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!

cheers!

Philippe

 

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.

Wicked Clinical Case: POCUS & Prone save the day! #FOAMed, #FOAMcc, #FOAMer

So I get a call from a colleague in the ED at about 2am, telling me about a 39 yr old woman post-arrest. So I start putting on my boots and warming up the car (it’s January in Montreal folks).  Apparently she had presented earlier in severe acidosis, the diagnosis is unclear, but she apparently got 2 units for an Hb of 49, then went into respiratory failure and got intubated. She arrested about 30 minutes later, cause unknown.

I tell the ICU to prepare a bed but I want to see her in the ED first. Twenty minutes later I put probe to patient and see a full IVC with spontaneous echo contrast. On that I tell the nurse to hold the fluids – there was a bag and tubing and a pump with 100ml/hr on it – and turn into a subxiphoid view to see a normal RV and a hypokinetic LV with some WMAs. She has marked consolidations  in both posterior lung fields and B lines laterally, with small effusions and dynamic air bronchograms (indicating patent airways). At this point she has a HR of about 120, but there is neither perceptible BP (by NIBP) nor saturation. She’s on levophed at 20mcg. She’s about an hour post arrest which was witnessed and brief (<10min to ROSC).

The theories about the arrest are possible hyperkalemia: she was intubated with succinylcholine before the K of 6.1 was back from the lab, and her pre-intubation pH was 7.0, and post-intubation she was only ventilated at 400 x 18, possibly precipitating a drop in pH and a rise in K. Her EKG had some nonspecific signs at this point, but also a poor anterior R wave.

So we head to the ICU, as instrumentation was needed. Cerebral saturation (SctO2) is 42% and ETCO2 is 20mmhg, which reassures me that the BP is probably in the measurable range (normal SctO2 is >60% and varies, but 47% is certainly viable)…  A jugular CVC with continuous ScVo2 and a femoral arterial line goes in:

screen-shot-2017-01-05-at-10-44-50-pm

So with a BP of 59/44 (ignore the 100/46, not sure whose arm that was on!) I start epinephrine, as the POCUS is similar, as I want some added beta-agonism. ScVO2 matches SctO2 in the 40’s. We get the BP up the the 90-1oo range, the ETCO2 goes to 30, the SctO2 and ScVo2 go up into the high 40’s, which is very reassuring, because with this I know that my epi drip is improving perfusion and NOT over-vasoconstricting. Without looking at a real-time tissue perfusion index of some sort or other, it is nearly impossible to know rapidly whether your therapy is helping or harming (will discuss tissue saturation & resuscitation monitoring in more detail in another post sometime soon).

screen-shot-2017-01-05-at-10-46-31-pm

So now the sat finally starts to record in the low 60’s. We have a PEEP of 5, so start bringing it up. We hit 16 before the BP starts to drop, and that only gets us to the mid 70’s sat%. She actually squeezes my hand to command.

screen-shot-2017-01-05-at-10-45-21-pm

At this point I take a few seconds to recap in my mind. I’d spoken to the husband briefly and she had had recurrent episodes of feeling unwell with headache, nausea and diaphoresis, and that had been out for dinner earlier and she felt fine until later in the evening when this came on and eventually brought her to hospital. There was also a notion of hypertension at an ER visit a couple of weeks ago. Her history was otherwise not significant. Nonsmoker.

Pheo? Maybe, but shock?  I repeat the EKG, and now, in I and AVL, there is perhaps a 1mm ST elevation. She’s 39 and essentially dying. Lactate comes back >15, pH 6.9.  I give her a few more amps of NaHCO3. You can see the BP respond to each amp. I decide we need to go to the cath lab and get the cardiologist on call to get on the horn with the interventional team at a nearby hospital with a cath lab and ECMO, which is what I think she needs. Hb comes back at 116, making that initial 49 that prompted 2 PRBCs probably a technical or lab error…very unfortunate. There are no visible signs of significant bleeding.

But back to the patient, because this isn’t really a transferrable case.

