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Nur 265 exam 3 study guide 2025
Increased icp (939-940, chart 941)
• Normal icp 10-15 mmhg, pressures >20 mmhg impair cerebral circulation
• Iicp is leading cause of death from head trauma in pts who reach the hospital alive.
• Cerebral perfusion pressure (cpp) o blood flow required to provide adequate oxygenation & glucose for brain
metabolism o maintenance above 70 mmhg o cpp= map-icp
map= (2xd) + s map needs to be atleast 80
3
• Compensation
o First response – csf is shunted or displaced into the spine (compliance) o next – reduction
of blood volume in the brain (autoregulation)
o As icp continues to increase cerebral perfusion decreases leading to brain tissue ischemia,
edema, vasodilation then acidosis which causes further increases icp
o In edema remains untreated the brain may herniate into spinal canal – death from brain
stem compression
• Assessment findings o changes in loc – first sign of iicp is declining loc & includes restlessness or confusion to
stuporous
w/o glucose & 02, brain shuts down. Ex. Pt knew who you were in am & now don’t remember o
headache – quite environment may have photophobia so keep room lights very low.
o Change in speech pattern – aphasia, slurred speech o changes in pupil size – 2 cm change
in either direction is significant, dilated or constricted, notify dr
Normal is 6 mm. Getting better if going back toward normal from dilated or constricted
Uneven pupils tx as iicp until proven otherwise; pinpoint - brain stem (pons) dysfunction o abnormal
posturing – decorticate (flexion) or decerebrate (extensor)
Decorticate – arms drawn to core, legs straight
Decerebrate – arms straight and stiff, pts rarely survive o hyperthermia – followed later by
hypothermia
When hypothermic – be concerned, pressure on hypothalamus located next to brain stem o cardiac
& respiratory rate/rhythm changes
Tachy first – increased hr & rr before brady hr & rr o n/v – common in iicp
o Cushing’s triad – severe htn, widened pulse pressure, bradycardia
Late response & indicates severe iicp w/loss of autoregulation, imminent death
Systolic bp increases bc decreased blood flow to brain
Pressure on vagus nerve and brainstem = bradycardia
• Managing iicp o elevate hob 30-45 degrees (unless contraindicated)
if hypotension, elevate hob where cpp >70 o
maintain head in a midline neutral position
o Avoid sudden and acute hip or neck flexion during positioning – log roll pt o avoid
clustering of care (bath followed by linen change) o coughing and suctioning increase icp o
decrease cerebral edema – osmotic diuretics (mannitol) & fluid restriction
Mannitol is hypertonic- pulling fluid into vascular space- will inc. Fluid output & monitor bp for htn
Furosemide used in adjunct to reduce incidence of rebound from mannitol. Helps reduce edema &
blood volume, decrease na uptake by the brain, & decrease production of csf at choroid plexus.
o Low csf using intraventricular drain system o control fever w/antipyretics or cooling
blanket – do not allow pt to shiver as will increase icp
When febrile every cell in body needs more 02 and glucose
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o Oxygenation – hyperventilate on a vent to decrease co2 which causes vasodilation o
Reduce cellul n (coma)
t
raumatic brain injury (946-957)
• Primary brain injury o occurs at time of injury
o Open – head fractured or penetrated; closed – blunt trauma, shaken baby o open head
injuries
Skull fractures
• Linear fx – thin line on x-ray, no tx unless underlying brain tissue damaged
• Depressed fx – brain damage from bruising (contusion), laceration from bone fragments basilar skull fx – fx of bones
of the base of skull & results in csf leak from nose & ears. O may not be seen on plain x-ray, r/f infection w/ csf leak
o Manifested by bruises around eyes(raccoon eyes) or behind ears (battle’s sign)
o has potential for hemorrhage if it damages the internal carotid
o Closed head injuries
Caused by blunt force trauma
Contusion – bruising to brain tissue @ site of impact (coup) or opposite (contercoup)
Laceration – tearing of the cortical surface vessels, lead to secondary hemorrhage, cerebral
edema and inflammation
Diffuse axonal injury (dai) – tissue of entire brain from high speed acel/decel mvc
• Impaired cognitive functioning, results in disorganization, impaired memory
• Severe will present with immediate coma, survivors require lone-term care
o Classified as
Mild – gcs 13-15 (concussion)
• Blow to head, transient confusion, or feeling dazed or disoriented
• Loss of consciousness for up to 30 min, loss of memory before and after accident
• No evidence of brain damage, sx resolve w/i 72 hrs
• Sx: ha, n/v, fatigue, foggy, balance off, irritable, sad, nervous, emotional, visual probs
moderate – gcs 9-12
• Loss of consciousness 30 min – 6 hrs w/ memory loss up to 24 hrs. short hospital stay to
prevent secondary injury memory loss up to 24 hrs.
