Abstract 12447: Early Coronary Reperfusion Improves Cerebral and Systemic Hemodynamics After Ischemic Refractory Cardiac Arrest and Extracorporeal Resuscitation in Pigs
Introduction: Extracorporeal cardiopulmonary resuscitation (ECPR) is widely proposed for the treatment of refractory cardiac arrest. It should be associated to etiologic determination, especially if acute coronary artery occlusion is suspected. However, prioritization of care remains unclear in this situation.
Hypothesis: Our goal was to determine whether reperfusion should be instituted as soon as possible during ischemic refractory cardiac arrest treated by extracorporeal cardiopulmonary resuscitation (ECPR) in pigs.
Methods: Pigs were instrumented and submitted to coronary artery occlusion prior to ventricular fibrillation. After 5 min of untreated cardiac arrest, life support was started using external chest compression (ECC) during 15 min followed by ECPR during 240 min, respectively. Animals randomly underwent either early or late coronary reperfusion after 20 or 120 min of ECPR, respectively. Return of spontaneous circulation (ROSC) was determined as organized ECG rhythm with systolic blood pressure above 80 mmHg.
Results: Hemodynamic parameters were not different between groups at baseline or during ECC. Since the onset of ECPR, carotid blood flow was improved by ≈70% vs ECC in both groups. No animal (0/7) elicited ROSC after late reperfusion vs 4/7 after early reperfusion (p<0.05). Hemodynamic parameters, such as mean arterial pressure and carotid blood flow, were improved in early vs late reperfusion groups (Figure), along with infarct size decrease (71±4 vs 84±2 % of the risk zone, respectively; p<0.05).
Conclusions: Early reperfusion improved hemodynamic status and increased ROSC chances after ischemic refractory cardiac arrest treated by ECPR. This supports the need of rapid reperfusion in this situation.
Figure: Carotid blood flow after extracorporeal cardiopulmonary resuscitation (ECPR) and successful defibrillation (*, p<0.05 between groups; comparisons were only made at the end of the follow-up).
Author Disclosures: A. Hutin: None. L. Lamhaut: None. F. Lidouren: None. M. Kohlhauer: None. N. Mongardon: None. P. Carli: None. A. Berdeaux: None. B. Ghaleh: None. R. Tissier: None.
- © 2016 by American Heart Association, Inc.