Research ArticleOriginal Research

Adaptive Support Ventilation and Lung-Protective Ventilation in ARDS

Elias N Baedorf Kassis, Andres Brenes Bastos, Maximillian S Schaefer, Krystal Capers, Benjamin Hoenig, Valerie Banner-Goodspeed and Daniel Talmor
Respiratory Care December 2022, 67 (12) 1542-1550; DOI: https://doi.org/10.4187/respcare.10159

Abstract

BACKGROUND: Adaptive support ventilation (ASV) is a partially closed-loop ventilation mode that adjusts tidal volume (VT) and breathing frequency (f) to minimize mechanical work and driving pressure. ASV is routinely used but has not been widely studied in ARDS.

METHODS: The study was a crossover study with randomization to intervention comparing a pressure-regulated, volume-targeted ventilation mode (adaptive pressure ventilation [APV], standard of care at Beth Israel Deaconess Medical Center) set to VT 6 mL/kg in comparison with ASV mode where VT adjustment is automated. Subjects received standard of care (APV) or ASV and then crossed over to the alternate mode, maintaining consistent minute ventilation with 1–2 h in each mode. The primary outcome was VT corrected for ideal body weight (IBW) before and after crossover. Secondary outcomes included driving pressure, mechanics, gas exchange, mechanical power, and other parameters measured after crossover and longitudinally.

RESULTS: Twenty subjects with ARDS were consented, with 17 randomized and completing the study (median PaO2/FIO2 146.6 [128.3–204.8] mm Hg) and were mostly passive without spontaneous breathing. ASV mode produced marginally larger VT corrected for IBW (6.3 [5.9–7.0] mL/kg IBW vs 6.04 [6.0–6.1] mL/kg IBW, P = .035). Frequency was lower with patients in ASV mode (25 [22–26] breaths/min vs 27 [22–30)] breaths/min, P = .01). In ASV, lower respiratory-system compliance correlated with smaller delivered VT/IBW (R2 = 0.4936, P = .002). Plateau (24.7 [22.6–27.6] cm H2O vs 25.3 [23.5–26.8] cm H2O, P = .14) and driving pressures (12.8 [9.0–15.8] cm H2O vs 11.7 [10.7–15.1] cm H2O, P = .29) were comparable between conventional ventilation and ASV. No adverse events were noted in either ASV or conventional group related to mode of ventilation.

CONCLUSIONS: ASV targeted similar settings as standard of care consistent with lung-protective ventilation strategies in mostly passive subjects with ARDS. ASV delivered VT based upon respiratory mechanics, with lower VT and mechanical power in subjects with stiffer lungs.

Introduction

Adaptive support ventilation (ASV) is a partially closed-loop mode of mechanical ventilation that continuously performs breath-by-breath evaluation of respiratory mechanics and patient effort to target a set minute ventilation by adjusting the breathing frequency (f) and tidal volume (VT).1,2 ASV determines the f-VT combination aiming to minimize mechanical work of breathing and the applied force with each breath (using a proprietary interpretation and application of Otis and Mead equations) and the total peak pressures that can be directly limited by the clinician.3 The ASV algorithm provides individual adjustment to the patient’s specific pathophysiology secondary to variability in compliance, resistance, and expiratory time constant (RCexp) between different disease states, resulting in patients with high compliance and resistance receiving lower f and larger VT, whereas patients with low compliance receive lower VT and higher f.4

Treatment of ARDS is defined by lung-protective ventilation,5 minimizing VT and plateau pressures,6 with a goal to reduce ventilation-induced lung injury7 and improve mortality.8 Additionally, retrospective analysis suggests that lower driving pressure (ΔP)9,10 and mechanical power11-13 are associated with improved outcomes. Whereas ASV has been extensively investigated during weaning and has demonstrated potential improved speed of extubation and shorter ICU length of stay,2 many of the potential benefits remain speculative including pilot data suggesting that ASV reduces applied mechanical power.14 Despite lack of existing evidence, the underlying mechanism in ASV employing mechanical work, ΔP, and peak pressure limitation, which lowers VT and limits applied pressures in response to low-compliance states, provides motivation to consider this mode during lung-protective ventilation in patients with ARDS. Preliminary data suggest that ASV may be safely applied in ARDS.15 However, this requires further investigation and larger studies.

