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Ann Thorac Surg 2000;70:1515-1520
© 2000 The Society of Thoracic Surgeons

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Original articles: cardiovascular

Venous saturation and the anaerobic threshold in neonates after the Norwood procedure for hypoplastic left heart syndrome

^a Department of Anesthesiology, Children’s Hospital of Wisconsin and Medical College of Wisconsin, Milwaukee, Wisconsin, USA
^b Department of Pediatric Critical Care Medicine, Children’s Hospital of Wisconsin and Medical College of Wisconsin, Milwaukee, Wisconsin, USA
^c Department of Pediatric Cardiology, Children’s Hospital of Wisconsin and Medical College of Wisconsin, Milwaukee, Wisconsin, USA
^d Department of Cardiovascular Surgery, Children’s Hospital of Wisconsin and Medical College of Wisconsin, Milwaukee, Wisconsin, USA

Address reprint requests to Dr Hoffman, Department of Pediatric Anesthesiology and Critical Care Medicine, Children’s Hospital of Wisconsin #735, 9000 West Wisconsin Ave, Milwaukee, WI 53226
e-mail: ghoffman{at}mcw.edu

Presented at the Thirty-sixth Annual Meeting of The Society of Thoracic Surgeons, Fort Lauderdale, FL, Jan 31–Feb 2, 2000.

	Abstract

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Background. Reduction in oxygen delivery can lead to organ dysfunction and death by cellular hypoxia, detectable by progressive (mixed) venous oxyhemoglobin desaturation until extraction is limited at the anaerobic threshold. We sought to determine the critical level of venous oxygen saturation to maintain aerobic metabolism in neonates after the Norwood procedure (NP) for the hypoplastic left heart syndrome (HLHS).

Methods. A prospective perioperative database was maintained for demographic, hemodynamic, and laboratory data. Invasive arterial and atrial pressures, arterial saturation, oximetric superior vena cava (SVC) saturation, and end-tidal CO₂ were continuously recorded and logged hourly for the first 48 postoperative hours. Arterial and venous blood gases and cooximetry were obtained at clinically appropriate intervals. SVC saturation was used as an approximation of mixed venous saturation (SvO₂). A standard base excess (BE) less than -4 mEq/L (BElo), or a change exceeding -2 mEq/L/h (BElo), were used as indicators of anaerobic metabolism. The relationship between SvO₂ and BE was tested by analysis of variance and covariance for repeated measures; the binomial risk of BElo or BElo at SvO₂ strata was tested by the likelihood ratio test and logistic regression, with cutoff at p < 0.05.

Results. Complete data were available in 48 of 51 consecutive patients undergoing NP yielding 2,074 valid separate determinations. BE was strongly related to SvO₂ (model R² = 0.40, p < 0.0001) with minimal change after adjustment for physiologic covariates. The risk of anaerobic metabolism was 4.8% overall, but rose to 29% when SvO₂ was 30% or below (p < 0.0001). Survival was 100% at 1 week and 94% at hospital discharge.

Conclusions. Analysis of acid-base changes revealed an apparent anaerobic threshold when SvO₂ fell below 30%. Clinical management to maintain SvO₂ above this threshold yielded low mortality.

	Introduction

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Perioperative management of neonates after surgical repair of congenital cardiac defects is directed at optimization of oxygen delivery to maintain end-organ function and promote wound healing. Increased metabolic demands related to extent of surgery and compromised cardiorespiratory function increase the risk of perioperative morbidity and mortality. Patients with hypoplastic left heart syndrome (HLHS) have high perioperative risk because of the intersection of those risk factors. These patients historically have high rates of cardiogenic shock, impaired oxygen delivery, end-organ dysfunction, and death, even after palliation of their circulatory defect by the Norwood procedure (NP) [1, 2]. Examination of oxygen transport and metabolism in this patient population is thus likely to reveal examples of both oxygen supply-independent (aerobic) and oxygen supply-dependent (anaerobic) metabolism. Because our perioperative management strategy uses continuous arterial (SaO₂) and venous (SvO₂) oximetry to assess circulatory physiology [3, 4], we sought to determine the SvO₂ threshold for anaerobic metabolism in this high-risk patient population.

