Neurophysiology Flashcards
1
Q
the brain receives blood from two distinct arteries which are
A
internal carotid artery (anterior circulation) vertebral arteries (posterior circulation)
2
Q
blood traveling through the vertebral arteries
A
branches of subclavian artery, enter base of skull through the foramen magnum and run along the medulla and join in the pons forming the basilar artery which then branches into 2 posterior cerebral arteries
3
Q
the 2 posterior cerebral arteries primarily supply which lobes of the brain
A
occipital
4
Q
blood traveling through the internal carotid branches
A
enter through base of skull pass through the cavernous sinus and divided into anterior and middle cerebral artery
5
Q
a major site of aneurysm and atherosclerosis is
A
middle cerebral artery
6
Q
cerebral blood flow varies with
A
metabolic activity 10-300 mL/100g/min
7
Q
total cerebral blood flow in adults averages
A
750 mL/min
8
Q
brain receives ___ of cardiac output
A
15-20%
9
Q
average cerebral blood flow to the gray matter is
A
80 mL/100g/min
10
Q
average cerebral blood flow to the white matter is
A
20 mL/100g/min
11
Q
cerebral impairment occurs when cerebral blood flow is
A
20-25 mL/100g/min
12
Q
flat EEG occurs when cerebral blood flow is
A
15-20 mL/100g/min
13
Q
irreversible brain damage is associated with cerebral blood flow below
A
10 mL/100g/min
14
Q
how can we assess CBF in the clinical setting?
A
transcranial doppler, brain tissue oximetry, intracerebral microdialysis, and near infrared spectroscopy
15
Q
near infrared spectroscopy
A
receptors detect the reflected light from superficial and deep structures
largely reflects the absorption of venous hemoglobin
NOT pulsatile arterial flow
16
Q
neuro events can occur when rSO2
A
rSO2 <40% or change in rSO2 of >25% from baseline
17
Q
CPP =
A
MAP - ICP
CVP may be substituted for ICP
18
Q
ICP normal value
A
< 10-15 mmHg
19
Q
CPP normal value
A
80-100 mmHg
20
Q
CPP < 50 =
A
slowing eeg
21
Q
CPP 25 - 40 =
A
flat eeg
22
Q
CPP maintained < 25 =
A
irreversible brain damage
23
Q
increase in CPP =
A
cerebral vasoconstriction (limit CBF)
24
Q
decrease in CPP =
A
cerebral vasodilation (increase CBF)
25
myogenic autoregulation
intrinsic response of smooth muscle in cerebral arterioles
26
metabolic autoregulation
metabolic demands determine arteriolar tone
| tissue demand > blood flow
27
release of tissue metabolites causes
vasodilation = increase flow
28
CBF remains nearly constant between MAPs of
60-160 mmHg
29
MAP greater than ____ can disrupt the BBB and may result in ____
150-160 mmHg; cerebral edema and hemorrhage
30
factors effecting CBF
PaCO2, PaO2, temperature, viscosity, autonomic influences, age
31
the most important extrinsic influences on CBF are
respiratory gas tensions-particularly PaCO2
32
CBF directly proportionate to PaCO2 between
tensions 20-80 mmHg
33
blood flow changes ____ per 1 mmHg change in PaCO2
1-2 mL/100g/min
34
What happens if you give HCO3?
