Potential for the Lung Recruitment and the Risk of Lung Overdistension During 21 Days of Mechanical Ventilation in Patients With COVID-19 After Noninvasive Ventilation Failure: the COVID-VENT Observational Trial

doi:10.21203/rs.3.rs-646124/v1

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Potential for the Lung Recruitment and the Risk of Lung Overdistension During 21 Days of Mechanical Ventilation in Patients With COVID-19 After Noninvasive Ventilation Failure: the COVID-VENT Observational Trial

https://doi.org/10.21203/rs.3.rs-646124/v1

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published 04 Mar, 2022

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Background: Data on the lung respiratory mechanics and gas exchange in the time course of COVID-19-associated respiratory failure is limited. This study aimed to explore respiratory mechanics and gas exchange, the lung recruitability and risk of overdistension during the time course of mechanical ventilation.

Methods: This was a prospective observational study in critically ill mechanically ventilated patients (n=116) with COVID-19 admitted into Intensive Care Units of Sechenov University. The primary endpoints were: «optimum» positive end-expiratory pressure (PEEP) level balanced between the lowest driving pressure and the highest SpO₂ and number of patients with recruitable lung on Days 1 and 7 of mechanical ventilation. We measured driving pressure at different levels of PEEP (14, 12, 10 and 8 cmH₂O) with preset tidal volume, and with the increase of tidal volume by 100 ml and 200 ml at preset PEEP level, and calculated static respiratory system compliance (C_RS), PaO₂/FiO₂, alveolar dead space and ventilatory ratio on Days 1, 3, 5, 7, 10, 14 and 21.

Results: The «optimum» PEEP levels on Day 1 were 11.0 (10.0-12.8) cmH₂O and 10.0 (9.0-12.0) cmH₂O on Day 7. Positive response to recruitment was observed on Day 1 in 27.6% and on Day 7 in 9.2% of patients. PEEP increase from 10 to 14 cmH₂O and VT increase by 100 and 200 ml led to a significant decrease in C_RS from Day 1 to Day 14 (p<0.05). Ventilatory ratio was 2.2 (1.7-2,7) in non-survivors and in 1.9 (1.6-2.6) survivors on Day 1 and decreased on Day 7 in survivors only (p<0.01). PaO₂/FiO₂ was 105.5 (76.2-141.7) mmHg in non-survivors on Day 1 and 136.6 (106.7-160.8) in survivors (p=0.002). In survivors, PaO₂/FiO₂ rose on Day 3 (p=0.008) and then between Days 7 and 10 (p=0.046).

Conclusion: Lung recruitability was low in COVID-19 and decreased during the course of the disease, but lung overdistension occurred at «intermediate» PEEP and VT levels. In survivors gas exchange improvements after Day 7 mismatched C_RS.

Trial registration: ClinicalTrials.gov, NCT04445961. Registered 24 June 2020 - Retrospectively registered, http://https://clinicaltrials.gov/ct2/show/NCT04445961?cond=COVID-19&cntry=RU&city=Moscow&draw=3&rank=23

Anesthesiology & Pain Medicine

COVID-19

PEEP

volutrauma

lung recruitability

lung strain

acute respiratory distress syndrome

Most patients with COVID-19-associated acute respiratory failure fulfil the criteria of the acute respiratory distress syndrome (ARDS) and often require invasive mechanical ventilation (1-18). In these patients it may be crucial to understand the principal features of gas exchange abnormalities, respiratory mechanics and lung recruitability in order to provide an appropriate adjustment of the positive end-expiratory pressure (PEEP), the tidal volume and the use of recruitment maneuvers. Gattinoni L et al. recently proposed two phenotypes of COVID-19-related ARDS: L-phenotype (low lung elastance and low recruitability) and H-phenotype (high lung elastance and high recruitability) at the late stage (1). On the contrary, in comparative studies the COVID-related ARDS was similar to the primary non-COVID-related ARDS (2-3, 18). However, observational studies have shown high variability in the optimum PEEP levels and in the lung recruitability in these patients, and covered predominantly the first 7 days of mechanical ventilation (3-5, 7, 9, 10-11, 15-17).

The goal of the study was to investigate respiratory mechanics and gas exchange during the first 21 days of mechanical ventilation with the aim for selection of the «optimum» positive end-expiratory pressure (PEEP), evaluation of recruitability and a risk of volutrauma in COVID-19-associated acute respiratory failure.

