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NUR 250 > Intracranial Regulation > Flashcards

Intracranial Regulation Flashcards

1
Q

maintaining homeostasis in the cns

A

o2
glucose
csf
filtration

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2
Q

big suppliers of blood to brain

A

carotid

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3
Q

big drainers of blood from the brain

A

jugular

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4
Q

monro-kellie hypothesis

A

no room fr swelling
something has to give

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5
Q

factors that impair ICR

A

impaired puerfusion
compromised neurotransmission
glkucose regulation
pathology

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6
Q

cerebral autoregulation

A

Ability of the brain to maintain blood flow
fairly constant rate of 1000ml/min.
MAP > 130 can be lost

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7
Q

compliance

A

Shunting of cerebrospinal fluid and venous blood to make room for expanding brain tissue
The brain can shift to make space, but this is delicate and dangerous

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8
Q

cerebral edema

A

increased brain water content

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9
Q

hydrocephalus

A

Increased CSF- dilated ventricles- impaired absorption or obstruction

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10
Q

what cna cause hydrocephalus

A

CSF Obstruction
Clogged arachnoid villi
Impaired CSF reabsorption
SAH and TBI can be a cause
Temporary vs. Long-term treatments

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11
Q

hematoma

A

collection of blood outside of bvs
mostly clotted
“bruise”
subdural hematoma

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12
Q

hemorrhage

A

activw ongoing bleeding
subarachnoid hemorrhage

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13
Q

cerebral perfusion pressure

A

pressure necessry to supply adequate blood flow to brain

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14
Q

intracranial pressure normal

A

Normal ICP is 7-10

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15
Q

causes of increased icp

A

cerebral edema
hematomas/blood clots
hydrocephalus
increased bp
incerased paco2-hypercapnia
decreased pa02-hypoxia
vasodilators
hyperthermia- fevers
coughing/suctioning
sneezing/blowing nose
valslva maneuvers
straining
PEEP
supine position w/ hOB flat
bending over
head/neck flexion and rotation
knee and hip flexion

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16
Q

what does increased icp look like

A

Change in LOC (1st) & Behavior changes
Restlessness, confusion or drowsiness, lethargy
Stuporous (serious impairment)
Coma- posturing or flaccidity
Headache
Neurological changes
Vomiting

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17
Q

what is a late sign of increased icp

A

cushings triad

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18
Q

what is cushings triad

A

3 primary signs that often indicate an increased in intracranial pressure
increased systolic bp
decreased pulse
decreased respiration
SIGN OF ABOUT TO HERNIATE

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19
Q

cva

A

Cerebrovascular disorders is an umbrella term for a functional abnormality of the central nervous system (CNS) that occurs when the blood supply to the brain is disrupted
Stroke is the most common cerebrovascular disorder in the United States

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20
Q

ichemic stroke

A

Cerebral blood flow disrupted due to obstruction of blood vessel
Infarction vs. penumbra

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21
Q

core

A

not getting tissue back

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22
Q

penumbra

A

might get tissue back

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23
Q

what to symptoms of cva depend on

A

Location of the infarction
Size of infarction
Amount of collateral blood flow

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24
Q

ischemic stroke clinical manifestations

A

Motor loss
Communication loss
Perceptual disturbances
Sensory loss
Cognitive impairment and psychological effects

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25
Q

befast

A

balance
eyes
face
arms
speech
time

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26
Q

last known well

A

last time they felt like themselves

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27
Q

hemiplegia

A

paralysis of one side of the body

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28
Q

hemiparesis

A

weakness on one side of body

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29
Q

dysarthria

A

diffuclutly speaking

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30
Q

aphasia

A

cant undertsadn or express speech

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31
Q

apraxia

A

word salad
words they want to say don’t come out correctly

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32
Q

hemianopsia

A

perceptual disturbances

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33
Q

agnosia

A

sensory loss
loss of proprioception

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34
Q

psychological effects

A

damage to the frontal lobe
might not be able to balance checkbooks, simple math, etc

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35
Q

neuro deficit: what do we want to know

A

Last known well
Rapid focused physical and neurologic exam
PRIORITY: Airway patency, cardiovascular status, and gross neurologic deficits

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36
Q

transient ichemic attack

A

A neurologic deficit that complete resolves in 24 hours (most last less than 1 hour)
MUST be evaluated!
stroke might follow

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37
Q

gold standard of cva diagnostic findings

A

non contrast ct scan within 20 minutes from presenting to ED
Sometimes further diagnostic studies completed to determine location of thrombi/emboli (client may benefit from mechanical intervention/clot removal

