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Background: APRV has been used for ARDS in the past. Little is known about the risk of ventilator- induced lung- injury (VILI) in APRV vs. BIPAP in the management of in COVID19-associated ARDS (CARDS). This study aimed to compare transpulmonary pressures (TPP) in APRV vs. BIPAP in CARDS in regard to lung protective ventilator settings. Methods: This retrospective, monocentric cohort study (ethical approval: 21-1553) assessed all adult ICU- patients with CARDS who were ventilated with BIPAP vs. APRV and monitored with TPP from 03/2020 to 10/2021. Ventilator-settings / -pressures, TPP, hemodynamic and arterial blood gas parameters were compared in both modes. Results: 20 non- spontaneously breathing patients could be included in the study: Median TPPendexpiratory was lower / negative in APRV (-1.20mbar; IQR − 4.88 / +4.53) vs. positive in BIPAP (+ 3.4mbar; IQR + 1.95 / +8.57; p <.01). Median TPPendinspiratory did not differ. In APRV, mean tidal- volume per body- weight (7.05 ± 1.28 vs. 5.03 ± 0.77 ml; p <.01) and mean airway- pressure (27.08 ± 1.67 vs. 22.68 ± 2.62mbar; p <.01) were higher. There was no difference in PEEP, peak-, plateau- or driving- pressure, compliance, oxygenation and CO2- removal between both modes. Conclusion: Despite higher tidal- volumes / airway-pressures in APRV vs. BIPAP, TPPendinspiratory was not increased. However, in APRV median TPPendexpiratory was negative indicating an elevated risk of occult atelectasis in APRV- mode in CARDS. Therefore, TPP- monitoring could be a useful tool for monitoring a safe application of APRV- mode in CARDS. [ABSTRACT FROM AUTHOR]

Background: Recruitment maneuvers are used in patients with ARDS to enhance oxygenation and lung mechanics. Heterogeneous lung and chest-wall mechanics lead to unpredictable transpulmonary pressures and could impact recruitment maneuver success. Tailoring care based on individualized transpulmonary pressure might optimize recruitment, preventing overdistention. This study aimed to identify the optimal transpulmonary pressure for effective recruitment and to explore its association with baseline characteristics. Methods: We performed post hoc analysis on the Esophageal Pressure Guided Ventilation (EpVent2) trial. We estimated the dose-response relationship between end-recruitment end-inspiratory transpulmonary pressure and the change in lung elastance after a recruitment maneuver by using logistic regression weighted by a generalized propensity score. A positive change in lung elastance was indicative of overdistention. We examined how patient characteristics, disease severity markers, and respiratory parameters predict transpulmonary pressure by using multivariate linear regression models and dominance analyses. Results: Of 121 subjects, 43.8% had a positive change in lung elastance. Subjects with a positive change in lung elastance had a mean ± SD transpulmonary pressure of 15.1 ± 4.9 cm H2O, compared with 13.9 ± 3.9 cm H2O in those with a negative change in lung elastance. Higher transpulmonary pressure was associated with increased probability of a positive change in lung elastance (adjusted odds ratio 1.35 per 1 cm H2O of transpulmonary pressure, 95% CI 1.13–1.61; P =.001), which indicated an S-shaped dose-response curve, with overdistention probability > 50% at transpulmonary pressure values > 18.3 cm H2O. The volume of recruitment was transpulmonary pressure–dependent (P <.001; R2 = 0.49) and inversely related to a change in lung elastance after adjusting for baseline lung elastance (P <.001; R2 = 0.43). Negative correlations were observed between transpulmonary pressure and body mass index, PEEP, Sequential Organ Failure Assessment score, and PaO2/FIO2, whereas baseline lung elastance showed a positive correlation. The body mass index emerged as the dominant negative predictor of transpulmonary pressure (ranking 1; contribution to R2 = 0.08), whereas pre-recruitment elastance was the sole positive predictor (contribution to R2 = 0.06). Conclusions: Higher end-recruitment transpulmonary pressure increases the volume of recruitment but raises the risk of overdistention, providing the rationale for transpulmonary pressure to be used as a clinical target. Predictors, for example, body mass index, could guide recruitment maneuver individualization to balance adequate volume gain with overdistention. [ABSTRACT FROM AUTHOR]

Purpose: Personalized positive end-expiratory pressure (PEEP) might foster lung and diaphragm protection in patients with acute respiratory distress syndrome (ARDS) who are undergoing pressure support ventilation (PSV). We aimed to compare the physiologic effects of personalized PEEP set according to synchronized electrical impedance tomography (EIT) and driving transpulmonary pressure (∆PL) monitoring against a classical lower PEEP/FiO2 table in intubated ARDS patients undergoing PSV. Methods: A cross-over randomized multicenter study was conducted in 30 ARDS patients with simultaneous recording of the airway, esophageal and transpulmonary pressure, together with EIT during PSV. Following a decremental PEEP trial (18 cmH2O to 4 cmH2O), PEEPEIT-∆PL was identified as the level with the smallest difference between lung overdistension and collapse. A low PEEP/FiO2 table was used to select PEEPTABLE. Each PEEP strategy was applied for 20 min, and physiologic data were collected at the end of each step. Results: The PEEP trial was well tolerated. Median PEEPEIT-∆PL was higher than PEEPTABLE (10 [8–12] vs. 8 [5–10] cmH2O; P = 0.021) and, at the individual patient level, PEEPEIT-∆PL level differed from PEEPTABLE in all patients. Overall, PEEPEIT-∆PL was associated with lower dynamic ∆PL (P < 0.001) and pressure–time product (P < 0.001), but there was variability among patients. PEEPEIT-∆PL also decreased respiratory drive and effort (P < 0.001), improved regional lung mechanics (P < 0.05) and reversed lung collapse (P = 0.007) without increasing overdistension (P = 0.695). Conclusion: Personalized PEEP selected using synchronized EIT and transpulmonary pressure monitoring could be associated with reduced dynamic lung stress and metabolic work of breathing in ARDS patients undergoing PSV. [ABSTRACT FROM AUTHOR]

Abstract Background Transpulmonary pressure is the effective pressure across the lung parenchyma and has been proposed as a guide for mechanical ventilation. The pleural pressure is challenging to directly measure in clinical setting and esophageal manometry using esophageal balloon catheters was suggested for estimation. However, the accuracy of using esophageal pressure to estimate pleural pressure is debated due to variability in the mechanical properties of respiratory system, esophagus and esophageal catheter. Furthermore, while a vertical pleural pressure gradient exists across lung regions, esophageal pressure balloon provides a single value, representing, at most, the pressure surrounding the esophagus. Methods In a swine model with a preserved esophagus and a single homogenous, easily measurable intrathoracic pressure, we evaluated esophageal pressure’s agreement with intrathoracic pressure at different positive end-expiratory pressure (PEEP) levels (0, 5, 10, 15 cmH2O). We assessed the improvement of measurement accuracy by correcting absolute esophageal values using a previously described technique, that accounts for the pressure generated by the esophageal wall in response to esophageal balloon inflation. The study involved five swine, wherein two different esophageal catheters were used alongside the four distinct PEEP levels. Swings, uncorrected and corrected absolute esophageal pressures (end-inspiratory, end-expiratory) were compared with their respective intrathoracic pressures. The effect of correction technique was assessed with manual incremental step inflation procedure. Results We found that both catheters significantly overestimated absolute esophageal pressure compared to intrathoracic pressure (5.01 ± 3.32 and 6.06 ± 5.62 cmH2O at end-expiration and end-inspiration, respectively), with error increasing at higher positive end-expiratory pressure levels (end-expiration: 2.36 ± 2.03, 3.77 ± 1.37, 6.24 ± 2.51 and 7.69 ± 4.02 for each PEEP level, P

