Intravenous Anaesthetic Agents (excluding ketamine) Ketamine Volatile Anaesthetic Agents (excluding N2O) N2O Opioids NMBA Propofol, thiopentone and etomidate all reduce CMRAs a result of flow–metabolism coupling they all result in a fall in cerebral blood...
There is a linear correlation between cerebral blood flow and CMR Known as ‘flow–metabolism coupling’ Exact mechanisms are unclear but are likely due to accumulation of vasodilatory metabolic by-products (e.g. CO2, H+, K+ and adenosine Occurs on a local level to match...
At ‘normal’ PaO2 of >8 kPa there is minimal effect on cerebral blood flow As PaO2 falls below this level there is a rapid rise in cerebral blood flow: Mediated by hypoxia-induced vasodilation Results in a CBF of around 110ml/100g/min at a PaO2 of 4.0...
Increases linearly between a PaCO2 range of 3-10 kPa: Due to CO2 mediated vasodilatation Below 3.5 kPa, cerebral vasoconstriction leads to tissue hypoxia with subsequent reflex vasodilatation and maintenance of blood flow Above 10 kPa vasodilatation is maximal with no...
The autoregulatory vessel calibre changes are mediated by interplay between myogenic, neurogenic, metabolic and endothelial mechanisms: Myogenic Tone Metabolic Response Neurogenic Response Endothelial Response Thought to be the primary mechanism behind cerebral...
