124 research outputs found
Facteurs associés à la survie des patients présentant une hypothermie sévÚre
Dans cette Ă©tude rĂ©trospective sur 10 ans, nous avons Ă©valuĂ© l ensemble des patients prĂ©sentant une hypothermie accidentelle sĂ©vĂšre admis au dĂ©choquage du centre de traumatologie de rĂ©fĂ©rence de l arc alpin. L objectif de l Ă©tude Ă©tait de dĂ©terminer les facteurs associĂ©s Ă la survie des patients admis avec une tempĂ©rature centrale infĂ©rieure Ă 28C. Les facteurs de mauvais pronostic que nous avons mis en Ă©vidence Ă©taient un arrĂȘt cardiaque survenu avant l arrivĂ©e des secours et par rapport au patient ayant survĂ©cu, un pH et un TP abaissĂ© et une augmentation de la natrĂ©mie, de la kaliĂ©mie, des lactates, de la crĂ©atinĂ©mie et du TCA Ă l admission. Le rescue collapse , dĂ©fini comme un arrĂȘt cardiaque survenu pendant la prise en charge des secours notamment lors de la mobilisation, n est pas un facteur de pronostic pĂ©joratif. La rĂ©animation des patients prĂ©sentant un rescue collapse devrait ĂȘtre poursuivie. L orientation devrait s effectuer vers un centre Ă©quipĂ© d Extracorporeal Life Support (ECLS) de rĂ©chauffement mĂȘme si le dĂ©lai de transport est extrĂȘmement long. A l inverse, la constatation d un arrĂȘt cardiaque survenu avant l arrivĂ©e des secours est un Ă©lĂ©ment pĂ©joratif, mĂȘme en hypothermie, et pourrait constituer un Ă©lĂ©ment de dĂ©cision pour la non mise sous ECLS. Cette Ă©tude met en Ă©vidence des facteurs pouvant aider les cliniciens dans leurs dĂ©cisions pour prendre en charge des patients prĂ©sentant une hypothermie sĂ©vĂšre. Du fait de l effet protecteur de l hypothermie, il est important de noter que la survie dans des conditions exceptionnelles est parfois possible et peut dĂ©pendre de l orientation des patients vers un centre disposant d un plateau technique adaptĂ©.GRENOBLE1-BU MĂ©decine pharm. (385162101) / SudocSudocFranceF
Ăvaluation de la gravitĂ© ressentie par les familles des patients pris en charge en intervention SMUR aprĂšs information mĂ©dicale
Objectif: Le but de notre travail est d Ă©valuer pour des patients pris en charge en prĂ©hospitalier par un SMUR la comprĂ©hension de l information mĂ©dicale par la famille en ce qui concerne la gravitĂ© de leur proche et de dĂ©terminer les facteurs qui l altĂšrent. MĂ©thodes : Il s agit d une Ă©tude observationnelle prospective multicentrique rĂ©alisĂ©e dans 4 SMUR de RhĂŽne-Alpes de juin Ă octobre 2012. Les donnĂ©es ont Ă©tĂ© recueillies Ă l aide de questionnaires immĂ©diatement aprĂšs l intervention. La Classification Clinique des Malades du SMUR (CCMS) et sa traduction validĂ©e comprĂ©hensible pour les proches ont Ă©tĂ© utilisĂ©es comme critĂšre de jugement. RĂ©sultats : 184 proches et mĂ©decins ont complĂ©tĂ© le questionnaire. Leur anxiĂ©tĂ© (6 [Intervalle de Confiance (IC) 95% 5,6-6,5] en moyenne sur une Ă©chelle de 0 Ă 10) est sous-estimĂ©e par le mĂ©decin (4,2 [IC95% 3,8-4,5]). Nous retrouvons une faible corrĂ©lation entre la CCMS cotĂ©e par la famille et celle dĂ©crite par le mĂ©decin (kappa pondĂ©rĂ©=0,32). Une analyse multivariĂ©e a permis d isoler trois facteurs d altĂ©ration de la comprĂ©hension : l anxiĂ©tĂ© (odds ratio (OR) 1,35, IC95% [1,1-1,7], p=0,014), un faible niveau d Ă©ducation (OR 4,6, IC95% [1,3-16,3], p=0,018) et une gravitĂ© Ă©levĂ©e de l Ă©tat du patient (OR 2,35, IC95% [1,2-3,8], p=0,009). Conclusion: Nos donnĂ©es suggĂšrent que les mĂ©decins doivent s efforcer de rapidement identifier les situations Ă risque de faible comprĂ©hension Ă savoir : un proche anxieux, un proche tĂ©moignant d un faible niveau d Ă©ducation ou un patient grave. La traduction de la CCMS en langage comprĂ©hensible par les proches a Ă©tĂ© validĂ©e et pourrait dĂ©sormais ĂȘtre un outil employĂ© en intervention.Objective: The aim of our study was to evaluate patients, supported by Mobile Intensive Care Unit (MICU), and their families understanding of medical information regarding the severity of their loved ones state and to determine the factors that affect them most. Methods: We conducted a prospective, multicenter observational study in four MICU of the RhĂŽne-Alpes region from June to October 2012. Data were collected using questionnaires immediately after the intervention. Clinical Classification of Patients of SMUR (CCMS) and its translation validated understandable for relatives were used as primary endpoint judgment criteria. Results: 184 relatives and physicians completed the questionnaire. Their anxiety (6 [95% confidence interval (CI) 5.6 to 6.5] on average on a scale of 0 to 10) is underestimated by the physician (4.2 [95% CI 3.8 to 4.5]). We found a weak correlation between CCMS listed by family and described by the doctor (weighted kappa = 0.32) and only 43% of family perceived severity accurately. Multivariate analysis was used to isolate three factors of impaired comprehension: anxiety (odds ratio (OR) 1.35, 95% CI [1.1-1.7], p = 0.014), low level of education (OR 4.6, 95% CI [1.3-16.3], p = 0.018) and a high severity of the patient's condition (OR 2.35, 95% CI [1.2-3.8], p = 0.009). Conclusion: Our data suggests that physicians should strive to quickly identify situations at risk of poor understanding namely an anxious relative, a relative indicating a low level of education or a critical patient. Translation of CCMS in language understandable by relatives has been validated and could now be used as a tool.GRENOBLE1-BU MĂ©decine pharm. (385162101) / SudocSudocFranceF
Head and thorax elevation prevents the rise of intracranial pressure during extracorporeal resuscitation in swine
Aim: Head and thorax elevation during cardiopulmonary resuscitation improves cerebral hemodynamics
and ultimate neurological outcome after cardiac arrest. Its effect during extracorporeal cardiopulmonary resuscitation
(E-CPR) is unknown. We tested whether this procedure could improve hemodynamics in swine treated by E-CPR.
