Introduction
Respiratory mechanics is a key element in clinical practice to monitor mechanically ventilated patients and guide ventilator settings [
1]. Respiratory system compliance (
CRS) has been shown to correlate with the amount of aerated lung [
2]. In addition, an increased respiratory system driving pressure (DP
RS) has been shown to be associated with an increased risk of mortality in patients with ARDS [
3,
4]. Beside this “basic” respiratory mechanics assessment, some more complex explorations, including in particular the evaluation of chest wall mechanics and the detection of complete airway closure, may allow to better characterize respiratory mechanics and personalize ventilator settings [
5‐
7]. Instead of considering the respiratory system as a whole, partitioning it into the lung and the chest wall using esophageal pressure measurements has thus been proposed to estimate transpulmonary pressures and determine the amount of applied airway pressure, which is spent to inflate the lung and the one spent to displace the chest wall [
8‐
10]. The airway closure, a phenomenon recently highlighted in ARDS patients, may also impact respiratory mechanics assessment and ventilatory management [
5]. Complete airway closure leads to an absence of communication between proximal airways and alveoli when airway pressure is below the level of the so-called airway opening pressure (AOP). Practically, in case of complete airway closure, no gas enters the lung during insufflation until AOP has been overcome. Complete airway closure may thus lead to driving pressure overestimations and compliance underestimations when AOP is not considered in their calculations. In addition, a PEEP setting below the AOP level may promote inflammation due to cyclic airway closure and favor atelectasis [
11]. Its detection at the bedside requires performing a low flow pressure–volume or pressure–time curve [
5]. Some data suggest that this “advanced” respiratory mechanics assessment may be particularly relevant in obese patients [
12‐
14]. Obesity is a major public health issue with a prevalence around 35% in adults in the United States of America and 13% worldwide and impacts critically ill patients’ management [
15‐
17]. Most of the literature describing respiratory mechanics in obese patients comes however from the postsurgical setting and data concerning respiratory mechanics and in particular chest wall mechanics of critically ill obese patients remain scarce. Furthermore, the impact of obesity on respiratory mechanics has not been specifically assessed in patients fulfilling or not ARDS criteria. The main aim of this study was to comprehensively assess respiratory mechanics in obese and non-obese patients with or without ARDS and to study the additional value of an advanced respiratory mechanics evaluation (including esophageal pressure measurements and complete airway closure detection) in these patients compared to a basic evaluation (based on airway pressure monitoring). For this purpose, we prospectively measured gas exchange and respiratory mechanics in standardized conditions with the same positive end-expiratory pressure (PEEP) level and the same normalized tidal volume (Vt) in all intubated patients in two ICUs.
Discussion
The main results of the study can be summarized as follows:
(1)
Oxygenation, CRS, CL, and EELV were similarly altered in obese patients without ARDS and patients with ARDS (either obese or non-obese).
(2)
Peso expi was higher in obese patients than in non-obese patients but CCW did not differ between these groups of patients. Chest wall contribution to CRS expressed by the EL/ERS ratio was widely distributed and was not predictable by patient’s general characteristics.
(3)
Complete airway closure was observed in all groups of patients but was more frequently found in obese than in non-obese patients and in ARDS than in non-ARDS patients. Ignoring airway closure led to an overestimation of DPRS in almost 17% of obese patients.
In the present series, gas exchange, CRS, CL, and EELV were similarly affected by obesity and ARDS in comparison with non-obese non-ARDS patients. These original findings can be explained by the reduction in lung volumes reported in both obese and ARDS patients. Chest wall mechanics differ however between obese and ARDS patients with higher Peso expi in obese patients despite similar CCW. This increased Peso expi may be related to the decreased EELV and the increased frequency of complete airway closure in these patients.