HCO3 ions do not passively cross BBB so HCO3 doesn't acutely affect CBF
35
acute metabolic acidosis has ____ on CBF
little effect
36
CBF is directly proportional to PaCO2 until PaCO2 is
< 25 mmHg
37
sensitivity of CBF to changes in PaCO2 is
positively correlated with resting levels of CBF
38
inhaled anesthetics ___ CBF
increase which increases cerebrovascular reactivity to carbon dioxide
39
marker hyperventilation shifts the oxy-hemoglobin dissociation curve to the ___
left which may result in EEG changes suggestive of cerebral impairment
40
alkalosis causes ____ affinity of Hgb for O2 and therefore ____ release of O2
increased; decreased
41
acute restoration of a normal PaCO2 value will result in
a significant CSF acidosis (after sustained period of hyperventilation/hypocapnia)
42
CSF acidosis results in ___ CBF after surgery
increased which will increase ICP
43
PaO2 less than ___ rapidly increases CBF
50 mmHg
44
vasodilation mediated via
release of neuronal nitric oxide, open ATP dependent K+ channels, rostral ventrolateral medulla
45
CBF changes ___ per 1 degree C
5-7%
46
CMR decreases by ___ per 1 degree C
6-7%
47
CMRO2 decreases by ____ per 1 degree C
7%
48
____ determines viscosity
hematocrit
49
a decrease in Hct = ____ viscosity and ____ CBF
decrease; increase
50
optimal cerebral oxygen delivery may occur at Hct of
30%
51
sympathetic innervation = ____ CBF
decrease
52
parasympathetic innervation = ____ CBF
increase
53
how does age affect the brain
progressive loss of neurons = loss of myelinated fibers = loss of white matter = loss of synapses
54
at age 80 CBF and CMRO2 decrease by
15-20%
55
the brain normally consumes ___ of total body oxygen
20%
56
cerebral metabolic rate
3-3.8 mL/100g/min = 50 mL/min
57
O2 is mostly consumed in the
gray matter
58
interruption of cerebral perfusion =
unconsciousness in 10 seconds
59
if O2 is not restored in 3- 8 minutes
depletion of ATP and irreversible cellular injury
60
which areas are most sensitive to hypoxic injury
hippocampus and cerebellum
61
brain glucose consumption
5 mg/100g/min
| 90% is metabolized aerobically
62
hypoglycemia =
brain injury
63
hyperglycemia =
exacerbated hypoxic injury
64
blood brain barrier
lipid soluble substances freely pass, ionized molecules restricted, large molecules restricted
65
what freely crosses the blood brain barrier
o2, co2, lipid soluble molecules, water
66
what is restricted through the blood brain barrier
ions, plasma proteins, large molecules
67
things that could disrupt the blood brain barrier
HTN, tumor, trauma, stroke, infection, marked hypercapnia, hypoxia, and sustained seizure
68
where is csf formed
in the choroid plexus by ependymal cells
69
how much csf is produced
21 mL/hr, 500 mL/day
total volume 150 mL
replaced 3-4x per day
70
role of csf
protect the CNS from trauma
71
formation of csf
involves active secretion of sodium in the choroid plexuses = isotonic fluid despite lower K+, bicarb, and glucose concentration
72
csf production is inhibited by
carbonic anhydrase inhibitors (Acetazolamide), corticosteroids, spironolactone, furosemide, isoflurane, and vasoconstrictors
73
csf absorption
translocation from arachnoid granulations into cerebral sinuses
74
the monro-kellie hypothesis states that
the cranial compartment is incompressible and the volume inside the cranium is a fixed volume
so any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another to prevent a rise in ICP
75
brain composition in the cranial vault
80%
76
blood composition in the cranial vault
12%
77
csf composition in the cranial vault
8%
78
major compensatory mechanisms with intracranial elastance
initial displacement of csf from the cranial to spinal compartment, increase in csf absorption, decrease in csf production, decrease in total cerebral blood volume
79
provider goals for a closed cranium
maintain CPP, prevent herniation
80
provider goals for an open cranium
facilitate surgical access, reverse ongoing herniation
81
causes of intracranial hypertension
expanding tissue or fluid mass, interference with csf absorption, excessive csf production, systemic disturbances promoting edema
82
signs and symptoms of increased ICP