Methods and Results: Pigs were anesthetized and submitted to 15 minutes of untreated ventricular fibrillation followed
by E-CPR. Animals randomly remained in flat position (flat group) or underwent head and thorax elevation since E-CPR
institution (head-up group). Electric shocks were delivered after 30 minutes until the return of spontaneous circulation (ROSC).
They were followed during 120 minutes after ROSC. After 30 minutes of E-CPR, ROSC was achieved in all animals, with no difference regarding blood pressure, heart rate, and extracorporeal membrane of oxygenation flow among groups. The head-up
group had an attenuated increase in ICP as compared with the flat group after cardiac arrest (13 ± 1 vs. 26 ± 2 mm Hg at the
end of the follow-up, respectively). Cerebral perfusion pressure tended to be higher in the head-up versus flat group despite
not achieving statistical difference (66 ± 1 vs 46 ± 1 mm Hg at the end of the follow-up). Carotid blood flow and cerebral oxygen
saturation were not significantly different among groups. Conclusion: During E-CPR, head and thorax elevation prevents ICP
increase. Whether it could improve the ultimate neurological outcome in this situation deserves further investigation.The study was supported by grants LIVE-RESP and AREG-SHOCK from Agence Nationale pour la Recherche. Y. Levy was supported by ADEREMVeterinari
Intranasal sufentanil versus intravenous morphine for acute severe trauma pain: A double-blind randomized non-inferiority study.
BACKGROUND: Intravenous morphine (IVM) is the most common strong analgesic used in trauma, but is associated with a clear time limitation related to the need to obtain an access route. The intranasal (IN) route provides easy administration with a fast peak action time due to high vascularization and the absence of first-pass metabolism. We aimed to determine whether IN sufentanil (INS) for patients presenting to an emergency department with acute severe traumatic pain results in a reduction in pain intensity non-inferior to IVM. METHODS AND FINDINGS: In a prospective, randomized, multicenter non-inferiority trial conducted in the emergency departments of 6 hospitals across France, patients were randomized 1:1 to INS titration (0.3 ÎŒg/kg and additional doses of 0.15 ÎŒg/kg at 10 minutes and 20 minutes if numerical pain rating scale [NRS] > 3) and intravenous placebo, or to IVM (0.1 mg/kg and additional doses of 0.05 mg/kg at 10 minutes and 20 minutes if NRS > 3) and IN placebo. Patients, clinical staff, and research staff were blinded to the treatment allocation. The primary endpoint was the total decrease on NRS at 30 minutes after first administration. The prespecified non-inferiority margin was -1.3 on the NRS. The primary outcome was analyzed per protocol. Adverse events were prospectively recorded during 4 hours. Among the 194 patients enrolled in the emergency department cohort between November 4, 2013, and April 10, 2016, 157 were randomized, and the protocol was correctly administered in 136 (69 IVM group, 67 INS group, per protocol population, 76% men, median age 40 [IQR 29 to 54] years). The mean difference between NRS at first administration and NRS at 30 minutes was -4.1 (97.5% CI -4.6 to -3.6) in the IVM group and -5.2 (97.5% CI -5.7 to -4.6) in the INS group. Non-inferiority was demonstrated (p < 0.001 with 1-sided mean-equivalence t test), as the lower 97.5% confidence interval of 0.29 (97.5% CI 0.29 to 1.93) was above the prespecified margin of -1.3. INS was superior to IVM (intention to treat analysis: p = 0.034), but without a clinically significant difference in mean NRS between groups. Six severe adverse events were observed in the INS group and 2 in the IVM group (number needed to harm: 17), including an apparent imbalance for hypoxemia (3 in the INS group versus 1 in the IVM group) and for bradypnea (2 in the INS group versus 0 in the IVM group). The main limitation of the study was that the choice of concomitant analgesics, when they were used, was left to the discretion of the physician in charge, and co-analgesia was more often used in the IVM group. Moreover, the size of the study did not allow us to conclude with certainty about the safety of INS in emergency settings. CONCLUSIONS: We confirm the non-inferiority of INS compared to IVM for pain reduction at 30 minutes after administration in patients with severe traumatic pain presenting to an emergency department. The IN route, with no need to obtain a venous route, may allow early and effective analgesia in emergency settings and in difficult situations. Confirmation of the safety profile of INS will require further larger studies. TRIAL REGISTRATION: ClinicalTrials.gov NCT02095366. EudraCT 2013-001665-16
Physiopathologie cardio-pulmonaire sur un modĂšle porcin d'arrĂȘt cardiaque rĂ©fractaire en hypothermie profonde traitĂ© par assistance circulatoire
