Dissociation between airway and transpulmonary pressures during external chest wall restriction: a prospective self-controlled physiological study

Abstract

Background

External chest wall restriction can alter how airway pressure is transmitted to the lung. This may make airway pressure an unreliable surrogate for lung stress during mechanical ventilation. We aimed to determine whether short-term chest strapping dissociates airway pressure from transpulmonary pressure by increasing chest wall elastance in mechanically ventilated postoperative intensive care unit (ICU) patients.

Methods

This was a single-center, prospective, self-controlled physiological study. Postoperative ICU patients receiving invasive mechanical ventilation were screened for eligibility. Ventilator settings were kept constant. A chest strap was tightened for 30 minutes as a model of acute external chest wall restriction. Airway and esophageal pressures were recorded before and during strapping, and transpulmonary pressure (P_L) was derived. This post hoc re-analysis was restricted to patients without chronic obstructive pulmonary disease (COPD) or an acute pulmonary diagnosis at ICU admission (n=21).

Results

During strapping, gas exchange and hemodynamics remained stable, whereas peak and plateau airway pressures, along with airway driving pressure (ΔP), increased. End-inspiratory and end-expiratory esophageal pressures rose, while the corresponding P_L decreased. Transpulmonary driving pressure (ΔP_L) decreased numerically but did not reach statistical significance. Respiratory system compliance (C_rs) decreased, driven mainly by reduced chest wall compliance (C_cw). The elastance ratio (E_lung/E_rs) declined. Mechanical power increased, with a significant increase in the elastic component but no significant change in the resistive part.

Conclusions

In sedated, volume-controlled postoperative ICU patients undergoing short-term external chest wall restriction, chest strapping increased airway pressures mainly through chest wall loading. Higher airway pressures did not correspond to higher P_L, and ΔP_L did not increase significantly. Esophageal pressure monitoring may help interpret airway pressures when C_cw is externally restricted.

Highlight box.

Key findings

• Chest strapping increased airway pressures and respiratory system elastance, with a large increase in chest wall elastance.

• Transpulmonary pressures (P_Ls) decreased despite higher airway pressures; transpulmonary driving pressure did not increase significantly in patients without chronic obstructive pulmonary disease (COPD) or an acute pulmonary diagnosis at intensive care unit (ICU) admission.

• Mechanical power increased, with a significant increase in the elastic component but no significant change in the resistive component.

What is known and what is new?

• Chest wall restriction has been reported to affect airway pressures and compliance in acute respiratory distress syndrome, but results vary across studies.

• In a restricted cohort without COPD or an acute pulmonary diagnosis at ICU admission, we show that chest strapping primarily loads the chest wall and can lower P_L even when airway pressures rise.

What is the implication, and what should change now?

• When external chest wall restriction is present (straps, binders, positioning), airway pressures may overestimate lung stress.

• Esophageal pressure monitoring can separate chest wall and lung mechanics and may prevent over-interpretation of airway pressure alone.

Introduction

Limiting lung stress is a core aim of lung-protective ventilation, particularly in acute respiratory distress syndrome (ARDS) (1-3). Airway plateau pressure (P_plat) and airway driving pressure (ΔP) are used to assess ventilator load, but they reflect the combined mechanics of the lung and chest wall rather than lung stress alone (4).

Transpulmonary pressure (P_L) describes the distending pressure applied to the lung. Esophageal pressure is commonly used as a bedside surrogate for pleural pressure and allows partitioning of lung and chest wall mechanics during ventilation (4,5). In ARDS, P_L-based assessment has been used to interpret lung stress and to guide positive end-expiratory pressure (PEEP) in selected patients (6,7), and transpulmonary mechanics have been associated with outcomes in observational analyses (8).

Chest wall mechanics can change with positioning and external thoracoabdominal compression (9-12). For example, chest strapping is routinely used after surgery to support the chest wall. External restriction has also been reported as a physiologic maneuver in ARDS, but prior findings are mixed. Classic physiology suggests that rib cage or abdominal restriction increases airway pressures and reduces respiratory system compliance (C_rs) by stiffening the chest wall (13,14). In contrast, continuous anterior chest compression and abdominal compression have been reported to improve compliance in selected ARDS patients (15,16), suggesting phenotype-dependent effects (17).

