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Neuro Dr. Mosier > Quiz 2 > Flashcards

Quiz 2 Flashcards

1
Q

Is ANS afferent, efferent, or both?

A

All Efferent

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2
Q

What does SNS do to…

  • CO
  • SVR
  • Lungs
  • Glucose
  • Pupils
  • Hunger and Procreation
A 
>CO
>SVR
Bronchodilation
>Serum glucose
Dilates pupils
Inhibits eating and procreating
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3
Q

The is the SNS also known as?

A

Thoracolumbar system: all neurons are in lateral horn of gray matter from T1-L2.

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4
Q

What neurotransmitter is released by most postganglionic “adrenergic” fibers in the SNS?

A

Norepinephrine (aka noradrenaline)

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5
Q

What does the Parasympathetic NS do to …

  • Eat and procreation
  • CO and SVR
  • Lungs
  • Pupils
A

Prepares body to eat and procreate.

< CO

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6
Q

What is the Parasympathetic VS also known as?

A

Craniosacral system bc all preganglionic neurons are in the brain stem or sacral levels of the spinal cord

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7
Q

What neurotransmitter is associated with Parasympathetic NS?

A

Acetylcholine at end organ as well as at preganglionic synapse “cholinergic”

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8
Q

T/F The PNS is continuously active while the SNS is active only when it is activated.

A

False, both systems are continuously active.

Inhibition of one branch allows the other branch to dominate

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9
Q

What is autonomic tone?

A

The balance between the SNS and PNS. In adults tone is dominated by the SNS. In children under 10, tone is dominated by the PNS.

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10
Q

__________ neurons leave CNS to synapse with the _____________ neurons, __________ neurons extends to their target ______.

A

Preganglionic, Postganglionic, postganglionic, organs.

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11
Q

(PNS fibers)The preganglionic neurons originate in the _________ or __________ and are relatively long.

A

Brain stem or sacral spinal cord.

The preganglionic neurons synapse with postganglionic neurons in ganglia near the effector organ or in the wall of the effector organ.

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12
Q

(SNS) Where do pregangliionic neurons originate from?

A

Lateral horn of gray matter from T1-L2.

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13
Q

Where do preganglionic neurons synapse with postganglionic neurons?

A

Sympathetic chain, or
Sympathetic ganglia, or
Adrenal Glands.

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14
Q

Presynaptic neurotransmitter is what and what is its target receptor?

A

Acetylcholine

Nicotinic receptor

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15
Q

What is the postsynaptic neurotransmitter of the SNS?

A

Norepinephrine

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16
Q

What are the receptors of the target organs in the SNS?

A

Alpha and Beta

Autonomic innervation of the Adrenal Glands in the exception

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17
Q

What is the post-synaptic neurotransmitter of the PNS?

A

Acetylcholine

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18
Q

What are the receptors of the target organs in the PNS?

A

Muscarinic

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19
Q

Where does myelination occur?

A

Preganglionic axons of SNS and PNS

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20
Q

What is the captain of the Autonomic Nervous System.

A

Hypothalamus

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21
Q

SNS is found where in the CNS?

A

T1-L2

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22
Q

PNS is found where in the CNS?

A

Cranial nerve VII, IX, X

S2-S4

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23
Q

Alpha-1 Adrenergic Receptors do what?

A 
Smooth muscle contraction
Vasoconstriction
Bronchoconstriction
Phenylephrine
NE>Epi
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24
Q

Alpha-2 Adrenergic Receptors do what?

A

Inhibits release of NE (Vasodilation)
Clonidine
Dexmetatomidine

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25
Q

Beta-1 Adrenergic Receptors do what?

A 
> HR (+chronotrope)
>AV node conduction (+dropotrope)
>contractility (+inotrope)
>diastolic relaxation (+lusitrope)
Isoproterenol (Isuprel) >EPI=NE
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26
Q

Beta-2 Adrenergic Receptors do what?

A 
Smooth muscle relaxation
Vasodilation
Bronchodilation
Uterine muscle relaxation
Isuprel>Epi>NE
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27
Q

Cholinergic Receptor (Nicotinic)

A

Autonomic Ganglia
Adrenal Medulla
(NMJ skeletal muscle)

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28
Q

Cholinergic Receptors (Muscarinic)

A

< HR

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29
Q

Spinal Cord Injury (SCI) occurs in what ways?

