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The levels of selected neuroregulatory proteins that inhibit or promote apoptotic cell death were measured in the striatum of piglets subjected to precisely controlled 1 h hypoxic insult followed by 0, 2 and 4 h recovery and compared to sham operated animals. The anti-apoptotic proteins: there were increases in Survivin at 0 (157%, P = 0.031) and 4 h (171%, P = 0.033), in Bcl-XL at 0 (138%, P = 0.028) and 4 h (143%, P = 0.007), in VEGF at 4 h (185%, P = 0.019) and Hsp27 at 2 h (144%, P = 0.05) and 4 h (143%, P = 0.05). The pro-apoptotic proteins: caspases-1 and 7 increased at 4 h (135%, P = 0.05) and (129%, P = 0.038), respectively. Bim increased after 4 h (115%, P = 0.028), Apoptosis Inducing Factor after 2 h (127%, P = 0.048) and Calpain after 4 h (143% of control, P = 0.04). Hypoxia causes increase in levels of both anti- and pro-apoptotic proteins. Their relative activity determines the outcome in terms of cell damage and neuronal deficit.

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Responses of selected neuroregulatory proteins that promote (Caspase 3 and Bax) or inhibit (Bcl-2, high Bcl-2/Bax ratio) apoptotic cell death were measured in the brain of piglets subjected to precisely controlled hypoxic and ischemic insults: 1 h hypoxia (decreasing FiO2 from 21 to 6%) or ischemia (ligation of carotid arteries and hemorrhage), followed by 0, 2 and 4 h recovery with 21% FiO2. Protein expression was measured in cortex, hippocampus and striatum by Western blot. There were no significant differences in expression of Caspase-3 between sham operated, hypoxic and ischemic groups. There were significant regional differences in expression of Bcl-2 and Bax in response to hypoxia and ischemia. The changes in Bcl-2/Bax ratio were similar for hypoxia and ischemia except for striatum at zero time recovery, with ischemia giving lower ratios than hypoxia. The Bcl-2/Bax ratio was also lower for the striatum than for the other regions of the brain, suggesting this region is the more susceptible to apoptotic injury.

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BACKGROUND: The objective of this study was to determine whether serum lactate levels predict mortality in children less than 1 year of age who have undergone cardiopulmonary bypass and operations for complex congenital heart disease. METHODS: The initial lactate, maximum lactate, and lactate levels at 4 to 6 hours after operation were analyzed for each of 48 children less than 12 months of age who underwent cardiopulmonary bypass. RESULTS: Data were analyzed for the 6 patients who died and the 42 patients who survived. For the patients who died, the initial postoperative serum lactate, maximum lactate, and 4- to 6-hour lactate levels were significantly higher than those in the patients who survived. All patients with an initial lactate less than 7 mmol/L, a maximum lactate less than 9 mmol/L, or a 4- to 6-hour lactate level less than 4 mmol/L survived to hospital discharge. CONCLUSIONS: Serum lactate levels may be a useful predictor of mortality in children less than 1 year of age who have undergone cardiopulmonary bypass. An elevation in serum lactate level after a complex operation for congenital heart disease should be taken as a serious indicator of potential mortality.

