Anesthesia III: Effects of Anesthesia on IOM
EEG is a measure of spontaneous synaptic function
Why N20 is the worst, Effect of N20 on the CMAP
- EEG with anesthesia progression
- Alpha; High, Medium, Low
- Fast
- Rhythmic
- Complex
- Burst Suppression (early)
- Burst Suppression (late)
- Suppression
Why N20 is the worst, Effect of N20 on the CMAP
*Create conditions that are favorable to neuromonitoring
*From Anesthesia Protocols for Surgery during Neuromonitoring; Todd Sloan
*From Anesthesia Protocols for Surgery during Neuromonitoring; Todd Sloan
need more molecular interaction of what each drug does to a person, the molecular interactions of each and visually communicate the importance. fundamentally explain what is happening to a persons brain function enough that you can put needles in their body and take all of these measurements. talk about the hallucinogenic effects of certain drugs and how they can numb pain. presti and the ethnobotonist
EMG - Electromyography - No muscle relaxants (No other anesthetic constraints)
NCV - Nerve Conduction Velocity - No anesthetic constraints
ABR - Auditory Brainstem Response - No anesthetic constraints but sensitive to ischemia
EEG - Electroencephalography - Complex effects depending on agent, Burst suppression lowers CMRO2 (cerebral metabolic rate of oxygen); can typically watch a transition from active to burst to isoelectric activity;
SEP - Somatosensory Evoked Potentials - Most common agents can lower the amplitude, increase latency (which are similar effects to compromise of the DCML pathway) sensitive to cortical and thalamic ischemia
MEP - Motor Evoked Potentials - No muscle relaxants which reduce action of the neuromuscular junction to zero, anesthetic fade for increased Propofol concentration, Inhalation agents, bolus of narcotic, sensitive to ischemia and related to blood pressure, MAP (mm Hg)
Nitrous Oxide - suppresses EEG and EP activity, MOST POTENT per MAC
Halogenated Agents - suppresses EEG, usually ok if < 0.3 - 0.5 MAC
Propofol - suppresses EEG, anesthetic build-up can suppress SEP and MEP
Opiods - little or no effect but boluses can suppress MEP
Neuromuscular blockade, can improve SEP (with reduced EMG artifact/noise) but cannot use if EMG/MEP recordings are necessary
Ketamine
Lidocaine
Dexmetatomadine
Typical scenarios: TIVA, 100 mcg/kg/min Propofol, 0.2 mcg/kg/min
Anesthetic requirements for SSEP monitoring
Effects on evoked potentials can cause a dose dependent decrease in amplitudes and increase in latencies of SEP cortical waveforms. with nitrous, the changes occur rapidly and are highly destructionve. the potency is based of lipid soluability. isolfurane is readily store d in the fat and has rapid changes but is less potent. The site of action in the central nervous system is the cortex, thalamus, brainstem and spinal cord which cause suppression of synaptic neuronal transmission.
Propofol
Propofol effects on evoked potentials causes a dose dependent decrease in SEP cortical amplitude, and dose dependent increase in SEP latencies, less sever than inhalation agents.
Muscle relaxant
They effect the neuromuscular junction so no EMG or MEP
Narcotics
The effects of narcotics on EPs cause increased cortical latencies, mild decreases in cortical amplitudes, the maximum latency and amplitude effect 3-5 minutes following bolus injection.
Benzodiazepines IOM
Can cause latency increase in SEP waves, or amplitude decrease in cortical SeP waveforms, less sever than inhalation agents
Induction Barbituates
The effects on EPs can cause dose dependent cortical amplitude decreased, dose dependent cortical latency increases, they are less severe than inhalation agents.
Etomidate
the effect on evoked potentials can increase SeP cortical amplitudes at low does, can increase SEP cortical latencies.
Ketamine
it can have a positive effect where in increases SEP amplitudes.
Dexmedetomidine
it has no diminutive effect on SEP cortical amplitudes.