A

Injury to cord
Compression
Hemorrhage
Traumatic Vasospasm

All of there may result in ischemia/infarction

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30
Q

What should be avoided and contributes to secondary ischemic neurologic injury?

A

Systemic hypotension, and reduced spinal cord perfusion pressure.

Secondary injury may be exacerbated by hypotension due to hemorrhage or neurogenic shock, and can peak in 4-6 days.

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31
Q

FYI (Acute phase SCI)

Systemic vasodilation from loss of SNS tone occurs in increasingly severity with ascending levels of SCI above L2, leading to hypotension

A

FYI

Bradycardia complicates the picture with injuries above T6 due to compromise of SNS cardiac accelerator fibers.

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32
Q

FYI (Chronic Phase, Autonomic Hyperreflexia)

A neurologic disorder that occurs in association with resolution of spinal shock and a return of spinal cord reflexes.

A

Cutaneous or visceral stimulation (such as distention of the urinary bladder or rectum) below the level of the spinal cord transection initiates afferent impulses that are transmitted to the spinal cord at this level.

This stimulation elicits a reflex SNS response that results in intense generalized vasoconstriction and HTN.

Bradycardia occurs secondary to activation of baroreceptor reflexes.

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33
Q

Approximately 85% of pts w/ a spinal cord transection above the ___ dermatome will exhibits autonomic Hyperreflexia.

Incidence of AH during general anesthesia depends on the level of spinal cord transection.

A

T6

In contrast, it is difficult to elicit this reflex in pts with spinal cord transection below T10 dermatome.

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34
Q

How do you Tx Autonomic Hyperreflexia

A

PREVENTION: Neuralaxial block, SAB or Epidural

Direct Acting Vasodilators:
Nitroprusside
Nitroglycerine

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35
Q

Upper motor neuron injuries

A

Spastic paralysis
Not associated with muscle atrophy
Hyperreflexia
Cerebral Palsy is an example

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36
Q

Lower motor neuron injury (peripheral nerves)

A

Flaccid paralysis
Associated with muscle atrophy
Hyporeflexia

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37
Q

What does injury to L2 and above cause?

Lumbar injury (L1-S5)

A

Spastic paralysis of lower extremities

Injury causes bowel, bladder, and sexual dysfunction.

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38
Q

What deficits does thoracic injury (T1-T12) cause?

A

Same deficits as lumbar injury

T9-T12 injury causes loss of trunk of abd muscle control.

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39
Q

What type of injuries occur above T6?

A

Autonomic Dysreflexia
Neurogenic Shock: loss of vascular tone. T1-T4 are the cardiac accelerator fibers. Can cause disruption of body temperature regulation.

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40
Q

What type of injury occurs in cervical injuries (C1-C8)

C3-5
C1-4
C5 and above.

A

Same deficits as thoracic injury
C3-5: innervate diaphragm.
C1-4: quadriplegia, need for mechanical ventilation.
>C5: difficulty clearing secretions.

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41
Q

3 main components of the intracranial vault and what are their %’s?

A

CSF 10-15%
Brain 80-85%
Blood 5-10%

The adult cranium is a rigid, non-expandable structure that protects the brain.

42
Q

What is the normal ICP?

A

5-15 mmHg.

43
Q

Where is CSF produced and what does it surround?

A

Choroid Plexus in the cerebral ventricles.

Surrounds the brain and spinal cord

44
Q

How much CSF is produced in 24 hrs and what is the total volume of CSF?

A

500ccs / day

150cc total volume

45
Q

FYI

Is CSF is drained with VP shunts for chronic hydrocephalus

Is drained when there is acute increase in ICP with ventriculostomies

A

FYI

Can be drained during aortic aneurysm surgery to improve spinal cord perfusion.

46
Q

What > brain volume?

A
  • Tumor (Meningioma, Glioblastoma, Pituitary Tumor)

- Swelling (edema, HACE, ect..)

47
Q

What to use when acutely correcting cerebral edema?

A

Mannitol (osmotherapy)

Corticosteroids (lower ICP in vasogenic edema bc of their beneficial effect on the blood vessel.

48
Q

What effect does hyponatremia have on the brain?

