Neuro and neuromuscular measurement Flashcards
How do potentials compare between the brain and heart in terms of amplitude?
Brain are smaller and therefore difficult to detect
How many electrodes in an EEG
16
What size are the potentials in an EEG
50 microvolts
What is an evoked potentials?
change observed in continuous EEG recording immediately after a stimulus
What types of evoked potentials can be used in EEG
Auditory - clicks in the ear
Visual - flashing lights
Somatosensory - peripheral nerve stimulated
A normal EEG has what type of signal
high frequency against a low frequency background
What effect does anaesthetic have on EEG
Suppresssed high frequency bursts in a dose dependent manner
What does burst suppression mean?
Brain at minimum metbabolic rate, hgih amplitude activity obliteraded
What is a compressed spectral array?
Processing EEG - measurement period broken down into several epochs of fixed duration, and the frequency spectrum is characterised durnig each epoch using Fourier analysis and each spectrum is stacked to form a 3D representation of how different features evolve over time
BIS is what in the context of EEG?
bispectral analysis - EEG from fronttemporal region analysed and dimensionless number displayed aiming to correlate with awareness - 0 no brain acitvity, 100 awake
What are the 5 EEG signals in order of frequency
Delta lowest
THeta
Alpha
Beta
Gamma
Give the frequency of each EEG band designation
Describe the features of each EEG wave and its interpretation
If someone were drowsy but awake, not focused then what band designation and frequency would they fall in?
If I am intensely focusing for short term memory recall or using multiple senses what EEG wave would I have and what frequency
What frequency and task might I be doing if I had beta waves on an EEG
In slow wave sleep what band designation in EEG would I be in? What characteristics and frequency would it have
At what rate is CSF produced
0.4ml/min and 24mL/hr —> 576 per day. 160ml at any one time
How much CSF is there t any one time
160ml
CSF reabsorption subsides and ceases at what pressure
ICP <5
Normal ICP
5 - 15 - Chambers
8 - 12 in equipment and anaesthesia
CPP =
MAP - (ICP + CVP)
What is the gold standard of ICP montoring
EVD
What is an EVD
fine plastic catheter through a burr hole passing through he meninges and brain into the lateral ventricle (frontal horn), connected to a drainage bag and pressure transducer through a 3 way stopcock
How does an EVD measure pressure
continuous fluid column connected to a strain gauge transducer/Wheatstone bridge via fluid filled non compressible tubing. The ICP may also be read using a simple manometer using the vertical height of the CSF columns above a zero calibration point
How is an EVD calibrated
zero point is taken to the be the patients mastoid process, external auditory canal, tragus (foramen of Monro); and can be re-calibrated after insertion to atmospheric presssure
What functions does an EVD fulfill aside from ICP measurement
◦ Character of CSF can be assessed
◦ Allows drainage to assist regulation of ICP especially in the context of hydrocephalus, drainage above a set pressure can be set up
◦ CSF sampling
Advantages of an EVD
◦ Accurate and can be recalibrated
◦ Treatment and monitoring concurrently
◦ Cheaper
Disadvantages of an EVD
◦ Require a general anaesthetic to insert and special expertise (12% still end up in the wrong position)
◦ Difficult to insert in patients with collapsed ventricles e.g. DAI in young patients
◦ Risk of infection higher than intraparenchymal devices - 3-5% vs 1-2%
‣ Ventriculitis rates increased after 5 days
◦ Prone to blockage which may impair drainage but also measurement
◦ Greater risk of trauma due to size and insertion location/depth i.e. risk of IVH; contraindicated if coagulopathic
‣ 5-7% risk of haemorrhagic complications in absence of coagulopathic
◦ No therapeutic benefit found for use of EVDs or any intracranial pressure monitoring
What is a Codman device an example of
an intraparenchymal fibreoptic pressure monitor
What is the anatomical site of measurement of a Codman catheter?