Chest strapping provides a pragmatic model of acute external chest wall restriction. It does not reproduce the chronic and complex respiratory mechanics of morbid obesity. However, it resembles clinical situations in which external devices or postoperative support restrict chest wall motion, such as chest support straps, binders, and other forms of thoracoabdominal restriction. In these settings, clinicians may observe higher airway pressures but still need to know whether the lung is exposed to higher distending pressure.

We hypothesized that chest strapping would primarily increase chest wall elastance and increase the transmission of airway pressure to pleural pressure, as reflected by esophageal pressure. We therefore expected airway pressures and respiratory system elastance to increase, the elastance ratio (E_lung/E_rs) to decrease, and airway pressure to dissociate from P_L. We conducted a prospective self-controlled study with esophageal pressure monitoring to test this hypothesis. We present this article in accordance with the TREND reporting checklist (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2026-1010/rc).

Methods

Ethics

This trial was conducted at the Department of Critical Care Medicine, Zhongshan Hospital, Fudan University, Shanghai, China. Written informed consent was obtained from all patients or their surrogates. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments, and was approved by the institutional research committee of Zhongshan Hospital, Fudan University (No. B2018-322). The study was registered at ClinicalTrials.gov (NCT03947476; principal investigator: Minjie Ju; date of registration: May 8, 2019).

Study design and population

This was a single-center, prospective, self-controlled physiologic study in postoperative intensive care unit (ICU) patients receiving invasive mechanical ventilation. During the study period, patients were screened from the postoperative mechanically ventilated ICU population. Eligible patients were adults (age ≥18 years) with body mass index (BMI) 18–40 kg/m² who were hemodynamically stable under deep sedation and analgesia to suppress spontaneous breathing, and were expected to require invasive mechanical ventilation for at least 12 hours. Exclusion criteria included BMI <18 or >40 kg/m², pregnancy, pneumothorax, severe hypoxemia defined as partial pressure of oxygen in arterial blood/fractional inspiratory oxygen concentration (PaO₂/FiO₂) <100 mmHg at screening, intra-abdominal hypertension, end-stage disease, and contraindications to esophageal catheter placement (e.g., inability to place a nasogastric tube) or recent thoracic trauma or surgery.

The study focused on short-term changes in respiratory mechanics during a standardized chest strapping intervention. During the study period, 36 patients had complete paired measurements before and during chest strapping and were included in the initial descriptive analyses. Alignment between trial registration and the analyses reported here is summarized in Table S1.

Ventilation protocol

All enrolled patients were ventilated in a volume-assist control mode with constant square flow and a tidal volume of 7 mL/kg predicted body weight (PBW) using the Mindray ventilator (Mindray SV800, Shenzhen, China). PEEP was adjusted between 5–10 cmH₂O and the respiratory rate was adjusted to ensure a normal partial pressure of carbon dioxide. The above settings remained unchanged during the intervention. After the intervention, the attending physician could adjust the parameters in response to other conditions during ICU stay.

In this study, the Richmond Agitation-Sedation Scale (RASS) was used to assess the depth of sedation. Continuous infusion of remifentanil with midazolam or propofol was used to achieve a RASS score of −3 to −2.

Chest strapping

The tightening procedure was performed by trained staff following a consistent routine. When hemodynamic and respiratory parameters were stable after ICU admission, chest circumference was measured around the rib cage and the closest-fitting thoracic band was selected (available sizes 75–120 cm in 5 cm increments). The band was then tightened to maximal feasible tightness and maintained for 30 minutes while ventilator settings were kept unchanged (Figure S1). The 30-minute duration was chosen to allow cardiorespiratory variables to stabilize and to minimize confounding from concurrent clinical interventions.

Esophageal and PL measurements

An esophageal manometer tube (Mindray SDY-1, Guangzhou, China) was placed and positioned according to established guidance (18). An end-inspiratory occlusion of 2 s allowed the measurement of P_plat and inspiratory P_es (P_{es insp}), while an end-expiratory occlusion hold of 5 s allowed the measurement of total PEEP and expiratory P_es (P_{es exp}). The following measurements and calculations were performed before chest strapping and after 30 minutes of chest strapping, respectively.

