Pesquisa de abordagem qualitativa que consistiu em avaliar o potencial de leigos para atuar como circunstantes nos procedimentos de reanimação cardiorrespiratória e no manejo do desfibrilador externo automático (DEA). Teve como objetivos: descrever o perfil dos participantes; realizar um processo de capacitação dos participantes sobre os primeiros atendimentos à PCR, utilizando o protocolo de atendimento à PCR da AHA para leigos; destacar as habilidades apontadas por eles e analisar suas percepções sobre o processo de atendimento inicial à PCR e o manejo do DEA. Pela especificidade do objeto de estudo, a metodologia utilizada foi pesquisa-ação. A investigação foi realizada na cidade de Marília/SP. O local foram selecionados por meio de mapeamentos específicos e de acordo com a legislação estadual e municipal sobre quais deveriam atender as exigências ao disponibilizar pessoas com capacitação específica, além da manutenção do dispositivo DEA. Selecionou-se um local público, o Terminal de Transporte Urbano de Marília/SP, segundo o número de circulação de pessoas por dia. Os sujeitos deste estudo foram pessoas voluntárias, leigas, trabalhadores de diversas categorias profissionais e ocupacionais do Terminal. Os sujeitos participaram de reuniões informativas sobre a pesquisa e a importância dos procedimentos iniciais à PCR. Realizou-se-se o curso de capacitação e, em seguida, um grupo focal para coleta de dados. Focou-se nas percepções dos participantes sobre o atendimento inicial à PCR, os sentimentos e habilidades relatadas em relação ao processo preconizado como um todo, incluindo o manejo dos materiais envolvidos nessa situação simulada. Posterior à coleta, os dados foram categorizados, tendo sido usada a técnica de análise de conteúdo descrita por Bardin. Os dados foram analisados e discutidos à luz dos referenciais teóricos e pedagógicos propostos por Paulo Freire, a teoria do modelo de crenças em saúde do campo da promoção da saúde e o papel do Estado democrático. Como resultados obteve-se os Grupos 1 e 2, compostos por 11 participantes, em sua maioria constituído de homens. Observaram-se diferenças relacionadas a escolaridade, capacidade comunicativa e intensidade na participação. As principais categorias empíricas foram: as percepções sobre cidadania; as vivências antes do curso; a percepção sobre o processo de capacitação e a não operacionalização do preceito legal. Em síntese, verificou-se o desconhecimento sobre a existência do arcabouço legal, assim como direito de acesso aos serviços e bens públicos decorrentes dos princípios normativos no resgate à cidadania. Emergiram expressões inusitadas de medo de agir por desconhecimento e por temer consequências do insucessos enfrentamento de processos judiciais, em contraste à solidariedade. Sobre habilidade antes do curso de simulação, os participantes relataram alguma vivência na preparação para o advento mal súbito, sobressaindo a insuficiência no aprendizado das habilidades manuais. Após a simulação, houve relatos de possibilidade e de enfrentamento da situação como circunstante, valorizando a oportunidade de aprendizado e apontando a necessidade de maior tempo para a assimilação de conteúdo, com foco nas habilidades em massagem cardíaca e segurança na condução da situação. Quanto à tecnologia DEA, foram unânimes quanto à facilidade interativa com o circunstante. Enfatizaram a necessidade de implementar processos de capacitação para leigos com o uso do DEA, condicionados à mobilização da sociedade civil n a operacionalização dos dispositivos legais por meio de reordenamento das políticas públicas locais. / Qualitative research, which was to assess the potential for laymen to act as bystanders in CPR procedures and management of the automated external defibrillator (AED). Aimed to describe the profile of the participants, conduct a training process with the participants on the first calls to PCR using the PCR protocol compliance with AHA for laymen; highlight the skills mentioned by participants and analyze the perceptions of participants about the process of initial care and management of the PCR DEA. The specificity of the object of study, the methodology was action research and the test was performed in the city of Marilia / SP. The sites were selected through specific mappings and in accordance with state law and city where they should meet the requirements to provide people with specific training in addition to maintaining the device DEA. We selected the public place, Terminal Urban Transport Marilia/SP according to the number of movements of people per day. The subjects of this study were secular groups, made up of volunteers / workers of various professional and occupational this Terminal. Proceeded methodological following