What’s one thing you wish your IR guys/gal know?

[deleted950463]

As title. IRs deal with a lot of ICU pts. Are there one or more things you wish to have us know about critical care?

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[sluggs]

Obstructing uretral calculus with septic shock/instability is a source control emergency, even at 3am-- please come stent it.
Cirrhotics not on warfarin with elevated INR don't usually need reversal before procedures.
Thank you for your help-- we appreciate you!

 

[deleted950463]

Obstructing uretral calculus with septic shock/instability is a source control emergency, even at 3am-- please come stent it.
Cirrhotics not on warfarin with elevated INR don't usually need reversal before procedures.
Thank you for your help-- we appreciate you!

1.There is a big variablity in response to septic obstructed stones. Personally those are immediate action cases for me. I have heard some IR say that they would sit on those if HD stable. Not sure if I agree

2. our societal guideline have something about cirrhotics now days. Again chronically elevated INR does not portend increased bleeding risk to the degree of acute inr rises.

there are two sides to one story. At my shop the primary team sometimes give product hoping to make us do a case which is just downright wasteful as giving product today at 9pm instead of tomorrow at 7am for something nonemergent isnt going to make the call team come in when the call team needs to be available for trauma, stroke etc.

Don’t even get me started on the team that wanted to give kcentra for an INR of 1.8 for a paracentesis....

 

[jdh71]

IF you want to restrict who can put in PICCs (or midlines) (I know not every location doesn’t this where I’ve been) by policy then plenty of patients will need one on the weekend. I’m not asking for a 2am PICC. But at 9am on a Sunday? Tell your tech to stop giving us a bunch of **** - call me and talk man to man if you are going to say no so I can tell you personally what I think about it.

Don’t tell the ED a patient can/will get catheter directed lytics to a limb without FIRST asking a vascular surgeon about it. Don’t tell the ED a patient will get catheter directed lyrics for submissive PE until you have talked to the Intensivist about it first and there is an echocardiogram read from a cardiologist with a real assessment of the RV.

 

[vector2]

Don’t tell the ED a patient will get catheter directed lyrics for submissive PE until you have talked to the Intensivist about it first and there is an echocardiogram read from a cardiologist with a real assessment of the RV.

To be fair, a CT has approximately the same specificity and a better sensitivity for picking up RV strain than TTE. If on the CT the RV:LV ratio is decently increased, septum is flattened, there's venous contrast reflux, and the BP is only borderline normal, I'd have no problem sending to IR before the official TTE read comes back.

 

[CCM-MD]

There is more to the decision making process than RV strain alone. And the evidence isn't amazing for catheter based therapies in comparison to anticoagulation alone in hemodynamically stable patients. There aren't great guidelines for intermediate risk/submassive PEs and there is enormous institutional variation... I trained at one that was conservative about catheter based therapies and our patients did fine with systemic anticoagulation alone. Having some kind of multidisciplinary approach to this or a PE response team is probably best.

 

[jdh71]

To be fair, a CT has approximately the same specificity and a better sensitivity for picking up RV strain than TTE. If on the CT the RV:LV ratio is decently increased, septum is flattened, there's venous contrast reflux, and the BP is only borderline normal, I'd have no problem sending to IR before the official TTE read comes back.

I cant even find methods of the study they cite.

But it doesn’t matter you need to see the RV moving or not to get an assessment of it’s FUNCTION.

 

[vector2]

I cant even find methods of the study they cite.

But it doesn’t matter you need to see the RV moving or not to get an assessment of it’s FUNCTION.

Lmgtfy

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And no, you don't absolutely need to see the RV "moving" with echo to say that its function has been compromised. By definition, RV dilatation to the point where it's approaching the size of the LV is always abnormal, means it's under strain, and in the case of a PE, unable to pump against the high afterload. A snapshot of flattening or bowing of the interventricular septum automatically means that RV systolic motion will be deranged from baseline. Reflux of contrast into the IVC that's extensive enough to be picked up on CT means that RVSP/PAP have become very high and the RV is under significant strain with likely distortion of the tricuspid annulus. There is enough data on many CTs (in addition to the fact that there is a big PE) to obviate the need to wait on the echo report.

 

[deleted547339]

There is more to the decision making process than RV strain alone. And the evidence isn't amazing for catheter based therapies in comparison to anticoagulation alone in hemodynamically stable patients. There aren't great guidelines for intermediate risk/submassive PEs and there is enormous institutional variation... I trained at one that was conservative about catheter based therapies and our patients did fine with systemic anticoagulation alone. Having some kind of multidisciplinary approach to this or a PE response team is probably best.

I don’t know if having said team is best. I know that having said team results in doing more for these patients, particularly catheter directed lytics - but there’s no data on that.

 

[CCM-MD]

I don’t know if having said team is best. I know that having said team results in doing more for these patients, particularly catheter directed lytics - but there’s no data on that.

I feel like I’ve been able to prevent catheter lyrics if I’m involved. There are situations where I’m not involved and IR/cards/vascular have made the decision to do it in situations it seems totally unnecessary. They are financially motivated to do more.

 

[deleted950463]

I find it very surprising when IR would pursue thrombolysis without input of others.

I don’t know if having said team is best. I know that having said team results in doing more for these patients, particularly catheter directed lytics - but there’s no data on that.

PERT team is becoming the standard of care in my opinion. Those catheter therapy can be high risk but high reward as well and there is a lack in high quality evidence because it’s an ongoing investigation. I think those procedure should involve more than IR in decision making.

 

[deleted950463]

I feel like I’ve been able to prevent catheter lyrics if I’m involved. There are situations where I’m not involved and IR/cards/vascular have made the decision to do it in situations it seems totally unnecessary. They are financially motivated to do more.

it depends on your set up. In the setup i am familiar with the doc do not get call pay (IR docs usually do not get call pay in academia). Nor do academic IR doc get paid more on production.

if you are in an academic shop, IR is pushing for thrombolysis because we see how well it can work.

 

[Siggy]

We just introduced a PERT team at my hospital and it seems like catheter based lysis is all the rage, especially with EKOS. Out of the 3 interventionalists (2 IR, 1 interventional cardiology), 2 are huge supporters of catheter based lysis and one is not a huge fan. From a critical care standpoint, I'm a bit agnostic because there really is no long term evidence of benefit. The best I can find for catheter based lysis are the EKOS trials, which either show no benefit vs heparin at 90 days (RV:LV ratio of 0.92 for EKOS vs 0.96 for Heparin. No mortality difference. 59 patients total in the study) or controlled against itself (OPTALYSE had 4 arms and essentially showed that 4mg TPA over 2 hours = 4mg over 4 hours = 6 mg over 6 hours = 12 mg over 6 hours. This too had a whopping 100 patients).

At this point, I think catheter based lysis might have benefit, but EKOS, and possibly catheter based too, is a fad that will be gone in less than a decade.

 

[CCM-MD]

it depends on your set up. In the setup i am familiar with the doc do not get call pay (IR docs usually do not get call pay in academia). Nor do academic IR doc get paid more on production.

if you are in an academic shop, IR is pushing for thrombolysis because we see how well it can work.

