The effect of electrolyte imbalance on weaning from cardiopulmonary bypass: an experimental study.

An imbalance in electrolyte concentration during separation from cardiopulmonary bypass (CPB) may lead to a disruption in excitation-contraction coupling resulting in a failure to wean. The etiology of myocardial dysfunction is multifactorial, and includes alterations in acid-base balance, glucose metabolism, and cellular function. The purpose of this study was to assess the effect of hyperkalemia on myocardial function during separation from CPB. A porcine model (n = 5) of hypothermic (32 degrees C) CPB was used where hyperkalemia [K+ (6.5 +/- 1.0)] was created before weaning. A 3-minute weaning process was initiated once normothermia was achieved. Mixed venous and arterial samples were obtained during CPB, weaning, and 10 minutes postbypass. Samples were assayed for [K+], [Ca++], glucose, pH, CPK-MB, and lactic acid levels. Hyperkalemia resulted in the generation of severe arrhythmias in all animals. During the immediate prewean period, there was a significant correlation between venous [K+] and pH (p < .01, r2 =.891). Arterial pH did not change during the weaning or post-CPB period, while venous pH declined significantly throughout the same period (7.35 +/- 0.75 to 7.20 +/- 0.17, p < .05). No other measured variables correlated with hyperkalemia. In summary, hyperkalemia caused a significant decline in venous pH evidenced in the early separation period, but had no effect on other variables. Therefore, measurement of venous pH may be an early marker indicating myocardial dysfunction and dysrhythmia.

Expanding perfusion services through mobile point-of-care coagulation monitoring.

Current trends in cardiac surgery have challenged perfusionists to seek diversification of services. Point-of-care coagulation (POCC) monitoring represents a desirable area of perfusion service expansion. The purpose of the study was to create a series of hemostatic conditions to assess the functionality of POCC monitors to identify specific coagulopathies with identifiable profiles for algorithm development. Fresh (< 4 h) bovine blood, anticoagulated with anticoagulant citrate dextrose, was adjusted to a hematocrit of 30.0 +/- 2.0%. Hypofibrinogenemia < or = 90 mg/dL), thrombocytopenia (< or = 70,000/mm3), platelet dysfunction (850 microg/mL of nitroglycerin/mL of blood) and hyperfibrinolysis (0.40 units of urokinase/mL of blood) were created. Five POCC devices were used to evaluate activated clotting time, thrombin time, fibrinogen, platelet function, prothrombin time, activated partial thromboplastin time and thromboelastograph. Results are reported as percentage change from control for each test (abtract table). [table: see text] Each test performed showed specificity and sensitivity for certain coagulopathies, however variability amongst monitors was encountered. In conclusion, the development of a mobile cart incorporating POCC monitors with knowledge of specific coagulopathic conditions may expand perfusion service.

The effects of ultrafiltration on e-aminocaproic acid: an in vitro analysis.

Blood conservation strategies have become a standard of practice in cardiac surgery, with the use of antifibrinolytic agents and ultrafiltration two popular techniques. The purpose of this study was to evaluate the effects of continuous ultrafiltration on e-aminocaproic acid (EACA) utilizing functional coagulation analysis. A fibrinolytic assay was developed to detect EACA using the thromboelastograph (TEG) and urokinase (0.138 units 0.360 mL(-1)). Fresh bovine blood (23 +/- 1% hematocrit) was pumped (100 mL min(-1)) through an ultrafiltrator (HPH 400) at 37 degrees C with a transmembrane pressure of 280 mmHg. EACA (0.065 mg mL(-1)) was circulated for 10 minutes before initiating ultrafiltration. Samples (pre- and postultrafiltrator) were obtained at baseline, 5, and 10 min of ultrafiltration and analyzed via the fibrinolytic assay for EACA determination. TEG profiles significantly decreased from concentrations of 0.065 mg to 0.0325 mg of EACA mL(-1) blood (maximum amplitude MA, 75.4 +/- 4.0 versus 63.3 +/- 2.9, p < .05, TEG index 5.4 +/- 0.7 versus 4.0 +/- 0.3, p < .05). Fibrinolysis at 30 min increased as EACA concentrations declined (0.065 mg, 0% versus 0.032 mg, 16.4 +/- 2.8%, p < .05). During ultrafiltration the MA increased significantly from baseline to 10 min postultrafiltrator (68.2 +/- 3.0 versus 75.8 +/- 10.0, p < .05) and from 5 min pre- to 10 min postultrafiltrator (69.7 +/- 4.2 versus 75.8 +/- 10.0, p < .05). The TEG index showed no significant change, and no fibrinolysis was detected at 30 min from any datapoint during ultrafiltration. In conclusion, this study demonstrates that the antifibrinolytic properties of EACA are maintained during ultrafiltration with a 25% reduction in total circulating volume.

