Skip to main content
Download PDF

Driving pressure-guided ventilation decreases the mechanical power compared to predicted body weight-guided ventilation in the Acute Respiratory Distress Syndrome

Critical Care volume 26, Article number: 185 (2022) Cite this article

Abstract

Background

Whether targeting the driving pressure (∆P) when adjusting the tidal volume in mechanically ventilated patients with the acute respiratory distress syndrome (ARDS) may decrease the risk of ventilator-induced lung injury remains a matter of research. In this study, we assessed the effect of a ∆P-guided ventilation on the mechanical power.

Methods

We prospectively included adult patients with moderate-to-severe ARDS. Positive end expiratory pressure was set by the attending physician and kept constant during the study. Tidal volume was first adjusted to target 6 ml/kg of predicted body weight (PBW-guided ventilation) and subsequently modified within a range from 4 to 10 ml/kg PBW to target a ∆P between 12 and 14 cm H2O. The respiratory rate was then re-adjusted within a range from 12 to 40 breaths/min until EtCO2 returned to its baseline value (∆P-guided ventilation). Mechanical power was computed at each step.

Results

Fifty-one patients were included between December 2019 and May 2021. ∆P-guided ventilation was feasible in all but one patient. The ∆P during PBW-guided ventilation was already within the target range of ∆P-guided ventilation in five (10%) patients, above in nine (18%) and below in 36 (72%). The change from PBW- to ∆P-guided ventilation was thus accompanied by an overall increase in tidal volume from 6.1 mL/kg PBW [5.9–6.2] to 7.7 ml/kg PBW [6.2–8.7], while respiratory rate was decreased from 29 breaths/min [26–32] to 21 breaths/min [16–28] (p < 0.001 for all comparisons). ∆P-guided ventilation was accompanied by a significant decrease in mechanical power from 31.5 J/min [28–35.7] to 28.8 J/min [24.6–32.6] (p < 0.001), representing a relative decrease of 7% [0–16]. With ∆P-guided ventilation, the PaO2/FiO2 ratio increased and the ventilatory ratio decreased.

Conclusion

As compared to a conventional PBW-guided ventilation, a ∆P-guided ventilation strategy targeting a ∆P between 12 and 14 cm H2O required to change the tidal volume in 90% of the patients. Such ∆P-guided ventilation significantly reduced the mechanical power. Whether this physiological observation could be associated with clinical benefit should be assessed in clinical trials.

Background

The major goal of lung-protective ventilation in the Acute Respiratory Distress Syndrome (ARDS) is to reduce ventilator/ventilation-induced lung injuries (VILI) by minimizing strain and stress applied to the lung by mechanical ventilation [1, 2]. As ARDS patients are characterized by a dramatical decrease in aerated lung volume, lowering the tidal volume (VT) down to 6 ml/kg of predicted body weight (PBW) has been shown more than 20 years ago to improve their survival [3] and has become the cornerstone of lung protective ventilation [4]. In such patients, the decrease in respiratory system compliance (CRS) is correlated to the decrease in the lung volume available for ventilation [5,6,7]. The driving pressure (ΔP), defined as the difference between the plateau pressure and the positive end expiratory pressure (PEEP), represents the ratio between the VT and the CRS [8]. Therefore, the ΔP normalizes the VT to a surrogate of the aerated lung, rather than to the theoretical lung size as is the case when VT is related to PBW. In a post hoc analysis of nine randomized control trials, Amato et al. found that high ΔP was a better predictor of mortality than high VT [9], with an increased risk of death when the ΔP exceeded 14 cm H2O. These findings have been confirmed in a subsequent meta-analysis [10] and reinforced by large-scale observational data [11,12,13]. More recently, it has been shown that the mortality benefit of lowering VT in ARDS varied according to the CRS: the patients with lower CRS were likely to have a greater mortality benefit, whereas patients with higher CRS were likely to have a lower mortality benefit [14]. All these data argue for targeting ΔP rather than VT scaled to PBW in ARDS.

