Neuro Physiology Flashcards
(129 cards)
1
Q
What are the two distinct arteries that supply the brain?
A
internal carotid artery
veretebral arteries
2
Q
What circulation does the internal carotid artery create?
A
anterior circulation
85% of blood flow
supplies anterior 2/3 surface of brain
3
Q
What circulation does the vertebral arteries create?
A
posterior circulation
15% blood flow
supplies posterior 1/3 surface of brain
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
5
Q
Describe the circulation of the basilar artery
A
the basilar artery then branches into two posterior cerebral arteries
6
Q
What do the two posterior cerebral arteries supply?
A
occipital lobes of the brain
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
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
9
Q
What happens if one portion of the circle of willis becomes obstructed?
A
other blood flow will compensate and give collateral flow
10
Q
What is a major site for aneurysm and atherosclerosis?
A
the circle of willis
Middle cerebral artery
11
Q
What varies with metabolic activity?
A
cerebral blood flow
10-300ml/100g/min
12
Q
What is the average TOTAL cerebral blood flow in adults?
A
750ml/min
13
Q
what % of cardiac output is CBF?
A
15-20%
14
Q
What is the average cerebral blood flow?
A
50ml/100g/min
15
Q
Grey matter average CBF
A
80ml/100g/min
16
Q
White matter average CBF
A
20ml/100g/min
17
Q
What is the main function of the Circle of Wilis?
A
to provide redundancy of blood flow in the brain
18
Q
How does venous blood exit the brain?
A
paired jugular veins
19
Q
Cerebral impairment on an EEG
A
20-25ml/100g/min
20
Q
Flat EEG
A
15-20ml/100g/min
21
Q
Associated with irreversible brain damage EEG recording
A
below 10ml/100g/min
22
Q
How do you assess CBF in a clinical setting
A
Transcranial doppler
brain tissue oximetry
intracerebral microdialysis
Near infrared Spectroscopy
23
Q
What is transcranial doppler?
A
ultrasound
middle cerebral artery
24
Q
What is brain tissue oximetry?
A
bolt with clark electrode oxygen sensor
25
What is intracerebral microdiaylsis?
assesses brain tissue chemistry
26
What is NIRS?
near infrared spectroscopy
receptors detect the reflected light from superficial and deep structures
27
What does NIRS reflect?
absorption of venous hemoglobin
NOT pulsatile arterial flow
28
What are considered neuro events with NIRS monitoring?
rSO2 <40% or change in rSO2 of >25% from baseline
29
What surgery does not have a cut off for rSO2?
carotid endarectomy
30
What is the physics law associated withe NIRS?
beer lambert law
reflectance spectroscopy
O2 and de-O2 Hgb absorb light at different frequencies
31
What is cerebral perfusion pressure?
difference in mean arterial pressure and intracranial pressure
32
What is the equation for CPP?
MAP-ICP=CPP
33
What can be substituted for ICP?
CVP, if CVP is greater then ICP
34
What is CPP primarily dependent on?
MAP
35
What are reference values for CPP and ICP?
ICP- <10-15mmHg
CPP: 80-100mmHg
(>60 okay for alseep healthy individuals)
36
What are critical CPPs?
Low BP + elevated ICP
CPP<50 + slowing EEG
CPP 25-40= Flat EEG
37
What is cerebral autoregulation?
myogenic regulation
Vascular smooth muscles
cerebral vascular rapidly adapts to changes in CPP
38
What does autoregulation cause when CPP is increased?
Cerebral vasoconstriction (limiting CBF)
39
What does autoregulation cause when CPP is decreased?
Cerebral vasodilation (increasing CBF)
40
Metabolic autoregulation
metabolic demands determine arteriole tone
41
Myogenic autoregulation
intrinsic response of smooth muscles in cerebral arteries
42
Both myogenic and metabolic autoregulation determine
tissue demand> blood flow
release tissue metabolites causing vasodilation= increase flow
43
Autoregulation remains nearly constant between MAPS of
60-160
70-150
50-150
60-140mmHg
44
What happens when MAP is outside these ranges?
blood flow becomes pressure dependent
45
MAP >150-160mmHg will cause
disruption in BBB and may result in cerebral edema and hemorrhage
46
Patients with chronic hypertension have autoregulation curves shifted
Right because the flow becomes more pressure dependent at low "normal" arterial pressures in return for cerebral protection at higher arterial pressures
47
What factors effect CBF?
