In light of the potential morbidity associated with transfusion of blood products, a reliable preoperative screening test to identify cardiothoracic surgical patients who are at potential risk for increased intraoperative blood loss would be useful. Accordingly, we examined the efficacy of a variety of coagulation tests to predict intraoperative blood loss in 60 patients presenting for coronary artery bypass surgery (CABG). A complete coagulation screen, activated clotting time (ACT), and thromboelastograph (TEG) were performed before surgery. Intraoperative blood loss was determined by weighing sponges and measuring the quantity of blood in suction canisters. The duration of cardiopulmonary bypass was 100 +/- 4 min, and total surgery time was 5.0 +/- 0.1 h. Total crystalloid and colloid requirements were 5.5 +/- 0.2 and 1.4 +/- 0.1 L. Forty-eight percent of the patients required blood with an average requirement of 2.5 +/- 0.5 units. Total intraoperative blood loss averaged 1590 +/- 95 mL with a range from 640 to 3928 mL. Using multiple linear regression, all coagulation and TEG variables were used to model perioperative blood loss. Results showed that all components of the TEG failed to predict blood loss (r < 0.25, P > 0.78). However, three components of the routine coagulation assay, including bleeding time, prothrombin time, and platelet count could be modeled to predict perioperative blood loss (r = 0.75, P < 0.05). Although TEG has been shown to have potential in identifying postcardiopulmonary bypass coagulopathies, these results suggest that it does not appear to be useful in determining the coagulation status of CABG patients preoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)

Propofol is being used more often in cardiac surgery, particularly after hypothermic, hyperkalemic cardioplegic arrest (HHCA). The purpose of this study was to examine the effects of propofol on isolated myocyte contractile function under both normothermic conditions and after simulated HHCA and rewarming. Myocytes were isolated from the left ventricle of eight pigs. Myocyte contractile function was measured under both normothermic conditions and after simulated HHCA (incubation at 4 degrees C for 2 h in crystalloid cardioplegia; K+ = 24 mEq/L) using computer-assisted videomicroscopy in the presence of 2, 4, and 6 micrograms/mL propofol (11.2, 22.4, and 33.6 microM/L, respectively). Isoproterenol (25 nM) was then added and contractile function measurements repeated. Propofol caused significant dose-dependent reductions in myocyte velocity of shortening (baseline = 67 +/- 2 microns/s; propofol = 2 micrograms/mL, 45 +/- 4 microns/s; and propofol = 6 micrograms/mL, 27 +/- 3 microns/s; P < 0.05). HHCA and rewarming caused a significant reduction in myocyte velocity of shortening (29 +/- 0.9 microns/s, P < 0.05), with further significant dose-dependent reductions in contractile function after the addition of propofol. Propofol caused a decrease in beta-adrenergic responsiveness under normothermic conditions, but not after simulated HHCA. Results from the present study demonstrated for the first time that the reduction in isolated myocyte contractile function after simulated HHCA is further decreased by propofol administration.

The direct and interactive effects of phosphodiesterase inhibition (PDEI) and beta-adrenergic receptor (beta AR) stimulation on isolated myocyte contractile function were examined after hypothermic, hyperkalemic, cardioplegic arrest (HHCA) and under normothermic conditions. Left ventricular (LV) myocytes were isolated from porcine hearts and myocyte contractile function was measured under normothermic conditions (37 degrees C in standard media) and after HHCA (2 h at 4 degrees C in Ringer's solution with 24 mEq KCl) with subsequent rewarming. Myocytes were then randomly assigned to treatment with the beta AR agonist isoproterenol (25 nM), the phosphodiesterase inhibitor amrinone (50 microM), or a combination of these compounds and contractile function measurements repeated. Baseline myocyte contractile function was reduced by 32% after HHCA. Isoproternol alone increased myocyte contractile function more than 100% under both normothermic conditions and after HHCA, whereas amrinone alone significantly (60%) improved myocyte contractile function only after HHCA. Amrinone preincubation followed by isoproterenol improved contractile function after HHCA to a greater extent than all other treatment protocols. In contrast, combination treatment under normothermic conditions did not augment myocyte contractile function relative to isoproterenol alone. These findings suggest that amrinone has differential effects on contractile processes. Moreover, the marked improvement of contractile function after HHCA with PDEI pretreatment followed by beta AR stimulation may have implications in treatment strategies for improving myocardial function after cardiopulmonary bypass and provide insight into contractile dysfunction after HHCA.

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