Portal vein pulsatility can occur in normal subjects and cirrhotic patients without cardiac disease, driven by mechanisms beyond retrograde atrial pulsations.
The literature indicates that Doppler demonstration of pulsatile flow in the portal vein suggests heart disease, and that retrograde transsinusoidal transmission of atrial pulsations is the mechanism. We noninvasively investigated portal vein pulsatility (PVP) in normal subjects and in patients with cardiac and liver disease, and performed invasive studies in cirrhotic humans and normal pigs. We found that accentuated PVP occurred in some normal subjects and in some patients with cirrhosis, and that mechanisms other than transsinusoidal transmission of atrial pulsations contributed to PVP. Determinants of PVP may include pulsatile portal inflow, transmission of pulsations from the vena cava (IVC) and location of the Doppler sample volume relative to the IVC.
Wachsberg et al. (1995) studied this question.