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OBJECTIVE: Following the use of deep hypothermic circulatory arrest in cardiac surgery, cerebral blood flow and cerebral oxygen metabolism are impaired. These may result from abnormal cerebral vasospasm. Powerful vasoconstrictors including endothelins and thromboxane A2 could mediate these processes. We investigated possible involvement of these two factors by assessing the effects of (a) phosphoramidon-an inhibitor of endothelin converting enzyme, and (b) vapiprost (GR32191B)-a specific thromboxane A2-receptor antagonist, on the recovery of cerebral blood flow and cerebral oxygen metabolism following deep hypothermic circulatory arrest. METHODS: A total of 18 1-week-old piglets were randomised into three groups (n = 6 per group). At induction, the control group received saline; group PHOS received phosphoramidon 30 mg kg-1 intravenously. Group VAP received vapiprost 2 mg kg-1 at induction and at 30 min intervals thereafter. All groups underwent cardiopulmonary bypass cooling to 18 degrees C, exposed to 60 min of deep hypothermic circulatory arrest, rewarmed and reperfused for 1 h. Cerebral blood flow was measured with radio-labeled microspheres: cerebral oxygen metabolism was calculated at baseline before deep hypothermic circulatory arrest and at 1 h of reperfusion and rewarming. RESULTS: In the control group, cerebral blood flow decreased to 40.2 +/- 2.0% of baseline after deep hypothermic circulatory arrest and cerebral oxygen metabolism decreased to 50.0 +/- 5.5% (P < 0.0005). The responses in group PHOS were similar. In group VAP, cerebral blood flow and cerebral oxygen metabolism were 64.3 +/- 10.6 and 80.1 +/- 9.8% of baseline, respectively, after deep hypothermic circulatory arrest. Thus, treatment with vapiprost significantly improved recovery of cerebral blood flow (P = 0.046) and cerebral oxygen metabolism (P = 0.020) following deep hypothermic circulatory arrest. No such improvement was seen after treatment with phosphoramidon. CONCLUSIONS: Thromboxane A2 mediates impairments in cerebral perfusion and metabolism following deep hypothermic circulatory arrest. These changes were attenuated by blockade of thromboxane A2-receptors using vapiprost. Endothelins are not shown to be involved. Better knowledge of injury mechanisms will enable development of more effective cerebral protection strategies and allow safer application of deep hypothermic circulatory arrest.

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BACKGROUND: For many congenital heart defects, hospital mortality is no longer a sensitive parameter by which to measure outcome. Although hospital survival rates are now excellent for a wide variety of lesions, many patients require expensive and extensive hospital-based services during the perioperative period to enable their convalescence. These services can substantially increase the cost of care delivery. In today's managed care environment, it would be useful if risk factors for higher cost could be identified preoperatively so that appropriate resources could be made available for the care of these patients. The focus of this retrospective investigation is to determine if risk factors for high cost for repair of congenital heart defects can be identified. METHODS: We assessed financial risk by tracking actual hospital costs (not charges) for 144 patients undergoing repair of atrial septal defect (58 patients), ventricular septal defect (48 patients), atrioventricular canals (14 patients), or tetralogy of Fallot (24 patients) at Duke University Medical Center between July 1, 1992, and September 15, 1995. Furthermore, we were able to identify where the costs occurred within the hospital. Financial risk was defined as a large (> 60% of mean costs) standard deviation, which indicated unpredictability and variability in the treatment for a group of patients. RESULTS: Cost for atrial septal defect repair was predictably consistent (low standard deviation) and was related to hospital length of stay. There were factors, however, for ventricular septal defect, atrioventricular canal, and tetralogy of Fallot repair that are identifiable preoperatively that predict low- and high-risk groups using cost as an outcome parameter. Patients undergoing ventricular septal defect repair who were younger than 6 months of age at the time of repair, who required preoperative hospital stays of longer than 7 days before surgical repair, or who had Down's syndrome had a less predictable cost picture than patients undergoing ventricular septal defect repair who were older than 2 years, who had short (< 4 days) preoperative hospitalization, or who did not have Down's syndrome ($48,252 +/- $42,539 versus $15,819 +/- $7,219; p = 0.008). Patients with atrioventricular canals who had long preoperative hospitalization (> 7 days), usually due to pneumonia (respiratory syncytial virus) with preoperative mechanical ventilation had significantly higher cost than patients with atrioventricular canals who underwent elective repair with short preoperative hospitalization ($83,324 +/- $60,138 versus $26,904 +/- $5,384; p = 0.05). Patients with tetralogy of Fallot had higher costs if they had multiple congenital anomalies, previous palliation (combining costs of both surgical procedures and hospital stays), or severe "tet" spells at the time of presentation for operation compared with patients without these risk factors ($114,202 +/- $88,524 versus $22,241 +/- $7,071; p = 0.0005). One patient (with tetralogy of Fallot) with multiple congenital anomalies died 42 days after tetralogy of Fallot repair of sepsis after a gastrointestinal operation. Otherwise, hospital mortality was 0% for all groups. CONCLUSIONS: Low mortality and good long-term outcome for surgical correction of congenital heart defects is now commonplace, but can be expensive as some patients with complex problems receive the care necessary to survive. This study demonstrates that it is possible to identify factors preoperatively that predict financial risk. This knowledge may facilitate implementation of risk adjustments for managed care contracting and for strategic resource allocation.

