Elevated serum lactate correlates with intracranial hemorrhage in neonates treated with extracorporeal life support.

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.

Blood gas management and degree of cooling: effects on cerebral metabolism before and after circulatory arrest.

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.

Liquid ventilation improves pulmonary function and cardiac output in a neonatal swine model of cardiopulmonary bypass.

OBJECTIVE: Neonatal and infant cardiopulmonary bypass results in multiorgan system dysfunction. Organ protective strategies have traditionally been directed at the myocardium and brain while neglecting the sometimes severe injury to the lungs. We hypothesized that liquid ventilation would improve pulmonary function and cardiac output in neonates after cardiopulmonary bypass. METHODS: Twenty neonatal swine were randomized to receive cardiopulmonary bypass with or without liquid ventilation. In the liquid-ventilated group, a single dose of perflubron was administered before bypass. The control group was conventionally ventilated. Each animal was placed on nonpulsatile, hypothermic bypass. Low-flow cardiopulmonary bypass was performed for 60 minutes. The flow rate was returned to 125 ml/kg per minute, and after warming to 37 degrees C, the animals were removed from bypass. Hemodynamic and ventilatory data were obtained after bypass to assess the effects of liquid ventilation. RESULTS: Without liquid ventilation, cardiopulmonary bypass resulted in a significant decrease in cardiac output, oxygen delivery, and static pulmonary compliance compared with prebypass values. Input pulmonary resistance and characteristic impedance increased in these control animals. At 30, 60, and 90 minutes after bypass, the animals receiving liquid ventilation showed significantly increased cardiac output and static compliance and significantly decreased input pulmonary resistance and characteristic impedance compared with control animals not receiving liquid ventilation. CONCLUSIONS: Liquid ventilation improved pulmonary function after neonatal cardiopulmonary bypass while increasing cardiac output. The morbidity associated with cardiopulmonary bypass may be significantly reduced if the adverse pulmonary sequelae of bypass can be diminished. Liquid ventilation may become an important technique to protect the lungs from the deleterious effects of cardiopulmonary bypass.

Routine use of intraoperative epicardial echocardiography and Doppler color flow imaging to guide and evaluate repair of congenital heart lesions. A prospective study.

Routine epicardial two-dimensional echocardiography, Doppler, and Doppler color flow imaging studies were performed before and after cardiopulmonary bypass in 328 patients undergoing operations for congenital heart disease. Ages ranged from 1 day to 59 years (mean 5.9 years); the smallest patient was 1.8 kg. Complete examinations were conducted in 3.6 +/- 1.7 minutes. Prebypass examinations demonstrated previously unappreciated details of anatomy in 60 patients (18%), which did not relate to whether catheterization had been performed, and they were believed to play a role in surgical planning in 143 patients (44%). Discovery of previously unrecognized features of anatomy increased the impact of echo-Doppler color flow imaging on operative planning by 2.5 times. After bypass, echo-Doppler color flow imaging disclosed unsuspected residual defects in 22 patients (7%) who were doing well clinically and enabled an attempt at immediate revision of the procedure. When ultimate clinical outcome was compared to postbypass findings of echo-Doppler color flow imaging, the presence of a residual defect, right or left ventricular dysfunction, or any concern with the heart by echo-Doppler color flow imaging appeared to serve as a predictor of unfavorable outcome (p less than 0.001 for each when compared with absence of these difficulties). Thus routine intraoperative echo-Doppler color flow imaging is useful in aiding the planning, conduct, and assessment of results in operations for congenital heart disease.

Cerebral blood flow response to changes in arterial carbon dioxide tension during hypothermic cardiopulmonary bypass in children.