Study design

This was a prospective observational clinical study (ClinicalTrials.gov NCT04445961) conducted in intensive care units (ICUs) at three hospitals of Sechenov University (Moscow, Russia) from May 1 to August 14, 2020. The study was approved by the Institutional Ethics Committee (reference number: 16-20). Written informed consent was waived owing to the observational nature of the study.

Patients

All mechanically ventilated patients (both invasive and non-invasive) were daily screened for eligibility. We included patients with COVID-19-associated respiratory failure requiring invasive mechanical ventilation after noninvasive ventilation (NIV) failure. Exclusion criteria were: 1)peripheral oxygen saturation (SpO₂) > 93%, no visible work of auxiliary respiratory muscles (sternocleidomastoid and scalene), no fatigue on conventional oxygen therapy (oxygen flow < 15 l/min) or non-invasive ventilation; 2) life-threatening heart rhythm abnormalities and/or systolic blood pressure < 80 mmHg despite norepinephrine at a dose > 2 µg/kg/min; 3) ICU stay less than 24 hours for any reason; 4) primary lung diseases (e.g. interstitial lung diseases, lung emphysema) or tumour metastases in lungs; 5) chronic decompensated diseases with extrapulmonary organ dysfunction (tumour progression, liver cirrhosis, congestive heart failure); 6) atonic coma.

Measurements

At the start of the study all patients were on mechanical ventilation in the assisted pressure-controlled volume-guaranteed mode in supine position with the tidal volume (VT) set at 6-8 ml/kg of the predicted body weight (PBW) and positive end-expiratory pressure set at 8 cmH₂O, inspiratory time 0,8-1,1 s to prevent air trapping at exhalation, respiratory rate (RR) set at 16-28 to reach arterial carbon dioxide tension (PaCO₂) 35-50 mmHg and inspiratory fraction of oxygen (FiO₂) set at minimal level to reach SpO₂ 93-96%. Patients were sedated with a propofol infusion up to the Richmond Agitation-Sedation Score (RASS) -3-4 points and paralyzed if they had inspiratory swings on pressure-time curve and/or visible work of auxiliary respiratory muscles besides RASS-4.

We measured plateau pressure (Pplat) with the inspiratory hold maneuver for 3 seconds at PEEP levels of 14, 12, 10 and 8 cmH₂O and calculated driving pressure (DP) as Pplat-PEEP and static respiratory system compliance (C_RS) on Days 1, 3, 5, 7, 10, 14, 21 and 28 (if applicable) («PEEP trial»). We set the PEEP level at mentioned time points at the balance point of the lowest DP and the highest SpO₂. After the PEEP setting, we increased tidal volume by 100 ml and 200 ml in 2 steps, respectively, and measured Pplat on each step with DP and C_RS calculation (on Days 1 and 7 as part of recruitment maneuver)(«volume trial»). For the correct calculation of C_RS during a volume increase we computed the «normalized» C_RS by dividing the tidal volume in ml/kg of the predicted body weight to driving pressure.

Also, on Days 1 and 7, we used the recruitment maneuver (RM) doubling tidal the volume for 15 respiratory cycles at a preset PEEP level (the doubled tidal volume was reached by several steps of 100 ml each). Before the maneuver we set FiO₂ that corresponds to SpO₂ 90%. Prior to and at the end of the maneuver we measured the plethysmography variability index (PVI) by Radical-7 monitor (Masimo Corp, Irvine, CA, USA). We defined RM as effective if SpO₂ rose to 95% and higher in 5 minutes after RM.

Patients were placed in the prone position for at least 16 hours per day if it led to an increase in SpO₂ by more than 5% except for patients with body mass index > 40 kg/m² (they were placed in lateral positions) and patients in whom the prone position led to an increase in driving pressure. The ventilation mode was switched to the Pressure Support mode if a patient was conscious or sedated up to RASS 0-2, had a stable respiratory and hemodynamic state, no visible work of auxiliary respiratory muscles and a stable respiratory pattern after switching. The pressure support level was set according to Pplat and corrected to achieve the Tobin index (respiratory rate/VT) of less than 70. Tracheostomy was performed on the 3rd day of mechanical ventilation.

