Catherine V. Koffel and Maximilien J. Gourdin
SV ¼ VTI LVOT AREA LVOT
Ejection fraction(EF): This can be calculated from SV and LVEDV. The normal range for EF is 50–70%.
EF¼ ðSV=LVEDVÞ 100
Pulsed-wave (PW) tissue Doppler imaging (TDI) of the basal myocardium can provide a quick method to estimate LV contractile function (Figure 25.4). An S’ value greater than 8 cm s1 is associated with an ejection fraction above 50%.
Regional systolic function
Following coronary artery occlusion systolic wall thickening and endocardial inward motion are reduced within five cardiac cycles. These signs pre- cede ECG changes and increases in PAWP, making TEE a more sensitive indicator of myocardial ische- mia. The regional wall motion abnormality (RWMA) is determined by the coronary artery involved. The
S⬘
E⬘
A⬘ (a)
10 cm/s
5
–5
–10 (b)
Figure 25.4 (a) Mid-esophageal two-chamber view with pulsed- wave tissue Doppler in the anterior and inferior basal myocardium.
(b) Myocardial spectral tissue Doppler signal, showing systolic (S’), early diastolic (E’) and atrial contraction (A’) waves.
(a) (b) Figure 25.3Transgastric mid-papillary
short-axis views of the left ventricle, giving (a) the LVEDA and (b) LVESA, used to calculate the fractional area change.
RCA
LCx
LAD
Figure 25.5Transgastric mid-SAX view of the LV showing the distribution of coronary artery supply.
Chapter 25: Intraoperative assessment of ventricular function
155
Apical
L IL IL
I IS
AL
IS AL I
IL A
AS A
(a)
AS AL
A AS
IS I
S
A I
3-chamber 2-chamber
4-chamber
Mid-papillary Basal
(b)
Figure 25.6The LV segments: (a) mid- esophageal and TG views at basal, mid- papillary and apical levels, with anterior (A), antero-septal (AS), infero-septal (IS), inferior (I), infero-lateral (IL) and antero- lateral (AL) walls. (b) Seventeen-segment model.
Table 25.1 Classification and scoring of regional wall motion abnormalities (RWMAs)
Class Score Myocardial thickening Wall excursion
Normal 1 >50% Inward>30%
Hypokinesia 2 10–50% Inward 0–30%
Akinesia 3 <10% None
Dyskinesia 4 None/thinning Outward
Aneurysmal 5 Thinning/aneurysmal None/outward
156
TG mid-SAX view displays myocardium supplied by all three major coronary arteries (Figure 25.5).
For the purposes of RWMA evaluation, the LV myocardium is now divided into a 17-segment model.
At basal and mid-papillary levels there are six segments;
at the apical level there are four segments; the 17th segment is the true apex of the LV (Figure 25.6)–rarely visualized with TEE. Each segment is scored according to degree of dysfunction (Table 25.1). The sum for all the segments is divided by the number of segments visualized to produce awall motion index score.
Diastolic function
Normal diastolic function allows for adequate LV filling with low LVEDP. Diastole extends from AV closure to MV closure. The phases of diastole include isovolumic relaxation time (IVRT), early rapid filling, late filling (diastasis) and atrial systole (Figure 25.7).
Indices of myocardial relaxation include:
Isovolumic relaxation time(IVRT): the initiation of myocardial relaxation occurs at the time of peak systolic pressure. When the pressure in the aorta exceeds that in the LV the AV closes and IVRT starts.
When LV pressure falls below LA pressure the MV opens and IVRT ends. A normal IVRT is 70–90 ms.
Impaired relaxation leads to an increase in IVRT
>90 ms. With restrictive pathophysiology the IVRT decreases below 70 ms.
Transmitral flow (TMF): placing a PW Doppler sampling window at the tips of the MV leaflets as they open into the LV gives a typical TMF pattern. TMF starts as the MV opens and comprises three phases (Figure 25.8): rapid early filling (E wave), late filling (L wave) and atrial systole (A wave). LV filling is determined by the pressure gradient between the LA and LV when the MV opens, LV compliance, LV relaxation, atrial contraction and MV orifice area.
Diastolic dysfunction leads to changes in the ratio of the amplitude of the transmitral E and A waves (Figure 25.9). Initially E wave velocity decreases, but as dysfunction progresses, the E:A ratio reverts to that of a normal pattern (pseudo-normalization). When dysfunction becomes severe (restrictive pathology) the E wave velocity increases markedly.