Intraparenchymal - 15-20mm below the surface with the fibreoptic transducer measuring from the tip
What is the measurement system of pressure utilised by a Codman catehter
◦ Fibreoptic pressure transducers - small enough to be catheter mounted, the light from the fibreoptic cable is passed onto a mirror which reflects it onto a detector. The mirror is distorted by increased pressure which alters the amount of light reaching the detector. —> the amount of reflection detected is used to calculate pressure
◦ Piezoelectric strain gauge pressure sensor is intracranial connected to monitor via fibreoptic cable
◦ Wire stain gauge - mounted on the end of the catheter and the system arranged so increase in pressure causes the wire to be stretched and electrical resistance through it is used to generate the pressure
At what stage does a Codman start to drift
5-7 days
Advantages of a Codman style catheter system for ICP measurement
◦ Easier to insert/reduced expertise required
◦ Do not always require a general anaesthetic
◦ Reduced risk of infection (1%)
◦ Reduced risk of haemorrhage (1.1%) - smaller catheter. Relatively contraindicated in coagulopathic but not absolute
◦ Can be used in severe cerebral oedema or DAI where ventricles are collapsed
Disadvantages of a Codman catheter
◦ Reduced accuracy - intraparenchymal pressure locally may be different to global ICP
◦ Nil capacity for treatment or drainage
◦ Cannot be recalibrated, readings subject to drift (this has been shown to be as little as 1mmHg at 5 days)
◦ expensive
How does ICP affect people clincially?
generally well tolerated if the pressure rise is slow over time
How does clinical assessment compared with direct measurement
non inferior when it comes to mortality in general trauma population
Cardinal features of raised ICP clinically
Decreased LOC - early sign but late in pathological terms
bradycardia/hypertension
Papilloedema
Unilateral or bilateral pupillary dilation
Associated
- Headache
- Vomiting
- Seiuzires
- ST segment changes and TWI
Why does LOC fall with high ICP
Reduced blood flow as CPP falls and generally seen once CPP 30-35 (ICP > 40)
How useful is the cushing reflex
‣ 40% sensitive and 73% specific at a CPP of 30; and doesn’t seem to occur if CPP > 40mmHg independent of intracranial pressure. The ICP has to be enormous and CPP 15mmHg
How does raised ICP affect vision
axoplasmic flow in the optic nerve as well as retinal venous blood flow is towards the head and usually no pressure gradient against this, as IOP is the same as IC. Order of changes
‣ Decreased and eventually absent retinal venous pulsation
‣ Engorgement of retinal veins
‣ Loss of border of optic disc
‣ Enlarging scotoma
‣ Concentric loss of vision - peripheral first
Why does pupil dilation occur in raised ICP
‣ Third nerve stretched over petroclinoid ligament or crush against it in uncal herniation - uncal herniation occurs on the same side as the lesion
‣ When herniation is central pupils are small and mid dilate when the brain stem is completely destroyed
Signs requiring a CT prior to LP
◦ Immunocompromised - HIV or AIDs, on immunosuppressants including steriods, post transplant of any sort, post splenectomy
◦ History of focal CNS disease - tumour, stroke, known focal infection
◦ New onset of seizures - within 1 week
◦ Ongoing or recent seizures - prolonged or within 30 minutes of last seizure - seizures cause an increased ICP
◦ Papilloedema or lost venous pulsations
◦ Decreased LOC
◦ Focal neurological signs - partial seizures, cranial nerve signs, unilateral weakness, dilated unreactive pupil
Who clinically gets ICP monitoring placed
Abnormal CT and GCS 3-8
Normal CT and GCS 3-8 if SBP <90, motor posturing or age >40
Advantages of an ICP monitor being placed
◦ Prediction of outcome - average ICP for the first 48 hours is a good independent predictor of both mortality and neuropsychological outcome
◦ Improvement in mortality with ICP monitor use in severe TBI in some studies
◦ Response to ICP lowering therapies or lack thereof is a useful predictor of outcome
◦ ICP does not prolong length of stay or intensity of brain specific treatments in NEJM 2012 study (Chestnut)
◦ BTF recommends it
◦ EVD can monitor and manage ICP
◦ ICP monitoring continuous, while clinical exam intermittent, thus ICP monitoring can result in earlier detection of new onset intracranial hypertension from new incidents
Why is ICP monitoring problematic
◦ Routine ICP monitoring for all TBI patients may no influence mortality outcomes or at least lack of good evidence for mortality reducing role
◦ Some studies suggest prolonged length of stay and treatment intensity without positive influence on outcome
◦ BEST:TRIP trial 2012 - absence of mortality benefit
◦ Risk of
‣ Anaesthesia, craniotomy
‣ Haemorrhage
‣ Infection
‣ Device failure, malposition, poor monitoring, incorrect readings leading to incorrect management
Describe the waveforms of an ICP trace and their signfiicance
What happens to an ICP waveform as ICP increases
Increasing amplitude of the ICP waveform, morphology unchanged, lost breathing variations
