Neuro Flashcards
Main CNS inhibitory neurotransmitter
GABA
- Opens Cl channels
- Reduces excitability of neurons by hyperpolarizing them
Main CNS excitatory neurotransmitter
Glutamate
- Activates NMDA receptor (opens Na channel)
- When activated it depolarizes neurons, making them more likely to fire action potentials
3 classification actions of neurons
Sensory (afferent, toward posterior root)
Motor (efferent, away from anterior root)
Interneuron
Gyri vs Sulci
Gyri: Outer 3mm area of cerebral structure that is convoluted to increase surface area
Sulci: Grooves that separate Gyri
4 cerebral structure lobes and their functions
Frontal -Motor, thought Parietal -Pain, pressure, temperature, touch Temporal -Hearing, smelling, recognition, memory Occipital -Visual
Brainstem: Midbrain, Pons, and Medulla
Contain reticular activating system
-Consciousness, arousal, alertness
Pons: connects midbrain and medulla oblongata
Medulla: Respiratory and cardiovascular centers
3 meningeal layers and spaces in between them
Cover brain and spinal cord
- Epidural space is above dura
- Dura: thickest, providers structural support
- Subdural space
- Arachnoid: thin cobweb like, major pharmacologic barrier (BBB), avascular
- Subarachnoid space, contains CSF
- Pia: thin, highly vascular
Cranial nerve pneumonic and sensory/motor pneumonic
Olfactory:On:Some Optic:Occasion:Say Oculomotor:Our:Money Trochlear:Trusty:Matters Trigeminal:Truck:But Abducens:Acts:My Facial:Funny:Brother Vestibulocochlear:Very:Says Glossopharyngeal:Good:Big Vagus:Vehicle:Brains Accessory:Any:Matter Hypoglossal:How:More
2 main arteries to brain
Carotid arteries: Anterior portion of brain
Vertebral arteries: Posterior portion
Circle of Willis
Anastomosis formed by arteries giving blood supply to the brain
Cerebral blood flow (normal ml/g/min and percentage of cardiac output the brain receives)
50mL/100g/min of brain tissue
-700-750mL/min
15-20% of CO
-Disproportionately large b/c high metabolic rate, inability to store energy
Cerebral Perfusion Pressure calculation and normal number, ICP where CPP/CBF compromised
MAP-ICP/CVP
-ICP vs CVP=whichever is higher (CVP at ear canal)
Normally 10-15 mmHg
>30 even if MAP is normal CPP/CBF can be compromised
Cerebral metabolic rate of oxygen
CMRO2
Glycolysis -> ATP =90% aerobic process
-Parallels glucose consumption
-Influences CBF directly
How long cellular injury can occur in without oxygen stores/ATP store depletion
3-8 minutes
What CPP/MAP that CBF will remains constant with
50-150mmHg
-Can shift in chronic hypertension
O2/CO2 effect on CBF
O2 has little effect unless its <50mmHg
CO2=Most important regulator
-CBF changes 3% for every 1mmHg change in PaCO2
Steal phenomenon
Hypoventilation/hypercarbia -> increased CBF to normal areas
Temperature effect on CBF
1C decrease -> 5-7% decrease in CBF
-also decreased CMRO2
Blood viscosity impact on CBF
Increased viscosity (Hct) -< decreased CBF Optimal Hct for O2 delivery to brain =30%
Autonomic influence on CBF
Sypathetic -> Vasoconstriction/decreased CBF
Parasympathetic -> Vasodilation/increased CBF
CSF (where produced, rate of production, total volume present at a time, normal CSF pressure)
- Produced at choroid plexus, secreted by ependymal cells there
- Produced at 30mL/hr
- 150mL present at a time (recycles every 3-4 hours)
- Normal CSF pressure: 5-15mmHg
Brain percentages of brain vs blood vs CSF
Brain: 80%
Blood: 12%
-ICF, ECF
CSF: 8%
ICP level considered intracranial HTN
> 15mmHg
Cushing reflex
HTN, bradycardia, respiratory irregularities
- Brain ischemia if ICP is too high
- Increases MAP to compensate but then CPP falls further -> more ischemia
- Last ditch effort by the body to maintain homeostasis in the brain (usually ends up making things worse)
