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Indications and Utility in The Intensive Care Unit: Neuromonitoring

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116 views11 pages

Indications and Utility in The Intensive Care Unit: Neuromonitoring

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philip
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Feature

Neuromonitoring
Indications and Utility in
the Intensive Care Unit
CATHERINE HARRIS, PhD, MBA, CRNP

Information on the use of neuromonitoring in intensive care units is scattered but significant. Nurses who do
not care for neurologically impaired patients on a daily basis may not have a strong understanding of the util-
ity of various neuromonitoring techniques, why they are used, or how they are interpreted. Two main types of
neuromonitoring that are frequently seen but poorly understood are reviewed here: transcranial Doppler sono-
graphy and electrophysiology. Information on these 2 techniques tends to be either superficial with limited
applicability to the critical care setting or very technical. This review provides information about neuromoni-
toring to help guide critical care nurses providing care to neurologically impaired patients. (Critical Care Nurse.
2014;34[3]:30-40)

N
euromonitoring is an umbrella term used to describe the various invasive and nonin-
vasive techniques that are available for monitoring functioning of the central nervous
system. Neuromonitoring techniques are essential tools used in evaluating patients with neu-
rological injury in critical care settings. Neuromonitoring is typically used when a clinical neurological
examination is either difficult or not practical to perform, such as during an operative procedure or
when the patient’s mental status has deteriorated. Depending on the technique used, neuromonitoring
allows the health care staff to evaluate motor and sensory function, brain activity, blood flow, and
intracranial pressures. Nurses must be able to use various neuromonitoring techniques and interpret
their results to provide the best care for their patients. However, useful and user-friendly information
on the indications and utility of neuromonitoring is scarce. In this article, I review 2 pertinent types of
noninvasive neuromonitoring techniques encountered in intensive care units, transcranial Doppler
monitoring and electrophysiology, for their indications, use, and applicability to patient care. Invasive
monitoring such as intracranial monitoring is not covered here.

CNE Continuing Nursing Education


This article has been designated for CNE credit. A closed-book, multiple-choice examination follows this article, which tests your knowledge
of the following objectives:

1. Describe neuromonitoring with transcranial Doppler monitoring and electrophysiology for the neurologically impaired patients
2. Identify normal and abnormal findings with transcranial Doppler monitoring and electrophysiology
3. Discuss the indications, use, and applicability of transcranial Doppler monitoring and electroencephalography in the neurocritical patient

©2014 American Association of Critical-Care Nurses doi: [Link]

30 CriticalCareNurse Vol 34, No. 3, JUNE 2014 [Link]


Transcranial Doppler Monitoring
Transcranial Doppler (TCD) monitoring is a nonin-
Table 1 Uses for transcranial Doppler imaginga

vasive technique that uses ultrasonic waves to measure Conventional Experimental


the velocity of blood flow in the brain.1 A pulsed Doppler Assessment for intracranial Detection of cerebral venous
2-MHz portable ultrasound machine can be used at the stenosis thrombosis
Detection of cerebral emboli Evaluation of autoregulation
bedside to measure changes in blood flow. TCD moni- Assessment for collateral flow Evaluation of arteriovenous
toring is most frequently used to detect and follow the patterns malformations
course of vasospasm in patients with aneurysmal sub- Assessment for cerebral blood Continuous monitoring
flow during angiography
arachnoid hemorrhage.2,3 However, TCD monitoring can Evaluation of stroke risk in chil- Evaluation of blood flow
be used any time that knowledge of cerebral circulation dren with sickle cell disease during a migraine
and the state of blood flow to the brain is of importance. a Based
on information from the American Institute of Ultrasound in Medicine,4
Marshall et al,5 and Tsivgoulis et al.6
Table 1 lists both conventional and experimental uses of
TCD monitoring.4-6 Advantages of using TCD monitor-
ing include the following: it allows real-time detection swooshing sound corresponding to each heartbeat,
of changes in blood flow, it is relatively inexpensive, it which the technician can hear and see on the TCD
can be repeated frequently or used continuously if needed, screen (Figure 2). If the swooshing sound is dampened,
and most hospital systems already have an ultrasound the technician may attempt to relocate the artery.
department. Table 2 provides important information regarding
In order to perform TCD monitoring, an ultrasound normal values of TCDs. In the first column is the name
probe is placed on specific locations on the skull where of the cranial window. The second column lists the asso-
the bone is very thin, called cranial windows. The 3 main ciated arteries that can be identified in that window, and
cranial windows are temporal, orbital, and occipital. the third col-
Each window allows access to different arteries. These umn shows at Neuromonitoring allows motor and sensory
bony windows must be thin enough to allow insonation what depth function, brain activity, blood flow, and
of the artery. Insonation refers to the exposure of the the arteries intracranial pressures to be evaluated.
artery to ultrasound waves. Thick skull bones do not would be
allow passage of an ultrasound signal from the transducer. expected. The last column is the anticipated mean flow
In the case of no signal return, the technician reports that velocity of the arteries. Higher values or no value may
there are “no windows” on TCDs. If the windows are acces- indicate abnormal flow or lack of flow.
sible, the TCD transducer will insonate or expose an artery After performing TCD monitoring, the technician
to an ultrasound signal through the bone (Figure 1). prints out an output sheet of various numbers (Figure 3)
The ultrasound beam bounces off erythrocytes in the that indicate the different arteries that were insonated in
insonated artery and returns the signal to the transducer.8 both hemispheres. Each artery may be repeated several
The signal is interpreted by software and presented as times on both the right and left sides because of the vari-
a series of numbers, which are then used to determine ation in flow rates. The important numbers are the ones
flow velocity. There is also an auditory confirmation of that reflect the depth at which each artery was insonated
insonation of the artery, as the flowing blood makes a and the mean flow velocities. If there is a large deviation
from normal depth or from the patient’s baseline, the
TCD numbers should be viewed with some skepticism.
Author
Findings on clinical examination should always take pri-
Catherine Harris is an assistant professor at Jefferson School of
Nursing and an acute care nurse practitioner in the neurocritical ority, and other imaging techniques such as computed
care unit at Jefferson Hospital for Neuroscience in Philadelphia, tomographic angiography may be warranted.
Pennsylvania. The mean flow velocity reflects the average rate of
Corresponding author: Catherine Harris, PhD, MBA, CRNP, Thomas Jefferson University,
School of Nursing, 901 Walnut Street, Suite 823, Philadelphia, PA 19107 (e-mail: blood flow through the artery. The peak flow velocity is
[Link]@[Link]). significantly higher than the mean flow velocity and is
To purchase electronic or print reprints, contact the American Association of Critical- subject to fluctuations in the patient’s heart rate and
Care Nurses, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or (949)
362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints@[Link]. blood pressure. Therefore, the peak flow velocity varies