Abstract Background We previously showed in animals that transpulmonary driving pressure (PL) can be estimated during Neurally Adjusted Ventilatory Assist (NAVA) and Neural Pressure Support (NPS) using a single lower assist maneuver (LAM). The aim of this study was to test the LAM-based estimate of PL (PL_LAM) in patients with acute respiratory failure. Methods This was a prospective, physiological, and interventional study in intubated patients with acute respiratory failure. During both NAVA and simulated NPS (high and low levels of assist), a LAM was performed every 3 min by manually reducing the assist to zero for one single breath (by default, ventilator still provides 2 cmH2O). Following NAVA and NPSSIM periods, patients were sedated and passively ventilated in volume control and pressure control ventilation, to obtain PL during controlled mechanical ventilation (PL_CMV). PL using an esophageal balloon (PL_Pes) was also compared to PL_LAM and PL_CMV. We measured diaphragm electrical activity (Edi), ventilator pressure (PVent), esophageal pressure (Pes) and tidal volume. PL_LAM and PL_Pes were compared to themselves, and to PL_CMV for matching flows and volumes. Results Ten patients were included in the study. For the group, PL_LAM was closely similar to PL_CMV, with a high correlation (R 2 = 0.88). Bland–Altman analysis revealed a low Bias of 0.28 cmH2O, and 1.96SD of 5.26 cmH2O. PL_LAM vs PL_Pes were also tightly related (R 2 = 0.77). Conclusion This physiological study in patients confirms our previous pre-clinical data that PL_LAM is as good an estimate as PL_Pes to determine PL, in spontaneously breathing patients on assisted mechanical ventilation. Trial registration The study was registered at clinicaltrials.gov (ID NCT05378802) on November 6, 2021

Abstract Background Understanding the characteristics of pulmonary resistance and elastance in relation to the location of airway narrowing, e.g., tracheal stenosis vs. intrapulmonary airway obstruction, will help us understand lung function characteristics and mechanisms related to different airway diseases. Methods In this study, we used ex vivo sheep lungs as a model to measure lung resistance and elastance across a range of transpulmonary pressures (5–30 cmH2O) and ventilation frequencies (0.125–2 Hz). We established two tracheal stenosis models by inserting plastic tubes into the tracheas, representing mild (71.8% lumen area reduction) and severe (92.1%) obstructions. For intrapulmonary airway obstruction, we induced airway narrowing by challenging the lung with acetylcholine (ACh). Results We found a pattern change in the lung resistance and apparent lung elastance as functions of ventilation frequency that depended on the transpulmonary pressure (or lung volume). At a transpulmonary pressure of 10 cmH2O, lung resistance increased with ventilation frequency in severe tracheal stenosis, whereas in ACh-induced airway narrowing the opposite occurred. Furthermore, apparent lung elastance at 10 cmH2O decreased with increasing ventilation frequency in severe tracheal stenosis whereas in ACh-induced airway narrowing the opposite occurred. Flow-volume analysis revealed that the flow amplitude was much sensitive to ventilation frequency in tracheal stenosis than it was in ACh induced airway constriction. Conclusions Results from this study suggest that lung resistance and apparent elastance measured at 10 cmH2O over the frequency range of 0.125-2 Hz can differentiate tracheal stenosis vs. intrapulmonary airway narrowing in ex vivo sheep lungs.

Abstract Background Right ventricle impairment (RVI) is common during acute respiratory distress syndrome (ARDS) in adults and children, possibly mediated by the level of transpulmonary pressure (P L). We sought to investigate the impact of the level of P L on ARDS-associated right ventricle impairment (RVI). Methods Adults and children (> 72 h of life) were included in this two centers prospective study if they were ventilated for a new-onset ARDS or pediatric ARDS, without spontaneous breathing and contra-indication to esophageal catheter. Serial measures of static lung, chest wall, and respiratory mechanics were coupled to critical care echocardiography (CCE) for 3 days. Mixed-effect logistic regression models tested the impact of lung stress (ΔP L) along with age, lung injury severity, and carbon dioxide partial pressure, on RVI using two definitions: acute cor pulmonale (ACP), and RV dysfunction (RVD). ACP was defined as a dilated RV with septal dyskinesia; RVD was defined as a composite criterion using tricuspid annular plane systolic excursion, S wave velocity, and fractional area change. Results 46 patients were included (16 children, 30 adults) with 106 CCE (median of 2 CCE/patient). At day one, 19% of adults and 4/7 children > 1 year exhibited ACP, while 59% of adults and 44% of children exhibited RVD. In the entire population, ACP was present on 17/75 (23%) CCE. ACP was associated with an increased lung stress (mean ΔP L of 16.2 ± 6.6 cmH2O in ACP vs 11.3 ± 3.6 cmH2O, adjusted OR of 1.33, CI95% [1.11–1.59], p = 0.002) and being a child. RVD was present in 59/102 (58%) CCE and associated with lung stress. In children > 1 year, PEEP was significantly lower in case of ACP (9.3 [8.6; 10.0] cmH2O in ACP vs 15.0 [11.9; 16.3] cmH2O, p = 0.03). Conclusion Lung stress was associated with RVI in adults and children with ARDS, children being particularly susceptible to RVI. Trial registration Clinical trials identifier: NCT0418467.

