critical care medicine
Cardiac Arrest
Pathophysiology of Cardiac Arrest
Cardiac arrest causes global ischemia with consequences at the cellular level that adversely affect organ function even after resuscitation and restoration of perfusion. The main consequences involve direct cellular damage and edema formation. Edema is particularly harmful in the brain, which has minimal room to expand, and often results in increased intracranial pressure and corresponding decreased cerebral perfusion postresuscitation. A significant proportion of successfully resuscitated patients have short-term or long-term cerebral dysfunction manifested by altered alertness (from mild confusion to coma), seizures, or both. Decreasedadenosinetriphosphate (ATP) production leads to loss of membrane integrity with efflux of potassium and influx of sodium and calcium. Excess intracellular sodium is one of the initial causes of cellular edema. Excess calcium damages mitochondria (depressing ATP production), increases nitric oxide production (leading to formation of damaging free radicals), and, in certain circumstances, activates proteases that further damage cells. Abnormal ion flux also results in depolarization of neurons, releasing neurotransmitters, some of which are damaging (eg, glutamate activates a specific calcium channel, worsening intracellular calcium overload). Inflammatory mediators (eg, interleukin-1B, tumor necrosis factor-alpha) are elaborated; some of them may cause microvascular thrombosis and loss of vascular integrity with further edema formation. Some mediators trigger apoptosis, resulting in accelerated cell death. 