Laboratory tests

Before the PEEP and volume trials we measured partial pressure of oxygen in arterial blood (PaO₂), partial pressure of carbon dioxide in arterial blood (PaCO₂), arterial pH, and end-expiratory carbon dioxide tension (PetCO₂), and calculated PaO₂/FiO₂ ratio, alveolar dead space (VDalv/VT) according to Bohr-Enghoff equation and ventilatory ratio (VR) (19).

Routine blood examinations included 1) complete blood count, 2) coagulation profile - fibrinogen, activated partial thromboplastin time, international normalized ratio and D-dimers, 3) serum biochemical tests (C-reactive protein, albumin, creatinine, blood urea nitrogen, total bilirubin, alanine transaminase and aspartate transaminase, lactate dehydrogenase, electrolytes and serum ferritin). The frequency of tests was determined by the attending physician (everyday, as usual).

Endpoints and statistical analysis

The primary endpoints were: 1. «Optimum» PEEP level on Days 1 and 7 of mechanical ventilation balanced between the lowest DP and the highest SpO₂; 2. Number of patients with recruitable lung defined as SpO₂ changed from 90% to 95% and more after recruitment maneuver on Days 1 and 7 of mechanical ventilation.

Secondary endpoints included: 1. «Optimum» PEEP level on Days 3, 5, 10, 14 and 21 (set as described above); 2. Driving pressure at different PEEP levels (8, 10, 12, 14 mbar) and different tidal volumes (initial, +100 ml and + 200 ml) at a set PEEP level on Days 1, 3, 5, 7, 10, 14, 21 of the mechanical ventilation; 3. Alveolar dead space on Days 1, 3, 5, 7, 10, 14, 21 of the mechanical ventilation; 4. Plethysmography variation index before PEEP and volume trials and at the end of the recruitment maneuver on Days 1 and 7 of the mechanical ventilation or during the volume trial on Days 3, 5,10 and 21; 5. PaO₂/FiO₂ ratio and ventilatory ratio on Days 1, 3, 5, 7, 10, 14, 21 of the mechanical ventilation.

Descriptive statistics included proportions for categorical and median (interquartile range) for continuous variables. No imputation was made for missing data. To assess differences between survivors and non-survivors, we performed the Mann-Whitney U test for continuous variables, and Chi-square or Fisher exact test for categorical variables. The Friedman test was used for variable dynamics within group. A two-sided p< 0.05 was considered statistically significant. Statistical analyses were performed using SPSS Statistics version 19.0 (IBM, Armonk, NY, USA).

We consecutively identified 176 and enrolled 116 patients (Figure 1). Baseline demographic and laboratory characteristics, comorbidities and medications of all patients and subgroups of survivors and non-survivors are summarised in Table 1.

The «PEEP trial» (Figure 2, Table E1) showed that the PEEP increase from 10 to 14 cmH₂O resulted in a significant increase in driving pressure on Days 3, 5, 7, 10 and 14 both in survivors and non-survivors. Driving pressure decreased with PEEP increase from 8 to 12 cmH₂O in survivors on Day 1. Driving pressure levels were significantly higher in non-survivors on Days 5, 7 and 10. Driving pressure rose at equal PEEP levels during the study period and it reached 48 cmH₂O at PEEP 14 cmH₂O in 1 non-survivor at day 28.

Volume increase by 100 ml and 200 ml from the set volume and PEEP («volume trial») resulted in a significant decrease in normalized Cstaton Days 1, 3, 5, 7, 10 and 14 in all patients and on Day 21 in non-survivors (Figure 3, Table E1). Differences between normalized Cstat in survivors and non-survivors were significant on Days 5, 7 and 10. At day 21 minimal normalized Cstat in non-survivor at tidal volume +200 ml was 8 cmH₂O/ml and driving pressure reached 74 cmH₂O (Table E1).

Static compliance at a preset tidal volume and PEEP showed a mild-to-moderate decrease and was not significantly different within and between survivors and non-survivors in dynamics (Figure 4, Table 2). Driving pressure differed significantly between survivors and non-survivors on Days 5, 7 and 10 and didn’t change significantly within survivors but increased in non-survivors on Day 21 (p=0.046).

