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J Thorac Cardiovasc Surg 2008;135:83-90
© 2008 The American Association for Thoracic Surgery

Surgery for Congenital Heart Disease

The influence of systemic hemodynamics and oxygen transport on cerebral oxygen saturation in neonates after the Norwood procedure

Jia Li, MD, PhDa,*, Gencheng Zhang, MD, PhDa, Helen Holtby, MDa, Anne-Marie Guerguerian, MDa, Sally Caib, Tilman Humpl, MDa, Christopher A. Caldarone, MDa, Andrew N. Redington, MDa, Glen S. Van Arsdell, MDa

a Heart Center, the Hospital for Sick Children, Toronto, Ontario, Canada
b Data Center, Congenital Heart Surgeon’s Society, Toronto, Ontario, Canada.

Received for publication April 27, 2007; revisions received June 8, 2007; accepted for publication July 9, 2007.

* Address for reprints: Jia Li, MD, PhD, Division of Cardiology, Hospital for Sick Children, 555 University Ave, Toronto, Ontario, Canada M5G 1X8. (Email: jia.li{at}sickkids.ca).


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Discussion
 Limitations
 Conclusions
 References
 
Objectives: Ischemic brain injury is an important morbidity in neonates after the Norwood procedure. Its relationship to systemic hemodynamic oxygen transport is poorly understood.

Methods: Sixteen neonates undergoing the Norwood procedure were studied. Continuous cerebral oxygen saturation was measured by near-infrared spectroscopy. Continuous oxygen consumption was measured by respiratory mass spectrometry. Pulmonary and systemic blood flow, systemic vascular resistance, oxygen delivery, and oxygen extraction ratio were derived with measurements of arterial, and superior vena cava and pulmonary venous gases and pressures at 2- to 4-hour intervals during the first 72 hours in the intensive care unit.

Results: Mean cerebral oxygen saturation was 66% ± 12% before the operation, reduced to 51% ± 13% on arrival in the intensive care unit, and remained low during the first 8 hours; it increased to 56% ± 9% at 72 hours, still significantly lower than the preoperative level (P < .05). Postoperatively, cerebral oxygen saturation was closely and positively correlated with systemic arterial pressure, arterial oxygen saturation, and arterial oxygen tension and negatively with oxygen extraction ratio (P < .0001 for all). Cerebral oxygen saturation was moderately and positively correlated with systemic blood flow and oxygen delivery (P < .0001 for both). It was weakly and positively correlated with pulmonary blood flow (P = .001) and hemoglobin (P = .02) and negatively correlated with systemic vascular resistance (P = .003). It was not correlated with oxygen consumption (P > .05).

Conclusions: Cerebral oxygen saturation decreased significantly in neonates during the early postoperative period after the Norwood procedure and was significantly influenced by systemic hemodynamic and metabolic events. As such, hemodynamic interventions to modify systemic oxygen transport may provide further opportunities to reduce the risk of cerebral ischemia and improve neurodevelopmental outcomes.

Abbreviations and Acronyms CPB = cardiopulmonary bypass; DO 2 = oxygen delivery; ERO 2 = oxygen extraction ratio; ICU = intensive care unit; NIRS = near-infrared spectroscopy; PaO 2 = arterial oxygen tension; Qp = pulmonary blood flow; Qs = systemic blood flow; ScO 2 = cerebral oxygen saturation; SVR = systemic vascular resistance; VO 2 = oxygen consumption


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Discussion
 Limitations
 Conclusions
 References
 
There has been a dramatic reduction in mortality after surgery for complex congenital heart defects. Consequently, much attention is now being directed to neurologic outcomes among survivors.1Go The incidence of measurable neurologic sequelae is as high as 25%, including both early postoperative seizures2,3Go and long-term neurodevelopmental impairment such as cognitive, attentional, behavioral, and neuromuscular disabilities.4-8Go Studies on neurologic outcomes have largely focused on specific intraoperative risk factors, such as hemodilution, pH management,9Go and deep hypothermic circulatory arrest.2-5,8,10Go Others have reported preoperative reduction of cerebral blood flow and ischemic injury (in turn related to anatomic and functional features), being most severe in neonates with hypoplastic left heart syndrome.11-14Go Postoperative hemodynamic instability may further affect the vulnerable brain. Prolonged stay in the intensive care unit (ICU) has been found to be associated with poorer neurologic outcomes.15Go Ischemic lesions early after cardiac surgery, in the form of periventricular leukomalacia, have been seen in more than 50% of neonates and have been attributed to postoperative hypoxia and diastolic hypotension.16,17Go

