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AS - N934 Advanced Principles II > Neurophysiology > Flashcards

Neurophysiology Flashcards

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 = ___ %

A

30%

24
Q

Sympathetic impact on CBF

A

Vasoconstriction

25
Q

Parasympathetic impact on CBF

A

Vasodilation

26
Q

Age Impact

A

Progressive loss neurons
Loss myelinating fibers
Synapses loss
↓CBF & CMRO2 by 15-20% at 80yo

27
Q

Brain normally consumes ___ % total body oxygen

A

20% (60% used to generate ATP)

28
Q

Cerebral Metabolic Rate

A

CMRO2 3-3.8 mL/100g/min = 50mL/min

80% O2 consumed in the gray matter

29
Q

Cerebral perfusion interruption = unconsciousness w/in ___ seconds

A

10 seconds

O2 not restored w/in 3-8 minutes → ATP depletion → irreversible cellular injury

30
Q

What areas are most sensitive to hypoxic injury?

A

Hippocampus & cerebellum

31
Q

What is the primary cerebral energy source?

A

GLUCOSE
Brain glucose consumption 5mg/100g/min
90% metabolized aerobically

32
Q

Hypoglycemia

A

→ brain injury

33
Q

Hyperglycemia

A

→ exacerbate hypoxic injury

34
Q

Blood-Brain Barrier

A

Vascular endothelial cell junctions tight (essentially fused together)
- O2, CO2, & lipid-soluble molecules freely cross the blood-brain barrier

35
Q

What impacts molecules/drugs that are able to cross the blood-brain barrier?

A 
Size & charge
- Ions (electrolytes Na+)
Lipid solubility
Plasma protein binding
Large molecules such as Mannitol
36
Q

What causes disruptions to the blood-brain barrier?

A

HTN, tumor, trauma/stroke, infection, hypercapnia, hypoxia, sustained seizure

37
Q

CSF

A

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
Q

How many mL CSF produced in adults per hour & day?

A

21mL/hr

500mL/day

39
Q

Total CSF Volume

A

≈ 150mL

1/2 cranium & 1/2 spinal space

40
Q

CSF Circulation

A

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
Q

Cranial Vault

A

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
Q

Brain/Blood/CSF

A

Brain 80%
Blood 12%
CSF 8%

43
Q

ICP

A

Supratentorial CSF pressure measured in the lateral ventricles over the cerebral cortex

44
Q

ICP Compensatory Mechanisms

A

CSF displacement from cranium to spinal compartment
↑CSF absorption
↓CSF production
↓total cerebral blood volume

*Major compensatory mechanisms`

45
Q

Closed Cranium Goals

A

Maintain CPP

Prevent herniation

46
Q

Open Cranium Goals

A

Facilitate surgical process

Reverse ongoing herniation

47
Q

Intracranial HTN

A

Sustained ICP 20-25mmHg

48
Q

Intracranial HTN

Causes

A

Expanding tissue or fluid mass
Interference w/ CSF absorption
Excessive CSF production
Systemic disturbances promoting edema

49
Q

↑ICP S/S

A 
Headache
Nausea/vomiting
Papilledema
Focal neurological deficit
↓LOC
Seizures
Coma
CUSHING TRIAD
50
Q

CUSHING TRIAD

A
  1. HTN
  2. Bradycardia
  3. Irregular respirations
51
Q

Herniation Types

A
  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
Q

Most common herniation type _____

A

Cerebellar tonsils through foramen magnum

53
Q

Cerebellar Tonsillar S/S

A 
No specific clinical manifestations
Arches stiff neck
Paresthesias in shoulder
↓LOC
Respiration abnormalities
Pulse rate variations
54
Q

Uncal & Central S/S

A

↓LOC
Sluggish pupils or fixed & dilated
Cheyne-Stokes respirations
Decorticate → decerebate posturing

55
Q

Cingulate Gyrus S/S

A

Minimal known about S/S

56
Q

Transcalvarial S/S

A

Potential to occur during surgery

57
Q

Intracranial HTN

Treatment

A

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)

AS - N934 Advanced Principles II (18 decks)

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