Severe – gcs 3-8
• Loss of consciousness >6 hrs
• High risk for secondary brain injury from cerebral edema, hemorrhage, reduced perfusion
• Pupil changes, bradycardia, papilledema, htn w/wide pp, nuchal rigidity if csf leak
o Glasgow coma scale
Score from 3-15; score 3-8 in a coma
A change of 2 points requires immediate notification to hcp
• Secondary brain injury o any process that occurs after the initial injury and worsen
or negatively influences patient outcomes.
While trying to recover from initial event, something else happens (ex: meningitis) o
most common result from hypotension, hypoxia, iicp, & cerebral edema
Damage to brain tissue due to delivery of o2 and glucose to brain is interrupted
Low blood flow and hypoxemia contribute to cerebral edema o hypotension & hypoxia
Hypotension (map <70), hypoxia (pao2 <80)
Hypotension may be from shock & hypoxia from resp. Failure, loss of airway, or impaired
ventilation o increased intracranial pressure (iicp)
See increased icp section above
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O hemorrhage
Begins at moment of impact & potentially life threatening
Epidural hematoma – arterial bleeding between dura and inner skull, from fx of
temporal bone
• Have “lucid intervals” – pt awake & talking then momentary unconsciousness
Subdural hematoma – venous bleeding into space beneath dura & above arachnoid
• From laceration of brain tissue, bleeding is slower than epidural, highest mortality rate
• Acute sdh – w/i 48 hrs after impact
• Subacute sdh – 48 hrs – 2 weeks
• Chronic sdh – 2 weeks to several months
A loss of consciousness from an epidural or subdural hematoma is a neurological emergency!
O hydrocephalus – abnormal increase in csf volume
Caused by impaired reabsorption or blockage with outflow of csf, leads to iicp o brain herniation
Uncus- dilated non-reactive pupils, ptosis, decreased loc
Central – down shift brain stem – cheyne-stokes, pinpoint & nonreactive pupils, hemodynamic
instability. Notify physicial immediately
• Etiology o young males, play more sports, take more risks when driving
(mvc) , consume more alcohol o falls most common in older adults.
• Assessment/interventions o hx – did pt lose consciousness? Drug or alcohol
consumption? All screened for abuse/neglect o physical
First priority is assessment of abcs - report any sign of respiratory problems
immediately!
Suspect neck injury until proven otherwise, stabilize w/ c-collar and backboard
• Skin breakdown & pressure ulcer formation are concern with spine board &
c-collar
• Once board removed, spinal precautions maintained until hcp indicates it is
safe o (1) bedrest; (2) no neck flexion with a pillow or roll; (3)no thoracic or
lumbar flexion w/hob elevation (reverse t acceptable); (4) manual control of
c spine anytime collar removed; (5) log roll
Prevent secondary brain injury – o2 & lowering icp, vent if needed, do not want co2
to rise as it causes vasodilation & iicp.
o Vital signs
Monitor vs q 1-2 hrs – may be hypotensive or hypertensive (iv fluids to maintain above 90)
Central fever caused by hypothalamic damage – no sweating, high, last days-weeks
• Responds better to cooling (sponge bath, cool air)
• Fever from any cause is associated w/higher mortality rates
Cushing’s triad – htn, wide pp, & bradycardia – late sign of iicp and indicates imminent death
Hypotension and tachycardia indicate hypovolemic shock
o Neuro gcs
Most important variable to assess w/any brain injury is loc
Dec or change in loc is first sign of deterioration (behavior changes, restlessness, disorientation)
assess pupils
• Pinpoint - & nonresponsive – brainstem dysfunction @ level of ponds
• Asymmetric, loss of light reaction, unilateral or bilateral dialed – herniation o late
signs of iicp – severe ha, n/v, seizures, papilledema - always sign of iicp
Motor response - decorticate or decerebrate posturing o psychosocial
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Nur 265 exam 3 study guide 2025
Increased icp (939-940, chart 941)
• Normal icp 10-15 mmhg, pressures >20 mmhg impair cerebral circulation
• Iicp is leading cause of death from head trauma in pts who reach the hospital alive.
