PaCO2: 35-45 mmHg

ICP
; if PaCO2 is INC > BV is dilated > DEC O2
ICP is a symptom like LOC; not the disease and INC vol of blood
process itself.
POSTURE
BRAIN IS ENCLOSE IN A RIGID SKULL;
protects the brain from the outside; the COMPENSATORY
scalp and skull after skull meninges DURA
STAGE 1:
ARACHNOID PIA (closest to the brain is
PIA) 1. Autoregulation
8- cranial bones ; alteration depends on the BP
14- facial bones INC CSF ABSORPTION
NORMAL ICP:  By channeling it down to the central
canal of the SC
6-15 mmHg
DEC CSF FORMATION
10-15 mmHg
 CSF secretion is DEC it is secreted in the
0-15 mmHg
choroid plexus in the lateral ventricle
FACTORS IT WILL COMPENSATE SO THERE’S NO
N; 120/80 mmHg if the BP falls below this MANIFESTATION
the blood circulation is not adequate, means
the O2 decrease and will affect the pressure
inside. 2. METABOLIC REQUIREMENT

HIGH BP the pressure is also ineffective. > GLUCOSE is needed for action potential

VENOUS
Passing from the brain is passing to the 3. MEAN ARTERIAL PRESSURE
jugular veins, and shouldn’t be interrupted
MAP < 50= DILATED> DEC O2 deliver >
to the heart.
ischemia; ma DILATE > ma taas blood
INTRA-THO-AB volume>

Can cause impairment in the enhancement

of respi exchange
MAP < 50= DILATED> DEC O2 deliver=
TEMPERATURE ischemia > C02 INC> it will compensate to
dilate the blood vessels in effort to INC the
Dilated BV > INC volume of blood > INC O2> VASODILATE (ACIDIC
pressure ENVIRONMENT)> INC BLOOD VOLUME >
So nd pwede na mag last high fever sang INC ICP
patient for 8 hours
BLOOD GASSES MAP > 150= CONSTRICTED
PaO2: 80-100 mmHg
CPP= PRESSURE NECESSARY TO PUSH 5. HEMATOMA
BLOOD into q 100g of brain tissue per min;
SUBDURAL HEMATOMA:
range 70-100 mmHg
Tearing of the bridging vein; build up of the
If there’s ICP INC
hematoma is slower so the manifestation is
If 50-60 mmHg also slower
< 50 mmHg= ischemia 6. INTRACRANIAL SURGERY
< 30 mmHg= neural death After surgery the nursing intervention is
prevention of INC ICP
In 2 minutes without oxygenation the
metabolism of the brain will stop 7. Hydrocephalus
In 4-6 minutes without O2, the neurons will If it happens in a child the suture is soft
die hence there’s enlargement of the head; if
adult there’s no room for expansion
How long is the CPR? 2 minutes
8. Radiation therapy
Pressure change
COMPLICATIONS OF INC ICP
STAGE 1:
STAGE 2: early signs of ICP as it is now
less able to expand CINGULATE: hematoma moves the
structure of the brain in the center
STAGE 3: severe manifestation; critical
period Cushing’s triad is seen Structure of the center brain
STAGE 4: Basal ganglia, thalamus, insula, corona
radiate
CAUSES OF INCREASE ICP
ASSESSMENT
1. Cerebral edema
Severe hypoxia
BREATHING PATTERN

