Time-Domain Analysis

Traditional display of the EEG is a graph of biopotential voltage (y-axis) as a function of time and, consequently, is described as a time-domain process. The objective of a diagnostic EEG is to identify the most likely cause of a detected abnormality at one moment in time. Typically, a diagnostic EEG is obtained under controlled conditions, using precisely defined protocols. Recorded EEG appearance is visually compared with reference patterns. Interpretation is based on recognition of unique waveform patterns that are pathognomonic for specific clinical conditions.¹³ In contrast, the goal of EEG monitoring is to identify clinically important change from an individualized baseline. Unlike diagnostic EEG interpretation, monitoring requires immediate assessment of continuously fluctuating signals in an electronically hostile, complex, and poorly controlled recording environment. Therefore, of necessity, interpretation relies less on pattern recognition and more on statistical characterization of change. Simple numerical descriptors thus may appropriately form an integral part of EEG monitoring.

Both EEG diagnostic and monitoring interpretations are based, in part, on the “Law of the EEG” (Box 16-3). It states that amplitude and dominant frequency are inversely related. As described earlier, synchronously generated postsynaptic potentials may produce large-amplitude biopotentials. However, long membrane time constants limit the number of changes that may occur per second (e.g., high amplitude, low frequency). Conversely, summation of spatially distributed asynchronous potentials results in EEG signals of low amplitude but relatively high frequency. Thus, the inverse relation between amplitude and frequency generally is maintained during unchanging cerebral metabolic states. Parallel increases in both may occur in some hypermetabolic states such as seizure activity, whereas decreases may be seen in hypometabolic states such as hypothermia. In the absence of these influences, simultaneous decreases in both amplitude and frequency may indicate ischemia or anoxia (Figure 16-9), whereas a parallel increase may be artifact (Figure 16-10).

Figure 16-9 This two-channel electroencephalographic recording was made immediately after induction of anesthesia, before head repositioning for insertion of a central venous catheter. Anesthetic induction apparently uncovered a preexisting asymmetry that was not evident in the waking electroencephalogram. Although the patient had a history of an earlier mild cerebrovascular accident and transient ischemic attacks, he appeared neurologically normal at preoperative assessment.

(Modified from Yli-Hankala A [ed]: Handbook of four-channel EEG in anesthesia and critical care. Helsinki, Finland: GE Medical, Datex-Ohmeda Division, 2004, p 31.)

Figure 16-10 The large-amplitude 2-Hz triangular waves in the left frontotemporal derivation (top trace) are the result of temporalis muscle activation with a nerve stimulator. Current spread from the stimulating to the electroencephalographic recording electrodes may be minimized with use of the appropriate facial nerve stimulation site at the jaw angle.

(Modified from Yli-Hankala A [ed]: Handbook of four-channel EEG in anesthesia and critical care. Helsinki, Finland: GE Medical, Datex-Ohmeda Division, 2004, p 18.)

Time-domain analysis of traditional electroencephalography uses linear amplitude voltage and time scales. The amplitude range of EEG signals is quite large (several hundred microvolts), and univariate statistical measures of its central tendency and dispersion may contain clinically useful information.¹⁴ Furthermore, amplitude variation may present clinically significant changes in reactivity that can be obscured by frequency-domain analysis.¹⁵ Advances in the technology of EEG amplitude integration have prompted a resurgent interest in this attractively simple approach, particularly in pediatrics.¹⁶

Frequency-Domain Analysis

An alternative method, frequency-domain analysis, is exemplified by the prismatic decomposition of white light into its component frequencies (i.e., color spectrum). As the basis of spectral analysis, the Fourier theorem states that a periodic function can be represented, in part, by a sinusoid at the fundamental frequency and an infinite series of integer multiples (i.e., harmonics). The Fourier function at a specific frequency equals the amplitude and phase angle of the associated sinusoid. Graphs of amplitude and phase angle as functions of frequency are called Fourier spectra (i.e., spectral analysis). The EEG amplitude spectral scale (Figure 16-11) squares voltage values to eliminate troublesome negative values. Squaring changes the unit of amplitude measure from microvolts to either picowatts (pW) or nanowatts (nW). However, a power amplitude scale tends to overemphasize large-amplitude changes. Clinically important changes in lower amplitude components that are readily discernible in the linearly scaled unprocessed EEG waveform may become invisible in power spectral displays.

Figure 16-11 The traditional analog electroencephalographic (EEG) signal shown in the upper left is a time-domain graph of scalp-recorded amplitude (μV) as a function of time. Digitized EEG segments (epochs) are computer-processed using the fast Fourier transform (FFT), which, like a prism, decomposes a complex electromagnetic signal into a series of sinusoids, each with a discrete frequency. The instantaneous relation is then graphically depicted by the power spectrum (bottom left), a frequency-domain plot of power (μV² or pW) as a function of frequency. The spectral edge frequency (SEF) defines the signal amplitude upper boundary. The three-dimensional compressed spectral array (CSA) plots successive power spectra with time on the z-axis (upper middle). The density spectral array (upper right) improves data compression by using dot-density to represent signal amplitude (i.e., power). Amplitude resolution is improved through color coding in the color density spectral array (CDSA) shown at bottom right. SEF is shown as the white vertical line. Note the EEG suppression at the bottom of each spectral trend.

Simplification of the large amount of spectral information generally has been achieved through the use of univariate numeric descriptors. Most commonly, the power contained in a specified traditional EEG frequency band (delta, theta, alpha, or beta) is calculated in absolute, relative, or normalized terms. Relative amplitude represents the fraction of total power contained in a specified frequency band (relative delta power = delta [−0.5 to 2 Hz] power/total [0.5 to 55 Hz] power). Normalization equalizes the total power of successive epochs to that of some arbitrary reference before the calculation of relative power (the delta power is described as Z-score change from a previous individualized baseline). The latter two derived measures are particularly useful in minimizing misinterpretation of spectral changes. For example, during the production of hypothermia, absolute delta power declines in parallel with cerebral metabolism, whereas the fraction of the total power in the delta band remains unchanged. In this circumstance, exclusive focus on absolute delta power may lead to the erroneous conclusion that the hypnotic state is decreasing.

The most widely used univariate frequency descriptors (Box 16-4) are (1) peak power frequency (the single frequency of the spectrum that contains the highest amplitude), (2) median power frequency (frequency below which 50% of the spectral power occurs), (3) mean spectral frequency (sum of power contained at each frequency of the spectrum times its frequency divided by the total power), (4) spectral edge frequency (SEF; frequency below which a predetermined fraction, usually 95%, of the spectral power occurs), and (5) suppression ratio (SR; percentage of flatline EEG contained within sampled epochs). The performance of two descriptors in characterizing clinically important EEG changes is compared (Figure 16-12). Note that at anesthetic induction, the large transient decrease in SEF and reciprocal SR increase. However, later transient SR increases signifying marked EEG suppression were not detected by SEF, apparently because of low-level radiofrequency contamination.

