By definition, ‘suspended animation’ is a hypometabolic state characterized by the “the slowing of life processes by external means without termination” [1]. Various mammalian species are capable of nearly completely shutting down their vital functions in order to survive otherwise lethal environmental conditions, such as prolonged impairment of O2 supply and/or extreme temperatures. First described and studied in patients as “hibernation artificielle” induced by the so-called “cocktail lytique” during the Indochina war in the early 1950 s, for obvious reasons the concept of inducing such a hypometabolic condition has attracted special interest in intensive care and emergency medicine. Originally, organ-protection, in particular for the central nervous system (CNS), was demonstrated when suspended animation was induced by rapidly cooling experimental animals to core body temperatures of about 10–15 °C using ice-cold infusions and/or cardiopulmonary bypass (CPB). Given the potential undesired adverse effects of hypothermia per se, e. g., metabolic acidosis, coagulopathy, prolonged inflammation, and impaired host defense, any pharmacological measure allowing for a therapeutic on-demand induction of suspended animation would be of particular interest. Moreover, more recently, it was suggested that the reduced visceral organ function present in critically ill patients and/or after overwhelming hyperinflammation could be referred to as an adaptive mechanism to maintain ATP-homeostasis due to reduced energy expenditure rather than to irreversible organ failure [2]. A landmark paper by Blackstone et al. produced much excitement among researchers in the field of shock and critical illness: These authors demonstrated that mice inhaling hydrogen sulfide (H2S) reversibly decreased their energy expenditure, which was associated with a fall in core temperature [3]. In the meantime, numerous pre-clinical studies have been published on the possible organ-protective effects of H2S, the available data being equivocal depending on the model used and the type of shock investigated. In this context in particular, the impact of H2S effects on energy metabolism remains a matter of debate. Therefore, the present chapter reviews the available data on H2S-induced on-demand hypometabolism, and its relation (directly as well as a possible consecutive drop in body temperature) to organ-protective properties of H2S.