In this pilot investigation of subjects with ARDS, we aimed to compare the automated ASV settings with standard-of-care lung-protective ventilation strategy at Beth Israel Deaconess Medical Center (BIDMC) in Boston, Massachusetts, comparing VT and other ventilator and mechanics parameters in a randomized open-label crossover study.

QUICK LOOK

Current Knowledge

Adaptive support ventilation (ASV) is an automated partially closed-loop ventilation mode that adjusts breathing frequency and tidal volume (VT) to maintain a set minute ventilation. Lung-protective ventilation settings are required in ARDS to prevent ventilator-induced lung injury, with limitation of VT representing the highest-quality evidence for reduction of mortality.

What This Paper Contributes to Our Knowledge

This crossover study randomizing to order of ventilation mode compared standard-of-care lung-protective ventilation with VT manually set to 6 mL/kg ideal body weight with ASV where VT adjustment was automated. ASV targeted similar although marginally larger VT compared with standard-of-care mode as well as similar driving pressures, plateau pressures, mechanics, and gas exchange. Notably, ASV targeted lower VT than standard-of-care mode in subjects with low respiratory-system compliance as well as lower mechanical power. ASV settings were similar overall to the standard of care, as were individual adjustments based on subject physiology. Larger studies are needed to determine if this individual titration has clinical benefits.

Methods

Study Design and Population

This was a crossover study with randomization to order of intervention that was conducted between February 2018–November 2020 in ICUs of BIDMC, Boston, Massachusetts. The study was approved by the local institutional review board and registered in ClinicalTrials.gov under identifier NCT03715751. The study protocol is available in the supplementary material (Appendix 1 and 2, see related supplementary materials at http://www.rcjournal.com).

Subjects were eligible when undergoing mechanical ventilation, who were 18 y or older, and if they met the Berlin criteria for ARDS.5 Although passive breathing was not a specific inclusion criteria, none of the subjects were triggering spontaneous breaths at the time of enrollment, with one demonstrating spontaneous breathing during data collection on day 1. Clinical team refusal, esophageal injury, or contraindication precluding placement of the esophageal balloon were the main exclusion criteria. Informed consent for enrollment was obtained from the legally authorized representative for each subject.

Study Interventions and Protocol

An esophageal balloon was inserted, if not already being used for clinical care, and positioning confirmed using depth, cardiac oscillations, and manual thoracic compressions to assure optimal placement.16,17 Esophageal pressures (Pes) were used to estimate transpulmonary pressures (PL = airway opening pressure [Pao] − Pes), whereas flow and volume were recorded simultaneously.

Baseline measurements were obtained prior to randomization. Before initial randomization to a study group, all subjects were clinically optimized per standard-of-care lung-protective ventilation settings. This included adjustment of PEEP using the esophageal balloon data, targeting an end-expiratory PL 0 cm H2O as per standard practice at BIDMC. Further adjustments were allowed if clinically indicated by the treating team; however, PEEP was required to be kept the same before and after crossover. As per standard of care at BIDMC, the VT was changed to 6 mL/kg ideal body weight (IBW) if not already set. If the VT was changed to target a different VT, f was changed to target consistent minute ventilation. Lastly, FIO2 was adjusted to achieve SpO2 95% to reduce need for further adjustment during the pre- and post-crossover data collection.

