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NSCC 7520 Critical Care Theory 4 > Neuro > Flashcards

Neuro Flashcards

1
Q

What makes up the CNS

A

brain
spinal cord
CN I and II

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2
Q

what do sensory neurons inervate

A 
skin
muscle 
joints
viscera
provide sensory info to CNS
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3
Q

what are the nerves of the PNS separated into

A

sensory

motor

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4
Q

what do motor nerves innervate

A 
skeletal muscle (somatic)
and ANS
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5
Q

what are the two components of the autonomic nervous system

A

sympathetic

parasympathetic

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6
Q

T or F the SNS and PNS work together

A

false

they work in opposition to one another

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7
Q

how many cranial nerves are there? how many spinal nerves are there

A

12

13

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8
Q

are the cranial and spinal nerves part of the CNS or PNS?

A

predominantly PNS

exception: CN I and II are part of CNS

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9
Q

What is cranial nerve II? what is it’s function?

A

Optic (part of the CNS)

Function: vision, detection of light

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10
Q

How do we test CN II

A

read eye chart
detect objects/movement from corner of eyes
shine light into pupil

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11
Q

what is CN III? what is it’s fn?

A

oculomotor
Function: eye movement (up, down and in)
pupil dilation and constriction
raise eyelids

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12
Q

how do we test CN III

A

ask person to follow moving target
pupil response to light
check for ptsosis (drooping)

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13
Q

What is CN IX? what is its function?

A

Glossopharyngeal

Function: swallowing, gag reflex, speech

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14
Q

What is cranial nerve X? what is its fn?

A

vagus

swallowing, gag reflex and speech; control of muscle in internal organs

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15
Q

How do you test CN IX and X

A

ask person to swallow
say aah to check movement
have pt speak and cough - ability to protect airway

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16
Q

are reflexes part of the CNS or PNS

A

PNS

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17
Q

do reflexes involve the brain

A

no

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18
Q

what are the 5 components of a reflex arc

A

receptor - sensory fibers sensitive to stimulus

sensory neuron- afferent neuron relays impulse via posterior/dorsal root of spinal cord

interneuron - connecting center within CNS

Motor neuron - efferent neuron that relays impulse via anterior/ventral root of spinal cord to effector organ

effector- specific organ that responds

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19
Q

What is the brainstem composed of (5)

A 
midbrain
pons
medulla
reticular formation
RAS
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20
Q

What is responsible for involuntary actions such as HR, RR, BP

A

brainstem

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21
Q

what is the area where the motor fibers cross? What kind of findings do we see below this area

A

brainstem

changes on contralateral side

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22
Q

What is the pons

A

relay center btw cerebellum and cerebrum

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23
Q

where does the brainstem connect to the spinal cord

A

through the foramen magnum to become the medulla

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24
Q

what makes up the cerebrum

A 
cerebral hemispheres
diencephalon 
thalamus
hypothalamus
basal ganglia
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25
Q

what makes up the diencephalon

A

thalamus
hypothalamus
basal ganglia

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26
Q

Where are CN I and II rooted

A

cerebrum

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27
Q

What are the 4 lobes of the brain

A

Frontal
parietal
temporal
occipital

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28
Q

What is the fn of the frontal lobe

A 
high level cognitive fn
personality
behavior
emotions
motor control of speech (Broccas area)
control of voluntary motor fxn
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29
Q

what is the fn of the parietal lobe

A

interprets sensory info
position
visuospatial processing

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30
Q

what is the fn of the temporal lobe

A 
auditory (Wernicke's area)
smell
complex stimuli (e.g. faces)
memory
speech
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31
Q

what is the fn of the occiptal lobe

A

visual perception
smooth eye movement
sight

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32
Q

What is the fn of the cerebellum

A

control of fine movement
coordination and balance
proprioception

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33
Q

What is the name of the fold of dura that separates cerebellum and occipital lobe? What area of the brain is this located?

A

tentorium cerebella –> located in cerebellum

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34
Q

What is the tentorium cerebella

A

fold of dura that separates cerebellum and occipital lobe

encloses process/plate of skull

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35
Q

what CN can be affected by the tentorium cerebella

A

III; if ICP increases it can cause the brain to herniate through the tentorium as it is a hard structure putting pressure on CN III

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36
Q

Where is the reticular formation located? What is its function

A

core brainstem

sensation, movement, reflexive behaviors, consciousness

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37
Q

Where is the reticular activating system located

A

located in the ascending reticular formation

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38
Q

what is the function of the reticular activating system in the brainstem

A

sleep and wakefullness

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39
Q

what is the fn of the reticular activing system in the thalamic region

A

cognition and attention

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40
Q

what is the thalamus part of? where is it located

A

diencephalon

below cerebral cortex - mass of gray matter

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41
Q

what is the fn of the thalamus

A

gatekeeper for motor/sensory stimuli

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42
Q

what is the hypothalamus part of? where is it located

A

diencephalon

response to emotion
maintain homeostasis via ANS and endocrine
temp regulation
food/water intake
hormone release
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43
Q

Where is the basal ganglia located? what does it do?

