#FOAMresus Case from Amand Thind (@Thind888)

So #MedTwitter is truly an incredible forum for case discussion, where you get to exchange with literally some of the best medical minds on the planet who often also happen to be front-line clinicians in the nitty-gritty therapeutic decision-making. Here’s a discussion which I think was great. Recently, Dr. Thind has been generating some great cases and hemodynamic discussions. I thought this one was worth highlighting!
Dr Thind is an internist and currently Critical Care Hospitalist (and upcoming ICU fellow) at the Cleveland Clinic, and tweets out some great #FOAM from @Thind888 on twitter.
Case:
OK, let’s give this a shot. Here’s a ‘hemodynamics special’. Saw this case a couple weeks ago. A lot of decision making was based on educated guesses so it should be a good one for discussion. – 51 yo woman being worked up on the floor for chronic diarrhea, moved to ICU for hypoxia.
Dyspnea progressed over few hours. Vitals significant for tachycardia (140s) and hypotension (MAP in low 60s). On arrival, SBP 60s – improved with fluid bolus. CXR attached. Patient has H/O of pericardial effusion for several months that has been managed conservatively. 
The patient has an official ECHO performed on arrival in ICU (images attached). IVC difficult to assess but about 2cm without collapse. Lung US – diffuse B lines. 
OK so right there a flag goes up for me. A plethoric IVC means something is wrong. Sounds too vague maybe, but you need to find the reason for this, as it likely has therapeutic implications. Let’s see what comes up.
Modifed A5C.
LVOT doppler

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CXR

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Pressing questions –
(i) Is it hydrostatic or increased permeability pulmonary edema?
(ii) Fluids, diuresis, or none?
(iii) Would CPAP help?
(iv) Drain the pericardial effusion?
(v) What about that LVOT doppler? 
Mitral inflow velocities and TDI attached. M-mode through PLAX almost uninterpretable. Lung infiltrates are new so less likely lymphangitic carninomatosis. Note: ScVo2 = 40s. Another Q to ponder on –
(vi) Is tamponade typically associated with hydrostatic pulmonary edema?

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Perhaps this slowed up (0.5x) A3C loop will help with that LVOT doppler!

Great discussion as expected. Lets discuss:
Q4. Is it tamponade? – This is not a slam dunk. Chamber collapse can sometimes be controversial. In these situations I try my best to get MV E-wave variation. I think our tech got a decent signal. But note these are fused E/A waves.
The first thing I look at to screen for tamponade is the IVC. Tamponade is an obstructive form of shock, dependant on the intrapericardial pressure exceeding the right atrial pressure. If it does, unless respiratory efforts are extreme, the IVC should become plethoric. Hence, the absence of such would make the effusion – given the current RA pressure – NOT tamponade. Yet again, another point scored by the IVC for usefulness.
Although I don’t see why we can’t use fused waves for this purpose (couldn’t find anything on it in the literature). Note that in spite of the cardiac motion, the mitral inflow variation is <25% (~23%). It’s close though, and certainly seems to have increased from 3 days ago.

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The cardiologist (understandably) was non-committal and read it as “possible early tamponade”.
Q5. What about LVOT doppler? A good M-mode could not be obtained but the A3C in 6/ shows SAM. The report mentioned “chordal SAM” but I think you can clearly see “valvular SAM” too.
Chordal SAM is SAM of the chordal apparatus (you could see it bumping against the septum in 6/). It is (typically) NOT hemodynamically significant (PMID: 27241937). – When we see mitral SAM, it is important to quantify its hemodynamic effects – with LVOT peak gradient via CW.
In HOCM, DLVOTO is defined by an LVOT gradient of >30; >50 is considered severe. Our patient had a gradient of ~70. Although classically a/w HCM, SAM can be seen in anyone with thick, hypercontractile, underfilled LV. Tachycardia further hampers LV filling (PMID: 27726435).
Mitral SAM is often a/w MR – this acute MR can cause flash pulmonary edema. These patients may actually need fluids (to help with SAM) to fix there hydrostatic pulmonary edema!! (PMID: 20661209). However, our patient only had trace MR (you could see it in 1-2 CD frames).
Working theory (similar to Lars) – Chronic stable pericardial effusion –> diarrhea (pt had 15 BMs the day before the admission) –> reduced venous return –> brought the patient at the verge of low-pressure tamponade (PMID: 16923755) –> further reduction in LV filling  —> reduced stroke volume –> adrenergic drive causing tachycardia and increased inotropy –> all factors culminating in mitral SAM and DLVOTO.
This also explains the low ScVO2. Note – CPAP would further reduce venous return (Q3) so wouldn’t help, may hurt.
Now the most important Qs: why pulmonary edema and what to do about it (Q1 and 2). As tamponade causes impedance to venous return, it is not typically associated with high LAP and hydrostatic pulmonary edema (Q6).
But first, let’s check out another CW tracing. Any thoughts?