routes: the subjects participated in briefings on the research procedures and the importance of the initial PCR. Proceeded to the training course and programming focus group data collection. Focused on participants\' perceptions about the initial care to PCR, feelings and skills reported in relation to the process advocated as a whole, including the handling of the materials involved in this situation simulated. After collection, the data were categorized, relying on the technique of content analysis described by Bardin. Data were analyzed and discussed in the light of theoretical / pedagogical proposed by Paulo Freire\'s, theory of health belief model in the field of health promotion and the role of the democratic state. The results obtained Groups 1 and 2, comprising 11 participants, mostly consisting of men. Observed among members, differences related to education: communication ability and intensity of participation. The main categories were: perceptions of citizenship; experiences before the course, the perception about the training process and not operationalize the legal precept. In summary there was ignorance about the existence of the legal framework for the majority, as well as right of access to public goods and services resulting in the rescue of normative principles to citizenship. Emerged unusual expressions of fear to act by ignorance and/or fear the consequences of failure to act and facing lawsuits contrast with the predominance of either solidarity. About skills before the course simulation, emerged on experience in preparation for the event sudden illness, highlighting the inadequacy of learning with regard to craftsmanship. After the simulation showed reports of chance and face the situation as bystander, valuing the learning opportunity and pointing the need for more time in the assimilation of content focusing on skills in CPR and driving safety of the situation. As for technology DEA was unanimous to its ease interactive with the bystander. It was emphatically the need to implement the processes of training lay people using the DEA, conditioned the mobilization of civil society in the operationalization of legal devices through reorganization of local public policies.

Le refroidissement in vivo du myocarde jusqu'à 32-34°C est une stratégie cardioprotectrice extrêmement puissante expérimentalement. La ventilation liquide totale (VLT) par des perfluorocarbones permet d'induire cette hypothermie très rapidement en utilisant le poumon comme bioéchangeur thermique, tout en maintenant des échanges gazeux normaux. L'objectif de notre travail de thèse a été d'étudier les effets de la VLT hypothermisante sur les lésions d'ischémie-reperfusion dans des modèles d'ischémie myocardique régionale et d'arrêt cardiorespiratoire chez le lapin. Dans une première étude, nous avons démontré que l'instauration per-ischémique d'un épisode de VLT hypothermisante permettait d'atteindre la température cible de 32-33°C en seulement 5 min chez des lapins chroniquement instrumentés soumis à 30 min d'occlusion coronaire. Cela permettait d'atténuer non seulement la taille d'infarctus mais également la dysfonction contractile post-infarctus. La taille d'infarctus était ainsi respectivement réduite de 89 et 71% lorsque la VLT était débutée à la 5ème ou à la 15ème min d'occlusion coronaire par rapport au groupe Témoin. Cette protection était associée à un effet bénéfique sur la fonction mitochondriale dont la capacité de rétention calcique était significativement accrue par l'hypothermie.Dans une seconde étude, nous avons montré que cet effet cardioprotecteur de la VLT hypothermisante n'était pas limité par un plateau de cardioprotection puisqu'il persistait lors d'ischémies prolongées (60 min) chez des lapins anesthésiés. Les tailles de l'infarctus et du no-reflow étaient en effet respectivement diminuées de 45 et 74% dans un groupe d'animaux soumis à une VLT hypothermisante à partir de la 5ème min d'occlusion coronaire par rapport au groupe Témoin. Lorsque la VLT était instaurée plus tardivement (20ème min d'occlusion coronaire), ces réductions restaient significatives (respectivement -30% et -60%) alors qu'un refroidissement conventionnel par application de couvertures froides n'induisait aucun bénéfice, même lorsqu'il était débuté dès la 5ème min d'occlusion coronaire.Grâce aux travaux précédents, nous avons obtenu la preuve de concept de l'effet cardioprotecteur de la VLT hypothermisante au cours d'une ischémie myocardique régionale. Cependant, la translation clinique de cette stratégie est probablement délicate dans la situation de l'infarctus du myocarde. Il nous a en revanche semblé qu'elle pourrait être également bénéfique au cours de la réanimation post-arrêt cardiaque. Pour