Ann Thorac Surg 2006;81:S2373-S2380
© 2006 The Society of Thoracic Surgeons
Supplement
Neurologic Monitoring on Cardiopulmonary Bypass: What Are We Obligated to Do?
George M. Hoffman, MD
*
Department of Anesthesiology and Critical Care Medicine, Children's Hospital of Wisconsin, Medical College of Wisconsin, Milwaukee, Wisconsin
* Address correspondence to Dr Hoffman, Department of Anesthesiology and Critical Care Medicine, Children's Hospital of Wisconsin, Medical College of Wisconsin, Milwaukee, WI 53226 (Email: ghoffman{at}mcw.edu).
Presented at the Symposium on Harnessing the Effects of Neonatal Cardiopulmonary Bypass at the Fourth World Congress of Pediatric Cardiology and Cardiac Surgery, Buenos Aires, Argentina, Sept 21, 2005.
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Abstract
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Improving survival from congenital cardiac repairs using cardiopulmonary bypass has appropriately shifted focus to neurologic outcomes. Hypoxic–ischemic mechanisms are the major cause of neurologic injury in neonatal cardiac surgery, and modifications of techniques of cardiopulmonary bypass can affect organ oxygen delivery and the propensity to injury both during and after surgery. Through successive refinements in the techniques of cardiopulmonary bypass, the risk factors for hypoxic–ischemic injury have been reduced, but not eliminated. The application of specific monitoring to enhance detection of hypoxic conditions associated with neurologic injury would both allow intervention on individual patients and drive refinements in strategies to further reduce risk. Specific neurologic monitoring techniques that can be used during cardiopulmonary bypass include near-infrared spectroscopy, transcranial Doppler ultrasonography, and electroencephalographic techniques. Of these, only near-infrared spectroscopy provides a continuous quantitative signal of the physiologic variable most related to injury and most amenable to intervention. This review will advocate wide adoption of near-infrared spectroscopy monitoring throughout the perioperative period, to enhance detection of hypoxic conditions and to drive patient-specific interventions.
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Introduction
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Recognition of the brain as a potential target of injury during cardiopulmonary bypass (CPB) has been magnified as the early mortality risk for CPB and associated procedures has declined [1]. The magnitude of the problem is large, with estimates of post-CPB neurologic injury ranging from 2% to 30% in neonates [2, 3]. The absolute incidence will never be definable because of limitations in functional assessment in neonates and small children, and the potential for alterations in neurologic plasticity only evident after years of follow-up [4]. Because of the lifetime burden of neurologic injury to the neonate, the payoff from investment that prevents even a small fraction of neurologic disability is socially and individually worthwhile [5]. On a per-case basis, the cost of intensive neurologic monitoring during CPB is a fraction of the disposable cost for CPB, and should be viewed as a priority on the basis of available data. This manuscript briefly reviews the scientific rationale for neurologic monitoring during CPB.
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Pathophysiology of Neurologic Injury
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Perioperative neurologic dysfunction can result from preexisting injury, from potentially reversible organ dysfunction as a manifestation of ongoing pathophysiology, or from a spectrum of irreversible, reversible, and potential injuries related to modifiable and unmodifiable risk factors. The magnitude of the problem is large; signs of overt neurologic injury occur in 2% to 25% of cardiac neonates, with double risk in arch abnormalities, resulting in decreased developmental potential (based on parental and sibling models) in as many as 33% of survivors [2]. Magnetic resonance imaging abnormalities are present preoperatively in 33% of cardiac neonates, and in as many as 93% postoperatively [6]. The early perioperative imaging changes may reveal both completed and potential injury, and thus provide an estimate of risk, with the potential for modification of risk factors. Complexity of plasticity in the neonatal central nervous system implies that, just as new symptoms may occur in the perioperative period as a manifestation of prior injury, perioperative injury may not become symptomatic for years. Thus neurologic injury associated with CPB should be viewed in the context of the risk factors for injury preceding and subsequent to the operative event.
The pathophysiology of intraoperative injury is now understood with increasing knowledge about risk factors: congenital abnormalities in both central nervous system ultrastructure and cerebral vasculature, and the immaturity of the neonatal brain, may conspire to increase the sensitivity to hypoxic–ischemic conditions. Although perioperative events do not completely determine the range of neurodevelopmental outcome, many factors in the perioperative period, particularly CPB, present intense pathophysiologic stress. Neurologic monitoring during this period can expose processes associated with central nervous system injury, and therefore provide a model for exploration of strategies to improve perioperative care.