A

white matter of cerebral hemispheres

integrates movement and involuntary motor fn

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44
Q

What bones are frequently involved in basal skull #s

A

sphenoid, ethmoid, temporal bones

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45
Q

what are the three layers of the meninges from innermost to outmost

A

Pia mater
Arachnoid mater
Dura mater

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46
Q

T or F the Pia mater adheres to the brain

A

yes

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47
Q

what are 2 characteristics of pia mater

A

embedded in brain structure and ventricles

rich in small blood vessels

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48
Q

what is the fn of pia mater

A

production of CSF in choroid plexus in lateral 3rd and 4th ventricles

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49
Q

where is the subarachnoid space? what does is its purpose

A

btw pia mater and arachnoid mater

contains CSF - cushins/shock absorption

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50
Q

What are 3 characteristics of arachnoid mater

A

delicate, fragile membrane thin spider like
contains vascular supply
looseley surrpound brain btwn pia and dura

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51
Q

what is the fn of arachnoid mater

A

absorption of CSF via arachnoid villi into venous sinuses

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52
Q

what type of blood flow occurs in a subarachnoid hemorrhage? where does it occur

A

arterial

subarachnoid space

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53
Q

what type of blood flow is involved in a subdural hematoma

A

venous

subdural space

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54
Q

what are 3 characteristics fo dura mater

A

forms tentorium
double-layered
tough fibrous membrane

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55
Q

what is the fn of dura mater

A

support nerves and vasculature

venous sinus for CSF drainage

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56
Q

where is the epidural space

A

space btwn skull and dura mater

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57
Q

what type of blood is involved in an epidural hemorrhage

A

arterial

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58
Q

what is CSF

A

cerebral spinal fluid

clear colorless solution that fills ventricles and subarachnoid space of spinal cord

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59
Q

what is the purpose of CSF

A

acts as shock absorber against injury

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60
Q

where is CSF produced

A

choroid plexus in 3rd and 4th ventricle

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61
Q

how much CSF is produced a day

A

~500 mL

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62
Q

what is the amount of CSF circulating in the ventricle system

A

125-150 mL

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63
Q

What is monro’s Foramen

A

small opening that connects lateral/3rd and 4th ventricle

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64
Q

what is munro’s foramen used for

A

landmark for levelling EVDs

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65
Q

where is the common lumbar puncture site

A

btw L4 and L5

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66
Q

What is the BBB

A

network of endothelial cells and astrocytes that prevent substances from reaching the brain

endothelial cells which for tight junctions w astrocytes

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67
Q

What does the BBB do

A

regulates transport of nutrients, ions, water and waste through selective permeability

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68
Q

what must drugs be to pass the BBB

A

lipid soluble

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69
Q

what is the BBB very permeable to

A 
H2O
O2
CO2
glucose
lipid soluble compounds
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70
Q

T or F blood flow rates do not directly correspond to metabolism of cerebral tissue

A

false
blood flow rates respond directly to metabolsim of cerebral tissu - parts that are the busiest receive the most blood flow

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71
Q

what percentage of CO does the brain receive

A

~20%

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72
Q

Does the brain have a reserve of O2 or glucose

A

no

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73
Q

where does cerebral blood supply stem from

A

aortic arch

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74
Q

cerebral blood supply stems from the aoritc arch as pair vessels and branches into what

A

anterior circulation via L & R carotid arteries

posterior circulation via L and R vertebral arteries

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75
Q

The L and R carotid arteries bifurcate into what

A

external and internal carotid arteries

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76
Q

what do the external carotids supply

A

face
scalp
extra-cranial structures

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77
Q

what do the internal carotids supply

A

most of the brain

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78
Q

anterior circulation provides what percentage of blood flow to cerebral hemisphers

A

80%

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79
Q

What is anterior circulation comprised of

A

rt and left carotids which bifurcate into the internal and external carotids

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80
Q

where does posterior circulation originate from

A

subclavian artery

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81
Q

what does the subclavian artery lead into

A

R & L vertebral artery

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82
Q

what are the components of the posterior circulation

A

subclavian –> L&R vertebral –> basilar artery –> two main posterior inferior cerebellar arteries (PICA)

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83
Q

What does posterior circulation supply

A

cerebellum, brainstem, spinal cord, occipital/temporal lobes, posterior diencephalon

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84
Q

what blood vessels unite at the circle of willis

A

branches of basilar and internal carotid arteries

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85
Q

What arteries make up the circle of willis

A

2 anterior cerebral arteries - connect by anterior communicating artery

middle cerebral arteries - connect directly to anterior and posterior cerebral arteries (via communicating arteries)

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86
Q

What is the circle of Willis?

