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Thanks, I’m aware of the guidelinesBelow is a link to the guidelines on repair of valvular heart disease under TEE. There is mention of CVP tracings and PA pressures in these guidelines, but they are certainly not emphasized. In most cases I have seen, these measurements do not play a major role in deciding intervention or not. Also in my experience, the severity (especially severe cases) of tricuspid pathologies is pretty obvious on TEE.
Your mention of symptomatology is also addressed in the guidelines specifically. If it's primary dysfunction, you're probably there to address the TV already, so discussion is gonna be mostly moot in the context of being under anesthesia as the vascular resistance and cardiac function variables have all changed. If secondary (most cases of TR), there are specific recommendations on intervention laid out in the guidelines.
It's worth noting that whatever we talk about is always in context of guidelines being studied and written by cardiologists who do TTE/TEE all day, every day, and see the effects of these valvular lesions on patient's long term outcomes in clinics and inpatient areas. Every TEE/CVP/PA pressure that's done intraoperatively is going to be confounded by the patient being under anesthesia, so in these cases of whether to intervene or not it's more appropriate imo to confirm findings with an available cardiologist. If what you're doing is complex enough where CVPs/PAs are the deciding factor, a cardiologist should be available for consultation either preoperatively or intraoperatively. You will never, ever go wrong getting a second set of eyes on a TEE that is equivocal.
Here's the algorithm:
View attachment 364027
And I fully agree with your points about the guidelines being written by cardiologists with long-term effects in mind, and the fact that GA affects loading conditions and hemodynamics in such a fashion that any grading of valvular lesion severity needs to be done with caution and in context of the preop findings.
To @T-burglar ’s point, his mention of hemodynamics in relation to severe TR was not about slam dunk cases where the TR was obviously massive or torrential and/or where the imaging or tricuspid annular dilatation was so obvious that repair was definitely indicated. And in regard to symptomatology, almost every adult surgical TVR/r performed is actually the second procedure being done during a pump run…since most TVR/r’s are occurring at the time of left sided heart surgery for the main symptomatic lesion. Indeed, intervention for primary symptomatic severe TR is vanishingly rare, which is why I don’t find the guidelines or the relative lack of class I indications to be the most helpful in the operating room.
Ultimately, we need to be asking ourselves, what are we actually worried about with a severe regurgitant valvular lesion? What actually kills the patient? In the case of MR, the hemodynamic and volume loading effects are deleterious upon 1. The LV, 2. The LA/pulmonary vasculature, and 3. The RV. And in the case of MR if you look at the echo guidelines, one of the most specific findings (other than the obvious 2d appearance of flail with a large flail gap/width) is holosystolic reversal of flow in the pulmonary veins, aka the echocardiographic representation of MR’s real hemodynamics. Analogously, in the case of AI, what’s most specific echo finding? Holodiastolic reversal of flow in the distal descending aorta.
And in the case of TR, as I alluded to in my earlier post, one of the most specific findings is holosystolic reversal of flow in the hepatic veins. This finding (in context of the preop findings, the effects of GA, the rest of the echo/ability to exclude other causes like RV cardiomyopathies, RV diastolic dysfunction, significant arrhythmias, constrictive processes) lets you know in an instant that the RV is moving so much blood forward and backward that it will have deleterious effects upon the RV, the pulmonary vasculature, the RA, and the rest of the body if left unchecked long enough. So it’s not just CVP in isolation that has value, but if you look at the CVP and it’s as high as the PAD, and there are obvious V waves, you are looking at the true hemodynamic representation of one of the most specific echocardiographic findings of severe TR, and I don’t think that can be ignored when advising a surgeon, especially if the echo isn’t of top tier quality.