The impairments in lung volumes and chest wall mechanics that we measured in critically ill obese ARDS and non-ARDS patients are consistent with the observations previously reported by Coudroy et al
. in a post hoc pooled analysis of two small cohorts of patients with ARDS [
13]. In this work,
Peso expi, but not C
CW, was shown to correlate with BMI. Airway closure was also found to be more frequently observed in patients with higher BMI [
13]. Based on CT scan analyses, Chiumello et al
. reported lower lung gas volume and higher total superimposed pressure in obese ARDS compared to non-obese ARDS patients [
34]. Noticeably, in this series, C
CW was similar in obese and non-obese ARDS patients, which is consistent with our observations but P
L expi did not differ.
In addition, our observations in critically ill patients are consistent with those reported in obese surgical patients [
35‐
37]. Pelosi et al
. found however a lower C
CW in morbidly obese patients [
36]. This discrepancy with our results may be related to the higher BMI, and the strict supine position in which measurements were performed in Pelosi et al
. study [
36].
Our study is the first to systematically assess, soon after intubation, and according to a well-standardized protocol, the complete respiratory mechanics in a large series of non-selected patients including ARDS and non-ARDS patients. This methodological strength is of particular relevance to appreciate properly the roles played by obesity and ARDS since respiratory mechanics have been shown to significantly change over time under mechanical ventilation due to several confounding factors as the progressive increase in lung weight.
Our findings have important clinical implications especially since obesity is frequent in ICU patients [
15]. The respiratory mechanics features observed in both obese and ARDS patients suggest that lung protective ventilation strategy could overall be similarly managed in these patients but no interventional study has so far specifically evaluated the potential benefit of such a strategy in obese non-ARDS patients [
14]. In addition, our data suggest that advanced explorations may be of particular value to better assess respiratory mechanics and individualize ventilator settings. Interestingly, whereas basic respiratory mechanics assessments showed similar alterations in obese non-ARDS and non-obese ARDS patients, advanced explorations revealed that mechanisms involved were different in these two groups of patients. Differences in
Peso expi may thus lead to different PEEP settings when a positive
PL expi is considered as a goal to optimize ventilation [
38,
39]. Moreover, our study shows that the
EL/
ERS ratio may significantly differ between patients and cannot be easily predicted by the main patients’ characteristics. Esophageal pressure monitoring is thus needed to assess the contribution of C
CW to
CRS. Furthermore, an assessment of airway closure may be systematically considered as this phenomenon impacts driving pressure measurements in around 10% of the patients (and even 17% of obese patients). Such alterations in obese patients respiratory mechanics may contribute to explain the absence of association between DP
RS and mortality observed in obese ARDS patients contrary to what was observed in non-obese ARDS patients [
40]. In addition, a PEEP level set below the AOP may be associated with a higher risk of ventilator induced lung injury because of the heterogeneity of tidal ventilation distribution and atelectrauma [
11].
Our study has several limitations. First, gas exchange and respiratory mechanics were assessed at only one PEEP level and lung recruitability was not directly evaluated. Higher PEEP could have been associated with different observations, but our study design allowed to assess all the patients in similar standardized and safe conditions. Second, we did not deduct the estimated pressure generated by the esophagus wall from the directly measured esophageal pressure [
21]. However, our calibration procedure allowed to adjust the balloon filling volume to limit the risk of balloon overstretching, and the amplitude of the difference between the directly measured non-corrected esophageal pressure and the corrected value using the strategy proposed by Mojoli et al. is likely to be very small in this setting. Third, obesity may appear as a heterogeneous disease and some features may be observed only in morbidly obese (BMI > 40 kg m
−2) or may vary according to the distribution of fat tissue. ARDS may also be considered as a heterogenous syndrome, and we did not distinguish ARDS caused by pulmonary and non-pulmonary disease. Last, ARDS Berlin definition may be difficult to apply in obese patients who are often hypoxemic and for whom condensations may be difficult to assess on chest X-rays. This difficult classification may contribute to explain why some authors found that obesity was associated with a higher risk of ARDS development [
41]. Interestingly, in our study in which chest X-rays were independently assessed by two experienced investigators, and ARDS diagnosis was defined by an adjudication committee, ARDS was not found to be more frequent in obese than in non-obese patients.
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