In this study, we hypothesized that a ΔP-guided tidal ventilation strategy (ΔP-Vent), targeting a ΔP between 12 and 14 cm H2O, may reduce the risk of VILI as compared to a PBW-guided tidal ventilation strategy (PBW-Vent) in ARDS patients. Such ∆P-vent approach could protect against excessive driving pressure in patients with lower CRS while permitting higher driving pressure in patients with higher CRS, allowing a concomitant decrease in the respiratory rate. Interestingly, recent data suggest that both driving pressure and respiratory rate are predictors of mortality in ARDS [15]. Their combined effect may depend on CRS with potential value in increasing tidal volume while decreasing respiratory rate in patients with higher CRS. The mechanical power represents the energy applied to the respiratory system by the ventilator and has been considered as a surrogate for the risk of VILI [16,17,18]. It is associated with mortality during controlled mechanical ventilation in ARDS [15, 19] and has the advantage of taking into account both an elastic component related to the driving pressure and the possible impact of respiratory rate. Thus, the aim of our study was to compare, in ARDS patients, the mechanical power resulting from a ΔP-Vent versus that resulting from a PBW-Vent.

Methods

Study design

This is an ancillary report of an ongoing prospective monocentric observational study on ventilator settings and respiratory mechanics assessment in patients with ARDS, conducted in the Henri Mondor University Hospital medical ICU, Créteil, France. The study was approved by the ethics committee “CPP Sud Ouest et Outre Mer III” (2018-A00867–48). According to the French law, non-opposition to participate in the study from the patient or his/her next of kin was collected prior to inclusion.

Patients

Inclusion criteria were as follows: moderate-to-severe ARDS according to the Berlin definition [20], less than 5 days since the onset of ARDS, and passive ventilation, i.e., no clinical detection of spontaneous respiratory effort. Non-inclusion criteria were the followings: age < 18 years, pregnancy, extra-corporeal membrane oxygenation, the need for strict control of PaCO2 (e.g., severe neurological impairment) and patients under law protection. Exclusion criteria was the impossibility to achieve ΔP-Vent (see below).

Ventilator settings

Positive end-expiratory pressure (PEEP) and fraction of inspired oxygen (FiO2) were set by the attending physician and kept constant during the study. As per our clinical routine (see below), the PEEP set by the clinician was equal or above the airway opening pressure, while ensuring a plateau pressure below 30 cm H2O. The tidal volume was routinely set at 6 mL/kg of PBW, with the respiratory rate adjusted to maintain the pH between 7.20 and 7.45 [21, 22], which corresponds to the PBW-Vent. Respiratory mechanics was assessed during PBW-Vent, including the ΔP (see below). The principle of the ΔP-Vent was to target a ΔP between 12 and 14 cm H2O. Thus, if the ΔP measured during PBW-Vent was below 12 or above 14 cm H2O, the tidal volume was readjusted within a range from 4 to 10 ml/kg PBW to target a ΔP between 12 and 14 cm H2O without exceeding a plateau pressure of 30 cm H2O. The respiratory rate was then modified within a range from 12 to 40 breaths/min until the end-tidal CO2 (EtCO2) returned to its baseline value observed during PBW-Vent, defining the ΔP-Vent.

Measurements

At baseline during PBW-Vent, the potential airway closure phenomenon was detected by measuring the airway opening pressure during a low flow (< 6 L/min) insufflation, as previously described [23]. The potential for lung recruitment was assessed using recruitment-to-inflation ratio (R/I ratio) obtained with a drop in PEEP over a single breath maneuver, as previously detailed [23]. By default, R/I ratio was assessed between 15 and 5 cmH2O of PEEP. However, in case of airway closure, the low PEEP was set above the airway opening pressure. Ventilator’s settings and respiratory mechanics were collected during PBW-Vent and after at least 30 min of ΔP-Vent application. For that purpose, a 0.3 s end-inspiratory pause and a one to two second end-expiratory occlusion maneuver were performed to record both the plateau pressure and total PEEP. From these data, the mechanical power (in Joules per minute) was computed as the algebraic sum of elastic and resistive power [15, 16]:

$$\begin{aligned} & {\text{Elastic power}}\,({\text{J}}/\min ): \, \,0.098 \, \times {\text{ RR }} \times \, V_{T} \times \, \left( {{\text{PEEP }} + \, 0.5 \, \times \, \Delta P} \right) \\ & {\text{Resistive power}}\,({\text{J}}/\min ):\, \, 0.098 \, \times {\text{ RR }} \times \, V_{T} \times \, \left( {{\text{Ppeak }}{-}{\text{ Pplat}}} \right) \\ \end{aligned}$$

where RR is the respiratory rate, VT the tidal volume, Ppeak the peak airway pressure, and Pplat the plateau pressure.

