Cereberal Protection Strategies following Cardiopulmonary Resuscitation

Abstract

Cardiac arrest, the process where the mechanical pumping activity of the heart stops, represents the final step in a common pathway which, without intervention, leads to death (Baskett et al., 1996). When the cause is known or suspected, therapy can be individualized and directed at the cause. In all cases management has two priorities; rapid restoration of cardiopulmonary functions and minimization of ischemic damage to end organs (Sulivan, 2011). Irrespective of those events leading to cardiac arrest, when the heart’s pumping activity stops and forward blood flow through the body ceases, ischaemic injury from tissue hypoxia and stoppage of normal aerobic metabolism occurs within seconds (Schneeberger et al., 2007). The brain is the organ most susceptible to ischaemic injury. The rate of development of irreversible brain injury in a patient with cardiac arrest depends upon Cardiopulmonary Resuscitation (CPR) and the resultant blood flow and oxygenation that ensues (Land, 2004). The whole body ischemia/reperfusion of cardiac arrest with associated oxygen debt causes generalised activation of immunologic and coagulation pathways which increases the risk of multiple organ failure and infection (Adams, 2006). Post-cardiac arrest brain injury is a common cause of morbidity and mortality. In one study of patients who survived to ICU admission but subsequently died in the hospital, brain injury was the cause of death in 68% after out-of- hospital cardiac arrest and in 23% after in-hospital cardiac arrest (Laver et al., 2004).