Central Nervous System (ICP) Flashcards
What are the two components of the nervous system?
Central nervous system
Peripheral nervous system
What makes up the central nervous system?
Cerebrum (cerebral hemispheres)
Brain stem
Cerebellum
Spinal cord
- Ascending tracts
- Descending tracts
- Lower motor neurons
- Upper motor neurons
- Reflex arc
What are the major three components of the brain?
Cerebrum
Cerebellum
Brain stem
What makes up the cerebrum?
Frontal lobe
Temporal lobe
Parietal lobe
Occipital lobe
What does the frontal lobe do?
Controls higher cognitive functions, memory, voluntary movements,
Broca’s area in (L) hemisphere (for expressive speech & language)
What does the temporal lobe do?
Integration of somatic, visual, and auditory data and Wernicke’s area (responsible for receptive language)
What does the parietal lobe do?
Composed of sensory cortex
Controls and interprets spatial formation
What does the occipital lobe do?
process visual data
What does the cerebrum enclose?
encloses basal ganglia, thalamus, hypothalamus, and limbic system.
Why is it important to know what the different lobes do?
If something is not working then you know which lobe is affected and what symptoms to look for
What does the brain stem consist of?
Consists of:
Midbrain
Pons
Medulla
- vital centres concerned with respiratory, vasomotor, and cardiac function are located in medulla (PROTECT) - can stop breathing
Cerebellum
Located inferior to occipital lobe
Coordinates voluntary movement & maintains trunk stability, and equilibrium
Receives information from cerebral cortex, muscles, joints and inner ear
Ventricles
4 cavities within the brain, filled with CSF
Cerebro-spinal fluid
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
Cerebral circulation
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)
Protective structures of the brain
Meninges (dura matter, arachnoid, pia mater) - surround brain and spinal cord
Skull
Vertebral column
Dura matter
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)
Arachnoid matter
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)
Pia matter
Delicate, innermost layer of meninges
how does the skull affect ICP?
- 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
Primary injury ICP
initial time of injury
Secondary injury ICP
results from hypoxia, Ischemia, hypotension, edema, increased intracranial pressure
Regulation of ICP
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)
Measure of ICP
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)
Compensatory mechanisms
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
Cerebral blood flow (CBF)
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
Brain autoregulation
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
When does cerebral ischemia occur?
If MAP < 50 mmHg, CBF ↓ and cerebral ischemia occurs
If MAP > 150 mmHg, cerebral vessels are maximally constricted, and further response is lost
What are additional factors besides autoregulation that affect CBF?
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
What can CBF be indirectly reflected by?
CPP - cerebral perfusion pressure
What is CPP?
the pressure needed to ensure adequate perfusion to brain tissue
How do we calculate CPP?
MAP - ICP
MAP = SBP + 2 (DBP) /3
What is normal CPP?
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 ↑
What is the mechanisms of increased ICP?
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
What are the different types of ICP?
Vasogenic cerebral edema
Cytotoxic cerebral edema
Interstitial cerebral edema
What is Vasogenic cerebral edema?
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
What is Cytotoxic edema?
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
what is Interstitial cerebral edema?
Result of diffusion of ventricular CSF in an uncontrolled hydrocephalus (ventricles of the brain enlarge)
What are the manifestations of increased ICP
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
What is crushings triad?
decreased HR, decreased RR/irreg., widening pulse pressure
medical emergency
means brain stem is involved
Early signs of increased iCP
(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
Late signs of increased ICP
[↓ 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
Terminal signs of increased ICP
Coma
Bilaterally fixed and dilated pupils
Resp. Arrest
Absence of motor response
When does crushings triad come in?
Late and terminal signs
Patho if increased ICP
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
What are the causes of cerebral edema?
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
Complications of increased ICP
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
What are the different types of herniation?
Cingulate herniation (moves past midline where brain should be)
Tentorial herniation
Cerebellar tonsillar herniation (pushes brain down into brain stem)
Diagnostic studies of increased ICP
MRI
CT scan
MRA
CTA
Above tests are used to differentiate many conditions that can cause ↑ ICP and to evaluate therapeutic options
Goal of care of increased ICP
identify and treat the underlying cause of increased ICP and to support brain function
Care of increased ICP
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)
GCS scale
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
When would you not be able to use GCS?
Sleeping, pain meds
What is key with GCS?
change
Score less than or equal to 8 at 6 hours post injury - 50% die
Nursing management
- GCS
- 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
