Study of the Effects of 3 h of Continuous Cardiopulmonary Resuscitation at 27°C on Global Oxygen Transport and Organ Blood Flow

Abstract

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

WITHDRAWN: Carbon Monoxide Releasing Molecule-2 Protects Intestinal Mucosal Barrier Function of Rat Undergoing Cardiopulmonary Resuscitation via Attenuation of TNF-α/NF-κB Signaling

“…Cold shock is typically mediated by endogenous vasoconstrictors, e.g. noradrenaline, which is considered as a physiological compensatory mechanism in order to provide and stabilize the perfusion of the majority of vital organs, including brain, heart, and lung [4]. Thus, the gut plays a pivotal role in the development of systemic in ammation and multiple organ failure after CPR, therefore further research is needed to prevent gut from IRI during CPR.…”

Effects of Rewarming with Extracorporeal Membrane Oxygenation to Restore Oxygen Transport and Organ Blood Flow After Hypothermic Cardiac Arrest in a Porcine Model.

“…The results of this study also demonstrate that 3-h of continues CPR at 27 °C maintained MAP, CO, and blood ow to the brain, heart, liver, and spleen at the same reduced level, with adequate O 2 delivery to enable aerobic metabolism. In this respect, the ndings of the present study are consistent with those of a previous study [21].…”

“…In this model we previously have reported that after successful rewarming from 3-h at 27 °C with maintained spontaneous circulation, due to patency of adequate physiologic compensatory responses [19] blood ow distribution and O 2 availability was preserved in vital organs despite the existence of a signi cantly reduced CO [19,20]. In this model we recently have documented that after 15 min of CPR for ventricular brillation at 38 °C vs. 27 °C, hemodynamic function, global O 2 delivery, and organ blood ow were generated at the same reduced levels irrespective of core temperature [21]. Furthermore, in contrast to the circulatory collapse that occurs by 45 min of CPR at 38 °C, continued CPR for up to 3-h at 27 °C provided adequate O 2 delivery to support aerobic metabolism in critical organs, apparently due to a patency of adequate physiologic compensatory responses even during these circumstances [21].…”

“…The animals were then rewarmed to a blood temperature of 38 °C (max heat exchanger temperature 38 °C), Thereafter, blood sampling and recordings were repeated and cardioversion was tried again. Based on the occurrence of multiple costae and sternal fractures made in our previous experiment after 3-h CPR [21], if cardioversion was unsuccessful after 3 shocks, a sternotomy was made to evacuate extravascular blood, followed by internal de brillation (5-15 J). The experiment was then concluded and the animals euthanized.…”

“…In this model we recently have documented that after 15 min of CPR for ventricular brillation at 38 °C vs. 27 °C, hemodynamic function, global O 2 delivery, and organ blood ow were generated at the same reduced levels irrespective of core temperature [21]. Furthermore, in contrast to the circulatory collapse that occurs by 45 min of CPR at 38 °C, continued CPR for up to 3-h at 27 °C provided adequate O 2 delivery to support aerobic metabolism in critical organs, apparently due to a patency of adequate physiologic compensatory responses even during these circumstances [21]. The reason for testing 3-h CPR is that our hospital is located in a scarcely populated catchment area, above the Arctic Circle, making evacuation and transportation time with air ambulance typically 3-4 h for patients with hypothermic cardiac arrest in need of in-hospital rewarming.…”