I work outside of academia and my understanding is they are usually paid based on production or there is some kind of incentive for doing more "work".

And in academia, I feel like everyone wants to "do stuff". Full of little gunner kids running around trying to poke anyone or anything... screaming "My specialty can poke better than yours!"

 

[jdh71]

Lmgtfy

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And no, you don't absolutely need to see the RV "moving" with echo to say that its function has been compromised. By definition, RV dilatation to the point where it's approaching the size of the LV is always abnormal, means it's under strain, and in the case of a PE, unable to pump against the high afterload. A snapshot of flattening or bowing of the interventricular septum automatically means that RV systolic motion will be deranged from baseline. Reflux of contrast into the IVC that's extensive enough to be picked up on CT means that RVSP/PAP have become very high and the RV is under significant strain with likely distortion of the tricuspid annulus. There is enough data on many CTs (in addition to the fact that there is a big PE) to obviate the need to wait on the echo report.

Thank you. I did go to the link YOU originally provided. And the best way to be super snakry about googling something for someone is to use the actual LMGTFY link.

Yes. You DO need to see the RV function as a clinician. The study you cite only uses the definition of right ventricular strain (RVS) as found here in the AHA guidelines. And that is only defined as being big. The only problem with that CLINICALLY is that just being big doesn't actually often mean anything. Regardless of the size of the RV it is still working fine enough. You need to evaluate more than a simple snapshot of the size of the RV and this includes at minimum, what the patient actually looks like, are they hypoxic and or getting more hypoxic, how much obstructive hypotension is present, and is there any chemical evidence of that the RV is actually under real strain with troponin and BNP. You need to know all of this prior to committing the patient to an intervention without great evidence of great benefit (in all of these patients) in patients who simply have big RVs.

A very important part of that evaluation is the echocardiogram and how the RV is ACTUALLY functioning, not that it is just big. Most of these patient do not need their RV, even if big, more rapidly offloaded, and are fine with heparin. Starting catheter direct lytics based on CT imaging alone is practicing bad medicine.

 

[jdh71]

I don’t know if having said team is best. I know that having said team results in doing more for these patients, particularly catheter directed lytics - but there’s no data on that.

Our experience has been the opposite. Much, much fewer catheter directed lytic patients since starting our PERT. I mean they used to literally just show up after only the ED and the rads guys came up with a plan.

 

[vector2]

Thank you. I did go to the link YOU originally provided. And the best way to be super snakry about googling something for someone is to use the actual LMGTFY link.

Yes. You DO need to see the RV function as a clinician. The study you cite only uses the definition of right ventricular strain (RVS) as found here in the AHA guidelines. And that is only defined as being big. The only problem with that CLINICALLY is that just being big doesn't actually often mean anything. Regardless of the size of the RV it is still working fine enough. You need to evaluate more than a simple snapshot of the size of the RV and this includes at minimum, what the patient actually looks like, are they hypoxic and or getting more hypoxic, how much obstructive hypotension is present, and is there any chemical evidence of that the RV is actually under real strain with troponin and BNP. You need to know all of this prior to committing the patient to an intervention without great evidence of great benefit (in all of these patients) in patients who simply have big RVs.

A very important part of that evaluation is the echocardiogram and how the RV is ACTUALLY functioning, not that it is just big. Most of these patient do not need their RV, even if big, more rapidly offloaded, and are fine with heparin. Starting catheter direct lytics based on CT imaging alone is practicing bad medicine.

Don't strawman me and put words into my mouth. No one was saying that we are to forgo clinical judgment or the entire clinical picture (especially in submassive where things are many times equivocal) and just make a decision based on one test. You made a statement that the TTE with an official cardiologist read is one of the things you require before telling the ED that a catheter directed lytic is appropriate. I am simply telling you and have supported with the evidence that you can make a determination of RV strain (and even significant RV compromise) as part of the clinical picture without an official TTE read back.

 

[jdh71]

Don't strawman me and put words into my mouth. No one was saying that we are to forgo clinical judgment or the entire clinical picture (especially in submassive where things are many times equivocal) and just make a decision based on one test. You made a statement that the TTE with an official cardiologist read is one of the things you require before telling the ED that a catheter directed lytic is appropriate. I am simply telling you and have supported with the evidence that you can make a determination of RV strain (and even significant RV compromise) as part of the clinical picture without an official TTE read back.

And I’m telling you that you absolutely actually cannot have that based on the CT scan.

RV strain is actually a fairly useless concept clinically as currently defined.

Simply saying something is big is meaningless. Ok. So what? It’s only a problem if it is a problem. And you can’t tell anything about the actual function of the RV from the CT.

 

[vector2]

And I’m telling you that you absolutely actually cannot have that based on the CT scan.

RV strain is actually a fairly useless concept clinically as currently defined.

Simply saying something is big is meaningless. Ok. So what? It’s only a problem if it is a problem. And you can’t tell anything about the actual function of the RV from the CT.

You don't understand the RV, its method of muscular contraction, interventricular dependence, or its main function as a volume, not pressure, chamber if you believe that "something is big is meaningless" in regard to that structure. Being significantly enlarged is automatically pathologic, and there is a reason that "Normal Variant" is not listed as a cause of RV dilatation.. In the case of a CT where one sees significant clot burden and RV dilatation (or the other things that I mentioned earlier like IVC contrast reflux, bowed septum) we know the mechanism. You have RV pressure overload, and the RV really, really doesn't like missing out on the luxury systolic coronary perfusion that it normally receives. While "big" does matter, "how big" probably is a more important question because we see that once RV:LV ratios start getting over 1.1, people start dying a lot faster.

At the end of the day, though, we know what to do with massive PE. We also know what to do with "comfortable on RA satting 100%, SBP 138, HR 65" PEs. Submassive PEs are really the crux of the issue, and treatment algorithms take a variety of data into account, not just one data point. In the case of submassive PE, an RV:LV ratio of exactly 0.9 on a CT doesn't mean boom, go to cath lab stat. However, if a patient is uncomfortable, diaphoretic, slightly hypoxic, slightly tachycardic, small troponin leak, the RV:LV ratio is >=0.9 on CT (+- the other CT findings I mentioned), but the SBP is >90 for 15 minutes and therefore it's technically not "massive," are you going to tell me that catheter directed thrombolytics are not indicated unless you've ordered a TTE, it's been performed, and a cardiologist has read it? Is it going to change your management significantly in this patient if the TAPSE is 17mm instead of 11mm? What about if the S' is 11 instead of 9?

 

[jdh71]

You don't understand the RV, its method of muscular contraction, interventricular dependence, or its main function as a volume, not pressure, chamber if you believe that "something is big is meaningless" in regard to that structure. Being significantly enlarged is automatically pathologic, and there is a reason that "Normal Variant" is not listed as a cause of RV dilatation.. In the case of a CT where one sees significant clot burden and RV dilatation (or the other things that I mentioned earlier like IVC contrast reflux, bowed septum) we know the mechanism. You have RV pressure overload, and the RV really, really doesn't like missing out on the luxury systolic coronary perfusion that it normally receives. While "big" does matter, "how big" probably is a more important question because we see that once RV:LV ratios start getting over 1.1, people start dying a lot faster.