Background: Transpulmonary pressure is the effective pressure across the lung parenchyma and has been proposed as a guide for mechanical ventilation. The pleural pressure is challenging to directly measure in clinical setting and esophageal manometry using esophageal balloon catheters was suggested for estimation. However, the accuracy of using esophageal pressure to estimate pleural pressure is debated due to variability in the mechanical properties of respiratory system, esophagus and esophageal catheter. Furthermore, while a vertical pleural pressure gradient exists across lung regions, esophageal pressure balloon provides a single value, representing, at most, the pressure surrounding the esophagus. Methods: In a swine model with a preserved esophagus and a single homogenous, easily measurable intrathoracic pressure, we evaluated esophageal pressure's agreement with intrathoracic pressure at different positive end-expiratory pressure (PEEP) levels (0, 5, 10, 15 cmH2O). We assessed the improvement of measurement accuracy by correcting absolute esophageal values using a previously described technique, that accounts for the pressure generated by the esophageal wall in response to esophageal balloon inflation. The study involved five swine, wherein two different esophageal catheters were used alongside the four distinct PEEP levels. Swings, uncorrected and corrected absolute esophageal pressures (end-inspiratory, end-expiratory) were compared with their respective intrathoracic pressures. The effect of correction technique was assessed with manual incremental step inflation procedure. Results: We found that both catheters significantly overestimated absolute esophageal pressure compared to intrathoracic pressure (5.01 ± 3.32 and 6.06 ± 5.62 cmH2O at end-expiration and end-inspiration, respectively), with error increasing at higher positive end-expiratory pressure levels (end-expiration: 2.36 ± 2.03, 3.77 ± 1.37, 6.24 ± 2.51 and 7.69 ± 4.02 for each PEEP level, P < 0.0001; end-inspiration: 1.71 ± 2.10, 3.70 ± 1.73, 7.67 ± 3.62 and 11.14 ± 7.60 for each PEEP level, P = 0.0004). Applying the correction technique significantly improved agreement for absolute values (0.82 ± 1.62 and 1.86 ± 3.94 cmH2O at end-expiration and end-inspiration, respectively). Esophageal pressure swings accurately estimated intrathoracic pressure swings at low-medium intrathoracic pressures (-0.64 ± 0.62, -0.07 ± 0.53, 1.43 ± 1.51, and 3.45 ± 3.94 at PEEP 0, 5, 10 and 15 cmH2O, respectively; P = 0.0197). Conclusions: The correction technique, based on the mechanical response of esophageal wall to the balloon inflation, is fundamental for obtaining reliable estimations of absolute intrathoracic pressure values, and for ensuring its correct application in clinical setting. [ABSTRACT FROM AUTHOR]

The use of transpulmonary pressure monitoring based on measurement of esophageal pressure has contributed importantly to the personalization of mechanical ventilation based on respiratory pathophysiology in critically ill patients. However, esophageal pressure monitoring is still underused in the clinical practice. This technique allows partitioning of the respiratory mechanics between the lungs and the chest wall, provides information on lung recruitment and risk of barotrauma, and helps titrating mechanical ventilation settings in patients with respiratory failure. In assisted ventilation modes and during non-invasive respiratory support, esophageal pressure monitoring provides important information on the inspiratory effort and work of breathing. Nonetheless, several controversies persist on technical aspects, interpretation and clinical decision-making based on values derived from this monitoring technique. The aim of this review is to summarize the physiological bases of esophageal pressure monitoring, discussing the pros and cons of its clinical applications and different interpretations in critically ill patients undergoing invasive and non-invasive respiratory support. [ABSTRACT FROM AUTHOR]

Background: We previously showed in animals that transpulmonary driving pressure (PL) can be estimated during Neurally Adjusted Ventilatory Assist (NAVA) and Neural Pressure Support (NPS) using a single lower assist maneuver (LAM). The aim of this study was to test the LAM-based estimate of PL (PL_LAM) in patients with acute respiratory failure. Methods: This was a prospective, physiological, and interventional study in intubated patients with acute respiratory failure. During both NAVA and simulated NPS (high and low levels of assist), a LAM was performed every 3 min by manually reducing the assist to zero for one single breath (by default, ventilator still provides 2 cmH2O). Following NAVA and NPSSIM periods, patients were sedated and passively ventilated in volume control and pressure control ventilation, to obtain PL during controlled mechanical ventilation (PL_CMV). PL using an esophageal balloon (PL_Pes) was also compared to PL_LAM and PL_CMV. We measured diaphragm electrical activity (Edi), ventilator pressure (PVent), esophageal pressure (Pes) and tidal volume. PL_LAM and PL_Pes were compared to themselves, and to PL_CMV for matching flows and volumes. Results: Ten patients were included in the study. For the group, PL_LAM was closely similar to PL_CMV, with a high correlation (R2 = 0.88). Bland–Altman analysis revealed a low Bias of 0.28 cmH2O, and 1.96SD of 5.26 cmH2O. PL_LAM vs PL_Pes were also tightly related (R2 = 0.77). Conclusion: This physiological study in patients confirms our previous pre-clinical data that PL_LAM is as good an estimate as PL_Pes to determine PL, in spontaneously breathing patients on assisted mechanical ventilation. Trial registration The study was registered at clinicaltrials.gov (ID NCT05378802) on November 6, 2021 [ABSTRACT FROM AUTHOR]

Background: Right ventricle impairment (RVI) is common during acute respiratory distress syndrome (ARDS) in adults and children, possibly mediated by the level of transpulmonary pressure (PL). We sought to investigate the impact of the level of PL on ARDS-associated right ventricle impairment (RVI). Methods: Adults and children (> 72 h of life) were included in this two centers prospective study if they were ventilated for a new-onset ARDS or pediatric ARDS, without spontaneous breathing and contra-indication to esophageal catheter. Serial measures of static lung, chest wall, and respiratory mechanics were coupled to critical care echocardiography (CCE) for 3 days. Mixed-effect logistic regression models tested the impact of lung stress (ΔPL) along with age, lung injury severity, and carbon dioxide partial pressure, on RVI using two definitions: acute cor pulmonale (ACP), and RV dysfunction (RVD). ACP was defined as a dilated RV with septal dyskinesia; RVD was defined as a composite criterion using tricuspid annular plane systolic excursion, S wave velocity, and fractional area change. Results: 46 patients were included (16 children, 30 adults) with 106 CCE (median of 2 CCE/patient). At day one, 19% of adults and 4/7 children > 1 year exhibited ACP, while 59% of adults and 44% of children exhibited RVD. In the entire population, ACP was present on 17/75 (23%) CCE. ACP was associated with an increased lung stress (mean ΔPL of 16.2 ± 6.6 cmH2O in ACP vs 11.3 ± 3.6 cmH2O, adjusted OR of 1.33, CI95% [1.11–1.59], p = 0.002) and being a child. RVD was present in 59/102 (58%) CCE and associated with lung stress. In children > 1 year, PEEP was significantly lower in case of ACP (9.3 [8.6; 10.0] cmH2O in ACP vs 15.0 [11.9; 16.3] cmH2O, p = 0.03). Conclusion: Lung stress was associated with RVI in adults and children with ARDS, children being particularly susceptible to RVI. Trial registration Clinical trials identifier: NCT0418467. [ABSTRACT FROM AUTHOR]

