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In This Article

  • Some physicians have alleged, mostly on social media and in the popular press, that COVID-19–associated respiratory failure is the result of a novel pathophysiology and is therefore not ARDS
  • A published editorial by Gattinoni and colleagues suggests there are distinct phenotypes of severe COVID-19, one of which is distinct from ARDS and could be treated with large tidal volumes
  • That hypothesis ignores decades of evidence for gentle ventilation, including in non-ARDS hypoxemic respiratory failure
  • Gattinoni and colleagues appear to agree that large distending pressures in the inflamed lung can be injurious and lead to worsening of gas exchange and pulmonary mechanics—the essential pathophysiology of ARDS

In recent weeks some have argued that COVID-19–associated respiratory failure is distinct from acute respiratory distress syndrome (ARDS). Most of these comments were made in social media or the popular press, but one group of clinicians published a letter in the American Journal of Respiratory and Critical Care Medicine and an editorial in Intensive Care Medicine.

Corey Hardin, MD, PhD, physician in the Division of Pulmonary and Critical Care at Massachusetts General Hospital, critiques multiple allegations that it is different in a fast literature update posted on April 10, 2020.

Distinct COVID-19 Phenotypes?

Without speculating on the mechanism, Dr. Gattinoni and colleagues suggest there are distinct phenotypes of severe COVID-19, including:

  • Type L (low elastance/near-normal compliance, low ventilation-to-perfusion ratio, low lung recruitability) is distinct from ARDS and could be treated with large tidal volumes
  • Type H (high parameters) is severe ARDS with widespread alveolar collapse

The authors of the editorials say patients with type L can tolerate large tidal volumes and noninvasive respiratory support. That hypothesis ignores decades of evidence for lung-protective ventilation, including in non-ARDS hypoxemic respiratory failure.

Ventilation for COVID-19

Recruitment maneuvers may improve shunt or ventilation–perfusion mismatch in some lung units. However, they can also cause overdistention of well-inflated lung units. Therefore, ventilatory strategies for COVID-19 (outlined in a previous fast literature update) stress low tidal volumes and cautious use of positive end-expiratory pressure.

Noninvasive support is frequently avoided in COVID-19 because it can cause increased tidal volumes—the dyspneic patient vigorously contracts the diaphragm, generating large negative pleural pressures and therefore large transpulmonary pressures. Early intubation is advocated to limit distending pressures.

A Contradiction

Dr. Gattinoni and colleagues acknowledge that large distending pressures in the inflamed lung can be injurious and cause "type L" to become "type H." The authors are therefore in the perverse position of insisting that the pathophysiology of ARDS is present in COVID-19, but urging abandonment of the most successful evidence-based treatment for ARDS.

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During the COVID-19 pandemic, many novel approaches to acute respiratory distress syndrome (ARDS) have been suggested for immunomodulation and targeting the host response to SARS-CoV-2. However, these novel therapies must be evaluated in the context of the history of failed investigational therapies for ARDS.

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Researchers at Massachusetts General Hospital report that "dry lungs are happy lungs" in patients with acute respiratory distress syndrome, including cases related to COVID-19.