Bridging Systemic and Intracranial Circulations using a 1D-0D Arterio-Venous Model
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We present a 1D-0D closed-loop computational model describing the coupling between systemic blood circulation and the intracranial dynamics, with specific focus on cerebrovascular physiology. The systemic arterial–venous circulation is modeled employing the ADAVN cardio-respiratory model (Müller et al., 2023; Dalmaso et al., 2025), a one-dimensional representation of the major systemic vessels, in which the interaction between arterial and venous networks is mediated through lumped-parameter models of the peripheral vascular beds. In addition, we consider cardiopulmonary interactions to account for the impact of respiration on intracranial dynamics, and the influence of local control mechanisms that regulate cerebral blood flow. The intracranial domain is described using a compartmental formulation accounting for cerebral blood volume, cerebrospinal fluid (CSF), and brain parenchyma dynamics. Building upon the models proposed in (Linninger et al., 2019; Toro et al. 2022), the present framework introduces two key extensions: (i) the explicit inclusion of the spinal canal as a co-axial one-dimensional compliant domain (Toro et al., 2019), enabling a more faithful anatomical representation and the capture of spatially distributed CSF dynamics; and (ii) the relaxation of the Monro–Kellie hypothesis through the introduction of a pressure–volume constitutive relationship for the brain parenchyma, allowing for small but physiologically relevant cranial deformations. The resulting model constitutes an anatomically detailed multi-system {\it in-silico} laboratory capable of quantifying the impact of inter- and intra-individual variability factors in systemic circulation—such as heart rate variability, stroke volume modulation, and respiratory-induced pressure fluctuations—on intracranial pressure dynamics, CSF volume patterns, among other biomarkers. This framework provides a robust computational basis for investigating cerebrovascular regulation mechanisms and their sensitivity to systemic hemodynamic perturbations.