Anesthetic requirements for SEP monitoring 1.0 MAC or less inhalation agent (0.5 MAC), avoid N2O, TIVA is recommended with patients with myelopathy or significant neurological compromise
Inhalational Agents Effects on Evoked Potentials
Effect of Barbituates on EP's
Effects of Etomidate on EP's
Effect of Dexmedetomidine on EPs
Effect of NMBs on EPs
Induction with propofol, use short to intermediate acting relaxants (succinylcholine, vecuronium, rocuronium), basic maintenance with TIVA; propfol/sufentanil/remifentanil/fentanyl, use EEG to guide propofol, no muscle relaxation
Work with the anesthesiologist to develop an anesthetic plan based on the case and monitoring techniques used
Start the case with the best anesthesia possible and begin monitoring and review the responses, refine the monitoring technique, liberalize or adjust anesthesia, hold the physiology and the anesthesia steady, evaluate the anesthesia, develop an anesthesia protocol, keep in constant awareness/communication with the anesthesiologist so one can quickly notice changes and or make adjustments that do not disrupt the overall awareness of the patient status; keep it in real-time; stay vigiliant
Can see observational effects of low blood pressure on monitoring
100mcg/kg/min Propofol, 0.2 mcg/kg/min Sufentanil, 100 mcg/kg/hr Fentanyl, 1.5 mcg/kg/min, Remifentanil, Lidocaine. 0.5 MAC Sevoflurane (MACS are different) boluses of XX PRN, how much rocuronium, low dose versus high dose and when they need it for instance ALIFs, Dexmedetomidine amount, What's the average MAP, typically want them around or above 80,
NCV - Nerve Conduction Velocity - No anesthetic constraints
ABR - Auditory Brainstem Response - No anesthetic constraints but sensitive to ischemia
EEG - Electroencephalography - Complex effects depending on agent, Burst suppression lowers CMRO2 (cerebral metabolic rate of oxygen); can typically watch a transition from active to burst to isoelectric activity;
SEP - Somatosensory Evoked Potentials - Most common agents can lower the amplitude, increase latency (which are similar effects to compromise of the DCML pathway) sensitive to cortical and thalamic ischemia
MEP - Motor Evoked Potentials - No muscle relaxants which reduce action of the neuromuscular junction to zero, anesthetic fade for increased Propofol concentration, Inhalation agents, bolus of narcotic, sensitive to ischemia and related to blood pressure, MAP (mm Hg)
Nitrous Oxide - suppresses EEG and EP activity, MOST POTENT per MAC
Halogenated Agents - suppresses EEG, usually ok if < 0.3 - 0.5 MAC
Propofol - suppresses EEG, anesthetic build-up can suppress SEP and MEP
Opiods - little or no effect but boluses can suppress MEP
Neuromuscular blockade, can improve SEP (with reduced EMG artifact/noise) but cannot use if EMG/MEP recordings are necessary
Ketamine
Lidocaine
Dexmetatomadine
Typical scenarios: TIVA, 100 mcg/kg/min Propofol, 0.2 mcg/kg/min
Anesthetic requirements for SSEP monitoring
- 1.0 MAC or less inhalation agent; limited narcotic and sedative (propofol and benzodiazepines) support is acceptable
- would use 0.5 MAC in the operating room
- N20 should be avoided if other inhalation agents are used
- TIVA - total intravenous anesthetic is recommended for patients with myelopathy or significant neurological compromise
Effects on evoked potentials can cause a dose dependent decrease in amplitudes and increase in latencies of SEP cortical waveforms. with nitrous, the changes occur rapidly and are highly destructionve. the potency is based of lipid soluability. isolfurane is readily store d in the fat and has rapid changes but is less potent. The site of action in the central nervous system is the cortex, thalamus, brainstem and spinal cord which cause suppression of synaptic neuronal transmission.
Propofol
Propofol effects on evoked potentials causes a dose dependent decrease in SEP cortical amplitude, and dose dependent increase in SEP latencies, less sever than inhalation agents.
Muscle relaxant
They effect the neuromuscular junction so no EMG or MEP
Narcotics
The effects of narcotics on EPs cause increased cortical latencies, mild decreases in cortical amplitudes, the maximum latency and amplitude effect 3-5 minutes following bolus injection.
