Response to "COVID 19 conundrum: Clinical phenotyping based on pathophysiology as a promising approach to guide therapy in a novel illness" and "Strengthening the foundation of the house of CARDS by phenotyping on the fly" and "COVID 19 phenotypes: leading or misleading?"

Our interest derives from a simple fact: the debate on terms like “typical acute respiratory distress syndrome (ARDS)” or “atypical ARDS” is not just a question of semantics; these terms represent concepts linked to specific clinical, mechanical and radiological criteria, and are not merely based on the severity of gas exchange. It should not be a surprise to the authors that different radiological patterns and mechanical characteristics should suggest different ventilatory strategies, each with possible benefits and harm. The management of individual patients needs to take into consideration various factors, and not just the gas exchange that currently defines ARDS. This is precisely the point of bringing attention to the novel “L” and “H” phenotypes of coronavirus disease 2019 (COVID-19) that bracket the extremes of the clinical encounter [2]. Usually, there is overlap, depending in large part on disease duration. The “L” and “H” were not intended to be tightly prescriptive nor mutually exclusive “bins” into which each patient falls, as we clearly stated previously [3]. Rather, the object was to alert clinicians, in order to avert potential harm from assuming usual ARDS associations between hypoxaemia and mechanics at all stages. In so doing, we hoped to help prevent use of high positive end-expiratory pressure when there is no benefit and, equally important, to avoid maintaining low pressures when higher pressures can be beneficial.