We’ve explored several POCUS concepts in bits and pieces over time, and many have asked how all of this actually comes together at the bedside. This series is an attempt to bring those pieces together through real clinical scenarios. The focus is not on rare or flashy cases, but on the ones we see in everyday practice.

The idea here is not to get into the weeds with technical details or pitfalls, but to walk through the thinking behind each step and what to look for in that context. Relevant articles are linked along the way for those who want to go deeper. Patient consent has been obtained.

The Clinical Question

Here we have a patient who recently underwent liver transplantation, required perioperative CRRT, and is now off CRRT but receiving intravenous diuretics. The patient has mild bilateral edema, a slight rise in creatinine compared to yesterday, and no meaningful change in symptoms. Cumulative fluid balance + 2.5 L. So, the question is simple but clinically important: what is the patient’s hemodynamic status right now? Should we give fluids, or should we continue diuretics? And is this a situation where congestion is evolving despite a rising creatinine, similar to what we often see in heart failure physiology?

Is there increased extravascular lung water?

On lung ultrasound, I mostly see A-lines, with a few B-lines at the bases that likely represent mild basal atelectasis. Overall, the pattern is predominantly A-lines. So, there is no significant increase in extravascular lung water. Below are a couple of representative images.

How does global cardiac function look?

On focused cardiac ultrasound, the LV appears to be squeezing well, with a normal E-point septal separation, suggesting a qualitatively normal ejection fraction. On the parasternal short-axis view, there is no interventricular septal flattening, so the LV maintains a round shape without a D-sign. In the apical four-chamber view, the RV is smaller than the LV, which argues against significant RV enlargement. The tricuspid annular motion toward the apex looks good, so even without measuring TAPSE, RV systolic function appears preserved.  There is a trace pericardial effusion, which does not look hemodynamically significant. The left atrium appears borderline enlarged on visual assessment, although the linear dimension in the parasternal long axis view measures around 3.8 cm, which is within normal range.

Next, I move to Doppler to get a better sense of stroke volume, LV filling pressures, and right atrial pressure.

What is the stroke volume?

The LVOT VTI is in the range of 25-29 cm, which is on the higher side. This does not necessarily mean a high-output state, but it makes volume depletion unlikely. Instead of assuming a standard LVOT diameter of 2 cm, I measured it and found it to be 1.77 cm. Using that, the stroke volume comes out to about 66.4 mL, translating to a cardiac output of roughly 4.6 L/min, which is within normal range. In general, a truly volume-depleted patient is unlikely to maintain a normal stroke volume at a normal heart rate.

What about LV filling pressures?

Looking at mitral inflow and tissue Doppler, the E/e′ ratio on the lateral side is 15.8 with a reduced e′ of 7 cm/s, and on the medial side the E/e′ is 18.5 with an e′ of 6 cm/s. As a rule of thumb, an average E/e′ greater than 14 suggests elevated LV filling pressures, and reduced e′ values in this range further support that (generally, lateral e’ less than 8 or septal e’ less than 7 is considered significantly low). So overall, the LV filling pressures are likely elevated.

Even though the lungs do not show significant extravascular lung water, this profile suggests a high likelihood of developing it if fluids are given. The mitral E velocity is also above 100 cm/s, which can be thought of as a surrogate for preload. When you put this together with a preserved stroke volume, it argues strongly against low preload as the problem here. One caveat is that significant mitral regurgitation can elevate the E velocity, but in this case, there is no meaningful MR on color Doppler, so that does not apply.

In addition to E/e′, and left atrial size, the tricuspid regurgitant jet velocity is another parameter we often use when thinking about diastolic function. A value of 2.8 m/s or higher is generally considered elevated. In this case, the TR was mild, and the Doppler envelope was not perfect, but the peak velocity measured around 2.74 m/s, which is quite close to that threshold. Practically, I would report this as ‘at least’ a peak gradient of 29 mmHg. This is based on the simplified Bernoulli equation where the pressure gradient = 4 V². If you add right atrial pressure to this, you get right ventricular systolic pressure (RVSP). While elevated TR velocity can reflect RV dysfunction or pulmonary hypertension, that seems unlikely here as the primary problem – this is more likely a downstream effect of left-sided filling pressures.

