Central Nervous System Ischaemic Response explained

Kia ora team. Let's breakdown the central nervous system ischaemic response following a traumatic brain injury or a hemorrhagic stroke. We will talk about the early and late phases and the equations for cerebral perfusion pressure and blood pressure. We will discuss the Monroe Kelly hypothesis and Cushing's Triad. Early phase Cranial insult will result in haemorrhage and vasogenic oedema This increases intracranial pressure . Increased intracranial pressure will compress cerebral blood vessels. Cerebral perfusion pressure = MAP -ICP. Therefore Cerebral perfusion pressure will decrease The Monroe-Kelly Hypothesis states that an increase in one compartment of the skull means there must be a decrease in another compartment therefore Cerebrospinal fluid shifts into the spinal cavity to attempt to decrease ICP Ischaemia leads to hypoxia and hypercapnia which causes vasodilation of cerebral blood vessels Late phase To increase CPP, the Sympathetic nervous system causes systemic vasoconstriction. This increases Total peripheral resistance and therefore BP because BP = CO x TPR . Baroreceptors in the aortic arch and carotid sinus sense increased BP, so they stimulate the parasympathetic nervous system via the vagus nerve to decrease HR As ICP continues to increase, the Brainstem gets compressed. This causes irregular respirations. Prolonged hypoxia and hypercapnia lead to excitotoxicity and neuronal death. Cushing’s triad consists of Increased systolic BP Bradycardia Irregular respirations Happy studying team.