Blood brain barrier (how it’s formed, what passes through well vs not well)
Formed from tight junctions between endothelial cells
Passes through well: Lipid soluble molecules
Not well: Large, highly charged, water soluble
Intra vs extracranial causes of HTN
Intracranial -Brain tumor -Trauma -Intracerebral hemorrhage -Stroke -Hydrocephalus Extracranial -Hypercarbia -Hypoxia -HTN -Hyperpyrexia -Venous outflow obstruction (jugular pressure, intrathoracic pressure)
Compensatory mechanisms for increased ICP
- Decreased CSF production/increase reabsorption
- Translocate CSF to spinal column
- Decrease CBF
Gold standard for ICP monitoring
Intraventricular catheter
-Also allows for drainage of CSF
Volatile agent effect on CBF/CMRO2
Low dose -CBF unchanged or slightly increased Higher dose -Vasodilated -> increased CBF *Autoregulation impaired at 1MAC -Decreased CMRO2 -Iso increases the most, sevo the least
Coupling CBF and CMRO2
In normal patients:
<1 MAC = coupling
-CMRO2 decreases along with CBF (coupled reductions)
>1 MAC = uncoupling
-CBF increases but CMRO2 doesn’t
-Volatile agents alter the coupling effect (don’t disengage it) by redistributing the blood flow
Robin Hood vs Circulatory Steal Phenomenon
How volatile agents change coupling effect (normal brain tissues can vasoconstrict, ischemic tissue can’t)
- Circulatory Steal: Increased blood flow in normal areas but ischemic areas are dilated so blood flow is redistributed away from the ischemic area
- Robin Hood: Normal parts of brain vasoconstrict to decrease flow to normal area to give to ischemic area
- Barbiturates will cause this vasoconstriction
Which inhaled anesthetic increases CBF the least
Isoflurane, also decreases CMRO2 the most
Then sevo
N2O use in neurosurgery
Controversial
-Increases ICP, CMRO2, CBF (but this doesn’t happen when its used with IV anesthetics or hypocapnea)
Propofol use in neurosurgery
Decreases CBF and CMRO2 (dose dependent)
“Relaxes brain”
Etomidate use in neurosurgery
Decreases CMRO2, CBF, ICP
Ketamine use in neurosurgery
Dilates cerebral vasculature and increases CBF 60-80%
Opioid use in neurosurgery
Have minimal effect on CBF, CMRO2, and ICP
Benzo use in neurosurgery
Decreases CBF and CMRO2 (to a lesser extent than barbiturates)
Precedex use in neurosurgery
Decreases CBF without a decrease in CMRO2 (could limit adequate cerebral oxygenation)
Muscle relaxant use in neurosurgery
Succs
-May increase ICP, CBF, CMRO2 (increased muscle spindle activity)
-Nonfasciculating dose of NMDA will help blunt this increase
NMDAs
-No effect on ICP, CBF, CMRO2
-Histamine release may cause vasodilation -> increased ICP
-Can’t do if cranial nerve monitoring is needed
Vasoactive agent use in neurosurgery
Labetalol/Esmolol
-No effect on CBF, CMRO2
Nipride/Nitro/Hydralazine
-Dilate cerebral vessels -> increased CBV/ICP
Phenylephrine
-Possibly causes decreased CBF, some studies don’t support this
IV agent that dilates cerebral vasculature
Ketamine
Anti-seizure medication effect on NDMRs
Patients on phenytoin and anti-seizure medications have hepatic enzyme induction
- Rapidly metabolize NDMRs
- Need increased dose and will have a decreased DOA
Barbiturate use in neurosurgery
Decrease CMRO2 - coupled with reducing CBF/CBV
End point for maximal brain protection
Burst suppression
Steroid use during neurosurgery
Dexamethasone 4mg q6h
Decrease edema associated with lesions/tumors
-Penetrate BBB
Anticonvulsant use during neurosurgery
Dilantin: Usually administered prophylactically
-Acute irritation of cortical surface can result in seizures
Diuretic use during neurosurgery
Loop diuretics -Decrease CSF production/cerebral edema Osmotic diuretics -Decrease water content of brain -Mannitol: Rapid admin may produce vasodilation/increased CBF/increase ICP. *Administer 0.25-1g/kg slowly over 10-15 mins -Check Na levels regularly
