Pe

obiwan said:

have a case i was hoping to get some thoughts particularly from you pulm/cc guys

basically female comes in with central massive pe (not saddle) but is fairly asymptomatic and hemodynamically stable.

echo is done which shows some decreased RV function, RVSP 55 consistent with mod pulm HTN, and LV with D shaped septum

is this someone you would go with the tPA route? also, is this someone who you would completely avoid IV fluids in?

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I wouldn't tPA a patient without more symptoms (ie. hypotension or hypoxia).

There is enough data on what you're describing which based on the echo finding that we would call a "sub-massive" PE that you can make the case for tPE in that situation. But stable is stable. Most of us get the tPA ready and watch that patient in the MICU, but otherwise don't pull the trigger, use heparin instead of lovenox (or similar) so that it can be stopped, and give the tPA only if the patient de-compensates.

I see no reason to avoid IV fluids if you think you need IV fluids.

If this patient wasn't symptomatic, what brought her in and why'd she get scanned?

obiwan said:

i guess with the read of a higher RVSP that would make me more cautious with fluid administration or entirely avoid if patient were to go into obstructive shock.

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If you've got pressure on the left side, then your parameters in the right side are going to generally be fine for fluid administration IF you think the patient needs it and it doesn't sound like this is a case when you'd even need to have anything outside of TKO going.

If you get into an obstructive shock picture from PE, well . . .that's a really, really bad thing and the only intervention that really helps is removing the obstruction, lytics or surgery. V-A echmo, if available, can help tremendously in these patients, if not available, then kick the RV with dobutamine and afterload reduce the PA with inhaled nitric or epoprostenol, while praying for the lytics to work.

Almost always if it gets this bad, these patients just die despite our best efforts. A BIG clot in the PA is on the wrong side of basically all the physiology.

obiwan said:

have a case i was hoping to get some thoughts particularly from you pulm/cc guys

basically female comes in with central massive pe (not saddle) but is fairly asymptomatic and hemodynamically stable.

echo is done which shows some decreased RV function, RVSP 55 consistent with mod pulm HTN, and LV with D shaped septum

is this someone you would go with the tPA route? also, is this someone who you would completely avoid IV fluids in?

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Fluids usually help in RV failure from PE. Just like RV failure from MI, it is very pre-load dependent.

Instatewaiter said:

Fluids usually help in RV failure from PE. Just like RV failure from MI, it is very pre-load dependent.

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Fluids can make it worse. The failing RV is probably the most tricky bitch out of any and all pathophysiology. Preload isn't the problem with PE. It's the big honking clot in the PA. Forcing in fluids on the venous side could be completely catastrophic in this setting the RV handles large increasing fluid shifts quite well at baseline but what it doesn't handle well are acute change in PRESSURE. So once the RV has reached it's distensibility pressures head up precipitously and in the setting of big PE are already high. And once this begins to occur the forward feeding cycle of sh8t know as RV dysfunction and ischemia feed in on themselves until the RV fails and the patient dies. Besides if you're not getting a little bit if blood through an obstructing clot, what makes you think you'll be getting MORE fluid past the same obstruction given the physics of the situation?

In the setting of PE you MIGHT be in a situation there you have some room from a frank-starling perspective to optimize preload with a small bolus, but don't start dumping in fluids. The RV compensates to an increased loads mostly with an increase in contractilty. So your best bet in dealing with the RV in PE is to kick with dobutamine and afterload reduce with inhaled vasodilators.

Be very careful of fluids and DO NOT treat PE like RV infarct.

I would like more details on the admission.

Pt was 'mildly dyspneic but not hypoxic"..whay was she scanned then?

Was she a youngs 30 something on OCPs or an old gomer or a longstanding COPDr?

Does she have any history of left or right heart failure?

Does she have a previously normal ECHO?

Does she have any ekg changes or elevation in the cardiac biomarkers?

What did the ECHO show in terms of contracility of the RV? Was it big and globally hypocontractile or just a mildly enlarged chamber with normal squeeze?

As JDH said, you have described a "central/massive but not saddle", to use your words, embolus, with RV dilatation and elevated right sided pressures. this is by definiton a submassive PE and thus has a 2b recommendation to lyse. However I would not pull the trigger on lysing her without answers to the above questions. I have seen what was described as small segmental PE cause RV failure and another pt with a near saddle embolus with normal echo tolerating room air....the clinical picture is very important here.

