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Ann Thorac Surg 2007;84:1301-1311
© 2007 The Society of Thoracic Surgeons
a Herma Heart Center and Children’s Research Institute, Children’s Hospital of Wisconsin, Milwaukee, Wisconsin
b Division of Cardiothoracic Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin
c Department of Surgery, The Section of Critical Care, Medical College of Wisconsin, Milwaukee, Wisconsin
d Department of Cardiology, Medical College of Wisconsin, Milwaukee, Wisconsin
e Department of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin
f Department of Anesthesia, Medical College of Wisconsin, Milwaukee, Wisconsin
Accepted for publication May 1, 2007.
* Address correspondence to Dr Tweddell, Children’s Hospital of Wisconsin, 9000 W. Wisconsin Ave, Milwaukee, WI 53226 (Email: jtweddell{at}chw.org).
Presented at the Forty-third Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Jan 29–31, 2007.
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Abstract |
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 Top Abstract IntroductionPatients and MethodsResultsCommentDiscussionReferences |
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Methods: Since July 1996, we have performed stage 1 palliation (S1P) in 178 patients. Within this group is a consecutive cohort of 116 patients with true hypoplastic left heart syndrome that underwent S1P with a modified Blalock-Taussig shunt. A prospective database containing postoperative hemodynamic data was maintained on all patients. Studied were the incidence of organ failure, extracorporeal membrane oxygenation (ECMO), and mortality, as well as the relationship between these outcomes and postoperative hemodynamics.
Results: Hospital survival for this cohort was 93% (108/116). Patients who died after S1P had a lower superior vena cava oxygen saturation (SvO 2) level compared with survivors (53.1% ±10.6% versus 59.3% ±9.2%, p = 0.034). Renal failure developed in 2 (1.7%) of the 116 patients, necrotizing enterocolitis developed in 1 (0.9%), and 5 (4.3%) had clinical seizures. ECMO support was instituted in 12 patients (10.3%). The SvO 2 level was lower in patients requiring ECMO (54.0% ± 9.7% versus 59.9% ± 9.2%, p = 0.031).
Conclusions: Goal-directed therapy with SvO 2 as an indicator of systemic oxygen delivery is associated with excellent early survival and a low incidence of organ failure after S1P. Inability to optimize SvO 2 in the early postoperative period is associated with an increased risk of organ failure, ECMO, and death.
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Introduction |
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TopAbstractIntroductionPatients and MethodsResultsCommentDiscussionReferences |
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Historically, monitoring during this period has included physical exam, blood pressure, heart rate, central venous pressure (CVP), and measurement of systemic arterial oxygen saturation (SaO 2) using pulse oximetry. We hypothesized that objective measurement of systemic oxygen delivery would permit better management of the patient during this vulnerable period after the Norwood procedure. For the last 10 years we have used continuous venous oximetry from the superior vena cava (SvO 2) as an objective assessment of systemic oxygen delivery and as a means to guide management. This study reviews our experience using SvO 2 monitoring to manage this complex group of patients.
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Patients and Methods |
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TopAbstractIntroductionPatients and MethodsResultsCommentDiscussionReferences |
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The focus of this review is 116 of the 178 patients with HLHS as defined by International Working Group for Mapping and Coding of Nomenclatures for Paediatric and Congenital Heart Disease, the Nomenclature Working Group, who underwent S1P with a modified Blalock-Taussig shunt [2]. The study excluded 37 patients who underwent S1P for hypoplastic left heart variants, specifically single-ventricle anatomy with systemic outflow obstruction with arch obstruction such as single left ventricle with transposed great vessels, unbalanced atrioventricular canal, and double-outlet right ventricle with mitral atresia. Also excluded were 25 patients who met the definition of HLHS but underwent S1P with a right ventricle–to–pulmonary artery conduit. The aim was to isolate a cohort with a uniform diagnosis undergoing a standardized operation.
