The Resus Tracks: Trans-Pulmonary Dilution Catheters in the ED…myth or reality? #FOAMed, #FOAMer

So anyone who knows Korbin (@khaycock2) realizes he is a true trailblazer in the ED, essentially doing cutting edge critical care from the get go in his shock patients. In my mind this should be the goal for any critically ill patients, that they get the highest level care right at entry and for however long they may be staying in the ED until they get to the ICU.

So today, I was really happy to corner Korbin lounging somewhere in sunny California (as 6 inches of snow come down hard in Montreal) to tell me how he is using this technology in his resus patients.

 

 

So this has got me interested in using this technology. I see it as an early warning signal that your patient may be less fluid tolerant than you may think, and that the signs of pulmonary fluid intolerance I use (oxygen requirement, appearance of B lines (FALLS Protocol-style), etc…) have yet to manifest.

So I’m looking forward to hearing Korbin explain this further (during H&R2020!) and in actual cases where the change in management is clear.

 

cheers

 

Philippe

 

 

 

 

#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

RV Doppler: Resistance vs. Back Pressure. Jon-Emile Kenny & Korbin Haycock! #FOAMed #FOAMer #FOAMcc #POCUS

So I’m still trying to digest the RVOT Doppler physiology and working my hand at generating the best views and Doppler angles I can (See previous post on RVOT Doppler here). Not sure yet how this will fit in to my clinical practice but I think it’s worth shining a light into this murky pseudo-science of resuscitation. These guys are helping define its potential use… Naturally, this is bleeding-edge stuff. Use it to try to understand what’s going on with your patient’s physiology, don’t use this on board exams! My comments in bold.

Now for the big guns…

 

Jon-Emile Kenny (@heart_lung), pulmccm.org, heart_lung.org

Hey Guys – great discussion as always!
One thing that I find confusing on this topic, and is helpful – i think – when scrutinizing the literature, is the difference between ‘impedance’ and ‘resistance.’ Elevated vascular ‘resistance’ is often used too broadly; for example, true/pure WHO II pulmonary venous hypertension [say from acute left atrial pressure hypertension, but before chronic, compensatory pulmonary arterial changes] is actually typified by a *decrease* in resistance, but an increase in *impedance.* To make things more confusing, acute left atrial hypertension will often display a high “resistance” mathematically … even though, the true resistance can be low. What am i saying? if you imagine an acute increase in the left atrial pressure, the pulmonary venous beds and pulmonary vascular beds “recruit and dilate” backwards [why we see cephalization on the CXR] typically from the bottom to the top of the lungs up the hydrostatic gradient. Recruitment and dilation actually *increases* the cross-sectional radius/area of the vascular beds — a true decrease in resistance [Poiseuille what?]! But, as these vascular beds are engorged, they reach that infamous, hockey-stick-shaped compliance curve point [go leafs go!], where the vessels become really stiff … that is, the compliance falls such that each ejection the RV throws into this dilated circulation, the pressure rises dramatically [especially the systolic pulmonary pressure] …

This I think is a key concept to understand and keep in mind when analyzing the venous system. The physical characteristics are more akin to a floppy plastic bag or balloon, with little rise in pressure until a certain point, then a sharp one – Jon’s “hockey stick.”  It was Jon who made me realize that, with exposure to chronically elevated right atrial pressures, one could have a very big IVC (say 25-30mm, but in fact a low CVP, whereas in normal IVCs exposed to normal CVPs, that sharp rise in pressure probably occurs somewhere around 20mm. Hence, the + value we use in the PAP calculation using TR Vmax for the RAP may be very inaccurate in chronically elevated PAP… Food for thought.

