Abstract 338: Impact of No-Flow Time on the Coagulopathy of Prolonged Cardiac Arrest

Abstract

Introduction: Prolonged cardiac arrest (CA) eligible for ECPR has pathologic features that are more pronounced than CA durations in which ROSC is typically achieved. One such feature is consumptive coagulopathy resulting in microvascular thrombosis and no-reflow. In this study we examined the impact of no-flow time on CA coagulopathy during prolong CPR in swine Hypothesis: No-flow time amplifies the coagulopathy of prolonged cardiac arrest. Methods: Animals were anesthetized and instrumented for hemodynamic monitoring. After 4 or 8 min of untreated ventricular fibrillation (groups CA-4 and CA-8, n=5/group), goal-directed CPR was initiated and continued for a total arrest time of 45 minutes. Viscoelastic properties of clot formation and fibrinolysis were measured by TEG in whole blood at baseline and at the end of resuscitation protocol. Rate of fibrin activation (Angle alpha), Maximum amplitude (MA), Time to MA (TMA), and reduction of clot after 30 min (CL30) were measured to describe coagulation status. Results: TEG showed reduction in clot strength after the CPR protocol. For groups CA-4 and CA-8, Alpha declined from 71(4) to 55(7) and from 68(5) to 51(9) deg, MA reduced from 75(2) to 58(7) and from 73(3) to 53(11) mm and TMA prolonged from 21(2) to 27(4) and from 20(4) to 25(2) min. CL30 increased from 95(2) to 97(2) and from 96(2) to 100(1) % (all p<0.05). Clot lysis was more reduced in CA-8 (p<0.05) but other parameters did not significantly vary between groups. Overall, platelets declined from 328(86) to 138(81) thousands/mm3 while hematocrit increased (all p<0.01). Conclusion: In this clinically relevant model of prolonged CA with consumptive coagulopathy, the reduction of clot formation and clot strength after 45 minutes of CA and CPR was not significantly different with 4 and 8 min no-flow time. However, clot lysis was more reduced after 8-min no-flow. Further studies are needed to determine the impact of no-flow time on CA coagulopathy at the microvascular level.