Operative Technique and Postoperative Management
The operative technique and postoperative management have been previously described in detail [1, 3–5]. High-dose aprotinin was used in all patients and 110 received phenoxybenzamine. Cardiopulmonary bypass (CPB) strategies for arch reconstruction included predominately deep hypothermic circulatory arrest (DHCA) in 54 patients and continuous cerebral perfusion in 62. In general, arch reconstruction included a coarctectomy and augmentation of the arch and ascending aorta using pulmonary homograft. Shunt sizing was based on the patient’s weight and age. Patients who weighed less than 3.2 kg generally received a 3.0-mm shunt, and those heavier than 3.2 kg received a 3.5-mm shunt. For patients who presented after 2 weeks of life, a larger shunt was used. Modified ultrafiltration and delayed sternal closure were routine.
Monitoring and Data Collection
Standardized postoperative monitoring for this cohort included heart rate, continuous invasive arterial blood pressure, central venous pressure (CVP), SaO
2, SvO
2, and end-tidal carbon dioxide. Postoperative management targets of SaO
2 exceeding 75%, SvO
2 exceeding 50%, mean arterial blood pressure (MAP) exceeding 45 mm Hg, diastolic blood pressure exceeding 30 mm Hg, and hematocrit exceeding 45% were achieved by titration of vasoactive drugs, red cell transfusion, analgesia, sedation, and controlled ventilation.
This study was approved by the Children’s Hospital of Wisconsin Human Research Review Board and was conducted in accordance with all human research regulatory requirements. Informed written consent was obtained from the parents of the most recent 110 patients reported in this study for prospective data collection of hemodynamic and outcome data after surgery for HLHS. The first 6 patients in this study had prospective collection of hemodynamic data in 1996 before human studies approval was generally required for reporting of anonymous data. The Children’s Hospital of Wisconsin Human Research Review Board approved the inclusion of these 6 additional patients and waived the need for parental consent.
For all patients, recording of SvO
2, SaO
2, MAP, heart rate, CVP, and inspired oxygen fraction (FIO
2) are made upon arrival in the intensive care unit and hourly for 48 hours. Additional data collected during the first 48 postoperative hours include hemoglobin level, arterial partial pressure of carbon dioxide (PaCO
2), arterial partial pressure of oxygen (PaO
2), and inotropic support. Derived variables include pulmonary-to-systemic flow ratio (Qp/Qs), arterial-venous oxygen content difference (
AVO
2), the indices for systemic (SVRI) and pulmonary vascular resistance (PVRI), assuming an oxygen consumption of 160 mL/(m2
· min), and ventilation index [ventilator rate x (peak inspiratory pressure – end expiratory pressure) x PaCO
2/1000]. Demographics, preoperative support, intraoperative support, shunt size, and outcome data were available for all patients.
The impact of a variety of factors (Appendix) on outcome end points was determined. International Classification of Diseases, 9th revision (ICD-9), diagnostic and procedural coding for all patients at time of discharge after S1P was reviewed for death and evidence of postoperative complications. Complications were categorized by organ system and are summarized in Table 1. Validity of diagnosis and procedure coding was confirmed by a review of all medical records. One of three end points was assigned to each patient: uncomplicated survival, survival with complications (as defined in Table 1), or early death (mortality within 30 days of S1P or within the primary S1P hospitalization).
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2 and the likelihood ratio test were used for categoric variables. Adjustment for multiple comparisons was performed using the Tukey honestly significant difference method with a significance cutoff at p < 0.05. Multivariable analysis was performed to determine factors related to outcome using stepwise ordered logistic regression with a threshold for rejection at p > 0.2 and cutoff for significance at p < 0.05. Actuarial survival analysis was performed using Kaplan-Meier methods. Data are reported as mean ± standard deviation for continuous variables and count with percentage for categoric variables. Time series regression techniques were used to derive time-weighted mean values. Median values are included where appropriate. |
Results |
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TopAbstractIntroductionPatients and MethodsResultsCommentDiscussionReferences |
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Figure 1 outlines the surgical progress and outcomes for these patients. There were eight (6.9%) early deaths. Mean time to death after S1P was 30.4 ± 13 days (range, 10 to 50 days), and the mean age at death was 37.6 ± 17 days (range, 15 to 68 days). Seven of the 8 patients who died had significant postoperative complications, and 3 had multiple complications. Causes of early death included cardiac failure in 6, shunt obstruction in 1, and sudden death at home while feeding in 1 patient on day 29 of life.