Figure 16-12 Certain univariate electroencephalographic (EEG) descriptors are particularly susceptible to the confounding influence of electronic interference. Note the peak in the suppression ratio (SR) trend at 17:00, correctly identifying marked EEG suppression. In contrast, the spectral edge frequency remains unchanged because of the presence of low-intensity electronic noise.

Pronk¹⁷ evaluated computer-processed univariate descriptors of EEG changes occurring before, during, and after CPB. Mean spectral frequency alone was sufficient to adequately describe all EEG changes except those occurring at very low amplitudes. Addition of a single-amplitude factor improved agreement with visual interpretation to 90%. Further factor addition did not improve agreement.

Multivariate (i.e., composed of several variables) descriptors have been developed to improve simple numeric characterization of clinically important EEG changes. With this approach, algorithms are used to generate a single number that represents the pattern of amplitude-frequency-phase relations occurring in a single epoch. Several commercially available monitors provide unitless numbers that have been transformed to arbitrary (i.e., 0 to 100) scales. Each monitor provides a different probability estimate of patient response to verbal instruction. Current monitors designed for use by anesthesia providers are listed in Box 16-5. BIS-XP, NT, PSI, and SNAP II are rule-based proprietary indices empirically derived from patient data. In contrast, CSI uses a fuzzy logic-based algorithm, whereas state entropy (SE) applies standard entropy equations to EEG analysis. Each product is designed to require the use of proprietary self-adhesive forehead sensors. Collectively, these products are now in widespread use as objective measures of hypnotic effect.

These hypnotic indices appear to provide clinically useful information. However, their fundamental differences may result in distinctly unique performances. Close agreement among these measures should not be expected. Thus, it is inappropriate and unjustified to apply clinical evidence of improved outcome obtained with one of these measures to a competing index. To date, adequately powered, prospective, randomized evidence of a statistically significant (i.e., 82%) reduction in risk for intraoperative awareness in adult noncardiac surgery has been achieved only with BIS-XP.²⁴ A recent meta-analysis review of the extensive peer-reviewed BIS literature concluded that “BIS could reduce the incidence of perioperative recall in surgical patients with high risk of awareness.”²⁵ In addition, the review authors opined that anesthesia guided by BIS monitoring could decrease anesthetic consumption and enhance recovery from relatively deep anesthesia. These findings suggest that prevention of intraoperative awareness may represent only the tip of the iceberg of potential clinical and economic benefit to be derived from routine quantitative EEG perioperative monitoring.

Scalp-recorded cerebral biopotentials are complex physiologic signals representing the algebraic summation of voltage changes produced from cortical synaptic activity (i.e., EEG), upper facial muscle activity (i.e., facial electromyogram [fEMG]), and eye movement (i.e., electro-oculogram [EOG]). During consciousness and light sedation, high-frequency gamma power (i.e., 25 to 55 Hz) is a mixture of EEG and subcortically influenced facial electromyogram. Muscle activity makes a larger contribution because of the closer proximity of signal generators to the recording electrodes. Hypnotics and analgesics typically suppress both cerebral and muscle activities, resulting in reduced gamma power. Because the upper facial muscles are relatively insensitive to moderate neuromuscular blockade, they may remain reactive to noxious stimuli.²⁶ Nociception results in sudden gamma power increase, independent of activity in the lower frequency classical EEG bands.

The EEG analyzers just described either provide separate quantitative estimates of the high-frequency information or incorporate it into the hypnotic index. For example, the Datex-Ohmeda Entropy Module separately analyzes the 32- to 47-Hz band and terms the signal “response entropy.” Addition of response entropy to the lower frequency SE is claimed by the manufacturer to facilitate distinction between changes in hypnosis and analgesia, although supporting evidence for this proposition awaits carefully designed and adequately powered randomized, prospective studies. EEG suppression decreases both entropy indices because noise-free flatline EEG segments are generally thought to have near-zero entropy. However, during cardiac surgery, EEG signals that appear to be totally suppressed may be associated with paradoxically very high entropy values. To minimize this problem, SE uses a special algorithm that assigns zero entropy to totally suppressed EEG epochs.

In addition to the quantitative EEG numeric indices, many monitors also display pseudo-three-dimensional plots of successive power spectra as a function of time. This frequency-domain approach was originated by Joy²⁷ and popularized by Bickford, who coined the term compressed spectral array (CSA).²⁸ Popularity stems, in part, from enormous data compression. For example, the essential information contained in a 4-hour traditional EEG recording consuming more than 1000 pages of unprocessed waveforms can be displayed in CSA format on a single page.

With CSA (see Figure 16-11), successive power spectra of brief (2- to 60-second) EEG epochs are displayed as smoothed histograms of amplitude as a function of frequency. Spectral compression is achieved by partially overlaying successive spectra, with time represented on the z-axis. Hidden-line suppression improves clarity by avoiding overlap of successive traces. Although the display is esthetically attractive, it has limitations. The extent of data loss caused by spectral overlapping depends on the nonstandard axial rotation that varies among EEG monitors. More important, epoch duration and the frequency with which each is measured (i.e., update rate) may critically affect the presentation of clinically important change. For example, there are three distinctly different burst-suppression CSA patterns: high-amplitude bursts, flat line, or a combination of the two.²⁹

Fleming and Smith³⁰ designed an alternative to the CSA display to reduce data loss. Density-modulated spectral array (DSA) uses a two-dimensional monochrome dot matrix plot of time as a function of frequency (see Figure 16-11). The density of dots indicates the amplitude at a particular time-frequency intersection (e.g., an intense large spot indicates high amplitude). Clinically significant shifts in frequency may be detected earlier and more easily than with CSA. However, the resolution of amplitude changes is reduced. Therefore, the color density-modulated spectral array (CDSA) has been developed to enhance amplitude resolution (see Figure 16-11). The CSA, DSA, and CDSA displays are not well-suited for the detection of nonstationary or transient phenomena like burst-suppression or epileptiform activity.

In summary, a quick assessment of EEG change in either the time or frequency domain focuses on the following: (1) maximal peak-to-peak amplitude, (2) relation of maximal amplitude to dominant frequency, (3) amplitude and frequency variability, and (4) new or growing asymmetry between homotopic (i.e., same position on each cerebral hemisphere) EEG derivations. These objectives are generally best achieved through the viewing of both unprocessed and processed displays with a clear understanding of the characteristics and limitations of each (Box 16-6).

Documentation of Preexisting Electroencephalographic Abnormalities

Because there is a high likelihood of latent cerebrovascular disease in many older cardiac surgery patients, it is essential to examine the waking EEG for signs of marked asymmetry before the induction of anesthesia. This serves to alert the anesthesia provider to the patient’s increased vulnerability and to document the previously unappreciated risk.