Pulmonary venous flow (PVF): the use of PW Doppler in the left or right upper pulmonary veins gives a PVF pattern (Figure 25.10), consisting of two systolic waves (S1and S2), a diastolic wave (D) and an atrial systole wave (A).
Diastolic dysfunction causes changes to the normal PVF pattern (Figure 25.11). As diastolic function worsens, the D wave initially decreases, then becomes greater than the S wave as restrictive pathophysiology predominates. The size and duration of the A wave increase as diastolic dysfunction progresses.
Figure 25.7 The four phases of ventricular diastole: isovolumic relaxation time (IVRT), early rapid filling (E), late filling (L) and atrial contraction (A). The pressure curves of the LA and LV show the timing of the opening (O) and closing (C) of the AV and MV.
Figure 25.8A normal transmitral flow pattern, consisting of early (E), late (L) and atrial contraction (A) waves.
Chapter 25: Intraoperative assessment of ventricular function
157
Tissue Doppler imaging(TDI): PW Doppler inter- rogation of the lateral mitral annulus reveals typical E’ and A’ waves. An E’ wave less than 8 cm s1 is associated with diastolic dysfunction.
Right ventricle
The RV is a complex structure – a triangular, crescent-shaped chamber containing muscle ridges (trabeculae carneae). This makes accurate measure- ment of volumes a difficult and time-consuming task in the intraoperative setting. Simpson’s method can be used to determine RV volume, with the use of an ellipsoid or pyramidal model instead of a series of discs. Because RVEDV > LVEDV (50–100 ml m2 versus 45–90 ml m2), normal RVEF is 10% less than the LVEF. RV stroke volume is dependent on preload and contractility and is very sensitive to changes in RV afterload. The mid-esophageal 4-chamber (Figure 25.12) and TG mid-SAX views are used to assess RV volume status and free-wall contractility.
RV hypertrophy is defined as RVED wall thick-
ness >5 mm. RV systolic pressure can be estimated
using continuous-wave Doppler interrogation of a TV regurgitation jet and applying the simplified Bernoulli equation (P¼4V2).
Systolic function
RV systolic function may be assessed using:
Fractional area change (RVFAC): using the mid- esophageal 4-chamber view, RVEDA and RVESA are traced to give the RVFAC. A normal value is 30–60%.
Tricuspid annular plane systolic excursion (TAPSE): using M mode in the mid-esophageal 4-chamber view, the longitudinal motion of the lateral TV annulus is measured. A distance >15 mm indi- cates normal systolic function.
Tissue Doppler imaging(TDI): a systolic (S’) wave velocity of the lateral TV annulus >12 cm s1 is associated with normal RV contractility.
Diastolic function
Assessment of RV diastolic dysfunction is complex and still to be fully studied. It may be estimated
Figure 25.10 Normal pulmonary venous flow pattern. Systolic waves S1(atrial relaxation) and S2(mitral annular systolic excursion);
diastolic wave (D) and atrial contraction (A) wave.
Figure 25.11 Changes in pulmonary venous flow pattern with diastolic dysfunction.
d3 71–79 mm d2 27–33 mm
d1 22–28 mm
d2 d1
d3
Figure 25.12 Mid-esophageal four-chamber view with normal values for RV dimensions.
Normal function
E:A 1-2:1
E:A
< 1:1 E:A
1-2:1 E:A
> 2:1 Impaired
relaxation
Pseudo- normal
Restrictive pathology
Figure 25.9 Changes in transmitral flow pattern with diastolic dysfunction.
158
by observing the RV filling pattern and hepatic vein flow profile.
Key points
TEE provides a better estimate of preload than CVP or PCWP in ventricles with abnormal diastolic function.
TEE is a sensitive indicator of myocardial ischemia.
TEE allows direct visualization of LV and RV systolic and diastolic function.
Although TEE can be used to measure CO, in practice the PAC is easier to use.
Further reading
Funk DJ, Moretti EW, Gan TJ. Minimally invasive cardiac output monitoring in the perioperative setting.Anesth Analg2009;108(3): 887–97.