[Link] CriticalCareNurse Vol 34, No. 3, JUNE 2014 31


2
Suboccipital
Ophthalmic
window:
artery
Vertebral artery
Basilar artery

ACA
MCA
ICA

1 PCA
Temporal window:
3
MCA
Transorbital
ACA, PCA Basilar artery
window:
ICA
Ophthalmic artery

4
Jaw angle window: Vertebral
ICA artery
ECA, CCA

Figure 1 Transcranial Doppler imaging windows and insonated arteries.


Abbreviations: ACA, anterior cerebral artery; CCA, common carotid artery; ECA, external carotid artery; ICA, internal carotid artery; MCA, middle cerebral artery;
PCA, posterior cerebral artery.

Reprinted from Schell et al,7 with kind permission from Springer Science+Business Media B.V.

L-EX-ICA 50 2
Mean
R-EX-ICA 50 2
Mean
Table 2 Normal findings on transcranial Doppler
-24.6 -23.5 imaging
Peak
Peak
-58.1 -56.2
Flow velocity,
L-EX-ICA 52 2 R-EX-ICA 50 2 Depth, mean (SD),
Mean
-23.5
Mean
-22.7
Window Artery mm cm/s
Peak Peak
-52.4 -60.1
Temporal Middle cerebral 30-60 55 (12)
L-OA 50 2 BA 80 2 R-EX-ICA 52 2
19.6 Mean Mean Temporal Anterior cerebral 60-85 50 (11)
Mean -27.7 -25.4
39.7 Peak Peak Temporal Posterior cerebral 60-70 40 (10)
Peak -57.4 -69.3
L-Siphon 60 2 BA 80 2 R-OA 50 2 Temporal Terminal internal 55-65 39 (9)
Mean Mean 18.1
32.7 -30.8 Mean
carotid
-20.4
Peak Peak 36.2
62.8
-43.1 -66.6 Peak
Orbital Internal carotid 60-80 45 (15)
L-Siphon 60 2 BA 80 2 R-OA 50 2 artery siphon
25.4 Mean 21.2
Mean -28.1 Mean Orbital Ophthalmic 40-60 20 (10)
53.5 Peak 38.1
Peak -68.1 Peak
Occipital Vertebral 60-80 38 (10)
L-MCA 50 2 R-Siphon 66 2
55.8 36.2
Mean Mean
Occipital Basilar 80-110 41 (10)
115 65.8
Peak Peak

Figure 2 Transcranial Doppler imaging output. After subarachnoid hemorrhage, TCD monitoring
Abbreviations: BA, basilar artery; Ex, external; ICA, internal carotid artery; may be ordered daily or twice daily to assess the mean
L, left; MCA, middle cerebral artery; OA, ophthalmic artery; R, right.
flow velocity. Primary providers who order TCD moni-
toring will be most interested in the mean flow velocity
more widely than the mean flow velocity. The mean flow of the middle cerebral artery (MCA), the anterior cere-
velocity is considered more stable and thus a more reli- bral artery (ACA), and the basilar artery because they
able indicator of blood flow in the brain, so it has been are the largest vessels and thus have the potential to
established as the criterion to follow.9 cause the most devastating strokes. They are also the 3