HA, N/V, papilledema, focal neurological deficit, decrease LOC, seizures, coma, cushing triad: irregular respirations, HTN, bradycardia
83
where do we mainly see herniation
cerebellotonsillar
84
signs and symptoms of uncal and central herniation
decrease LOC, pupils sluggish, cheyne stokes respirations, posturing
85
signs and symptoms of cerebellar tonsillar herniation
no specific manifestations, arched stiff neck, paresthesias in shoulder, decrease LOC, respiratory abnormalities, pulse rate variations
86
treatment of intracranial hypertension
brain tissue - surgical removal of mass
csf - no effective pharmacological manipulation so need a drain
fluid - steroids, osmotics/diuretics
blood - decrease arterial flow or increase venous drainage
reduce PaCO2
CMR suppression
87
inhaled anesthetics affect CMRO2, CBF, ICP
decrease CMRO2
increase CBF
increase ICP
88
iv anesthetics affect CMRO2, CBF, ICP
all decrease
89
LA affect CMRO2, CBF, ICP
all decrease
90
ketamine affect on CMRO2, CBF, ICP
+/- CMRO2, increase CBF and ICP
91
opioids affect on CMRO2, CBF, ICP
+/- for all
92
nitrous oxide
34 x more soluble than nitrogen in blood
| increases everything but can be inhibited by barbs, benzos, narcotics, and propofol
93
intracranial tumors with 66% N2O average ICP increases
13 to 40 mmhg
94
alpha 1 agonists on CBF
bolus - transiently change CBF and cerebral SaO2
| continuous infusion - little effect
95
alpha 2 agonists on CBF
decreases CBF up to 25-30%
| results from reduced CMRO2 leading to reduced CBF
96
beta agonists on CBF
small doses- little effect
large doses + physiologic stress - increased CMRO2 and CBF
ex. large dose epi is >0.05 mcg/kg/min
response exaggerated with BBB defect
97
beta blockers on CBF
little to no effect on CBF and CMRO2
98
ACE inhibitors and ARBs on CBF
little to no effect on CBF and CMRO2
| autoregulation is maintained
99
barbiturates on CBF
dose dependent reduction until isoelectric EEG (max 50%)
effective in lowering ICP
robin hood/reverse steel phenomenon (CBF to ischemic areas)
CMR is decreased more than CBF (supply > demand)
anticonvulsant
100
benzos on CBF
dose dependent reduction (less than barbiturates, propofol, and etomidate but more than narcotics)
Midazolam is agent of choice
may prolong emergence
anticonvulsant
101
propofol on CBF
dose dependent reduction in CBF and CMR
anticonvulsant
short elimination half life
commonly used for maintenance phase of anesthesia for neuro cases/intracranial hypertension
102
etomidate on CBF
decreases CMR, CBF, and ICP
myoclonic movements on induction
has been used to treat seizures (not first choice though)
**small doses can activate seizure foci in patients with epilepsy**
103
What is the only IV anesthetic that dilates cerebral vasculature and increases CBF?
Ketamine by 50-60%
104
Ketamine
increases CBF and ICP (potentially if they have decreased intracranial compliance)
can be blunted if given with other anesthetics
CMR does not change (debatable)
105
Ketamine and CMR debate
In 1997: subanesthetic doses (0.2-0.3 mg/kg) can INCREASE global CMR by 25%
In 2005: subanesthetic and anesthetic doses increased CBF without altering CMRO2
106
what may be appealing about ketamine in neuroanesthesia?
NMDA antagonist - neuroprotective
107
NMDA antagonist
dissociates the thalamus from limbic cortex
thalamus - relays sensory impulses from the reticular activating system to cerebral cortex-limbic cortex
limbic cortex -involved with the awareness of sensation
increases HR, BP, CO, and secretions
analgesic and hallucinogenic properties
108
NMDA antagonism in brain injury patients may be protective against
neuronal cell death
109
opioids on CBF
minimal effects on CBF, CMR, and ICP (unless increase PaCO2)
avoid Morphine - poor lipid solubility, slow onset and long DOA
avoid Meperidine- active metabolite can cause seizures especially in renal patients
110
hyperventilation and PaCO2 blunts increase of CBF/ICP from
ketamine and volatile agents
111
in general, anesthetic agents ____ the CMR with exception of ___ and ____
suppress; ketamine; nitrous oxide
112
control and manipulation of ____ are central to the management of ICP
CBF
113
when does CBF not parallel with cerebral blood volume?