We examined the relationship of changes in partial pressure of carbon dioxide on cerebral blood flow responsiveness in 20 pediatric patients undergoing hypothermic cardiopulmonary bypass. Cerebral blood flow was measured during steady-state hypothermic cardiopulmonary bypass with the use of xenon 133 clearance methodology at two different arterial carbon dioxide tensions. During these measurements there was no significant change in mean arterial pressure, nasopharyngeal temperature, pump flow rate, or hematocrit value. Cerebral blood flow was found to be significantly greater at higher arterial carbon dioxide tensions (p less than 0.01), so that for every millimeter of mercury rise in arterial carbon dioxide tension there was a 1.2 ml.100 gm-1.min-1 increase in cerebral blood flow. Two factors, deep hypothermia (18 degrees to 22 degrees C) and reduced age (less than 1 year), diminished the effect carbon dioxide had on cerebral blood flow responsiveness but did not eliminate it. We conclude that cerebral blood flow remains responsive to changes in arterial carbon dioxide tension during hypothermic cardiopulmonary bypass in infants and children; that is, increasing arterial carbon dioxide tension will independently increase cerebral blood flow.

Modified ultrafiltration improves cerebral metabolic recovery after circulatory arrest.

Modified ultrafiltration uses hemofiltration of the patient and bypass circuit after separation from cardiopulmonary bypass to reverse hemodilution and edema. This study investigated the effect of modified ultrafiltration on cerebral metabolic recovery after deep hypothermic circulatory arrest. Twenty-six 1-week-old piglets (2 to 3 kg) were supported by cardiopulmonary bypass (37 degrees C) at 100 ml.kg-1.min-1 and cooled to 18 degrees C. Animals underwent 90 minutes of circulatory arrest followed by rewarming to 37 degrees C. After being weaned from cardiopulmonary bypass, animals were divided into three groups: controls (n = 10); modified ultrafiltration for 20 minutes (n = 9); transfusion of hemoconcentrated blood for 20 minutes (n = 7). Global cerebral blood flow was measured by xenon 133 clearance methods: stage I--before cardiopulmonary bypass; stage II--5 minutes after cardiopulmonary bypass; and stage III--25 minutes after cardiopulmonary bypass. Cerebral metabolic rate of oxygen consumption, cerebral oxygen delivery, and hematocrit value were calculated for each time point. At point III, the hematocrit value (percent) was elevated above baseline in the ultrafiltration and transfusion groups (44 +/- 1.8, 42 +/- 1.8 versus 28 +/- 1.7, 30 +/- 0.7, respectively, p < 0.05). Cerebral oxygen delivery (ml.100 gm-1.min-1) increased significantly above baseline at point III after ultrafiltration (4.98 +/- 0.32 versus 3.85 +/- 0.16, p < 0.05) or transfusion (4.59 +/- 0.17 versus 3.89 +/- 0.06, p < 0.05) and decreased below baseline in the control group (2.77 +/- 0.19 versus 3.81 +/- 0.16, p < 0.05). Ninety minutes of deep hypothermic circulatory arrest resulted in impaired cerebral metabolic oxygen consumption (ml.100 gm-1.min-1) at point III in the control group (1.95 +/- 0.15 versus 2.47 +/- 0.07, p < 0.05) and transfusion group (1.72 +/- 0.10 versus 2.39 +/- 0.15, p < 0.05). After modified ultrafiltration, however, cerebral metabolic oxygen consumption at point III had increased significantly from baseline (3.12 +/- 0.24 versus 2.48 +/- 0.13, p < 0.05), indicating that the decrease in cerebral metabolism immediately after deep hypothermic circulatory arrest is reversible and may not represent permanent cerebral injury. Use of modified ultrafiltration after cardiopulmonary bypass may reduce brain injury associated with deep hypothermic circulatory arrest.

pH-stat cooling improves cerebral metabolic recovery after circulatory arrest in a piglet model of aortopulmonary collaterals.

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.

The effect of hypothermic cardiopulmonary bypass and total circulatory arrest on cerebral metabolism in neonates, infants, and children.