Objective Measurement of Hypnotic Effect

Recording the transition from wakefulness to unresponsiveness permits detection of unusual sensitivity or resistance to general anesthetics (Figure 16-13). Such information is vital during fast-track anesthesia protocols to avoid excessive or inadequate anesthesia. Although no available neurophysiologic monitoring modality is an infallible predictor of anesthetic inadequacy, characteristic changes in the EEG frequency pattern provide an easily recognized warning of potential patient awareness. EEG detection of excessive or inadequate hypnosis during cardiac surgery may be aided by the multivariate EEG descriptors.

Figure 16-13 The panels containing unprocessed bilateral electroencephalogram (EEG; top left) and bispectral index (BIS) trend (bottom left) illustrate right hemisphere (red) EEG high-frequency loss after head rotation after anesthetic induction. The right panel bilateral color density spectral array (CDSA) trend depicts global power increase (i.e., high-amplitude, low-frequency waves) during anesthetic induction and later left hemisphere high-frequency loss associated with placement of a left common carotid clamp. Note prompt return of the high-frequency activity with insertion of an intravascular shunt. The EEG return documented proper shunt function, whereas maintenance of the high-frequency activity established that blood pressure was sufficient to prevent cerebral cortical hypoperfusion.

(Courtesy of Covidien/Aspect Medical Systems, Inc.)

Head Position

Because of the diffuse nature of atherosclerotic vascular disease, many elderly patients are at increased risk for positional focal or regional cerebral ischemia that may occur before incision. Head rotation for surgical positioning or insertion of a pulmonary artery catheter may compress a vital carotid or vertebral artery. Such ischemia is generally identified by marked depression in the affected frontotemporal EEG derivation (see Figure 16-13).

Vascular Obstruction and Flow Misdirection

Manipulation or torsion of the aorta or vena cava may result in regional or global cerebral ischemia. During CPB, the aortic cannula can misdirect either cardiac or pump flow away from one or more head vessels while leaving the radial artery pressure unaltered. Alternatively, a malpositioned venous cannula may impair return from the head without noticeable change in central venous pressure or return flow to the venous reservoir.³⁹ Resulting intracranial hypertension leads to ischemic depression of the EEG (Figure 16-14).

Figure 16-14 Insertion of a 14-French venous cannula in this pediatric patient during repair of an atrial septal defect caused a sudden diffuse electroencephalographic (EEG) slowing. The heart rate and blood pressure remained unchanged, although the central venous pressure increased from 6 to 45 mm Hg. Cannula repositioning restored both the former EEG pattern and central venous pressure. SVC, superior vena cava.

(Modified from Rodriguez RA, Cornel G, Semelhago L, et al: Cerebral effects in superior vena caval obstruction: The role of brain monitoring. Ann Thorac Surg 65:1820, 1997.)

Nonpulsatile Perfusion

Nonpulsatile perfusion used with CPB and some new left ventricular assist devices may result in microcirculatory collapse in susceptible regions of the cerebral cortex despite “acceptable” radial artery pressures. EEG-guided increases in arterial pressure, circulating volume, or both may be necessary to restore perfusion in the microvasculature.

Hemodilution

Hemodilution is used to improve vital organ perfusion by reducing viscosity. However, it may cause inadequate delivery of oxygenated hemoglobin to a high-demand brain, even though hematocrit and systemic venous oxygen saturation are within normal limits.⁴⁰ EEG deterioration may thus serve as an objective indicator for transfusion.

Hypocarbia and Hypercarbia

Cerebral arteries normally constrict in response to decreased carbon dioxide tension or hydrogen ion concentration. With reactive arteries, hypocarbia may lead to cerebral ischemia because flow is reduced 4%/mm Hg [CO₂]. In this circumstance, return to normocarbia can markedly improve cerebral perfusion.⁴¹ Conversely, hypercarbia may steal blood from the dilated vessels of an already underperfused region, resulting in focal EEG slowing. This circumstance may be exacerbated by the use of volatile anesthetics causing cerebral vasodilation.

Cooling

During cardiac surgery requiring deep hypothermic circulatory arrest, the EEG provides an effective method for assessing the effects of cooling. Optimal brain temperature may be viewed as a balance between decreased cerebral oxygen consumption and increased risk for coagulopathy. Actual brain temperature cannot be measured directly and appears to be influenced by many variables including the rate of cooling, as well as acid-base and anesthetic management. The EEG is often used to assess the functional consequences of brain cooling because a flat line pattern signifies cortical synaptic quiescence. The wide interpatient variation in flat line temperature is the rationale for EEG guidance of the cooling process.³⁴ Alternative use of a fixed temperature criterion increases the risks for both excessive and inadequate brain cooling.

As nasopharyngeal or tympanic temperature decreases (Figure 16-15), there is a gradual loss of absolute spectral power across all frequency bands.³⁴ Although the reversible decreases in absolute spectral band power are quite large, computing these changes as relative spectral band power minimizes them suggesting that initial brain cooling exerts a similar decrease in spectral power across all frequency bands and cortical regions.⁴² Cooling below 28°C leads to progressive slowing of the residual EEG until the EEG waveform becomes a flat line.

Figure 16-15 Progressive temperature-related electroencephalographic (EEG) suppression is shown in this bilateral color density spectral array (CDSA) display. Following the onset of cooling at 22:07, note the gradual decline in the power of the 9-Hz (orange) frequency band. Establishment of moderately deep hypothermia at 22:27 results in near-total EEG suppression. The spectral edge frequency (white vertical lines) does not fall to baseline because of the presence of background electrical contamination of the EEG signal.

(Courtesy of Covidien/Aspect Medical Systems, Inc.)

Rewarming

After circulatory arrest, the EEG documents the recovery of synaptic function during rewarming. However, rapid rewarming may result in cerebral ischemia because of cold-triggered vasoparesis, which uncouples cerebral blood flow and metabolism. In this case, rewarming-induced increase in metabolic demand may outpace the lagging delivery of essential nutrients.⁴³ This situation is indicated by a loss of EEG high-frequency activity accompanying the increase in cranial temperature. Although the practice is controversial, administration of a metabolic suppressant drug such as propofol, dosed to EEG burst suppression, may facilitate balancing cerebral perfusion with metabolic demand.⁴⁴

Myocardial Revascularization without Extracorporeal Support

Avoidance of CPB during myocardial revascularization may protect patients from the many potential hazards of this nonphysiologic insult.⁴⁵ EEG stability during beating-heart coronary revascularization is often observed, despite transient hypotension and bradycardia. Nevertheless, some surgeons believe that neuromonitoring is mandatory because the combination of controlled hypotension and vascular torsion can suddenly disrupt cerebral perfusion. In the absence of the neuroprotective effects of mild hypothermia, even relatively brief episodes of cerebral ischemia may result in injury.

