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(Circulation. 2001;103:2699.)
© 2001 American Heart Association, Inc.

Clinical Investigation and Reports

Unrecognized Pulmonary Venous Desaturation Early After Norwood Palliation Confounds p:s Assessment and Compromises Oxygen Delivery

Roozbeh Taeed, MD; Steven M. Schwartz, MD; Jeffrey M. Pearl, MD; Jenni L. Raake, RRT; Robert H. Beekman, III, MD; Peter B. Manning, MD; David P. Nelson, MD, PhD

From the Divisions of Cardiology and Cardiothoracic Surgery, The Heart Center, Children’s Hospital Medical Center, Cincinnati, Ohio.

Correspondence to David P. Nelson, MD, PhD, Division of Pediatric Cardiology, Children’s Hospital Medical Center, 3333 Burnet Ave, OSB-4, Cincinnati, OH 45229-3039. E-mail davenelson{at}chmcc.org

	Abstract

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Background—Hemodynamic stability after Norwood palliation often requires manipulation of pulmonary vascular resistance to alter the pulmonary-to-systemic blood flow ratio (p:s). p:s is often estimated from arterial saturation (SaO₂), a practice based on 2 untested assumptions: constant systemic arteriovenous O₂ difference and normal pulmonary venous saturation.

Methods and Results—In 12 patients early (3 days) after Norwood palliation, simultaneous arterial, superior vena caval (SsvcO₂), and pulmonary venous (SpvO₂) oximetry was used to test whether SaO₂ accurately predicts p:s. Stepwise multiple regression assessed the contributions of SaO₂, SsvcO₂, and SpvO₂ to p:s determination. SaO₂ correlated weakly with p:s (R²=0.08, P<0.05). Inclusion of SsvcO₂ and SpvO₂ improved p:s prediction accuracy. Pulmonary venous desaturation (SpvO₂ <95%) was observed frequently (30%), especially at FiO₂ 0.21, but normalized with higher FiO₂ or PEEP in all patients. In 6 patients, FiO₂ was increased incrementally from 0.17 to 0.50 to determine whether this was an effective means to manipulate p:s. p:s failed to change predictably with increased FiO₂. In 5 of 6 patients, however, higher SpvO₂ and SaO₂ enhanced systemic oxygen delivery, as demonstrated by improvement in oxygen extraction.

Conclusions—SaO₂ correlated poorly with p:s because of variability in SsvcO₂ and SpvO₂. A novel observation was that pulmonary venous desaturation occurred frequently early after Norwood palliation but normalized with higher FiO₂ or PEEP. Because unrecognized pulmonary venous desaturation confounds p:s assessment and compromises SaO₂ and oxygen delivery, judicious use of inspired oxygen and PEEP may be beneficial in selected patients early after Norwood palliation.

Key Words: heart defects, congenital • lung • surgery • hypoplastic left heart syndrome • Norwood operation

	Introduction

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Hemodynamic stability in the early postoperative period after Norwood palliation for hypoplastic left heart syndrome is largely dependent on maintaining a balance between pulmonary blood flow (p) and systemic blood flow (s).¹ Ventilation strategies that alter pulmonary vascular resistance are routinely used to manipulate the ratio of p to s (p:s).^{1 2} Estimation of the p:s ratio is thus vitally important for accurate assessment of an unstable hemodynamic state and to determine the effects of interventions designed to alter the p:s. It has long been accepted that arterial oxygen saturation (SaO₂) is reflective of p:s after the Norwood operation.²

The assertion that p:s can be estimated from SaO₂ alone in single-ventricle physiology is based on a simplification of the Fick equation that is not well founded. Because p is supplied by a systemic-to–pulmonary artery shunt, pulmonary and systemic arterial oxygen saturations are equivalent, so that p:s can be calculated as p:s=(SaO₂-SmvO₂)/(SpvO₂-SaO₂), where mv is mixed-venous and pv pulmonary venous. This equation has been further simplified on the basis of 2 untested assumptions: (1) that systemic arteriovenous oxygen saturation difference (A-V O₂) is constant (commonly assumed to be 25), and (2) that the pulmonary venous (PV) blood is fully oxygen saturated (ie, SpvO₂95%).¹ These assumptions yield the simplified equation: p:s=25/(95-SaO₂). This equation has been used to estimate p:s from SaO₂ alone.