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This is a CW beam through LV apex and mitral valve – typically performed to assess mitral inflow and MR velocities and is part of the standard ECHO exam. However, the tracing is not typical for MR (late peaking, dagger shape). Remember, CW does not have depth resolution.

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This is likely mid-cavitay/intra-ventricular obstruction. This is caused by complete mid-systolic obliteration of LV cavity (see PSAX) causing obstruction to the apical systolic flow. Again, seen in hypercontractile, underfilled, thick LV – e.g. sepsis (PMID: 26082197).
Finally – what does the ECHO tell us about LV filling pressures? – E/A ratio: As Lars pointed out, an E/A < 0.8 usually means normal LAP. However, the exception to this is sinus tach. This was shown in a study by none other than Dr. Nagueh (PMID: 9778330). (Also, see image)

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The idea is that when early filling (E) is incomplete due to short diastolic time, the LA remains “full” at the time of the atrial kick – causing higher A velocities. NB: In that paper, E/E’ > 10 had a specificity of 95% for elevated LAP in ST. In our case: E/E’ = 75/5 = 15!

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Potential contributors of high LAP – (i) SAM-associated MR – ‘trace’ in this ECHO but maybe we didn’t catch it. (ii) Tachycardia – E’ is 5 suggestive of delayed relaxation. Tachycardia causes “incomplete relaxation”. (iii) High afterload – high-grade dynamic obstructions.

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So at this point, it’s still contentious but I have my money on hydrostatic pulmonary edema. Will detail our interventions and the remaining course in a bit. …Sorry to make this long but I think it’s worth it!
Now for the home stretch, the remaining course: We realized pericardiocentesis may be required soon but wanted to see if volume helps with (i) Peri-tamponade (ii) Dynamic obstructions. It helped a little – O2 requirements went from 60% HF to 6L NC. BP okay but still tachy.
Day 2: We pushed 2.5 mg metop x2 with concurrent ECHO. LVOT gradient improved from 70s to ~10! (I did not compare mid-cavitary gradient, apologies). Started on 25 bid of PO metop later that night. HR now 90s Day 3: Official ECHO shows improved but persistent gradients.

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Evaluation of tamponade was similar to previous ECHO but E-wave velocity variation now 38% –> elective pericardiocentesis: 550 cc removed. Fluid was transudate We also tapped a small pleural effusion pocket: transudate, cx negative (again goes with hydrostatic pulmonary edema).

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Day 3 (contd): inc metop to 50 Q12H to blunt the gradients.
Day 4 – HR in 80s. ECHO shows no DLVOTO and non-significant mid-cavitary gradient. Oxygenation improved but still not normal. Why?! Check the E-velocity post-pericardiocentesis: it has jumped to 120 with E/A > 1.

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So why is the LAP still high despite no significant dynamic obstruction? – Patients with chronic pericardial effusion may have chronically impaired diastolic filling –> low output –> volume retention (basic CHF physiology). When pericardial restraint suddenly released ––> increased LV preload –> high LAP.
Originally discussed elegantly here: PMID 6877287.
This is especially true if the LV has some baseline dysfunction. Day 5 – We started diuresis! The obvious risk was to precipitate the dynamic obstructions –> metop increased to 50 Q8H.
Day 7: Excellent diuresis (~2-3L negative per day). Hemodynamics stable (SvCO2 normal). Resting HR 60s – 70s. Follow-up ECHO confirmed no dynamic obstructions (see image). Day 8: Finally on room air. Pulmonary infiltrates improved (image). All cx remained negative.

