Respiratory mechanics and gas exchanges in the early course of COVID-19 ARDS: a hypothesis-generating study
Respiratory mechanics and gas exchanges in the early course of COVID-19 ARDS: a hypothesis-generating study
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DOI：
10.1186/s13613-020-00716-1
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发表时间：
2020-07-16
影响因子：
8.1
通讯作者：
Smadja, D. M.
中科院分区：
文献类型：
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作者：
Diehl, J-L;Peron, N.;Smadja, D. M.
COVID-19 ARDS可能与该综合征的典型形式不同。目的肺微血管损伤和血栓形成越来越多地被报道为COVID-19呼吸衰竭的组成特征。我们的目的是研究COVID-2019 ARDS患者在启动保护性有创机械通气后早期研究的肺力学和气体交换，寻求相应的病理生理学和生物学特征。方法2020年3月22日至3月30日期间，在插管后1 [1-4]天（中位数[IQR]），对22例中重度COVID-19 ARDS患者的呼吸力学、气体交换、作为内皮损伤标志物的循环内皮细胞（CEC）和D-二聚体进行了研究。测量和主要结果13名中度和9名重度COVID-19 ARDS患者在开始高PEEP保护性机械通气后进行了研究。我们观察到呼吸系统顺应性中度降低：39.5 [33.1-44.7] mL/cmH（2）O和呼气末肺容积：2100 [1721-2434] mL。气体交换的特征为高碳酸血症55 [44-62] mmHg，高生理死腔（V-D/V-T）：75 [69-85.5] %和舒张比（VR）：2.9 [2.2-3.4]。V-D/V（T）和VR显著相关：r（2）= 0.24，p = 0.014。测量时未怀疑肺栓塞。与正常值相比，CEC和D-二聚体升高：分别为24 [12-46]个细胞/mL和1483 [999-2217] ng/mL。结论我们观察到COVID-19 ARDS病程早期的高V（D）/V（T）与内皮损伤和血栓形成的生物标志物相关。高V（D）/V（T）可以通过高PEEP设置和增加的仪器死腔来解释，可能与COVID-19引发的肺微血管内皮损伤和微血栓形成过程相关。
Rationale COVID-19 ARDS could differ from typical forms of the syndrome. Objective Pulmonary microvascular injury and thrombosis are increasingly reported as constitutive features of COVID-19 respiratory failure. Our aim was to study pulmonary mechanics and gas exchanges in COVID-2019 ARDS patients studied early after initiating protective invasive mechanical ventilation, seeking after corresponding pathophysiological and biological characteristics. Methods Between March 22 and March 30, 2020 respiratory mechanics, gas exchanges, circulating endothelial cells (CEC) as markers of endothelial damage, and D-dimers were studied in 22 moderate-to-severe COVID-19 ARDS patients, 1 [1-4] day after intubation (median [IQR]). Measurements and main results Thirteen moderate and 9 severe COVID-19 ARDS patients were studied after initiation of high PEEP protective mechanical ventilation. We observed moderately decreased respiratory system compliance: 39.5 [33.1-44.7] mL/cmH(2)O and end-expiratory lung volume: 2100 [1721-2434] mL. Gas exchanges were characterized by hypercapnia 55 [44-62] mmHg, high physiological dead-space (V-D/V-T): 75 [69-85.5] % and ventilatory ratio (VR): 2.9 [2.2-3.4].V-D/V(T)and VR were significantly correlated:r(2) = 0.24,p = 0.014. No pulmonary embolism was suspected at the time of measurements. CECs and D-dimers were elevated as compared to normal values: 24 [12-46] cells per mL and 1483 [999-2217] ng/mL, respectively. Conclusions We observed early in the course of COVID-19 ARDS highV(D)/V(T)in association with biological markers of endothelial damage and thrombosis. HighV(D)/V(T)can be explained by high PEEP settings and added instrumental dead space, with a possible associated role of COVID-19-triggered pulmonary microvascular endothelial damage and microthrombotic process.