Cardiopulmonary bypass management in neonates, infants, and children often requires the use of deep hypothermia at 18 degrees C with occasional periods of circulatory arrest and represents marked physiologic extremes of temperature and perfusion. The safety of these techniques is largely dependent on the reduction of metabolism, particularly cerebral metabolism. We studied the effect of hypothermia on cerebral metabolism during cardiac surgery and quantified the changes. Cerebral metabolism was measured before, during, and after hypothermic cardiopulmonary bypass in 46 pediatric patients, aged 1 day to 14 years. Patients were grouped on the basis of the different bypass techniques commonly used in children: group A--moderate hypothermic bypass at 28 degrees C; group B--deep hypothermic bypass at 18 degrees to 20 degrees C with maintenance of continuous flow; and group C--deep hypothermic circulatory arrest at 18 degrees C. Cerebral metabolism significantly decreased under hypothermic conditions in all groups compared with control levels at normothermia, the data demonstrating an exponential relationship between temperature and cerebral metabolism and an average temperature coefficient of 3.65. There was no significant difference in the rate of metabolism reduction (temperature coefficient) in patients cooled to 28 degrees and 18 degrees C. From these data we were able to derive an equation that numerically expresses a hypothermic metabolic index, which quantitates duration of brain protection provided by reduction of cerebral metabolism owing to hypothermic bypass over any temperature range. Based on this index, patients cooled to 28 degrees C have a predicted ischemic tolerance of 11 to 19 minutes. The predicted duration that the brain can tolerate ischemia ("safe" period of deep hypothermic circulatory arrest) in patients cooled to 18 degrees C, based on our metabolic index, is 39 to 65 minutes, similar to the safe period of deep hypothermic circulatory arrest known to be tolerated clinically. In groups A and B (no circulatory arrest), cerebral metabolism returned to control in the rewarming phase of bypass and after bypass. In group C (circulatory arrest), cerebral metabolism and oxygen extraction remained significantly reduced during rewarming and after bypass, suggesting disordered cerebral metabolism and oxygen utilization after deep hypothermic circulatory arrest. The results of this study suggest that cerebral metabolism is exponentially related to temperature during hypothermic bypass with a temperature coefficient of 3.65 in neonates infants and children. Deep hypothermic circulatory arrest changes cerebral metabolism and blood flow after the arrest period despite adequate hypothermic suppression of metabolism.

The brain uses mostly dissolved oxygen during profoundly hypothermic cardiopulmonary bypass.

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.

Coagulation defects in neonates during cardiopulmonary bypass.

We examined components of the coagulation system in 30 neonates (age, 1 to 30 days) undergoing deep hypothermic cardiopulmonary bypass (CPB). A coagulation profile consisting of activated clotting time; prothrombin time; partial thromboplastin time; factors II, V, VII, VIII, IX, X, and I (fibrinogen); antithrombin III; platelet count; and heparin levels was evaluated before bypass, at three intervals during bypass (1 minute after initiation of bypass, stable hypothermic CPB, warm CPB), after weaning from CPB and administration of protamine, and 2 to 3 hours after skin closure. The initiation of CPB resulted in a 50% decrease in circulating coagulation factors and antithrombin III levels. Platelet counts were reduced by 70% with CPB initiation. Neither deep hypothermic temperatures nor prolonged exposure to extracorporeal surfaces had any additional effect on the coagulation profiles. This suggests that the coagulation system of a neonate undergoing CPB is profoundly and globally effected by hemodilution. We believe that treatment of post-CPB coagulopathy in neonates must address these global deficits.

Effect of deep hypothermia and circulatory arrest on cerebral blood flow and metabolism.

