Cerebral perfusion Flashcards
3 components of neuro assessment
level of consciousness
pupillary reaction
vital signs (MAP)
components of pupillary assessment
size
equality
shape
degree of reactivity to light
apraxia
inability to perform learned movement
cerebral cortex injury
ataxia
lack of coordination
cerebellar injury
dyskinesia
impaired voluntary movements
hemiplegia
paralysis on 1 side of body
lesion of contralateral cortex
nystagmus
jerking-bobbing of eyes when trying to track
drugs/ETOH, brainstem injury
anesthesia
complete absence of sensation
paresthesia
alteration of sensation
posterior column
cranial nerve 1
olfactory
sensory: nose
cranial nerve 2
optic
sensory: eye
cranial nerve 3
oculomotor
motor: all eye muscles except those supplied by 4 and 5
cranial nerve 4
trochlear
motor: superior oblique muscle
cranial nerve 5
trigeminal
sensory: face, sinuses, teeth, etc
motor: muscles of mastication
cranial nerve 6
abducens
motor: external rectus muscle
cranial nerve 7
facial
motor: muscles of the face
cranial nerve 8
vestibulocochlear
sensory: inner ear
cranial nerve 9
glossopharyngeal
motor: pharyngeal musculature
cranial nerve 10
vagus
motor: heart, lungs, bronchi, GI tract
sensory: heart, lungs, bronchi, trachea, larynx, pharynx, GI tract, inner ear
cranial nerve 11
accessory
motor: sternocleidomastoid and trapezius muscles
cranial nerve 12
hypoglossal
motor: muscles of the tounge
airway assessment
maintain c-spine precautions
loose teeth, vomitus, bleeding
edema, neck swelling
LOC
breathing assessment
skin color
breathing spontaneously
respiratory rate/pulse oximetry/ETCO2
chest rise and fall, symmetry
breath sounds
circulation assessment
skin color
temp
pulse
blood pressure
obvious bleeding
components of GCS
eye opening
verbal response
motor response
2 types of traumas for TBI
blunt
penetrating
blunt TBI
injury with no opening in the skin or communication with the environment
motor vehicle crash, assault, fall
penetrating TBI
foreign object penetrates the body
gunshot, stabbing, impalement
types of blunt TBIs
skull fracture
concussion
contusion
hematoma: epidural, subdural, intracerebral
diffuse axonal injury
linear skull fracture
break in bone but no displacement
usually from low velocity injury
depressed skull fracture
inward indentation of the skull, requires a powerful impact
simple skull fracture
can be linear or depresses
no fragmentation or communicating lacerations
from low/moderate impact
comminuted skull fracture
multiple linear fractures with fragmentation of bone into many pieces
from direct, high momentum impact
compound skull fracture
depressed fracture and scalp laceration with communicating pathway into the intracranial cavity, severe injury
two tale tell signs of basilar skull fracture
racoon eyes
battle sign
concussion
occurs after the blow to the head hard enough to move the brain within the skull
contusion
occurs after a more severe injury when the brain rebounds against the skull from the force of a blow
injury is directly underneath site of impact
coup-contracoup injury
brains hits both sides of skull, side on injury and opposite side
diffuse axonal injury
shearing damage to the pathways (axons) that connect the different areas of the brain
occurs when there is twisting and turning of the brain tissue at the time of injury
brain messages are slowed or lost
torn axons cannot be repaired
two types of stroke
hemorrhagic
ischemic
2 types of ischemic stroke
embolic
hemorrhagic
causes of a ischemic stroke
thrombosis (develops in brain)
embolism (travels to brain)
causes of a hemorrhagic stroke
subarachnoid hemorrhage
intracerebral hemorrhage
rupture of a stressed cerebral vessel, aneurysm, or vascular malformation
assessment of stroke
decreased consciousness
changing personality
drooping mouth and eyelid
paralysis or weakness on one or both sides
arm drift, possible seizures
pupillary changes
increased BP, HR, RR
nausea and vomiting
pain
stroke assessment tools
BE FAST
NIH Stroke Scale
BE FAST stroke assessment
balance
eyes (vision)
facial droop
arm drift
speech difficulty
time to call
stroke diagnostic testing
CT scans
MRI
lumbar puncture
doppler ultrasound and duplex imaging
echocardiogram
24 hrs of continuous cardiac monitoring
CT angiography
stroke ambulance and portable CT scan
medical management of a stroke
optimize cerebral oxygenation
maintain a patent airway
restore cerebral blood flow with thrombolytic therapy, tPA
manage BP and temp
minimize risk of stroke recurrence with anti-coagulant/platelet meds
prevent aspiration
PT/OT asap
seizure precautions
medical management of ischemic stroke
infusion of rTPA (tissue plasminogen activator)
mechanical thrombectomy
anticoagulant medications
mannitol for cerebral edema
surgical management of ischemic stroke
mechanical thrombectomy
catheters to deliver TPA to site of clot and/or deploy a retrieval device
types of mechanical clot removal
coil retrievers
aspiration devices
medical management for hemorrhagic stroke and its vasospasm