Decreased p1 on an ICP waveform implies
decreased cerebral perfusion - as arterial systolic pressure transmission through the choroid reduces. Can sugest vasospasm in the absence of rising ICP
Increased P2 on an ICP waveform implies
decreased compliance, hyperventilation increases compliance decreasing amplitude and worsening oedema increases the P2. P2 can appear more prominent due to P1 being less so could be representative of vasospasm
What is an A wave or plateau wave and what does it imply in the context of ICP monitoring
- A waves or plateau waves suggest intact cerebral blood flow auto regulation - these are seen over several minutes
What is an EEG
recording of spontaneous electrical activity of the brain measured against time using 19 scalp electrodes to detect potential difference between 16 combinations of these. It measured the activity generated by cortical pyramidal cells and the thalmus with modulation by the reticular activiating system
What does an EEG actually measure
- electrical potential generated by depolarisation of a single neuron is too small to be detected at the scalp, therefore the EEG represents synchronised depolarisation o f groups of neutrons
- Generated primarily from the superficial layer of pyramidal cells by changes in post synaptic potentials in the dendrites orientated perpendicular to the cortical surface - the current is the aggregate/summation of Excitatory post synaptic potentials (EPSPs) and IPSPs for neurons running perpendicular to the cortical surface
Where is the rhythm of cortical acitvitiy controlled?
Thalamus - which has its activity modulated by the reticular activating system
What does thalamic EEG activity look like
regular
What effect does the reticular activating system have on thalamic EEG activity
Interrupts it, desynchronises the cortical impulses
What voltage characteristics do EEGs have?
◦ Recorded potentials from 0 - 200 microvolts (generally 50 - 200)
What frequencies do EEG rhythms have
2 seconds to 100 per second
EEG between hemispheres is symmetrical or assymetrical?
Symmetrical
Delta wave
- Frequency
- Synchornous or assynchronous
- High or low frequency
- When do they occur?
- Originate from?
0-4 Hz - deep sleep regular synchronised, high voltage waves of low frequency
‣ During
* Deep sleep
* Anaesthesia
* Organic brain disease
‣ Originate in cerebral cortex independent of lower brain centres - therefore occur when cortex is severed from the RAS
Theta wave
- Frequency
- Arise from which areas
- Occur when in relation to acitivty?
4-8Hz - from parietal and temporal areas and occur most commonly in the first stage of sleep, general anaesthesia and deep medication
Alpha waves
- Freqeuncy
- Amplitude
- Synchronous or assynchronous
- Correspond to what level of alertness
- originate from
8-13 Hz -low voltage <50 microvolts
‣ Synchronous activity in the parietoocciptal cortex - i.e. symmetrical
‣ Normal awake state with eyes closed, i.e. rhythm of inattention or idle brain
‣ Thalamocortical activity and abolished when cortex disconnected from the thalamus
Beta waves
- Freqeuncy
- Amplitude
- Synchronous or assynchronous
- Correspond to what level of alertness
- originate from
> 13 Hz (14-30) - high frequency low voltage (<50microV), seen when awake (30-80 microvolts)
Symmetrical
‣ irregular assynchronous waves
‣ Frontal area
‣ Require intact thalamocortical projections and functional ascending reticular input to the thalamus
‣ Replace a waves in presence of visual stimulation and increased mental activity (arousal response or desynchronisation) - conscious effort, awake alert
Gamma waves
- Frequency
- Corresponding activity
30-80Hz
Focused attention
Increasing order of frequency for EEG waves
Delta
Theta
Alpha
Beta
Gamma
Use of EEG
- Diagnosis fo epilepsy and non convulsive status
◦ And target depth of sedation in patients - burst suppression is where there is a burst of activity followed by a period of almost isoelectric EEG, electrical activity subsequently resumes - Diagnosis of encephalopathy - progressive increase in slow wave activity
◦ Cerebral ischaemia - loss of high frequency alpha and beta waves and appearance of large low voltage delta waves
◦ Prolonged ischaemia produces low voltage slow waves and EEG may become isoelectric - Adjunct test in brain death testing - isoelectric
- Measure of depth of anaesthesia
◦ 16 channel EEG has limitations due to technical issues, noisy environment electrically, expert interpretation required. Not specific as hypothermia, hypoxaemia, hypocarbia, deep anaesthesia and ischaemia all produce similar findings. Processed EEG systems e.g. BIS has aimed to correct this - Somatosensory evoked potentials -used in spinal surgery to reduce the risk of damage to the spinal cord. Involves stimulating a peripheral nerve and detecting a response int he somatosensory cortex through scalp electrodes. SSEPs are usually combined with motor evoked potentials. Loss of amplitude or increased latency suggests injury
What is a somatosensory evoked potential and when might it be used?