The ability to determine p:s from SaO₂ is highly desirable, given the ease with which SaO₂ can be obtained in clinical practice. The assumptions that underlie this simplified Fick equation may be false, however, in the immediate postoperative Norwood period. A-V O₂ will be significantly greater than 25 if systemic blood flow is low, a common occurrence in the postoperative period. Rossi and colleagues^{3 4} reported the importance of monitoring superior vena cava (SVC) oxygen saturation (SsvcO₂) after Norwood palliation as a means of assessing s. The assumption that PV blood is fully saturated has never been tested in the postoperative Norwood circulation; however, it is a potentially dangerous assumption, given the routine use of minimal inspired oxygen (even subambient oxygen) and controlled hypercarbia in postoperative management of these infants. Failure to account for a decrease in SpvO₂ will result in an important underestimation of p:s based on SaO₂ alone. If reduced levels of inspired oxygen result in PV desaturation without a significant decrease in p:s, the associated decrease in SaO₂ may be detrimental to overall systemic oxygen delivery.

The purpose of this study was to use simultaneous oximetry of arterial, SVC, and PV blood to test the hypothesis that SaO₂ alone is an accurate predictor of p:s in the early postoperative Norwood circulation. We thus hoped to evaluate the validity of common assumptions regarding A-V O₂ and SpvO₂ in postoperative Norwood patients. A second aim was to determine whether changes in fraction inspired oxygen (FiO₂) are an effective means to alter p:s.

	Methods

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Patient Enrollment
Infants with single-ventricle anatomy and aortic arch obstruction undergoing stage I Norwood palliation with functional SVC and PV catheters were eligible for inclusion. These catheters are routinely placed intraoperatively during the Norwood procedure at our institution. Exclusion criteria included weight <2 kg, clinical or radiographic evidence of pulmonary disease, or the inability to draw samples from SVC or PV catheters. The study was approved by the Institutional Review Board of Children’s Hospital Medical Center, and informed consent was obtained from a parent or legal guardian before the study.

Intraoperative Procedure
A narcotic anesthetic was used for optimal myocardial function. After sternotomy and bypass initiation, dissection was completed during cooling. An atrial septectomy was performed via atriotomy, the aortic arch was reconstructed with a homograft patch,^{2 5} and the pulmonary artery bifurcation was closed primarily. Retrograde cardioplegia was administered during circulatory arrest. A Gore-tex shunt was placed during rewarming. Intracardiac catheters were inserted by the transatrial approach and the tips directed into the SVC and left lower pulmonary vein under direct visualization.

Postoperative Management
Patients were returned to the Cardiac Intensive Care Unit with open sternotomy on a fentanyl infusion and neuromuscular blockade. Postoperative monitoring included atrial and systemic arterial pressures, ECG, pulse oximetry, and end-tidal CO₂. Patients were ventilated with volume control ventilation at a tidal volume of 20 mL/kg and positive end-expiratory pressure (PEEP) of 4 cm H₂O. The ventilator rate was adjusted to control PaCO₂. Inotropic support and volume were administered as needed. Diuretic therapy was initiated routinely on the first morning after surgery.

