The Resuscitation Tracks 1: Portal Vein POCUS with Dr. Andre Denault. #FOAMed, #FOAMcc, #FOAMus

So this is one of the key discussions I wanted to have in my process of synthesizing my resuscitation algorithm. Dr. Denault is the one guy I’d call a mentor, and I think one of the rare and true clinician-scholar, who is just as comfortable being the anaesthetist/intensivist at the bedside of the crashing patient as he is being the keynote speaker in major conferences, or writing the textbooks that lead the field in acute care/perioperative TEE and critical care POCUS.

So to put some perspective to this discussion, back in 2014 I organized a resuscitation afternoon for internists with Andre and another awesome guy you probably all know, Haney Mallemat (@criticalcarenow). In a quick 15 minute discussion between talks, he shared with me the most recent of his discoveries, portal vein POCUS as a marker of right-sided failure/volume overload in his post-op cardiac patients, and how aggressively managing these resulted in much improved post-operative courses in terms of weaning, vasopressors and even delirium.

Interesting stuff.

So here you are:

So I’ll let you all ponder that and I would really like to hear comments and ideas. Sometime in the next few weeks I’ll be finalizing my resus algorithm – which will not be a recipe approach, as you might suspect if you have been following this blog, and will rely heavily on POCUS and the clinical exam.

cheers and thanks for reading and listening!

Don’t miss Andre running a POCUS workshop on PV/HV at  next april!



A Discussion on Fluid Management Protocols with Rory Spiegel. #FOAMed, #FOAMcc, #POCUS


So Rory (@EMnerd) is in the process of working on a fluid resus protocol for Shock-Trauma, and asked me if we could have a chat about it, which I feel very honored for – and had a brief impostor syndrome crisis – but it’s always great to chat with people who are really bright, really physiological and after the same goal, to make patients better. Always a pleasure to chat with Rory, so here it is.

I really can’t wait to see their protocol, because I think this is a huge and complex endeavor, but has to be done.  I will try to put pen to paper (probably really pixels to a screen but that doesn’t sound as good) and put what I try to do for fluid resus on a diagram of sorts.

Love to hear comments and questions.

PS please skip the first 30 seconds which are a technical blank… Ièm not tech saavy so can’t trim it!




A great comment by Dr. Korbin Haycock

One issue to consider is the degree of pulmonary vascular leakage. If, as in the case of sepsis, the pulmonary vasculature is more prone to the development of lung interstitial edema, lower LVEDP’s possibly will still result in as much lung wetness as higher LVEDP’s. Therefore, reliance of E/e’ ratios may not be the best measure of a fluid resuscitative endpoint in sepsis (and aren’t we really talking about sepsis resuscitation here?). I believe that it’s relatively clear that EVLW will adversely affect outcomes, but pushing for every bit of increased stroke volume/fluid responsiveness is less clear to be beneficial, even if it makes sense from a DO2/VO2 perspective (which may not be the real issue in sepsis anyway, as mitochondrial utilization of the DO2 provided may be the real problem, rather than DO2/VO2 balance). If the assumption is that the kidneys and lungs are the most delicate organs and most at risk to over aggressive fluid administration, and will impact mortality/LOS in the ICU, perhaps a combined strategy of attention to E/e’ ratios, development of B-lines, or the renal resistive index increasing would be a signal for a different strategy rather than fluids to increase venous return (i.e. switching from crystalloids to norepinephrine or vasopressin if the CO is elevated and will tolerate a minor ding from the increase in SVR). If any of those three variables indicate a problem, stop the fluids, switch to a vasopressor. If the issue is the CO rather than the SVR, use an inotrope instead. Of course RV/LV interactions as mentioned in the comments above must be considered. No point in giving fluids to an empty LV if the RV is failing–you’ll just congest the kidneys.

Bedside Ultrasound Case: Control the source. #POCUS #FOAMed, #FOAMcc, #FOAMus

So this morning a 65yr old man with shock and respiratory failure was admitted to the ICU, hypotensive on levophed and vasopressin, with a lactate over 10.

