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N934: Advanced Principles of Anesthesia > Neuro Physiology > Flashcards

Neuro Physiology Flashcards

1
Q

What are the two distinct arteries that supply the brain?

A

internal carotid artery
veretebral arteries

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2
Q

What circulation does the internal carotid artery create?

A

anterior circulation
85% of blood flow
supplies anterior 2/3 surface of brain

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3
Q

What circulation does the vertebral arteries create?

A

posterior circulation
15% blood flow
supplies posterior 1/3 surface of brain

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4
Q

Describe the two vertebral arteries to til they form the basilar artery

A

Enter the base of the skull through the foramen magnum
runs along the medulla
join in the pons to form the basilar artery

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5
Q

Describe the circulation of the basilar artery

A

the basilar artery then branches into two posterior cerebral arteries

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6
Q

What do the two posterior cerebral arteries supply?

A

occipital lobes of the brain

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7
Q

Describe the internal carotid artery branches

A

enter through the base of the skull pass through the cavernous sinus and divide into the anterior and middle cerebral artery

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8
Q

What is the Circle of Willis?

A

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

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9
Q

What happens if one portion of the circle of willis becomes obstructed?

A

other blood flow will compensate and give collateral flow

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10
Q

What is a major site for aneurysm and atherosclerosis?

A

the circle of willis
Middle cerebral artery

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11
Q

What varies with metabolic activity?

A

cerebral blood flow
10-300ml/100g/min

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12
Q

What is the average TOTAL cerebral blood flow in adults?

A

750ml/min

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13
Q

what % of cardiac output is CBF?

A

15-20%

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14
Q

What is the average cerebral blood flow?

A

50ml/100g/min

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15
Q

Grey matter average CBF

A

80ml/100g/min

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16
Q

White matter average CBF

A

20ml/100g/min

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17
Q

What is the main function of the Circle of Wilis?

A

to provide redundancy of blood flow in the brain

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18
Q

How does venous blood exit the brain?

A

paired jugular veins

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19
Q

Cerebral impairment on an EEG

A

20-25ml/100g/min

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20
Q

Flat EEG

A

15-20ml/100g/min

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21
Q

Associated with irreversible brain damage EEG recording

A

below 10ml/100g/min

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22
Q

How do you assess CBF in a clinical setting

A

Transcranial doppler
brain tissue oximetry
intracerebral microdialysis
Near infrared Spectroscopy

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23
Q

What is transcranial doppler?

A

ultrasound
middle cerebral artery

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24
Q

What is brain tissue oximetry?

A

bolt with clark electrode oxygen sensor

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25
Q

What is intracerebral microdiaylsis?

A

assesses brain tissue chemistry

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26
Q

What is NIRS?

A

near infrared spectroscopy
receptors detect the reflected light from superficial and deep structures

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27
Q

What does NIRS reflect?

A

absorption of venous hemoglobin
NOT pulsatile arterial flow

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28
Q

What are considered neuro events with NIRS monitoring?

A

rSO2 <40% or change in rSO2 of >25% from baseline

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29
Q

What surgery does not have a cut off for rSO2?

A

carotid endarectomy

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30
Q

What is the physics law associated withe NIRS?

A

beer lambert law
reflectance spectroscopy
O2 and de-O2 Hgb absorb light at different frequencies

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31
Q

What is cerebral perfusion pressure?

A

difference in mean arterial pressure and intracranial pressure

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32
Q

What is the equation for CPP?

A

MAP-ICP=CPP

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33
Q

What can be substituted for ICP?

A

CVP, if CVP is greater then ICP

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34
Q

What is CPP primarily dependent on?

A

MAP

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35
Q

What are reference values for CPP and ICP?

A

ICP- <10-15mmHg
CPP: 80-100mmHg
(>60 okay for alseep healthy individuals)

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36
Q

What are critical CPPs?

A

Low BP + elevated ICP
CPP<50 + slowing EEG
CPP 25-40= Flat EEG

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37
Q

What is cerebral autoregulation?

