Download Applied Physiology Lecture 3

Applied Physiology Lecture 3: Neuromonitoring, TBSI
9-19-11
When you do cardiac, you need to read an EKG. This is not enough for neuro. You need an EEG also. It
takes many years to learn how to read an EEG, but we’ll try to learn it in ½ an hour.
EEG latencies…ask Will
SSEP latencies: (N means it’s a negative wave, but it actually gives a positive peak when monitoring b/c
it’s opposite. Ex: ulnar cortical will have a negative peak that goes up to 20, followed by a positive peak
(P) that goes down to 23)
Ulnar – subcortical –N 13
Cortical – N20-P23
Posterior Tibial – subcortical -N 30
Cortical – P37-N45
EVOKED
POTENTIAL
LATENCY
ANESTHETIC
INTERACTION
BAER’s
2 msec
Barely affected
SSEP’s (median
nerve)
20 msec
Somewhat affected
SSEP’s (posterior
tibial nerve)
40 msec
Somewhat affected
VER’s
70-100 msec
Very inhibited
If you know how and when to monitor the patient, you will be able to fix it when something goes wrong.
Knowing physiology doesn’t help if you cannot monitor and understand what is happening.Apply what
we’ve learned about the O2 and CO2 curves to EEGs.
Neuroanesthesiology now exists where they do their own monitoring (EEGs, MEPs, SSEPs, BAEPs, etc.)
and sleep studies. SOAP is a fellowship of OB anesthesiologists who take care of OB with the mom and
the neonate. However, if the mom passes, there’s a legal liability for the child, so they really only focus
on taking care of the mom now, even though they are qualified to do both.
EEG waves are associated with frequencies:
Wave type
δ (delta)
θ (theta)
Associated frequency
0-3
4-7
α (alpha)
β (beta)
8-13
14-30
The latency/ frequency= the distance from spike to spike.
The amplitude = the height of the spike.
↑ frequency:
↑ amplitude:
↓ frequency and amplitude:
Interpretation
Deep anesthesia/
General anesthesia/
hyperventilation
Awake, relaxed, eyes closed
Wide awake
The stuff you give affects the brain waves. Ex: the effects of hypoxia on the brain waves depend on the
level of hypoxia. You can also use the waves to map out the areas which are affected by hypoxia based
on which areas have changes in the wave frequencies, etc.
At this point, we should be thinking: what is the effect of hyperventilation? ↓PCO2 ↓CBF ↓CBV
↓ICP. We expect these waves. We monitor both sides/ hemispheres of the brain and, if we know the
frequencies, we can identify the waves we are seeing and know what’s going on inside the brain based
on what is shown on the EEG. If we establish a baseline before the case gets started, then we can know
that any deviations from this baseline will signify a problem with the patient. If the frequency and the
amplitude both ↓, we probably have a lack of blood flow, ischemia, etc. ↑ activity is also an issue b/c it
be a seizure, etc. The ↑ activity also occurs with the use of certain drugs (ketamine, etomidate,
inhalational agents, etc.).
Usually, ↑ CBF causes an ↑ BMR. These 2 factors are usually tied together, a phenomenon which is
known as “coupling”. However, the use of inhalational agents causes “uncoupling”, which means you
get ↑ CBF and a ↓ BMR.
Blood is supplied to the brain via the carotid artery. If there is a plaque in the carotid, then the blood
flows through the vertebral arteries, which are the collateral blood vessels (but are thinner) that supply
blood flow to the brain. Occlusion of a blood vessel leads to a ↓ in blood flow.
TIAs (transient ischemic attacks) are little ministrokes that occur when little bits of the plaque break off
and go into the brain. They then occlude a smaller vessel and cause ischemia to an area. This sometimes
manifests as Amaurosis Fugax (transient loss in vision/ temporary blindness) due to carotid occlusion. To
treat the occlusion, they have to open the artery, clean out the plaque and close the vessel with a patch.
To do this, they must temporarily disrupt the blood flow to the brain, so you have to monitor the brain
activity and make sure you keep the CPP at an adequate level to perfuse the tissue. If one vessel is
occluded, the chance that the other side is also occluded is rather high, even if it isn’t as bad.
