Respiratory mechanics and gas exchanges in the early course of COVID-19 ARDS: a hypothesis-generating study

J.‑L. Diehl 1,2*, N. Peron 3, R. Chocron 4,5, B. Debuc 6 , E. Guerot 3, C. Hauw‑Berlemont 3, B. Hermann 3 , J. L. Augy 3 , R. Younan 3 , A. Novara 3, J. Langlais 3, L. Khider 7, N. Gendron1,8, G. Goudot 5, J.‑F. Fagon 3 , T. Mirault 4,9 and D. M. Smadja 1,8.

Abstract

Rationale: COVID-19 ARDS could difer 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 patho‑ physiological 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/cmH2O and end-expiratory lung volume: 2100 [1721–2434] mL. Gas exchanges were characterized by hypercapnia 55 [44–62] mmHg, high physiological dead-space (VD/VT): 75 [69–85.5] % and ventila‑ tory ratio (VR): 2.9 [2.2–3.4]. VD/VT and VR were signifcantly 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 high VD/VT in association with biological markers of endothelial damage and thrombosis. High VD/VT 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.
Keywords: ARDS, COVID-19, Physiological dead-space, Ventilatory ratio .

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Respiratory mechanics and gas exchanges in the early course of COVID-19 ARDS: a hypothesis-generating study

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