used in spinal surgery to reduce the risk of damage to the spinal cord. Involves stimulating a peripheral nerve and detecting a response int he somatosensory cortex through scalp electrodes. SSEPs are usually combined with motor evoked potentials. Loss of amplitude or increased latency suggests injury
What EEG changes occur with encephalopathy?
Cerebral ischaemia? Prolonged ischaemia and brain death?
- Diagnosis of encephalopathy - progressive increase in slow wave activity
◦ Cerebral ischaemia - loss of high frequency alpha and beta waves and appearance of large low voltage delta waves
◦ Prolonged ischaemia produces low voltage slow waves and EEG may become isoelectric
What happens with anaesthesia to EEG? Equate this to MAC for a volatile agent?
change from fast wave small amplitude (beta wave) trace of wakefulness to slow wave large amplitude delta waves
◦ Volatile anaesthetics - dose dependent changes in the EEG
‣ <MAC 0.4 - excitement stage of general anaesthesia with increased frequency and voltage. There’s an abrupt shift of high voltage activity from the poerstioer to the anterior regions of the brain
‣ 0.4 MAC reflects transition from wakefulness to unconsciousness - EEG frequency and voltage reduced and continues to reduce as volatile approaches 1 MAC
‣ 1.5 MAC Burst suppression occurs with sevofluorane and desfluorane - higher concentrations produce decreased voltage and increasing periods of electrical silence
‣ 1.5 - 2 MAC Isoelectric
Nitrous oxide does what to EEG
Similar effects to desfluorane but not additive
Opioid effect on EEG
nil
What monitors utilise EEG
◦ BIS
◦ Entropy monitor
◦ Power spectral analysis PSA monitor
◦ Compressed spectral array CSA
◦ Auditory evoked potential monitor
What does BIS stand for
Bispectral index
What is BIS? Why was it made? How does it work?
◦ Simplify EEG to a dimensionless number to help assess depth of anaesthesia and avoid intraoperative awareness
‣ Bispectral analysis is a complex statistical analysis where phase relations between different frequency components derived by Fourier transformation are calaculated
‣ Utilises the fact that as anaesthesia occurs biochoerence of different parts of the brain is lost - there relationship lies somewhere on a scale of 0 being total randomness, and 1 being total coherence
◦ BIS is calculated using a proprietary algorithm based on
‣ CSA
‣ Biocoherence
‣ Level of burst suppression
‣ Other
◦ Set up
‣ 3-4 electrodes placed on the forehead
What is the output of a BIS system of EEG and what do these outputs correlate to?
◦ Converts frontal EEG to a dimensionless number from 0 -100 where 40-60 is considered optimal
‣ 85-100 awake and risk of recall
‣ 60-85 light sedation or hypnosis reusable with stimulation, impaired memory processing
‣ 60 moderate hypnosis - aim for less than this to reduce awareness risk
‣ <40 deep hypnosis and burst suppression
‣ 0 =isoelectric
What does a suppression ratio on a BIS monitor mean?