	Material and methods

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Patient population and management strategy
Patients undergoing the NP for single-ventricle defects were eligible for inclusion in this study. After appropriate preoperative stabilization, all patients underwent surgical palliation consisting of relief of arch obstruction, anastomosis of the pulmonary artery to the ascending aorta combined with augmentation of the ascending aorta, transverse arch and proximal descending aorta with pulmonary homograft, placement of a systemic to pulmonary artery shunt, and creation of a nonrestrictive atrial septal defect [4]. This procedure was performed using synthetic opioid-based perioperative anesthesia [5], hypothermic cardiopulmonary bypass (CPB) with pH-stat blood gas management to facilitate cooling to a temperature of 26°C, alpha-stat management before and after circulatory arrest at 16°C to 18°C, and modified ultrafiltration. Phenoxybenzamine 0.25 mg/kg was administered to 43 of 51 infants upon initiation of cardiopulmonary bypass (CPB) according to a protocol with Food and Drug Administration and Internal Review Board approval and parental informed consent. During rewarming, all patients received milrinone 50 µg/kg followed by infusions of milrinone at 0.5 µg/kg/min and dopamine at 3 µg/kg/min. Oximetric catheters (4F OxyCath; Abbott Laboratories, North Chicago, IL) were placed in the superior vena cava (SVC) to allow continuous monitoring of SvO₂. Before separation from CPB, infusions of nitroprusside or norepinephrine were titrated to achieve an approximate systemic vascular resistance (SVR) of 12 Wood Units (mean arterial pressure of 40 mm Hg at CPB flow index of 3.2 L/m²/min), and epinephrine was added for additional inotropic support if necessary. Patients were transported to the pediatric intensive care unit (ICU) after hemostasis for postoperative management, which included delayed sternal closure.

Postoperative management targets included mean arterial blood pressure (MABP) greater than 45 mm Hg, SvO₂ greater than 50%, SaO₂ 70% to 80%, and clinical evidence of end-organ function. All patients received continuous fentanyl infusions at 5 to 10 µg/kg/h, and neuromuscular blockade was maintained by vecuronium infusion until postoperative day 1. Patients were maintained at normothermia in servo-controlled infant warmers (Ohio Infant Warmer System; Ohmeda Inc, Columbia, MD). Ventilator settings were adjusted to maintain arterial normocapnia (PaCO₂ 35 to 45 torr) with the lowest FiO₂ that did not reduce SaO₂ or SvO₂. Pulmonary-to-systemic flow ratio (Qp/Qs) was calculated from SaO₂ and SvO₂ using an assumed pulmonary capillary saturation of 97% [1, 3, 4]. Low SvO₂ with high Qp/Qs was addressed by attempts to lower SVR with additional analgesia or sedation, nitroprusside, or initiation of phenoxybenzamine infusion. Low SvO₂ with balanced Qp/Qs was addressed by transfusion of red cells to achieve a hematocrit in the 45% to 50% range, and increased inotropic support when necessary.

Arterial blood gases were obtained hourly for the first 4 postoperative hours, and then at intervals dependent upon patient condition. The standard base excess, calculated without temperature correction, was used to identify metabolic acidosis. Persistent or worsening metabolic acidosis not explainable by electrolyte abnormalities was interpreted as evidence of systemic hypoperfusion [6], and interventions to increase systemic oxygen delivery were initiated. Treatment with buffer (NaHCO₃ 1 mEq/kg) was reserved for worsening metabolic acidosis after interventions to optimize circulation, and was administered in 11 instances. Circulatory support with extracorporeal membrane oxygenation (ECMO) was initiated in 1 patient with persistent metabolic acidosis and profound venous desaturation at the seventh postoperative hour.

Monitoring and data collection
A prospective perioperative database for all patients undergoing the Norwood repair of HLHS since July 1996 was maintained for demographic, surgical, and 48-hour postoperative hemodynamic and laboratory data. Physiologic parameters included invasive arterial (MABP) and atrial pressures (RAP), arterial saturation (N-200; Nellcor, Haywood, CA), inspired oxygen and end-tidal carbon dioxide tension, and SvO₂ as an approximation of mixed venous saturation [7, 8]. These parameters were continuously displayed, digitally acquired, and averaged using either a dedicated PC-based monitoring cart (DAP-102; Microstar Labs, Belleview, WA; and DasyLab; DasyTec GmBH, Concord, NH) or a multichannel clinical information system (Solar 3000; Marquette Electronics, Milwaukee, WI). Arterial and venous blood gases and cooximetry (ABL; Radiometer, Copenhagen, Denmark) were obtained at clinically appropriate intervals. The physiologic parameters, laboratory data, ventilator parameters, and medication infusion rates were recorded hourly for the first 48 postoperative hours using a standardized, prospective format.