Haddad F, Couture P, Tousignant C,et al. The right ventricle in cardiac surgery, a perioperative perspective:
I. Anatomy, physiology and assessment.Anesth Analg 2009;108(2): 407–21.
Lang RM, Bierig M, Devereux RB,et al. Recommendations for chamber quantification: a report from the American Society of Echocardiography Guidelines and Standards Committee and the Chamber Quantification Writing Group.J Am Soc Echocardiogr2005;18(12): 1440–63.
Nagueh SF, Appleton CP, Gillebert TC,et al.
Recommendations for the evaluation of left ventricular diastolic function by echocardiography.J Am Soc Echocardiogr2009;22(2): 107–33.
Skubas N. Intraoperative Doppler tissue imaging is a valuable addition to cardiac anesthesiologists’
armamentarium: a core review.Anesth Analg2009;
108(1): 48–66.
Weyman AE (Ed.).Principles and Practice of
Echocardiography, 2nd edition. Philadelphia: Lea &
Febiger; 1994.
Chapter 25: Intraoperative assessment of ventricular function
159
Chapter
26
Neurologic monitoring
Joseph E. Arrowsmith
Injury to the brain, spinal cord and peripheral nerves represents a significant cause of morbidity and disabil- ity after cardiac surgery. Although monitors of neuro- logic function have been available since the 1950s, their use remains uncommon and largely limited to enthusi- asts and academic centers. The reason is undoubtedly the perception that neuromonitors are complex and costly devices that produce spurious results, and merely document neurologic injury – rather than allow prevention. Emerging evidence, however, sug- gests that modern neuromonitoring technologies – particularly when used together–can be used both to predict and to modify clinical outcome. Neurologic monitoring includes routine clinical observation, monitors of cerebral substrate (O2, blood flow) and monitors of cerebral function (Table 26.1)
Clinical monitoring
The risk of neurologic injury is reduced by early detection of aortic cannula displacement and venous air entrainment, as well as the avoidance of hypoxia, hypoglycemia, acidosis, gross anemia, prolonged cerebral hypoperfusion and cerebral hyperthermia (Figure 26.1).
It should be borne in mind that cerebral perfusion pressure (CPP) is dependent upon MAP, intracranial pressure (ICP) and CVP. A marked elevation in CVP, even in the presence of a seemingly adequate MAP, may result in significant cerebral hypoperfusion. As continuous invasive hemodynamic monitoring is a mandatory component of cardiac anesthesia, the accuracy of the equipment used should be critically assessed at regular intervals.
Cerebral perfusion pressure CPPð Þ ¼MAP ðICPþCVPÞ
Temperature
Cerebral perfusion pressure
PaCO2
PaCO2 Glucose
[H+] [Hb]
Emboli
Figure 26.1Factors affecting cerebral function during cardiac surgery. [Hb], hemoglobin concentration; [Hþ], hydrogen ion concentration.
Table 26.1Neurologic monitoring during cardiac surgery Clinical Arterial pressure
Central venous pressure CPB pump flow rate
Arterial oxygen saturation (SaO2) Temperature
Hemoglobin concentration Pupil size
Arterial PCO2
Substrate delivery
Transcranial Doppler (TCD) sonography
Near infrared spectroscopy Jugular venous oxygen saturation Cerebral
activity
Electroencephalography (EEG) Somatosensory evoked potentials (SSEP)
Auditory evoked potentials (AEP) Motor evoked potentials (MEP) Other Epiaortic ultrasound
Transesophageal echocardiography
Core Topics in Cardiac Anesthesia, Second Edition, ed. Jonathan H. Mackay and Joseph E. Arrowsmith. Published by Cambridge University Press. © Cambridge University Press 2012.
160
At temperatures >30C cerebral autoregulation (flow-metabolism coupling) is essentially preserved so that cerebral blood flow (CBF) across a wide range of MAP is governed by PaCO2. At PaCO2<23 mmHg (3.0 kPa) CBF may be reduced by more than half, leading to cerebral ischemia. Conversely, at PaCO2
>68 mmHg (9 kPa) CBF may be more than doubled, resulting in the delivery of greater numbers of micro- emboli to the cerebral circulation. At lower tempera- tures, autoregulation is gradually lost and progressive cerebral“vasoparesis”renders CBF pressure-passive
Substrate delivery
Transcranial Doppler (TCD) sonography
Although the intact adult skull is impervious to the transmission of conventional ultrasound (5–10 MHz), insonation of the basal cerebral arteries is possible using low-frequency ultrasound (2 MHz) directed through regions of the skull where bone is thinnest (the temporal bones) or absent (the orbit and fora- men magnum; Figure 26.2). Thus pulsed-wave TCD provides a non-invasive means of measuring cerebral artery blood flow velocity (CBFV)–an indirect meas- ure of CBF (Figure 26.3).
