Is severe COVID-19 pneumonia a typical or atypical form of ARDS? And does it matter?
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EDITORIAL
Is severe COVID‑19 pneumonia a typical or atypical form of ARDS? And does it matter? Ewan C. Goligher1,2,3 , V. Marco Ranieri4 and Arthur S. Slutsky1,5* © 2020 Springer-Verlag GmbH Germany, part of Springer Nature
The coronavirus disease 2019 (COVID-19) pandemic has proven remarkable for many reasons, among them its capacity to provoke controversy and debate. One hotly debated question is whether severe COVID-19 pneumonia should be classified simply as another cause of acute respiratory distress syndrome (ARDS), or as a particular subtype of ARDS with pathophysiological features so unique that a different approach to ventilatory management is needed. Does severe COVID-19 pneumonia fall within the usual pathophysiological spectrum of ARDS or is it a qualitatively different disease state? And what consequences might the answer to this question hold for the optimal ventilatory management of severe COVID-19? In a recent article, Chiumello et al. approach these questions by comparing the respiratory pathophysiological features of patients with early COVID-19 ARDS to historical controls with classical (non-COVID-19) ARDS [1]. A hallmark of classical ARDS is that hypoxemia results predominantly from atelectasis and consolidation, with a consequent increase in physiological shunt fraction [2, 3]. In the matched cohort study, Chiumello et al. demonstrated exactly this in patients with classical ARDS: both venous admixture and hypoxemia (PaO2/ FiO2 ratio) were correlated to the fraction of non-aerated lung. In their patients with COVID-19 pneumonia, by contrast, they found that venous admixture and PaO2/ FiO2 were not correlated to the fraction of non-aerated lung, suggesting a different mechanism of hypoxemia. Moreover, the severity of hypoxemia appeared to be out of proportion to the impairment in lung mechanics.
*Correspondence: [email protected] 5 Keenan Centre for Biomedical Research, Li Ka Shing Knowledge Institute, St. Michael’s Hospital, 30 Bond Street, Toronto, ON M5B 1W8, Canada Full author information is available at the end of the article
When matched on compliance, patients with COVID-19 ARDS had more severe hypoxemia; and when matched on hypoxemia, they had relatively preserved compliance compared to patients with classical ARDS. The authors concluded that COVID-19 ARDS should be regarded as an “atypical subset of ARDS.” These conclusions accord with the pathological findings revealing unusual involvement of the pulmonary microvasculature and associated coagulopathy [4, 5]. As Chiumello et al. point out, patients in their COVID19 ARDS cohort seem to have strikingly “vasocentric” disease compared to classical ARDS (although the pulmonary microcirculation is clearly affected in classical ARDS as well). Computational models of deranged pulmonary microcirculatory function have been able to reproduce the depth of hypoxemia observed in COVID19 ARDS in the absence of significant pure shunt [6]. Nevertheless, before generalizing the results of Chiumello et al. it’s important to note that
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