From measurements of SaO₂, SvO₂, MABP, RAP, and hemoglobin concentration, hemodynamic and oxygen transport indices were derived according to standard formulae, assuming pulmonary capillary saturation of 97% and oxygen consumption of 160 mL/min/m² [1, 3, 4, 9]. These derived parameters included arteriovenous O₂ difference in saturation (Sa-vO₂) and content (Ca-vO₂), oxygen extraction ratio (O₂ER), pulmonary blood flow (Qp), systemic blood flow (Qs), pulmonary/systemic flow ratio (Qp/Qs), systemic vascular resistance index (SVRI), and total pulmonary vascular resistance index (PVRI).

Statistical analysis
Data were summarized as mean ± standard deviation (SD) when continuous, or number and percent when discrete, unless otherwise specified. Blood gas data were subjected to linear interpolation between determinations, and excluded from analysis if coincident with buffer administration. Oximetric data were excluded when the arterial venous saturation difference was less than 8%, or during ECMO support. Anaerobic conditions were defined by a standard base excess (BE) less than -4 mEq/L (BElo), or a change exceeding -2 mEq/L/h (BElo) [6, 10–12]. Differences in physiologic data between anaerobic and aerobic conditions were tested by one-way analysis of variance (ANOVA), and z scores for these statistics at anaerobic conditions were computed. After creation of equal-width strata from continuous variables, relationships were tested by quantile (median) regression, categorical ANOVA with post-hoc contrasts by the Tukey WSD method, and the likelihood ratio test for proportions. Anaerobic risk across the range of SvO₂ was predicted by logistic regression. Risk estimates were calculated with and without adjustment for covariates that had univariate relation to anaerobic indicators. All statistical calculations were performed with correction for repeated measures, and with significance cutoff at p < 0.05 after correction for multiple comparisons, using a standard statistical package (Stata Statistical Software, Release 6; StataCorp, College Station, TX).

	Results

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Data from 51 consecutive patients undergoing the NP were available for analysis. Patient characteristics are summarized in Table 1. Of these patients, 48 had functioning oximetric catheters upon ICU admission, and catheter faults occurred in 45 of 2,304 (1.95%) hours of monitoring. The SvO₂ was below the target of 50% for 643 of 2,259 (28%) monitored hours; the hourly risk of low SvO₂ was 38% during postoperative hours 1 to 24, and 19% during hours 25 to 48. These periods of physiologic vulnerability were successfully managed by medical intervention in all but 1 patient whose progressive venous desaturation and metabolic acidosis prompted initiation of ECMO support at postoperative hour 7. Survival was 100% at 1 week and 94% to hospital discharge.

A summary of hemodynamic, respiratory, acid-base, and support modalities appears in Table 2. Physiologic parameters with greater changes at anaerobic conditions are indicated by high z scores and significance tests by ANOVA. No significant differences in SaO₂, SVRI, PVRI, PaO₂, or PaCO₂ occurred with anaerobic conditions. The highest anaerobic z score (-0.71) occurred for SvO₂.

View larger version (17K): [in this window] [in a new window]   Fig 1. SvO2 at BE strata. The strong positive relationship between SvO2 and BE, as mean and 95% CI for SvO2 by strata of standard base excess. Relationship is indicated by test for trend (p < 0.001). Clusters are evident with significant differences, indicated by horizontal lines, at SvO2 < 50%, SvO2 50% to 54%, and SvO2 > 54% (adjusted model R2 = 0.30, p < 0.001).

View larger version (15K): [in this window] [in a new window]   Fig 2. Anaerobic Risk by SvO2 strata. The risk of anaerobic conditions at different SvO2, expressed as binomial risk and 95% CI of anaerobic indicators versus strata of SvO2. The overall anaerobic risk of 4.8% is indicated by the horizontal line. The risk increases sharply and significantly at SvO2 < 30% (*p < 0.0001 by likelihood ratio test; model adjusted R2 = 0.40, p < 0.0001).

View larger version (17K): [in this window] [in a new window]   Fig 3. Prediction of anaerobic risk from SvO2. Predicted anaerobic risk and 95% CI by logistic regression from SvO2 over range 20% to 70%, after adjustment for covariates. The 95% CI exceeds the baseline 4.8% risk, indicated by the horizontal line, as SvO2 approaches 30% (model R2 = 0.28; p < 0.0001).