A

interconnecting network allowing blood to circulate btw hemispheres and from anterior/posterior parts of the brain

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87
Q

T or F the cirlce of willis allows for some degree of collateral circulation if one of the vessels is occluded

A

T

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88
Q

What percentage of people have a complete circle of willis

A

~50%

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89
Q

which cerebral artery is most common for ischemic strokes

A

middle cerebral artery

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90
Q

where is the most common sites of aneurysms in the brain

A

circle of willis occur at the bifurcations

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91
Q

when you are testing when you check pupillary response

A

focus of injury and CN III oculomotor

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92
Q

what is normal pupil size and reaction

A

2-6mm and brisk

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93
Q

what is the point in the medulla where the motor fibers cross

A

decussation of pyramids

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94
Q

what CN is involved in pupil reaction to light

A

II optic

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95
Q

what CN is involed in pupil restriction

A

III oculomotor

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96
Q

do SCI patients lose parasympathetic responses below their level of injury

A

no they lose sympathetic

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97
Q

what 3 bones are typically involved in basal skull #s

A

sphenoid, ethmoid and temporal bones

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98
Q

the internal carotid artery branches into what vessels

A

anterior communicating artery
middle cerebral artery
posterior communicating artery

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99
Q

The L&R vertebral arteries unite to form what

A

basilar artery

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100
Q

the basilar re-subdivides into which vessels

A

posterior inferior cerebellar arteries (PICAS)

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101
Q

what does posterior circulation supply

A 
cerebellum
occipital lobe
part of the temporal lobes
posterior diencephalon
spinal cord and brain stem
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102
Q

what are the 5 components of a neuro assesment

A 
pts story
LOC
CN
peripheral nerves - motor strength 
VS
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103
Q

What does GCS access

A

LOC

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104
Q

what is the max score you can get for eye opening

A

4

spont, voice, pain, none

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105
Q

what is the max score for verbal

A

5, ox3, confused, incomprehensible words, sounds, none

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106
Q

what is the max score for motor

A

6, obeys, localizes, normal flexion, abnormal flexion, abnormal extension, none

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107
Q

What would you chart if there eyes were swollen shut for GCS

A

E1C

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108
Q

what is the first sign of neurological deterioration

A

any decrease in LOC

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109
Q

which CN are vulnerable to inc ICP

A

CN II and III - why we check them frequently

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110
Q

what is the term used to describe the same side

A

ipsilateral

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111
Q

what will you see regarding pupil assessment if there is increased ICP

A

dilated non-reactive pupil same side

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112
Q

what does consensual mean regarding pupil assesment

A

both eyes constrict

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113
Q

what does a patient need to be able to do to test for accomidation

A

follow commands

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114
Q

What nerves are responsible for cough and gag

A

CN IX glossopharyngeal and X vagus

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115
Q

does everyone have a gag reflex

A

no

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116
Q

if a pt is unable to cough what does this indicate

A

they are unable to protect their own airway

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117
Q

what CN are tested for corneal reflex

A

CN V (trigeminal) and CN VII (facial)

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118
Q

how do you test corneal reflex

A

manually open eye and touch eyelashes with corner of gauze or Kleenex - look for blinking

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119
Q

where does the spinal cord finish and and become the cauda equina

A

L@

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120
Q

how far do the meingeal layers continue to on the spine

A

S2

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121
Q

Does CSF circulate below spinal cord

A

yes

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122
Q

where is a common LP site

A

L4/L5

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123
Q

what are dermatones used for

A

to determine where injury is based on what sensory input is collected form which spinal cord level

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124
Q

strength changes are seen on what side from the injury

A

contralteral

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125
Q

T or F pupil changes are contralteral to injury and strength changes are ipsilateral

A

false
strength contralateral
pupil ipsilateral

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126
Q

what must you see a patient do in order to document “localizes to pain”

A

pt must lift hand and CROSS the midline of their body

OR rise above clavicle

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127
Q

if a patient does not localize to pain what do you do next

A

stand on the OPPOSITE side, apply nail bed presure

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128
Q

if a patient is trying to pull out their IV/ETT/NG what can you document for their GCS

A

localizing

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129
Q

What is cheyne-stokes breathing

A

cyclical episodes of apnea and hyperventilation

130
Q

what is a common manifestation of intracranial injury regarding BP

A

systemic hypertenion

131
Q

what can happen regarding autoregulation in intracranial injury? what does this result in?