CBFV can be calculated using the modified Doppler equation:
CBFV¼cðFS FTÞ 2FT Cosy
wherec¼the speed of sound in human tissue ~1540 m s 1, FS¼the frequency of reflected sound, FT¼the frequency of
transmitted sound–typically 2 MHz, andθ¼the angle of incidence or insonation angle. In the absence of vasospasm or vessel stenosis, the pulsatility or Gosling Index is a reflection of cerebrovascular resistance.
Gosling Index¼VSYS VDIAS VMEAN
where VSYSis systolic flow velocity, VDIASis diastolic flow velocity, and VMEANis weighted mean flow velocity.
Near infrared spectroscopy
Cerebral near infrared spectroscopy (NIRS) provides a non-invasive means of estimating regional cortical cerebral oxygenation. The physical principles under- lying NIRS are summarized in Table 26.3.
Devices for clinical use typically employ self- adhesive sensors, applied to the skin on the sides of the forehead, away from the midline, and a remote processing and display unit. Between two and four wavelengths of infrared light are generated by photo- diodes, and light emerging from the scalp is detected by optodes (Figure 26.4). NIRS algorithms typically assume that there is a fixed ratio of arterial:venous
Transorbital ICA
Transtemporal
MCA, ACA, PCA ACoA
PCoA
ACA MCA
ICA PCA VA
BA
Basilar BA, VA
Figure 26.2 TCD ultrasound windows for examination of the basal cerebral arteries (the Circle of Willis)–submandibular approach not shown. ACA, anterior cerebral artery; ACoA, anterior communicating artery; MCA, middle cerebral artery; ICA, internal carotid artery; PCoA, posterior communicating artery; BA, basilar artery; PCA, posterior cerebral artery; VA, vertebral arteries.
Table 26.2 Clinical applications of transcranial Doppler sonography
Detection of cerebral embolism during carotid endarterectomy and cardiac surgery
Detection of endoaortic balloon clamp migration during port access cardiac surgery
Diagnosis of circulatory arrest in raised ICP Assessment of cerebral autoregulation Assessment of CBFV in migraine
Detection and monitoring of post subarachnoid hemorrhage vasospasm
Hemodynamic assessment of vessels feeding arteriovenous malformations
Assessment of vertebrobasilar insufficiency
Chapter 26: Neurologic monitoring
161
blood (e.g. 1:3) in the sample volume; actual arterial:
venous blood ratios are likely to be subject to both intra- and inter-individual variation. The use of more than one optode allows correction for the
contribution made by blood in the scalp and skull, such that around 85% of the signal is from the brain. In contrast to conventional pulse oximetry, cerebral NIRS does not rely on the pulsatile com- ponent of the signal and can, therefore, be used during non-pulsatile CPB and deep hypothermic circulatory arrest (DHCA).
Cerebral NIRS has found a number of clinical applications in the setting of cardiac surgery: detec- tion of cerebral ischemia; assessment of selective cere- bral perfusion; and the prediction of perioperative neurologic injury, postoperative cognitive dysfunc- tion, and duration of intensive care unit and hospital stay. In animal models, cerebral NIRS appears to provide a monitor of safe DHCA duration.
Jugular venous oximetry
Jugular venous oxygen saturation (SJVO2) is an invasive method of estimating the balance between
Table 26.3 Physical principles underlying near infrared spectroscopy
Light in the visible spectrum (450–750 nm) penetrates biological tissues to a depth of only 10 mm, due to attenuation By contrast, biological tissue is relatively translucent to infrared (650–1100 nm) radiation
Light traversing the brain is both scattered and absorbed
Absorption of light by colored substances (“chromophores”) is concentration-dependent Oxyhemoglobin (HbO2) and deoxyhemoglobin (Hb) have different absorption spectra The absorption of infrared light by HbO2and Hb is similar at 810 nm–the isobestic point Hb has greater absorption at shorter wavelengths
HbO2has great absorption at longer wavelengths
Figure 26.3 TCD examination of the MCA during CABG surgery; before (left), during (center), and immediately after (right) CPB.
