Cardiopulmonary bypass (CPB) exposes blood to artificial surfaces, resulting in mechanical damage to the formed elements of the blood. The purpose of this study was to examine the effect of poly(2-methoxyethylacrylate) coating (PMEA, X-Coating™) on coagulation and inflammation under various prime conditions. An in vitro analysis was conducted utilizing fresh whole human blood (2 units) and a CPB circuit (n 18) consisting of a venous reservoir, oxygenator, and arterial filter. Nine nontreated circuits were used in a control group (CTR) and an equal number of tip-to-tip PMEA circuits for treatment (TRT). Each group was divided into three subgroups based upon prime: crystalloid, hetastarch (6%), and albumin (5%). CPB was conducted with a hematocrit 30% ± 2, temperature 37°C ± 1, and a flow of 4L/min. Samples were collected at 0, 60, 120, and 240 minute intervals. Endpoint measurements included thromboelastograph index (TI), and markers of inflammation and coagulation. The TI was significantly depressed in both groups when hetastarch was used in the prime. The TRT had significantly higher TI levels in both the crystalloid (0.3 ± 0.1 vs. −3.3±[1.2, P < .05) and albumin (0.6 ± 0.2 vs−3.9± −1.1. P < .03) subgroups compared to CTR groups. Platelet count was significantly higher in TRT as compared to CTR groups, except for both hetastarch groups. SEM demonstrated significant fibrin deposition on nontreated circuitry but little to no detection in the TRT group. In conclusion, both surface coating and prime components significantly effect coagulation, with PMEA circuits resulting in more favorable preservation of function.

Increasing, the colloid osmotic pressure (COP) of blood cardioplegia (BCP) may reduce myocardial edema and preserve cardiac function following cardiopulmonary bypass (CPB). The purpose of this study was to quantify the effects of albumin (ALB) supplementation on cardioplegia COP through an in vitro analysis. A self-contained cardioplegia delivery system administered supplemental ALB to four BCP ratios (1:1, 4:1, 8:1, and 20:1). In Group A, 25% ALB was combined with BCP at four delivery rates (0,13, 25, and 50 mL ALB/L BCP), with a delivery rate of 0 mL ALB/L BCP serving as the control for all groups. Twenty-five percent ALB was added to crystalloid to create carrier solutions containing 12.5, 25, or 50 g ALB/L in Group B, while Group C combined an ALB delivery rate of 50 mL ALB/L BCP with each of the three carrier solutions. Endpoints included initial and post-supplementation hematocrit, total serum protein (TSP), and COP. Without supplemental ALB, TSP was less affected with increasing blood to crystalloid ratios (1:1-81.7 ± 6.2%, 4:1-40.6 ± 5.1%, 8:1-20.6 ± 4.1%, 20:1-6.0 ± 5.7%). The TSP of 1:1 and 4:1 BCP increased (p < .0003 and p < .02) across all methods of supplementation, while 8:1 BCP was similarly increased (p < .008), except with 12.5 and 25 g ALB/L carrier solutions. The greatest change from baseline COP was seen with the lower blood to crystalloid ratios (1:1-64.3 ± 5.0% and 4:1-39.5 ± 10.5%). In higher ratios, the effects of dilution were less profound (14.6 ± 4.2 ± 4.2% and 20:1-6.0 ± 1.9%). COP of 1:1 BCP increased (p < .008) whenever ALB was added. In conclusion, TSP and COP of blood cardioplegic solutions is increased by supplemental albumin administration with quantitative enhancement dependent upon the dilutional effects of the blood to crystalloid ratio.

