Neuro Quizlet Flashcards
Brain usually consumes _ % of total body O2, and _mL/100g/min is the normal CMRO2 ( ~ _ mL/min)
20%
3.8mL/100g/min
~ 50mL/min
CMRO2 is greatest in _ matter of the cerebral cortex at _ mL/100g/min
gray
80mL/100g/min
2 areas of the brain most sensitive to hypoxic injury of the brain:
-hippocampus
-cerebellum
Primary source of energy for neuronal cells and how much is consumed:
glucose
5mg/100g/min
T/F Most glucose in the brain is metabolized anaerobically
false
aerobic
Normal CBF
-mL/100g/min
-total mL/min
-%CO
50mL/100g/min
750mL/min
15-20% CO
Regional CBF parallels metabolic activity and can vary from _ to _ mL/100g/min
10-300mL/100g/min
Gray matter receives _ mL/100g/min of CBF and white matter receives _mL/100g/min
gray: 80mL/100g/min
white: 20mL/100g/min
Which CBF will you see EEG slowing, flattening, and irreversible damage?
slowing: 20-25mL/100g/min
flattening: 15-20mL/100g/min
damage: <10-15mL/100g/min
Transcranial doppler measures the _ CBF in the _ artery
velocity
MCA
Normal CBF velocity on transcranial doppler:
-what does it mean if number is high?
55mm/sec
>120 can mean vasospasm
Which artery has a higher velocity flow when measured with a transcranial doppler, MCA or ICA?
MCA (3x)
Does infrared spectroscopy reflect cerebral arterial or cerebral venous O2 sat?
venous
Which receives more CBF, cortical or subcortical region of the brain?
cortical
5 determinants of CBF:
-CMRO2
-CPP
-Venous pressure
-PaCO2
-PaO2
Is more CMRO2 used for electrical or cellular integrity?
Electrical
Brain autoregulates between CPP of _ - _ and a MAP of _ - _
CPP 50-150
MAP 60-160
What happens below the lower limit of cerebral autoregulation? Above the upper limit?
Below lower limit: vessels become maximally dilated and risk hypoperfusion and ischemia
Above upper limit: vessels are maximally constricted and risk cerebral edema and hemorrhage
CMRO2 drops by _ % for every 1*C drop in temperature.
7%
EEG suspension occurs at _ - _ *C
18-20
Hyperthermia beyond _ *C destroys neurons and denatures proteins
42*C
What controls cerebral vascular resistance?
pH of CSF around the arterioles
_ has a linear relationship with CBF
PaCO2
At a PaCO2 of 40, CBF is _ mL/100g/min. For every _ mm increase or decrease in PaCO2, CBF will increase/decrease by _ mL/100g/min
50mL/100g/min
1-2mL/100g/min
Max vasodilation occurs when PaCO2 is at _ - _ and max vasoconstriction occurs at _
80-100 vasodilation
25 vasoconstriction
Effects on CBF:
-resp. acidosis
increases CBF
Effects on CBF
-resp alkalosis
decreases CBF
Effects on CBF
-met acidosis
no effects
PaO2 < _ - _ causes cerebral vasodilation and increases CBF
50-60
PaO2> 60 does not affect CBF
60
Normal ICP
5-15mmHg
Avg brain wt, blood volume, CSF volume
brain wt: 1350g
blood volume: 50mL
CSF: 75mL
T/F Brain has a large O2 reserve
false
LOC in < _ sec without O2, ATP stores deplete in _ minutes.
10 sec
3-8min
CPP formula and normal value
CPP = MAP - ICP or CVP (whichever is greater)
CPP (n) = 80-100 mmHg
At which CPP will you see EEG slowing, flattening, and irreversible damage of the brain?
slowing: CPP < 50
flat: CPP 25-45
damage: CPP < 25
Cerebral autoregulation curve is shifted to the _ in patients with HTN
right
What is the myogenic mechanism of cerebral autoregulation?
Intrinsic response of smooth muscle cells in cerebral arterioles to changes in MAP
What is the metabolic mechanism of cerebral autoregulation?
cerebral metabolic demands determine the arterial tone
-when demand > CBF metabolites are released > vasodilation and increases CBF
Hypotonicity moves water (in/out of) the brain, where hypertonicity moves water (in/out)
hypo - into
hyper- out of
When the resting CBF is low, the reduction of CBF from hypocapnia is (more/less) effective
less
Why is the decreased CBF from hypocapnia not sustained
pH of CSF normalizes with 6-8hr from dissociation of HCO3 from H2CO3
What effect will an abrupt increase in CO2 have on CBF?
increased CBF and ICP, will also cause CSF acidosis
What effect will an abrupt decrease in CO2 have on CBF?
potential ischemia
-decreased CBF
-also causes CSF alkalosis
Effect on CBF?
