Schanche, Torstein

New Findings What is the central question of this study? Detailed guidelines for volume replacement to counteract hypothermia‐induced intravascular fluid loss are lacking. Evidence suggests colloids might have beneficial effects compared to crystalloids. Are central haemodynamic function and level of hypothermia‐induced calcium overload, as a marker of cardiac injury, restored by fluid substitution during rewarming, and are colloids favourable to crystalloids? What is the main finding and its importance? Infusion with crystalloid or dextran during rewarming abolished post‐hypothermic cardiac dysfunction, and partially mitigated myocardial calcium overload. The effects of volume replacement to support haemodynamic function are comparable to those using potent cardio‐active drugs. These findings underline the importance of applying intravascular volume replacement to maintain euvolaemia during rewarming. AbstractPrevious research exploring pathophysiological mechanisms underlying circulatory collapse after rewarming victims of severe accidental hypothermia has documented post‐hypothermic cardiac dysfunction and hypothermia‐induced elevation of intracellular Ca2+ concentration ([Ca2+]i) in myocardial cells. The aim of the present study was to examine if maintaining euvolaemia during rewarming mitigates cardiac dysfunction and/or normalizes elevated myocardial [Ca2+]i. A total of 21 male Wistar rats (300 g) were surface cooled to 15°C, then maintained at 15°C for 4 h, and subsequently rewarmed to 37°C. The rats were randomly assigned to one of three groups: (1) non‐intervention control (n = 7), (2) dextran treated (i.v. 12 ml/kg dextran 70; n = 7), or (3) crystalloid treated (24 ml/kg 0.9% i.v. saline; n = 7). Infusions occurred during the first 30 min of rewarming. Arterial blood pressure, stroke volume (SV), cardiac output (CO), contractility (dP/dtmax) and blood gas changes were measured. Post‐hypothermic changes in [Ca2+]i were measured using the method of radiolabelled Ca2+ (45Ca2+). Untreated controls displayed post‐hypothermic cardiac dysfunction with significantly reduced CO, SV and dP/dtmax. In contrast, rats receiving crystalloid or dextran treatment showed a return to pre‐hypothermic control levels of CO and SV after rewarming, with the dextran group displaying significantly better amelioration of post‐hypothermic cardiac dysfunction than the crystalloid group. Compared to the post‐hypothermic increase in myocardial [Ca2+]i in non‐treated controls, [Ca2+]i values with crystalloid and dextran did not increase to the same extent after rewarming. Volume replacement with crystalloid or dextran during rewarming abolishes post‐hypothermic cardiac dysfunction, and partially mitigates the hypothermia‐induced elevation of [Ca2+]i.

Abstract Background: We recently documented that cardiopulmonary resuscitation (CPR) for hypothermic cardiac arrest maintains cardiac output (CO) and mean arterial pressure (MAP) to the same reduced level during normothermia (38°C) vs. hypothermia (27°C). Furthermore, continuous CPR at 27°C maintains CO and MAP throughout a 3-h period, and provides O2 delivery to support aerobic metabolism. The aim of the present study was to investigate the effects of extracorporeal membrane oxygenation (ECMO) rewarming to restore O2 delivery and organ blood flow. Methods: 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. Results: 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, O2 delivery 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, O2 delivery, and blood flow to the heart and to parts of the brain, whereas flow to kidneys, stomach, liver and spleen remained significantly reduced. Conclusions: CPR for 3-h at 27°C with sustained lower levels of CO and MAP and maintained aerobic metabolism sufficient to support O2 delivery. 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.

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