ACTIVATION OF BLOOD-COAGULATION AFTER CARDIAC-ARREST IS NOT BALANCED ADEQUATELY BY ACTIVATION OF ENDOGENOUS FIBRINOLYSIS

Background Animal studies have demonstrated that hemostatic disorders occurring after cardiac arrest affect outcome. We investigated hemosta tic changes during and after cardiopulmonary resuscitation (CPR) in hu mans. Methods and Results The prospective study included 23 patients ( 29 to 86 years) who underwent out-of-hospital CPR for nontraumatic cau ses. Blood samples were drawn immediately and 15 and 30 minutes after initiation of CPR. In the case of restoration of spontaneous circulati on (ROSC; n=7), additional blood samples were taken immediately, 30 mi nutes, and 2, 8, 24, 48, and 72 hours after ROSC A marked activation o f blood coagulation was found in all patients. The specific markers of activated blood coagulation and fibrin formation, thrombin-antithromb in complex (TAT; median during CPR, 260 mu g/L; median after ROSC, 57 mu g/L; normal range, 1.0 to 4.1 mu g/L), and fibrin monomers (FM; med ian during CPR, 34.3 mu g/mL; median after ROSC, 65.4 mu g/mL; normal range, 0 to 3.6 mu g/mL) were markedly increased during and in the ear ly phase after CPR. When patients survived for 48 hours, TAT and FM va lues returned to the normal range. In most patients, the plasma levels of D-dimer, an indicator of endogenous fibrinolytic activity, were no t markedly increased during CPR (median, <0.25 mu g/mL; normal range, <0.25 mu g/mL) but increased moderately after ROSC (median, 0.56 mu g/ mL). Levels of plasminogen activator inhibitor type 1 (normal range, 0 .3 to 3.5 U/mL), a marker for endogenous inhibition of fibrinolytic ac tivity, were moderately increased in most patients (median during CPR, 4.22 U/mL; median after ROSC, 8.08 U/mL). Conclusions Our data clearl y demonstrate that there is a marked activation of blood coagulation a nd fibrin formation after prolonged cardiac arrest and CPR in humans t hat is not balanced adequately by concomitant activation of endogenous fibrinolysis. These changes may contribute to reperfusion disorders, such as the cerebral ''no-reflow'' phenomenon, by inducing fibrin depo sition and formation of microthrombi.