Speakers
Description
Impaired cerebrovascular reactivity (CVR), the ability of cerebral blood vessel tone to respond to stimuli for regulating blood flow and metabolism in the brain, has been linked to many acute and chronic cardiovascular and neurological diseases. In one mechanism of cerebrovascular reactivity, the cerebral blood vessels dilate to lower resistance in response to increased arterial carbon dioxide (CO2), thereby increasing blood flow to wash out the CO2. However, the integration of this with other regulatory processes and the implications for the systemic circulation are still not fully understood. Since the ability to measure the cerebral vasculature is inherently limited, a computational model that incorporates multiple possible factors underlying cerebrovascular blood flow regulation with patient-specific noninvasive data can help determine what most influences dynamics and regulation at the individual level. We present a mechanistic representation of cerebrovascular resistance as a function of partial pressure of CO2 together with a first-order control equation within a closed-loop whole-body circulation framework. We also incorporate functional representations of additional systemic and cerebral responses to CO2 and pressure. The current model is calibrated against experimental blood flow, pressure, and end-tidal CO2 from a cohort of control subjects and patients during a CO2 rebreathing protocol. These model adaptations will improve understanding of the system-level integration of mechanisms underlying CVR.