After baseline optimization, subjects were randomized with a nonsequential 1:1 utilizing a computer-generated randomization list to order of intervention, receiving either ASV mode or standard of care followed by crossover to the alternate mode. The randomization was performed by study team within a REDCap database. Standard-of-care ventilation mode at BIDMC was a pressure-regulated, volume-targeted mode called adaptive pressure ventilation (APV), a mode similar to pressure-regulated volume control modes. The randomization list was created by an independent statistician. Research and clinical teams were unblinded to the result of randomization. Of note, sedation and analgesic medications were maintained at the same levels before and after crossover. After randomization, a strict protocol was followed (with the schema in Fig. 1) (further detail in Appendix 1 and 2, see related supplementary materials at http://www.rcjournal.com).

Fig. 1.
Fig. 1.

Study schema. ASV = adaptive support ventilation.

After randomization to order of intervention, stable minute ventilation was maintained before and after crossover while in APV or ASV. Subjects were studied for 1–2 h in the initial mode and then switched to the alternate regimen for an additional 1–2 h. When in ASV, the VT and f were determined by the automated mode. When returned to or continued on standard of care (APV), the VT was set to 6 mL/kg and f adjusted to maintain consistent minute ventilation to prior. Mechanics, VT, and blood gases were recorded at the end of each study period, which lasted up to 2 h. Blood gas measurements were provided to the clinical team for safety, with plans to restart data collection and crossover if the clinical team needed to make any changes to assure consistency before and after crossover.

After completion of day 1 measurements, the clinical team dictated all further care but subjects could be left on ASV if desired. Subjects on APV were titrated to support ventilation as deemed ready by treating team. For subjects on ASV after crossover, the treating team was encouraged to continue on ASV when weaning to support mode and to allow the algorithm to automatically make this transition. Subjects were followed with serial Pao, PL, Pes, flow, volume, and mechanics.

Outcomes

The primary end point was VT (corrected for IBW) compared between standard-of-care lung-protective ventilation (APV set to 6 mL/kg) and ASV mode before and after crossover on day 1. At the termination of each 1–2 h recording before and after crossover, expiratory VT was recorded in each mode as the average obtained from 10 sequential breaths.

The secondary end points comparing day 1 before and after crossover data included driving pressure, end-inspiratory and end-expiratory pressures of respiratory system, chest wall and transpulmonary systems, f, oxygenation, PaCO2, pH, PaO2, PaO2/FIO2, and PaCO2 after 1–2 h in each mode before and after crossover. Additionally, inspiratory work of breathing was calculated from continuous recordings for each single breath from the area under the inspiratory limb of the airway pressure/volume curves. Averaged inspiratory work of breathing was then multiplied with f to calculate mechanical power in joules per minute as previously described18 (Appendix 3, see related supplementary materials at http://www.rcjournal.com). Subjects were monitored after day 1 with collection of mechanics and VT, but these were not included as part of the primary analysis due to the small numbers and lack of crossover.

Adverse events were assessed by monitoring for events related to study procedures or ventilation mode, which included death, any life-threatening events believed to be related to study procedures, persistent disability greater than expected, esophageal injury, hemodynamic compromise, barotrauma, and any other complication related to the placement of the esophageal balloon (see Appendix 1 for full list of adverse events reporting, see related supplementary materials at http://www.rcjournal.com). Lastly, time to extubation, ICU length of stay, and in-hospital mortality as ascertained by medical record review were compared between subjects continuing on ASV and subjects receiving standard of care (APV) after the initial crossover period.

Statistical Analysis

The target sample size was determined utilizing previous data indicating mean VT 6.2 mL/kg IBW (SD 0.9)17 in standard volume control modes as well as preliminary data using ASV that reported mean VT 6.4 mL/kg (SD 1.1). With an estimated correlation 0.30 between measurements pre- and post-crossover, alpha 0.05, and 80% power, and allowing for a margin up to 1 mL/kg in ASV to be considered equivalent, we calculated a need to recruit a total of 16 subjects with complete day 1 measurements. Assuming loss of roughly 4 subjects, we planned to enroll 20 for this pilot study. Sample size estimation was performed using SAS software (SAS Institute, Cary, North Carolina) by an independent statistician.