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Follow-up was complete on 100% of patients to a mean age of 57.1 ± 37.2 months (median, 59.8 months; range, 0.5 to 126.5 months). Actuarial survival for this cohort of 116 patients is 80% at 5 years and is shown in Figure 2.
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Between 1997 and 2000, 5 patients were cannulated for cardiac failure independent of shunt occlusion, 3 of whom required cardiopulmonary resuscitation (CPR) just before cannulation. Two patients with evidence of low cardiac output syndrome were cannulated without CPR. Three of the 5 patients were decannulated but died of progressive cardiogenic shock 7, 14, and 16 days later. Two of the 5 patients had support withdrawn while on ECMO owing to persistent multiorgan failure.
Between 1998 and 2005, 5 patients were supported with ECMO due to acute shunt occlusion, of which 3 received CPR before cannulation, and 4 survived S1P. Overall S1P mortality for patients placed on ECMO was 50%, and all ECMO survivors have undergone successful completion Fontan.
CPR was required in 12 patients (10.3%) during S1P hospitalization: 4 as a result of acute shunt occlusion, 1 after a respiratory arrest, and 7 for cardiac failure. Five of the 7 patients who received CPR for cardiac failure are included in the group who went on to ECMO before 2000. Two additional patients had CPR and were not placed on ECMO: 1 as a result of a hyperkalemic arrest and 1 for cardiac tamponade. Six (50%) of the 12 patients who received CPR survived S1P; 4 had completion Fontan and 2 underwent cardiac transplantation.
Most of the postoperative complications were within the circulatory system. Additional complications included renal failure requiring dialysis in 2 patients (1.7%), renal insufficiency necessitating treatment for oliguria with hyperkalemia in 2 (2.5%), necrotizing enterocolitis in 1 (0.9%), and clinical seizures in 5 (4.3%). One patient with seizures had a documented embolic stroke. These results are summarized in Table 1.
The results of univariate analysis are summarized in Table 3. Complications were associated with longer duration of intraoperative cardiopulmonary support, wider AVO
2, lower MAP, lower pH, and lower base deficit. A borderline association was found between complications and higher Qp/Qs. Mortality was associated with a lower SvO
2, higher hemoglobin level, and wider AVO
2. There was a borderline association between the use of a higher FIO
2 and mortality.
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AVO
2 (5.5 ± 1.7 mL/dL versus 4.5 ± 1.6 mL/dL, p = 0.014). Use of ECMO was associated with a lower SvO
2 (54.0% ± 9.7% versus 59.9% ± 9.2%, p = 0.031) and wider AVO
2 (5.5 ± 1.8 mL/dL versus 4.4 ± 1.5 mL/dL, p = 0.014). Patients who died after S1P had a lower SvO
2 (53.1% ± 10.6% versus 59.3% ± 9.2%, p = 0.034) and wider AVO
2 (5.4 ± 1.8 mL/dL versus 4.4 ± 1.7 mL/dL, p = 0.035). The risk of outcome end points at incremental ranges of SvO 2 is illustrated in Figure 5. The SvO 2 was inversely related to the risk of any complication, CPR, ECMO at any time, and early and late death. Table 5 summarizes the relative risk of ECMO, CPR, and mortality rate for patients with an SvO 2 that was more or less than 55%, the 25th percentile for average 48 hour postoperative SvO 2. An SvO 2 of less than 55% was associated with the need for ECMO during the first 48 postoperative hours, the use of any ECMO during S1P hospitalization, CPR, and early death.