32 CriticalCareNurse Vol 34, No. 3, JUNE 2014 [Link]


Left Right

Label Depth Mean Peak Edv PI RI Label Depth Mean Peak Edv PI RI
2 MHz
L-EX-ICA 50 -24.6 -58.1 -14.9 1.73 0.74 R-EX-ICA 50 -23.5 -56.2 -4.21 2.21 0.91
L-EX-ICA 52 -23.5 -52.4 -14.2 1.61 0.72 R-EX-ICA 50 -22.7 -60.1 -4.17 2.40 0.92
L-OA 50 19.6 39.7 6.17 1.64 0.81 R-EX-ICA 52 -25.4 -69.3 -7.50 2.39 0.88
L-Siphon 60 32.7 62.8 18.1 1.34 0.71 R-OA 50 18.1 36.2 4.39 1.72 0.87
-20.4 -43.1 -5.87 1.68 0.77 R-OA 50 21.2 38.1 5.45 1.52 0.85
L-Siphon 60 25.4 53.5 7.09 1.79 0.85 R-Siphon 66 36.2 65.8 14.2 1.39 0.77
L-MCA 50 55.8 115 34.6 1.43 0.69 R-VA 60 -20.0 -34.6 -7.28 1.28 0.76
L-MCA 52 64.3 137 39.8 1.51 0.71 R-VA 62 -25.8 -65.8 -4.56 2.33 0.92
L-MCA 56 61.2 132 38.5 1.51 0.70 R-VA 66 -16.6 -57.4 -3.99 3.09 0.91
L-MCA 58 70.1 139 45.4 1.32 0.67 R-VA 66 -15.8 -58.9 -3.62 3.17 0.91
L-MCA 58 68.1 142 43.2 1.44 0.69 R-VA 66
L-MCA 58 73.2 139 46.6 1.26 0.66 R-MCA 50 42.7 89.3 25.4 1.47 0.71
L-MCA 58 62.8 133 39.1 1.48 0.70 R-MCA 52 33.9 69.3 14.5 1.58 0.78
L-MCA 58 70.8 139 44.1 1.33 0.68 R-MCA 54 40.8 79.7 22.3 1.39 0.71
L-MCA 60 66.6 134 44.3 1.34 0.67 R-MCA 54 55.8 104 29.0 1.29 0.70
L-MCA/ACA 66 71.6 184 44.1 1.95 0.75 R-MCA 54 65.8 131 41.2 1.34 0.68
-40.8 -67.4 -25.1 1.02 0.62 R-MCA 58 65.8 167 37.0 1.95 0.77
L-MCA/ACA 66 61.2 161 37.2 2.00 0.74 R-MCA/ACA 64 43.5 82.0 28.9 1.21 0.64
-40.0 -72.8 -25.9 1.16 0.62 -50.8 -97.4 -30.5 1.30 0.68
L-ACA 66 -42.4 -72.0 -28.0 1.03 0.57 R-MCA/ACA 66 46.6 85.5 26.6 1.20 0.66
L-ACA 66 -44.3 -77.8 -28.9 1.09 0.59 -37.0 -67.0 -20.4 1.23 0.68
L-ACA 70 -44.7 -80.1 -30.7 1.09 0.61 R-ACA 70 -43.1 -87.0 -27.4 1.36 0.68
L-T-ICA 50 23.1 62.0 3.05 2.50 0.94 R-ACA 68 -39.7 -75.5 -24.6 1.27 0.67
L-PCA P1 70 43.9 70.8 20.7 1.11 0.68 R-MCA 50 64.7 146 37.5 1.66 0.72
L-PCA P1 70 46.2 68.5 25.4 0.91 0.62 R-MCA 56 75.1 138 48.8 1.18 0.64
L-PCA P1 68 43.5 72.0 23.4 1.10 0.67 R-MCA 56 73.9 144 44.7 1.33 0.68
L-VA 60 -26.2 -76.6 -9.41 2.32 0.60 R-T-ICA 56 20.0 45.4 4.71 2.00 0.89
L-VA 64 -20.0 -30.4 -12.4 0.89 0.58 R-T-ICA 56 23.5 54.7 4.97 2.02 0.87
L-VA 60 -21.9 -31.2 -15.8 0.69 0.49 R-PCA P1 56 18.1 45.0 2.61 2.28 0.92
L-VA 64 -21.2 -30.0 -14.6 0.72 0.51 R-PCA P1 64 22.7 40.8 13.3 1.19 0.66
L-VA 66 -20.4 -32.0 -12.8 0.92 0.59 R-PCA P1 66 21.9 41.6 12.6 1.30 0.68
L-VA 66 -21.2 -31.2 -14.4 0.78 0.53 R-PCA P1 72 20.0 45.4 6.74 1.80 0.79

BA 80 -27.7 -57.4 -6.13 1.73 0.83


BA 80 -30.8 -66.6 -13.1 1.76 0.77
BA 80 -28.1 -68.1 -13.9 1.91 0.79
Left Lindegaard ratio = 2.97 Right Lindegaard ratio = 2.95

Figure 3 Transcranial Doppler imaging output numbers.