	Comment

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

The concept of anaerobic threshold implies alteration of cellular metabolism from oxygen supply limitation, usually associated with metabolic acidosis and increased lactate production [13, 14]. Although we did not routinely measure lactate in this study, the appearance of lactate, pyruvate, or other strong acids as products of anaerobic metabolism will reduce the base excess stoichiometrically [6, 10, 11, 15]. The fall in BE may exceed the rise in lactate because of the production of other anions under anaerobic conditions [6, 12]. Similarly, the BE may fall during splanchnic hypoperfusion from the failure of hepatic and renal clearance of anions [16] which are substrates for intermediary metabolism without increased production of lactate. Conversely, in experimental cardiogenic shock, the rise in lactate in venous blood may indicate reperfusion after critical hypoperfusion [17, 18]. Thus, the presence or development of a significant metabolic acidosis (BElo or BElo) in a patient population with an overall increasing metabolic alkalosis (mean BE 3.8 mEq/L; mean BE + 0.1 mEq/L/h) will indicate a significantly altered metabolic state as a result of critical organ hypoperfusion.

Some physiologic variables included in this analysis have been derived using assumptions that must be emphasized. In this patient population, no single blood sample can represent mixed venous blood. Although inferior vena cava sampling should be more sensitive to splanchnic hypoperfusion [19], repeated measurements are more variable because of blood streaming. Assumed values for VO₂ and pulmonary venous saturation may characterize the study population more accurately than individuals within it. Despite these limitations, these parameters are commonly used to characterize pulmonary and systemic hemodynamics [1–3, 7, 8, 20, 21].

Direct treatment of metabolic acidosis with buffer, although infrequent, was more likely to occur in patients with acid-base abnormalities that would fit our definition of anaerobic conditions. The relationship between SvO₂ and anaerobic indicators was actually stronger without exclusion of these data points, because our correction of metabolic acidosis was rarely complete. However, we chose to exclude them because such treatment altered the relationship under study.

SvO₂ monitoring can reveal deterioration in oxygen transport and guide treatment before supply–dependent conditions develop [14]. Other investigations have revealed an apparent anaerobic threshold at a SvO₂ of 15% to 25% in neonatal piglets subject to hypoxic hypoxia, and higher in anemic hypoxia [10, 22–24]. The relationship between oxygen transport and utilization is probably less predictable in distributive shock [25], and 2 patients in our series did have persistent biochemical evidence of anaerobic metabolism at high SvO₂, but maldistribution is not the predominant pathophysiologic mechanism in the early postoperative course in this patient population. Examination of Table 2 reveals that the predominant hemodynamic abnormality in our patients was low total cardiac output (more precisely, low oxygen supply/demand relationship) with relatively balanced Qp/Qs. SvO₂ monitoring can reveal changes in oxygen supply/demand relationships even under supply-dependent conditions [24], and our data support its use in prediction of pathologic cellular oxygen status in this patient population.

Low SvO₂ can predict poor outcome of patients after myocardial infarction [26], adult cardiac surgery [27], and NP for HLHS [1]. Interventions to increase low SvO₂ can improve outcome [4, 28, 29]. Knowledge of an approximate value for critical SvO₂ can guide thresholds for intervention that target either SvO₂ itself or derived parameters such as available oxygen [20, 21] before pathologic oxygen supply conditions develop.

Our management target of SvO₂ greater than 50% yielded low mortality and revealed a period of physiologic risk in the first 24 postoperative hours for both low SvO₂ and biochemical indication of anaerobic metabolism. The adjusted odds ratio for anaerobic metabolism was 8.0 for SvO₂ less than 30% compared with higher SvO₂. Because this threshold was not apparent by examination of the relationship of SaO₂ or MABP to anaerobic indicators, we have concluded that SvO₂ monitoring is essential to guide management strategies that avoid the risk of cellular hypoxia and resultant mortality after the NP for HLHS.

	Acknowledgments

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
This work was supported in part by the Children’s Hospital Foundation, Milwaukee, WI, and the Medical College of Wisconsin Departments of Anesthesiology and Surgery. We acknowledge the support of the nurses, physicians, technicians, and therapists in the intensive care units and operating rooms at Children’s Hospital, without whose help this study would not have been completed.

	References

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 

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