PaCO2, PaO2, temperature, viscosity, autonomic interference, age
48
How are CBF an PaCO2 related?
directly proportional between tensions 20-80mmHg
49
What are the most important extrinsic influences on CBF?
respiratory gas tensions
particularly PaCO2
50
Since CBF and PaCO2 are directly proportional what are the approximate blood flow changes?
1-2ml/100g/min per mmHg in PaCO2
51
What does not cross the BBB?
ions, HCO3
52
What are changes in PaCO2 reflective of?
respiratory tensions and secondary to pH changes in CSF and cerebral tissue
53
Why does metabolic acidosis not have a readily effect on cerebral perfusion (CBF)?
because Hydrogen ions can not readily cross the BBB
54
Describe cerebral blood flow when you hyperventilate a patient?
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
What happens to cerebral blood flow with severe hyperoxia?
great increases in CBF
56
Does PaO2 have a large influence on CBF?
no
57
What happens in 24-28 hour in the brain with an metabolic acidosis?
CSF HCO3 compensates (active transport) for changes in PaCO2
effects of hypocapnia and hypercapnia are diminished
58
What is the ceiling effect for PaCO2 in CBF?
response of decrease in cerebral blood flow is attenuated at a PaCO2 <25mmHg
59
The sensitivity of CBF to changes in PaCO2 (deltaCBF/deltaPaCO2) are
positively corrleated with resting levels of CBF
60
At normocarbia, VAs do what to the cerebral vessels?
dilate cerebral vessels and impair autoregulation in a concentration dependent manner
61
What occurs to the hemoglobin oxygenation dissociation curve when the patient is hyperventilated?
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
What does the shift of the hemoglobin dissociation curve imply in an EEG?
can suggest cerebral impairment even in normal individuals
63
What occurs after an acute restoration normal PaCO2 after surgery?
significant CSF acidosis
which causes increased CBF and increased ICP
64
How do you prevent an increased ICP post-operatively?
slowly increase CO2 during the case
65
What range does PaO2 have little range on CBF?
50-300mmHg
66
When does PaO2 change CBF and how?
<50mHg
rapid increase in CBF
67
How does vasodilation occur when PaO2 <60mmHG in the brain?
Mediated by release of neural nitric oxide
open ATP dependent K channels
Rostral ventrolateral medulla (RVM)
brain's O2 sensory stimulation
68
How does temperature effect CBF and CMRO2?
hypothermia decreases CBF and CMRO2
hyperthermia increases CBF and CMRO2
69
How does viscosity effect CBF?
decrease in viscosity can improve CBF
70
What determines viscosity?
hematocrit (Hct)
71
Describe the relationship of viscosity, hematocrit and the brain
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
When does optimal cerebral oxygen delivery occur? (Hct level?)
30%
73
When there is variation in HCT (33-45%) what happens to CBF
only modest alternations
74
What happens to CBF in anemia?
cerebral vascular resistance decreases, CBF increases
75
What can occur in elevated hematocrits?
polycythemia
reduced CBF
76
Do you manipulate viscosity with ischemic strokes?
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
How does the sympathetic system affect CBF?
vasoconstriction, decreases CBF
78
How was the parasympathetic system affect CBF
vasodilation, increases CBF
79
What does autonomic innervation play an important role in after a brain injury or stroke?
cerebral vasospasms
80
How does age affect a patient's neurological function?
progressive loss of neurons with aging
loss of myelinated fibers, loss of white matter
loss of synapes
81
How much does CBF and CMRO decrease by 80 Y?
CBF and CMRO2 decreases by 15%-20%
82
What is the normal consumption of total blody oxygen by the brain?
20% of total body oxygen
83
How much of the 20% of total body oxygen is used to make ATP?
60%
84
What is the cerebral metabolic rate?
3-3.8mL/100g/min (CMRO2)
50ml/min
85
Where is O2 mostly consumed?
gray matter
86
WHen will you become unconcious due to interruption of cerebral perfusion?
