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Cardiorespiratory failure just before surgery in critically ill thoracic transplant patients can have catastrophic consequences. We judged the cardiorespiratory condition in three of 160 thoracic transplant procedures performed in our center too unstable for a safe induction of anesthesia. In these 3 patients, extracorporeal membrane oxygenation support was installed before induction of anesthesia to maintain an adequate cardiorespiratory state. This strategy was successful for all 3 patients, and long-term survival was achieved with a good quality of life. Guidelines for indications to follow this strategy are discussed.

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BACKGROUND: Extreme dilution of clotting factors, as may occur during pediatric or neonatal cardiopulmonary bypass, often leads to inadequate monitoring of anticoagulation with activated clotting time (ACT). In this study we postulate that the high-dose thrombin time (HiTT) is less influenced by extreme dilution of clotting factors because it stimulates clotting through the common pathway. METHODS: Heparinized prebypass blood was obtained from 30 adult cardiac surgical patients and was diluted in a laboratory setting with saline solution to mimic the clinical clear prime solution (group I; n = 10), with saline solution containing similar heparin as in the prebypass blood (group II; n = 10), and with fresh frozen plasma to substitute clotting factors in the diluted blood (group III; n = 10). Blood was diluted to four different degrees: a control without dilution, 25%, 50%, and 75% dilution. The ACT and HiTT were measured and compared. RESULTS: In group I, significant prolongation of ACT was observed in blood diluted to 75% as compared with the nondiluted blood (p < 0.01). In contrast, HiTT was not prolonged at any degree of dilution but reduced proportionally to dilution up to 75%, reflecting the concomitant reduction of heparin. In group II, ACT increased at 25% dilution (p < 0.01) whereas HiTT increased at 50% dilution (p < 0.01). In group III, no prolongation of ACT or HiTT was found in any degree of dilution. Furthermore, adding fibrinogen to the diluted blood (n = 4) did not cause ACT to recover at 75% dilution, suggesting that dilution of other factors in the early clotting cascade rather than fibrinogen alone increases ACT. CONCLUSIONS: These results imply that when blood is extremely diluted during cardiopulmonary bypass with a clear prime without substituted clotting factors, HiTT is a better test than ACT for anticoagulation monitoring.

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Since aprotinin has become extensively used during cardiopulmonary bypass the maintenance of safe anticoagulation is a concern. Aprotinin affects anticoagulation measurement by the activated clotting time. Therefore, a reliable new measurement is needed to monitor anticoagulation during cardiopulmonary bypass. In the present study, we tested the efficacy of two alternative measurements in which whole blood clotting was stimulated by high-dose thromboplastin or by high-dose thrombin. During cardiopulmonary bypass under standardized heparinization, the activated clotting time was twofold longer in the aprotinin group than in control group (p < 0.05), whereas high-dose thromboplastin and high-dose thrombin groups were not significantly affected by aprotinin. In laboratory tests using blood from healthy volunteers, all methods showed linear correlation with heparin concentration in the absence of aprotinin (p < 0.05). However, the activated clotting time measurement was prolonged more by heparin when aprotinin was present (p < 0.05), whereas high-dose thromboplastin and high-dose thrombin measurements were not. Moreover, these measurements were faster and more dependable than the activated clotting time. Therefore, high-dose thromboplastin time and high-dose thrombin time seem to be reliable for monitoring anticoagulation when aprotinin is used during cardiopulmonary bypass.

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Monitoring of anticoagulation during cardiopulmonary bypass by means of the activated coagulation time (ACT) has become questionable due to the prolongation in the clotting time of patients receiving aprotinin. Because the celite-based ACT only indicates intrinsic coagulation, and sufficient anticoagulation is needed to also prevent extrinsic coagulation, the ACT may not be reliable. Three different clotting times, the celite-based ACT, the kaolin-based activated coagulation time (AKT) and the high-dose thrombin time (HITT), were compared in a prospective, double-blind, placebo-controlled study of 20 patients who were to undergo cardiopulmonary bypass. As expected, neither the kaolin-based assay nor the high-dose thrombin time was influenced by aprotinin, whereas the celite-based ACT was significantly prolonged in aprotinin-treated patients as compared to control patients (P < 0.05). This study confirms that both kaolin-based and thrombin-based tests provide a reliable means of determining the degree of heparinization in the presence of aprotinin during cardiopulmonary bypass.

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Cardiopulmonary bypass generates a systemic inflammatory response including the activation of the complement cascade and leukocytes contributing to postoperative morbidity. To evaluate whether the use of heparin-coated extracorporeal circuits could reduce these activation processes, we performed a study on 30 patients undergoing coronary artery bypass grafting who were randomly perfused with a heparin-coated circuit (Duraflo II, n = 15) or with a similar noncoated circuit (control, n = 15). Standardized systemic heparinization was applied for every patient before cardiopulmonary bypass. The use of heparin-coated circuits resulted in a reduction of systemic leukocyte activation during cardiopulmonary bypass reflected by reduced elastase release (p < 0.05) and tumor necrosis factor generation (p < 0.05) manifest after release of the aortic cross-clamp. In addition, blood samples taken from both the right and left atria after reperfusion revealed that the elastase release from the pulmonary microcirculation was absent in the Duraflo II group in contrast to the control group (p < 0.05). The pattern of complement activation, likely initiating this inflammatory reaction, was modified by heparin coating in two different aspects. There was a significant reduction of C3a generation after protamine administration in patients perfused with heparin-coated circuits, and there was a decrease of complement hemolytic capacity in pooled human serum incubated with heparin-coated tubing. These observations suggest that heparin coating might bind some of the complement components from the classic pathway, thereby reducing the inflammatory response to cardiopulmonary bypass.

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