At the end of the day, though, we know what to do with massive PE. We also know what to do with "comfortable on RA satting 100%, SBP 138, HR 65" PEs. Submassive PEs are really the crux of the issue, and treatment algorithms take a variety of data into account, not just one data point. In the case of submassive PE, an RV:LV ratio of exactly 0.9 on a CT doesn't mean boom, go to cath lab stat. However, if a patient is uncomfortable, diaphoretic, slightly hypoxic, slightly tachycardic, small troponin leak, the RV:LV ratio is >=0.9 on CT (+- the other CT findings I mentioned), but the SBP is >90 for 15 minutes and therefore it's technically not "massive," are you going to tell me that catheter directed thrombolytics are not indicated unless you've ordered a TTE, it's been performed, and a cardiologist has read it? Is it going to change your management significantly in this patient if the TAPSE is 17mm instead of 11mm? What about if the S' is 11 instead of 9?

Now who is knocking over strawmen?! Lol.

I understand the RV fine. Just being big IS meaningless even if it "abnormal" or even "pathologic". If the patient is doing fine enough with that big RV they are doing fine enough. And YES I am going to tell you that slightly hypoxic, slightly tachycardic, small troponin leak will not go for catheter directed lytics unless there is evidence on a real time study that function is actually down. I don't care about your other strawman varibales. What does the RV actually look like.

 

[vector2]

Now who is knocking over strawmen?! Lol.

I understand the RV fine. Just being big IS meaningless even if it "abnormal" or even "pathologic". If the patient is doing fine enough with that big RV they are doing fine enough. And YES I am going to tell you that slightly hypoxic, slightly tachycardic, small troponin leak will not go for catheter directed lytics unless there is evidence on a real time study that function is actually down. I don't care about your other strawman varibales. What does the RV actually look like.

Lol, you were the one just strawmanning my position by telling me that the CT needs to be integrated into the total picture of the patient's clinical condition (duh), but simultaneously you're trying to state that one particular test (and an often finicky test to boot), with no explanation what precisely on that test constitutes useful information, is required to make a clinical decision. Can you describe the evidence that your patient needs to have a cardiologist interpreted TTE assessment of the RV before proceeding to cathlab, or is it merely your opinion? And if you do need that echo, what exactly defines "good" vs "bad" function vis a vis a clinical trigger to go to cathlab?

 

[jdh71]

Lol, you were the one just strawmanning my position by telling me that the CT needs to be integrated into the total picture of the patient's clinical condition (duh), but simultaneously you're trying to state that one particular test (and an often insensitive test to boot), with no explanation what precisely on that test constitutes useful information, is required to make a clinical decision. Can you describe the evidence that your patient needs to have a cardiologist interpreted TTE assessment of the RV before proceeding to cathlab, or is it merely your opinion? And if you do need that echo, what exactly defines "good" vs "bad" function vis a vis a clinical trigger to go to cathlab?

Can you give me the evidence that patients have any long term benefit with catheter directed lytics in the scenario you described and seemed incredulous that someone would not do catheter directed lytics?

What I am asking for is an opinion from a specialist that states there is actually a worrisome decline in RV function based on a real time analysis before spending money and patient risk on a procedure that has not been shown to benefit these submassive patients as a group in total - I am not looking for a specific variable, I am looking for an expert opinion on the matter. This is my opinion and that of my group based on the available evidence that we find very valuable in the context of the other important clinical variables. There is ZERO good data to support your approach any more than mine with a RCT. Though your approach does put patients at more risk but for little evidence of any benefit at increased cost with the submassive PE cohort.

 

[leviathan]

Please call me if you don't think something should be or can be done. Our IR guy refused to put a pigtail in a loculated parapneumonic effusion because it was loculated, so there would be "no point", but I didn't know until hours later when the report came up. That was the very reason we wanted to put it in, so we could give tPa/DNAse to try to avoid a surgical decortication.

But on that note, I have much love for our IR team. It really helps free me up to do other things in a busy ICU.

 

[vector2]

There is ZERO good data to support your approach any more than mine with a RCT.

This is EXACTLY my point. You are the one who has been saying over and over and over that you "DO" absolutely need to have a cardiologist read TTE before going to the cathlab, but there is no good evidence to support that assertion if the submassive clinical picture is bad enough. All I have pointed out is that RV dilatation on CT is essentially synonymous with some degree of RV dysfunction, and the case is even stronger when combined with septal bowing, contrast reflux into the IVC secondary to TR, or an RV:LV ratio >=1.1-1.2 instead of 0.9. I'm not incredulous that someone wouldn't take the pt to the cathlab in the scenario I described- I'm incredulous at the fact that anyone would absolutely require a cards echo to do so (or worse, that a borderline normal echo would prevent them from doing so) if the patient's HR, bnp, trop, O2 req, and CT, etc are all consistent with a submassive requiring treatment.

Further, you are likely sidestepping this whole problematic issue of "submassive" if what you want from cards is an expert opinion of a worrisome decline in RV function. By the time a cardiologist tells you that the decline is worrisome (at least at my shop and a couple others), you've probably already reached the stage where we'd all be calling it massive and where we would have missed the window to do a lytic in a safer and timelier manner. Ultimately, what it really sounds like is that you'd rather have one more consultant for CYA purposes rather than clinical decision making.

 

[jdh71]

This is EXACTLY my point. You are the one who has been saying over and over and over that you "DO" absolutely need to have a cardiologist read TTE before going to the cathlab, but there is no good evidence to support that assertion if the submassive clinical picture is bad enough. All I have pointed out is that RV dilatation on CT is essentially synonymous with some degree of RV dysfunction, and the case is even stronger when combined with septal bowing, contrast reflux into the IVC secondary to TR, or an RV:LV ratio >=1.1-1.2 instead of 0.9. I'm not incredulous that someone wouldn't take the pt to the cathlab in the scenario I described- I'm incredulous at the fact that anyone would absolutely require a cards echo to do so (or worse, that a borderline normal echo would prevent them from doing so) if the patient's HR, bnp, trop, O2 req, and CT are all consistent with a submassive requiring treatment.

Further, you are likely sidestepping this whole problematic issue of "submassive" if what you want from cards is an expert opinion of a worrisome decline in RV function. By the time a cardiologist tells you that the decline is worrisome (at least at my shop and a couple others), you've probably already reached the stage where we'd all be calling it massive and where we would have missed the window to do a lytic in a safer and timelier manner. Ultimately, what it really sounds like is that you'd rather have one more consultant for CYA purposes rather than clinical decision making.

The consultant can't cover my ass but that comment was an attempt at a weak cheap shot.

I told you why - perhaps reading comprehension isn't your best quality? - in a situation where you are talking about doing a costly procedure with the increased risks that come form a procedure that shows NO as in ZIP, ZERO group benefit for submassive patients, there needs to something more that points to enough dysfunction that the RV needs to be offloaded sooner than you will get with a heparin drip alone. I'm interested in the least harm to the patient.

