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Advanced Principles 2 > Neurophysiology > Flashcards

Neurophysiology Flashcards

1
Q

Describe the vascular supply to the brain.

A

blood from two distinct arteries:
internal carotid artery- anterior circulation
vertebral arteries- posterior circulation

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2
Q

The internal carotid artery branches enter through the base of skull- pass through cavernous sinus and divide into

A

anterior and middle cerebral artery

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3
Q

The basilar artery then branches (at the midbrain) into

A

2 posterior cerebral arteries* which primarily supply the occipital lobes of the brain

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4
Q

The circle of willis is a major site of

A

aneurysm and atherosclerosis, especially the middle cerebral artery

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5
Q

The Circle of Willis is important because if

A

one portion of cerebral blood flow becomes obstructed, other blood flow will compensate and give collateral flow

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6
Q

Cerebral blood flow varies with

A

metabolic activity 10-300 mL/100 g/min.

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7
Q

Total cerebral blood flow in adults averages

A

750 mL/min.

-15 to 20% of cardiac output

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8
Q

Describe the difference in cerebral blood flow for gray vs. white matter

A

gray matter- 80 mL/100 g/min

white matter- 20 mL/100 g/min

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9
Q

Cerebral blood flow of 20-25 mL/100 g/min shows up on EEG as

A

cerebral impairment

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10
Q

Cerebral blood flow of 15-20 mL/100 g/min shows up as

A

flat EEG

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11
Q

Cerebral blood flow below 10 mL/100 g/min is

A

associated with irreversible brain damage

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12
Q

Cerebral blood flow monitoring can be achieved through use of

A 
transcranial doppler (TC): ultrasound- middle cerebral artery
Brain tissue oximetry: bolt with a Clark electrode oxygen sensor
Intracerebral microdialysis: assesses brain tissue chemistry 
*Near infrared spectroscopy
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13
Q

Near infrared largely reflects the

A

**absorption of venous hemoglobin

NOT pulsatile arterial flow

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14
Q

Near infrared spectroscopy receptors detect the

A

reflected light from superficial & deep structures

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15
Q

Neuro events will appear on near infrared spectroscopy as:

A

rSO2 <40%

or change in rSO2 of >25% from baseline*****

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16
Q

Cerebral perfusion pressure equation is

A

MAP-ICP= CPP

*CVP may be substituted for ICP

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17
Q

Normal ICP is

A

<10-15 mmHg

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18
Q

Normal CPP is

A

80-100 mmHg

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19
Q

CPP < 50 mmHg is reflected on EEG as

A

slowing EEG

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20
Q

CPP 25-40 mmHg is reflected as a

A

flat EEG

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21
Q

CPP maintained <25 mmHg causes

A

irreversible brain damage

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22
Q

Increased cerebral perfusion pressure leads to

A

cerebral vasoconstriction to limit CBF

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23
Q

Decreased cerebral perfusion pressure leads to

A

cerebral vasodilation to increase CBF

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24
Q

Autoregulation originates in

A

vascular smooth muscles

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25
Q

Autoregulation can be explained by

A

myogenic- intrinsic response of smooth muscle in cerebral arterioles
metabolic- metabolic demands determine arteriolar tone
-tissue demand> blood flow
-release of tissue metabolites causes vasodilation and increases flow

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26
Q

CBF remains nearly constant between MAPS of

A

60-160 mmHg**

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27
Q

MAPs >150-160 mmHg can disrupt the

A

BBB and may result in cerebral edema & hemorrhage

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28
Q

In patients with chronic hypertension, the autoregulation curve is

A

right shifted

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29
Q

Factors that effect cerebral blood flow include

A 
PaCO2
PaO2
temperature
viscosity
autonomic influences
age
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30
Q

The most important extrinsic influences on CBF are

A

respiratory gas tensions- particularly PaCO2

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31
Q

CBF is directly proportionate to

A

PaCO2 between tensions 20-80 mmHg

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32
Q

Blood flow changes ______ per 1 mmHg change in PaCO2

A

1-2 mL/100 g/min

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33
Q

ACUTE metabolic acidosis has

A

little effect on CBF

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34
Q

In 24-48 hours, CSF bicarb compensates for

A

change in PaCO2**

bottom line: bicarb compensation probably happens in the ICU… not the OR

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35
Q

CBF is _______ to PaCO2

A

DIRECTLY PROPORTIONATE

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36
Q

CBF is attenuated at a PaCO2 of

A

<25 mmHg (ceiling effect)

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37
Q

Sensitivity** of CBF to changes in PaCO2 is _______ with resting levels of CBF

A

positively correlated

38
Q

Marked hyperventilation (defined as PaCO2 <20 mmHg**) shifts the oxyhemoglobin dissociation curve

A

to the LEFT and with changes in CBF may result in EEG changes suggestive of cerebral impairment** even in normal individuals

39
Q

Alkalosis causes _______ affinity of hemoglobin for

A

increases; O2 and therefore decreased release of O2

40
Q

Acute restoration of a normal PaCO2 value will result in a

A

significant CSF acidosis (after “sustained period” of hyperventilation/hypocapnia)

41
Q

CSF acidosis results in

A

increased CBF

42
Q

Increased CBF results in

A

increased ICP

43
Q

A PaO2 of

A

50 mmHg

44
Q

With a PaO2 of <60 mmHg vasodilation is mediated via

A

release of neuronal nitric oxide
open ATP-dependent K+ channels
rostral ventrolateral medulla**
Brain’s O2 sensor stimulation= increase CBF, but not CMRO2