SaO₂, SpvO₂, SsvcO₂, and p:s
Simultaneous oximetry of arterial, SVC, and PV blood was performed as clinically indicated in all patients with functional SVC and PV catheters. Because there is no site to sample true mixed-venous blood in patients with single-ventricle physiology, blood sampled from the SVC line was considered the mixed-venous sample. It was also assumed that samples from the left lower pulmonary vein were representative of overall PV blood. To reduce potential erroneous sampling of atrial blood, the SVC and PV lines were cleared, and samples were drawn slowly with 1-mL syringes (unit protocol). True p:s was determined as (CaO₂-CsvcO₂)/(CpvO₂-CaO₂), where CaO₂ is arterial oxygen content (1.36xHgbxSaO₂), CsvcO₂ is mixed-venous oxygen content (1.36xHgbxSsvcO₂), and CpvO₂ is PV oxygen content (1.36xHgbxSpvO₂+0.003xPpvO₂). Hemoglobin was determined oximetrically for each data set. Estimated p:s was determined from SaO₂ alone by the formula 25/(95-SaO₂). A-V O₂ was determined as CaO₂-CsvcO₂, and the oxygen extraction ratio was determined as (CaO₂-CsvcO₂)/CaO₂, where CaO₂ and CsvcO₂ represent arterial and mixed-venous oxygen content, respectively.

FiO₂ Effects on p:s
To determine whether changes in FiO₂ are an effective means to alter true p:s, data were collected in a subset of patients as FiO₂ was systematically manipulated. Patients were studied 48 to 72 hours after surgery, when gas exchange and hemodynamics were steady state, usually just before sternal closure. Chest radiograph confirmed the correct position of intracardiac catheters and absence of pulmonary parenchymal changes. No manipulations in inotropic support or minute ventilation were made during the changes in FiO₂. After administration of fentanyl (10 µg/kg) and vecuronium (0.1 mg/kg) and endotracheal tube suctioning, baseline oximetric data (SaO₂, SsvcO₂, and SpvO₂) were obtained at an FiO₂ of 0.21. Hemodynamic and oximetric data were subsequently collected as FiO₂ was adjusted incrementally to 0.17, 0.21, 0.30, and 0.50. Hemoglobin was measured for each oximetric data set. After each change in FiO₂, patients were allowed 10 minutes for equilibration before oximetric data were collected.

Oximetric data were analyzed to determine the effects of changes in FiO₂ on p:s. As surrogates of systemic oxygen delivery, alterations in A-V O₂ and the oxygen extraction ratio were examined.

Data Analysis and Statistical Methods
Data were analyzed with Statview software (Abacus Concepts). For the purpose of correlating SaO₂ with true p:s, all measurements were assumed to be independent, and stepwise linear multiple regression was used to determine the contributions of SaO₂, SsvcO₂, and SpvO₂ to the determination of p:s. Data are presented as mean±SD. Statistical significance was defined as a value of P<0.05.

	Results

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From April 1997 to December 1998, 20 patients underwent Norwood palliation at Children’s Hospital Medical Center. Twelve patients were included in this study. Of the remaining 8 patients, there was 1 intraoperative death, 1 patient weighed <2 kg, and another patient developed Gram-negative sepsis/pneumonia. In 5 patients, the PV or SVC catheter was not placed successfully or could not be used for sampling, including 1 patient who was excluded because of atrial contamination of PV blood, as evidenced by SpvO₂ data that closely approximated the SaO₂. Oximetric data from the 12 study patients were used to test the assumptions underlying the simplified Fick equation, and in 6 of these patients, FiO₂ was systematically altered to determine the effect of FiO₂ on p:s. One patient was not studied at subambient oxygen (FiO₂=0.17) because of significant PV desaturation during baseline room air ventilation.

Patient characteristics are summarized in the Table. The median age at the time of surgery was 7 days (range 3 to 45 days). The median weight was 3.23 kg (range 2.2 to 4.1 kg). During the study period, 14 of 20 neonates (70%) were discharged home and subsequently returned for successful bidirectional Glenn anastomosis. Of the 12 infants included in the study, 2 infants died in the early postoperative period and 1 died 2 months after the Norwood procedure of persistent hepatic failure. All nonsurviving infants demonstrated marked pulmonary overcirculation, demonstrating the highest maximum p:s measurements recorded. Excessive pulmonary blood flow in these patients was associated with clinically important PV desaturation. PV desaturation (SpvO₂<95%) was observed in 11 of 12 patients but normalized with higher FiO₂ or PEEP in all patients.

