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

J-L Diehl, N Peron, R Chocron, B Debuc, E Guerot, C Hauw-Berlemont, B Hermann, J L Augy, R Younan, A Novara, J Langlais, L Khider, N Gendron, G Goudot, J-F Fagon, T Mirault, D M Smadja
Annals of Intensive Care 2020 July 16, 10 (1): 95

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/cmH2 O 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 ventilatory ratio (VR): 2.9 [2.2-3.4]. VD /VT and VR were significantly correlated: r2  = 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.

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