Cerebral perfusion
Autoregulation
Cerebral autoregulation refers to the ability of the cerebral vasculature to maintain a stable cerebral perfusion pressure (CPP) despite changes in systemic blood pressure. [23] [24]
Autoregulation is maintained through four mechanisms:
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Myogenic Tone: refers to changes in arteriole and smooth muscle tone in response to changes in pressure. [24] Increased pressures will cause increased myogenic tone, whereas decreased pressure will lessen myogenic tone. [24]
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Neurogenic Response: Neurogenic mediation of cerebral perfusion refers to the ability of cerebral blood vessels to adapt vasomotor tone in response to depolarisation of neurons. [24] Neurons (along with other cells such as astrocytes and microglia) secrete neurotransmitters with vasoactive properties. Some cause vasodilation, whilst others cause vasoconstriction. [24] Studies have shown that repeated depolarisation of single cortical interneurons causes precise and repeatable changes in vasomotor tone in neighbouring vessels. [24]
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Metabolic Mechanism: Refers to changes in autoregulation in response to changes in the local environment. [24] For example, the presence of carbon dioxide in blood causes vasodilation of the vessels. [23] [24] To put this in to context, for every 1mmHg increase in arterial CO2, cerebral blood flow increases by 4%. [24] Furthermore, it has been shown that increased levels of oxygen can cause cerebral vasoconstriction, and hypoglycaemic can cause vasodilation and hence an increase in cerebral blood flow. [24]
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Endothelial Mechanism: Endothelial control of autoregulation is another important aspect of cerebral blood flow. [24] In response to pressures exerted on blood vessels, the endothelium may secrete chemicals such as Nitric Oxide (vasodilator) or Thromboxane A2 (vasoconstrictor) to assist in controlling the neural perfusion. [24]
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Cerebral perfusion Pressure
Cerebral Perfusion Pressure (CPP) is the net gradient that drives oxygen delivery to neuronal tissue. It is the difference between systemic arterial pressure (MAP) and the intracranial pressure (ICP). [25]
In patients with neurological injury, it is critical to maintain the CPP at normal physiological levels (60-80mmHg). [25] Cerebral autoregulation aims to keep the CPP relatively constant despite changes in MAP. In normal circumstances, ICP is between 5-10mmHg. [25] Following a TBI, ICP may rise to dangerously high levels (may be attributed to bleeding or oedema). [26] As ICP increases, the gradient of cerebral blood flow changes leading to decreases in CPP. [25] [26]
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In the management of TBI, maintenance of the CPP is among the most important considerations. [26]
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Calculations:
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Mean Arterial Pressure (MAP) = [(2 x DBP) + SBP] / 3 [27]
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Cerebral Perfusion Pressure = MAP - ICP [25]
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Intracranial Pressure - Unable to measure in prehospital practice, however assume ICP >20mmHg in severe head injury. [26]
[31]
There are two sets of paired arteries that are responsible for blood flow to the brain.
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Internal Carotid Arteries [28] [29]
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Vertebral Arteries [28] [29]
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The internal carotid arteries branch off to form two major arteries - the anterior cerebral artery and middle cerebral artery.[29] The vertebral arteries arise from the subclavian arteries and eventually converge to form the basilar artery. [28] It is important to note that there are various arteries branching from these vessels. [29]
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Circle of Willis
The vertebral and internal carotid arteries eventually terminate and form a circular blood vessel, called the Circle of WIllis. [28] [29] This is an important aspect of cerebral blood flow, as it provides a “back-up” pathway in the case of damage or obstruction of cerebral blood vessels. [28]
Blood flow to the brain
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[30]