Recap: a 39yr old woman in cardiogenic shock AND in severe congestive heart failure exacerbated by fluids and packed red cells, with a PO2 in the 40’s and sat in the 70’s.

So I decide to prone her.

screen-shot-2017-01-05-at-10-47-44-pm

Along with draining tamponades, this had to be one of the most rapid and rewarding maneuvers I’ve done. There was a scry drop of sat to the 40’s for a few seconds (may have been a technical thing), but then within a few minutes: BP to the 130’s, SctO2 to 59% and sat 100%!

screen-shot-2017-01-05-at-10-46-46-pmscreen-shot-2017-01-05-at-10-47-31-pm

screen-shot-2017-01-06-at-12-08-05-am

 

We dropped the vasopressors, the FiO2, and all breathed a collective sigh of relief. Now for the novices out there, prone ventilation improves VQ mismatch by moving perfusion from diseased, posterior lung fields to now-dependant, relatively healthy, anterior lung fields.

So transfer at this point was in the works. I planned to leave her prone until the last minute. The miraculous effect started to slowly wane within about 30 minutes, with sat and BP creeping down. At the time of transfer, we were back up to 80% FiO2.

So why is this?  Simple enough, this being simple pulmonary edema – rather than consolidated pneumonia – it migrated to dependent areas  relatively quickly. This was confirmed by a quick POCUS check:screen-shot-2017-01-05-at-10-48-06-pmscreen-shot-2017-01-05-at-10-48-26-pm

So in the still shots, you see a pristine “A” profile (normal, no edema) from the patient’s back, and a severe consolidation or “C” profile with ultrasound bronchograms in the antero-lateral (now dependant) chest. Impressive. (for those wanting some POCUS pearls see other posts and here). This is the reverse of her initial POCUS exam.

So we flipped her back and transported her – lights & sirens – the the cath lab, where they were waiting with ECMO cannulae. As an aside, it was quite refreshing to speak to the ICU fellow who spoke POCUS as well as french and english – it’s not usually the case, but I’m glad to see the change. I do believe it to be a direct effect of the influence of my friend and mentor, Dr. Andre Denault, one of the POCUS deities.

So she turned out to have a normal cath and a large adrenal mass. She did well on ECMO, being weaned off it today, and is now alpha-blocked and waiting for surgery, neurologically intact for all intents and purposes. A big thanks to the interventionists and the ICU team at the Montreal Heart Institute. Puts a smile on my face.

 

Take Home Points:

  1. don’t resuscitate without POCUS. I wouldn’t want anyone guessing with my life on the line, would you?
  2. keep pheo in mind as a cause of “acute MI” and shock
  3. if you’re not using some form of realtime monitor of perfusion (continuous CO, SctO2, ETCO2, ScvO2) then all you’ve got is looking at the skin and mentation, so you are essentially flying blind. Lactate and urine output are not realtime in real life.
  4. get ECMO in the house, it’ll come in handy. I’m working on it.

 

Love to hear some comments!

cheers

 

Philippe

 

ps I’ll try to add more ultrasound clips from this case in the next few days.

Fluids in Sepsis: An EmCrit Webinar! #FOAMed, #FOAMcc

Screen Shot 2016-04-27 at 2.00.28 PM

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So a few weeks ago Scott (@EmCrit) asked me to be part of a pretty cool webinar organized by the Greater New York Hospital Association about fluids in sepsis. The gang consisted of David Gaiesky, Emmanuel Rivers and moderated by Scott himself. And for some obscure reason, he asked me to be part of it – much to my honour (terror, also), naturally.  It was only afterwards that he told me it was to help stir the pot and be controversial, challenge the “old school” etc… He seemed to have overlooked that I am Canadian, and inherently and perhaps overly polite and considerate – at least live and in “person”!

We talk about a bunch of stuff around fluids, which, how much, how to assess, etc.

Anyhow, I hope I got a few ideas across, but it was really cool to hear that these gurus do use ultrasound – don’t necessarily strictly adhere to, for instance, EGDT, and also advocate that guidelines are guidelines and not necessarily gold standards.