Baseline demographics as well as pre- and post-crossover measurements were displayed as median with interquartile range (IQR). Normality was assessed using Wilks-Shapiro test. Paired variables before and after crossover were compared with paired t test and Wilcoxon signed-rank test as indicated. Linear regression was used for comparison of continuous variables. Data from one subject were removed from linear regression comparing VT with compliance and RCexp as VT limitation occurred secondary to total pressure limits and was not secondary to usual ASV algorithm utilizing RCexp. Hierarchical mixed models were used for comparison of variables on subsequent study days (after day 1) with subject ID and day of measurement clustered with random effects. Estimated marginal means with 95% CI were used to display difference between study arms after day 1. Analysis was performed using Stata 14.2 (StataCorp, College Station, Texas).

Results

Study Population

A total of 20 subjects were consented; 17 were enrolled and underwent randomization and completed the study protocol with crossover comparison (Fig. 2). The 3 subjects who were consented but did not initiate the study and were not randomized were excluded because they were weaned off lung-protective ventilation to pressure support before study procedures were able to be initiated, and it was not clinically appropriate to re-sedate them for inclusion. Overall, subjects presented with moderate-severe ARDS (median PaO2/FIO2 146.6 [IQR 128.3–204.8]) and showed high morbidity with baseline Acute Physiology and Chronic Health Evaluation (APACHE) II 27 (21–32) and Sequential Organ Failure Assessment 12 (11–13). Baseline mechanics, driving pressure, and cause of ARDS are shown in Table 1.

Fig. 2.
Fig. 2.

Consort diagram with screened, eligible, and enrolled subjects.

View this table:
Table 1.

Characteristics of Study Subjects (N = 17)

Primary Outcome

VT adjusted for IBW was higher in subjects receiving ASV (6.29 [5.87–6.99] mL/kg IBW vs 6.04 [6.01–6.06] mL/kg IBW, P = .035), with no statistical difference in uncorrected VT (440.5 [393.4–497.4] mL vs 417.7 [392.7–440.8] mL, P = .058) (Table 2 and Fig. 3). During the period on ASV, there was a wider variability in VT than in subjects receiving standard-of-care ventilation (APV) (Fig. 3A–B). Variability in VT was primarily explained by range in compliance and RCexp between subjects (except in one subject where VT was limited by ASV peak pressure limits). In the remaining subjects, RCexp and compliance demonstrated correlation with VT (R2 = 0.52, P = .002; and R2 = 0.34, P = .02, respectively) and with VT/IBW (R2 = 0.33, P = .02; and R2 = 0.49, P = .002, respectively) (Fig. 4), demonstrating that VT was smaller in subjects with low compliance and larger in subjects with higher compliance.

View this table:
Table 2.

Comparison Between Ventilator Modes Before and After Crossover on Day 1

Fig. 3.
Fig. 3.

Distribution box plots comparing the crossover between standard of care at Beth Israel Deaconess Medical Center, a pressure-regulated volume-targeted mode called adaptive pressure ventilation (APV), and adaptive support ventilation (ASV) mode. A: Tidal volume (VT) (mL) comparison. P = .058. B: VT/ideal body weight (IBW) (mL/kg). P = .035. C: Plateau pressure (cm H2O). P = .14. D: Driving pressure (cm H2O). P = .29. N = 17 subjects with crossover measurements. Statistical comparison performed via paired t test (A, C, and D) and Wilcoxon paired signed-rank test (B) due to nonparametric distribution. Star indicates statistical significance.

Fig. 4.
Fig. 4.

Adaptive support ventilation (ASV) adjusts tidal volume (VT) and breathing frequency (f) on a breath-to-breath basis based upon expiratory time constant (RCexp), which is product of resistance and compliance. Figures include n = 16 subjects, with one patient not included due to VT being set by ASV pressure limits. A and B: VT and VT/IBW have strong linear correlation to respiratory-system compliance. C and D: Similarly, VT and VT/IBW also have strong linear correlation with RCexp. Correlations were performed using linear regression.