SR - suppression ratio - percentage of the last 63 seconds in which where has been an isoelectric ECG. Ideally 0
What are the problems with a BIS system
‣ Dose response relationship with some anaesthetic agents e.g. propofol, Inhalational agents, midazolam but not others nitric oxide and opioids
‣ Problems with
* Ketamine increases BIS number
* Nitrous oxide induces sedation without reflecting in the BIS score
* Opioids do not affect it
‣ Contradictory assessment fo efficacy
* B aware study found BIS guided anaesthesia reduced risk of awareness with recall by 82%
* B unaware trial found BIS guided anaesthesia provided no greater reduction in intraoperative awareness than using end tidal volatile concentration monitoring
What is SE on a BIS moniotr?
Spectral entropy
Level of signal unpredictability is measured on the EEG and frontalis EMG
‣ SE - state entropy - derived over frequency range 0.8 - 32 Hz reflects level of hypnosis * <60 corresponds to adequate anaesthesia ‣ RE - response entropy - calculated over frequency range 0.8 - 47 Hz of frontalis EMG is sensitive to facial muscle activity. Has a faster response time than SE and therefore predicts arousal earlier. <60 indicates anaesthesia
What is CSA in the context of EEG? How does it work? What is it used for?
◦ Method of analysing complex data from raw EEG
◦ Short periods of 5-10 seconds recorded - epochs
◦ Fourier transformation - complex waveforms to simpler sine waves fo different frequencies
◦ Low frequencies become more common as anaesthesia takes effect and the abundance of each frequency is reflectedi in a histogram called the CSA
◦ The spectral edge is the frequency below which 95% of CSA occurs and therefore a marker of the highest frequencies and can be monitored - does not correlate well with drug concentration or effect during emergence
◦ The median frequency has an improved correlation with drug concentration - it is the frequency below and above which 50% of CSA occurs - not consistent between patients or anaesthetic agents
PSA in the context of EEG is what? How does it work?
◦ EEG is analysed in epochs intervals of 2- 16 minutes
◦ Fourier transformation used - convert each epoch to constituent sine waves of varying amplitudes and frequencies
◦ Power spectrum calculated by amplitude of individual frequency processes being squared and then displayed graphically
◦ Power wave amplitude decreases as depth of anaesthesia increases
◦ Inter patient variability a major issue
What is normal cerebral blood flow
54mL/100g per minute
What is critical cerebral blood flow when awake? When asleep?
18-20mL/100g per minute when awake
10-18mL/100g /min when anaesthetised
What is an evoked potential?
the use of sensitive equipment to detect the signal produced from repeated sensory receptor stimulation in the cerebral cortex.
◦ Background noise can be averaged out after multiple stimuli
◦ Evoked potentials smaller amplitude than EEG 1-5 microV (as opposed to 10-20microV)
How does an evoked potential signal compare to EEG?
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◦ Evoked potentials smaller amplitude than EEG 1-5 microV (as opposed to 10-20microV)
What characteristics of evoked potentials are measured and matter? Which is more sensitive for changed in awareness?
◦ Latency - delay from stimuli to detection
◦ Amplitude - peak to trough voltage
◦ Waveform characteristic - positive or negative
- Volatile anaesthestics cause dose dependent decreases in the amplitude and increases in the latency of the cortical component of somatosensory evoked potentials
◦ Amplitude is more sensitive to changes than latency
What types of evoked potentials are used?
◦ Visual
◦ Auditory - used to monitor depth of anaesthesia based on it disappearing last when undergoing anaesthesia. Series of clicks are delivered as the patient is anaesthetised and result EEG analysed to give an AEP index using an algorithm to give arbitrary values of 0-100
‣ >80 = awake
‣ <50 = asleep
◦ brain stem auditory
◦ Somatosensory
What is impedence? Why is it important in the context of EEG? What factors are important in reducing impedence in EEG
Impedence is resistance to alternating current
EEG is a small signal 10-20microvolts, impedence will interrupt this
Factors which may account for increased impedence in EEG
- Lack of contact between skin and electrode
Impedence = <5kohms = good electrode placement
2.6 nanowatts on an EEG is equivalent to how many volts
26 microvolts
What is the signifiance of very high voltage or very low voltage EEG
Low amplitude <20 microvolts- ischaemia
High amplitude >59 microvolts - seizures
Burst suppression - coma
What does a spike denote on an EEG and what does it look like
Conventionally which side of the EEG is left and right
When you look at the screen EEG 1 - left; EEG 2 right
What does burst suppression look like
What is an epileptiform activity on an EEG
What criteria are required for determination fo an electrogrpahic seizure
How are EEG traces for seizures different in ICU patients to others?