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38
Q

other studies

A

CT angiography/CT perfusion
Magnetic resonance imaging (MRI)/ MRI angiography of the brain and neck
Transcranial Doppler flow studies
Transthoracic or transesophageal echocardiography
12-lead electrocardiogram (ECG)
Carotid ultrasound

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39
Q

NIH

A

rates severity of stroke

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40
Q

medical management ischemic stroke

A

Gold standard for ischemic stroke within 3-4.5 hours after symptoms
Tissue plasminogen activator (t-PA)
Breaks up the clot
Client must meet criteria to receive t-PA
Goal: Given within 45 minutes of presenting to ED

41
Q

considerations with tpa

A

Dosing: 0.9 mg/kg with a maximum of 90 mg
10% of dose given over 1 minute
90% given over an hour
Admitted to the ICU with continuous cardiac monitoring and frequent neurologic assessments
Blood pressure management (SBP<185, DBP<110)
Monitoring for bleeding

42
Q

treatment without tpa

A

Possible anticoagulant therapy (heparin) but comes with risks
Manage complications especially increased ICP
supplemental o2-no less than 95%
elevate hob

43
Q

endovascular therapy

A

Recommended that clients have the clot physically removed through a procedure if they meet the following criteria:
- Pre-stroke status of no deficits
- Acute ischemic stroke receiving IV t-PA within 4.5 hours of onset according to guidelines from professional medical societies
- Causative occlusion of the internal carotid artery or middle cerebral artery segment
- Age ≥18 years
- National Institutes of Health Stroke Scale (NIHSS) score of ≥6
- An Alberta Stroke Program Evaluation of Computed Tomography (ASPECT) score of ≥6 (a radiologic assessment of the CT scan), and treatment can be initiated (groin puncture) within 6 hours of symptom onset

44
Q

hemorrhagic stroke patho

A

Depends on cause and underlying type of cerebrovascular disorder
Bleeding puts pressure on nearby nerves/brain tissue
Brain metabolism is disrupted
Cerebral perfusion pressure is often inadequate
End result: infarction of brain tissue

45
Q

types of hemorrhagic stroke

A

Intracerebral Hemorrhage- bleeding into brain, trauma, blood thinners
Intracranial (cerebral) aneurysm- weakening of vessels
Arteriovenous malformation (AVM)
Subarachnoid hemorrhage- arterial bleeding into subarachnoid space

46
Q

diagnostic findings hemorhagic stroke

A

ct scan determine type of stroke, size, location of hematoma, presence or absence of ventricular blood of hydrocephalus
CT angiography confirms diagnosis of intracerebral aneurysm and/or AVM
Lumbar puncture can be used to confirm bleeding with a negative CT scan (as long as NO increased ICP)
Sometimes younger patients (less than 40 years old) are tested for illicit drug use

47
Q

clinical manifestations of hemorrhagic stroke

A

Similar neurologic deficits to ischemic stroke
Often complain of headache
If the bleeding stops, client may have no symptoms
High mortality in subarachnoid hemorrhage from a ruptured aneurysm

48
Q

managing complications of stroke

A

Maintain airway
Preventing UTI’s, cardiac arrhythmias and complications of immobility
Monitoring blood glucose closely

49
Q

primary prevention

A

managing htn

50
Q

risk factors for hemorrhagic stroke

A

elderly
male
latino, african american, and japenese
moderate or excessive alcohol intake

51
Q

medical management hemorrhagic stroke

A

Prevent rebleeding
Reverse anticoagulant agents- ffp
Treat seizures- prophylactic
Treat hyperglycemia
Surgical intervention not common (craniotomy if used) GET TO OR

52
Q

complications of hemorrhagic stroke

A

Rebleeding
Cerebral hypoxia and decreased blood flow
Vasospasm
Increased intracranial pressure
Hypertension

53
Q

seizures

A

Abnormal, sudden, excessive, uncontrolled electrical discharge of neurons within the brain that may result in a change in level of consciousness (LOC), motor or sensory ability and/or behavior

54
Q

epilepsy

A

Defined by two or more seizures experience by an individual
Repeated, unprovoked seizure activity occurs

55
Q

what can cause epilaepsy

A

Abnormality in electrical neuronal activity
Imbalance of neurotransmitters
Combination of both

56
Q

idiopathic epilepsy

A

Not associated with any specific cause or brain lesion
Genetics may play a role

57
Q

2ndary seizures

A

Underlying brain lesion – tumor or trauma
Metabolic Disorders
Acute Alcohol Withdrawal
Electrolytic Disturbances
High Fever
Stroke
Head Injury
Substance Abuse
Heart Disease

