High risk of patient self-inflicted lung injury in COVID-19 with frequently encountered spontaneous breathing patterns: a computational modelling study.
High risk of patient self-inflicted lung injury in COVID-19 with frequently encountered spontaneous breathing patterns: a computational modelling study.
复制标题
DOI：
10.1186/s13613-021-00904-7
复制
发表时间：
2021-07-13
影响因子：
8.1
通讯作者：
Bates DG
中科院分区：
文献类型：
--
作者：
Weaver L;Das A;Saffaran S;Yehya N;Scott TE;Chikhani M;Laffey JG;Hardman JG;Camporota L;Bates DG
对于患有COVID-19急性低氧性呼吸衰竭的自主呼吸患者，呼吸努力增加是否可能导致患者自伤肺损伤（P-SILI），目前仍存在争议。然而，将吸气努力增加与肺损伤联系起来的直接临床证据很少。我们采用心肺病理生理学的计算模拟器来量化在不同呼吸努力水平下可能导致P-SILI的机械力。根据最近的数据，人工调整模拟器参数以生成10名患者的人群，这些患者概括了某些COVID-19患者表现出的临床特征，即，严重低氧血症合并相对良好的肺力学，正在接受补充氧气治疗。在潮气量（VT）和呼吸率（RR）为7 ml/kg和14次呼吸/min的条件下进行模拟（代表正常呼吸努力）和VT/RR为7/20、7/30、10/14、10/20和10/30 ml/kg /次呼吸/min。虽然氧合随着呼吸努力的增加而改善，在测试的所有较高VT/RR组合中，观察到肺损伤可能性的多个指标显著增加。胸腔压摆幅从基线时的12.0 ± 0.3 cmH 2 O增加到VT/RR为7 ml/kg/30次呼吸/min时的33.8 ± 0.4 cmH 2 O，并在VT/RR为10 ml/kg/30次呼吸/min时增加到46.2 ± 0.5 cmH 2 O。跨肺压摆幅从基线时的4.7 ± 0.1 cmH 2 O增加到VT/RR为7 ml/kg/30次呼吸/min时的17.9 ± 0.3 cmH 2 O总肺应变从基线时的0.29 ± 0.006增加到10 ml/kg/30次呼吸/min时的0.65 ± 0.016。机械功率从基线时的1.6 ± 0.1 J/min增加到VT/RR为7 ml/kg/30次呼吸/min时的12.9 ± 0.2 J/min，在VT/RR为7 ml/kg/30次/min时，驱动压从基线时的7.7 ± 0.2 cmH 2 O增加到19.6 ± 0.2 cmH 2 O，在10 ml/kg/30次呼吸/min时，呼吸强度为26.9 ± 0.3 cmH 2 O。我们的研究结果表明，COVID-19中常见的吸气努力增加所产生的力，19急性低氧血症性呼吸衰竭与机械通气期间呼吸机诱导的肺损伤相关。应仔细监测和控制这些患者的呼吸努力，以尽量减少肺损伤的风险。在线版本包含补充材料，可通过10.1186/s13613-021-00904-7获得。
There is on-going controversy regarding the potential for increased respiratory effort to generate patient self-inflicted lung injury (P-SILI) in spontaneously breathing patients with COVID-19 acute hypoxaemic respiratory failure. However, direct clinical evidence linking increased inspiratory effort to lung injury is scarce. We adapted a computational simulator of cardiopulmonary pathophysiology to quantify the mechanical forces that could lead to P-SILI at different levels of respiratory effort. In accordance with recent data, the simulator parameters were manually adjusted to generate a population of 10 patients that recapitulate clinical features exhibited by certain COVID-19 patients, i.e., severe hypoxaemia combined with relatively well-preserved lung mechanics, being treated with supplemental oxygen. Simulations were conducted at tidal volumes (VT) and respiratory rates (RR) of 7 ml/kg and 14 breaths/min (representing normal respiratory effort) and at VT/RR of 7/20, 7/30, 10/14, 10/20 and 10/30 ml/kg / breaths/min. While oxygenation improved with higher respiratory efforts, significant increases in multiple indicators of the potential for lung injury were observed at all higher VT/RR combinations tested. Pleural pressure swing increased from 12.0 ± 0.3 cmH2O at baseline to 33.8 ± 0.4 cmH2O at VT/RR of 7 ml/kg/30 breaths/min and to 46.2 ± 0.5 cmH2O at 10 ml/kg/30 breaths/min. Transpulmonary pressure swing increased from 4.7 ± 0.1 cmH2O at baseline to 17.9 ± 0.3 cmH2O at VT/RR of 7 ml/kg/30 breaths/min and to 24.2 ± 0.3 cmH2O at 10 ml/kg/30 breaths/min. Total lung strain increased from 0.29 ± 0.006 at baseline to 0.65 ± 0.016 at 10 ml/kg/30 breaths/min. Mechanical power increased from 1.6 ± 0.1 J/min at baseline to 12.9 ± 0.2 J/min at VT/RR of 7 ml/kg/30 breaths/min, and to 24.9 ± 0.3 J/min at 10 ml/kg/30 breaths/min. Driving pressure increased from 7.7 ± 0.2 cmH2O at baseline to 19.6 ± 0.2 cmH2O at VT/RR of 7 ml/kg/30 breaths/min, and to 26.9 ± 0.3 cmH2O at 10 ml/kg/30 breaths/min. Our results suggest that the forces generated by increased inspiratory effort commonly seen in COVID-19 acute hypoxaemic respiratory failure are comparable with those that have been associated with ventilator-induced lung injury during mechanical ventilation. Respiratory efforts in these patients should be carefully monitored and controlled to minimise the risk of lung injury. The online version contains supplementary material available at 10.1186/s13613-021-00904-7.
登录
查看更多内容
DOI：
10.1186/s13054-014-0723-6
发表时间：
2015-01-12
期刊：
Critical care (London, England)
影响因子：
--
作者：
Das A;Cole O;Chikhani M;Wang W;Ali T;Haque M;Bates DG;Hardman JG
通讯作者：
Hardman JG
影响因子：
3.2
作者：
Grieco, Domenico L.;Menga, Luca S.;Antonelli, Massimo
通讯作者：
Antonelli, Massimo
DOI：
10.1164/rccm.201605-1081cp
发表时间：
2017-02-15
影响因子：
24.7
作者：
Brochard, Laurent;Slutsky, Arthur;Pesenti, Antonio
通讯作者：
Pesenti, Antonio
DOI：
10.1152/ajpheart.00230.2014
发表时间：
2016-04-01
影响因子：
4.8
作者：
Albanese, Antonio;Cheng, Limei;Chbat, Nicolas W.
通讯作者：
Chbat, Nicolas W.
影响因子：
3.4
作者：
DUNNILL, MS
通讯作者：
DUNNILL, MS