Background: Understanding the characteristics of pulmonary resistance and elastance in relation to the location of airway narrowing, e.g., tracheal stenosis vs. intrapulmonary airway obstruction, will help us understand lung function characteristics and mechanisms related to different airway diseases. Methods: In this study, we used ex vivo sheep lungs as a model to measure lung resistance and elastance across a range of transpulmonary pressures (5–30 cmH2O) and ventilation frequencies (0.125–2 Hz). We established two tracheal stenosis models by inserting plastic tubes into the tracheas, representing mild (71.8% lumen area reduction) and severe (92.1%) obstructions. For intrapulmonary airway obstruction, we induced airway narrowing by challenging the lung with acetylcholine (ACh). Results: We found a pattern change in the lung resistance and apparent lung elastance as functions of ventilation frequency that depended on the transpulmonary pressure (or lung volume). At a transpulmonary pressure of 10 cmH2O, lung resistance increased with ventilation frequency in severe tracheal stenosis, whereas in ACh-induced airway narrowing the opposite occurred. Furthermore, apparent lung elastance at 10 cmH2O decreased with increasing ventilation frequency in severe tracheal stenosis whereas in ACh-induced airway narrowing the opposite occurred. Flow-volume analysis revealed that the flow amplitude was much sensitive to ventilation frequency in tracheal stenosis than it was in ACh induced airway constriction. Conclusions: Results from this study suggest that lung resistance and apparent elastance measured at 10 cmH2O over the frequency range of 0.125-2 Hz can differentiate tracheal stenosis vs. intrapulmonary airway narrowing in ex vivo sheep lungs. [ABSTRACT FROM AUTHOR]

Abstract Heart–lungs interactions are related to the interplay between the cardiovascular and the respiratory system. They result from the respiratory-induced changes in intrathoracic pressure, which are transmitted to the cardiac cavities and to the changes in alveolar pressure, which may impact the lung microvessels. In spontaneously breathing patients, consequences of heart–lungs interactions are during inspiration an increase in right ventricular preload and afterload, a decrease in left ventricular preload and an increase in left ventricular afterload. In mechanically ventilated patients, consequences of heart–lungs interactions are during mechanical insufflation a decrease in right ventricular preload, an increase in right ventricular afterload, an increase in left ventricular preload and a decrease in left ventricular afterload. Physiologically and during normal breathing, heart–lungs interactions do not lead to significant hemodynamic consequences. Nevertheless, in some clinical settings such as acute exacerbation of chronic obstructive pulmonary disease, acute left heart failure or acute respiratory distress syndrome, heart–lungs interactions may lead to significant hemodynamic consequences. These are linked to complex pathophysiological mechanisms, including a marked inspiratory negativity of intrathoracic pressure, a marked inspiratory increase in transpulmonary pressure and an increase in intra-abdominal pressure. The most recent application of heart–lungs interactions is the prediction of fluid responsiveness in mechanically ventilated patients. The first test to be developed using heart–lungs interactions was the respiratory variation of pulse pressure. Subsequently, many other dynamic fluid responsiveness tests using heart–lungs interactions have been developed, such as the respiratory variations of pulse contour-based stroke volume or the respiratory variations of the inferior or superior vena cava diameters. All these tests share the same limitations, the most frequent being low tidal volume ventilation, persistent spontaneous breathing activity and cardiac arrhythmia. Nevertheless, when their main limitations are properly addressed, all these tests can help intensivists in the decision-making process regarding fluid administration and fluid removal in critically ill patients.

Heart–lungs interactions are related to the interplay between the cardiovascular and the respiratory system. They result from the respiratory-induced changes in intrathoracic pressure, which are transmitted to the cardiac cavities and to the changes in alveolar pressure, which may impact the lung microvessels. In spontaneously breathing patients, consequences of heart–lungs interactions are during inspiration an increase in right ventricular preload and afterload, a decrease in left ventricular preload and an increase in left ventricular afterload. In mechanically ventilated patients, consequences of heart–lungs interactions are during mechanical insufflation a decrease in right ventricular preload, an increase in right ventricular afterload, an increase in left ventricular preload and a decrease in left ventricular afterload. Physiologically and during normal breathing, heart–lungs interactions do not lead to significant hemodynamic consequences. Nevertheless, in some clinical settings such as acute exacerbation of chronic obstructive pulmonary disease, acute left heart failure or acute respiratory distress syndrome, heart–lungs interactions may lead to significant hemodynamic consequences. These are linked to complex pathophysiological mechanisms, including a marked inspiratory negativity of intrathoracic pressure, a marked inspiratory increase in transpulmonary pressure and an increase in intra-abdominal pressure. The most recent application of heart–lungs interactions is the prediction of fluid responsiveness in mechanically ventilated patients. The first test to be developed using heart–lungs interactions was the respiratory variation of pulse pressure. Subsequently, many other dynamic fluid responsiveness tests using heart–lungs interactions have been developed, such as the respiratory variations of pulse contour-based stroke volume or the respiratory variations of the inferior or superior vena cava diameters. All these tests share the same limitations, the most frequent being low tidal volume ventilation, persistent spontaneous breathing activity and cardiac arrhythmia. Nevertheless, when their main limitations are properly addressed, all these tests can help intensivists in the decision-making process regarding fluid administration and fluid removal in critically ill patients. [ABSTRACT FROM AUTHOR]

Transpulmonary pressure (PL) calculation requires esophageal pressure (PES) as a surrogate of pleural pressure (Ppl), but its calibration is a cumbersome technique. Central venous pressure (CVP) swings may reflect tidal variations in Ppl and could be used instead of PES, but the interpretation of CVP waveforms could be difficult due to superposition of heartbeat-induced pressure changes. Thus, we developed a digital filter able to remove the cardiac noise to obtain a filtered CVP (f-CVP). The aim of the study was to evaluate the accuracy of CVP and filtered CVP swings (ΔCVP and Δf-CVP, respectively) in estimating esophageal respiratory swings (ΔPES) and compare PL calculated with CVP, f-CVP and PES; then we tested the diagnostic accuracy of the f-CVP method to identify unsafe high PL levels, defined as PL>10 cmH2O. Twenty patients with acute respiratory failure (defined as PaO2/FiO2 ratio below 200 mmHg) treated with invasive mechanical ventilation and monitored with an esophageal balloon and central venous catheter were enrolled prospectively. For each patient a recording session at baseline was performed, repeated if a modification in ventilatory settings occurred. PES, CVP and airway pressure during an end-inspiratory and -expiratory pause were simultaneously recorded; CVP, f-CVP and PES waveforms were analyzed off-line and used to calculate transpulmonary pressure (PLCVP, PLf-CVP, PLPES, respectively). Δf-CVP correlated better than ΔCVP with ΔPES (r = 0.8, p = 0.001 vs. r = 0.08, p = 0.73), with a lower bias in Bland Altman analysis in favor of PLf-CVP (mean bias − 0.16, Limits of Agreement (LoA) -1.31, 0.98 cmH2O vs. mean bias − 0.79, LoA − 3.14, 1.55 cmH2O). Both PLf-CVP and PLCVP correlated well with PLPES (r = 0.98, p < 0.001 vs. r = 0.94, p < 0.001), again with a lower bias in Bland Altman analysis in favor of PLf-CVP (0.15, LoA − 0.95, 1.26 cmH2O vs. 0.80, LoA − 1.51, 3.12, cmH2O). PLf-CVP discriminated high PL value with an area under the receiver operating characteristic curve 0.99 (standard deviation, SD, 0.02) (AUC difference = 0.01 [-0.024; 0.05], p = 0.48). In mechanically ventilated patients with acute respiratory failure, the digital filtered CVP estimated ΔPES and PL obtained from digital filtered CVP represented a reliable value of standard PL measured with the esophageal method and could identify patients with non-protective ventilation settings. [ABSTRACT FROM AUTHOR]

