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NURS 412 > Central Nervous System (ICP) > Flashcards

Central Nervous System (ICP) Flashcards

1
Q

What are the two components of the nervous system?

A

Central nervous system
Peripheral nervous system

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2
Q

What makes up the central nervous system?

A

Cerebrum (cerebral hemispheres)
Brain stem
Cerebellum
Spinal cord
- Ascending tracts
- Descending tracts
- Lower motor neurons
- Upper motor neurons
- Reflex arc

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3
Q

What are the major three components of the brain?

A

Cerebrum
Cerebellum
Brain stem

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4
Q

What makes up the cerebrum?

A

Frontal lobe
Temporal lobe
Parietal lobe
Occipital lobe

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5
Q

What does the frontal lobe do?

A

Controls higher cognitive functions, memory, voluntary movements,
Broca’s area in (L) hemisphere (for expressive speech & language)

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6
Q

What does the temporal lobe do?

A

Integration of somatic, visual, and auditory data and Wernicke’s area (responsible for receptive language)

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7
Q

What does the parietal lobe do?

A

Composed of sensory cortex
Controls and interprets spatial formation

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8
Q

What does the occipital lobe do?

A

process visual data

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9
Q

What does the cerebrum enclose?

A

encloses basal ganglia, thalamus, hypothalamus, and limbic system.

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10
Q

Why is it important to know what the different lobes do?

A

If something is not working then you know which lobe is affected and what symptoms to look for

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11
Q

What does the brain stem consist of?

A

Consists of:
Midbrain
Pons
Medulla
- vital centres concerned with respiratory, vasomotor, and cardiac function are located in medulla (PROTECT) - can stop breathing

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12
Q

Cerebellum

A

Located inferior to occipital lobe
Coordinates voluntary movement & maintains trunk stability, and equilibrium
Receives information from cerebral cortex, muscles, joints and inner ear

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13
Q

Ventricles

A

4 cavities within the brain, filled with CSF

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14
Q

Cerebro-spinal fluid

A

clear, colourless
circulates with subarachnoid space
provides cushioning for brain and spinal cord
allows fluid shifts from cranial cavity to spinal cavity
carries nutrients
absorbed through arachnoid villi
CSF pressure is measured in pts with actual or suspected intracranial diseases
increase in CSF pressure indicates increase in intracranial pressure (ICP) which can lead to herniation of brain

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15
Q

Cerebral circulation

A

Blood-brain barrier
- Physiological barrier between blood capillaries and brain tissue
- Protects brain from certain harmful agents, while allowing nutrients
- Affects penetration of drugs → only certain ones enter
(Lipid-soluble drugs enter quickly)
(Water-soluble and ionized drugs enter slowly)

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16
Q

Protective structures of the brain

A

Meninges (dura matter, arachnoid, pia mater) - surround brain and spinal cord
Skull
Vertebral column

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17
Q

Dura matter

A

Outermost layer
falx cerebri → fold of dura two cerebral hemispheres
Tentorium cerebelli → a fold of dura that separate cerebral hemispheres from posterior fossa (which contains brain stem & cerebellum)

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18
Q

Arachnoid matter

A

Delicate, impermeable membrane, lies between dura matter & pia matter
Arteries, veins, and cranial nerves passing to and from brain must mass through subarachnoid space (space between arachnoid layer and pia matter)

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19
Q

Pia matter

A

Delicate, innermost layer of meninges

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20
Q

how does the skull affect ICP?

A
  • A closed space so pressure only rises so much and the brain is compressed and ischemia
  • volume from 3 components: CSF , blood and brain tissue
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21
Q

Primary injury ICP

A

initial time of injury

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22
Q

Secondary injury ICP

A

results from hypoxia, Ischemia, hypotension, edema, increased intracranial pressure

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23
Q

Regulation of ICP

A

Pressure exerted from total volume of 3 components within the skull
- Brain tissue, blood, CSF
If vol of any of 3 components ↑ without corresponding ↓ in another component → results in ↑ ICP (Monroe/Kelly hypothesis)

24
Q

Measure of ICP

A

In ventricles, subarachnoid space, subdural space, epidural space, or brain tissue using a pressure transducer
Normal ICP: 5- 15 mmHg
Sustained ICP >20 mmHg = abnormal (not contusive to life)

25
Q

Compensatory mechanisms

A

Mechanisms to resist ↑ in ICP by:
1. Changes in CSF volume
- by displacement of CSF, e.g., into spinal subarachnoid space, or
- altering production and absorption rates of CSF
2. Altering intracranial blood vol by compression of veins, or vasoconstriction/vasodilation, or changes in venous outflow
3. Brain tissue vol
- Distention of dura, or compression of brain tissue

However, compensatory adaptation are finite

26
Q

Cerebral blood flow (CBF)

A

amount of blood (mL) passing through 100 gms of brain tissue/min → approx. 750ml/min
Brain is unable to store oxygen and glucose - Need blood flow and oxygen to breath and function

27
Q

Brain autoregulation

A

Brain has ability to autoregulate its own blood flow in response to metabolic needs (= called autoregulation)
Automatic alteration in diameter of cerebral flow to maintain constant blood flow
Autoregulation does not work in extreme hypo/hypertension

28
Q

When does cerebral ischemia occur?

