress set of courses on may 9th, including:

EGLS (echo-guided life support)

Focused TEE

Bedside ultrasound for nurses (vascular access, IVC volume status assessment)

Critical Care Procedures (drains, tracheostomy, central lines)


Registration is not yet open but will be in the next few weeks, so for anyone interested please visit http://www.ccusinstitute.org and join (it’s free!) and we’ll email you when its up and running.

Please forward/link this to all your forward-thinking colleagues~




Bicarb: Myths and Facts…

So I was in the ED a few days ago as overheard a conversation between one of the staff internists and a resident, and how they were planning to correct a lactic acidosis using some bicarb.  I cringed under the surface, because the attending was explaining how this would buffer the acidosis, and the resident was nodding. The attending then turned to me and asked me how much I would give in this case.

I had a moment of hesitation because it was a particularly busy day and I hadn’t planned on an impromptu teaching session which I knew would have to happen if I opened my mouth. On the other hand my…academic principles (? – or something like that) wouldn’t allow me to agree…

I wouldn’t give any at all.

So I’ll spare you the play by play, but here is the gist of it.

Rewind first to 2001’s SCCM in San Diego and a talk by Dr. John Kellum about acid-base, and my introduction to the Stewart or physicochemical approach to acid base.  Somewhere in that hour was one of my few genuine lightbulb moments in medicine, and a sinking realization that a lot of stuff I’d been thought wasn’t really so.

Here’s a simple equation we all know:

CO2 + H20   <-> H2CO3 <-> H+ + HCO3-       this is mediated by carbonic anhydrase.


1. we have a LOT of CO2

2. we have a LOT of H2O

3. carbonic anhydrase is pretty ubiquitous…

thus…we have an (almost) endless supply of “bicarb.”    What????

Yup. I’m not particularly bright nor a chemist, and although I did read Peter Stewart’s original paper, much of it was over my head.  However smarter docs have distilled the principles (http://www.anaesthetist.com/icu/elec/ionz/Findex.htm) to make it palatable to the clinician. It does seem to make a lot of sense, and explains many clinical scenarios which didn’t seem to make physiological sense. In addition, the slow and steady growth of literature using the strong ion difference rather than traditional acid base theories is encouraging.

Most of all, being involved in education, I have had the privilege of exchanging ideas with some really bright people, and all the ones who are particularly physiological have changed their acid base understanding to the Stewart approach.

So, in super-summary, this approach tells us that the only role of HCO3 is to maintain electroneutrality, which is primarily filling the gap between sodium and chloride. Depending on what happens to sodium, chloride, or if there is another anion, HCO3 will either increase or decrease, mediated by carbonic anhydrase. We make as much or as little HCO3 depending on our needs. It is a dependant variable, and has no active role.

In fact, when we are administering “bicarb,” what we are really giving is sodium without chloride, thus increasing our strong ion difference. We can give sodium acetate or citrate and the bicarb will increase just the same – filling the gap.

So what does this mean clinically?

Well, first of all it is important to understand what we are doing if deciding to administer NaHCO3: attempting to change the pH (note that I’m not saying improve, because in varying scenarios, I’m not sure which pH is better…).

One of the common and sometimes almost subconscious beliefs is that bicarb “buffers” acids in a sense of neutralizing them. This is only true in the sense of electroneutrality, and not in a biological sense. The more important thing to realize is that none of these acids are directly “toxic” and require “buffering”…  Lactic acid isn’t toxic, it’s cellular fuel. Its the process behind it that can be and that sometimes needs to be excised!

So the question then becomes when is it truly important to increase the pH? When is there actual benefit?  I won’t argue that at some levels (<7) I get chicken too, and feel like giving some solo sodium (more commonly known as bicarb). But I think it is pretty clear (permissive hypercapnia data) that pH in the range of 7.20-7.35 is innocuous. How about 7.10-7.20?  Or 7.00 to 7.10?  I don’t know. But I do know that my DKA patients (6.85-7.20) are definitely not in cardiovascular collapse. Just a little tired from the Kussmauling…

So what am I doing with the NaHCO3?  Is increasing pH beneficial to my patient? Certainly to the one who is arresting from hyperkalemia it is, to shift the K a little, but what about my septic patient?

Well, in giving NaHCO3, I am increasing my CO2 load (equation vide supra), which my respiratory system now has to get rid of, else I am worsening my intracellular acidosis (CO2 diffuses freely).  I am also interfering with the adaptive response of the hemoglobin dissociation curve and impeding the right shift (below) which helps deliver more oxygen…hmm…and aren’t most of these patients to whom we consider giving “bicarb” having some degree or other of tissue hypoxia…? hmmm… what was the benefit again?

O2 Hb dissoc

Scott Weingart (emcrit.org) also gives a great podcast about his use of NaHCO3, especially the means (bolus vs infusion) and indications.

Personally, I think it’s reasonable to use in a mixed infusion when facing hyperchloremic acidosis, usually post-resuscitation due to overzealous use of NaCl, but never really in “treatment” of acute metabolic acidosis (especially not with the theory of “buffering”), and it is important to remember what we are trying to do, to what end and possibly at what price.