So, as usual, my first reflex was to reach for the probe to assess hemodynamics. He had been well resuscitated by a colleague, and the IVC was essentially normal, somewhere around 15 mm and still with some respiratory variation. However, scanning thru the liver, my colleague had noted a large hepatic lesion, which on CT scan (non-infused since patient had acute renal failure) the two radiologists argued whether it was solid, vascular or fluid filled.


Having the advantage of dynamic ultrasound, you can tell that there is some fluid motion within the structure, very suggestive of an abcess, especially in the context of severe septic shock:

So the next step was source control:


Pretty nasty. Pardon my french!

We got over 1.5 L of exceedingly foul pus.


Within a couple of hours the lactate dropped to 3 and the levophed was down by more than half.

I think this case illustrates once again, the power of POCUS in the hands of clinicians.  While I am certain that the diagnosis would have been made without POCUS, it probably would have taken additional time as the radiologists themselves were debating its nature, and without POCUS, bedside drainage in the ICU would have been out of the question. That liter might still be in there tonight…

For those interested in how to integrate POCUS in their daily rounds, I think I put together a fair bit of clinical know-how and tips in this little handbook.





Tom Woodcock: The Revised Starling Principle and The Glycocalyx! #FOAMed, #FOAMcc

Screen Shot 2016-08-05 at 11.57.11 PM

So today, I had the chance of having a private tutorial with Dr. Thomas Woodcock (@thomaswoodcock) about the glycocalyx and the revised Starling principles.  For anyone interested in fluid resuscitation, this is an area you have to delve into. The basic principles we all learned (which are still being taught) are basically the physiological equivalent of the stick man we all started drawing as toddlers: overly simplified and far from an accurate representation of reality.

Now my first disclaimer is that I have been a colloid supporter for many years. My physiological logic for that had been to minimize the crystalloid spillover into inflamed/septic areas, particularly the lungs and abdomen, when those are the septic sources. However, I was likely misled by my education and lack of knowledge about the endothelium.

So I stumbled upon the whole glycocalyx thing a couple years ago, and this prompted me to try more enteral fluids – the only way fluids normally ever enter the vasculature – but little else. Aware that it’s there, but unsure what to do about it.

Now a year and a half ago, Andre Denault, my closest thing to a mentor, casually dropped the line to me about albumin not working. “Don’t use it. It doesn’t act the way we think it does.”  But it was a brief chat, and I didn’t get to pick his brain about it.  Just a few weeks ago, I discuss with Jon Emile (Kenny), and he’s coming to the same conclusion.  Damn. I’m finding it a bit harder to hang on to my albumin use, which is beginning to look a bit dogmatic and religious.

Here is Jon-Emile’s take on it – a must-read.

Here is Tom Woodcock’s site and article – another must-read.

And here is my discussion (in two parts) with Tom (to skip the silence, skip forward to about 30 seconds into each – sorry my editing skills are limited!)


Bottom line?

Probably stick to isotonic crystalloids, and some hypertonics.


Love to hear some thoughts!






The NYC Tracks with Jon-Emile: The Glycocalyx – The Next Frontier. #FOAMed, #FOAMcc

I was really psyched when Jon-Emile mentioned he would like to talk about the glycocalyx.  I first blogged about it here, basically when I stumbled on the extensive literature on this huge organ we have been completely ignoring in terms of physiology and therapeutics. It lines our entire endothelium, which is where most of our therapeutic interventions go, and we only heard of it in passing, possibly in histology class as med 1’s.   Hmmm.  Anyhow, here, Jon-Emile and I talk about it a little, discuss possible clinical implications, but more importantly Jon mentions the relatively new blog of Dr. Thomas Woodcock (@thomaswoodcock),, who is one of the pioneer clinicians who have studied the glycocalyx, and who is now trying to bridge the bench to the bedside.

I’ve been fortunate enough to get in touch with him and we’re planning to record some discussions soon.