Preop eval for neurosurgery: Cardiac risks
- Delay surgery 2 weeks after simple balloon angio
- Delay 4-6 weeks after bare metal stent placement
- Delay 1 year after drug eluting stent
Preop eval for neurosurgery: meds/premeds
- Meds: Know anticonvulsant plan and last dose
- Premeds: Caution with benzos/opioids. Respiratory depression -> increased ICP
- No premeds in patients with midline shift or abnormal ventricular size
Paralysis or weakness with succs use
- In acute stroke/SCI succs is OK
- After 48-72 hours AcH receptors are upregulated -> hyperkalemia -> cardiac arrest
IV anesthetic that doesn’t interfere with electrophysiological (EP) mapping
Precedex
-Also provides hemodynamic stability
Anesthesia maintenance during neurosurgery
< 1 MAC with Propofol and narcotic
- Mannitol, hypertonic saline, TIVA
- Hypocapnea offsets cerebral vasodilation from inhalation agents
Hyperventilation in neurosurgery
Causes cerebral vasoconstriction/brain relaxation
- But can potentially exacerbate cerebral ischemia
- Avoid in TBI patients unless briefly necessary to manage acute increase in ICP
- gPaCO2=30-35
IVF in neurosurgery
Goal=euvolemia
Hypertonic saline
-Osmotic effect -> reduced ICP
-Low side effects but may cause electrolyte abnormalities/cardiac failure
Dextrose containing fluids
-Avoid
High glucose levels may exacerbate neurological injury during ischemia
Target blood sugar during neurosurgery
Normoglycemia or 140-180
Check q30mins
Variability in blood glucose can cause cerebral osmotic shifts
Neurosurgery emergence before/after closing dura
Before -PaCO2 allowed to return to normal -BP raised 120% above baseline so surgeon can assess the ability to withstand challenges After -Maintain BP at baseline
Where to zero A-line for neurosurgery
External auditory meatus
-Same as circle of willis
Overall methods to provide adequate brain relaxation
- Sub-MAC volatile anesthesia and/or TIVA
- Mild-moderate hyperventilation
- Minimize tumor edema with mannitol, dexamethasone, HTS
- Maximize venous drainage/minimize congestion/avoid excessive neck rotation
Venous air embolism often occurs when surgical site is ____
20cm above the heart
Paradoxic air embolism
If air enters venous circulation and travels through patent foramen ovale to arterial side
-May present as acute cerebral vascular or coronary event
Most sensitive monitor to detect VAE
TransEsophageal Echocardiography (TEE)
Pituitary
Tumors are rarely metastatic S/Sx: Neuro, *visual, hormonal changes -Amenorrhea -Galactorrhea -Cushins (increased ACTH) -Acromegaly (increased GH) -Hyperthyroid -Panhypopituitarism (hormone replacement with cortisol, levothyroxine, DDAVP) -Diabetes insipidus
Pituitary surgery transphenoidal vs craniotomy
Intracranial only when tumor>10mm
Transphenoidal=reduced morbidity and mortality
Diabetes insipidus associated with pituitary surgery
Common complication
- No ADH production, temporary or permanent, intraop or post op
- Tx: DDAVP
Hunt & Hess Classification
What surgeons use for SAH to indicate mortality rate
- Score 0-5
- 3=Mortality rate 5-10%
- 5=Mortality rate 30-40%
Rebleeding after SAH
50% chance of occurring in the first few days, life threatening
-Typically wait 2 weeks to do elective repair
Postponing surgical clipping of ruptured aneurysm
Shouldn’t be postponed unless hemodynamically unstable patient
-Once it’s done the risk of recurrent hemorrhage is gone
Vasospasm after SAH
Leading cause of morbidity and mortality after SAH (1/4 will get it)
- Reactive narrowing of cerebral arteries, impairs circulation -> ischemia and infarction
- Detected with angiography
- Peak 4-9 days postop
Vasospasm treatment