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Cardiopulmonary Bypass and Neurologic Injury
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Acute neurologic injury related to CPB can result from hypoxic–ischemic, embolic, reperfusion, and inflammatory mechanisms [7, 8]. The perioperative injury in neonates may be like premature periventricular leukomalacia with a superimposition of developmental susceptibility and critical reductions in cerebral blood flow and oxygen delivery in watershed vascular regions [9, 10]. Embolic events seem less significant in both children and adults as general CPB techniques improve [7]. Multimodal approaches to controlling the biologic response to CPB can reduce the inflammatory vasculopathy that has been implicated in delayed reperfusion defects [11, 12]. However, the most effective method of reducing the severity of reperfusion injury is to limit ischemia. Thus prevention of hypoxic–ischemic conditions, both by strategic modification of CPB technique and by detection of events in individual patients in real time, seems the most fruitful approach to reducing the risk of neurologic injury occurring through a variety of mechanisms.
Although many of determinants of cerebral oxygenation can be adversely affected by CPB, extracorporeal circulatory support may in itself be helpful in avoiding hypoxic conditions. For example, the outcome of profoundly hypoxic neonates with persistent pulmonary hypertension is improved by extracorporeal membrane oxygenation support [13]. Similarly, routine elective postoperative extracorporeal membrane oxygenation support has been applied as a cerebral protective strategy in children at high risk of low cardiac output syndrome [14]. The risk of hypoxic–ischemic cerebral injury may be lower after the initiation of well-conducted CPB as a support technique to deliver adequate systemic oxygen [15, 16]. The optimal monitoring would signal conditions likely to be associated with hypoxic–ischemic injury, and provide continuous feedback about the effectiveness of interventions, which may include continuation, weaning, or modification of CPB support in the perioperative period [14].
Cardiopulmonary bypass–related factors that reduce the ratio of cerebral blood flow to metabolism are linked to a higher risk of neurologic disability. Risk factors for decreased cerebral oxygen delivery include anemia, hypocarbia, alkalosis, lower flow rates, and duration of deep hypothermic circulatory arrest (DHCA). Factors related to increased metabolism include inadequate cooling time or target temperature, relative alkalosis, and anesthetic technique. Microvascular alterations that produce postoperative changes in cerebrovascular resistance include cold vasoplegia, edema, and inflammatory vasculopathy. Strategies that limit these risk factors are generally associated with improved outcomes [8, 17–25]. The safe limit for DHCA appears to be in the 30- to 40-minute range, although examination of data from the Boston Circulatory Arrest Study shows both good and bad outcomes on both sides of that time limit. Although examination of the hemoglobin–oxygen decay curve from near-infrared spectroscopy (NIRS) during DHCA suggests rate-limiting oxygen metabolism at 30 to 40 minutes [26], the theoretic oxygen flux is continually declining, and both local and interindividual variation in susceptibility to hypoxic injury during DHCA is likely to occur regardless of the specific strategies used.
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Rationale for Detection of Hypoxic–Ischemic Conditions
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Injury can be prevented only if monitoring detects potentially harmful conditions early enough to allow initiation of effective interventions before irreversible injury has occurred [27–29]. In neonates and children, hypoxic–ischemic mechanisms account for the majority of preventable injury [7, 8]. The pattern of abnormality after CPB in neonates is that of hypoxic–ischemic encephalopathy, with alterations in cerebral blood flow and metabolism occurring with far greater frequency than the appearance of overt neurologic signs [30]. The pattern is similar to periventricular leukomalacia in premature neonates who have had critical reductions in cerebral oxygen delivery as a mechanism [6, 9, 31]. Because the neurodevelopmental effects of central nervous system injury in a neonate may not be manifest until a number of years later, rational approaches to injury prevention will be based largely on strategies to avoid known pathophysiologic risk factors, particularly hypoxia.
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Monitoring Techniques
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Neurologic monitoring in the perioperative period has been extensively reviewed [32, 33]. Possible approaches include monitoring of superior vena cava or jugular venous oxyhemoglobin saturation (SvO
2), regional cerebral oxygen saturation by NIRS, cerebral blood flow velocity by transcranial Doppler, electroencephalography (EEG), and processed EEG. Each of these has different features, which will be briefly summarized.