Abbreviations: ACA, anterior cerebral artery; BA, basilar artery; Edv, end-diastolic velocity; EX, external; ICA, internal carotid artery; L, left; MCA, middle cerebral artery;
OA, ophthalmic artery; P1, first section of posterior cerebral artery; PCA, posterior cerebral artery; PI, pulsatility index; RI, resistance index; T, terminus; VA, vertebral artery.

[Link] CriticalCareNurse Vol 34, No. 3, JUNE 2014 33


arteries that are large enough for endovascular interven-
tion if warranted. Significant increases or decreases in Table 3 Mean flow velocities and Lindegaard ratios
by severity of vasospasm
the mean flow velocity should be reported to the primary
Vasospasm Flow velocity, Lindegaard
provider, as they may reflect important changes in circu- severity mean (SD), cm/s ratioa
lation in the brain. A significant increase in mean flow None <120 <2
velocity may be due to increasing severity of vasospasm Mild 120-150 2-3
or hyperemia. A significant decrease in mean flow veloc- Moderate >150-200 >3-6
ity may reflect an impending or completed stroke. An
Severe >200 >6
extremely important change to report is when a previ-
ously high mean flow velocity is no longer detectable, a Ratioof flow velocity in middle cerebral artery to flow velocity in internal
carotid artery.
again possibly indicating a stroke. Patients with consis-
tently high mean flow velocity in the MCA should be
monitored very closely for potential stroke. are combative and confused may need behavioral or
Another very important number to follow is the Lin- pharmacological intervention before the start of the pro-
degaard ratio. This ratio is the mean flow velocity in the cedure. Nurses who are aware of the timing of the study
MCA divided by the mean flow velocity in the ipsilateral can make sure that patients are in bed and prepared.
internal carotid artery (ICA).10 This ratio helps to distin- Nurses might also consider having a patient care assistant
guish between true vasospasm and hyperemia. Hyperemia stay with the patient to help assuage fears or redirect the
is an increase in blood flow, which increases mean flow patient’s attention. Because the procedure can be limited
velocity, possibly as a result of hypervolemia, but does not by movement or agitation, nurses can greatly facilitate
indicate the situation by using their organizational skills and some
Changes in the mean flow velocity of the vasospasm. In forethought about how the patient might respond. After
middle or anterior cerebral artery and the hyperemia, the procedure is completed, the nurse should review the
basilar artery are signs of trouble. the mean flow mean velocities of the MCA and compare those values
velocity in the with values from the previous day. If there are any signif-
MCA increases to more than 200 cm/s, but the Linde- icant categorical differences, such as an increase from
gaard ratio does not increase because an associated mild to moderate spasm or moderate to severe spasm,
increase in blood flow to the ICA also occurs. Table 3 the nurse should alert the provider. Also if there is an
shows the criteria for various degrees of vasospasm. increase in the Lindegaard ratio above 2 or loss of the
The output numbers on TCDs should not be used by ability to find the artery, the nurse should alert the
themselves as the sole criteria for making clinical deci- provider.
sions and should always be correlated with findings on
the patient’s neurological examination. Technical errors Electrophysiology
are common, especially if the technician does not per- Neurological electrophysiology includes monitoring
form TCD often. Results may be dependent on the skill of various electrical impulses in the body. In the intensive
of the technician. Often, results can change dramatically care unit, the most frequently encountered neuroelectro-
when the only difference is that a different technician is physiology techniques are electroencephalography (EEG)
performing the TCD monitoring. Alternatively, errors and one of its derivatives, bispectral (BIS) monitoring.
may occur if the bone windows are thickened or the ves- Other derivatives of EEG include somatosensory evoked
sels are difficult to access and/or the patient is uncoop- potentials (SSEPs) and brainstem auditory evoked poten-
erative, confused, or combative. tials (BAEPs). These last 2 studies are more frequently
used in the operating room; however, they may be used
TCD: Nursing Implications as adjunctive studies in assessing for brain damage and
Nurses at the bedside are responsible for ensuring brain death. SSEPs and BAEPs can be used to evaluate the
that TCD monitoring is done in a timely fashion and for extent of brain damage and assist providers in discussing
making sure that the patient is in optimal condition for prognoses with patients’ families. Some experimental
the technician to perform the procedure. Patients who studies11,12 have also been done to evaluate the utility of

34 CriticalCareNurse Vol 34, No. 3, JUNE 2014 [Link]


SSEPs and BAEPs in the intensive care unit, but at this
time those 2 techniques are not the standard of care. Table 4 Electroencephalography attributes