Thus, the calculated pressure gradient rises and and the calculated resistance falls, but what has actually happened is that compliance has fallen, not “resistance”. More broadly, the term “impedance” is composed of compliance, resistance and something called the characteristic impedance [the Windkessels!]. Typically what abnormal RV Doppler shows you is that *impedance* has risen. At the end, you are often still left with the why? Impedance can rise when “true resistance “falls, but compliance also falls [as above] – yet the calculated RVSP/regurgitant jet will also rise. The linked papers are fantastic, but they both excluded patients with left heart disease, so you can be more confident that the RVOT abnormalities seen are related to true ‘pre-capillary’ problems. I’d be willing to bet [and if there’s data, i’d be interested to read it] that patients with pure WHO II pulmonary venous hypertension have very similar abnormalities on the right side. The key means to distinguish – as Korbin talks about – is really looking at the left heart [E/e’] and clinical context to get a better sense of what’s going on.

What would also be interesting would be to look at acutely “decompensated” true left heart disease in volume overload and correlated with RVOT morphology and great vein Doppler velocimetry. My guess is that as you decongest the pulmonary veins [increase their compliance] that the RVOT envelope “pulsatility” goes away [the RV ejection envelope appears more rounded] as does the venous pulsatility in the great veins and intra-renal veins! It’s all about energy transfer … moving away from excessive potential energy trapped in distensible structures [i.e. congestion] to kinetic energy [normal, forward blood flow]

Jon.

 

Korbin (@khaycock2)

Thanks for the reply Jon-Emile, as usual you bring an incredible amount of intelligent well thought out points.

As you mentioned, afterload is much better described in terms of the 3-element Windkessel model as resistance is only one component of said model (the other factors being vascular compliance and characteristic impedance). Please correct me if I’m wrong, but I believe that the most practical and easiest way to non-invasively determine arterial load is to calculate the Ea (formula: (SBP*0.9)/SV). This would include all of the factors that determine afterloading conditions instead of simply using resistance as it is only one of those factors.

Clinically speaking, I think it is important to address why afterloading conditions are abnormal when we come across undifferentiated pulmonary HTN in the acute setting. Practically in my mind, this is simply finding if the pHTN is due to post-capillary “back pressure” from elevated left atrial pressures or due to elevated pre-capillary pulmonary vascular resistance (or could be some combination of both of course). Both of these conditions can cause elevated pulmonary artery pressures, as you have pointed out, and there are a few other contributors to the afterload as well that we are ignoring (or else we’d blissfully nerd out all day and forget to take care of the patients).

I agree with this concept. This is what may direct me to use pulmonary vasodilators, whether inhaled or even the choice of milrinone or vasopressin (not a vasodilator per se but a non-pulmonary vasoconstrictor). If all the pulmonary hypertension is post-capillary, there would be little or no benefit. This important decision point is what prompts me to look into this whole right-sided Doppler thing… Let’s see what else Korbin has to add! 

So how can find out the cause(s) of the elevated PAP? Is it resistance or back pressure from the left atrium? This is essentially the topic of the post. Because PVR=(mPAP-LAP)/CO, it has been suggested that the TR gradient can be a surrogate for the mPAP-LAP and RVOT VTI be a surrogate for CO. Thus if the ratio is high, we can assume that a significant component of the pHTN is due to resistance in addition to or to the exclusion of the contribution of LAP. You have rightly questioned and very well explained why you wonder if these are valid assumptions that translate to the finding the clinical causes of pHTN.

You pointed out that the cited papers in the post excluded patients with LV failure, thus bringing into question if the TR/VTI ratio methods and their permutations are actually detecting PVR as the primary etiology of the pHTN or are corrupted by elevations in LAP. Here are 3 papers that included a significant number of patients with pHTN and elevated PCWPs as measured by RHC that show that the TR/VTI methods do seem to work to detect PVR elevations themselves even if the LAP are high:

1) Am J Cardiol. 2013 September 15; 112(6): 873–882. doi:10.1016/j.amjcard.2013.05.016.
2) J Am Soc Echocardiogr 2013;26:1170-7.
3) J Am Coll Cardiol 2003;41:1021–7.