View this table: [in this window] [in a new window]   Table 1. Patient Characteristics

Prediction of p:s From SaO₂
A total of 115 complete, simultaneous sets of oximetric data (SaO₂, SsvcO₂, and SpvO₂) were available for analysis. True p:s calculated from simultaneous oximetry data ranged from 0.45 to 5.43 and correlated poorly with SaO₂ (R²=0.08,P<0.05). There is a particularly poor correlation between true p:s and SaO₂ at arterial saturations of 65% to 85%, where one might expect a "balanced" circulation on the basis of the usual clinical assumptions (Figure 1).

View larger version (18K): [in this window] [in a new window]   Figure 1. Regression analysis of SaO2 against true p:s. SaO2 is a poor predictor of p:s (R2=0.08, P<0.05). Variability in p:s is most pronounced at SaO2 values in range of 65% to 85%, usual target range for patients after Norwood palliation.

Stepwise linear regression using SaO₂, SsvcO₂, and SpvO₂ to predict p:s showed significant improvement in ability to estimate p:s with inclusion of each additional variable. SaO₂ alone accounted for only 8% of the variation in p:s (R²=0.08), a remarkably low finding. Addition of SsvcO₂ increased this to 56%, and the PV component accounted for the remaining variability in p:s.

Systemic A-V O₂
The mean A-V O₂ in the 115 samples was 30±11% (95% CI 8% to 52%). There was wide intrapatient and interpatient variability, with a range of 9% to 50%. Variation in SsvcO₂ contributed most significantly to alterations in systemic A-V O₂. Consistent with the observations of previous investigators,³ our data indicate that variability in the systemic A-V O₂ confounds bedside assessment of p:s from SaO₂ alone.

PV Desaturation Is Common in the Early Postoperative Period After Norwood Palliation
Measured SpvO₂ ranged from 76% to 100%, and PV desaturation (defined as SpvO₂ <95%) was observed in 35 of the samples (30%). SpvO₂ was <90% in 17 of the 115 samples (15%). All but 1 patient had 1 desaturated PV sample, and 8 of 9 samples taken during administration of subambient oxygen were <95%. Although PV desaturation was observed more frequently at lower FiO₂, it was also observed in 5 samples at FiO₂ of 0.30 (Figure 2). Desaturation of PV blood occurred without evidence of pulmonary edema, atelectasis, or infiltrates or catheter migration on repeated chest radiographs.

View larger version (19K): [in this window] [in a new window]   Figure 2. SpvO2 plotted as a function of FiO2 demonstrates that PV desaturation was observed relatively frequently. Desaturation of PV blood (SpvO2 <95%, points below dashed line) was observed in 35 of 115 samples (30%) without clinical or radiographic evidence of pulmonary edema or infiltrates. Although PV desaturation was most often observed at FiO2 0.21, it was also observed occasionally at higher FiO2.

To verify that these were true PV samples and not samples contaminated with atrial blood, an effort was made to normalize SpvO₂ in all patients who exhibited PV desaturation. By use of a combination of increased FiO₂ and PEEP, SpvO₂ was raised to 95% in all patients, and PpvO₂ was >200 mm Hg in all patients studied at an FiO₂ of 0.50. The minimum and maximum SpvO₂ values for each individual patient are displayed in the Table, and the interventions used to normalize SpvO₂ are noted.

FiO₂ and p:s
As FiO₂ was increased, SaO₂ increased in all patients (Figure 3, top). The corresponding PV blood, which was desaturated in 5 of 6 patients at 0.17 FiO₂, became fully saturated as FiO₂ was increased (Figure 3, second panel). Somewhat surprisingly, no significant relationship between FiO₂ and p:s was observed with systematic manipulation of FiO₂ (Figure 3, middle panel). As FiO₂ was increased from 0.17 to 0.50, only 1 patient ( symbols) demonstrated a clinically important increase in p:s with apparent reduction in systemic O₂ delivery (increased A-V O₂, decreased O₂ extraction ratio). Although the systemic-pulmonary shunt in this patient (patient 1, Table) was not excessively large, it is relevant that this patient had the highest p:s on subambient oxygen of all patients studied, suggesting excessive baseline pulmonary blood flow. In the remaining 5 patients, systematic increases in FiO₂ failed to cause a corresponding change in p:s. In these patients, changes in p:s and A-V O₂ with FiO₂ were minimal, but a reduced O₂ extraction ratio in these patients suggested more luxuriant systemic O₂ delivery (Figure 3, lower 3 panels). Improvement in SpvO₂ at higher FiO₂ helped to enhance oxygen delivery, demonstrating the importance of fully saturated PV blood to help optimize SaO₂ and systemic oxygen delivery. These data support the supposition that decreases in pulmonary vascular resistance may have minimal effect on p:s in patients in whom the aortopulmonary shunt limits pulmonary blood flow mechanically.