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BACKGROUND: During profoundly hypothermic cardiopulmonary bypass, cerebral venous oxygen saturation increases (eg, to 98% at 15 degrees C). We reanalyzed results of clinical studies to learn why. METHODS: One hundred sixty-eight cerebral oxygen transport measurements were available from 96 infants and children undergoing profoundly hypothermic cardiopulmonary bypass during repair of congenital heart defects. RESULTS: Dissolved oxygen accounted for 2% to 17% of arterial oxygen content, depending on the arterial oxygen partial pressure and hemoglobin concentration. The fraction of the cerebral metabolic rate for oxygen obtained from dissolved oxygen depended on pump flow, temperature, hemoglobin concentration, and arterial oxygen partial pressure (all p < 10(-3)). For "full-flow" cardiopulmonary bypass, temperatures less than 18 degrees C, and arterial oxygen partial pressure measurements more than 180 mm Hg, the mean +/- standard deviation of the fraction of cerebral metabolic rate for oxygen obtained from dissolved oxygen equaled 77% +/- 19%. CONCLUSIONS: Dissolved oxygen satisfies most of the brain's oxygen requirements during profound hypothermic cardiopulmonary bypass. This result reflects four properties of profound hypothermic cardiopulmonary bypass: (1) increases in hemoglobin's oxygen affinity due to profound hypothermia (which impairs oxygen transfer from hemoglobin to cerebral tissue), (2) use of hemodilution, (3) use of high arterial oxygen partial pressure, and (4) low cerebral metabolic rate of oxygen.

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OBJECTIVE: This study compares the total hospital cost (HC) for one-stage versus "two-stage" repair of tetralogy of Fallot (TOF) in infants younger than 1 year of age. SUMMARY BACKGROUND DATA: Total (one-stage) correction of TOF is now being performed with excellent results in infancy. Alternatively, a two-stage approach, with palliation of infants in the first year of life, followed by complete repair at a later time can be used. In some institutions, the two-stage approach is standard practice for infants younger than 1 year of age or is used selectively in patients with an anomalous coronary artery across the right ventricular outflow tract (RVOT), "small pulmonary arteries," multiple congenital anomalies, critical illnesses (CI), which increase the risk of bypass (e.g., sepsis or DIC), or severe hypercyanotic spells (HS) at the time of presentation. The cost implications of these two approaches are unknown. METHODS: The authors reviewed 22 patients younger than 1 year of age who underwent repair of TOF at their institution between 1993 and 1995. Eighteen patients had one-stage (1 degree) repair (mean age, 3.4 +/- 3.1 months; range, 3 days-9 months) and 4 patients were treated by a staged approach with initial palliation (1.6 +/- 0.4 month; range, 1.5-2 months) followed by later repair (14.75 +/- 1.5 months; range, 13-16 months). The reasons for palliation were severe HS at time of presentation (two patients), anomalous coronary artery (one patient) and CI (one patient). In the 18 patients undergoing 1 degree repair, 3 (16.6%) presented with HS, 6 (33.3%) had a transanular repair, and 6 (33.3%) were able to be repaired through an entirely transatrial approach (youngest patient, 1.5 months). The HC (1996 dollars) and hospital length of stay (LOS; days) were evaluated for all patients. The HCs were calculated using transition I, which is a cost accounting system used by our medical center since July 1992. Transition I provides complete data on all direct and indirect hospital-based, nonprofessional costs. RESULTS: There was no mortality in either group. The group undergoing 1 degree repair had an average LOS of 14.5 +/- 11.2 days compared to an average LOS for palliation of 14 +/- 6.4 days. When the palliated group returned for complete repair, the average LOS was 28.8 +/- 25 days, yielding a total LOS for the two-stage strategy of 43 +/- 30.8 days (p = 0.003 compared to 1 degree repair). The HC for 1 degree repair was $32,541 +/- $15,968 compared to $25,737 +/- $1900 for palliation (p = not significant compared to 1 degree repair) and $54,058 +/- $39,395 for subsequent complete repair (p = not significant compared to 1 degree repair) (total two-stage repair HC = $79,795 +/- $40,625; p = 0.001 compared to 1 degree repair). The LOS and HC for the two-stage group combine a total of palliation plus later repair and, as such, reflect two separate hospitalizations and convalescent periods. To eliminate cost outliers, a best-case analysis was performed by eliminating 50% of patients from each group. Using this analysis, the two-stage approach resulted in an average (total) LOS of 16.5 +/- 2.1 days compared to 8.5 +/- 1.4 days for the 1 degree group. Total cost for the two-stage strategy in this best-case group was $44,660 +/- $3645 compared to $22,360 +/- $3331 for 1 degree repair (p = 0.00001). CONCLUSIONS: The data from this review show that palliation alone generates HC similar to that from 1 degree infant repair of TOF, and total combined HC and LOS for palliation plus eventual repair of TOF (two-stage approach) are significantly higher than from 1 degree repair. Furthermore, these data do not include additional costs for care delivered between palliation and repair (e.g., outpatient visits, cardiac catheterization, serial echocardiography). Although there may be occasions when a strategy using initial palliation followed by later repair may seem prudent, the cost is clearly higher and use of health care resources greater.