calcium channel blockers: nimodipine, verapamil
triple H therapy: hypertension, hypervolemia, hemodilution
medical management for hemorrhagic stroke and its obstructive hydrocephalus
external ventricular drain (EVD)
aka “ventric”, “ventriculostomy”
surgical management of a hemorrhagic stroke
craniotomy
craniectomy
aneurysm clipping or coiling
burr holes
epidural hematoma location
between skull and the outer endosteal layer of the dura mater
is an epidural hematoma an arterial or venous bleed
arterial
source of epidural hematoma
temperoparietal locus: middle meningeal artery (most common)
frontal locus: anterior ethmoidal artery
occipital locus: transverse or sigmoid sinuses
vertex locus: superior sagittal sinus
why does an epidural hematoma form a biconvex lens
the expansion stops at skull’s sutures, where the dura mater is tightly attached to the skull
epidural hematoma symptoms
changes in level of consciousness
nausea and vomiting
focal deficits
treatment for epidural hematoma
rapid surgical evacuation of blood and stopping bleed
location of subdural hematoma
between the dura and the arachnoid layers
source of bleed in a subdural hematoma
bridging veins
what type of lens is present in a subdural hematoma on xray
concave, crescent-shaped lens
because bleed crosses suture lines
symptoms of a subdural hematoma
gradually increasing headache, confusion, and LOC change
location of a subarachnoid hemorrhage
bleeding into the subarachnoid space
diagnostic tests for subarachnoid hemorrhage
CT
lumbar puncture
MRU
subarachnoid hemorrhage causes
smoking, heavy drinking, illicit drugs
genetic
people between 30 and 40 years of age
more common in women than men
treatment of a subarachnoid hemorrhage
early neurosurgical intervention
nursing care for a subarachnoid hemorrhage
CLOSE observation
decrease BP
nimodipine for vasospams
drain care
decrease stimulation, do not cluster care
what is an intracerebral blled
bleeding anywhere in the brain
what causes an intracerebral bleed
trauma
severe head injury
abnormalities of the blood vessels
aneurysm
angioma
uncontrolled HTN
shearing injury in intracerebral hemorrhage
shear forces from brain movement commonly cause vessel laceration and hemorrhage into the parenchyma
monroe-kellie hypothesis
skull is a rigid compartment filled to capacity with essentially non-compressible contents
if volume rises in one compartment, there has to be a decrease in one of the other compartments for pressure to remain unchanged
percentages for the contents of the brain in regards to monroe-kellie hypothesis
brain 80%
blood 10%
CSF 10%
normal ICP
0-15 mmHg
increased ICP
life threatening
persistent increase 20mmHg or more for >5min
autoregulation
compensatory mechanism to keep cerebral blood flow constant
cerebral blood vessels automatically constrict or dilate to maintain adequate cerebral perfusion pressure (CPP)
factors that impact autoregulation
MAP, CO2, O2 levels
autoregulation response to increase in MAP
cerebral blood vessels constrict so the brain doesn’t get too much blood
autoregulation response to decreased MAP
cerebral blood vessels dilate to increase blood flow
autoregulation response to increase in CO2 or O2 decreases
cerebral blood vessels dilate
equation for cerebral perfusion pressure
CPP = MAP - ICP
normal CPP
80-100mHg
an increase in ICP does what to CPP
decreased CPP
what happens with a CPP less than 70
ischemia and death
what happens when MAP gets too high or too low
autoregulation does not work :(
primary injury
damage to the brain from the bio-mechanical effects of the trauma
secondary injury
the result of the hypotension, hypoxia, and elevated ICP
pathophysiology of secondary brain injury
primary brain injury ->
inflammatory response triggered by damaged cells ->
increased vascular permeability and vasodilation -> vasogenic edema -> cerebral ischemia and impaired autoregulation -> decreased ATP production and increased lactic acidosis -> increased intracellular influx of Na, Cl, Ca, H2O -> cytotoxic edema -> and repeat at cerebral ischemia
neurogenic fever
damage to the hypothalamus
core, rectal, and brain temperatures all differ, with brain temp the higheste
effects of a fever
increased cerebral blood flow and cerebral metabolic rate
increased ICP
increases O2 consumption
neurogenic fever nursing implications
targeted temp management
antipyretics
cooling devices: washcloths, blankets, fans
prevent shivering (increases O2 demand)
induced hypothermia
effects of seizures on the brain
increased cerebral metabolic rate and increased ICP
indications for dilantin
intracranial hemorrhage
witnessed seizure activity
depressed skull fracture
penetrating head wound
lorazepam indication
seizures
lorazepam + seizure nursing implications
maintain airway
monitor VS
note timing of seizure (onset + termination)
barbiturate coma (BI)
reduces cerebral blood flow and O2 consumption
effects of noxious stimuli are blunted thus stopping increases in ICP
care of the brain injured patient
oxygen delivery!