Introduction: Accidental hypothermia is associated with significant mortality and morbidity, especially when core temperature is under 28°C with an increased risk of cardiac arrest. Extracorporeal life support (ECLS) is the preferred treatment in case of cardiac arrest or hemodynamic instability not responding to medical treatment. There are no current guidelines concerning the optimal rewarming strategy. The aim of this work was to develop a porcine experimental model of deep hypothermic cardiac arrest (DHCA) in order to assess the cardiac and pulmonary pathophysiological response during cooling and rewarming with ECLS. We also aimed to assess the impact of different ECLS blood flow rates on cardiopulmonary lesions.Method: Two experimental protocols were performed. Pigs were cannulated for ECLS, cooled until DHCA occurred and subjected to 30 min of cardiac arrest. Protocol A (n = 24): during the rewarming phase, pigs were randomized into 4 groups with 2X2 factorial design. We compared a low blood flow rate of 1.5 L/min (group LF) vs. a normal flow rate of 3.0 L/min (group NF) and a temperature during ECLS adjusted to 5°C above the central core temperature vs. 38°C maintained throughout the rewarming phase. Protocol B (n = 20): Animals were also randomized in 2 groups during rewarming, a group NF and a group LF with a controlled temperature delta of 5°C. In order to assess the physiological impact of ECLS on cardiac output at the end of rewarming we measured flow in the pulmonary artery using a modified thermodilution technique using the Swan-Ganz catheter (injection site inserted in the right ventricle) controlled also by an echocardiographic measurement. Cardiac output, hemodynamics and pulmonary function parameters were evaluated. Biological markers of ischemia/reperfusion injuries were analyzed.Results: Protocol A : The final cardiac output was reduced in the low flow rate versus the high flow rate groups (1.96±1.4 versus 3.34±1.7 L/min, p=0.05). The increase in the serum RAGE concentration was higher in the 38°C rewarming temperature groups compared to 5°C above adjusted temperature.Protocol B: During the cooling phase, cardiac output, heart rhythm, and blood pressure decreased continuously. Pulmonary artery pressure tended to increase at 32°C compared to initial value (20.2 ± 1.7 vs. 29.1 ± 5.6 mmHg, p=0.09). During rewarming, arterial blood pressure was higher at 20° and 25°C in group NF vs. Group LF (p=0.003 and 0.05, respectively). After rewarming at 35°C, cardiac output was 3.9 ± 0.5 in the group NF vs. 2.7 ± 0.5 L/min in group LF (p=0.06). Under ECLS cardiac output was inversely proportional to ECLS flow rate. ECLS flow rate did not significantly change pulmonary vascular resistance.Conclusion: Our results suggest that ECLS rewarming for DHCA patients, using a normal inflow rate of ECLS and a controlled temperature with less than 5°C between ECLS and core temperature could be the less deleterious rewarming strategy to limit cardiac and pulmonary dysfunction. A normal inflow rate of ECLS decreased cardiac dysfunction after rewarming and did not increased pulmonary vascular resistance compared to a low flow rate. A non controlled temperature delta between core temperature and ECLS increased biomarkers level of lung injury. This experimental model on pigs bring some pathophysiological finding for the rewarming strategy of patients who suffer deep accidental hypothermia and could allow to assess different therapeutic strategy in this context.Introduction : Lâhypothermie accidentelle est associĂ©e Ă un taux important de morbiditĂ© et de mortalitĂ©, notamment en cas dâhypothermie accidentelle sĂ©vĂšre oĂč le risque dâarrĂȘt cardiaque est trĂšs Ă©levĂ©. LâExtracorporeal Life Support (ECLS) est le traitement de rĂ©fĂ©rence dans le cas dâhypothermie avec arrĂȘt cardiaque ou instabilitĂ© hĂ©modynamique rĂ©fractaire. Il nâexiste pas de recommandations concernant les modalitĂ©s optimales de rĂ©chauffement.Lâobjectif de ce travail Ă©tait de dĂ©velopper un modĂšle expĂ©rimental porcin dâarrĂȘt cardiaque en hypothermie profonde afin dâĂ©tudier la rĂ©ponse physiopathologique cardiaque et pulmonaire pendant le refroidissement et le rĂ©chauffement par ECLS. Nous avons Ă©galement Ă©valuĂ© lâimpact de diffĂ©rentes stratĂ©gies de rĂ©chauffement (en terme de dĂ©bit dâECLS et de delta de tempĂ©rature entre lâECLS et la tempĂ©rature centrale) sur les lĂ©sions cardiaques et pulmonaires.MĂ©thode : Deux protocoles expĂ©rimentaux ont Ă©tĂ© rĂ©alisĂ©s. Les animaux ont Ă©tĂ© canulĂ©s pour ECLS, refroidis jusquâĂ lâobtention dâun arrĂȘt cardiaque (AC) en hypothermie profonde et soumis Ă 30 minutes dâischĂ©mie complĂšte. Protocole A (n = 24) : durant la phase de rĂ©chauffement, les animaux Ă©taient randomisĂ©s en 4 groupes selon un plan factoriel 2x2 comparant un dĂ©bit normal dâECLS de 3l/min (groupe NF) Ă un dĂ©bit rĂ©duit de 1,5 l/min (groupe LF) ainsi quâun delta de tempĂ©rature entre la tempĂ©rature centrale et le circuit dâECLS limitĂ© Ă 5°C, ou une tempĂ©rature dâECLS Ă 38°C. Protocole B (n = 20) : les animaux ont Ă©tĂ© randomisĂ©s en 2 groupes pendant le rĂ©chauffement : un groupe NF et un groupe LF avec un delta de tempĂ©rature de 5°C. Lâimpact de lâECLS sur le dĂ©bit cardiaque en fin de rĂ©chauffement a Ă©tĂ© Ă©valuĂ© par une technique de thermodilution (site dâinjection du catheter positionnĂ© dans le ventricule droit) et contrĂŽlĂ© par une technique Ă©cho-doppler. Le dĂ©bit cardiaque, lâhĂ©modynamique et des paramĂštres de fonction pulmonaire Ă©taient Ă©valuĂ©s. Des marqueurs biologiques de lĂ©sions dâischĂ©mie/reperfusion Ă©taient mesurĂ©s.RĂ©sultats : Protocole A : Le dĂ©bit cardiaque final Ă©tait rĂ©duit dans les groupes LF