Autoregulation occurs 70-150mmHg, but for people who are getting this surgery it will usually be higher
b/c they usually have chronic HTN and have had a stroke. This means their autoregulation curve has
shifted up, so 70-150mmHg may not be good enough. You have to be able to know when the brain is
going ischemic (monitor) based on the frequency and amplitude of the EEG waves. Correlate the EEG
reading with what is going on and see if the CPP is being maintained at an adequate level.
Brain:
R-lobe
L-lobe
Temporal
T2
T3
Frontal
F4
F3
Parietal
P2
P3
Occipital
O4
O3
Channels on the R are even, channels on the L are odd. Ex: T1= channel in the left temporal lobe.
If you clamp the R carotid to do surgery, you see a flat line on the EEG for the R side after the artery is
clamped due to loss of blood flow. How the EEG is analyzed depends on the # of channels, etc.
The BIS monitor (Bispectral Index System) monitor the frontal lobe for brain activity. There is a big
controversy as to whether or not to use the BIS monitor b/c, if you have the technology to monitor this
way and you don’t and something happens, then they’ll claim you should have used it. However, the BIS
takes the raw frontal EEG and analyzes it. It then assigns numbers to try to say that a certain number
range means a certain amount of brain activity, as a way of dumbing it down. But, if you hyperventilate
the patient, you ↓ their CBF and BMR, which ↓ their brain activity, so you’ll get a ↓ in frequency and
amplitude, which will give you a lower #, but this doesn’t mean the pt is asleep. So, we can see how
these #s are not always completely accurate. They do not give you the whole picture.
If you look at the slides, we see the standards, guidelines and options. The standards are the ones that
have a lot of clinical evidence. The guidelines have some clinical evidence, and the options are
recommendations. So, for BIS to become a standard is an industry lobby, not a realistic implication.
If the patient’s blood pressure is 200/150, their HR is high, but the BIS number says they’re sleeping,
then they’re actually probably awake and paralyzed. Maybe you’re giving them a PCO2 which is
vasconstricting to harmful degrees. Everything must be considered together. To do this, do a lifescan
(periodic analysis), which can be seen as telephone poles or shades of gray. These different methods
have the same nomenclature, it’s just put as a different picture.
Hills and valleys:
Shades of Gray:
Telephone Poles:
The big deal for us is how the drugs we give affect the frequency and latency. If your latency ↑ or
frequency ↓by 10%, or if the amplitude ↓ by 50% or more, you know something is wrong. There could
be many reasons for this such as the medications given or an insult to the brain tissue, etc.
Normal ICP is <10mmHg. You have a patient with an ICP of 25mmHg, a ↓ frequency and a ↓ amplitude.
The patient is also lethargic, confused and unresponsive. This tells us that the ICV is ↑ b/c of ↑CBF.
What should you do? You will want to hyperventilate your patient, possibly use a diuretic (not if they are
on dialysis). But the first thing you should do is secure the airway (low GCS). How else can you ↓ICP?
Drain CSF through a catheter.
It is possible for the brain to herniate through the top where you are draining the CSF, but it is not nearly
as likely as the patient herniating through the foramen magnum if you drain CSF from the spinal cord
region. So, first put the head up before draining. How do you know how much to drain?
CPP= MAP- ICPor CVP ICP= 25 CVP= 16 bp= 120/80, so:CPP= 93-25= 69mmHg. The autoregulation
curve is 70-150mmHg. Should you drop it to 17 or 18? Drain the CSF until the CPP is WNL. ICP should
ideally be <10mmHg. To see if you are draining the right amount, you would drain a little, transduce
with the arterial line, and then repeat if necessary until it is where it needs to be.
EEG:
We’re looking for frequency, amplitude and symmetry. Are the R and L equal? We’re looking at waves δ,
θ, α, and β. (delta, theta, alpha and beta) (Don’t Touch A Bagel!).
Concept of coupling vs. uncoupling:
We use evoked potentials (we evoke and look for potentials). We may monitor sensory where we
stimulate peripherally(nerves of the body/ appendages) and look for a response centrally(in the brain);
or we may monitor motor where we evoke centrally and look for a response peripherally.The longer
distance means the evoked potential will take longer to show a response.
