In cases of fibrillation or cardiac arrest there is no cardiac output to the brain. At a physiological temperature and without sedation the brain integrity may be preserved for only a few minutes. When resuscitation is effective and leads to a timely recovery of circulation, brain ischemia does not necessarily lead to disability. However, resuscitation may not start straight away and a delay longer than on estimate 6 minutes may lead to permanent brain damage.
Brain ischemia becomes so pronounced that it leads to anoxic depolarisation of neurones. Anoxic depolarization leads to the intracellular cascade of apoptosis and, thereby, neuronal death. Those neurones most active at the moment of circulatory arrest are most vulnerable to permanent damage: usually the hippocampus and cerebellum suffer most from prolonged brain ischemia.
The theory of arterial acceleration gives a new perspective on the aim and technique or resuscitation. When properly executed, cardiac massage triggers the myogenic response in the arterial system, which helps to bring blood into motion in all the body's capillary systems, including the brain. The pressure on the chest wall may additionally result in blood volume being moved to the aorta, but when cardiac preload is low (due to a massive vaso-dilatation resulting from a loss of sympathetic tone) only a limited amount of blood volume may effectively be brought into motion.
Theoretically, cardiac massage should aim to trigger the myogenic response and, therefore, be executed rapidly and in a high frequency. Backflow to the heart may be promoted by lifting the legs or positioning the patient in Trendelenburg, whenever feasible. Artificial breathing only contributes when there is at least some form of blood circulation established.
In the cardiovascular simulation model, cardiac arrest can be simulated by playing off the scenario. Heart massage can be performed by placing the mouse over the heart and making repetitive mouse (or trackpad) compressions at high frequency. When properly executed the arterial Sys1 component can be shown to recur in the signal.