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Neurologic Monitoring. Mani K.C Vindhya M.D Asst Prof of Anesthesiology Nova Southeastern University. Introduction to EEG Interpretation. Basic EEG Interpretation. You basically study an EEG for three things -- frequency, amplitude, and symmetry.
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Neurologic Monitoring Mani K.C Vindhya M.D Asst Prof of Anesthesiology Nova Southeastern University
Introduction to EEG Interpretation • Basic EEG Interpretation. You basically study an EEG for three things --frequency, amplitude, and symmetry. • 1. Frequency.The electrical waveform of the EEG is divided into sinewaves of specific frequencies (cycles/sec or Hertz = Hz). The mnemonic I use to remember the frequencies is: • DON'T TOUCH A BRAIN, or DON'T TOUCH A BAGEL – D. T. A. B. • Delta waves = 0 to 3 Hz -- Deep Anesthesia or Deep "Stage 4"Sleep • Theta waves = 4 to 7 Hz -- general anesthesia andhyperventilation • Alpha waves = 8 to 13 Hz -- Awake but relaxed, eyes closed • Beta waves = 14 to 30 Hz -- awake and alert (eyes open) orexcitement phase of anesthesia
Amplitude -- measured in microvolts (uV). Sometimes amplitude isexpressed as power, which is the amplitude squared, (uV)2. • Low amplitude = < 20 microvolts (uV) • Medium amplitude = 20 to 50 uV • High amplitude = > 50 uV • Symmetry. Do the EEG waveforms look the same on each side?
Summary of Factors Affecting the EEG • Increased frequency • Barbiturates, benzodiazepines, etomidate, propofol (low dose) • Inhalational agents (< 1 MAC) • Nitrous oxide 30-70% (acts on NMDA receptors) • Ketamine (acts on NMDA receptors) • Hypoxia (initially) • Hypercarbia (mild) • Seizures • Decreased frequency/increased amplitude • Barbiturates, etomidate, propofol (moderate dose) • Opioids • Inhalation agents (> 1 MAC) • Hypoxia (mild) • Hypocarbia (moderate to extreme) • Hypothermia
Decreased frequency, decreased amplitude • Barbiturates (high dose) • Hypoxia (mild) • Hypercarbia (severe) • Hypothermia (< 35 oC) • Electrical silence • Barbiturates (coma dose) • Etomidate, propofol (high dose) • Isoflurane, desflurane, sevoflurane (2 MAC) • Hypoxia (severe) • Hypothermia (< 15-20 oC) • Brain death
Effects of anesthetics on the EEG: • 1. Can be expressed as graphs showing frequency on the x-axis and amplitude on the y-axis • 2. Awake individual -- alpha and beta activity, about 20 uV amplitude
Fentanyl and other narcotics -- classically produce high amplitude, low frequency delta wave activity
Inhalational anesthetics: • Low concentrations -- increase frequency & amplitude, or "EEG activation" • Higher concentrations -- high amplitude theta acticity • Isoflurane -- starts with "iso" because it produces an isoelectric "flat" EEG at > 2 MAC (This is true for sevoflurane and desflurane, too) • Enflurane -- starts with an "E" because it is Epileptogenic, especially with along with hyperventilation and hypocapnia. Seizures markedly increase frequency. • Sevoflurane – can also cause “seizure” activity (> 1.5 MAC)
Sodium pentothal and other barbiturates produce a whole spectrum of different effects, depending on the dose: • EEG activation -- in low doses • Barbiturate spindles • Slow delta wave activity • Burst suppression -- defined as an isoelectric EEG with < 6 bursts of EEG activity per minute = the desired endpoint for barbiturate coma (cerebral protection) • Isoelectric or "flat" EEG
Other intravenous anesthetics: • a. Many of the other IV anesthetics suppress the EEG, as does sodium pentothal: • Propofol • Etomidate • Ketamine • b. These IV anesthetics may show seizure-like (spike and wave) activity on the EEG.
To avoid peri-operative drug-induced seizures in epileptic patients: • Continue anti-convulsant therapy. • Consult with patient’s neurologist to discuss management. • Avoid etomidate. • Do not use sevoflurane routinely. • Limit maximum concentration to < 1.5 MAC.