Slowly evolving and low frequencies and amplitudes leading to false negatives
What Hz readings may lead to a suspciion of seizures if persisting for >10 seconds?
> /= 3Hz
If <3Hz but evolving or improves with AED it signifies seizure
What does non convulsive status epilepticus look like on EEG
- Rhtyhmic, generalised, symmetrical, spike and wave or polyspike at 2-3.5Hz
- Atypical spike and wave with lower frequency and less symmetry
- Multiple spike and wve
- High voltage, repititive, rhythmic delta activity with intermixed spikes and sharpes waves
What trace do you aim for in a thiopentone coma
Burst suppression - periodic hihg voltages, sharply contoured waveforms including spikes and polyspikes alternating with severe suppression or isoelectricity. Bursts lasting 1-10 secnods. Aiming for no more than 2-5 bursts per minute or burst suppression ratio >75% (i.e. at least 75% of trace suppression pattern)
What is a PLED on an ECG
What happens in cerebrla ischaemia on an EEG
loss of alpha and beta waves
Appearance of large voltage, slow delta waves
What is critical blood flow in the cerebral circulation
The blood flow below which ischaemic EEG changes will present within 3 minutes
Normal CBF is 54ml/100g tissue/per minute if awake
Critical blood flow is 18-20ml/100g per minute for awake and 10-18 if anaesthetised
What effect does a volatile anaesthetic have on EEG <0.4MAC
excitatory - an abrupt shift from an excitement stage of GA to high voltage activity from the posterior and anterior regions of the brain at 0.4MAC and above
At what MAC does burst suppression occur on an EEG
1.5 MAC
What is a nerve stimulator
produce direct current of specific amplitude, duration and frequency to produce depoalrisationo of nerves
What is the physiology of a nerve stimulator
Electrical energy delivered sufficent to cause a rise in membrane potential of a nerve such that it exceeds its threshold potential –> depolarisation.
Variables that can be manipulated
- Amplitude of current
- Duration and frequency of the stimulus
- Proximity of the electrode to the nerve
- Polarity
Energy delivered reflectino of current and duration
What is a supramaximal stimulus in the context of NMJ monitoring
sufficient current amplitude to cause 100% fo motor neurons within the nerve to depolarise
60-80mA square wave DC for 0.1-0.3 seconds
What level of stimulus is required in NMJ monitoring
Supra-maximal stimuli are required during monitoring of
neuromuscular blockade so that any variation in the twitch characteristics (for example, fade)
must be due to a factor other than the number of neurons recruited during repeated stimulation.
What impact does duration of stimulus have in NMJ monitoring
For a given current - short impulses preferentially stimulate large fibres, therefore action potentials can be stimulated in motor fibres which have larger mean diametres than sensory fibres if application of current 0.1 second
Longer impulses likely to cause pain
What impact does polarity have on NMJ monitoring
Interestingly, significantly less energy is needed to stimulate a nerve that is adjacent to the
cathode than one adjacent to the anode. Therefore the negative terminal should be connected to
the electrode closest to the target nerve or the stimulator needle.
What relationship does distance between impulse and nerve have?
The relationship between the energy required to
depolarize a neuron and the distance between
the neuron and electrode obeys the inverse
square law, meaning that four times the energy is
required if the distance is doubled.
What components are there to a nerve stimulator
How much current is used in NMJ monitoring
40-60mA
Single twitch neuromuscular blocking works how
Single square wave of current lasting 0.1-0.2msec is applied to the nerve - muscle twitch amplitude begins to fall when >70% of acetylcholine receptors are occupied
Neuromuscular blockade monitoring with train of 4 works how
4 single twitches are applied at a frequency of 2Hz - the ratio of the 4th twitch amplitude to thef irst provides a more sensitive indicator of level fo NMB than a single twitch
What methods of neuromuscular blockade monitoring are there?
