Lumped Parameter Modelling of Changes in Liver Hemodynamics due to Cirrhosis

Abstract

In this thesis, a lumped parameter hydraulic network model is used to simulate blood flow through the entire human liver to study the effects of cirrhosis on liver hemodynamics. Blood is transported from the hepatic artery and portal vein through the liver via a network of sinusoids, eventually draining into the hepatic artery. During cirrhosis, the resistance of the liver increases and blood may flow through recanalized vessels that bypass the liver, known as collaterals. Cirrhosis is implemented as a combination of increasing heterogeneity in the sinusoidal network, narrowing and blocking of lumped sinusoid channels, and increasing collateral dilation. We investigated the effects of increasing heterogeneity and narrowing the mean lumped sinusoid channel diameter and found that increasing heterogeneity results in blood being preferentially directed to a small fraction of sinusoid channels with the largest diameters. This reduces the efficiency of blood filtration, one of the key functions of the liver, and impairs liver function. We also increased collateral dilation and decreased mean lumped channel sinusoid diameter to study the resultant changes in volume flow rates and portal pressure. The results are validated by clinical observations of retrograde flow in the portal vein, and increase blood flow through collateral pathways. The results also verify observations of variceal dilation, and show that significant collateral dilation is required to maintain the portal vein pressure within biologically reasonable limits. Results from these simulations explain clinical observations that arise in cirrhotic patients through hemodynamics, and may help plan patient-specific optimal procedures for living donor liver transplant surgery.