The primary goal of monitoring cerebral blood flow and metabolism is to improve our understanding of the association with cardiopulmonary bypass and deep hypothermic circulatory arrest so that effective brain protection strategies can be developed and employed. A review of our cerebral blood flow/cardiopulmonary bypass database, presently totaling 275 neonates and infants, for the purposes of this publication, reveals certain trends and some conclusions that can be drawn. Deep hypothermic circulatory arrest continues to be a factor in the delayed recovery of cerebral blood flow and metabolism in these patients. Examining flow and metabolism serially in the postoperative period shows that in the majority of patients, flow, metabolism and autoregulation return to normal within 24 hours after operation. Some patients' cerebral oxygen metabolism is unable to exert a protective response of increasing extraction in the setting of low cerebral blood flow. We have also observed that in the setting of low cardiac output after cardiac repair, cerebral blood flow is low. It is therefore likely that low cardiac output and pressure-passive cerebral blood flow potentiate brain ischemia after cardiopulmonary bypass and operation in some patients. We have also examined in our series of 275 patients selective neuroprotection strategies for their potential for improving recovery of cerebral blood flow and cerebral metabolism. Duration of cooling on cardiopulmonary bypass correlates directly with suppression of metabolism due to hypothermia. Low-flow cardiopulmonary bypass instead of deep hypothermic circulatory arrest, and topical brain cooling with ice during deep hypothermic circulatory arrest, improve cerebral blood flow and cerebral metabolic recovery.

Temperature monitoring during CPB in infants: does it predict efficient brain cooling?

We examined jugular venous oxygen saturation data in 17 pediatric patients less than 1 year of age undergoing hypothermic cardiopulmonary bypass (CPB). Jugular venous oxygen saturations (JvO2SATS) were measured before bypass and during the active core cooling portion of CPB. The study intervals during CPB included 1 minute after initiation of CPB, at a tympanic membrane temperature of 15 degrees C, and at a rectal temperature of 15 degrees C. During these measurement intervals, there were no significant changes in mean arterial pressure, pump flow rate, arterial oxygen saturation, mixed venous oxygen saturation, carbon dioxide tension, or hematocrit. Six of the 17 patients (29%) demonstrated a significantly lower JvO2SAT (87.1% +/- 6.3% versus 98.1% +/- 0.9%) at a tympanic membrane temperature of 15 degrees C. Patients demonstrating jugular venous desaturation could not be predicted from continuous monitoring of tympanic membrane and rectal temperatures or through on-line measurements of mixed venous oxygen saturation. Low JvO2SAT suggests higher levels of cerebral metabolism and cerebral uptake of oxygen. In the presence of deep hypothermic CPB and stable anesthetic levels, the most likely cause of a low JvO2SAT is inadequate cerebral cooling. We believe JvO2SAT monitoring may be an important adjunct to conventional temperature monitoring in the patient undergoing deep hypothermic CPB or total circulatory arrest.

Effect of altering pump flow rate on cerebral blood flow and metabolism in infants and children.

The effects of reduced pump flow rate (PFR) on cerebral blood flow, cerebral oxygen consumption (CMRO2), oxygen extraction, cerebral vascular resistance, and total body vascular resistance were examined in 27 pediatric patients during hypothermic cardiopulmonary bypass (hCPB). During steady state hCPB the extracorporeal flows were randomly adjusted to a conventional PFR and a reduced PFR for each patient. The reduced pump flow rates were dictated by surgical needs. Cerebral blood flow measured using Xenon 133 clearance, and CMRO2 and oxygen extraction were calculated. Our results demonstrated that cerebral blood flow and CMRO2 are unchanged if pump flow rates are reduced by 35% to 45% of conventional PFRs at moderate and deep hypothermic temperatures. Reductions in PFR of 45%-70% from conventional PFRs affect the brain differently during either moderate or deep hCPB. At moderate hCPB (26 degrees to 29 degrees C), reductions in PFRs of 45% to 70% resulted in a significant decrease in cerebral blood flow and CMRO2, whereas oxygen extraction increased in a compensatory manner. During deep hCPB (18 degrees to 22 degrees C), PFR reductions of 45% to 70% of conventional PFR significantly reduced cerebral blood flow and CMRO2 but did not increase oxygen extraction, suggesting that at deep hypothermic temperatures, cerebral blood flow and CMRO2 exceed cerebral metabolic needs. Cerebral vascular resistance increased significantly with decreasing temperature but was not affected by pump flow reductions. We have derived indices for minimal acceptable low-flow cardiopulmonary bypass based on the known effects of temperature on cerebral metabolism and have speculated on its utility based on our limited data and a literature review.