Neonates with hypoplastic left heart syndrome undergoing the Norwood procedure, which involves reconstruction of the aortic arch to maintain unobstructed systemic blood flow (Qs) and limiting pulmonary blood flow (Qp) with a modified Blalock–Taussig shunt, may be particularly prone to neurologic insult, with hypoxic–ischemic lesions seen preoperatively in nearly half of these neonates.12,17Go Intraoperatively, the already vulnerable neonatal brain will be exposed to the effects of prolonged cardiopulmonary bypass (CPB), circulatory arrest, and variable hemodynamic and metabolic events. The effects of regional brain perfusion strategies remain to be demonstrated, but it is likely that intraoperative neuroprotection is less than complete.18Go In addition to these preoperative and intraoperative risk factors, our group has shown that the early postoperative period after the Norwood operation is characterized by hemodynamic instability with marginal systemic oxygen delivery (DO 2), with the injured neonatal single right ventricle supplying the parallel circulations and arterial oxygen desaturation.19,20Go At the same time, systemic oxygen consumption (VO 2) increases,19,20Go thus further impairing systemic oxygen transport and placing the cerebral circulation at risk. It has been recently reported that low systemic venous oxygen saturation is associated with childhood neurodevelopmental abnormality.21Go Clearly, a systematic assessment of the effects of systemic hemodynamics and oxygen transport on cerebral oxygenation during the early postoperative period is needed to understand the mechanisms of neurologic ischemic injury and to improve postoperative management and long-term neurologic outcomes.

Near-infrared spectroscopy (NIRS) provides a noninvasive, continuous method to monitor regional tissue oxyhemoglobin saturation.22,23Go It has been extensively used during CPB to determine the risk factors for poor cerebral perfusion.16,18,24Go In the present study, we hypothesized that cerebral oxygen transport might be influenced by systemic hemodynamics and oxygen transport during the early postoperative period after the Norwood procedure. We used NIRS to continuously measure cerebral oxygen saturation (ScO 2) and respiratory mass spectrometry to continuously measure VO 2 and to derive measurements of Qp and Qs, DO 2, and oxygen extraction ratio (ERO 2). We examined the effects of each of the systemic hemodynamic indices and oxygen transport variables on ScO 2 during the first 72 hours after the Norwood procedure.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Discussion
 Limitations
 Conclusions
 References
 
Patients
This study was approved by the Research Ethics Board at the Hospital for Sick Children, Toronto, Canada. Written informed consent was obtained from the parents of 16 neonates (14 boys, age range 4–16 days, median 7 days) undergoing the Norwood procedure between April 2004 and November, 2006. Patient demographics are shown in Table E1. Data from some of these patients were reported previously on systemic hemodynamics and oxygen transport early after the Norwood procedure.19,20Go


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  		TABLE E1 Clinical data for the 16 neonates
 
Operative Procedure
Neonates were intubated with a cuffed endotracheal tube (Microcuff-Heidelberg-Pediatric; Microcuff GmbH, Weinheim, Germany). General anesthesia was maintained with inhaled isoflurane, intravenous fentanyl, and pancuronium bromide. A standard Norwood procedure with regional cerebral circulation was used. All neonates had a 3.5-mm right modified Blalock–Taussig shunt with the distal anastomosis placed centrally on the intramediastinal pulmonary artery. CPB management consisted of a target flow of 125 mL · min–1 · kg–1 and a hematocrit value of 25% to 30% with modified pH-stat blood gas management for uniform cooling (18°C–20°C) at the esophageal site. Selected cerebral perfusion was performed in all neonates at pump flows of 30 to 35 mL · min–1 · kg–1. All neonates received aprotinin 1.7 x 106 KIU/m2 and methylprednisolone 10 mg/kg before CPB. Phenoxybenzamine 0.25 mg/kg was added to the pump prime. Separation from CPB occurred after initiation of infusions of milrinone (0.66 µg · min–1 · kg–1) and dopamine (5 µg · min–1 · kg–1). Modified ultrafiltration was used in all neonates immediately after separation from CPB. A pulmonary venous line was inserted into the orifice of the right upper pulmonary vein. The sternal incision was left open routinely in all the patients.