étudier ce phénomène, nous avons mis au point un modèle expérimental d'arrêt cardiaque et de réanimation cardiopulmonaire chez des lapins soumis à un épisode de fibrillation ventriculaire. Nous avons ainsi montré que la VLT hypothermisante permettait d'augmenter significativement la survie et d'atténuer le syndrome post-arrêt cardiaque par rapport à une réanimation conventionnelle. Après 10 min d'arrêt cardiaque, la survie était par exemple respectivement de 7/10 vs 0/10 chez les animaux soumis à la VLT hypothermisante par rapport au groupe Témoin. Ces effets bénéfiques étaient directement liés à la rapidité d'induction de l'hypothermie par la VLT puisqu'une hypothermie conventionnelle par refroidissement externe et perfusion de fluides refroidis n'a pas permis d'induire de protection significative.En conclusion, la VLT hypothermisante est une approche puissamment protectrice lors d'ischémie myocardique régionale et au décours d'un arrêt cardiaque. L'évaluation plus approfondie de cette stratégie nécessite à présent le développement de dispositifs sécurisés pouvant être utilisés sur un modèle gros animal.MOTS-CLES : Ventilation liquide totale, perfluorocarbone, hypothermie, infarctus, no-reflow, arrêt cardiaque. LABORATOIRE D'ACCUEIL : Laboratoire de pharmacologie, INSERM U955 équipe 3, Ecole nationale vétérinaire d'Alfort, Faculté de médecine de Créteil, Université Paris-Est, Créteil. / Cooling the ischemic myocardium to 32-34 °C is known to be potently cardioprotective. Total liquid ventilation (TLV) with perfluorocarbons can induce such an hypothermia very fastly using the lung as a heat exchanger while maintaining normal gas exchanges. The aim of this thesis was to investigate its beneficial effects in experimental models of myocardial ischemia and cardiac arrest in rabbits.In our first study, we demonstrated that the institution of hypothermic TLV allowed achieving a cardiac temperature of 32-33°C within only 5 min in chronically instrumented rabbits subjected to 30 min of coronary artery occlusion. This was associated with a significant reduction in infarct size along with a dramatic attenuation of the post-ischemic myocardial contractile dysfunction. As example, infarct size was reduced by 89 and 71% when TLV was initiated at the 5th or 15th min of coronary artery occlusion, respectively. This protection was associated with an attenuation of the mitochondrial dysfunction, as shown by an increased calcium restrain capacity.In a second study, we demonstrated that the protective effect of hypothermic TLV was not limited by a ceiling of cardioprotection since infarct size reduction persisted following prolonged ischemia (60 min) in anesthetized rabbits. Infarct and no-reflow sizes were indeed reduced by 45 and 74% in animals subjected to hypothermic TLV from the 5th min of coronary occlusion as compared to corresponding Controls, respectively. In comparison, a conventional external cooling with cold blankets did not reduce infarct size even when instituted since the 5th of ischemia.Thanks to the previous works, we obtained the proof of concept that hypothermic TLV could offer a dramatic cardioprotection during regional myocardial ischemia. However, the clinical translation of this strategy might be challenging in the clinical scenario of ST-elevation myocardial infarction. This might conversely be less challenging and also beneficial to prevent the post-cardiac arrest syndrome in patients resuscitated from cardiac arrest. In order to investigate this phenomenon, we developed an experimental model of cardiac arrest and cardiopulmonary resuscitation in rabbits submitted to an episode of ventricular fibrillation. Accordingly, we have demonstrated in this model that hypothermic TLV significantly increased survival and attenuated the post-cardiac arrest syndrome as compared to conventional resuscitation. After 10 min of cardiac arrest, survival was for example 7/10 vs 0/10 in animals subjected to hypothermic TLV vs corresponding Controls, respectively. These beneficial effects were directly related to the rapidity at inducing hypothermia with TLV since conventional hypothermia using external cooling and infusion of cold fluids failed to induce a significant protection.In conclusion, hypothermic TLV can induce a dramatic protection during regional myocardial ischemia or following cardiac arrest and resuscitation. In order to further investigate this strategy, we are now requiring a secured device that can be used in large animals.KEYWORDS: total liquid ventilation, perfluorocarbon, hypothermia, infarct, no-reflow, cardiac arrest.Laboratory: Laboratory of Pharmacology, INSERM U955 équipe 3, Ecole nationale vétérinaire d'Alfort, Faculté de médecine de Créteil, Université Paris-Est, Créteil.