• Cerebral perfusion pressure (cpp) o blood flow required to provide adequate oxygenation & glucose for brain
metabolism o maintenance above 70 mmhg o cpp= map-icp
map= (2xd) + s map needs to be atleast 80
3
• Compensation
o First response – csf is shunted or displaced into the spine (compliance) o next – reduction
of blood volume in the brain (autoregulation)
o As icp continues to increase cerebral perfusion decreases leading to brain tissue ischemia,
edema, vasodilation then acidosis which causes further increases icp
o In edema remains untreated the brain may herniate into spinal canal – death from brain
stem compression
• Assessment findings o changes in loc – first sign of iicp is declining loc & includes restlessness or confusion to
stuporous
w/o glucose & 02, brain shuts down. Ex. Pt knew who you were in am & now don’t remember o
headache – quite environment may have photophobia so keep room lights very low.
o Change in speech pattern – aphasia, slurred speech o changes in pupil size – 2 cm change
in either direction is significant, dilated or constricted, notify dr
Normal is 6 mm. Getting better if going back toward normal from dilated or constricted
Uneven pupils tx as iicp until proven otherwise; pinpoint - brain stem (pons) dysfunction o abnormal
posturing – decorticate (flexion) or decerebrate (extensor)
Decorticate – arms drawn to core, legs straight
Decerebrate – arms straight and stiff, pts rarely survive o hyperthermia – followed later by
hypothermia
When hypothermic – be concerned, pressure on hypothalamus located next to brain stem o cardiac
& respiratory rate/rhythm changes
Tachy first – increased hr & rr before brady hr & rr o n/v – common in iicp
o Cushing’s triad – severe htn, widened pulse pressure, bradycardia
Late response & indicates severe iicp w/loss of autoregulation, imminent death
Systolic bp increases bc decreased blood flow to brain
Pressure on vagus nerve and brainstem = bradycardia
• Managing iicp o elevate hob 30-45 degrees (unless contraindicated)
if hypotension, elevate hob where cpp >70 o
maintain head in a midline neutral position
o Avoid sudden and acute hip or neck flexion during positioning – log roll pt o avoid
clustering of care (bath followed by linen change) o coughing and suctioning increase icp o
decrease cerebral edema – osmotic diuretics (mannitol) & fluid restriction
Mannitol is hypertonic- pulling fluid into vascular space- will inc. Fluid output & monitor bp for htn
Furosemide used in adjunct to reduce incidence of rebound from mannitol. Helps reduce edema &
blood volume, decrease na uptake by the brain, & decrease production of csf at choroid plexus.
o Low csf using intraventricular drain system o control fever w/antipyretics or cooling
blanket – do not allow pt to shiver as will increase icp
When febrile every cell in body needs more 02 and glucose
Downloaded by NELSON KIIRU ()
, lOMoARcPSD|26582732
o Oxygenation – hyperventilate on a vent to decrease co2 which causes vasodilation o
Reduce cellul n (coma)
t
raumatic brain injury (946-957)
• Primary brain injury o occurs at time of injury
o Open – head fractured or penetrated; closed – blunt trauma, shaken baby o open head
injuries
Skull fractures
• Linear fx – thin line on x-ray, no tx unless underlying brain tissue damaged
• Depressed fx – brain damage from bruising (contusion), laceration from bone fragments basilar skull fx – fx of bones
of the base of skull & results in csf leak from nose & ears. O may not be seen on plain x-ray, r/f infection w/ csf leak
o Manifested by bruises around eyes(raccoon eyes) or behind ears (battle’s sign)
o has potential for hemorrhage if it damages the internal carotid
o Closed head injuries
Caused by blunt force trauma
Contusion – bruising to brain tissue @ site of impact (coup) or opposite (contercoup)
Laceration – tearing of the cortical surface vessels, lead to secondary hemorrhage, cerebral
edema and inflammation
Diffuse axonal injury (dai) – tissue of entire brain from high speed acel/decel mvc
• Impaired cognitive functioning, results in disorganization, impaired memory
• Severe will present with immediate coma, survivors require lone-term care
o Classified as
Mild – gcs 13-15 (concussion)
• Blow to head, transient confusion, or feeling dazed or disoriented
• Loss of consciousness for up to 30 min, loss of memory before and after accident
• No evidence of brain damage, sx resolve w/i 72 hrs
• Sx: ha, n/v, fatigue, foggy, balance off, irritable, sad, nervous, emotional, visual probs
moderate – gcs 9-12
• Loss of consciousness 30 min – 6 hrs w/ memory loss up to 24 hrs. short hospital stay to
prevent secondary injury memory loss up to 24 hrs.