So, in my view, the glycocalyx is a formidable force we have been ignoring, and have been damaging often with our interventions. I’m hoping to see some developments allowing glycocalyx assessment outside of the labs in order to give us the tools to reassess every fluid in terms of the relative damage it does to what is essentially the gatekeeper between the blood and the tissues.

Love to hear some comments!

Here is the chat with Jon:





Post-Arrest BP Study by Young et al (Resuscitation) – interesting & important, but not yet an N=1 answer! #FOAMed, #FOAMcc

Happy New Year to all!

So trying to catch up on some reading, here is an interesting paper I came across. Young et al did a retrospective study on post-arrest BP, in an attempt to answer the very pertinent and important question as to whether or not a higher MAP may confer better neurological recovery, which is a very sensical hypothesis. After all, a brain with potential swelling, both of tissue and endothelium, may “need” a higher BP. Some societies have advocated for a higher MAP than is usually targeted (i.e. 65) and in studies this has been anywhere from 60 to 100. In their particular institution (Vanderbilt) the protocol aimed for 80-90.

Here it is:

Young et al RESUS

So what did they find?

Basically, they were unable to demonstrate that a higher MAP – in this case defined as achieving 80 mmhm – improved anything, with a follow up to 3 months. There was also no increased mortality related to the use of vasopressors.

So, why might this be? Well, I think there are a couple of important principles to review, especially for the novices reading this.

1. Pressure does not equal flow. The relationship between pressure and flow is a complex one and depends on the interaction between the pump (CO) and the circuit resistance (SVR). Pressure rises when resistance is increased, output is increased, or both. If resistance is increased without increasing output – or by a disproportionate increase in resistance vs output, flow decreases. The effect of vasopressors such as norepinephrine is complex, with both vasoconstriction and increased cardiac output (both via beta stimulation and via increased venous return), and depends on volume status, alpha sensitivity and the recruitable cardiac reserve.

So…? This means that on the surface, a BP number tells you little about flow. The same MAP may represent a highly vasoconstrictor, low-flow state, or a normal flow state. Obviously, a certain minimum pressure is required, to drive the flow from artery down thru the capillaries, but what that number is is unclear. So when looking at any study using simply MAP without another assessment of flow, one cannot draw a conclusion that improving hemodynamics may not help the situation.  How does one assess this – in all likelihood  an integrated approach using ultrasound (volume status, cardiac function), tissue saturation (cerebral/somatic oximetry) and possibly other technologies, including simple physical exam looking at skin mottling.  This type of information could categorize patients into flow categories and make results much more interesting and applicable.

Note that this isn’t really criticism on the authors – it would be impossible to do this on a retrospective study, but simply food for thought for further studies to come.

2. The N=1 principle: remember that we are never treating hundreds of patients at once, and we do not have to decide what is best for most (which is what an RCT generally answers) but what is best for the one patient we are treating.  Hence, looking at any one patient and saying that the target BP should be 65 vs 80 based on this study is incorrect.  What we should be saying is that aiming for a higher MAP may not be necessary if we feel that the patient is well perfused at 65. How each of us figures that out will depend on individual skills and available technologies, but to simply aim for 65 without further thought and assessment is relinquishing your MD in favour of the printed word, essentially what any paper protocol could do.

In the next post I’ll discuss the use of tissue oximetry and how it can be used as part of a strategy to optimize vasopressor use and MAP targets.


Thanks and love to hear your opinions!


Oh, and don’t forget to register for CCUS 2015 at, and for more info at  In those couple of days, Paul Marik, Scott Weingart (@emcrit), Josh Farkas (@pulmcrit), and a bunch of other totally amazing speakers will be talking about this stuff, and more!


A Bedside Ultrasound Case & Poll: All Infiltrates are not created Equal: A Follow Up! #FOAMed #FOAMcc #FOAMus

Ok so so far, the votes show the following:

CHF 52%

PE 26%

Pneumonia 21%

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!

Bottom Line?

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.


Thanks for reading!