The images below were obtained from a young healthy fit-looking individual during a POCUS workshop. They appear concerning, right?

A dilated inferior vena cava (IVC) with minimal respiratory variation – does this imply elevated right atrial pressure (RAP)?

Pulsatile portal vein flow (close to 50%) – does this indicate significant systemic venous congestion?

For many clinicians learning VExUS, the initial instinct may be “yes.” After all, these are findings we often associate with elevated venous pressures and impaired venous compliance.

But physiology is more nuanced. The key clue here is the hepatic vein Doppler waveform.

Despite the dilated IVC and pulsatile portal flow, the hepatic vein demonstrates preserved systolic predominance with a normal systolic-to-diastolic relationship. This argues strongly against clinically significant venous congestion and instead suggests efficient transmission of physiological RAP oscillations into the portal vein. Focused cardiac ultrasound (not shown here) further supported a physiological rather than pathological state, demonstrating preserved biventricular systolic function with normal LVEF and normal tricuspid annular plane systolic excursion (TAPSE).

You may ask: how can we confidently identify the S and D waves in the absence of simultaneous EKG tracing? The answer lies in the rhythm itself. The subject had marked resting bradycardia, a common feature in endurance-trained individuals with high vagal tone. Because of the prolonged cardiac cycle length, there is a clearly visible gap between successive cardiac cycles (dotted line). That prolonged interval is highly unlikely to represent separation between S and D waves within the same cycle.

First, Why Is the IVC Dilated? It’s multifactorial.

1. Chronic Blood Volume Expansion: Endurance training induces a 20 to 25% expansion in circulating blood volume, initially through plasma volume expansion mediated by RAAS activation, vasopressin release, and renal sodium and water retention, followed later by increased red cell mass. Because veins are highly compliant capacitance vessels, with venous compliance exceeding arterial compliance by more than 20 fold, the IVC is particularly susceptible to chronic volume mediated distension.

2. Structural Venous Remodeling: Exercise does not simply increase venous filling. It remodels the venous system. Repeated increases in venous return and flow velocity → endothelial shear stress → flow mediated vascular remodeling over time. Similar adaptations are also seen in the lower extremity veins of endurance athletes, the so called “athlete’s vein” phenotype.

3. Right Heart Adaptation: The athletic heart itself also remodels. Endurance trained individuals commonly develop enlarged and highly compliant right sided chambers with increased end diastolic volumes. The result is a globally remodeled high flow system extending from the systemic veins to the right heart, with IVC enlargement occurring as part of this physiological continuum.

4. The Potential Role of Autonomic Tone: The sympathetic nervous system is the primary regulator of venous capacitance. Reduced resting sympathetic tone, together with enhanced vagal predominance commonly seen in athletes (remember, our subject was bradycardic), may allow veins to remain in a more relaxed and compliant state, facilitating greater passive venous distension.

5. What About IVC Collapsibility? Though the IVC is dilated, collapsibility is generally expected to be relatively preserved in physiological states, but this is not a strict rule. As demonstrated in our subject, the IVC barely collapsed with a sniff despite otherwise normal cardiac function and preserved hepatic venous systolic predominance.

Why Is the Portal Vein Pulsatile?

The pathway of retrograde RAP transmission is vena cava → hepatic veins → hepatic venous sphincters → sinusoids → portal vein

Importantly, RAP is only partially transmitted to the portal vein. The degree of transmission depends on intrahepatic vascular resistance, particularly at the level of the hepatic venous sphincter resistance sites, as well as the magnitude of rise in right atrial pressure itself.

1. Small RAP Changes Are Buffered Better Than Large Ones: Classic animal studies demonstrated that small rises in RAP are transmitted relatively inefficiently upstream. However, as RAP progressively rises, the hepatic venous resistance sites passively distend, allowing greater transmission of pressure into the sinusoids and eventually the portal vein. At low CVP values (<4.5 mmHg), less than 20% of the pressure rise is transmitted to sinusoidal pressure. In contrast, at markedly elevated CVP (~16 mmHg), nearly 75% may be transmitted upstream. This explains why mild portal pulsatility can occasionally occur in physiological states (undulations typically correspond to the A-wave of CVP), whereas marked pulsatility is much more suggestive of pathological venous congestion.

2. Sympathetic Tone Buffers Pressure Transmission: Sympathetic activation appears to reduce retrograde pressure transmission. Norepinephrine, histamine, and hepatic nerve stimulation cause contraction of the hepatic venous resistance sites, reducing their distensibility and limiting upstream transmission of RAP oscillations. This likely serves as a protective buffering mechanism against ‘normal fluctuations’ in central venous pressure (at high RAP, this cannot stop the transmission).

3. Could High Vagal Tone Do the Opposite? Possibly. Experimental data suggest that vagal efferent stimulation decreases intrahepatic vascular resistance. Theoretically, high vagal tone (as in our patient) could therefore facilitate greater retrograde transmission of physiological RAP oscillations into the portal venous system.

However, I would like to acknowledge that human data in this area remain extremely limited, and much of the physiological understanding comes from animal models. Interestingly, while animal studies demonstrate smooth muscle sphincters capable of active constriction within small intrahepatic veins, whether identical structures exist in humans with the same degree of functional significance remains less well established.

Below is another pulsatile portal vein waveform obtained from a normal subject.

Bottomline:

This case is another reminder of why isolated POCUS parameters can be misleading.

The IVC has long been the favorite parameter of isolated POCUS lovers, and now portal vein pulsatility is slowly joining the fan club. But physiology is rarely binary. Context is king (or queen). Examine the entire hemodynamic circuit and interpret the findings together.

Disclosure: If you have followed NephroPOCUS long enough, you already know I am a strong believer in eVExUS and will take every possible opportunity to bash isolated parameter assessment 😉