- Single twitch
- train of 4
- Tetanic stimulation
- Double burst
How does number of twitches seenn correlated with % blockage of nicotinic acetylcholine receptors at the NMJ
Methods of assessing response to stimulation
How is movement detected in neuromuscular monitoring? Where do the electrodes go? What is the measurement system ideal for
How does double birst non depolarising assessment work?
How does single twitch non depolarising blockade work in asssesment of NMJ
How does a TOF work for NMJ assessment?
How does tetany and post tetanic count NMJ monitoring work?
What clinical features suggest inadequate neuromuscular reversal or persisting blockade>
Unable to perform a sustained head lift for >5 seconds (<30% blockade)
Vt < 10ml/kg
Tongue protrusion unable to perform
Unabel to open eyes
Sustained hand grip for 5 seconds
What is an accelarometer
Acceleration is proportional to force for any given mass ( F=ma ), therefore an accelerometer taped to the thumb can be used to assess force of contraction.
Which muscle groups are most sensitive to neuromuscular blockade?
Smaller m
Where are the different leads placed in relation to nerve and muscle for neuromuscular monitoring
Negative electrode (black) over nerve
Positive electrod (red) away from muscle
Where to place electrodes for neuromuscular monitoring
Ulnar nerve
Electrodes are placed along the ulnar border of the wrist at the flexor crease, and thumb adduction is assessed. (adductor pollicus)
Facial nerve
The positive electrode is placed at the outer canthus, and the negative electrode is placed anterior to the tragus. Eyebrow twitching is assessed. (orbicularis oculi)
Posterior tibial nerve
Electrodes are placed posterior to the medial malleolus, and plantar flexion is assessed. (plantar flexion)
Train of 4 monitoring utilises stimulus at what frequency and how long does each stimulus last
Four single twitches (0.1ms) delivered at 2Hz (i.e. 1.5s for all 4).
What is fade in neuromuscular blockade monitoring
Number of observed twitches gives an indication of receptor occupancy
With increasing blockade, the amplitude and number of observed twitches decreases.
Fade is the reduction of twitch height with repeated stimuli during a partial neuromuscular block
Occurs due to the effect of non-depolarising agents on the presynaptic membrane, reducing ACh production.
What is the physiological mechanism of fade
Fade is the reduction of twitch height with repeated stimuli during a partial neuromuscular block
Occurs due to the effect of non-depolarising agents on the presynaptic membrane, reducing ACh production.
In train of 4 neuromuscular monitoring how does the amount of twitches relate to level of blockade?
What is a TOF ratio and what are some numbers of significance
The ratio of the amplitude of T1 to T4 (ToF ratio) can also be used as a measure of blockade:
ToF ratio > 90% is adequate for extubation
ToF ratio > 70% suggests adequate respiratory function
What is tetanic stimulation
High frequency (50-200Hz) supramaximal stimulus for 5 seconds.
Normal muscle will exhibit tetanic contraction
Partially paralysed muscle exhibits fade
Degree of fade is proportional to degree of blockade, and is very sensitive.
When might a post tetanic count be used? How is the stimulus given
Used in deep blockade when there is no response to ToF. A tetanic stimulus is given, followed 3s later by single twitches at 1Hz.
How is a double burst stimulus given in neuromuscular monitoring
Two 0.2ms 50Hz (tetanic) stimuli are applied 750ms apart.
What double burst ratio is required for adequate reversal?
> 0.9
How much neuromuscular blockade is required to cause a depressed response in single twitch neuromuscular stimulus
> 75% blockade
Single stimulsu lasts 0.2ms
3 Ways of objectively measuring neuromuscular stimulus
Mechanomyographer
Electromyography
Accelaromyography
Mechanomyography in the context of NMJ monitoring works how? Pros? Cons?
Strain gauge transducer attached to thumb and measures thumb force of contraction
Gold standard
Can be used for all types of stimulus
Cumbersome
Hand and arm must be fixed
Electromyography as NMJ monitoring works how? Pros? Cons?
Nerve stimulation and measurement of evoked compound muscle action potential
Pro - not bulky
Cons 0 diathermy, hand temperature and movement interfere
Acceleromyography as NMJ monitoring works how?
Piezoelectric crytal attached to thumbn and thumn movement causes measurement of accelaration of the crystal
Comparable to mechanomyography
Only for TOF ratio and PTC