Near-Infrared Spectroscopy
Near-infrared spectroscopy yields an approximation of oxyhemoglobin saturation of a volume of tissue beneath the probe. The measure is regional, not global or hemispheric, and thus provides information different from jugular bulb saturation. Near-infrared spectroscopy devices are validated in circulatory models that specify a 16:84 or 25:75 ratio of arterial to venous blood using measures of carotid arterial and jugular bulb venous saturation. Both the arterial to venous blood ratio and the complex physics of light scattering and absorption cause the signal to be highly weighted toward venous blood; thus the NIRS signal is highly related to the regional flow–metabolism relationship, for which it has been extensively used in both the clinical and laboratory setting.
The source–detector distance determines the depth of the light path, with a distance of at least 4 cm necessary for intracranial measurement about 2 cm below the probe. The available technologies operate on the assumption that hemoglobin is the major chromophore, but variation in nonheme pigments and geometry of the light path make absolute measurement of saturation less reliable. Errors attributable to differential path length variation and superficial scalp blood flow are minimized by a dual-detector subtraction technique in the Somanetics INVOS device. This device is currently the only US Food and Drug Administration–approved cerebral and tissue oximeter, which reports a value for regional relative oxyhemoglobin saturation (rSO
2). A three-wavelength device by Hamamatsu Instruments can provide an estimate of oxyhemoglobin relative concentration termed tissue oxygenation index, but it is less reliable in clinical application [34, 35]. Agreement between rSo2 and tissue oxygenation index is not absolute, but changes track well [36]. Near-infrared spectroscopy is especially suited to neonatal and pediatric use because the light path will traverse the at-risk deeper neural structures (Fig 1).
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Fig 1. Areas of potential hypoxic–ischemic injury in the neonatal brain include moderate and deep cortical structures. The light path of a near-infrared (NIR) spectroscopy device applied to the frontal forehead will traverse areas at risk between the short and long penetrating arteries. More of these regions will be in the monitored field in neonates with small head dimensions. (PVL = periventricular leukomalacia.)
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Transcranial Doppler
Transcranial Doppler provides a measure of blood flow velocity consistent with the angle of incidence to the direction of flow. The probe is typically placed over the middle cerebral artery, and provides an indirect measure of cerebral blood flow, under the assumption that vessel diameter is relatively invariant. Minor changes in probe position may result in significant signal alteration, limiting the robustness of this modality in prolonged clinical use.
A unique contribution of transcranial Doppler stems from the detection of high-intensity transient signals, which signify embolic phenomena. Available software can quantify these signals in terms of frequency and size. The relationship of small high-intensity transient signals to outcome has been obscure in children [32, 37]. Current CPB techniques may limit the importance of embolic injury even in adults [38].
The measure of cerebral blood flow velocity provides a useful signal of perfusion, and when combined with knowledge of hemoglobin, temperature, carbon dioxide tension, and arterial saturation, can approximate cerebral oxygen delivery. Because conducting vessels change diameter with a number of stimuli, transcranial Doppler may best be used as an adjunct to NIRS, with which it can enable inferences about metabolism from flow and saturation signals, and to help guide flow rates during mechanical circulatory support [32].
Electroencephalographic Techniques
Electroencephalographic-related technologies examine the electrical functional activity of the brain. The EEG activity is linked to cerebral metabolism, and thus will reveal changes as neuronal energy metabolism is limited by hypoxic–ischemic states [39]. The EEG is the best available method for detecting seizure activity, which may be subclinical in manifestation or obscured by neuromuscular blockade, which may be a later sign of injury, and which may cause further injury if protracted. Depending on the complexity of the monitoring montage, EEG may be very helpful in localizing the area of central nervous system injury or dysfunction. However, seizure activity on CPB has little predictive value for later neurologic outcome in neonates [39, 40].
In addition to changes with metabolism, the EEG is extremely dependent on the behavioral and anesthetic state of the patient. This dependence has been used to develop anesthetic state monitors using various processing algorithms. Advanced signal processing is a relative necessity to elucidate the complex interactions between behavior, anesthetic drugs, and biochemical changes that may result from hypoxia, and the differentiation is incomplete. Hypothermia may suppress brain electrical activity to a nearly isoelectric point, which may be indistinguishable from that produced by deep anesthesia or profound ischemia [40]. The EEG may be used to guide adequate extent and duration of cooling to achieve metabolic suppression before DHCA [41]. The latency of return of EEG activity after DHCA does predict later neurologic outcome [42]. Likewise, longer duration DHCA is associated with a higher incidence of postoperative seizures [43]. However, as late indicators of potential injury, neither EEG latency nor seizures help guide hemodynamic interventions to prevent ongoing hypoxic injury.