2. Abscess Cheyne stokes

3. Tumor > Fast, apnea, fast, apnea; cycle of

As this is growing cause by the mass effect
of cerebral edema
4. Infarct
Considered as space occupying lesion
(ischemic type of stroke)
LMCA= serves upper portion of temporal,
frontal, and parietal lobe.
hyperventilation and apnea; rapid and
regular followed of apnea; compromised is
at the level of diencephalon; it should be
intubated; hyperventilation means
compromised O2 with INC CO2
Central neurogenic hyperventilation
> compromised going down to the
brainstem; severe compromised of O2,
excessive high CO2; severe vasodilation
(there’s edema); compromised at the level
of the midbrain
Apneustic
> long inspiratory pause followed by long
expiratory pause; compromise pons
Cluster
> group of irregular breathing followed by
apnea; biot’s breathing; damaged in lower
pons and upper medulla which is the
breathing center; severe O2 compromised
Ataxic
> if the severe compromised reaches the
medulla oblongata; the breathing pattern will
be completely irregular; completely irregular
breathing pattern when there’s sever
compromised O2 @ the level of medulla
oblongata.
OCULAR SIGNS
> Compression of CN3 @ L so there’s
compression in the L side of the brain.
Anisocoria:
CN3 problem:
Drooping of the eyelid
Constriction of the pupil
OCULOCEPHALIC REFLEX
TEST OF CN 3 4 6
3; eyes downward
4; upward, inward, oblique
6; outward, lateral
PUPILLARY CHANGES
-KUNG DIIN ANG DAMAGE DIDTO MA
DILATE ANG PUPIL (ANISOCORIA)
-IMPENDING DEATH THE PUPIL GA
AMAT-AMAT NA DAKO (BLOWN PUPIL)
HEADACHE
> because of the INC pressure in the brain;
occurs early in the morning
Vomiting
> Projectile vomiting; medulla oblongata is
the vomiting center
If ma bunggo ulo ka px we admit the px for
24-48 hours for observation.
If with head injury, we do not give pain
medication immediately
Seizure
> if compromised O2 and glucose in the
brain it will make the brain cells
hyperexcitable; if they become
hyperexcitable together (synchronize) it’ll
cause seizure.
IMPLEMENTATION
MONITOR ABG if there’s INC CO2 there
will be respiratory acidosis
> pH IS LOW (< 7.35), PCO2 > 45
IF INC PCO2 will dilate the BV so the Dr.
will have administered; indicated if the ICP
INC is severe
> 30-45 degree to drain the venous
circulation therefore lower ICP and cerebral
edema
NGT is to relieve abdominal distention
(decompression) and can be used for
feeding (after acute phase)
Scheduled suctioning; 5-10 seconds
suctioning
RECTAL EXAMINATION: it’ll decrease the
HR as it will manipulate the vagal nerve
hydrate client but strictly monitor the MIO
OSMOLALITY: 275-300
NEED: Glucose, Na, K, BUN
SIGNIFICANCE: If the serum osmolality is < SHORT TERM (PRN): Benzodiazepine
275 it means dehydrated if > 300 it means group
fluid retention
ANTIULCERANTS: PPI/H2
ICP INCREASE:
> to prevent stress ulcer; whenever you
DIABETES INSIPIDUS have compromised O2 in the brain the 1st
system that will help the circulation of the
> Urine output is > 200 ml for 2 consecutive
brain is the GIT; in favor of the cerebral
hours (polyuria); decrease ADH
circulation; circulation for GIT will be
> Refer if the output is > and expect an shunted away for cerebral circulation, that is
order of ADH replacement such s why they’re prone for ulceration.
vasopressin
> Stool softeners
> Serum Na retained as not equal loss; INC
CRANIETOMY/CRANIOTOMY
Na it’ll stimulate hypothalamus to mobilize
thirst mechanism BURR HOLE
SIADH (syndrome of inappropriate They will then insert a catheter where the
antidiuretic hormones) CSF is following the catheter is then buried
subcutaneously. Indicated to patient with
> INC ADH; dilution hyponatremia ga kagto
hydrocephalus.
ang asin sa tissues nga naka retain damo