An EEG is the evaluation of spontaneous electrical Attribute Measures Evaluation


activity in the brain used to guide seizure management, Amplitude Microvolts (mV) Low or high
assess level of consciousness, detect cerebral ischemia, Latency Milliseconds (ms) Fast or slow
and monitor effects of medications such as barbiturates Frequency Hertz (Hz) Fast or slow
in coma induction. The brain consists of billions of neu-
rons, all of which release an electrical charge. Neurons
are charged by the constant flux of ions such as sodium measure of a time delay between a stimulus and its
and potassium across their membranes. The ions are response. The latency comes just before the amplitude
transferred in and out of the cell body by membrane on the EEG. Frequencies are oscillations that are syn-
transport proteins. Neurons send electrical impulses chronized activity corresponding to a series of neuronal
(action potentials) from the cell body via myelinated networks.13 Some commonly known frequency bands are
axons, which provide the signal to release neurotrans- delta, theta, alpha, beta, gamma, and mu waves (Table 5).14
mitters from synaptic vesicles. This process is how the Symmetry is assessed visually on EEGs to ascertain if
neurons communicate with the body to perform various both hemi-
functions. Although the electrical charge of 1 neuron is spheres are Patients with consistently high mean flow
too small for EEG to pick up alone, the synchronous roughly velocity in the middle cerebral artery should
activity of millions of neurons generates a measurable equivalent. be monitored very closely for potential stroke.
charge. Scalp electrodes can be used to monitor the fluc- Finally, pat-
tuations of the electrical charges of neurons. Evidence of terns can be identified, such as burst suppression, status
seizure activity can be seen on an EEG in the form of epilepticus, or brain death (Figure 4). Nurses can and
abnormal fluctuations of voltage displayed as spikes and should be taught to identify these 3 patterns, all of which
fluctuating waveforms. EEG features do not correspond are extremely important in treatment of patients.
to specific anatomy; rather, they correspond to territo- Status epilepticus can be either convulsive or non-
ries of brain activity that cluster together. Therefore, convulsive, so interpretation of EEG waves can be diffi-
EEG is often used as an adjunctive technique to validate cult and beyond the purview of bedside nurses.
results of other diagnostic tests. However, any change in mental status of a patient may
EEG features are measured in terms of amplitude, prompt the nurse to look at the EEG if it is being contin-
latencies, frequency, symmetry, and patterns (Table 4). uously monitored. Typical markings of status epilepti-
The amplitude of a variable is a measure of its change over cus are spikes in amplitude, although such spikes vary
time. The amplitude of an EEG feature is compared with widely depending on the type of seizure. Movement of
either known norms or a person’s baseline. The highest the EEG leads may also cause artifact that may mimic
value of an amplitude is called the peak. Latencies are a the look of seizure activity, so the nurse may receive a

Table 5 Frequency bandsa

Type Location Hertz (Hz) Amplitude Normal occurrence Pathological occurrence


Delta Frontal <4 High Slow-wave sleep Metabolic encephalopathy, diffuse
injury
Theta Random 4-8 High Drowsiness Metabolic encephalopathy
Alpha Posterior head 8-13 Low Eye closing, relaxed Coma
Beta Symmetrical 13-30 Alert, active, concentration Benzodiazepines
Gamma Somatosensory cortex 30-100 Cross-modal sensory Cognitive decline
Mu Sensorimotor cortex 8-13 Rest-state motor neurons Autism, social and cognitive deficits
a Based on information from Blanco et al.
14

[Link] CriticalCareNurse Vol 34, No. 3, JUNE 2014 35


Normal EEG

Status epilepticus

Burst suppression

Brain death

Figure 4 Electroencephalography (EEG) patterns.

call from the epileptologist who is monitoring the patient providers will typically ask the nurses to titrate the med-
for clarification. ications to a certain number of bursts per minute. For
Burst suppression is evidenced by voltage attenua- example, in an induced coma, the order may read to
tion with bursts of generalized activity. Burst suppres- titrate either a pentobarbital or propofol infusion to 4 to
sion is seen in clinical states such as anoxic brain injury 6 bursts per minute. If a standard EEG screen displays 15
or prolonged resuscitation or it can be induced with seconds of information, the nurse should see a minimum
medications such as pentobarbital or propofol. When of 1 burst of electrical activity on the screen at any given
burst suppression is pharmacologically induced, time, but no more than 2. An accurate assessment of

36 CriticalCareNurse Vol 34, No. 3, JUNE 2014 [Link]


burst suppression clearly depends on the time sequence
of the computer screen, which should be verified and Table 6 Index for bispectral monitoring devicea

documented. Index range Clinical state


Brain death is the cessation of any activity on EEG. >90-100 Awake
In this scenario, the nurses can alert providers that no >60-90 Light to moderate sedation
activity has been seen on EEG for an extended period. >40-60 General anesthesia
This information may prompt providers to initiate other 20-40 Burst suppression
evaluation methods to confirm brain death. <20 Isoelectric electroencephalogram
Despite an effort to identify the meaning of patterns, a Based on information from Kelly.16
their interpretation remains largely elusive and it is diffi-
cult to correlate EEG patterns with clinical condition.
One derived measure of EEG has been interpreted to
Table 7 Waves seen in brainstem auditory evoked
correlate with level of consciousness. The BIS monitor potentials
detects a slowed pattern of electrical activity and corre- Wave Probable anatomic correlate
lates to depth of anesthesia.15 BIS monitoring uses statis-
P1 (wave I) Distal acoustic wave
tically based and complex equations to derive a sum of
P2 (wave II) Proximal acoustic nerve/cochlear nucleus
EEG parameters that include time and frequency. These
P3 (wave III) Lower pons
composite measures are then assessed in relation to
P4 (wave IV) Mid/upper pons
various signal components. This process allows the BIS
monitor to detect certain patterns, which can then be P5 (wave V) Lower midbrain

