EEG and ICP Flashcards
Glasgow Coma Scale values
3: deep unconsciousness
3-9: severe brain injury
9-12: moderate brain injury
13: minor brain injury
Normal cerebral physiology (blood flow and O2 requirements)
3-5 mL O2/min/100g tissue (~15-20% of CO)
50 mL blood/min/100g tissue (which delivers ~150 mL O2/min) + ~750 mL blood flow/min to brain
O2 extraction: 35-50% (heart is 60%)
Cerebral perfusion pressure equation
CPP = MAP - ICP
Range of MAP at which CBF is autoregulated (maintained)
Normally between MAP of 60-160 mm Hg, CBF is maintained.
Post-trauma, this regulation is impaired and lower limit of auto-regulation is moved up.
CBF is reduced by..
Head injury Intracranial hypertension Hypotension Hyperventilation Vasospasm
Monroe-Kellie hypothesis
Skull is a fixed volume of brain (80%), blood (10%), and CSF (10%)
Cerebral Volume = Brain + Blood + CSF
When CV is compressed, CSF decreases first, then venous blood, then arterial blood, then brain (herniation due to non-compliance of brain)
**After venous blood leaves, any further increase in brain volume will result in large ICP changes
How does ICP monitoring work at the level of the transducer? (basic)
Note: requires a watertight fluid interface
Deformation of transducer membrane is converted to electrical pulsations, which is amplified and displayed as waveforms
Indications for ICP monitoring
-CT indicates hematoma, edema, contusion, or compressed cisterns
- Normal CT with GCS < 8 and 2 of:
- Age > 40
- Posturing
- SBP < 90 mm Hg
- Sedation that prevents clinical assessment
- Meningitis and strokes
Effect of GA on CBF autoregulation
autoregulation curve of CBF vs MAP becomes more linear
trend: higher BP = higher CBF = higher ICP
CBF is increased physiologically by..
dilation of cerebral vasculature due to increase in plasma CO2, which also increases ICP
Normal/abnormal ICP ranges
Normal: 7-15 mm Hg
Abnormal: >20 mm Hg
Requires aggressive management: >25 mm Hg
Intraventricular drain and transducer
ICP control by CSF drainage
Currently the most accurate transducer we have
External zeroing every time its hooked up to the monitor
Placement needs to be in the superior lateral ventricles 1 and 2 (not the more central ventricles)
Intraventricular drain/transducer risks
Bleeding
Blockage
Infection risk
Insertion difficulties
Intraparenchymal pressure monitor
- sits right in the brain (parenchyma = actual brain tissue/neurons+glia)
- lower infection risk and hemorrhage risk
- less “drifting” although this still occurs after several days
- less accurate (tends to underestimate ICP)
Contraindications of intraparenchymal pressure monitor
Intracranial infection
Coagulopathies
Severe skull fractures
Conditions where CSF drainage is necessary
Difference between compliant and noncompliant brain (herniation) in ICP vs Time wave
Noncompliant wave has high peak P2 rebound wave
see slide 23
Ways to manage high ICP by decreasing brain water
- Mannitol – filtered but not reabsorbed sugar (gets peed out by kidney); sucks fluid out of brain but only works with intact BBB [.25-1 g/kg]
- Worry about hypotension with fast mannitol admin - Lasix = loop diuretics (decreases overall body fluid)
- Corticosteroids
Ways to manage high ICP by decreasing CSF volume
CSF drainage (ventricular, lumbar subarachnoid)
Head elevation
Ways to manage high ICP by increasing cranial space
Cranionectomy
Autoregulation of CBF is impaired by these types of drugs that we use ..
Inhalational anesthetics
Direct acting vasodilators (Ca++ channel blockers, NTG, nitroprusside, adenosine, prostacyclin)
Continuous electroencephalogram monitoring
- Monitors superficial pyramidal cells of the cerebral cx ; represents dendritic potentials
- Reflects metabolic activity of the brain
- Very position dependent
Indications for EEG
- Craniotomy
- Carotid endarterectomy : one side (Carotid artery) is clamped down, EEG on either side used to figure out whether there is less CBF on clamped side
- Cardiopulmonary bypass
- Depression of brain for cerebral protection
- Extra cranial/intracranial bypass procedures
(generally any procedures in which blood flow to the brain may be significantly affected)
Disadvantages of EEG
- Rarely useful for figuring out why Cx dysfunction exists
- Low sensitivity and specificity
- Susceptible to electrical and physio artifacts (including drugs, state of alertness, eye movements, EKG, body movement etc..)
- Small or deep lesions may go undetected
EEG: signs of activation vs depression
Activation (light anesthesia, surgical stimulation): high frequency, low voltage
Depression (deep anesthesia, cerebral compromise): low frequency, high voltage
EEG: hypnotic states VS waves
Awake: beta waves dominant
Relaxation with eyes closed: alpha wave prominence
Light anesthesia: increased beta waves, decreased alpha waves (transition into Stage II)?
Deepening of anesthesia: increase in slow wave activity (delta and theta waves), decrease in alpha and beta waves
Cortical silence : burst suppression
EEG: agents and factors that activate
Low MAC volatiles
Low dose barbs and benzos
Low dose etomidate
N2O
Ketamine
Mild hypercapnia
Surgical stimulation
Early hypoxia
EEG: agents and factors that depress
1-2 MAC volatiles
Medium to high dose barbs, propofol, etomidate
Narcotics (dose dependent)
Hypocapnia
Hypothermia
Late hypoxia