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OBJECTIVE: To test the hypothesis that in a swine model of acute respiratory distress syndrome (ARDS) with permissive hypercapnia, inhaled nitric oxide would improve transpulmonary vascular mechanics and right ventricular workload while not changing intrinsic right ventricular contractility. DESIGN: Prospective, randomized, controlled laboratory trial. SETTING: University research laboratory. SUBJECTS: Eleven swine (30 to 46 kg). INTERVENTIONS: The swine were anesthetized, intubated, and paralyzed. After median sternotomy, pressure transducers were placed in the right ventricle, pulmonary artery, and left atrium. An ultrasonic flow probe was placed around the pulmonary artery. Ultrasonic dimension transducers were sutured onto the heart at the base, apex, left ventricle (anterior, posterior, free wall), and right ventricle (free wall). An additional transducer was placed in the interventricular septum. A surfactant depletion model of ARDS was created by saline lung lavage. Nitric oxide was administered at 2, 4, and 6 parts per million (ppm), in a random order, under the condition of permissive hypercapnia (Paco2 55 to 75 torr [7.3 to 10.0 kPa]). MEASUREMENTS AND MAIN RESULTS: We evaluated the pulmonary vascular and right ventricular effects of permissive hypercapnia, with and without inhaled nitric oxide, by measuring variables of transpulmonary vascular mechanics and right ventricular function. These variables included mean pulmonary arterial pressure, right ventricular total power, right ventricular stroke work, transpulmonary vascular efficiency, and right ventricular intrinsic contractility. Data were obtained after lung injury under the following conditions: a) normocapnia (Paco2 35 to 45 torr [4.7 to 6.0 kPa]) and nitric oxide at 0 ppm; b) hypercapnia and nitric oxide at 0 ppm; c) hypercapnia and nitric oxide at 2, 4, and 6 ppm; and d) repeat measurements with hypercapnia and nitric oxide at 0 ppm. In ARDS with permissive hypercapnia, inhaled nitric oxide therapy (2 to 6 ppm) improved transpulmonary vascular mechanics and right ventricular workload by lowering pulmonary arterial pressure (29.6 +/- 1.3 vs. 24.6 +/- 1.0 mm Hg, p = .0001), increasing transpulmonary vascular efficiency (13.9 +/- 0.5 vs. 16.1 +/- 0.7 L/W-min, p = .0001), decreasing right ventricular total power (142 +/- 9 vs. 115 +/- 9 mW, p = .001), and decreasing right ventricular stroke work (653 +/- 37 vs. 525 +/- 32 ergs x 10(3), p = .001). Inhaled nitric oxide did not change right ventricular contractility, as measured by preload-recruitable stroke work. CONCLUSIONS: Inhaled nitric oxide ameliorated any negative effects of hypoxic and hypercapnic pulmonary vasoconstriction. The beneficial effects of inhaled nitric oxide are related to alterations in right ventricular afterload and not intrinsic right ventricular contractility. The improved cardiopulmonary effects of inhaled nitric oxide with permissive hypercapnia potentially expand the use of nitric oxide in ARDS and other conditions in which this strategy is employed.