Here is the link to the webinar for those interested:

 

https://t.co/dbL03Vuqlj

 

And here is the figure for the section where I refer to fluid responsiveness/tolerance:

Screen Shot 2016-02-21 at 9.25.50 AM

I further talk about this in a previous post here.

Scott and I also recorded a debrief which should be coming up in the next weeks on EmCrit – link to follow!

cheers!

 

Philippe

Cerebral & Somatic NIRS (Near InfraRed Spectroscopy) in shock states: tailoring therapy. (PART 1) #FOAMed, #FOAMcc

So I’d mentioned using NIRS to monitor and tailor therapy a few months ago, and promised a more in-depth discussion to come, so here we go.

For this not familiar with the technology or the concept, NIRS measures tissue saturation, predominantly venous. Hence physiologically it is akin to central/mixed venous gases, but localized. Cerebral NIRS found its foothold in the OR with carotid and cardiac surgery, but its use is now expanding. Given typical knowledge translation time of a decade, it should end up joining ETCO2 as a routine vital in monitored units, but probably not soon enough.

So in our unit at Santa Cabrini Hospital in Montreal, we’ve had this technology for about a year (the INVOS system), and have been studying its uses. In this time, three applications have stood out:

  1. Finding the “Sweet Spot” for vasopressors.
  2. Confirmation that therapeutic interventions are hemodynamically appropriate.
  3. Cardiac arrest: CPR adequacy, prognostication and detecting ROSC.

 

  1. Finding the “Sweet Spot” – I think (hope) that anyone reading this with professional interest understands that pressure does not necessarily equal perfusion.  With that in mind, adjusting vasopressors to a pressure makes little sense, and represents at best a guesstimate of perfusion, which is what we really are after. We can all agree, however, that a certain minimum pressure is required, but whether that is 65, 55 or 45 MAP no one can say for sure.  So the way I like to use it is to establish a baseline and watch the direction of the tissue saturation with vasopressor therapy. If the saturation begins to drop off, we may have reached a point at which excessive vasoconstriction is worsening tissue perfusion, and that inflexion point may represent the upper beneficial limit of the vasopressor – this may happen to be under 60 or 65 of MAP.  However, it is key to understand that this inflexion point is reflective of the current state of hemodynamics, such that a change in volume status or cardiac output, in one direction or the other, would likely change the position of this physiological point.  For example,  a volume depleted patient may reach a decreasing tissue saturation point at 55 MAP, but, once volume replete, may reach a higher MAP of 65 or above before a drop in saturation is seen.  Conversely, a patient whose best tissue saturations were around 65 MAP who suffers an MI and sudden drop in cardiac output may now see his perfusion compromised at that same MAP, which would now be achieved with a greater vasoconstriction, less cardiac output and consequently, poorer flow… I posted a case discussion which illustrates this.
  2. Confirmation that therapeutic interventions are hemodynamically appropriate – I feel this is really important. When a patient’s life is literally on the line, and knowing that our interventions are seldom without potential nefarious side effects, it is poor medicine to be introducing a therapy without having some form of monitoring – preferably multiple – that we are headed in the right direction, or at least not making things worse. Of course, we already do this – with BP, sat, lactate, CCO, ultrasound, ETCO2 – but I think using a realtime measure of tissue saturation adds to this. It is also my firm opinion that integrated, multimodality monitoring is necessary – at least until someone develops some form of mitochondrial monitoring which tells us that the cytoenergetics are sufficient to survive. Until then we are stuck with surrogate markers and many of them (e.g. lactate) are the result of complex processes that preclude them being a simple indicator of perfusion adequacy. For instance, when giving a fluid bolus/infusion – after having determined that the patient is likely fluid responsive AND tolerant – one should expect to see an increase in ETCO2 (other parameters being constant), an increase in CO, an increase in NIRS values. The absence of such response should make one reconsider the intervention, because without benefit, we are left only with side effects.

Here is a patient’s cerebral (top) and and somatic (thigh – bottom) and CO values. This patient had an RV infarct and was in shock.