Primary outcomes

«Optimum» PEEP levels on Days 1 and 7 were 11.0 (10.0-12.8) cmH₂O and 10.0 (9.0-12.0) cmH₂O, respectively, with no differences between survivors and non-survivors (p=0.705 and p=0.835, respectively) (Figure 5). The recruitment maneuver was effective in 29.3% of patients on Day 1, and in 9.2 % on Day 7.

Secondary outcomes

«Optimum» PEEP levels on Days 1, 3, 5, 7, 10, 14 and 21 are presented in Table 2. The «optimum» PEEP levels and tidal volumes were not different between survivors and non-survivors and within groups throughout the study.

Table 2 displays respiratory parameters, ventilatory settings and adjunctive interventions on days 1, 3, 5, 7, 10, 14 and 21 in all patients, survivors and non-survivors. The first day of mechanical ventilation in our study was associated with PaO₂/FiO₂ levels corresponding to moderate-to-severe ARDS (moderate ARDS 51.7%, severe ARDS 41.4%), high alveolar dead space with hypercapnia and high ventilatory ratio with a relatively preserved respiratory system compliance (Figure 4, Table 2). Data on Day 1 was not significantly different between survivors and non-survivors except for the PaO₂/FiO₂ ratio that was lower in non-survivors (105.5 (76.2-141.7) mmHg vs 136.6 (106.7-160.8), p=0.002).

Differences in PaO₂/FiO₂ ratio were significant between survivors and non-survivors at all study points. In survivors, PaO₂/FiO₂ ratio rose on Day 3 (p=0.008) and then between Days 7 and 10 (p=0.046). In non-survivors, PaO₂/FiO₂ ratio rose on Day 3 only (p=0.013), decreased on Day 5 (p=0.009), and later was stable until Day 10 and again decreased on Day 14 (p=0.016 as compared to Day 10; p=0.002 - to Day 1).

Alveolar dead space was increased nearly two-fold in all patients, differences between survivors and non-survivors were significant on Days 7 and 10. Alveolar dead space decreased on Day 10 in survivors (p=0.046 as compared to Day 1) and didn’t change in non-survivors. Accordingly, the ventilatory ratio was increased about two-fold in all patients and reached a statistical significance between survivors and non-survivors on Days 10 and 14 (p=0.006 and p=0.009, respectively) but failed to reach significance within subgroups in dynamics.

Patents who survived 28 days demonstrated a continuous increase of PaO₂/FiO₂ with a stable ventilatory ratio in survivors (n=4), and a stable PaO₂/FiO₂ratio with an increase of the ventilatory ratio in non-survivors after Day 10 (n=4); survivors showed a relatively small decrease in static compliance after Day 7 with decrease in the «PEEP-dependency», while non-survivors showed a drop in static compliance with marked overdistension at «intermediate» PEEP levels (Table E1).

ICU and in-hospital mortality was 84.6% (n=99). Non-survivors had a higher prevalence of cardiovascular and renal failure (Table 2). In survivors the duration of mechanical ventilation was 15 (14-28) days and in non-survivors 7 (4-12) days. We didn’t find any significant differences between survivors and non-survivors in the «non-respiratory» characteristics at baseline.

ROC-analysis

ROC-analysis revealed that gas exchange parameters on Days 7 and 10 can be used as a prognostic point for survival prediction: PaO₂/FiO₂ AUROC on Day 7 was 0.82 (0.72-0.93), p<0.0001; VDalv/VT AUROC on Day 10 was 0.80 (0.67-0.93), p=0.001; Ventilatory ratio AUROC on Day 10 was 0.75 (0.61-0.89), p=0.006. ROC-analysis for the static compliance measured at the preset PEEP and tidal volume and during the PEEP and volume trials showed non-significant results at all time points.

Laboratory values are presented in Table E2.

The results of our study can be summarized as follows: 1. All patients on Day 1 of invasive mechanical ventilation had PaO₂/FiO₂ levels corresponding to moderate-to-severe ARDS, nearly two-fold alveolar dead space and a slightly decreased respiratory system compliance at the tidal volume level; 2. On Day 1, we detected significant differences between survivors and non-survivors only in PaO₂/FiO₂; after Day 7, survivors had increased PaO₂/FiO₂ and decreased alveolar dead space irrespective of C_RS that remained stable after Day 7; 3. The potential for lung recruitment and response to the PEEP increase in COVID-19 was low, and it further decreased over time; 4. PEEP levels more than 10 cmH₂O after Day 7 led to the lung overdistension in most patients; 4. Even a modest volume increase resulted in the lung overdistension that tended to increase over time.