comparĂ© aux groupes NF (1.96±1.4 vs. 3.34±1.7 L/min, p=0.05). Lâaugmentation de RAGE Ă©tait plus Ă©levĂ©e dans les groupes avec une tempĂ©rature dâECLS Ă 38°C comparĂ©e aux groupes avec delta contrĂŽlĂ©. Protocole B : Durant la phase de refroidissement, le dĂ©bit cardiaque, la frĂ©quence cardiaque et la pression artĂ©rielle ont diminuĂ© de façon continue. La pression artĂ©rielle pulmonaire avait tendance Ă augmenter Ă 32°c comparĂ©e Ă la valeur initiale (20.2±1.7 vs. 29.1±5.6 mmHg, p=0.09). Pendant le rĂ©chauffement, la pression artĂ©rielle moyenne Ă©tait plus Ă©levĂ©e dans le groupe NF vs. groupe LF Ă 20°C et 25°C (p=0.003 and 0.05, respectivement). AprĂšs rĂ©chauffement Ă 35°C, le dĂ©bit cardiaque Ă©tait de 3.9±0.5L/min dans le groupe NF vs. 2.7±0.5 L/min dans le groupe LF (p=0.06). Sous ECLS, le dĂ©bit cardiaque gauche Ă©tait inversement proportionnel au dĂ©bit dâECLS. En fin de rĂ©chauffement, le dĂ©bit ECLS nâavait pas dâimpact significatif sur les rĂ©sistances pulmonaires.Conclusion : Nos rĂ©sultats suggĂšrent que le rĂ©chauffement par ECLS des arrĂȘts cardiaques en hypothermie profonde, en utilisant un dĂ©bit dâECLS normal avec un delta de tempĂ©rature nâexcĂ©dant pas 5°C par rapport Ă la tempĂ©rature centrale, pourrait ĂȘtre la stratĂ©gie la moins dĂ©lĂ©tĂšre au niveau cardiaque et pulmonaire. LâECLS Ă dĂ©bit normal diminuait la dysfonction myocardique en fin de rĂ©chauffement et ne majorait pas les rĂ©sistances vasculaires pulmonaires par rapport au groupe avec un dĂ©bit dâECLS rĂ©duit. Un delta important entre la tempĂ©rature centrale et celle de lâECLS augmentait le taux du biomarqueur associĂ©s aux lĂ©sions pulmonaires. Ce modĂšle expĂ©rimental apporte des Ă©lĂ©ments physiopathologiques dans le choix des modalitĂ©s de rĂ©chauffement des patients victimes dâhypothermie accidentelle profonde et pourrait permettre dâĂ©valuer dâautres stratĂ©gies thĂ©rapeutiques dans ce contexte
Physiopathologie cardio-pulmonaire sur un modĂšle porcin d'arrĂȘt cardiaque rĂ©fractaire en hypothermie profonde traitĂ© par assistance circulatoire
Introduction: Accidental hypothermia is associated with significant mortality and morbidity, especially when core temperature is under 28°C with an increased risk of cardiac arrest. Extracorporeal life support (ECLS) is the preferred treatment in case of cardiac arrest or hemodynamic instability not responding to medical treatment. There are no current guidelines concerning the optimal rewarming strategy. The aim of this work was to develop a porcine experimental model of deep hypothermic cardiac arrest (DHCA) in order to assess the cardiac and pulmonary pathophysiological response during cooling and rewarming with ECLS. We also aimed to assess the impact of different ECLS blood flow rates on cardiopulmonary lesions.Method: Two experimental protocols were performed. Pigs were cannulated for ECLS, cooled until DHCA occurred and subjected to 30 min of cardiac arrest. Protocol A (n = 24): during the rewarming phase, pigs were randomized into 4 groups with 2X2 factorial design. We compared a low blood flow rate of 1.5 L/min (group LF) vs. a normal flow rate of 3.0 L/min (group NF) and a temperature during ECLS adjusted to 5°C above the central core temperature vs. 38°C maintained throughout the rewarming phase. Protocol B (n = 20): Animals were also randomized in 2 groups during rewarming, a group NF and a group LF with a controlled temperature delta of 5°C. In order to assess the physiological impact of ECLS on cardiac output at the end of rewarming we measured flow in the pulmonary artery using a modified thermodilution technique using the Swan-Ganz catheter (injection site inserted in the right ventricle) controlled also by an echocardiographic measurement. Cardiac output, hemodynamics and pulmonary function parameters were evaluated. Biological markers of ischemia/reperfusion injuries were analyzed.Results: Protocol A : The final cardiac output was reduced in the low flow rate versus the high flow rate groups (1.96±1.4 versus 3.34±1.7 L/min, p=0.05). The increase in the serum RAGE concentration was higher in the 38°C rewarming temperature groups compared to 5°C above adjusted temperature.Protocol B: During the cooling phase, cardiac output, heart rhythm, and blood pressure decreased continuously. Pulmonary artery pressure tended to increase at 32°C compared to initial value (20.2 ± 1.7 vs. 29.1 ± 5.6 mmHg, p=0.09). During rewarming, arterial blood pressure was higher at 20° and 25°C in group NF vs. Group LF (p=0.003 and 0.05, respectively). After rewarming at 35°C, cardiac output was 3.9 ± 0.5 in the group NF vs. 2.7 ± 0.5 L/min in group LF (p=0.06). Under ECLS cardiac output was inversely proportional to ECLS flow rate. ECLS flow rate did not significantly change pulmonary vascular resistance.Conclusion: Our results suggest that ECLS rewarming for DHCA patients, using a normal inflow rate of ECLS and a controlled temperature with less than 5°C between ECLS and core temperature could be the less deleterious rewarming strategy to limit cardiac and pulmonary dysfunction. A normal inflow rate of ECLS decreased cardiac dysfunction after rewarming and did not increased pulmonary vascular resistance compared to a low flow rate. A non controlled temperature delta between core temperature