I get reads on echos in 30-60 minutes. Perhaps the problem is your "shop" not my algorithm for making objective and informed decisions regarding directed lytics in the submassive PE cohort.

Ultimately, what it really sounds like is that you'd rather be a cowboy putting patients at increased risk with a procedure that shows no benefits in the entire group you are trying to treat. (This assuming the worst about each other stuff is fun).

 

[ShockIndex]

So many things in life age us - smoking, drinking, meth.

But only the internet can make grown adults look like children.

 

[vector2]

The consultant can't cover my ass but that comment was an attempt at a weak cheap shot.

I told you why - perhaps reading comprehension isn't your best quality? - in a situation where you are talking about doing a costly procedure with the increased risks that come form a procedure that shows NO as in ZIP, ZERO group benefit for submassive patients, there needs to something more that points to enough dysfunction that the RV needs to be offloaded sooner than you will get with a heparin drip alone. I'm interested in the least harm to the patient.

I get reads on echos in 30-60 minutes. Perhaps the problem is your "shop" not my algorithm for making objective and informed decisions regarding directed lytics in the submassive PE cohort.

Ultimately, what it really sounds like is that you'd rather be a cowboy putting patients at increased risk with a procedure that shows no benefits in the entire group you are trying to treat. (This assuming the worst about each other stuff is fun).

Curious that you're trying to pull off a "no benefit" argument in a critical care forum given that we're talking about a relatively new treatment for a relatively low incidence, controversially defined condition with HUGE clinical variability, especially if the diagnosis is anywhere between "stone cold normal vitals" PE and "massive" PE. But I guess some non-CCM trained people who have no clue about the statistics of CCM studies might be fooled...if that's what you're going for. Also, you should specify "no superiority in mortality" if that's the rhetorical point you're trying make, because catheter directed therapies reduce RV strain and lower PAPs faster than A/C, have essentially equivalent mortality, and also a low procedural complication rate.

My day to day is frequently performing cardiac anesthesia, I've passed the advanced periop TEE exam, and I'm more than capable of performing and interpreting a comprehensive or POCUS TTE when I round in the unit. I don't need cardiology to give me their interpretation of an echo, but importantly, the point I'm making is that the length of time it takes the echo to come back even if you did need them is irrelevant. To get back to where we started before you began all this goalpost shifting- you initially made the claim (and in quite an absolute fact fashion) that you need to see the RV moving with echo and you need a cardiologist to read it before we can pass go. You should be very clear and state that given the dearth of evidence, this is you and your group's opinion in regard to the decision-making surrounding the treatment of potentially deteriorating submassive PE, and that other radiologic signs of RV dysfunction combined with biochemical markers and the overall clinical picture may also serve as an appropriate indication for lytics pending more data or definitive RCTs.

 

[jdh71]

Curious that you're trying to pull off a "no benefit" argument in a critical care forum given that we're talking about a relatively new treatment for a relatively low incidence, controversially defined condition with HUGE clinical variability, especially if the diagnosis is anywhere between "stone cold normal vitals" PE and "massive" PE. But I guess some non-CCM trained people who have no clue about the statistics of CCM studies might be fooled...if that's what you're going for. Also, you should specify "no superiority in mortality" if that's the rhetorical point you're trying make, because catheter directed therapies reduce RV strain and lower PAPs faster than A/C, have essentially equivalent mortality, and also a low procedural complication rate.

My day to day is frequently performing cardiac anesthesia, I've passed the advanced periop TEE exam, and I'm more than capable of performing and interpreting a comprehensive or POCUS TTE when I round in the unit. I don't need cardiology to give me their interpretation of an echo, but importantly, the point I'm making is that the length of time it takes the echo to come back even if you did need them is irrelevant. To get back to where we started before you began all this goalpost shifting- you initially made the claim (and in quite an absolute fact fashion) that you need to see the RV moving with echo and you need a cardiologist to read it before we can pass go. You should be very clear and state that given the dearth of evidence, this is you and your group's opinion in regard to the decision-making surrounding the treatment of potentially deteriorating submassive PE, and that other radiologic signs of RV dysfunction combined with biochemical markers and the overall clinical picture may also serve as an appropriate indication for lytics pending more data or definitive RCTs.

I shifted exactly zero goal posts in this this discussion.

If there is no objective benefit to reducing RV strain and PAP faster, then there is no reason to adventure in the risk and cost. The ends points of RV strain and PAP pressure are not meaningful simply by themselves. Show me the benefit. If you cannot, then there is no good evidence that we should be doing catheter directed lytics in all of these patients.

I think I stated that ONLY having a CT scan was not enough. You need to see the RV moving to get a sense of its real function. Just being big doesn't mean anything by the mere virtue of being big. Which was my point about the discussion regarding moving to catheter directed lytics in the first place to the question form a RADIOLOGIST about what IR could do better or different. I haven't changed or moved off the point. It is my opinion echocardiogram is necessary to make a final decision on who gets catheter directed lytics for submassive PE. It is appears it your OPINION that this evaluation of RV function is not necessary for a decision to move forward with the risk and cost associated catheter directed lytics for submassive PE. Dueling opinions. Mine simply does it's best to triage who actually needs the intervention while yours does not.

 

[jdh71]

So many things in life age us - smoking, drinking, meth.

But only the internet can make grown adults look like children.

Edgy

 

[vector2]

I shifted exactly zero goal posts in this this discussion.

If there is no objective benefit to reducing RV strain and PAP faster, then there is no reason to adventure in the risk and cost. The ends points of RV strain and PAP pressure are not meaningful simply by themselves. Show me the benefit. If you cannot, then there is no good evidence that we should be doing catheter directed lytics in all of these patients.

I think I stated that ONLY having a CT scan was not enough. You need to see the RV moving to get a sense of its real function. Just being big doesn't mean anything by the mere virtue of being big. Which was my point about the discussion regarding moving to catheter directed lytics in the first place to the question form a RADIOLOGIST about what IR could do better or different. I haven't changed or moved off the point. It is my opinion echocardiogram is necessary to make a final decision on who gets catheter directed lytics for submassive PE. It is appears it your OPINION that this evaluation of RV function is not necessary for a decision to move forward with the risk and cost associated catheter directed lytics for submassive PE. Dueling opinions. Mine simply does it's best to triage who actually needs the intervention while yours does not.

Lol you haven't shifted the goal posts? We somehow moved from the simple point of contention that echo is the be-all-end-all of RV function assessment to me having to prove that catheter directed therapy has a mortality benefit to me having to prove a negative that echo isn't worthwhile...when you are the one upon whom the burden of proof lies when you affirmatively suggest/imply that an echo will improve the eligibility criteria and probability of success of the intervention.