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Comment |
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TopAbstractIntroductionPatients and MethodsResultsCommentDiscussionReferences |
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Monitoring during this period has historically included blood pressure, heart rate, CVP, and measurement of systemic arterial oxygen saturation using pulse oximetry. Clinical assessment of perfusion is used despite data suggesting that clinical assessment of cardiac output, even by trained clinicians, is often inaccurate [6]. Objective measurement of systemic oxygen delivery would permit better management of the patient during this vulnerable period after the Norwood procedure. For the last 10 years, we have used venous oximetry as an objective assessment of systemic oxygen delivery and to guide management.
The goal of postoperative management is to achieve oxygen delivery adequate to meet the metabolic demands of the tissues and enable healing. Physical examination is limited in its ability to accurately assess cardiac output, despite defining precise areas within the physical examination such as pulse amplitude, extremity temperature, and capillary refill [6–8]. Serial measurements of lactate have been used as a guide for the postoperative management of patients with HLHS. Decreasing lactate level was associated with an uncomplicated postoperative course and a rising level was shown to predict the need for ECMO [9]. Unfavorable changes in lactate would indicate that a period of oxygen delivery-dependent oxygen consumption is already in effect. Therefore, measurement of lactate does not predict a period of anaerobic metabolism but rather demonstrates that anaerobic metabolism is already in place. Assumptions concerning cardiac output based on the commonly measured parameters of arterial saturation and blood pressure are inaccurate [10, 11].
The mixed venous blood is a summary of the last blood in contact with the tissues at the capillary level and can be used as a guide to the tissue oxygen economy. Superior vena cava saturation is a close approximation of mixed venous saturation and has been validated as a target for intervention that will result in improved outcome. In a study to look at the impact of SvO 2 monitoring and shock, Rivers and colleagues [12] randomized patients to receive conventional monitoring (CVP, blood pressure, and urine output) or early goal-directed therapy that included SvO 2 monitoring. They showed a reduction in organ failure as well as early and late mortality in those patients in whom real-time oxygen delivery was assessed objectively and used in treatment.
Intermittent sampling of the superior vena cava blood has been used to assist with postoperative management of patients undergoing palliation for HLHS. Rossi and colleagues [13] used intermittent SVC blood samples to measure venous saturation and calculate both Qp/Qs and AVO
2. Survivors showed a gradual increase in venous saturation and a gradual decline in Qp/Qs during the first 24 hours. They noted that Qp/Qs could be elevated even in patients with an acceptable arterial saturation [13].
We reported the use of continuous superior vena cava saturation monitoring using a 4F oximetric catheter. Of importance was that we identified abrupt decreases in SvO 2, indicating a sudden decrease in systemic oxygen delivery that could not be identified by monitoring SaO 2, MAP, heart rate, or CVP. These sudden decreases in SvO 2 were mirrored by subtle increases in MAP and SaO 2 and represent acute increases in SVR. These observations led us to incorporate phenoxybenzamine into our routine management for patients undergoing SIP. In that study we demonstrated that continuous SvO 2 could identify patients with decreasing systemic oxygen delivery and that interventions could restore the venous saturation to an acceptable range [1].
In subsequent work we showed that subsets of patients with HLHS who have been considered high risk had decreased SvO 2 in the early postoperative period, suggesting that the increased risk was partly due to lower systemic oxygen delivery [14]. Although that study included a small number of patients, the low mortality suggested that careful attention to systemic oxygen delivery by use of continuous SvO 2 monitoring could improve the outcome of high-risk subtypes of HLHS. In an analysis of a broad group of HLHS and variants, we found that use of continuous SvO 2 favored survival of patients undergoing S1P [4]. Further work from our group showed an inverse correlation between SvO 2 and the development of metabolic acidosis.
Although we have targeted an SvO 2 of 50%, we failed to achieve this target in many patients, especially in the early postoperative period. Analysis of the relationship between SvO 2 and increasing metabolic acidosis revealed an anaerobic threshold when SvO 2 fell towards 30% [15]. The current study suggests that targeting an even higher threshold for SvO 2, in the 55% to 60% range, is optimal to achieve the lowest risk of death and complications.