Different forms of spectral analysis allow characterization of the frequency-power distribution, which may be useful in detection of global ischemic states [32, 37]. Global hypoxia severe enough to alter the EEG may be used in conjunction with NIRS to set a threshold for an individual patient, but the EEG has no value in detection of changes in brain oxygenation above the EEG threshold. Recovery of EEG activity after DHCA occurred while abnormalities in brain oxygenation by NIRS persisted, emphasizing that the EEG is generally less sensitive than NIRS in detecting more subtle conditions of hypoxia [44].
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Near-Infrared Spectroscopy, Cerebral Oxygenation, and Neurologic Injury
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Cerebral desaturation by NIRS generally precedes signs of neuronal dysfunction. In human adults undergoing implantable defibrillator testing, EEG changes during cardiac arrest occurred at NIRS rSO
2 of 47% [45]. In a neonatal piglet model, graded neuronal dysfunction was related to NIRS values observed during progressive hypoxia: lactate accumulated at rSO
2 of 44%; EEG changes occurred at rSO
2 of 42%; the EEG became silent at rSO
2 of 37%, and loss of adenosine triphosphate production resulted in biochemical failure at rSO
2 of 33% [46]. Thus NIRS can provide a graded signal over a range of hypoxia, resulting in progressive metabolic disturbance, functional deterioration, and actual biochemical failure.
Near-infrared spectroscopy has been extensively used in both laboratory and clinical settings to quantify the relationship between circulatory arrest and brain hypoxia. Using NIRS to follow the decay of oxyhemoglobin during circulatory arrest, Kurth and colleagues [47] found a critical reduction in oxygen flux at an rSO
2 near 40% in human neonates during DHCA. Sakamoto and colleagues [26] found that DHCA limited to an rSO
2 nadir time of less than 25 minutes did not produce detectable injury.
Factors related to inadequate oxygen delivery on CPB were recently evaluated using NIRS by Hagino and associates [48]. The authors found that the CPB-related factors of hemoglobin concentration, flow rate, and carbon dioxide tension were the determinants of both brain oxygenation by NIRS and histologic injury in a graded hypoxic–ischemic model. These data indicate that NIRS provides a signal highly related to injury, with a critical tissue oxygenation index value of 55% in neonatal piglets. In adults undergoing aortic arch repair using antegrade cerebral perfusion, Orihachi and coworkers [49] found that the neurologic outcome was determined by the rSO
2 pattern, not the duration of circulatory arrest, and also recommended intervention for rSO
2 less than 55%. This study underscores the importance of variation in individual biology and technical factors, rather than the usual CPB-related determinants of oxygen delivery, in determining outcome, and suggests that interventions based on NIRS monitoring would reduce injury.
The average NIRS value during CPB has been reported to predict the development of postoperative neurologic dysfunction [50]. However, a threshold effect is likely to apply, and measures such as time under a given saturation, or lowest measured rSO
2, may more likely be predictive of outcome [51]. Even in the absence of absolute threshold data, NIRS data can reveal changes in flow and metabolism before a threshold is reached, and thus provide a sensitive but not specific indicator of risk conditions [37, 52, 53].
The relationship of cerebral oxygenation to acute perioperative outcomes in children without circulatory arrest is more complex. Kurth and associates [54] found acute postoperative neurologic injury in 3 of 26 patients monitored intraoperatively with NIRS, and found lower rSO
2 on CPB in the injured patients. Austin and colleagues [5] found that 70% of 250 neonates and children had prolonged rSO
2 reductions (defined as 20% change from baseline) during CPB, associated with high (25%) risk of postoperative neurologic dysfunction, which could be reduced to 6% if these desaturations were effectively treated.
Periods of risk for cerebral hypoxia in the cardiac neonate extend throughout the perioperative period range [31, 55]. The risk of neurologic injury from cerebral hypoxia during DHCA rises with time, and techniques to provide continuous and intermittent cerebral perfusion have been developed as alternatives to DHCA [56–59]. Langley and colleagues [56] showed that intermittent brief reperfusion of the brain at 30-minute intervals prevented the abnormalities in reperfusion and metabolic recovery associated with prolonged circulatory arrest. This time interval corresponds with the 25- to 35-minute critical period of DHCA found by other authors [23, 26, 47], and suggests that reperfusion at intervals guided by NIRS might better account for individual differences in metabolism [60].