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Some dogmalysis offered by this case – – Fluids (probably) helped the pulmonary edema; CPAP/diuresis may have worsened. – IV metop contraindicated in hypotension? Not in this case – Sometimes you may have to diurese someone who recently had DLVOTO, as discussed above.
This case highlights the cognitive flexibility required to deal with hemodynamic puzzles. One thing I would’ve done different is be more aggressive with metop early on as it made a huge difference with DLVOTO. This was quite a ride. Hope you had fun. Feel free to share! 
Much kudos to the treating team, I think this was excellently managed. As Amand says, cognitive flexibility ias absolutely key in assessing hemodynamics, particularly in the grey zones when multiple processes occur and co-exist. Managing this type of case using a recipe-based approach and without POCUS could have let to a poor outcome. 
Now the POCUS used in this case is on another level. Very impressive and allowing incredible insight and certainly many potentially clinically useful Doppler analysis tips for LVOTO and LAP assessment. 
In the end, I think that there were three pathologies, (a) tamponade physiology, (b) dynamic LVOTO, exacerbated by (c) hypovolemia (diarrhea)  I might have approached this differently, had I seen a truly plethoric IVC. In such a case, one can easily see how tamponade physiology would contribute to LVOTO in two ways by creating intracardiac hypovolemia, hence worsening LVOTO both by decreasing LV preload and by the compensatory tachycardia. My first approach would probably have been to drain the pericardial effusion, and reassessing the hemodynamics afterwards, but correcting the intravascular deficit was necessary.
The other important thing this case re-emphasize is that tamponade is not a static diagnosis but a physiological spectrum. For the same given effusion (read intrapericardial pressure – IPP), it is the RA pressure that will determine whether overt tamponade develops. In this patient, it is very likely that a day earlier, there was no frank tamponade, but that after some diarrheal volume loss, the RAP dropped, and now IPP > RAP.  It is important to know this because if you have an effusion and a fairly full IVC, one needs to be very careful with anything that can drop the RAP, meaning diuretics and vasodilators, because these can easily turn pre-tamponade into overt shock.  And, as this case illustrates so well, you might even end up with LVOTO and pulmonary edema!  Which is one of the myriad reasons one should have a basic POCUS exam in every acutely ill patient. These are things a resucitationist needs to know and prepare for.
cheers and thanks again to Dr. Thind!
Philippe

H&R2020: The Hospitalist Course. #Hresus20

As with all continuing medical education events, this one will make you a better physician. But we know who you are: It’s 2am. Your pager is blowing up. You go to the floor with 3 simultaneously crashing patients. We’ve all been there. As a result, we’ve collectively designed this educational event to bring together an ultimate think-tank on how to improve your clinical management of all those things that make us scared at night, and even in the day… If it’s an organ that can fail, we’ve got you covered for a solid, easy, memorable approach to how to support it.

Mixed throughout the day will be cases to solidify your newly acquired clinical pearls & hands on stations with all the toys you need to stabilize your patients.

Hosted by The IBCC (Internet Book of Critical Care) co-creators Adam Thomas and Josh Farkas – also the man behind PulmCrit – this is going to be jam-packed with physiology, clinical pearls, interactive and case-based. If you take care of patients on the wards, this is one not to miss.

Co-directors: Adam Thomas & Josh Farkas.

PRELIMINARY PROGRAMME

Hypotension on the wards – Adam Thomas reviews the physiology of shock, the use of invasive & non-invasive monitoring, POCUS & “how your radiologist can help”, initial stabilization (hint, it is not just giving fluid), the hunt for & elimination of hypovolemic, cardiogenic, obstructive shock & distributive shock, as well reviewing the role of hormones and regulatory cytokines as well as how this can potentially be modulated.

Recognizing Illness at a Glance – in this interesting talk, Daniel Kaud shares his data-linkage and pattern recognition skills on common but important pathologies, to help clinicians develop rapid muscle memory and make elusive diagnoses.

Initial stabilization of respiratory failure – this can be one of the most harrowing and time-critical clinical scenarios facing the hospitalist, before the critical care team can take over or the patient can be transferred. Adam Thomas takes participants thru the identification of respiratory failure, the rule of 2s in type & treatment of respiratory failure and the right tools for the job on the wards.

Managing the Congestive Heart Failure Patient – here, Philippe Rola introduces a physiologic and POCUS-based approach to the management of the admitted CHF patient, particularly with the management of effusions and venous congestion.

Physiologic approach to Renal Failure – nephro-intensivist Sharad Patel drags the management of this common disease into this century and will share a rapid approach based on evidence, physiology and the efficiency that POCUS brings to bedside diagnosis and clinical decision-making.

The Biliary patient – whether neoplasia or lithiasis, these patients are often real puzzles. Echo? ERCP? MRCP? Drain? Stent? Fever? Jaundiced?  Let’s lay down a solid base for approaching these before calling for the GI SWAT team.

Cirrhosis for the Hospitalist – in this one, hepatologist Ahn Le reviews the most pertinent pearls related to the care of patients with cirrhosis, such as managing encephalopathy, ascites, coagulopathy and more.

ID pearls – microbiologist extraordinaire Silvana Trifiro runs us through some interesting cases to make sure we don’t overlook sometimes subtle symptoms and signs of unexpected infectious diseases.

Neuro pearls – Jeff Scott shares some interesting cases highlighting key elements of the examination and management of neurological emergencies.

Wound Management – microbiologist Marc Laroche sheds some light into what is for most of us a nebulous topic, and provides a thorough, but simple and practical approach to the dressings and management of the various wounds that hospitalists come across.