A

loss of autoregulation

As BP increases CBF and cerebral blood volume increases causing increase in ICP

132
Q

What are the 3 components of cushing’s triad

A 
systolic HTN (wide pulse pressure)
bradycardia
abnormal resps (bradypnea)
133
Q

what is a stroke

A

sudden loss of brain fn lasting longer than 24 hours

134
Q

what causes a stroke (2 types of stroke)

A

Ischemic - interruption of blood flow to the brain

hemorrhagic - rupture of blood vessels in the brain

135
Q

what are 7 stroke signs and symptoms

A 
HA
blurred vision/visual disturbances
dizziness
sudden confusion
difficulty speaking
facial droop
muscle weakness, especially one sided
136
Q

how do you differentiate between the two types of stroke

A

non-con CT

137
Q

What is the penumbra

A

zone of ischemic tissue surrounding infarcted area

138
Q

are we able to salvage the penumbra tissue

A

yes with treatment

139
Q

What type of stroke is more common

A

ischemic 87%

140
Q

if stroke symptoms less than 24 hours what is it termed

A

TIA

141
Q

what are the two types of ischemic stroke

A

embolic (20%) - clot from elsewhere in the body

thrombotic (80%) - build up of plaque in brain

142
Q

which is most common embolic or thrombotic

A

thrombotic

143
Q

what is the most common cause of embolic stroke

A

afib

144
Q

what are the two types of hemorrhagic stroke

A

intracerebral (10%)

Subarachnoid (3%)

145
Q

where is a subarachnoid hemorrhagic stroke located

A

subarachnoid space btw arachnoid mater and pia mater

146
Q

what can cause hemorrhagic stroke

A

trauma or structural malfomrations of blood vessels

147
Q

what are two structural malformations fo blood vessels that can result in hemorrhagic stroke

A 
aneurysms 
arteriovenous malformations (AVMs)
148
Q

what are aneurysms

A

weak area of vessel bulges with blood and can burst

149
Q

what are arteriovenous malfomations (AVM(

A

tangle of thin walled veins and arteries

congenital

150
Q

what is the most common cause for rupture of AVM

A

uncontrolled HTN

151
Q

what is the most common type of aneurysm

A

saccular

152
Q

how long is the window of time for fibrinolytic therapy (rtPA)

A

<4.5 hours of onset of symptoms

153
Q

what is the dosing for rtPA

A

0.9 mg/kg (max 90mg)

10% as a bolus, rest over an hour

154
Q

what meds cant be given with tpa

A

no asa, heparin, warfarin or any antithrombotic or antiplatelet

155
Q

what are contraindications for rtPA

A 
head trauam/stroke < 3months
AVM
aneurysm
recent intracranial or spinal sx 
active bleeding
BP >185/110
siezures
ICH < 6months
156
Q

how often are VS done during tPA administration

A

q15mins x 1 hour
q 30 x 7 hrs
q8hr

157
Q

how often are neuro checks done during tPA adminstration

A

q30 during infusion

q1hr x 8 hrs

158
Q

once a pts received tPA what must their BP be kept at

A

<180/105

159
Q

what is the pre-op/rtPA blood pressure control for stroke

A

<220/110 ischemic want high BP to optimize perfusion

160
Q

what is the BP parameters pre-op/rtPA for SAH

A

SBP ~140

lower BP to control bleeding

161
Q

post op/rtPA what are the difference in blood pressure monitoring for stroke vs SAH

A

stroke <180/105 control BP
SAH MAP >80
SBP 150-180

162
Q

what are 3 things that influence cerebral oxygen supply

A

Cerebral perfusion pressure CPP
cerebral vascular resistance CVR
Cerebral blood flow CBF

163
Q

How is CBF calculated

A

CPP/CVR

164
Q

What is CPP

A

cerebral perfusion pressure

blood pressure available to perfuse the brain

165
Q

what is ICP

A

intracranial pressure

pressure inside the head that MAP must overcome to provide cerebral perfusion

166
Q

how do you calculate CPP? What is the normal range?

