Minimizing hypoxic injury during cardiac arrest.

Abstract

Efforts to minimize hypoxic injury may gain insight from considering treatments directed at different levels of biological organization, from cellular physiology to societal norms. At the cellular level, it appears that cells do not actually die during ischemia, but rather during reperfusion or resuscitation. Free radicals are implicated because antioxidants reduce cell death from ischemia/reperfusion, but typically fail to protect when only given during reperfusion. In preliminary work, two synergistic antioxidants were seen to offer significant protection even if used only during reperfusion. These findings suggest some cell death may be treatable at reperfusion and antioxidants targeted specifically at radical generation hold promise as a future therapy. On the organism level, blood flow during cardiopulmonary resuscitation (CPR) may be improved with a new manual device that combines the advantages of active-decompression CPR with interposed-abdominal-compression CPR; preliminary hemodynamic data in animals are encouraging. Possible worsening of injury in the postarrest period may occur from overuse of beta-agonists, excessive defibrillation energy, untreated hypotension, and lack of attention to intensive care principals. At the societal level, we have failed to provide simple treatments that are known to save lives, particularly basic CPR and early defibrillation. Bystander CPR suffers from poor quality of performance and from lack of initiation due to concern over disease transmission. The technology for rapid public defibrillation exists, yet is not commonly employed. Collectively, survival likelihood may be predicted with a multifactor equation which may be useful as we develop future therapies.