In this post, we’ll discuss the diagnostic possibilities to consider when the hepatic vein waveform is abnormal, building on the short video I recently shared on hepatic vein waveform generation. To make things easier to follow, I’ve included summary slides for each waveform component below. Once you understand how each wave is generated, it becomes much easier to connect abnormal waveforms to the underlying physiology rather than relying on memorization.

Let’s start with the S-wave. Its main determinants are right atrial relaxation and the ability of the right ventricle to move downward during systole, reflecting right ventricular systolic function and tricuspid annular descent. Any process that impairs these mechanisms can alter the S-wave.

In general, when right atrial pressure (RAP) increases because of volume or pressure overload, the pressure difference that drives blood from the systemic veins into the RA becomes smaller. As a result, the hepatic vein S-wave decreases in amplitude. Tricuspid regurgitation is perhaps the most well-known cause of S-wave reduction. The mechanism is easy to understand – during systole, blood flows backward through the tricuspid valve into the RA, opposing the normal forward flow from the hepatic veins. This reduces the S-wave amplitude, and in severe cases, results in S-reversal. It is also worth noting that conditions such as volume overload and pulmonary hypertension are frequently accompanied by functional TR, which may improve with decongestive therapy. So, don’t look at a patient with TR and immediately think, “Well, the HV waveform is going to be abnormal, and there is nothing I can do about it.” As nephrologists and intensivists, we often modify loading conditions through fluid removal and other therapies. Re-POCUSing the patient afterward is a good idea.

Similarly, conditions associated with reduced longitudinal RV function, reflected by a lower TAPSE, can also decrease the HV S-wave. The reason is simple: during systole, the downward movement of the tricuspid annulus helps create space within the RA, facilitating forward venous flow from the hepatic veins. When this motion is reduced, the S-wave becomes smaller. A similar pattern may be seen in patients with RV infarction. A classic example is the period following cardiopulmonary bypass. If you compare HV Doppler tracings obtained before and after bypass using the transesophageal echocardiography probe already in place during surgery, the reduction in S-wave amplitude is often quite noticeable. This is believed to occur because RV contraction becomes less dependent on longitudinal shortening and more dependent on circumferential (transverse) shortening. Although overall RV stroke volume is usually preserved, the reduced descent of the tricuspid annulus results in a smaller S-wave.

Atrial fibrillation is another important cause of S-wave reduction. Remember that atrial relaxation is one of the major contributors to S-wave generation. In Afib, there is no organized atrial contraction and, consequently, no organized atrial relaxation. As a result, the S-wave is often reduced even in the absence of significant congestion.

Restrictive cardiomyopathy can also reduce the S-wave through two related mechanisms. First, impaired atrial relaxation results in a blunted x-descent. Second, longitudinal RV function is often reduced, leading to less tricuspid annular descent during systole. Together, these changes diminish the systolic pressure gradient that normally promotes venous return into the RA, resulting in a smaller S-wave.

Now let’s move on to the V-wave. The V-wave occurs at the end of systole and can be thought of as the transition between systole and diastole. It reflects the point at which the RA is maximally filled.

The V-wave becomes larger when more blood accumulates in the RA during systole or the RA compliance is reduced, or both. Common examples include TR, RV failure, Afib (low RA compliance), and other conditions associated with elevated right-sided filling pressures.

Next, let’s look at the D-wave. The two main determinants of D-wave amplitude are the conduit function of the RA and the ability of the RV to relax and accept blood during early diastole.

Logically, the amount of blood available within the RA and hepatic veins also affects the D-wave. As a result, the D-wave is typically reduced in hypovolemia. The same is true for the S-wave, so what you usually see is an overall low-velocity waveform with preservation of the normal S>D relationship. In theory, the D-wave may be affected to a greater extent because it is a passive, preload-dependent phenomenon that relies on an adequate venous reservoir to generate flow across the open tricuspid valve. That’s an interesting physiologic concept, although it rarely makes much difference in clinical practice.

In severe pulmonary hypertension, the D-wave may be reduced because the RV becomes both less compliant and slower to relax. As a result, the RV is less able to accept blood during early diastole. In simple terms, a stiff RV resists filling. Even after the tricuspid valve opens, RV pressure rises rapidly as blood enters, quickly narrowing the pressure gradient between the RA and RV and limiting forward flow. Consequently, the D-wave may be reduced and exhibit a short deceleration time, reflecting this rapid pressure equalization.

Cardiac tamponade is particularly interesting. Early in its course, it behaves somewhat like volume depletion because RV filling is impaired during diastole, resulting in a smaller D-wave. As tamponade progresses and chamber collapse develops, the D-wave may become markedly reduced and can even reverse during early expiration, typically on the first expiratory beat. The mechanism relates to exaggerated ventricular interdependence (see figure below). At the onset of expiration, increased LV filling (↑ intrathoracic pressure → ↑ pulmonary venous return → ↑ LV filling) shifts the interventricular septum toward the RV, further limiting RV filling. As a result, resistance to forward diastolic flow increases, causing the D-wave to diminish or reverse. This occurs at the same time that tricuspid inflow E-wave velocity reaches its lowest value, while mitral inflow E-wave velocity reaches its highest. In advanced tamponade, forward HV flow may be seen only during inspiration. At this stage, systemic venous and intracardiac pressures are approaching equalization, signaling impending circulatory collapse. At that point, stop worrying about VExUS and start reaching for the pericardiocentesis kit!

