Neuro Physiology Flashcards
brain receives blood from these two arteries
internal carotid artery
vertebral arteries
the internal carotid artery provides blood flow for the
anterior circulation
the vertebral arteries provide blood flow for the
posterior circulation
which structures does the anterior cerebral artery supply
basal ganglia, corpus callosum, medial surface of cerebral hemispheres, superior surface of frontal and parietal lobes
what conditions are caused by occlusion of the anterior cerebral artery
hemiplegia on contralateral side of body, greater in lower than in upper extremities
which structures does the middle cerebral artery supply
frontal lobe, parietal lobe, temporal lobe (primarily cortical surfaces)
what conditions are caused by occlusion of the middle cerebral artery
aphasia in dominant hemisphere and contralateral hemiplegia
which structures does the posterior cerebral artery supply
part of diencephalon and temporal lobe: occipital lobe
what conditions are caused by occlusion of the posterior cerebral artery
visual loss, sensory loss, contralateral hemiplegia if cerebral peduncle affected
path of two vertebral arteries
branches from subclavian, enters through foramen magnum, run along medulla, join in pons to form basilar artery. basilar artery then branches into 2 posterior cerebral arterries which primary supply occipital lobes of the brain
path of internal carotid arteries
pass through cavernous sinus and divided into anterior and middle cerebral artery
circle of willis
located at base of brain and forms anastomotic ring that includes vertebral (basilar) and internal carotid flow
artery that is most common site for aneurysm and atherosclerosis
MCA
total cerebral blood flow in adults averages how many mL/min? and takes up how much CO?
750mL/min, 15-20% of CO
average cerebral blood flow is how many ml/g/min?
50mL/100g/min
average cerebral blood flow of gray matter
80mL/100g/min
average blood flow of white matter
20mL/100g/min
varied cerebral blood flow range based on metabolic activity
10-300mL/100g/min
when EEG monitoring, what CBF is associated with cerebral impairment?
20-25ml/100g/min
when EEG monitoring, what CBF is associated with a flat EEG
15-20mL/100g/min
when EEG monitoring, what CBF is associated with irreversible brain damage
below 10mL/100g/min
how do we assess CBF (O2 delivery) in the clinical setting? (4 ways, and what they monitor)
- transcranial doppler: ultrasound- MCA
- brain tissue oximetry: bolt with a clark electrode oxygen sensor
- intracerebral microdialysis: assess brain tissue chemistry
- near infrared spectroscopy
near infrared spectroscopy (NIRS) how it works
receptors detect reflected light from superficial and deep structures
largely reflects absorption of venous HGB
not pulsatile arterial flow
NIRS changes that would indicate an acute neuro event
rSO2 <40% OR change in rSO2 >25% from baseline
what percentage would you expect on a NIRS monitor for a normal healthy patient versus a patient with co morbidities and decreased reserve?
80% versus near 60%
normal CPP
80-100mmHg (if they’ve got co morbidities, may need >80 but if theyre healthy >60 is fine)
normal ICP
10-15mmHg
when monitoring EEG, what CPP would reflect a “slowing EEG”
<50mmHg
when monitoring EEG, what CPP would reflect a “flat EEG”
25-40mmHg
when monitoring EEG, what CPP would reflect “irreversible brain damage”
CPP maintained <25mmHg
myogenic auto regulation: when CPP gets too high, the body
limits CBF via vasoconstriction
myogenic auto regulation, when CPP gets too low, the body
increases CBF via vasodilation
CBF remains nearly constant between MAPs of
60-160
what happens to CBF if MAP >150-160mmHg
BBB gets disrupted, cerebral edema and hemorrhage can result
factors affecting CBF (6)
PaCO2, PaO2, temperature, viscosity, autonomic influences, age
CBF is directly proportionate to PaCO2 between tensions of
20-80mmHg
blood flow changes how much per 1mmHg change in PaCO2?
1-2mL/100g/min
what happens if you give HCO3?
nada. ions dont passively cross BBB so its not an acute fix. but in 24-48h you can see some compensation
when does the directly proportional rate of CBF to PaCO2 increase or decrease attenuate
when the PaCO2 is <25mmHg.
what do we give that increases the cerebrovascular reactivity to carbon dioxide (CVR-CO2)
inhaled anesthetics. CBF increases, CVR-CO2 increases
what happens to even normal healthy individuals in the setting of marked hyperventilation (PaCO2 <20mmHg)
shifts oxygen hemoglobin dissociation curve to the left and could result in EEG changes suggestive of cerebral impairment
do we usually allow neuro patients’ PaCO2 to climb at the end of surgery so they get the hypoxic drive to breathe?
