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N934 Adv Principles Fa 21 > Neuro Physiology > Flashcards

Neuro Physiology Flashcards

1
Q

brain receives blood from these two arteries

A

internal carotid artery

vertebral arteries

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2
Q

the internal carotid artery provides blood flow for the

A

anterior circulation

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3
Q

the vertebral arteries provide blood flow for the

A

posterior circulation

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4
Q

which structures does the anterior cerebral artery supply

A

basal ganglia, corpus callosum, medial surface of cerebral hemispheres, superior surface of frontal and parietal lobes

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5
Q

what conditions are caused by occlusion of the anterior cerebral artery

A

hemiplegia on contralateral side of body, greater in lower than in upper extremities

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6
Q

which structures does the middle cerebral artery supply

A

frontal lobe, parietal lobe, temporal lobe (primarily cortical surfaces)

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7
Q

what conditions are caused by occlusion of the middle cerebral artery

A

aphasia in dominant hemisphere and contralateral hemiplegia

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8
Q

which structures does the posterior cerebral artery supply

A

part of diencephalon and temporal lobe: occipital lobe

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9
Q

what conditions are caused by occlusion of the posterior cerebral artery

A

visual loss, sensory loss, contralateral hemiplegia if cerebral peduncle affected

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10
Q

path of two vertebral arteries

A

branches from subclavian, enters through foramen magnum, run along medulla, join in pons to form basilar artery. basilar artery then branches into 2 posterior cerebral arterries which primary supply occipital lobes of the brain

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11
Q

path of internal carotid arteries

A

pass through cavernous sinus and divided into anterior and middle cerebral artery

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12
Q

circle of willis

A

located at base of brain and forms anastomotic ring that includes vertebral (basilar) and internal carotid flow

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13
Q

artery that is most common site for aneurysm and atherosclerosis

A

MCA

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14
Q

total cerebral blood flow in adults averages how many mL/min? and takes up how much CO?

A

750mL/min, 15-20% of CO

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15
Q

average cerebral blood flow is how many ml/g/min?

A

50mL/100g/min

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16
Q

average cerebral blood flow of gray matter

A

80mL/100g/min

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17
Q

average blood flow of white matter

A

20mL/100g/min

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18
Q

varied cerebral blood flow range based on metabolic activity

A

10-300mL/100g/min

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19
Q

when EEG monitoring, what CBF is associated with cerebral impairment?

A

20-25ml/100g/min

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20
Q

when EEG monitoring, what CBF is associated with a flat EEG

A

15-20mL/100g/min

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21
Q

when EEG monitoring, what CBF is associated with irreversible brain damage

A

below 10mL/100g/min

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22
Q

how do we assess CBF (O2 delivery) in the clinical setting? (4 ways, and what they monitor)

A
  1. transcranial doppler: ultrasound- MCA
  2. brain tissue oximetry: bolt with a clark electrode oxygen sensor
  3. intracerebral microdialysis: assess brain tissue chemistry
  4. near infrared spectroscopy
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23
Q

near infrared spectroscopy (NIRS) how it works

A

receptors detect reflected light from superficial and deep structures
largely reflects absorption of venous HGB
not pulsatile arterial flow

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24
Q

NIRS changes that would indicate an acute neuro event

A

rSO2 <40% OR change in rSO2 >25% from baseline

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25
Q

what percentage would you expect on a NIRS monitor for a normal healthy patient versus a patient with co morbidities and decreased reserve?

A

80% versus near 60%

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26
Q

normal CPP

A

80-100mmHg (if they’ve got co morbidities, may need >80 but if theyre healthy >60 is fine)

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27
Q

normal ICP

A

10-15mmHg

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28
Q

when monitoring EEG, what CPP would reflect a “slowing EEG”

A

<50mmHg

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29
Q

when monitoring EEG, what CPP would reflect a “flat EEG”

A

25-40mmHg

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30
Q

when monitoring EEG, what CPP would reflect “irreversible brain damage”

A

CPP maintained <25mmHg

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31
Q

myogenic auto regulation: when CPP gets too high, the body

A

limits CBF via vasoconstriction

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32
Q

myogenic auto regulation, when CPP gets too low, the body

A

increases CBF via vasodilation

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33
Q

CBF remains nearly constant between MAPs of

A

60-160

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34
Q

what happens to CBF if MAP >150-160mmHg

A

BBB gets disrupted, cerebral edema and hemorrhage can result

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35
Q

factors affecting CBF (6)

A

PaCO2, PaO2, temperature, viscosity, autonomic influences, age

36
Q

CBF is directly proportionate to PaCO2 between tensions of

A

20-80mmHg

37
Q

blood flow changes how much per 1mmHg change in PaCO2?

A

1-2mL/100g/min

38
Q

what happens if you give HCO3?

A

nada. ions dont passively cross BBB so its not an acute fix. but in 24-48h you can see some compensation

39
Q

when does the directly proportional rate of CBF to PaCO2 increase or decrease attenuate

A

when the PaCO2 is <25mmHg.

40
Q

what do we give that increases the cerebrovascular reactivity to carbon dioxide (CVR-CO2)

A

inhaled anesthetics. CBF increases, CVR-CO2 increases

41
Q

what happens to even normal healthy individuals in the setting of marked hyperventilation (PaCO2 <20mmHg)

A

shifts oxygen hemoglobin dissociation curve to the left and could result in EEG changes suggestive of cerebral impairment

42
Q

do we usually allow neuro patients’ PaCO2 to climb at the end of surgery so they get the hypoxic drive to breathe?