Somewhere in my files I have a study that shows that the mid systolic notch is fairly specific for high PVR and independent of LAP as well. but apologies, I’d have to look for it.

As I might have mentioned in the audio portion of the post (I can’t remember), there is a second method to flesh out PVR from LAP causes of pHTN. First, you need to find a good estimation of the LAP. ECHO has multiple ways of various accuracies to get a number. The formulas are listed above. I don’t believe any of them are validated in acutely sick patients though. Once you have a LAP number, turn your attention to the pulmonary valve regurgitant jet which will almost always be there if there’s pHTN. The wave form is sort of down-sloping trapezoidal lasting through diastole. The velocity at end-diastole can be squared, multiplied by 4, then added to the RAP to give you the end-diastolic PAP. This is normally < 6 mmHg higher than the LAP pressure measurement, if it is a bit more higher, there likely is increased PVR. This is the same principle used in a RHC, where the inflation of the balloon stops flow and therefore eliminates resistance so that the PCWP can be measured and differentiated from the dPAP. The problem with this method is that it doesn’t work as well as the TR/VTI methods

I really enjoyed your thoughts about how Doppler waveform patterns may be affected once compliance limits have been reached, and I’m sure there is something to this that is real as well no doubt! I thought it might be helpful to provide you with the additional studies that included the patients with high LAP, and do a bit of re-explaining/restating your points to anyone new to this stuff.

Thanks again Jon!

Jon replies:

Hey Korbin – thanks for the references – I’ll dig into them. My main concern is that the mPAP-LAP will disproportionately rise (mostly because the sPAP disproportionately rises) when the left atrial pressure is high … that is when it’s actually not a “resistance” problem but rather a back pressure problem, the mathematical resistance is high. As you mention, this is why there’s a push to move away from “PVR” with RHC and more towards the dPAP-PCWP gradient which should be less than 6 mmHg. I made a cartoon describing this in an old post (https://pulmccm.org/critical-care-review/icu-physiology-1000-words-folly-pulmonary-vascular-resistance/). Thanks for these references, I’ll read them and see if they make sense from the framework I’ve adopted – which is entirely stolen from this great article

Naeije, R., et al., The transpulmonary pressure gradient for the diagnosis of pulmonary vascular disease. Eur Respir J, 2013. 41(1): p. 217-23.

Maybe Phil should do a point-counterpoint podcast where Rory comes in at the end and shakes his head because nothing really matters in the end.

“Nihilism rules…”

Jon

Korbin:

Thanks Jon, I would like to see what you think. Thanks back at you for the reference you mentioned in your reply. And you’re hilarious!

Jon replies:

I had a read of the references that you provided, thank you. I think my concerns still apply, however. My main concern is what is being used as the gold standard for ‘pulmonary vascular resistance.’ An elevated calculated pulmonary vascular resistance (e.g. in WU) doesn’t actually tell you where the pathology is. the assumption is that an elevated calculated pulmonary vascular resistance is caused by a high pre-capillary resistance in the pulmonary circulation, but this isn’t necessarily true. as i showed in that post that i linked to (https://pulmccm.org/critical-care-review/icu-physiology-1000-words-folly-pulmonary-vascular-resistance/) … if one were to acutely cross-clamp the descending aorta, below the diaphragm, the calculated pulmonary vascular resistance would rise, even though the pathology is totally outside of the thorax!! i have no doubt that the TRV / RVOT-VTI would also rise in that very same patient with the cross-clamped descending aorta such that the good correlation between the calculated ‘pulmonary vascular resistance’ and the TRV / RVOT-VTI is maintained – but the pathology is in the abdomen – not the pulmonary vascular tree! So many exclamation marks; but i’m not yelling. In a hypothetical patient with a cross-clamped descending aorta, one might be tricked into giving a pulmonary vasodilator — but that would be the absolute wrong thing to do, even though the calculated pulmonary vascular resistance is high. The treatment is to afterload reduce the struggling LV (remove the cross clamp) — which would then lower the calculated “pulmonary” vascular resistance and the TRV / RVOT-VTI.