Seizure Detection

Certain anesthetics and adjuvants such as etomidate, sevoflurane, and the opioid analgesics may produce seizure-like EEG activity, although the clinical manifestations may be obscured by neuromuscular blockade (Figure 16-16).^46–48 The consequences of this anesthetic-induced seizure-like activity have not been established in adults. However, seizures may be deleterious to the developing brain. Bellinger et al⁴⁹ showed that perioperative EEG seizure activity in infant cardiac surgery patients was associated with a 10-point decline in expected IQ when subsequently measured in the patients’ fifth year after surgery (Box 16-8).

Figure 16-16 These epileptiform electroencephalographic (EEG) patterns are associated with mask induction of sevoflurane in adults. The patterns include: (1) slow delta monophasic activity with spikes, (2) burst suppression with spikes, (3) polyspikes, and (4) rhythmic polyspikes.

(Modified from Yli-Hankala A, Vakkuri A, Sarkela M, et al: Epileptiform EEG during induction of anesthesia with sevoflurane mask. Anesthesiology 91:1596, 1999.)

Peripheral Nerve Injury Detection

During cardiothoracic or vascular surgery, improper patient positioning or sternal retraction can lead to injury, respectively, of the ulnar nerve⁶⁷ and brachial plexus.⁶⁸ Unfortunately, the standard recording electrode configuration illustrated in Figure 16-20A does not permit distinction of ulnar injury from plexopathy.⁶⁶ For this purpose, additional recording sites above the elbow or adjacent to the axilla should be used.⁶⁶ Lorenzini and Poterack⁶⁹ proposed SSEP noteworthy change criteria that appear to minimize the incidence of false-positive and false-negative responses. In the absence of marked body temperature change, these criteria are either a 60% amplitude reduction or 10% latency increase in the peripheral nerve components of the SSEP response.

Cerebral Ischemia Detection

In contrast with the typically robust subcortical N13 response, during cardiac or vascular surgery many factors other than ischemia may influence the SSEP N20 cortical response. These include anesthetic effects, body temperature, acid-base management, arterial blood oxygen-carrying capacity and blood pulsatility.⁷⁰ Therefore, traditional criteria for new cortical SSEP abnormality (Figure 16-21) long-established for other types of surgery (50% amplitude reduction and 20% increase in N13-N20 interpeak latency)⁶⁴ may result in an unacceptably high incidence of false-positive results. To overcome this problem, Astarci et al⁷¹ proposed a more rigorous criterion of total N20 loss. A recent SSEP study during carotid endarterectomy supports this approach.⁷²

Figure 16-21 The upper traces represent normothermic, bihemispheric, anesthesia-suppressed electroencephalographic activity derived from scalp (Fpz, F3, F4, C3, and C4), cervical spine (C6sp), and earlobe (A1 and A2) recorded 2 minutes after left common carotid clamping (CCC). The lower traces represent contemporaneous bihemispheric upper-limb somatosensory-evoked potential (SSEP) responses. Electrophysiologic evidence of left hemispheric hypoperfusion is suggested only by the suppressed SSEP N20 component amplitude.

(Modified from Nuwer MR [ed]: Handbook of clinical neurophysiology, vol 8. New York: Elsevier, 2008, p. 787.)

Brain Thermometer

Cooling prolongs SSEP peak and interpeak latencies and suppresses amplitude of predominantly the cortical response (see Figure 16-20B). However, because subcortical SSEP responses involve far fewer synapses than EEG, they often persist when cortical neuronal activity is totally cold-suppressed. Thus, detection of cerebral ischemia via SSEP can be achieved during EEG quiescence (Figure 16-22). In addition, the differential effect of cooling on the cortical and subcortical SSEP components can be used to identify the patient-specific nasopharyngeal or tympanic temperature suitable for the optimal cooling strategy for hypothermic brain protection.⁶⁶ For example, Guérit et al⁷³ found that there were no neurologic complications in a group of patients who underwent deep hypothermic circulatory arrest guided by abolition of the subcortical SSEP response. In contrast, patients who exhibited SSEP loss because of non–temperature-related causes experienced postoperative neurologic sequelae.

Figure 16-22 The upper traces represent bihemispheric, cold-suppressed electroencephalographic (EEG) activity derived from scalp (Fpz, F3, F4, C3, and C4), cervical spine (C6sp), and earlobe (A1, A2, and linked A3) recorded at 24°C. The lower traces represent contemporaneous bihemispheric upper-limb somatosensory-evoked potential (SSEP) responses. Arrow points to left hemispheric N20 suppression accompanying left common carotid clamping (CCC). Blood pressure increase restored the N20 amplitude. Note that this regional cerebral hypoperfusion was not apparent in the hypothermia-suppressed EEG recording.

(Modified from Nuwer MR [ed]: Handbook of clinical neurophysiology, vol 8. New York: Elsevier, 2008, p. 835.)

Pulsed-Wave Spectral Display

Pulsed-wave Doppler samples the ultrasonic echoes at a user-selected distance (i.e., single gate) below the scalp. The frequency composition of these Doppler-shifted echoes is analyzed by Fourier analysis, the same technique used to quantify EEG frequency patterns (see Figure 16-26). The analysis produces a momentary amplitude spectrum displayed as a function of blood flow velocity (e.g., Doppler-shift frequency). This relation is mapped as one vertical strip in the spectrogram display (see Figure 16-26, upper right). Amplitude at each frequency is expressed as log change (i.e., dB) from the background composed of random echoes. The momentary analysis is repeated 100 times a second to produce a scrolling spectrogram of time-related changes in flow velocity.

Signal amplitude at each frequency shift–time intersection is indicated by monochromatic dot density or color coding. The maximum velocity, the upper edge (envelope) of the velocity spectrum (analogous to the EEG SEF), represents the maximum Doppler shift (erythrocyte velocity) in the vessel center. Peak systolic and end-diastolic velocities are derived from this spectral edge. Intensity-weighted mean velocity is calculated by weighted averaging of the intensity of all Doppler spectral signals in a vessel cross section. Sampling echoes at multiple loci (multigating) produces spectrograms for each of the different probe-to-sample site distances (Figure 16-27).

Figure 16-27 Multigating of pulsed-wave Doppler signals permits simultaneous display of echo spectra generated at several different intracranial loci. LACA, left anterior cerebral artery; LMCA, left middle cerebral artery; RACA, right anterior cerebral artery; RMCA, right middle cerebral artery.

Power M-Mode Doppler Display

An alternative method for processing pulsed-wave Doppler echoes is nonspectral power M-mode Doppler (PMD; Figure 16-28). Unlike the series of spectra generated with multigating, PMD creates one image with each depth represented by a plot of signal amplitude (i.e., power) and depth as functions of time. A color scale signifies flow direction (red is flow directed toward the probe; blue is flow away from the probe), whereas color intensity is directly related to signal power.