Patients with acute exacerbation of lung fibrosis with usual interstitial pneumonia (EUIP) pattern are at increased risk for ventilator-induced lung injury (VILI) and mortality when exposed to mechanical ventilation (MV). Yet, lack of a mechanical model describing UIP-lung deformation during MV represents a research gap. Aim of this study was to develop a constitutive mathematical model for UIP-lung deformation during lung protective MV based on the stress–strain behavior and the specific elastance of patients with EUIP as compared to that of acute respiratory distress syndrome (ARDS) and healthy lung. Partitioned lung and chest wall mechanics were assessed for patients with EUIP and primary ARDS (1:1 matched based on body mass index and PaO2/FiO2 ratio) during a PEEP trial performed within 24 h from intubation. Patient's stress–strain curve and the lung specific elastance were computed and compared with those of healthy lungs, derived from literature. Respiratory mechanics were used to fit a novel mathematical model of the lung describing mechanical-inflation-induced lung parenchyma deformation, differentiating the contributions of elastin and collagen, the main components of lung extracellular matrix. Five patients with EUIP and 5 matched with primary ARDS were included and analyzed. Global strain was not different at low PEEP between the groups. Overall specific elastance was significantly higher in EUIP as compared to ARDS (28.9 [22.8–33.2] cmH2O versus 11.4 [10.3–14.6] cmH2O, respectively). Compared to ARDS and healthy lung, the stress/strain curve of EUIP showed a steeper increase, crossing the VILI threshold stress risk for strain values greater than 0.55. The contribution of elastin was prevalent at lower strains, while the contribution of collagen was prevalent at large strains. The stress/strain curve for collagen showed an upward shift passing from ARDS and healthy lungs to EUIP lungs. During MV, patients with EUIP showed different respiratory mechanics, stress–strain curve and specific elastance as compared to ARDS patients and healthy subjects and may experience VILI even when protective MV is applied. According to our mathematical model of lung deformation during mechanical inflation, the elastic response of UIP-lung is peculiar and different from ARDS. Our data suggest that patients with EUIP experience VILI with ventilatory setting that are lung-protective for patients with ARDS. [ABSTRACT FROM AUTHOR]

Background and Objectives: Intra-abdominal hypertension (IAH) and acute respiratory distress syndrome (ARDS) are common concerns in intensive care unit patients with acute respiratory failure (ARF). Although both conditions lead to impairment of global respiratory parameters, their underlying mechanisms differ substantially. Therefore, a separate assessment of the different respiratory compartments should reveal differences in respiratory mechanics. Materials and Methods: We prospectively investigated alterations in lung and chest wall mechanics in 18 mechanically ventilated pigs exposed to varying levels of intra-abdominal pressures (IAP) and ARDS. The animals were divided into three groups: group A (IAP 10 mmHg, no ARDS), B (IAP 20 mmHg, no ARDS), and C (IAP 10 mmHg, with ARDS). Following induction of IAP (by inflating an intra-abdominal balloon) and ARDS (by saline lung lavage and injurious ventilation), respiratory mechanics were monitored for six hours. Statistical analysis was performed using one-way ANOVA to compare the alterations within each group. Results: After six hours of ventilation, end-expiratory lung volume (EELV) decreased across all groups, while airway and thoracic pressures increased. Significant differences were noted between group (B) and (C) regarding alterations in transpulmonary pressure (TPP) (2.7 ± 0.6 vs. 11.3 ± 2.1 cmH2O, p < 0.001), elastance of the lung (EL) (8.9 ± 1.9 vs. 29.9 ± 5.9 cmH2O/mL, p = 0.003), and elastance of the chest wall (ECW) (32.8 ± 3.2 vs. 4.4 ± 1.8 cmH2O/mL, p < 0.001). However, global respiratory parameters such as EELV/kg bodyweight (−6.1 ± 1.3 vs. −11.0 ± 2.5 mL/kg), driving pressure (12.5 ± 0.9 vs. 13.2 ± 2.3 cmH2O), and compliance of the respiratory system (−21.7 ± 2.8 vs. −19.5 ± 3.4 mL/cmH2O) did not show significant differences among the groups. Conclusions: Separate measurements of lung and chest wall mechanics in pigs with IAH or ARDS reveals significant differences in TPP, EL, and ECW, whereas global respiratory parameters do not differ significantly. Therefore, assessing the compartments of the respiratory system separately could aid in identifying the underlying cause of ARF. [ABSTRACT FROM AUTHOR]

Advanced respiratory monitoring encompasses a diverse range of mini- or noninvasive tools used to evaluate various aspects of respiratory function in patients experiencing acute respiratory failure, including those requiring extracorporeal membrane oxygenation (ECMO) support. Among these techniques, key modalities include esophageal pressure measurement (including derived pressures), lung and respiratory muscle ultrasounds, electrical impedance tomography, the monitoring of diaphragm electrical activity, and assessment of flow index. These tools play a critical role in assessing essential parameters such as lung recruitment and overdistention, lung aeration and morphology, ventilation/perfusion distribution, inspiratory effort, respiratory drive, respiratory muscle contraction, and patient–ventilator synchrony. In contrast to conventional methods, advanced respiratory monitoring offers a deeper understanding of pathological changes in lung aeration caused by underlying diseases. Moreover, it allows for meticulous tracking of responses to therapeutic interventions, aiding in the development of personalized respiratory support strategies aimed at preserving lung function and respiratory muscle integrity. The integration of advanced respiratory monitoring represents a significant advancement in the clinical management of acute respiratory failure. It serves as a cornerstone in scenarios where treatment strategies rely on tailored approaches, empowering clinicians to make informed decisions about intervention selection and adjustment. By enabling real-time assessment and modification of respiratory support, advanced monitoring not only optimizes care for patients with acute respiratory distress syndrome but also contributes to improved outcomes and enhanced patient safety. [ABSTRACT FROM AUTHOR]

Abstract Introduction Chest tube drainage is usually performed through an underwater seal at a level of 10–20 cmH2O. Based on the definition of transpulmonary pressure, continuous chest drainage creates continuous negative pressure, decreasing pleural surface pressure and increasing transpulmonary pressure. We investigated how unilateral chest drainage could affect the tidal volume or driving pressure during mandatory mechanical ventilation. Methods This study was an experimental study using a lung-thoracic model and anesthesia ventilator. Tidal volume was set to 300 mL with pressure-controlled ventilation or volume-controlled ventilation. Left tidal volume and right tidal volume were measured independently using respirometers with positive end-expiratory pressure (PEEP) levels of 0, 10, and 20 cmH2O. Simultaneously, left negative pressure of the chest drainage was changed to 0, 10, and 20 cmH2O. Results In all conditions, a tidal volume of 300 mL was achieved. In both pressure-controlled ventilation and volume-controlled ventilation, the left tidal volume increased with the application of chest drainage at 10 cmH2O when the PEEP level was 0 cmH2O, but left tidal volume decreased with the application of chest drainage at 20 cmH2O. Furthermore, when PEEP was 10 cmH2O, the left tidal volume decreased in proportion to the pressure of thoracic drainage. The right tidal volumes changed inversely with their counterpart left tidal volumes. Conclusion Unilateral chest drainage caused unbalanced ventilation of the left and right lungs regardless of pressure-controlled ventilation or volume-controlled ventilation.