Secondary Outcomes

Respiratory-system driving pressure (12.8 [9.0–15.8] cm H2O APV vs 11.7 [10.7–15.1] cm H2O ASV, P = .29) and plateau pressures (24.7 [22.6–27.6] APV vs 25.3 [23.5–26.8] ASV, P = .14) were similar (Table 2, Fig. 3C–D). Frequency was marginally lower in ASV (27 [22–30] breaths/min APV vs 25 [22–26] breaths/min ASV, P = .01). Lung and respiratory system mechanics including transpulmonary driving pressure, lung and respiratory-system compliance, plateau pressure, elastance, and RCexp were similar, as was gas exchange with PaCO2, PaO2, and PaO2/FIO2 before and after crossover (Table 2). Calculated mechanical power was also similar before and after crossover (Table 2). However, in subjects with lower compliance, ASV decreased the applied mechanical power (Fig. 5A) particularly in the subset of subjects where VT was reduced while in ASV (Fig. 5B).

Fig. 5.
Fig. 5.

Inspiratory work of breathing was calculated from continuous recordings for each single breath from area under inspiratory limb of airway pressure/volume curves. Averaged inspiratory work of breathing was then multiplied with breathing frequency to calculate mechanical power in joules per minute. A: Comparison of respiratory-system compliance with change in mechanical power from adaptive pressure ventilation (APV) (pressure-regulated, volume-targeted standard of care used at Beth Israel Deaconess Medical Center) to adaptive support ventilation (ASV) demonstrates linear correlation (R2 = 0.2337, P = .049). This correlation shows that in subjects with stiffer lungs ASV lowers delivered mechanical power. B: Bar graph comparing subjects with increased VT (n = 12) and subjects with decreased VT (n = 5) when transitioned to ASV mode, showing a significant decrease in applied mechanical power in this subgroup of subjects.

There were no study-related adverse events noted in any subjects. One subject was taken off ASV at discretion of clinical team when switched into prone position to target ultralow VT; however, this was not considered an adverse event, and the switch was performed after crossover measurements were obtained without impacting the primary and most of the secondary end points. Hemodynamics appeared to be similar in ASV and APV.

Three subjects completed the study with only day 1 measurements obtained (one due to prone positioning as above, one due to early extubation, and one due to being made comfort measures only with subsequent terminal extubation) and were included in the analysis of the primary end point. Eight of the remaining subjects who had been randomized were kept on ASV and were automatically transitioned within ASV mode from fully ventilator-controlled breathing to supported breaths at median 6 d (IQR 3–8). Subjects were followed for median 4 d (IQR 2–7), and there was no difference in VT between ASV and control arms of study over the course of subsequent follow-up (Appendix 4, Supplemental Table, see related supplementary materials at http://www.rcjournal.com).

Discussion

In our cohort of mechanically ventilated subjects with ARDS, ASV provided a minor but statistically significant increase in VT/IBW when compared to standard of care at BIDMC (APV). This difference was small in terms of absolute difference (∼0.25 mL/kg), and the authors consider this difference to not be clinically relevant. Importantly, VT during ASV ventilation were all within what is generally considered lung-protective ventilation range, <8 mL/kg.6 Indeed, in a subset of subjects with lower compliance and short RCexp, ASV targeted lower VT, demonstrating individual titration inherent to the ASV mode, tailoring lower VT in subjects with stiffer lungs. Of note, in subjects who received a higher VT in ASV, compliance was also higher with resulting driving pressures that remained at similar levels with control.10,19 Other markers for ventilation parameters including respiratory-system and transpulmonary driving pressures, plateau pressures, and mechanics in each mode were similar, while achieving similar effectiveness in gas exchange, further reiterating similar ventilation that ASV provides in addition to the individualized parameters unique to subject’s physiology and ventilation needs.