A

Cerebral edema

Increased ICP

49
Q

What it Central pontine myelinolysis (CPM)?

A

The most common cause is overly rapid correction of low blood sodium levels.

50
Q

What does CPP =?

A

CPP = MAP -ICP or CVP, whichever is greater.

51
Q

How much of CO is CBF?

A

14% of CO
50cc/100g/min

Cortical (75-80%)
Subcortical (20-25%)

CBF is tightly coupled to CMRO2. Increased CMRO2 leads to increased CBF.

52
Q

T/F: The brain has no significant O2 reserve.

A

True

53
Q

What CBF cause:
Ischemia
Abnormal EEG (Infarct)
Irreversible Damage

A

< 30ml/100gm/min = Ischemia
< 20ml/100gm/min = Abnormal EEG
< 15ml/100gm/min = Irreversible damage

54
Q

What all controls CBF?

A 
Autoregulation
CPP
PaCO2
H+, HCO3 concentration
PaO2
Temperature
Neurogenic
55
Q

What MAP range is CBF constant?

A

60-160 mmHg

56
Q

What 4 things does loss of Autoregulation occur with?

A

Acidosis
Hypoxia
Trauma
Volatile anesthetics

57
Q

CBF changes by ~ __% for each 1 mmHg change in PaCO2.

A

4%

58
Q

PaCO2 is a potent cerebral ____________.

A

Vasodilator

59
Q

T/F: If there is a decrease in PaO2, while the PaCO2 remains normal, CBF is unaffected.

A

True

Once the PaO2 drops below 50 mmHg, there is an increase in CBF even in the presence of hypocapnia

An increase in PaO2 within the normal range results in only a slight increase in cerebral vascular resistance or vasoconstriction.

60
Q

T/F: decreased pH —> decreased CBF (vasoconstriction)

Increased pH —> increased CBF (vasoconstriction)

A

False
Acidosis —> increased CBF (Vasodilation)

Alkalosis __> decreased CBF (Vasoconstriction)

61
Q

What is the CMRO2?

A

3.5cc/100g/min

Cerebral blood flow and CMRO2 are coupled in the absence of pathology and or various anesthetic drugs.

62
Q

Temperature and CMRO2/CBF

FYI

There is a decrease in CBF with a decrease in body temp.

CBF changes 7% per C in core body temp

A

FYI

Hypothermia decreases both CBF and CMRO2 EEG isoelectric at 20 C

Hyperthermia increases both CBF and CMRO2

There is a 50% decrease in CMRO2 with an 8 C temperature decrease

63
Q

T/F: Dose dependent increase in CBF, due to vasodilation, with a dose dependent decrease in CMRO2. (Uncoupled CBF and CMRO2)

A

True

64
Q

T/F: Nitrous Oxide leads to decreased CBF and decreased CMRO2.

A

False, Nitrous Oxide leads to INCREASED CBF and INCREASED CMRO2

65
Q

T/F: IV Anesthetics (propofol/etomidate/thiopental) will DECREASE CBF and DECREASE CMRO2.

A

True

Ketamine is the exception, it will INCREASE CBF and CMRO2

66
Q

T/F: There is minimal effects of CBF and no affect on CMRO2 when using opioids.

A

False, there is no affect on CBF with minimal effects on CMRO2.

67
Q

T/F: Benzodizapines cause a minimal change in CBF with reduction in CMRO2

A

True

68
Q

Is there any significant effect on CBF or CMRO2 when using NMBDs?

A

No

Succinylcholine: CBF/CMRO2 controversial, text books say that it leads to increased CBF and CMRO2 due to increased spindle activity; however, studies have shown this is not clinically significant.

69
Q

Do Alpha and Beta agonists and antagonists have any effect on CBF with the BBB intact?

A

No

70
Q

All vasodilators ________ CBF.

SNP, NTG, Trimethephan

A

Increase

71
Q

What all is Electroencephalogram used for?

A
  • Intraop monitoring and diagnosis
  • CNS function and ischemia
  • Burst suppression
  • Depth of anesthesia
72
Q

A progressive reduction in CBF will produce a reliable _________ _______ in the EEG.

A

Pattern change

Loss of high frequency activity
Loss of power
Eventual progression to EEG silence

73
Q

Noninvasive cerebral oxygenation measurement using _________________ technology.

