Mitochondria is often considered as the common nexus of cardiac and cerebral dysfunction after cardiac arrest. Here, our goal was to determine whether the time course of cardiac and cerebral mitochondrial dysfunction is similar after shockable vs nonshockable cardiac arrest in rabbits. Anesthetized rabbits were submitted to 10 min of no-flow by ventricular fibrillation (VF group) or asphyxia (non-shockable group). They were euthanized at the end of the no-flow period or 30 min, 120 min or 24 h after resuscitation for in vitro evaluation of oxygen consumption and calcium retention capacity. In the brain (cortex and hippocampus), moderate mitochondrial dysfunction was evidenced at the end of the no-flow period after both causes of cardiac arrest vs baseline. It partly recovered at 30 and 120 min after cardiac arrest, with lower calcium retention capacity and higher substrate-dependant oxygen consumption after VF vs non-shockable cardiac arrest. However, after 24 h of follow-up, mitochondrial dysfunction dramatically increased after both VF and non-shockable cardiac arrest, despite greater neurological dysfunction after the latter one. In the heart, mitochondrial dysfunction was also maximal after 24 h following resuscitation, with no significant difference among the causes of the cardiac arrest. During the earlier timing of evaluation, calcium retention capacity and ADP-dependant oxygen consumption were lower and higher, respectively, after non-shockable cardiac arrest vs VF. In conclusion, the kinetics of cardiac and cerebral mitochondrial dysfunction suggests that mitochondrial function do not play a major role in the early phase of the post-resuscitation process but is only involved in the longer pathophysiological events.