Neurophysiology Flashcards

(57 cards)

1
Q

Cerebral Vascular Blood Supply

A

Anterior - internal carotid artery

Posterior - vertebral arteries x2

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2
Q

Circle of Willis

A

Located at base of brain

Forms an anastomotic ring includes vertebral (basilar) & internal carotid flow

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3
Q

What site do aneurysms & atherosclerosis commonly occur?

A

Middle cerebral artery

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4
Q

CBF

A

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

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5
Q

Gray Matter CBF

A

80mL/100g/min

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6
Q

White Matter CBF

A

20mL/100g/min

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7
Q

EEG Activity

A

20-25mL/100g/min = cerebral impairment
15-20mL/100g/min = flatline EEG
< 10mL/100g/min = irreversible brain damage

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8
Q

NIRS

A

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

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9
Q

CPP

A

Cerebral perfusion pressure
MAP - ICP = CPP
CVP ≈ ICP

↑CPP = cerebral vasoconstriction (↓CBF)
↓CPP = cerebral vasodilation (↑CBF)
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10
Q

Normal ICP

A

ICP < 10mmHg (5-15mmHg)

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11
Q

Normal CPP

A

80-100mmHg

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12
Q

Cerebral Autoregulation

A

Myogenic - smooth muscle intrinsic response

Metabolic - tissue demand decreases arteriole tone & increases blood flow

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13
Q

CBF remains constant b/w what MAPs?

A

60-100mmHg

MAP > 150-160mmHg potentially results in cerebral edema & hemorrhage

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14
Q

What effects CBF?

A
PaCO2
PaO2
Temperature
Viscosity
Age
Autonomic
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15
Q

PaCO2 impact on CBF

A

CBF α PaCO2 b/w 20-80mmHg

Blood flow changes 1-2mL/100g/min per 1mmHg PaCO2 change

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16
Q

_____ metabolic acidosis has _____ effect on CBF

A

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

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17
Q

PaCO2 < 25mmHg

A

CBF α PaCO2
Effects attenuated at PaCO2 < 25mmHg (ceiling effect)
Left shift on oxyhemoglobin curve
Alkalosis causes ↑Hgb oxygen-affinity

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18
Q

PaCO2 AFTER Surgery

A

After sustained hyperventilation/hypocapnia
CSF acidosis → increase CBF
↑CBF ↑ICP
SLOWLY restore/increase PaCO2 back to baseline

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19
Q

PaO2 impact on CBF

A

50 to > 300mmHg minimal influence on CBF

< 50mmHg rapidly ↑CBF

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20
Q

PaO2 < 60mmHg

A

Vasodilation mediated via

  • Release neuronal nitric oxide
  • Open ATP-dependent K+ channels
  • Rostral ventrolateral medulla
  • Cerebral O2 sensor stimulation ↑CBF but not CMRO2
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21
Q

Temperature Impact (Cooling)

A

CBF ↓5-7% per 1°C
Cerebral metabolic rate ↓6-7% per 1°C
↓CMRO2 7% per 1°C

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22
Q

Viscosity Impact

A

Hct determines viscosity
↓Hct ↓viscosity ↑CBF
↓O2-carrying capacity → impaired oxygen delivery to brain tissue

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23
Q

Optimal cerebral oxygen delivery hematocrit = ___ %

24
Q

Sympathetic impact on CBF

A

Vasoconstriction

25
Parasympathetic impact on CBF
Vasodilation
26
Age Impact
Progressive loss neurons Loss myelinating fibers Synapses loss ↓CBF & CMRO2 by 15-20% at 80yo
27
Brain normally consumes ___ % total body oxygen
20% (60% used to generate ATP)
28
Cerebral Metabolic Rate
CMRO2 3-3.8 mL/100g/min = 50mL/min | 80% O2 consumed in the gray matter
29
Cerebral perfusion interruption = unconsciousness w/in ___ seconds
10 seconds | O2 not restored w/in 3-8 minutes → ATP depletion → irreversible cellular injury
30
What areas are most sensitive to hypoxic injury?
Hippocampus & cerebellum
31
What is the primary cerebral energy source?
GLUCOSE Brain glucose consumption 5mg/100g/min 90% metabolized aerobically
32
Hypoglycemia
→ brain injury
33
Hyperglycemia
→ exacerbate hypoxic injury
34
Blood-Brain Barrier
Vascular endothelial cell junctions tight (essentially fused together) - O2, CO2, & lipid-soluble molecules freely cross the blood-brain barrier
35
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 ```
36
What causes disruptions to the blood-brain barrier?
HTN, tumor, trauma/stroke, infection, hypercapnia, hypoxia, sustained seizure
37
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
38
How many mL CSF produced in adults per hour & day?
21mL/hr | 500mL/day
39
Total CSF Volume
≈ 150mL | 1/2 cranium & 1/2 spinal space
40
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
41
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
42
Brain/Blood/CSF
Brain 80% Blood 12% CSF 8%
43
ICP
Supratentorial CSF pressure measured in the lateral ventricles over the cerebral cortex
44
ICP Compensatory Mechanisms
CSF displacement from cranium to spinal compartment ↑CSF absorption ↓CSF production ↓total cerebral blood volume *Major compensatory mechanisms`
45
Closed Cranium Goals
Maintain CPP | Prevent herniation
46
Open Cranium Goals
Facilitate surgical process | Reverse ongoing herniation
47
Intracranial HTN
Sustained ICP 20-25mmHg
48
Intracranial HTN | Causes
Expanding tissue or fluid mass Interference w/ CSF absorption Excessive CSF production Systemic disturbances promoting edema
49
↑ICP S/S
``` Headache Nausea/vomiting Papilledema Focal neurological deficit ↓LOC Seizures Coma CUSHING TRIAD ```
50
CUSHING TRIAD
1. HTN 2. Bradycardia 3. Irregular respirations
51
Herniation Types
1. Cingulate gyrus under flax cerebri 2. Central 3. Uncal (transtentorial) 4. Cerebellar tonsils through foramen magnum* 5. Upward herniation of cerebellum 6. Transcalvarial
52
Most common herniation type _____
Cerebellar tonsils through foramen magnum
53
Cerebellar Tonsillar S/S
``` No specific clinical manifestations Arches stiff neck Paresthesias in shoulder ↓LOC Respiration abnormalities Pulse rate variations ```
54
Uncal & Central S/S
↓LOC Sluggish pupils or fixed & dilated Cheyne-Stokes respirations Decorticate → decerebate posturing
55
Cingulate Gyrus S/S
Minimal known about S/S
56
Transcalvarial S/S
Potential to occur during surgery
57
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)