Induced hypothermia after cardiopulmonary resuscitation provides organ protection and is currently considered standard of care in clinical practice. An increasing number of reports indicate that induced hypothermia is also beneficial in other conditions of hypoxia-induced organ injury, including brain injury, intestinal ischaemia-reperfusion injury and acute lung injury. The mechanism of the protective effect is thought to be caused by a reduction in metabolism. A hibernation-like state, characterised by hypothermia, bradypnoea and a reduction in metabolic rate, was induced in animals that normally do not hibernate, after inhalation of hydrogen sulphide. This state was termed a 'suspended animation-like state'. In critically ill patients, an exaggerated systemic inflammatory response is common, which often results in multiple organ injury. Inducing a hypometabolic state during critical illness may limit organ injury by reducing oxygen consumption, constituting a fascinating new therapeutic perspective for the treatment of critically ill patients. In this manuscript, we describe mitochondrial dysfunction during critical illness and preclinical data that suggest a potential therapeutic possibility of lowering metabolism. In addition, we discuss issues that warrant further research before clinical applicability.