Abstract
Cardiac arrest is unique among cardiac ischemic syndromes in that all circulation must be generated external to the heart. Although, chest compressions deliver limited blood flow, it may be possible to take advantage of this cardiopulmonary resuscitation (CPR) low-flow state to “prime” the heart in advance of return of restoration of spontaneous circulation. Prior investigation has demonstrated improved cardiac function after perfusing the globally ischemic heart with a cardioprotective agent under low-flow perfusion conditions (modeling CPR flow). These results raise the question as to whether CPR-generated flow can be utilized to induce pharmacological post-conditioning in the arrested heart.
Highlights
Cardiac arrest is unique among cardiac ischemic syndromes in that all circulation must be generated external to the heart
Recent studies in animal models and in patients undergoing percutaneous coronary intervention (PCI) have demonstrated intermittent short periods of reperfusion interspersed with ischemia prior to full reperfusion to reduce myocardial infarct size and improve functional recovery. [1,2] This reperfusion strategy for the heart, termed post-conditioning, was first described by Zhao et al [1] and consists of a stuttered on-off ischemia/reperfusion cycle instituted in the first minutes of cardiac reperfusion
The post-conditioning phenomenon has primarily been described in regional cardiac ischemia models and in PCI, under conditions in which reperfusion can be controlled
Summary
As cardiopulmonary resuscitation (CPR) is the only way to initially generate blood flow in the cardiac arrest victim; can this sub-normal flow provide some measure of cardioprotection or attenuation of reperfusion injury following restoration of spontaneous circulation (ROSC)? In several animal studies, controlled reperfusion at 70% of baseline in ischemic hearts has demonstrated cardioprotection, suggesting a post-conditioning benefit with lower than normal pressure/flow reperfusion. [6,7] This level of flow is significantly more than CPR generated flow. The data showing that interventions at the onset of reperfusion, such as controlled reperfusion, can improve cardiac outcome, constitutes a powerful argument in support of utilizing perfusion strategies for ameliorating reperfusion injury Whether such a strategy might be effective during cardiac arrest by CPR generated flow is still unknown. [10] there is some earlier evidence from clinical studies that a brief period of CPR may improve survival outcomes These studies reported that early survival rates were improved if 1.5 – 3 minutes of CPR was performed before defibrillation of ventricular fibrillation cardiac arrest patients. Recent studies have shown benefits of controlled low pressure reperfusion for post-ischemic hearts, [6] the required flow/perfusion pressure to induce protection is much higher than usual CPR-generated flow/pressure. We recently reported in our whole animal rat cardiac arrest model that 10 minutes of CPR preserved cardiac mitochondrial function compared with no-flow cardiac arrest. [15] If low-flow can activate cardioprotective pathways at the onset of reperfusion, further augmentation of these pathways during resuscitation can potentially improve post-arrest myocardial recovery
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
