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Apex > Brain > Flashcards

Brain Flashcards

1
Q

What is the most common cause of perioperative vision loss?

A

Ischemic optic neuropathy

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2
Q

What is the most common perioperative eye complication?

A

corneal abrasion

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3
Q

When does vision loss from ION occur?

A

Usually within 24-48 hours of surgery

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4
Q

Is ION painful?

A

No, it is not associated with pain

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5
Q

What are the procedural risk factors for developing ION?

A

Prone position
Wilson frame
Long anesthesia
Blood loss
Insufficient colloids with resuscitation
Hypotension

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6
Q

Which procedures carry the highest risk for ION?

A

Spinal surgery
CPB
Radical neck dissection

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7
Q

What is CRAO?

A

Central Retinal Artery Occlusion

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8
Q

What’s the difference between ION and CRAO?

A

ION is a problem with the nerve ischemia, usually due to venous congestion

CRAO is a problem with blood vessel occlusion

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9
Q

What are the risk factors for CRAO?

A

Horse shoe headrest
Using nitrous after retinal bubble placement
Embolism from CPB

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10
Q

Most brain tumors arise from _______ cells

A

glial

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11
Q

What is the role of astrocytes?

A

the most abundant type of glial cell
They regulate the metabolic environment and repair neurons after injury

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12
Q

What is the role of ependymal cells?

A

CSF production

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13
Q

What is the role of oligodendrocytes?

A

Form the myelin sheath in the CNS

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14
Q

What is the role of Schwann cells?

A

Form the myelin sheath in the PNS

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15
Q

What is the role of microglia?

A

Act as macrophages and phagocytize neuronal debris

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16
Q

What is Broca’s area?

A

Frontal lobe
motor control of speech

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17
Q

What is Wernicke’s area?

A

Temporal lobe
Understanding of speech

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18
Q

What structures are located in the diencephalon?

A
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19
Q
A
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20
Q

What cranial nerve is most likely to be compressed by a pituitary tumor?

A

Optic

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21
Q

What is the primary site of CSF production?

A

Choroid plexus

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22
Q

What is the primary site of CSF reabsorption?

A

Arachnoid villi

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23
Q

The BBB is composed of ______ junctions

A

tight junctions

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24
Q

What is approximate normal CSF volume?

A

About 150 ml

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25
Q

How quickly is CSF produced?

A

About 30ml/hr

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26
Q

Where in the brain is the BBB NOT present?

A

Chemoreceptor Trigger Zone
Hypothalamus
Pineal Gland
Posterior Pituitary
Choroid Plexus

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27
Q

What is the calculation for cerebral blood flow?

A
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28
Q

What percent of the cardiac output goes to the brain?

A

15%

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29
Q

What is a normal CMRO2?

A

3.0-3.8 ml/O2/100g Tissue

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30
Q

What percentage of brain oxygen is used for electrical activity?

A

60%

The other 40% maintains cellular integrity

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31
Q

How does temperature impact CMRO2?

A

Decreases 7% for every 1 degree C drop

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32
Q

CMRO2 is decreased by:

A
  • hypothermia
  • halogenated anesth.
  • propofol
  • etomidate
  • barbiturates
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33
Q

CMRO2 is increased by:

A
  • hyperthermia
  • ketamine
  • nitrous
  • seizures
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34
Q

What is the calculation for cerebral perfusion pressure?

A
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35
Q

Cerebral perfusion is generally autoregulated. What things abolish cerebral autoregulation?

A
  • Tumors
  • Trauma
  • Volatile anesthetics
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36
Q

The brain is able to autoregulated when the CPP is between _______ and ______

A

50 to 150 mmHg

37
Q

CPP autoregulation is generally maintained when the MAP is between ______ and _______

A

60 - 160

38
Q

Which patients are at greatest risk of developing cerebral ischemia intraop?

A

Patients with chronic hypertension

39
Q

For every 1mmHg increase in PaCO2, CBF will:

A

increase by 1-2 ml/100g tissue

40
Q

For every 1mmHg decrease in PaCO2, CBF will:

A

decrease by 1-2 ml/100g tissue

41
Q

Maximal cerebral vasodilation occurs at a PaCO2 of:

A

80-100 mmHg

42
Q

Maximal cerebral vasoconstriction occurs at a PaCO2 of:

A

~ 25 mmHg

43
Q

The relationship between CBF and PaCO2 is:

A

linear

44
Q

Will a patient with metabolic acidosis display changes in CBF?

A

NO!

Cerebral response is based on H+ ions in the CSF, but only CO2 can cross the BBB. Once across, it dissociates back into H+ ions

45
Q

What is the Robinhood effect?

A

Using hyperventilation to increase cerebral vasoconstriction in healthy tissue to cause increased perfusion to ischemic tissue (which is permanently vasodilated). Nice in theory, but not supported by evidence

46
Q

How does PaO2 impact CBF?