Critical Care
Infants received time-cycled pressure control/pressure support ventilation. Sedation and analgesia were given as a continuous intravenous infusion of morphine (20–40 µg · h–1 · kg–1), intermittent injections of lorazepam (0.1 mg/kg), and pancuronium (0.1 mg/kg). Pancuronium was discontinued when the patient achieved satisfactory hemodynamic stability.

The central esophageal temperature was monitored continuously and maintained at 36°C–37°C. Vasoactive agents (milrinone, dopamine, phenoxybenzamine, and vasopressin) and ventilatory settings were adjusted according to our standard protocol to achieve arterial carbon dioxide tension around 45 to 50 mm Hg and pH 7.3 to 7.4, mean arterial blood pressure 40 to 45 mm Hg with systolic pressure in the range of 55 to 65 mm Hg, arterial oxygen saturation 70% to 80%, and superior vena caval saturation of 44% to 55%.25Go Intravenous volume infusions (5% albumin or blood) were given to maintain filling pressures of 7 to 10 mm Hg. Transfusions were given for a hemoglobin of less than 14 mg/dL, and hemoglobin was generally maintained between 14 and 16 mg/dL (Figure 1).


Figure 1
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  		Figure 1. Mean ± SD values of cerebral oxygen saturation (ScO 2) and hemodynamics including systolic, diastolic, and mean arterial pressures, systemic vascular resistance (SVR), arterial oxygen saturation (SaO 2), arterial partial oxygen pressure (PaO 2), hemoglobin (Hb), pulmonary (Qp) and systemic blood flows (Qs), and oxygen transport including systemic oxygen consumption (VO 2), oxygen delivery (DO 2), and oxygen extraction ratio (ERO 2) during the first 72 hours after arrival in the intensive care unit. *After polynomial transformation, with time indicating the coefficient of the early trend, and time2 indicating the later trend. **Data were entered after logarithmic transformation.

 
Methods of Measurements
ScO 2
A NIRS probe, consisting of a near-infrared light emitter optode and a receiver optode with a distance of 5 cm, was placed on the patient’s midline forehead. The recordings were monitored by a dual-detector device (Somanetics INVOS 5100A, Troy, Mich) and recorded at 1-minute intervals.

VO 2
VO 2 was measured continuously with an AMIS2000 respiratory mass spectrometer (Innovision A/S, Odense, Denmark). This is a sensitive and accurate method that allows simultaneous measurements of multiple gas fractions. The detailed methodology used in this protocol has been published previously by our group.20Go

Calculations of hemodynamic and oxygen transport variables
Blood samples were taken from the arterial line, superior vena cava, and pulmonary vein lines for the measurements of blood gases and saturations. Qp and Qs were then calculated by the direct Fick method:


Formula



Formula

Systemic vascular resistance (SVR) was calculated by the following equation:


Formula

DO 2 and ERO 2 were calculated by standard equations:


Formula



Formula

where CaO 2, CpvO 2, and CvO 2 indicate systemic arterial (which is pulmonary arterial), pulmonary venous, and superior vena cava oxygen contents, respectively; MAP and MVP indicate the mean arterial and superior vena cava pressures. All values were indexed to body surface area as calculated before the operation.

Study Protocol
ScO 2 was continuously monitored after anesthesia introduction, during the operation, and 72 hours after the operation. Intraoperative clinical data (including esophageal temperature, systemic arterial blood pressure, and blood gases) were collected before the operation as baseline, before selective cerebral perfusion (CPB cooling), during selective cerebral perfusion, before separation from CPB (CPB rewarming), and at the end of the operation. Postoperative study recordings were prospectively performed during the first 72 hours after arrival in the ICU. Values of hemodynamic and oxygen transport variables and central body temperature were collected at 2-hour intervals during the first 24 hours and at 4-hour intervals in hours 25 through 72. Sampling was avoided if a change in sedation, paralysis, ventilatory, or hemodynamic treatment was made within 15 minutes. The treating physicians were blinded to NIRS values during the postoperative period.