I don't have the guidelines memorized (yet), but have been told a good rule of thumb is that where there is evidence of right heart failure, its time to pull out the big guns. No sense in waiting for death angel to come knocking on the door before you get busy correcting the underlying problem.

jdh71 said:

Fluids can make it worse. The failing RV is probably the most tricky bitch out of any and all pathophysiology. Preload isn't the problem with PE. It's the big honking clot in the PA. Forcing in fluids on the venous side could be completely catastrophic in this setting the RV handles large increasing fluid shifts quite well at baseline but what it doesn't handle well are acute change in PRESSURE. So once the RV has reached it's distensibility pressures head up precipitously and in the setting of big PE are already high. And once this begins to occur the forward feeding cycle of sh8t know as RV dysfunction and ischemia feed in on themselves until the RV fails and the patient dies. Besides if you're not getting a little bit if blood through an obstructing clot, what makes you think you'll be getting MORE fluid past the same obstruction given the physics of the situation?

In the setting of PE you MIGHT be in a situation there you have some room from a frank-starling perspective to optimize preload with a small bolus, but don't start dumping in fluids. The RV compensates to an increased loads mostly with an increase in contractilty. So your best bet in dealing with the RV in PE is to kick with dobutamine and afterload reduce with inhaled vasodilators.

Be very careful of fluids and DO NOT treat PE like RV infarct.

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I'm not saying dump them in willy-nilly or dump them in continuously, many (?most) guidelines say give 500cc - 1L initially. An empty ventricle doesn't respond too well to inotropes. I guess I should have said, preload sensitive.

Instatewaiter said:

I'm not saying dump them in willy-nilly or dump them in continuously, many (?most) guidelines say give 500cc - 1L initially. An empty ventricle doesn't respond too well to inotropes. I guess I should have said, preload sensitive.

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I know your training pedigree and that you are not an idiot so I hope it didn't sound like I was jumping on you, but for everyone reading, I just wanted it to be clear that we didn't want to treated PE with RV issues exactly the same with the huge amount of fluids you'll see used with other etiologies of RV dysfunction/failure

obiwan said:

oops forgot to adhere to the strict massive vs submassive nomenclature

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serious business

I'm not pushing it in a code unless I know I have a clot.

obiwan said:

are you guys big pushers of tPA during codes especially if you have a high suspicion for clot?

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I'm a little gunshy about pushing it.

Every code I have been a part of where it has been pushed has ended up with blood spewing from the mouth of the patient each time someone pressed on the chest. It is a pretty nasty thing to watch and it hasn't made a difference in the handful of times I've seen it pushed.

I have to be pretty suspicious of a clot.

jdh71 said:

I know your training pedigree and that you are not an idiot so I hope it didn't sound like I was jumping on you, but for everyone reading, I just wanted it to be clear that we didn't want to treated PE with RV issues exactly the same with the huge amount of fluids you'll see used with other etiologies of RV dysfunction/failure

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Nah, we're cool.

jdh71 said:

Fluids can make it worse. The failing RV is probably the most tricky bitch out of any and all pathophysiology. Preload isn't the problem with PE. It's the big honking clot in the PA. Forcing in fluids on the venous side could be completely catastrophic in this setting the RV handles large increasing fluid shifts quite well at baseline but what it doesn't handle well are acute change in PRESSURE. So once the RV has reached it's distensibility pressures head up precipitously and in the setting of big PE are already high. And once this begins to occur the forward feeding cycle of sh8t know as RV dysfunction and ischemia feed in on themselves until the RV fails and the patient dies. Besides if you're not getting a little bit if blood through an obstructing clot, what makes you think you'll be getting MORE fluid past the same obstruction given the physics of the situation?

In the setting of PE you MIGHT be in a situation there you have some room from a frank-starling perspective to optimize preload with a small bolus, but don't start dumping in fluids. The RV compensates to an increased loads mostly with an increase in contractilty. So your best bet in dealing with the RV in PE is to kick with dobutamine and afterload reduce with inhaled vasodilators.

Be very careful of fluids and DO NOT treat PE like RV infarct.

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100% agree. Fluid boluses in obstructive right heart failure can just pancake the LV and LV stroke volume. The only style difference is that I like Epinephrine +/- Vaso, Milrinone > Dobutamine, and Flolan.