• ❖ Driving pressure (ΔP) = P_plat − total PEEP

• ❖ End-inspiratory transpulmonary pressure (P_{L insp}) = P_plat − P_{es insp}

• ❖ End-expiratory transpulmonary pressure (P_{L exp}) = total PEEP − P_{es exp}

• ❖ Esophageal pressure swing (ΔP_es) = P_{es insp} − P_{es exp}

• ❖ Change in ΔP_es = ΔP_{es after} − ΔP_{es before}

• ❖ Transpulmonary driving pressure (ΔP_L) = P_{L insp} − P_{L exp} = ΔP − (P_{es insp} − P_{es exp})

• ❖ Respiratory system elastance (E_rs) = ΔP/V_t = 1/C_rs

• ❖ Chest wall elastance (E_cw) = (P_{es insp} − P_{es exp})/V_t = 1/C_cw

• ❖ Lung elastance (E_lung) = (P_{L insp} − P_{L exp})/V_t = 1/C_lung

• ❖ Mechanical power (MP) = 0.098 × RR × V_t × [P_peak − (P_plat − PEEP)/2]

• ❖ Elastic mechanical power (MP_e) = 0.098 × RR × V_t × (PEEP + ΔP/2)

• ❖ Resistive mechanical power (MP_r) = 0.098 × RR × V_t × (P_peak − P_plat)

In these formulas, RR is respiratory rate, Vt is tidal volume in liters, and PEEP refers to measured total PEEP.

Analytic cohort

No formal sample-size calculation was performed because this was a physiologic self-controlled study. All 36 patients with complete paired measurements underwent the same standardized chest strapping protocol. The present post hoc re-analysis was restricted to 21 patients without chronic obstructive pulmonary disease (COPD) or an acute pulmonary diagnosis at ICU admission to reduce clinical heterogeneity. The remaining 15 patients with COPD and/or an acute pulmonary diagnosis were included only in exploratory subgroup and effect-modification analyses reported in Tables S2-S4 and Figures S2,S3. Severe hypoxemia (PaO₂/FiO₂ <100 mmHg) was an exclusion criterion at enrollment; none of these 15 patients met this threshold at ICU admission.

Data collection

Demographics, ventilator settings, gas exchange, hemodynamics, and respiratory mechanics were recorded immediately before chest strapping and after 30 minutes of the intervention. The primary outcome was paired changes in respiratory mechanics before vs. during chest strapping. Paired comparisons were performed within each patient.

Statistical analysis

Continuous variables are summarized as median [interquartile range (IQR)]. Paired comparisons (after vs. before) were performed using two-sided Wilcoxon signed-rank tests. For key outcomes, effect magnitude was described using paired median changes with 95% confidence intervals (CIs) and rank-biserial correlations (Table S5). No post hoc power analysis was performed. Exploratory subgroup comparisons used Mann-Whitney U tests, and correlations used Spearman coefficients. A two-sided P<0.05 was considered statistically significant. All analyses were performed using R version 4.2.2 (R Foundation for Statistical Computing, Vienna, Austria).

Results

Study population

From May 2019 to April 2022, 64 postoperative patients receiving mechanical ventilation were screened. Ten patients were not enrolled because of refusal of informed consent (n=6) or enrollment in another study (n=4). Of the remaining 54 eligible patients, 18 were excluded, including 10 due to spontaneous breathing during the intervention. Thirty-six patients had complete paired measurements before and during chest strapping. The post hoc re-analysis cohort included 21 patients without COPD or an acute pulmonary diagnosis at ICU admission (Figure 1). Baseline characteristics and ventilator settings are shown in Table 1. The paired median changes with 95% CIs and rank-biserial correlations are summarized in Table S5.

Figure 1.

Participant flow diagram. Postoperative mechanically ventilated ICU patients screened between May 2019 and April 2022. Thirty-six patients had complete paired measurements before and during chest strapping. The post hoc re-analysis cohort included 21 patients without COPD and without an acute pulmonary diagnosis at ICU admission. Fifteen patients with an acute pulmonary diagnosis at ICU admission and/or COPD were excluded from the re-analysis. COPD, chronic obstructive pulmonary disease; ICU, intensive care unit.