10 seconds
87
What areas are most sensitive to hypoxic injury?
hippocampus and cerebellum
88
what is the primary energy source?
glucose
89
What is the brain's glucose consumption?
5mg/100g/min
90% metabolized aerobically metabolized
90
what parallels glucose consumption?
CMRO2
91
What are the effects of hypoglycemia?
brain injury
92
What are the effects of hyperglycemia?
exacerbate hypoxic injury
93
What is the role of the blood brain barrier?
isolates the brain and spinal cord extracellular compartment from intravascular compartment
94
What is the blood brain barrier?
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
What do CNS endothelial cells lack?
transport mechanisms
96
What does the lipid barrier allow to pass?
lipid soluble substances
-carbon dioxide, oxygen, most anesthetics
97
what is restricted by the lipid barrier?
ionized molecules
large molecules
ions, proteins, larger substances (mannitol)
98
What governs the movement of particles across the BBB?
size
charge
lipid solubility
plasma protein binding
99
What causes disruptions in the BBB?
HTN, tumor, infection, trauma, stroke, marked hypercapnia, hypoxia, sustained seizure
100
Where is CSF formed?
choroid plexus by ependymal cells
101
What is the average total volume of CSF?
150ml
102
how many times is CSF replaced a day?
3-4 times
103
Where is CSF found?
cerebral ventricles and cisterns and subarachnoid space surrounding the brain and spinal cord
104
What is the purpose of CSF?
to protect the CNS from trauma
105
CSF is ____ to plasma?
isotonic
106
What electrolyte concentrations are different in CSF?
lower potassium, bicarbonate, glucose concentrations
107
What is CSF production inhibited by?
carbonic anhydrase inhibitors (acetazolamide), corticosteroids, spironolaction, isoflurane, vasoconstriction
108
Describe the flow of CSF
lateral ventricles of the cerebral hemispheres-> through the foramen of monro-> 3rd ventricle-> through the aqueduct of sylvius (midbrain)-> into 4th ventricle
109
Describe how CSF leaves the ventricular system
the subarachnoid space through three openings in the roof of the fourth ventricle
110
What are openings which CSF leaves?
medial foramen of magendie and two lateral foramina of luschka
111
what is intracranial pressure (ICP)?
supratentorial CSF pressure measure in the lateral ventricles or over the cerebral cortex
112
What does the Monro Kellie hypothesis state?
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
What are the major compensatory mechanisms for intracranial elastance?
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
What size of ICP changes are well tolerated?
small increases
115
Describe herniation
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
What are the five types of brain herniation?
-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
What are signs and symptoms of cingulate gyrus hernination?
little known
118
What are signs and symptoms of uncal & central herniation?
decrease LOC
pupils sluggish -> fixed and dilated
Cheyne-strokes respirations
decorticate-> decerebrate posturing
119
What are signs and symptoms of cerebellar tonsillar herniation?
most common
no specific clinical manifestations
arched stiff neck
paresthesias in shoulder
decrease in LOC
respiration abnormalities
pulse rate variations
120
What are signs and symptoms of transcalvarial?
may occur during surgery
121
What is the provider's goal during a closed cranium?
maintain CPP
prevent herniation
122
What is the provider's goal during an open cranium?
facilitate surgical access
reverse ongoing herniation
123
What is intracranial hypertension?
sustained increase in ICP about 20-25mmHg
124
What causes ICP HTN?
expanding tissue or fluid mass
interference with CSF
excessive CSF production
systemic disturbances promoting edema
125
What can influence increase BV?
increased airway or intrathoracic pressure
increased jugular vein distention
increase PaCO2 or decreased PaO2
some anesthetics (vasodilators and seizures)
126
What can cause cellular compartment masses or leisons?
tumors
hematomas, subdural, extradural, intracerebral
127
What can cause increase in edema (increase fluid compartment)?
mechanical injury
ischemia
defective autoregulation
128
What are the signs and symptoms of increase in ICP?
headache
N/V
papilledema
focal neurological deficit
decreased LOC
seizures
coma
cushings: irregular respirations, HTN, bradycardia
posturing
decreased motor function
changes in speech
129
How do you treat intracranial hypertension?
-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)
