So these two had some follow up discussion in regards to this prior post, which is definitely worth a read. My editorial comments in bold.

Korbin:

Jon-Emile, thanks for your follow up and taking the time to look at the studies I referenced. I hadn’t seen your reply until Phil posted this. I gather your concerns primarily rest on the assumption that mPAP would rise higher (due to reaching the limits of the compliance of the pulmonary vasculature) than the rise in LAP, causing an increase in the delta mPAP-LAP and thus making the TRpg/RVOT VTI methods invalid as a way to know what the PVR is, as well as the concept of a calculated PVR in cases of significantly elevated LAP.

I absolutely believe you are right in postulating that this does indeed occur, but I think that the fact that the LAP  required to be significantly increased to cause this phenomenon would tend to “blunt” the delta between the mPAP and LAP as well, therefore also simultaneously helping to decrease the pressure/flow ratio that we are taking about to calculate PVR. In other words, the LAP required to cause what you are talking about also serves to pull back the error in PVR calculation a bit too. I’m sure there is a complex interplay between pulmonary vascular compliance and LAP that would make prediction of all this difficult in real life, but again I do agree with you that this is real and perhaps, common.

Having said that, I still think that the PVR estimation by the TR/VTI method works as there were enough patients with elevated LAPs included in the studies I showed you and the findings were replicated. After listening to your concerns, I will probably wonder a bit now about how close the predicted PVR is to the actual PVR when I see elevated LAP as well though!

Which brings me to my next point. I don’t think I would be fooled by a calculated PVR error scenario because I’m going to have a good idea about if there is elevated LAP or not due to the fact that I’m also seeing the left side of the heart dynamics on POCUS. Furthermore, I can get a relatively good idea about how high a LAP is by applying some Doppler techniques as well. Where this can get a bit murky is when I suspect elevated PVR and also see elevated LAPs on POCUS at the same time.

In an offline email exchange between you, I, and a group of people I thought would be interested, I presented one of these cases where I believed there to be both increased PVR and LAP. So the question at hand was what was causing the patient’s hemodynamic compromise. In the email, I purposely included information about the pulmonary valve regurgitant jet as it was very apropos to your points and the concerns you had described. The answer to the question of whether the PVR elevation was artifactual (due to what you have described) or real, was settled in both our minds by the fact that in the pulmonary valve regurgitant jet Doppler pattern, there was clear evidence that there was quite a gap between the LAP and the dPAP, thus pretty much proving a pre-capillary elevated PVR mechanism was in play as well as the elevation in LAP to the cause of the pulmonary HTN.

So I’d like to reinforce what you have pointed out, as it really is a key point: If you need to know if the PVR is real or not, the delta of the dPAP to LAP is really the only way to know for sure. However, I think I can still trust my assessment by looking at the echo as a whole and putting everything together in the occasional cases where a PR jet isn’t available to see as well.

Again, thanks so much Jon for pointing out where things may go sideways with your superior and deep understanding of physiology. You are really great to discuss these things with!

 

Jon-Emile:

Thanks for turning this into a dedicated post Phil.

I rambled my way around saying that my concern is the gold standard, not echo! If i were Rory, I would have called my post “The Case of The Flawed Gold Standard” (he may already have used this title).

The flawed gold standard is the calculated pulmonary vascular resistance from a right heart cath (note that in the pulmonary hypertension literature, that the PA Catheter-based definition does not include PVR!). One reason that PVR is not used is because of its many physiological/mathematical problems – probably first made explicit in the mid 1980s

Versprille A. Pulmonary vascular resistance. A meaningless variable. Intensive Care Med. 1984;10(2):51-3. PMID: 6715677

Korbin, I have no doubt that when you perform bedside TTE, that you have a very keen ability to discern left-sided PVR elevations from “true” pulmonary vascular PVR elevations – but not everyone is you! It actually doesn’t take very high left atrial pressures to cause the calculated PVR to rise and what i find most troubling is the nomenclature – because of the therapeutic implications. Calling it elevated “pulmonary vascular resistance” implies that **pulmonary vascular** resistance is high (even though it may not be) – so there may be the desire to give pulmonary vasodilators … which can make things worse! (see the SIOVAC trial).

That’s my clinical question exactly. Should I give pulmonary vasodilators or no?

What I’d really be interested to see … would be to measure the TRpg/RVOT VTI in patient with true hypertensive emergency (ideally without hypoxemia or significant pulmonary problems) – before, during and after treatment. I suspect that a very high LV afterload on presentation could cause the TRpg/RVOT VTI to be elevated (and if you put a right heart cath into the patient, the calculated PVR would also be high), even though the problem is, arguably, entirely in the systemic circulation. In theory, treatment with systemic vasodilators would lower impedance of the systemic circulation (the LV afterload) without any true ‘pulmonary vasodilation” — yet, I suspect that the TRpg/RVOT VTI would fall with therapy.

I know Korbin is now on the hunt for this exact patient. Looking forward to Part 3 of this discussion when he does find him or her!

 

cheers

 

Philippe