Benzodiazepines IOM
Can cause latency increase in SEP waves, or amplitude decrease in cortical SeP waveforms, less sever than inhalation agents
Induction Barbituates
The effects on EPs can cause dose dependent cortical amplitude decreased, dose dependent cortical latency increases, they are less severe than inhalation agents.
Etomidate
the effect on evoked potentials can increase SeP cortical amplitudes at low does, can increase SEP cortical latencies.
Ketamine
it can have a positive effect where in increases SEP amplitudes.
Dexmedetomidine
it has no diminutive effect on SEP cortical amplitudes.
Anesthetic requirements for SEP monitoring 1.0 MAC or less inhalation agent (0.5 MAC), avoid N2O, TIVA is recommended with patients with myelopathy or significant neurological compromise
Inhalational Agents Effects on Evoked Potentials
- cause a dose dependent decrease in amplitudes and increase latencies of SSEP cortical waveforms
- Nitrous; changes occur rapidly, most destructive of SSEP waveforms
- potency is based upon lipid/fat soluability
- isoflurane is readily stored in fat, slower changes, more potent
- desflurane is not readily stored in fat, rapid changes, less potent
- sites of action in the CNS are the cortex, thalamus, brainstem and spinal cord; cause suppression of synaptic neuronal transmission
- causes increased cortical latencies
- causes mild decreases in cortical amplitudes
- maximum latency and amplitude effect 3-5 minutes following bolus injection
- have seen decrease in motors
- causes latency increases in cortical SSEP waveforms
- causes amplitude decrease in cortical SSEP waveforms
- less severe effect than inhalation agents
Effect of Barbituates on EP's
- causes dose dependent cortical amplitude decreases
- causes dose dependent cortical latency increases
- less severe effect than inhalation agents
Effects of Etomidate on EP's
- increases SSEP cortical amplitudes at low doses
- increases SSEP cortical latencies
Effect of Dexmedetomidine on EPs
- has no diminutive effect on SSEP cortical amplitudes
Effect of NMBs on EPs
- reduces/eliminates EMG artifact/responses; will see stimulation removal
- no change in cortical amplitudes or latencies
- reduces/eliminates tcMEP amplitudes and may increase pedicle screw thresholds
- Suggamadex reversal; can test the validity of NMB with T04 and MEP, relay to anesthesia, there is a grading system if 1/4, 4/4 depeding on dose of suggamadex. depends on the molecular interaction. is typically a once per surgery kind of thing but i have been involved in surgeries where they as for it twice. just need to make sure you give enough.
Induction with propofol, use short to intermediate acting relaxants (succinylcholine, vecuronium, rocuronium), basic maintenance with TIVA; propfol/sufentanil/remifentanil/fentanyl, use EEG to guide propofol, no muscle relaxation
Work with the anesthesiologist to develop an anesthetic plan based on the case and monitoring techniques used
Start the case with the best anesthesia possible and begin monitoring and review the responses, refine the monitoring technique, liberalize or adjust anesthesia, hold the physiology and the anesthesia steady, evaluate the anesthesia, develop an anesthesia protocol, keep in constant awareness/communication with the anesthesiologist so one can quickly notice changes and or make adjustments that do not disrupt the overall awareness of the patient status; keep it in real-time; stay vigiliant
Can see observational effects of low blood pressure on monitoring
- causes a dose dependent decrease in SSEP cortical amplitudes
- causes a dose dependent increase in SSEP latencies
- less severe than inhalation agents
- can put patient into burst suppression; not a good thing long-term
100mcg/kg/min Propofol, 0.2 mcg/kg/min Sufentanil, 100 mcg/kg/hr Fentanyl, 1.5 mcg/kg/min, Remifentanil, Lidocaine. 0.5 MAC Sevoflurane (MACS are different) boluses of XX PRN, how much rocuronium, low dose versus high dose and when they need it for instance ALIFs, Dexmedetomidine amount, What's the average MAP, typically want them around or above 80,