-hypoxia (PaO2 <60)
causes rapid increase
What is the target Hct for ideal CBF and what happens if blood viscosity increases?
30-33% Hct
increased viscosity = decreased CBF
What happens in “steals” and what conditions can precipitate this?
vessels that supply ischemic areas in the brain lose their tone and become maximally dilated so that when cerebral vasodilation occurs, vessels that still have tone will vasodilate and “Steal” perfusion from the ischemic areas
-hypercapnia, hypoventilation, vasodilators
What happens in “inverse steal”?
hyperventilation is used to constrict cerebral vessels that supply healthy tissue, allowing flow to redistribute to ischemic regions
Another term for “steal”
luxury perfusion
Most important chemical regulator of CBF
PaCO2
CMRO2 decreases by _ % for every 10 degree in temp decrease
50%
CSF:
-total volume
-spec grav
-pH
Volume: 150mL
SG: 1.002-1.009
pH: 7.32
Normal CSF production is _mL/hr or _mL/day and it is replaced every _ hrs
21mL/hr
500mL/day
Q 3-4hr
Path of CSF flow:
- Lateral ventricles
- Intraventricular foramen of munro
- 3rd ventricle
- Aqueduct of Sylvius
- 4th ventricle
- Foramen of magendie, formaen of luschka
- Cisterna Magna
- SA space
- Arachnoid granulations of hemispheres
Name 6 drugs/types of drugs that decrease CSF production:
- acetazolamide (carbonic anhydrase inhibitors)
- corticosteroids
- spironolactone
- furosemide
- isoflurane
- vasoconstrictors
3 electrolytes that are higher in CSF than in plasma?
Na, Cl, Mg
Normal supratentorial ICP:
10mmHg
What is intracranial elastance and what determines it?
determined by measuring changes in ICP in response to volume change
-normally small changes in volume are well compensated for but eventually elastance decreases and ICP increases more
4 compensatory mechanisms of the intracranial vault:
-displacement of CSF from cranial to spinal compartment
-increase CSF absorption
-decrease CSF production
-decrease in total CBV
CBV increases by _ mL/100g per 1mmHg increase in PaCO2
0.5mL/100g
Which IA (sevo, iso, des) decreases CMR?
all of them
Which IA (sevo,iso,des) increases CSF absorption and which decreases it?
increased absorption : Iso
decreased absorption: Des
Which IA (sevo, iso, des) increases CBV the most?
Iso
What effect does IA(sevo/iso/des) have on ICP
increases ICP
What effect do all the IAs and N2O have on CBF?
increases it slightly
What does ketamine do to CSF absorption
decreases
When used alone, what effect does N2O have on CBF, CMR, and ICP?
increases them
Which is greater with the use of N2O, the increase in CBV or the increase in CBF?
CBF increases more
Which IA produces the greatest depression of CMRO2?
Iso
T/F At normocarbia, volatile agents, dilate cerebral vessels and impair autoregulation in a dose-dependent manner
true
Which volatile agent produces the LEASE cerebral vasodilation?
sevo
T/F Volatile agents impair CO2 responsiveness of cerebral vasculature
false
_ can blunt the increase in CBV associated with volatile agents
hypocapnia
T/F VAs uncouple the relationship between CBF and CMRO2
false- they alter it but don’t uncouple it
The net effect of volatile agents on ICP (increase it) is the result of what 3 things:
- immediate changes in CBV
- delayed alterations of CSF dynamics
- arterial CO2 tension
What are the two VAs of choice in patients with decreased intracranial compliance?
Iso and Sevo
CBF vs CBV: changes are larger
CBF
CBF vs CBV: does NOT reliably predict increases in ICP
CBF
CBF vs CBV: responds to PaCO2
both but CBV less so
T/F there is a direct 1:1 relationship between CBF and CBV?
false it is direct but not 1:1
How do NDMRs affect cerebral physiology?
no effect unless histamine is released
T/F Both barbs and lidocaine reduce CBF via increasing cerebral vascular resistance
true
T/F Ketamine increases CMRO2
False CMRO2 is unchanged (everything else increased - CBF, CSF, ICP)
What is the only type of vasodilating agent that has little or no effect on CBF and CBV
ganglionic blocker (Trimethaphan)
What effect does remifentanil have on CBF and CMR alone vs as an adjunct?
