VExUS is better thought of as a Doppler signature of elevated right atrial pressure (RAP) and reduced systemic venous compliance. We keep emphasizing that VExUS is not a volume-status gauge. Why? Because volume is not the only determinant of RAP. Multiple cardiac factors, including but not limited to tricuspid regurgitation (TR), can raise RAP independent of volume, as we discussed previously in the post on the IVC and volume status. But RAP is only part of the story. Venous compliance also influences how elevated pressure is transmitted through the venous system, and it is not static. Sympathetic activation can reduce venous compliance, particularly in acute heart failure, shifting blood from the venous reservoir toward the central circulation. In other words, significant congestion can develop through volume redistribution even when there is little actual gain in total body volume. What happens around the veins matters too, for example, renal interstitial edema or increased intra-abdominal pressure. In addition, how RAP is transmitted to an individual vein depends on its proximity to the heart and what lies between. The portal vein, for example, is not directly exposed to systemic venous pressure; hepatic sinusoids and sphincter-like regulatory mechanisms lie between the portal and systemic venous circulations and can modify pressure transmission.
A recent study in JACC: Cardiovascular Interventions caught my attention because it provides a nice illustration of this concept. Investigators studied 64 patients with severe TR undergoing transcatheter tricuspid valve intervention and assessed VExUS before and after the procedure. The change was striking. VExUS grade 3 decreased from 45/64 patients (70%) before intervention to only 11/64 (17%) at 24 hours, with 66% of patients reaching VExUS grade 0–1. The improvement generally persisted over 12 months. Here is the particularly interesting part: body weight did not change significantly, and inpatient furosemide doses were actually lower than baseline outpatient doses. In other words, VExUS improved dramatically without evidence of substantial net fluid removal.
This is an important reminder that intravascular volume is not the sole determinant of congestion. As a corollary, congestion can improve without removing fluid – the key is addressing the underlying cause of the elevated venous pressure. Also, the organs don’t care why they are congested. Whether the elevated venous pressure results from severe tricuspid regurgitation, RV dysfunction or exogenous fluid loading, the downstream consequences of congestion are still relevant. I say “exogenous” fluid overload deliberately, because TR can be thought of as a form of “endogenous volume overload”. Most TR in fact is functional but once established it can participate in a vicious cycle: TR begets TR. Regurgitant volume contributes to progressive RV and annular dilation, which worsens leaflet coaptation and tethering, leading to more TR, further right-sided volume overload, and potentially worsening systemic venous congestion.
There is another interesting observation. Among the 11 patients who remained VExUS grade 3 after the procedure, 9 (81.8%) had at least moderate residual TR, compared with 23/53 (43.4%) among patients with VExUS grades 0-2 (P = 0.043). Persistent significant TR therefore appears to be associated with persistent severe VExUS abnormalities, although this observational finding does not establish direct causality.
But could VExUS grade 3 hide meaningful improvement?
Among patients who remained VExUS grade 3, could the renal venous stasis index (RVSI) nevertheless have improved? Absolutely possible though it was not reported. An intrarenal venous waveform may remain monophasic while the proportion of the cardiac cycle devoid of flow decreases. The waveform would still qualify as severely abnormal for conventional VExUS grading, yet the RVSI could show meaningful improvement in renal venous flow. If you’re not familiar with RVSI, below illustrations might help.
Also, a patient can have substantial improvement in portal vein pulsatility and still remain VExUS grade 3 if the hepatic and intrarenal venous Doppler patterns remain severely abnormal. So, among those 11 patients with persistent grade 3 VExUS, did portal vein pulsatility improve? Did RVSI improve despite persistence of a monophasic renal waveform? – We simply don’t know.
And if you ask me whether an improvement in RVSI translates into better renal function when the intrarenal venous waveform remains monophasic, I honestly don’t know at this point. We need more data on that. That said, it is worth noting that renal function in this study remained stable through the end of follow-up. I would still consider that a positive finding, especially since prior studies suggest that untreated significant TR is associated with progressive worsening of renal function over similar follow-up periods.
The portal vein may be particularly useful in severe TR
This is also a good opportunity to revisit an important point about portal vein Doppler in patients with severe persistent TR. I want to emphasize “persistent” because much of the functional TR we encounter on medical wards improves with fluid removal, unless there is underlying chronic severe pulmonary hypertension or advanced right-sided heart disease. Putting the interventional aspect aside, portal vein pulsatility can improve with fluid removal even when severe TR itself persists. A prospective study by Sergio M. Alday-Ramírez and colleagues, with our friend Eduardo Argaiz as senior author, enrolled 42 patients with TR undergoing decongestive therapy. Despite persistent severe TR and right ventricular dysfunction, portal vein pulsatility fraction frequently improved with volume removal, reaching <50% in most patients, and appeared more responsive to decongestion than intrarenal venous Doppler.
The case below illustrates the same concept. This patient had end-stage kidney disease, chronic pulmonary hypertension, and severe TR and was undergoing dialysis. With fluid removal, the portal venous Doppler essentially normalized despite persistent systolic flow reversal in the hepatic vein.
And then there are patients in whom improvement is much less dramatic.
In another case of severe pulmonary hypertension and torrential TR, we removed approximately 10 liters of fluid. Ten liters! And yet portal vein pulsatility improved only from about 250% to 140%. The hepatic and intrarenal venous waveforms remained severely abnormal, and by strict criteria, even the portal vein was still severely abnormal.
But sometimes, this is as good as it gets. Of course, this is an extreme example rather than the rule, but it nicely illustrates that complete Doppler normalization may not always be achievable.
There comes a point where chasing a normal or near-normal Doppler waveform with further fluid removal may do more harm than good. You may reduce preload enough to compromise forward flow, worsen hypotension, and increase vasopressor requirements, all while the underlying mechanical problem remains unchanged. In advanced right-sided heart disease, the goal cannot always be normalization of venous Doppler. The next step here is referral for tricuspid intervention or, in patients with advanced disease who are not candidates for intervention, a shift toward palliative goals of care. Whether you’re a nephrologist or a critical care physician, don’t hesitate to get your cardiology colleagues on board sooner rather than later to figure out whether an intervention is needed. At the end of the day, it’s always a team sport!
So, the next time someone says, “VExUS is useless in TR,” remind them that it’s not. It still provides useful information about severity of congestion, and individual components such as portal vein Doppler or the RVSI may still be helpful when interpreted cautiously and alongside measures of forward flow. Also remember that not all TR is persistent as discussed above, TR itself may improve during the course of hospitalization with fluid removal. Very few things in medicine are truly “useless.” The key is knowing when to use them, how to interpret them, and what their limitations are.
That’s all for now! And if you’re coming to ASN Kidney Week next month in Denver, whether you’re attending the POCUS pre-course or catching our POCUS session during the main meeting, come say hi. Always happy to meet fellow POCUS enthusiasts in person.