AIMS: Coagulopathy is often present after resuscitation from cardiac arrest but plays an undefined role in the post cardiac arrest syndrome. The aim of this study was to characterize coagulation changes during cardiac arrest and post-resuscitation care in order to direct further focused study. METHODS: Ventricular fibrillation (VF) was induced electrically in immature male swine, followed by normothermic American Heart Association Advanced Cardiac Life Support and a uniform post-resuscitation goal-directed resuscitation protocol. PT, aPTT, fibrinogen, Thrombelastography (TEG), platelet contractile force (PCF), clot elastic modulus (CEM), and collagen-induced platelet aggregation were compared at baseline, at 8 min of VF, during the 3rd round of chest compressions (CPR), and at 15, 90, 180, and 360 min after return of circulation using repeated measures ANOVA. RESULTS: 8/18 (44%) animals were resuscitated after 10.9 ± 0.9 min of VF and 7.6 ± 3.4 min of CPR. TEG revealed a significant impairment in clot strength (MA) and clot formation kinetics (K, alpha angle) arising during CPR, followed by a brief prolongation of clot onset times (R) after return of circulation. Both PCF and CEM fell significantly during CPR (PCF by 50%, CEM by 47% of baseline) and platelet aggregation was significantly decreased during CPR. Coagulation changes were partially recovered by 3h of post-resuscitation care. CONCLUSION: Whole blood coagulation was rapidly impaired during CPR after electrically induced VF in this swine model by impaired platelet aggregation/contractile function and clotting kinetics. Further platelet-specific study is indicated.
AIMS: Coagulopathy is often present after resuscitation from cardiac arrest but plays an undefined role in the post cardiac arrest syndrome. The aim of this study was to characterize coagulation changes during cardiac arrest and post-resuscitation care in order to direct further focused study. METHODS:Ventricular fibrillation (VF) was induced electrically in immature male swine, followed by normothermic American Heart Association Advanced Cardiac Life Support and a uniform post-resuscitation goal-directed resuscitation protocol. PT, aPTT, fibrinogen, Thrombelastography (TEG), platelet contractile force (PCF), clot elastic modulus (CEM), and collagen-induced platelet aggregation were compared at baseline, at 8 min of VF, during the 3rd round of chest compressions (CPR), and at 15, 90, 180, and 360 min after return of circulation using repeated measures ANOVA. RESULTS: 8/18 (44%) animals were resuscitated after 10.9 ± 0.9 min of VF and 7.6 ± 3.4 min of CPR. TEG revealed a significant impairment in clot strength (MA) and clot formation kinetics (K, alpha angle) arising during CPR, followed by a brief prolongation of clot onset times (R) after return of circulation. Both PCF and CEM fell significantly during CPR (PCF by 50%, CEM by 47% of baseline) and platelet aggregation was significantly decreased during CPR. Coagulation changes were partially recovered by 3h of post-resuscitation care. CONCLUSION: Whole blood coagulation was rapidly impaired during CPR after electrically induced VF in this swine model by impaired platelet aggregation/contractile function and clotting kinetics. Further platelet-specific study is indicated.
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