Blood gases were performed under PBW-Vent and after 30 min of ΔP-Vent if an arterial line was present.

A transthoracic echocardiography was conducted under PBW-Vent and ΔP-Vent for the last 24 patients included in the study in order to assess the potential effects of ΔP-Vent on cardiac output and right ventricle function. These echocardiography tests were performed using an S7 or E9 ultrasound system (GEMS, Buc, France). Pulsed-wave Doppler were obtained at aortic valve to assess aortic velocity–time integral for cardiac output computation. Right ventricle preload was assessed using the maximal diameter of inferior vena cava on long-axis M-mode view. Right ventricle systolic function assessment relied on tricuspid annulus plane systolic excursion (TAPSE) and on tissue Doppler peak systolic wave at tricuspid lateral annulus (tricuspid S’ wave). Relative size of right and left ventricles was assessed on apical four-chamber view using the end-diastolic right ventricle/left ventricle area ratio. The systolic pulmonary arterial pressure was assessed using the peak velocity of tricuspid regurgitation on continuous-wave Doppler.

Endpoints

The primary endpoint was the mechanical power. Secondary endpoints were the followings: mechanical power normalized to PBW (norMP), ΔP, tidal volume, respiratory rate, minute ventilation, compliance and resistance of the respiratory system, PaO2/FiO2 ratio, PaCO2, ventilatory ratio [24], cardiac output and right ventricle function.

Statistics

Data were analyzed using SPSS Base 20.0 statistical software package (SPSS, Chicago, IL). Sample size calculation was made using the “pwr” package in R (version 4.0.1). To be able to show a potential difference in mechanical power between VT-Vent and ΔP-Vent with a medium effect size—the effect size being the difference between the means divided by the pooled standard deviation; a value of 0.5 defining a medium effect size for paired comparisons [25]—a type I error of 0.05 and a statistical power of 90%, 44 patients were needed using two-sided tests. We therefore chose to include at least 50 patients. Continuous data were expressed as medians (25th–75th percentiles) and compared using Mann–Whitney test for independent variables and Wilcoxon signed rank test for related variables. Categorical variables, expressed as percentages, were evaluated using Chi-square or Fisher exact tests as appropriate. A p < 0.05 was considered significant.

Results

Patients’ characteristics

Fifty-one patients were included between December 2019 and May 2021. One patient was secondarily excluded because ΔP-Vent was impossible to achieve with the predefined boundaries of VT (≥ 4 mL/kg) and RR (≤ 40/min). ΔP-Vent was feasible in the remaining 50 (98%) patients, whose main characteristics are reported in Table 1. The basal ΔP during PBW-Vent was already within the target range of ΔP-Vent in five patients (10%), above in nine (18%) and below in 36 (72%). Thus, the VT was left unchanged in five patients, decreased in nine and increased in 36. In all patients in whom tidal volume was increased, the increase was possible to meet the target ΔP before the plateau pressure limit was reached.

Table 1 Characteristics of patients who underwent predicted body weight- and driving pressure-guided ventilation
Full size table

Primary endpoint

Compared to PBW-Vent, ΔP-Vent was accompanied by a significant decrease in mechanical power from 31.5 J/min [28–35.7] to 28.8 J/min [24.6–32.6] (p < 0.001, Table 2 and Fig. 1), corresponding to a relative decrease of 7% [0–16].

Table 2 Ventilatory and hemodynamic changes between tidal volume-guided ventilation and driving pressure-guided ventilation
Full size table
Fig. 1
figure 1

Change in mechanical power between predicted body weight-guided ventilation (PBW-Vent) and driving pressure-guided ventilation (ΔP-Vent). A The violin plots represent the mechanical power (thick horizontal line: median; thin horizontal dashed lines: 25th and 75th percentiles). *Denotes statistical significance. B Individual data

Full size image

Individual data showed that the mechanical power strictly decreased with ΔP-Vent in 36 patients (from 31.5 J/min [27.8–35.8] to 26.4 J/min [24.1–32.9]), and remained unchanged or increased in 14 patients (from 30.7 J/min [28.7–35.4] to 31.9 J/min [30.4–35.4]).

