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410 Patho Exam 4 > Increased Intracranial Pressure > Flashcards

Increased Intracranial Pressure Flashcards

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1
Q

This powerpoint is going to be from the recording from the increased intracranial pressure

A
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2
Q

First thing is we must understand what is in our head before we start talking about the fluid that will increase the pressure in our head.

The skull has 3 essential components which are ?

A

Brain tissue
Blood
Cerebrospinal fluid (CSF)

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3
Q

what are some factors that influence increased intracranial pressure ?

A

arterial pressure
venous pressure
intraabdominal and intrathoracic pressure
posture
temperature
blood gases (co2 levels)

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4
Q

something we need to understand and know is something called the

monro-kellie doctrine

what is this ?

A

if one of the three component of the skull, so blood, brain tissue or CSF increases, the other two will decrease in order to maintain balance of intracranial pressure

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5
Q

monro-kellie doctrine only works if what?

A

the skull is closed

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6
Q

what is normal intracranial pressure ?

A

5-15

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7
Q

when is our concern for intracranial pressure, like at what number ?

A

more than 20 and its sustained

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8
Q

what are some normal compensatory adaptations your body does in order to help maintain normal intracranial pressure? (3)

think of the 3 components again

A

changes CSF volume

changes in intracranial blood volume

changes in tissue brain volume

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9
Q

its very important to note that the body ability to compensate is what?

A

very limited

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10
Q

once our ability to compensate is gone, or if intracranial pressure increases, we are going to do what?

A

decompensation

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11
Q

we do look at something called cerebral blood flow when the patient is having increase intracranial pressure.

what does cerebral blood flow mean ?

A

the amount of blood in milliliters passing through 100g of brain tissue in 1 minute

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12
Q

typically what is the normal cerebral blood flow ?

A

50ml/min per 100g of brain tissue

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13
Q

the brain uses __% of the body oxygen

the brain uses __% of its glucose

A

20

25

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14
Q

something to add here, its important to note that we keep talking about perfusion and glucose levels, why do think that?

A

the reason why we keep mentioning about perfusion is because of the fact that when the body is struggling to maintain adequate circulation , the body will shunt oxygen from “unimportant areas.” and focus mainly on the important ones, like the brain and the heart, which is why we see that the brain uses 20% of oxygen

we mentioned before for glucose that a diabetic patient is in more critical care due to hypoglycemia than hyper, and the reason is for the fact that we are using over 25% of our glucose in our brain to function, so when we dont have enough, we have those neuro changes

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15
Q

what is auto regulation ?

this is something the body will do on its own to compensate by the way before we begin to decomp

A

adjusts diameters of blood vessels to ensure consistent blood flow

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16
Q

auto regulation is only effective when ?

A

the mean arterial pressure (map) is 70-150mm hg

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17
Q

what does cerebral perfusion pressure mean ?

A

the amount of pressure needed to ensure blood flow to the brain

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18
Q

what is normal cerebral perfusion pressure ?

A

60-100

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19
Q

less than 50 cerebral blood flow is associated with what 2 things ?

A

ischemia
death of neurons

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20
Q

there are 4 stages of increased intrancranial pressure, which are ?

A

stage 1 : total compensation

stage 2: decrease compensation and risk for increase intracranial pressure

stage 3 : failing to compensate ; clinical manifestations of increase intracranial pressure ( Cushing triad )

stage 4 : herniation imminent -> death

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21
Q

stage 1 its the total compensation, what are the 2 things that are happening ?

A

accommodation and auto regulation intact

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22
Q

stage 3 is the failing to compensate and clinical manifestations are becoming present for increase intracranial pressure

stage 3 is also known for what other situation ?

A

Cushing’s triad

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23
Q

what are the 3 factors that affect cerebral blood vessel tone ?