RV tissue Doppler and right atrial pressure:

I also looked a bit more closely at RV function. In addition to a qualitative assessment, I prefer using tissue Doppler of the tricuspid annulus rather than TAPSE (M-mode parameter), as I find it more reproducible, though both correlate reasonably well with RV systolic function. The tricuspid S′ in this case is 15 cm/s, which is clearly normal (>9.5 to 10 cm/s).

Finally, I looked at the tricuspid E/e′ ratio, which is not routinely measured but can be helpful as an adjunct to other parameters for estimation of right atrial pressure – values below 6 are typically consistent with non-elevated right atrial pressure. In this case, it was 5.4. Since I was already obtaining the S′, the e′ was right there below the baseline on the same tracing, so it was easy to capture and adds one more hemodynamic piece.

Since we are already thinking about right atrial pressure, the most commonly used parameter is the inferior vena cava. However, this is a liver transplant patient, and in my experience, the IVC in these patients does not always behave the way we expect. Because of the surgical anastomosis and local structural changes, the usual cutoffs we rely on, such as a diameter above or below 2.1 cm or more than 50% collapsibility with inspiration, may not be directly applicable. In this case, the IVC is less than 2.1 cm in diameter but shows minimal respiratory variation. You can also appreciate the anastomotic site, and if you look closely, the respiratory motion appears more preserved in the intrahepatic segment and closer to the hepatic vein. Taken together, this makes the IVC less reliable – would not completely disregard it, but interpret it with caution. That is exactly where having additional parameters, such as the tricuspid E/e′, becomes helpful in building a more complete picture of right atrial pressure.

Additionally, I looked at the right internal jugular vein – the patient did not have a dialysis catheter in the neck, so the IJV was easily accessible. Here, the vein at the base of the neck appears almost fully collapsible with respiration, which supports the impression of non-elevated right atrial pressure (head angle <30°).

VExUS

For completeness, I also looked at VExUS, although it would not typically be pursued in a case like this where right atrial pressure appears normal. The hepatic vein Doppler looks normal with a dominant systolic wave compared to the diastolic wave. The portal vein flow is fairly continuous, and the internal jugular vein Doppler also shows a normal pattern with systolic and diastolic components in expected proportions. All of this is reassuring and does not suggest systemic venous congestion.

The interesting part is the intrarenal Doppler. The arterial waveform shows diminished diastolic flow → elevated resistive index. The venous signal is not very crisp, but it appears somewhat discontinuous, closer to a biphasic pattern. This is where contextual interpretation really matters. If one were to look only at the intrarenal venous pattern, it would be tempting to assume congestive nephropathy and push diuresis. But these findings can also be explained by persistent interstitial edema or intrinsic kidney injury, and the elevated resistive index supports that possibility. This is well described in the setting of acute tubular injury.

Putting it all together

This patient does not show sonographic features of overt volume depletion, and there is no evidence of pulmonary or systemic venous congestion. At the same time, the left-sided filling pressures appear to be elevated.

So where does that leave us? This is not a patient who needs fluids, but it is also not someone in whom I would push aggressive diuresis. A reasonable approach here is to continue gentle or maintenance level diuresis. However, the creatinine has worsened compared to yesterday, and the patient is on a calcineurin inhibitor, which already affects renal autoregulation. So, I would lean toward down-titrating diuretics. The overall picture suggests underlying tubular injury rather than a purely hemodynamic problem. And if that is the case, there is little value in adding further hemodynamic stress to the kidneys when it can be avoided.

Time? The entire scan took me about 20 minutes, including setting up ECG leads. Of course, this level of detailed hemodynamic assessment is not needed for every patient. In a typical day, maybe 3-4 patients truly require all these parameters, so spending 15 to 20 minutes per patient feels worthwhile. An added benefit of doing POCUS is that it creates an opportunity to engage with the patient and explain what we are seeing in real-time. It also reduces cognitive load and improves diagnostic confidence. Instead of making empiric decisions, we are acting with a better understanding of the underlying physiology.