Correlation between mechanical power and lung ultrasound score and association with clinical outcomes in acute respiratory distress syndrome

Abstract

BACKGROUND

Mechanical power (MP) integrates tidal volume, airway pressures, flow, and respiratory rate into a single estimate of ventilatory energy delivery and serves as an integrative physiologic marker of ventilator-induced lung injury. Lung ultrasound score (LUS) is a bedside tool that quantifies lung aeration loss, reflecting the structural expression of lung injury in acute respiratory distress syndrome (ARDS). However, data correlating MP with LUS and clinically relevant outcomes in ARDS remain limited.

AIM

To explore whether MP is associated with lung ultrasound–derived aeration loss and clinical outcomes in moderate-to-severe ARDS.

METHODS

This prospective observational study enrolled adult patients with moderate-to-severe ARDS requiring invasive mechanical ventilation for more than 48 hours. MP and LUS were assessed at 0, 24, 48, and 72 hours. Their association was evaluated using Pearson correlation analysis. Associations between MP and 28-day mortality and weaning outcomes were analyzed using logistic regression and receiver operating characteristic curve analysis. Mean MP was defined as the arithmetic mean across the four time points.

RESULTS

Forty-four patients were included. MP was strongly correlated with LUS at baseline (r = 0.84, 95%CI: 0.72-0.91), 24 hours (r = 0.83, 95%CI: 0.71-0.91), 48 hours (r = 0.91, 95%CI: 0.85-0.95), and 72 hours (r = 0.93, 95%CI: 0.87-0.96) (all P < 0.001). In exploratory analyses, higher mean MP was associated with increased mortality [odds ratio (OR) = 2.11 per J/minute increase, 95%CI: 1.31-3.39] and demonstrated numerically higher area under the receiver operating characteristic curve than driving pressure (0.98, 95%CI: 0.94-1.00 vs 0.91, 95%CI: 0.82-0.98). Higher mean MP was also associated with difficult (OR = 2.20, 95%CI: 1.11-4.36) and prolonged weaning (OR = 1.61, 95%CI: 1.04-2.50).

CONCLUSION

MP parallels lung ultrasound-derived aeration loss in ARDS and demonstrates associations with mortality and adverse weaning, supporting its potential role as an integrative physiologic marker in individualized ventilatory management.

Key Words: Acute respiratory distress syndrome; Mechanical power; Lung ultrasound; Lung aeration loss; Ventilator-induced lung injury; Mechanical ventilation; Mortality; Weaning outcomes; Prognosis

Core Tip: This prospective observational study demonstrates a close association between mechanical power (MP), an integrative measure of ventilatory energy delivery, and lung aeration loss assessed by lung ultrasound score in patients with moderate-to-severe acute respiratory distress syndrome. Higher MP exposure was also associated with mortality and poor weaning outcomes. By linking ventilatory energy burden with bedside structural assessment of lung injury, this study highlights the potential value of combining MP and lung ultrasound to support physiologically informed and individualized ventilatory care.

INTRODUCTION

Acute respiratory distress syndrome (ARDS) remains a major cause of acute hypoxemic respiratory failure requiring invasive mechanical ventilation and continues to be associated with substantial morbidity and mortality despite advances in supportive care. While mechanical ventilation is essential to maintain gas exchange, ventilation applied to an injured, heterogeneously aerated lung may paradoxically exacerbate damage through ventilator-induced lung injury (VILI), driven by excessive mechanical stress, strain, and repetitive alveolar opening and collapse[1,2].

To mitigate VILI, lung-protective ventilation strategies emphasizing lower tidal volumes, limitation of airway pressures (including plateau pressure), appropriate positive end-expiratory pressure (PEEP), and attention to driving pressure are widely recommended. However, individual ventilatory variables considered in isolation may not fully represent the cumulative mechanical burden delivered to the injured lung, particularly as respiratory rate, flow, and pressure interact dynamically over time.

In this context, mechanical power (MP) has emerged as an integrative physiologic construct that quantifies the total energy transferred from the ventilator to the respiratory system per unit time by incorporating tidal volume, airway pressures, respiratory rate, and inspiratory flow[3-6]. Observational data suggest that higher MP is associated with increased risk of VILI and adverse outcomes, even when conventional lung-protective thresholds for individual variables are maintained[3-6].

Lung ultrasound has become an established bedside tool for assessing pulmonary aeration in critically ill patients. In ARDS, the lung ultrasound score (LUS) provides a semi-quantitative measure of regional aeration loss, reflecting both disease severity and dynamic changes in aeration over time[7-9]. As aeration heterogeneity amplifies regional stress and strain, LUS offers a physiologically relevant complement to ventilatory metrics that quantify applied mechanical energy.