A

carbon dioxide
oxygen
hydrogren ion concentration

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24
Q

how does carbon dioxide affect cerebral blood vessel tone ?

what happens when its increased

what happens when its decreased

A

increase co2 causes smooth muscle relaxation, dilation of vessels, improved CBF
- slow deep breaths, slower respiratory rate
- improved blood flow

decreased co2 causes vasoconstriction and decreased CBF
- hyperventilation
- decreased blood flow

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25
how does oxygen affect our cerebral blood vessel tone ?
low levels of oxygen causes dilation, but will cause anaerobic metabolism and lactic acid build up and then cellular death
26
how does hydrogen ion concentration affect cerebral blood vessel?
results from lactic acid build up, acidosis and vasodilation - auto regulation is lost usually a result from low oxygen and then goes into metabolic acidosis then with that lactic acid build up, we have acidosis and vasodilation of the vessels and the ability to compensate is gone pretty much
27
increased intracranial pressure is life threatening its caused by an increased in any of the 3 components, which are ?
brain tissue, blood, CSF cerebral edema hypercapnia, cerebral acidosis, impaired auto regulation, hypertension
28
in the powerpoint she uses a good diagram to describe the steps of having increased intracranial pressure there are 5 steps what is the 5 steps. first one to start us off is brain injury
1. brain injury 2. tissue edema causing increased intracranial pressure 3. compression of brain tissue and decreased blood flow 4. necrotic tissue and edema 5. increased CO2 causing vasodilation and increase intracranial pressure
29
what are some clinical manifestations that we see in a patient who has cerebral edema ? (2) think very broad
change in level of consciousness change in vital signs
30
how does the patient appear when they have a change in level of consciousness when they have cerebral edema?
flattening of affect -> coma ( no emotion, no facial expression, tone of voice is very flat, avoid eye contact, very bored and uninterested ) - confusion, agitation, combativness
31
what are some changes in vital signs when we see a patient who has cerebral edema? (2)
Cushing's triad change in body temperature
32
what is Cushing's triad in cerebral edema Clincal manifestation ? we do need to know this 5 things apart of this
systolic hypertension with widened pulse pressure, bradycardia with bounding pulses, irregular respirations
33
Cushing's triad is a what?
medical emergency
34
why do we have a change in body temperature when the patient is having cerebral edema? usually its a what?
the hypothalamus regulates our body temperature, so when we have increased pressure, our hypothalamus can regulate it and will cause us to be unable to maintain a good body temp hyperthermia ( hot, fever )
35
patients can have a compression of oculomotor nerve, what do we check for ? (4)
unilateral pupil dilation ( occurs on ipsilateral (same) side as the lesions ) - dilation of the pupil of the side of the injury sluggish or no response to light inability to move eye upward eyelid ptosis (drooping of the eyelid)
36
clinical manifestations other cranial nerves - diplopia, blurred vision, eom changes central herniations can manifest as ___ uncle herination causes ____ papilledema presents with __
sluggish but equal pupils dilation of unilateral pupil ( one pupil ) persistent increased in intracranial pressure ( can also be seen with severe hypertension )
37
patients may also experience decrease in motor function what is contralateral hemiparesis/hemiplegia ?
a patient may find it very hard to move, typically the opposite side of the lesion so like I hurt the right side of my brain, so I can't move anything on my left side of the body
38
posturing a very important indictor on the severity of the brain injury or overall increased intracranial pressure. we have 4 types, what are they called ?
decorticating posturing decerebrate posturing mixed-decorticate opisthotonic
39
what is decorticating posturing?
flexing the upper extremities extension of the lower extremities
40
what is decerebrate posturing?
stiff extensions of arms hyperpronation ( hyper extend arms and legs )
41
which out of the 2 main posture is worse? decorticating or decerebrate? and why?
decerebrate reason is because at least your body is trying to protect its core, when in decorticating
42
what is mixed-decorticate/decebreate ?
one side can be decorticate and the other side can be decerebrate
43
what is opisthotonic posture?
bowing of the body with head and heels bent back so like the heels of the feet and your head are on the bed, but the rest of the body is lifted up in the arm
44
just to go back into the powerpoint, its in the other one and not in the recording, what is an indication of a brain herniation? what is like the neurologic emergencies we can see with the eyes ?
fixed, unilateral, dilated pupil
45
patients usually will have a headache, which makes sense cause of the pressure - mainly worsen in the morning - last all day - never get better yet they will gave vomiting without what and what type?
not preceded by nausea and projectile
46
vomiting usually is not preceded by nausea, but why do patients vomit though with increased intracranial pressure?
