BACKGROUND: The purpose of this study was to determine (1) the role of emergency cardiopulmonary bypass (CPB) after prolonged cardiac arrest and failed cardiopulmonary resuscitation, and (2) the use of systemic hyperkalemia during CPB to convert intractable ventricular fibrillation (VF). METHODS: Thirty-one pigs (34 +/- 2 kg) underwent 15 minutes of cardiac arrest after induced VF, followed by 10 minutes of cardiopulmonary resuscitation-advanced life support. Peripheral CPB was used if cardiopulmonary resuscitation failed to restore stable circulation. Damage was assessed by evaluating hemodynamics, biochemical variables (creatine kinase-MB, neuron-specific enolase), neurologic deficit score, and brain magnetic resonance imaging. RESULTS: Cardiopulmonary resuscitation alone was successful in only 19% (6 of 31 pigs). Cardiopulmonary bypass was initiated in 81% of animals (25 of 31 pigs) either for hypotension (5 of 25 pigs) or intractable VF (20 of 25 pigs). Defibrillation was successful in 7 of 20 animals during the first 10 minutes after initiating CPB. Ventricular fibrillation persisted more than 10 minutes in 13 of 20 pigs, and animals were treated either with repeated defibrillation (6 of 13 pigs) or with a potassium bolus (7 of 13 pigs) to induce transient cardiac arrest. Overall survival at 24 hours was 84% with cardiopulmonary resuscitation (100% of pigs with hypotension; 71% in CPB-VF < 10 minutes). Despite CPB, fatal myocardial failure occurred after VF duration of more than 10 minutes in all pigs treated with electrical defibrillation, whereas hyperkalemia allowed 100% cardioversion and 86% survival. Biochemical variables remained elevated in all groups. Similarly, severe brain injury was present in all animals as confirmed by neurologic deficit score (197 +/- 10) and magnetic resonance imaging. CONCLUSIONS: Emergency CPB after prolonged cardiac arrest improves survival and allows systemic hyperkalemia to convert intractable VF, but fails to reduce neurologic damage. 2010 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.
BACKGROUND: The purpose of this study was to determine (1) the role of emergency cardiopulmonary bypass (CPB) after prolonged cardiac arrest and failed cardiopulmonary resuscitation, and (2) the use of systemic hyperkalemia during CPB to convert intractable ventricular fibrillation (VF). METHODS: Thirty-one pigs (34 +/- 2 kg) underwent 15 minutes of cardiac arrest after induced VF, followed by 10 minutes of cardiopulmonary resuscitation-advanced life support. Peripheral CPB was used if cardiopulmonary resuscitation failed to restore stable circulation. Damage was assessed by evaluating hemodynamics, biochemical variables (creatine kinase-MB, neuron-specific enolase), neurologic deficit score, and brain magnetic resonance imaging. RESULTS: Cardiopulmonary resuscitation alone was successful in only 19% (6 of 31 pigs). Cardiopulmonary bypass was initiated in 81% of animals (25 of 31 pigs) either for hypotension (5 of 25 pigs) or intractable VF (20 of 25 pigs). Defibrillation was successful in 7 of 20 animals during the first 10 minutes after initiating CPB. Ventricular fibrillation persisted more than 10 minutes in 13 of 20 pigs, and animals were treated either with repeated defibrillation (6 of 13 pigs) or with a potassium bolus (7 of 13 pigs) to induce transient cardiac arrest. Overall survival at 24 hours was 84% with cardiopulmonary resuscitation (100% of pigs with hypotension; 71% in CPB-VF < 10 minutes). Despite CPB, fatal myocardial failure occurred after VF duration of more than 10 minutes in all pigs treated with electrical defibrillation, whereas hyperkalemia allowed 100% cardioversion and 86% survival. Biochemical variables remained elevated in all groups. Similarly, severe brain injury was present in all animals as confirmed by neurologic deficit score (197 +/- 10) and magnetic resonance imaging. CONCLUSIONS: Emergency CPB after prolonged cardiac arrest improves survival and allows systemic hyperkalemia to convert intractable VF, but fails to reduce neurologic damage. 2010 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.
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