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Volume removal in right heart distension

economycian

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Posted this thread to get other people’s viewpoints on this. I have trouble convincing some of my colleagues that in the shocked, cold patient with a grossly distended right ventricle and septal flattening (presumed acute rather than chronic) that volume removal will improve hemodynamics. They cite the fear of “dropping the preload” too much.

To be clear I don’t advocate volume removal in other situations eg LV failure, diastolic dysfunction or RV failure without massive dilatation or that is chronic. In these situations I think sometimes optimal CO is at an elevated EDV/EDP.

Keen to hear more experienced peoples thoughts on this. We’re talking of course about the cold shocked pt.
 
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deleted547339

Posted this thread to get other people’s viewpoints on this. I have trouble convincing some of my colleagues that in the shocked, cold patient with a grossly distended right ventricle and septal flattening (presumed acute rather than chronic) that volume removal will improve hemodynamics. They cite the fear of “dropping the preload” too much.

To be clear I don’t advocate volume removal in other situations eg LV failure, diastolic dysfunction or RV failure without massive dilatation or that is chronic. In these situations I think sometimes optimal CO is at an elevated EDV/EDP.

Keen to hear more experienced peoples thoughts on this. We’re talking of course about the cold shocked pt.

The right heart likes to be dry. I don’t understand the question.
 
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Tipsy McStagger

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I may be missing the spirit of the question entirely here... but assuming acute right heart failure I'd be looking for the underlying etiology in a hurry. For example: PE ➔ thrombolysis vs whatever your pert team (if you have one) will do

If we're talking about a right heart that is already poor, say due to longstanding pHTN of whichever group you like, and now they're worse and you don't suspect a new offending factor then yes I'd start pulling fluid any way that I could. This, in addition to whatever other interventions I thought were prudent given the diagnosis like inotropes / prostacyclin / ECMO...
 
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MediMike

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What setting do you work in? I've run across that mentality in the community centers where they keep bolusing aRHF with the thought of an RV always being preload responsive.

Agree with above. An overdistended RV leads to worse function, worse strain and an underfilled malformed LV.
 
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ShockIndex

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What setting do you work in? I've run across that mentality in the community centers where they keep bolusing aRHF with the thought of an RV always being preload responsive.

Agree with above. An overdistended RV leads to worse function, worse strain and an underfilled malformed LV.


I think there is overall poor understanding of ventricular interdependence and pericardial constraint as it pertains to right heart failure in the medical community as a whole. It leads to a “1 stop shopping” mentality on treatment.

I suspect that the thinking you witness comes from 1 approach to acute right heart failure due to RV MI, but not even all of those patients respond to fluids and the crystalloids should be judicious.

On the other end of the acute right heart failure spectrum with higher PVR or obstruction from massive PE (dilated RV with thin wall on echo), I’m reaching for Epi + inhaled pulmonary vasodilator while I try to address the cause of the condition. I don’t muck with preload in the first few hours which means that I avoid fluids, diuretics, and PPV if at all possible up front. My focus is on reducing RV afterload while supporting systemic circulation. We can pull fluid off later.

If it is a acute on chronically failing RV from cor pulmonale that has finally met its match (big RV with thick wall and a pulmonary history to match), then I’m putting them on inhaled vasodilators, an inodilator (Milrinone, low dose epi, etc.), and gentile diureses.

Bottomline - approaches to a failed RV needed be varied and anyone who insists on one size fits all approach is probably going to have problems. However, a common theme will be limiting fluids on the front end (except select cases of RV MI) and diuretics on the back end.
 
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deleted171991

Posted this thread to get other people’s viewpoints on this. I have trouble convincing some of my colleagues that in the shocked, cold patient with a grossly distended right ventricle and septal flattening (presumed acute rather than chronic) that volume removal will improve hemodynamics. They cite the fear of “dropping the preload” too much.

To be clear I don’t advocate volume removal in other situations eg LV failure, diastolic dysfunction or RV failure without massive dilatation or that is chronic. In these situations I think sometimes optimal CO is at an elevated EDV/EDP.

Keen to hear more experienced peoples thoughts on this. We’re talking of course about the cold shocked pt.
"Some of your colleagues" should probably not be practicing critical care.