58
Q

electrolyet that causes seizures when imbalanced

A

sodium

59
Q

generalized seizures

A

Widespread electrical discharge that involves both hemispheres of the brain
impacts every wavelength of eeg

60
Q

generalized tonic clonic tonic phase

A

Stiffening or rigidity of the muscles
Primarily affecting the arms and legs
Immediate loss of consciousness

61
Q

clonic phase of generalized tonic clonic

A

Rhythmic jerking of all extremities
Lasting from 2-5 minutes
May bite tongue or become incontinent of urine and feces

62
Q

post ictal generalized tonic clonic

A

Fatigue, acute confusion, and lethargy may last up to an hour after the seizure

63
Q

generalized myloclonic

A

Brief jerking or stiffening of the extremities

May occur in a single episode or in groups

Contractions may be symmetric (both sides) or asymmetric (one side)

awake- don’t lose consciousness

64
Q

generalized absence seizures

A

Common in children → familial tendency
Brief periods of loss of consciousness and blank staring
Automatisms (involuntary behaviors) may occur
Lip smacking, eye fluttering, picking at clothes
Return to baseline after seizure
May occur numerous times per day

65
Q

generalized atonic seizure

A

Sudden loss of muscle tone followed by post-ictal confusion
Only lasts a few seconds
Causes the patient to fall → leads to injury
Most resistant to drug therapy

66
Q

partial seizures

A

Focal/local seizures that begin in one hemisphere of the brain
only some leads in eeg

67
Q

complex partial

A

Common in older adults
May cause loss of consciousness or “blackout” for 1-3 minutes
Automatisms may occur
Unaware of environment – can lead to wandering
Amnesia may occur after the seizure
Often involves the temporal lobe

68
Q

simple partial

A

Remains conscious
Reports an aura
Unusual sensation before the seizure takes place
One-sided movement of extremities
Autonomic symptoms
Changes in heart rate, skin flushing, and epigastric discomfort

69
Q

seizure diagnostics

A

EEG (electroencephalogram)
CT Scan
MRI
PET Scan
Labs → assess for metabolic causes

70
Q

pet scan

A

tpyically for cancer
areas of brain utilizing more glucose

71
Q

treatment for primary epilepsy

A

Managed with Drug Therapy

72
Q

treatment for 2ndary seizures

A

Remove or treat the underlying cause

73
Q

antiepileptic drugs

A

“Anticonvulsants”
Introduce one drug at a time
If this one drug is not effective, provider may:
Increase dose
Introduce another AED
For some, combination therapy is needed
Doses are adjusted to achieve therapeutic blood levels without causing major side effects

74
Q

pt teaching on aeds

A

Compliance – right dose at the same time every day
Follow up laboratory testing
Drug Decline and Sensitivity
Continue to take drug, even if no seizure activity
Drug-Drug interactions
Drug-Food interactions

75
Q

first line acute treament

A

valium and ativan: benzos

76
Q

care of pt during seizure

A

Turn client on their side for airway protection
Maintain airway and suction as needed
Protect from injury
DO NOT force anything into mouth
Loosen clothing
Do not restrain or try to stop movement
Document
Time seizure started and ended

77
Q

status epilepticus

A

Medical Emergency
Prolonged seizure lasting longer than 5 minutes OR repeated seizures over the course of 30 minutes
Potential complication of all seizures

78
Q

causes of status epilepticus

A

sudden w/draw of aeds
acute alc or drug w/draw
head trauma
infection
cerebral edema
metablic disturbances

79
Q

status epilepticus treatmetn

A

1 – Establish or Maintain the Airway

#2 – Diazepam or Lorazepam – doses may be repeated
#3 – Loading dose of an AED (Phenytoin/Fosphenytoin or Levetiracetam)
Other Interventions:
IV access -> IV fluids
ABG/Bloodwork

80
Q

pt education status epilepticus

A

Take medications as directed
Educate about potential side effects
Educate about missed doses and concurrent illnesses
Importance of blood draws if applicable
Medical alert bracelet
Follow-up care
Education for family members, roommates, friends, coworkers etc.
Avoid alcohol and excessive fatigue
Seizure log
Driving -> know state laws.