And to also weight in on the original post -> submassive PE doesn't get lytics. the only utility of knowing that there's some RV strain without shock is that it has some prognostic value.

souljah1 said:

100% agree. Fluid boluses in obstructive right heart failure can just pancake the LV and LV stroke volume. The only style difference is that I like Epinephrine +/- Vaso, Milrinone > Dobutamine, and Flolan.

And to also weight in on the original post -> submassive PE doesn't get lytics. the only utility of knowing that there's some RV strain without shock is that it has some prognostic value.

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Any particular reason you prefer the milrinone?

jdh71 said:

Any particular reason you prefer the milrinone?

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Like Epi so if I need additional inotropy I reach for milrinone as opposed to another drug with a similar mechanism of action to Epi (B agonist). Not sure how much benefit there is to adding dobutamine to epinephrine.

souljah1 said:

Like Epi so if I need additional inotropy I reach for milrinone as opposed to another drug with a similar mechanism of action to Epi (B agonist). Not sure how much benefit there is to adding dobutamine to epinephrine.

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Roger that. Makes sense.

I too like Milrinone over Dobutamine for massive PE if needed. Milrinone Inhibits cAMP phosphodiesterase which also dilates pulmonary arteries.

because of the mechanism difference milrinone is also highly unlikely to produce arrythmia and tachyphylaxis like dobutamine. Seeing as we are adding to epi, which itself can cause tachy, dobutamine on top could really make things worse. Milrinone is renally cleared and has to be dose adjusted for renal failure, which a lot of shock pts have, so that needs to be factored in as well.

Bostonredsox said:

because of the mechanism difference milrinone is also highly unlikely to produce arrythmia and tachyphylaxis like dobutamine. Seeing as we are adding to epi, which itself can cause tachy, dobutamine on top could really make things worse. Milrinone is renally cleared and has to be dose adjusted for renal failure, which a lot of shock pts have, so that needs to be factored in as well.

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I would not say that tachyarrythmias are highly unlikely on milrinone. They definitely happen.

In my experience, with milrinone, they happen pretty damn commonly. We used to call it kill-rinone.

somewhere out there, there is a study between milrinone and dobutamine and they found similar rates of arrhythmia. I don't remember the specifics. I'll look for it somewhere

souljah1 said:

I would not say that tachyarrythmias are highly unlikely on milrinone. They definitely happen.

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I'd love to see some data on it. My experience is fewer arrhythmia's with milrinone than dobutamine. But my N isn't a huge number and just anecdotal from what I've seen.

Instatewaiter said:

somewhere out there, there is a study between milrinone and dobutamine and they found similar rates of arrhythmia. I don't remember the specifics. I'll look for it somewhere

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I don't have any data to back this up, but from my experience, dobu will get you tachycardic in a hurry, then maybe give you an arrhythmia later -- gives you lots of warning and usually people switch out of it coz of the tachycardia. Primacor will make you think everything's hunkydory then warn you a little with some PVCs and NSVTs here and there, then get you into VT if you're not paying attention.

And what I think? Too many people avoid using either when they are really needed because they are afraid of rhythm issues.

Also, just because a patient is tachy at 120-130 on one of these is not some reason to worry, especially in younger, structurally normal hearts.

jdh71 said:

And what I think? Too many people avoid using either when they are really needed because they are afraid of rhythm issues.

Also, just because a patient is tachy at 120-130 on one of these is not some reason to worry, especially in younger, structurally normal hearts.

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In PE, fine. Not sure we have data one way or the other (perhaps someone can correct me) but maybe it is just like in heart failure...

In regular ole heart failure though, I think they are used way, way too much. In residency it was used like water for severely decompensated heart failure. I think this is a common experience. We thought, if we can just get them over this hump then we will pull off the intropes and can justify it. But, when you think about it, the data really doesn't support it. It's like giving blood when the hemoglobin is 10. The numbers get better but in the end, you are doing more harm than good. Perhaps inotropes are the same in PE...

Anyone have studies?

Instatewaiter said:

In PE, fine. Not sure we have data one way or the other (perhaps someone can correct me) but maybe it is just like in heart failure...

In regular ole heart failure though, I think they are used way, way too much. In residency it was used like water for severely decompensated heart failure. I think this is a common experience. We thought, if we can just get them over this hump then we will pull off the intropes and can justify it. But, when you think about it, the data really doesn't support it. It's like giving blood when the hemoglobin is 10. The numbers get better but in the end, you are doing more harm than good. Perhaps inotropes are the same in PE...