Although the physiologic association between MP and lung aeration loss is conceptually distinct from its potential prognostic utility, evidence directly linking MP to lung ultrasound–derived aeration loss in ARDS remains limited. To the best of our knowledge, only a single-center observational study from China has evaluated the correlation between MP and LUS at serial time points, demonstrating a positive association and suggesting potential prognostic value for 28-day mortality[10]. However, the reported correlation strengths were modest, weaning-related outcomes were not evaluated, and MP was not compared with established ventilatory indices such as driving pressure. Consequently, the temporal evolution, strength, and clinical relevance of the MP-LUS relationship during early ARDS remain insufficiently characterized. Furthermore, whether increased ventilatory energy burden translates into clinically meaningful outcomes, including difficult and prolonged weaning, warrants systematic investigation.

Accordingly, we conducted a prospective observational study to evaluate the physiologic association between MP and LUS at predefined time points in patients with moderate-to-severe ARDS receiving invasive mechanical ventilation. Secondary exploratory objectives were to examine the relationship between MP and clinically relevant outcomes, including 28-day mortality and weaning patterns, and to compare its prognostic performance with driving pressure. We hypothesized that higher MP would be associated with greater lung aeration loss and adverse short-term clinical outcomes.

MATERIALS AND METHODS

Study design and setting

This prospective observational study was conducted between January 2023 and June 2024 in the intensive care unit of the Acute Care and Emergency Medicine Unit, Department of Internal Medicine, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India. PGIMER is a large tertiary-care academic referral center serving patients from multiple states in North India.

Sample size

Sample size estimation was based on detecting a Pearson correlation between MP and LUS. Assuming an expected correlation of 0.414 from prior published data, with two-sided α = 0.05 and 80% power, the minimum required sample size was 44, using Fisher’s z (arctanh) transformation[10,11].

Study population

Adult patients with moderate-to-severe ARDS requiring invasive mechanical ventilation were consecutively screened for eligibility. Patients aged ≥ 18 years who fulfilled the Berlin definition of moderate-to-severe ARDS (ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen (PaO₂/FiO₂) < 200 mmHg with a minimum PEEP of 5 cm H₂O) and remained on invasive mechanical ventilation for > 48 hours were eligible for inclusion[12].

Patients were excluded if they had conditions likely to confound respiratory mechanics or lung ultrasound interpretation, including older age (> 70 years), pregnancy, chest trauma, thoracic deformities, pneumothorax, massive pleural effusion, or known chronic alveolar lung disease. Additional exclusion criteria included severe hemodynamic instability, advanced heart failure, brain death, end-of-life care status, or refusal of consent.

Ventilatory management

All patients received standard-of-care management for ARDS in accordance with institutional protocols and accepted international guidelines[13]. Volume-controlled ventilation was the predominant ventilatory mode; other ventilatory modes were used at the discretion of the treating intensivist. Ventilator mode, tidal volume, airway pressures, respiratory rate, PEEP, and FiO₂ were adjusted according to clinical judgment. Adjunctive therapies, including prone positioning, neuromuscular blockade, and recruitment maneuvers, were permitted at the discretion of the treating team and were not used as exclusion criteria. Ventilatory strategies and adjunctive interventions were not protocolized and were not adjusted for in the primary analyses.

Measurements

MP was derived from routinely recorded ventilatory parameters and calculated offline using the simplified equation proposed by Gattinoni et al for controlled mechanical ventilation with constant inspiratory flow[3,4]: MP (J/minute) = 0.098 × respiratory rate (minute^-1) × tidal volume (L) × [peak inspiratory pressure (cm H₂O) - ½ × driving pressure].

Driving pressure was calculated as plateau pressure minus PEEP. Plateau pressure was measured using an end-inspiratory pause of at least 0.5 seconds during passive mechanical ventilation, with the absence of spontaneous respiratory effort confirmed by ventilator waveforms and lack of patient triggering at the time of assessment. All measurements were recorded only at time points fulfilling these controlled conditions.