alone: increases CBF and CMR
adjunct: no effect
Does fentanyl have any effect on CBF and CMR?
no
Lidocaine effects on CMR and CBF?
decreases
T/F: IV induction agents cause parallel decreases in CMR and CBF but preserve flow-metabolism coupling, autoreg, and CO2 responsiveness
true
T/F: Propofol reduces CMRO2 and CBF the same degree as barbiturates
true
All vasodilators cause _ _ but catecholamine agonists only effect CBF/CMR when the _ is disrupted
cerebral vasodilation
BBB
Which 2 agents may elicit seizures?
ketamine
etomidate
T/F Benzos have no effect on CMR/ CBF
false; moderate reduction
How do inhaled agents differ from IV agents at >1 MAC?
they increase ICP and CBF and abolish autoreg but they also decrease CMRO2 (uncoupling)
Which primarily determines ICP, CBF or CBV?
CBV
Patients having an ischemic stroke can have tPA within _ hrs of symptom onset
3hr
HTN is common after a CVA; a target pressure should be < _ / _
185/110
Altered area of brain after an ischemic CVA is called the _ _
ischemic penumbra
Hypothermia is good for which type of ischemia?
global/complete
for protective hypothermia, body temp is reduced to _ *C for 24hr
32-34
In incomplete ischemia, where should MAP be maintained? How long should surgery be delayed?
MAP 70-80
delay for 6wks
Effect on EEG: MAC <1
activation
Effect on EEG: barbs, benzos and etomidate
dose dependent
Effect on EEG: opioids
depression
Effect on EEG: propofol
depression
Effect on EEG: N2O
activation
Effect on EEG: hypercapnia
activation
Effect on EEG: hypothermia
depression
Effect on EEG: early v late hypoxia
early: activation
late: depression
Which IA produces an isoelectric EEG at high doses (1-2MAC)
Iso
Which IAs produce burst suppression but not electrical silence at high clinical doses?
Des and Sevo
How does N2O impact EEG?
increases BOTH frequency and amplitude
What are the only agents capable of producing burst suppression AND electrical silence at high doses (3)?
Propofol
Barbs
Etomidate
How does ketamine affect EEG?
unusual activation consisting of a rhythmic high-amplitude theta activity followed by very high amp gamma and low amp beta
What is cushings triad and what causes it?
HTN
Bradycardia
Cheyne-Stokes respirations
caused by SNS outflow from brainstem compression
Define intracranial HTN
sustained increase in ICP >15
What is intracranial compliance? What does it mean if ICP is increasing?
compliance is the ability of the compartment to accommodate increased volume without major changes in pressure
increased ICP = decreased compliance
What is cushings response?
periodic increases in MAP with reflex slowing of the HR lasting 1-15 min
Tx of intracranial HTN and cerebral edema
corticosteroids control BG
decrease swelling: fluid restriction, osmotic agents, loop diuretics
Moderate hyperventilation (PaCO2 30-33) can help with exposure IV agents
T/F hyperventilation should be used universally
false
VAE s/s
decrease in EtCO2 of SpO2 (before hemodynamic changes), ETN2, sudden HoTN, ST changes, decreased CO, changes in BP and heart sounds are LATE SIGNS
VAE can cause acute _ - sided HF
right
Tx of VAE in neurosurgery:
- tell surgeon and flood field
- 100% FiO2, no N2O
- Aspirate 60mL from multi orifice CVC
- IVF to increase CVP
- Valsalva 5-10 sec
- head down, left tilt position
True or false: mayfield pins should be removed while patient is in sitting position
false VAE risk
Risk of VAE is higher during spontaneous or mechanical ventilation? why?
spontaneous - negative inspiratory pressure
What is a paradoxical air embolism and who is at risk?
develops with air entry into systemic circulation
people with connections between right and left heart (PFO)
when R>L pressure, systemic air may enter arterial circulation
If patients who are going to have surgery in the sitting position have a murmur, what should be done pre-op to minimize VAE risk?
An echo, if a PFO is present, then surgery should be done in a different position
What is the standard of care for VAE detection?
precordial doppler, ETCO2 monitoring
Where is precordial doppler placed?
right of sternum, 3rd-6th intercostal (over RA)
What is the most sensitive test of VAE that can detect presence of a paradoxical embolus in presence of a pFO?