I had a similar patient in fellowship; the local IM stepdown idiots had pumped her full of water for "hypotension" and "preload", despite being a known chronic RV failure. She was still hypotensive when I admitted her to the MICU. Saved her with two days of TLC; didn't even need a central line. And that was without echo, just based on the (hi)story (i.e. talking to the patient, for the padawans).

In your patient, you need to increase systemic BP first, with pressors (even just a touch of phenylephrine). That will increase coronary perfusion (which may be the source of the acute RV/?LV failure) and also LV pressures, resulting in an increase in RV ejection. Then, if the volume overload is real, you can start diuresing.

People tend to forget how essential the LV is for RV ejection. The number one cause of (non-isolated) RV failure is (undiagnosed) LV failure, not cor pulmonale/OSA. (Actually, the PHTN in OSA/OHS is pretty reversible, AFAIK.)

Do not fall into the mistake of using (just) inodilators. Make sure it's not the low MAP that's driving all of this, first. Also, don't assume low-dose phenylephrine will necessarily hurt a heart failure patient (we use it all the time in the OR, it usually works).

If it's not ischemic (i.e. increasing MAP doesn't really increase CO and fix the problem), consider adding an inodilator, and treating it like secondary to PHTN. As @ShockIndex said, there are multiple scenarios. There is one thing that's frequent, though: people tend to confuse type 2 PHTN with type 3 (or others). And the treatment for type 2 is diuresis to euvolemia.

Just make sure you're not confusing an euvolemic PE with fluid overload.

Also: when in doubt, don't be afraid to diurese. Even if you're wrong, they cannot pee as fast as you can replace the fluids through an 18G PIV.
 
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BIGphysician

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"Some of your colleagues" should probably not be practicing critical care.

I had a similar patient in fellowship; the local IM stepdown idiots had pumped her full of water for "hypotension" and "preload", despite being a known chronic RV failure. She was still hypotensive when I admitted her to the MICU. Saved her with two days of TLC; didn't even need a central line. And that was without echo, just based on the (hi)story (i.e. talking to the patient, for the padawans).

In your patient, you need to increase systemic BP first, with pressors (even just a touch of phenylephrine). That will increase coronary perfusion (which may be the source of the acute RV/?LV failure) and also LV pressures, resulting in an increase in RV ejection. Then, if the volume overload is real, you can start diuresing.

People tend to forget how essential the LV is for RV ejection. The number one cause of (non-isolated) RV failure is (undiagnosed) LV failure, not cor pulmonale/OSA. (Actually, the PHTN in OSA/OHS is pretty reversible, AFAIK.)

Do not fall into the mistake of using (just) inodilators. Make sure it's not the low MAP that's driving all of this, first. Also, don't assume low-dose phenylephrine will necessarily hurt a heart failure patient (we use it all the time in the OR, it usually works).

If it's not ischemic (i.e. increasing MAP doesn't really increase CO and fix the problem), consider adding an inodilator, and treating it like secondary to PHTN. As @ShockIndex said, there are multiple scenarios. There is one thing that's frequent, though: people tend to confuse type 2 PHTN with type 3 (or others). And the treatment for type 2 is diuresis to euvolemia.

Just make sure you're not confusing an euvolemic PE with fluid overload.

Also: when in doubt, don't be afraid to diurese. Even if you're wrong, they cannot pee as fast as you can replace the fluids through an 18G PIV.

Obviously important aspect to realize. I don’t know if I would go for fluid removal, maybe conservative fluids moving forward and then optimize all factors that can increase PA pressures. Temperature, lung volumes, peak and plateau pressures, avoid hypercarbia. Consider milrinone and vasopressin to maintain afterload but not effect the PA like norepi. I guess some places use flolan also.


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chocomorsel

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Obviously important aspect to realize. I don’t know if I would go for fluid removal, maybe conservative fluids moving forward and then optimize all factors that can increase PA pressures. Temperature, lung volumes, peak and plateau pressures, avoid hypercarbia. Consider milrinone and vasopressin to maintain afterload but not effect the PA like norepi. I guess some places use flolan also.


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If the RV is truly dilated and distended, pushing on the LV and causing back up of fluids into the liver, then increase the SVR and diurese. Because if the RV can’t pump forward, the LV will not get fed.

As someone said the RV prefers a dry state and of course low pressures.

Assuming we aren’t talking of a PE as a cause that is.
 
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MediMike

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Assuming we aren’t talking of a PE as a cause that is.

