Abstract 294: Thrombolytics Improve Extracorporeal Cardiopulmonary Resuscitation After 30 Minutes of Untreated Cardiac Arrest
Introduction: Extracorporeal cardiopulmonary resuscitation (ECPR) after prolonged cardiac arrest (CA) often fails to restore cardiac and cerebral function. The primary limiting factor is presumed to be ischemia duration. An alternative hypothesis is that intravascular coagulation prevents tissue reperfusion.
Hypothesis: Adding thrombolytics to ECPR after prolonged untreated CA improves cardiac and cerebral recovery when compared to ECPR alone.
Methods: We developed a porcine model of 30 minute untreated ventricular fibrillation followed by ECPR for 6 hours. Animals were instrumented for hemodynamic and intracranial pressure (ICP) monitoring and continuous EEG. Two groups were studied: t-ECPR (n=7) with streptokinase 1 MU added to prime circuit; c-ECPR (n=6) with no streptokinase. ECPR goals included: flow >50 ml/kg/min, MAP >70 mmHg, PaO2 150±50 mmHg, PaCO2 40±5 mmHg, core temperature 33±1 °C. Recovery of heart function was assessed by echocardiography and weanability from ECPR. After 6 hours, animals were euthanized and brain harvested for quantification of intracerebral hemorrhage and neuronal injury.
Results: Recovery of heart function following defibrillation occurred in 1/6 c-ECPR and 7/7 t-ECPR animals (p <0.05). Successful weaning from ECPR within 6 hours was achieved in 1/6 c-ECPR and 4/7 t-ECPR animals. Six-hour lactate clearance was significantly lower in c-ECPR than in t-ECPR (18±2 % vs 40±15 %, p <0.05). Marked increase in post-arrest ICP occurred in c-ECPR but not in t-ECPR (19±13 mmHg vs 1±3 mmHg, p <0.05). Quantitative EEG analysis revealed no recovery of brain activity in either group. Thrombolytics did not result in increased intracerebral hemorrhage (c-ECPR 0.011±0.001 % vs 0.003±0.002 % t-ECPR, p <0.05). Composite histologic damage score (scale 0 to 5) was not different between groups (c-ECPR 3.2±0.9 vs. 3.2±1.1 t-ECPR, p >0.05).
Conclusions: Thrombolytic enhanced ECPR after prolonged untreated CA improves recovery of cardiac function and reduces brain edema without increasing bleeding. However, we detected no effect on early EEG recovery or ischemic neuronal injury. Additional studies are needed to determine if thrombolytic enhanced ECPR improves long-term survival and neurologic outcomes after prolonged CA.
- Cardiopulmonary resuscitation
- Cardiac arrest
- Extracorporeal circulation
- Ischemia reperfusion
Author Disclosures: E. Spinelli: None. R.P. Davis: None. X. Ren: None. A. Iyengar: None. P. Sheth: None. T. Tooley: None. B. Sowell: None. W.C. Stacey: None. R.H. Bartlett: None. A. Rojas-Pena: None. R.W. Neumar: None.
- © 2014 by American Heart Association, Inc.