81
Q

loc tbi

A

The most important indicator of neurologic function is Level of Consciousness!!
The most sensitive indicator of a patient’s neurological status.
Lethargy, agitation, irritability

82
Q

cerebral edema

A

Is defined as increased brain water content and can be either intracellular or extracellular.
Brain is susceptible to injury from edema
Located in confined space
Cannot expand
No lymphatic pathways within CNS
to carry away fluid that accumulates.
Cytotoxic, Vasogenic, Interstitial

83
Q

cerebral perfusion presure

A

Brain dependent on blood
supply for oxygen
Dependent on cerebral
perfusion pressure
CPP = MAP – ICP
Normal ICP < 15 mmHg
Normal CPP= 80-100 mmHg (70-100)
CPP < 60 = cell injury
CPP < 30 = cell death- neuronal hypoxia

84
Q

cycle of malugnat progressive brain swelling

A

increased icp
decreased cerebral brain flow
tissue hypoxia
increase pco2 and decreased ph
cerebral vasodilation and edema

85
Q

causes of increased icp

A

Hypoxia
Elevated pCO2
Suctioning, PEEP
Head/neck, knee & hip flexion
Clustering activities
Noxious stimuli &/or pain
Agitation
Trendelenburg
Sneezing, Coughing
Blowing nose
Straining, Bending over
↑ Temperature (↑ CMR)
Seizures (↑ CMR)
Vasodilating meds – nitrates, antihistamines, anesthetics

86
Q

icp s&s

A

Change in LOC
Cushing’s Triad
Severe HTN
Widened pulse pressure
Bradycardia
Papilledema
Headache
Pupil changes
Vomiting
Projectile
Motor changes
Posturing
Hemiplegia
Hyperthermia
Seizures
Visual & extraocular movement abnormalities
Weakness or Paralysis
Loss of brainstem reflexes (late)
VS changes (late)

87
Q

gcs

A

used for tbi
can this pt be rehabed

88
Q

decorticate

A

pull to CORE

89
Q

decerebrate

A

stiffen up and psuh OUT

90
Q

management of increased icp

A

Intracranial Bolt
Subarachnoid space
Simple to place; rapid insertion
Intraventricular Catheter
MOST ACCURATE
Placed in the lateral ventricle
Can drain if ICP ↑
Can withdraw CSF specimens
INCREASED RISK OF INFECTION

91
Q

treament if increased icp

A

Elevate HOB
IVF – maintain euvolemia
Prevent hypovolemia
BP management
Prevent hypoTN & HTN
Osmotic diuretics
Hypertonic saline
CSF drain
Oxygen
Sedation, Analgesics
Neuromuscular Blocking agents
Hypothermia
Control shivering
Hyperventilation
Prevention – control temps, control glucose, acetaminophen, anticonvulsants
Barbiturate Coma (last resort)
NEVER PUT ANYTHING IN THE NOSE

Glucocorticoids ARE NOT recommended

92
Q

nsg intervention for increased icp

A

Frequent neuro checks
Monitor ICP & CPP
Keep fevers down
Hyperventilation
Hyperoxygenate before suctioning/careful suctioning
Rest a few minutes between suctioning passes
Keep neck straight
No flexion or extension of the head
Logroll, avoid hip or knee flexion
Maintain head in neutral position (alignment)
HOB at least 30% or ↑
No Valsalva
No coughing/sneezing
No nose blowing
Cluster care Yes? No?
Limit patient stimulation/ decrease stimuli
Keep room quiet & dark
Prevent seizures

93
Q

hydrocephalus

A

Develops as a result of edema or bleeding
into the subarachnoid space
Blood blocks the reabsorption of CSF
Arachnoid villi become clogged and cannot reabsorb
Blockage of CSF outflow from the ventricular system
There is not enough or there are insufficient
arachnoid villi to reabsorb CSF
SAH and TBI can be a cause
Treatment is ventriculostomy to drain CSF temporarily
Long-term would require a shunt.

94
Q

brain herniation

A

brain dead
brainstem doesnt work

95
Q

brain death

A

State of irreversible brain damage characterized by:
No cognitive function
Inability to maintain vital functions
Absence of isoelectric activity on EEG

96
Q

requirements for brain death diagnostics

A

Coma of known cause
GCS 3
Absent response to noxious stimuli
Absent muscle movements
Loss of brain stem reflexes
Corneal, oculocephalic, oculovestibular
Absent cough/gag reflex
No pupil response, Pupils fixed, dilated, midposition
Apnea
At least one physician neuro exam; some states require two
Apnea test
Adjunctive neurodiagnostic testing not required, but usually done
2 PHYSICIANS SIGN OFF-SET PERIOD OF TIME INBETWEEN

97
Q

factors inpacting brain death

A

Factors impacting brain death diagnosis
Normal body temp (>36˚ C)
No meds (CNS depressants or neuromuscular blockades)
Encephalopathy & electrolyte imbalances reversed
Normal SBP (no shock state) or > = to 100 mm Hg
Ethical
Patient’s wishes
Ethics committee
Legal
Gift of Life
Patient’s wishes

98
Q
A

NUR 250 (6 decks)

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