It's great and all that you said that ONLY having a CT scan was not enough, but as I pointed out, that was you strawmanning me because I originally said "If on the CT the RV:LV ratio is decently increased, septum is flattened, there's venous contrast reflux, and the BP is only borderline normal..." It is not a point of contention that RV function is worrisome with a dilated RV, flattened septum, and readily apparent significant tricuspid regurgitation in the setting of a CT confirmed PE. I then followed up by stating that obviously any decision is made based on the overall clinical picture, which implies that there needs to be some other supporting evidence wrt to pt's vitals, labs, oxygen requirement, appearance, etc. If you could use your reason for one second instead of just reflexively being obstinate, you'd see that I never said nor ever meant "GET CT, RV:LV 0.9, CATHLAB NOW."

If you'd like to continue strawmanning me by implying that I don't want any echo (when my actual point of contention is really the cards official read since 97% of us here are capable of a sufficient POCUS exam), or continuing to say that using radiological data as one of a multitude of data points is bad triaging, that is certainly your prerogative.

 

[vector2]

For those of you who haven't seen what MDCT is capable of....imagine in the future if multidetector gated CT is done simultaneously as part of (high suspicion) PE protocol...

 

[sluggs]

Great debate, folks.
Correct me, please, if my understanding is wrong:
If a patient has a PE and is in shock or going into shock (hypotensive, not fluid responsive, or requiring a lot of fluid +/- pressor), this is an emergency and you push thrombolytic to avoid a code (or abort a code if it is happening).
If a patient has a submassive PE on CTA (acute) and evidence of riight heart strain or elevated RVSP, you assess for candidacy for catheter directed thrombolytic, with the outcome measure being a lower PA pressure at 90 days (outcome measure in the second scenario being reduced incidence of long-term pulmonary hypertension).
function with normal RVSP, so I typically use echo to assess for EKOS candidacy.
Please tell me if my approach is wrong and give me an article or 2...?
Thanks

 

[jdh71]

Lol you haven't shifted the goal posts? We somehow moved from the simple point of contention that echo is the be-all-end-all of RV function assessment to me having to prove that catheter directed therapy has a mortality benefit to me having to prove a negative that echo isn't worthwhile...when you are the one upon whom the burden of proof lies when you affirmatively suggest/imply that an echo will improve the eligibility criteria and probability of success of the intervention.

It's great and all that you said that ONLY having a CT scan was not enough, but as I pointed out, that was you strawmanning me because I originally said "If on the CT the RV:LV ratio is decently increased, septum is flattened, there's venous contrast reflux, and the BP is only borderline normal..." It is not a point of contention that RV function is worrisome with a dilated RV, flattened septum, and readily apparent significant tricuspid regurgitation in the setting of a CT confirmed PE. I then followed up by stating that obviously any decision is made based on the overall clinical picture, which implies that there needs to be some other supporting evidence wrt to pt's vitals, labs, oxygen requirement, appearance, etc. If you could use your reason for one second instead of just reflexively being obstinate, you'd see that I never said nor ever meant "GET CT, RV:LV 0.9, CATHLAB NOW."

If you'd like to continue strawmanning me by implying that I don't want any echo (when my actual point of contention is really the cards official read since 97% of us here are capable of a sufficient POCUS exam), or continuing to say that using radiological data as one of a multitude of data points is bad triaging, that is certainly your prerogative.

I haven’t “strawmaned” you anywhere.

You’ve made a lot of incorrect assumptions about what I’ve been saying and I do find your accusations of straw man amusingly ironic and hypocritical.

And I haven’t moved a single goal post. You were basically asking why the echo end point was so important here. If I misunderstand that question then perhaps you can clarify? My point that you seemed to be demanding an answer to was that in a situation where not all those with submissive PE benefit from catheter directed lyrics that I picked an end point of real time dynamic RV dysfunction as a reasonable point in the algorithim for patients who should have a quicker improvement in RV pressures than a heparin infusion can provide.

 

[chocomorsel]

Ok, ok, whose cojones are bigger? @jdh71 yours are bigger. @vector2 your anaconda is bigger.

But now, can we please get back to giving the IR guy/gal some other pointers now? You guys can go on an on and on for pages and pages.

Agree to disagree? Thousand ways to skin a cat?

 

[vector2]

I haven’t “strawmaned” you anywhere.

You’ve made a lot of incorrect assumptions about what I’ve been saying and I do find your accusations of straw man amusingly ironic and hypocritical.

And I haven’t moved a single goal post. You were basically asking why the echo end point was so important here. If I misunderstand that question then perhaps you can clarify? My point that you seemed to be demanding an answer to was that in a situation where not all those with submissive PE benefit from catheter directed lyrics that I picked an end point of real time dynamic RV dysfunction as a reasonable point in the algorithim for patients who should have a quicker improvement in RV pressures than a heparin infusion can provide.

I'm guessing you don't know what the word means, because you have clearly misrepresented my position on CTs repeatedly just to knock down something which no one said in the first place.

And I haven't made a single incorrect assumption about what you're saying. You've made it very clear that 100% of the time you need a cardiologist-read TTE before you'd ever think of proceeding to a catheter directed lytic for submassive PE. I understand the logic and the reasoning behind it. You've also made it clear that you think significant RV dysfunction or compromise can't be discerned on a CT. I simply just disagree with both statements. And even though I'm an echo junkie, I do think that just the pt's radiological studies, clot burden, clinical picture, and labs can provide enough evidence of a deteriorating submassive PE to go to cathlab.

 

[jdh71]

I'm guessing you don't know what the word means, because you have clearly misrepresented my position on CTs repeatedly just to knock down something which no one said in the first place.

And I haven't made a single incorrect assumption about what you're saying. You've made it very clear that 100% of the time you need a cardiologist-read TTE before you'd ever think of proceeding to a catheter directed lytic for submassive PE. I understand the logic and the reasoning behind it. I just disagree with the conclusion if the pt's radiological studies, clot burden, clinical picture, and labs provide enough evidence of a deteriorating submassive PE.

I am familiar with the term straw man and I never misrepresented your position.

You did say this, which was at least a SINGLE incorrect assumption about what I was saying . . .

Ultimately, what it really sounds like is that you'd rather have one more consultant for CYA purposes rather than clinical decision making.

And yes in the case of submissive PE there needs to a real time assessment of the dynamic RV function before initiating catheter directed lyrics for the reasons now given multiple time. I suppose it matters little if it necessarily a cardiologist.

If a patient is deteriorating that is different situation than what I've been discussing.

 

[jdh71]

Ok, ok, whose cojones are bigger? @jdh71 yours are bigger. @vector2 your anaconda is bigger.

But now, can we please get back to giving the IR guy/gal some other pointers now? You guys can go on an on and on for pages and pages.

Agree to disagree? Thousand ways to skin a cat?

Has the unmoving object met the unstoppable force?

I admit I am not very familiar with this vector guy

 

[chocomorsel]

Has the unmoving object met the unstoppable force?

I admit I am not very familiar with this vector guy

Haha, you guys are really going at it. It’s interesting though. But has the potential to never end.
I lost track of who’s moving goal posts and who’s straw manning it.

 

[jdh71]

Haha, you guys are really going at it. It’s interesting though. But has the potential to never end.
I lost track of who’s moving goal posts and who’s straw manning it.