```
cerebral ischemia - CBV increases but CBF decreases
normal BP (MAP 70-150 mmHg) - autoregulation intact
initial increases in CBV doesn't increase CBF - compensatory responses from venous blood shifting to extracerebral vessels and CSF shifting to spinal compartment
```
114
CBV is ___ mL/___g of brain
5mL/100g (70mL)
115
types of intracranial neurosurgeries
craniotomy, interventional radiology, trauma
116
types of functional neurosurgeries
epilepsy, movement, pain
117
types of spine neurosurgeries
anterior, posterior, and transoral
118
preoperative neurological assessment includes
always get a baseline!
- LOC
- reflexes
- motor/sensory function
- evaluate for S/S of increased ICP
- document pre-existing neurological deficits
119
preoperative considerations for medications
anticonvulsants (frequency, continue intraop)
antibiotics (vanc and ancef)
diuretics
steroids
120
hypothermia ____ amplitude of EEG tracing
suppresses
121
MEP neuromonitoring
used in surgeries where motor tract is at risk
more sensitive to ischemia than SSEP by 15 minutes and degree detection
difficult to obtain due to pre-existing conditions or anesthetic conditions
122
SSEP neuromonitoring
Most common method
stimulation of peripheral sensory nerve
mapping in spinal cord and sensory cortex
ischemia detection in cortical tissue
reduce risk of spinal cord/brainstem insults
123
EMG neuromonitoring
records muscle electrical activity using needle pairs
| used to detect nerve irritation, nerve mapping, assess nerve function, and monitor cranial nerves
124
what do we use to assess posterior corticospinal tract
MEP and SSEp
125
etomidate and ketamine ___ amplitude of neuromonitoring tracing
increase
126
stereotactic neurosurgery
applies rules of geometry to radiologic images to allow for precise localization within the brain, providing up to 1mm accuracy
allows surgeons to perform certain intracranial procedures less invasively
interferes with pulse ox
127
craniotomy medications
cleviprex, mannitol, keppra, phenylephrine sticks, precedex, epi
propofol gtt at 40-100 mcg/kg/min ABW
remifentanil gtt at 0.2 mcg/kg/min IBW
phenylephrine gtt at 0.2 mcg/kg/min
induction: fentanyl, propofol, rocuronium
128
craniotomy meds to decrease ICP
10mg decadron
50-100mg mannitol (0.25-0.5 mg/kg)
lasix
129
antiepileptics for craniotomy
1g keppra
| vimpat
130
awake craniotomy specific drugs
caffeine (adenosine receptor antagonist)
| physotigmine (Anticholinesterase)
131
types of intracranial mass lesions
congenital, neoplastic, infectious, and vascular
132
typical presentation of an intracranial mass lesions
HA, seizures, focal neurological deficits, sensory loss, cognitive dysfunction
133
frontal supratentorial intracranial mass lesion
personality changes, increased risk taking, difficulty speaking (damage to Broca's area)
134
parietal supratentorial intracranial mass lesion
sensory problems
135
temporal supratentorial intracranial mass lesion
problems with memory, speech perception, and language skills
136
occipital supratentorial intrcranial mass lesion
difficulty recognizing objects, an inability to identify colors, and trouble recognizing words
137
cerebellar dysfunction infratentorial/posterior fossa intracranial mass lesion
ataxia, poor balance, nystagmus, dysarthria, cannot perform rapid alternating movements, loss of muscle coordination
138
brainstem compression infratentorial/posterior fossa intracranial mass lesion
cranial nerve palsy, altered LOC, abnormal respiration, edema, obstructive hydrocephalus at 4th ventricle
139
primary intracranial tumor locations
glial cells, ependymal cells, supporting tissues
140
glial cell primary tumor
astrocytoma, oligodendroglioma, glioblastoma
141
ependymal cell primary tumor
ependymoma
142
supporting tissue primary tumor
meningioma, schwannoma, choroidal papilloma
143
major considerations for intracranial mass lesions
tumor location - determines position, EBL, risk for hemodynamic changes intraop
growth rate and size- slow growing tumors are often asymptomatic
ICP elevated
144
anesthetic goals for intracranial mass lesion
control ICP
maintain CPP
protect from position related injuries
rapid emergence for neuro assessment
145
intraoperative considerations for monitoring for intracranial mass lesion
```
standard monitors
a line
foley
+/- central line
PNS
+/- ventriculostomy
neuromonitoring potentially
```
146
where do you zero for a ventriculostomy?