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BACKGROUND: Use of deep hypothermic circulatory arrest (DHCA) in infant cardiac surgery is associated with reduced cerebral perfusion and metabolism during the recovery period. We investigated the impairment of nitric oxide production as a possible cause. METHODS: A group of 1-week-old piglets underwent normothermic cardiopulmonary bypass (group A); three other groups (B, C, and D; n = 6 per group) underwent 60 minutes of DHCA at 18 degrees C and 60 minutes of rewarming. The animals were then treated as follows: Groups A and B received L-omega-nitro-arginine-methyl-ester (L-NAME, 50 mg.kg-1); group C, saline solution; and group D, L-arginine (600 mg.kg-1). RESULTS: In group A, global cerebral blood flow decreased to 37.3% +/- 4.2% of baseline after L-NAME administration (p < 0.005). In group B, global cerebral blood flow decreased to 44.6% +/- 4.4% of baseline after DHCA and 28.9% +/- 3.4% after L-NAME administration (p < 0.001). Following L-arginine treatment after DHCA (group D), global cerebral blood flow increased from 43.8% +/- 3.0% of baseline to 61.6% +/- 9.1% (p < 0.05); cerebral oxygen metabolism increased from 1.93 +/- 0.16 mL.min-1.100 g-1 after DHCA to 2.42 +/- 0.25 mL.min-1.100 g-1 (p < 0.05). CONCLUSIONS: Tonal production of nitric oxide is impaired in the brain after DHCA and is partly responsible for the circulatory and metabolic changes observed. Stimulation of nitric oxide production (L-arginine) significantly improved recovery of cerebral blood flow and cerebral oxygen metabolism after DHCA.

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Extracorporeal membrane oxygenation (ECMO) is widely used in the treatment of respiratory and cardiovascular failure in neonatal patients. The authors present a case of a child with hemoglobin SS disease who was treated with ECMO after acute chest syndrome and acute respiratory distress syndrome developed. They also present data from the Extracorporeal Life Support Organization on this use of ECMO from other centers. To date, there have been 15 pediatric patients with acute chest syndrome treated with ECMO. Survival rate has been 26%. In selected patients with severe disease, ECMO can provide support at a lower mean airway pressure, allow for aggressive pulmonary lavage, and maintain adequate tissue oxygen delivery until the patient is more stable. Patients who might benefit include those with poor ventilation secondary to mucous plugging and barotrauma. The best success with these patients might be anticipated from venoarterial ECMO. Patients with severe cardiac or neurologic deterioration may constitute a group less likely to survive.

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OBJECTIVES: a) To determine if cerebral blood flow is symmetric after internal carotid artery and ipsilateral internal jugular vein ligation in infants during venoarterial extracorporeal life support. b) To determine the cerebral CO2 reactivity (delta cerebral blood flow/delta torr CO2) of neonates during venoarterial extracorporeal life support and its correlation to neurodevelopmental outcome. DESIGN: Prospective, clinical study. SETTING: University hospital pediatric intensive care unit. PATIENTS: Fourteen neonates with respiratory failure who were receiving venoarterial extracorporeal life support. INTERVENTIONS: PaCO2 was altered by adjusting the CO2 gas flow through the membrane oxygenator. Cerebral blood flow was measured over both parietal-temporal regions at three PaCO2 values using xenon-133 clearance methodology. Cerebral blood flow measurements were made early (< or = 12 hrs of extracorporeal life support, n = 10) or late (> or = 48 hrs of extracorporeal life support, n = 10). In six of 14 infants, both early and late cerebral blood flow rates were measured. PaO2, mean arterial pressure, pump flow rate, and temperature were stable during each study period. Neurodevelopmental outcome was assessed in the neonatal follow-up clinic. MEASUREMENTS AND MAIN RESULTS: Right and left hemispheric cerebral blood flow rates were significantly correlated with each other during early and late extracorporeal life support (p = .0001; r2 = .91). Overall, hemispheric cerebral blood flow was statistically symmetric. There was no association of CO2 reactivity (delta cerebral blood flow/delta torr PCO2, range 0.04 to 1.36 mL/min/100 g/torr) with short-term neurodevelopmental outcome. Infants with normal neurodevelopmental outcome had variable CO2 reactivity (range 0.04 to 0.67 mL/min/100 g/torr). Normal short-term neurodevelopmental outcome was observed in two infants with cerebral blood flow of < 10 mL/min/100 g. CONCLUSIONS: Hemispheric cerebral blood flow was symmetric in infants during early and late venoarterial extracorporeal life support. Some subgroups showed a trend toward decreased right hemispheric cerebral blood flow, but the small number of patients limited interpretation of this finding. CO2 reactivity and cerebral blood flow were highly variable in this population, and were not predictive of short-term neurodevelopmental outcome. Stressed neonates with extremely low cerebral blood flow rates may have relatively normal short-term neurodevelopmental outcome after venoarterial extracorporeal life support.