Ex: it take 20msec. to see an ulnar response, but it takes 37-40msec to see a response in the foot.
The spinal cord has motor neurons in the ventral column/ on the anterior portion. It has sensory
neurons on the dorsal column/ posterior portion. If you are monitoring motor potentials, you cannot
paralyze the patient. If you are monitoring sensory, you are monitoring the posterior/ dorsal column.
You actually record the response at the end of wherever the signal is being sent to. SSEPs
(somatosensory evoked potentials) have latencies ( b/c of the distance they have to travel) and
morphologies (usually M-shaped, but tibial is usually W-shaped) built in to the waves.
We’re doing all of this b/c we are operating on the spinal cord (SC). We could be working on the bone
around the cord or on a SC tumor. We have to give them enough anesthetic to keep them still w/o
paralyzing them b/c they are recording MEPs (motor-evoked potentials). We could paralyze the patient
for SSEPs, but we would have to keep our gases low. This is b/c the gases we give ↓ the amplitude and
frequency. How do you know if it’s really a problem or if it’s just the gases if you have your gases high? If
you are recording both SSEPs and MEPs, you would use both.
How do we take care of this patient? We can’t paralyze them b/c we’re monitoring MEPs. We can’[t
have our gases high b/c we are monitoring SSEPs. If you get too muych anesthetic, you’ll get δ or θ
waves and lose our baseline tracings. So, we need to establish a baseline waveform for SSEPs and MEPs.
Sevoflurane, isoflurane, desflurane, and other inhalational agents affect amplitude and frequency of the
waves recorded. We need to back off the gas, but we can’t go too light or the BIS (bispectral index) will
say he is awake. There are #s for the ranges to maintain. Usually you need to stay belwo 1 MAC to kleep
the proper BIS #s.
MAC is the amount of gas given to keep ½ the people anesthetized. MAC was actually decided through
an experiment on mice where they were given IAs and was recorded as the concentration of gas given
that kept 50% of mice from moving when their tails were clamped.
NO2 is bad b/c it ↓ amplitude and ↓ latency, so it makes it look like the spinal cord is already paralyzed.
Once a baseline is established, the change from there is really what’s important. However, it is very hard
to tell someone to get their baseline and then turn on NO2. It is also hard to defend this legally, so it
could get you into trouble. Just stay away from NO2 in these cases.
How do we do this? Well, we need to take in other factors as well. Ex: if the patient has acute EtOH, that
is going to ↓ the necessary MAC for their case. If they have chronic EtOH, that will ↑ their MAC. If you
have a patient who is chronic EtOH and a drug abuser, and you have to do a 0.5MAC w/o a paralyzer,
what would you do? You can’t use a combination of sevoflurane, desflurane and NO2 b/c there is a
locking mechanism on the anesthesia machine that preevnts it. NO2 is out of the question b/c it would
require way too much. You need to supplement with something else, so you could use propofol.
Etomidate is good b/c it ↑ the amplitude but we can’t do an etomidate infusion b/c it suppresses the
renal cortex/ adrenal gland. The adrenal gland has 2 parts: the cortex and the medulla. One of these
secretes cortisol which converts NE to epi to maintain the blood pressure. An etomidate infusion would
result in HTN, which makes the EEG tracings ↓. So, you want to consider gases, drugs and the
physiology (including hypothermia, hyperthermia, anemia, etc.).
Ex: Kyphoscoliosis repair is done to straighten out the vertebral column. This procedure causes tension
on the SC, so you need to monitor and notify the surgeon of changes in waveforms (↓ from baseline,
etc). You have:






Normal carbic readings
Normal blood volume
Good O2 sats
Good temperature
Good bp (hypotension ↓ amplitude)
Good Hct, etc
If you have all of this at good levels and there is no muscle relaxant on board, you have documented
twicthes, etc., and theirs is still a problem happening with the EEG waves, then you know it is because of
tension on the SC and you need to tell the surgeon.
BAEP: Anesthetics do not affect the BAEP (brainstem auditory evoked potentials), whiched are evoked
with a clicking sound.
