The fatal circulatory derangements often observed when resuscitating victims of accidental hypothermia by rewarming are recognized as a falling cardiac output and a sudden drop in blood pressure, termed "rewarming shock". The real cause of this rewarming shock, or rewarming collapse, is, so far, unknown. This review presents current information exploring different aspects of the compromised circulatory function during hypothermia and especially after rewarming and supports the hypothesis that posthypothermic circulatory instability may be caused by cardiac insufficiency and alteration of the peripheral vascular bed. Cellular calcium overload, disturbed calcium homeostasis, changes in myocardial myofilament responsiveness to intracellular calcium as well as impaired high energy phosphate homeostasis could all be proposed as important factors leading to the changes observed in the hypothermic heart. Together with alteration of capillary function, increased capillary leakage of plasma protein, changes in intra- and extravascular volume-homeostasis and alteration of autonomous vascular control they all contribute to a maintained low cardiac output during and after rewarming which is associated with a fatal outcome.