For decades, conventional wisdom held that brain and organ damage following cardiac arrest was solely caused by the direct effects of oxygen deprivation. However, some of the most significant findings in resuscitation science over the past two decades have indicated that much of the cellular damage that is observed after cardiac arrest may not occur when the heart is stopped and the body remains deprived of oxygen. Rather, it may result from the toxic effects of oxygen returning to the body after a period of oxygen deprivation. This phenomenon, known as reperfusion injury, has been described in other conditions such as in stroke and heart attack, but is now known to be equally applicable in cardiac arrest.1

Reperfusion injury is one of a constellation of complications that can follow cardiac arrest and the restoration of the heartbeat. Commonly referred to as post-cardiac arrest syndrome or post-resuscitation syndrome, this condition includes brain and cardiac dysfunction, massive systemic inflammation, and organ failure, and is a leading cause of death following resuscitation.2 Together, cardiac arrest and post-cardiac arrest syndrome constitute a two-step injury process, in which the duration of the secondary injury process (reperfusion injury, systemic inflammation, organ failure) is directly proportional to the severity of the first (cardiac arrest and oxygen deprivation/ischemia). The relationship can be analogized to that of an earthquake and the tsunami that follows, whereby the magnitude of the tsunami is directly proportional to the magnitude of the earthquake; much of the damage observed after an earthquake actually occurs from the tsunami.

The first 24 to 72 hours following resuscitation are the most critical, and approximately 75 percent of people who are resuscitated after having their hearts restarted die during this period, often from damage arising from post-cardiac arrest syndrome. Protective therapies are urgently needed to help manage post-cardiac arrest syndrome and any potential brain damage. Current national and international evidence-based medical recommendations have been established by the American Heart Association and others since 2008. These include limiting oxygen delivery to minimize oxidative damage in the brain and organs, interventions to manage and regulate blood pressure, avoidance of seizures, early cardiac catheterization especially for those suffering cardiac arrest outside of hospitals, and careful regulation of blood glucose and carbon dioxide.3

This is an active area of research, and trials are needed to identify additional pharmacological interventions that may improve survival outcomes. Increased awareness of the significance of post-cardiac arrest syndrome and its treatment among clinicians and other healthcare providers is vital to help improve patient care and increase survival without brain damage.

References

1. Neumar RW … Vanden Hoek T. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. Circulation. 2008. DOI. Opens in a new tab.
2. Sekhon MS … Griesdale DE. Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a "two-hit" model. Critical Care. 2017. DOI. Opens in a new tab.
3. Chalkias A … Xanthos T. Post-cardiac arrest brain injury: pathophysiology and treatment. Journal of the Neurological Sciences. 2012. DOI. Opens in a new tab.