na water= cerebral edema Behind the hairline is the supratentorial
> Osmotic diuretic (mannitol, furosemide) > If we remove the bone flap and the
intention is to decompress, it is buried
MEDICATION subcutaneous on the stomach of the
WE DON’T GIVE STEROIDS TO PX WITH patient. Now we have bone bag.
HEAD INJURY
NURSING RESPONSIBILITIES AFTER
> BARBITURATES (SEDATE) SURGERY
DEC O2 the brain cells become hyperactive Support the head with a small pillow under
(as neurons can be: excited, conduct the neck to maintain alignment of the head
impulses, influence other neurons) and torso
We need to prevent seizure to limit its
metabolic requirements.
> OSMOTIC DIURETICS
Hypertonic solution ---- effect so ma suyop
siya water from compartment of lesser
concentration to higher concentration
solution kay ma upod ang fluid sa plasma to
be excreted to urine.
Check BP shouldn’t be < 90
> ANTICONVULSANTS
 TRAUMATIC BRAIN
INURY
> Blood vessels in the scalp are less
constrictive than other part of the body,
hence, they bleed more.
MECHANISM OF INJURY
> CLOSE HEAD INJURY
no opening but there’s injury
> OPEN HEAD INJURY
TYPES OF BRAIN INJURY
LINEAR: no fragmentation on the bones no
separation align dyapon so no need for
surgery
There’s a danger of development of
subdural hematoma
COMMINUTED: fragmentation, it will
compress the brain.
CONTUSION: major TBI
Diffuse axonal injury (DAI):
STRETCHING, TWISTED, COMPRESSED,
OR SHEARED AXONS
Damage axon will swell, hence, there’s
cerebral edema development amo na ga
coma ang patient
HEMATOMA:
EPIDURAL= outside of the dura mater;
damage in the artery (middle meningeal
artery); profuse bleeding so build up is
faster
SUBDURAL= Bridging veins
CLINICAL MANIFESTATION
If there’s dischargers in the nose rhinorrhea
which indicates a frontal bone fracture and
in need of assessment if the discharges
contain CSF as there might be leakage.
CEREBROVASCULAR
ACCIDENT
Aging: Less elastic and it may harder also
called “Arteriosclerosis”
Cadmium: can interfere with absorption of
vitamins B complex, C, A, zinc
DM: increase viscosity of the blood, polyuria
dec h2o and Na decreasing the blood
volume increasing viscosity of the blood that
will predispose to clot formation.
Oral contraceptive: contraindicated to
people over 35 y/o and above because of
risk for HPN, as the BLOOD VOLUME is
increasing and if the women is smoking the
BLOOD VESSEL is constricting with
constricting BLOOD VESSEL (from
SMOKING) and increasing blood volume
(from PILLS) > HYPERTENSION.
TYPE OF STROKE
THROMBOTIC: Not related to activity
HEMORRHAGIC: the patient is active; 50%
cases; this occur during activity, this will be
the time that the pressure increases the
blood vessels will dilate and then will
rupture; if there’s weakness in blood vessel
it becomes more permeable hence blood
leaks which causes headache.
> High blood pressure may cause
outpouching of blood vessels
Because of the high pressure it will cause
weakening of the blood vessels and may
results outpouching called aneurysm; these
weak blood vessels may thin and whenever
the person is active with high pressure it
may rupture (blood vessel). Aneurysm is the
outpouching of the blood vessels, fusiform
type nag habok gid ang bilog na
circumference of BV.
Hemorrhagic type of strokes may results
from hypertension and rupture aneurysm.
To differentiate hemorrhagic stroke from
ischemic stroke is the headache and INC
BP.
Poor prognosis; if able to survive px will be
left with disabling manifestations
MANAGEMENT:
PNSS 0.9% Na 154 Na and Cl
PLR 130 Na
Cerebral vasopasm: Is it possible that this
will still results to an ischemic type of
stroke? Yes
Medication:
CCB: prevent cerebral vasospasm
THROMBOLYTIC: > Dose recommended
0.9 mg per body weight; max dose 90 mg