A

MAP - ICP

60-100 mmHg

167
Q

What must the MAP do in terms of ICP to perfuse brain

A

overcome ICP

168
Q

if CPP is too high what can that cause

A

cerebral hyperperfusion Inc ICP

169
Q

if CPP is too low what can happen

A

brain hypoxia

170
Q

what is normal ICP

A

0-15 mmHg

171
Q

can brain hypoxia occur despite adequate CPP

A

yes so must consider CVR

172
Q

What is CVR

A

amt of resistance created by cerebral vessels to blood flow

173
Q

what incluences CVR

A

vessel diameter

ICP

174
Q

what is vessel diameter influenced by in the brain

A

autoregulation and cereebral metabolic demand

175
Q

what is autoregulation

A

regulatory mechanism that ensures constant CBF despite changes in arterial pressure

176
Q

how does autoregulation work

A

changes vessel size dependent on MAP
constrict when MAP >100
dilate when MAP <60

177
Q

what are the 3 conditions required for autoregulation to work

A

CPP >60
ICP <30
MAP 60-150

178
Q

what are the two theories on how atuoregulation works

A

biophysical - controlled by precence of stretch receptors in blood vessels triggered by CBF

chemical
CO2 and H+ ions cause vasodiation
O2 levels PaO2 <50 causes vasodialtion

179
Q

what can happen to autoregulation in TBI patients

A

they can lose autoregulation

CBP will increase with inc MAP and cause inc ICP

180
Q

what is a common symptom in SAH

A

thunderclap HA worst HA of your life

181
Q

what are 5 risk factors for SAH

A 
pre-menopausal women
smokers
undiagnosed HTN
genetics
previous SAH
182
Q

what grading scale is used in dx of SAH? how many grades are there?

A

Hunt & Hess Grading Scale

5

183
Q

what are the survival percentages for each grade for SAH

A 
1 - 70%
2 - 60%
3 - 50%
4 - 20%
5 - 10%
184
Q

What grade of SAH would a patient presenting in deep coma, decerberate rigidity and moribound appearance have

A

5

185
Q

what grade of SAH would a patient be if they precented with drowsiness, confusion and mild focal deficits be? do they have a good prognosis

A

grade 3

yes

186
Q

what grades can go to the OR for clip or coil

A

2 and 3

187
Q

what grade of SAH would a pt be if they had minimal or no bleed, slight HA and no neuro deficits

A

grade 1 - 70%

188
Q

what grade SAH would a pt who is in a stupor with mild-to-severe hemiparesis and poss early decerbrate rigidity be

A

grade 4 -20%

189
Q

what grade of SAH would a pt be if they had a mild bleed, moderate to severe HA, awake and alert, some nuchal ridigity

A

2 60% good prognosis

190
Q

what are two types of imaing used for SAH dx

A

CT scan

cerebral angiography

191
Q

what are 2 surgical interventions for brain aneurysms

A

clip or coil

192
Q

What are the 3 components of the cranial vault

A

brain (80%)
blood (10%)
csf (10%)

193
Q

what is the monroe-kellie hypothesis

A

ICP = cerebral blood volume + brain tissue + CSF volume
closed box
if one component increases then one or both of the other components must decrease in volume

194
Q

if there is an increase in one of the 3 compnents of the cranial vault what are 6 compensation mechanisms

A

displacement of CSF down spinal cord to venous system
decreased CSF production (timely)
insertion of a drain to remove CSF
vasoconstriction of cerebral vasculature
surgery to remove blood clot or tumor
displacement of brain itself (herniation)

195
Q

what does mannitol do? when is it used

A

reduces cerebral edema

osmotic diuretic pulls H2O out of the brain tissue reducing brain volume

196
Q

what are 4 examples of increaesd brain volume

A

tumors
hematomas
abcesses
cerebral edema

197
Q

What are 3 examples of things that can obstruct CSF circulation

A

spina bifida
tumors
pus/abcess

198
Q

what can cause a block of CSF reabsorption

A

SAH

199
Q

is it possible to cause an overproduction of CSF

A

yes but it is rare

200
Q

what are 4 ways blood volume can be increased

A

vasodilation
elevated PaCO2/acidosis
loss of autoregulation
venous outflow obstruction

201
Q

what are 3 ways venous outflow obstruction can occur

A

ETT ties
PEEP
position

202
Q

How would you manage increased brain volume causing inc ICP

A

mannitol

203
Q

how would you manage increased blood volume causing inc ICP

A

sedation/analgesia
HOB @ 30
reduce stimulation

204
Q

how would you manage increased CSF causing inc ICP

A

EVD

205
Q

what must you be mindful of regarding PaO2 for TBI pts

A

PEEP affects ICP

decide between PEEP and FiO2

206
Q

What is meant by good intracranial compliance

A

pressure increases in the intracranial vault and there is no change in ICP
e.g. cough in healthy person or slow growing tumor

207
Q

what is meant by poor intracranial compliance

A

small pressure is added and there is alarge change in ICP

208
Q

what are 4 nursing responsibilities pre-op SAH

A

BP control minimize further bleeding
ensure adequate CVP and MAP - support perfusion
provide quiet environment/reduce stimulus
manage pain

209
Q

Do we expect a fever to occur in SAH pts pre op? why or why not?

