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

Abstract

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/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 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.

Response to Damiani and colleagues

“…However, it must be pointed out that VR was not originally designed to be used as a surrogate of dead space [4]. Accordingly, although highly significant, we found only a moderate level of correlation between VR and physiological dead space (V D /V T ) [5]. The level was even lower than the values found in the non-COVID-19 ARDS literature.…”

Prevalence and characteristics of pulmonary embolism in 1042 COVID-19 patients with respiratory symptoms: A nested case-control study

“…The disease rapidly spread into a global pandemic of public health worldwide leading to more than 617,000 deaths (data from July 22, 2020). The main failure in COVID-19 was atypical acute respiratory distress syndrome (ARDS) because of the dissociation between well-conserved lung compliance and severe hypoxemia, attributed to pulmonary vasoregulation disruption and local thrombogenesis [ 2 , 3 ]. Furthermore, COVID-19 outbreak coagulopathy has been described with unusual high levels of D-dimer in a large majority of patients [ 1 , [4] , [5] , [6] ].…”

Behandlungsempfehlungen zur Beatmung von COVID‑19-Patienten

“…Viele Patienten mit COVID-19-Pneumonie zeigen im Verlauf ein respiratorisches Versagen Typ 2. Die Hyperkapnie ist am ehesten durch einen erhöhten Totraum zu erklären [33,34]. Wenn eine schwere Hyperkapnie trotz einer Erhöhung der Atemfrequenz bis maximal 35/min bei begleitender Minimierung des apparativen Totraums nicht beherrschbar ist, so kann die Erhöhung des TV erwogen werden, um die alveoläre Ventilation weiter zu erhöhen.…”