All alligator rolls eventually end. Eventually.

I feel like I'm having a discussion with one some who only has a surface understanding of the terms, like a sophomore in his first few weeks of a rhetoric class. Don't worry about it too much.

You're probably right. It's all stupid now.

 

[vector2]

I am familiar with the term straw man and I never misrepresented your position.

Weird you say that when you also said "Starting catheter direct lytics based on CT imaging alone is practicing bad medicine. " as if that were my argument.

And yes in the case of submissive PE there needs to a real time assessment of the dynamic RV function before initiating catheter directed lyrics for the reasons now given multiple time. I suppose it matters little if it necessarily a cardiologist.

Every one of these patients has an official TTE ordered by the ED or the ICU when they're admitted.

If a patient is deteriorating that is different situation than what I've been discussing.

The whole crux of this stupid argument has been which imaging modality(ies) do deteriorating submassive PE pts need before lytics. Obviously someone who has CT proven PE, a 0.08 troponin and a RV:LV of 0.9 (or a TAPSE of 14 or something) - but who is stable from a hemodynamic and respiratory standpoint - isn't automatically going to the cathlab....even though they technically meet the definition of a "submassive PE" (no systemic hypotension + evidence of either or both RV dysfunction or myocardial necrosis). As I said earlier, PE spans a massive (no pun intended) spectrum which ranges from normal vitals/chamber size/function/biochemical markers PE all the way to there-is-no-pulse PE.

To be very clear, it is my opinion that there are patients who are subPE but on the border who are appropriate for catheter directed lytics- without the formal read back from the TTE, assuming they have sufficient other radiologic, biochemical, and/or clinical data.

 

[vector2]

Haha, you guys are really going at it. It’s interesting though. But has the potential to never end.
I lost track of who’s moving goal posts and who’s straw manning it.

You just finished CCM fellowship this past year right? Did you ever have one of those rigid, patronizing AF attendings who only had one way of doing things and would just ramble endlessly from point to point without ever making a coherent, consistent argument...

 

[jdh71]

Weird you say that when you also said "Starting catheter direct lytics based on CT imaging alone is practicing bad medicine. " as if that were my argument.



The whole crux of this stupid argument has been which imaging modality(ies) do deteriorating submassive PE pts need before lytics. Obviously someone who has CT proven PE, a 0.08 troponin and a RV:LV of 0.9 (or a TAPSE of 14 or something) but who is stable from a hemodynamic and respiratory standpoint isn't automatically going to the cathlab....even though they technically meet the definition of a "submassive PE" (no systemic hypotension + evidence of either or both RV dysfunction or myocardial necrosis). As I said earlier, PE spans a massive (no pun intended) spectrum which ranges from normal vitals/chamber size/function/biochemical markers PE all the way to there-is-no-pulse PE.

To be very clear, it is my opinion that there are patients who are subPE but on the border who are appropriate for catheter directed lytics- without the formal read back from the TTE, assuming they have sufficient other radiologic, biochemical, and/or clinical data.

When I made the CT alone comment you were only discussing CT finding and had made no mention of other clinical factors. This was all in the context of my original statement that radiologist should not be putting in catheters for directed lytics based on CT imaging alone. Also I never said that was your argument. I said it’s bad medicine to only use that. You clearly made some assumptions there and found yourself indignant.

This discussion from my end was not about “deteriorating” patients. We were talking about who which submissive patients should get catheter directed lytics. I’m sorry you misunderstood that and again made some assumptions that clearly confused you. Trying clarifying better next time.

 

[vector2]

When I made the CT alone comment you were only discussing CT finding and had made no mention of other clinical factors. This was all in the context of my original statement that radiologist should not be putting in catheters for directed lytics based on CT imaging alone. Also I never said that was your argument. I said it’s bad medicine to only use that. You clearly made some assumptions there and found yourself indignant.

This discussion from my end was not about “deteriorating” patients. We were talking about who which submissive patients should get catheter directed lytics. I’m sorry you misunderstood that and again made some assumptions that clearly confused you. Trying clarifying better next time.

That's a good try with the "sorry you're confused" nonsense, but in the very first post I ever made about the topic I said "If on the CT the RV:LV ratio is decently increased, septum is flattened, there's venous contrast reflux, and the BP is only borderline normal, ..." From the beginning, I have intimated that the clinical picture has importance and we are talking about a borderline picture at that, even though you desperately wish (and act) as if the only statement I made was RV:LV 0.9 or BUST.

Also, I gathered from your previously stated need to have an official read back from cards that you're not really that facile or knowledgeable about echocardiography or alternative cardiac imaging modalities, but yet you bizarrely continue to disagree authoritatively with me (and without sourcing) when I tell you that RV:LV ratio, IVC contrast reflux, and abnormal septum position are synonymous with significant RV dysfunction, not to mention prognostic of adverse outcomes. Even worse, you can't even specify what it is you do want the official cardiology TTE read to say about the RV other than "worrisome." We may both be bringing our opinions to the table, but at least I can tell everyone what I'm looking for before making the clinical decision with more specificity than "worrisome."

 

[vector2]

--------
"To evaluate the ability to identify right ventricular (RV) dysfunction, and to predict adverse outcomes of chest computed tomography (CT), we compared CT and echocardiography in acute pulmonary embolism patients. We analyzed 56 patients diagnosed by CT with acute pulmonary embolism, who underwent echocardiography within 48 h of CT scan from January 2004 to December 2008. From the CT scan, the ratio of RV diameter to left ventricular diameter (RVd/LVd), the presence of septal bowing and embolus location were determined. RVd/LVd (P < 0.001), septal bowing (P < 0.001) and proximal embolism (P = 0.016) were associated with echocardiographic RV hypokinesia. The odds ratio for adverse clinical outcomes was 19.2 for the combination of three CT parameters (RVd/LVd > 1, septal bowing, and proximal embolism), and 13.4 for RV hypokinesia (each P = 0.001). The positive predictive value (PPV) for adverse clinical outcomes for echocardiographic RV hypokinesia was 55.0%, and the negative predictive value (NPV) was 96.2%. The three-parameter combination predicted adverse clinical outcomes with a PPV of 54.5%, and a NPV of 94.1%. CT parameters including RV dysfunction were significantly associated with poor outcomes. Rapid risk stratification of patients with acute pulmonary embolism based on chest CT appears to be comparable with echocardiography, is clinically reliable, and may be useful in guiding management strategy. "

Evaluation of right ventricular dysfunction and prediction of clinical outcomes in acute pulmonary embolism by chest computed tomography: comparisons with echocardiography - PubMed

To evaluate the ability to identify right ventricular (RV) dysfunction, and to predict adverse outcomes of chest computed tomography (CT), we compared CT and echocardiography in acute pulmonary embolism patients. We analyzed 56 patients diagnosed by CT with acute pulmonary embolism, who...