The high-amplitude signals (center and right) represent cerebral microemboli.
Periosteal dura mater
Superior sagittal sinus
Light source Bone
Brain Skin tissue
40 mm 30 mm
Figure 26.4 Cerebral near infrared spectroscopy (NIRS).
(Courtesy of Somanetics Inc.)
162
global cerebral metabolism (CMRO2) and cerebral oxygenation. The method is analogous to the use of mixed venous oximetry (SVO2) as a measure of whole body oxygen consumption and the adequacy of the systemic circulation.
CMRO2CBFðSaO2 SJVO2Þ
Using the Seldinger technique, a retrograde catheter is inserted into the internal jugular vein and advanced cephalad into the jugular bulb at the base of the skull.
A lateral radiograph of the neck is required to con- firm correct catheter placement. SJVO2 can be meas- ured intermittently by drawing serial blood samples for blood gas analysis or continuously by using a fiberoptic catheter. The latter is prone to calibration drift. Normal values for SJVO2 are in the range 60– 75%. Increased cerebral O2 delivery or #CMRO2 ! SJVO2, whereas#cerebral O2 delivery or CMRO2 ! SJVO2.
In neurosurgical critical care, SJVO2 monitoring has been used to guide the management of raised ICP and cerebral hyperemia. In the setting of head injury SJVO2<50% has been shown to be associated with a doubling of mortality.
In cardiac surgery, SJVO2 measurement may be particularly useful during CPB when systemic hypo- tension, cerebral hypoperfusion and anemia may have a significant impact on cerebral oxygenation. Exces- sive or rapid rewarming may produce cerebral hyper- thermia and reduced SJVO2. The magnitude of
cerebral arterio-venous oxygen difference (DAVO2) during rewarming has been shown to correlate with cognitive dysfunction (Figure 26.6).
Cerebral function monitoring Electroencephalography
The EEG is a representation of the spontaneous elec- trical activity of the cerebral cortex recorded through a series of scalp electrodes (Figure 26.7).
The potential differences (typically 20–200 μV) between pairs of electrodes or between each electrode and a common reference point are displayed continu- ously on up to 16 channels. The resulting output is
35 45 55 65 75 85 95
08:44 09:10 09:36 10:02 10:28 10:54 11:20 11:46 12:12 12:38 13:04 13:30 13:56 14:22 14:48 15:14 15:40 16:06 16:32 16:58 17:24 17:50
Time Left Right CPB
DHCA
Rewarming
Figure 26.5Near infrared spectroscopy monitoring during pulmonary
thromboendarterectomy. Significant cerebral desaturation is seen at the onset of CPB, during four periods of
hypothermic circulatory arrest (DHCA), and during rewarming.
Table 26.4Common causes of changes in cerebral oxygen delivery and consumption
O2delivery O2consumption
" Hypercapnia Hypertension Gross hypoxia
Vasodilators (e.g. isoflurane)
Hyperthermia Pain
Light anesthesia Seizures
# Hypocapnia (<3.5 kPa) Vasospasm
Drugs
(e.g. thiopental)
Hypotension Stroke
Low cardiac output Coma
Hypoxia Hypothermia
Anemia Brainstem death
Chapter 26: Neurologic monitoring
163
usually described in terms of location, amplitude and frequency. EEG frequency is conventionally grouped into one of four bands: δ, θ, α and β (Table 26.5). A normal awake adult has a posteriorly
located, symmetrical EEG frequency of around 9 Hz (i.e.αrhythm).
Opioids and most anesthetic agents produce dose- dependent EEG slowing (#αandδandθ) culminating
Maximum C(a-v)O2 on rewarming (ml/dI)
< 3 0
10 20 30 40 50 60 70
21.7
% Cognitive dysfunction
31.4 34.8
44.3
57.1
n=28 n=61
n=92 n=51
n=23
3–4 4–5 5–6 >6
Figure 26.6 The frequency of cognitive dysfunction in relation to maximum cerebral arterial-venous oxygen content difference at normothermia in 96 patients with postoperative cognitive dysfunction.
From Croughwellet al.Ann Thorac Surg 1994; 58(6): 1702–8. With permission.