and ECLS increased biomarkers level of lung injury. This experimental model on pigs bring some pathophysiological finding for the rewarming strategy of patients who suffer deep accidental hypothermia and could allow to assess different therapeutic strategy in this context.Introduction : Lâhypothermie accidentelle est associĂ©e Ă un taux important de morbiditĂ© et de mortalitĂ©, notamment en cas dâhypothermie accidentelle sĂ©vĂšre oĂč le risque dâarrĂȘt cardiaque est trĂšs Ă©levĂ©. LâExtracorporeal Life Support (ECLS) est le traitement de rĂ©fĂ©rence dans le cas dâhypothermie avec arrĂȘt cardiaque ou instabilitĂ© hĂ©modynamique rĂ©fractaire. Il nâexiste pas de recommandations concernant les modalitĂ©s optimales de rĂ©chauffement.Lâobjectif de ce travail Ă©tait de dĂ©velopper un modĂšle expĂ©rimental porcin dâarrĂȘt cardiaque en hypothermie profonde afin dâĂ©tudier la rĂ©ponse physiopathologique cardiaque et pulmonaire pendant le refroidissement et le rĂ©chauffement par ECLS. Nous avons Ă©galement Ă©valuĂ© lâimpact de diffĂ©rentes stratĂ©gies de rĂ©chauffement (en terme de dĂ©bit dâECLS et de delta de tempĂ©rature entre lâECLS et la tempĂ©rature centrale) sur les lĂ©sions cardiaques et pulmonaires.MĂ©thode : Deux protocoles expĂ©rimentaux ont Ă©tĂ© rĂ©alisĂ©s. Les animaux ont Ă©tĂ© canulĂ©s pour ECLS, refroidis jusquâĂ lâobtention dâun arrĂȘt cardiaque (AC) en hypothermie profonde et soumis Ă 30 minutes dâischĂ©mie complĂšte. Protocole A (n = 24) : durant la phase de rĂ©chauffement, les animaux Ă©taient randomisĂ©s en 4 groupes selon un plan factoriel 2x2 comparant un dĂ©bit normal dâECLS de 3l/min (groupe NF) Ă un dĂ©bit rĂ©duit de 1,5 l/min (groupe LF) ainsi quâun delta de tempĂ©rature entre la tempĂ©rature centrale et le circuit dâECLS limitĂ© Ă 5°C, ou une tempĂ©rature dâECLS Ă 38°C. Protocole B (n = 20) : les animaux ont Ă©tĂ© randomisĂ©s en 2 groupes pendant le rĂ©chauffement : un groupe NF et un groupe LF avec un delta de tempĂ©rature de 5°C. Lâimpact de lâECLS sur le dĂ©bit cardiaque en fin de rĂ©chauffement a Ă©tĂ© Ă©valuĂ© par une technique de thermodilution (site dâinjection du catheter positionnĂ© dans le ventricule droit) et contrĂŽlĂ© par une technique Ă©cho-doppler. Le dĂ©bit cardiaque, lâhĂ©modynamique et des paramĂštres de fonction pulmonaire Ă©taient Ă©valuĂ©s. Des marqueurs biologiques de lĂ©sions dâischĂ©mie/reperfusion Ă©taient mesurĂ©s.RĂ©sultats : Protocole A : Le dĂ©bit cardiaque final Ă©tait rĂ©duit dans les groupes LF comparĂ© aux groupes NF (1.96±1.4 vs. 3.34±1.7 L/min, p=0.05). Lâaugmentation de RAGE Ă©tait plus Ă©levĂ©e dans les groupes avec une tempĂ©rature dâECLS Ă 38°C comparĂ©e aux groupes avec delta contrĂŽlĂ©. Protocole B : Durant la phase de refroidissement, le dĂ©bit cardiaque, la frĂ©quence cardiaque et la pression artĂ©rielle ont diminuĂ© de façon continue. La pression artĂ©rielle pulmonaire avait tendance Ă augmenter Ă 32°c comparĂ©e Ă la valeur initiale (20.2±1.7 vs. 29.1±5.6 mmHg, p=0.09). Pendant le rĂ©chauffement, la pression artĂ©rielle moyenne Ă©tait plus Ă©levĂ©e dans le groupe NF vs. groupe LF Ă 20°C et 25°C (p=0.003 and 0.05, respectivement). AprĂšs rĂ©chauffement Ă 35°C, le dĂ©bit cardiaque Ă©tait de 3.9±0.5L/min dans le groupe NF vs. 2.7±0.5 L/min dans le groupe LF (p=0.06). Sous ECLS, le dĂ©bit cardiaque gauche Ă©tait inversement proportionnel au dĂ©bit dâECLS. En fin de rĂ©chauffement, le dĂ©bit ECLS nâavait pas dâimpact significatif sur les rĂ©sistances pulmonaires.Conclusion : Nos rĂ©sultats suggĂšrent que le rĂ©chauffement par ECLS des arrĂȘts cardiaques en hypothermie profonde, en utilisant un dĂ©bit dâECLS normal avec un delta de tempĂ©rature nâexcĂ©dant pas 5°C par rapport Ă la tempĂ©rature centrale, pourrait ĂȘtre la stratĂ©gie la moins dĂ©lĂ©tĂšre au niveau cardiaque et pulmonaire. LâECLS Ă dĂ©bit normal diminuait la dysfonction myocardique en fin de rĂ©chauffement et ne majorait pas les rĂ©sistances vasculaires pulmonaires par rapport au groupe avec un dĂ©bit dâECLS rĂ©duit. Un delta important entre la tempĂ©rature centrale et celle de lâECLS augmentait le taux du biomarqueur associĂ©s aux lĂ©sions pulmonaires. Ce modĂšle expĂ©rimental apporte des Ă©lĂ©ments physiopathologiques dans le choix des modalitĂ©s de rĂ©chauffement des patients victimes dâhypothermie accidentelle profonde et pourrait permettre dâĂ©valuer dâautres stratĂ©gies thĂ©rapeutiques dans ce contexte
Cardiac and pulmonary physiopathology in a porcine model of deep hypothermic refractory cardiac arrest treated by extracorporeal life support