VER (visual evoked responses): this is the most sensitive type of evoked potential and it disappears as
soon as the patient is induced. At this point, they can hear things, but they cannot see. This does not
mean they are paralyzed and awake. If they are aware during anesthesia, it could be b/c of this. The
instance of recall is highest in the PACU. They are awake and listening and they think they are awake
and paralyzed. Document everything!! If you put an A-line in a patient in the PACU, they may remember.
This state usually shows α waves. BAEP goes away in θ b/c the brain is so sedated, not b/c the pathway
is inhibited.
There is really not a clear cut effect that benzodiazepines have because the effects change with the
dosing sizes. If too little benzodiazepine is given, it only affects the EEG wave amplitude. However, if too
much is given, the benzos affect both the amplitude and the frequency.
Depending on the drug you’re using,
you can plot where they stand. It
could be a wide range depending on
where they stand.
Brain and SC Trauma (the slides for this are mostly literature review)
TBI (traumatic brain injury) and SCT (spinal cord trauma): How do you maintain this patient? It is not cut
and dry, but you must decide on a case by case basis what is best for the patient. Some cases, we give
mannitol (this is a last resort); we can give steroids for SCT or a solid tumor (i.e. pituitary). One way to
take out the pituitary tumor is via a transphenoidal path (through the nose). You give steroids to shrink
the tumor, but now the surgeon cannot operate b/c it has shrunk down too much. So, it is not cut and
dry. You would instead do the steroids at the end of or after the case so you could still give them and
the surgeon could still successfully operate on an area still big enough to see.
Slides: Neuromonitoring: We’re looking for frequency and amplitude of the EEG waves. You could look
at a raw 16-lead EEG and see if something happened on, say, the left side (odd leads), like where the
carotid was clamped, etc. You have to know the EEG basics so you can tell when things go bad. We give
some medicines that make things go bad. (Here he showed some lists in the slides)Don’t memorize the
lists b/c you really can’t…they’re all over the place.
Ex: high dose barbiturates will ↓ your EEG amplitude and ↓ the temperature. If you want to get to a
point where the pt’s brain is only functioning enough to stay alive, you can achieve this via temperature
(17⁰C) or drugs, but you still need an EEG either way. Once you have achieved this, you will get 6 spikes/
min on the EEG. You can do drug supp________ in patients who bleed out of their head do a
medically induced coma with a combination of drugs while making sure there’s not too much blood flow
or glucose. The next step below this level of sedation is an isoelectric EEG line, or brain dead/ flat line.
So, we want a level that is above suppression.
When a blood vessel is weak, it dilates and can form an aneurysm. They used to go in and clip the
aneurysm, but they don’t do as many of these intracranial surgeries now. When they do do them,
however, they use a temporary clip and a permanent clip afterwards (they’re color-coded gold and
silver). You have to drop the blood pressure before the clip is placed on the aneurysm or the aneurysm
will burst. Sometimes it is dropped as low as 40/20, which causes a ↓ in CPP. We need to protect the
brain, so we induce a coma with drugs or temperature. This ↓ the CMRO2.
The problem with ↓ temperature is that the patient is hypocoagulate, which means they bleed more, so
we use barbiturates, which give us a hypoelectric EEG.
Most of the aneurysm surgeries are now done with ________________ radiology where they go
through the groin all the way to the brain and put a coil in. The blood then clots around the foreign
object so it doesn’t rupture. When we put catheters in, the blood will also clot, so we have to give
heparin. Then, when we puncture the aneurysm, the patient is going to bleed, so we need to have
prot__________ ready to reverse it.
Barbiturates/ thiopental is good for
14 days after you draw it up. A coma
dose given of this will produce an
isoelectric EEG.
 Barbiturate graph
With a narcotic infusion, you will get a low frequency
and high amplitude. You will see δ waves with minimum
change in the waves. It is good to be able to read an EEG
plotted as a agraph. It shows us the effects on frequency
and amplitude.
Seizure Graph (above)
Narcotic Infusion graph
It is also able to tell you, as in the figure below, when
you get a significant ↑ in frequency and amplitude. This
burst in electrical activity may signify a seizure. With the
↑ activity, you would need to use an anti-convulsant
drug (isoflurane). Sevoflurane is usually ok to use, but it
can cause non-obvious seizures which cannot be seen
b/c the pt is paralyzed. However, they can be seen as
↑spike amplitudes on EEG, which lead to ↑ pressures,
etc. A pt who is on anti-seizure medications should
continue their medications the day of surgery.