Anyone have studies?

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Well. It's all first principles when it comes to this kind of thing. You'll never get a randomized anything for massive PE, right? RV respond to an increased load most effectively by an increase in contractility, therefore the ionotropes on top of pulmonary vascular afterload reduction.

When it comes to heart failure, I'm sure this is much more nuanced.

I have been meaning to ask this. In cardiogenic shock if the patient is tachycardic to compensate what can one do? The tachy is doing no good cuz less filling time. But would you still add dobutamine say even if pt is tachy to say 130s?

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jdh71 said:

Well. It's all first principles when it comes to this kind of thing. You'll never get a randomized anything for massive PE, right? RV respond to an increased load most effectively by an increase in contractility, therefore the ionotropes on top of pulmonary vascular afterload reduction.

When it comes to heart failure, I'm sure this is much more nuanced.

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Why not? They have randomized studies for STEMI, ICH and a host of other life threatening things- why not massive PE?

I think my point was that just because it makes sense physiologically and you have surrogate end points doesn't mean it works. Just like the RV responds to increased contractility in PE, in severe decompensated HF all the numbers improve with inotropy. If you use BP or CO or stroke volume or mixed venous sats or SVR it looks like you can do no wrong with dobutamine or milrinone. The problem is when they actually studied inotropes, it killed people. Might as well give IV beta blockers to them because you're doing about as much good.

redy said:

I have been meaning to ask this. In cardiogenic shock if the patient is tachycardic to compensate what can one do? The tachy is doing no good cuz less filling time. But would you still add dobutamine say even if pt is tachy to say 130s?

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For the most part Nipride and Balloon pump should be your go to. If you have to levophed.

If you do it carefully and slowly, nipride can be used even when the BP is very, very low.

/agree with instate. If there so tachy from failure on cardiogenic shock that I think it's further worsening their CO/CI because of decreasing ventricular filling times, then it's time for an IABP.

Instatewaiter said:

Why not? They have randomized studies for STEMI, ICH and a host of other life threatening things- why not massive PE?

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Why not? You're cute sometimes, because: 1) the study would take too long - not a large number of massive PEs requiring salvage in any given year, even if you could get multiple centers together, coupled together with just how tricky it is to randomize ANY crazy sick patient to ANY kind of differing therapy by informed consent [you should really try and do some of this sometime, "Hey I know your loved one is really scary sick, I want to talk to you about some experimental stuff we want to try with them . . ." - been there, done that, have the t-shirt, you do it . . .] and 2) who exactly do you think is going to pay for it?

Do the math. Connect some dots. And because I think you're a smart guy, I think you'll begin to understand just exactly WHY that study is NEVER going to be done. Of course it's technically possible, but then there is the real world of clinical research. Wish into one hand, crap into the other, tell me which one fills up quick.

I think my point was that just because it makes sense physiologically and you have surrogate end points doesn't mean it works.

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And my point was that is ALL we have - first principles here. So you can wax philosophical about anything you want, but you're not in the trenches taking care of these patients. The bunch of nice trials in the cardio literature is basically non-existent anywhere else in the same manner. So I can agree just because it makes sense physiological doesn't necessarily mean it will work out, and I'd counter just because that point is true . . . doesn't mean it won't work!! This is fun. But ultimately not helpful.

Just like the RV responds to increased contractility in PE, in severe decompensated HF all the numbers improve with inotropy. If you use BP or CO or stroke volume or mixed venous sats or SVR it looks like you can do no wrong with dobutamine or milrinone. The problem is when they actually studied inotropes, it killed people. Might as well give IV beta blockers to them because you're doing about as much good.

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Agreed. But that's NOT what we are talking about here . . .

Is it . . . ?

jdh71 said:

Why not? You're cute sometimes,

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Are you coming on to me? Flattered as I am, I'm gonna see how this whole heterosexual thing works out for me.

JDH said:

2) who exactly do you think is going to pay for it?

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The rainbow and unicorn coallition has deep pockets. Fine, you make a valid point.

JDH said:

] So I can agree just because it makes sense physiological doesn't necessarily mean it will work out, and I'd counter just because that point is true . . . doesn't mean it won't work!! This is fun. But ultimately not helpful.

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As I told you previously, that is what cardiology is here for. To ultimately not be helpful