<p>Ischemic neuronal injury continues to be a major delimiting factor in achieving successful clinical outcomesafter resuscitation from cardiac arrest. In this thesis, a pig model of cardiopulmonary resuscitation (CPR) wasused to address the effects of different interventions on cerebral blood flow and oxygenation during CPR and theinitial postresuscitation period. A novel technique is presented to quantify the reperfusion oxidative injury.</p><p>Maximization of cerebral blood flow during CPR by open-chest cardiac compression, continuous aortic balloon occlusion, and intra-aortic administration of hypertonic saline-dextran (HSD) did not ameliorate thepostresuscitation hypoperfusion or improve the cerebral oxygen extraction ratio or tissue pH. These findings disaffirm earlier studies suggesting that conserving brain viability after global ischemia is mostly a question ofmaintaining high perfusion pressure.</p><p>Despite an increased cerebral perfusion pressure during CPR, intra-aortic administered epinephrineabove the aortic balloon occlusion did not further improve cerebral blood flow and oxygenation. This findingmay indicate adverse effects of epinephrine on cerebral vascular beds, possibly induced by a relatively highconcentration of epinephrine when administered above the site for aortic balloon occlusion.</p><p>The IV administration of equipotent doses of epinephrine or vasopressin during CPR resulted incomparable hemodynamic changes. The peak increase in cerebral cortical blood flow, however, was reachedapproximately 30 sec later by vasopressin. Furthermore, the second bolus of vasopressin during CPR did notaugment cerebral perfusion, whereas epinephrine did. Consequently, reports suggesting that vasopressin issuperior to epinephrine with respect to its effects on central hemodynamics and vital organ blood flow may bebiased by the pharmacodynamic differences between the drugs, depending on the time point at which blood flowmeasurements are performed.</p><p>In comparison with IV vasopressin, vasopressin administered above the aortic balloon occlusion resulted in a significant increase in cerebral perfusion pressure during CPR, but not after restoration of spontaneous circulation (ROSC). Cerebral cortical blood flow was, however, not improved <i>during</i> CPR, whereas a significant increase was recorded <i>after</i> ROSC. Relatively higher concentrations of vasopressin above the sitefor intra-aortic balloon occlusion may, therefore, predominantly induce cerebral cortical vasoconstriction duringCPR but induce vasodilatation after ROSC.</p><p>Assessment of oxidative stress or inflammation have been extremely difficult to attain. In our pig model of resuscitation, an association wasobserved between the duration of cardiac arrest and jugular bulb levels of 8-iso-PGF_2α, a major isoprostane and a novel index of oxidative injury. 8-iso-PGF_2α, and the prostaglandin 15-K-DH-PGF_2α, increased within 5 min after ROSC and remained so up to 2 h, indicating the interval of time during which cerebral reperfusion oxidative injury and inflammatory response may occur and are potentially preventable.</p>

Ischemic neuronal injury continues to be a major delimiting factor in achieving successful clinical outcomesafter resuscitation from cardiac arrest. In this thesis, a pig model of cardiopulmonary resuscitation (CPR) wasused to address the effects of different interventions on cerebral blood flow and oxygenation during CPR and theinitial postresuscitation period. A novel technique is presented to quantify the reperfusion oxidative injury. Maximization of cerebral blood flow during CPR by open-chest cardiac compression, continuous aortic balloon occlusion, and intra-aortic administration of hypertonic saline-dextran (HSD) did not ameliorate thepostresuscitation hypoperfusion or improve the cerebral oxygen extraction ratio or tissue pH. These findings disaffirm earlier studies suggesting that conserving brain viability after global ischemia is mostly a question ofmaintaining high perfusion pressure. Despite an increased cerebral perfusion pressure during CPR, intra-aortic administered epinephrineabove the aortic balloon occlusion did not further improve cerebral blood flow and oxygenation. This findingmay indicate adverse effects of epinephrine on cerebral vascular beds, possibly induced by a relatively highconcentration of epinephrine when administered above the site for aortic balloon occlusion. The IV administration of equipotent doses of epinephrine or vasopressin during CPR resulted incomparable hemodynamic changes. The peak increase in cerebral cortical blood flow, however, was reachedapproximately 30 sec later by vasopressin. Furthermore, the second bolus of vasopressin during CPR did notaugment cerebral perfusion, whereas epinephrine did. Consequently, reports suggesting that vasopressin issuperior to epinephrine with respect to its effects on central hemodynamics and vital organ blood flow may bebiased by the pharmacodynamic differences between the drugs, depending on the time point at which blood flowmeasurements are performed. In comparison with IV vasopressin, vasopressin administered above the aortic balloon occlusion resulted in a significant increase in cerebral perfusion pressure during CPR, but not after restoration of spontaneous circulation (ROSC). Cerebral cortical blood flow was, however, not improved during CPR, whereas a significant increase was recorded after ROSC. Relatively higher concentrations of vasopressin above the sitefor intra-aortic balloon occlusion may, therefore, predominantly induce cerebral cortical vasoconstriction duringCPR but induce vasodilatation after ROSC. Assessment of oxidative stress or inflammation have been extremely difficult to attain. In our pig model of resuscitation, an association wasobserved between the duration of cardiac arrest and jugular bulb levels of 8-iso-PGF2α, a major isoprostane and a novel index of oxidative injury. 8-iso-PGF2α, and the prostaglandin 15-K-DH-PGF2α, increased within 5 min after ROSC and remained so up to 2 h, indicating the interval of time during which cerebral reperfusion oxidative injury and inflammatory response may occur and are potentially preventable.

Hypothermia therapy (HT) is used clinically following global cerebral ischemia (GCI) but its therapeutic mechanisms are not completely understood. An elucidation of such mechanisms may lead to novel therapeutic approaches that improve patient outcome. Using a murine model of GCI, we determined the effect of HT on the expression of inflammatory proteins in the hippocampus and serum. We also examined its effect on microglia/macrophage activation and neurodegeneration in the brain at 72 hours following ischemia, and its effect on long-term spatial memory/learning and contextual fear response. GCI led to increased neurodegeneration and microglia/macrophage activation in the hippocampus, and increased IL-1β and KC protein expression in the hippocampus at 72 hours. Hypothermia therapy attenuated these inflammatory responses. It also improved spatial learning/memory at 7 and 21 days, and preserved contextual fear response 21 days post-ischemia. Hypothermia therapy attenuated the post-ischemic inflammatory response, protected hippocampal neurons, and preserved long-term memory and learning.

Hypothermia therapy (HT) is used clinically following global cerebral ischemia (GCI) but its therapeutic mechanisms are not completely understood. An elucidation of such mechanisms may lead to novel therapeutic approaches that improve patient outcome. Using a murine model of GCI, we determined the effect of HT on the expression of inflammatory proteins in the hippocampus and serum. We also examined its effect on microglia/macrophage activation and neurodegeneration in the brain at 72 hours following ischemia, and its effect on long-term spatial memory/learning and contextual fear response. GCI led to increased neurodegeneration and microglia/macrophage activation in the hippocampus, and increased IL-1β and KC protein expression in the hippocampus at 72 hours. Hypothermia therapy attenuated these inflammatory responses. It also improved spatial learning/memory at 7 and 21 days, and preserved contextual fear response 21 days post-ischemia. Hypothermia therapy attenuated the post-ischemic inflammatory response, protected hippocampal neurons, and preserved long-term memory and learning.

Cerebral ischemia is a life-threatening condition associated with a substantial morbidity and mortality. Hyperglycemia, a common coexisting phenomenon in both stroke and cardiac arrest (CA), may further aggravate ischemic brain injury. To date, the therapeutic possibilities are lim-ited and the search for new treatment modalities is warranted. One aspect of such a research could be to better understand the cerebral pathogenesis induced by hyperglycemic ischemia-reperfusion. We investigated the combination of ischemia and hyperglycemia in two experimental models of stroke and CA. The aims were to test the neuroprotective potential of the sulfonated nitrone 2-sulfophenyl-N-tert-butylnitrone (S-PBN) in focal hyperglycemic cerebral ischemia (1), to outline the short-terms effects of hyperglycemia in prolonged (2) and short CA (3) and to performed a global transcriptome analysis of brain from hyperglycemic and normoglycemic CA (4). In a stroke model rats were made hyperglycemic prior to transient middle cerebral artery oc-clusion and randomized to S-PBN or saline. We found that S-PBN may ameliorate hyperglyce-mic-ischemic brain damage by improving the neurological performance after 1 day of survival, but did not reduce the infarct size. To study the cerebral oxidative state and perfusion after CA, pigs were randomized and clamped at blood glucose levels of 8.5 ̶ 10.0 mmol/L (high) and 4.0 ̶ 5.5 mmol/L (normal), sub-jected to 12 ̶ min of CA, followed by 8 min of cardiopulmonary resuscitation (CPR), and ob-served for 180 min. Increased oxygenation was found at higher glucose levels measured by near-infrared light spec-troscopy after CA. Tendencies toward increased protein S100β and 15-keto-dihydro-prostaglandin F2α were observed in the hyperglycemic group. We hypothesized that in combination with a brief period of CA, the preischemic hyperglycemia would worsen the cerebral injury compared with normoglycemia. We used a glycemic protocol similar to that in Paper II, whereby pigs were subjected to 5 ̶ min of CA, followed by 8 min of CPR, and observed for 180 mins. An increased level of the cerebral marker S100β was found in hyperglycemic pigs compared with normoglycemic pigs after CA. Global transcriptome analysis using microarray analysis revealed a different early metabolic gene expression in hyperglycemic CA compared with normoglycemic CA.

Bakgrund: Dödligheten vid hjärtstopp utanför sjukhus är hög och endast några få procent av de som drabbas räddas till livet. Tidig behandling är en avgörande faktor för överlevnad. Överlevnaden kan ökas markant av att människor på platsen, bystanders, ingriper med hjärt-lungräddning (HLR). Att vårda och utföra vårdhandlingar är inte exklusivt för sjuksköterskor. Vid hjärtstopp utanför sjukhus är det istället bystandern som förväntas utföra vårdhandlingen. I många fall sker dock inget ingripande trots att hjärtstoppet bevittnas och den vårdande handlingen uteblir därför. Syfte: Syftet med arbetet var att identifiera faktorer som påverkar människors vilja att ingripa vid hjärtstopp utanför sjukhus. Metod: Arbetet designades som en litteraturstudie där artiklar med både kvantitativ och kvalitativ ansats ingick. Resultat: Resultatet baserades på potentiella bystanders antaganden av hur de skulle agera och faktiska bystanders erfarenheter av att ha agerat. Skillnader i faktorer som påverkade viljan observerades mellan dessa. Viljan påverkades till stor del av rädslor, bristande HLR-kunskaper samt scenariot kring hjärtstoppet där bland annat en familjerelation mellan den drabbade och bystandern utgjorde en påverkande faktor. Slutsats: Resultatet visar att hindrande faktorer för viljan skulle kunna påverkas positivt genom förbättrad HLR-utbildning. Klinisk betydelse: Med hjälp av identifierade faktorer kan befintlig HLR-utbildning ses över och eventuellt förbättras. Detta skulle kunna öka antalet ingripanden och därigenom överlevnaden vid hjärtstopp utanför sjukhus. / Background: The lethality is high in out-of-hospital cardiac arrests and only a few percent of the victim’s lives are saved. Early treatment is crucial for survival. People at the scene can increase the survival significantly through CPR interventions. To care and the act of caring is not exclusively for nurses. In cases of out-of-hospital cardiac arrest, the bystander could be the one that performs the act of caring. In many cases, however, no interventions are made although the arrest is witnessed and therefore no act of caring is being performed. Objective: The aim of this essay was to identify factors that influence people's willingness to intervene in out-of-hospital cardiac arrest. Method: This study was designed as a literature study and both quantitative and qualitative research articles were included in the analysis. Results: The result was based on potential bystander's assumptions of how they would act and actual bystanders experience having acted. Differences in factors affecting the willingness were observed between them. The will seemed influenced by fears, lack of CPR skills and the scenario surrounding the arrest. A family tie between the victim and the bystander appeared also as an influencing factor. Conclusion: The findings show that the non-willingness to act could be affected positively by improved CPR training. Clinical significance: In light to the identified factors, improvement of the existing CPR training and increased education could improve the probability of intervention by bystanders and out-of-hospital cardiac arrest survival.