Hypoxia has degree-dependant effects. Giving more meds in this situation can cause brain death.
For the EEG, we separate the waves forms, smooth them out, compress them and make a 3D image
(hills and valleys), which is just another way to read them. It gives us the same thing as the previous
methods and lets us see where something goes wrong.
This will be a test question: How does anesthesia affect BAER, SSEP, MEP, VER? Know the chart!
Evoked Potential
Latency
Anesthetic Interaction
2 msec
Barely affected
BAERs
20msec
Somewhat affected
SSEPs (median nerve)
40msec
Somewhat affected
SSEPs (posterior tibial nerve)
70-100msec
Very inhibited
VERs
SSER depends on where you get it from on what shape it has and the time it takes to get it.
6
“I”s that inhibit SSEPs:
 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) (can also be a disconnected lead)
N2O has some very marked effects on EEG. You can see
the baseline at the bottom, and as we move up the
chart, we have ↑ our N2O, so the line flattens a bit,
then it’s ↑ to the point that we lose our EEG waves, so
we back off a bit and ↓ back down to get our reading
back.
Anesthesia is not a cookbook. You can mix propofol with phenylephrine and ketamine and run a narcotic
infusion. This is just one mix that you could do. The only problem with the narcotic infusion is that is is
long-acting, so it may delay awakening and cause hypotension. The best test to monitor any possible
motor deficits is the wake up test, where you wake the patient up and see if they can move their
extremities, etc.
You should give such good anesthesia that, with the back flayed open, the guy can wake up relatively
quickly and be lying face down with his back open and not be screaming and still able to follow
commands. If there’s a problem, put him back to sleep and fix it. You don’t have to even move the
patient.
This will be a test question: know how to organize visuals, motors, SSEPs and _______ in order of
sen___________ (sensitivity?).
Know about the spinal column and tracts, the blood supply to the SC, and 2 anterior spinal arteries. You
can use a TCD (Transcranial Doppler). You’ll be able to hear if they have collateral blood flow, if they
have a bunch of crap in the artery (it will sound like a sandstorm). Can’t do anything about it (?).
__________________ measures velocities of blood. A narrower lumen= faster flow.
Slides: Traumatic Brain Injury and SCI
How do we maintain the pressure in these pts? Do we keep it low b/c they’re bleeding out? Do we keep
it high to maintain perfusion? Don’t know.
GCS (Glascow Coma Scale)- a low score is usually associated with cervical spinal cord injuries (SCI). If the
pt has a GCS of <8, we need to intubate them b/c they cannot maintain their own airway. The problem is
that most of these patients also have cervical spine injuries, so you cannot move them too much. Cricoid
pressure can displace the ________________ and cause paralysis, but it is still done.
Many of these pts come in a neck collar (c-collar) b/c this is prophylactically done. They could have a
ligamentous tissue injury that is not picked up, even if the c-spine looks clear on the CT scan. So, you
leave the c-collar on until the patient is cleared radiologically and clinically, meaning there is no sign of
an injury radiologically and he does not feel any injury clinically. However, the clearance clinically cannot
be established until at least a few days later, when the patient does not have so many injuries
distracting him from any pain a ligamentous injury may have caused. If you ask him the first day, the
pain from that injury may simply blend in with the pain from all the other injuries and you wont really
know if he has one or not.
ER patient: guy with full stomach, drunk, c-collar, c-spine injury. If you manipulate his airway, you may
cause injury/ paralysis. If you intubate him awake, he’s going to throw up, which will ↑ his ICP and
cause a bleed in his head. What do you do? We’ll talk about it later, but it helps to have the statistics in
the literature backing up your decisions.
Look up this document: Marlow, T.J., Goltra, D.D.  Google IC placement of nasotracheal…. If the pt is
getting CSF out of their ears, then you know they have a basal skull fracture, so don’t put anything in
there.