A

myogenic regulation
Vascular smooth muscles
cerebral vascular rapidly adapts to changes in CPP

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38
Q

What does autoregulation cause when CPP is increased?

A

Cerebral vasoconstriction (limiting CBF)

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39
Q

What does autoregulation cause when CPP is decreased?

A

Cerebral vasodilation (increasing CBF)

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40
Q

Metabolic autoregulation

A

metabolic demands determine arteriole tone

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41
Q

Myogenic autoregulation

A

intrinsic response of smooth muscles in cerebral arteries

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42
Q

Both myogenic and metabolic autoregulation determine

A

tissue demand> blood flow
release tissue metabolites causing vasodilation= increase flow

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43
Q

Autoregulation remains nearly constant between MAPS of

A

60-160
70-150
50-150
60-140mmHg

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44
Q

What happens when MAP is outside these ranges?

A

blood flow becomes pressure dependent

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45
Q

MAP >150-160mmHg will cause

A

disruption in BBB and may result in cerebral edema and hemorrhage

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46
Q

Patients with chronic hypertension have autoregulation curves shifted

A

Right because the flow becomes more pressure dependent at low “normal” arterial pressures in return for cerebral protection at higher arterial pressures

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47
Q

What factors effect CBF?

A

PaCO2, PaO2, temperature, viscosity, autonomic interference, age

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48
Q

How are CBF an PaCO2 related?

A

directly proportional between tensions 20-80mmHg

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49
Q

What are the most important extrinsic influences on CBF?

A

respiratory gas tensions
particularly PaCO2

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50
Q

Since CBF and PaCO2 are directly proportional what are the approximate blood flow changes?

A

1-2ml/100g/min per mmHg in PaCO2

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51
Q

What does not cross the BBB?

A

ions, HCO3

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52
Q

What are changes in PaCO2 reflective of?

A

respiratory tensions and secondary to pH changes in CSF and cerebral tissue

53
Q

Why does metabolic acidosis not have a readily effect on cerebral perfusion (CBF)?

A

because Hydrogen ions can not readily cross the BBB

54
Q

Describe cerebral blood flow when you hyperventilate a patient?

A

hyperventilation leads to PaCO2 <20mmHg
lower partial pressure of carbon dioxide in the blood therefore you have an a decrease in cerebral blood flow

55
Q

What happens to cerebral blood flow with severe hyperoxia?

A

great increases in CBF

56
Q

Does PaO2 have a large influence on CBF?

A

no

57
Q

What happens in 24-28 hour in the brain with an metabolic acidosis?

A

CSF HCO3 compensates (active transport) for changes in PaCO2
effects of hypocapnia and hypercapnia are diminished

58
Q

What is the ceiling effect for PaCO2 in CBF?

A

response of decrease in cerebral blood flow is attenuated at a PaCO2 <25mmHg

59
Q

The sensitivity of CBF to changes in PaCO2 (deltaCBF/deltaPaCO2) are

A

positively corrleated with resting levels of CBF

60
Q

At normocarbia, VAs do what to the cerebral vessels?

A

dilate cerebral vessels and impair autoregulation in a concentration dependent manner

61
Q

What occurs to the hemoglobin oxygenation dissociation curve when the patient is hyperventilated?

A

The curve shifts left
Decrease in cerebral blood flow, therefore alkalosis causes increased affinity for Hgb for O2 and therefore decreased release of O2

62
Q

What does the shift of the hemoglobin dissociation curve imply in an EEG?

A

can suggest cerebral impairment even in normal individuals

63
Q

What occurs after an acute restoration normal PaCO2 after surgery?

A

significant CSF acidosis
which causes increased CBF and increased ICP

64
Q

How do you prevent an increased ICP post-operatively?

A

slowly increase CO2 during the case

65
Q

What range does PaO2 have little range on CBF?

A

50-300mmHg

66
Q

When does PaO2 change CBF and how?

A

<50mHg
rapid increase in CBF

67
Q

How does vasodilation occur when PaO2 <60mmHG in the brain?