trying to remove all the fluid, it is projectile - its forceful vomit !!
47
what is the 2 complications that can occur from increased intracranial pressure?
inadequate cerebral perfusion cerebral herniation
48
what are the 3 types of herniation ?
tentorial herniation uncal herniation cingulate herniation
49
what is each//describe tentorial herniation uncal herniation cingulate herniation
downward herniation through opening for brain stem lateral and downward herniation lateral displacement
50
what are some diagnostic studies we are going to do for patients who have increase intracranial pressure?
ct scan/ mri / pet eeg cerebral angiography icp and brain tissue oxygenation measurement doppler and evoked potential studies
51
what is a heavy heavy contraindication, NO! for diagnostic studies for increased intracranial pressure?
no lumbar puncture
52
why is lumbar puncture a big no no when it comes to testing a patient with ICP?
because its an instant herniation and death for patients
53
what is the objective assessment tool we may use to help assess a patient with ICP?
glasgow coma scale
54
Glasgow coma scale score ranges from what ?
3-15 ( the higher the number the better )
55
what are the 3 things the Glasgow coma scale measures?
eyes, verbal, Motor responses
56
eyes go from ___ to ___ verbal response go from ___ to ____ motor response go from ___ to ___
spontaneous to non opening to any stimulus talking to not even making sound with painful stimulus obey commands to no response
57
typically when you have a score of ___ or lower, we are worried for what ___and usually you are going to be ___
8 respiratory compromise intubated
58
when we are measuring the amount of increased intracranial pressure in the brain, what are we actually using as a measuring unit?
the mean pressure
59
if there is any elevation from the previous measurement of intracranial pressure, you want to what?
immediately report it
60
remember when we are placing the device to monitoring the mean pressure, or pretty much the increased intracranial pressure in the brain, it is an invasive procedure, its literally going into their skull the risk of infection is possible, so we should what out for ? if the monitor is there for more than 5 days, its more than likely infection can occur
csf leak or systemic
61
if there is an increased intracranial pressure in the patient, what do you want to look at first, the patient or the machine ?
always the patient
62
you can always get inaccurate readings of increased intracranial pressure caused by what? test question, look at the patient first - then look at the system
CSF leaks obstruction in catheter/kinks difference in height of bolt incorrect heigh of drainage bubbles/air in tubing
63
how can we as nurses control increased intracranial pressure ?
we can remove it by the ventricular catheter with intermittent or continuous drainage
64
when we are draining out the CSF, we have to what?
monitor and essential to keep track cause we dont want to remove too much
65
when we have a patient who have ICP, typically there is an underlying cause, so we obviously are going to treat the underlying cause in order to stop the ICP. ICP IS A SYMPTOM, NOT A CONDITION. what are some things that we can do to help aid this?
oxygenation - intubation and mechanical ventilation surgery possible
66
what are the 3 drug therapies we are going to be using for these patients with ICP?
mannitol (osmitrol) hypertonic saline corticosteroids
67
what does mannitol do? hypertonic saline does the same thing by the way ^
brain fluid into your vessels, and dilation of your blood viscosity - improvement of perfusion to the brain as we balance out the fluid
68
why do we use corticosteroids ?
mainly help with inflammation
69
take corticosteroids with ___ dont take during what point of the day ? and why? ___your blood sugar can cause ____blood pressure
food cause ulcers can occur night because it can cause increase activity increase blood sugar increase blood pressure
70
when taking a corticosteroids, we usually want to take it with what other medications ?
h2 receptor blockers proton pump inhibitors concurrent antacids
71
if a patient has a fever, seizures can increase, what medications can we use to aid with this ?
antipyretics - help with fever anti seizure medications sedatives analgesics - pain barbiturates - calm them
72
what 2 nutritional states do you end up having when you have increased intracranial pressure ?
hyper metabolic and hyper catabolic state with increase need for glucose break down of muscles and fat
73
how are we going to feed patient ?
enteral or parenteral nutrition early feedings normal saline keep fluid volume normal
74
notes nursing assessment - assess history of ICP - level of consciousness - glasgow coma assessment - assess perfusion, ventilation and gas exchange ( bun/creatinine, blood pressure, gas exchange, respiratory rate/depth/rythem, pulse ox)
75
we are also going to do some cranial nerves assessment eye movement alert and orientation symmetrical gait extra ocular movement we can do corneal reflect? we can do oculocephalic reflex? we can do oculovestibular (caloric stimulation)?