This individualization is of particular interest considering recent focus moving beyond VT alone to identify improved markers of lung stress. ASV uses an underlying proprietary algorithm that determines best combination of VT and f to limit degree of driving pressure applied to the lungs as well as to limit the applied mechanical work. Driving pressure initially gained interest in a large retrospective study demonstrating a strong link between driving pressure and mortality.19 A recent paper furthered this concept in a retrospective data set including subjects randomized to high versus low VT strategies, which suggested that limitation of VT to target lower driving pressures only provides benefit in subjects with stiffer lungs.20 Strict limitation of VT in all subjects may not provide benefits we hope to achieve and may indeed result in increased sedation requirements to allow tolerance of these settings. A dynamic approach that tolerates larger VT in some patients with higher compliance, with highly protective VT in other patients with stiffer lungs, may be the future of personalized ventilation management. Extrapolation of our findings from this pilot study, the growing understanding of driving pressure as a clinical target, and the underlying algorithm of ASV, together illustrate the potential for individualized partially closed-loop modes such as ASV.

The concept of mechanical power has recently gained attention as a possible cause of lung injury as it incorporates not only the energy required to inflate the lung during a single breath but also the effect of total applied energy to the respiratory system over time.12,21,22 Power is calculated by integration of pressure over volume change during a breath, multiplied by f, and can be directly calculated via waveforms or through a simple formula. Mechanical power is independently associated with higher in-hospital mortality, hospital length of stay, and fewer ventilator-free days even in subjects receiving low VT,12 and limitation of applied power has been postulated to decrease the risk for developing lung injury. The application of the Otis formula in ASV has serendipitously gained interest due to the formula solving for f that minimizes the work of breathing in spontaneously breathing patients. Whereas this is clearly a different work of breathing measurement than energy applied from the ventilator (the newer concept), this has raised interest in examining ASV for its ability to provide limitations in applied mechanical power.14 In our study, although mechanical power was overall similar between modes, lower compliance correlated with decrease in mechanical power while in ASV. This decrease in power seemed to be primarily driven by decrease in VT. Targeted limitation of mechanical power and ventilation strategies that facilitate this warrant further large-scale investigation.

Notably, the secondary outcomes including driving pressure, end-inspiratory and expiratory respiratory system, chest wall and PL, VT, f, oxygenation, and CO2 clearance were similar before and after crossover, making the argument again that ASV seems to be generally equivalent to the standard of care within this population of ARDS during passive mechanical ventilation.

Whereas safety was not specifically tested for in this study, there were no adverse events during use of ASV. Additionally, the similar overall settings compared with standard of care (APV) were suggestive that ASV could be applied as a reasonable alternative in subjects with ARDS with parameters within clinically acceptable goal ranges. Of note, the mode was less commonly applied in the very sickest subjects (with only 2 subjects with PaO2/FIO2 < 100 mm Hg), although this was not intentional by study team. Additionally, study did not look at use during prone positioning, although there is no reason to suspect that the mode would not perform as expected. Nonetheless, eliminating clinician control of specific VT was felt by some providers as a barrier for its use. The authors believe this is more an issue of education and experience with the mode rather than a weakness specific to the mode itself.

There are several important limitations to this study that bear mentioning. The total number of subjects who were enrolled was small; however, the crossover allowed for improved ability to directly compare modes and address the primary end point. Although there were no adverse events with the mode, as mentioned the duration of each crossover period and enrolled numbers preclude any true comparison of safety. Additionally, use in sickest subjects with very low PaO2/FIO2 and prone positioning was not validated in this study, although there is no reason to suspect that the mode would perform differently under these circumstances. This was a single-center study, potentially limiting its generalizability; however, ASV was not commonly used at start of study, suggesting ease of implementation over time. There was minimal spontaneous activity during day 1 measurements before and after crossover, so parameters during spontaneous breathing were not tested for in primary and secondary end points. This study was not powered to detect differences in VT beyond the initial study day, nor was it powered to detect differences in other parameters including outcomes as this was not the purpose of this pilot study. Extrapolations based upon mechanical power and driving pressure remain speculative but important to discuss.