This thesis investigated whether out­come after in-hospital cardiac arrest patients could be improved by a cardiopulmonary resuscitation (CPR) educational intervention focusing on all hospital healthcare professionals. Annually in Sweden, approximately 3000 in-hospital patients suffer a cardiac arrest in which CPR is attempted, and which 900 will survive. The thesis is based on five papers: Paper I was a methodological study concluding in a reliable multiple choice questionnaire (MCQ) aimed at measuring CPR knowledge. Paper II was an intervention study. The intervention consisted of educating 3144 healthcare professionals in CPR. The MCQ from Paper I was answered by the healthcare professionals both before (82% response rate) and after (98% response rate) education. Theoretical knowledge improved in all the different groups of healthcare professionals after the intervention. Paper III was an observational laboratory study investigating the practical CPR skills of 74 healthcare professionals’. Willingness to use an automated external defibrillator (AED) improved generally after educa­tion, and there were no major differences in CPR skills between the different healthcare professions. Paper IV investigated, by use of a questionnaire, the attitudes to CPR of 2152 healthcare professionals (82% response rate). A majority of healthcare professionals reported a positive attitude to resuscitation. Paper V was a register study of patients suffering from cardiac arrest. The intervention tended not to reduce the delay to start of treatment or to increase overall survival. However, our results suggested indirect signs of an improved cerebral function among survivors. In conclusion, CPR education and the introduction of AEDs in-hospital – improved healthcare professionals knowledge, skills, and attitudes – did not improve patients’ survival to hospital discharge, but the functional status among survivors improved.

Malgré de très nombreuses études expérimentales et cliniques dans le domaine de l'arrêt circulatoire, seulement 2% à 12% des patients quittent l'hôpital avec une bonne récupération neurologique. Il est donc nécessaire de proposer de nouvelles thérapeutiques pour tenter d'augmenter la survie après un arrêt circulatoire. Pour atteindre ce but il semble indispensable d'améliorer la qualité du massage cardiaque durant la réanimation et de protéger le myocarde et le cerveau contre les phénomènes d'ischémie-reperfusion. Dans la première partie de ce travail, nous avons évalués dans une étude pré hospitalière l'utilisation d'un dispositif innovant de massage cardiaque interne par minithoracotomie et montré une amélioration de l'hémodynamique en comparaison avec le massage cardiaque standard. Dans la deuxième partie, nous avons testés les possibles effets protecteurs de l'EPO (érythropoïétine) dans deux types d'arrêt circulatoire. Dans un modèle d'arrêt cardiaque expérimental chez le rat nous avons démontré que lorsque l'EPO était injectée avant l'arrêt cardiaque, la réanimation initiale était améliorée et la survie des animaux augmentée ce qui pouvaient suggérer un effet cardio et/ou neuroprotecteur de l'EPO contre les effets délétères de l'ischémie reperfusion. Dans une étude clinique en chirurgie cardiaque sous circulation extra corporelle, nous n'avons pas pu démontré d'effet bénéfique de l'EPO ni sur l'ischémie myocardique, ni sur l'ischémie cérébrale ni sur les paramètres de l'inflammation. Sur la base de ces deux études, il est donc difficile de conclure sur le potentiel rôle bénéfique de l'EPO dans l'arrêt circulatoire. Néanmoins, sur la seule base des résultats expérimentaux, l'EPO pourrait faire partie de l'arsenal thérapeutique pour mieux protéger le myocarde et le cerveau contre les effets délétères de l'ischémie reperfusion après un arrêt cardiaque. / Despite extensive experimental and clinical research on cardiac arrest, only 2-12% of resuscitated patients are discharged from hospital in good neurological conditions. There is, therefore, a dear need for new therapies that improve survival after cardiac arrest. It ‘s necessary to improve the quality of cardiac massage and to protect against cardiac and cerebral ischemia occurring during cardiac arrest. In a first part, we evaluated the prehospital feasibility of performing a new method of minimally invasive direct cardiac massage (MID-CM®) and we suggested that better haemodynamic results can be obtained than with standard cardiopulmonary resuscitation. In a second part, we tested erythropoietin (EPO) against placebo in two model of cardiac arrest. In an experimental model of cardiac arrest, we demonstrated that EPO, when administrated before cardiac arrest, improved initial resuscitation and increased the duration of post-resuscitation survival. In a second model of circulatory arrest during cardiac surgery with cardiopulmonary bypass, EPO administration did not protect against cerebral ischemia and inflammatory response occurring during cardiac surgery with CPB. It is difficult to make definitive conclusion on the potential role of EPO in myocardial and cerebral protection after circulatory arrest. We can hope that EPO administration will represent pharmacological approach in upcoming years to additional myocardial salvage of the reperfused myocardium after cardiac arrest.