IMG_7948IMG_7946

 

Following initiation of dobutamine, this is what occurred:

IMG_7951IMG_7949

Given that we cannot always predict the response to an inotrope – depending on the amount of recruitable myocardium, it is reassuring to see an improving trend. This enabled us to decrease the vasopressor dose significantly.

Note that, so far, and unless some good evidence comes out, I don’t use a goal value, and so far, I have not identified a value that is predictive of prognosis. However, downward trends usually bode very poorly. For instance, I had a severe chronic cardiomyopathy patient whose cerebral saturation was 15%!!!  But more surprisingly, she was awake, alert and hemodynamically stable. Adaptation.

Part 2 and the stuff on cardiac arrest coming soon!

Please, anyone using NIRS in shock, share your experience!

 

cheers

 

Philippe

A Bedside Ultrasound Case & Poll: All Infiltrates Are Not Created Equal. #FOAMed, #FOAMcc, #FOAMus

So I get an early morning call from a really good ER guy informing me of a likely ICU admission: a young guy (30’s) with a bilateral pneumonia and fever whom he suspected might get worse before he got better. He’s given him some fluids and started ceftriaxone and azithromycin. Sounds good to me. Sold. I tell him I’ll come take a look as soon as I roll into work (we do home call).

An hour or so later I head to the ED and see a him, in bed at 30 degrees or so with nasal prongs, maybe a little tachypneic but certainly not in severe distress and not particularly toxic. The nurse informs me that his temperature was apparently 40 degrees. The CXR (I’ll try to put it up soon) shows bilateral infiltrates, more predominant in the lower two thirds of the lung fields. WBC is 14, lactate 2.3.

So this guy had been short of breath for about 2 weeks, having some cough and localized left sided pain associated with movement, cough and pressure. The cough was non-productive.  As I was getting this history (yup, generally bedside ultrasound is simultaneous with history-taking for me), this is what I see:

(parasternal long axis)

(parasternal short axis)

(right lower costal margin)

(you can see this in most of the lung fields)

He has no past medical history or notable family history, drinks occasional wine, has not traveled of late and works as an electrician. He is active and played soccer – the last time a few weeks ago. He came to the ED for dyspnea, but had still been able to go up several flights of stairs, albeit with more dyspnea than he normally would have.

 

 

 

check back tomorrow and let’s see what happens!

 

cheers!

 

Philippe

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

Bedside Ultrasound Clip Quiz: The Incidentaloma! #FOAMed, #FOAMcc, #FOAMus

Ok, so in the process of doing a little bedside ultrasound teaching, I was scanning this lady in the ER who was being worked up for urosepsis. She had been previously a little hypotensive, apparently, and had gotten some fluid boluses, but was not looking quite comfortable with a BP of about 90 systolic.

So her IVC was pretty normal, about 10-12 mm with visible respiratory variation.

Then I saw something funny in the parasternal views (short axis at the level of the aortic valve)…

 

 

 

Any takers?

Hint:  as I scanned around the patient for the possible cause of this, I noted a pressure bag hanging with an empty bag of NS (argh! NS!)… Really empty. I mean, not a drop left in the tubing…

 

Scroll below.

 

 

 

 

 

This is iatrogenic air embolism.  You can see the bulk of the air is in the RA (left side of the screen), and air bubbles make it into the RV (inflow-outflow) at the top, and some into the PA (curving to the bottom right).

This is not elegant. There is always some air in the drip chamber, so, especially on a pressure bag, an IV bag can’t be allowed to be totally empty…

When we agitate saline to do a bubble study, you get a few seconds of bubble persistence. In this case, two separated examinations about 10 minutes apart revealed little or no change.

Fortunately for the patient, the amount if air is not really enough to cause pulmonary vascular obstruction, as you generally need upwards of 150cc to cause an arrest, and, as we can see by the normal IVC/RV, there was no evidence of even pulmonary hypertension.  I left her in the left lateral decubitus position and she remained monitored, recovering uneventfully. I’ll review the management of venous air embolism in the next post!

Here is another clip, a bit of a reverse and hybrid parasternal short axis view but for some reason gave me the best images:

 

cheers

 

Philippe