correlated with depth of anesthesia. In an awake patient,


the BIS monitor would detect a small amplitude with a the function of the system could be due to a malfunction
fast frequency, whereas in moderate sedation, the BIS in the neuromonitoring system, the presence of central
monitor would detect an increase in amplitude at a slower nervous system depressants/paralytic agents, or spinal
frequency. In a patient under general anesthesia, the BIS cord injury or brain injury. SSEPs might be used in the
monitor would detect a large amplitude at a very slow intensive care unit in a patient who does not wake up
frequency. In a patient under deep anesthesia, the BIS after surgery or as an adjunctive diagnostic tool in deter-
monitor would detect an isoelectric charge that looks mining brain death. In brain death, no response would
similar to an EEG consistent with brain death (Figure 4). be captured through the scalp electrodes despite an
BIS monitoring is commonly used in intensive care intact spine.
units to ascertain the level of consciousness of the patient. BAEPs are used to evaluate the function and integrity
Sedative and anesthesia can be titrated on the basis of the of the brainstem. BAEPs also entail the placement of
BIS monitoring, depending on the needs of the patient. electrodes on the scalp. BAEPs are elicited by the appli-
The lower the number on the BIS monitor, the deeper cation of brief transient stimuli such as audible clicks in
the level of anesthesia16 (Table 6). the ears. The response is then received and recorded via
BAEPs and SSEPs are also derivatives of EEG that electrodes. Five
correlate with specific electrical impulses. SSEPs are used common types The lower the number on the BIS monitor,
to monitor spinal cord ascending pathways and their of waves that the deeper the level of anesthesia.
functional integrity. Tiny needle electrodes are placed in are recorded
the skin along the medial nerve and the posterior tibial from BAEPs correspond to anatomic locations (Table 7).
nerve. Scalp electrodes capture the response of an elec- BAEPs are more robust than SSEPs because BAEPs are
trical stimulation that is generated through the needles. more resistant to effects of medications or anesthesia.
Once the stimulus is given peripherally, there is a certain Disorders of the ear such as labyrinthitis do not affect
amount of time that is expected to elapse before the scalp BAEPs. Even hearing loss does not preclude the use of
electrodes record the response. If there is a delay or no BAEPs. Wave V is used to assess hearing loss in the clini-
response is recorded, a break in the integrity of the ascend- cal setting; however, waves I through IV can still be
ing pathways of the spinal cord is indicated. A break in assessed for a baseline. BAEPs are largely affected only

[Link] CriticalCareNurse Vol 34, No. 3, JUNE 2014 37


by a structural abnormality such as a stroke, tumor, or
cerebral edema in the brainstem. Signal changes may Now that you’ve read the article, create or contribute to an online discussion about
start to occur when intracranial pressures exceed 30 mm this topic using eLetters. Just visit [Link] and select the article you want
to comment on. In the full-text or PDF view of the article, click “Responses” in the
Hg.17 The presence of BAEPs will disappear in more than middle column and then “Submit a response.”

