Neurophysiology Flashcards
Cerebral Vascular Blood Supply
Anterior - internal carotid artery
Posterior - vertebral arteries x2
Circle of Willis
Located at base of brain
Forms an anastomotic ring includes vertebral (basilar) & internal carotid flow
What site do aneurysms & atherosclerosis commonly occur?
Middle cerebral artery
CBF
Cerebral blood flow varies based on metabolic activity
10-300 mL/100g/min
Average CBF = 50 mL/100g/min
Adult averages 750 mL/min
Receives 15-200% CO
Gray Matter CBF
80mL/100g/min
White Matter CBF
20mL/100g/min
EEG Activity
20-25mL/100g/min = cerebral impairment
15-20mL/100g/min = flatline EEG
< 10mL/100g/min = irreversible brain damage
NIRS
Near infrared spectroscopy
Normal = 80%
Reflects venous Hgb absorption
NOT pulsatile arterial blood flow
Neuro events associated w/ rSO2 <40% or >25% change from baseline
CPP
Cerebral perfusion pressure
MAP - ICP = CPP
CVP ≈ ICP
↑CPP = cerebral vasoconstriction (↓CBF) ↓CPP = cerebral vasodilation (↑CBF)
Normal ICP
ICP < 10mmHg (5-15mmHg)
Normal CPP
80-100mmHg
Cerebral Autoregulation
Myogenic - smooth muscle intrinsic response
Metabolic - tissue demand decreases arteriole tone & increases blood flow
CBF remains constant b/w what MAPs?
60-100mmHg
MAP > 150-160mmHg potentially results in cerebral edema & hemorrhage
What effects CBF?
PaCO2 PaO2 Temperature Viscosity Age Autonomic
PaCO2 impact on CBF
CBF α PaCO2 b/w 20-80mmHg
Blood flow changes 1-2mL/100g/min per 1mmHg PaCO2 change
_____ metabolic acidosis has _____ effect on CBF
Acute metabolic acidosis has minimal effect on CBF
HCO3¯ does NOT acutely effect CBF
- Unable to passively cross the blood-brain barrier
- 24-48hrs CSF HCO3¯ compensates via active transport to buffer PaCO2 (PACU or ICU)
- Hypo/hypercapnia are diminished
PaCO2 < 25mmHg
CBF α PaCO2
Effects attenuated at PaCO2 < 25mmHg (ceiling effect)
Left shift on oxyhemoglobin curve
Alkalosis causes ↑Hgb oxygen-affinity
PaCO2 AFTER Surgery
After sustained hyperventilation/hypocapnia
CSF acidosis → increase CBF
↑CBF ↑ICP
SLOWLY restore/increase PaCO2 back to baseline
PaO2 impact on CBF
50 to > 300mmHg minimal influence on CBF
< 50mmHg rapidly ↑CBF
PaO2 < 60mmHg
Vasodilation mediated via
- Release neuronal nitric oxide
- Open ATP-dependent K+ channels
- Rostral ventrolateral medulla
- Cerebral O2 sensor stimulation ↑CBF but not CMRO2
Temperature Impact (Cooling)
CBF ↓5-7% per 1°C
Cerebral metabolic rate ↓6-7% per 1°C
↓CMRO2 7% per 1°C
Viscosity Impact
Hct determines viscosity
↓Hct ↓viscosity ↑CBF
↓O2-carrying capacity → impaired oxygen delivery to brain tissue
Optimal cerebral oxygen delivery hematocrit = ___ %
30%
Sympathetic impact on CBF
Vasoconstriction
Parasympathetic impact on CBF
Vasodilation
Age Impact
Progressive loss neurons
Loss myelinating fibers
Synapses loss
↓CBF & CMRO2 by 15-20% at 80yo
Brain normally consumes ___ % total body oxygen
20% (60% used to generate ATP)
Cerebral Metabolic Rate
CMRO2 3-3.8 mL/100g/min = 50mL/min
80% O2 consumed in the gray matter
Cerebral perfusion interruption = unconsciousness w/in ___ seconds
10 seconds
O2 not restored w/in 3-8 minutes → ATP depletion → irreversible cellular injury
What areas are most sensitive to hypoxic injury?