A

yes, blood irritates subarachnoid space

210
Q

What must pts BP be maintained at post-op SAH

A

higher BP SBP 150-180

MAP >80 to maintain CPP

211
Q

What medication is commonly given post op SAH? why?

A

statins - improve endothelial fn
increase endothelial nitric oxide synthase
helps prevent vasospasm

212
Q

what is important to remember regarding ventilation in SAH patients

A

avoid excessive or inadequate ventilation to avoid changes in PaCO2

213
Q

T or F magnesium may be given for 10 days in SAH pts post op

A

T

214
Q

do you want to excessively sedate post op SAH pts

A

No, avoid it

215
Q

what do you want to do with HOB for SAH pts

A

up to promote venous drainage

216
Q

What are 3 complications of surgically treated aneurysms

A

seizures
hydrocephalus
vasospasm

217
Q

when does vasospasm occur post surgery for SAH

A

3-12 days after

218
Q

what is vasospasm

A

narrowing of lumen of cerebral arteries in response to blood clots
caused by chemical mechanism

219
Q

what is the most common complication of surgically treated aneurysms

A

vasospasm

220
Q

why do seizures occur as a complication of surgically treated aneurysms

A

irritation from blood in subarachnoid space causing increased ICP

221
Q

why does hydrocephalus occur as a complication of surgically treated aneurysms

A

d/t blocking of CSF reabsorption by arachnoid vili causing increased ICP

222
Q

T or F blood mixing in the CSF can impair reabsoption of CSF in the arachnoid villi causing inc ICP

A

T

223
Q

what is the cornerstone prevention and treatment of vasospasm

A

Triple H therapy!
Hypervolemia
Hemodilution
Hypertension

224
Q

in triple H therapy what do we do/want regarding hypervolemia

A

NS
CVP 8-10
increases blood flow

225
Q

in triple H therapy what do we do/want regarding hemodilution

A

HCT 0.32 - 0.35

easier for blood flow

226
Q

in triple H therapy what do we do/want regarding hypertension

A

levophed (30% increase in MAP)

increase MAP and CPP

227
Q

What is a common drug used prophylactically for vasospasm

A

nimodipine
Ca2+ channel blocker
may alleviate abnormal contraction of smooth muscle and vasodilates

228
Q

what must we look out for when administering nimodipine

A

hypotension

229
Q

T or F Milrinone is a new therapeutic intervention for vasospasm

A

true

230
Q

If there is a promeblem with increased ICP what might the doctor order

A

insertion of intra ventricular catheter

231
Q

what do IVC’s allow us to assess

A

characteristics of CSF
drain excess CSF
monitor ICP when transduced
early identification of intracranial HTN

232
Q

What is the purpose of having an IVC with an EVD

A

allow CSF drainage via external shunt

provide a method of monitoring ICP with or without an ICP transducer

233
Q

what is the range for normal drainage of ventricular drains

A

5-15 mL/hr

234
Q

if a pt drains > __ mL/hr or an increase of __ mL/hr more than usual you should notify the MD

A

30

10

235
Q

what anatomical structure is an EVD levelled to

A

Foramen of Munro

236
Q

where is the foramen of monro

A

central in brain and opening of tentorium; btw lateral and 3rd ventricle

237
Q

what are external landmarks for foramen of monroe

A

outer corner of eye, temple, tragus

238
Q

when should you flush the transducer on an EVD

A

NEVER

239
Q

Which one of newtons law do we consider when analyzing mechanism of injury

A

mass x acceleration

faster the force is applied the faster the energy is released resulting in more tissue damage

240
Q

4 examples of mechanisms of injury

A

acceleration
acceleration-deceleration
coup countercoup
rotation

241
Q

What is primary vs secondary injury

A

primary injury happens at the accident

secondary - psysiological response to primary injury

242
Q

what are 4 examples of primary injuries

A

concussion
contusion
fractures
blunt/penetrating trauams

243
Q

what are 4 examples of secondary injuries

A

cerebral edema, hemorrhage, herniation, cerebral ischemia

244
Q

what is index of suspicion

A

suspected injuries or complications based on mechanism

245
Q

T or F basal skull freactures are able to be seen on CT

A

False need MRI

246
Q

What are three symptoms of basal skull #s

A

rhinorrhea (CSF from nose)
Otorrhea (CSF from ear)
RAccoon eyes, battle’s sign (hematoma behind ear

247
Q

T or F basak skull # pts are at increased risk of infection

A

true

248
Q

Can you put an NG in a patient with suspected basal skull fracture

A

no

249
Q

what is DAI how is diagnosed

A

diffuse axonal injury
causes stretching, tearing and shearing of nerve fibers
dx by immediate and severe decrease in LOC
widespread neurological dysfunction

