People often claim that tricuspid regurgitation (TR) makes VExUS useless, assuming the regurgitation itself distorts the waveforms—especially causing hepatic S-reversal—rather than reflecting pressure changes. However, the portal vein remains a reliable marker to track the effectiveness of decongestive therapy in these patients, as highlighted by recent findings from our colleagues. At the end of the day, congestion is congestion—whether it’s due to volume overload, regurgitation, pericardial effusion, or chronic pulmonary hypertension. Moreover, in these cases, femoral vein Doppler can be a valuable addition to traditional waveforms. Check out our recent case report that illustrates this point: CASE journal.

In the early stages of TR, the right atrium (RA) and inferior vena cava (IVC) are still fairly compliant, so they can absorb the kinetic energy from the regurgitation. This causes the RA and IVC to dilate with only a small increase in right atrial pressure (RAP), which might lead to overestimating RAP on echocardiography. But as TR progresses and becomes more severe, the RA and IVC lose their compliance, and the kinetic energy drives RAP up more rapidly. At this point, patients with RAP over 15 mm Hg may not be accurately assessed by current echocardiographic algorithms, which can underestimate non-invasive RAP compared to invasive measurements (Est. pressure is 15 if IVC is >2.1 cm, <50% collapsible per ASE guidelines).

VExUS (venous waveforms) gives a better picture of congestion because it reflects the interplay between RAP and the compliance of the right atrium and veins, plus local factors like renal interstitial edema. This makes it more reliable than just looking at the IVC or even invasive pressures. Invasive (pulmonary artery catheter) pressures, while useful, can be tricky to interpret and prone to errors, like issues with leveling or zeroing, which can happen in everyday practice. While venous waveforms aren’t perfect and many ‘unknowns’ remain, they’re a great, non-invasive way to visually track congestion.

Let’s dive into a case. A patient with end-stage renal disease on hemodialysis via an AV fistula presented after missing a dialysis session. The patient had mild shortness of breath with exertion and mild pedal edema but was otherwise asymptomatic. Acute coronary syndrome was ruled out. Physical examination (= POCUS) findings showed preserved stroke volume (assessed via LVOT VTI) but revealed qualitatively severe TR, a severely dilated RV that was visibly larger than the LV on the apical four-chamber view, and interventricular septal flattening on the parasternal short-axis view. Additionally, the IVC was plethoric, indicating elevated right-sided pressures.

Here are the VExUS waveforms. Renal Doppler wasn’t performed due to the patient’s ESRD, but femoral vein Doppler was used as an alternative. The patient was in atrial fibrillation. The hepatic vein waveform showed S-wave reversal, the portal vein exhibited pulsatility >50%, and the femoral vein showed a severely increased stasis index (gaps in flow, as we’ve discussed before). The patient’s blood pressure was low, with MAP ~55-60 mmHg. Low-dose norepinephrine was initiated, and continuous renal replacement therapy was started for decongestion.

In any ESRD patient with pulmonary hypertension or RV failure, we should maintain a high suspicion for a high-flow AV fistula. High-flow fistulas increase preload and reduce afterload (via direct arteriovenous shunting), leading to a high-output cardiac state that can eventually progress to cardiac failure with elevated filling pressures. Unsurprisingly, Doppler ultrasound of the patient’s AV fistula revealed a flow >2 L/min, far exceeding the expected range. When the fistula was manually occluded, the patient’s blood pressure significantly increased, reflecting a rise in peripheral vascular resistance.

The patient was referred for AV fistula ligation—a complex decision requiring a multidisciplinary approach and subject to delays. However, the fascinating part of this case is the change in venous waveforms after volume removal despite TR. After approximately 5-6 liters of ultrafiltration, here’s what happened: The portal vein waveform normalized completely. The hepatic vein still showed S-wave reversal, but the reverse amplitude was reduced. The femoral vein stasis index improved significantly.

Interestingly, the TR appeared qualitatively similar to initial assessment, with the TR jet velocity remaining unchanged. The IVC remained plethoric, though its diameter slightly decreased. According to current guidelines, both pre- and post-decongestion IVC measurements corresponded to an RAP of 15 mmHg, highlighting the limitations of relying solely on IVC measurements in such cases.

What’s striking to me was the dramatic reduction in the right internal jugular vein diameter/area at the neck base. After decongestion, the IJV essentially collapsed at a 30-degree head angle. This observation reinforces my experience that IJV ultrasound may offer a more accurate estimation of RAP in patients like this or those on mechanical ventilation—a promising area for future research.

In summary, portal and femoral vein waveforms can serve as valuable tools to monitor the response to decongestive therapy in patients with severe TR. Future studies should consider developing an extended scoring system that incorporates multiple veins to improve assessment in these complex cases.