Studies Of The Changes Of Haemostatic Mechanisms In Peri-Cardiopulmonary Bypass

Objective The changes of hemostatic mechanisms in peri-cardiopulmonary bypass (peri-CPB) vary greatly, which have two main complications:blood loss and thromboembolism. This study was to continually measure and observe the variants related to hemostatic mechanisms (coagulation, fibrinolysis and anticoagulation), and to analyze correlation between post CPB blood loss and the above mechanisms, and to observe prolonged CPB duration affected by these hemostatic variants.Through this study, we intend to find the different characteristics and regularity above the changes of the mechanisms. The factors affecting the blood loss and thromboembolism peri-CPB may be discovered. Thereby this study may provide theoretical basis for the prophylaxis and treatment of clinical complications, and may play a guiding role in treatment of post CPB anticoagulation.Methods Fifty patients undergoing CPB cardiac surgery between April 2013 and April 2014 were studied consecutively. Twenty variants were consecutively measured at 8 time-interval during 72h from pre-CPB to post CPB. The differences of post CPB between each time-intervals were compared with pre-CPB basis data. The relationship between each other hemostatic system, and between post CPB-blood loss and each hemostatic variants were analyzed. According to CPB duration, the patients were divided into two groups. The difference of each variant between two groups at 8 time intervals was compared. Out of this, the facts affecting post CPB blood loss increased and hemostatic variants disorder should be discovered.Results 1. Blood coagulation function:Blood coagulation factors decreased during early CPB, the extrinsic coagulation factors obviously reduced to 56%, at 1h post CPB, the level of F Ⅱ, F V and F X were significantly lower than that of pre-CPB (P<0.05), withD-Dimer elevated and PT prolongation. After 24h post CPB, all blood coagulation factors increased, especially inttinsic factors which reached to 20° above pre-CPB(P<0.05).2. Fibrinolytic system:tPA rose significantly during CPB[from (11.72±6.6)ng/ml to (18.33±7.7)ng/ml, P<0.01]. tPA reached peak at 6h post CPB[(23.7±4.3)ng/ml],which was two times of the amount pre-CPB. PAI change versus tPA:pre-CPB was (28.9±6.1)ng/ml, dropped sharply to (16.0±16.5) ng/ml(P<0.05) at 1h post CPB, which was only 45% of pre-CPB amount. and remained low level(P<0.05) till 72h post CPB. PLG varied samely with ATPL. They reduced to 45% of pre-CPB levels during CPB(P<0.01),and remained lower level at 1h post CPB. But they rosed up more after 24h post CPB than pre-CPB level(P<0.05).3.Anticoagulative system:P C reduced after 48h post CPB, and reached to (77.1±25.8)% 72h post CPB, which reduced significantly in comparing with pre-CPB basis data (98.1±27.4)% (P<0.05).AP C first elevated post CPB (1.16± 0.42),then reduced to 0.79±0.28 and 0.82±0.40 at 24h and 48h post CPB, which reduced significantly less than pre-CPB level 1.03±0.13(P<0.01).Analysis of correlation between P C system and fibrinolytic system showed negative correlation between AP C and PAI(r=-0.2556, P<0.001), positive correlation between AP C and tPA (r=0.3927, P<0.001). Heparin elevated significantly at 1h post CPB[(0.14±0.15) U/ml], which was 1.6 times of pre-CPB level [(0.086±0.200)U/ml] (P<0.05), and returned to pre-CPB level at 6h and 24h post CPB. But heparin increased again to (0.13±0.29)U/ml and (0.30±0.39)U/ml at 48h and 72h post CPB, which was 2.1-3.4 times of pre-CPB pre-CPB level(P<0.05).4. The amount of blood loss within 12h post CPB was 72% of the total amount of within 72h post CPB. The blood loss showed negative correlation with PAI(r= 0.2657, P<0.01),and positive correlation with extrinsic coagulation factors(P<0.001), and positive correlation with heparin(r=0.3939, P<0.001).5.Comparison with two groups showed:CPB duration effected on fibrinolysis significantly, but no influence of coagulation factors and anticoagulative system. tPA in group Ⅱ (CPB≥120min during CPB elevated significantly more than that in group Ⅰ (CPB<120min), respectively group Ⅱ(21.9±7.0)ng/ml and group Ⅰ(13.1±6.1)ng/ml (P<0.01). There were no significant difference between the two groups at each time-interval post CPB. PAI in group Ⅱ was significantly higher than that in group I at pcri-CPB[respectively group Ⅱ(31.5±5.7)ng/ml and group Ⅰ(25.7±5.3)ng/ml, P<0.05], no significant difference was found during CPB. PAT in group Ⅱ dropped sharply to (8.2±7.2) ng/ml and (10.5±13.3)ng/ml within 1 h and 6h post CPB. But PAI in group Ⅰ remained same level to pre-CPB. The difference was signif(?) between group Ⅱ and group Ⅰ (P<0.05).Conclusions:1.Hyperfibrinolysis is the main cause of disfunction of hemostatic mechanisms pre-CPB.The mechanism of hyperfibrinolysis is imbalance between tPA and PAI.Reduced PAI is the main factor causing increase of blood loss post CPB. Prolonging CPB duration can significantly effect on changes of PAI.2. Activity of PC system elevates post CPB early phase, which is related to hyperfibrinolysis. AP C negatively correlates with PAI, and positively correlates with tPA, which indicated PC system can promotes fibrinolysis.3. It is recommanded that measuring PAI peri-CPB may help to predict blood loss or thromboembolism. Observing D-Dimer, PT and APTT may help to diagnose hypercoagulable state and thrombosis trend.