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Neurophysiology (1).pptx
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- 4. Overview 1. Neuroanatomy 2. Cerebral circulation 3. CSF circulation 4. Monroe-Kellie Doctrine 5. Cerebral blood flow 6. Cerebral perfusion pressure 7. 4
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- 12. 12 Cerebral Blood Flow ● Direct relationship between: ○ Flow. ○ CPP ○ Calibre of cerebral vessels. ● Where ○ π is the mathematical constant. ○ P the pressure gradient which is the CPP. ○ r the radius/calibre of blood vessel. ○ η the dynamic viscosity of blood. ○ l the length of the blood vessel.
- 13. 13 Cerebral autoregulation Radius of cerebral arterial blood vessels regulated by: – Cerebral metabolism rate of O2 – Carbon dioxide and oxygen – Autoregulation – Neurohumeral factors
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- 20. References 20 1. Cipolla MJ. The Cerebral Circulation. San Rafael (CA): Morgan & Claypool Life Sciences; 2009. 2. Cerebral physiology. Alifia Tameem. Anaesth Crit Care Pain. 2013;13(4):113-118 3. Physiology. Linda S Costanzo, 2nd edition;2002. 4. Pre-Interview Assessment for Emergency Medicine Master of Medicine (PIAEM) Preparatory course 2017 notes 5. Pre-Interview Assessment for Emergency Medicine Master of Medicine (PIAEM) Preparatory course 2016 notes
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- • Extracellular fluid in the ventricles and subarachnoid space. • Produced at a rate of 0.3-0.4ml/min (500ml/day) by the choroid plexus in the lateral, third and fourth ventricles. • CSF formation is dependent on the CPP and when this falls below 70mmHg, CSF production also falls because of the reduction in cerebral and choroid plexus blood flow. • CSF circulates through the ventricular system and the subarachnoid spaces, aided by ciliary movements of the ependymal cells. • Resorption takes place mostly in the arachnoid villi and granulations into the circulation: – mechanism: difference between the CSF pressure and the venous pressure. • Obstruction in CSF circulation, overproduction of CSF or inadequate resorption results in hydrocephalus. CSF functions • Mechanical protection by buoyancy. The low specific gravity of CSF (1.007) reduces the effective weight of the brain from 1.4kg to 47g (Archimede’s principle) - protects it against deformation caused by acceleration or deceleration forces • Provides a constant chemical environment for neuronal activity • Important for acid-base regulation for control of respiration • Provides a medium for nutrients after they are transported actively across the blood-brain-barrier
- The normal adult skull can be considered as a bony box of fixed volume and it contains brain, blood and cerebrospinal fluid (CSF). An increase in the volume of any one of the three components will be at the expense of the other two beyond the autoregulation. • Major compensatory mechanism include i. Displacement of CSF from cranial to spinal compartment. ii. An increase in CSF resorption. iii. Decrease in CSF production. iv. Decrease in total cerebral blood volume. Brain is the least compressible among the three. Cerebral blood flow is autoregulated. Autoregulation persist when CPP is between 60-160mmHg When CPP is <60mmHg, CBF decreases. When compensatory mechanisms are exhausted, small increases in the volumes of intracranial constituents cause large increases in ICP to the point of causing global ischaemia Normal ICP is between 5 - 13mmHg. • Constituents within the skull: – the brain (80%/1400ml), – Blood (10%/150ml) and – cerebrospinal fluid (CSF 10%/150ml)
- • Normal CPP is about 70 to 90mmHg. • More dependant on MAP – CBF is constant. • ICP > 30mmHg compromise CPP. • Decrease in CPP will affect electrical activity: ü<50mmHg – slowing of EEG ü25 – 40 mmHg – flat EEG ü<25 mmHg – irreversible brain damage • Cerebrovascular resistance (CVR) predominantly determine by calibre of the vessels: üVasodilatation – ↑ radius, ↓ CVR, ↑ CBF. üVasoconstriction – ↓ radius, ↑ CVR, ↓ CBF. Map = 1/3sbp + 2/3dbp – MAP is usually around 80-110mmHg – ICP is normally 5-13mmHg. – CPP is normally about 70-90mmHg
