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a closed box w. 3 essential volume components: 1. Brain Tissue [78%] 2. Blood [12%] 3. CSF [10%]
Factors That Influence ICP Under Normal Circumstances Are Changes In:
1. arterial pressure 2. venous pressure 3. intraabdominal & intrathoracic pressure 4. posture 5. temperature 6. blood gases [CO2 levels]
Monro-Kellie Doctrine
- non-expandable, non-contractable, freely communicating space, the pressure of fluid contents & brain itself, must be directly porportional to eachother in order to maintain a constant pressure - if one of these pressures increases, another must decrease in order to compensate
Normal Compensatory Adaptations
- initially an increase in CSF volume produces no increase in ICP - however, ability to compensate to changes in volume is limited; as volume increase continues, ICP rises & decompensation ultimately occurs = compression & ischemia
Measuring ICP
- measured in ventricles, subarachnoid space, subdural space, epidural space, or brain parenchymal tissue using a PRESSURE TRANSDUCER
Normal ICP
0 to 15 mm Hg
Pt who becomes acutely unconscious, regardless of the cause:
- is suspected of having increased ICP - ICP monitoring in ICU, except for pt's w. irreversible problems or advanced neurologic disease - goals: preservation of cerebral oxygenation & perfusion, early identification of neurologic changes, & prevention of complications
Cerebral Blood Flow [CBF]
- amount of blood in mL passing through 100g of brain tissue in 1 min - global CBF ~ 50mL/min per 100g - white matter has a slower blood flow = 25 mL/min per 100g - gray matter has a faster blood flow = 75 mL/min per 100g
Autoregulation Of CBF
- automatic adjustment in diameter of cerebral blood vessels by brain to maintain a constant blood flow during changes in arterial BP - purpose: ensure a consistent CBF to provide for metabolic needs of brain tissue & maintain cerebral perfusion WNLs
Autoregulation is effective when:
- MAP of 50 mmHg - MAP of 150 mmHg
- if MAP is less than 50 = cerebral ischemia; syncope & blurred vision - if MAP is greater than 150 = vessels are maximally constricted, & further vasoconstrictor response is lost
Cerebral Perfusion Pressure [CPP]
- pressure needed to ensure blood flow to brain - CPP = MAP-ICP - MAP = SBP+2(DBP)/3
Cerebral Perfusion Pressure [CPP]
- Normal CPP: 70 - 100 mmHg - less than 50 = ischemia & neuronal death - less than 30 = ischemia & is incompatible w. life
Cerebral Perfusion Pressure [CPP]
- critical to maintain MAP when ICP is elevated - if CPP decreases, autoregulation fails & CBF decreases
- expandability of brain - represented as volume increase for each unit increase in pressure - w. low compliance, small changes in volume = greater increases in pressure - compliance = volume/pressure
Pressure-Volume Curve
represents stages of increased ICP
Increased ICP: Stage 1
- high compliance - brain in total compensation, w. accomodation & autoregulation intact - an increase in volume [in brain tissue, blood, or CSF] doesn't increase ICP
Increased ICP: Stage 2
- compliance beginning to lessen - an increase in volume places pt @ risk of increased ICP
Increased ICP: Stage 3
- significant reduction in compliance - any small addition of volume causes a great increase in ICP - compensatory mechanisms fail: loss of autoregulation & pt will show s/s of increased ICP [HA, ALOC, or pupil responsiveness]
Increased ICP: Stage 3
- loss of autoregulation = rise in systolic BP - decompensation is imminent = Cushing's Triad
Cushing's Triad
Characterized by: - systolic HTN w. widening pulse pressure - bradycardia w. a full & bounding pulse - altered respirations
Increased ICP: Stage 4
- ICP rises to lethal levels w. little increase in volume - herniation occurs as brain tissue is forcibly shifted from compartment of greater pressure to a compartment of lesser pressure
Factors That Affect CBF
- carbon dioxide - oxygen - hydrogen ion concentration
Carbon Dioxide in Arterial Blood [PaCO2]
- an increase in PaCO2 relaxes smooth muscle, dilates cerebral vessels, decreases cerebrovascular resistance, & increases CBF
Carbon Dioxide in Arterial Blood [PaCO2]
- a decrease in PaCO2 constricts cerebral vessels, increases cerebrovascular resistance, & decreases CBF
Cerebral O2 Tension Oxygen
- cerebral o2 tension below 50 mmHg = cerebral vascular dilation - this dilation decreases cerebral vascular resistance, increases CBF, & raises o2 tension
Cerebral O2 Tension Oxygen
- if o2 tension is not raised, anaerobic metabolism begins = accumulation of lactic acid - as lactic acid increases & hydrogen ions accumulate = acidosis - acidosis = further vasodilation
Cerebral O2 Tension Oxygen
- combination of severely low partial pressure of PaO2 & an elevated hydrogen ion concentration [acidosis], both potent cerebral vasodilators, may produce a state wherein autoregulation is lost & compensatory mechanisms fail to meet tissue metabolic demands
Regional or Global Autoregulation
When regional or global autoregulation is lost, CBF is no longer maintained @ a constant level but is directly influenced by changes in systemic BP, hypoxia, or catecholamines
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