William J. Greeley

Hemofiltration during cardiopulmonary bypass in pediatric cardiac surgery. Effects on hemostasis, cytokines, and complement components.

BackgroundThis prospective study was intended to determine in a homogeneous population of children whether hemofiltration, performed during cardiopulmonary bypass rewarming, is able to Improve hemodynamics and biologic hemostasis variables, to reduce postoperative blood loss, time to extubation, and plasma cytokines, and complement fragments. MethodsThirty-two children undergoing surgical correction of tetralogy of Fallot were randomly assigned to a hemofiltration or control group. Hemofiltration was performed with a polysulphone hemofilter during rewarming of cardiopulmonary bypass. Plasma clotting factors, D-dimers, antithrom-bin-III, complement fragments C3a and C5a, interleukin-lβ, interleukln-6, interleukin-8, and tumor necrosis factor-a were measured before and after hemofiltration. Systemic mean arterial pressure, left atrial pressure, time to extubation, and postoperative blood loss were monitored. ResultsIn the hemofiltration group, significant reductions in 24-h blood loss (250 (176–356) vs. 319 (182–500) ml/m2, median (minimum-maximum)), time to extubation (15 (9–22) vs. 19 (11–24) h), plasma concentrations of C3a, C5a, interleukin-6, and tumor necrosis factor-α were observed compared to control. Arterial oxygen tension on admission to the intensive care unit was significantly greater in the hemofiltration group (136 ± 20 vs. 103 ± 25 mmHg, mean ± SD). Significant increases in mean arterial pressure, clotting factors, and antithrombin-III were noted for the hemofiltration group. No intergroup difference was observed in left atrial pressure, platelets count, D-dimers, lnterleukin-8, and duration of stay in the Intensive care unit. ConclusionsHemofiltration during cardiopulmonary bypass in children Improves hemodynamics and early postoperative oxygenatlon and reduces postoperative blood loss and duration of mechanical ventilation. Hemofiltration is able to remove some major mediators of the inflammatory response.

Cerebral blood flow and metabolism during cardiopulmonary bypass

Although much has been learned about cerebral physiology during CPB in the past decade, the role of alterations in CBF and CMRO2 during CPB and the unfortunately common occurrence of neuropsychologic injury still is understood incompletely. It is apparent that during CPB temperature, anesthetic depth, CMRO2, and PaCO2 are the major factors that effect CBF. The systemic pressure, pump flow, and flow character (pulsatile versus nonpulsatile) have little influence on CBF within the bounds of usual clinical practice. Although cerebral autoregulation is characteristically preserved during CPB, untreated hypertension, profound hypothermia, pH-stat blood gas management, diabetes, and certain neurologic disorders may impair this important link between cerebral blood flow nutrient supply and metabolic demand (Figure 5). During stable moderate hypothermic CPB with alpha-stat management of arterial blood gases, hypothermia is the most important factor altering cerebral metabolic parameters. Autoregulation is intact and CBF follows cerebral metabolism. Despite wide variations in perfusion flow and systemic arterial pressure, CBF is unchanged. Populations of patients have been identified with altered cerebral autoregulation. To what degree the impairment of cerebral autoregulation contributes to postoperative neuropsychologic dysfunction is unknown. It must be emphasized that not the absolute level of CBF, but the appropriateness of oxygen delivery to demand is paramount. However, the assumption that the control of cerebral oxygen and nutrient supply and demand will prevent neurologic injury during CPB is simplistic. A better understanding of CBF, CMRO2, autoregulation and mechanism(s) of cerebral injury during CPB has lead to a scientific basis for many of the decisions made regarding extracorporeal perfusion.

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.

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.

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 (

The use of intraoperative echo with Doppler color flow imaging to predict outcome after repair of congenital cardiac defects.

94,180.28 +/-

The learing curve for intraoperative echocardiography during congenital heart surgery

33,881.63 versus

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

21,415.79 +/-

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

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.

Population pharmacokinetics of milrinone in neonates with hypoplastic left heart syndrome undergoing stage I reconstruction

Surgical repair of congenital cardiac defects (CCD) has undergone a remarkable evolution in the past decade. Major defects are now often completely corrected in early infancy with continually improving rates of survival. It has become clear that the next major focus will be improvements in the long-term quality of life and this has promoted many innovations in surgical technique and approach. One advance is the use of intraoperative echo with Doppler color flow imaging (echo-DCFI) to evaluate the exactness of operative repair. Aside from anecdotal reports, very little information is available regarding the interpretation of images produced by this technology in the operating room. Furthermore there have been no studies addressing the predictive value of intraoperative echo-DCFI findings with respect to outcome for patients undergoing repair of CCD. The prospective data obtained by following the course of 273 patients receiving intraoperative echo-DCFI has been reviewed after repair of a variety of CCD (age range, 1 to 53 years; mean 5.3 years; smallest patient, 1.8 kg). Forty-seven patients (17%) had initially unacceptable results, by echo, at the completion of their repair. Eighteen of these patients (7% of entire series) had no clinical problems and the defects were discernible only by echo. Twenty-six patients with initially unacceptable results had their repairs revised in the operating room and left with an acceptable result by echo. Twenty-one patients were allowed to leave the operating room with echo-discernible defects. Follow-up of these patients demonstrated a significantly higher (p less than 0.006) rate of reoperation (42% vs. 3%) and of early death (29% vs. 10%) for those patients whose defects were left unrepaired compared to those whose problems were corrected before leaving the operating room. Sixty-eight patients (25%) had some alteration of ventricular function (compared to their prebypass evaluation) at the completion of their repair. Regardless of whether the dysfunction was limited to the right ventricle, left ventricle, or was biventricular, patients in this group had a significantly higher incidence (p less than 0.004) of early, but not late, death compared to patients without alteration of ventricular function (35% vs. 4%). Patients who left the operating room with no problems of concern by echo-DCFI had a greater than 90% likelihood of a long-term acceptable outcome compared to patients who had any problem of concern (residual defect, anatomic or technical imperfection, ventricular dysfunction, and so on) whose long-term likelihood of an acceptable outcome approached 50% (p less than 0.0125).(ABSTRACT TRUNCATED AT 400 WORDS)