Effects of Anesthetics and Hypoxia on the EEG • Hypoxia and many anesthetics: • IV anesthetics (pentothal, propofol, etomidate) • Inhaled anesthetics (isoflurane, sevoflurane, desflurane) • Share similar effects on EEG: • High frequency, high amplitude • Low frequency, high amplitude • EEG burst suppression • Isoelectric EEG
Types of processed EEGs • Processed EEGs use power spectrum analysis to break the EEG down into its component frequencies.
Bispectral index (BIS) is generated in part by power spectrum analysis. • Compressed Spectral Array (CSA) expresses EEG as “hills and valleys.” • Frequency – on the x-axis • Amplitude – shown as height of the hill, or y-axis • Time. The “hills and valleys” are stacked over time on a 3-D z-axis.
Arrow marks time of left carotid artery occlusion • Example of effect of carotid occlusion on CSA:
Density Spectral Array (DSA) • Similar to CSA • Expresses “hills and valleys” as “dark and light.”
Lifescan (Periodic Analysis) – expressed EEG activity as “telephone poles”
Introduction to Evoked Potentials • Sensory evoked potentials (or responses) • Brainstem auditory evoked responses • Somatosensory evoked potentials • Visual evoked responses
Brainstem auditory evoked potentials or responses (BAEP's or BAER’s) • Specialized form of EEG monitoring • Background EEG activity is electronically subtracted out. • The EEG waveform evoked by auditory stimulus (clicking • in ear) remains.
Shape of a typical BAEP = seven peaks • Latency = time to first peak (usually 2 msec) • Amplitude = height of the peaks
The seven peaks of the BAEP are believed to correspond to passage of astimulus through "generators" in the auditory nerve, brainstem and cortex.
What do we look for during surgery? • Mainly two things: • Increase in latency (> 10%) • Decrease in amplitude (<50%) These two changes could be indicative of impending injury or ischemia in the BAEP pathway
BAER's are barely affected by anesthetics: • 1. No anesthetic drug produces a change in BAER’s that could be mistaken for a surgically induced change. • 2. Etomidate decreases amplitude and increases latency (but this is not clinically significant).
Somatosensory evoked potentials • Upper extremity:Median nerve SSEP has “M” shape
What do we look for during surgery? • Decrease in SSEP amplitude • Increase in latency (time to first peak or dip) • Six I’s that inhibit SSEP’s: • Inhaled anesthetics, including isoflurane • N2O doesn’t decrease amplitude alone, but has a synergistic effect with volatile agents. • IV agents, but to a lesser extent than inhaled anesthetics • Etomidate = the exception; it increases SSEP amplitude • Ischemia/hypoxia • Injury, to the spinal cord or anywhere in SSEP pathway • “Ice cold” temperatures (< 34.5 oC) • Incompetence (observer foul-ups)
Summary of effects of anesthetics on SSEP’s: • Inhaled anesthetics – dose-related decrease in amplitude and increase in latency • Use less than 1 MAC volatile agent • Nitrous oxide – profound depressant effect on SSEPs, especially when used in combination with volatile agent
Intravenous agents • a. Propofol and thiopental • Small decrease in amplitude and increase in latency • Propofol is commonly used for TIVA (total IV anesthetic technique) • Opioids – negligible effects on SSEPs • Ketamine and etomidate – increase SSEP amplitude • (Etomidate is exceptional. It increases SSEP amplitude but decreases BAEP amplitude.) • Anesthesia for SSEP’s (progression from routine to desperate) • Volatile agent / N2O / narcotic • Volatile agent / narcotic • Volatile agent / propofol / narcotic • TIVA: total IV anesthetic with propofol and narcotic • Etomidate / narcotic (really desperate) • Increases amplitude • Adrenocortical suppression with etomidate
Other Evoked Potentials • Visual evoked potentials • M shape • Long latency • Sensitive to all anesthetics except opiates
Motor evoked potentials • Evoked by transcranial electrical or magnetic stimulation • Effects of anesthetics are profound. • Same anesthetic progression as with SSEP’s
Why bother to test motor function? • SSEP’s mainly test for dorsal (posterior) spinal cord function. • Motor EP’s mainly test for ventral (anterior) spinal cord function.
Transcranial Doppler (TCD) • A. Carotid endarterectomy -- might be used during CEA cross-clamping todetect emboli or decreased cerebral blood flow velocity
Vasospasm • TCD can be used to detect vasospasm after aneurysmal SAH. • Vasospasm causes an increase in cerebral blood flow velocity.