Table 1. Baseline characteristics and ventilator settings.

Characteristic	N=21
Age, years	74 [65, 80]
Male sex	12 (57.1)
Height, cm	165 [160, 168]
Weight, kg	60 [55, 67]
BMI, kg/m2	22.0 [18.6, 25.7]
APACHE II	16 [12, 19]
Primary diagnosis category
Abdominal surgery	11 (52.4)
Neurosurgical surgery	7 (33.3)
Cardiac surgery	3 (14.3)
FiO2	0.40 [0.40, 0.40]
Respiratory rate, breaths/min	12 [12, 12]
Tidal volume, mL	480 [460, 480]
PEEP, cmH2O	7 [5, 8]
Tidal volume/PBW, mL/kg	7.9 [7.5, 8.8]

Data are presented as number (%), or median [interquartile range]. APACHE II, acute physiology and chronic health evaluation II score; BMI, body mass index; FiO₂, fractional inspiratory oxygen concentration; PBW, predicted body weight; PEEP, positive end-expiratory pressure.

Among the 21 patients in the re-analysis cohort, 12 (57.1%) were male. Median age was 74 [65, 80] years and median BMI was 22.0 [18.6, 25.7] kg/m². Upon ICU admission, the median acute physiology and chronic health evaluation II (APACHE II) score was 16 [12, 19]. Primary diagnosis categories were abdominal surgery/gastrointestinal (n=11, 52.4%), neurosurgical/neurologic (n=7, 33.3%), and cardiac (n=3, 14.3%) (Table 1).

Mechanical ventilation

All patients were ventilated in a volume-assist control mode. Remifentanil was administered intravenously in all patients. Ventilator settings were kept unchanged during the 30-min intervention {FiO₂ 0.40 [0.40, 0.40], tidal volume 480 [460, 480] mL, PEEP 7 [5, 8] cmH₂O, respiratory rate 12 [12, 12] breaths/min}.

Effects of chest strapping

Effects on ventilation and hemodynamics

Gas exchange and hemodynamics showed no significant change during the intervention (Table 2). After chest strapping, patients had similar arterial pH 7.40 [7.38, 7.43] vs. 7.41 [7.38, 7.43] (P=0.20), PaO₂/FiO₂ 380 [315, 425] vs. 380 [340, 428] mmHg (P=0.44), PaCO₂ 38 [36, 41] vs. 38 [37, 41] mmHg (P=0.66), mean arterial pressure 70 [69, 73] vs. 71 [69, 73] mmHg (P=0.82), and heart rate 89 [79, 93] vs. 88 [79, 92] bpm (P=0.23).

Table 2. Changes in respiratory mechanics before and after chest strapping (paired analysis).

Characteristic	Before (n=21)	After (n=21)	P value
Gas exchange and hemodynamics
pH	7.40 [7.38, 7.43]	7.41 [7.38, 7.43]	0.20
PaO2, mmHg	152 [126, 170]	152 [136, 171]	0.44
PaCO2, mmHg	38 [36, 41]	38 [37, 41]	0.66
PaO2/FiO2, mmHg	380 [315, 425]	380 [340, 428]	0.44
Mean arterial pressure, mmHg	70 [69, 73]	71 [69, 73]	0.82
Heart rate, bpm	89 [79, 93]	88 [79, 92]	0.23
Airway pressures
Ppeak, cmH2O	24.0 [19.0, 29.0]	28.0 [21.0, 31.0]	<0.001
Pplat, cmH2O	18.0 [14.0, 20.0]	18.0 [17.0, 22.0]	0.003
ΔP, cmH2O	10.0 [8.0, 13.0]	12.0 [10.0, 14.0]	0.003
Esophageal and transpulmonary pressures
End-Pes insp, cmH2O	15.0 [10.0, 18.0]	17.0 [16.0, 23.0]	<0.001
End-Pes exp, cmH2O	11.0 [8.5, 14.0]	14.0 [11.0, 18.0]	<0.001
ΔPes, cmH2O	3.0 [2.0, 3.6]	5.0 [3.0, 6.1]	0.002
End-PL insp, cmH2O	3.0 [2.0, 4.0]	0.0 [−1.0, 1.0]	<0.001
End-PL exp, cmH2O	−4.4 [−7.0, −3.0]	−6.0 [−10.0, −4.0]	<0.001
ΔPL, cmH2O	7.1 [6.0, 9.0]	6.0 [6.0, 8.0]	0.19
Compliance and elastance
Crs, mL/cmH2O	46 [40, 56]	37 [34, 50]	0.002
Ccw, mL/cmH2O	160 [128, 240]	92 [76, 153]	0.005
Clung, mL/cmH2O	64 [53, 75]	71 [54, 80]	0.08
Ers, cmH2O/L	21.7 [18.0, 25.0]	27.1 [20.0, 29.2]	0.005
Ecw, cmH2O/L	6.2 [4.2, 7.8]	10.9 [6.5, 13.2]	0.002
Elung, cmH2O/L	15.6 [13.4, 18.8]	14.0 [12.5, 18.4]	0.21
Elung/Ers	0.70 [0.67, 0.80]	0.58 [0.46, 0.69]	0.002
MP
MP, J/min	10.01 [8.47, 12.14]	11.29 [8.93, 12.98]	<0.001
Elastic MP, J/min	7.20 [5.68, 7.90]	7.34 [6.21, 8.38]	0.002
Resistive MP, J/min	3.39 [2.16, 4.33]	3.95 [3.39, 5.08]	0.21