Wouldn't volume overload of the RV due to an downstream (PVR) related problem be deleterious regardless of whether it is due to a PE, pHTN, hypoxia, hypercarbia etc? Or am I misinterpreting your statement?

My understanding is anything resulting in further distension increases transmural stress, decreasing coronary perfusion pressure as well as the sequelae noted above with LV underfilling etc.

Although I guess our conversation point hinges on the definition of "dry"...
 
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BIGphysician

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If the RV is truly dilated and distended, pushing on the LV and causing back up of fluids into the liver, then increase the SVR and diurese. Because if the RV can’t pump forward, the LV will not get fed.

As someone said the RV prefers a dry state and of course low pressures.

Assuming we aren’t talking of a PE as a cause that is.

Agree but that would be pretty rare to be so acute you don’t have time to correct the underlying mechanism before it gets to that level.


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chocomorsel

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Wouldn't volume overload of the RV due to an downstream (PVR) related problem be deleterious regardless of whether it is due to a PE, pHTN, hypoxia, hypercarbia etc? Or am I misinterpreting your statement?

My understanding is anything resulting in further distension increases transmural stress, decreasing coronary perfusion pressure as well as the sequelae noted above with LV underfilling etc.

Although I guess our conversation point hinges on the definition of "dry"...
I was more responding to the OP as far as the patient has fluid overload and the interdependence of the LV and RV and the increased LV wall/transmural stress is preventing proper forward flow.

In either case, yes, always keep pulm pressures down, but in a PE you need to bust up or fish out the clot too for definitive care. Diuresing there won't do much.
 
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chocomorsel

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Agree but that would be pretty rare to be so acute you don’t have time to correct the underlying mechanism before it gets to that level.


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It happens with people taking care of these patients on the floor keep pushing more and more fluids in them to fix the lactate and the hypoperfusion and by the time you get them, they are pretty full up with a distended RV. I doubt that it's that rare. I see balloons all the time in the ICU, so fluid overloading someone is very common. And if they had unknow RV failure where the doc didn't know.... It takes time, but for an intensivist, by the time you get them, it's now an acute problem.
 
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economycian

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Thanks guys for all the replies.

We can all agree on the general principles but I guess what’s come out of the discussion are exactly the subtleties I’m trying to tease apart. How is it different for pulmonary HTN vs acute PE? What is your definition of dry and what parameters do you use to decide that? What happens when the problem of fluid overload is iatrogenic?

Helpful to hear every bodies approach.
 

chocomorsel

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If you know it's an acute massive PE, then you know those right heart pressures have acutely increased and that thin walled RV cannot handle those high pulmonary pressures. Aside from TPA/Thrombectomy, the treatment would be similar. Keep the pulmonary pressures low by preventing hypoxia, acidosis, and hypercarbia, support the SVR using pressors known to keep PVR low, and then use pulmonary vasodilators if needed. You Keep the B/P and SVR high so as not to go down a death spiral and keep the gradient pushing the blood forward and left heart pressures higher than right hear. If patient doesn't get better because you can't for some reason get TPA or Thrombectomy, then you may be screwed if you can't get them on ECMO. Transfer them.

With pulmonary HTN, the Right heart has adapted to those higher pressures. So you may have a little more time before decompensation, but again, gotta keep the left heart pressures high and pulmonary pressures low. But there comes a point where the right heart pressures now exceed the capacity to pump forward. It is nice to obviously have an echo or swan to assist with management. You got a D sign, swollen IVC, reflux hepatopathy, hypoperfusion not improving with more and more fluids you need to think of diuresing.

As far as definition of "dry" my thing is to keep the patient euvolemic to maintain as normal pressures as possible. Obviously if they are overall too dry we get into hypoperfusion, hypotension so do your baby fluid challenges if you got known high RV. Blind man's Echo. If they respond, are getting better, keep challenging them, but when they no longer start responding, stop, because now you have filled the tank.

We have a lot of iatrogenic fluid overload, especially in sepsis and trauma. That's just life as when you are rescusitating the patient doesn't blow up as you are pumping fluids in them right then and there. It takes a few days to equilibrate and see the effects of vascular leak i.e see the Michellin man.
I would then treat it as above.
 
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Phillipe Rola and the folks over at EMCRIT have done a lot of work into venous congestion, hepatic portal vein flow pulsatility and the downstream effects of venous congestion (a primary manifestation of RV dysfunction).

