Improved understanding of the respiratory drive pathophysiology could lead to earlier spontaneous breathing in severe acute respiratory distress syndrome

F. Petitjeans, Sandrine Leroy, C. Pichot, M. Ghignone, L. Quintin, D. Longrois, J. Constantin
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引用次数: 1

Abstract

Optimisation of the respiratory drive, as early as possible in the setting of severe acute respiratory distress syndrome (ARDS) and not its suppression, could be a new paradigm in the management of severe forms of ARDS. Severe ARDS is characterised by tachypnoea and hyperpnoea, a consequence of a high respiratory drive. Some patients require endotracheal intubation, controlled mechanical ventilation (CMV) and paralysis to prevent overt ventilatory failure and self-inflicted lung injury. Nevertheless, intubation, CMV and paralysis do not address per se the high respiratory drive, they only suppress it. Optimisation of the respiratory drive could be obtained by a multimodal approach that targets attenuation of fever, agitation, systemic and peripheral acidosis, inflammation, extravascular lung water and changes in carbon dioxide levels. The paradigm we present, based on pathophysiological considerations, is that as soon as these factors have been controlled, spontaneous breathing could resume because hypoxaemia is the least important input to the respiratory drive. Hypoxaemia could be handled by combining positive end-expiratory pressure (PEEP) to prevent early expiratory closure and low pressure support to minimise the work of breathing (WOB). ‘Cooperative’ sedation with alpha-2 agonists, supplemented with neuroleptics if required, is the pharmacological adjunct, administered immediately after intubation as the first-line sedation regimen during the multimodal approach. Given relative contraindications (hypovolaemia, auriculoventricular block, sick sinus syndrome), alpha-2 agonists can help attenuate or moderate fever, increased oxygen consumption VO2, agitation, high cardiac output, inflammation and acidosis. They may also help to preserve microcirculation, cognition and respiratory rhythm generation, thus promoting spontaneous breathing. Returning the physiology of respiratory, ventilatory, circulatory and autonomic systems to normal will support the paradigm of optimised respiratory drive favouring early spontaneous ventilation, at variance with deep sedation, extended paralysis, CMV and use of the prone position as therapeutic strategies in severe ARDS. Glossary and Abbreviations_SDC, http://links.lww.com/EJAIC/A55
提高对呼吸驱动病理生理的认识,可使严重急性呼吸窘迫综合征患者早期自主呼吸
在严重急性呼吸窘迫综合征(ARDS)的情况下,尽早优化呼吸驱动,而不是抑制呼吸驱动,可能是严重急性呼吸窘迫综合征(ARDS)管理的新范式。严重的ARDS以呼吸急促和呼吸急促为特征,这是高呼吸驱动的结果。一些患者需要气管插管,控制机械通气(CMV)和麻痹,以防止明显的呼吸衰竭和自我造成的肺损伤。然而,插管、巨细胞病毒和麻痹本身并不能解决高呼吸驱动,它们只是抑制它。呼吸驱动的优化可以通过多模式方法来实现,该方法针对发热、躁动、全身和周围性酸中毒、炎症、血管外肺水和二氧化碳水平变化的衰减。基于病理生理学的考虑,我们提出的范例是,一旦这些因素得到控制,自发呼吸就可以恢复,因为低氧血症是呼吸驱动最不重要的输入。低氧血症可以通过结合呼气末正压(PEEP)来防止早期呼气关闭和低压支持来最小化呼吸功(WOB)来处理。配合α -2激动剂镇静,必要时辅以抗精神病药,是一种药理学辅助手段,在多模式方法中,作为一线镇静方案,插管后立即给予。考虑到相对禁忌症(低血容量、耳室传导阻滞、病态窦性综合征),α -2激动剂可以帮助减轻或中度发热、耗氧量增加、躁动、心输出量高、炎症和酸中毒。它们还可能有助于维持微循环、认知和呼吸节奏的产生,从而促进自发呼吸。恢复呼吸、通气、循环和自主系统的生理机能将支持优化的呼吸驱动模式,有利于早期自发通气,这与深度镇静、延长麻痹、巨细胞病毒和使用俯卧位作为严重ARDS的治疗策略不同。缩略语s_sdc, http://links.lww.com/EJAIC/A55
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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