Secondary endpoints

Switching from PBW-Vent to ΔP-Vent required a significant increase in VT, and a significant decrease in respiratory rate (Table 2). As compared to PBW-Vent, ΔP-Vent was characterized by a significant increase in ΔP, plateau pressure and PaO2/FiO2 ratio, and a significant decrease in minute ventilation, auto-PEEP, and ventilatory ratio, while PaCO2 was similar between the two ventilation strategies (Table 2). The hemodynamic parameters, cardiac output and right ventricle function were not altered by the change in ventilation strategy.

At baseline during PBW-Vent, patients whose mechanical power decreased with ΔP-Vent (n = 36) had a significantly higher SAPS II, SOFA score and respiratory system compliance and a significantly lower driving pressure, plateau pressure, R/I ratio and alveolar dead space (Table 3). In these patients, switching to ΔP-Vent was accompanied by a significant increase in ΔP and VT and a significant decrease in respiratory rate, minute ventilation and ventilatory ratio (Fig. 2). In patients whose mechanical power did not decrease with ΔP-Vent (n = 14), applying ΔP-Vent was not associated with a significant change in respiratory pattern or ventilatory ratio compared with PBW-Vent (Fig. 2).

Table 3 Baseline and ventilatory characteristics according to the evolution of mechanical power with driving pressure-guided ventilation
Full size table
Fig. 2
figure 2

Change in ventilatory parameters according to the change in mechanical power with ΔP-Vent. MP ↘ with ΔP-Vent: patients in whom the mechanical power strictly decreased with ΔP-Vent compared with PBW-Vent (n = 36). MP → or ↗ with ΔP-Vent: patients in whom the mechanical power remained unchanged or increased with ΔP-Vent compared with PBW-Vent (n = 14). ΔP: driving pressure; Vt: tidal volume. *Denotes statistical significance

Full size image

Discussion

The main findings of our study are the followings: a ∆P-guided ventilation targeting a ∆P between 12 and 14 cm H2O represented a distinct strategy from a conventional PBW-guided ventilation as it required VT changes in 90% of the patients; the direction of the change in VT was an increase in the majority of cases (72%), accompanied by a concomitant decrease in respiratory rate; such ∆P-guided ventilation led to a significant decrease in mechanical power while PaO2/FiO2 and ventilatory ratio improved; the decrease in mechanical power was mainly driven by patients with higher respiratory system compliance, thus in whom the VT increased during ∆P-guided ventilation.

A ΔP-limited strategy (aiming at minimizing the ΔP) has been proposed and seems feasible [28]. However, decreasing the ΔP at the price of an increase in respiratory rate may be at higher risk of unfavorable outcome in patients with higher compliance [19]. In this study, we rather assessed a ΔP-Vent strategy targeting a ΔP range below the threshold identified as associated with an increased risk of death. If the ΔP was above the threshold during PBW-Vent, the VT was decreased in order to avoid excessive strain. However, the ΔP at baseline during PBW-Vent in our series was below the predefined target range in a majority of patients, in accordance with values usually observed in ARDS patients when the VT is set at 6–8 ml/kg of PBW [11]. VT was therefore most often increased to achieve ΔP-Vent. One may assume that allowing some increase in VT in patients with higher compliance during the ΔP-Vent strategy could be associated with favorable physiological effects as promotion of recruitment and decrease in alveolar dead space [29], improvement of oxygenation [30], unloading of respiratory muscles, attenuation of respiratory drive [31, 32], relief of dyspnea [14], decreased risk of occurrence of breath stacking [33, 34] and decreased need for sedative drugs [35]. Of note, in our study, ΔP-Vent was accompanied by an increase in PaO2/FiO2 ratio, and a decrease in ventilatory ratio. Whether such physiological effects could be associated with improvement in clinical outcome warrants further research.