Data Analysis
Data are expressed as mean ± standard deviation. Mixed linear regression analysis for repeated measures was used to determine the nature of any time trend of the measures over the 72-hour study period. For some measures, various transformations of time (logarithmic and polynomial) were tested regarding the best fit for the time course. Correlations between the variables were sought also using mixed linear regression analysis for repeated measures. The extent of correlation was indicated by the intercept, parameter estimate, and P value. Further comparisons of the extents of correlations between the 2 periods in the first 24 hours and the following 48 hours were made and indicated by the parameter estimates of the interactions of time period and the variables and P values. All data analyses were performed with SAS statistical software version 9.2 (SAS Institute, Inc, Cary, NC).


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Discussion
 Limitations
 Conclusions
 References
 
Patients
There was no incidence of circulatory collapse or death during the study period. All neonates survived to hospital discharge except for one who died of cardiac failure on the 25th postoperative day (patient 13). Complete data sets were collected in all neonates for 72 hours except in one (patient 8) owing to weaning from mechanical ventilation at 48 hours. The standard neonatal physical examination at the time of discharge did not demonstrate abnormal neurologic findings.

Intraoperative Changes of ScO 2
ScO 2 values differed markedly between the different periods of perfusion and surgical repair. Preoperative baseline ScO 2 was 66% ± 12%. ScO 2 increased to 88% ± 6% at the end of cooling and was 90% ± 7% during selective cerebral perfusion. It decreased to 64% ± 9% during rewarming, and further to 54% ± 6% after separation from CPB, significantly lower than the preoperative baseline level (P = .02).

Postoperative Changes of ScO 2 and Systemic Hemodynamic and Oxygen Transport Variables
Table E2 and Figure 1 show the results of ScO 2 and its temporal relationship with systemic hemodynamic, and oxygen transport variables during the 72 hours after arrival in the ICU. All the variables showed substantial intraindividual and interindividual variations over the study period, with marked differences in the time course and extent of change.


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  		TABLE E2 Statistical analysis results of the changes of ScO 2, systemic hemodynamics, and oxygen transport in the 16 neonates during the 72-hour study period using mixed linear regression method
 
ScO 2
ScO 2 further decreased to 51% ± 13% on arrival in the ICU and remained at the low level in the initial 8 hours. Over the first 72 hours, ScO 2 was significantly related to time in a complex polynomial function, with an increase in the first 48 hours (P < .0001) and a subsequent small but significant decrease in 48 to 72 hours (P < .0001). The mean value of ScO 2 at 72 hours was 56% ± 9%, significantly lower than the preoperative baseline level (P = .02). When all data were pooled together, the values ranged from 27% to 79%, with 28% of the measurements lower than the reported critical level of 48%.26-28Go

Systemic hemodynamics and oxygen transport
Systolic and mean arterial pressures were significantly related to time after a logarithmic transformation, being initially low in the first 24 hours, followed by a rapid increase between 24 and 48 hours, and remained at that level thereafter (P < .0001 for both). Diastolic arterial pressure significantly and linearly increased over the study period (P = .004). SVR was significantly related to time in a complex polynomial function, being initially high in the first 8 hours, followed by a rapid decrease in the first 24 hours (P < .0001), and a subsequent small but significant increase (P = .0001). Hemoglobin showed a small linear decrease over time (P < .0001). SaO 2 and arterial oxygen tension (PaO 2) were significantly related to time after logarithmic transformation, with a rapid increase in the first 24 hours and thereafter a slow increase (P < .0001). Qp showed a linear significant increase over time (P < .0001). Qs and DO 2 were significantly related to time in a complex polynomial function, with an initial rapid increase in the first 24 hours followed by a slow increase (P < .0001 for both), and a subsequent small but significant decrease at around 28 hours (P = .0001 for Qs and P < .0001 for DO 2). VO 2 and ERO 2 were significantly related to time after logarithmic transformation, showed a rapid decrease in the first 8 hours, and a subsequent slow decrease (P = .0005 for VO 2, and P < .0001 for ERO 2).