Lung ultrasound examinations were performed by trained clinicians using a convex probe and a standardized scanning protocol. Each hemithorax was divided into six regions (anterior, lateral, and posterior zones, each subdivided into superior and inferior areas), yielding a total of 12 lung regions per patient. Aeration loss in each region was graded on a four-point scale (0-3) according to established criteria: Normal aeration (0), moderate loss with B-lines (1), severe loss with coalescent B-lines (2), and consolidation (3)[7,8]. The total LUS was calculated as the sum of regional scores, ranging from 0 to 36, with higher values indicating greater aeration loss. Serial ultrasound examinations for a given patient were preferably performed by the same operator whenever feasible. Operators were not blinded to ventilator settings or clinical status, reflecting real-world practice in critically ill patients.

MP and LUS were assessed concurrently at predefined time points following initiation of invasive mechanical ventilation: Baseline, 24 hours, 48 hours, and 72 hours. Relevant clinical and laboratory data were collected at the same time points.

Outcomes

The primary objective was to evaluate the association between MP and lung ultrasound–derived aeration loss at predefined time points (baseline, 24, 48, and 72 hours) following initiation of invasive mechanical ventilation.

Secondary objectives included exploratory analyses to examine the association of MP with short-term clinical outcomes, including 28-day mortality, duration of invasive mechanical ventilation, and weaning outcomes. Weaning outcomes were categorized as simple, difficult, or prolonged according to the international consensus weaning classification[14]. Patients who underwent tracheostomy were analyzed using the same weaning outcome definitions. Patients who died before liberation from mechanical ventilation were excluded from weaning outcome analyses. Comparative exploratory analyses were also performed to evaluate the prognostic performance of mean MP relative to mean driving pressure for 28-day mortality.

Statistical analysis

Statistical analyses were performed using SPSS version 25 (IBM Corp., Armonk, NY, United States). Continuous variables are presented as mean ± SD or median [interquartile range (IQR)], as appropriate. Categorical variables are expressed as n (%).

Associations between MP and LUS at predefined time points were assessed at each predefined time point (0, 24, 48, and 72 hours) using Pearson correlation analysis, with correlation coefficients (r) and corresponding 95%CIs reported. Correlation analyses were unadjusted and were not corrected for physiologic severity indices or longitudinal modeling, consistent with the exploratory study design. Mixed-effects or repeated-measures models were not used because the limited sample size and repeated observations per patient would risk model instability and overfitting.

All outcome analyses were exploratory and restricted to univariable models. For prognostic analyses, mean MP and mean driving pressure were calculated as the average of values measured at 0, 24, 48, and 72 hours, representing cumulative early ventilatory exposure. Associations with 28-day mortality were examined using univariable logistic regression and receiver operating characteristic curve analysis, with discrimination quantified by the area under the receiver operating characteristic curve (AUROC) and 95%CIs. A formal statistical comparison of AUROC values was not performed, and differences are reported descriptively. Associations between mean MP or mean driving pressure and duration of invasive mechanical ventilation were assessed using Spearman rank correlation (ρ).

Weaning outcomes were categorized as simple, difficult, or prolonged. Associations between mean MP and weaning outcomes were evaluated using separate univariable binary logistic regression models, with simple weaning as the reference category. All statistical tests were two-tailed, and a P value < 0.05 was considered statistically significant.

RESULTS

Study participants

A total of 103 patients with moderate-to-severe ARDS were screened. Of these, 59 were excluded for predefined reasons, and 44 patients were included in the final analysis (Figure 1). The mean age was 37.07 ± 11.47, and 27 (61.4%) were male. Moderate and severe ARDS were equally distributed (n = 22, each), with a mean PaO₂/FiO₂ ratio of 113.36 ± 28.52 (range 65-161) at admission. Baseline illness severity was moderate, with a Sequential Organ Failure Assessment score of 8.32 ± 3.02 and an Acute Physiology and Chronic Health Evaluation II score of 13.86 ± 4.73. The most common ARDS etiologies were community-acquired pneumonia (n = 24), sepsis-related ARDS (n = 15), and Pneumocystis jirovecii pneumonia (n = 5). Prone positioning was used during ARDS management in 20 patients (45.5%).

Figure 1 Flow diagram showing patient screening, exclusions, and inclusion in the final analysis. ARDS: Acute respiratory distress syndrome.

Ventilatory parameters, MP, and LUS

Ventilatory parameters, MP, and LUS over the first 72 hours of invasive mechanical ventilation are summarized in Table 1. Tidal volume and airway pressures remained broadly stable over time, while oxygen requirements showed a gradual decline. MP demonstrated a progressive increase across time points, accompanied by a corresponding rise in LUS. The overall mean MP was 20.41 ± 6.61 J/minute, and the mean driving pressure was 15.55 ± 5.41 cm H₂O. No patient died during the first 72 hours of observation, and ventilatory parameters, MP and LUS data were available for all patients at each predefined time point.