Figure 16-28 The transcranial Doppler (TCD) continuous-wave M-mode (top left) and pulsed-wave spectral (bottom left) displays are compared. The horizontal bands of the M-mode display represent a series of Doppler-shift echoes. Signals in the 30- to 50-mm-depth range (top red band) represent flow in the right middle cerebral artery (MCA) ipsilateral to the ultrasonic probe. Red color signifies flow directed toward the probe (right). Echoes arising between 55 and 70 mm from the probe emanate from the ipsilateral anterior cerebral artery (ACA). They are shown in the middle blue band of the M-mode display. Signals in the 72- to 85-mm range arise from the contralateral ACA with flow directed toward the probe (lower red band). The M-mode yellow line at a depth of 50 mm indicates the measurement site for the TCD frequency spectral display shown at the bottom left.

(Courtesy of Dr. Mark Moehring, Spencer Technologies, Seattle, WA.)

Embolus Detection

Erythrocytes (approximately 5 million/mL) are the most acoustically reflective, nonpathologic blood elements (i.e., high acoustic impedance). However, gaseous and particulate emboli are better reflectors of sound than erythrocytes. The presence of high-intensity transient signals (HITSs) within either the PMD or spectral TCD display may signify the presence of an embolus.^85,86 Because a gaseous or particulate embolus cannot simultaneously appear at all distances from the probe, either PMD or a multigated spectral display may be used to distinguish them from acoustic artifact (tapping on the ultrasonic probe produces a high-intensity transient acoustic artifact at all distances).

Figure 16-29 illustrates the appearance of HITSs in the two TCD display formats. The bottom spectral displays are generated from a small vascular segment at a distance of 50 ± 3 mm (6-mm sample volume) from the probe surface. The midpoint of the spectral sample is indicated on the top PMD displays as a light horizontal line at a 50-mm depth. An embolic track labeled “a” is a single embolus that is shown in the top PMD display moving toward the probe (i.e., decreasing distance from the probe face over time). Embolic tracks “b” and “d” display the characteristic “lambda” acoustic signature in the spectral display. The PMD shows that this pattern is due to embolus direction reversal within the spectral sample volume. The true behavior of the spectrally paradoxical track “c” (start and end points of the single acoustic signature are not connected) becomes clear in the PMD view. Track “c” direction reversal is invisible on the spectral display because it occurs outside the sampling region. Currently available spectral or PMD TCD monitors can determine neither the size nor composition of emboliform material responsible for HITSs. TCD devices designed for surgical monitoring typically provide a semiquantitative estimate of aggregate HITSs, irrespective of their origin (Box 16-11).

Figure 16-29 The appearance of emboliform high-intensity transient signals (HITSs) is compared using the M-mode and frequency spectral displays. White horizontal line at a depth of 50 mm depicts the site of the spectral measurement along the axis of the vessel. HIT_a (white transient) represents linear migration of an embolus in the M2 segment of the ipsilateral middle cerebral artery. A single HIT (white dot) is noted on the spectral display as the embolus passes through the 50-mm measurement site. In contrast, emboli in the remaining panels suddenly change direction as they pass into a smaller branch vessel. HIT_b and HIT_d direction changes are noted on the spectral displays as the characteristic “lambda” sign. However, the HIT_c behavior is misidentified as two emboli because the direction change occurs outside the spectral sample volume.

(Courtesy of Dr. Mark Moehring, Spencer Technologies, Seattle, WA.)

Intervention Threshold

Because erythrocyte velocity and flow may be differentially influenced by vessel diameter,⁸⁷ blood viscosity,^88,89 and pH,⁸⁹ as well as temperature,⁸⁹ TCD does not provide a reliable measure of cerebral blood flow. However, in the absence of hemodilution, change in TCD velocity does correlate closely with change in blood flow.⁸⁷ Sudden large changes in velocity or direction are readily detected by continuous TCD monitoring. The clinical significance of velocity changes has been assessed in conscious patients during implantable cardioverter-defibrillator and tilt-table testing.^90,91 In both circumstances, clinical evidence of cerebral hypoperfusion was accompanied by a mean velocity decline of greater than 60% and absent diastolic velocity. During nonpulsatile CPB, the ischemia threshold appears to be an 80% decrease below the preincision baseline.⁹²

In general, reduction of flow velocity indicating severe ischemia is associated with profound depression of EEG activity.⁹² However, with adequate leptomeningeal collateral flow, cerebral function may remain unchanged in the presence of a severely decreased or absent middle cerebral artery flow velocity.⁹³ Together, these findings form the rationale for a TCD-based intervention threshold. During cardiac surgery, mean velocity reductions of greater than 80% or velocity loss during diastole suggest clinically significant cerebral hypoperfusion.

Before Cardiopulmonary Bypass

TCD provides cerebral hemodynamic information for the timely detection and correction of perfusion abnormalities that may occur before the onset of CPB. Vascular torsion during neck extension or axial head rotation may result in regional cerebral hypoperfusion detectable by TCD.⁹⁴ Cerebral blood flow obstruction may also be detected by TCD during endovascular repair of aortic dissection.⁹⁵ Excessive hyperventilation may result in inadvertent cerebral ischemia because blood flow declines by 4%/mm Hg Paco₂ in normally reactive cerebral arteries.⁸⁷ Cerebral dysautoregulation is often seen in hypertensive and diabetic patients.⁹⁶ This abnormality may result in pressure-dependent brain perfusion and place the patient at risk for ischemic brain injury during even moderate hypotension. TCD may be used to identify pressure dependency and facilitate appropriate individualization of acceptable perfusion pressure.⁹⁷ In addition, TCD has been used to identify the optimal aortic cannulation site.⁹⁸ For example, Mullges et al⁹⁹ observed that the mean aggregate middle cerebral artery embolic load was significantly lower with a distal arch cannulation compared with the traditional ascending aorta site. These results are consistent with the studies using epiaortic ultrasound. Detection of malpositioned aortic or superior vena caval perfusion cannula is rapidly achieved with TCD monitoring.¹⁰⁰ In the former case, the malposition results in a sudden profound decrease in the peak systolic velocity (Figure 16-30), whereas in the latter, diastolic velocity is compromised (Figure 16-31).

Figure 16-30 Malposition of an aortic perfusion cannula before the onset of cardiopulmonary bypass was identified on its insertion by the sudden large decrease in peak systolic velocity. Repositioning led to a prompt recovery of cerebral perfusion.

Figure 16-31 Malposition of a superior vena cava perfusion cannula before the onset of cardiopulmonary bypass was identified shortly after its insertion by the loss of end-diastolic velocity. Repositioning led to a prompt recovery of cerebral perfusion.