the problem in reasoning lies in what happens with the left atrial pressure rises (as would happen if one acutely cross-clamped the descending aorta). it is assumed that as the LAP rises that the mPAP – LAP gradient stays the same or rises in proportion. but what happens when the LAP rises is that the mPAP rises disproportionately because of pulmonary vascular engorgement/stiffening (in fact, the pulmonary vascular resistance has fallen because of recruitment and dilation of the pulmonary tree). what *does* rise in proportion is the dPAP – LAP gradient [should stay below 7 mmHg]. i strongly suspect that the ability of the TTE to detect/calculate the dPAP – LAP gradient is not yet refined enough because there is a lot of supposition and inference when making dPAP and LAP measurements with pulsed wave Doppler.

alas, with either an elevated TRV / RVOT-VTI (or calculated pulmonary vascular resistance from a RHC), one still doesn’t know if it’s purely a left-sided problem (e.g. purely elevated LV afterload) – which could seriously alter management. to know that, i think that a full interrogation of the left heart and pulmonary veins must be done before knowing exactly what an elevated TRV / RVOT-VTI specifically identifies. in addition to that vascular resistance post above, i dug into some more of this in a discussion on the SIOVAC trial a while back (https://pulmccm.org/randomized-controlled-trials/choose-wisely-avoid-sildenafil-pulmonary-hypertension-corrected-left-heart-valvular-disease-siovac-trial/) – which, in my opinion, should never have passed ethics.

Jon

So this is really fascinating stuff. I must admit both Korbin and Jon make excellent points, and for now am not sure if and how to use RV Doppler in clinical decision-making, but until then will be sure to polish up these skills so that they are ready for prime time, and use them in observation of physiology in my shock patients. We’ll see what conclusions I draw.

cheers

 

Philippe

Exploring the Pulmonary Vasculature with Korbin Haycock: RVOT Doppler. #FOAMed, #FOAMcc, #POCUS

