4 Nervous System Alterations Part 2 Flashcards

1
Q

Increased ICP late signs

A

Cushings triad:
—Widening pulse pressure (HTN present)
—Bradycardia
—Cheyne-stokes respirations

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2
Q

Cerebral edema tx

A

Prevention is key

Corticosteroids
Osmotic diuretics (pulls fluid off brain)

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3
Q

Causes of ICP (vasogenic edema)

Most common what?
What does it do?
Common causes? (4)

A

Most common reason of increased ICP

A disruption in the BBB with increased capillary permeability (increased ECF)

Causes:
—brain tumors
—cerebral abscess
—ischemic/hemorrhagic stroke

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4
Q

Causes of increased ICP (cytotoxic edema)

What happens
Causes (2)

A

Swelling of neurons and endothelial cells
(Increased ICF)

Causes:
—anocia
—hypoxic injury

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5
Q

Worries with increased ICP

A

Herniation:
—displaced tissue through opening
—compresses the CNS

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6
Q

ICP and CPP goals

Nursing interventions (4)

A

ICP <20
CPP >70

Interventions:
—HOB 30
—head midline
—pre-oxygenate prior to suctioning
—avoid excess stimulation

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7
Q

ICP

—adequate oxygenation labs (3)
—intervention to do it
—what a short term to remove CO2
—normal CO2

A

PaO2 >80
Normal hgb and Hct

Mechanical vent

Normal co2 35-45
Hyperventilation decreases co2 short term

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8
Q

Management of ICP

—2 main things to watch/do and how to do that
—GOALS
—What meds

A

Fluids:
—all fluids and piggybacks in NS
(no hypotonic/dextrose)
(Monitor CVP/BP/BUN/Creat/UOP)

BP:
Arterial BP (GOAL MAP: 70-90, CPP >70)

CBB: calcium channel blockers

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9
Q

What calcium channel blockers for ICP

A

Nimodipine:
—PO
—prevents vasospasms w/ SAH

Nicardipine:
—IV
—decrease BP

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10
Q

Interventions to reduce metabolic demands in ICP:

—Temp
—Sedation

A

temp:
—34-35 degree for 24-72hrs

Sedation:
—decreased ICP r/t agitation
—propofol/fentanyl/morphine/benzodiazepines

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11
Q

Interventions to reduce metabolic demands in ICP:

—Seizure prophylaxis
—Barbiturate coma

A

Seizure prophylaxis:
—phenytoin/fosphenytoin/levetiracetam

—SE: bradycardia/HOTN

Barbiturate coma:
—purposeful coma to decrease metabolic demands

—SE: HOTN/apnea

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12
Q

ICP monitoring

What we use
Risk

A

Intraventricular monitoring device

Risk of infection

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13
Q

Spinal drain:

Drains with what:
Location of lazer for zeroing

A

Drains to gravity

Zero to tragus of ear (foreman of monroe)

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14
Q

EVD (Extra-ventricular drain)

—inserted where to do what
—can be done where with what?
—inserted at what point

A

—Inserted into hemipheres to drain CSF d/t hydrocephaly

Done at bedside with a crank drill

Inserted at kocher’s point

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15
Q

When do we start using ICP monitoring (criteria)

Contra indications for ICP monitoring

A

do it:
—TBI w/GCS <9

CI:
—systemic infection
—infection at insertion site
—CNS infection
—coagulopathy

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16
Q

At what ICP are the ICP treatments initiated?

17
Q

1st tier of ICP treatment? (4)

A

Mannitol
Hypertonic saline solutions (3%-7.5& NaCl)
Respiratory support
Analgesia and sedation (reduce agitation)

18
Q

1st tier ICP tx

—mannitol:
What does it do
May lower what d/t what

—hypertonic saline solutions
What solutions
What they do
Long term does what

A

mannitol:
—diuretic to decrease ICP
—may lower CPP d/t decreaseing BP
So you need to moniro BP/UOP w/FC

hypertonic saline solutions:
—3%-7.5%
—ICF pulled out and shrinks brain = decreased ICP
—increased MAP and CPP in the long term

19
Q

1st tier ICP treament

Respiratory support:
-keep what

Analgesia/sedation:
-does what
-meds

A

Keep adequate oxygenation
(increase PEEP by increasing mean airway pressure)

Analgesia/sedation:
—reduce agitation
—mechanical vent
—opiods are drug of choice (fentanyl/morphine)

20
Q

2nd tier ICP treatment

2 things

A

Hypothermia:

Barbiturate coma

21
Q

2nd tier ICP tx

Hypothermia

—temp
—what increase in C = what increase demand
—what is does

A

36-37.7C

every 1C increase body metabolic demands increases 5-10%

decreased cerebral metabolic rate = decreased CO2 and lactate build up

22
Q

2nd tier ICP treatment

Barbiturate coma

—what is it
—meds
—decreases what 3 things
—what hour we start it
—when to d/c

A

36-37.7C

every 1C increase body metabolic demands increases 5-10%

decreased cerebral metabolic rate = decreased CO2 and lactate build up

23
Q

Hyperventilation

—increased PaCO2 leas to what 2 things
—what does PaCO2 do to ICP by doing what to CBF

—diminished blood flow may do what

—only do for what

A

Increased PaCO2 = increased CBF/vasodilation

PaCO2 = decreased ICP d/t decreased CBF

Diminished blood flow may compromise cerebral oxygenation

—only do it for immediate neurological emergencies

24
Q

Why is hyperventilation short term for decreasing CO2 and ICP

A

It decreased CBF which decreases oxygenation to brain (NOT GOOD)

25
Cerebral vascular accident —acute stroke -2types -what is happening
Decreased blood supply to brain —ischemic —hemorrhagic
26
Both strokes have the same s/s —what are the other ways to diagnose which type it is?
CT MRI Ateriography Doppler/carotid US Coagulation studies CBC
27
Ischemic stroke tx
Thrombolytic therapy (time sensitive) Non-thrombolytic therapy: —monitoring/meds to decrease ICP Anticogulants/antiplt therapy
28
Hemorrhagic stroke tx
—early sx within 24hrs —STOP bleed
29
Signs of stroke
BEFAST Balance Eyes Face Arms Speech Time Sudden HA (worst HA of life)
30
Things to assess stroke
NIH ABC CT scan to r/o hemorrhagic stroke
31
What BP goal Ischemic Hemorrhagic
Ischemic: —SBP <220 —DBP <120 Hemorrhagic: —MAP <130
32
Thrombolytic therapy for ischemic stroke —what is the name? —inclusion criteria —exclusion criteria
tPA (ischemic stroke only) Inclusion: —onset under 3hrs Exclusion: —onset over 3hrs —bleeding
33
Non-thrombolytic candidates (Who cant have thrombolytic tx) (2) (What we do) (4)
WHO: —waited over 3hrs —on anticoagulants WHAT: —clot removal —avoid rapid drops in BP —do not administer any fluids w/dextrose —anticoag/antiplt if no hemorrhage
34
Aneurysm tx 2tx 2risks
Clip or endovascular coil Risk: —ischmeic if vasospasms —rebleeding
35
Malignant MCA infarct (Middle cerebral artery/main blood flow to brain) —s/s —mortality rate
—rapid neuro deterioration —80% mortality