The pathophysiological consequence associated with cardiopulmonary bypass (CPB) has generated a movement away from this technology in the treatment of heart disease. The negative outcomes are multifactorial in origin and may be associated both with the conduct of CPB and the instrumentation of extracorporeal flow. The purpose of this study was twofold. First, to develop a bedside patient risk assessment to aid in the development of a perfusion care plan. Second, to identify the controllable variables used during CPB that contribute to overall morbidity. Controllable perfusion-related variables that were positively linked to improved patient outcomes were identified from randomized, peer-reviewed human studies. Such variables as hematocrit, mean arterial pressure, thermic perfusion, blood lactate, colloid osmotic pressure, pulsatile perfusion, acid base homeostasis, oxygenation, and coated circuitry were included. Patient risk assessment was developed using the Society of Thoracic Surgeon database, where 61 variables affecting postoperative morbidity were identified. These variables were used to develop a bedside tool, Mortality Assessment Perfusion Score (MAPS), to guide the perfusion patient care plan. The MAPS generates a specific value that may predict patient morbidity and mortality based on past mortalities. In conclusion, the improvement in patient outcome may be associated with both the change in conduct of CPB and the quantitative assessment of patient risk stratification and a patient treatment algorithm.

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.

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.