Introduction : Lâhypothermie accidentelle est associĂ©e Ă un taux important de morbiditĂ© et de mortalitĂ©, notamment en cas dâhypothermie accidentelle sĂ©vĂšre oĂč le risque dâarrĂȘt cardiaque est trĂšs Ă©levĂ©. LâExtracorporeal Life Support (ECLS) est le traitement de rĂ©fĂ©rence dans le cas dâhypothermie avec arrĂȘt cardiaque ou instabilitĂ© hĂ©modynamique rĂ©fractaire. Il nâexiste pas de recommandations concernant les modalitĂ©s optimales de rĂ©chauffement.Lâobjectif de ce travail Ă©tait de dĂ©velopper un modĂšle expĂ©rimental porcin dâarrĂȘt cardiaque en hypothermie profonde afin dâĂ©tudier la rĂ©ponse physiopathologique cardiaque et pulmonaire pendant le refroidissement et le rĂ©chauffement par ECLS. Nous avons Ă©galement Ă©valuĂ© lâimpact de diffĂ©rentes stratĂ©gies de rĂ©chauffement (en terme de dĂ©bit dâECLS et de delta de tempĂ©rature entre lâECLS et la tempĂ©rature centrale) sur les lĂ©sions cardiaques et pulmonaires.MĂ©thode : Deux protocoles expĂ©rimentaux ont Ă©tĂ© rĂ©alisĂ©s. Les animaux ont Ă©tĂ© canulĂ©s pour ECLS, refroidis jusquâĂ lâobtention dâun arrĂȘt cardiaque (AC) en hypothermie profonde et soumis Ă 30 minutes dâischĂ©mie complĂšte. Protocole A (n = 24) : durant la phase de rĂ©chauffement, les animaux Ă©taient randomisĂ©s en 4 groupes selon un plan factoriel 2x2 comparant un dĂ©bit normal dâECLS de 3l/min (groupe NF) Ă un dĂ©bit rĂ©duit de 1,5 l/min (groupe LF) ainsi quâun delta de tempĂ©rature entre la tempĂ©rature centrale et le circuit dâECLS limitĂ© Ă 5°C, ou une tempĂ©rature dâECLS Ă 38°C. Protocole B (n = 20) : les animaux ont Ă©tĂ© randomisĂ©s en 2 groupes pendant le rĂ©chauffement : un groupe NF et un groupe LF avec un delta de tempĂ©rature de 5°C. Lâimpact de lâECLS sur le dĂ©bit cardiaque en fin de rĂ©chauffement a Ă©tĂ© Ă©valuĂ© par une technique de thermodilution (site dâinjection du catheter positionnĂ© dans le ventricule droit) et contrĂŽlĂ© par une technique Ă©cho-doppler. Le dĂ©bit cardiaque, lâhĂ©modynamique et des paramĂštres de fonction pulmonaire Ă©taient Ă©valuĂ©s. Des marqueurs biologiques de lĂ©sions dâischĂ©mie/reperfusion Ă©taient mesurĂ©s.RĂ©sultats : Protocole A : Le dĂ©bit cardiaque final Ă©tait rĂ©duit dans les groupes LF comparĂ© aux groupes NF (1.96±1.4 vs. 3.34±1.7 L/min, p=0.05). Lâaugmentation de RAGE Ă©tait plus Ă©levĂ©e dans les groupes avec une tempĂ©rature dâECLS Ă 38°C comparĂ©e aux groupes avec delta contrĂŽlĂ©. Protocole B : Durant la phase de refroidissement, le dĂ©bit cardiaque, la frĂ©quence cardiaque et la pression artĂ©rielle ont diminuĂ© de façon continue. La pression artĂ©rielle pulmonaire avait tendance Ă augmenter Ă 32°c comparĂ©e Ă la valeur initiale (20.2±1.7 vs. 29.1±5.6 mmHg, p=0.09). Pendant le rĂ©chauffement, la pression artĂ©rielle moyenne Ă©tait plus Ă©levĂ©e dans le groupe NF vs. groupe LF Ă 20°C et 25°C (p=0.003 and 0.05, respectivement). AprĂšs rĂ©chauffement Ă 35°C, le dĂ©bit cardiaque Ă©tait de 3.9±0.5L/min dans le groupe NF vs. 2.7±0.5 L/min dans le groupe LF (p=0.06). Sous ECLS, le dĂ©bit cardiaque gauche Ă©tait inversement proportionnel au dĂ©bit dâECLS. En fin de rĂ©chauffement, le dĂ©bit ECLS nâavait pas dâimpact significatif sur les rĂ©sistances pulmonaires.Conclusion : Nos rĂ©sultats suggĂšrent que le rĂ©chauffement par ECLS des arrĂȘts cardiaques en hypothermie profonde, en utilisant un dĂ©bit dâECLS normal avec un delta de tempĂ©rature nâexcĂ©dant pas 5°C par rapport Ă la tempĂ©rature centrale, pourrait ĂȘtre la stratĂ©gie la moins dĂ©lĂ©tĂšre au niveau cardiaque et pulmonaire. LâECLS Ă dĂ©bit normal diminuait la dysfonction myocardique en fin de rĂ©chauffement et ne majorait pas les rĂ©sistances vasculaires pulmonaires par rapport au groupe avec un dĂ©bit dâECLS rĂ©duit. Un delta important entre la tempĂ©rature centrale et celle de lâECLS augmentait le taux du biomarqueur associĂ©s aux lĂ©sions pulmonaires. Ce modĂšle expĂ©rimental apporte des Ă©lĂ©ments physiopathologiques dans le choix des modalitĂ©s de rĂ©chauffement des patients victimes dâhypothermie accidentelle profonde et pourrait permettre dâĂ©valuer dâautres stratĂ©gies thĂ©rapeutiques dans ce contexte.Introduction: Accidental hypothermia is associated with significant mortality and morbidity, especially when core temperature is under 28°C with an increased risk of cardiac arrest. Extracorporeal life support (ECLS) is the preferred treatment in case of cardiac arrest or hemodynamic instability not responding to medical treatment. There are no current guidelines concerning the optimal rewarming strategy. The aim of this work was to develop a porcine experimental model of deep hypothermic cardiac arrest (DHCA) in order to assess the cardiac and pulmonary pathophysiological response during cooling and rewarming with ECLS. We also aimed to assess the impact of different ECLS blood flow rates on cardiopulmonary lesions.Method: Two experimental protocols were performed. Pigs were cannulated for ECLS, cooled until DHCA occurred and subjected to 30 min of cardiac arrest. Protocol A (n = 24): during the rewarming phase, pigs were randomized into 4 groups with 2X2 factorial design. We compared a low blood flow rate of 1.5 L/min (group LF) vs. a normal flow rate of 3.0 L/min (group NF) and a temperature during ECLS adjusted to 5°C above the central core temperature vs. 38°C maintained throughout the rewarming phase. Protocol B (n = 20): Animals were also randomized in 2 groups during rewarming, a group NF and a group LF with a controlled temperature delta of 5°C. In order to assess the physiological impact of ECLS on cardiac output at the end of rewarming we measured flow in the pulmonary artery using a modified thermodilution technique using the Swan-Ganz catheter (injection site inserted in the right ventricle) controlled also by an echocardiographic measurement. Cardiac output, hemodynamics and pulmonary function parameters were evaluated. Biological markers of ischemia/reperfusion injuries were analyzed.Results: Protocol A : The final cardiac output was reduced in the low flow rate versus the high flow rate