A

If MAP < 50 mmHg, CBF ↓ and cerebral ischemia occurs
If MAP > 150 mmHg, cerebral vessels are maximally constricted, and further response is lost

29
Q

What are additional factors besides autoregulation that affect CBF?

A

Increased Carbon Dioxide in the blood (↑ PaCO2 ) causes cerebral vasodilation, ↓ vascular resistance, and ↑ cerebral blood flow (CBF) if carbon dioxide is decreased in the blood this is reversed and CBF is decreased.
PaO2 <50 mmHg → vascular dilation, increasing CBF.
In acidotic environment, further vasodilation in attempt to ↑ blood flow

30
Q

What can CBF be indirectly reflected by?

A

CPP - cerebral perfusion pressure

31
Q

What is CPP?

A

the pressure needed to ensure adequate perfusion to brain tissue

32
Q

How do we calculate CPP?

A

MAP - ICP

MAP = SBP + 2 (DBP) /3

33
Q

What is normal CPP?

A

70-100 mmHg

Min of CPP 50-60 mmHg required for adequate cerebral perfusion
CPP < 50 mmHg → cerebral ischemia
CPP < 30 mmHg → incompatible with life
Note: CPP does not reflect perfusion pressure in ALL parts of the brain
Imperative to maintain MAP when ICP is ↑

34
Q

What is the mechanisms of increased ICP?

A

Cerebral edema - ↑ accumulation of fluid in extravascular spaces of brain tissue
Contusion – bruise to brain (swelling)
Cerebral abscess – puss filled pocket of infection in the brain. EMERGENCY treatment, causes swelling, bacteria enters – infected ears can cause it)
Cerebral neoplasm (tumor, cancerous or non-cancerous)

Crucial factor → preservation of brain tissue by maintaining cerebral blood flow

35
Q

What are the different types of ICP?

A

Vasogenic cerebral edema
Cytotoxic cerebral edema
Interstitial cerebral edema

36
Q

What is Vasogenic cerebral edema?

A

Most common type
From changes in endothelial lining of cerebral capillaries
↑ in permeability of blood-brain barrier and ↑ extracellular fluid vol
Occurs mainly in white matter

37
Q

What is Cytotoxic edema?

A

From disruption of integrity of cell membrane
Results from destructive lesions or trauma to brain tissue, leading to cerebral hypoxia/anoxia, Na+ depletion, syndrome of inappropriate antidiuretic hormone (SIADH)
Fluid and protein shift from extracellular space into cells
- Hyponatremia (results in)
Most often in grey matter

38
Q

what is Interstitial cerebral edema?

A

Result of diffusion of ventricular CSF in an uncontrolled hydrocephalus (ventricles of the brain enlarge)

39
Q

What are the manifestations of increased ICP

A

Change in LOC (may be subtle, flattening affect, confusion, reduced level of attention)
Change in VS
- crushings triad (decreased HR, decreased RR/irreg., widening pulse pressure)
Ocular signs
- dilation of pupil ipsilateral – same side of affected side
- sluggish or no response to light
- inability to move eye upward, drooping of eyelid
- fixed unlarteray dialated pupil – EMERGENCY (BRAIN HERNIA)
Decreased motor function
- Decorticate (flexor)
- Decerebrate (extensor) - More serious damage
Headache - From compression of intracranial structures, e.g., arteries, veins, nerves, Pain is continuous
Vomiting
- Not proceeded by nausea
- From direct pressure on vomiting center in 4th ventricle in medulla.
- Vomiting associated with ↑ ICP is projectile

40
Q

What is crushings triad?