We studied changes in regional oxygenation during hypothermic CPB with selective cerebral perfusion (SCP) with NIRS, to assess vulnerable periods for central nervous system injury, and found that cerebral rSO
2 was maintained during SCP with an average flow rate of 47 mL/min at a temperature of 20°C [61]. However, variations in the interactions of temperature, hemoglobin, carbon dioxide tension, and variable runoff resistance created a need for wide adjustments in flow rates to maintain cerebral rSO
2. Data from transcranial Doppler about cerebral blood flow velocity may be combined with rSO
2 from NIRS to help guide perfusion variables during SCP [29].
Aside from providing a target for management of oxygen-delivery variables during CPB and SCP, our intraoperative NIRS data [61] showed that the risk of cerebral desaturation rose after hypothermic CPB with SCP, as predicted by studies of cerebral blood flow and metabolism after hypothermic CPB [18]. We found evidence for altered autoregulation after CPB with SCP, with a shift in the slope of the carbon dioxide tension to rSO
2 relationship acutely after CPB with SCP [61].
By extending this monitoring modality postoperatively, we have shown that the conduct of CPB can affect postoperative cerebral perfusion also [44]. The altered cerebral autoregulation induced by hypothermic CPB did not return to preoperative values until after 24 hours (Fig 2). Low cerebral rSO
2 was observed across a wide range of blood pressure, arterial saturation, and superior vena cava SvO
2, suggesting that usual hemodynamic indices do not predict cerebral oxygenation after CPB, and emphasizing the concept that perioperative risk does not reside entirely intraoperatively.
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Fig 2. The conduct of cardiopulmonary bypass (CPB) affects postoperative cerebral hemodynamics. The relationship between carbon dioxide tension (pCO2) and cerebral regional oxygen saturation (rSO
2) is shown before (pre-CPB), immediately after (post-CPB), and at 24 and 48 hours after surgery. Cerebral autoregulation is altered after hypothermic selective cerebral perfusion, persists for at least 24 hours, and returns to baseline by 48 hours. Data are from 26 neonates over 48 hours after stage I palliation of hypoplastic left heart syndrome. (ICU = intensive care unit.)
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Few neonatal data show a direct relationship between measures of cerebral oxygenation and late neurologic outcome. We systematically examined the relationship between hemodynamics after neonatal stage I palliation of hypoplastic left heart syndrome and neurodevelopmental outcome at preschool age, finding that low values of superior vena cava SvO
2 after neonatal surgery contributed substantially to adverse neurologic development [62]. Superior vena cava SvO
2 is highly determined by brain blood flow and metabolism, and moves closely with brain NIRS [63, 64]. In our multivariate model, DHCA time and postoperative SvO
2 accounted for 30% and 20% of the variance in late outcome, respectively, with a breakpoint at SvO
2 less than 40% (Fig 3). Postoperative hypercapnia modified the post-DHCA relationship of SvO
2 to late neurologic outcome, probably by altering the distribution of limited cardiac output to the brain (Fig 4). These data indicate that SvO
2 is a rough proxy for cerebral oxygenation and that targeting cerebral oxygenation in the perioperative period is likely to affect neurologic injury and long-term outcome. Recent data from a similar patient population show that prolonged cerebral desaturation detected by NIRS (more than 90 minutes with rSO
2 less than 45%) in the postoperative period is associated with new abnormalities on early postoperative magnetic resonance imaging [65]. Late neurodevelopmental outcome data from our cohort in an era of continuous perioperative NIRS monitoring is still a few years away.
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Fig 3. Perioperative systemic oxygen delivery affects neurologic injury. In the first 48 hours after stage I palliation of hypoplastic left syndrome, critical reduction in venous oxygen saturation (SvO
2) to less than 40% is associated with poor neurodevelopmental outcome assessed at age 4 to 5 years. (ANOVA = analysis of variance; CI = confidence interval.) (Reprinted from [62] with permission of the American Association for Thoracic Surgery.)
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Fig 4. Perioperative management strategy affects neurologic injury. Hypercapnia ameliorates the effect of low systemic oxygen delivery on cerebral injury. (CI = confidence interval; pCO2 = carbon dioxide tension; SvO
2 = venous oxygen saturation.) (Reprinted from [62] with permission of the American Association for Thoracic Surgery.)