Severe – gcs 3-8
• Loss of consciousness >6 hrs
• High risk for secondary brain injury from cerebral edema, hemorrhage, reduced perfusion
• Pupil changes, bradycardia, papilledema, htn w/wide pp, nuchal rigidity if csf leak
o Glasgow coma scale
Score from 3-15; score 3-8 in a coma
A change of 2 points requires immediate notification to hcp
• Secondary brain injury o any process that occurs after the initial injury and worsen
or negatively influences patient outcomes.
While trying to recover from initial event, something else happens (ex: meningitis) o
most common result from hypotension, hypoxia, iicp, & cerebral edema
Damage to brain tissue due to delivery of o2 and glucose to brain is interrupted
Low blood flow and hypoxemia contribute to cerebral edema o hypotension & hypoxia
Hypotension (map <70), hypoxia (pao2 <80)
Hypotension may be from shock & hypoxia from resp. Failure, loss of airway, or impaired
ventilation o increased intracranial pressure (iicp)
See increased icp section above
Downloaded by NELSON KIIRU ()
, lOMoARcPSD|26582732
O hemorrhage
Begins at moment of impact & potentially life threatening
Epidural hematoma – arterial bleeding between dura and inner skull, from fx of
temporal bone
• Have “lucid intervals” – pt awake & talking then momentary unconsciousness
Subdural hematoma – venous bleeding into space beneath dura & above arachnoid
• From laceration of brain tissue, bleeding is slower than epidural, highest mortality rate
• Acute sdh – w/i 48 hrs after impact
• Subacute sdh – 48 hrs – 2 weeks
• Chronic sdh – 2 weeks to several months
A loss of consciousness from an epidural or subdural hematoma is a neurological emergency!
O hydrocephalus – abnormal increase in csf volume
Caused by impaired reabsorption or blockage with outflow of csf, leads to iicp o brain herniation
Uncus- dilated non-reactive pupils, ptosis, decreased loc
Central – down shift brain stem – cheyne-stokes, pinpoint & nonreactive pupils, hemodynamic
instability. Notify physicial immediately
• Etiology o young males, play more sports, take more risks when driving
(mvc) , consume more alcohol o falls most common in older adults.
• Assessment/interventions o hx – did pt lose consciousness? Drug or alcohol
consumption? All screened for abuse/neglect o physical
First priority is assessment of abcs - report any sign of respiratory problems
immediately!
Suspect neck injury until proven otherwise, stabilize w/ c-collar and backboard
• Skin breakdown & pressure ulcer formation are concern with spine board &
c-collar
• Once board removed, spinal precautions maintained until hcp indicates it is
safe o (1) bedrest; (2) no neck flexion with a pillow or roll; (3)no thoracic or
lumbar flexion w/hob elevation (reverse t acceptable); (4) manual control of
c spine anytime collar removed; (5) log roll
Prevent secondary brain injury – o2 & lowering icp, vent if needed, do not want co2
to rise as it causes vasodilation & iicp.
o Vital signs
Monitor vs q 1-2 hrs – may be hypotensive or hypertensive (iv fluids to maintain above 90)
Central fever caused by hypothalamic damage – no sweating, high, last days-weeks
• Responds better to cooling (sponge bath, cool air)
• Fever from any cause is associated w/higher mortality rates
Cushing’s triad – htn, wide pp, & bradycardia – late sign of iicp and indicates imminent death
Hypotension and tachycardia indicate hypovolemic shock
o Neuro gcs
Most important variable to assess w/any brain injury is loc
Dec or change in loc is first sign of deterioration (behavior changes, restlessness, disorientation)
assess pupils
• Pinpoint - & nonresponsive – brainstem dysfunction @ level of ponds
• Asymmetric, loss of light reaction, unilateral or bilateral dialed – herniation o late
signs of iicp – severe ha, n/v, seizures, papilledema - always sign of iicp
Motor response - decorticate or decerebrate posturing o psychosocial
Downloaded by NELSON KIIRU ()