at the external auditory meatus
147
why do we not monitor PNS on hemiplegic side of patients?
may end up overdosing on paralytics
148
awake-awake for craniotomy for tumor
no infusions until closing
| prop bolus for pins
149
asleep-awake for craniotomy for tumor
start under GA with LMA/ETT
wake the patient up once tumor is exposed
prop gtt 40 mcg/kg/min ABW
remi gtt 0.2-0.4 mcg/kg/min IBW
150
asleep craniotomy for tumor
TIVA with neuromonitoring
| GETA with no neuromonitoring
151
awake craniotomies are useful for
epilepsy and resection of tumors in frontal lobes and temporal lobes when speech and motor are to be assessed intraop
152
types of cases for iMRI
```
awake tumor resection
laser ablation
cytokine delivery
ROSA
clearpoint
```
153
monteris medical LITT interventions for
epilepsy, glioblastomas, recurrent brain metasstases, and radiation necrosis
154
MR thermography
uses phase change to calculate real time temperature data at and around probe
thermal dose confirmed in real time using bio thermodynamic theory
white line - 43 C - 60 min (vaporized)
blue line - 43 C - 10 min (dead)
yellow line- 43 C - 2 min (recoverable)
155
contents of posterior fossa
cerebellum- movement and equilibrium
brainstem - autonomic nervous system, CV and respiratory centers, RAS, motor/sensory pathways
cranial nerves I - XII
large venous sinuses
156
brainstem injuries
bradycardia and hypertension - trigeminal nerve stimulation (Cushing's reflex)
bradycardia and hypotension - glossopharyngeal or vagus nerve stimulation
respiratory centers may be damaged and necessitate mechanical ventilation postop
tumors around glossopharyngeal and vagus nerves may impair gag reflex and increase risk of aspiration
cranial nerves IX, X, and XI control pharynx and larynx
157
advantages of sitting position
improved surgical exposure, less retraction and tissue damage, less bleeding, less cranial nerve damage, better resection of the lesion, access to airway, chest, and extremities
158
disadvantages of sitting position
1. CV compromise - postural hypotension, arrhythmias, venous pooling
2. pneumocephalus- open dura (CSF leak, air enters), after dural closure air can act as a mass lesion as CSF reaccumulates, usually resolves spontaneously, tension pneumocephalus = burr holes, symptoms (delayed awakening, HA, lethargy, confusion)
3. nerve injuries - ulnar compression, sciatic nerve stretch, lateral peroneal compression, brachial plexus stretch
4. venous air embolism
159
venous air embolism signs and symptoms
decreased EtCO2, decreased PaO2, decreased SaO2, spontaneous ventilation, mill wheel murmur, detection of ET nitrogen, increased PaCO2, hypotension, dysrhythmias
160
monitoring for VAE
capnography, CVP/PA line, precordial doppler
| do not rely on one monitor!
