Thrombin-antithrombin appearance in out-of-hospital cardiac arrest

Intravascular thrombosis induced during out-of-hospital cardiac arrest (OOHCA) may contribute to the pathophysiology of cardiac arrest and complicate resuscitation. We characterized the prevalence of thrombogenesis during OOHCA by measuring plasma levels of thrombin-antithrombin complexes (TAT).

An observational cohort study of medical OOHCA patients in an urban emergency medical services (EMS) system. Subjects were patients>or=18 years suffering medical OOHCA. Citrated blood samples were drawn in the prehospital setting either directly from venous blood or during the placement of a central venous catheter and frozen (-70 degrees C). The EMS physician documented age, gender, time intervals, return of spontaneous circulation (ROSC), therapies administered and time of blood draw. TAT assays were performed by commercial ELISA.

Eighty-eight patients (58% male) aged 63.4+/-15.9 years were enrolled in the study. Median [interquartile range IQR] TAT values in 80 samples (8 samples were grossly clotted and excluded) were 159.2 [38, 2, 522, 8] and ranged from 0.79 to 1,343.9. Patients transported to the hospital had lower TAT levels than those pronounced in the field (p=0.014). Of four EMS-witnessed arrests, three had return of pulses with TAT values of 0.79, 6.8, and 17.9. The fourth had a TAT over 525 after a long unsuccessful resuscitation. For subjects with TAT below 50 (n=23), all but three were witnessed arrests or received bystander CPR.

Except for a single case witnessed by EMS and immediately defibrillated into a perfusing rhythm, all cases of OOHCA exhibited increased thrombotic state. Intravascular thrombosis may represent a global barrier to resuscitation and ultimately, end-organ perfusion.