Li and colleagues [11] have shown that oxygen consumption is highly variable in the postoperative patient and that improvement in the postoperative oxygen economy can be achieved through strategies that limit oxygen consumption, such as control of hyperthermia and sedation. Fundamental management of patients after S1P now includes not only the usual strategies of optimizing rhythm, rate, preload, and contractility but also the routine use of sustained afterload reduction, a FIO 2 high enough to prevent pulmonary venous desaturation, red cell transfusion to maximize oxygen carrying capacity, and efforts to minimize oxygen consumption [3, 16, 17]. Continuous monitoring of oxygen economy has allowed the identification of shock states and has provided a real-time guide to the efficacy of intervention.
In this group of patients with the most agreed upon anatomic definition of HLHS, SvO 2 was shown to identify those at risk for mortality and complications. The early mortality in this group was 7% and compares favorably with any contemporary series. Commonly measured hemodynamic parameters such as blood pressure were not predictive of outcome. Other commonly cited risk factors such as the presence of additional diagnoses, aortic atresia versus aortic stenosis, low birth weight, and prematurity were not identified as risk factors for mortality [18, 19]. In this series, no patient with low birth weight, prematurity, or additional extracardiac diagnosis died. These findings suggest that SvO 2 monitoring may have ameliorated the impact of these commonly identified risk factors for death.
The incidence of CPR and ECMO was similar to other recent series of patients undergoing S1P of HLHS. The need for CPR and ECMO as rescue therapy for cardiac failure has been eliminated since the year 2000 and reflects an increasing reliance on SvO 2 to guide management of low cardiac output syndrome. It is important to note that SvO 2 monitoring has not eliminated the need for CPR or ECMO due to acute shunt occlusion.
The incidence of noncardiac complications was low in this series. There was a single incident of stroke in this cohort. Clinically evident seizures occurred in 5 patients (4.3%), which compares favorably with the 18% incidence of seizures reported by Clancy and colleagues [20]. Our own experience relating SvO 2 with late neurodevelopment outcome indicates that the potential for neurologic injury is inversely related to SvO 2 [21].
The incidence of renal failure was low in this series, with only 2 patients (1.7%) requiring dialysis. Three patients (2.5%) had renal insufficiency, defined as oliguria with hyperkalemia, requiring therapy. This incidence of renal failure compares favorably with the incidence of renal failure in other series of patients with congenital heart disease, including those with less severe forms [22, 23].
Our series was unique for a very low incidence of gastrointestinal complications. Only 1 patient in our series had necrotizing enterocolitis, and this patient did not require surgical intervention. A higher incidence of gastrointestinal complications has been reported by other experienced centers. McElhinney and colleagues [24] reported a 7.6% incidence of necrotizing enterocolitis in patients with HLHS, and Jeffries and colleagues [25] reported an 18% incidence. There is no dispute that decreased cardiac output is a risk factor for both renal insufficiency and necrotizing enterocolitis.
Continuous SvO 2 monitoring has shortcomings. It is invasive, with potential complications of bleeding and vessel thrombosis. We have had one episode of bleeding requiring reexploration but no episodes of thrombosis. To minimize the risk of thrombosis, we avoid placing any additional catheters in the superior vena cava.
In cases of anomalous pulmonary venous drainage to the superior vena cava, saturations will not reflect the tissue oxygen economy. In cases of distributive shock, venous saturations may appear satisfactory but oxygen delivery may be maldistributed at the tissue level. Continuous SvO 2 monitoring is of little additional benefit to conventional monitoring in identifying shunt thrombosis. The abrupt decrease in arterial saturation and change in the shunt murmur are generally diagnostic.
Likewise, lethal arrhythmias are seen in the postoperative Norwood patient and can be diagnosed by continuous electrocardiograph monitoring and hypotension. Nonetheless, if a prodrome of decreased cardiac output preceded the lethal arrhythmias, SvO 2 monitoring may identify patients at risk.