www.ncbi.nlm.nih.gov

-------------

--------
CONCLUSIONS:
Three-dimensional ventricular volume measurement on chest CT is a predictor of early death in patients with acute PE, independent of clinical risk factors and comorbidities. Abnormal position of the interventricular septum, inferior vena cava contrast reflux, and RVD(4-CH)/LVD(4-CH) ratio are predictive of adverse outcomes, whereas RVD(axial)/LVD(axial) ratio >1.0 is not

CT signs of right ventricular dysfunction: prognostic role in acute pulmonary embolism - PubMed

Three-dimensional ventricular volume measurement on chest CT is a predictor of early death in patients with acute PE, independent of clinical risk factors and comorbidities. Abnormal position of the interventricular septum, inferior vena cava contrast reflux, and RVD(4-CH)/LVD(4-CH) ratio are...

www.ncbi.nlm.nih.gov

---------------


---------------
RESULTS:
A total of 49 studies with 13,162 patients with acute pulmonary embolism (median age of 61 years, 55.1% were women) who underwent diagnostic CT imaging were included in the analysis. An abnormally increased RV/LV diameter ratio measured on transverse sections was associated with an approximately 2.5-fold risk for all-cause mortality (pooled odds ratio [OR], 2.5; 95% confidence interval [CI], 1.8-3.5) and adverse outcome (OR, 2.3; 95% CI, 1.6-3.4) and a 5-fold risk for pulmonary embolism-related mortality (OR, 5.0; 95% CI, 2.7-9.2). Thrombus load (OR, 1.6, 95% CI, 0.7-3.9; P = .2896) and central location (OR, 1.7; 95% CI, 0.7-4.2; P = .2609) were not predictive for all-cause mortality, although both were associated with adverse clinical outcome.

CONCLUSIONS:
Across all end points, the RV/LV diameter ratio on transverse CT sections has the strongest predictive value and most robust evidence base for adverse clinical outcomes in patients with acute pulmonary embolism.

Predictive Value of Computed Tomography in Acute Pulmonary Embolism: Systematic Review and Meta-analysis - PubMed

Across all end points, the RV/LV diameter ratio on transverse CT sections has the strongest predictive value and most robust evidence base for adverse clinical outcomes in patients with acute pulmonary embolism.

www.ncbi.nlm.nih.gov

-----------------


----------------
Abstract
There is variability in guideline recommendations for assessment of the right ventricle (RV) with imaging as prognostic information after acute pulmonary embolism (PE). The objective of this study is to identify a clinical scenario for which normal CT-derived right-to-left ventricular (RV/LV) ratio is sufficient to exclude RV strain or PE-related short-term death. This retrospective cohort study included 579 consecutive subjects (08/2003-03/2010) diagnosed with acute PE with normal CT-RV/LV ratio (<0.9), 236 of whom received subsequent echocardiography. To identify a clinical scenario for which CT-RV/LV ratio was considered sufficient to exclude RV strain or PE-related short-term death, a multivariable logistic model was created to detect factors related to subjects for whom subsequent echocardiography detected RV strain or those who did not receive echocardiography and died of PE within 14 days (n = 55). The final model included five variables (c-statistic = 0.758, over-fitting bias = 2.52 %): congestive heart failure (adjusted odds ratio, OR 4.32, 95 % confidence interval, CI 1.88-9.92), RV diameter on CT >45 mm (OR 3.07, 95 % CI 1.56-6.03), age >60 years (OR 2.59, 95 % CI 1.41-4.77), central embolus (OR 1.96, 95 % CI 1.01-3.79), and stage-IV cancer (OR 1.94, 95 % CI 0.99-3.78). If these five factors were all absent (37.1 % of the population), the probability that "CT-RV/LV ratio is sufficient to exclude RV strain/PE-related short-term death" was 0.97 (95 % CI = 0.95-0.99). Normal CT-RV/LV ratio plus readily obtained five clinical predictors were adequate to exclude RV strain or PE-related short-term mortality.

Normal ventricular diameter ratio on CT provides adequate assessment for critical right ventricular strain among patients with acute pulmonary embolism - PubMed

There is variability in guideline recommendations for assessment of the right ventricle (RV) with imaging as prognostic information after acute pulmonary embolism (PE). The objective of this study is to identify a clinical scenario for which normal CT-derived right-to-left ventricular (RV/LV)...

www.ncbi.nlm.nih.gov

-------------------

 

[jdh71]

That's a good try with the "sorry you're confused" nonsense, but in the very first post I ever made about the topic I said "If on the CT the RV:LV ratio is decently increased, septum is flattened, there's venous contrast reflux, and the BP is only borderline normal, ..." From the beginning, I have intimated that the clinical picture has importance and we are talking about a borderline picture at that, even though you desperately wish (and act) as if the only statement I made was RV:LV 0.9 or BUST.

Also, I gathered from your previously stated need to have an official read back from cards that you're not really that facile or knowledgeable about echocardiography or alternative cardiac imaging modalities, but yet you bizarrely continue to disagree authoritatively with me (and without sourcing) when I tell you that RV:LV ratio, IVC contrast reflux, and abnormal septum position are synonymous with significant RV dysfunction, not to mention prognostic of adverse outcomes. Even worse, you can't even specify what it is you do want the official cardiology TTE read to say about the RV other than "worrisome." We may both be bringing our opinions to the table, but at least I can tell everyone what I'm looking for before making the clinical decision with more specificity than "worrisome."

Im sorry you were confused.

“Borderline normal” sure seems like a nice way to try and hide now. What does that mean?

I’m sure if YOU can learn echo in training I could have easily as well but I wasn’t trained with echo to more than a rough estimate on bedside echo. That is no crime. Nor is it anything to be ashamed about. You trying to beat me over the head with it Is cute but it changes nothing hero. The actual function when I decide to make my decision about treating submissive PE is important to me.

 

[vector2]

Im sorry you were confused.

“Borderline normal” sure seems like a nice way to try and hide now. What does that mean?

I’m sure if YOU can learn echo in training I could have easily as well but I wasn’t trained with echo to more than a rough estimate on bedside echo. That is no crime. Nor is it anything to be ashamed about. You trying to beat me over the head with it Is cute but it changes nothing hero. The actual function when I decide to make my decision about treating submissive PE is important to me.

You’re presumably a critical care physician and you’re not familiar with the term “borderline” in relation to vitals, labs, tests? Yowsers, good thing I didn’t use the word “equivocal.” However, to explain it at a level simple enough for you to comprehend, traditional definitions of submassive PE use an SBP of 90 as a cutoff. A borderline normal SBP would be something like 95- technically not meeting the definition but certainly not reassuring from a clinical standpoint. Ergo, from the beginning I never advocated CT parameters as the sole criteria for taking a submassive to the cathlab.

You not being trained in echo certainly isn’t a crime. The crime is you insisting you want the cardiologist to give you an official read but the most specific he has to be about RV function to satisfy you is “worrisome.” The crime is you going around telling people who have way more experience in echo and dynamic evaluation of cardiac function that X modality is definitely better or more useful than Y, or that one “absolutely actually cannot” evaluate RV function from CT ....without providing a shred of evidence or really anything more than the opinion of you and your group.