groups (1.96±1.4 versus 3.34±1.7 L/min, p=0.05). The increase in the serum RAGE concentration was higher in the 38°C rewarming temperature groups compared to 5°C above adjusted temperature.Protocol B: During the cooling phase, cardiac output, heart rhythm, and blood pressure decreased continuously. Pulmonary artery pressure tended to increase at 32°C compared to initial value (20.2 ± 1.7 vs. 29.1 ± 5.6 mmHg, p=0.09). During rewarming, arterial blood pressure was higher at 20° and 25°C in group NF vs. Group LF (p=0.003 and 0.05, respectively). After rewarming at 35°C, cardiac output was 3.9 ± 0.5 in the group NF vs. 2.7 ± 0.5 L/min in group LF (p=0.06). Under ECLS cardiac output was inversely proportional to ECLS flow rate. ECLS flow rate did not significantly change pulmonary vascular resistance.Conclusion: Our results suggest that ECLS rewarming for DHCA patients, using a normal inflow rate of ECLS and a controlled temperature with less than 5°C between ECLS and core temperature could be the less deleterious rewarming strategy to limit cardiac and pulmonary dysfunction. A normal inflow rate of ECLS decreased cardiac dysfunction after rewarming and did not increased pulmonary vascular resistance compared to a low flow rate. A non controlled temperature delta between core temperature and ECLS increased biomarkers level of lung injury. This experimental model on pigs bring some pathophysiological finding for the rewarming strategy of patients who suffer deep accidental hypothermia and could allow to assess different therapeutic strategy in this context
Physiopathologie cardio-pulmonaire sur un modĂšle porcin d'arrĂȘt cardiaque rĂ©fractaire en hypothermie profonde traitĂ© par assistance circulatoire
Introduction: Accidental hypothermia is associated with significant mortality and morbidity, especially when core temperature is under 28°C with an increased risk of cardiac arrest. Extracorporeal life support (ECLS) is the preferred treatment in case of cardiac arrest or hemodynamic instability not responding to medical treatment. There are no current guidelines concerning the optimal rewarming strategy. The aim of this work was to develop a porcine experimental model of deep hypothermic cardiac arrest (DHCA) in order to assess the cardiac and pulmonary pathophysiological response during cooling and rewarming with ECLS. We also aimed to assess the impact of different ECLS blood flow rates on cardiopulmonary lesions.Method: Two experimental protocols were performed. Pigs were cannulated for ECLS, cooled until DHCA occurred and subjected to 30 min of cardiac arrest. Protocol A (n = 24): during the rewarming phase, pigs were randomized into 4 groups with 2X2 factorial design. We compared a low blood flow rate of 1.5 L/min (group LF) vs. a normal flow rate of 3.0 L/min (group NF) and a temperature during ECLS adjusted to 5°C above the central core temperature vs. 38°C maintained throughout the rewarming phase. Protocol B (n = 20): Animals were also randomized in 2 groups during rewarming, a group NF and a group LF with a controlled temperature delta of 5°C. In order to assess the physiological impact of ECLS on cardiac output at the end of rewarming we measured flow in the pulmonary artery using a modified thermodilution technique using the Swan-Ganz catheter (injection site inserted in the right ventricle) controlled also by an echocardiographic measurement. Cardiac output, hemodynamics and pulmonary function parameters were evaluated. Biological markers of ischemia/reperfusion injuries were analyzed.Results: Protocol A : The final cardiac output was reduced in the low flow rate versus the high flow rate groups (1.96±1.4 versus 3.34±1.7 L/min, p=0.05). The increase in the serum RAGE concentration was higher in the 38°C rewarming temperature groups compared to 5°C above adjusted temperature.Protocol B: During the cooling phase, cardiac output, heart rhythm, and blood pressure decreased continuously. Pulmonary artery pressure tended to increase at 32°C compared to initial value (20.2 ± 1.7 vs. 29.1 ± 5.6 mmHg, p=0.09). During rewarming, arterial blood pressure was higher at 20° and 25°C in group NF vs. Group LF (p=0.003 and 0.05, respectively). After rewarming at 35°C, cardiac output was 3.9 ± 0.5 in the group NF vs. 2.7 ± 0.5 L/min in group LF (p=0.06). Under ECLS cardiac output was inversely proportional to ECLS flow rate. ECLS flow rate did not significantly change pulmonary vascular resistance.Conclusion: Our results suggest that ECLS rewarming for DHCA patients, using a normal inflow rate of ECLS and a controlled temperature with less than 5°C between ECLS and core temperature could be the less deleterious rewarming strategy to limit cardiac and pulmonary dysfunction. A normal inflow rate of ECLS decreased cardiac dysfunction after rewarming and did not increased pulmonary vascular resistance compared to a low flow rate. A non controlled temperature delta between core temperature and ECLS increased biomarkers level of lung injury. This experimental model on pigs bring some pathophysiological finding for the rewarming strategy of patients who suffer deep accidental hypothermia and could allow to assess different therapeutic strategy in this context.Introduction : Lâhypothermie accidentelle est associĂ©e Ă un taux