- • Brain only able to withstand very short periods of lack of blood supply (ischaemia), because neurones produce energy (ATP) almost entirely by oxidative metabolism of substrates including glucose and ketone bodies, with very limited capacity for anaerobic metabolism. • Without oxygen, energy-dependent processes cease leading to irreversible cellular injury if blood flow is not reestablished rapidly (3 to 8 minutes under most circumstances). • Therefore, adequate cerebral blood flow must be maintained to ensure a constant delivery of oxygen and substrates and to remove the waste products of metabolism. • CBF is dependent on factors a. those affecting cerebral perfusion pressure b. those affecting the radius of cerebral blood vessels Hagen-Poiseuille law CBF = CPP/CVR • CBF = 50ml/100g/min (ranging from 20ml/100g/min in white matter to 70ml/100g/min in grey matter) • The adult brain weighs 1400g or 2% of the total body weight. But CBF is 700ml/min or 15% of the resting cardiac output • This reflects the high oxygen consumption of the brain of 3.3ml/100g/min which is 20% of the total body consumption. • Referred as the cerebral metabolic rate for oxygen or CMRO2
- Radius of cerebral arterial blood vessels regulated by: – Cerebral metabolism rate of o2 – Carbon dioxide and oxygen – Autoregulation – Neurohumeral factors CMRO2 • Local or global increases in metabolic demand are met rapidly by an increase in CBF and substrate delivery and vice versa • Controlled by several vasoactive metabolic mediators including hydrogen ions, potassium, CO2, adenosine, glycolytic intermediates, phospholipid metabolites and nitric oxide. CO2 • A decrease in brain extracellular pH bought the change in PaCO2 • Moderate hypotension impairs the response of the cerebral circulation to changes in PaCO2, and severe hypotension abolishes it • Hyperventilation reduces PaCO2 causes vasoconstriction of the cerebral vessels. reduces cerebral blood volume and ICP. • If PaCO2 is reduced too much, vasoconstriction will reduce CBF causing worsening cerebral ischaemia. • Hypercapnia resulting vasodilatation, increase in ICP must be avoided. • Useful in manage patients with – raised intracranial pressure, Eg TBI – PaCO2 is therefore best maintained at low-normal (35-40mmHg, 4.7- 5.3kPa). O2 • CBF increases once PaO2 drops below 50mmHg (6.7kPa) so that cerebral oxygen delivery remains constant. • Hypoxia acts on cerebral tissue to promote the release of adenosine, and prostanoids that contribute to cerebral vasodilatation. • Hypoxia also acts directly on cerebrovascular smooth muscle to produce hyperpolarisation and reduce calcium uptake, both mechanisms enhancing vasodilatation. Autoregulation • Autoregulation is thought to be a myogenic mechanism, whereby vascular smooth muscle constricts in response to an increase in wall tension and to relax to a decrease in wall tension. • Pressure autoregulation impaired in brain tumour, subarachnoid haemorrhage, stroke, or head injury. • CBF is kept constant over a wide range of MAP (50 – 150 mmHg) • CPP = MAP – ICP • If increase MAP, cerebral vasoconstriction. • If decrease MAP, cerebral vasodilation. • Constant CBF is maintained. • If pressure above 160mmHg, -Disrupt blood brain barrier. -Cerebral oedema. -Haemorrhage. Neurohumeral factors • Relative lack of humoral and autonomic control on normal cerebrovascular tone. • Sympathetic nerves causes vasoconstriction that protects the brain by shifting the autoregulation curve to the right in hypertension. • Parasympathetic nerves contribute to vasodilatation and play a part in hypotension and reperfusion injury • Blood viscosity - optimal haematocrit 30% • Temperature: CMRO2 decreases by 7% for each 1°C fall in body temperature – At 27°C, CBF is approximately 50% of normal. By 20°C, CBF is about 10% of normal. • Drugs: Barbiturate thiopentone - Cerebral metabolism can be manipulated (reduced) and consequently CBF, cerebral blood volume and ICP is reduced - control high ICP after head injury. • Anaesthetic drugs; volatile agents cause reduction in the tension of cerebral vascular smooth muscle resulting in vasodilatation and an increase in CBF. • Vasodilatation can be countered by hyperventilation, without serious risk of cerebral ischaemia.
- 1. Temporal lobe herniation beneath tentorium cerebelli (uncal herniation) – causes cranial nerve III palsy (dilatation of pupil followed by movement of eye down and out). 2. Herniation of cerebellar peduncles through foramen magnum (tonsillar herniation). Pressure on the brainstem causes the Cushing reflex – hypertension, bradycardia and Cheyne- Stokes respiration (periodic breathing). 3. Subfalcine herniation occurs when the cingulate gyrus on the medial aspect of the frontal lobe is displaced across the midline under the free edge of the falx cerebri and may compress the anterior cerebral artery. 4. Upward, or cerebellar herniation occurs when either a large mass or increased pressure in the posterior fossa occurs. The cerebellum is displaced in an upward direction through the tentorial opening and causes significant upper brainstem compression.