Correlations of ScO 2 With Systemic Hemodynamics and Oxygen Transport
The statistical analysis results of the correlations between ScO 2 and systemic hemodynamics and oxygen transport during the whole study period are seen in Table E3 and Figure 2.


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  		TABLE E3 Statistical analysis results of the correlations of ScO 2 as the dependent variable with the systemic hemodynamics and oxygen transport as the independent variables in the 16 neonates during the first 72 hours after the Norwood procedure using mixed linear regression method
 

Figure 2
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  		Figure 2. Correlations between cerebral oxygen saturation (ScO 2) and systemic hemodynamic and oxygen transport variables of systolic, diastolic, and mean arterial pressures, systemic vascular resistance (SVR), arterial oxygen saturation (SaO 2), arterial partial oxygen pressure (PaO 2), Hemoglobin (Hb), pulmonary (Qp) and systemic blood flows (Qs), systemic oxygen consumption (VO 2), oxygen delivery (DO 2), and oxygen extraction ratio (ERO 2) in neonates during the first 72 hours after arrival in the intensive care unit (ICU).

 
ScO 2 was closely and positively correlated with systolic, diastolic, and mean arterial pressures (parameter estimate 0.31, 0.26, and 0.48, respectively; P < .0001, P = .0003, and P < .0001, respectively) and with SaO 2 and PaO 2 (parameter estimate 0.41 and 0.69, respectively; P < .0001 for both). ScO 2 was also closely and negatively correlated with ERO 2 (parameter estimate –31.0; P < .0001). It was moderately and positively correlated with Qs (parameter estimate 2.1; P < .0001) and DO 2 (parameter estimate 0.023; P < .0001). It was weakly but significantly and positively correlated with Qp (parameter estimate 1.8; P = .001) and negatively with SVR (parameter estimate –0.15; P = .003). It was not correlated with VO 2 (P > .05).

Additionally, PaO 2 and SaO 2 were weakly correlated with Qp (parameter estimate 0.05; P < .0001 for both), Qp/Qs (parameter estimate 0.03 and 0.04, respectively; P < .0001 for both), and DO 2 (parameter estimate 3.7, P = .002 for PaO 2; parameter estimate –0.16; P > .05 for SaO 2). The extents of correlations of ScO 2 with hemodynamics and oxygen transport variables were not significantly different between the period of the first 24 hours and that of the later period (P > .05 for all).


   Discussion
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
Limitations
 Conclusions
 References
 
This is the first study to examine the consequences of postoperative systemic hemodynamics and oxygen transport on cerebral oxygenation in neonates with hypoplastic left heart syndrome after the Norwood procedure. We found that ScO 2 fell during the first 8 hours after surgery and then increased in neonates during the first 72 hours after the Norwood procedure. Critically low levels of ScO 2 occurred frequently. The changes in ScO 2 were significantly related to the changes in systemic hemodynamics and oxygen transport variables.

NIRS was used to estimate cerebral oxygenation in our study. The dual-path length device we used measures the percentage of oxyhemoglobin to total hemoglobin in the mixture of arteries, capillaries, and veins in a slice of tissue approximately 1.5 to 2.5-cm deep.22Go Because the predominant venous portion may account for approximately 70% to 80% in NIRS signals,29Go the changes in ScO 2 can estimate the cerebral flow–metabolism relationships. In heavily sedated subjects, as in these neonates, in whom aerobic metabolism of the brain is relatively low and stable, ScO 2 may act as surrogate for cerebral blood flow and DO 2.