keep CPP 80-100mmHg
what to do in the event of decreased CPP
increase MAP with fluids, vasopressors (dopamine)
decrease ICP with CSF drainage, surgery, nursing interventions, osmotic diuretics
early symptoms of increased ICP
decreased level of consciousness
irritabilty, restlessness, lethargy, confusion, “goofy”
headache
pupillary changes: ipsilateral changes in size, shape, or reactivity
visual abnormalities: blurred or double vision
later symptoms of increased ICP
marked changes in LOC
pupils: ipsilateral pupil becomes fixed and dilated (CN III)
motor function changes
abnormal flexion: decorticate posturing
abnormal extension: decerebrate posturing
last symptoms of increased ICP
cushing’s triad
hyperthermia
loss of cranial nerve function
death
Cushing’s triad
increased SBP (widened pulse pressure)
bradycardia
altered respiratory pattern
respiratory variations associated w/ Cushing’s triad
Cheyne-Stokes
Central neurogenic hyperventilation
Apneustic breathing
Cluster breathing
Ataxic breathing
epidural catheter
least invasive
can’t recalibrate or zero after placement
can’t drain CSF fluid
indirect method of ICP measurement
subdural catheter and subarachnoid screw or bolt
subdural drain
screw or bolt into the SAS
may or may not have access for CSF drainage & sampling
direct method of ICP measurement
parenchymal fiberoptic catheter
placed directly in to brain tissue just below subarachnoid space
useful for patients with compressed or dislocated ventricles
very accurate
does not require fluid-filled transducer
no CSF can be withdrawn
ventriculostomy
most invasive
most accurate
higher risk of infection
direct method of ICP measurement
frequent calibration is required
catheter can become occluded with blood or brain tissue and cause false readings
inserted on right side of brain to not affect speech and language center
ICP monitoring
monitor ICP
drain CSF
watch for infection
some systems require zeroing
ventricular drainage
quick way to decrease ICP and increase CPP transiently
“closed” system
“zero” and calibrate system qs and prn
document amount drained
assess color and clarity of CSF
assess ventriculostomy site
P1 wave on an intracranial pressure waveforms
P1: percussion (systolic) wave
produced by systolic pressure
P2 wave on an intracranial pressure waveform
elastance (tidal) wave
produced by the restriction of ventricular expansion from rigid dura and skull
measures compliance of brain
P3 wave on intracranial pressure waveform
dicrotic wave
produced by closure of the aortic valve
on normal intracranial pressure waveforms should p1 or p2 be higher
p1
jugular venous oxygen saturation (SjvO2) monitoring
normal 55-75%
measures supply and demand of cerebral O2
indicator of cerebral metabolism
place on side of injury
electroencephalogram (EEG) monitoring
can detect seizure activity
transcranial doppler
assess cerebral blood flow noninvasively
neuro nursing care
treat primary injury
prevent or minimize secondary injury
treat the patient and don’t forget the family and/or significant others
serial assessment is vital
positioning
fluid volume status
ICP management
ventilation & Oxygenation
temperature management
glucose control
seizure prevention
barbiturate coma
ICP management nursing care
ventricular drainage
sedatives, analgesics, paralytics
reduce noxious stimuli
mannitol
positioning
elevate HOB
usually avoid supine position because it can increase ICP
HOB is individualized to pt response
prevent jugular venous drainage obstruction
individualize to patient response
how to prevent jugular venous drainage obstruction
keep head/neck in neutral position
avoid tight cervical collars
avoid tight ETT taping
avoid raising HOB with hips flexed
why is monitoring glucose so important
brain injury releases glutamate (molecule that increases metabolic activity and increases breakdown of glucose) -> glycolysis produces lactic acid -> acidosis increases capillary membrane permeability -> increases cerebral edema
benefits of sedative, analgesics, and paralytics
reduce agitation and discomfort
decrease ICP
decrease cerebral O2 consumption
facilitate mechanical ventilation
reduce response to noxious stimuli (suctioning)
cons of sedatives, analgesics, and paralytics
limits ability to follow neuro exam
some drugs can cause hypotension and decrease CPP
how to reduce noxious stimuli
avoid hyperinflation pre-suctioning (still hyperoxygenate though!)
avoid bundling of nursing activities
reduce environmental stimuli (dim lights, quiet)
family at bedside may decrease ICP
mannitol
osmotic diuretic of choice
hyperosmolar fluid pulls fluid from cells to vascular space
decreases blood viscosity
decrease ICP
reduced edema
mannitol nursing implications
monitor serum osmolality to prevent renal failure
maintain euvolemia (BP, CVP, PAWP)
monitor urine output
REALLY watch blood pressure
monitor electrolytes
ventilation/oxygenation considerations
hyperventilating is no longer recommended
maintain PaCO2 35-45 mmHg
PEEP can raise ICP and should be used cautiously
maintain PaO2 > 70 mmHg
corticosteroids
NOT helpful in TBI
effective with brain and spinal cord tumors in reducing vasogenic edema
goals in the care of the brain injured patient
keep CPP >70mmHg
keep ICP <15 mmHg
keep PaO2 >80mmHg
keep PaCO2 between 35-40mmHg
keep other lab indices WNL
provide adequate analgesia and sedation
provide sufficient nutrition
prevent iatrogenic injury
provide information & support to patient and family
priorities of care
ineffective cerebral tissue perfusion
ineffective breathing patterns
ineffective airway clearance
body image disturbance
ineffective coping