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Rationale for Standardized Near-Infrared Spectroscopy Monitoring
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Given the multiple linkages between hypoxic–ischemic risk and reduced neurodevelopmental outcome, we have chosen a straightforward perioperative strategy: increase the detection, treatment, and prevention of brain hypoxia throughout the period of physiologic risk. The rationale for this approach is to improve outcomes by interrupting the pathway from risk to reversible dysfunction to irreversible injury, while cognizant of the fact that absolute thresholds for injury do not exist. Strategic improvements in both survival and oxygen delivery at Children's Hospital of Wisconsin have been gained through the use of phenoxybenzamine on CPB and SCP instead of DHCA for complex neonatal repairs [66]. Using regressive multivariable modeling, we have evidence that perioperative cerebral oxygenation has also improved with improvements in global oxygen delivery. However, even in the current era, periods of cerebral desaturation occur, requiring aggressive management, and neither arterial oxygen saturation, arterial blood pressure, nor SvO
2 adequately predict cerebral desaturation [67]. In our patient population, episodes of cerebral desaturation as detected by NIRS were associated with a wide range of measures of arterial blood pressure, arterial oxygen saturation, and Svo2, despite management strategies to optimize systemic oxygen delivery and SvO
2 (Fig 5). As a result, we have adopted a strategy of universal NIRS monitoring to detect cerebral desaturation events that occur without complete predictability, but which usually do respond to intervention [27]. Data-driven individualized patient management would not be possible without an online monitor of cerebral oxygenation; see Figure 6
for an example. The standardized use of perioperative NIRS will promote both further strategic reduction in cerebral hypoxic risk and individualized treatments that can account for interpatient variability [32].
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Fig 5. Cerebral oxygenation is only partly predictable by the usual variables, and low cerebral regional oxygen saturation (rSO
2) occurs over a range of arterial blood pressure, arterial oxygen saturation (SaO
2), and venous oxygen saturation (SvO
2). Data are from 26 neonates over 48 hours after stage I palliation of hypoplastic left heart syndrome.
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Fig 6. Intraoperative record of cerebral and somatic regional oxygen saturation (rSO
2) during stage I palliation of hypoplastic left heart syndrome with a right ventricle-to-pulmonary artery shunt, showing the expected rapid reduction in cerebral oxygenation during brief periods of circulatory arrest before and after a period of selective cerebral perfusion. The more gradual but prolonged and otherwise silent critical cerebral desaturation events occurred during weaning from cardiopulmonary bypass and before transfer from the operating room, but were correctable by modification of determinants of cerebral blood flow and metabolism.
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The adoption of NIRS as a routine monitor has been slow, in part because of the lack of absolute thresholds for injury. However, no other monitored variable has such a threshold established. What blood pressure, hematocrit, or carbon dioxide tension is too low for any individual patient? We make decisions constantly based only on approximation of certainty. As a single factor, rSO
2 has the highest likelihood of detecting conditions associated with cerebral hypoxia. In concert with other variables known from population studies to be associated with injury, rSO
2 can lead to informed decisions about intervention to a greater degree than other monitored variables to date. Difficult questions are raised when cerebral monitoring data indicate potentially dangerous conditions in a case that is otherwise according to plan. Yet we will continue to have the responsibility of making the best choices with incomplete data on a minute-by-minute, case-by-case, and strategy-by-strategy basis.
Assiduous attention to CPB technique is a critical foundation for specific neurologic monitoring. Risk factors for inadequate cerebral oxygen delivery include hemodilution, hypocarbia, normothermia, lower pump flows, and hypotension. Although a high-flow, hypercarbic, hypothermic, limited-dilution CPB technique will in general reduce the likelihood of hypoxic–ischemic injury, decisions about how to modify such factors could be more appropriately driven by patient-specific data. In this perspective, NIRS can provide a guide to management of CPB factors associated with oxygen delivery even without identification of critical desaturation, just as a pulse oximeter can provide continuous information about pulmonary gas exchange, allowing modification of ventilation strategies before critical arterial desaturation occurs. The weight of the evidence supports NIRS as an effective modality to reduce the incidence of hypoxic–ischemic conditions associated with neurologic injury, if the data are actually incorporated into practice [53]. We should use it routinely in the operating room, with an open eye and mind for information that can drive improvements in current practice extending throughout the perioperative period [1].
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Abstract
Introduction