80% of patients who are clinically brain dead. Because


BAEPs are not 100% sensitive and specific for brain
death, they can be used as an adjunctive diagnostic tool, To learn more about neuromonitoring, read “Intracranial Pressure
but they cannot be used alone to declare brain death. Waveform Morphology and Intracranial Adaptive Capacity” by Fan
et al in the American Journal of Critical Care, November 2008;17:545-
554. Available at [Link].
Electrophysiology: Nursing Implications
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neurointensive care. Neurosurgery. 2001;48:249-261.
sciousness. Therefore, it is important for nurses to 3. Oyama K, Criddle L. Vasospasm after aneurysmal subarachnoid hemorrhage.
Crit Care Nurse. 2004;24:58-60,62,64-67.
understand how these techniques work. Furthermore, 4. American Institute of Ultrasound in Medicine. AIUM practice guideline
knowledge of these techniques assists nurses in explain- for the performance of a transcranial Doppler ultrasound examination for
adults and children. J Ultrasound Med. 2012;31:1489-1500.
ing to patients’ families what is going on and educating 5. Marshall SA, Nyquist P, Ziai WC. The role of transcranial Doppler ultra-
sonography in the diagnosis and management of vasospasm after aneurys-
them on what it all means. Nurses are instrumental in mal subarachnoid hemorrhage. Neurosurg Clin North Am. 2010;21:291-303.
this process, but educating patients’ families requires a 6. Tsivgoulis G, Alexandrov AV, Sloan MA. Advances in transcranial
Doppler ultrasonongraphy. Curr Neurol Neurosci Rep. 2009;9:46-54.
solid understanding of the technology. 7. Schell R, Cole D, Lichtor JL, Miller RD. Neurophysiologic monitors. In:
Miller RD, Lichtor JL, eds. Atlas of Anesthesia. Vol. 3. New York, NY:
Springer Publishing; 2002:chap 10.
Summary 8. Padayachee TS, Kirkham FJ, Lewis RR, et al. Transcranial measurement of
blood velocities in the basal cerebral arteries using pulsed Doppler ultrasound:
This article reviewed 2 important noninvasive neu- a method of assessing the circle of Willis. Ultrasound Med Biol. 1986;12:5-14.
romonitoring techniques that are commonly used in 9. Sloan MA, Alexandrov AV, Tegeler CH, et al. Transcranial Doppler ultra-
sonography in 2004: a comprehensive evidence-based update. Neurology.
neurocritical care settings. For nurses who work in a 2004;62(9):1468-1481.
10. Lindegaard KF, Nornes H, Bakee SJ, Sorteberg W, Nakstad P. Cerebral
general critical care setting and do not encounter neuro- vasospasm after subarachnoid haemorrhage investigated by means of tran-
critical care patients on an everyday basis, understand- scranial Doppler ultrasound. Acta Neurochir Suppl (Wien). 1988;42:81-84.
11. Amantini A, Amadori A, Fossi S. Evoked potentials in the ICU. Eur J
ing key techniques in neurocritical care is essential. EEG Anaesthesiol Suppl. 2008;42:196-202.
12. Emerson RG, Pedley TA. Clinical neurophysiology: electroencephalography
and TCD play a major role in understanding a patient’s and evoked potentials. In: Bradley WG, Daroff RB, Fenichel GM, Jankovic J,
overall neurological status and prognosis. Nurses must eds. Neurology in Clinical Practice. 6th ed. Philadelphia, PA: Butterworth-
Heinemann: 2012:chap 32A.
understand the importance of these techniques, how 13. Andrade-Valenca LP, Dubeau F, Mari F, Zelmann R, Gotman J. High-frequency
oscillations recorded on scalp EEG. Neurology. 2011;77:524-531.
they work, and how to interpret their meaning in the 14. Blanco JA, Stead M, Krieger A, et al. Data mining neocortical high-frequency
context of the individual patient. Understanding neu- oscillations in epilepsy and controls. Brain. 2011;134(10):2948-2959.
15. Olson D, Chioffi SM, Macy GE, Meek LG, Cook HA. Potential benefits of
romonitoring is an essential aspect of working with criti- bispectral index monitoring in critical care: a case study. Crit Care Nurse.
2003;23(4):45-52.
cally ill neurological patients. CCN 16. Kelly SD. Monitoring Consciousness: Using the Bispectral Index during Anes-
thesia. 2nd ed. Boulder, CO: Covidien; 2010.
Financial Disclosures 17. Im JJ, Park BR. Does oxygen deficit to the cerebral blood flow caused by
None reported.
subdural hematoma and/or increased intracranial pressure affect the vari-
ations in auditory evoked potentials in white New Zealand rabbits? Neu-
rosci Lett. 2002;317:139-142.

38 CriticalCareNurse Vol 34, No. 3, JUNE 2014 [Link]


CCN Fast Facts CriticalCareNurse
The journal for high acuity, progressive, and critical care nursing

Neuromonitoring Indications and


Utility in the Intensive Care Unit
Facts depth the arteries would be expected. The last column is the
Neuromonitoring techniques are essential tools used anticipated mean flow velocity of the arteries. Higher val-
in evaluating patients with neurological injury in critical ues or no value may indicate abnormal flow or lack of flow.
care settings. Nurses must be able to use various neu- • Nurses should ensure that TCD monitoring is done in a
romonitoring techniques and interpret their results in timely fashion and make sure that the patient is in optimal
order to provide the best care for their patients. condition for the technician to perform the procedure.
After the procedure is completed, the nurse should review
Transcranial Doppler Monitoring the mean velocities of the middle cerebral artery and com-
• Transcranial Doppler (TCD) monitoring is a nonin- pare those values with values from the previous day. If
vasive technique that uses ultrasonic waves to meas- there are any significant categorical differences, the nurse
ure the velocity of blood flow in the brain. A pulsed should alert the provider. Also if there is an increase in the
Doppler 2-MHz portable ultrasound machine can be Lindegaard ratio above 2 or loss of the ability to find the
used at the bedside to measure changes in blood flow. artery, the nurse should alert the provider.
• To perform TCD monitoring, an ultrasound probe
is placed on specific locations on the skull where the Electrophysiology
bone is very thin, called cranial windows. The 3 main • In the intensive care unit, the most frequently encountered
cranial windows are temporal, orbital, and occipital. neuroelectrophysiology techniques are electroencephalog-
Each window allows access to different arteries. raphy (EEG) and one of its derivatives, bispectral (BIS)
• The Table provides important information regarding monitoring.
normal values of TCDs. In the first column is the • An EEG is the evaluation of spontaneous electrical activity
name of the cranial window. The second column in the brain used to guide seizure management, assess
lists the associated arteries that can be identified in level of consciousness, detect cerebral ischemia, and mon-
that window, and the third column shows at what itor effects of medications such as barbiturates in coma
induction.
• EEG features are measured in terms of amplitude, latencies,
Table Normal findings on transcranial Doppler imaging frequency, symmetry, and patterns.
Flow velocity, • It is difficult to correlate EEG patterns with clinical condi-
Depth, mean (SD),
Window Artery mm cm/s tions. One derived measure of EEG has been interpreted
to correlate with level of consciousness. The BIS monitor
Temporal Middle cerebral 30-60 55 (12)
detects a slowed pattern of electrical activity and correlates
Temporal Anterior cerebral 60-85 50 (11) to depth of anesthesia.
Temporal Posterior cerebral 60-70 40 (10) • Nurses are typically not responsible for reading or inter-
Temporal Terminal internal 55-65 39 (9)
preting EEGs; however, they do monitor continuous EEG
carotid for burst suppression and follow BIS recordings to determine
a patient’s level of consciousness. Knowledge of these
Orbital Internal carotid 60-80 45 (15)
artery siphon techniques assists nurses in explaining to patients’ families
what is going on and educating them on what it all means.
Orbital Ophthalmic 40-60 20 (10)
Nurses are instrumental in this process, but educating
Occipital Vertebral 60-80 38 (10) patients’ families requires a solid understanding of the
Occipital Basilar 80-110 41 (10) technology. CCN