In our study, ΔP-Vent was associated with a significant decrease in both the resistive and elastic component of the mechanical power, as compared to PBW-Vent. Mechanical power, which represents the energy delivered to the respiratory system, could be considered as a target for VILI prevention [18]. Cressoni et al. conducted an experimental study on piglets suggesting that neither the VT alone nor the respiratory rate could generate VILI, which instead was induced by their combination when the mechanical power produced was higher than a certain threshold [17]. Therefore, paying attention to mechanical power might help broaden our focus on VILI, taking into account not only VT and ΔP, but also respiratory rate and their combination. In an analysis of more than 8000 critically ill patients from the MIMIC-III and eICU databases, Serpa Neto et al. retrieved that high mechanical power was independently associated with high in-hospital mortality, even at low tidal volumes [19]. More recently, a retrospective analysis of 4549 patients included in six randomized clinical trials of protective ventilation showed that mechanical power was a significant predictor of mortality at 28 or 60 days [15]. In our study, the ΔP-Vent induced a relative decrease in mechanical power of 7% [0–16]. In a prospective cohort study involving 13,408 patients, Urner et al. reported a significant increase in the hazard of death with each daily increment in mechanical power over the whole duration of mechanical ventilation, suggesting that even a small decrease in mechanical power could be relevant if maintained over time. However, a causal relationship between mechanical power and clinical outcome has not been demonstrated to date. High mechanical power may be a marker of lung injury rather than inappropriate ventilator settings. Indeed, during conventional protective ventilation, the mechanical power increases in case of CRS impairment and decreases during resolution of the lung disease. Thus, the clinical impact of a ventilation strategy that is accompanied by a decrease in mechanical power remains unclear and deserves future clinical trials.

Our study has some limitations. First, this was a single-center study with a significant proportion of COVID-19-related ARDS among the included patients. Conflicting data have been reported about potential differences in the respiratory system compliance in the early phase of COVID-19-related ARDS compared to ARDS of other origins [36,37,38,39,40]. However, the ΔP at baseline during PBW-Vent in our population was consistent with reports prior to COVID-19 pandemics [11], suggesting external validity. Second, PEEP management in our unit may have influenced the value of mechanical power. In fact, mechanical power is modeled with a positive linear relationship with PEEP. However, we did not modify PEEP between PBW-Vent and ΔP-Vent. The difference in mechanical power was therefore exclusively related to variations in VT and respiratory rate, and should be reproducible as long as the PEEP level remains of the same order of magnitude. Third, our PEEP management may also have influenced the plateau pressure values. Excessive plateau pressure may be associated with higher mortality even with limited driving pressure [41]. In our study however, the plateau pressure remained below 30 cm H2O during both ventilation strategies in all patients. Lastly, the ΔP value is influenced by the chest wall compliance and a high ΔP may be related to a low chest wall compliance rather than an excessive lung strain. We did not record the esophageal pressure and were thus unable to measure the chest wall compliance. However, we aimed at assessing a pragmatic approach that could be easily translated into clinical practice. As the ΔP-Vent was feasible and different from PBW-Vent in 90% of our patients, designing clinical trials comparing the two strategies is attainable.

Conclusion

As compared to a conventional PBW-guided ventilation, a ∆P-guided ventilation strategy targeting a ∆P between 12 and 14 cm H2O significantly reduced the mechanical power.

Availability of data and material

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

References

  1. Brochard L, Slutsky A, Pesenti A. Mechanical ventilation to minimize progression of lung injury in acute respiratory failure. Am J Respir Crit Care Med. 2017;195(4):438–42.

    Article  PubMed  Google Scholar 

  2. Nieman GF, Satalin J, Andrews P, Habashi NM, Gatto LA. Lung stress, strain, and energy load: engineering concepts to understand the mechanism of ventilator-induced lung injury (VILI). Intensive Care Med Exp. 2016;4(1):16.

    Article  PubMed  PubMed Central  Google Scholar 

  3. Acute Respiratory Distress Syndrome Network, Brower RG, Matthay MA, Morris A, Schoenfeld D, Thompson BT, et al. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342(18):1301–8.

    Article  Google Scholar 

  4. Papazian L, Aubron C, Brochard L, Chiche JD, Combes A, Dreyfuss D, et al. Formal guidelines: management of acute respiratory distress syndrome. Ann Intensive Care. 2019;9(1):69.

    Article  PubMed  PubMed Central  Google Scholar 

  5. Gattinoni L, Pesenti A. The concept of «baby lung». Intensive Care Med. 2005;31(6):776–84.

    Article  PubMed  Google Scholar 

  6. 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(3):730–6.