Mixed venous saturation monitoring may be relatively insensitive to significant regional hypoperfusion, which can occur during early shock states, for which gastric tonometry or near infrared spectroscopy may provide better information.
All of the patients in this study had SvO
2 monitoring, and no control group was used to prove the efficacy of SvO
2 monitoring. We did not quantify our ability to increase a low SvO
2. We used assumed values for both pulmonary venous saturation and oxygen consumption. We rarely used a FIO
2 of less than 30%, and therefore, it is unlikely that pulmonary venous desaturation complicated our calculations. Although it has been shown that oxygen consumption can vary greatly in the early postoperative period, the major findings of this study are related to SvO
2 and AVO
2 and therefore did not require any assumptions.
A large proportion of the data in this study were prospectively collected; however, data concerning many of the complications were retrospectively collected. The complications selected were those used by other authors and were fairly easy to identify by electronic database review methods. It would unlikely to miss any patients who required dialysis or needed an operation for necrotizing enterocolitis.
Goal-directed therapy with SvO 2 as an indicator of systemic oxygen delivery is associated with excellent early survival and a low incidence of organ failure in infants after S1P for HLHS. Inability to optimize SvO 2 in the early postoperative period is associated with an increased risk of organ failure, ECMO, and death.
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Appendix |
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Discussion |
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TopAbstractIntroductionPatients and MethodsResultsCommentDiscussionReferences |
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You and I have talked about this before about the role of near-infrared spectroscopy, which I guess one could view as a complimentary modality to SvO 2. Do you think that using the NIRS technology would ever replace putting a catheter in the SVC, or would you think that it would just be something where you would continue to do both?
DR TWEDDELL: Near-infrared spectroscopy is an excellent adjunct to SvO 2 monitoring. It is a terrific trend monitor.
In addition, near infrared spectroscopy permits identification of changes in regional perfusion. We place one probe on the forehead and one probe on the back at around the L2 level. In this way, we can monitor changes in the relative distribution of cardiac output to the cerebral and splanchnic circulations.
I think you need to combine NIRS monitoring with venous saturation monitoring. Will it eventually take over? I think that is possible. Certainly it would be nice to have a noninvasive device and something you could use more long term as well.
DR JACOBS: But right now you still put the SVC catheter in all the stage 1s?
DR TWEDDELL: Yes.
DR CARL L. BACKER (Chicago, IL): Jim, that is a great series, and I really think you may be changing the standard of care for postoperative follow-up after the Norwood operation. I have heard Nancy Ghanayem, one of your coauthors, talk about this, and she made the statement, and I think I heard her correctly, that she would prefer to have the NIRS monitoring than an arterial line. Do you agree with that or is she "out on a limb"?
DR TWEDDELL: The NIRS monitoring does provide some very useful information. It is best as a trend monitor, and we use it more and more. If we have any concerns about a patient, we will place the probes on the patient and get an idea of what is going on.
Some of the changes that occur as a result of abrupt events are pretty dramatic and are picked up by NIRS instantaneously. It is a powerful tool. Exactly how it is going to be used and so on is a little difficult to predict right now.
To answer your question, I want the A-line, I want the SvO2 monitor, I want the whole thing because the more objective data you are able to gather, the less likely you are to be fooled. If we had all the information, we’d all be more likely to make the same correct decisions in a more timely manner and we would all achieve the best possible outcomes.
DR BACKER: The other question I have is given all this data, I mean, your reliance on the SvO 2, when you see that it is not coming up or is going down, are you now, in the last quartile of your study going to ECMO much sooner than you were earlier in the series?
Also, what is going through your mind when this happens? What kind of changes are you making when you see that SvO 2 going down into the basement?
DR TWEDDELL: That is an excellent question. In addition to our studies, we paid a lot of attention to some of the terrific work that Dr Li has done in Toronto and the work that was done in Cincinnati by Taeed and colleagues. In addition to the usual measures of optimizing rate, rhythm, filling pressures, inotropy, afterload reduction is absolutely essential. It doesn’t have to be phenoxybenzamine, but you should be using something such as milrinone to control the SVR.