Nitric oxide production affects cerebral perfusion and metabolism after deep hypothermic circulatory arrest.

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.

Serum lactates correlate with mortality after operations for complex congenital heart disease.

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.

Comparing two strategies of cardiopulmonary bypass cooling on jugular venous oxygen saturation in neonates and infants.

BACKGROUND: Cerebral protection during deep hypothermic circulatory arrest is predicted on efficient and complete cerebral cooling. Institutions approach cooling quite differently. We compared two different cooling strategies in terms of measured jugular venous bulb saturations in 39 infants undergoing deep hypothermic cardiopulmonary bypass to evaluate the effect of institutional cooling practices on jugular venous bulb saturation, an indirect measure of cerebral cooling efficiency. METHODS: The patients were grouped based on the method of core cooling. In group A (n = 17), core cooling was achieved rapidly by setting the water bath temperature of the heat exchanger at 4 degrees to 5 degrees C, and the patient was cooled until rectal temperature and nasopharyngeal temperature were 15 degrees C or lower. In group B (n = 22), the heat exchanger was initially set at 18 degrees C and slowly lowered to 12 degrees C. Hypothermic temperatures of 12 degrees C were maintained until the nasopharyngeal temperature was 18 degrees C or less and the rectal temperature was 20 degrees C or lower. Once cooling was complete, blood samples were analyzed by cooximetry for determination of arterial oxygen saturation and jugular venous bulb saturation. RESULTS: In group A, the measured jugular venous bulb saturation was 98.0% +/- 0.9% and the oxygen saturation to jugular venous bulb saturation difference was 0.3% +/- 0.5%, measured at the time that institutional cooling objectives were achieved (total cooling time, 15.0 +/- 0.45 minutes). In group B, jugular venous bulb saturation was 86.2% +/- 12% and the oxygen saturation to jugular venous bulb saturation difference was 10.8% +/- 12.2%, measured at the time that institutional cooling objectives were achieved (total cooling time, 17.5 +/- 1.1 minutes (p < 0.01). CONCLUSIONS: Differences in cardiopulmonary bypass cooling techniques may alter the rate at which jugular bulb saturations rise. We believe this represents an indirect measure of the efficiency of brain cooling and therefore of cerebral protection.

Intraoperative echocardiography during congenital heart operations: experience from 1,000 cases.

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.

Thromboxane A2-receptor blockade improves cerebral protection for deep hypothermic circulatory arrest.

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.

Cerebral monitoring during cardiopulmonary bypass in children.

Although cerebral monitoring during CPB remains primarily investigational, recent data support its clinical utility. In particular, it is cerebral metabolic monitoring that provides meaningful information in terms of preparing the brain for dhCPB and dhCA. Cerebral blood flow or cerebral blood flow velocity monitoring is less beneficial due to the presence of luxuriant cerebral blood flow at deep hypothermic temperatures. Conventional temperature monitoring can be improved upon by adding jugular venous oxygen saturation monitoring to satisfy the primary goal of cerebral protection--uniform cerebral cooling and metabolic suppression. Although online measures of cerebral cellular metabolism are not widely available, early experience with near infrared technology suggests that it is a feasible and reliable monitor of cerebral metabolic activity and is likely to represent an important noninvasive continuous monitor in the near future. CMRO2 recovery data have suggested that cerebral metabolic suppression is more severe the longer the period of dhCA. Cerebral protection strategies, such as intermittent cerebral perfusion have demonstrated less metabolic suppression of dhCA in animal models and are currently undergoing clinical evaluation in our institution. Finally, the postoperative period remains a high-risk period for neurologic injury because temperatures are normothermic, cardiac output is reduced, cerebral autoregulation is impaired, and management strategies, such as hyperventilation, are commonly used to increase pulmonary blood flow with little knowledge on its effects on cerebral perfusion.