So some recent twitter discussions, particularly involving my friend Korbin (@khaycock2) and Lars (@LMSaxhaug) – whom I am trying to get on the podcast soon – were really fascinating in regards to RV and pulmonary hypertension assessment. So time to dig into this a little.
The basic POCUS RV assessment is RV:LV ratio and TAPSE, along with RV free wall thickness (should be below 5mm) and the D sign in parasternal SAX. This is a solid start to screen for significant RV dysfunction.
The next level should be to measure PAP using TR Vmax, in order to assess the degree of pulmonary hypertension. Thats pretty much where I’ve been at for the last few years and wasn’t sure there was really a lot more that was necessary from an acute care standpoint where your immediate questions are fluids/pressors/inotropes and some inhalational pulmonary dilators. I wasn’t convinced I needed more.
But of course Korbin and Lars are on another level, and started to talk about doing RVOT doppler and looking at TR Vmax to RVOT VTI ratios to estimate pulmonary vascular resistance. Is there any difference there? Is my PAP not enough? Well, turns out there may be some useful information there, so I will let Korbin do the talking, and my apologies for my dumb questions during this discussion!
So I will be toying with RVOT doppler and trying to see if this is something that warrants a place in acute care management. I suspect it may be something that may tip towards earlier inhaled vasodilator therapy, or else make not using them a more confident choice. I do like the waveform analysis. I think we generally overlook a lot of good info by focusing on numbers over morphology!
So far, images using the PS SAX view have been quite good:
Additionally, RVOT notching could be suggestive of an acute PE – makes sense (study link here!)
Here are a couple of excellent references:
So thanks to Korbin and Lars for forcing me to up my doppler game some more!
cheers
Philippe
Formula Fun:
Tricuspid regurgitation pressure gradient for sPAP:
sPAP=4*(TRvelocity^2) + RAP or
sPAP=TRpg +RAP
mPAP=(sPAP)*0.61 + 1.9
Acceleration time equations for sPAP and mPAP:
sPAPlog= -0.004(AT) + 2.1
mPAP=90 – (0.62*AT)
Pulmonary Regurgitation pressure gradient:
mPAP=4*(Peak initial velocity^2) +RAP
dPAP=4*(End velocity^2) + RAP
dPAP-PCWP should be about <6mmHg or else PVR is likely, see PCWP equations below
PVR equation to screen for increased PVR, or if PVR < 3 WU:
PVR=10*(TRvelocity/RVOT VTI) + 0.16. TR velocity is in m/sec, if <2 WU, no increased PVR.  This equation is accurate up to 3 WU
PVR equations for increased PVR > 3 WU.  These equations less accurate if PVR < 3 WU:
PVR=5.19*(TRvelocity^2) – 0.4, or more simplified: 5 * (TRvelocity^2). Note that the 5 * (TRvelocity^2 is almost sPAP equation (4 * TRvelocity^2)=sPAP
PVR=sPAP/RVOT VTI if no RVOT notch present
PVR=(sPAP/RVOT VTI) + 3 if RVOT notch is present
PCWP equations (for detection of group 2 pHTN to elevated sPAP), as you know, this is a whole other area, and gets a quite a bit more complicated, but to summarize:
PCWP likely elevated if E/e’>15, unlikely if E/e'<8
In NSR, PCWP=1.24 * (E/lateral e’) + 1.9
In ST, PCWP=1.5 * (E/lateral e’) + 1.5
In atrial fibrillation averaged over 5 beats, PCWP=0.8 * (E/lateral e’) +6
Using color M-mode and propagation velocity: PCWP=5.27 * (E/Vp) + 4.6

Venous Congestion from different Clinical Standpoints. #FOAMed, #FOAMcc, #FOAMus

 

So last week sometime we had an interesting twitter exchange which made me realize it is important to explain how some of us are using venous POCUS in different clinical scenarios, which is key, because the development of monosynaptic clinical reflexes with POCUS findings is a rabbit hole we should try not to go down. Instead, POCUS should be about asking the right question and taking that answer as a piece of the pathophysiologic puzzle facing us, which may mean intervening sometimes, and sometimes not, for the same given finding, but with different surroundings.

Here is the twitter exchange.

Thanks to those involved in that discussion – it is how we grow!

And here are some thoughts:

For those not up to speed on venous congestion POCUS I put up the chapter that Korbin Haycock, Rory Spiegel and I worked on in this earlier post.

Here are Korbin’s thoughts on this:

I’m very glad Dr. Eduardo Argaiz pointed this case out, as it brings up considerations apropos both chronic venous congestive cases as well as management of acute illness, particularly in sepsis, where we would expect patients to most likely be fluid responsive, but fluid tolerance is largely overlooked with current management strategies by the majority of clinicians.

Phil’s above audio commentary points out the difference is these two broad categories very nicely. If you didn’t listen to it–you should.

With respect to chronic venous congestive conditions, the knowledge and application of Doppler assessment to therapy will hopefully be the next advance in management at large. Already, I think there is more than adequate research available to show the value of Doppler POCUS (D’POCUS, D/POCUS, or DPOCUS?) in managing these patients. It’s only a matter of clinicians willing to commit to learning and integrate this technology into their skill set.

With respect to resuscitation of the acutely ill patient, there is by far less data, and we are probably into the realm of N=1 here, in terms of how to manage these patients. But, I personally believe–and I understand this is my opinion–that current trends in resuscitation (especially sepsis resuscitation), largely ignores the effect of over volume resuscitation and the potential downstream damage inflicted on our patients.

