Background: Patients with liver cirrhosis develop symptoms comparable to those of patients with sepsis, who have increased total vascular compliance, which may cause blood pooling in the venous pool. No previous studies have evaluated the effect of using norepinephrine on the intravascular blood volume. We investigated the norepinephrine infusion's effect on the mean systemic filling pressure, venous return, and cardiac preload in patients undergoing liver transplantation.
Methods: Overall, 33 patients who underwent living donor liver transplantation were included in this study. Cardiac output (CO) was measured using a PiCCO device (Pulsion Medical Systems, Munich, Germany). The mean systemic filling pressure was calculated using the inspiratory hold maneuver at four time intervals - at baseline, 10 min after the norepinephrine infusion, 5 min after norepinephrine discontinuation, and after infusion of 500 cc of 5% albumin. Other hemodynamic parameters, including the mean arterial pressure (MAP), pulse pressure variation, stroke volume variation, global end-diastolic volume, and mitral inflow velocity (E wave), were also evaluated.
Results: The norepinephrine infusion increased MAP and systemic vascular resistance in all patients. Moreover, it increased CO, mean systemic filling pressure, and global end-diastolic volume in 20 patients (60%), whereas there were no changes in these variables in 13 patients (40%). In all patients, norepinephrine infusion discontinuation caused a significant decrease in MAP, CO, resistance to venous return, and mean systemic filling pressure. Infusion of 500 cc colloid increased CO; however, interestingly, it was associated with a significant decrease in systemic vascular resistance; hence, MAP and mean systemic filling pressure showed no changes.
Conclusions: The norepinephrine infusion at 0.1 µg-1 kg-1 min-1 was associated with an increase in CO in patients with liver cirrhosis undergoing liver transplantation. Norepinephrine's effect on CO was primarily attributable to an increase in venous return due to an increase in mean systemic filling pressure.