A

slowly increase back to normal PaCO2, do not allow this to happen quickly so be apprised of PaCO2 and permissive hypercapnia is much much more limited if at all allowed.

43
Q

what range of PaO2 can a normal CBF rate be sustained

A

30->300mmHg

44
Q

what PaO2 level can rapidly increase CBF

A

<50mmHg

45
Q

what happens when PaO2 is <60mmHg to create a vasodilated environment

A

release of neuronal nitric oxide
open ATP dependent K channels
rostral ventrolateral medulla (RVM), pressure area of medulla, senses increase in pressure
while CBF increases, CMRO2 does not

46
Q

at what temperature would you assume neuronal cell injury

A

> 42c

47
Q

what is the goal temperature for neuro patients

A

normothermia

48
Q

what determines viscosity

A

HCT

49
Q

decreased HCT in relation to CBF

A

decreases viscosity, increases CBF

50
Q

optimal cerebral oxygen delivery happens at a HCT of

A

30%

51
Q

age means a loss of

A

neurons, myelinated fibers (white matter), synapses

52
Q

what two things decrease by 15-20% at 80 years

A

CBF and CMRO2

53
Q

the brain normally consumes how much of the total body oxygen

A

20%

54
Q

how much of the total body oxygen consumed by the brain is used to generate ATP

A

60%

55
Q

what is the baseline cerebral metabolic rate

A

3-3.8mL/100g/min or 50mL/min

56
Q

O2 is mostly consumed in the

A

gray matter

57
Q

interruption of the cerebral perfusion creates unconsciousness in

A

10 seconds

58
Q

irreversible cellular injury happens if the O2 is not restored in the brain in

A

3-8 minutes. its because of a depletion in ATP

59
Q

which areas of the brain are most sensitive to hypoxic injury

A

hippocampus and cerebellum

60
Q

baseline brain glucose consumption

A

5mg/100g/min

61
Q

primary energy source for brain

A

glucose

62
Q

hypoglycemia does what to the brain

A

creates a brain injury

63
Q

hyperglycemia does what to the brain

A

exacerbates hypoxic injury

64
Q

what cannot pass through the blood brain barrier

A

ionized molecules (electrolytes), plasma proteins, large molecules (mannitol)

65
Q

what can freely cross the BBB

A

O2, CO2, lipid soluble molecules (most anesthetics)

66
Q

what can cause disruptions in the BBB

A

HTN, tumor, trauma, stroke, infection, marked hypercapnia, hypoxia, sustained seizure

67
Q

CSF is formed in

A

the choroid plexuses by the ependymal cells

68
Q

adults make CSF at ___/hr and ___/day

A

21ml/h and 500ml.day

69
Q

total volume of CSF is usually ____ and can be found ______

A

~150ml, half in cranium and half in spinal space

70
Q

CSF is replaced how many times per day

A

3-4

71
Q

tonicity of CSF and makeup

A

isotonic with plasma. lower K, HCO3, and glucose concentration

72
Q

production of CSF is inhibited by

A

carbonic anhydrase inhibitors (acetazolamide), corticosteroids, spironolactone, furosemide, isoflurane, and vasoconstrictors

73
Q

flow of CSF

A

lateral ventricles through intraventricular foramen (of monro), 3rd ventricle, 4th ventricle (foramen of magendie), cisterns magna, subarachnoid space where it circulates around brain and spinal cordd, then absorbed in arachnoid granulations

74
Q

monro kelly and cranial vault: components and %

A

brain (80%), blood (12%), CSF (8%). increase in one means another has to decrease to prevent increase in ICP

75
Q

where is supratentorial CSF pressure measured

A

in the lateral ventricles or over the cerebral cortex

76
Q

major compensatory mechanisms for intracranial elastane includes (4)

A

initial displacement of CSF from cranial to spinal compartment
increase in CSF absorption
decrease in CSF production
decrease in total cerebral blood volume

77
Q

intracranial HTN is a sustained increase in ICP

A

about 20-25mmHg

78
Q

intracranial HTN causes

A

expanding tissue or fluid mass
interference with CSF absorption
excessive CSF production
systemic disturbances promoting edema

79
Q

s/sx of increased ICP

A

HA, n/v, papilledema, focal neurological deficit, decrease LOC, seizures, coma, bushings (irreg resp, bradycardia, HTN)

80
Q

cushings happens when ICP is

A

> 20 ICP for 1-15min

81
Q

most common type of herniation

A

cerebellar tonsils through foramen magnum

82
Q

s/sx of cerebellar tonsilar herniation

A 
no specific clinical manifestations
arched stiff neck
parasthesias in shoulder
decrease LOC
respiratory abnormalities
pulse rate variations
83
Q

treatment of intracranial HTN

A

brain tissue: surgical removal of mass
CSF: no effective pharmacological management, only practical management is a drain
fluid: steroids, osmotics/diuretics
blood: most amenable to rapid alterations: decrease arterial flow or increase venous drainage (pt position)
reduction of PaCO2 (to not <23-25mmHg)
CMR suppression (barbs, prop, hypothermia)

84
Q

normal CBV

A

~5ml/100g of brain (70mL)

85
Q

when does CBF not parallel CBV

A

cerebral ischemia (CBV increases, but CBF decreases)

N934 Adv Principles Fa 21 (23 decks)

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