Physical hemodynamic interaction between portal venous and hepatic arterial blood flow in humans

The hepatic arterial end-diastolic velocity (HAEDV) is normally equal to portal vein peak velocity (PVPV). However, there is no report of quantitative measurement that HAEDV was equal to PVPV. We investigated the interaction in PVPV and HAEDV in both chronic and acute hepatic hemodynamic changes.

One hundred and nineteen patients (54 with cirrhosis, 23 with chronic hepatitis, and 42 with no diffuse liver disorder) were enrolled. We investigated the differences in PVPV and HAEDV among the patients with and without liver disorder. In addition, we measured the intraindividual changes in HAEDV when PVPV was mechanically changed by percutaneous isolated hepatic perfusion in six patients and by percutaneous transhepatic portal embolization (PTPE) in six more.

HAEDV was nearly equal to PVPV not only in patients with both normal and hepatitis but also in those with cirrhosis (PVPV-HAEDV = 3.0 +/- 5.2, 2.2 +/- 5.4, 2.3 +/- 6.5 cm/s, respectively). In the intraindividual study, both PVPV and HAEDV decreased during hepatic mechanical perfusion and HAEDV was equal to PVPV (8.2 +/- 2.8, 10.5 +/- 1.5 cm/s, respectively). After PTPE, PVPV was increased and hepatic arterial peak systolic velocity was reciprocally decreased. However, HAEDV was nearly equal to PVPV 7 days after PTPE (PVPV-HAEDV = 5.9 +/- 5.1 cm/s).

Since arterial end-diastolic velocity depends on the downstream vascular resistance, lower HAEDV in patients with cirrhosis was considered to reflect a high outflow resistance. If there is no collateral pathway, we consider that HAEDV may actually reflect sinusoidal resistance to the same degree as PVPV.