View larger version (18K): [in this window] [in a new window]   Figure 3. Effect of FiO2 on SaO2 and SpvO2, p:s, A-V O2, and O2 extraction ratio. Shown are data sets from 6 patients collected during systematic manipulation of FiO2. Data symbols represent same patient consistently in all panels. As FiO2 was increased, SaO2 increased in all patients. Corresponding PV blood, which was desaturated (<95%) in 5 of 6 patients at 0.17 FiO2, became fully saturated as FiO2 was increased. Although changes in p:s and A-V O2 with FiO2 were unpredictable, O2 extraction decreased in all but 1 patient, suggesting improvement in systemic O2 delivery. One patient observed to have an important increase in p:s also demonstrated a corresponding increase in A-V O2 and decrease in O2 extraction, indicating a reduction in O2 delivery.

	Discussion

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The fragile early postoperative course after Norwood palliation is exquisitely sensitive to the balance of systemic and pulmonary blood flow.^{1 2 6 7} Bedside estimation of p:s from SaO₂ alone has been advocated on the basis of 2 untested assumptions: constant systemic A-V O₂ and normal SpvO₂ (95%). This study demonstrates that SaO₂ is a poor predictor of p:s after Norwood palliation; SaO₂ alone predicted only 8% of the variability in p:s. Inaccuracy in p:s estimation was caused by variability in both SmvO₂ and SpvO₂, thus challenging the dual assumptions used by clinicians for rapid bedside assessment of p:s.

Although others have demonstrated variability in SmvO₂ after Norwood palliation,^{3 8} this is the first study to demonstrate that PV desaturation is also common. PV desaturation was observed in 30% of PV samples even though there was no evidence of pulmonary edema, atelectasis, or infiltrates on chest radiograph. The data thus suggest that postoperative Norwood patients may have pulmonary gas exchange abnormalities resulting from cardiopulmonary bypass, circulatory arrest, and the extensive surgical procedure. Furthermore, ventilatory maneuvers used to manipulate pulmonary vascular resistance in these patients (ie, controlled hypoventilation, low FiO₂) may predispose patients to microatelectasis and ventilation-perfusion mismatch.

The presence of unrecognized PV desaturation may contribute to substantial errors in p:s estimated from SaO₂ alone. The data indicate that p:s is underestimated at higher levels of true p:s, when it is most clinically relevant (Figure 4A). Our observations (Figure 4B) provide clinical evidence to substantiate the computer modeling predictions of Barnea and colleagues.^{6 7} If PV blood is assumed to be fully saturated (95%), the error in p:s estimation can be substantial if true SpvO₂ falls below 95%. p:s is underestimated by 20% to 25% when SpvO₂ is 90%, and the underestimation error is as large as 30% to 70% if SpvO₂ falls below 90%. The data also suggest that the frequency and degree of PV desaturation may be intensified by use of reduced levels of FiO₂ (Figures 2 and 3), as commonly used in the perioperative management of single-ventricle patients. Reduced or subambient FiO₂ can lower SaO₂ by decreasing SpvO₂ without a concomitant decrease in p:s. The resultant decrease in systemic oxygen delivery may not be recognized, because the patient is assumed to be "better" on the basis of the decrease in SaO₂.

