CO2 response without CNS ischemic response active (with only cerebral and systemic metabolic response active).
The CNS ischemic response has long been known to cause an increase in arterial blood pressure. Its pathways are largely unknown. In physiology textbooks this response is thought to be active only under extreme conditions when normal hemostatic mechanisms have failed.
In the model the CNS ischemic response is hypothetically introduced as a variation of the venous capacitance in response to changes in central pCO2: when central pCO2 increases venous capacitance is reduced causing an increase in cardiac output and when it decreases, mutatis mutandis, venous capacitance is increased.
This response can be simulated by selecting "hyperventilation" or "CO2 retention" in the scenario box. In the model, this will increase or decrease the effectiveness of lung perfusion in eliminating blood CO2. The activity of the CNS ischemic response will have a stabilizing effect on central pCO2, since the changes in cardiac output cause the tissue perfusion to follow changes in metabolic activity (or respiratory effectiveness).
CO2 response with CNS ischemic response active.
In the above graph the CBF changes dramatically with changes in pCO2. There is hysteresis during the test because the changes in blood pCO2 caused by changes in respiratory activity take time to reach the brain (circulation time): the CNS ischemic response lags upon changes in blood pCO2.