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38 Cards in this Set

  • Front
  • Back
Equation for flow
Equation for cerebral blood flow
CPP = cerebral perfusion pressure
CVR = cerebral vascular resistance (experimental)
Equation for cerebral perfusion pressure
MAP = mean arterial pressure
ICP = inctracranial pressure
Poiseulle's law
States that the major determinants of cerebral blood flow are: vessel radius, pressure gradient, and blood viscosity
Factors regulating cerebral blood flow via resistance changes
– Pressure [autoregulation]
– Arterial PCO2 and PO2
– Cerebral metabolism
– Neurogenic
Describe pressure autoregulation
At pressures between 50 –160mmHg MAP, a constant flow of blood to the brain is maintained
– Pre-capillary arterioles dilate or contract
– Myogenic
Describe the mechanisms of myogenic pressure autoregulation
Stretch sensitive calcium channels respond to changes and systemic blood pressure
Describe the influence of PCO2 on cerebral blood flow
– 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]
Describe the influence of PO2 on cerebral blood flow
– 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
What recieves more bloodflow:
White or gray matter
Gray matter
Role of astrocytes and cerebral blood flow
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
Neurogenic control of blood flow
No major role.
What is the normal cerebral blood flow (in cc/100g/min) at rest, in gray matter and in white matter?
– Normal brain that rest 45 – 65
– Grey matter 75 – 80
– White matter 20 – 30
What are some ways that cerebral blood flow can be measured clinically
– PT
– Xenon CT
– CT perfusion
– MRI perfusion
How does the PET work for measuring CBF
Advantages of using PET for measuring CBF
– High spatial resolution (5mm^3)
– Most quantitative method
How does a SPECT work and measuring CBF
– Uses lipophilic tracers that cross the blood brain barrier and are fully extracted on first pass through cerebral circulation
Advantages/ disadvantages of SPECT
+ High spatial resolution (9mm^3) but less than PET
– Semi-quantitative
How does a Xenon CT work?
– 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
Advantages to using CT perfusion method
Allows analysis of:
– Mean transit time
– Cerebral blood volume
– Cerebral blood flow
Disadvantages to using CT perfusion method
- IV bolus of iodinated contrast
- acquisition is limited to 2 cm slab
How does MRI perfusion method for measuring CBF work
– 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
Normal values for intracranial pressure
Adults: <15cm H20
Children: <5cm H20
Advantages of the anatomy of the skull
Provides excellent protection for the brain
Disadvantages to the anatomy of the skull
Intolerant to internal volume changes
Skull contents
80% brain
10% CSF
10% blood
Monro-kellie doctrine
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
What pathological processes contribute to ICP
– Neoplasm
– Stroke
– Head injury
– Infection
What pathological situations can increased volume in brain and increase icp
– Tumor
– Cerebral edema
– Hemorrhage
– Abscess
How to the cranial contents respond to an added volume
– 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
Intracranial hypertension
– 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
What are some general and focal neurologic or effects of intracranial hypertension
General (diffuse increased ICP):
– Headache
– Nausea
– Vomiting
– Papilledema
– Cushing's response [HTN, bradycardia]

Focal (compression):
– Paralysis
– Aphasia
– Cranial
– Nerve palsy
– Drowsiness
– Apnea
Consequences of acute and severe increased ICP
– Focal areas of the brain shift along pathways of least resistance --> herniate
– Herniation syndromes
Types of herniation syndromes
– 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
Consequences of uncal herniation
Pressure on CN III and midbrain peduncle
– Can cause immediate death and is it true medical emergency
Monitoring ICP
– External ventricular drain
– Fiber-optic pressure transducers
What is contraindicated in cases of elevated ICP
Lumbar puncture
Management of intracranial hypertension
– Head elevation
– Diuretics
– Hyperventilation
– Sedation/paralysis
– Barbiturates
– Surgery [CSF drainage, evacuate the mass, craniectomy]