Harris C. Neuromonitoring Indications and Utility in the Intensive Care Unit. Critical Care Nurse. 2014;34(3):30-40.

[Link] CriticalCareNurse Vol 34, No. 3, JUNE 2014 39


CNE Test Test ID C143: Neuromonitoring Indications and Utility in the Intensive Care Unit
Learning objectives: 1. Describe neuromonitoring with transcranial Doppler monitoring and electrophysiology for the neurologically impaired patients
2. Identify normal and abnormal findings with transcranial Doppler monitoring and electrophysiology 3. Discuss the indications, use, and applicability of
transcranial Doppler monitoring and electroencephalography in the neurocritical patient

1. Which of the following is an experimental use of transcranial Doppler 7. Which of the following is not a derivative of electroencephalography (EEG)?
(TCD) imaging? a. Bispectral monitoring
a. Assessment for collateral flow patterns b. Somatosensory evoked potentials
b. Assessment for cerebral blood flow c. Brainstem auditory evoked potentials
c. Detection of cerebral emboli d. Transcutaneous nerve stimulation
d. Evaluation of arteriovenous malformations
8. An EEG is the evaluation of spontaneous electrical activity in the brain
2. Which of the following is not a cranial window for TCD monitoring? used to guide which of the following?
a. Temporal a. Nutritional management
b. Orbital b. Seizure management
c. Parietal c. Vasopressor therapy
d. Occipital d. Hypothermia therapy

3. Which of the following velocities are established as the criterion to follow 9. Which of the following are the typical markings of status epilepticus on
to assess blood flow in the brain? the EEG?
a. Mean flow velocity a. Amplitude spikes
b. Peak flow velocity b. Latency spikes
c. Mode flow velocity c. Frequency spikes
d. Median flow velocity d. Delta spikes

4. A significant decrease in mean flow velocity may reflect which of the 10. What can an EEG help diagnose when there is cessation of any activity?
following complications? a. Level of sedation
a. Increasing severity of vasospasm b. Brain death
b. Impending or competed stroke c. Level of anesthesia
c. Increasing severity of hyperemia d. Brain hypoxia
d. Rupture of a cerebral aneurysm
11. What does the bispectral monitoring device indicate if the index range
5. The Lindegaard ratio examines the mean flow velocity in which of the number is 20-40?
following? a. Awake
a. Middle cerebral artery divided by the mean flow velocity in the ipsilateral b. Light to moderate sedation
internal carotid artery (ICA) c. General anesthesia
b. Anterior cerebral artery divided by the mean flow velocity in the ipsilateral d. Burst suppression
ICA
c. Posterior cerebral artery divided by the mean flow velocity in the ipsilat- 12. Brainstem auditory evoked potentials may show signal changes when the
eral ICA patient’s intracranial pressure is at what level?
d. Basilar cerebral artery divided by the mean flow velocity in the ipsilateral ICA a. 15-19 mm Hg
b. 20-24 mm Hg
6. A Lindegaard ratio of >3-6 indicates which degree of vasospasm severity? c. 25-29 mm Hg
a. None d. >30 mm Hg
b. Mild
c. Moderate
d. Severe
Test answers: Mark only one box for your answer to each question. You may photocopy this form.
1.  a 2.  a 3.  a 4.  a 5.  a 6.  a 7.  a 8.  a 9.  a 10.  a 11.  a 12.  a
b b b b b b b b b b b b
c c c c c c c c c c c c
d d d d d d d d d d d d
Test ID: C143 Form expires: June 1, 2017 Contact hours: 1.0 Pharma hours: 0.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 9 correct (75%)
Synergy CERP Category A Test writer: Lynn C. Simko, PhD, RN, CCRN

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