New Findings 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. Abstract 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 (DnormalO2) 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 DnormalO2 and O2 consumption (V̇normalO2) were made. During hypothermia, there was a reduction in organ blood flow, V̇normalO2 and DnormalO2. After rewarming, there was a 40% reduction in stroke volume and cardiac output, causing a global reduction in DnormalO2; 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 DnormalO2 and V̇normalO2 returned to control values. After hypothermia and rewarming there is a significant lowering of DnormalO2 owing to heart failure. However, compensatory mechanisms preserve O2 transport, blood flow and V̇normalO2 in most organs. Nevertheless, these results indicate that hypothermia‐induced heart failure requires therapeutic intervention.

Aims: Complete restitution of neurologic function after 6 h of pre-hospital resuscitation and in-hospital rewarming has been reported in accidental hypothermia patients with cardiac arrest (CA). However, the level of restitution of circulatory function during longlasting hypothermic cardiopulmonary resuscitation (CPR) remains largely unknown. We compared the effects of CPR in replacing spontaneous circulation during 3 h at 27 • C vs. 45 min at normothermia by determining hemodynamics, global oxygen transport (DO 2), oxygen uptake (VO 2), and organ blood flow. Methods: Anesthetized pigs (n = 7) were immersion cooled to CA at 27 • C. Predetermined variables were compared: (1) Before cooling, during cooling to 27 • C with spontaneous circulation, after CA and subsequent continuous CPR (n = 7), vs. (2) before CA and during 45 min CPR in normothermic pigs (n = 4). Results: When compared to corresponding values during spontaneous circulation at 38 • C: (1) After 15 min of CPR at 27 • C, cardiac output (CO) was reduced by 74%, mean arterial pressure (MAP) by 63%, DO 2 by 47%, but organ blood flow was unaltered. Continuous CPR for 3 h maintained these variables largely unaltered except for significant reduction in blood flow to the heart and brain after 3 h, to the kidneys after 1 h, to the liver after 2 h, and to the stomach and small intestine after 3 h. (2) After normothermic CPR for 15 min, CO was reduced by 71%, MAP by 54%, and DO 2 by 63%. After 45 min, hemodynamic function had deteriorated significantly, organ blood flow was undetectable, serum lactate increased by a factor of 12, and mixed venous O 2 content was reduced to 18%. Conclusion: The level to which CPR can replace CO and MAP during spontaneous circulation at normothermia was not affected by reduction in core temperature in our

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We recently documented that cardiopulmonary resuscitation (CPR) generates the same level of cardiac output (CO) and mean arterial pressure (MAP) during both normothermia (38 °C) and hypothermia (27 °C). Furthermore, continuous CPR at 27 °C provides O2 delivery (ḊO2) to support aerobic metabolism throughout a 3-h period. The aim of the present study was to investigate the effects of extracorporeal membrane oxygenation (ECMO) rewarming to restore ḊO2 and organ blood flow after prolonged hypothermic cardiac arrest. Eight male pigs were anesthetized and immersion cooled to 27 °C. After induction of hypothermic cardiac arrest, CPR was started and continued for a 3-h period. Thereafter, the animals were rewarmed with ECMO. Organ blood flow was measured using microspheres. After cooling with spontaneous circulation to 27 °C, MAP and CO were initially reduced to 66 and 44% of baseline, respectively. By 15 min after the onset of CPR, there was a further reduction in MAP and CO to 42 and 25% of baseline, respectively, which remained unchanged throughout the rest of 3-h CPR. During CPR, ḊO2 and O2 uptake (V̇O2) fell to critical low levels, but the simultaneous small increase in lactate and a modest reduction in pH, indicated the presence of maintained aerobic metabolism. Rewarming with ECMO restored MAP, CO, ḊO2, and blood flow to the heart and to parts of the brain, whereas flow to kidneys, stomach, liver and spleen remained significantly reduced. CPR for 3-h at 27 °C with sustained lower levels of CO and MAP maintained aerobic metabolism sufficient to support ḊO2. Rewarming with ECMO restores blood flow to the heart and brain, and creates a “shockable” cardiac rhythm. Thus, like continuous CPR, ECMO rewarming plays a crucial role in “the chain of survival” when resuscitating victims of hypothermic cardiac arrest.