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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
Autoregulation can be explained by
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
26
CBF remains nearly constant between MAPS of
60-160 mmHg**
27
MAPs >150-160 mmHg can disrupt the
BBB and may result in cerebral edema & hemorrhage
28
In patients with chronic hypertension, the autoregulation curve is
right shifted
29
Factors that effect cerebral blood flow include
``` PaCO2 PaO2 temperature viscosity autonomic influences age ```
30
The most important extrinsic influences on CBF are
respiratory gas tensions- particularly PaCO2
31
CBF is directly proportionate to
PaCO2 between tensions 20-80 mmHg
32
Blood flow changes ______ per 1 mmHg change in PaCO2
1-2 mL/100 g/min
33
ACUTE metabolic acidosis has
little effect on CBF
34
In 24-48 hours**, CSF bicarb** compensates for
change in PaCO2** | bottom line: bicarb compensation probably happens in the ICU... not the OR
35
CBF is _______ to PaCO2
DIRECTLY PROPORTIONATE
36
CBF is attenuated at a PaCO2 of
<25 mmHg (ceiling effect)
37
Sensitivity**** of CBF to changes in PaCO2 is _______ with resting levels of CBF
positively correlated
38
Marked hyperventilation (defined as PaCO2 <20 mmHg**) shifts the oxyhemoglobin dissociation curve
to the LEFT and with changes in CBF may result in EEG changes suggestive of cerebral impairment**** even in normal individuals
39
Alkalosis causes _______ affinity of hemoglobin for
increases; O2 and therefore decreased release of O2
40
Acute restoration of a normal PaCO2 value will result in a
significant CSF acidosis (after "sustained period" of hyperventilation/hypocapnia)
41
CSF acidosis results in
increased CBF
42
Increased CBF results in
increased ICP
43
A PaO2 of
50 mmHg
44
With a PaO2 of <60 mmHg vasodilation is mediated via
release of neuronal nitric oxide open ATP-dependent K+ channels rostral ventrolateral medulla** Brain's O2 sensor stimulation= increase CBF, but not CMRO2
45
Hyperthermia causes
more energy usage | typically keep patients normothermic unless surgeon wants them cooler
46
CMR decreases by ________
6% to 7% per 1 degree C
47
Hematocrit determines
viscosity
48
Decreased hematocrit decreases
viscosity & increases CBF
49
Decreased hematocrit also decreases
O2 carrying capacity | -impaired oxygen delivery to brain tissue
50
Some studies suggest that optimal cerebral oxygen delivery**** may occur
at HCT of 30%
51
Sympathetic innervation causes
vasoconstriction leading to decreased CBF
52
Parasympathetic innervation causes
vasodilation leading to increased CBF
53
Autonomic innervation may also play an important role in
cerebral vasospasm following brain injury & stroke
54
Progressing aged leads to
decreased CBF due to progressive loss of neurons, loss of myelinated fibers, & loss of synapses
55
At 80 years of age, _____ & ______ decrease by 15-20%
CBF & CMRO2
56
The brain normally consumes
20% of total body oxygen*** | -60% is used to generate ATP
57
Interruption of cerebral perfusion results in
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
O2 is mostly consumed in
the gray matter***
59
____ is the primary energy source in the brain
glucose
60
Hypoglycemia can lead to
brain injury****
61
Hyperglycemia can lead to
exacerbation of hypoxic injury***
62
Brain glucose consumption is
5 mg/100g/min
63
______ is responsible for the blood brain barrier
paucity of pores****
64
With the lipid barrier,
lipid soluble substances freely pass ionized molecules are restricted large molecules are restricted
65
The following freely cross the blood brain barrier
O2 & CO@ | lipid soluble molecules (e.g. most anesthetics)
66
The following are restricted across the blood brain barrier
ions (electrolytes e.g. Na+) plasma proteins large molecules (e.g. Mannitol)
67
Disruptions from the blood brain barrier may be a result of
HTN, tumor, trauma, stroke, infection, marked hypercapnia, hypoxia, sustained seizure
68
Cerebral spinal fluid is
formed in the choroid plexuses by ependymal cells
69
Adult production of cerebral spinal fluid is
21 mL/hr. or 500 mL/day total volume is ~150 mL
70
Cerebral spinal fluid protects
CNS from trauma
71
Cerebral spinal fluid is found in the
cerebral ventricles and cisterns & subarachnoid space surrounding the brain and spinal cord
72
CSF production is inhibited by
carbonic anhydrase inhibitors (acetazolamide), corticosteroids, spironolactone, furosemide, isoflurane, and vasoconstrictors
73
Absorption of CSF is the result of
translocation from arachnoid granulations into cerebral sinuses
74
Formation of the CSF involves
active secretion of sodium in the choroid plexuses | resulting fluid is isotonic with plasma (despite lower K, bicarb, & glucose concentrations)
75
The cranial vault is composed of
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
Intracranial pressure is the
supratentorial CSF pressure measured in the lateral ventricles or over the cerebral cortex
77
Major compensatory mechanisms for changes in ICP include
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
With a closed cranium, the provider's goal is to
maintain CPP | prevent herniation
79
With an open cranium, the provider's goal is to
facilitate surgical access | reverse ongoing herniation
80
Intracranial hypertension is defined as
sustained increase in ICP about 20-25 mmHg
81
Causes of intracranial hypertension is a result of
expanding tissue or fluid mass interference with CSF absorption excessive CSF production systemic disturbances promoting edema
82
Signs & symptoms of increased intracranial pressure include
headache, N/V, papilledema, focal neurological deficit, decreased LOC, seizures, coma, cushing's triad: irregular respirations, hypertension, bradycardia
83
Herniation is typically seen as
cerebellar tonsils through foramen magnum
84
Signs and symptoms of transcalvarial herniation include
may occur during surgery
85
Signs & symptoms of cerebellar tonsillar herniation include
most common - no specific clinical manifestations - arched stiff neck - paresthesias in shoulder - decrease LOC - respiratory abnormalities - pulse rate variations
86
Signs & symptoms of uncal & central herniation include
decrease LOC pupils sluggish > fixed & dilated Cheyne-Stokes respirations Decorticate--> decerebrate posturing
87
Treatment of intracranial hypertension includes:
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
Describe how inhaled anesthetics affect CMRO2, CBF, & ICP.
CMRO2 decreased expect N2O CBF increased due to vasodilation ICP increased
89
Describe how intravenous anesthetics affect CMRO2, CBF, & ICP.
decreased CMRO2 decreased CBF decreased ICP
90
Describe how local anesthetics affect CMRO2, CBF, & ICP.
decreased CMROs decreased CBF decreased ICP
91
Describe how ketamine affects CMRO2, CBF, & ICP
+/- for CMRO2 increased CBF increased ICP
92
Nitrous oxide leads to
increased CMRO2, CBF, CBV, and ICP... more dramatic if sole agent******

Advanced Principles 2 (42 decks)

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