This article discusses a study on the use of esophageal balloon catheters to measure respiratory effort and mechanics in patients receiving mechanical ventilation. The researchers used a system identification approach to improve the accuracy of these measurements. They conducted tests in a controlled setting and with patient data, and found that correcting the dynamic response of the balloon catheter improved the accuracy of resistance and compliance estimates. The study acknowledges limitations and suggests further investigation, but concludes that using esophageal pressure measurements can improve ventilator settings and decision-making. The data from the study are available upon request. [Extracted from the article]

Introduction: Chest tube drainage is usually performed through an underwater seal at a level of 10–20 cmH2O. Based on the definition of transpulmonary pressure, continuous chest drainage creates continuous negative pressure, decreasing pleural surface pressure and increasing transpulmonary pressure. We investigated how unilateral chest drainage could affect the tidal volume or driving pressure during mandatory mechanical ventilation. Methods: This study was an experimental study using a lung-thoracic model and anesthesia ventilator. Tidal volume was set to 300 mL with pressure-controlled ventilation or volume-controlled ventilation. Left tidal volume and right tidal volume were measured independently using respirometers with positive end-expiratory pressure (PEEP) levels of 0, 10, and 20 cmH2O. Simultaneously, left negative pressure of the chest drainage was changed to 0, 10, and 20 cmH2O. Results: In all conditions, a tidal volume of 300 mL was achieved. In both pressure-controlled ventilation and volume-controlled ventilation, the left tidal volume increased with the application of chest drainage at 10 cmH2O when the PEEP level was 0 cmH2O, but left tidal volume decreased with the application of chest drainage at 20 cmH2O. Furthermore, when PEEP was 10 cmH2O, the left tidal volume decreased in proportion to the pressure of thoracic drainage. The right tidal volumes changed inversely with their counterpart left tidal volumes. Conclusion: Unilateral chest drainage caused unbalanced ventilation of the left and right lungs regardless of pressure-controlled ventilation or volume-controlled ventilation. [ABSTRACT FROM AUTHOR]

Background: Although patients with interstitial pneumonia pattern (ILD-UIP) and acute exacerbation (AE) leading to severe acute respiratory failure may require invasive mechanical ventilation (MV), physiological data on lung mechanics during MV are lacking. We aimed at describing the physiological effect of lung-protective ventilation in patients with AE-ILD-UIP compared with primary ARDS. Methods: Partitioned lung and chest wall mechanics were assessed in a series of AE-ILD-UIP patients matched 1:1 with primary ARDS as controls (based on BMI and PaO2/FiO2 ratio). Three PEEP levels (zero = ZEEP, 4–8 cmH2O = PEEPLOW, and titrated to achieve positive end-expiratory transpulmonary pressure PL,EE = PEEPTITRATED) were used for measurements. Results: Ten AE-ILD-UIP patients and 10 matched ARDS were included. In AE-ILD-UIP median PL,EE at ZEEP was − 4.3 [− 7.6– − 2.3] cmH2O and lung elastance (EL) 44 [40–51] cmH2O/L. At PEEPLOW, PL,EE remained negative and EL did not change (p = 0.995) versus ZEEP. At PEEPTITRATED, PL,EE increased to 0.8 [0.3–1.5] cmH2O and EL to 49 [43–59] (p = 0.004 and p < 0.001 compared to ZEEP and PEEPLOW, respectively). ΔPL decreased at PEEPLOW (p = 0.018) and increased at PEEPTITRATED (p = 0.003). In matched ARDS control PEEP titration to obtain a positive PL,EE did not result in significant changes in EL and ΔPL. Conclusions: In mechanically ventilated AE-ILD-UIP patients, differently than in patients with primary ARDS, PEEP titrated to obtain a positive PL,EE significantly worsened lung mechanics. [ABSTRACT FROM AUTHOR]

Acute respiratory distress syndrome (ARDS) is a common disease in intensive critical care(ICU), and the use of positive end-expiratory pressure(PEEP) during mechanical ventilation can increase the right heart afterload and eventually cause right heart dysfunction. For these factors causing acute cor pulmonale(ACP), especially inappropriate mechanical ventilation settings, it is important to explore the effect of PEEP on right heart function. To investigate the effects of three titration methods on right heart function and prognosis in patients with ARDS. Observational, prospective study in which ARDS patients were enrolled into three distinct PEEP-titration strategies groups: guide, transpulmonary pressure-oriented and driving pressure-oriented. Prognostic indicators, right heart systolic and diastolic echocardiographic function indices, ventilatory parameters, blood gas analysis results, and respiratory mechanics Monitoring indices were collated and analyzed statistically by STATA 15 software. A total of 62 ARDS patients were enrolled into guide (G) group (n=40) for whom titrated PEEP values were 9±2cm H 2 O, driving pressure-oriented (DPO) group (n=12) with titrated PEEP values of 10±2cm H 2 O and transpulmonary pressure-oriented (TPO) group (n=10) with titrated PEEP values of 12±3cm H 2 O. Values were significantly higher for TPO than for G (p=0.616) or DPO (p=0.011). Compliance was significantly increased after 72 h in the TPO and DPO groups compared with the G group (p<0.001). Mean airway pressure at end-inspiratory obstruction (p=0.047), tricuspid annular plane systolic excursion (TAPSE, p<0.001) and right ventricular area change fraction (RVFAC, p=0.049) were all higher in the TPO and DPO groups than in the G group. E/A indices were significantly better in the TPO group than in the G or DPO groups (p=0.046). No significant differences in 28 day mortality were found among the three groups. Multivariate logistic regression analysis revealed that lung compliance and transpulmonary pressure-oriented PEEP titration method was negatively correlated to the increase in right ventricular systolic dysfunction. Transpulmonary pressure-oriented PEEP titration improves oxygenation and pulmonary function and causes less right heart strain when compared to other PEEP-titration methods during mechanical ventilation of ARDS patients. [ABSTRACT FROM AUTHOR]

Abstract Transpulmonary pressure is an essential physiologic concept as it reflects the true pressure across the alveoli, and is a more precise marker for lung stress. To calculate transpulmonary pressure, one needs an estimate of both alveolar pressure and pleural pressure. Airway pressure during conditions of no flow is the most widely accepted surrogate for alveolar pressure, while esophageal pressure remains the most widely measured surrogate marker for pleural pressure. This review will cover important concepts and clinical applications for esophageal manometry, with a particular focus on how to use the information from esophageal manometry to adjust or titrate ventilator support. The most widely used method for measuring esophageal pressure uses an esophageal balloon catheter, although these measurements can be affected by the volume of air in the balloon. Therefore, when using balloon catheters, it is important to calibrate the balloon to ensure the most appropriate volume of air, and we discuss several methods which have been proposed for balloon calibration. In addition, esophageal balloon catheters only estimate the pleural pressure over a certain area within the thoracic cavity, which has resulted in a debate regarding how to interpret these measurements. We discuss both direct and elastance-based methods to estimate transpulmonary pressure, and how they may be applied for clinical practice. Finally, we discuss a number of applications for esophageal manometry and review many of the clinical studies published to date which have used esophageal pressure. These include the use of esophageal pressure to assess lung and chest wall compliance individually which can provide individualized information for patients with acute respiratory failure in terms of setting PEEP, or limiting inspiratory pressure. In addition, esophageal pressure has been used to estimate effort of breathing which has application for ventilator weaning, detection of upper airway obstruction after extubation, and detection of patient and mechanical ventilator asynchrony.