Triple H method: -HTN (MAP 20-30 above baseline) -Hypervolemia -Hemodilution (Hct ~30%) Nimodipine PO decreases morbidity from cerebral ischemia
Anesthesia for endovascular treatment of aneurysms
- Patient movement is devastating: *keep relaxed
- Avoid hyperventilation! (makes access more challenging)
Awake epilepsy surgery or awake craniotomy anesthetic considerations
Pt is sedated but able to respond
- Done to facilitate monitoring of the region of the brain the surgeon is operating on
- Contraindications: anxiety, claustrophobia, psych disorders, difficult airway, OSA, orthopnea
- Propofol or precedex drip
Asleep awake asleep technique
Used for epilepsy and tumor resection surgery
General with LA infiltration on skull
Pt emerges in middle of surgery
-Neurosurgeon applies electrical stimulation to map which allows for maximal tumor resection and minimizes neurologic deficits
*Preop pt education of what to expect
Head trauma goal
Secure the airway rapidly and efficiently with minimal/no neck movement
- Increases difficulty of intubation
- Incorrectly applied CP may displace cervical fractures
Glascow coma scale possible scores and categories
3 (bad) - 15
Eye opening 1-4
Verbal response 1-5
Motor response 1-6
Cerebral autoregulation after head trauma (and goal CPP)
Impaired
-Avoid hypotension (->ischemia) and HTN (->hemorrhage)
-Albumin -> higher mortality rate/unfavorable outcomes. Don’t use it unless pts are hypoalbuminemic
-Can cause cerebral edema
-Use mannitol or hypertonic saline
Goal CPP 50-70
Goal PaO2 ETCO2 and temp in head trauma with increased ICP patients
PaO2 >60 SpO2>90
ETCO2 30-35
Moderate hypothermia (controversial, some studies say no benefit)
Barbiturate use in head trauma/elevated ICP patients
Only if they’re hemodynamically stable and have been adequately volume resuscitated
-Not if MAP and CPP can’t be maintained
Normal cerebral oximetry (SctO2)
60-80%
BP goal during carotid endarterectomy (CEA)
Controlled 20% over baseline
-Usually with phenylephrine drip
SBP>180 may be associated with CVA
Nerve injuries or hematoma after carotid endarterectomy
Nerve injury: Hypoglossal, sublingual, or RLN (hoarseness)
Wound hematoma: Worry about tracheal deviation, immediate action required (secure airway in OR)
-Usually precipitated by HTN in PACU
Carotid artery stenting typical anesthesia and complication/what to do
Performed under sedation, done for patients who are poor surgical candidates
Near vagal nerve, may get bradycardia or asystole during balloon angioplasty of internal carotid artery
-Don’t give atropine-don’t want tachycardia
-Have surgeon infiltrate lidocaine-will prevent
EEG: Deep anesthesia vs cerebral ischemia
Both produce similar changes
Meds/labs that cause EEG activation
Inhalation agents -subanesthetic Barbiturates -small dose Benzos -small doses Etomidate -small doses N2O Ketamine Mild hypercapnia Stimulation Hypoxia -early
Meds/labs that cause EEG depression
Inhalation agents -1-2MAC Barbiturates Opioids Propofol Etomidate Hypocapnia Marked hypercapnia Hypothermia Hypoxia -Late Ischemia
Somatosensory evoked potentials (SSEP)
Test the integrity of the dorsal spinal column, ascending tract, and sensory cortex supplied to posterior spinal artery
-Used for spinal, CEA, and aortic surgery
Anesthetic effect on SSEPs
Volatile agents have greatest effect
-Influenced by all anesthetics except MRs
Motor evoked potentials (MEPs)
Assess function of motor cortex/descending tracts supplied by anterior spinal artery (vs SSEP=posterior/ascending tract)
Anesthetic effect on MEPs
Volatiles, N2O, and NMDAs all suppress the response
-TIVA recommended
Electromyography (EMG)
Recording of electrical activity of muscle that is irritated or injured
- Identifies nerves and tests their integrity
- Assesses motor function of facial nerve and CN III, IV, X, XI