During Cardiopulmonary Bypass

TCD is the only available method to continuously assess changes in cerebral hemodynamics associated with CPB. Despite the confounding influences of hemodilution, altered acid-base management, and cooling on absolute flow velocity, TCD nevertheless indicates the presence and direction of cerebral blood flow. A sudden large decrease, increase, or asymmetry indicates, respectively, inadvertent occlusion of a great vessel, hyperperfusion of a single cranial artery, or misdirection of aortic cannula flow (Figure 16-32).

Figure 16-32 During total cardiopulmonary bypass with nonpulsatile perfusion, cerebral malperfusion was identified by asymmetric left/right hemisphere velocity decline. A slight change in the position of the aortic perfusion cannula corrected the problem.

During surgical repair of the aortic arch, TCD documents cerebral artery flow direction during attempts at supplemental retrograde (Figure 16-33) or antegrade (Figure 16-34) cerebral perfusion during systemic circulatory arrest.^101,102 Because peak velocity changes in large basal cerebral arteries are directly related to peak flow changes, TCD may aid in the determination of safe upper and lower limits for pump flow and perfusion pressure.¹⁰³ Deep cooling and circulatory arrest may produce a transient cerebral vasoparesis and result in uncoupling of cerebral blood flow and metabolism.¹⁰² TCD identifies this phenomenon as an unchanging flow velocity during rewarming. Emboli detection by TCD can improve surgical and perfusion technique, as well as facilitate correction of technical problems such as an air leak^104–106 (see Figure 16-34 and Box 16-12).

Figure 16-33 These two transcranial Doppler (TCD) frequency spectral displays show changes in left (top) and right (bottom) middle cerebral artery (MCA) flow velocity during attempted retrograde cerebral perfusion via the superior vena cava with carotid drainage. Spectral patterns above the zero-velocity baselines indicate antegrade blood flow directed toward the ultrasound probe.

Figure 16-34 Hyperperfusion of the right middle cerebral artery was identified by transcranial Doppler during attempted supplemental antegrade cerebral perfusion during total circulatory arrest. Repositioning of the right axillary perfusion cannula led to a reduction in velocity followed shortly thereafter by the accidental introduction of a small amount of air. The leak was quickly identified and corrected.

Baseline rSo₂

Surgical cerebral oximetric monitoring should be initiated immediately after patient entry to the operating room. Self-adhesive patches containing the infrared light source with shallow (proximate) and deep (distant) sensors are fixed on the forehead on both sides of the midline. The initial objective is the establishment of a reference baseline before preoxygenation and anesthetic induction (Figure 16-37).

Figure 16-37 Right and left regional oxygen saturations (rSo₂) were symmetric and within normal limits (WNL) before anesthetic induction. Symmetric postinduction increase suggested intact CO₂ reactivity of the cerebral arterioles. Patient positioning resulted in a transient left hemisphere rSo₂ decline, whereas the right hemisphere decline was persistent and severe. Because all other physiologic signals were WNL, a patient malposition was suspected. Adjustment of the shoulder roll and head repositioning to correct a neck extension immediately resolved the regional desaturation. CABG, coronary artery bypass graft; DM, diabetes mellitus; HTN, hypertension.

A high cerebral metabolic demand for oxygen may result in abnormally low rSo₂ values despite normal pulse oximetry readings. For example, the cerebral oximeter detected oxygen imbalance during high-altitude trekking that was unrecognized by pulse oximetry.¹⁷⁴ Similarly, patients in heart failure often have preoperative baseline values far below the normative range.^175–178 Abnormally high rSo₂ values may signify a silent infarction because injured or dead neurons consume little oxygen. Abnormal (>10 scale units) right-left rSo₂ may be caused by unrecognized carotid or intracranial arterial stenosis, intracranial space-occupying lesion, old infarction, skull defect, or extracranial sources such as a hemangioma, sinusitis, or artifactual interference from an infrared-emitting device.^179–182 An asymmetry or abnormal rSo₂ baseline, high or low, alerts the operative team to the increased potential for cerebral oxygen imbalance during surgical challenge.

Developing rSo₂ Asymmetry

A new asymmetry, signifying cerebral dysoxygenation, may develop quickly during anesthetic induction, pulmonary artery catheter insertion, or final patient positioning. During head positioning, an asymmetric rSo₂ decrease warns of developing regional cerebral hypoperfusion that otherwise may remain unrecognized.^139,155,183 Axial head rotation displaces the lateral mass of the contralateral atlas forward behind the internal carotid artery, just below its entrance into the carotid canal at the skull base. If this process is prolonged or if the artery is adherent to adjacent tissue, it can be compressed from behind, resulting in decreased flow.^184–186 Furthermore, volatile anesthetics may interfere with the regulatory mechanisms that normally maintain effective cerebral perfusion bilaterally during head rotation in conscious patients.¹⁸⁷

The cerebral oximeter has detected potentially catastrophic cerebral desaturation because of great vessel torsion during cardiac manipulation.^188–192 Desaturation often appears to be the result of compromised venous return. Particularly in pediatric cardiac operations and in myocardial revascularization without CPB, cardiac manipulation may produce sudden large rSo₂ decreases without any appreciable change in mean arterial pressure (MAP) or arterial oxygen saturation.

Numerous reports have described rSo₂ detection of perfusion cannulae malposition^193–195 or regional malperfusion development during surgery involving the aortic arch or great vessels.^194–204 Malperfusion-related cerebral ischemia may be identified by EEG or SSEP, but these signals are susceptible to compromise by electrocautery, deep anesthesia, and hypothermia.²⁰⁵ Similarly, TCD signals are susceptible to radiofrequency, acoustic, and movement artifact. Cerebral oximetry is also used during extracorporeal membrane oxygenation to detect regional deficiencies in brain perfusion associated with carotid cannulation.²⁰⁶

rSo₂ Responsiveness to CO₂

Induction of anesthesia and its attendant apnea during tracheal intubation often transiently alter the brain oxygen supply-demand relation. Hypnotic agents may transiently suppress cerebral metabolism more than blood flow; resulting relative hyperperfusion leads to an rSo₂ increase.²⁰⁷ With normally reactive cerebral arterioles, ventilation disruption and CO₂ accumulation during tracheal intubation further increase rSo₂ as a result of the increased delivery of hyperoxygenated blood to a metabolically suppressed brain. Under these circumstances, even mild hypercapnia augments cerebral perfusion and oxygenation through local vasodilation.^208–211 Several investigators have demonstrated an rSo₂ increase (see Figure 16-37) associated with hypercapnia.^{139,140,150,171}

Absence of rSo₂ increase with increasing arterial CO₂ tension suggests impairment of both CO₂ reactivity and cerebral autoregulation. Asymmetry warns of a potential vasculopathy (e.g., intracranial stenosis or silent infarction) and may prompt alterations in anesthetic and perfusion management to maintain cerebral perfusion in both hemispheres.²¹¹

Acid-base management during CPB remains controversial, particularly during deep cooling. Some propose that the greater CO₂ tension afforded by pH-stat acid-base management results in fewer neurologic complications.²¹² Vijay et al²¹³ observed that during adult near- normothermic myocardial revascularization, vasopressor-induced perfusion pressure increases alone were sometimes inadequate to correct decreased rSo₂ occurring during CPB. In this situation, judiciously applied permissive hypercapnia often was effective in restoring rSo₂ to baseline.

