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38 Cards in this Set
- Front
- Back
Equation for flow
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Pressure/Resistance
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Equation for cerebral blood flow
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CPP/CVR
CPP = cerebral perfusion pressure CVR = cerebral vascular resistance (experimental) |
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Equation for cerebral perfusion pressure
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MAP - ICP
MAP = mean arterial pressure ICP = inctracranial pressure |
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Poiseulle's law
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States that the major determinants of cerebral blood flow are: vessel radius, pressure gradient, and blood viscosity
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Factors regulating cerebral blood flow via resistance changes
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– Pressure [autoregulation]
– Arterial PCO2 and PO2 – Cerebral metabolism – Neurogenic |
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Describe pressure autoregulation
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At pressures between 50 –160mmHg MAP, a constant flow of blood to the brain is maintained
– Pre-capillary arterioles dilate or contract – Myogenic |
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Describe the mechanisms of myogenic pressure autoregulation
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Stretch sensitive calcium channels respond to changes and systemic blood pressure
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Describe the influence of PCO2 on cerebral blood flow
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– Cerebral vessels are very sensitive to changes in PCO2
– Hypercarbia causes vasodilation increases CBF – Hypocarbia causes vasoconstriction and decreases CBF – Changes mediated by extracellular [H] |
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Describe the influence of PO2 on cerebral blood flow
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– CBF does not very with small variations in PaO2
– When PaO2 falls below 50mmHg --> CBF begins to rise exponentially – hypoxia --> NO and Adenosine production --> vasodilation |
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What recieves more bloodflow:
White or gray matter |
Gray matter
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Role of astrocytes and cerebral blood flow
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Coupling of neuronal activity and CBS
– Send processes to synapses and blood vessels --> Increase neuronal activity --> increased blood flow to area - communicate with other astrocytes through gap junctions |
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Neurogenic control of blood flow
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No major role.
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What is the normal cerebral blood flow (in cc/100g/min) at rest, in gray matter and in white matter?
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– Normal brain that rest 45 – 65
– Grey matter 75 – 80 – White matter 20 – 30 |
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What are some ways that cerebral blood flow can be measured clinically
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– PT
– SPECT – Xenon CT – CT perfusion – MRI perfusion |
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How does the PET work for measuring CBF
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– USES A OXYGEN LABELED WATER AS A TRACER
– MEASURES OXYGEN UTILIZATION/EXTRACTION |
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Advantages of using PET for measuring CBF
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– High spatial resolution (5mm^3)
– Most quantitative method |
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How does a SPECT work and measuring CBF
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– Uses lipophilic tracers that cross the blood brain barrier and are fully extracted on first pass through cerebral circulation
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Advantages/ disadvantages of SPECT
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+ High spatial resolution (9mm^3) but less than PET
– Semi-quantitative |
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How does a Xenon CT work?
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– Xenon gas is inhaled, dissolves in the blood and readily cross BBB
– High atomic number of xenon allows it to the measured on CT – Wash out method employed: steady-state is achieved and then the rate of decay relates to superfusion |
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Advantages to using CT perfusion method
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Allows analysis of:
– Mean transit time – Cerebral blood volume – Cerebral blood flow |
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Disadvantages to using CT perfusion method
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- IV bolus of iodinated contrast
- acquisition is limited to 2 cm slab |
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How does MRI perfusion method for measuring CBF work
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– IV injection of paramagnetic contracts followed by rapid acquisition of images
– Dephasing of immediately adjacent tissues and the signal loss closely related to cerebral perfusion |
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Normal values for intracranial pressure
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Adults: <15cm H20
Children: <5cm H20 |
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Advantages of the anatomy of the skull
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Provides excellent protection for the brain
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Disadvantages to the anatomy of the skull
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Intolerant to internal volume changes
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Skull contents
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80% brain
10% CSF 10% blood |
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Monro-kellie doctrine
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Vk = Vbrain + Vcsf + Vblood
As long as the volume relationship is maintained, the pressure inside this skull will remain normal – Any added volume to the skull will displace the normal three constituents and can eventually cause an increase in pressure |
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What pathological processes contribute to ICP
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– Neoplasm
– Stroke – Head injury – Infection |
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What pathological situations can increased volume in brain and increase icp
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– Tumor
– Cerebral edema – Hemorrhage – Abscess |
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How to the cranial contents respond to an added volume
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– Compensation depends on how fast the volume is added
Rapid addition: two phases - Phase 1: CSF and blood redistribute, ICP unchanged – Phase 2: maximal redistribution reached, ICP rises |
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Intracranial hypertension
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– One compensation is exhausted, pressure is exerted onto the brain
– Cellular effects: mechanical compression on neurons, glia, and cerebral blood vessels – Neurological effects: general and focal |
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What are some general and focal neurologic or effects of intracranial hypertension
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General (diffuse increased ICP):
– Headache – Nausea – Vomiting – Papilledema – Cushing's response [HTN, bradycardia] Focal (compression): – Paralysis – Aphasia – Cranial – Nerve palsy – Drowsiness – Apnea |
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Consequences of acute and severe increased ICP
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– Focal areas of the brain shift along pathways of least resistance --> herniate
– Herniation syndromes |
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Types of herniation syndromes
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– Subfalcine herniation: herniation of frontal lobe under the falx
– Midline shift: movement of one hemisphere towards other – Tonsillar herniation: herniation of cerebral tonsils through foramen magnum – Uncal herniation a.k.a. transtentorial herniation: herniation of uncus (medial temporal lobe) through tentorial hiatus and against brainstem |
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Consequences of uncal herniation
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Pressure on CN III and midbrain peduncle
– Can cause immediate death and is it true medical emergency |
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Monitoring ICP
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– External ventricular drain
– Fiber-optic pressure transducers |
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What is contraindicated in cases of elevated ICP
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Lumbar puncture
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Management of intracranial hypertension
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– Head elevation
– Diuretics – Hyperventilation – Sedation/paralysis – Barbiturates – Surgery [CSF drainage, evacuate the mass, craniectomy] |