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首页> 外文期刊>Temperature >Hypothesis: Fever control, a niche for alpha-2 agonists in the setting of septic shock and severe acute respiratory distress syndrome?
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Hypothesis: Fever control, a niche for alpha-2 agonists in the setting of septic shock and severe acute respiratory distress syndrome?

机译:假设:发热控制,α-2激动剂的菌株在脓毒症休克和严重的急性呼吸窘迫综合征的环境中?

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During severe septic shock and/or severe acute respiratory distress syndrome (ARDS) patients present with a limited cardio-ventilatory reserve (low cardiac output and blood pressure, low mixed venous saturation, increased lactate, low Pa02/Fi02 ratio,etc.), especially when elderly patients or co-morbidities are considered. Rescue therapies (low dose steroids, adding vasopressin to noradrenaline, proning, almitrine, NO, extracorporeal membrane oxygenation, etc.) are complex. Fever, above 38.5-39.5°C, increases both the ventilatory (high respiratory drive: large tidal volume, high respiratory rate) and the metabolic (increased 02 consumption) demands, further limiting the cardio-ventilatory reserve. Some data (case reports, uncontrolled trial, smallrandomized prospective trials) suggest that control of elevated body temperature ("fever control") leading to normothermia (35.5-37°C) will lower both the ventilatory and metabolic demands: fever control should simplify critical care management when limited cardio-ventilatory reserve is at stake. Usually fever control is generated by a combination of general anesthesia ("analgo-sedation", light total intravenous anesthesia), antipyretics and cooling. However general anesthesia suppresses spontaneous ventilation, making the management more complex. At variance, alpha-2 agonists (clonidine, dexmedetomidine) administered immediately following tracheal intubation and controlled mandatory ventilation, with prior optimization of volemia and atrio-ventricular conduction, will reduce metabolic demand and facilitate normothermia. Furthermore, after a rigorous control of systemic acidosis, alpha-2 agonists will allow for accelerated emergence without delirium, early spontaneous ventilation, improved cardiac output and micro-circulation, lowered vasopressor requirements and inflammation. Rigorous prospective randomized trials are needed in subsets of patients with a high fever and spiraling toward refractory septic shock and/or presenting with severe ARDS.
机译:在严重的化脓性休克和/或严重的急性呼吸窘迫综合征(ARDS)患者患有有限的心通风储备(低心输出和血压,低混合静脉饱和度,增加乳酸,低PA02 / FIO2比例等),特别是当考虑老年患者或共同病态时。救援疗法(低剂量类固醇,将血管加压素添加到去甲肾上腺素,牙酮,阿仑膦,NO,体外膜氧合等)是复杂的。发烧,高于38.5-39.5°C,增加了通风(高呼吸驱动:大潮气量,高呼吸速率)和代谢(02个消费量增加)的需求,进一步限制了心通风储备。一些数据(案例报告,不受控制的试验,小型化前瞻性试验)表明,控制升高的体温(“发热控制”)导致常温(35.5-37°C)将降低通气和代谢要求:发热控制应简化至关重要有限的心通风储备有限的护理管理。通常发热控制是通过全身麻醉(“丙镇镇静”,光总静脉内麻醉),退析性和冷却的组合产生的。然而,全身麻醉抑制自发通风,使管理更加复杂。在变异性下,在气管插管后立即施用的α-2激动剂(Clonidine,Dexmedetomidine),在气管插管和受控的强制性通风后,先前优化vlemia和Atrio-心室传导,将减少代谢需求并促进常温。此外,在对全身酸中毒的严格控制后,α-2激动剂将允许加速出苗而没有谵妄,早期自发通风,改善的心输出和微循环,降低血管加压器要求和炎症。在高发烧患者的亚组中需要严格的前瞻性随机试验,并朝着难治性化脓性休克和/或具有严重的ARDS呈现。

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