Some of the most satisfying patients are those who have RV dysfunction requiring vasopressors that rapidly improve with volume removal. It's a sight to behold and makes a believer out of anybody. That said, this is where TTE comes into play. Systolic function and size of the RV are somewhat different issues that are very easily delineated on echocardiography. Simply comparing TAPSE/S' and RV dimensions can guide your management. Especially in the acute setting:

1) Diminished RV function (TAPSE/S') but a normal RV:LV ratio? This is the patient that may actually benefit from judicious and titrated amounts of volume, RV afterload reduction (inhaled epoprostenol, milrinone) and ionotropy.

2) Preserved RV function, but RV > LV? Get the volume off in any way you can before your function takes a hit

3) Diminished RV function and RV > LV? These are some of the sickest patients and need very aggressive measures to reverse the death spiral. Think cor pulmonale from severe ARDS or even acute severe MI.

The fact that we "resuscitate" patients into RV failure on a regular basis is a topic for another day.
 
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deleted547339

In a massive one, yes. Possibly even a submassive one if it's causing hemodymic compromise.

It was more a tongue in cheek statement. Although by definition if a PE is causing hemodynamic compromise, it’s massive. But lots of folks like to do something about these submissive PEs - maybe it works, but I’d like to see data. We shouldn’t be doing unproven therapies outside of the context of clinical trials, yet we do.
 
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chocomorsel

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It was more a tongue in cheek statement. Although by definition if a PE is causing hemodynamic compromise, it’s massive. But lots of folks like to do something about these submissive PEs - maybe it works, but I’d like to see data. We shouldn’t be doing unproven therapies outside of the context of clinical trials, yet we do.
But when you see someone die of a submassive PE days after admission that you were doing conservative management with, I can understand why people become more aggressive.
They teeter on the edge sometimes.
 
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deleted171991

Phillipe Rola and the folks over at EMCRIT have done a lot of work into venous congestion, hepatic portal vein flow pulsatility and the downstream effects of venous congestion (a primary manifestation of RV dysfunction).

Some of the most satisfying patients are those who have RV dysfunction requiring vasopressors that rapidly improve with volume removal. It's a sight to behold and makes a believer out of anybody. That said, this is where TTE comes into play. Systolic function and size of the RV are somewhat different issues that are very easily delineated on echocardiography. Simply comparing TAPSE/S' and RV dimensions can guide your management. Especially in the acute setting:

1) Diminished RV function (TAPSE/S') but a normal RV:LV ratio? This is the patient that may actually benefit from judicious and titrated amounts of volume, RV afterload reduction (inhaled epoprostenol, milrinone) and ionotropy.

2) Preserved RV function, but RV > LV? Get the volume off in any way you can before your function takes a hit

3) Diminished RV function and RV > LV? These are some of the sickest patients and need very aggressive measures to reverse the death spiral. Think cor pulmonale from severe ARDS or even acute severe MI.

The fact that we "resuscitate" patients into RV failure on a regular basis is a topic for another day.
It's not so hard to diagnose abdominal venous congestion, for anyone who can do a PW Doppler on a vein:


Abdominal vein congestion POCUS.png


Now, ultrasound skills don't replace a proper knowledge of physiology, hence my contention that people who would never diurese a RV failure don't belong in critical care.
 
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deleted171991

I have attached an excellent paper about the RV, written (among others) by Dr. Eric Jacobsohn, the Canadian anesthesiology professor who's 2015 ASA national meeting presentation I credit with opening my eyes about the RV.


One thing they say:
The commonly held belief that the ailing RV should be aggressively volume-loaded is not accurate. Overfilling will stretch the tricuspid valve annulus, increase TR, aggravate organ congestion, decrease TSG, and decrease CO. In contrast, underfilling places the RV on a deleterious part of the Frank-Starling curve.
 
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deleted171991

It was more a tongue in cheek statement. Although by definition if a PE is causing hemodynamic compromise, it’s massive. But lots of folks like to do something about these submissive PEs - maybe it works, but I’d like to see data. We shouldn’t be doing unproven therapies outside of the context of clinical trials, yet we do.
Critical care is among the most experimental specialties I know, at least the good type.

My "evidence-based" critical care sounds like this: if I give something a brief try and it works in the patient, that's all the evidence I need (for that individual).