Lytes, a Pot-Pourri – Josh Farkas, inventor of the “Nephron Bomb,” brings his unique, hard-hitting physiological approach to electrolyte management.  This is the thinking doc’s approach, not a check-the-box one.

Clinical Cases – tying everything together, Sharad Patel, Adam Thomas, Silvana Trifiro and Josh Farkas will discuss several cases bringing together several of the key concepts and skills explored during the day.

WORKSHOPS:

  • Airway: sharpen your airway skills with BVM technique, intubation, and for the bold, emergency surgical airway! Never know when you’ll need it!
  • POCUS – assess the IVC and basic cardiac views for hemodynamics, assess kidneys and bladder as part of your AKI workup, assess lungs for B lines and effusions. These abilities are sine qua non for acute care at any level.
  • Non-invasive Ventilation – learn how to setup and check high-flow nasal nasal cannulae, cPAP and BiPAP for your hypoxic patients.
  • Pleural pigtail catheters – a simple, but important skill that should be in the skill set of all hospitalists.
  • …and more on request!

 

We reserve the right to make the programme even more awesome by adding to or modifying the above, and promise you’ll come out of this one with a few extra notches on your belt!

But wait…only 30 spots. So don’t wait till the last minute!

click here to register!

Hope to see you there!

…and of course, if you stumbled on this, do make sure to check out the main event, H&R2020!

Adam, Josh, Philippe & The H&R2020 Team.

H&R2019 Lecture Series: Denault on POCUS and Delirium! #FOAMed, #FOAMcc

So the pundits still try to claim the lack of evidence for the use of POCUS, bla, bla bla. Just wait till they get a load of this: POCUS in delirium? Master Andre Denault introduces us here to a completely new way of assessing a little known potential aetiology of acute delirium.

 

Here it is, certainly one of the most interesting and forward-thinking lectures of H&R2019:

Denault on POCUS and Delirium.

 

 

 

Don’t forget The Hospitalist & The Resuscitationist H&R2020 is happening May 20-22 and registration is open! Seating is limited…

cheers!

Philippe

A few words on venous congestion, thresholds, and physiology. #FOAMed

 

So I’m really glad to see that recently, a lot of discussion has been taken place on the topic of right sided failure and venous congestion, which has huge clinical applications. Even more so, the fact that a lot of individual practitioners have taken this on and have been applying it clinically with physiological results is really amazing.

So a common question that has been popping up revolves around clinical thresholds of significance, and I thought it was worth clarifying that we need to stay away from a pure threshold approach, but rather try to embrace a holistic cardio pulmonary and whole body assessment.

So here’s my two cents:

Thank you, love to hear any comments!

Philippe

ps obviously, this type of discussion will be what H&R2020 will be chock full of!

 

H&R2019 Lecture Series: Felipe Teran on Intra-Arrest Hemodynamics! #FOAMed, #FOAMcc

Here is an awesome lecture by Felipe Teran from this year’s H&R:

 

 

In resus, there is no one size fits all.

 

 

For anyone who missed H&R2019, you can still catch the Essentials!

 

 

But more importantly don’t forget that registration for H&R2020 is now open!

 

cheers!

 

Philippe

The Resus Tracks: Josh Farkas on Sepsis Metabolic Resuscitation and the CITRUS-ALI Study. #FOAMed

 

So metabolic resuscitation is a topic that both Josh (@Pulmcrit) and I are really interested in. We were looking forward to the CITRUS-ALI study. The results, to me, are good. They continue to establish the fact that there are no real side effects, particularly renal, as this was a concern to some (despite the already large data sets – particularly in the Matsuda study), and in an even higher dose than the Marik study.

Of course since the study was not designed to show a mortality benefit, it wouldn’t be clean to tout their results from that angle, but it certainly should be hypothesis-generating (imagine the cheers from the pundits who would certainly have used it in reverse had the mortality been increased instead!!!).  So for me, it changes nothing, because – if my institution hadn’t decreed (for no legitimate reason I can see) that I cannot use it in patients that I feel would benefit – I would still use it as an adjunct to septic shock management.

There are more studies around the corner, and hope they will come out before next may, so that Josh can give us an update for H&R2020 (#Hresus20)!

Here is our chat:

 

cheers

 

Philippe

H&R2019 Lecture Series: Weimersheimer (@VTEMsono) on Massive Transfusion. #FOAMed, #FOAMer

Sorry for the delay, been bogged down in getting H&R2020 off the ground! But here is another goodie from H&R2019, my good friend Peter W. on an ever-important trauma topic.  Enjoy!

Weimersheimer on MT – H&R2019.

 

cheers

 

Philippe

ps for anyone interested, H&R2019 On Demand can be found here!