Let’s try something different. Does anyone have any questions about acute and critical care echocardiography? If I can’t answer I’ll try to bring in someone who can. #emimcc #cccsky #pocus
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If I may, 2nd question. Say RV failure with consequential LV failure resulting in circulatory shock. Say you fixed whatever you can to optimise RV, PVR, RV afterload etc (ie., max medical Rx) yet see septum bowing & obliterating LV (almost like SAM)what’s your thought process / further Rx ? Thanks
Say you have a septic patient with diastolic dysfunction, how does that change your management ? And what do you then track to guide management further down the line
That's a whole big theme. When we usually talk about diastolic dysfunction we conflate filling pressure with actual function. We assume that if we find signs of elevated diastolic pressure at rest, then the patient has diastolic dysfunction.
We have evidence that echocardiography is fair at detecting elevated diastolic pressure at rest (essentially correlation across individuals), but we have very little and conflicting evidence for ability to track diastolic pressure within individuals over time and with change in conditions.
So I think we should be very careful about making judgements about diastolic function and pressure in acute illness, and the ability to track pressure and function over time is an area ripe for research.
If you know that this patient has poor diastolic function, truly restrictive physiology, and you have a baseline, I think many think that tachycardia is more detrimental than it is. In the extreme patients will have a fixed stroke volume, and bradycardia may actually increase LAP and reduces CO.
What is your aim? As I mentioned to @teddyhla.bsky.social diastology was primarily developed for the outpatient setting, to diagnose heart failure with preserved EF. It’s unclear what it’s use is in the acute/critical care setting.
I'd say the best resource is likely the diastolic guideline that you are recommended using, and which you will asked for I imagine. The ASE 2016 gives a good description of limitations and a succinct summary of the physiology.
I've struggled to find literature on this. It's mostly on valsalva manoeuvre in stable patients, or CPAP in healthy volunteers.
Even for IVC it's murky, some guidelines advocate "sniffing" to judge variation, others spontaneous calm breathing which is obviously very different.
In patients with an impella whats the best way to estimate CO/CI? Lets say you dont have a PA cath. Is there any utility in looking at VTI estimates of SV/CO and combining it with your impella and /or ecmo flows
Im trying to wrap my head around best methods to estimate CO/CI in pts with MCS devices
Excellent question. Hard to get reliable VTI from LVOT with an Impella in there in my experience (which is limited as rarely as we use it). A case for using RVOT VTI for assessing relative change in SV i think? I would love to hear what @drfreeze.bsky.social and others from #cccsky do.
On high support artefacts are a big nuisance in my limited experience, perhaps worsened by the 4vc probe's suboptimal doppler qualities?
I'm sceptical of the VTI when the doppler spectrum isn't crisp, when there's turbulence or flow convergence.
I dont know. Anecdotally i find you can often get a pretty crisp ejection doppler envelope under the artifact. But youre right. If you cant its not useful.
Another scenario may be when you have VAECMO and an impella in, your PAC estimates of CI are kind of unreliable so was wondering if VTI + flows from MCS devices may be the way. Gets tricky ya know.
No real clinical question specifically. Just another data point for titrating inotropes and assessing readiness for MCS weaning and liberation.
Had a situation the other day where the PAC and Fick CIs were wildly disparate and the PAC was finicky so i was trying to get a third eye to adjudicate🤷🏻♂️
Great point abt RVOT. Thats def useful in pts w ecmo/impella for sure. Anecdotally in pts w impellas i have compared LVOTVTI CI estimates (plus impella flow) to FICK and/or TD and as pulsatility improves and as native ejection returns it seems like its in the ballpark. Would be a cool study.
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Even for IVC it's murky, some guidelines advocate "sniffing" to judge variation, others spontaneous calm breathing which is obviously very different.
Im trying to wrap my head around best methods to estimate CO/CI in pts with MCS devices
RVOT VTI also good (in theory you could use transmitral or suprasternal VTI too)
If you have access to a 3D probe and good images I’d consider volumetrics
What’s the clinical question though?
I'm sceptical of the VTI when the doppler spectrum isn't crisp, when there's turbulence or flow convergence.
Had a situation the other day where the PAC and Fick CIs were wildly disparate and the PAC was finicky so i was trying to get a third eye to adjudicate🤷🏻♂️