45
Q

Hyperthermia causes

A

more energy usage

typically keep patients normothermic unless surgeon wants them cooler

46
Q

CMR decreases by ________

A

6% to 7% per 1 degree C

47
Q

Hematocrit determines

A

viscosity

48
Q

Decreased hematocrit decreases

A

viscosity & increases CBF

49
Q

Decreased hematocrit also decreases

A

O2 carrying capacity

-impaired oxygen delivery to brain tissue

50
Q

Some studies suggest that optimal cerebral oxygen delivery** may occur

A

at HCT of 30%

51
Q

Sympathetic innervation causes

A

vasoconstriction leading to decreased CBF

52
Q

Parasympathetic innervation causes

A

vasodilation leading to increased CBF

53
Q

Autonomic innervation may also play an important role in

A

cerebral vasospasm following brain injury & stroke

54
Q

Progressing aged leads to

A

decreased CBF due to progressive loss of neurons, loss of myelinated fibers, & loss of synapses

55
Q

At 80 years of age, _____ & ______ decrease by 15-20%

A

CBF & CMRO2

56
Q

The brain normally consumes

A

20% of total body oxygen***

-60% is used to generate ATP

57
Q

Interruption of cerebral perfusion results in

A

unconsciousness in 10 seconds
-O2 not restored in 3-8 min= depletion of ATP= irreversible cellular injury
hippocampus & cerebellum are most sensitive to hypoxic injury

58
Q

O2 is mostly consumed in

A

the gray matter***

59
Q

____ is the primary energy source in the brain

A

glucose

60
Q

Hypoglycemia can lead to

A

brain injury**

61
Q

Hyperglycemia can lead to

A

exacerbation of hypoxic injury***

62
Q

Brain glucose consumption is

A

5 mg/100g/min

63
Q

______ is responsible for the blood brain barrier

A

paucity of pores**

64
Q

With the lipid barrier,

A

lipid soluble substances freely pass
ionized molecules are restricted
large molecules are restricted

65
Q

The following freely cross the blood brain barrier

A

O2 & CO@

lipid soluble molecules (e.g. most anesthetics)

66
Q

The following are restricted across the blood brain barrier

A

ions (electrolytes e.g. Na+)
plasma proteins
large molecules (e.g. Mannitol)

67
Q

Disruptions from the blood brain barrier may be a result of

A

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

68
Q

Cerebral spinal fluid is

A

formed in the choroid plexuses by ependymal cells

69
Q

Adult production of cerebral spinal fluid is

A

21 mL/hr.
or 500 mL/day
total volume is ~150 mL

70
Q

Cerebral spinal fluid protects

A

CNS from trauma

71
Q

Cerebral spinal fluid is found in the

A

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

72
Q

CSF production is inhibited by

A

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

73
Q

Absorption of CSF is the result of

A

translocation from arachnoid granulations into cerebral sinuses

74
Q

Formation of the CSF involves

A

active secretion of sodium in the choroid plexuses

resulting fluid is isotonic with plasma (despite lower K, bicarb, & glucose concentrations)

75
Q

The cranial vault is composed of

A

brain (80%), blood (12%), and CSF (8%) in a fixed vault

-any increase in one component must be offset by an equivalent decrease in another to prevent rise in ICP

76
Q

Intracranial pressure is the

A

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

77
Q

Major compensatory mechanisms for changes in ICP include

A

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

78
Q

With a closed cranium, the provider’s goal is to

A

maintain CPP

prevent herniation

79
Q

With an open cranium, the provider’s goal is to

A

facilitate surgical access

reverse ongoing herniation

80
Q

Intracranial hypertension is defined as

A

sustained increase in ICP about 20-25 mmHg

81
Q

Causes of intracranial hypertension is a result of

A

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

82
Q

Signs & symptoms of increased intracranial pressure include

A

headache, N/V, papilledema, focal neurological deficit, decreased LOC, seizures, coma,
cushing’s triad: irregular respirations, hypertension, bradycardia

83
Q

Herniation is typically seen as

A

cerebellar tonsils through foramen magnum

84
Q

Signs and symptoms of transcalvarial herniation include

A

may occur during surgery

85
Q

Signs & symptoms of cerebellar tonsillar herniation include

A

most common

  • no specific clinical manifestations
  • arched stiff neck
  • paresthesias in shoulder
  • decrease LOC
  • respiratory abnormalities
  • pulse rate variations
86
Q

Signs & symptoms of uncal & central herniation include

A

decrease LOC
pupils sluggish > fixed & dilated
Cheyne-Stokes respirations
Decorticate–> decerebrate posturing

87
Q

Treatment of intracranial hypertension includes:

A

brain tissue: surgical removal of mass (i.e. lobectomy or removal of bone flap)
CSF: no effective pharmacological manipulation; only practical management is a drain
Fluid: steroids; osmotics/diuretics
Blood: most amenable to rapid alteration; decrease arterial flow** or increase venous drainage*** (pt. position)
reduction of PaCO2
CMR suppression (barbiturates, propofol, hypothermia)

88
Q

Describe how inhaled anesthetics affect CMRO2, CBF, & ICP.

A

CMRO2 decreased expect N2O
CBF increased due to vasodilation
ICP increased

89
Q

Describe how intravenous anesthetics affect CMRO2, CBF, & ICP.

A

decreased CMRO2
decreased CBF
decreased ICP

90
Q

Describe how local anesthetics affect CMRO2, CBF, & ICP.

A

decreased CMROs
decreased CBF
decreased ICP

91
Q

Describe how ketamine affects CMRO2, CBF, & ICP

A

+/- for CMRO2
increased CBF
increased ICP

92
Q

Nitrous oxide leads to

A

increased CMRO2, CBF, CBV, and ICP… more dramatic if sole agent****

Advanced Principles 2 (42 decks)

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