250
Q

what are signs and symptoms of DAI

A

deep prolonged coma
inc ICP, BP and temp
defict in cognition, memory, speech, motor function and personality

251
Q

What are possible complications of TBI (8)

A 
prolonged immobility - skin breakdown, DVTs
prolonged invasive devices - risk for infection 
hypermetabolism and hypercatabolism
coagulation disorders
VAP, ARDS, PE
delayed gastric emptying
seizures
fluid and electrolyte disorders
252
Q

what is diabetes insipidus

A

decreased secretion of ADH aka vasopressin d/t damage of hypothalamus or pituaty gland

253
Q

what does DI cause

A

polydipsia and polyuria d/t bodys inability to concentrate urine

254
Q

what is CSW

A

cerebral salt wasting

255
Q

What is SIADH

A

syndrome of imapprorpiate ADH
dilutional hyponatremia d/t excess of ADH secreted inot bloodstream
excessive water reabsorbed

256
Q

what is the difference in urine output btwn DI, SIADH, CSW

A

DI increased
SIADH dec
CSW increased

257
Q

serium sodium is increased or decreased in DI? SIADH?

A

DI increased

SIADH decreased

258
Q

what is the treatment of DI

A

vasopressin and fluid replacement

259
Q

what is the treatment for SIADH

A

fluid restriction
3% saline
diuretics

260
Q

what is the urine osmo/serum osmo in DI SIADH and CSW

A

DI decrased
SIADH increased/decreased
CSW decrased

261
Q

what is volume status for DI, SIADH, CSW

A

DI decreased
SIADH increased
CSW decrased

262
Q

what head injury do you commonly see DI or SIADH

A

basal skull #

263
Q

When does cerebral edema begin to show? when does it peak

A

shows 24-48 hrs

peaks at 72 hours

264
Q

what are three things we can do to stop brain herniation

A

mannitol
craniectomy
control ICP and ensure adequate cerebral oxygenation

265
Q

What is the most common type of ICP monitoring/drain device

A

intra-ventricular catheter

266
Q

what are 5 benefits of ICP monitoring

A 
reliable and accurate ICP measurment
assess ICP with sedated/paralyzed pt
determine CPP
evaluate waveform to assess compliance
immediate reassesment of effectiveness of intervnetions
267
Q

what are the 6 questions you must ask when working with an IVC and EVD with ICP monitoring

A 
is it leveled and zeroed to foramen of monroe?
ordered to be open or closed?
order for what it should be set at?
safety check - secure position
CSF fluctuation and characteristics 
good waveform?
268
Q

how many peaks in one wave should you observe on an ICP wavefrom?

A

3

269
Q

what does P1 mean

A

percussion wave - represents arterial pulation

270
Q

what does P2 represent

A

Tidal wave

represents intracranial compliance

271
Q

what does P3 represent

A

dichroitic wave

represents aortic valve closure

272
Q

what does a normal ICP waveform look like

A

P1 highest, then P2, then P3

273
Q

what would a poor compliance ICP waveform look like

A

P2 higher than P1 - small changes in volume can cause ICP to skyrocket - ICP rises with MAP

274
Q

If you have IVC with an EVD and your ICP is 35 but your waveform doesnt look right what do you do (4)

A

focused neuro assesment
validate transducer placement
re-zero transducer
check for EVD fluctuation

275
Q

What does hyperventilating a pt do?

A

removes CO2 which is a potent vasodilator causing vasoconstriction of cerebral vessels

276
Q

What is a negative concequence of hyperventilating a pt

A

limits O2 supply ischemia & secondary injury

277
Q

What are the 3 rules for hyperventilating brain injured pts

A

if PaCO2 is in normal range
only as a temp measure (on the way to the OR)
only if the pt is deteriorating despite interventions

278
Q

Aside from hyperventilation how else can you manage cerebral O2 supply? give 6 examples

A 
decrease cerebral metabolism thus decreasing O2 demand
heavy sedation
normothermia or slightly low temp
HOB 30-45%
quiet enviornment
avoid restraints
neuromuscular blockade
279
Q