important de morbiditĂ© et de mortalitĂ©, notamment en cas dâhypothermie accidentelle sĂ©vĂšre oĂč le risque dâarrĂȘt cardiaque est trĂšs Ă©levĂ©. LâExtracorporeal Life Support (ECLS) est le traitement de rĂ©fĂ©rence dans le cas dâhypothermie avec arrĂȘt cardiaque ou instabilitĂ© hĂ©modynamique rĂ©fractaire. Il nâexiste pas de recommandations concernant les modalitĂ©s optimales de rĂ©chauffement.Lâobjectif de ce travail Ă©tait de dĂ©velopper un modĂšle expĂ©rimental porcin dâarrĂȘt cardiaque en hypothermie profonde afin dâĂ©tudier la rĂ©ponse physiopathologique cardiaque et pulmonaire pendant le refroidissement et le rĂ©chauffement par ECLS. Nous avons Ă©galement Ă©valuĂ© lâimpact de diffĂ©rentes stratĂ©gies de rĂ©chauffement (en terme de dĂ©bit dâECLS et de delta de tempĂ©rature entre lâECLS et la tempĂ©rature centrale) sur les lĂ©sions cardiaques et pulmonaires.MĂ©thode : Deux protocoles expĂ©rimentaux ont Ă©tĂ© rĂ©alisĂ©s. Les animaux ont Ă©tĂ© canulĂ©s pour ECLS, refroidis jusquâĂ lâobtention dâun arrĂȘt cardiaque (AC) en hypothermie profonde et soumis Ă 30 minutes dâischĂ©mie complĂšte. Protocole A (n = 24) : durant la phase de rĂ©chauffement, les animaux Ă©taient randomisĂ©s en 4 groupes selon un plan factoriel 2x2 comparant un dĂ©bit normal dâECLS de 3l/min (groupe NF) Ă un dĂ©bit rĂ©duit de 1,5 l/min (groupe LF) ainsi quâun delta de tempĂ©rature entre la tempĂ©rature centrale et le circuit dâECLS limitĂ© Ă 5°C, ou une tempĂ©rature dâECLS Ă 38°C. Protocole B (n = 20) : les animaux ont Ă©tĂ© randomisĂ©s en 2 groupes pendant le rĂ©chauffement : un groupe NF et un groupe LF avec un delta de tempĂ©rature de 5°C. Lâimpact de lâECLS sur le dĂ©bit cardiaque en fin de rĂ©chauffement a Ă©tĂ© Ă©valuĂ© par une technique de thermodilution (site dâinjection du catheter positionnĂ© dans le ventricule droit) et contrĂŽlĂ© par une technique Ă©cho-doppler. Le dĂ©bit cardiaque, lâhĂ©modynamique et des paramĂštres de fonction pulmonaire Ă©taient Ă©valuĂ©s. Des marqueurs biologiques de lĂ©sions dâischĂ©mie/reperfusion Ă©taient mesurĂ©s.RĂ©sultats : Protocole A : Le dĂ©bit cardiaque final Ă©tait rĂ©duit dans les groupes LF comparĂ© aux groupes NF (1.96±1.4 vs. 3.34±1.7 L/min, p=0.05). Lâaugmentation de RAGE Ă©tait plus Ă©levĂ©e dans les groupes avec une tempĂ©rature dâECLS Ă 38°C comparĂ©e aux groupes avec delta contrĂŽlĂ©. Protocole B : Durant la phase de refroidissement, le dĂ©bit cardiaque, la frĂ©quence cardiaque et la pression artĂ©rielle ont diminuĂ© de façon continue. La pression artĂ©rielle pulmonaire avait tendance Ă augmenter Ă 32°c comparĂ©e Ă la valeur initiale (20.2±1.7 vs. 29.1±5.6 mmHg, p=0.09). Pendant le rĂ©chauffement, la pression artĂ©rielle moyenne Ă©tait plus Ă©levĂ©e dans le groupe NF vs. groupe LF Ă 20°C et 25°C (p=0.003 and 0.05, respectivement). AprĂšs rĂ©chauffement Ă 35°C, le dĂ©bit cardiaque Ă©tait de 3.9±0.5L/min dans le groupe NF vs. 2.7±0.5 L/min dans le groupe LF (p=0.06). Sous ECLS, le dĂ©bit cardiaque gauche Ă©tait inversement proportionnel au dĂ©bit dâECLS. En fin de rĂ©chauffement, le dĂ©bit ECLS nâavait pas dâimpact significatif sur les rĂ©sistances pulmonaires.Conclusion : Nos rĂ©sultats suggĂšrent que le rĂ©chauffement par ECLS des arrĂȘts cardiaques en hypothermie profonde, en utilisant un dĂ©bit dâECLS normal avec un delta de tempĂ©rature nâexcĂ©dant pas 5°C par rapport Ă la tempĂ©rature centrale, pourrait ĂȘtre la stratĂ©gie la moins dĂ©lĂ©tĂšre au niveau cardiaque et pulmonaire. LâECLS Ă dĂ©bit normal diminuait la dysfonction myocardique en fin de rĂ©chauffement et ne majorait pas les rĂ©sistances vasculaires pulmonaires par rapport au groupe avec un dĂ©bit dâECLS rĂ©duit. Un delta important entre la tempĂ©rature centrale et celle de lâECLS augmentait le taux du biomarqueur associĂ©s aux lĂ©sions pulmonaires. Ce modĂšle expĂ©rimental apporte des Ă©lĂ©ments physiopathologiques dans le choix des modalitĂ©s de rĂ©chauffement des patients victimes dâhypothermie accidentelle profonde et pourrait permettre dâĂ©valuer dâautres stratĂ©gies thĂ©rapeutiques dans ce contexte
Performance diagnostique des signes cliniques et électriques en présence d'un sus décalage du segment et en préhospitalier (à propos d'une année d'activité du SAMU 38)
Objectifs : situation frĂ©quente en mĂ©decine d'urgence que d'ĂȘtre confrontĂ© Ă un Ă©lectrocardiogramme (ECG) prĂ©sentant un sus dĂ©calage du segment ST durant une intervention du Service Mobile d'Urgence et de RĂ©animation (SMUR). Quels sont les signes cliniques et Ă©lectrocardiographiques utiles Ă la dĂ©marche diagnostique de l'urgentiste ? Quelle est sa facultĂ© de reconnaĂźtre l'Ă©tiologie d'un tel trouble de la repolarisation ? Conclusion : l'association de l'interrogatoire et de la clinique Ă l'analyse de l'ECG est essentielle dans la dĂ©marche diagnostique de toute douleur thoracique en intervention SMUR. Les critĂšres actuels de thrombolyse prĂ©hospitaliĂšre du SMUR 38 cadrent efficacement l'urgentiste dans sa dĂ©cision thĂ©rapeutique. Toutefois, il paraĂźt fondamental de former les mĂ©decins urgentistes aux pathologies induisant des sus dĂ©calages du segment ST, afin d'optimiser la prise en charge et de minimiser les risques de thrombolyse inadĂ©quate.GRENOBLE1-BU MĂ©decine pharm. (385162101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF
- âŠ