A number of intensivists tend to forget that this specialty requires an excellent knowledge of MODERN physiology, pathophysiology, pharmacology and resuscitation, not just good old internal medicine (and other stuff that can be looked up as needed). That's the HUGE difference between the fellowship-trained MD and the "critical care" midlevel. </rant>
 
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deleted547339

Critical care is among the most experimental specialties I know, at least the good type.

My "evidence-based" critical care sounds like this: if I give something a brief try and it works in the patient, that's all the evidence I need (for that individual).

A number of intensivists tend to forget that this specialty requires an excellent knowledge of MODERN physiology, pathophysiology, pharmacology and resuscitation, not just good old internal medicine (and other stuff that can be looked up as needed). That's the HUGE difference between the fellowship-trained MD and the "critical care" midlevel. </rant>

In some ways I agree and others I disagree. There are certainly times when I try someone and it works - higher map goal for a patient, different sedation or vent strategy, etc. The problem is that there are plenty of things that “work” - giving larger tidal volumes, higher transfusion thresholds, etc - they may temporarily make the patient look better but he associated with mortality. I think it’s ok to “experiment” in the absence of data, but only in the absence.

I agree, we aren’t as lucky as the cardiologists are to have pointless 30,000 patient students for the third time on the same topic, but that doesn’t mean we shouldn’t study it. At my institution, intervening on a submissive PE is practically sacrosanct. I’m not saying it doesn’t work, but it’s not that hard to study. The problem is that the people believe in the intervention so don’t want to study it. I think this logic is dangerous.
 
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deleted171991

In some ways I agree and others I disagree. There are certainly times when I try someone and it works - higher map goal for a patient, different sedation or vent strategy, etc. The problem is that there are plenty of things that “work” - giving larger tidal volumes, higher transfusion thresholds, etc - they may temporarily make the patient look better but he associated with mortality. I think it’s ok to “experiment” in the absence of data, but only in the absence.

I agree, we aren’t as lucky as the cardiologists are to have pointless 30,000 patient students for the third time on the same topic, but that doesn’t mean we shouldn’t study it. At my institution, intervening on a submissive PE is practically sacrosanct. I’m not saying it doesn’t work, but it’s not that hard to study. The problem is that the people believe in the intervention so don’t want to study it. I think this logic is dangerous.
I mostly don't disagree, except with the emphasized part, and to point out that many people don't know the quality of "evidence" they base their practice on.

Hence they are practicing mostly expert opinion and dogma, not science that's based on good quality evidence (which is actually pretty rare in intensive care). They just don't know where their knowledge is coming from; monkey see monkey do, four feet good two feet bad. The original post of this thread is a perfect example for that.

Also, the centuries-old wisdom "every patient is different" should make one think twice before blindly following EBM, especially when it's clearly not working in a particular patient (errare humanum est, perserverare autem diabolicum).

If we think about every paper as a theorem, even in proven true, it was proven true within the constraints of certain hypotheses (including a certain population). Applying that theorem to an even slightly different set of hypotheses may lead to a different conclusion. Just food for thought for the EBM fanatics (which I used to be one of).
 
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I don't disagree, except to point out that many people don't know the quality of "evidence" they base their practice on.

Hence they are practicing mostly expert opinion and dogma, not based on good quality evidence (which is actually pretty rare in intensive care). They just don't know where their knowledge is coming from. The original post of this thread is a perfect example for that.

Dogma at one institution is often dog shiit at another.
 
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deleted547339

I mostly don't disagree, except with the emphasized part, and to point out that many people don't know the quality of "evidence" they base their practice on.

Hence they are practicing mostly expert opinion and dogma, not science that's based on good quality evidence (which is actually pretty rare in intensive care). They just don't know where their knowledge is coming from; monkey see monkey do, four feet good two feet bad. The original post of this thread is a perfect example for that.

Also, the centuries-old wisdom "every patient is different" should make one think twice before blindly following EBM, especially when it's clearly not working in a particular patient (errare humanum est, perserverare autem diabolicum).

If we think about every paper as a theorem, even in proven true, it was proven true within the constraints of certain hypotheses (including a certain population). Applying that theorem to an even slightly different set of hypotheses may lead to a different conclusion. Just food for thought for the EBM fanatics (which I used to be one of).

I don’t disagree.
 

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I mostly don't disagree, except with the emphasized part, and to point out that many people don't know the quality of "evidence" they base their practice on.