Now I know some people really, really disagree with this, so please let me know your (physiological) thoughts!


Philippe Rola

Ultrasound-guided central venous catheter insertion: standard of care or preventing procedural skills? #FOAMed, #FOAMcc

Ok, so let me preface this with the fact that I walk around with a handheld ultrasound rather than a stethoscope, and that I examine ALL patients with a focused cardiopulmonary and abdominal exam. My bias towards bedside ultrasound is ridiculously huge. I think practicing without it, once the skill is acquired, is unethical.

Having said that, I have an issue with the fact that it now seems to be “standard of care” for all lines to be ultrasound guided.

Hmm…here are the problems as I see them:

1.      I have come across junior staff intensivists who have never inserted a jugular or subclavian catheter without ultrasound, using landmark techniques. That is an utter shame and worse, a possible disaster in an instance of technology failure (ie the ultrasound is out for repair, etc…).   Intensivists who would be unable to put in a line???

2.      I have been teaching bedside ultrasound for the last 5 years, and practicing it for over a decade.  I teach ultrasound-guided line workshops. The ability to safely and properly follow a needle tip to venous puncture is an expert-level skill. I cannot count how many times a participant has sworn that his beam is right at the tip of the needle and been befuddled when I point to the blue phantom and show him how he is scanning just a bit beyond the hub and that the tip is in fact several centimetres into the blue phantom (better the phantom than the lung!).  The problem comes from a false sense of confidence and security that the procedure being “guided” provides. I’ve already seen several carotid insertions and pneumothoraces with IJ and SC guided procedures…

3.      The evidence is shabby in the following sense:  if you look at the papers comparing blind to guided, the stats on the blind procedures are not exactly very impressive to start with (time and number of attempts)… Also, did all trainees who are out there doing guided procedures receive the same training that those in the study did?  All residents with a probe are not trained/created equal, hate to break it to you…

So…what is my preference?  I spot all lines, meaning that I scan both sides of the neck for jugular size, position relative to the carotid and anomalies.  I then do the IJ line blind, unless it is particularly small or really anomalous (eg right on top of the carotid), then I would do it guided. I use ultrasound for ventilated subclavians.

In the interest of science I have timed myself and recorded stats. I can generally get a functional line (puncture to catheter insertion – not including suture time) in 60-90 seconds, with an average of about 1.1 punctures (eg 1 in 10 times I need to widthdraw and re-angle/puncture).   Obviously this comes with about 18 years of doing central lines (since I was an R1), but I know I’m not the only one out there with this type of skill – there are a lot of CC/ED/anasthesia..etc docs who can do the same.  But it does take practice.

My suggestion would be for trainees to spot the vein and keep a ready ultrasound probe (sheathed and sterile), and do a blind puncture.  If they find it on a first pass, then great. If not, then go ahead with the ultrasound (but here I would hope that they would have had some good training in guided insertion and not just that given by a senior resident who’s done all of 5 lines…).

So I think that this is yet another example of N=1, in this case the 1 being the physician rather than the patient, and I think we are in a bit of a tough spot with these recommendations, as the skills will deteriorate in time, and within a generation there will be few if any physicians well-versed in landmark insertion, which would be a shame. It has served us well in the last decades and, unlike the stethoscope, I don’t think its time has passed…

let me know what you think!


ps when I have the opportunity, I will record a demo on my blind technique, for interested trainees.

Hi Philippe

just read your post on central line insertion. One of the things you mention is:

I cannot count how many times a participant has sworn that his beam is right at the tip of the needle and been befuddled when I point to the blue phantom and show him how he is scanning just a bit beyond the hub and that the tip is in fact several centimetres into the blue phantom 
This is one of the critical issues that we face with our hands-on intervention course…we’ve made videos, taken photos regarding ‘fanning the beam’ to keep the needle tip in view, etc … and still there are those whose spatial conception are challenged by the imaging…. many understand, but some do not ( my best guess is that it’s the narrow-window 2D image of a 3D structure that throws some people off ) 
Do you have any suggestions on how we can modify our approach to teaching this skill ? 
thanks for the great blog postings 
Tough question. The only way i get around that is one on one when a resident/student/attending is acutally rounding with me and we have time to really teach that 2d/3d relationship. You’re right some just have a hard time. Sometimes the long axis in plane works for those people, especially in subclavian access where this problem is more concerning. But its a tough issue, which i’m sure is happening everywhere.
Good question to ask some of the other faculty at CCUS 2014.
Cheers and looking forward to meeting you in a couple months!

Bedside Ultrasound & the patient with Acute Renal Failure – an N=1 Podcast #3, #FOAMed, #FOAMcc


So here is a quick and dirty approach to the patient with ARF using bedside ultrasound, which enables the rapid diagnosis or ruling out of two important and time-dependant conditions with significant clinical impact: hypovolemic and post-renal/obstructive renal failure.

Let me know what you think!

Philippe Rola