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急性呼吸窘迫综合征中的反向触发现象。

Reverse Trigger Phenotypes in Acute Respiratory Distress Syndrome.

机构信息

Division of Pulmonary and Critical Care.

Harvard Medical School, Boston, Massachusetts; and.

出版信息

Am J Respir Crit Care Med. 2021 Jan 1;203(1):67-77. doi: 10.1164/rccm.201907-1427OC.

Abstract

Reverse triggering is an underexplored form of dyssynchrony with important clinical implications in patients with acute respiratory distress syndrome. This retrospective study identified reverse trigger phenotypes and characterized their impacts on Vt and transpulmonary pressure. Fifty-five patients with acute respiratory distress syndrome on pressure-regulated ventilator modes were included. Four phenotypes of reverse triggering with and without breath stacking and their impact on lung inflation and deflation were investigated. Inflation volumes, respiratory muscle pressure generation, and transpulmonary pressures were determined and phenotypes differentiated using Campbell diagrams of respiratory activity. Reverse triggering was detected in 25 patients, 15 with associated breath stacking, and 13 with stable reverse triggering consistent with respiratory entrainment. Phenotypes were associated with variable levels of inspiratory effort (mean 4-10 cm HO per phenotype). Early reverse triggering with early expiratory relaxation increased Vts (88 [64-113] ml) and inspiratory transpulmonary pressures (3 [2-3] cm HO) compared with passive breaths. Early reverse triggering with delayed expiratory relaxation increased Vts (128 [86-170] ml) and increased inspiratory and mean-expiratory transpulmonary pressure (7 [5-9] cm HO and 5 [4-6] cm HO). Mid-cycle reverse triggering (initiation during inflation and maximal effort during deflation) increased Vt (51 [38-64] ml), increased inspiratory and mean-expiratory transpulmonary pressure (3 [2-4] cm HO and 3 [2-3] cm HO), and caused incomplete exhalation. Late reverse triggering (occurring exclusively during exhalation) increased mean expiratory transpulmonary pressure (2 [1-2] cm HO) and caused incomplete exhalation. Breath stacking resulted in large delivered volumes (176 [155-197] ml). Reverse triggering causes variable physiological effects, depending on the phenotype. Differentiation of phenotype effects may be important to understand the clinical impacts of these events.

摘要

反向触发是一种未被充分探索的失同步形式,对急性呼吸窘迫综合征患者具有重要的临床意义。本回顾性研究确定了反向触发表型,并对其对潮气量和跨肺压的影响进行了特征描述。纳入了 55 例接受压力调节通气模式的急性呼吸窘迫综合征患者。研究了有和无呼吸堆积的四种反向触发表型及其对肺充气和放气的影响。通过呼吸活动的坎贝尔图确定充气量、呼吸肌压力产生和跨肺压,并对表型进行区分。25 例患者存在反向触发,其中 15 例存在相关呼吸堆积,13 例存在与呼吸同步一致的稳定反向触发。表型与吸气努力的不同水平相关(每个表型平均为 4-10cmH2O)。具有早期呼气松弛的早期反向触发增加了潮气量(88 [64-113]ml)和吸气跨肺压(3 [2-3]cmH2O),与被动呼吸相比。具有延迟呼气松弛的早期反向触发增加了潮气量(128 [86-170]ml),并增加了吸气和平均呼气跨肺压(7 [5-9]cmH2O 和 5 [4-6]cmH2O)。中期周期反向触发(在充气期间开始并在放气期间最大努力)增加了潮气量(51 [38-64]ml),增加了吸气和平均呼气跨肺压(3 [2-4]cmH2O 和 3 [2-3]cmH2O),并导致呼气不完全。晚期反向触发(仅在呼气期间发生)增加了平均呼气跨肺压(2 [1-2]cmH2O)并导致呼气不完全。呼吸堆积导致输送的大体积(176 [155-197]ml)。反向触发会根据表型产生不同的生理效应。区分表型效应可能对理解这些事件的临床影响很重要。

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