So some recent twitter discussions, particularly involving my friend Korbin (@khaycock2) and Lars (@LMSaxhaug) – whom I am trying to get on the podcast soon – were really fascinating in regards to RV and pulmonary hypertension assessment. So time to dig into this a little.

The basic POCUS RV assessment is RV:LV ratio and TAPSE, along with RV free wall thickness (should be below 5mm) and the D sign in parasternal SAX. This is a solid start to screen for significant RV dysfunction.

The next level should be to measure PAP using TR Vmax, in order to assess the degree of pulmonary hypertension. Thats pretty much where I’ve been at for the last few years and wasn’t sure there was really a lot more that was necessary from an acute care standpoint where your immediate questions are fluids/pressors/inotropes and some inhalational pulmonary dilators. I wasn’t convinced I needed more.

But of course Korbin and Lars are on another level, and started to talk about doing RVOT doppler and looking at TR Vmax to RVOT VTI ratios to estimate pulmonary vascular resistance. Is there any difference there? Is my PAP not enough? Well, turns out there may be some useful information there, so I will let Korbin do the talking, and my apologies for my dumb questions during this discussion!

So I will be toying with RVOT doppler and trying to see if this is something that warrants a place in acute care management. I suspect it may be something that may tip towards earlier inhaled vasodilator therapy, or else make not using them a more confident choice. I do like the waveform analysis. I think we generally overlook a lot of good info by focusing on numbers over morphology!

So far, images using the PS SAX view have been quite good:

Additionally, RVOT notching could be suggestive of an acute PE – makes sense (study link here!)

Here are a couple of excellent references:

So thanks to Korbin and Lars for forcing me to up my doppler game some more!

cheers

Philippe

Tricuspid regurgitation pressure gradient for sPAP:

sPAP=4*(TRvelocity^2) + RAP or

sPAP=TRpg +RAP

mPAP=(sPAP)*0.61 + 1.9

Acceleration time equations for sPAP and mPAP:

sPAPlog= -0.004(AT) + 2.1

mPAP=90 – (0.62*AT)

Pulmonary Regurgitation pressure gradient:

mPAP=4*(Peak initial velocity^2) +RAP

dPAP=4*(End velocity^2) + RAP

dPAP-PCWP should be about <6mmHg or else PVR is likely, see PCWP equations below

PVR equation to screen for increased PVR, or if PVR < 3 WU:

PVR=10*(TRvelocity/RVOT VTI) + 0.16. TR velocity is in m/sec, if <2 WU, no increased PVR.  This equation is accurate up to 3 WU

PVR equations for increased PVR > 3 WU.  These equations less accurate if PVR < 3 WU:

PVR=5.19*(TRvelocity^2) – 0.4, or more simplified: 5 * (TRvelocity^2). Note that the 5 * (TRvelocity^2 is almost sPAP equation (4 * TRvelocity^2)=sPAP

PVR=sPAP/RVOT VTI if no RVOT notch present

PVR=(sPAP/RVOT VTI) + 3 if RVOT notch is present

PCWP equations (for detection of group 2 pHTN to elevated sPAP), as you know, this is a whole other area, and gets a quite a bit more complicated, but to summarize:

PCWP likely elevated if E/e’>15, unlikely if E/e'<8

In NSR, PCWP=1.24 * (E/lateral e’) + 1.9

In ST, PCWP=1.5 * (E/lateral e’) + 1.5

In atrial fibrillation averaged over 5 beats, PCWP=0.8 * (E/lateral e’) +6

Using color M-mode and propagation velocity: PCWP=5.27 * (E/Vp) + 4.6