A

decreased HR, decreased RR/irreg., widening pulse pressure
medical emergency
means brain stem is involved

41
Q

Early signs of increased iCP

A

(Altered LOC)
Unilateral pupil changes in size, equality, and/or reactivity
Altered respiratory pattern, e.g., bradypnea, or irregular
Unilateral hemiparesis (weakness to one side of the body)
Focal findings (e.g, speech difficulty
Papiledema (swelling behind eye)
Vomiting, headache, seizures

42
Q

Late signs of increased ICP

A

[↓ LOC (stupor)]
Unilateral or bilateral pupillary changes, i.e. size, equality, and/or reactivity
Cheyne-Stokes respiration (period of fast shallow breathing, periods of deeper breathing and slowed, periods of apnea)
Decorticate or decerebrate posturing

43
Q

Terminal signs of increased ICP

A

Coma
Bilaterally fixed and dilated pupils
Resp. Arrest
Absence of motor response

44
Q

When does crushings triad come in?

A

Late and terminal signs

45
Q

Patho if increased ICP

A

insult to brain
tissue edema
increased ICP
compression of ventricles
compression of blood vessels
decreased cerebral blood flow
decreased o2 with death of brain cells
edema around necrotic tissues
increased ICP with compression of brain stem and resp centre
accumulation of CO2
vasodilation
increased ICP resulting from increased blood volume
death

46
Q

What are the causes of cerebral edema?

A

Mass lesions
- Brain abscess, brain tumor, Hematoma, hemorrhage
Head injuries
- Contusion, Diffuse axonal injury, Hemorrhage, post-traumatic brain swelling
Cerebral infections
- Meningitis, Encephalitis
Brain surgery
Vascular insult
- Anoxic & ischemic episodes, Cerebral infarction (thrombotic or embolic), Venous sinus thrombosis (blood clot, blood is unable to drain)
Toxic or metabolic encephalopathic conditions
- Hepatic encephalopathy, Lead or arsenic intoxication, Uremia

47
Q

Complications of increased ICP

A

1, Inadequate cerebral perfusion
2. Cerebral herniation (occurs as brain tissue is shifted from high to low pressure, intense pressure is put on the brain stem)

Falx cerebri
Tentorium cerebelli
Tentorial incisura

48
Q

What are the different types of herniation?

A

Cingulate herniation (moves past midline where brain should be)
Tentorial herniation
Cerebellar tonsillar herniation (pushes brain down into brain stem)

49
Q

Diagnostic studies of increased ICP

A

MRI
CT scan
MRA
CTA

Above tests are used to differentiate many conditions that can cause ↑ ICP and to evaluate therapeutic options

50
Q

Goal of care of increased ICP

A

identify and treat the underlying cause of increased ICP and to support brain function

51
Q

Care of increased ICP

A

Drug therapy
- Mannitol – diuretic (osmotic affect, fluids move from brain tissue to vessels, goes to kidneys)
- Hypertonic saline (draws fluid into blood)
- Corticosteroids (decreased swelling)
- Pain control (decreased responses in GCS), can not give much pain meds
Nutritional therapy
-Pts with ↑ICP are in hypermetabolic & hypercatabolic state → ↑need for glucose for fuel among other considerations
Supportive therapy
- Metabolic demands such as fever, agitation, shivering, pain, and seizures can ↑ICP – increases metabolism (can use Antipyretics, cooling, seizure meds, Induced coma – decreases metabolic demand, keeps patient calm, Inducing hypothermia to suppress cerebral metabolism. This is often done for several days but extended hypothermia makes the patient susceptible to systemic infections and hypotension)

52
Q

GCS scale

A

Eyes:
4 - eyes open spontaneously
3 - Eyes open to verbal command, speech or shout
2 - eyes open to pain
1 - no eye opening

Verbal response:
5 - oriented
4 - confused conversation, but able to answer questions
3 - inappropriate responses
2 - Incomprehensible sounds or speech
1 - no verbal response

Motor response
6 - obeys commands
5 - purposeful movement to painful stimulus
4 - withdrawals from pain
3 - abnormal (spastic) flexion, decorticate posture
2 - extensor (rigid) response, decerebrate posture
1 - no motor response

53
Q

When would you not be able to use GCS?

A

Sleeping, pain meds

54
Q

What is key with GCS?

A

change
Score less than or equal to 8 at 6 hours post injury - 50% die

55
Q

Nursing management

A
  1. GCS
  2. Neurological assessment
    - Pupils compared for size, movement, and response (use penlight).
    - Evaluate cranial nerves.
    - For unconscious patients, observe their spontaneous movement.
    - If no spontaneous movement, painful stimuli are applied.
    - VS.

Respiratory function
Fluid & electrolyte balance
Monitoring ICP
Body position- HOB at least up 30 degrees, head midline, turn slowly
Protection from injury- confusion, agitation, seizures ( meds)
Psychological consideration (how is it affecting them and their family)
Meet nutritional needs

NURS 412 (21 decks)

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