Conclusions

ASV is a partially closed-loop mechanical ventilation mode that applies patient-specific tailored ventilation that continuously evolves with the patient’s mechanics. In this cohort of subjects with ARDS, ASV was found to provide marginally larger VT but otherwise similar ventilation parameters to what is considered standard of care at BIDMC. These preliminary pilot data suggest that this mode could be used in many patients with ARDS interchangeably with the current standard of care. Automated modes of ventilation may represent an important future direction of mechanical ventilation; demonstrating application of these modes in ARDS is important. ASV appeared to provide similar overall care to standard lung-protective ventilation in passive subjects, while also providing individually titrated care. These pilot data provide rationale for larger studies focusing on automated modes in subjects with ARDS.

Footnotes

  • Correspondence: Elias N Baedorf Kassis MD. E-mail: enbaedor{at}bidmc.harvard.edu

  • Drs Baedorf Kassis and Talmor disclose a relationship with Hamilton Medical. The remaining authors have disclosed no conflicts of interest.

  • This work was performed via internal departmental funding at Beth Israel Deaconess Medical Center, Boston, Massachusetts.

  • Supplementary material related to this paper is available at http://www.rcjournal.com.

REFERENCES

  1. 1.↵
    1. Fernández J,
    2. Miguelena D,
    3. Mulett H,
    4. Godoy J,
    5. Martinón-Torres F
    . Adaptive support ventilation: state-of-the-art review. Indian J Crit Care Med 2013;17(1):16-22.
    OpenUrl
  2. 2.↵
    1. Rose L,
    2. Schultz MJ,
    3. Cardwell CR,
    4. Jouvet P,
    5. McAuley DF,
    6. Blackwood B,
    7. et al
    . Automated versus non-automated weaning for reducing the duration of mechanical ventilation for critically ill adults and children: a Cochrane systematic review and meta-analysis. Crit Care 2015;19(1):1-12.
    OpenUrlCrossRefPubMed
  3. 3.↵
    1. Becher T,
    2. Adelmeier A,
    3. Frerichs I,
    4. Weiler N,
    5. Schädler D
    . Adaptive mechanical ventilation with automated minimization of mechanical power-a pilot randomized crossover study. Crit Care 2019;23(1).
  4. 4.↵
    1. Bialais E,
    2. Wittebole X,
    3. Vignaux L,
    4. et al
    . Closed-loop ventilation mode (IntelliVent-ASV) in intensive care unit: a randomized trial. Minerva Anestesiol 2016;82(6).
  5. 5.↵
    The ARDS Definition Task Force. Acute respiratory distress syndrome: the Berlin definition. JAMA 2012;307(23).
  6. 6.↵
    Acute Respiratory Distress Syndrome Network. 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).
  7. 7.↵
    1. Beitler JR,
    2. Malhotra A,
    3. Thompson BT
    . Ventilator-induced lung Injury. Clin Chest Med 2016;37(4).
  8. 8.↵
    Acute Respiratory Distress Syndrome Network. 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).
  9. 9.↵
    1. Bellani G,
    2. Laffey JG,
    3. Pham T,
    4. Fan E,
    5. Brochard L,
    6. Esteban A,
    7. et al
    ; for the LUNG SAFE Investigators and the ESICM Trials Group. 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.
    OpenUrlCrossRefPubMed
  10. 10.↵
    1. Baedorf Kassis E,
    2. Loring SH,
    3. Talmor D
    . Mortality and pulmonary mechanics in relation to respiratory system and transpulmonary driving pressures in ARDS. Intensive Care Med 2016;42(8):1206-1213.
