What is the central question of this study? Absence of hypothermia-induced cardiac arrest is a strong predictor for a favourable outcome after rewarming. Nevertheless, detailed knowledge of preferences in organ blood flow during rewarming with spontaneous circulation is largely unknown. What is the main finding and its importance? In a porcine model of accidental hypothermia, we find, despite a significantly reduced cardiac output during rewarming, normal blood flow and O2 supply in vital organs owing to patency of adequate physiological compensatory responses. In critical care medicine, active rewarming must aim at supporting the spontaneous circulation and maintaining spontaneous autonomous vascular control. ⋯ The absence of hypothermia-induced cardiac arrest is one of the strongest predictors for a favourable outcome after rewarming from accidental hypothermia. We studied temperature-dependent changes in organ blood flow and O2 delivery ( DO2 ) in a porcine model with spontaneous circulation during 3 h of hypothermia at 27°C followed by rewarming. Anaesthetized pigs (n = 16, weighing 20-29 kg) were randomly assigned to one of two groups: (i) hypothermia/rewarming (n = 10), immersion cooled to 27°C and maintained for 3 h before being rewarmed by pleural lavage; and (ii) time-matched normothermic (38°C) control animals (n = 6), immersed for 6.5 h, the last 2 h with pleural lavage. Regional blood flow was measured using a neutron-labelled microsphere technique. Simultaneous measurements of DO2 and O2 consumption ( V̇O2 ) were made. During hypothermia, there was a reduction in organ blood flow, V̇O2 and DO2 . After rewarming, there was a 40% reduction in stroke volume and cardiac output, causing a global reduction in DO2 ; nevertheless, blood flow to the brain, heart, stomach and small intestine returned to prehypothermic values. Blood flow in the liver and kidneys was significantly reduced. Cerebral DO2 and V̇O2 returned to control values. After hypothermia and rewarming there is a significant lowering of DO2 owing to heart failure. However, compensatory mechanisms preserve O2 transport, blood flow and V̇O2 in most organs. Nevertheless, these results indicate that hypothermia-induced heart failure requires therapeutic intervention.