Figure 26.7 The internationally standardized 10–20 system of EEG electrode placement. F, frontal; Fp, frontal polar; C, central; O, occipital; P, parietal;
T, temporal; A, ear lobe; Pg, nasopharyngeal.
Right-sided placements are indicated by even numbers, left-sided placements by odd numbers and midline placements by Z. In addition, intermediate electrodes located at 10% positions may also be used.
The location and nomenclature of these electrodes is standardized by the American Clinical Neurophysiology Society formerly the American Electroencephalographic Society. (Adapted with permission from Malmivuo J, Plonsey R.Bioelectromagnetism– Principles and Applications of Bioelectric and Biomagnetic Fields. New York: Oxford University Press; 1995.)
Table 26.5 EEG waveforms Waveform Frequency
(Hz)
Amplitude (μV)
Comments
Delta (δ) 1.5–3.5 >50 Normal during sleep and deep anesthesia, indication of neuronal dysfunction
Theta (θ) 3.6–7.5 20–50 Normal in children and elderly, normal adults during sleep, produced by hypothermia
Alpha (α) 7.6–12.5 20–50 Awake, relaxed, eyes open, mainly over occiput
Beta (β) 12.6–25 <20 Awake, alert, eyes open, mainly in parietal cortex, produced by barbiturates, benzodiazepines, phenytoin, alcohol
Gamma (g) 25.1–50 <20
164
in periods of very low EEG amplitude–burst suppres- sion. Nitrous oxide induces high-frequency frontal activity and decreased amplitude. Ketamine increases EEG amplitude at low doses, and slows the EEG at higher doses.
The EEG has long been regarded as the “gold standard” for the detection of cerebral ischemia. At constant temperature and depth of anesthesia, pro- gressive ischemia produces a reduction in total power and slowing–decreasedαandβpower and increased δandθpower. However, these changes typically only become apparent when CBF falls below half the normal value of 50 ml 100 g 1min 1. EEG amplitude attenuation of<50% or increasedδpower is regarded as being indicative of mild ischemia, whereas>50%
attenuation or a doubling inδ power is regarded as being indicative of severe ischemia. An isoelectric or
“silent” EEG is seen when CBF falls below 7–15 ml 100 g 1 min 1. While the EEG is sensitive to subtle changes in neuronal electrophysiology, it should be borne in mind that it is not specific for pathology.
Because the interpretation of continuous intrao- perative multi-channel EEG monitoring is complex and time-consuming, a number of automated pro- cessed EEG systems have been developed. In the cere- bral function monitor (CFM), the EEG signal is filtered to remove low-frequency activity and rectified to produce a single trace representing EEG power varying with both amplitude and frequency. The cere- bral function analyzing monitor (CFAM) overcomes many of the shortcomings of CFM by displaying signal amplitude and frequency separately (Figure 26.8). A further method of EEG processing is power spectrum analysis.
100
20 0 90%
10%
Mean
Muscle Beta Alpha Theta Delta Suppr KΩ
Line 10
1
vlf
A1 B3
mV
[100%]
Figure 26.8 Typical CFAM tracing.
The left trace displays the log-weighted- mean raw EEG amplitude distribution inμV, 10th and 90th centiles, and maximum and minimum amplitudes. The right trace displays; electromyography (“Muscle”), percentageα,β,θ,δand very–low- frequency (“vlf”<1 Hz) activity, percentage of suppression (“Suppr.”)<1μV peak-to- peak, and electrode impedance in KΩ.
I II
III IV V
Po
P1 P2 Pa
Nb Na N0
N1
N2
Brainstem response
Early cortical response
Late cortical response
1 2 5 10 20 50 100 200 500 1000
Time (ms) mV
Figure 26.9Auditory evoked potentials (AEPs). An auditory stimulus or“click”is repeated at regular intervals and signal averaging over several cycles is used to extract the AEP from background EEG activity. Short-latency (<10 ms) brainstem auditory evoked responses (BAERs) reflect neural activity between the cochlear nucleus (I) and the inferior colliculus (V).
BAERs are unaffected by anesthesia but are temperature-sensitive, making them useful for monitoring the effects of cooling and rewarming. Mid-latency (10–100 ms) AEPs represent cortical processing–necessary for awareness and recall of auditory events. Analysis of early cortical AEPs forms the basis of“depth of anesthesia”monitors such as the bispectral index (BIS) monitor.
Chapter 26: Neurologic monitoring