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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
what percentage would you expect on a NIRS monitor for a normal healthy patient versus a patient with co morbidities and decreased reserve?
80% versus near 60%
26
normal CPP
80-100mmHg (if they've got co morbidities, may need >80 but if theyre healthy >60 is fine)
27
normal ICP
10-15mmHg
28
when monitoring EEG, what CPP would reflect a "slowing EEG"
<50mmHg
29
when monitoring EEG, what CPP would reflect a "flat EEG"
25-40mmHg
30
when monitoring EEG, what CPP would reflect "irreversible brain damage"
CPP maintained <25mmHg
31
myogenic auto regulation: when CPP gets too high, the body
limits CBF via vasoconstriction
32
myogenic auto regulation, when CPP gets too low, the body
increases CBF via vasodilation
33
CBF remains nearly constant between MAPs of
60-160
34
what happens to CBF if MAP >150-160mmHg
BBB gets disrupted, cerebral edema and hemorrhage can result
35
factors affecting CBF (6)
PaCO2, PaO2, temperature, viscosity, autonomic influences, age
36
CBF is directly proportionate to PaCO2 between tensions of
20-80mmHg
37
blood flow changes how much per 1mmHg change in PaCO2?
1-2mL/100g/min
38
what happens if you give HCO3?
nada. ions dont passively cross BBB so its not an acute fix. but in 24-48h you can see some compensation
39
when does the directly proportional rate of CBF to PaCO2 increase or decrease attenuate
when the PaCO2 is <25mmHg.
40
what do we give that increases the cerebrovascular reactivity to carbon dioxide (CVR-CO2)
inhaled anesthetics. CBF increases, CVR-CO2 increases
41
what happens to even normal healthy individuals in the setting of marked hyperventilation (PaCO2 <20mmHg)
shifts oxygen hemoglobin dissociation curve to the left and could result in EEG changes suggestive of cerebral impairment
42
do we usually allow neuro patients' PaCO2 to climb at the end of surgery so they get the hypoxic drive to breathe?
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
what range of PaO2 can a normal CBF rate be sustained
30->300mmHg
44
what PaO2 level can rapidly increase CBF
<50mmHg
45
what happens when PaO2 is <60mmHg to create a vasodilated environment
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
at what temperature would you assume neuronal cell injury
>42c
47
what is the goal temperature for neuro patients
normothermia
48
what determines viscosity
HCT
49
decreased HCT in relation to CBF
decreases viscosity, increases CBF
50
optimal cerebral oxygen delivery happens at a HCT of
30%
51
age means a loss of
neurons, myelinated fibers (white matter), synapses
52
what two things decrease by 15-20% at 80 years
CBF and CMRO2
53
the brain normally consumes how much of the total body oxygen
20%
54
how much of the total body oxygen consumed by the brain is used to generate ATP
60%
55
what is the baseline cerebral metabolic rate
3-3.8mL/100g/min or 50mL/min
56
O2 is mostly consumed in the
gray matter
57
interruption of the cerebral perfusion creates unconsciousness in
10 seconds
58
irreversible cellular injury happens if the O2 is not restored in the brain in
3-8 minutes. its because of a depletion in ATP
59
which areas of the brain are most sensitive to hypoxic injury
hippocampus and cerebellum
60
baseline brain glucose consumption
5mg/100g/min
61
primary energy source for brain
glucose
62
hypoglycemia does what to the brain
creates a brain injury
63
hyperglycemia does what to the brain
exacerbates hypoxic injury
64
what cannot pass through the blood brain barrier
ionized molecules (electrolytes), plasma proteins, large molecules (mannitol)
65
what can freely cross the BBB
O2, CO2, lipid soluble molecules (most anesthetics)
66
what can cause disruptions in the BBB
HTN, tumor, trauma, stroke, infection, marked hypercapnia, hypoxia, sustained seizure
67
CSF is formed in
the choroid plexuses by the ependymal cells
68
adults make CSF at ___/hr and ___/day
21ml/h and 500ml.day
69
total volume of CSF is usually ____ and can be found ______
~150ml, half in cranium and half in spinal space
70
CSF is replaced how many times per day
3-4
71
tonicity of CSF and makeup
isotonic with plasma. lower K, HCO3, and glucose concentration
72
production of CSF is inhibited by
carbonic anhydrase inhibitors (acetazolamide), corticosteroids, spironolactone, furosemide, isoflurane, and vasoconstrictors
73
flow of CSF
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
monro kelly and cranial vault: components and %
brain (80%), blood (12%), CSF (8%). increase in one means another has to decrease to prevent increase in ICP
75
where is supratentorial CSF pressure measured
in the lateral ventricles or over the cerebral cortex
76
major compensatory mechanisms for intracranial elastane includes (4)
initial displacement of CSF from cranial to spinal compartment increase in CSF absorption decrease in CSF production decrease in total cerebral blood volume
77
intracranial HTN is a sustained increase in ICP
about 20-25mmHg
78
intracranial HTN causes
expanding tissue or fluid mass interference with CSF absorption excessive CSF production systemic disturbances promoting edema
79
s/sx of increased ICP
HA, n/v, papilledema, focal neurological deficit, decrease LOC, seizures, coma, bushings (irreg resp, bradycardia, HTN)
80
cushings happens when ICP is
>20 ICP for 1-15min
81
most common type of herniation
cerebellar tonsils through foramen magnum
82
s/sx of cerebellar tonsilar herniation
``` no specific clinical manifestations arched stiff neck parasthesias in shoulder decrease LOC respiratory abnormalities pulse rate variations ```
83
treatment of intracranial HTN
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
normal CBV
~5ml/100g of brain (70mL)
85
when does CBF not parallel CBV
cerebral ischemia (CBV increases, but CBF decreases)

N934 Adv Principles Fa 21 (23 decks)

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