Over a wide range of blood pressure cerebral blood flow remains constant if metabolic demands are unchanged, Fig 2. This means that normally if blood pressure falls cerebral vasodilation occurs to increase flow and thus maintain cerebral oxygen and nutrient delivery. Conversely, if blood pressure is excessively high the cerebral vessels vasoconstrict, maintaining cerebral oxygen and nutrient delivery whilst protecting the brain. This does not always pertain to the ill patient. Trauma, inflammation, seizure activity and conditions causing raised ICP may abolish auto-regulation and the CPP therefore becomes linearly dependent on MAP.
Figure 2. Cerebral autoregulation. Blood flow remains constant over a wide range of blood pressure.
Think of the last unconscious patient you looked after. What was their MAP ? Did you know their ICP ? Probably not. In many causes of unconsciousness the ICP will be raised.
So if BP was 90/60mmHg and ICP modestly raised at 15mmHg the CPP would be:
MAP (DBP plus 1/3 pulse pressure) = 70
CPP= 70-15 thus 55mmHg
If you add hypoxaemia or reduced DO2 to this the potential for secondary cerebral damage is major.
Think ICP and CPP in the unconscious patient!
Carbon dioxide is a potent vasodilator. Patients with type II respiratory failure have morning headache because of cerebral vasodilation caused by hypercapnia. So if there is a risk of raised ICP keeping CO2 down will help to control it. The corollary to this is that low PaCO2 will cause potentially detrimental cerebral vasoconstriction. So as a rescue therapy in severe circumstances with high ICP and incipient coning hyperventilation can save the situation but further therapeutic measures to lower ICP must be instituted to permit limitation of the period of hypocapnia. Control of PaCO2 can be achieved by bag-valve-mask ventilation as well as by hyperventilation of the intubated patient. Even if pupils have dilated the process is reversible if caught early enough.