Studies have shown that the airway pressures displayed on the screen of the ventilator monitor do not correlate with the actual alveolar distending pressures known as transpulmonary pressure or stress. The change in tidal volume (Vt) on top of the available functional residual capacity (FRC), also known as strain, is an essential factor directly related to stress. Even the correlation of driving pressure (DP) with ventilator-induced lung injury (VILI) needs to be interpreted in the background of what Vt, respiratory compliance (Crs) and at what positive end-expiratory pressure (PEEP) is that DP calculated and at what was the chest wall compliance, and the flow rate at that time. Stress and strain are related to all these factors, either directly or indirectly. The impact of stress and strain should be interpreted in “dynamic terms” over time rather than at one point. Hence, VILI is minimized by optimizing the Strain (using appropriate PEEP and Vt against available FRC) and stress (transpulmonary inspiratory and expiratory pressures), applied at an optimal respiratory rate and flow. In the pediatric age group, pulmonary mechanics also change as age changes. Moreover, children respond differently to lung injury than adults, adding another layer of complexity to the concept of stress and strain in the pediatric population. Despite this, most knowledge about stress and strain has come from studies in the adult population. Therefore, more extensive studies focussing on pediatric age groups are needed to improve our understanding of stress and strain in pediatric ventilated patients.

Esophageal pressure is the closest estimate of pleural pressure. Changes in esophageal pressure reflect changes in intrathoracic pressure and affect transpulmonary pressure, both of which have multiple effects on right and left ventricular performance. During passive breathing, increasing esophageal pressure is associated with lower venous return and higher right ventricular afterload and lower left ventricular afterload and oxygen consumption. In spontaneously breathing patients, negative pleural pressure swings increase venous return, while right heart afterload increases as in passive conditions; for the left ventricle, end-diastolic pressure is increased potentially favoring lung edema. Esophageal pressure monitoring represents a simple bedside method to estimate changes in pleural pressure and can advance our understanding of the cardiovascular performance of critically ill patients undergoing passive or assisted ventilation and guide physiologically personalized treatments. [ABSTRACT FROM AUTHOR]

OBJECTIVE: This study aimed to investigate the effect of mechanical ventilation guided by transpulmonary pressure in patients diagnosed with acute respiratory distress syndrome (ARDS). MATERIALS AND METHODS: Randomized control trials of ARDS patients that received mechanical ventilation guided by transpulmonary pressure vs. mechanical ventilation guided by traditional lung protective ventilation strategies in adults were retrieved by two reviewers independently from PubMed, EMBASE, The Cochrane Library, The China National Knowledge Infrastructure, and Wan-Fang database before October 2022. The protocol has been registered on PROSPERO (CRD42022307816). The primary outcome was mortality. The secondary outcomes included mechanical ventilation days, oxygenation function and ventilation parameters, hemodynamics, and cytokines level. RESULTS: Thirteen articles (819 patients) were finally included through our search strategy. The total mortality (RR, 0.68; 95% CI, 0.54-0.85; p = 0.0006) and mechanical ventilation days (MD, -2.77; 95% CI, -4.60 - -0.94; p = 0.003) reduced when compared with the control group. Patients in the transpulmonary pressure group had higher oxygen index (MD, 40.74; 95% CI 9.81-71.68, p = 0.010) and lung compliance (MD, 7.98; 95% CI 4.55-11.41, p < 0.00001). Positive end-expiratory pressure (PEEP) was higher in the transpulmonary pressure group (MD, 5.47; 95% CI, 3.59 - 7.35; p < 0.00001). The Interlukin-6 (IL-6) level in the control group decreased obviously compared with that in the transpulmonary pressure group (SMD, -2.03; 95% CI, -3.50 - -0.56; p = 0.007). CONCLUSIONS: Mechanical ventilation guided by transpulmonary pressure tended to have a beneficial prognosis on ARDS patients. Oxygenation and lung mechanics parameters were also improved. The clinical effect of mechanical ventilation directed by transpulmonary pressure was superior to the traditional lung protective ventilation strategies in ARDS patients. [ABSTRACT FROM AUTHOR]

Introduction: The driving pressure (ΔP) has an independent association with outcome in patients with acute respiratory distress syndrome (ARDS). INTELLiVENT-Adaptive Support Ventilation (ASV) is a closed-loop mode of ventilation that targets the lowest work and force of breathing. Aim: To compare transpulmonary and respiratory system ΔP between closed-loop ventilation and conventional pressure controlled ventilation in patients with moderate-to-severe ARDS. Methods: Single-center randomized cross-over clinical trial in patients in the early phase of ARDS. Patients were randomly assigned to start with a 4-h period of closed-loop ventilation or conventional ventilation, after which the alternate ventilation mode was selected. The primary outcome was the transpulmonary ΔP; secondary outcomes included respiratory system ΔP, and other key parameters of ventilation. Results: Thirteen patients were included, and all had fully analyzable data sets. Compared to conventional ventilation, with closed-loop ventilation the median transpulmonary ΔP with was lower (7.0 [5.0–10.0] vs. 10.0 [8.0–11.0] cmH2O, mean difference − 2.5 [95% CI − 2.6 to − 2.1] cmH2O; P = 0.0001). Inspiratory transpulmonary pressure and the respiratory rate were also lower. Tidal volume, however, was higher with closed-loop ventilation, but stayed below generally accepted safety cutoffs in the majority of patients. Conclusions: In this small physiological study, when compared to conventional pressure controlled ventilation INTELLiVENT-ASV reduced the transpulmonary ΔP in patients in the early phase of moderate-to-severe ARDS. This closed-loop ventilation mode also led to a lower inspiratory transpulmonary pressure and a lower respiratory rate, thereby reducing the intensity of ventilation. Trial registration Clinicaltrials.gov, NCT03211494, July 7, 2017. https://clinicaltrials.gov/ct2/show/NCT03211494?term=airdrop&draw=2&rank=1. [ABSTRACT FROM AUTHOR]

