EEG and ICP Flashcards

0
Q

What is normal cerebral blood flow? How much O2 does this deliver?

A

50 ml/min/100g tissue

Delivers 150 ml O2/min

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1
Q

What is the energy requirement of the brain?

A

3-5 ml O2/min/100g tissue

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2
Q

How much O2 does the brain extract?

A

35-50%

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3
Q

What is the equation of cerebral perfusion pressure?

A

CPP = MAP - ICP

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4
Q

Cerebral blood flow is impaired

A

Post trauma

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5
Q

Auto regulation of cerebral blood flow

A

Increases at the lower limit

Graph - as MAP increases, so does CBF… But plateaus in the middle…?

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6
Q

CBF is reduced by

A
Head injury
Intracranial hypertension
Hypotension
Vasospasm
Hyperventilation
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7
Q

Intracranial pressure can be directly monitored by

A

Subdural/subarachnoid bolts
Epidural transducers
Intraparenchymal fiber optic devices
Ventricular catheters

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8
Q

What is the Monroe-Kellie hypothesis?

A

The skull is a fixed volume and changes in one unit is balanced by the others.

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9
Q

What are the three components of the Monroe-Kellie hypothesis?

A

Blood, brain, cerebral spinal fluid

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10
Q

What are the percentages of the units that make up ICP?

A

Brain mass - 80%
Blood flow - 10%
CSF - 10%

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11
Q

T or F. ICP monitoring does not require a watertight fluid interface?

A

False

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12
Q

How is brain activity converted to a waveform?

A

Deformation of transducer membrane
Converted to electrical pulsations
Amplified
Displayed as a waveform

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13
Q

T or F. Catheter tip transducers need to be zeroed prior to insertion.

A

True

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14
Q

External transducers are zeroed

A

Anytime

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15
Q

Monitoring ICP is important in

A
Head injury
Poor grade subarachnoid hemorrhage
Intracerebral hematoma
Meningitis
Stroke
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16
Q

What are normal ICP values? Abnormal?

A

Normal: 7-15 mmHg
Abnormal: >20 mmHg

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17
Q

Aggressive management of ICP is indicated at what value?

A

> 25 mmHg

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18
Q

Elevated ICP causes

A

Herniation of internal and external brain
Distortion of cranial nerves and vital neurological centers
Impeded cerebral perfusion
Loss of CSF
Reduced venous blood flow

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19
Q

What are the pros of intraventricular drain and transducer?

A

Gold standard
ICP control by CSF draining
External zeroing

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20
Q

What are the cons of intraventricular drain and transducer?

A

Bleeding
Blockage
Infection

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21
Q

What is the correct placement of intraventricular catheters?

A

Lateral ventricle (frontal horn)

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22
Q

What is the position of the transducer?

A

Level with the meatus of the ear

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23
Q

What are the pros of the intraparenchymal pressure monitor?

A

Less infection risk
Less risk of hemorrhage
Excellent metro logical properties (less drift)

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24
What are the cons of the intraparenchymal pressure monitor?
Underestimates very high ICP | Drift becomes a problem after several days
25
What are contraindications for using intraparenchymal pressure monitoring?
Intracranial infections Coagulopathies Severe skull fracture CSF drainage necessary
26
What are the three phases of ICP waveforms?
P1: percussion wave (arterial pulsations) P2: rebound wave (intracranial compliance) P3: dichrotic wave (venous pulsations)
27
How is ICP managed?
Decrease brain water | Reduce CSF volume
28
What are ways to decrease brain water?
Hyperosmolar diuretics: mannitol w/ intact BBB Loop diuretics: Lasix Corticosteroids
29
What is the dosage of mannitol?
.25-1g per kg
30
CSF can be reduced from drainage by
Ventricular Lumbar subarachnoid Head elevation
31
Auto regulation is impaired by
Inhaled anesthetics | Direct acting vasodilators
32
What are examples of direct acting vasodilators?
``` Adenosine Prostacyclin Calcium channel blockers Nitroglycerin Nitroprusside ```
33
Transcranial Doppler Ultrasonography
Continuous or intermittent monitoring of CBF velocity
34
What is Transcranial Doppler Ultrasonography most useful for?
Vasospasm post subarachnoid hemorrhage
35
Does vasospasm cause increased or decreased CBF velocity?
Increased (due to Posseiulle's Law)
36
For TCD, what allows for monitoring independent of rising ICP?
ICA:MCA flow Ratio of internal carotid artery to middle cerebral artery flow
37
What is electroencephalogram monitoring?
Summation and recording of postsynaptic potentials from the pyramidal cells of the cerebral cortex Reflects the metabolic activity of the brain
38
EEG was first used by
Hans Berger in 1924
39
A tracing of voltage fluctuations versus time recorded from electrodes placed over scalp in a specific array
EEG
40
EEG
Represents fluctuating dendritic potentials from superficial cortical layers Required amplification
41
Part of the brain not sampled well by EEG
Deep parts of the brain
42
International 10-20 system of electrode placement
Electrodes spaces at ten or twenty percent of distances between specified anatomical landmarks
43
More than 21 electrodes can be added on an EEG to
Increase spatial resolution Record from specific areas Monitor electrical activity
44
Odd electrodes are placed Even electrodes are placed
On the left On the right hemisphere
45
Disadvantages of EEG
Detects cortical dysfunction, but not etiology Low sensitivity and low specificity Subject to electrical and physiologic artifacts Influenced by alertness, hypoglycemia, and drugs Small or deep lesions might not produce EEG abnormality Limited time sampling and spatial sampling
46
Indications for EEG
Craniotomy for cerebral aneurysm clipping when a temporary clip is used Carotid endarterectomy under GA Cardiopulmonary bypass Extra cranial intracranial bypass Pharmacological depression of brain for "cerebral protection"
47
Beta waves
13-30 Hz Awake and alert
48
Alpha waves
8-13 Hz Closed eyes, relaxed
49
Theta waves
4-7 Hz Young children Drowsiness in older children or adults
50
Delta waves
0-4 Hz Deep sleep, deep sedation
51
Suppression event
Very deep sedation, hypothermia, and ischemia
52
EEG artifact
``` Eye induced - blinks, movement, extra ocular muscle activity Gloss kinetic artifacts Poor grounding IV drips Body movement EKG artifact ```
53
Relaxation with eyes closed
Alpha waves predominance
54
Light anesthesia
Increase in beta | Decrease in alpha
55
Deepening of anesthesia
Increase in slow wave activity, delta 5 and theta 8
56
Cortical silence
Burst suppression
57
EEG is not
An output of the spinal cord or predictor of movement
58
Activation
High frequency Low voltage Light anesthesia Surgical stimulation
59
Depression
Low frequency High voltage Deep anesthesia Cerebral compromise
60
Most anesthetics produce
A biphasic pattern... Initial activation... Followed by dose dependent depression
61
Agents that activate EEG
``` Sub anesthetic inhalationals Low dose barbs and benzos Small doses of etomidate N2O Ketamine ```
62
Agents that depress EEG
1-2 MAC gases Barbs/propofol/etomidate Narcotics - dose dependent
63
Other things that influence - activate
Mild hypercapnia Surgical stimulation Early hypoxia
64
Other things that depress
Hypocapnia Hypothermia Late hypoxia