slowly increase back to normal PaCO2, do not allow this to happen quickly so be apprised of PaCO2 and permissive hypercapnia is much much more limited if at all allowed.
what range of PaO2 can a normal CBF rate be sustained
30->300mmHg
what PaO2 level can rapidly increase CBF
<50mmHg
what happens when PaO2 is <60mmHg to create a vasodilated environment
release of neuronal nitric oxide
open ATP dependent K channels
rostral ventrolateral medulla (RVM), pressure area of medulla, senses increase in pressure
while CBF increases, CMRO2 does not
at what temperature would you assume neuronal cell injury
> 42c
what is the goal temperature for neuro patients
normothermia
what determines viscosity
HCT
decreased HCT in relation to CBF
decreases viscosity, increases CBF
optimal cerebral oxygen delivery happens at a HCT of
30%
age means a loss of
neurons, myelinated fibers (white matter), synapses
what two things decrease by 15-20% at 80 years
CBF and CMRO2
the brain normally consumes how much of the total body oxygen
20%
how much of the total body oxygen consumed by the brain is used to generate ATP
60%
what is the baseline cerebral metabolic rate
3-3.8mL/100g/min or 50mL/min
O2 is mostly consumed in the
gray matter
interruption of the cerebral perfusion creates unconsciousness in
10 seconds
irreversible cellular injury happens if the O2 is not restored in the brain in
3-8 minutes. its because of a depletion in ATP
which areas of the brain are most sensitive to hypoxic injury
hippocampus and cerebellum
baseline brain glucose consumption
5mg/100g/min
primary energy source for brain
glucose
hypoglycemia does what to the brain
creates a brain injury
hyperglycemia does what to the brain
exacerbates hypoxic injury
what cannot pass through the blood brain barrier
ionized molecules (electrolytes), plasma proteins, large molecules (mannitol)
what can freely cross the BBB
O2, CO2, lipid soluble molecules (most anesthetics)
what can cause disruptions in the BBB
HTN, tumor, trauma, stroke, infection, marked hypercapnia, hypoxia, sustained seizure
CSF is formed in
the choroid plexuses by the ependymal cells
adults make CSF at ___/hr and ___/day
21ml/h and 500ml.day
total volume of CSF is usually ____ and can be found ______
~150ml, half in cranium and half in spinal space
CSF is replaced how many times per day
3-4
tonicity of CSF and makeup
isotonic with plasma. lower K, HCO3, and glucose concentration
production of CSF is inhibited by
carbonic anhydrase inhibitors (acetazolamide), corticosteroids, spironolactone, furosemide, isoflurane, and vasoconstrictors
flow of CSF
lateral ventricles through intraventricular foramen (of monro), 3rd ventricle, 4th ventricle (foramen of magendie), cisterns magna, subarachnoid space where it circulates around brain and spinal cordd, then absorbed in arachnoid granulations
monro kelly and cranial vault: components and %
brain (80%), blood (12%), CSF (8%). increase in one means another has to decrease to prevent increase in ICP
where is supratentorial CSF pressure measured
in the lateral ventricles or over the cerebral cortex
major compensatory mechanisms for intracranial elastane includes (4)
initial displacement of CSF from cranial to spinal compartment
increase in CSF absorption
decrease in CSF production
decrease in total cerebral blood volume
intracranial HTN is a sustained increase in ICP
about 20-25mmHg
intracranial HTN causes
expanding tissue or fluid mass
interference with CSF absorption
excessive CSF production
systemic disturbances promoting edema
s/sx of increased ICP
HA, n/v, papilledema, focal neurological deficit, decrease LOC, seizures, coma, bushings (irreg resp, bradycardia, HTN)
cushings happens when ICP is
> 20 ICP for 1-15min
most common type of herniation
cerebellar tonsils through foramen magnum
s/sx of cerebellar tonsilar herniation
no specific clinical manifestations arched stiff neck parasthesias in shoulder decrease LOC respiratory abnormalities pulse rate variations
treatment of intracranial HTN
brain tissue: surgical removal of mass
CSF: no effective pharmacological management, only practical management is a drain
fluid: steroids, osmotics/diuretics
blood: most amenable to rapid alterations: decrease arterial flow or increase venous drainage (pt position)
reduction of PaCO2 (to not <23-25mmHg)
CMR suppression (barbs, prop, hypothermia)
normal CBV
~5ml/100g of brain (70mL)
when does CBF not parallel CBV
cerebral ischemia (CBV increases, but CBF decreases)