If we suspect stroke immediately we ask for
CT scan without contrast medium; to
differentiate ischemic and hemorrhagic
stroke. Qualify patient if eligible for
thrombolytic therapy > no surgery 3 mons
before treatment, wala ga use
anticoagulants, no bleeding history.
Monitor 24 hours after R-tpa administration
Perform blood studies, lipid profile
ANTICOAGULANT: Oral route is preferred
ASSESSMENT FINDINGS:
Corticobulbar tracts innervate the motor
nuclei of CN @ the brainstem and may
affect CN7 which is responsible for
contraction of the muscles on the face
Corticospinal tract carries voluntary motor
movement and innervate in the cervical
spine; from cerebral cortex the corticospinal
tract will be send down to the cervical spine
and before it crosses to the level of medulla
oblongata
BROCA: expressive
WERNICKES: receptive/fluent aphasia
> CN2; problems on the ophthalmic artery
> EARLY MANIFESTATION of the dec o2 in
brain is restlessness and confuse
CLINICAL MANIFESTATION
Speech centers is in the L part of the brain;
broca’s is serves of MCA and the wernickes
is located in the L temporally
RIGHT BRAIN DAMAGE
 Once damage because of the
decussation of the corticospinal tract that
carries the voluntary motor movement to
spinal cord from the brainstem (medulla) ma
cross ang corticospinal to different segment
of the spinal cord > cervical, thoracic,
lumbar, sacral ma sugpon siya sa lower
motor neurons located in the spinal cord
that carries voluntary motor movement,
hence, if affected ang R side sang brain this
will results to L side hemiplegia/hemiparesis
(contralateral)
 L sided neglect: not aware that there is
problem in the left as he lost his spatial
orientation. Because of this loss he will
neglect the L side.
LEFT BRAIN DAMAGE
Right sided weakness
 results to different types of aphasia as
broca’s and wenicke’s can be damaged
Graphestesia: cortical discrimination in the
parietal lobe
Stereognosis:
 LONG TERM DISABILITIES
Motor or speech apraxia
FLACCID: damage in medulla oblongata
DYSPHAGIA: CN9 (glossopharyngeal) and
10 (vagus) both innervating the pharynx for
coughing, gagging, and swallowing.
AFFECT: secondary to change in body
image
ELIMINATION: Hyporeflexing state
HOMONYMOUS HEMIANOPSIA
LEFT EYE: when half of the L eye is blind
and the blind part is the R eye
RIGHT EYE: blindness on ½ of the R eye
and the side that is blind id in the R
¼ quadrant anopsia
½ hemianopsia
Whole eye, anopsia
DIAGNOSTIC
MRI: extent of the injury
Cerebral angiography: FEMORAL
ARTERY; MONITOR FOR BLEEDING
LUMBAR: with consent; empty bladder
Spinal cords ends L1-L2, HENCE, THE
SITE FOR LUMBAR TAP IS L3-L4
Lie flat for 6-8 hours
SPINAL CORD
INJURY
17:53
> 18 inches’ long
Vertebral: 7 cervical, 12 thoracic, 5 lumbar,
5 sacral, 1 coccyx
Meninges: Dura, arachnoid, pia
> Permanent or temporary damage below
the level of injury
> controls and coordinate the body
SPINAL CORD: SWOGI
ANTERIOR MOTOR; POSTERIOR
SENSORY
SPINAL NERVES 31 pairs: part of
peripheral nervous system
Consist BOTH motor and sensory
CNS: brain and spinal cord
ABOVE UMBILICAL AREA: T9-T10
SIDE: T10-T11
DOWN: T11-T12
LUMBAR NERVES: extension L2-L4
Plantar flexion S1-S2
SECONDARY
LEUKOTRINES: is a mediator which is
more potent than histamine; INC
vasopermeability, vasodilation, can cause
bronchospasm
IF PERMEABLE: it dilates the blood
vessels; anatomical remodeling > dilate >
losses the junction of the walls in the BV >
permeable > leakage or shifting of the fluid
from inside to outside > go to the interstial
space > edema
SHIFTING FLUID FROM INSIDE AND
OUTSIDE: Dec BV > hypovolemia >
hypotension > STIMULATE BARO
RECEPTORS and RAAS > ANGIOTENSIN
2 > VASOSPASM
PLATELET AGGREGATION: vasodilate
and vasopermeability > hypovolemia >
hypotension 1;15;06