    OpenUrl
  11. 11.↵
    1. Parhar KKS,
    2. Zjadewicz K,
    3. Soo A,
    4. et al
    . Epidemiology, mechanical power, and 3-year outcomes in acute respiratory distress syndrome patients using standardized screening: an observational cohort study. Ann Am Thorac Soc 2019;16(10).
  12. 12.↵
    1. Serpa A Neto,
    2. Deliberato RO,
    3. Johnson AEW,
    4. Bos LD,
    5. Amorim P,
    6. Pereira SM,
    7. et al
    ; PROVE Network Investigators. 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):1914-1922.
    OpenUrlPubMed
  13. 13.↵
    1. Zhang Z,
    2. Zheng B,
    3. Liu N,
    4. Ge H,
    5. Hong Y
    . Mechanical power normalized to predicted body weight as a predictor of mortality in patients with acute respiratory distress syndrome. Intensive Care Med 2019;45(6):856-864.
    OpenUrl
  14. 14.↵
    1. Buiteman-Kruizinga LA,
    2. Mkadmi HE,
    3. Schultz MJ,
    4. Tangkau PL,
    5. van der Heiden PLJ
    . Comparison of mechanical power during adaptive support ventilation versus non-automated pressure controlled ventilation-a pilot study. Crit Care Explor 2021;3(2):e0335.
    OpenUrl
  15. 15.↵
    1. Dai Y-L,
    2. Wu C-P,
    3. Yang G-G,
    4. et al
    . Adaptive support ventilation attenuates ventilator-induced lung injury: human and animal study. Int J Mol Sci 2019;20.
  16. 16.↵
    1. Beitler JR,
    2. Sarge T,
    3. Banner-Goodspeed V,
    4. et al
    . Lung mechanics to guide positive end-expiratory pressure in acute respiratory distress syndrome: the EPVent-2 randomized clinical trial. 2019.
  17. 17.↵
    1. Talmor D,
    2. Sarge T,
    3. Malhotra A,
    4. O’Donnell CR,
    5. Ritz R,
    6. Lisbon A,
    7. et al
    . Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med 2008;359(20):2095-2104.
    OpenUrlCrossRefPubMed
  18. 18.↵
    1. Schaefer M,
    2. Loring SH,
    3. Talmor D,
    4. et al
    . Comparison of mechanical power estimations in mechanically ventilated patients with the acute respiratory distress syndrome: a secondary data analysis from the EPVent study. Intensive Care Med 2020;47(1).
  19. 19.↵
    1. Amato MBP,
    2. Meade MO,
    3. Slutsky AS,
    4. Brochard L,
    5. Costa ELV,
    6. Schoenfeld DA,
    7. et al
    . Driving pressure and survival in the acute respiratory distress syndrome. N Engl J Med 2015;372(8):747-755.
    OpenUrlCrossRefPubMed
  20. 20.↵
    1. Goligher EC,
    2. Costa ELV,
    3. Yarnell CJ,
    4. Brochard LJ,
    5. Stewart TE,
    6. Tomlinson G,
    7. 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):1378-1385.
    OpenUrl
  21. 21.↵
    1. Gattinoni L,
    2. Tonetti T,
    3. Cressoni M,
    4. Cadringher P,
    5. Herrmann P,
    6. Moerer O,
    7. et al
    . Ventilator-related causes of lung injury: the mechanical power. Intensive Care Med 2016;42(10):1567-1575.
    OpenUrlCrossRefPubMed
  22. 22.↵
    1. Schaefer MS,
    2. Loring SH,
    3. Talmor D,
    4. Baedorf Kassis EN
    . Comparison of mechanical power estimations in mechanically ventilated patients with ARDS: a secondary data analysis from the EPVent study. Intensive Care Med 2021;47(1):130-132.
    OpenUrl
Back to top

In this issue

 

Print
Download PDF
Article Alerts
Email Article
Citation Tools

Jump to section

Related Articles

Cited By...

Keywords