TEE
Symptoms of VAE develop at >____mL of air
50mL
What is the most sensitive NON-INVASIVE monitor for VAE?
pre-cordial doppler
Which is a more sensitive detector of VAE, PA catheter or EtCO2?
PA catheter
Cerebral aneurysms typically occur where?
Bifurcation of the large arteries at the base of the brain i the ANTERIOR circle of willis
What is the most common cause of SAH
rupture of saccular aneurysm
What is the hallmark symptom of cerebral aneurysm rupture?
sudden severe headache (without focal deficit)
What EKG changes may you see with cerebral aneurysm rupture?
ST depression, T wave inversion
What is the most common symptoms and sign of an UNRUPTURED aneurysm?
Symptom: headache
Sign: third-nerve palsy
Aneurysm rupture is most likely to occur at what points during repair?
Dissection and clipping
Transmural pressure calculation? What does it mean if it’s increased?
MAP - ICP
increased risk of rupture
In aneurysm repair, arterial line should be placed when?
before induction
Where should you keep MAP during aneurysm repair and why?
high normal to maintain perfusion and avoid vasospasm
What is the leading cause of morbidity and mortality in patients with SAH after rupture, and what happens physiologically?
Vasospasm; delayed and sustained contraction of cerebral arteries causing decreased blood flow and lower CPP
Neuro deterioration after SAH peaks when and resolves when
peak: 13-14th day
resolve: 2-3 weeks
What is the only medication known to decrease vasospasm?
Nimodipine
3 signs of SEVERE vasospasm
- increased flow velocity >200 cm/sec
- lindegaard ratio >3
- brain tissue O2 tension <20mm Hg
How do you treat patients with symptomatic vasospasm who have an inadequate response to nimodipine, IV expansion, and induced HTN?
Triple H therapy!
-induce HTN
-hypervolemia (fluids)
-hemodilution
What does “triple H” therapy consist of?
Hypervolema, hemodilution, HTN
Hypervolemia = CVP>_______, PAWP>_______
12;14
SSEP vs. MEP: measures electrical CNS responses to peripheral electrical stimuli
SSEPs
SSEP vs. MEP: tests peripheral motor response to transcranial stimuli
MEPs
SSEP vs. MEP: measures dorsal horn of spinal cord
SSEP
SSEP vs. MEP: measures anterior horn of spinal cord
MEP
SSEP vs. MEP: muscle relaxants restricted
MEP
SSEP vs. MEP: more sensitive to anesthetic agents
MEP
SSEP vs. MEP: electrodes placed over median and posterior tibial nerves
SSEP
SSEP vs. MEP: require bite block
MEP
SSEP vs. MEP: amplitude and latency change indicate potential spinal cord injury
SSEP
How does midazolam affect SSEPs?
increased latency
How does Diazepam affect SSEPs?
decreased amplitude
How does Etomidate affect SSEPs?
decreases latency AND amplitude
How does an Opioid bolus affect SSEPs?
may interefere, avoid during critical monitoring
What induction agent is acceptable with SSEPs?
propofol
How doe IHA and N2O affect SSEPs?
Depress them in a dose-dependent manner
How does hypothermia of 2-3 degrees impact SSEPs? What about hyperthermia
hypothermia: increases latency
Hyperthermia: suppresses amplitude by 85%!
EMG monitors which cranial nerves
3, 4, 10, 11, 12
CNS is made up of the _____ and ______; PNS is made up of _______ and __________.
brain and spinal cord
cranial/spinal nerves and their receptors
CNS is derived from 2 cell types, what are they?
neurons and glial cells
Stimulation of multiple dendrites in the _______mater produce an impulse towards the cell body, and then conduction away from the cell body via the _______.
gray ; axon
A single axon (_______ mater) emerges from the cell body and branches to form collateral nerves
white
Multipolar vs. Pseudounipolar: motor neurons
Motor neurons
Multipolar vs. Pseudounipolar: sensory neurons
pseudounipolar
Multipolar vs. Pseudounipolar: interneurons
pseudounipolar
Where are unipolar cell bodies found?
Lower vertebrae
Where are bipolar cell bodies found?
retina, ear, olfactory mucosa
The majority of CNS neurons are ______polar
multi
Glial cells support the neuron function in what 4 ways
- creating healthy ion environment
- modulating nerve conduction
- controlling re-uptake of neurotransmitters
- repairing neurons following neuronal injury
Name that glial cell type: most abundant, regulates metabolic environment and repairs neurons after injury
astrocytes
Name that glial cell type: involved in CSF production, concentrated in the roof of the 3rd and 4th ventricles
ependymal cells
Name that glial cell type: form myelin sheath of CNS, increase conduction velocity
oligodendrocytes
Name that glial cell type: act as macrophages and phagocytize neuronal debris
microglia
True or false: glial cells participate in neuronal signaling
false
In an unmyelinated axon (PNS), in order to double the speed of impulse conduction, what must happen?
axon must double in size
Brain blood supply originates from ________ arteries for anterior circulation, and ________ arteries from posterior circulation.