After the publication on COVID-19-related L- and H-phenotypes (1), such phenotypes were identified in primary non-COVID ARDS (2). In our study, we were unable to distinguish these phenotypes in mechanically ventilated patients but observed a slightly decreased compliance in all patients which is consistent with previous COVID reports (3-5) and the lung overdistension at intermediate tidal volumes.

According to Gattinoni L et al., L-phenotype lungs are not recruitable; later, after the development of ARDS (H-phenotype), dependent lung zones collapse and become susceptible to the PEEP rising (1). In our patients, we observed a completely different picture, low recruitability at the beginning with completely non-recruitable lungs after one week of mechanical ventilation. Few data is available on the respiratory mechanics and response to PEEP in COVID-19 patients with acute respiratory failure (1, 3, 9-10, 14-17). Our results contradict previous data from Beloncle FM et al., where the majority of intubated patients were highly recruitable (10). Although we used a different approach to assessing recruitment opportunities, this difference can be due to the fact that our study mainly included patients after NIV failure, while in the study by Beloncle et al mechanical ventilation was the only treatment option. Of note, the high recruitability may be caused by the airway closure, rather than by lung recruitability per se (2, 11). Haudeborg AF et al. observed that about 30% of COVID patients had recruitable lung (3), but 40% of these patients had airway closure (3, 11) as a marker of compression atelectasis, not alveolar collapse.

Observational studies comparing COVID with primary non-COVID ARDS found that COVID-ARDS was very close to ARDS due to bacterial and another virus pneumonia: slightly decreased compliance and driving pressure around 10 cmH₂O with the disproportionately low PaO₂/FiO₂ (2). Near-normal compliance in COVID-ARDS is in line with «baby lung» concept because «healthy» lung zones (in which the tidal volume is distributed (ventral parts predominantly)) have normal compliance (12). This concept explains why the prone position can be effective in primary ARDS.

We hypothesized that SARS-CoV-2- pneumonia is a primary non-recruitable lung injury that results in a gradual decrease in the total vital lung capacity. To test this hypothesis, we conducted a «stress test» (PEEP trial) and a «strain test» (increase in the tidal volume). We found marked lung overdistension at the intermediate PEEP and volume levels, which can be a marker of severe lung restriction («baby lung»)(13) that tends to increase with time (we can call it «newborn lung» in the most severe cases).

So, COVID-19 patients are at the high risk of ventilation-induced lung injury at intermediate PEEP or tidal volume levels like in other primary ARDS where PEEP generates injurious transpulmonary pressures and has a higher transmission to the pleura causing an increase in alveolar dead space (14). Our data on PEEP levels is consistent with previous reports in similar respiratory mechanics, gas exchange at inclusion, and NIV usage before intubation which showed that higher PEEP levels (as in «higher» PEEP/FiO₂ table) cause lung overdistension (6, 14-15). Studies on electro impedance tomography that looked for balance between lung recruitment and overdistension, revealed similar results: “optimum” PEEP levels around 12 cmH₂O, lung overdistension at higher PEEP levels and the need in a personalized PEEP titration (16-18). We agree with Sella N et al. (16) that PEEP/FiO₂ tables should not be used in COVID-19-associated ARDS. Comparing primary ARDS of non-COVID and COVID origins Brault C et al., Grieco DL et al. and Chiumello D et al. found no major differences between them in the respiratory mechanics and gas exchange, high heterogeneity and the need for a personalized ventilation strategy (18, 20-21), but they didn’t perform a «strain test» that can reveal the great volume differences in the rest of the «baby lung». Our “volume trial” found volutrauma at “intermediate” lung volumes that is rarely seen in secondary ARDS. Similar results were obtained in primary ARDS with the upper inflection point on the pressure-volume curve at tidal volumes around 600 ml (22).

Ventilation-perfusion mismatch and high alveolar dead space are of special interest in COVID-19 (23–24). We found a discrepancy between respiratory compliance and gas exchange in dynamics as survivors showed an increase in oxygenation and a decrease in the ventilatory ratio with a stable or even decreased respiratory compliance that can be partly explained by the restoration of lung perfusion and a ventilation-perfusion mismatch in survivors. Patel BV et al found no correlations between computer tomography findings, PaO₂/FiO₂ or ventilatory ratio (24).

