Coming back to this, doesn’t VTI tell you the same thing?
06.01.2025 10:02
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Coming back to this, doesn’t VTI tell you the same thing?
Obviously I am not actively doing things and ignoring negative trials, some times despite negative trials, a particular intervention is all you have. For example Ecmo - trials are not particularly supportive yet we do it when it’s necessary.
Yes and no…. I have a problem with the current paradigm of research. Our population is never homogenous. And positive trials are fine but negative trials don’t necessarily mean the intervention isn’t useful but it gets thrown in the bin.
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Great right heart 101 skytorial with references and samples.
#echofirst
My practice and what I have observed: When using for pneumonia, almost always 50mg QDS. When doing it for shock- infusion. When pneumonia with shock, infusion.
Sema-GLU-tide. Obviously.
I am
Not sure about that. I have been involved in 3 and 2 survived the procedure - 1 walked out the hospital
And the other died later.
Experience of doing them?
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But we see contrast reflux into IVC in RV “strain” following acute PE. I am not sure fluid removal is the right choice here…
But we see severe RV dilation in cases of acute pulmonary embolism.
But RV won’t be down because of regurgitation!
Because removing fluid may bring total cardiac output down - the question is where the balance lies, does removing fluid and bringing back forward flow improve cardiac output to offset the volume loss- perhaps trial and error?
Yes but my problem with that is prior to onset of scute pulmonary hypertension, the patient had a normovolaemic state. The same fluid status is now too much for the patient because of acute pulmonary hypertension, the treatment should be reduce PVR not remove fluid.
Not sure I follow. Fluid removal
Would increase the gradient between RV and CVP no?
And isn’t the solution here still more inotropy/pulmonary vasodilators
Ok so now different question @drfreeze.bsky.social @load-dependent.bsky.social @zentensivist.bsky.social lets say aspiration pneumonia, severe ARDS, acute pulmonary hypertension with RV dilation and new tricuspid regurgitation - wouldn’t fluid removal also increase regurgitation fraction?
Yes the tachycardia will help, but even without tachycardia, inotropy should help.
But it’s difficult to justify this when the LV is “hyperdynamic”. However, I think the nuance that this is in context of regurgitation is lost.
This strategy puts you at risk of DLVOTO but you can watch out for that
The context is that the patient is presenting with septic shock.
I think the solution is less focus on removing fluid and more focus on forward flow. So I think inotropy is useful, such as milrinone or dobutamine, which should reduce regurgitation fraction and improve forward EF
How about MR causing pulmonary hypertension resulting in RV dilation and functional TR?
Ok next question. When there is severe tricuspid regurgitation (and normal RV function) in a patient with septic shock, and you have a high CVP, pulsatile flow in hepatic vein and distended IVC, how do you take fluid off without increasing regurgitating fraction? Isn’t the elevated cvp helping?
I love that idea!
Question for echo gurus, how do you interpret hyperdynamic or normal ventricular function in the context of severe regurgitation(mitral or tricuspid)? @load-dependent.bsky.social @zentensivist.bsky.social @drfreeze.bsky.social
Just to repeat the point made many times before, you have to individualise care. The current research paradigm doesn’t allow that so studies have to be taken in that context. If you have cardiogenic shock and you are bradycardic, dobutamine is better than milrinone. And if it doesn’t work, move on.
This is absolutely brilliant
This is exactly the scenario I have in my mind when thinking about vasopressin use. In my opinion, the inotropic effect of high dose noradrenaline is not appreciated enough and patients get more and more tachycardic. And not enough people are thinking about DLVOTO.
It’s obviously more nuanced and you can’t set one rule for a heterogenous population…which is the original point you were making anyway but I think it’s important to say that sometimes it’s ok to have vasopressin