Evidence from adult humans26Go and neonatal piglets28Go indicates that aerobic metabolism may be impaired when ScO 2 decreases below 44% to 47%. In a recent study of neonates after the Norwood procedure, prolonged exposure to low postoperative ScO 2 (<45% for >180 minutes) was associated with the development of ischemic lesions on magnetic resonance imaging.27Go In our neonates, the preoperative baseline ScO 2 was 66% ± 12%, similar to the range reported by Hoffman and associates.18Go The intraoperative changes also showed a similar pattern.18Go ScO 2 increased during cooling, was well maintained during selective cerebral perfusion, and decreased after rewarming and separation from bypass to be lower than preoperative baseline values, at an average of 54% ± 6%. There was a further decrease in ScO 2 in the first 8 hours after arrival in the ICU. Despite the subsequent increase, at 72 hours ScO 2 was still significantly lower than preoperative baseline levels.

This study shows that the vulnerable brain is dependent on unstable hemodynamics and oxygen transport seen in the early postoperative period after the Norwood procedure. DO 2 is characteristically low and highly variable. Qs and DO 2 are most depressed during the first 12 to 24 hours; at the same time, VO 2 is high, further compounding the imbalance of oxygen transport.19,20Go Thus the first 12 to 24 hours represents a critical period for not only cardiovascular but also neurologic morbidity. Low ScO 2 was associated with depressed hemodynamics and impaired balance of oxygen transport, as seen in the low arterial blood pressure, SaO 2, PaO 2, Qp, Qs, and DO 2 and a high VO 2 and ERO 2. Thereafter, ScO 2 improved with the gradual recovery in hemodynamics and oxygen transport.

ScO 2 showed wide interindividual and intraindividual variations throughout the study period (27%–79%). The frequency of a critically low level (<48%) was substantial, representing about 28% of all the measurements. Correlation analysis revealed that the changes in ScO 2 were influenced by the different elements of systemic hemodynamics and oxygen transport measurements to different degrees. The close and positive correlation between ScO 2 and SaO 2 may be expected because of the intrinsic arterial contribution to the NIRS signals. An arterial contribution of 16% ± 21% to the NIRS signals has been reported by Watzman and associates29Go in a group of children with congenital heart disease of varied arterial oxygen saturations. The explanation for the close positive correlation with PaO 2 may be less clear-cut. Arterial hypoxemia is known to increase cerebral blood flow when PaO 2 is reduced to less than 30 to 50 mm Hg in models of acute hypoxemia.30Go This regulation may be impaired in subjects exposed to chronic hypoxemia31Go and further compounded by anesthesia and hypothermic CPB. This may be the case in our patient population. Although speculative, with the loss of such compensation mechanism, a decrease in PaO 2 may lead to a direct decrease in cerebral DO 2. Arterial oxygenation has little impact on Qp and Qp/Qs and little contribution to systemic DO 2.20Go It does, however, appear to have significant impact on cerebral DO 2. Therefore, limiting arterial oxygenation as a means of favorably balancing the parallel circulations may be suboptimal, but may have an unnecessary detrimental impact on the brain. Indeed, the judicious use of inspired oxygen may be beneficial to cerebral oxygenation and metabolism without compromising systemic circulation. ScO 2 was positively correlated with hemoglobin in these neonates. A positive correlation has been found between ScO 2 and hemoglobin during mild-to-moderate hemodilution32,33Go and is further supported in our data in subjects with relatively high levels of hemoglobin.

The intercorrelations of ScO 2, systemic arterial pressure, SVR, and Qs are also important to note for these neonates. ScO 2 was significantly and positively correlated with systolic, diastolic, and mean arterial pressures. This may indicate impaired cerebrovascular autoregulation or a pressure-passive cerebral circulation after CPB.34,35Go The low diastolic pressure in the presence of a Blalock–Taussig shunt may further render the brain vulnerable to hypoperfusion or hypoxic insult. Loss of cerebrovascular autoregulation and low diastolic arterial pressure have previously been shown to be risk factors for the occurrence of severe periventricular leukomalacia in premature infants34Go and in neonates after cardiac surgery.16Go Interestingly, the close and positive interrelationships between ScO 2 and arterial pressure and, in turn, between arterial pressure and SVR did not necessarily lead to positive correlation between ScO 2 and SVR. In fact, ScO 2 was negatively and significantly correlated with SVR. This is largely due to the negative correlation between SVR and Qs and DO 2; Qs and DO 2 were significantly and positively correlated with ScO 2.