    Article  CAS  PubMed  Google Scholar 

  7. Gattinoni L, Pesenti A, Baglioni S, Vitale G, Rivolta M, Pelosi P. Inflammatory pulmonary edema and positive end-expiratory pressure: correlations between imaging and physiologic studies. J Thorac Imaging juill. 1988;3(3):59–64.

    Article  CAS  Google Scholar 

  8. Henderson WR, Chen L, Amato MBP, Brochard LJ. Fifty years of research in ARDS. Respiratory mechanics in acute respiratory distress syndrome. Am J Respir Crit Care Med. 2017;196(7):822–33.

    Article  PubMed  Google Scholar 

  9. Amato MBP, Meade MO, Slutsky AS, Brochard L, Costa ELV, Schoenfeld DA, et al. Driving pressure and survival in the acute respiratory distress syndrome. N Engl J Med. 2015;372(8):747–55.

    Article  CAS  PubMed  Google Scholar 

  10. Aoyama H, Pettenuzzo T, Aoyama K, Pinto R, Englesakis M, Fan E. Association of driving pressure with mortality among ventilated patients with acute respiratory distress syndrome: a systematic review and meta-analysis*. Crit Care Med. 2018;46(2):300–6.

    Article  PubMed  Google Scholar 

  11. Urner M, Jüni P, Hansen B, Wettstein MS, Ferguson ND, Fan E. Time-varying intensity of mechanical ventilation and mortality in patients with acute respiratory failure: a registry-based, prospective cohort study. Lancet Respir Med. 2020;8(9):905–13.

    Article  PubMed  PubMed Central  Google Scholar 

  12. Bellani G, Laffey JG, Pham T, Fan E, Brochard L, Esteban A, et al. Epidemiology, patterns of care, and mortality for patients with acute respiratory distress syndrome in intensive care units in 50 countries. JAMA. 2016;315(8):788–800.

    Article  CAS  PubMed  Google Scholar 

  13. The LUNG SAFE Investigators and the ESICM Trials Group, Laffey JG, Bellani G, Pham T, Fan E, Madotto F, et al. Potentially modifiable factors contributing to outcome from acute respiratory distress syndrome: the LUNG SAFE study. Intensive Care Med. 2016;42(12):1865–76.

    Article  CAS  Google Scholar 

  14. Goligher EC, Costa ELV, Yarnell CJ, Brochard LJ, Stewart TE, Tomlinson G, et al. Effect of lowering tidal volume on mortality in ARDS varies with respiratory system elastance. Am J Respir Crit Care Med. 2021;203(11):1378–85.

    Article  CAS  PubMed  Google Scholar 

  15. Costa ELV, Slutsky A, Brochard LJ, Brower R, Serpa-Neto A, Cavalcanti AB, et al. Ventilatory variables and mechanical power in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med. 2021;204(3):303–11.

    Article  PubMed  Google Scholar 

  16. Gattinoni L, Tonetti T, Cressoni M, Cadringher P, Herrmann P, Moerer O, et al. Ventilator-related causes of lung injury: the mechanical power. Intensive Care Med. 2016;42(10):1567–75.

    Article  CAS  PubMed  Google Scholar 

  17. Cressoni M, Gotti M, Chiurazzi C, Massari D, Algieri I, Amini M, et al. Mechanical power and development of ventilator-induced lung injury. Anesthesiology. 2016;124(5):1100–8.

    Article  PubMed  Google Scholar 

  18. Tonetti T, Vasques F, Rapetti F, Maiolo G, Collino F, Romitti F, et al. Driving pressure and mechanical power: new targets for VILI prevention. Ann Transl Med. 2017;5(14):286.

    Article  PubMed  PubMed Central  Google Scholar 

  19. Serpa Neto A, Deliberato RO, Johnson AEW, Bos LD, Amorim P, Pereira SM, et al. Mechanical power of ventilation is associated with mortality in critically ill patients: an analysis of patients in two observational cohorts. Intensive Care Med. 2018;44(11):1914–22.

    Article  CAS  PubMed  Google Scholar 

  20. ARDS Definition Task Force, Ranieri VM, Rubenfeld GD, Thompson BT, Ferguson ND, Caldwell E, et al. Acute respiratory distress syndrome: the Berlin definition. JAMA. 2012;307(23):2526–33.