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Cardiopulmonary bypass with deep hypothermic circulatory arrest increases the risk of neurologic injury in patients with aortopulmonary collaterals. Experimental studies have demonstrated that such collaterals decrease the rate of cerebral cooling before arrest and cerebral metabolic recovery after circulatory arrest. Use of pH-stat blood gas management has been shown to increase cerebral blood flow during cooling. The current study was designed to test whether cooling with pH-stat blood gas management can decrease the cerebral metabolic impact of aortopulmonary collaterals. Twenty 4- to 6-week-old piglets underwent placement of a shunt between the left subclavian artery and main pulmonary artery. In control animals (n = 10) the shunts were immediately ligated, whereas in the shunt animals (n = 10) the shunts were left patent. All animals were supported with cardiopulmonary bypass, cooled to 18 degrees C by means of either alpha-stat (five control and five shunt animals) or pH-stat (five control and five shunt animals) blood gas management, subjected to circulatory arrest for 90 minutes, and rewarmed to 37 degrees C. The cerebral metabolic rate of oxygen consumption (a marker for neurologic function) was significantly lower after circulatory arrest in the shunt animals cooled with alpha-stat blood gas management than in the control animals subjected to alpha-stat management (1.2 +/- 0.2 vs 2.3 +/- 0.2 ml oxygen per 100 gm/min, p < 0.05). By contrast, there was no difference between the pH-stat shunt animals and either control group (2.1 +/- 0.2 vs 2.3 +/- 0.2 [alpha-stat] and 2.0 +/- 0.3 [pH-stat] ml oxygen per 100 gm/min, p = not significant). pH-Stat cooling protected the brain from shunt-related injury. When circulatory arrest is used in the presence of aortopulmonary collaterals, the use of pH-stat blood gas management during cooling results in better cerebral protection than alpha-stat blood gas management.

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This study investigated the effects of different cooling strategies on cerebral metabolic response to circulatory arrest. In particular, it examined the impact of blood gas management and degree of cooling on cerebral metabolism before and after deep hypothermic circulatory arrest. Sixty-nine 1-week-old piglets (2 to 3 kg) were placed on cardiopulmonary bypass (37 degrees C) at 100 ml/kg per minute. Animals were cooled to 18 degrees or 14 degrees C as follows: alpha-stat strategy to 18 degrees C (n = 9) or 14 degrees C (n = 6), pH-stat strategy to 18 degrees C (n = 12) or 14 degrees C (n = 10). Animals underwent 60 minutes of circulator arrest followed by rewarming with alpha-stat strategy to 36 degrees C. Control animals were cooled with alpha-stat strategy to 18 degrees C (n = 10) or 14 degrees C (n = 3) and then maintained on cold cardiopulmonary bypass (100 ml/kg per minute) for 60 minutes. Three animals were excluded (see text). With the use of xenon 133 clearance methods, cerebral blood flow was measured at the following points: point I, cardiopulmonary bypass (37 degrees C); point II, cardiopulmonary bypass before circulatory arrest or control flow (18 degrees or 14 degrees C); and point III, cardiopulmonary bypass after rewarming (36 degrees C). Cerebral metabolic rate of oxygen consumption was calculated for each point. At point II, cerebral metabolism was more suppressed at 14 degrees C compared with that at 18 degrees C. At any given temperature (18 degrees or 14 degrees C), pH-stat strategy provided the greatest suppression of of cerebral metabolism. In control animals, cerebral metabolic oxygen consumption of point III returned to baseline values after 60 minutes of cold bypass. Sixty minutes of circulatory arrest resulted in a significant reduction in cerebral metabolic oxygen consumption at point III compared with that at point I regardless of cooling temperature or blood gas strategy. The amount of cerebral metabolic recovery was significantly reduced in the pH-stat 14 degrees C group compared with that in the pH-stat 18 degrees C group at point III. The use of pH-stat strategy followed by a switch to alpha-stat at 14 degrees C provided better cerebral metabolic recovery compared with either strategy used alone. The use of pH-stat strategy during initial cooling may provide the animal with maximal cerebral metabolic suppression. The cerebral acidosis produced with pH-stat cooling may worsen cerebral metabolic injury from circulatory arrest, but this affect is eliminated with the use of alpha-stat just before the period of circulatory arrest.