Table 1 Ventilatory parameters, mechanical power, and lung ultrasound score over time, mean ± SD.

Parameter (unit)	0 hours	24 hours	48 hours	72 hours
FiO2 (%)	85.23 ± 16.56	78.18 ± 20.29	76.93 ± 21.89	73.63 ± 26.46
Tidal volume (mL)	355.34 ± 37.10	354.00 ± 31.80	350.68 ± 28.89	354.43 ± 34.05
Respiratory rate (per minute)	25.34 ± 4.30	26.05 ± 3.69	26.43 ± 4.66	26.91 ± 6.54
Minute ventilation (L/minute)	9.11 ± 1.94	9.22 ± 1.39	9.37 ± 1.53	9.99 ± 4.30
PEEP (cm H2O)	10.27 ± 2.30	11.08 ± 2.56	11.38 ± 3.44	11.89 ± 4.50
Peak inspiratory pressure (cm H2O)	30.09 ± 6.00	29.64 ± 6.90	30.05 ± 8.64	29.43 ± 10.86
Plateau pressure (cm H2O)	26.77 ± 6.19	26.34 ± 6.72	26.68 ± 8.16	26.39 ± 10.49
Respiratory system compliance (mL/cm H2O)	23.93 ± 8.08	26.53 ± 9.47	26.45 ± 10.41	28.93 ± 13.97
Driving pressure (cm H2O)	16.63 ± 5.83	15.15 ± 5.06	15.28 ± 5.72	15.13 ± 6.67
Mechanical power (J/minute)	19.20 ± 4.84	19.99 ± 6.07	20.70 ± 7.92	21.76 ± 10.95
Lung ultrasound score	18.18 ± 4.40	19.18 ± 5.91	20.00 ± 7.91	20.43 ± 9.57

All values represent measurements from the entire study cohort (n = 44) at each time point. Values are presented descriptively to demonstrate temporal trends; no formal statistical comparisons across time points were performed, consistent with the exploratory study design. FiO₂: Fraction of inspired oxygen; PEEP: Positive end-expiratory pressure.

Correlation between MP and LUS

MP demonstrated a strong positive correlation with LUS at all predefined time points (Figure 2). At baseline (0 hours), MP was strongly correlated with LUS (r = 0.84; 95%CI: 0.72-0.91; P < 0.001). This association persisted at 24 hours (r = 0.83; 95%CI: 0.71-0.91; P < 0.001) and further strengthened at 48 hours (r = 0.91; 95%CI: 0.85-0.95; P < 0.001) and 72 hours (r = 0.93; 95%CI: 0.87-0.96; P < 0.001). Visual inspection of scatter plots did not reveal disproportionate influence of extreme outliers.

Figure 2 Scatter plots showing the association between mechanical power and lung ultrasound score at predefined time points. A: Baseline; B: 24 hours; C: 48 hours; D: 72 hours. Pearson correlation coefficients (r) and two-tailed P values are shown. All correlations were based on the complete cohort (n = 44) at each time point.

MP and clinical outcomes

At 28 days, 23 of 44 patients (52.3%) had died. In exploratory analyses, both mean MP and mean driving pressure were significantly associated with 28-day mortality. On univariable logistic regression, each 1 J/minute increase in mean MP was associated with higher odds of 28-day death [odds ratio (OR) 2.11, 95%CI: 1.31-3.39; P = 0.002]. Similarly, each 1 cm H₂O increase in mean driving pressure was associated with increased mortality risk (OR = 1.66, 95%CI: 1.23-2.24; P < 0.001). In exploratory analyses, mean MP showed numerically higher discrimination for 28-day mortality than mean driving pressure, with AUROCs of 0.98 (95%CI: 0.94-1.00) vs 0.91 (95%CI: 0.82-0.98), respectively (Figure 3).

Figure 3 Receiver operating characteristic curves showing the discriminative performance mean mechanical power and mean driving pressure for prediction of 28-day mortality (n = 44). MP: Mechanical power; DP: Driving pressure; AUROC: Area under the receiver operating characteristic curve.

The median duration of invasive mechanical ventilation was 5 days (IQR: 4-9). Mean MP demonstrated a weak inverse correlation with duration of invasive mechanical ventilation (Spearman’s ρ = -0.31, P = 0.042). Mean driving pressure showed a similar but non-significant trend (ρ = -0.27, P = 0.080).

