Abstract P28: Clotting Function is Impaired Within Minutes of Return of Spontaneous Circulation in a Swine Model of Cardiac Arrest
Introduction: Coagulopathy predicts mortality during the post-cardiac arrest syndrome and coagulation’s role during the post-arrest period has been identified as a critical knowledge gap by the International Liaison Committee on Resuscitation. The objective of this study was to describe changes in clotting function taking place during and after cardiac arrest.
Methods: Ventricular fibrillation (VF) was induced electrically in 6 immature male swine (weight 47 +/−2.4 kg) for 12 minutes followed by standard normothermic American Heart Association Advanced Cardiac Life Support. Resuscitated animals underwent a uniform post-resuscitation (ROSC) goal directed hemodynamic support protocol. PT, PTT, fibrinogen, Thrombelastography (TEG), platelet contractile force (PCF), and clot elastic modulus (CEM) were compared at baseline prior to arrest, at 10 minutes of VF, and at 15, 30, 90, 120, and 180 minutes of ROSC using repeated measures ANOVA.
Results: Five of six swine achieved ROSC and were analyzed. PCF (Mean, 95% CI) was 15.0 Kilodynes [11.7, 18.3] at baseline, increased to 16.1 Kilodynes [12.8, 19.4] during VF, fell to 5.7 Kilodynes [2.4, 9.0] by 15 min post ROSC and remained so thereafter (p=0.0001). CEM was 53.3 Kilodynes/cm2 [40.2, 66.3] at baseline, 45.3 Kilodynes/cm2 [32.2, 58.4] during VF, fell to 23.9 Kilodynes/cm2 [10.9, 37.0] at 15 min ROSC and remained depressed at 180 min ROSC (p=0.0016). Clotting time (R) by TEG was 5.6 min [4.0, 7.2] at baseline, decreased to 4.0 min [2.4, 5.6] during VF, increased to 8.5 min [6.9, 10.1] at 15 min ROSC and remained elevated at 180 min (p=0.005). Clot strength by TEG (MA) increased from 70.9 mm [66.3, 75.4] at baseline to 74.8 mm [70.3, 79.4] during VF, then fell to 63.3 mm [58.8, 67.9] at 15 min ROSC and remained depressed thereafter (p=0.028). PT, PTT, fibrinogen, and platelet counts were normal and did not change significantly during VF or ROSC (all p>0.12).
Conclusion: In this swine model of cardiac arrest, clotting function tended to become enhanced during VF and was significantly impaired during resuscitation. These changes were due to reduced platelet contraction and delayed clot initiation that occurred within minutes of ROSC. Future studies will examine the effect of hypothermia on post-resuscitation coagulation.