This theoretical damage of over aggressive fluid resuscitation is multifactorial, including glycocalyx shedding issues/endothelial dysfunction, positive fluid balance and EVLW causing increased mortality (which there is ample evidence for, I think), venous congestion leading to perfusion injuries to encapsulated organs, such as the kidney (AKI) and brain (congestive encephalopathy), and end organ edema leading to the perpetuation of a malignant inflammatory syndrome (portal HTN and gut edema).

In the case called out by Dr. Argaiz, (which can be reviewed by the previous post on this website) my patient had an IVC that whilst not plethoric, was not an IVC that one would expect to find in a patient with a typical distributive shock pattern (i.e. increased cardiac output, decreased SVR, and decreased RAP). Firstly, the complicating factor of atrial fibrillation with RVR was central to the patient’s shock state, however this was quickly addressed with rate control. However, in addition, this particular patient did exhibit additional signs of venous congestion. The portal vein was pulsatile and the intrarenal Doppler pattern was interrupted/bi-phasic in nature. Granted, a pulsatile PV Doppler could be interpreted as related to the hyper dynamic nature of septic shock (as the esteemed Dr. Denault correctly cautioned in his comments on the original post), however a less than flat IVC and the intrarenal findings gave weight to a venous congestive hypothesis as a cause the PV findings as well as a possible cause for his AKI evident on his initial labs.

With this particular case, given my personal global POCUS/FOCUS assessment of his increased LAP (high E/e’), RV dysfunction, RAP, PV, and intrarenal Doppler venous pattern, AND that fact that the RRI was insanely high with an AKI, I elected to treat my hypothetical construct of his renosarca with furosamide and his RRI with vasopressin (as the NE infusion did increase his MAP, BUT NOT decrease his RRI–which the vasopressin infusion did decrease, or so I presume as no other therapeutic interventions were given with respect to the time frame the RRI decreased).

In the end his kidneys had recovered by the next morning, which I’m sure that any intensivist will admit is the opposite of the norm, as the kidneys usually get, at least transiently worse initially-being the delicate sissies/whimps that they are. Whether this was because of the diuretic or the vasopressin, or something else, is debatable for sure, but it sure didn’t get better by 30 cc/kg of crystalloid mandated by CMS, because he got not a drop more than what was needed to push the diltiazem, the lasix, the antibiotics, and the vasopressors.

So to summarize, in the case of chronic cardiogenic venous congestion, clinician realization and adoption of Doppler assessment of this entity will likely be the next leap in improvement in the management of these patients. In the case of acute resuscitation, venous congestion may be a bit more nuanced, and a more comprehensive evaluation is in order in a case by case fashion. However, I think recognition of the issues of over aggressive volume administration will probably be the next frontier in sepsis resuscitation.

 

Love to hear your thoughts!

Cheers

 

Philippe

Another interesting question from @JCHCheung! #FOAMed, #FOAMcc

So here’s another interesting question as a follow up to the previous discussions:

Most people would probably agree that florid congestive signs on POCUS means the RV is unable to pass any more extra volume to the left heart; whilst the absence of those signs mean that the patient may be able to cope with some additional volume without immediately engorging the vital organs.

And my question is: what about those in between? i.e. the patients who start to develop some mild congestive features on POCUS.

For those who are on the verge of congestion, diuresis would push the RV to the left (i.e. steep part) of Starling curve resulting in significant CO drop; conversely, extra volume pushes the RV to the right (i.e. flat part) leading to congestion or even D-shape LV, directly hindering CO as well. This margin becomes even smaller in patients whose RV starts to fail (i.e. entire Starling curve shifted downwards)

Great, great question. The crux of this, I think, is deciding which is the greater issue, congestion or poor perfusion. Obviously they are intertwined, so the decision will be on a case by case basis. Jonathan alludes here to a narrow “balance point” between congestion and preload dependancy. My feeling – and we’ll see if we can get some consensus – is that this indeed narrow in patients with marked pulmonary hypertension. When patients have pure pump failure congestion, my clinical experience is that you can decongest plenty without drop in systemic CO, in fact it often improves, likely related to ventricular interdependance. So let’s go on…

I’ll illustrate my point with the following scenario:

for previously healthy middle aged patients intubated and admitted to the ICU for ARDS from severe pneumonia, they quite often develop some acute cor pulmonale after mechanically ventilated for several days even if the PEEP/driving pressure isn’t exceptionally high; and they usually have resp failure and shock to start with.