Recent studies have shown significantly lower mortality with early ECMO (25-27). We suggest that COVID-19 patients without improvement in gas exchange and with signs of lung overdistension on «common» ventilatory settings on Day 7 should be considered for ECMO.

At a first glance, our study had higher mortality than others (4, 6). We used invasive mechanical ventilation as the last step in the respiratory support chain after NIV failure in the conditions of ECMO shortage, not as the primary treatment option after low flow oxygen therapy had failed. Too many questions arose when we used intubation as the only option in primary ARDS based only on the PaO₂/FiO₂ ratio in patients without extrapulmonary organ failure and signs of impaired lung mechanics such as excessive respiratory muscle load on NIV or high-flow oxygen (28-29).

Our study had several limitations. First of all, because it’s observational design. Second, it covered only patients in whom noninvasive ventilation failed and/or organ dysfunction, i.e. the most severe patients. Third, we didn’t measure additional physiologic parameters such as transpulmonary pressure, end-expiratory lung volume etc. Unfortunately, patients can die because of multiple organ failure due to resource shortage during a pandemic (ECMO, renal replacement therapy).

Lung overdistension in COVID-19-associated acute respiratory distress syndrome occurs at «intermediate» positive end-expiratory pressures and tidal volume levels; it reflects severe lung restriction and a very high risk of volutrauma. In survivors gas exchange improvements occurred after Day 7 of mechanical ventilation and mismatched the respiratory compliance which didn’t increase but even decreased. Further research is warranted in order to decrease volutrauma and improve survival in COVID-19-associated ARDS.

ARDS - acute respiratory distress syndrome

C_RS - static respiratory system compliance

DP - driving pressure

FiO₂ - inspiratory fraction of oxygen

ICU - intensive care unit

PaCO₂ - arterial carbon dioxide tension

PaO₂ - partial pressure of oxygen in arterial blood

PBW - predicted body weight

PEEP - positive end-expiratory pressure

PetCO₂ - end-expiratory carbon dioxide tension

Pplat - plateau pressure

PVI - plethysmography variability index

RASS - Richmond Agitation-Sedation Score

RM - recruitment maneuver

SpO₂ - peripheral oxygen saturation

VDalv/VT - alveolar dead space

VR- ventilatory ratio

VT - tidal volume

Ethics approval and consent to participate

The study was approved by the Institutional Ethics Committee of Sechenov University (approval number: 16-20). Written informed consent was waived owing to the observational nature of the study. The waiver was approved by the Institutional Ethics Committee of Sechenov University (approval number: 16-20)

Consent for publication

Not applicable

Availability of data and materials

The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request

Competing interests

AIY reported personal fees from GE, Philips Respironics, Covidien, Fisher & Paykel, Drager, Triton Electronics, Mindray, Pfizer, BBraun, Gilead outside the submitted work. SNA reported personal fees from Behringer Ingelheim, Pfizer, Novartis, AstraZeneca, Chiesi outside the submitted work. No other disclosers were reported.

Funding

No funding source.

Author contributions:

AIY: study design, data collection, analysis and interpretation, script writing and revision; SNA: study design, data interpretation, manuscript revision, MEP: data collection; VGB: data collection; YDS: data collection, VDK: data analysis and interpretation; APK: data collection; ZMM: data collection; NVT: data collection; IAM: data analysis and interpretation; AGY: data analysis and interpretation. All authors revised the drafted manuscript, and all read and approved its final version.

