35 mL/cm H2O,
28 mL/cm H2O,
and 32 mL/cm H2O
) that are consistent or even lower than the values observed by Chiumello and colleagues (48 mL/cm H2O [SD 16] and 42 mL/cm H2O [14])
,
and Gattinoni and colleagues (44 mL/cm H2O [17])
in classical ARDS. In addition, Panwar and colleagues recently showed that patients with classical ARDS had a wide range of compliance, with about one in eight patients (136 [12·2%] of 1117 patients) having compliance of at least 50 mL/cm H2O, and that the ratio of partial pressure of arterial oxygen to fractional concentration of oxygen in inspired air (PaO2/FiO2) and static compliance were almost completely dissociated.
We used a linear regression model to analyse the relationship between static compliance and PaO2/FiO2 in COVID-19 ARDS
and in classical ARD.
This analysis can be quantified in terms of R2 (ie, the percentage of the PaO2/FiO2 variation that is explained by changes in compliance) and p values (to test the null hypothesis—ie, that the equation coefficient is equal to zero and that changes on PaO2/FiO2 have no effect on changes in compliance). In COVID-19 ARDS, the relationship was not significant (p=0·160) and R2 was 0·007 (appendix). In classical and pneumonia ARDS, results were statistically significant (pR2 were low (0·059 and 0·040, respectively; appendix). Thus, only 6% of the variability of PaO2/FiO2 is explained by the variability of compliance (p2/FiO2 depends on something else.
We agree with Camporota and colleagues and Tsolaki and colleagues that positive end-expiratory pressure (PEEP) should be individualised to the specific patient in COVID-19 ARDS, as in all other patients with ARDS. We believe the current methods, such as the lower PEEP–high FiO2 table, should be used until evidence of improved outcomes with other explicit strategies becomes available.
Regarding the potential imbalance in the distribution of potential confounders, values of SOFA score at baseline and use of steroids and anticoagulation did not vary among our four patient groups.
We also acknowledge that ventilatory ratio is only a proxy of dead space fraction and that other methods are available to measure specifically this relevant parameter, and that chest CT scans were obtained only in a small number of patients based on compelling clinical indications.
Finally, we agree with Michael Dandel that, given the relevant role of filling defects or occlusions of the pulmonary vasculature, particular attention should be paid to right ventricular dysfunction in patients with COVID-19 ARDS.
GG reports personal fees and non-financial support from Getinge and Biotest; personal fees from Thermofisher and Draeger Medical, and grants and personal fees from Fisher&Paykel, outside of the submitted work. AP reports personal fees from Maquet, Novalung/Xenios, Baxter, and Boehringer Ingelheim, outside of the submitted work. All other authors declare no competing interests.
Supplementary Material
References
- 1.
Epidemiology, clinical course, and outcomes of critically ill adults with COVID-19 in New York City: a prospective cohort study.
Lancet. 2020; 395: 1763-1770
- 2.
Clinical features, ventilatory management, and outcome of ARDS caused by COVID-19 are similar to other causes of ARDS.
Intensive Care Med. 2020; ()
- 3.
Respiratory mechanics and gas exchange in COVID-19 associated respiratory failure.
Ann Am Thorac Soc. 2020; 17: 1158-1161
- 4.
Ventilation management and clinical outcomes in invasively ventilated patients with COVID-19 (PRoVENT-COVID): a national, multicentre, observational cohort study.
Lancet Respir Med. 2020; ()
- 5.
Hysteresis and lung recruitment in acute respiratory distress syndrome patients: a CT scan study.
Crit Care Med. 2020; 48: 1494-1502
- 6.
Lung stress and strain during mechanical ventilation for acute respiratory distress syndrome.
Am J Respir Crit Care Med. 2008; 178: 346-355
- 7.
Lung recruitment in patients with the acute respiratory distress syndrome.
N Engl J Med. 2006; 354: 1775-1786
- 8.
Compliance phenotypes in early ARDS before the COVID-19 pandemic.
Am J Respir Crit Care Med. 2020; 202: 1244-1252
- 9.
Pathophysiology of COVID-19-associated acute respiratory distress syndrome: a multicentre prospective observational study.
Lancet Respir Med. 2020; 8: 1201-1208
- 10.
Epidemiology, Patterns of care, and mortality for patients with acute respiratory distress syndrome in intensive care units in 50 countries.
JAMA. 2016; 315: 788-800
Article Info
Publication History
Published: November 13, 2020
Identification
Copyright
© 2020 Elsevier Ltd. All rights reserved.