Internal carotid; vertebral
Vasospasm is thought to be caused by the breakdown of products of _______ that has accumulated around the vessels of the circle of willis after SAH
Hgb
Which lobe of the brain has motor control?
frontal
Which lobe of the brain has pain and touch?
parietal
Which lobe of the brain has the auditory cortex?
temporal
Which lobe of the brain has the visual cortex?
occipital
Which lobe of the brain is separated from the frontal and parietal lobes by the sylvian fissure?
temporal
Walk through the anterior circulation of the brain from aorta to cerebrum?
Aorta - carotid arteries - internal carotid - circle of willis - cerebral hemispheres
Walk through the posterior circulation of the brain from aorta to spinal cord?
aorta- subclavian artery - vertebral artery - basilar artery - posterior fossa structures and cervical spinal cord
Name the arteries of the circle of willis
- ant. communicating
- ant. cerebral
- middle cerebral
- post. communicating
- post. cerebral
- basilar artery
- vertebral arteries
All venous blood exits the brain via the _______ veins
jugular
Pons contains which cranial nerves
V and VII
Medulla contains which cranial nerves
8,9,10,11,13
________ separates the cerebral hemispheres, while _______ separate the occipital lobe and the cerebellum
falx cerebri; tentorium cerebellum
Distance from skin to epidural space
3-8 cm
Gray matter is enlarged in what 2 areas of the spinal cord?
C5-C7 (upper extremities)
L3-S2 (lower extremities)
Dorsal white matter is composed of _________fiber tracts, while lateral and ventral white matter contains ________ tracts.
ascending sensory; descending motor
Order these fibers from fastest to slowest: A-beta, A-gamma, A delta, A alpha, C fibers, B fibers
- a alpha
- a beta
- a gamma
- a delta
- b
- c
Which 3 cranial nerves are only sensory?
Olfactory CN I
Optic CN II
Vestibulocochlear CN VIII
Spinal cord receives blood from ________ (1/2) anterior spinal artery(s) and ________(1/2) posterior spinal artery(s)
1;2
Where does the artery of adam-whatever enter the cord and what does it supply?
T7; lumbosacral segment
Excitatory neurotransmitters increase the permeability of ________, inhibitory neurotransmitters increase the permeability of ________.
Sodium; chloride
What are the 3 inhibitory neurotransmitters?
GABA, glycine, dopamine
Which CN is responsible for taste to the anterior 2/3 of the tongue?
Facial CN VII
Eye movement is controlled by which 3 CNs? What about vision?
Vision = Optic CN II
Eye movement = CN III, IV, VI
Which CN is responsible for somatic sensation to the anterior 2/3 of the tongue
Trigeminal CN V
What is autonomic hyperreflexia?
Stimulation below the level of a SCI triggers SNS reglex causing vasoconstriction below the injury and vasodilation above the injury
What happens to HR in autonomic hyerreflexia?
slows due to baroreceptor reflex
SCI lesions above ________ are at risk for autonomic hyperreflexia?
T5-T8
Which happens first, spinal shock or autonomic hyperreflexia?
Spinal shock lasting 1-3 weeks
How do you treat autonomic hyperreflexia?
- remove the stimulus
- deepen the anesthsia
- administer direct vasodilators
ICP Waveform: what’s the first peak correspond to?
Percussion wave - SBP
ICP Waveform: what’s the second peak correspond to?
Tidal wave - dicrotic notch
ICP Waveform: whats the third wave correspond to?
dicrotic wave - will surpass P1 as ICP increases
What do plateau waves indicate on ICP waveform?
critically low intracranial compliance thought to be caused by brief episodes of decreased CPP leading to exaggerated cerebral vasodilation, and then increased CBV
First tier vs. second tier treatment for increased ICP
First tier: controlled hypocapnia (PaCO2 35), hyperosmolar therapy
Second tier: forced hyperventilation (PaCo2 25), barb coma, induced hypothermia, emergent surgery
What is an appropriate bolus dose of 3% saline?
Mannitol?
250mL
0.25-1mg/kg