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BACKGROUND: This article provides an overview of the application of intraoperative echocardiography during repair of congenital heart defects based on our experience with 1,000 patients. METHODS: The patients in this study all underwent repair of a congenital heart defect between 1987 and 1994 at Duke University Medical Center. Echocardiography was performed on all patients in the operating room both before and after repair using epicardial or transesophageal imaging (or both). Hospital costs and outcome data were obtained for all patients. RESULTS: Overall, 44 patients (4.4%) underwent intraoperative revision of their repair based on echocardiographic findings. There was an initial learning phase during which 8.5% of repairs needed to be revised. With experience, the number of revisions fell to as low as 3% to 4%, but need for revision continued to occur throughout the series. Thirty-nine patients (88.6%) had a successful revision. It was not possible for the surgeon to predict the need for a revision based on his confidence in the repair: in 2.6% of patients thought by the surgeon to have a good repair, intraoperative echocardiography revealed the need for operative revision. The average cost for patients who return to the operating room during their hospitalization for revision of a repair is significantly greater than for those whose repairs are revised before they leave the operating room ($94,180.28 +/- $33,881.63 versus $21,415.79 +/- $8,215.74). There were no significant complication attributable to intraoperative echocardiography. CONCLUSIONS: In an era where complete repair of congenital heart defects is emphasized, intraoperative echocardiography provides information that can guide successful operative revision so that babies leave the operating room with optimal results.

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OBJECTIVES: To correlate the initial and maximal lactate levels with the occurrence of intracranial hemorrhage (ICH) and survival in patients treated with extracorporeal life support (ECLS). DESIGN: Retrospective chart review. SETTING: Pediatric intensive care unit. PATIENTS: Eighty-two neonatal patients placed on ECLS for respiratory failure due to sepsis, meconium aspiration, or persistent pulmonary hypertension of the newborn. MEASUREMENTS: The initial lactate level measured within 6 hours of initiating ECLS and the maximal lactate level measured throughout the ECLS course were collected. Lactate levels were described as mean lactate +/- SE (mM). Head ultrasound reports and survival were reviewed. Platelet counts and activated clotting times (ACTs) were examined. RESULTS: The mean initial and maximal lactate levels were higher in ECLS patients who developed ICH (initial: 10 +/- 1.7 mM vs 6.4 +/- 0.8 mM, p = .05 and maximal: 12.4 +/- 2.5 mM vs 7.9 +/- 0.8 mM, p = .04). Initial and maximal lactate levels were also elevated in nonsurvivors (initial: 11.7 +/- 3 mM vs 6.4 +/- 0.7 mM, p = .01 and maximal: 14.8 +/- 3.3 mM vs 7.8 +/- 0.8 mM, P < .01). Platelet counts and ACT did not differ in patients with and without ICH. CONCLUSIONS: Lactate is a useful marker for the development of ICH in ECLS patients. In addition, elevated lactates during ECLS identify a subgroup of patients with poor outcome. Prospective studies are needed to determine whether the incorporation of this information into pre-ECLS and ECLS management will decrease the occurrence of ICH and improve survival.