Hippocampus & cerebellum
What is the primary cerebral energy source?
GLUCOSE
Brain glucose consumption 5mg/100g/min
90% metabolized aerobically
Hypoglycemia
→ brain injury
Hyperglycemia
→ exacerbate hypoxic injury
Blood-Brain Barrier
Vascular endothelial cell junctions tight (essentially fused together)
- O2, CO2, & lipid-soluble molecules freely cross the blood-brain barrier
What impacts molecules/drugs that are able to cross the blood-brain barrier?
Size & charge - Ions (electrolytes Na+) Lipid solubility Plasma protein binding Large molecules such as Mannitol
What causes disruptions to the blood-brain barrier?
HTN, tumor, trauma/stroke, infection, hypercapnia, hypoxia, sustained seizure
CSF
Cerebral spinal fluid formed in the choroid plexuses by ependymal cells
Replaced 3-4x per day
Found in cerebral ventricles, cisterns, & subarachnoid space surrounding the brain & spinal cord
Isotonic w/ plasma
Serves as a cushion to protect CNS from trauma
How many mL CSF produced in adults per hour & day?
21mL/hr
500mL/day
Total CSF Volume
≈ 150mL
1/2 cranium & 1/2 spinal space
CSF Circulation
Lateral ventricles → intraventricular foramina of Monroe → 3rd ventricle → cerebral aqueduct of Sylvius → 4th ventricle → medial (foramen of Magendie) or lateral (foramen of Luschka) apertures → subarachnoid space → arachnoid villi → superior sagittal sinus
Cranial Vault
RIGID structure
Monroe-Kellie hypothesis
Cranial compartment = incompressible
Volume inside cranium remains FIXED volume
Any increase in one volume requires compensatory decrease in another volume to prevent ↑ICP
*Small volume increases are initially well-compensated
Brain/Blood/CSF
Brain 80%
Blood 12%
CSF 8%
ICP
Supratentorial CSF pressure measured in the lateral ventricles over the cerebral cortex
ICP Compensatory Mechanisms
CSF displacement from cranium to spinal compartment
↑CSF absorption
↓CSF production
↓total cerebral blood volume
*Major compensatory mechanisms`
Closed Cranium Goals
Maintain CPP
Prevent herniation
Open Cranium Goals
Facilitate surgical process
Reverse ongoing herniation
Intracranial HTN
Sustained ICP 20-25mmHg
Intracranial HTN
Causes
Expanding tissue or fluid mass
Interference w/ CSF absorption
Excessive CSF production
Systemic disturbances promoting edema
↑ICP S/S
Headache Nausea/vomiting Papilledema Focal neurological deficit ↓LOC Seizures Coma CUSHING TRIAD
CUSHING TRIAD
- HTN
- Bradycardia
- Irregular respirations
Herniation Types
- Cingulate gyrus under flax cerebri
- Central
- Uncal (transtentorial)
- Cerebellar tonsils through foramen magnum*
- Upward herniation of cerebellum
- Transcalvarial
Most common herniation type _____
Cerebellar tonsils through foramen magnum
Cerebellar Tonsillar S/S
No specific clinical manifestations Arches stiff neck Paresthesias in shoulder ↓LOC Respiration abnormalities Pulse rate variations
Uncal & Central S/S
↓LOC
Sluggish pupils or fixed & dilated
Cheyne-Stokes respirations
Decorticate → decerebate posturing
Cingulate Gyrus S/S
Minimal known about S/S
Transcalvarial S/S
Potential to occur during surgery
Intracranial HTN
Treatment
Brain tissue - surgical mass removal (lobectomy or bone flap)
CSF - no effective pharmacological manipulation; drain placement
Fluid - steroids; osmotics/diuretics
Blood - most amenable to rapid alteration ↓arterial flow or ↑venous drainage (patient positioning)
Hyperventilation ↓PaCO2 25-35mmHg
CMR pharmacological suppression (i.e. barbiturates or Propofol) or hypothermia (therapeutic cooling)