It is our routine management of these neonates to use phenoxybenzamine and milrinone to sustain a relatively low SVR and to maintain an adequate Qs and DO 2.25,36Go The current study shows that this approach may also be beneficial to improve cerebral oxygenation. Furthermore, phenoxybenzamine can cross the blood–brain barrier and may have a direct and important effect on reducing cerebral vascular resistance.37Go Phenoxybenzamine may also contribute to maintaining cerebral blood flow during hypotension induced by bleeding38Go and enhance cerebrovascular response to carbon dioxide.39Go These properties of phenoxybenzamine are appealing in the care of neonates after the Norwood operation, in whom the goal is to optimize both systemic and cerebral oxygen transport. Further studies are necessary to quantify the potential effect of redistribution of blood flow between cerebral and systemic vascular beds caused by this and other medications.

The lack of correlation between ScO 2 and VO 2 is likely due to the deep sedation used to minimize cerebral VO2. Nonetheless, the improvement in ScO 2 was most pronounced when VO 2 was most rapidly decreased. As we have demonstrated, VO 2 is the most important contributor to the improvement in the balance of oxygen transport during the early hours after the Norwood procedure.22Go The close and negative correlation between ScO 2 and ERO 2 indicates the important influence of the balance of systemic oxygen transport on cerebral oxygenation during the early postoperative period after the Norwood procedure. Strategies to limit VO 2 may therefore improve overall oxygen balance and may be particularly relevant to neonates after the Norwood procedure, in whom DO 2 is tenuous.

Of note, whereas the low ScO 2 during the first 24 hours was associated with depressed systemic hemodynamics and impaired balance of oxygen transport, the influence of the systemic hemodynamics and oxygen transport variables on ScO 2 was of equal significance between the period of the first 24 hours and the following 48 hours. This may indicate that cerebral oxygen transport is vulnerable to systemic hemodynamic and oxygen transport fluctuations during the early days after the Norwood procedure.


   Limitations
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 Limitations
Conclusions
 References
 
The superior vena cava was used to measure systemic venous saturation for the calculations of Qs and DO 2. This measure does not account for potential differences in the inferior vena cava saturation.40Go Conversely, it could be argued that by sampling upper body venous saturation, we have a more representative measurement, incorporating cerebral blood flow.

NIRS was used to estimate cerebral oxygenation in our study. As mentioned earlier, NIRS measures oxygen saturation in the mixture of arteries, capillaries, and veins in a small part of underlining cerebral tissue and thus may not precisely reflect overall balance of cerebral oxygen transport. The value of the critically low ScO 2 was derived from subjects with biventricular circulation26-28Go and may not be generalizable to subjects with single ventricle and parallel circulations. Further assessments of cerebral oxygen and lactate extractions with a jugular bulb venous probe may be more precise to reflect cerebral oxygen transport. This, in combination with electroencephalography and cerebral magnetic resonance imaging, will provide further information about the influence of postoperative hemodynamics and oxygen transport on cerebral oxygen transport, ischemic injuries, and functional outcomes in this high-risk group of neonates.


   Conclusions
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 Limitations
 Conclusions
References
 
ScO 2 decreases significantly in neonates during the early postoperative period after the Norwood procedure. A critically low level of ScO 2 occurs frequently and is significantly influenced by the systemic hemodynamic instability and the imbalance of systemic oxygen transport. Interventions to optimize hemodynamic stability and to achieve an adequate balance of oxygen transport, including maintaining a low SVR and adequate Qs and DO 2, a relatively high hemoglobin, and in addition, judicious use of high inspired oxygen, may provide further opportunities to reduce the risk of cerebral ischemic injury and improve neurodevelopmental outcomes. Future studies correlating systemic hemodynamics and oxygen transport and cerebral oxygen transport to functional neurologic outcome may yield important insights of neurologic injury.


   Footnotes
 
This work was supported by the Heart and Stroke Foundation of Canada and the Canadian Institute of Health Research (J.L., A.M.G., A.N.R., and G.S.V.).


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 Limitations
 Conclusions
 References
 

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