A

Near infrared spectroscopy (NIRS)

74
Q

When in NIRS used?

A

In any procedure where there may be vascular compromise to the brain from restriction of blood flow or patient positioning.

(Cerebral Oximetry)

75
Q

A decrease of ___% from NIRS baseline is significant.

A

20%

Cerebral oximetry

76
Q

What is the BIS monitor used for?

A

Used to measure depth of anesthesia.

77
Q 
What is the MIS index range?
0
20
40
60
80
100
A 
0   Flat Line EEG
20 Burst suppression
40 Deep Hypnotic State
60 General Anesthesia
80 Responds to loud commands or mild shaking
100 responds to normal voice / Awake
78
Q

What does _____ stand for?

SSEP
BAEP
VEP
MEP

A

Somatosensory Evoked Potential

Brainstem Auditory Evoked Potential

Visual Evoked Potential

Motor Evoked Potential

79
Q

What is the benefit of EP monitoring?

A

It identifies the deterioration of neuronal function, thus providing an opportunity to correct offending factors before they are irreversible

80
Q

What are 4 potential offending factors of EP signal?

A

Position of patient
Hypotension
Hypothermia
Surgical intervention

81
Q

SSEP is a signal that is detectable on EEG monitoring the promary somatosensory cortex, and is generated by a __________ electrical stimulation of a ________ sensory nerve, or a _______ nerve with a sensory pathway.

A

Cutaneous, peripheral, cranial

82
Q

SSEP is described by:

A

Polarity-direction of wave deflection

Latency-time required for a signal to be detected after a stimulus has been applied

83
Q

SSEP is quantified by:

A

Amplitude of the resulting signal

Latency of the resulting signal

84
Q

T/F: Ischemic change is more common than mechanical disruptive change

A

True

85
Q

Ischemia causes the amplitude of the signal to _______ and the latency of the signal to _______.

A

Decrease, Increase

86
Q

When are % changes of amplitude and latency clinically significant?

A

50% decrease in signal amplitude.

10% increase in signal latency.

87
Q

What does MEP evaluate?

A

Descending motor pathways

88
Q

MEP acts as a complement to ______, particularly in the setting of spine surgery.

A

SSEP

The two modalities provide information about the integrity of anatomically different areas of the spinal cord.

89
Q

MEP stimulus is applied in a transcranial fashion over the ________ ________.

A

Motor cortex

90
Q

The deflection, essentially an electromyographic signal, is then detected by electrode embedded in the _______ _______.

A

Muscle belly.

MEP

91
Q

FYI MEP

A

Transcranial electrical stimulus is usually delivered as a rapid train of four of more stimuli, the voltage is then adjusted to achieve adequate signal in both the upper and lower extremities.

92
Q

T/F: Inhalation agents including nitrous oxide generally have less depressant effects on EP monitoring than IV agents.

A

False, More depressant effects.

93
Q

Volatile anesthetic agents can have a profound influence on the ________ and _______ of EP.

A

Amplitude and latency

94
Q

Signals are obtainable under volatile anesthesia, but the anesthetic is typically kept at ___ -MAC doses to avoid degradation in quality.

A

Sub-MAC

95
Q

How can propofol and thiopental effect EP signals?

A

They can reduce the amplitude of all modalities of EP but do not obliterate them.

96
Q

What effect does Ketamine and Etomidate have with EP?

A

Can enhance the quality of SSEP signals in patients with a weak baseline, although the clinical significance remains unclear.

97
Q

How do opioids, benzo’s, and dexmedetomidine effect EP signals?

A

Negligible effects on recording of EP.

98
Q

What is the ideal anesthetic for monitoring MEP?

A

TIVA without nitrous oxide.

MEP are exquisitely sensitive to the depressant effects of inhalation anesthetics including nitrous oxide.

99
Q

Can monitoring of MEP occur with the use of paralytics?

A

NO?

100
Q

T/F: MEP is monitored continuously throughout the procedure.

A

False: MEP can cause patient movement, so MEP signals are typically obtained intermittently at points during surgery.

101
Q

A _____ _____ is mandatory to prevent injury to the tongue during transcranial stimulation.

A

Bite block

Neuro Dr. Mosier (2 decks)

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