• Lys Darbera, Mourad Chenoune, Fanny Lidouren, Matthias Kohlhauer, Clovis Adam, Patrick Bruneval, Bijan Ghaleh, Jean-Luc Dubois-Randé, Pierre Carli, Benoit Vivien, Jean-Damien Ricard, Alain Berdeaux, and Renaud Tissier.
• 1INSERM, U955, Equipe 3, Créteil, France. 2Université Paris-Est, UMR_S955, UPEC, Créteil, France. 3Université Paris-Est, Ecole Nationale Vétérinaire d'Alfort, Maisons-Alfort, France. 4Assistance Publique, Hôpitaux de Paris, Hôpital du Kremlin-Bicêtre, Service d'Anatomie Pathologique, Le Kremlin-Bicêtre, France. 5INSERM, U970, Paris, France. 6SAMU de Paris, Département d'Anesthésie Réanimation, CHU Necker Enfants Malades, Université Paris Descartes-Paris V, Paris, France. 7INSERM, U722, UFR de Médecine Paris Diderot, Paris, France. 8Assistance Publique, Hôpitaux de Paris, Hôpital Louis Mourier, Service de Réanimation Médico-chirurgicale, Colombes, France.
• Crit. Care Med.. 2013 Dec 1;41(12):e457-65.

ObjectivesUltrafast and whole-body cooling can be induced by total liquid ventilation with temperature-controlled perfluorocarbons. Our goal was to determine whether this can afford maximal cardio- and neuroprotections through cooling rapidity when coronary occlusion is complicated by cardiac arrest.DesignProspective, randomized animal study.SettingAcademic research laboratory.SubjectsMale New Zealand rabbits.InterventionsChronically instrumented rabbits were submitted to coronary artery occlusion and ventricular fibrillation. After 8 minutes of cardiac arrest, animals were resuscitated and submitted to a normothermic follow-up (control group) or to 3 hours of mild hypothermia induced by total liquid ventilation (total liquid ventilation group) or by combination of cold saline infusion and cold blankets application (saline group). Coronary reperfusion was permitted 40 minutes after the onset of occlusion. After awakening, rabbits were followed up during 7 days.Measurements And Main ResultsTen animals were resuscitated in each group. In the control group, all animals secondarily died of cardiac/respiratory failure (8 of 10) or neurological dysfunction (2 of 10). In the saline group, the target temperature of 32°C was achieved within 30-45 minutes after cooling initiation. This slightly reduced infarct size versus control (41% ± 16% vs 54% ± 8% of risk zone, respectively; p < 0.05) but failed to significantly improve cardiac output, neurological recovery, and survival rate (three survivors, six death from cardiac/respiratory failure, and one from neurological dysfunction). Conversely, the 32°C temperature was achieved within 5-10 minutes in the total liquid ventilation group. This led to a dramatic reduction in infarct size (13% ± 4%; p < 0.05 vs other groups) and improvements in cardiac output, neurological recovery, and survival (eight survivors, two deaths from cardiac/respiratory failure).ConclusionsAchieving hypothermia rapidly is critical to improve the cardiovascular outcome after cardiac arrest with underlying myocardial infarction.

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