Data are median [interquartile range]. P values are from two-sided Wilcoxon signed-rank tests. C_cw, chest wall compliance; C_lung, lung compliance; C_rs, respiratory system compliance; E_cw, chest wall elastance; E_lung, lung elastance; E_lung/E_rs, elastance ratio; E_rs, respiratory system elastance; FiO₂, fractional inspiratory oxygen concentration; MP, mechanical power; PaCO₂, partial pressure of arterial carbon dioxide; PaO₂, partial pressure of oxygen in arterial blood; P_es, esophageal pressure; P_{es exp}, end-expiratory esophageal pressure; P_{es insp}, end-inspiratory esophageal pressure; P_{L exp}, end-expiratory transpulmonary pressure; P_{L insp}, end-inspiratory transpulmonary pressure; P_peak, peak airway pressure; P_plat, plateau pressure; ΔP, driving pressure; ΔP_L, transpulmonary driving pressure.

Effects on respiratory mechanics

Airway pressures increased after chest strapping. P_peak increased from 24.0 [19.0, 29.0] to 28.0 [21.0, 31.0] cmH₂O (paired median change, 2.0 cmH₂O; 95% CI: 1.0 to 3.0; P<0.001), P_plat from 18.0 [14.0, 20.0] to 18.0 [17.0, 22.0] cmH₂O (paired median change, 1.0 cmH₂O; 95% CI: 1.0 to 2.0; P=0.003), and ΔP from 10.0 [8.0, 13.0] to 12.0 [10.0, 14.0] cmH₂O (paired median change, 1.0 cmH₂O; 95% CI: 1.0 to 2.0; P=0.003). Mechanical power increased from 10.01 [8.47, 12.14] to 11.29 [8.93, 12.98] J/min (paired median change, 0.56 J/min; 95% CI: 0.28 to 0.85; P<0.001). The elastic component increased from 7.20 [5.68, 7.90] to 7.34 [6.21, 8.38] J/min (paired median change, 0.31 J/min; 95% CI: 0.28 to 0.56; P=0.002), while the resistive component showed no significant change {3.39 [2.16, 4.33] to 3.95 [3.39, 5.08] J/min; paired median change, 0.00 J/min; 95% CI: 0.00 to 0.56; P=0.21}.