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BACKGROUND: Aortopulmonary collaterals (APC) have been associated with an increased risk of choreoathetosis after deep hypothermic circulatory arrest (DHCA). To study the effects of APC on cerebral hemodynamics and metabolism before and after DHCA, a piglet model was developed. METHODS AND RESULTS: Protocol 1: Eight 4- to 6-week-old piglets underwent placement of a left subclavian-to-main pulmonary artery shunt. Control shunts (n = 4) were ligated, APC shunts (n = 4) were left patent. All animals were placed on cardiopulmonary bypass (CPB) and cooled in identical fashion for 20 minutes. Temperature probes were placed in the nasopharynx, cortex, and deep brain. Control animals achieved significantly lower temperatures in all three areas by the end of cooling (17.5 degrees C versus 20.1 degrees C, 19.0 degrees C versus 22.3 degrees C, and 17.5 degrees C versus 21.0 degrees C, respectively, P < .005). Protocol 2: Six control and six APC animals were instrumented as described. All were placed on CPB, cooled to 18 degrees C, arrested for 90 minutes, and rewarmed to 37 degrees C. Cerebral blood flow (CBF) was measured with radioactive microspheres while warm on CPB, after cooling, and after rewarming. Arterial and sagittal sinus blood gases and CBF were used to calculate the cerebral metabolic rate of oxygen consumption (CMRO2). Both CBF and CMRO2 were significantly higher after rewarming to 37 degrees C in control versus APC animals (28 +/- 3 versus 14 +/- 2 mL/100 g per minute and 1.72 +/- 0.21 versus 1.04 +/- 0.14 mL O2/100 g per minute, respectively, P < .05). CONCLUSIONS: APC decrease the rate of cerebral cooling on CPB and even if temperature is controlled result in increased cerebral metabolic derangement after DHCA. Patients with such collaterals may need additional measures to optimize cerebral protection.

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OBJECTIVES: To answer the following questions: a) Does jugular venous ligation (simulating venovenous extracorporeal life support) alter proximal jugular venous pressure, intracranial pressure, hemispheric cerebral blood flow, or cerebral metabolism? b) Does release of ligation reverse these effects? and c) What are the comparative effects of venous ligation alone vs. venous ligation in combination with arterial ligation? DESIGN: Prospective, randomized, laboratory investigation. SETTING: Multidisciplinary laboratory setting. SUBJECTS: Sixteen swine, weighing 8.1 to 12.1 kg, 3 to 4 wks of age. INTERVENTIONS: Sixteen swine were randomly assigned to two groups, utilizing a random sequence of vessel ligation. Nine swine underwent occlusion of the right internal and external jugular veins alone (venovenous ligation) followed by release of the occlusion and then occlusion of the right common carotid artery and the right internal and external jugular veins together (venoarterial ligation). The remaining seven swine underwent venoarterial ligation, followed by release of the occlusion and then venovenous ligation. In the experimental group in which venovenous ligation was performed first, the 5, and 30-min release periods after ligation were taken to represent the effects of draining the right jugular vein during venovenous extracorporeal life support. MEASUREMENTS AND MAIN RESULTS: Data were obtained at baseline, 5, and 30 mins after each ligation/release period. Intracranial pressure, right and left internal jugular pressures/flow rates, and cerebral sinus lactate concentrations were measured. Cerebral blood flow was determined using 133Xe clearance methodology, and the cerebral metabolic rate was calculated. There were no significant differences between the ipsilateral internal jugular pressure or extracorporeal life support at 5 or 30 mins after venovenous or venoarterial ligation compared with baseline values or compared with the release of the ligation at 5 or 30 mins. There was a significant increase in right-side (44.7 +/- 2.0 vs. 38.8 +/- 2.4 mL/kg/min; p < .05) and left-side (42.9 +/- 2.3 vs. 38.7 +/- 1.9 mL/kg/min; p < .05) cerebral blood flow 5 mins after venovenous ligation when compared with baseline values. Similarly, after venoarterial ligation, there was a significant increase in right-side (44.6 +/- 2.2 vs. 38.8 +/- 2.4 mL/kg/min; p < .05) and left-side (43.9 +/- 1.5 vs. 38.7 +/- 1.9 mL/kg/min; p < .05) and cerebral blood flow. Cerebral oxygen consumption was significantly increased after venovenous (2.7 +/- 0.2 to 3.2 +/- 0.2 mL/kg/min; p < .05) and venoarterial (2.7 +/- 0.2 to 3.1 +/- 0.2 mL/kg/min; p < .05) ligation at 5 mins after ligation. This increase persisted at the 30-min period and after release of ligation. CONCLUSIONS: Ligation of the right jugular veins alone (venovenous ligation) or jugular veins and right carotid artery (venoarterial ligation) does not increase jugular venous pressures or intracranial pressure. However, this procedure does increase cerebral blood flow and cerebral oxygen consumption. These findings demonstrate that there is adequate decompression of the venous system by the cerebrovascular system and retrograde decompression during extracorporeal life support appears unwarranted.

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