The effect of controlled aprotinin administration through cardiotomy suction during cardiopulmonary bypass.

Cardiotomy suction enhances inflammation and fibrinolysis during cardiopulmonary bypass (CPB). Aprotinin has been shown to reduce the generalized inflammatory insults associated with CPB. The purpose of this study was to evaluate the effect of Aprotinin administration through cardiotomy suction on the inflammatory and fibrinolytic responses during CPB. A pig model of CPB was utilized including 8 animals divided into control and treatment groups. In the treatment group, Aprotinin was infused into the cardiotomy suction (3000 KIU/min), while the same volume of saline was infused in the control group. D-dimer, platelet count, and IL-8 level were analyzed from systemic and cardiotomy suction. It was found that Aprotinin significantly suppressed the increase in D-dimer levels in the systemic (476.3 +/- 341.2 vs. 1218.8 +/- 281.3 ng/ml, p < 0.05) and the cardiotomy suction (565.0 +/- 192.5 vs. 1875.0 +/- 125.0 ng/ml, p < 0.05). Platelet count fell in both groups during CPB, although the reduction was greater in the control (13.1 +/- 5.1 vs. 37.9 +/- 13.8%, p < 0.05). In addition, IL-8 level in the suction solution was significantly lower in the Aprotinin group (56.5 +/- 18.0 vs. 136.3 +/- 14.8 pg/ml, p < 0.05). In conclusion, this study suggested that Aprotinin treatment of the cardiotomy solution might be an effective way of reducing fibrinolysis, platelet reduction, and inflammation associated with CPB.

Effects of increasing FiO2 on venous saturation during cardiopulmonary bypass in the swine model.

Adequacy of perfusion during cardiopulmonary bypass (CPB) is dependent on nutrient delivery and waste removal from the tissue. A recent study showed that over 75% of cardiopulmonary bypass procedures are completed using continuous venous saturation (SvO2) monitoring. The purpose of this study was to determine the effect of changing FiO2concentration on SvO2. A total of eight mixed gender 45-kg swine were placed on CPB under moderate hypothermic conditions. Animals were divided evenly into two groups: Experimental, where FiO2 was increased to 100% and blood flow decreased to an SvO2 level of prechange in FiO2, and Control, where the same condition was created except no change in blood flow. Variables measured include hemodynamic, blood gas, intramyocardial pH, and lactic acid concentrations. In the experimental group, percentage change of blood flow was decreased from baseline 28.4% +/- 12.5% (p < .005) as well as percentage change of oxygen delivery 23.9% +/- 14.7% (p < .005). Systemic venous saturation percentage change was increased in both the experimental 14.4% +/- 6.8% (p < .05) and control 11.2% +/- 7.1% (p < .05) groups. Jugular venous saturation percentage change was decreased in the experimental group 7.8% +/- 6.34% (p < .02), but not in the control animals. Myocardial venous saturation percentage change decreased in the experimental group to 3.73% +/- 8.34% (p < .004). Experimental manipulation, however, did not significantly change jugular lactic acid concentrations or intramyocardial pH values. In conclusion, these results suggest that decreased blood flow adjusting for increased SvO2 associated with high PaO2 did not result in significant reduction of adequacy of perfusion markers for organs studied.