Myocardial protection during resuscitation from cardiac arrest

Successful treatment of cardiac arrest requires that an electrically stable and mechanically competent cardiac activity be promptly reestablished. However, many interventions used to attempt to reestablish cardiac activity may also inflict additional myocardial injury and, in turn, compromise resuscitability. In this review, we examine mechanisms of such myocardial injury and discuss potential new strategies for myocardial protection during resuscitation from cardiac arrest.

Efforts are currently directed at understanding underlying mechanisms of myocardial injury associated with current resuscitation methods, with the purpose of developing alternative approaches that are safer and more effective. These new approaches include, among others, the development of alternative low-energy defibrillation waveforms, methods for optimizing the timing for attempting defibrillation, and the use of vasopressor agents devoid of beta-agonist effects. There is also interest in understanding the role that activation of pathways of ischemic and reperfusion injury could play during resuscitation from cardiac arrest. To this end, activation of the sarcolemmal sodium-hydrogen exchanger isoform 1 seems to play an important role. Other potentially important pathways involve adenosine metabolism, activation of potassium ATP channels, and generation of oxygen radical species. These pathways may become novel pharmacologic targets for cardiac resuscitation.

The growing body of research in these areas is bringing hope that in a not so distant future new approaches and interventions for cardiac resuscitation could be available for resuscitation of humans in various clinical settings.