A

Mediated by release of neural nitric oxide
open ATP dependent K channels
Rostral ventrolateral medulla (RVM)
brain’s O2 sensory stimulation

68
Q

How does temperature effect CBF and CMRO2?

A

hypothermia decreases CBF and CMRO2
hyperthermia increases CBF and CMRO2

69
Q

How does viscosity effect CBF?

A

decrease in viscosity can improve CBF

70
Q

What determines viscosity?

A

hematocrit (Hct)

71
Q

Describe the relationship of viscosity, hematocrit and the brain

A

Decrease in HCt, decreases viscosity, but improves CBF
Decrease in HCT, decrease in oxygen carrying capacity therefore possible impaired oxygen delivery to brain tissue

72
Q

When does optimal cerebral oxygen delivery occur? (Hct level?)

A

30%

73
Q

When there is variation in HCT (33-45%) what happens to CBF

A

only modest alternations

74
Q

What happens to CBF in anemia?

A

cerebral vascular resistance decreases, CBF increases

75
Q

What can occur in elevated hematocrits?

A

polycythemia
reduced CBF

76
Q

Do you manipulate viscosity with ischemic strokes?

A

no despite the idea that hemodiluation increases CBF, but you will decrease oxygen carrying capacity.
Only manipulate viscoscity if the patient has high hematocrit values

77
Q

How does the sympathetic system affect CBF?

A

vasoconstriction, decreases CBF

78
Q

How was the parasympathetic system affect CBF

A

vasodilation, increases CBF

79
Q

What does autonomic innervation play an important role in after a brain injury or stroke?

A

cerebral vasospasms

80
Q

How does age affect a patient’s neurological function?

A

progressive loss of neurons with aging
loss of myelinated fibers, loss of white matter
loss of synapes

81
Q

How much does CBF and CMRO decrease by 80 Y?

A

CBF and CMRO2 decreases by 15%-20%

82
Q

What is the normal consumption of total blody oxygen by the brain?

A

20% of total body oxygen

83
Q

How much of the 20% of total body oxygen is used to make ATP?

A

60%

84
Q

What is the cerebral metabolic rate?

A

3-3.8mL/100g/min (CMRO2)
50ml/min

85
Q

Where is O2 mostly consumed?

A

gray matter

86
Q

WHen will you become unconcious due to interruption of cerebral perfusion?

A

10 seconds

87
Q

What areas are most sensitive to hypoxic injury?

A

hippocampus and cerebellum

88
Q

what is the primary energy source?

A

glucose

89
Q

What is the brain’s glucose consumption?

A

5mg/100g/min
90% metabolized aerobically metabolized

90
Q

what parallels glucose consumption?

A

CMRO2

91
Q

What are the effects of hypoglycemia?

A

brain injury

92
Q

What are the effects of hyperglycemia?

A

exacerbate hypoxic injury

93
Q

What is the role of the blood brain barrier?

A

isolates the brain and spinal cord extracellular compartment from intravascular compartment

94
Q

What is the blood brain barrier?

A

cerebral blood vessels that are unique in junctions between vascular endothelial cells are nearly fused. The paucity of the pores is what creates the BBB

95
Q

What do CNS endothelial cells lack?

A

transport mechanisms

96
Q

What does the lipid barrier allow to pass?

A

lipid soluble substances
-carbon dioxide, oxygen, most anesthetics

97
Q

what is restricted by the lipid barrier?

A

ionized molecules
large molecules
ions, proteins, larger substances (mannitol)

98
Q

What governs the movement of particles across the BBB?

A

size
charge
lipid solubility
plasma protein binding

99
Q

What causes disruptions in the BBB?

A

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

100
Q

Where is CSF formed?

A

choroid plexus by ependymal cells

101
Q

What is the average total volume of CSF?

A

150ml

102
Q

how many times is CSF replaced a day?

A

3-4 times

103
Q

Where is CSF found?

A

cerebral ventricles and cisterns and subarachnoid space surrounding the brain and spinal cord

104
Q

What is the purpose of CSF?