Weaning outcomes were classified as simple (n = 13, 29.5%), difficult (n = 21, 47.7%), or prolonged (n = 10, 22.7%). Higher mean MP was associated with less favorable weaning outcomes. Compared with patients who achieved simple weaning, increasing mean MP was associated with higher odds of difficult weaning (OR = 2.20; 95%CI: 1.11-4.36; P = 0.024) and prolonged weaning (OR = 1.61; 95%CI: 1.04-2.50; P = 0.033).

DISCUSSION

In this prospective observational study of patients with moderate-to-severe ARDS, we demonstrate a strong and consistent association between MP and lung ultrasound–derived aeration loss during the first 72 hours of invasive mechanical ventilation. MP showed a strong positive correlation with LUS at all predefined time points, with correlation coefficients progressively increasing from baseline to 72 hours. In addition, higher mean MP was strongly associated with adverse clinical outcomes, including 28-day mortality and unfavorable weaning patterns, and demonstrated numerically higher discriminatory performance compared with driving pressure.

Because MP represents the cumulative energy load delivered to the injured lung, its strong association with lung ultrasound–derived aeration loss reflects parallel changes in ventilatory demand and structural lung injury in ARDS. Higher LUS values, reflecting alveolar collapse, interstitial edema, and consolidation, indicate increased lung inhomogeneity conditions known to amplify regional stress and strain during mechanical ventilation[3,15]. In heterogeneously aerated lungs, ventilatory energy quantified by MP is unevenly distributed, resulting in regional amplification of stress and strain at interfaces between aerated and nonaerated lung units, a central mechanism underlying VILI that is structurally captured by LUS.

As lung aeration deteriorates, maintaining adequate gas exchange typically requires higher pressures, respiratory rates, or both, thereby increasing MP[3,15]. The progressive strengthening of the MP-LUS correlation from baseline to 72 hours likely reflects a dynamic interaction between evolving lung injury and escalating ventilatory requirements, whereby progressive loss of aeration over time necessitated higher airway pressures and/or respiratory rates in patients with non-resolving or worsening ARDS[16]. Overall, because both MP and LUS reflect underlying disease severity, the magnitude of correlation should be interpreted cautiously, as part of the observed association may arise from shared dependence on ARDS severity rather than a direct mechanistic linkage alone.

A prior study demonstrated a positive correlation between MP and LUS at serial time points in patients with ARDS and suggested prognostic relevance for both parameters[10]. However, the correlations reported were modest and increased gradually over time, whereas the associations observed in our cohort were substantially stronger, particularly at later time points. Differences in study design such as timing of measurements, MP calculation methods, ventilatory mode restrictions, and outcome definitions, in addition to patient characteristics, may account for this discrepancy. Importantly, our findings are consistent with a broader body of literature linking higher MP to VILI and adverse outcomes, as well as studies demonstrating that lung ultrasound–derived aeration loss reflects lung inhomogeneity and structural injury in ARDS[4,15-17]. Collectively, these data reinforce the physiologic coherence between cumulative ventilatory energy delivery and bedside lung ultrasound–derived aeration loss in ARDS.

Beyond its association with lung aeration loss, persistently elevated MP during the first 72 hours was associated with increased mortality and unfavorable weaning patterns. These findings are broadly consistent with prior observational studies reporting higher mortality and fewer ventilator-free days among patients exposed to elevated MP[4,15,18,19]. However, given the relatively small sample size and limited number of outcome events, the observed AUROC estimates for mortality are susceptible to overfitting and should be interpreted as hypothesis-generating rather than confirmatory. In our cohort, MP also demonstrated relatively higher prognostic discrimination than driving pressure. This likely reflects the integrative nature of MP, which incorporates respiratory rate and inspiratory flow in addition to pressure and volume, rather than superiority over established lung-protective parameters.

The association between higher MP and unfavorable weaning outcomes may indicate delayed lung recovery related to sustained ventilatory energy burden; however, this interpretation cannot be separated from underlying disease severity. Notably, higher MP was inversely correlated with the duration of invasive mechanical ventilation in our cohort, an apparent discordance that likely reflects the competing risk of early mortality. Difficult or prolonged weaning was assessed only among patients who survived to undergo liberation attempts, whereas ventilation duration reflects the entire cohort and is therefore influenced by early death. Overall, these associations should be interpreted as reflecting the interaction between disease severity and ventilatory strategy, rather than implying a direct causal effect of MP alone[15].