Hence they are practicing mostly expert opinion and dogma, not science that's based on good quality evidence (which is actually pretty rare in intensive care). They just don't know where their knowledge is coming from; monkey see monkey do, four feet good two feet bad. The original post of this thread is a perfect example for that.

Also, the centuries-old wisdom "every patient is different" should make one think twice before blindly following EBM, especially when it's clearly not working in a particular patient (errare humanum est, perserverare autem diabolicum).

If we think about every paper as a theorem, even in proven true, it was proven true within the constraints of certain hypotheses (including a certain population). Applying that theorem to an even slightly different set of hypotheses may lead to a different conclusion. Just food for thought for the EBM fanatics (which I used to be one of).
Here's an anecdote (and I present it with knowledge of all the fallacies associated with anecdote):

Recent patient, 60 something year old with COVID infection on VVECMO. 4 pressor shock. Negative work-up (TTE/sepsis/steroids/abx/CT). Hgb 9.5 and difficulty oxygenating despite ECMO (PO2 ~60). Not responsive to crystalloid or albumin. Ended up receiving a few units of blood to augment O2 carrying capacity and pressors come off within hours. Still have absolutely no explanation for it.

Best thing about going to an ivory tower for fellowship was the stick they had up their ass. No paper was good enough for them but they always knew the specific population of each and every study and the particulars of the study protocol. Once you see it, it's eye-opening how limited the scope of data we have is.
 
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deleted547339

Here's an anecdote (and I present it with knowledge of all the fallacies associated with anecdote):

Recent patient, 60 something year old with COVID infection on VVECMO. 4 pressor shock. Negative work-up (TTE/sepsis/steroids/abx/CT). Hgb 9.5 and difficulty oxygenating despite ECMO (PO2 ~60). Not responsive to crystalloid or albumin. Ended up receiving a few units of blood to augment O2 carrying capacity and pressors come off within hours. Still have absolutely no explanation for it.

Best thing about going to an ivory tower for fellowship was the stick they had up their ass. No paper was good enough for them but they always new the specific population of each and every study and the particulars of the study protocol. Once you see it, it's eye-opening how limited the scope of data we have is.

I don’t disagree. I was simply trying to point out my problem with “standards of care” that have been recently adopted but not studied.
 

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In a massive one, yes. Possibly even a submassive one if it's causing hemodymic compromise.


It was more a tongue in cheek statement. Although by definition if a PE is causing hemodynamic compromise, it’s massive. But lots of folks like to do something about these submissive PEs - maybe it works, but I’d like to see data. We shouldn’t be doing unproven therapies outside of the context of clinical trials, yet we do.

Jeff Kline and Bill Barsan’s group at Michigan are designing a trial of reduced dose tPA for submissive PE. The idea is to find the right dose of tPA that improves mortality (primary outcome) and morbidity (secondary) without causing bleeding complications that erase those gains. Since RV:LV is easily measured at bedside and rough correlates with risk of cardiovascular collapse, I think they will be looking at multiple doses of tPA and multiple RV:LV ratios. Thus, this will be one of Barsan’s adaptive trials using Bayesian analysis.

I think it’s a cool concept. My concern is the size and number of centers that will be needed for enrollment for a relatively rare disease. Lots of centers gets expensive, harder to run, etc.

If that doesn’t work, maybe we can spend a few more million looking to see if EKOS will actually improve a patient-oriented outcome...
 
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chocomorsel

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May 24, 2006
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somewhere always warm
  1. Attending Physician
Look what I had in my reading list (so on topic):

For the padawans wondering about fellowships, she's a graduate of the Stanford anesthesia-CCM program.
She’s so hyper and excited about CCM. Listened to her in the past. Good stuff on CCM. So many podcasts out there with good stuff.
 

NITRAS

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Mar 26, 2018
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  1. Attending Physician
Dogma at one institution is often dog shiit at another.

I’m stealing this one.

Look what I had in my reading list (so on topic):

For the padawans wondering about fellowships, she's a graduate of the Stanford anesthesia-CCM program.

I recently listened to this. Made be realize just how poor my right heart failure understanding was.
 
D

deleted171991

I recently listened to this. Made be realize just how poor my right heart failure understanding was.
Read Jacobsohn's paper from above, too. I still remember watching his presentation at the ASA meeting in 2015, with my mouth open in an Aha! moment.

Once you understand RV anatomy and (patho)physiology, it all just falls into place so nicely. Completely different animal than the LV.
 
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