A
47
Q

How does the CVP impact ICP?

A
48
Q

What conditions impair venous drainage from the brain?

A
49
Q

What is a normal ICP?

A

5-15 mmHg

50
Q

Intracranial HTN occurs when ICP exceeds:

A

20 mmHg

51
Q

Cushing’s triad includes:

A

Hypertension
Bradycardia
Irregular Respirations

52
Q

The most common site of herniation is:

A

at the temporal uncus

53
Q

Why does herniation result in fixed and dilated pupils?

A

herniation applies pressure to CN III (Occulomotor)

54
Q

What is pseudotumor cerebri?

A

a condition where ICP is reduced for no apparent reason

55
Q

Which fluids should be avoided in patients with increased ICP?

A

Anything with Glucose

In ischemic settings, any extra glucose in the brain is converted to lactic acid, making things worse

56
Q
A
57
Q

Anterior circulation in the brain is supplied by:

A
58
Q

Posterior circulation of the brain is supplied by:

A
59
Q

Venous blood from the cerebral cortex and cerebellum drains via:

A

The superior sagittal sinus and the dural sinuses

60
Q

Venous blood from the basal brain structures drains via:

A

the inferior sagittal sinus, the vein of Galen, and the straight sinuses

61
Q

Both of the brain’s venous pathways converge at _______ and exit the brain via ________

A

the confluence of the sinuses

the jugular veins

62
Q

tPA must be given within _______ hours of an inschemic stroke

A

4.5 hours

63
Q

In patients with ischemic stroke, what is the goal BP?

A

Their BP will likely be high in order to maintain CPP

Just keep it below 185/110

64
Q

What is the leading cause of morbidity and mortality after a SAH?

A

Vasospasm

65
Q

What is the best prevention of vasospasm in patients with SAH?

A

The three H’s:

Hemodilution
Hypervolemia
Hypertension

66
Q

What is the most common cause of SAH?

A

Aneurysm rupture, usually in the circle of willis

67
Q

Why does Nimodipine reduce morbidity from vasospasm?

A

It does NOT relieve the spasm,

BUT it does increase collateral flow

68
Q

When a venous aneurysm ruptures, bleeding usually occurs in:

A

the subdural space

69
Q

When an arterial aneurysm ruptures, bleeding usually occurs in:

A

the subarachnoid space

70
Q

What is the treatment for SAH?

A

Endovascular coiling or clipping

71
Q

What are the anesthesia goals when performing an aneurysm clipping or coiling?

A

Maintain SBP between 120 and 150

72
Q

Patients with SAH are at risk for _________ syndrome

A

Cerebral salt wasting

73
Q

What is Cerebral Salt wasting syndrome?

A

The brain releases natriuretic peptides, leading to sodium wasting by the kidney.
Causes hyponatremia and hypovolemia

Unlike SIADH, it does not cause hypervolemia

74
Q

What are the two most common signs of cerebral vasospasm?

A

New neurological deficit
Altered LOC

75
Q

When is cerebral vasospasm most likely to occur?

A

Within 4-9 days of the SAH

76
Q

What are anesthetic considerations in the patient with TBI?

A

CPP> 70
Hypertonic saline
No steroids
No nitrous
No albumin
No glucose

77
Q

Status Epilepticus is defined as:

A

Seizure > 30 min

OR

2 grand mal seizures without regaining consciousness in between

78
Q

What are signs of a seizure under general anesthesia?

A

Tachycardia
Hypertension
Increased etCO2

79
Q

Which IV anesthetic should be avoided in patients with seizures?

A

Ketamine

80
Q

Which three IV anesthetics increase EEG activity and are used to locate seizure foci?

A

Etomidate
Methohexital
Alfentanil

81
Q

How does carbamazepine impact hepatic enzymes?

A

Induces

82
Q

How does valproic acid impact hepatic enzymes?

A

Inhibits

83
Q

How does phenytoin impact hepatic enzymes?

A

Induces

84
Q

How does gabapentin impact hepatic enzymes?

A

It doesn’t. It’s excreted unchanged by the kidneys

85
Q

How does hepatic enzyme induction impact NMBA action?

A

It causes resistance, because NMBAs are being metabolized at a higher rate

86
Q

What is the MOA of Valproic Acid, Carbamazepine, and Phenytoin?

A

Block voltage gated sodium channels, leading to membrane stabilization

87
Q

Which anticonvulsant can cause purple glove syndrome?

A

Phenytoin, if it extravasates

88
Q

Patients being treated for Alzheimer’s may have increased sensitivity to which NMBA?

A

They are usually taking cholinesterase inhibitors, which slows the metabolism of succinylcholine, mivacurium, and ester LAs

Apex (46 decks)

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