    Google Scholar 

  21. Papazian L, Forel JM, Gacouin A, Penot-Ragon C, Perrin G, Loundou A, et al. Neuromuscular blockers in early acute respiratory distress syndrome. N Engl J Med. 2010;363(12):1107–16.

    Article  CAS  PubMed  Google Scholar 

  22. Guérin C, Reignier J, Richard JC, Beuret P, Gacouin A, Boulain T, et al. Prone positioning in severe acute respiratory distress syndrome. N Engl J Med. 2013;368(23):2159–68.

    Article  PubMed  CAS  Google Scholar 

  23. Chen L, Del Sorbo L, Grieco DL, Junhasavasdikul D, Rittayamai N, Soliman I, et al. 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(2):178–87.

    Article  PubMed  Google Scholar 

  24. Radermacher P, Maggiore SM, Mercat A. Fifty years of research in ARDS. Gas exchange in acute respiratory distress syndrome. Am J Respir Crit Care Med. 2017;196(8):964–84.

    Article  CAS  PubMed  Google Scholar 

  25. Cohen J. Statistical power analysis for the behavioral sciences. 2nd ed. New York: Lawrence Erlbaum; 1988. p. 567.

    Google Scholar 

  26. Le Gall JR, Lemeshow S, Saulnier F. A new Simplified Acute Physiology Score (SAPS II) based on a European/North American multicenter study. JAMA. 1993;270(24):2957–63.

    Article  PubMed  Google Scholar 

  27. Vincent JL, Moreno R, Takala J, Willatts S, De Mendonça A, Bruining H, et al. The SOFA (Sepsis-related Organ Failure Assessment) score to describe organ dysfunction/failure. On behalf of the Working Group on Sepsis-Related Problems of the European Society of Intensive Care Medicine. Intensive Care Med. 1996;22(7):707–10.

    Article  CAS  PubMed  Google Scholar 

  28. Pereira Romano ML, Maia IS, Laranjeira LN, Damiani LP, Paisani DDM, Borges MDC, et al. Driving pressure–limited strategy for patients with acute respiratory distress syndrome. A pilot randomized clinical trial. Ann Am Thorac Soc. 2020;17(5):596–604.

    Article  PubMed  Google Scholar 

  29. Richard JC, Maggiore SM, Jonson B, Mancebo J, Lemaire F, Brochard L. Influence of tidal volume on alveolar recruitment: respective role of PEEP and a recruitment maneuver. Am J Respir Crit Care Med. 2001;163(7):1609–13.

    Article  CAS  PubMed  Google Scholar 

  30. Network ARDS. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342(18):1301–8.

    Article  Google Scholar 

  31. Vaporidi K, Akoumianaki E, Telias I, Goligher EC, Brochard L, Georgopoulos D. Respiratory drive in critically ill patients. pathophysiology and clinical implications. Am J Respir Crit Care Med. 2020;201(1):20–32.

    Article  PubMed  Google Scholar 

  32. Spinelli E, Mauri T, Beitler JR, Pesenti A, Brodie D. Respiratory drive in the acute respiratory distress syndrome: pathophysiology, monitoring, and therapeutic interventions. Intensive Care Med. 2020;46(4):606–18.

    Article  PubMed  PubMed Central  Google Scholar 

  33. Chanques G, Kress JP, Pohlman A, Patel S, Poston J, Jaber S, et al. Impact of ventilator adjustment and sedation-analgesia practices on severe asynchrony in patients ventilated in assist-control mode*. Crit Care Med. 2013;41(9):2177–87.

    Article  PubMed  Google Scholar 

  34. Thille AW, Rodriguez P, Cabello B, Lellouche F, Brochard L. Patient-ventilator asynchrony during assisted mechanical ventilation. Intensive Care Med. 2006;32(10):1515–22.

    Article  PubMed  Google Scholar 

  35. Shah FA, Girard TD, Yende S. Limiting sedation for patients with acute respiratory distress syndrome—time to wake up. Curr Opin Crit Care. 2017;23(1):45–51.