Blood pressure management in TBI: after autoregulation stops working, you get an ↑ in blood flow,
which ↑ pressure linearly. There are different theories as to why this happens:
Lund theory is that the relationship b/w CBF and
MAP stays linear.
Birm states that the relationship stays linear,
but at a lower rate
Edin states that it continues to autoregulate, but
at a lower rate.
Approach
Assumption About Autoregulation
“Lund” Approach
Abolished (steep rise)
“Edinburgh” Approach
Abolsihed (gradual rise)
“Birmingham” Approach
Intact (but plateau lower)
Total
Normotension/
Normoxia
Hypotension (SBP<90)
Hypoxia (PaO2<60)
Hypoxia and
Hypotension
Assumption About
MAP
Avoid hyperemia, keep
MAP down
Avoid ↓ CBF, keep MAP
up
Avoid ↓ CBF, keep MAP
up
Number
699
456
% Good/ Moderate
43%
51%
% Poor/ Dead
57%
49%
113
78
52
24%
45%
6%
76%
55%
94%
We don’t actually know which of these is correct, but we do know that too much blood flow =
_______________________. Hypoxia and hypotension is the worst combination b/c 94% die if the
airway and blood flow are not managed properly.
We sedate more and more to intubate the patient awake, which leads to hypoxia, etc. Surgeons did a
study that said that the neuro problems arose b/c anesthesia kept the blood pressure too low. The
problem with this study is that surgeons were reading anesthesia records.
TBI hyperventilate and they get worse b/c when you hyperventilate, you ↓ blood flow and get
ischemia. What you actually want is normal ventilation.
___________________ affects: it goes down, but only lasts for 6-8hrs. Mannitol is given if the BBB is
assumed to be intact.
EDC take to surgery and put burr holes in the head so they can bleed out instead of having an ↑ ICP.
Fluid management: keep them even. NS is better than LR (we talked about this before). We used to
think hypothermia was good for TBI, but it actually causes more bleeding, so keep them at a normal
temperature.
SCI at C3-C5 means the diaphragm is injured, so the patient will no longer be able to breathe on their
own. Ex: Shoulder surgery often requires an interscalene block. However, this block gives a high chance
that the anesthetic will reach C3-C5. Would you do this for post-op pain for a patient with COPD or give
them morphine (narcotics ↓ respiratory drive)?
If a guy has had a L pneumonectomy and is here for a R shoulder surgery, you would not do the block at
all.
When there is a SCI, the sympathetic stimulation gives way and the parasympathetic stimulation takes
dominance, which means the pt will have low blood pressure. If the SC is transected high up, everything
below it will see a pooling of blood, which is a condition known as spinal shock. SCI pt can be
hypotensive due to spinal shock.
T1-T4 is also very important. If a short pt is dosed a little higher for a c-section, they may have
bradycardia. You want the level of the nipples (T4) to not be anesthetized b/c this is where the vagus
nerve is (it’s the heart accelerator/ keeps the heart fast). If the spinal goes too high, you’ll see
bradycardia. You can also get asystole (cardiac arrest).
If you are dealing with a little baby, the spinal would go too high, so you do an epidural instead. The
effects of SCI at these levels have these same clinical implications.
24-48hrs after a SCI, you can still use sux. However, you cannot use it in this situation any later than that
b/c it will cause hyperkalemic arrest when combined with all of the potassium out of the dead tissue. All
the muscles of a quadriplegic patient are flaccid. HKA will show tall, peaked T-waves on the EKG. If you
have absolutely no other choice and you have to give sux, give the pt Ca2+ first b/c Ca2+ protects the
heart from ongoing hyperkalemia. Ca2+ is not a cure for HK, but it protects against it.
**Make sure you know the treatment for HK by heart!!!**
It could also cause chronic renal failure. Don’t use sux with MH (malignant hyperthermia). Also, a high
dose of methylprednisolone can improve ________________.
A quadriplegic patient cannot feel pain, but you still give them anesthetic b/c of autonomic
hyperreflexia, which is where their ANS still reacts to pain in the form of extreme HTN &
_____________. Usually happens with dissection above T6. No parasympathetic , only sympathetic
response. You can only cut this loop by giving anesthesia. Steroids improve this outcome.
**Know this stuff!!**