The preoperative use of platelet inhibitors has increased the risk of bleeding during cardiac surgery. Aprotinin has been shown to preserve hemostatic function in patients undergoing CPB. The purpose of this study was to investigate the effect of aprotinin on coagulation in blood exposed to eptifibatide. Freshly collected bovine blood was used in an in vitro model of extracorporeal circulation. Blood was separated into two groups: activated (60 minutes exposure to bubble oxygenation) and nonactivated. Within each group there were four subgroups: control (n = 3), eptifibatide (2.8 µg/mL, n = 3), aprotinin (250 KIU/mL, n = 3), and eptifibatide with aprotinin (2.8 µg/mL, 250 KIU/mL, n = 3). Twenty-four modified extracorporeal circuits utilizing a hard-shell venous reservoir and cardioplegia heat exchangers were used. Blood flow was maintained at a rate of 1.25 L/min for a total of 170 minutes, at 37 ± 1°C. Samples were collected at 0, 20, 50, and 110 minutes with the following variables measured: thromboelastograph (TEG), activated clotting time (ACT), and hematocrit (Hct). Results demonstrated that at 110 minutes, the TEG index (TI) was decreased by fourfold in the activated group compared to the nonactivated group (−4.6 ± 1.2 vs. 1.4 ± 1.5, p. < .05). The administration of aprotinin resulted in preservation of the TI as compared to eptifibatidetreated blood (−4.9 ± 1.2 vs. −7.9 ± 1.2, p < .05). Aprotinin combined with eptifibatide reduced coagulation derangements when compared to eptifibatide alone (−5.2 ± 1.2 vs. −7.9 ± 1.2, p < .05). In conclusion, aprotinin attenuated the platelet inhibition effect of eptifibatide during in vitro CPB, resulting in improved coagulation.

Cancellation of on-pump coronary artery bypass grafting after the circuit is primed may result in the discarding of unused circuits. In some off-pump cases, a surgeon may request that the circuit be primed, but complete the surgical procedure without utilizing the circuit. The major concerns about the unused circuit are its sterility and the performance of the oxygenator after it has been primed for a long period of time. The goal of this study is to determine whether prepriming of the circuit with and without albumin has an effect on the gas transfer efficiency of oxygenators during simulated cardiopulmonary bypass. Monolyth integrated membrane lungs (Sorin Biomedical, Arvada, CO) were used to deoxygenate and oxygenate the bovine blood. Oxygenators were preprimed for 72 (N = 6) and 24 (N = 6) hours before testing. In control group (N = 6), oxygenators were tested immediately (0 h) after they were primed. Three different priming solutions were used: physiological saline solution (Group A); 1.25% of human albumin (Group B); and 5% human albumin (Group C). The blood was modified to the American Association of Medical Instrumentation Standards before testing. The blood flow through the oxygenators was set at 2 Lpm and 4 Lpm, with gas (FiO2 at 1.0) to blood flow ratio at 1:1. Cultures were also obtained from preprimed oxygenators to test circuit sterility. Oxygen transfer in oxygenators primed for 0 h at blood flow of 4 Lpm were 203 mL/min ± 9.7 (Group A), 263.1 mL/min ± 52.9 (Group B), and 270.5 mL/min ± 13.1(Group C, p < .01 vs. Group A). In oxygenators preprimed for 72 h, the CO2 transfers were 135.0 mL/min ± 21.8 (Group A), 104.9 mL/ min ± 2.4 (Group B), and 148.9 ± 26.6 (Group C, p < .006 vs. Group B). In addition, the pressure drops were 56.5 mmHg ± 5.5 (Group A), 82.6 mmHg ± 13.4 (Group B), and 67.6 mmHg ± 15.3 (Group C, p < .05 vs. Group B). In group A, O2 transfer were 203.5 mL/min ± 9.7 (0 h), 272.4 mL/min ± 66.6 (24 h), and 260.8 mL/min ± 31.1 (72 h, p < .01 vs. 0 h). In group B, O2 transfer were 263.1 mL/min ± 52.0 (0 h), 302.7 mL/min ± 77.4 (24 h), and 235.2 mL/min ± 16.5 (72 hr, p < .02 vs. 24 hr). Cultures obtained from 12 preprimed oxygenators presented no organism growth for up to 5 days. In conclusion, oxygen transfer increases in oxygenators preprimed with albumin immediately after they were primed. However, gas transfer decreased after they were primed with albumin for 72 h. Oxygenators preprimed for 24 h and 72 h with 0.9% saline had better O2 transfer than those primed for 0 h.