Computational modeling of HHH therapy and impact of blood pressure and hematocrit.

Abstract

After an aneurysmal subarachnoid hemorrhage, cerebral microcirculatory changes occur as a result cerebral vasospasm. The objective of this study is to investigate, with a computational model, how various degrees of vasospasm are influenced by increasing the mean blood pressure and decreasing the blood viscosity. Using ANSYS CFX software, a computational model was constructed to simulate steady-state fully developed laminar blood flow through a rigid wall system consisting of the internal carotid artery (ICA), anterior cerebral artery, posterior cerebral artery, and middle cerebral artery (MCA). The MCA was selected for the site of a single acute vasospasm. Five severities of vasospasm were studied: 3 mm (normal), 2.5, 2, 1.5, and 1 mm. The ICA was assumed to have a constant inlet flow rate of 315 mL/min. The anterior cerebral artery and posterior cerebral artery were assumed to have constant outlet flow rates of 105 mL/min and 30 mL/min, respectively. The MCA was assumed to have a constant outlet pressure of 92 mL/min. Two different hematocrits, 45% and 32%, were simulated using the models. For a hematocrit of 45, the mean ICA inlet pressure required to pump blood through the system was 104 mm Hg for the 3-mm diameter MCA and 105, 108, 116, and 158 mm Hg for vasospasm diameters of 2.5, 2, 1.5, and 1 mm, respectively. For a hematocrit of 32, the mean ICA inlet pressure required was 102, 103, 105, 113, and 152 mm Hg, respectively. The MCA required a large increase in mean ICA inlet pressure for vasospasm diameters less than 1.5 mm, which suggests that for vasospasms more than 50% diameter reduction, the blood pressure must be increased dramatically. Decreasing the hematocrit had minimal impact on blood flow in a constricted vessel.