Acknowledgements

Not applicable

Authors information

Not applicable

Gattinoni L, Chiumello D, Caironi P, Busana M, Romitti F, Brazzi L, Camporota L. COVID–19 pneumonia: different respiratory treatments for different phenotypes? Intensive Care Med 2020;46:1099–1102.
Panwar R, Madotto F, Laffey JG, van Haren FMP. Compliance Phenotypes in Early Acute Respiratory Distress Syndrome before the COVID–19 Pandemic. Am J Respir Crit Care Med 2020;202:1244–1252.
Haudebourg AF, Perier F, Tuffet S, de Prost N, Razazi K, Mekontso Dessap A, Carteaux G. Respiratory Mechanics of COVID–19- versus Non-COVID–19-associated Acute Respiratory Distress Syndrome. Am J Respir Crit Care Med 2020;202:287–290.
Ziehr DR, Alladina J, Petri CR, Maley JH, Moskowitz A, Medoff BD, Hibbert KA, Thompson BT, Hardin CC. Respiratory Pathophysiology of Mechanically Ventilated Patients with COVID–19: A Cohort Study. Am J Respir Crit Care Med 2020;201:1560–1564.
Diehl JL, Peron N, Chocron R, Debuc B, Guerot E, Hauw-Berlemont C, Hermann B, Augy JL, Younan R, Novara A, Langlais J, Khider L, Gendron N, Goudot G, Fagon JF, Mirault T, Smadja DM. Respiratory mechanics and gas exchanges in the early course of COVID–19 ARDS: a hypothesis-generating study. Ann Intensive Care 2020;10:95.
Laverdure F, Delaporte A, Bouteau A, Genty T, Decailliot F, Stéphan F. Impact of initial respiratory compliance in ventilated patients with acute respiratory distress syndrome related to COVID–19. Crit Care 2020;24:412.
Pan C, Chen L, Lu C, Zhang W, Xia JA, Sklar MC, Du B, Brochard L, Qiu H. Lung Recruitability in COVID–19-associated Acute Respiratory Distress Syndrome: A Single-Center Observational Study. Am J Respir Crit Care Med 2020;201:1294–1297.
Gattinoni L, Coppola S, Cressoni M, Busana M, Rossi S, Chiumello D. COVID–19 Does Not Lead to a “Typical” Acute Respiratory Distress Syndrome. Am J Respir Crit Care Med 2020;201:1299–1300.
Schenck EJ, Hoffman K, Goyal P, Choi J, Torres L, Rajwani K, Tam CW, Ivascu N, Martinez FJ, Berlin DA. Respiratory Mechanics and Gas Exchange in COVID–19-associated Respiratory Failure. Ann Am Thorac Soc 2020;17:1158–1161.
Beloncle FM, Pavlovsky B, Desprez C, Fage N, Olivier PY, Asfar P, Richard JC, Mercat A. Recruitability and effect of PEEP in SARS-Cov–2-associated acute respiratory distress syndrome. Ann Intensive Care 2020;10:55.
Chen L, Del Sorbo L, Grieco DL, Junhasavasdikul D, Rittayamai N, Soliman I, Sklar MC, Rauseo M, Ferguson ND, Fan E, Richard JM, Brochard L. Potential for Lung Recruitment Estimated by the Recruitment-to-Inflation Ratio in Acute Respiratory Distress Syndrome. A Clinical Trial. Am J Respir Crit Care Med 2020;201:178–187.
Gattinoni L, Meissner K, Marini JJ. The baby lung and the COVID–19 era. Intensive Care Med 2020;46:1438–1440.
Gattinoni L, Pesenti A, Avalli L, Rossi F, Bombino M. Pressure–volume curve of total respiratory system in acute respiratory failure. Computed tomographic scan study. Am Rev Respir Dis 1987;136:730–736.
Tsolaki V, Siempos I, Magira E, Kokkoris S, Zakynthinos GE, Zakynthinos S. PEEP levels in COVID–19 pneumonia. Crit Care 2020;24:303.
Tsolaki V, Zakynthinos GE, Makris D. The ARDSnet protocol may be detrimental in COVID–19. Crit Care 2020;24:351.
Sella N, Zarantonello F, Andreatta G, Gagliardi V, Boscolo A, Navalesi P. Positive end-expiratory pressure titration in COVID–19 acute respiratory failure: electrical impedance tomography vs. PEEP/FiO2 tables. Crit Care 2020;24:540.
Bonny V, Janiak V, Spadaro S, Pinna A, Demoule A, Dres M. Effect of PEEP decremental on respiratory mechanics, gasses exchanges, pulmonary regional ventilation, and hemodynamics in patients with SARS-Cov–2-associated acute respiratory distress syndrome. Crit Care 2020;24:596.
