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Coronavirus Disease 2019 Acute Respiratory Distress Syndrome: Guideline-Driven Care Should Be Our Natural Reflex.

In December 2019, a novel virus, the severe acute respiratory syndrome coronavirus 2, arose and spread globally over the ensuing months (1). This new human pathogen causes coronavirus disease 2019 (COVID-19) associated respiratory failure and acute respiratory distress syndrome (ARDS), creating a substantial challenge to both public health and critical care medicine as a specialty. Patients with severe COVID-19 respiratory disease present with bilateral patchy opacities and hypoxemia, meeting criteria for ARDS (1–3). Early reports have, at times, proposed a variety of disease phenotypes, suggesting that the clinical manifestations of COVID-19 ARDS are unique when compared with traditional ARDS (4, 5). Some patients are noted to have only minor limitations in respiratory compliance yet significant hypoxemia, sometimes considered out of proportion to the degree of alveolar infiltrates and overall severity of illness, raising concerns about novel pathophysiologic mechanisms specific to COVID-19 (6). Others have noted significant ventilation/perfusion mismatch and significant pulmonary vascular involvement (7). Questions have been raised as to whether the classical description of ARDS, as a disease of low compliance and severe alveolar injury with shunt-related hypoxemia, even applies to COVID-19. This has led to some calls for the reevaluation of mechanical ventilation strategies and proposals for unconventional treatment approaches for patients with ARDS from COVID-19 (8) that focus on treating a “disparate physiology” as compared with traditional ARDS. While the variation in severity of lung injury and respiratory mechanics among patients with COVID-19 ARDS is notable and should prompt further investigation, similar degrees of compliance and lung injury are seen in previously described ARDS cohorts (9, 10). Bhatraju et al (3), in a case series of 24 patients with COVID-19 ARDS in the Seattle region of the United States found that the median compliance on day 1 of mechanical ventilation was 29 cm H 2 O (interquartile range [IQR], 25–36 cm H 2 O) with a median lowest PaO 2 :FIO 2 of 142 (IQR, 94–177). All patients in the case series also had bilateral infiltrates on imaging, meeting criteria per the Berlin definition of ARDS. Similar severity of lung injury has been described in larger cohorts of patients with COVID-19 ARDS (11). In the landmark trial of low tidal volume ventilation in ARDS, degree of lung injury defined by PaO 2 :FIO 2 was similar to that seen thus far in descriptions of COVID-19 ARDS. Similar wide ranges of respiratory compliance were also described (12). In this seminal ARDS Network study, low tidal volume ventilation improved mortality regardless of compliance. Additionally, disordered coagulation, endothelial function, and thrombosis are well-known in ARDS prior to the COVID-19 pandemic (13). Increased pulmonary dead space fraction (i.e., ventilation of nonperfused regions of lung) early in ARDS is also common and associated with mortality (14). Maldistribution of pulmonary blood flow to areas with limited participation in gas exchange has also been described in ARDS (15) with attenuated hypoxic vasoconstriction being a potential mechanism (16). In each of these respects, the pathophysiology of COVID-19 ARDS disease varies, but thus far, it has not been shown to differ qualitatively enough from already established scientific literature describing traditional ARDS to justify abandoning established guidelines and protocols. Based on these early clinical observations and physiologic reasoning, new phenotypes for COVID-19 ARDS have been proposed along with guidance recommending alternative approaches to mechanical ventilation based on the proffered phenotypes (17). Interest in phenotyping ARDS even prior to 1 Division of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN.