Quiz 3 - Module 5 Flashcards
Main vessels of cerebral circulation and the general areas of the brain they feed
internal carotid –> common carotid –> ACA, MCA
basilar artery –> vertebral –> PCA
Vessels involved in epidural bleed + S/S
arterial
Vessels involved in subdural bleed + S/S
venous
Vessels involved in subarachnoid bleed + S/S
arterial
Circle of Willis + collateral circulation
where pca, aca, mca join at the base of brain
protects against ischemia
CPP
CPP = MAP - ICP
Determinants of ICP
brain volume 80%
CSF 10%
blood 10%
Normal ICP
<10 mmHg
(some sources state 5-15)
Cerebral autoregulation
ability of cerebral blood vessels to vasodilate/vasoconstrict to maintain metabolic demand
vasoconstriction when BP too high
vasodilation when acidosis, hypercapnia, hyperglycemia, temperature
RAS function
level of consciouss
circadian rhythm
sleep-wake cycle
AEIOUTIPS
acidosis, alcohol
epilepsy, encephalitis, electrolytes, hepatic encephalopathy
infection
overdose
uremia, underdose
trauma, tumor, temperature
insulin (hypo or hyperglycemia)
psychosis, poisoning
stroke (ischemic/hemorrhage), seizure, syncope
A&P cerebrum
frontal lobe (executive function, memory, problem-solving, personality)
parietal (somatosensation)
temporal (listening/comprehension, memory)
occipital (vision
A&P brainstem
pons
midbrain
medulla
A&P cerebellum
muscle coordination/balance
Layers of meninges
dura mater
arachnoid mater
pia mater
Epidural space
between dura and skull
Subarachnoid space
between dura and arachnoid mater
where CSF circulates
Where is CSF produced?
in the ventricles
chondroid plexus
S/S encephalitis
focal neurologic deficit (slurred speech, blurry vision, muscle weakness)
fever
headache
N/V
neck stiffness
S/S meningitis
triad: fever >38, stiff neck, altered LOC usually sudden onset (<24 hours)
other S/S: headache, nausea/vomiting, vision changes
**usually DOES NOT have neurological deficits)
Differential diagnoses
meningitis
stroke (ischemic or hemorrhage)
traumatic intracranial hemorrhage
concussion
overdose
alcohol intoxication
Normal pupil size
2-6 mm
Which cranial nerves does extraocular movement test
3, 4, 6
Cushings triad
late sign of impending brain herniation
irregular resps
bradycardia
widened pulse pressure (elevated SBP)
Decorticate positioning
abduction of arm at shoulder
elbows flex inwards
legs extended
Decerebrate positioning
extended, adducted, internal rotation of arm
wrists pointed outwards
legs extended
feet plantar flexed
Subdural hematoma
between dura mater + arachnoid mater
venous bleed
Epidural hematoma
between dura + skull
arterial bleed
Frontal lobe
personality
emotions/arousal
intelligence
concentration, executive function, problem solving
self awareness
voluntary movement
speak/write
behavior control
Where is broca’s area located
in the frontal cortex
damage –> expressive aphasia
Where is wernicke’s area located
in the temporal lobe
damage –> comprehension aphasia
S/S of stroke
facial droop
slurred speech
arm drift
hemiparesis
loss of sensation to one side of body
sudden trouble seeing/blurred vision/loss of sight
S/S of increased ICP
headache
N/V
altered LOC
S/S of impending brain herniation
pupillary asymmetry
unilateral/bilateral fixed + dilated pupils
decorticate/decerebrate positioning
respiratory depression
Normal CPP
60-80
min 60 needed to maintain cerebral perfusion
At what map does cerebral autoregulation fail?
map <60 or >150
Target MAP for ICP
90
Normal ICP
5-15
max <20
How does fever affect metabolism?
an increase of one degree increases O2 demand by 6-10%
ICP components
brain 80%
blood 10%
CSF 10%
brain can compensate for increased ICP by causing cerebral vasoconstriction and increasing CSF absorption
S/S of increased ICP
change in LOC
loss of detail/orientation
forgetfulness
restlessness (hypercapnia, acidosis, hypoxia)
sudden quietness
pupillary changes (sluggish, fixed + dilated = BAD)
motor changes
How long does it take for brain cells to die without perfusion?
