Vignon Philippe
Medical-surgical ICU and Inserm CIC 1435, Dupuytren University Hospital, Limoges, France.
Faculty of Medicine, University of Limoges, Limoges, France.
Front Physiol. 2023 Sep 7;14:1275100. doi: 10.3389/fphys.2023.1275100. eCollection 2023.
Weaning a critically-ill patient from the ventilator is a crucial step in global management. This manuscript details physiological changes induced by altered heart-lung interactions during the weaning process, illustrates the main mechanisms which could lead to weaning failure of cardiac origin, and discuss a tailored management based on the monitoring of changes in central hemodynamics during weaning. The transition from positive-pressure ventilation to spontaneous breathing results in abrupt hemodynamic and metabolic changes secondary to rapidly modified heart-lung interactions, sudden changes in cardiac loading conditions, and increased oxygen demand. These modifications may elicit an excessive burden on both the respiratory and cardiovascular systems, result in a rapid and marked increase of left ventricular filling pressure, and ultimately result in a weaning-induced pulmonary oedema (WIPO). The T-piece trial induces the greatest burden on respiratory and cardiocirculatory function when compared to spontaneous breathing trial using pressure support ventilation with positive or zero end-expiratory pressure. Since LV overload is the mainstay of WIPO, positive fluid balance and SBT-induced acute hypertension are the most frequently reported mechanisms of weaning failure of cardiac origin. Although the diagnosis of WIPO historically relied on an abrupt elevation of pulmonary artery occlusion pressure measured during right heart catheterization, it is nowadays commonly documented by echocardiography Doppler. This non-invasive approach is best suited for identifying high-risk patients, depicting the origin of WIPO, and tailoring individual management. Whether this strategy increases the success rate of weaning needs to be evaluated in a population at high risk of weaning failure of cardiac origin.
使重症患者脱机是整体治疗中的关键一步。本文详细阐述了脱机过程中因心肺相互作用改变而引起的生理变化，阐明了可能导致心源性脱机失败的主要机制，并讨论了基于脱机期间中心血流动力学变化监测的针对性管理方法。从正压通气过渡到自主呼吸会导致血流动力学和代谢的突然变化，这继发于心肺相互作用的快速改变、心脏负荷条件的突然变化以及氧需求增加。这些改变可能给呼吸和心血管系统带来过重负担，导致左心室充盈压迅速显著升高，并最终引发脱机诱发的肺水肿（WIPO）。与使用正压或零呼气末压力的压力支持通气进行自主呼吸试验相比，T管试验对呼吸和心脏循环功能造成的负担最大。由于左心室超负荷是WIPO的主要原因，正性液体平衡和自主呼吸试验诱发的急性高血压是最常报道的心源性脱机失败机制。尽管WIPO的诊断在历史上依赖于右心导管检查期间测得的肺动脉闭塞压突然升高，但如今通常通过超声心动图多普勒检查来记录。这种非侵入性方法最适合识别高危患者、描述WIPO的病因并制定个体化管理方案。这种策略是否能提高脱机成功率需要在有较高心源性脱机失败风险的人群中进行评估。