161
most sensitive to detecting VAE to least sensitive
TEE --> precordial doppler --> etco2 --> PAP --> CVP --> PaCO2 --> MAP
162
VAE treatment
100% O2, notify surgeon to flood field or pack wound, call for help, aspirate from CVP line with 30-60 mL syringe, volume load, inotropes/vasopressors, jugular vein compression, PEEP, position left lateral decubitus and trendelenburg, CPR
163
craniocervical decompression (chiari malformation)
cerebellum protrudes through foramne magnum compressing brainstem and cervical spinal cord
types 1-4
syringomyelia
164
deceleration injuries
coup and contrecoup lesions
165
linear skull fracture
subdural or epidural hematomas
166
basilar skull fracture
CSF rhinorrhea, penumocephalus, and cranial nerve palsies (battle's sign, racoon/panda eyes)
depressed skull fracture
167
primary head injury
biomechanical effect of forces on the brain at time of insult
contusion concussion, laceration, hematoma
168
secondary head injury
represents complicating processes related to primary injury
| intracranial hematoma, increased ICP, seizures, edema, vasospasm
169
glasgow coma scale
classifies severity of head injury
prognosis (type of lesion, age, and severity of injury)
mortality = initial GCS score
170
blind nasal intubation is contraindicated in presence of
basilar skull fracture
171
head injury anesthetic consideration
hypotension, bradycardia, maintain Hct >30%, seizure prophylaxis, DIC with severe injuries (treat with plts, FFP, cryo), pituitary dysfunction (DI, SIADH), remains intubated
172
nonfunctioning/nonsecretory pituitary tumors
arise from growth of transformed cells of anterior pituitary
| generally well tolerated until 90% of gland is nonfunctional
173
functioning/secretory pituitary tumors
cushing's disease (ACTH)
acromegaly (GH)
prolactinomas (prolactin)
TSH adenomas
174
macroadenoma
>1 cm
175
microadenoma
<1 cm
176
transsphenoidal approach necessitates
HOB elevated 10-20 degrees
177
intraop considerations for pituitary surgery
avoid hyperventilation (reduction in ICP result in retraction of pituitary into teh sella tursica)
use oral RAE or reinforced ETT
potential for mass hemorrhage as the carotid arteries lie adjacent to the suprasellar area
mouth and throat pack
avoid positive pressure upon extubation
178
preop eval of pituitary surgery
```
visual field evaluation
S/S of increased ICP
endocrine labs
electrolytes
steroids?
```
179
postop management after pituitary surgery
DI is common and is usually self limiting (resolves in one week)
treat with vasopressin or DDAVP
SIADH
180
cerebral aneurysm is the leading cause of
nontraumatic intracranial hemorrhage
181
cerebral aneurysm is commonly located in
the anterior circle of willis
182
how can a cerebral aneurysm lead to subarachnoid hemorrhage
aneurysm fills with blood and can rupture, spilling blood into the subarachnoid space, creating the subarachnoid hemorrhage
183
unruptured cerebral aneurysm
HA, unsteady gait, visual disturbances, facial numbness, pupil dilation, drooping eyelid, pain above or behind eye
184
ruptured cerebral aneurysm
sudden, extremely severe HA, NV, LOC, prolonged coma, focal neuro deficits, hydrocephalus, seizure, S/S of increased ICP
185
vasospasm
causes ischemia or infarction
digital subtraction angiogrpahy is gold standard
(not detectable until 72 hours after SAH)
use calcium channel blockers
186
rebleeding following initial SAH
peaks 7 days post incident
major threat during delayed surgery
antifibrinolytic therapy
187
vasospasm treatment
```
triple H therapy
hypertension (SBP 160-200)
hemodilution (hct 33%)
hypervolemia
intended to increase CBF in ischemic brain areas
```
188
endovascular coiling
```
GETA with complete muscle paralysis
control CPP
minimal narcotics
a line
minimal to no blood loss
heparin may be used for ACT 200-250
```
189
advantages of endovascular aneurysm coiling
shorter stay, less anesthetic requirements, uncomplicated positioning, minimally invasive
190
complications of endovascular aneurysm coiling
aneurysm rupture/SAH
vasospasm
CVA
incomplete coiling
191
cerebral aneurysm in the OR
most commonly treated by microsurgical clip ligation
| deep circulatory arrest may be necessary for large aneurysms
192
likely times of rupture intraoperatively
dural incision, excessive brain retraction, aneurysm dissection, during clipping or releasing of clip
193
treatment of intraop aneurysm rupture
immediate aggressive fluid resuscitation, replace blood loss, propofol bolus, decrease MAP to 40-50mmHg
194
AVM treatment
intravascular embolization, surgical excision, or radiation
195
cranial nerve decompression treats disorders of which cranial nerves
trigeminal, hemifacial, glossopharyngeal