4-6 minutes
Types of cerebral edema
vasogenic
cytotoxic
interstitialV
Vasogenic edema
caused by inflammation + disruption of blood brain barrier
vasodilation + increased vascular permeability = fluid + proteins move into tissue
Cytotoxic edema
damage to cells/loss of ATP
malfunction of Na/K pump
increase in intracellular sodium = water moves in = intracellular edema
Factors causing increased ICP
hypercapnia
hypoxia
acidosis
hyperglycemia
temperature
loss of autoregulation (MAP <60 or >150)
impaired venous outflow (neck flexion)
anemia
Interventions for ICP
airway –> intubate if necessary
ATP –> adequate glucose (NG feed, SLP ax for dysphagia)
blood pressure –> maintain adequate MAP (IV fluids, pressors, inotropes, beta blockers)
cervical collar –> if c-spine injury suspected (can inhibit venous outflow)
calm environment –> decrease stress/stimuli
gastric decompression –> improve intraabdo/intrathoracic pressure to promote breathing
dim the lights
HOB 30 degrees, neck in neutral alignment, avoid flexion
therapeutic hyperventilation (blow off CO2 to prevent acidosis)
hypertonic IV fluids (mannitol)
avoid hyperthermia
avoid hip flexion –> increases ICP by changing intraabdo pressure
surgical –> resection, CSF drainage with catheter
IV steroids –> for brain tumors
hypertonic normal saline
barbiturate coma –> refractory ICP
sedation = decrease O2 demand
neuromuscular blocking agents = decrease peripheral O2 consumption
Adverse fx of mannitol
hyperglycemia
decreased hematocrit + blood viscosity
dehydration
fluid overload
hypo/hyper natremia or kalemia
can cross BBB –> vasogenic edema
Jugular vein anatomy
does not have veins
fluid moves from areas of high to low pressure
drainage facilitated by gravity
Interstitial edema
CSF leaks from ventricles into interstitial tissue
*occurs in meningitis
Anticoagulant reversal agents:
warfarin: PCC (blood infusion), Vitamin K
DOAC: none in canada
heparin/LWMH: protamine sulfate
Hypoxia
poor oxygenation of tissue with normal blood flow
low arterial oxygen content
Ischemia
decreased/interrupted blood flow –> poor oxygenation
Water shed areas
areas of the brain that lie between border zones
not supplied by major arteries
vulnerable to ischemia
Etiology of vasogenic edema
vasogenic edema = disrupted BBB
hemorrhage
brain injury
infection
Etiology of cytotoxic edema
cytotoxic edema = intracellular swelling
hypoosmotic state (hyponatremia, water intoxication)
failure of Na/K pump (ischemia, low ATP)
LOC continuum
alert
confusion
lethargy
obtunded
stupor
coma
Hydrocephalus
increase in ventricles d/t increase in CSF
1) overproduction of CSF
2) impaired reabsorption
3) obstruction
Traumatic Brain Injury
caused by a/d forces
brain makes contact with skull –> damage to tissue, hematoma, contusions
Brain contusion
bruising of brain surface
lacerations
tearing of brain tissue
Brain hematoma
vascular injury/bleeding
location can be:
epidural (arterial)
subdural
subarachnoid (intracerebral)
Concussion
transient neurological dysfunction caused by mechanical injury to brain
may have temporary loss of consciousness or amnesia
brain imaging negative
usually recovers within 24 hours
side fx can last months
Types of stroke
ischemic (>80%)
hemorrhagic (AV malformation, ruptured aneurysm, spontaneous bleed)
Ischemic stroke treatment
tPA within 3 hours
thrombectomy
Contraindications to tPA
BP >185/110
bleeding RF (genetic dx, low platelets, prolonged clotting times)
>3 hours
hx of stroke/head injury within last 3 months
hx of recent GI/GU bleed in last 21 days
hemorrhagic stroke
oral anticoagulants
major surgery last 14 days
active internal bleed
Medications that increase ICP + catecholaminse
nifedipine
nitric oxide
nitroprusside
Medications to treat BP in ICP
beta-blockers
a-receptor antagonists
VAN (stroke sequelae)
vision (hemiparesis)
aphasia
neglect (touch pt bilaterally, they cannot detect sensation on one side)
How quickly should you drop BP during a stroke
15-25% in first 24 hours