Esophageal pressures increased after chest strapping. End-P_{es insp} rose from 15.0 [10.0, 18.0] to 17.0 [16.0, 23.0] cmH₂O (paired median change, 4.0 cmH₂O; 95% CI: 3.0 to 5.0; P<0.001), end-P_{es exp} from 11.0 [8.5, 14.0] to 14.0 [11.0, 18.0] cmH₂O (paired median change, 2.6 cmH₂O; 95% CI: 2.0 to 3.0; P<0.001), and ΔP_es from 3.0 [2.0, 3.6] to 5.0 [3.0, 6.1] cmH₂O (paired median change, 2.1 cmH₂O; 95% CI: 1.0 to 3.0; P=0.002). In contrast, P_L shifted downward. End-P_{L insp} decreased from 3.0 [2.0, 4.0] to 0.0 [−1.0, 1.0] cmH₂O (paired median change, −2.0 cmH₂O; 95% CI: −3.2 to −2.0; P<0.001), and end-P_{L exp} became more negative {−4.4 [−7.0, −3.0] to −6.0 [−10.0, −4.0] cmH₂O; paired median change, −2.6 cmH₂O; 95% CI: −3.0 to −2.0; P<0.001}. ΔP_L showed a downward trend but did not reach statistical significance {7.1 [6.0, 9.0] to 6.0 [6.0, 8.0] cmH₂O; paired median change, −0.5 cmH₂O; 95% CI: −1.0 to 0.0; P=0.19}. Supplementary analyses showed heterogeneity by pulmonary status (Table S3 and Figure S2) and an exploratory interaction between baseline ΔP_L and paired change in ΔP_L (Table S4 and Figure S3). BMI showed no strong association with change in ΔP_L or change in elastance ratio (Table S6 and Figure S4).

Effects on respiratory compliance and elasticity

C_rs decreased from 46 [40, 56] to 37 [34, 50] mL/cmH₂O (paired median change, −6 mL/cmH₂O; 95% CI: −8 to −4; P=0.002), driven by a marked reduction in C_cw {160 [128, 240] to 92 [76, 153] mL/cmH₂O; paired median change, −73 mL/cmH₂O; 95% CI: −91 to −36; P=0.005}. Lung compliance (C_lung) increased numerically {64 [53, 75] to 71 [54, 80] mL/cmH₂O} but was not statistically significant (paired median change, 5 mL/cmH₂O; 95% CI: 0 to 15; P=0.08). E_rs increased from 21.7 [18.0, 25.0] to 27.1 [20.0, 29.2] cmH₂O/L (paired median change, 2.1 cmH₂O/L; 95% CI: 2.1 to 4.2; P=0.005), and E_cw increased from 6.2 [4.2, 7.8] to 10.9 [6.5, 13.2] cmH₂O/L (paired median change, 4.2 cmH₂O/L; 95% CI: 2.1 to 6.2; P=0.002). E_lung showed no significant change {15.6 [13.4, 18.8] to 14.0 [12.5, 18.4] cmH₂O/L; paired median change, −1.0 cmH₂O/L; 95% CI: −2.2 to 0.0; P=0.21}. The E_lung/E_rs decreased from 0.70 [0.67, 0.80] to 0.58 [0.46, 0.69] (paired median change, −0.151; 95% CI: −0.238 to −0.057; P=0.002) (Figure 2). The paired change in P_peak was inversely associated with the paired change in E_lung/E_rs (Spearman ρ=−0.43, P=0.054; Figure 3).

Figure 2.

Raincloud plots of paired changes in respiratory mechanics before and after chest strapping. Panels show (A) E_rs, (B) E_cw, (C) E_lung, and (D) E_lung/E_rs. Points represent individual patients with paired lines; half-violins show distributions. Median and interquartile range are indicated. P values are from two-sided Wilcoxon signed-rank tests; r denotes rank-biserial correlation. E_cw, chest wall elastance; E_lung, lung elastance; E_lung/E_rs, elastance ratio; E_rs, respiratory system elastance.

Figure 3.

Association between changes in peak airway pressure and E_lung/E_rs after chest strapping. Scatterplot of the paired change (after-before) in P_peak vs. the paired change (after-before) in E_lung/E_rs. Spearman correlation: ρ=−0.43, P=0.054 (two-sided). E_lung/E_rs, elastance ratio; P_peak, peak airway pressure.

Discussion

In this post hoc re-analysis restricted to patients without COPD or an acute pulmonary diagnosis at ICU admission, chest strapping increased airway pressures but lowered absolute P_L. The mechanical response was dominated by chest wall loading, with a marked increase in chest wall elastance and a lower E_lung/E_rs. These findings support the hypothesis that acute external chest wall restriction can dissociate airway pressures from P_L.

These findings highlight a practical point: when the chest wall is externally constrained (e.g., straps, binders, positioning), airway pressures may not reflect lung stress. Esophageal pressure monitoring helps separate lung and chest wall mechanics and may prevent over-interpretation of plateau pressure alone (18,19).

