What have we learned ventilating COVID-19 patients?
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EDITORIAL
What have we learned ventilating COVID‑19 patients? Uriel Trahtemberg1, Arthur S. Slutsky2,3 and Jesús Villar3,4,5* © 2020 Springer-Verlag GmbH Germany, part of Springer Nature
The spectrum of coronavirus disease 19 (COVID-19) ranges from asymptomatic to mild respiratory disease, pneumonia, acute respiratory distress syndrome (ARDS), multiorgan failure, and death. About 5% of COVID19 patients require ICU admission and ~ 3.5% develop ARDS, although this number depends on reporting bias, practice patterns, and resource availability. In this Editorial, we present a viewpoint on the ventilatory management of COVID-19-induced ARDS, based on the underlying pathophysiology. Our message is simple: after almost a year of treating ARDS caused by COVID-19, everything—and nothing—has changed [1].
Pathophysiology of COVID‑19 ARDS The angiotensin-converting enzyme 2 (ACE2) receptor is the functional SARS-CoV-2 receptor, and along with the transmembrane serine protease 2 (TMPRSS2) is required for viral entry into cells [2]. The ubiquity of this receptor can explain many manifestations of COVID-19. The lung is a prime target for SARS-CoV-2 because of its huge surface area which is in direct contact with the inspired air (and possible SARS-CoV-2 virions), and the expression of ACE2 in surfactant-producing alveolar type-II cells. Infection of the latter likely explains the atelectasis and pneumonia observed in COVID-19 patients. ACE2 expression in many cell types can also explain other organ involvement in COVID-19 (e.g., heart, kidney, blood vessels, skin), and perhaps some of the more unique findings including anosmia (olfactory support cells) and “happy hypoxemia” (carotid body).
*Correspondence: [email protected] 5 Research Unit, Hospital Universitario Dr. Negrín, Barranco de la Ballena s/n, 4th Floor South Wing, 35019 Las Palmas de Gran Canaria, Spain Full author information is available at the end of the article
The available pathological findings of COVID-19 ARDS suggest diffuse alveolar damage along with pulmonary vasculature involvement [3], which have been recognized as important features of ARDS for decades. Widespread pulmonary macro/microthrombi are commonly found in autopsies of patients with ARDS from any etiology at any phase of the disease. The biggest controversy is whether the pathophysiology of COVID-19 ARDS is different from non-COVID-19 (classical) ARDS. A number of editorials, opinion pieces, and small reports have suggested that COVID-19 ARDS is atypical, since some patients with severe hypoxemia had relatively normal respiratory compliance, with implications for ventilatory management [4, 5]. However, the heterogeneity of classical ARDS is well documented, and alterations of gas-exchange and respiratory system compliance in COVID-19 ARDS [6– 8] appear comparable to, and within the range of values reported for classical ARDS [9], including in a case series published in 2006 [10]. Some of the differences found may be due to differences in setting PEEP, reinforcing the need to individuali
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