Despite these seeming benefits, hypercapnia has potentially deleterious effects. Hypercapnia-induced cardiac output and heart rate also increase myocardial oxygen demand, whereas cerebral vasodilation may exacerbate preexisting intracranial hypertension. Cerebral oximetry provides a convenient method to document appropriate bihemispheric CO₂ reactivity. In addition, continuous measurement of brain oxygen saturation permits CO₂ titration to achieve optimal tissue perfusion at the lowest risk.^214–216

rSo₂ as a Transfusion Trigger

Two important determinants of tissue oxygenation are hemoglobin availability and plasma volume.^217,218 Madl et al²¹⁹ examined the relation between hemoglobin and rSo₂ in patients with septic shock. If a low hemoglobin (<8.5 mg/dL) was associated with an rSo₂ less than the normative range (i.e., <60%), transfusion consistently increased both variables. However, transfusion had no effect on rSo₂ values greater than 65%. Blas et al²²⁰ described profound desaturation accompanying hemodilution with all other physiologic measures within normal limits. Brain saturation responded immediately to 2 units of packed red cells in this patient with bilateral carotid artery occlusions.

Due to the apparent association between rSo₂ and hemoglobin, transient brain oxygen desaturation is to be expected at the onset of CPB because the pump prime solution briefly displaces hemoglobin in the cerebral circulation. Vijay et al²²¹ demonstrated that the magnitude of this transient desaturation was related directly to the volume of crystalloid prime. Use of a blood prime in the arterial limb of the perfusion circuit appears to eliminate the transient rSo₂ decline accompanying CPB onset.²²² The hemoglobin influence on rSo₂ is the basis for use of cerebral oximetry as both a transfusion trigger²²³ and a strategy to reduce or completely avoid administration of homologous blood.^224,225

rSo₂ and Blood Volume

Tissue oximetry has been used to visualize the effect of volume expansion on cerebral perfusion during tilt-table diagnostic testing for syncope.²²⁶ An rSo₂ sensor was placed on the gastrocnemius muscle to measure upright tilt-induced desaturation resulting from lower limb venous pooling. In susceptible patients, extensive pooling resulted in cerebral dysoxygenation and syncope. Crystalloid volume expansion reduced lower limb hemoglobin sequestration and prevented syncope. This same concept may be applied to cardiac surgery. Vasopressor ineffectiveness in the correction of an rSo₂ decline may indicate compromised microcirculatory gas exchange because of hypovolemia. In this circumstance, low rSo₂ values often respond to volume augmentation.

rSo₂ and Autoregulation

Numerous studies have concluded that cerebral autoregulation remains intact during cardiac operations, both before and during CPB. Although this conclusion may be correct for large groups of patients, it does not necessarily apply to each individual. Cerebral oximetry can identify the lower limit of autoregulation, the point at which brain blood flow and tissue oxygenation become pressure dependent.^139,227 The independence of MAP and cerebral oxygen saturation establishes intact cerebral autoregulation.^228,229

Figure 16-38 illustrates the use of rSo₂ measurement in the determination of the lower autoregulatory limit. The rSo₂-versus-MAP relation in the top graph depicts intact autoregulation. The rSo₂ values remain independent of MAP over a wide pressure range. The bottom graph, generated later the same day in the same operating room by the same surgical team, depicts dysautoregulation because rSo₂ declines each time MAP declines to less than 80 mm Hg. Examination of MAP-rSo₂ relations from a large series of cardiac operations resulted in two findings.²³⁰ First, the lower limit of autoregulation varies widely among patients, from a MAP of less than 40 to more than 100 mm Hg. Second, a substantial proportion of cardiac patients do not, in fact, maintain autoregulation throughout the entirety of the operation. These observations illustrate the potential benefit of continuously monitoring the adequacy of cerebral perfusion during cardiovascular surgery.

Figure 16-38 Relation between regional oxygen saturation (rSo₂) and mean arterial pressure during cardiopulmonary bypass is depicted.

Each symbol represents a single point paired measurement obtained at 5-minute intervals. Top, Intact cerebral autoregulation with clear independence of rSo₂ and mean arterial pressure (MAP) over a wide range. The patient’s outcome was uneventful. In contrast, the bottom panel depicts dysautoregulation with the classic appearance of a vascular waterfall. Each time the MAP declined to less than 80 mm Hg, a marked rSo₂ decrease occurred, indicating that the cerebral perfusion pressure had declined to less than the lower limit of autoregulation. Presumably, as a result of suboptimal cerebral perfusion, the patient experienced a prolonged recovery complicated by delirium. CABG, coronary artery bypass graft; ICU, intensive care unit.

The driving force for hemoglobin through the gas-exchanging microvasculature is not arterial pressure per se, but the arterial-venous pressure difference. Factors that increase cerebral venous pressure will compromise oxygen delivery, even if the arterial pressure remains in the normally acceptable range. It is most useful to examine a trend of the relation between rSo₂ and cerebral perfusion pressure (MAP − [the higher of central venous or intracranial pressure]).

Vasoactive drugs may have distinctly different effects on cerebral and systemic perfusion. These disparate pharmacologic actions further confound cerebral perfusion estimates on the basis of systemic blood pressure. Both vasodilators and vasoconstrictors may disrupt the expected brain blood flow-systemic blood pressure relation. Vasodilator nitrates may increase cerebral rSo₂ whereas systemic blood pressure is unchanged or declines.^231,232 Conversely, vasoconstrictors may increase cerebral rSo₂ only when MAP is below the lower limit of autoregulation.²³³

rSo₂ and Brain Temperature

Temperature has important effects on tissue oxygenation.²³⁴ Because standard temperature monitoring during CPB does not accurately characterize the efficacy of brain cooling, cerebral oximetry may facilitate management of hypothermic neuroprotection.^235–238 In theory, temperature with CPB and alpha-stat acid-base management results in a linear decrease in cerebral blood flow and an exponential decline in metabolic rate.²³⁹ Consequently, predicted “luxury” flow should ensure adequate cerebral oxygenation during cooling. However, Daubeney et al¹⁵¹ demonstrated that other variables were also involved in the maintenance of adequate tissue oxygenation during deep hypothermia in pediatric patients. The rSo₂ at a 20°C target cooling temperature varied inversely with the cooling rate by the equation: rSo₂ = −20.5 (cooling rate, °C/min) + 97.4. In addition, they found that the rate of desaturation during total circulatory arrest was a function of the nasopharyngeal temperature at arrest onset, described by the equation: desaturation rate = 0.19 (nasopharyngeal temp, °C) − 2.5. At 20°C, the mean desaturation rate was 0.25% min, although decay was not linear. At temperatures slightly greater than 20°C (21°C to 26°C), desaturation rate increased nearly 10-fold (2.0%/min). In normothermic infants, transient disruption of cerebral perfusion resulted in another 10-fold increase (i.e., ≈︀20% min) in the rate of desaturation.²⁴⁰ The desaturation rates in hypothermic pediatric patients are somewhat less than those reported in adults.^{215,216,238,241}

Deep hypothermia may also produce transient cerebral vasoparesis.^239,242 Consequently, rewarming may result in desaturation as the temperature-induced increase in cerebral metabolism is unsupported by adequate flow increase. Daubeney et al¹⁸⁸ described an inverse relation between rSo₂ and nasopharyngeal temperature during rewarming in pediatric patients, given by the equation: rSo₂ = −2.9 (nasopharyngeal temp) + 148. Liu et al²⁰⁷ observed similar cerebral desaturation during rewarming in adult cardiac surgery patients. Small perfusion deficits decreased rSo₂ as oxygen extraction is increased to meet rising demand. When the oxygen extractive capacity is exceeded, functional compromise will be manifested by EEG or evoked potential abnormalities.²⁴³

rSo₂ Guides Supplemental Cerebral Perfusion

Several studies have demonstrated that rSo₂-guided retrograde cerebral perfusion may extend the “safe time” for hypothermic circulatory arrest during adult aortic arch reconstruction.^101,244,245 Blas et al²²⁰ reported on the use of cerebral oximetry for detection of a superior vena cava cannula malposition during retrograde cerebral perfusion.

Higami et al²⁴⁶ found rapid desaturation with total circulatory arrest, slow continual desaturation with retrograde cerebral perfusion, and no desaturation with supplemental antegrade cerebral perfusion (Figure 16-39). There was a high incidence of neurologic deficit in patients whose saturation declined more than 30% below the conscious baseline. Subsequently, many studies have found cerebral oximetry to be a useful guide for the management of regional low-flow perfusion and selective antegrade cerebral perfusion.^247–259

Figure 16-39 Cerebral oximetry provides continuous objective assessment of supplemental antegrade cerebral perfusion (ACP) during deep hypothermic systemic circulatory arrest. In this case, a single perfusion cannula for ACP was located in the right axillary artery. The stable regional oxygen saturation (rSo₂) value in the right hemisphere and falling rSo₂ in the left hemisphere document that ACP was only partially successful. Had a longer arrest period been anticipated, this information would have prompted the surgeon to perfuse through the left carotid as well. CPB, cardiopulmonary bypass; MAP, mean arterial pressure.

rSo₂ Improves Systemic Hypoxemia Detection

The high oxygen demand of the brain means that signs of developing hypoxemia may first appear in regional cerebral measurements. Several reports have noted rSo₂ to decline earlier than Spo₂ at the onset of hypoxia.^260,261 Furthermore, continuous cerebral rSo₂ monitoring has provided the first indication of impaired oxygen delivery during nonpulsatile CPB.^262,263

rSo₂ Facilitates Regional Tissue Hypoxia Detection

In 2004, Edmonds et al²⁶⁴ reported on simultaneous brain and perivertebral rSo₂ monitoring during thoracoabdominal aneurysm repair. Desaturation occurring below the level of the aortic cross-clamp was interpreted as hypoperfusion within the extensive vertebrovenous plexus.²⁶⁵ This preliminary observation was subsequently confirmed in a laboratory investigation using human adult-size swine²⁶⁶ and a clinical study in pediatric aortic coarctation repair.²⁶⁷ Now many reports document the value of multisite tissue oximetry.^268–276 Hepatic, perirenal, and splanchnic tissue perfusion have been successfully assessed in neonates, whereas limb perfusion monitoring has been achieved in both pediatric and adult cardiac surgery and intensive care patients. Harel et al²⁷⁷ used strain-gauge and radionuclide plethysmography to validate the latter application of tissue oximetry.

rSo₂ and Anesthetic Adequacy

Another important determinant of tissue oxygenation is pain-induced stress.²⁷⁸ With inadequate hypnosis or analgesia, pain-induced stress may result in cerebral oxygen consumption exceeding delivery and decreasing rSo₂. Hypnosis and analgesia monitoring by EEG and facial electromyogram can facilitate the prompt identification and correction of this source of cerebral dysoxygenation (Box 16-14).

Until recently, the inability to integrate neuromonitoring information from different modalities (Box 16-15) into a unified display has inhibited clinical studies using a multimodality approach in cardiac surgery. As a result, currently only three outcome studies have examined the impact of multimodality neuromonitoring using a combination of EEG, TCD, and cerebral oximetry. The study involving pediatric cardiac patients noted significant reductions in both neurologic complications and hospital cost in the neuromonitored cohort.²⁷⁹ Both adult cardiac surgery studies^280,281 found a 2.7-day reduction in length of stay associated with multimodality neuromonitoring. Edmonds’s²⁸⁰ study also noted an 11% reduction in hospital expenses. In addition to the substantial reductions in hospital stay, charges, and neurologic complications, the results suggested possible benefit to other vital organ systems. This finding is not unexpected because the same processes that injure the brain may also injure other organs.^131,140 Future studies of neuromonitoring efficacy should not overlook these important accessory benefits. In addition, Lozano and Mossad²⁸² reviewed studies of neuromonitoring during pediatric cardiac surgery and showed that the monitoring was associated with enhanced outcomes (see Box 16-15).

The recent technologic developments address this limitation. New analysis and display systems (Figures 16-40A and B) can integrate multimodality neurophysiologic information, additional physiologic signals from anesthesia or critical care monitors, and information from ventilators, infusion pumps, and so forth into single, unified displays.

Figure 16-40 A, Multimodality neuromonitoring signals may be viewed on a single computer screen. In this case, the bilateral information includes: (1) a color density spectral array electroencephalographic (EEG) trend (top left), (2) traditional EEG (middle left), (3) EEG spectral edge frequency (SEF) and brain regional oxygen saturation (rSo₂) trends (bottom left), (4) upper limb somatosensory-evoked potentials to median nerve stimulation (middle right), and (5) transcranial Doppler (TCD) M-mode and frequency spectral displays (top right). B, Other multimodality analysis and display systems permit integration of information from many different physiologic monitors, ventilators, infusion pumps, and so on, into a unified, single time-base display. For example, this new FDA-approved system illustrates the integration of bilateral cerebral oximetry data with key physiologic signals from a neonatal critical care monitor.

(A, Courtesy of Axon Systems, Hauppauge, NY; the Vital Synch^TM display is courtesy of Somanetics Corporation and was modified with permission.)