 

[jdh71]

You’re presumably a critical care physician and you’re not familiar with the term “borderline” in relation to vitals, labs, tests? Yowsers, good thing I didn’t use the word “equivocal.” However, to explain it at a level simple enough for you to comprehend, traditional definitions of submassive PE use an SBP of 90 as a cutoff. A borderline normal SBP would be something like 95- technically not meeting the definition but certainly not reassuring from a clinical standpoint. Ergo, from the beginning I never advocated CT parameters as the sole criteria for taking a submassive to the cathlab.

You not being trained in echo certainly isn’t a crime. The crime is you insisting you want the cardiologist to give you an official read but the most specific he has to be about RV function to satisfy you is “worrisome.” The crime is you going around telling people who have way more experience in echo and dynamic evaluation of cardiac function that X modality is definitely better or more useful than Y, or that one “absolutely actually cannot” evaluate RV function from CT ....without providing a shred of evidence or really anything more than the opinion of you and your group.

I don't know what is so necessarily clinically unsettling about a SBP of 95.

It's no "crime" to want an up to date assessment of RV function in real time. Which is what the echo gives me.

I'm sorry you didn't like being challenged. It has clearly brought out the "best" you here complete with cries of being severely wronged. This must have been really hard for you. You can't tell me what the actual RV function is from the CT scan. There are plenty of RVs that don't look great on CT scan but look fine on echo and have otherwise fine enough clinical variables. I don't have to provide you with randomized trial or other "evidence". The RV on CT is a slice, a snap shot. It isn't an analysis of function.

 

[vector2]

I don't know what is so necessarily clinically unsettling about a SBP of 95.

If you don’t understand why a SBP of 95 isn’t the most reassuring of vitals in the context of a confirmed PE with poor CT prognostic signs, I shudder to think of how little vigilance you have for the other marginal or at-risk pts in your unit. But hey, not everyone understands the gestalt of the critically ill.

It's no "crime" to want an up to date assessment of RV function in real time. Which is what the echo gives me.

I'm sorry you didn't like being challenged. It has clearly brought out the "best" you here complete with cries of being severely wronged. This must have been really hard for you. You can't tell me what the actual RV function is from the CT scan. There are plenty of RVs that don't look great on CT scan but look fine on echo and have otherwise fine enough clinical variables. I don't have to provide you with randomized trial or other "evidence". The RV on CT is a slice, a snap shot. It isn't an analysis of function.

You can challenge all you want, but it’s an embarrassing attempt and utterly toothless when your reasoning begins and ends with “because I said so.” Firstly, it’s not “real time” because you have to wait for an echo tech to come and then wait for the turn around time and final read, which even under the best conditions isn’t that speedy in an evolving submassive PE who already had concerning signs on his admission CT. Secondly, it’s clear that you don’t have the foundational knowledge (aka a fking clue) to understand the implications of RV dilatation / D-shaped septum / septal bowing / interventricular dependence / presence of tricuspid regurgitation / RV pressure overload in the setting of heavy clot burden- all things which can be picked up or inferred on CT (as a side note, you also keep saying snapshot but maybe you don’t realize that rapid injection contrast studies also have some temporal information due to bolus tracking). But even if we were talking about a snapshot, look at this:

It's just a still image. There's no dynamic clips for you to get all excited about. I know you don't know much about echo, but would you like to take a guess on what this pt's LVEF is? Is there a chance on earth that it's 55%? The answer is no, and we know this based on the fundamental properties of what myocardium that is dilated to this absurd extend can do. We don't know if the LVEF is 12% or 18%, but we know it's bad. Similarly, even though our knowledge of the RV isn't as good, we know that its function is significantly compromised by gross dilation from RV pressure overload, septal distortion/bowing into the LV, and significant tricuspid regurgitation, all of which can be picked on CT and all of which are associated with a much higher risk of death in PEs. However, similarly to that dilated LV still, we don't know from a CT if the RV TAPSE is 9 or 10, but we know that a RV:LV volume ratio of 1.6:1 with septal bowing and supportive clinical signs means the function is bad enough to not need further quantitation before intervention.

I know you're so blinded but some strange desire to keep one-upping me that it probably won't matter, but just consider for a moment that your anecdote about "don't look great on CT but look fine on echo" might just be an incomplete description of what CT can tell us about ventricular function.




E:
vvvvvvvvvv
Good stuff, good stuff. I’m guessing it’s not the first time you’ve acted like an graceless ass after getting thoroughly educated, considering you’ve somehow managed to accrue 70,000 posts of what I assume is similarly inane bullsht

 

[jdh71]

If you don’t understand why a SBP of 95 isn’t the most reassuring of vitals in the context of a confirmed PE with poor CT prognostic signs, I shudder to think of how little vigilance you have for the other marginal or at-risk pts in your unit. But hey, not everyone understands the gestalt of the critically ill.

You can challenge all you want, but it’s an embarrassing attempt and utterly toothless when your reasoning begins and ends with “because I said so.” Firstly, it’s not “real time” because you have to wait for an echo tech to come and then wait for the turn around time and final read, which even under the best conditions isn’t that speedy in an evolving submassive PE who already had concerning signs on his admission CT. Secondly, it’s clear that you don’t have the foundational knowledge (aka a fking clue) to understand the implications of RV dilatation / D-shaped septum / septal bowing / interventricular dependence / presence of tricuspid regurgitation / RV pressure overload in the setting of heavy clot burden- all things which can be picked up or inferred on CT (as a side note, you also keep saying snapshot but maybe you don’t realize that rapid injection contrast studies also have some temporal information due to bolus tracking). But even if we were talking about a snapshot, look at this:

It's just a still image. There's no dynamic clips for you to get all excited about. I know you don't know much about echo, but would you like to take a guess on what this pt's LVEF is? Is there a chance on earth that it's 55%? The answer is no, and we know this based on the fundamental properties of what myocardium that is dilated to this absurd extend can do. We don't know if the LVEF is 12% or 18%, but we know it's bad. Similarly, even though our knowledge of the RV isn't as good, we know that its function is significantly compromised by gross dilation from RV pressure overload, septal distortion/bowing into the LV, and significant tricuspid regurgitation, all of which can be picked on CT and all of which are associated with a much higher risk of death in PEs. However, similarly to that dilated LV still, we don't know from a CT if the RV TAPSE is 9 or 10, but we know that a RV:LV volume ratio of 1.6:1 with septal bowing and supportive clinical signs means the function is bad enough to not need further quantitation before intervention.

I know you're so blinded but some strange desire to keep one-upping me that it probably won't matter, but just consider for a moment that your anecdote about "don't look great on CT but look fine on echo" might just be an incomplete description of what CT can tell us about ventricular function.

are you still all worked up about this?

 

[deleted547339]

I find it very surprising when IR would pursue thrombolysis without input of others.



PERT team is becoming the standard of care in my opinion. Those catheter therapy can be high risk but high reward as well and there is a lack in high quality evidence because it’s an ongoing investigation. I think those procedure should involve more than IR in decision making.

I dont think you know what standard of care means. And if you do, you are pretty loose with it.