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Abstract Introduction Current knowledge on the use of extracorporeal membrane oxygenation (ECMO) in COVID‐19 remains limited to small series and registry data. In the present retrospective monocentric study, we report on our experience, our basic principles, and our results in establishing and managing ECMO in critically ill COVID‐19 patients. Methods A cohort study was conducted in patients with severe acute respiratory distress syndrome (ARDS) related to COVID‐19 pneumonia admitted to the ICU of the Geneva University Hospitals and supported by VV‐ECMO from March 14 to May 31. The VV‐ECMO implementation criteria were defined according to an institutional algorithm validated by the local crisis unit and the Swiss Society of Intensive Care Medicine. Results Out of 137 ARDS patients admitted to our ICU, 10 patients (age 57 ± 4 years, BMI 31.5 ± 5 kg/m2, and SAPS II score 56 ± 3) were put on VV‐ECMO. The mean duration of mechanical ventilation before ECMO and mean time under ECMO were 7 ± 3 days and 19 ± 11 days, respectively. The ICU and hospital length of stay were 26 ± 11 and 35 ± 10 days, respectively. The survival rate for patients on ECMO was 40%. The comparative analysis between survivors and non‐survivors highlighted that survivors had a significantly shorter mechanical ventilation duration before ECMO (4 ± 2 days vs. 9 ± 2 days, p = 0.01). All the patients who had more than 150 h of mechanical ventilation before the application of ECMO ultimately died. Conclusion The present results suggest that VV‐ECMO can be safely utilized in appropriately selected COVID‐19 patients with refractory hypoxemia. The main information for clinicians is that late VV‐ECMO therapy (i.e., beyond the seventh day of mechanical ventilation) seems futile.

Abstract Background Chronic obstructive pulmonary disease (COPD) exacerbation and protective mechanical ventilation of acute respiratory distress syndrome (ARDS) patients induce hypercapnic respiratory acidosis. Main text Extracorporeal carbon dioxide removal (ECCO2R) aims to eliminate blood CO2 to fight against the adverse effects of hypercapnia and related acidosis. Hypercapnia has deleterious extrapulmonary consequences, particularly for the brain. In addition, in the lung, hypercapnia leads to: lower pH, pulmonary vasoconstriction, increases in right ventricular afterload, acute cor pulmonale. Moreover, hypercapnic acidosis may further damage the lungs by increasing both nitric oxide production and inflammation and altering alveolar epithelial cells. During an exacerbation of COPD, relieving the native lungs of at least a portion of the CO2 could potentially reduce the patient's respiratory work, Instead of mechanically increasing alveolar ventilation with MV in an already hyperinflated lung to increase CO2 removal, the use of ECCO2R may allow a decrease in respiratory volume and respiratory rate, resulting in improvement of lung mechanic. Thus, the use of ECCO2R may prevent noninvasive ventilation failure and allow intubated patients to be weaned off mechanical ventilation. In ARDS patients, ECCO2R may be used to promote an ultraprotective ventilation in allowing to lower tidal volume, plateau (Pplat) and driving pressures, parameters that have identified as a major risk factors for mortality. However, although ECCO2R appears to be effective in improving gas exchange and possibly in reducing the rate of endotracheal intubation and allowing more protective ventilation, its use may have pulmonary and hemodynamic consequences and may be associated with complications. Conclusion In selected patients, ECCO2R may be a promising adjunctive therapeutic strategy for the management of patients with severe COPD exacerbation and for the establishment of protective or ultraprotective ventilation in patients with ARDS without prognosis-threatening hypoxemia.