View larger version (15K): [in this window] [in a new window]   Figure 4. A, Plot of true p:s against estimated p:s demonstrating errors in p:s estimation resulting from false assumptions that SpvO2 95% and A-V O2 is 25%. B, Lower panel graphically demonstrates effect of unrecognized PV desaturation on this p:s estimation error. Error in p:s estimate was calculated as (true p:s-estimated p:s)/true p:s and plotted against measured SpvO2. If PV blood is assumed to be fully saturated (95%), error in p:s estimation increases progressively as measured SpvO2 falls below 95%. For example, p:s is underestimated by 20% to 25% when SpvO2 is 90%. As measured SpvO2 falls below 90%, error in p:s estimation was as high as 70%.

The observation that high FiO₂ and/or a mild respiratory alkalosis after Norwood palliation may not result in significant hemodynamic instability is supported by the work of Mosca and colleagues.⁹ Our data support the conjecture that p:s may be insensitive to manipulations in pulmonary vascular resistance when the systemic-to-pulmonary shunt limits pulmonary blood flow mechanically. As FiO₂ was systematically increased, we did not observe consistent changes in p:s, and the oxygen extraction ratio improved in 5 of 6 patients (Figure 3). These findings support the judicious use of higher PEEP and/or FiO₂ in select patients after Norwood palliation. In a similar manner, it may not be beneficial to aggressively induce respiratory acidosis in all postoperative Norwood patients, because controlled hypoventilation may predispose patients to microatelectasis and ventilation-perfusion mismatch. Because clinical recognition of PV desaturation is difficult in the absence of a pulmonary vein catheter, the consequences of any ventilatory maneuvers must be assessed cautiously by determining their effect on SaO₂ and SmvO₂ and global end-organ perfusion.

The conclusions of this study are contingent on accurate sampling of PV blood. To verify that atrial contamination of PV samples was minimal, an effort was made to normalize SpvO₂ in all patients exhibiting PV desaturation. With a combination of increased FiO₂ and PEEP, SpvO₂ was raised to 96% in all patients, and the PV PO₂ was >200 mm Hg in all patients studied at an FiO₂ of 0.50 (Table). The substantial improvements in PV PO₂ with increases in FiO₂ and/or PEEP indicate minimal atrial contamination of PV samples. Another limitation of the study is the assumption that SVC and PV samples reflect SmvO₂ and mixed SpvO₂, respectively. Although these assumptions are commonly used during catheterization of single-ventricle patients, they may be inaccurate. Finally, we would caution that the findings should not be generalized too broadly. These data represent only a small sample of postoperative Norwood patients, and the observations reported are specifically relevant to the early postoperative period. The data should be interpreted carefully and should not be applied broadly to all single-ventricle patients. Low-level or subambient inspired oxygen is presumably not detrimental for patients with preoperative single-ventricle physiology and healthy lungs in whom pulmonary blood flow is limited by pulmonary vascular resistance alone. We do not advocate use of high FiO₂ in single-ventricle patients with obvious pulmonary overcirculation, especially those with preoperative single-ventricle physiology. Similarly, unnecessarily high PEEP in single-ventricle patients may reduce venous return and thus be detrimental to overall cardiac output.

In summary, this study demonstrates that systemic SaO₂ alone is a poor predictor of p:s in the early postoperative period after Norwood palliation. Because inaccuracy in p:s estimation resulted from variability in both SsvcO₂ and SpvO₂, the data challenge the dual assumptions used by clinicians for rapid bedside assessment of p:s. The novel observation that PV desaturation is common in the early postoperative period after Norwood palliation raises the possibility that undetected pulmonary gas exchange defects may adversely affect systemic oxygen delivery in some patients after Norwood palliation. Because unrecognized PV desaturation confounds p:s assessment and compromises SaO₂ and oxygen delivery, judicious use of inspired oxygen and PEEP in the early postoperative period after Norwood palliation may be beneficial in selected patients.

	Acknowledgments

 
This study was supported by The Children’s Heart Association of Cincinnati.

Received February 15, 2001; revision received March 21, 2001; accepted March 26, 2001.

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