Patho/Pharm
INTRACRANIAL PRESSURE
COMPONENTS OF THE BRAIN
1. Brain tissue
2. Blood
3. CSF
Balance of these components maintain the ICP under normal conditions
ICP
o Hydrostatic force measured in the brain CSF compartment (the balance
among the 3 components)
o 5-15 is normal
o Sustained >5 min, >20mm = treatment
Increase in pressure can be due to hemorrhage, space occupying tumor, edema,
mass
FACTORS THAT INFLUENCE ICP
o Arterial and venous pressure
o Intrabdominal pressure (coughing, sneezing, BMs, straining)
o Posture (flexion increases ICP)
o Temperature (hyperthermia = NOT good (hot = increase ICP)
o Blood gases (particularly CO2 levels)
CEREBRAL BLOOD FLOW
o Alteration in diameter of cerebral blood vessels to maintain constant
blood flow in response to changes in arterial pressure
o 50 mL/min per 100g of brain tissue (brain uses 20% of O2 and 25% of
glucose)
,CEREBRAL PULSE PRESSURE
o Pressure needed to push blood flow to the brain
o CPP = MAP – ICP
o NORMAL = 60-100 mmHg
o MAP = 70-150
o <50 mmHg = ischemia and neuronal death
o <30 mmHg incompatible with life
FACTORS AFFECTING CBF
o PaCo2: vasoactive
• Increase rate on vent to decrease CO2 and decrease ICP
• If elevated à vasodilation, increased CBF (increased ICP)
• If low à vasoconstriction, decreased CBF (decreased ICP)
o PaO2
• Increase O2 on vent to decrease CO2 and decrease ICP
• <50 mmHg à vasodilation, increased CBF (increased ICP) (if it
does not increase à anaerobic metabolism)
o PaO2 + acidosis
• Causes increase ICP
• Lost autoregulation
INCREASED ICP
o Increased ICP = ischemia à decrease CBV = decreased CPP
o Brain does not like decreased blood flow so it responds by…
• Increase systolic blood pressure to push more blood to brain
• If this continues over time = decreased O2 to brain results in
swelling, edema, increased ICP, Cheyne – Stokes respirations
= increase CO2 retention = increase ICP
2
, CLINICAL MANIFESTATIONS OF INCREASED ICP
o MIND CRUSHED
• M – mental status change (confusion/drowsy, restlessness,
anxiousness) FIRST SIGN
• I – irregular breathing à hyperventilation then apnea (Cheyne-
Stokes) LATE SIGN
• N – Nerve changes à optic/oculomotor, diplopia, unequal pupils,
Doll’s eyes, swelling of the optic nerve on retina exam
(papilledema)
• D – Decorticate/Deceberate positioning à deceberate is the worst
of the two
• C – Cushing Triad à LATE SIGN à EMERGENCY à Cheyne -
Stokes widened pulse pressure, bradycardia
• R – reflexes à return of Babinskis reflex
• U – unconscious à LATE SIGN
• S – seizures
• E – emesis à projectile, early a.m. no nausea
• D – deterioration
COMPLICATIONS
o Inadequate cerebral perfusion
o Cerebral herniation
• Irreversible à fatal
• Compression of brainstem and cranial nerves
• Force the cerebellum and brainstem down through the foramen
magnum
• Will cause respiratory arrest due to compression of the
respiratory control center in the medulla
3
INTRACRANIAL PRESSURE
COMPONENTS OF THE BRAIN
1. Brain tissue
2. Blood
3. CSF
Balance of these components maintain the ICP under normal conditions
ICP
o Hydrostatic force measured in the brain CSF compartment (the balance
among the 3 components)
o 5-15 is normal
o Sustained >5 min, >20mm = treatment
Increase in pressure can be due to hemorrhage, space occupying tumor, edema,
mass
FACTORS THAT INFLUENCE ICP
o Arterial and venous pressure
o Intrabdominal pressure (coughing, sneezing, BMs, straining)
o Posture (flexion increases ICP)
o Temperature (hyperthermia = NOT good (hot = increase ICP)
o Blood gases (particularly CO2 levels)
CEREBRAL BLOOD FLOW
o Alteration in diameter of cerebral blood vessels to maintain constant
blood flow in response to changes in arterial pressure
o 50 mL/min per 100g of brain tissue (brain uses 20% of O2 and 25% of
glucose)
,CEREBRAL PULSE PRESSURE
o Pressure needed to push blood flow to the brain
o CPP = MAP – ICP
o NORMAL = 60-100 mmHg
o MAP = 70-150
o <50 mmHg = ischemia and neuronal death
o <30 mmHg incompatible with life
FACTORS AFFECTING CBF
o PaCo2: vasoactive
• Increase rate on vent to decrease CO2 and decrease ICP
• If elevated à vasodilation, increased CBF (increased ICP)
• If low à vasoconstriction, decreased CBF (decreased ICP)
o PaO2
• Increase O2 on vent to decrease CO2 and decrease ICP
• <50 mmHg à vasodilation, increased CBF (increased ICP) (if it
does not increase à anaerobic metabolism)
o PaO2 + acidosis
• Causes increase ICP
• Lost autoregulation
INCREASED ICP
o Increased ICP = ischemia à decrease CBV = decreased CPP
o Brain does not like decreased blood flow so it responds by…
• Increase systolic blood pressure to push more blood to brain
• If this continues over time = decreased O2 to brain results in
swelling, edema, increased ICP, Cheyne – Stokes respirations
= increase CO2 retention = increase ICP
2
, CLINICAL MANIFESTATIONS OF INCREASED ICP
o MIND CRUSHED
• M – mental status change (confusion/drowsy, restlessness,
anxiousness) FIRST SIGN
• I – irregular breathing à hyperventilation then apnea (Cheyne-
Stokes) LATE SIGN
• N – Nerve changes à optic/oculomotor, diplopia, unequal pupils,
Doll’s eyes, swelling of the optic nerve on retina exam
(papilledema)
• D – Decorticate/Deceberate positioning à deceberate is the worst
of the two
• C – Cushing Triad à LATE SIGN à EMERGENCY à Cheyne -
Stokes widened pulse pressure, bradycardia
• R – reflexes à return of Babinskis reflex
• U – unconscious à LATE SIGN
• S – seizures
• E – emesis à projectile, early a.m. no nausea
• D – deterioration
COMPLICATIONS
o Inadequate cerebral perfusion
o Cerebral herniation
• Irreversible à fatal
• Compression of brainstem and cranial nerves
• Force the cerebellum and brainstem down through the foramen
magnum
• Will cause respiratory arrest due to compression of the
respiratory control center in the medulla
3