    Article  PubMed  PubMed Central  Google Scholar 

  36. Grasselli G, Tonetti T, Protti A, Langer T, Girardis M, Bellani G, et al. Pathophysiology of COVID-19-associated acute respiratory distress syndrome: a multicentre prospective observational study. Lancet Respir Med. 2020;8(12):1201–8.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  37. Chiumello D, Busana M, Coppola S, Romitti F, Formenti P, Bonifazi M, et al. Physiological and quantitative CT-scan characterization of COVID-19 and typical ARDS: a matched cohort study. Intensive Care Med déc. 2020;46(12):2187–96.

    Article  CAS  Google Scholar 

  38. Grieco DL, Bongiovanni F, Chen L, Menga LS, Cutuli SL, Pintaudi G, et al. Respiratory physiology of COVID-19-induced respiratory failure compared to ARDS of other etiologies. Crit Care. 2020;24(1):529.

    Article  PubMed  PubMed Central  Google Scholar 

  39. Grasselli G, Cattaneo E, Florio G, Ippolito M, Zanella A, Cortegiani A, et al. Mechanical ventilation parameters in critically ill COVID-19 patients: a scoping review. Crit Care déc. 2021;25(1):115.

    Article  Google Scholar 

  40. Haudebourg AF, Perier F, Tuffet S, de Prost N, Razazi K, Mekontso Dessap A, et al. Respiratory mechanics of COVID-19- versus non-COVID-19–associated acute respiratory distress syndrome. Am J Respir Crit Care Med. 2020;202(2):287–90.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  41. Villar J, Martín-Rodríguez C, Domínguez-Berrot AM, Fernández L, Ferrando C, Soler JA, et al. A quantile analysis of plateau and driving pressures: effects on mortality in patients with acute respiratory distress syndrome receiving lung-protective ventilation*. Crit Care Med mai. 2017;45(5):843–50.

    Article  Google Scholar 

Download references

Acknowledgements

Not applicable.

Funding

No financial support for this study.

Author information

Authors and Affiliations

  1. CHU Henri Mondor-Albert Chenevier, Service de Médecine Intensive Réanimation, Assistance Publique- Hôpitaux de Paris, 51, Avenue du Maréchal de Lattre de Tassigny, 94010, Créteil Cedex, France

    Anne-Fleur Haudebourg, Samuel Tuffet, François Perier, Keyvan Razazi, Nicolas de Prost, Armand Mekontso Dessap & Guillaume Carteaux

  2. Groupe de Recherche Clinique CARMAS, Faculté de Santé, Université Paris Est-Créteil, 94010, Créteil Cedex, France

    Anne-Fleur Haudebourg, Samuel Tuffet, François Perier, Keyvan Razazi, Nicolas de Prost, Armand Mekontso Dessap & Guillaume Carteaux

  3. INSERM U955, Institut Mondor de Recherche Biomédicale, 94010, Créteil Cedex, France

    Samuel Tuffet & Guillaume Carteaux

Authors
  1. Anne-Fleur Haudebourg
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Samuel Tuffet
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. François Perier
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Keyvan Razazi
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Nicolas de Prost
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. Armand Mekontso Dessap
    View author publications

    You can also search for this author in PubMed Google Scholar

  7. Guillaume Carteaux
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

AFH was involved in study design, data collection, analysis, and interpretation, and script writing. ST was involved in data collection. FP was involved in data collection. NDP was involved in data interpretation. KR was involved in data interpretation. AMD was involved in study design, data interpretation, and script writing. GC was involved in study design, data analysis and interpretation, and script writing. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Anne-Fleur Haudebourg.

Ethics declarations

Ethics approval and consent to participate

This study was set in compliance with Helsinki Declaration and was approved by the ethics committee “CPP Sud Ouest et Outre Mer III” (2018-A00867-48). According to the French law, non-opposition to participate in the study from the patient or his/her next of kin was collected prior to inclusion.

Consent for publication

Not applicable.

Competing interests

The authors declare that they have no competing interests.

Additional information

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Haudebourg, AF., Tuffet, S., Perier, F. et al. Driving pressure-guided ventilation decreases the mechanical power compared to predicted body weight-guided ventilation in the Acute Respiratory Distress Syndrome. Crit Care 26, 185 (2022). https://doi.org/10.1186/s13054-022-04054-5

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s13054-022-04054-5

Keywords

Critical Care

ISSN: 1364-8535