You want to use an FIO 2 that will prevent pulmonary venous desaturation, ventilating a very low FIO 2 is a mistake.
You want to augment the oxygen carrying capacity by increasing the hematocrit. We push the hematocrit up to at least 45% in the uncomplicated patient, and in the sicker patient, an hematocrit over 50% may be necessary.
You need to reduce oxygen consumption if you can. You want to avoid hyperthermia, use sedation and paralysis to decrease oxygen consumption, and try to match oxygen delivery and consumption.
But if all that doesn’t work, you should go on ECMO. I would prefer to go on ECMO before chest compressions are initiated to limit neurologic injury.
DR BACKER: One final question. What about stress dose steroids? Are you giving that to some of the neonates? All of the neonates? Just the ones that have a low SvO 2?
DR TWEDDELL: We give preoperative steroid Solu-Medrol to everybody, and we give Solu-Medrol at midnight and 6 AM the day before surgery.
DR BACKER: But what about post-op?
DR TWEDDELL: On a per-patient basis.
Just one more point about the low SvO 2, George Hoffman published a paper about a year ago looking at late neurodevelopmental outcome and relating it to this perioperative database, and one of his findings was that a low SvO 2 in the early postoperative period, not surprisingly, predicted a poor neurodevelopmental outcome. So that may be another reason as Ross Ungerleider has suggested to use postcardiotomy support not simply to prevent mortality but to limit neurologic morbidity.
DR BACKER: It’s a great contribution.
DR CHRISTOPHER A. CALDARONE (Toronto, Ontario, Canada): Jim, just one question. We can’t challenge your results, of course, but can we challenge one of your conclusions today?
About 10% of your patients were on ECMO. Your program is well known for having a very standardized approach to patient management. If threshold SvO 2 is used to trigger putting a patient on ECMO, then is it fair to make the conclusion that low SvO 2 is associated with complications because you said ECMO is listed as one of your complications, as an end point of a complication. It is kind of self-fulfilling if low SvO 2s result in ECMO, then it is going to look like low SvO 2 results in the basket term of complications which includes ECMO.
So my question is, if you took ECMO out of the analysis as an end point as a complication, does low SvO 2 predict all those other complications that you saw?
DR TWEDDELL: We tried to pick complications that were related to low output.
I understand your point, but I think ECMO is a marker for inadequate cardiac output certainly.
DR MUHAMMAD A. MUMTAZ (Cleveland, OH): Just a very brief question. I may have missed that on your slides, but when the SvO 2 was where you desired it to be, about 45, how often did you have complications? I mean, is that a time when you can just go home and sleep and say things are nice?
DR TWEDDELL: We didn’t present the data here, but it is in the manuscript—we dichotomized at about 55% to see how that did with predicting outcome, and it certainly predicted the use of ECMO/CPR and mortality.
But if you really wanted to avoid complications, have complication-free survival, you needed a higher SvO 2, really greater than 60%. So it suggests that at least at the tissue oxygen economy level, the single-ventricle patient may not have any more tolerance for low output and a decreased oxygen delivery than any other baby. Thank you.
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This article has been cited by other articles:
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  H. M. Phelps, W. T. Mahle, D. Kim, J. M. Simsic, P. M. Kirshbom, K. R. Kanter, and K. O. Maher Postoperative cerebral oxygenation in hypoplastic left heart syndrome after the Norwood procedure. Ann. Thorac. Surg., May 1, 2009; 87(5): 1490 - 1494. [Abstract] [Full Text] [PDF]
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B. A. Johnson, G. M. Hoffman, J. S. Tweddell, J. R. Cava, M. Basir, M. E. Mitchell, M. C. Scanlon, K. A. Mussatto, and N. S. Ghanayem Near-infrared spectroscopy in neonates before palliation of hypoplastic left heart syndrome. Ann. Thorac. Surg., February 1, 2009; 87(2): 571 - 579. [Abstract] [Full Text] [PDF]
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