Brault C, Zerbib Y, Kontar L, Fouquet U, Carpentier M, Metzelard M, Soupison T, De Cagny B, Maizel J, Slama M. COVID–19- versus non-COVID–19-related Acute Respiratory Distress Syndrome: Differences and Similarities. Am J Respir Crit Care Med 2020;202:1301–1304.
Sinha P, Calfee CS, Beitler JR, Soni N, Ho K, Matthay MA, Kallet RH. Physiologic Analysis and Clinical Performance of the Ventilatory Ratio in Acute Respiratory Distress Syndrome. Am J Respir Crit Care Med 2019;199:333–341.
Grieco DL, Bongiovanni F, Chen L, Menga LS, Cutuli SL, Pintaudi G, Carelli S, Michi T, Torrini F, Lombardi G, Anzellotti GM, De Pascale G, Urbani A, Bocci MG, Tanzarella ES, Bello G, Dell'Anna AM, Maggiore SM, Brochard L, Antonelli M. Respiratory physiology of COVID–19-induced respiratory failure compared to ARDS of other etiologies. Crit Care 2020;24:529.
Chiumello D, Busana M, Coppola S, Romitti F, Formenti P, Bonifazi M, Pozzi T, Palumbo MM, Cressoni M, Herrmann P, Meissner K, Quintel M, Camporota L, Marini JJ, Gattinoni L. Physiological and quantitative CT-scan characterization of COVID–19 and typical ARDS: a matched cohort study. Intensive Care Med 2020; 46: 2187–2196.
Roupie E, Dambrosio M, Servillo G, Mentec H, el Atrous S, Beydon L, Brun-Buisson C, Lemaire F, Brochard L. Titration of tidal volume and induced hypercapnia in acute respiratory distress syndrome. Am J Respir Crit Care Med 1995;152:121–128.
Mauri T, Spinelli E, Scotti E, Colussi G, Basile MC, Crotti S, Tubiolo D, Tagliabue P, Zanella A, Grasselli G, Pesenti A. Potential for Lung Recruitment and Ventilation-Perfusion Mismatch in Patients With the Acute Respiratory Distress Syndrome From Coronavirus Disease 2019. Crit Care Med 2020;48:1129–1134.
Patel BV, Arachchillage DJ, Ridge CA, Bianchi P, Doyle JF, Garfield B, Ledot S, Morgan C, Passariello M, Price S, Singh S, Thakuria L, Trenfield S, Trimlett R, Weaver C, Wort SJ, Xu T, Padley SPG, Devaraj A, Desai SR. Pulmonary Angiopathy in Severe COVID–19: Physiologic, Imaging, and Hematologic Observations. Am J Respir Crit Care Med 2020;202:690–699.
Barbaro RP, MacLaren G, Boonstra PS, Iwashyna TJ, Slutsky AS, Fan E, Bartlett RH, Tonna JE, Hyslop R, Fanning JJ, Rycus PT, Hyer SJ, Anders MM, Agerstrand CL, Hryniewicz K, Diaz R, Lorusso R, Combes A, Brodie D, for the Extracorporeal Life Support Organization. Extracorporeal membrane oxygenation support in COVID–19: an international cohort study of the Extracorporeal Life Support Organization registry. Lancet 2020; 396:1071–1078.
Mustafa AK, Alexander PJ, Joshi DJ, Tabachnik DR, Cross CA, Pappas PS, Tatooles AJ. Extracorporeal Membrane Oxygenation for Patients With COVID–19 in Severe Respiratory Failure. JAMA Surg 2020;155: 990–992.
Le Breton С, Besset S, Freita-Ramos S, Amouretti M, Billiet PA, Dao M, Dumont LM, Federici L, Gaborieau B, Longrois D, Postel-Vinay P, Vuillard C, Zucman N, Lebreton G, Combes A, Dreyfuss D, Ricard JD, Roux D. Extracorporeal membrane oxygenation for refractory COVID–19 acute respiratory distress syndrome. J Crit Care 2020; 60:10–12
Tobin MJ. Basing respiratory management of COVID–19 on physiological principles. Am J Respir Crit Care Med 2020;201:1319–1320.
Yaroshetskiy AI, Avdeev SN, Konanykhin VD. Acute Respiratory Distress Syndrome in COVID–19: Do All These Patients Definitely Require Intubation and Mechanical Ventilation? Am J Respir Crit Care Med 2020;202:1480–1481.

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Potential for the Lung Recruitment and the Risk of Lung Overdistension During 21 Days of Mechanical Ventilation in Patients With COVID-19 After Noninvasive Ventilation Failure: the COVID-VENT Observational Trial

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