This study has several clinical implications. Our results highlight MP as a pragmatic, integrative bedside marker that contextualizes ventilatory settings in relation to the evolving condition of the lung. When interpreted alongside lung ultrasound–derived aeration loss, MP provides complementary information on the mechanical and structural dimensions of lung injury. While MP quantifies the energetic burden of ventilation, LUS provides real-time assessment of aeration loss and lung inhomogeneity[16,17]. Integrating both parameters may assist clinicians in interpreting whether rising ventilatory energy reflects potentially modifiable mechanical contributors or progression of structural lung injury. Concordant increases in MP and LUS may indicate persistent lung inhomogeneity with heightened vulnerability to VILI, whereas elevated MP in the presence of stable or improving LUS may suggest excess ventilatory demand driven predominantly by adjustable components such as respiratory rate or inspiratory flow rather than worsening parenchymal injury. Conversely, high LUS values despite relatively low MP may reflect severe intrinsic lung pathology rather than injurious ventilatory load. Accordingly, serial assessment of MP and LUS together may provide a physiologically coherent framework to interpret ventilatory burden in relation to lung recruitability and disease evolution, supporting individualized decision-making. Importantly, the lack of a consistently validated safe MP threshold across patient cohorts underscores the need for individualized ventilatory strategies rather than reliance on fixed cutoffs[19-21]. Overall, MP and lung ultrasound should be viewed as complementary tools that augment, rather than replace, established lung-protective ventilation principles[15,22].

Limitations

This study has several limitations. First, it was a single-center study with a relatively small sample size, which may limit generalizability and precluded multivariable adjustment for potential confounders, including baseline comorbidities, illness severity, and treatment-related factors. Second, the observational design does not permit causal inference, and the associations observed between MP, LUS, and clinical outcomes may reflect underlying disease severity and clinician-driven ventilatory decisions rather than a direct causal relationship with VILI.

Third, although serial assessments were obtained at predefined time points, longitudinal correlations may have been influenced by persistence of lung injury over time, as patients with non-resolving or worsening ARDS required continued ventilatory support. This enrichment of more severe physiology at later time points may have contributed to stronger MP-LUS associations, independent of a direct mechanistic relationship.

Fourth, ventilatory management was not protocolized and was guided by treating clinicians, reflecting real-world practice but introducing variability in ventilatory settings and adjunctive therapies such as prone positioning. These factors may have acted as unmeasured confounders influencing both ventilatory energy delivery and clinical outcomes.

Fifth, MP is a composite measure derived from multiple ventilatory parameters, and collinearity between MP and its individual components (including respiratory rate, airway pressures, and tidal volume) cannot be ruled out. In addition, MP reflects respiratory system mechanics rather than lung mechanics alone; direct assessment of chest wall mechanics, transpulmonary pressure, or obesity-related effects was not performed, which may influence interpretation in selected patients.

Sixth, although lung ultrasound was performed using a validated scoring system, interobserver and intraobserver variability were not formally assessed. In addition, variability in ultrasound protocols and ventilatory practices across centers may affect reproducibility. The absence of external validation further limits generalizability of these findings to other patient populations and care settings.

Finally, this study was not designed to establish threshold values for “safe” MP, and the findings should not be interpreted as defining specific MP cutoffs for clinical practice.

Future directions

Future studies should validate these findings in larger, multicenter cohorts across diverse ARDS etiologies and physiologic phenotypes, while also assessing whether alternative MP formulations-such as normalization to compliance, predicted body weight, or aerated lung volume-improve risk stratification and comparability across studies. The absence of a consistently validated safe MP threshold across different clinical settings reinforces the need for prospective validation and standardized reporting[19]. Finally, integrating MP with more granular physiologic assessment (e.g., transpulmonary pressure–guided approaches using esophageal manometry) may further clarify mechanisms and distinguish ventilatory energy delivery from true lung stress, enabling more individualized ventilation targets[23]. Future research may also explore integration of MP and LUS with additional biomarkers, advanced imaging modalities, and machine-learning models based on serial physiologic trajectories to enhance risk stratification and support individualized ventilatory care.

CONCLUSION

In patients with moderate-to-severe ARDS receiving invasive mechanical ventilation, MP correlates with lung aeration loss and is associated with mortality and adverse weaning outcomes. These findings suggest that ventilator energy burden and structural lung injury may evolve in parallel during the early course of ARDS and may have prognostic relevance. However, prospective interventional studies are required before MP-guided strategies can be recommended for individualized ventilatory management.

ACKNOWLEDGEMENTS

The authors thank Mrs. Sunaina Verma for statistical assistance.