ΔP_L decreased numerically but was not statistically significant in this restricted cohort. Given the sample size, the analysis is likely underpowered for small changes in ΔP_L. In exploratory analyses, patients with an acute pulmonary diagnosis or COPD (excluded from the re-analysis) showed a larger decrease in ΔP_L (Table S3 and Figure S2), suggesting heterogeneity by pulmonary status (16,20).

Mechanical power increased during strapping, with a significant increase in the elastic component and no significant change in the resistive component. Mechanical power is an integrated measure of the energy delivered from the ventilator to the respiratory system and has been discussed in relation to ventilator-induced lung injury (VILI) (4,21). In the setting of chest wall restriction, however, this value does not necessarily represent energy delivered to the lung alone. Part of the additional elastic work may be spent inflating a stiffer chest wall rather than increasing lung-directed stress. Thus, increased airway-pressure-based mechanical power may overestimate lung-directed mechanical load when chest wall elastance is markedly increased. However, a possible contribution to VILI cannot be excluded, especially if regional ventilation becomes uneven.

In patients with spontaneous breathing, respiratory drive and inspiratory effort can alter lung stress and patient-ventilator interaction, and these variables can be assessed at the bedside (22). In the present cohort, patients were deeply sedated and spontaneous breathing was suppressed. Thus, neuromechanical coupling could not be assessed directly. The relevant issue here is mechanical coupling among the ventilator, chest wall, and lung. Chest wall stiffening may change how airway pressure is transmitted to esophageal and P_L, and may also affect regional ventilation distribution even when global ΔP_L does not increase. Because regional ventilation and aeration were not measured using electrical impedance tomography (EIT) or imaging, this mechanism remains untested.

End-expiratory P_L was negative at baseline and became more negative during strapping. Absolute P_es and P_L values in the supine position can be influenced by mediastinal weight and other factors (18,19,23). Although a more negative P_{L exp} could raise concern for derecruitment, gas exchange remained stable over the 30-minute intervention and no new atelectasis was observed on routine bedside assessment. Similar physiological studies have combined esophageal or P_L monitoring with EIT to assess regional ventilation distribution (24). Without such monitoring, we could not determine whether chest wall stiffening changed regional ventilation despite stable global gas exchange. Longer exposures may also behave differently (7).

This study has several limitations. First, it was a single-center physiologic study with a short intervention and a modest sample size. No formal power calculation was performed, and the analysis may be underpowered to detect small but relevant changes, especially for ΔP_L. Second, the re-analysis cohort was defined post hoc. This may introduce selection bias and limits generalizability. Patients with COPD or acute pulmonary diagnoses had different baseline mechanics and may respond differently to external chest wall restriction. Third, strap tension was not directly quantified with a force transducer or pressure sensor. Although the procedure was standardized by chest circumference-based band selection, trained staff application, fixed exposure duration, and unchanged ventilator settings, the lack of direct tension measurement limits reproducibility and prevents assessment of dose-response relationships. Finally, regional ventilation or aeration was not assessed using EIT or imaging. Recent reviews emphasize that these tools can help assess regional ventilation, overdistension, collapse, and patient-specific respiratory mechanics (25,26). Future studies should quantify compression intensity and combine esophageal pressure monitoring with regional ventilation assessment, particularly in patients with ARDS, obesity, or other conditions associated with altered chest wall mechanics.

Conclusions

In sedated, volume-controlled postoperative ICU patients undergoing short-term external chest wall restriction, chest strapping increased airway pressures primarily through increased chest wall elastance. Despite higher airway pressures, absolute P_L decreased and ΔP_L did not increase significantly. These findings suggest that, when chest wall compliance is externally restricted, airway pressures may be unreliable surrogates for lung stress. Esophageal pressure monitoring may help distinguish lung loading from chest wall loading in this setting.

Supplementary

The article’s supplementary files as

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the institutional research committee of Zhongshan Hospital, Fudan University (No. B2018-322). Written informed consent was obtained from all patients or their surrogates.

Data Sharing Statement

Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2026-1010/dss

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DOI: 10.21037/jtd-2026-1010