What are the 3 types of brain bleeds

A

epidural
subdural
intracerebral

280
Q

cause and s&S of epidural hematomas

A

Skull #s and lacs to middle meningeal artery

ipsilateral dilated/fixed pupil

281
Q

does an epidural hematoma require surgery

A

yes

282
Q

is epidural hematoma from a vein or artery

A

artery

283
Q

what causes a subdural hematoma

A

rupture of bridging veins in cerebral contusions and intracerebral hemorrhage

284
Q

what causes an intracerebral hematoma

A

depressed skull #
penetrating injuries
sudden accel-decel motion

285
Q

what is CBF influenced by

A

cerebral vascular resistance

286
Q

What is PbtO2

A

brain tissue oxygenation monitoring

287
Q

what is used to determinme PbtO2

A

device like pulse ox that continously monitors regional tissue oxygenation
probe inserted into area of injury and attached ot bedside monitor

288
Q

what is the goal value for PbtO2

A

> 20 mmHg

289
Q

what central line can be inserted to allow us to calculate cerebral oxygen extraction ratio

A

Jub Bulb Catheter

290
Q

What does a jug bulb catheter allow us to calculate

A

cerebral oxygen extraction ratio

291
Q

how does a jub bulb catheter work

A

central line fed into jugular vein upward into venous circulation
allows access to jugular venous blood draining from the brain only

292
Q

T or F you cant do continuous reading from a jug bulb

A

false, can use a transducer to provide continous monitoring of the jub bulb O2 saturation

293
Q

What is the normal range for SjO2

A

55-75%

294
Q

what is CERO2? how is it calculated

A

cerebral oxygen extraction ratio

(SaO2-SjO2)/SaO2 x 100

295
Q

what is normal range for CERO2

A

25-35%

296
Q

if you have a low value for CERO2 what does this mean

A

high supply low demand

297
Q

if you have a high value for CERO2 what does this mean

A

high demand low supply

298
Q

what must occur in apnea test

A

CO2 must rise above 60 mmHg or at least 20mmHg higher than the start point of the test

pH must be less than 7.28

must receive 100% FiO2 applied to airway throughout the test
physician must watch for any sign of respiratory effort

299
Q

T or F Brain death can be diagnosed by one physician

A

false

must be done by 2 physicians independently of each other

300
Q

What are the 3 minimum criteria to declare brain deat

A

pupils fixed and non-responsive to light (> mid size)
absent brain stem reflexes
absent reflexes

301
Q

What are 4 reflexes must be absent to declare brain death

A

bilateral corneals
gag, cough and swallow
oculo cephalic - dolls eyes
oculo vestibular - ice water

302
Q

what are the 2 types of death that can allow for organ donation

A

neurological determination of death (NDD)

donation after cardiac death (DCD)

303
Q

what type of injury is suspected in any trauma pt who has absent movement or sensation, any unconscious pt or pt with head injury

A

spinal cord injury

304
Q

What are common causes of SCI

A

hyperflexion (head on collisions)

hyperextension (whiplash)

305
Q

True or false parasympathetic response is lost below level of injury in SCI

A

false

sympathetic

306
Q

What spinal cord level innervates the diaphragm

A

C4

307
Q

injury at what spinal cord level results in tetra/quadriplegia

A

C1-T1

308
Q

injruy at what level of the spinal cord causes paraplegia

A

T2-L1

309
Q

what causes SCI

A

any mechanical force that disrupts neurologic and/or vascular supply

310
Q

What is used to determine level of injury

A

ASIA - standard neurological classification of spinal cord injury

311
Q

how are SCI categorized

A

by the lowest segment of the cord with normal sensory/motor function on both sides

312
Q

what is primary injury in SCI

A

compression of cord by bone displacement
disruption of axons d/t lacerations
transaction or disruption of blood supply

313
Q

what are secondary injuries in SCI

A

ongoing progressive damage for instability or inflammation

SIRS-like, ischemia, hypoxiea, edema

314
Q

what are immediate complications of SCI

A

spinal shock

neurogenic shock

315
Q

what is spinal shock

A

loss of motor, sensory, reflex and autonomic fn below level of injury
flassic paralysis
loss of bowel/bladder fn, temp control
sudden cessation of impulses from the higher brain centers

316
Q

when does spinal shock occur

A

immediately or w/in several hours of injury

317
Q

what type of shock is neurogenic shock

A

distributive

318
Q

what can occur with severe cervical and upper thoracic injuries

A

neurogenic shock

319
Q

What happens with neurogenic shock

A

loss of sympathetic input to the systemic vasculature of the heart and subsequent decreased peripheral vascular resistnace

320
Q

what are the parasympathetic signs of nuerogenic shock

A

hypotension
severe bradycardia
loss of ability to sweat below the level of injuries - warm, dry extremeites)

321
Q

what are the 6 SCI best practice guidelines

A

cervical immobilization
spinal xray series and CT/MRI in first 48 hours
MAP maintained 85-90 mmHg for first 7 days
DVT prophylaxis - anticoagulants and SCDs

NSCC 7520 Critical Care Theory 4 (5 decks)

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