A

to protect the CNS from trauma

105
Q

CSF is ____ to plasma?

A

isotonic

106
Q

What electrolyte concentrations are different in CSF?

A

lower potassium, bicarbonate, glucose concentrations

107
Q

What is CSF production inhibited by?

A

carbonic anhydrase inhibitors (acetazolamide), corticosteroids, spironolaction, isoflurane, vasoconstriction

108
Q

Describe the flow of CSF

A

lateral ventricles of the cerebral hemispheres-> through the foramen of monro-> 3rd ventricle-> through the aqueduct of sylvius (midbrain)-> into 4th ventricle

109
Q

Describe how CSF leaves the ventricular system

A

the subarachnoid space through three openings in the roof of the fourth ventricle

110
Q

What are openings which CSF leaves?

A

medial foramen of magendie and two lateral foramina of luschka

111
Q

what is intracranial pressure (ICP)?

A

supratentorial CSF pressure measure in the lateral ventricles or over the cerebral cortex

112
Q

What does the Monro Kellie hypothesis state?

A

cranial compartments are incompressible and the volume inside the cranium is a fixed volume.
The cranium and its constituents (blood, CSF, adn brain tissue) create a state of volume equilibrium, such that any increase in volume of one of the cranial constituents must be compressed by a decrease in volume of another to prevent a rise in ICP

113
Q

What are the major compensatory mechanisms for intracranial elastance?

A

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

114
Q

What size of ICP changes are well tolerated?

A

small increases

115
Q

Describe herniation

A

brain tissue from one compartment to another (or into the surgical field) with resultant mechanical injury to brain tissue, or in reduction of perfusion pressure, leading to ischemic injury

116
Q

What are the five types of brain herniation?

A

-cingulate gyrus under falx cerebri
-central
-uncinate gyrus through tentorium cerebelli
-cerebellar tonsils through foramen magum
-upward herniation of cerebellum
-any area beneath defect in the skull (transcalvarial)

117
Q

What are signs and symptoms of cingulate gyrus hernination?

A

little known

118
Q

What are signs and symptoms of uncal & central herniation?

A

decrease LOC
pupils sluggish -> fixed and dilated
Cheyne-strokes respirations
decorticate-> decerebrate posturing

119
Q

What are signs and symptoms of cerebellar tonsillar herniation?

A

most common
no specific clinical manifestations
arched stiff neck
paresthesias in shoulder
decrease in LOC
respiration abnormalities
pulse rate variations

120
Q

What are signs and symptoms of transcalvarial?

A

may occur during surgery

121
Q

What is the provider’s goal during a closed cranium?

A

maintain CPP
prevent herniation

122
Q

What is the provider’s goal during an open cranium?

A

facilitate surgical access
reverse ongoing herniation

123
Q

What is intracranial hypertension?

A

sustained increase in ICP about 20-25mmHg

124
Q

What causes ICP HTN?

A

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

125
Q

What can influence increase BV?

A

increased airway or intrathoracic pressure
increased jugular vein distention
increase PaCO2 or decreased PaO2
some anesthetics (vasodilators and seizures)

126
Q

What can cause cellular compartment masses or leisons?

A

tumors
hematomas, subdural, extradural, intracerebral

127
Q

What can cause increase in edema (increase fluid compartment)?

A

mechanical injury
ischemia
defective autoregulation

128
Q

What are the signs and symptoms of increase in ICP?

A

headache
N/V
papilledema
focal neurological deficit
decreased LOC
seizures
coma
cushings: irregular respirations, HTN, bradycardia
posturing
decreased motor function
changes in speech

129
Q

How do you treat intracranial hypertension?

A

-surgical removal of mass
-drainage of CSF
-steroids, osmotic/diuretics
-decrease arterial BF or increase venous drainage (ie patient position)
-reduction in PaCO2
-CMR suppression (barbiturates, propofol, hypothermia)

N934: Advanced Principles of Anesthesia (16 decks)

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