Constrictive pericarditis can also produce D-wave reversal, but the timing is different from tamponade. In constrictive pericarditis, early diastolic filling is brisk and relatively unimpeded. The problem arises later in diastole, when ventricular filling abruptly encounters the constraint imposed by the noncompliant pericardium. As a result, D-wave reversal is classically a late-diastolic phenomenon. Also, in constrictive pericarditis, it typically appears in late expiration and may persist throughout expiration. In tamponade, it is often most pronounced during the first expiratory beat. Think of it this way: tamponade is a fluid-filled hydraulic system, so pressure changes are transmitted to the heart almost instantaneously. Constrictive pericarditis, on the other hand, is a rigid shell insulating cardiac chambers. As expiration continues, LV filling progressively increases (↑ intrathoracic pressure → ↑ pulmonary venous return as pulmonary veins are outside the pericardial constraint) → the septum shifts further rightward → RV filling space becomes progressively more restricted. In other words, the ventricular interdependence effect builds with each expiratory beat, which is why D-wave reversal is classically a late-expiratory finding.

Restrictive cardiomyopathy can also cause D-wave reversal, but typically during inspiration. As venous return increases with inspiration, a stiff, noncompliant RV is unable to accommodate the additional inflow. RV pressure rises rapidly, limiting forward flow and resulting in diastolic flow reversal in the hepatic veins.

A couple of additional points are worth mentioning here. During tachycardia, the D-wave may merge with the S-wave because diastole shortens disproportionately as heart rate increases. Without ECG gating, the above-baseline A-wave can then be mistaken for systolic flow reversal if the fused S-D wave is incorrectly identified as the D-wave. Also, hepatic vein waveform blunting is common in cirrhosis and fatty liver disease, sometimes producing a nearly monophasic pattern. However, this is not universal. Some patients retain just enough HV phasicity to identify the cardiac cycles, while others may have waveforms that appear surprisingly close to normal. Elevated intraabdominal pressure (IAP) can also blunt the HV waveform. A useful clue (in the appropriate context) is that the waveform often becomes very low amplitude, even when Doppler alignment is excellent.

Now let’s move on to the A-wave, which occurs due to atrial contraction.

The A-wave amplitude increases when RV end-diastolic pressure is elevated. This makes intuitive sense because atrial contraction occurs towards the end of diastole. When the RV is stiff or non-compliant, it cannot easily accommodate the additional blood delivered by atrial contraction. As a result, pressure rises within the RA and some blood is pushed backward into the hepatic veins, producing a larger A-wave. This pattern is commonly seen in conditions associated with impaired RV filling, such as pulmonary hypertension with RV hypertrophy, restrictive cardiomyopathy, and RV infarction.

Also, tricuspid stenosis is a classic cause of a large A-wave. Because the tricuspid valve is narrowed, the RA must generate higher pressure to push blood into the RV during atrial contraction. Some of that pressure is transmitted backward into the hepatic veins, producing a prominent A-wave. More generally, whenever the atrium contracts against a closed tricuspid valve, the force of atrial contraction has nowhere to go forward and is directed backward into the hepatic veins, resulting in giant (“cannon”) A-waves. This is typically seen in complete heart block, where atrial and ventricular contractions occur independently. When atrial contraction happens to coincide with ventricular systole, a cannon A-wave is produced. Because the timing varies from beat to beat, these waves are intermittent and irregular. A similar phenomenon can occur with PVCs. If atrial contraction coincides with a PVC beat, a cannon A-wave may appear – better appreciated with simultaneous ECG. The post-PVC compensatory pause often results in larger forward-flow waves (S and D) on the following beat because of the longer filling time.

A short PR interval can also produce a prominent A-wave, albeit by a different mechanism. When ventricular contraction begins very shortly after atrial depolarization, the tricuspid valve may close before atrial contraction is complete. The remaining atrial contraction then occurs against a partially or completely closed valve, causing pressure to be redirected backward into the hepatic veins and augmenting the A-wave.

On the other hand, A-wave is absent in atrial fibrillation because there is no organized atrial contraction to produce it. No effective atrial kick, no A-wave. Atrial flutter is a bit different. Rather than a single A-wave, you may see multiple ‘small’, rapid reversal waves (“flutter waves”) riding on top of the underlying S-D waveform.

It’s a long post, but I hope it helps illustrate the wealth of information hidden in the hepatic vein Doppler waveform. And don’t forget the most important rule: always use ECG when doing VExUS. Below is a summary slide.