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Intracranial pressure
Nursing Care- Complex Health Problems II (11-63-375)
University of Windsor
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COMPLEX II: FINAL: Intracranial pressure Brain - Cannot store oxygen or glucose - Is a closed vault, not much room for change - Accounts for 2% of body weight - Uses 20% of body’s oxygen; 25% of its glucose ICP - Pressure in cranial vault - Three components inside skull that contribute to volume/pressure: o Brain (78% of volume) o Blood (12%) o CSF (10%) Physiologic concepts of ICP - Normal ICP is <15 mmHg (0-10 mmHg) - Cerebral perfusion pressure (CPP)- normal is 60-100. CPP less then 50 mm Hg indicates impaired neuronal functioning o How to calculate it: mean arterial pressure – ICP = CPP - Monroe-kellie hypothesis o To maintain equilibrium, there cannot be an increase in one component w/o a compensatory decrease in the other two o If volume of one increases without a corresponding decrease in another, the result is elevated ICP Compensatory mechanisms - Displacement/shunting of CSF - ↓ CSF production; ↑ absorption of CSF - shunting of venous blood out of skull - collapse of ventricles and cisterns - brain volume – distension of dura or compression of brain tissue - responses are finite – progressive increases exhaust compensation Compliance Curve (Monroe-kellie hypothesis) - ICP - Flat part of curve - ↑s in volume are not associated w/ ↑ ICP bc volume displacement compensates *Graph below is used to make a point* Cerebral blood flow (CBF) - brings oxygen and nutrients to brain; removes waste - CBF varies with changes in cerebral perfusion pressure and diameter of cerebrovascular bed - The brain is the only organ were over perfusion can cause harm because if we get too much blood flow it would increase the pressure - autoregulation – automatic changes in diameter of cerebral vessels to maintain constant CBF during changes in BP Autoregulation - changes in cerebral vessel diameters to maintain constant CBF during changes in BP - autoregulation fails in extreme high/low BP: - MAP <50: CBF falls causes hypoperfusion (cerebral ischemia) - MAP >150, cerebral vessels cannot constrict further CBF increases ↑ICP - When ICP approaches MAP, CPP approaches zero no cerebral blood flow - increased volume of CSF (can be shunted down into the cord therefore this one is the easiest to compensate) o decrease in CSF absorption o increase in CSF production Compensatory Mechanisms - attempts to maintain a constant cerebral blood flow - types of compensatory mechanism: o displacement of CSF (easiest for the body to do) o collapse of ventricles and cisterns o increase absorption of CSF in arachnoid villa and decrease secretion of CSF o autoregulation Decompensation-herniation - supratentorial - infratentorial - herniation into surgical site Downward cerebellar herniation- LP/ICP Types of Herniation Supratentorial a) cingulate expanding lesion in one hemisphere b) uncal expanding lesion (most common) in middle fossa or temporal lobe causing lateral displacement. Unilateral (one side)-ipsilateral (same side) pupil dilation (same side we have expanding lesion one) c) central, frontal, parietal or occipital lesion d) transcalarial KEY POINT HERNIATION IS THE MOST SIGNIFICANT COMPLICATION FROM INCREASE ICP WHICH CAN LEAD TO DEATH AND THE MOST COMMON TYPE OF HERNIATION IS UNCAL IN THE MIDDLE FOSSA AND CAUSING LATERAL DISPLACEMENT EXAMPLE: if a pt. has lateral displacement to the right (pushing to the right) then they would have ipsilateral pupil dilation (only one pupil) OVERALL PICTURE: pt. gets head trauma of some sort tissue edema (swelling) increases ICP compression of arteries decrease cerebral flow decrease 02 with death of brain cells edema around necrotic tissue increase ICP with compression of brainstem and respiratory center CO2 accumulates vasodilation increase ICP due to increase blood volume = DEATH - Assessment o Signs and symptoms of increased ICP Changes in mental status Gross motor changes (hemiparesis, hemiplegia, localization, etc.) o Pupillary changes o Papilledema Optic disc swelling caused by IICP. Usually bilateral swelling, can occur over a period of hours to weeks Nonspecific sign associated w/ long standing elevated ICP Sx: visual disturbances, headache, vomiting o Changes in vital signs (cushing’s triad) o Cerebellar fxn o Headache o Vomiting – not preceded by nausea; projectile Clinical manifestations of increased ICP ICP monitoring device Surgical intervention - Remove focal mass or lesion (if tumor is not removeable they can do radiation) - Burr hole w/ ventriculostomy - Lobotomy (removes lobe to reduce amount of tissue this WILL lead the pt. with severe deficits) /craniotomy w/ bone flap (allows brain to swell, positioning is important with these patients no bone in certain area to protect the brain) Why Dilantin (is an anticonvulsant the generic name is phenytoin) or a phenobarbital coma to reduce metabolic activity Decompression/shunting Expected outcomes No deterioration in neurologic status ICP < 15 mmHg Hemodynamically stable with cerebral perfusion pressure 60-90 mmHg
Intracranial pressure
Course: Nursing Care- Complex Health Problems II (11-63-375)
University: University of Windsor
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