- touching their corneal and see if they blink - think of it as blowing into their eyes to get a blink reflex - doll eyes reflex, they turn their head sideways, there eyes turn to that side too - turn head to the right -> eyes move to the right squirt cold water in their ear, and when the cold water hits there ear drum, there eyes move away from the cold water, so like right ear -> move eyes to the left
76
to recap what is the reflex name for the blinking? what is the reflex name for doll eyes ? what is the reflex name for the ear drums water?
corneal oculocephalic reflex oculovestibular (caloric stimulation)
77
how can we assess their motor strength ? what test ?
pronator (palmar ) drift test squeeze hands too raise foot off bed and bend knees
78
what is the pronator (palmar) drift test?
lift there arms up with the palm facing up, on their weak side palm and arm will turn downward
79
typically we want to avoid causing any painful stimuli to a patient of any kind, but in neuro, when the patient isn't responding, we have to cause pain to see if they even can respond. so we can do something like what ?
sternal rub with their knuckles, see if they withdraw or anything
80
if you think a patient is faking their pain response, a good testing measure is how ?
lifting their arm above their face and letting it fall on their face, typically patients will move their arm away if they are faking it cause they dont want to get hit in the face
81
there are 5 abnormal respiratory patterns ill give you the names , you tell me the description of each cheyne-strokes central neurogenic hyperventilation apneustic breathing cluster breathing ataxic breathing
cycles of hyperventilation and apnea sustained, regular rapid, deep breathing prolonged inspiratory phases or pauses alternating with expiratory pauses clusters of breaths follow each other with irregular pauses between completely irregular with some breaths deep and some shallow. random, irregular pauses, slow rate
82
notes nursing diagnosis - decreased intracranial adaptive capacity - risk for ineffective cerebral tissue - risk for disuse syndrome - risk for injury nursing planning overall goals - maintain a patent airway - icp within normal limits - normal fluid and electrolyte balance - prevent complications secondary to immbolitiy and decreased LOC
83
nursing implementation respiratory Respiratory function -Maintain patent airway-at risk for airway occlusion. - Elevate head of bed 30 degrees. - Suctioning PRN - Minimize abdominal distention with NG tube placement - Monitor ABGs. - Maintain effective ventilation
84
the problem with elevating the head of the bed with ICP, we can decreased the perfusion, so we can only do what. (number) no semi or high fowlers
30 degrees
85
remember SUCTIONING AS ? what do we try first before suctioning to aid with secretions
NEEDED. - avoid it - try fluids first !
86
what are we going to help aid with pain and anxiety manamgent ?
opioids usage benzodiapzepines neuromuscular blocking agents
87
what is the issue with opioids when having a patient with ICP, or any neuro issue?
it makes you sleepy! it depresses your respiratory rate as well ! we need to assess their status frequently so be mindful when your giving opioids
88
we can give two medications called propofol (diprivan) what is the side effect? dexemedetomidine (precedex) used for ?
hypotension -> decreased cerebral perfusion pressure to aid patients who are on a vent to not fight with the vent so much
89
nursing implantation notes Fluid and electrolyte balance Monitor IV fluids. Daily electrolytes Monitor for DI or SIADH. Monitor and minimize increases in ICP. typically DI and SIADH are very common things we see in these patients
90
what is Diabetes insispidus ? (4 things )
cause by decreased ADH, leads to increased urine output and hyponatremia too little ADH pee too much too little salt dehydration
91
what is syndrome of inappropriate antidiuretic hormone (SIADH)? 4 main things
caused by increased ADH, leads to decreased urine output and hypernatremia too much ADH no pee too much salt fluid overload
92
how to help optimize ICP and CPP note - HOB elevated to 30 degrees - Head midline - Prevent extreme neck flexion. neutral chin, no chest chin or chin to air - Turn slowly. - Avoid coughing, straining, Valsalva. (holding breath and increase abdominal pressure) - stool softener & high fiber diet will aid that - Avoid hip flexion. hip flex can impair circulation and perfusion
93
Minimize complications of immobility. Protection from self-injury Judicious use of restraints; sedatives Seizure precautions, side rails up, padding side rails, lowest bed Quiet, nonstimulating environment Psychologic considerations
94
evaluation Expected Outcomes - Maintain ICP and CPP within normal parameters. - No serious increases in ICP during or following care activities - No complications of immobility
95
she doesn't mention this in the recording, but on the slideshow she has the babinski reflex what is this ? what is normal(negative)? what is abnormal (positve)?
the lateral aspect of the sole is stroked from the heel to the big toe planter flexion of all toes dorsiflexion of the big toe with the other toes fanning out
96
an abnormal positive for babinski reflex is only normal for who ?
infants through ages of 2
97
if the patient is positive of a babinski reflex, is often associate with what?
CNS disorders

410 Patho Exam 4 (5 decks)

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