Given that they don’t have pre-existing heart disease, the only signs suggesting the emergence of cor pulmonale could be subtle, without structural changes like dilated RV (RVEDD at most at upper normal range) nor abnormal septal movements. You may see TAPSE dropping to marginal level and portal vein PW signal may become a bit more pulsatile. IVC looks full and RVSP usually rises but not skyrocket. The MV inflow pattern & E/E’ suggest rather normal LA filling pressure, not surprising from a previously healthy heart.

In this case, it isn’t the LV diastolic dysfunction that overly afterloads the RV; and it isn’t the RV dilation that impairs the (D-shape) LV from ventricular interdependence. Therefore I’d consider the right heart circulation & left heart circulation running purely in series, whereby limiting the RV preload could reduce the LV CO.

Now, if this patient goes into shock, would you consider fluid challenge or diuretics? Everyone probably would also get other therapies on board, e.g pressor, inotrope, source control etc. But when the patient’s BP is 80/40mmHg, I am more prone to giving some fluid as I believe that reducing preload in a septic patient can precipitate arrest; and that RV only directly impairs LV CO once the IVS starts to shift, which should take more time and thereby easier to monitor.

Interesting case that happens commonly – if you do POCUS and look for it rather than blind-ish management. Here, you have congestion, likely due to pulmonary disease, fluids, on a normal-ish RV (which also means it is unable to mount a huge PAP).

So personally – and will full disclosure that this is not evidence-based (as if there was any evidence in our resuscitative practices!), I would consider this a relative contraindication to fluids, given the non-volume-tolerant state (ALI/pneumonia/ARDS and portal pulsatility) of the patient. With pulsatility and signs of organ dysfunction I would be diuresing or pulling fluid off. We’ll see if we can get Rory to comment, as he has been doing a fair bit of this.

So in this patient it would be either no fluids, or diurese.

I don’t think one should have a general conception that reducing preload in a septic patient category is an issue. That may be so if you do not have the capability to look, and hence feel you should behave more cautiously. A septic patient with a tiny IVC may indeed be tipped over into low CO by removing fluids, but another with a full tank post resuscitation may benefit. So with the ability to assess hemodynamics, individualized approaches trump general ides and protocols. Much more to come on this in the next weeks as we break down a lot of interesting concepts in regards to vascular tone assessment and cardiac efficiency. 

I fully appreciate how ambiguous this situation is and that in reality the only way to find out the treatment that works is often by trial and error. Serial assessment by POCUS is definitely needed and one may even put the entire fluid thing aside and focus on other treatments. But just want to know your take and the reasons behind.

Thanks again for all your work and these thought provoking posts; and my apologies for the supposedly quick question ending up being not so quick. It took me some effort to clearly delineate my question in mind.

Anyone interested in these topics should keep an eye out for the H&R2019 Tracks. A bunch of us are getting together before and during the conference and will be recording discussions on all these little cases and angles around hemodynamics and other fun resuscitationist topics.

 

cheers!

 

Philippe

 

The Hospitalist POCUS Course Participant Info.

 

So here is a little intro for those taking part in the course, or for those considering, though I don’t think there are many spots left.

 

The Hospitalist POCUS Course

Participants should receive course e-notes in the week prior, if you do not, please email hospresusconference@gmail.com to let the team know.

If you are thinking of registering the link is here.

cheers and see you there!

 

Philippe