Studies have shown that the airway pressures displayed on the screen of the ventilator monitor do not correlate with the actual alveolar distending pressures known as transpulmonary pressure or stress. The change in tidal volume (Vt) on top of the available functional residual capacity (FRC), also known as strain, is an essential factor directly related to stress. Even the correlation of driving pressure (DP) with ventilator-induced lung injury (VILI) needs to be interpreted in the background of what Vt, respiratory compliance (Crs) and at what positive end-expiratory pressure (PEEP) is that DP calculated and at what was the chest wall compliance, and the flow rate at that time. Stress and strain are related to all these factors, either directly or indirectly. The impact of stress and strain should be interpreted in "dynamic terms" over time rather than at one point. Hence, VILI is minimized by optimizing the Strain (using appropriate PEEP and Vt against available FRC) and stress (transpulmonary inspiratory and expiratory pressures), applied at an optimal respiratory rate and flow. In the pediatric age group, pulmonary mechanics also change as age changes. Moreover, children respond differently to lung injury than adults, adding another layer of complexity to the concept of stress and strain in the pediatric population. Despite this, most knowledge about stress and strain has come from studies in the adult population. Therefore, more extensive studies focussing on pediatric age groups are needed to improve our understanding of stress and strain in pediatric ventilated patients. [ABSTRACT FROM AUTHOR]

Hiccups-like contractions, including hiccups, respiratory myoclonus, and diaphragmatic tremor, refer to involuntary, spasmodic, and inspiratory muscle contractions. They have been repeatedly described in mechanically ventilated patients, especially those with central nervous damage. Nevertheless, their effects on patient-ventilator interaction are largely unknown, and even more overlooked is their contribution to lung and diaphragm injury. We describe, for the first time, how the management of hiccup-like contractions was individualized based on esophageal and transpulmonary pressure measurements in three mechanically ventilated patients. The necessity or not of intervention was determined by the effects of these contractions on arterial blood gases, patient-ventilator synchrony, and lung stress. In addition, esophageal pressure permitted the titration of ventilator settings in a patient with hypoxemia and atelectasis secondary to hiccups and in whom sedatives failed to eliminate the contractions and muscle relaxants were contraindicated. This report highlights the importance of esophageal pressure monitoring in the clinical decision making of hiccup-like contractions in mechanically ventilated patients. [ABSTRACT FROM AUTHOR]

Background and Objectives: Intra-abdominal hypertension (IAH) and acute respiratory distress syndrome (ARDS) are common concerns in intensive care unit patients with acute respiratory failure (ARF). Although both conditions lead to impairment of global respiratory parameters, their underlying mechanisms differ substantially. Therefore, a separate assessment of the different respiratory compartments should reveal differences in respiratory mechanics. Materials and Methods: We prospectively investigated alterations in lung and chest wall mechanics in 18 mechanically ventilated pigs exposed to varying levels of intra-abdominal pressures (IAP) and ARDS. The animals were divided into three groups: group A (IAP 10 mmHg, no ARDS), B (IAP 20 mmHg, no ARDS), and C (IAP 10 mmHg, with ARDS). Following induction of IAP (by inflating an intra-abdominal balloon) and ARDS (by saline lung lavage and injurious ventilation), respiratory mechanics were monitored for six hours. Statistical analysis was performed using one-way ANOVA to compare the alterations within each group. Results: After six hours of ventilation, end-expiratory lung volume (EELV) decreased across all groups, while airway and thoracic pressures increased. Significant differences were noted between group (B) and (C) regarding alterations in transpulmonary pressure (TPP) (2.7 ± 0.6 vs. 11.3 ± 2.1 cmH2O, p < 0.001), elastance of the lung (EL) (8.9 ± 1.9 vs. 29.9 ± 5.9 cmH2O/mL, p = 0.003), and elastance of the chest wall (ECW) (32.8 ± 3.2 vs. 4.4 ± 1.8 cmH2O/mL, p < 0.001). However, global respiratory parameters such as EELV/kg bodyweight (−6.1 ± 1.3 vs. −11.0 ± 2.5 mL/kg), driving pressure (12.5 ± 0.9 vs. 13.2 ± 2.3 cmH2O), and compliance of the respiratory system (−21.7 ± 2.8 vs. −19.5 ± 3.4 mL/cmH2O) did not show significant differences among the groups. Conclusions: Separate measurements of lung and chest wall mechanics in pigs with IAH or ARDS reveals significant differences in TPP, EL, and ECW, whereas global respiratory parameters do not differ significantly. Therefore, assessing the compartments of the respiratory system separately could aid in identifying the underlying cause of ARF.

Thirty years ago, the traditional approach to mechanical ventilation consisted of the normalization of PaCO2 and pH at the expense of using a tidal volume (VT) of 10–15 mL kg-1. But then, the use of 6–8 mL kg-1 became a dogma for ventilating patients either with acute respiratory distress syndrome (ARDS) or without lung disease in the operating theatre. It is currently recognized that even low tidal volumes may be excessive for some patients and insufficient for others, depending on its distribution in the aerated lung parenchyma. To carry out intraoperative protective mechanical ventilation, medical literature has focused on positive end expiratory pressure (PEEP), plateau pressure (Paw plateau), and airway driving pressure (ΔPaw). However, considering its limitations, other parameters have emerged that represent a better reflection of isolated lung stress, such as transpulmonary pressure (PL) and transpulmonary driving pressure (ΔPL). These parameters are less generalized in clinical practice due to the requirement of an oeso­phageal balloon for their measurement and therefore their cumbersome application in the operating theatre. However, its study helps in the interpretation of the rest of the ventilator pressures to optimize intraoperative mechanical ventilation. This article defines and develops protective ventilation parameters, breaks down their determinants, mentions their limitations, and offers recommendations for their use intraoperatively.

Abstract Background The use of pressure-controlled ventilation (PCV) for anesthesia management is becoming more commonly used. Chest drainage is commonly performed after thoracic surgery, and the negative pressure it generates might affect the transpulmonary pressure (TPP). In the present study, we investigated how chest drainage could affect ventilating conditions during PCV. Methods We created a hand-made simple thoracic and lung model, which was connected to an anesthesia machine. The tidal volume (TV) was measured with positive end-expiratory pressure (PEEP) 0 and no chest drainage (baseline), followed by 10 cmH2O PEEP/no drainage, 10 cmH2O PEEP/drainage with − 10 cmH2O and 10 cmH2O PEEP/drainage with − 20 cmH2O. Finally, TV with 20 cmH2O and 30 cmH2O PEEP/no drainage was measured. Driving (inspiratory) pressure was maintained at 20 cmH2O during the whole experiment. Results TV was significantly increased by applying 10 cmH2O PEEP compared with baseline, further increased by applying − 10 cmH2O by drainage, similar to the value with PEEP 20 cmH2O with no drainage (end-tidal TPP of 20 cmH2O for both). TV decreased to

Pneumothorax is a potentially fatal complication in patients with acute respiratory distress syndrome (ARDS), presenting challenges in determining the optimal positive end-expiratory pressure (PEEP) level to prevent atelectasis without exacerbating the pneumothorax. This case report describes the successful application of transpulmonary pressure and electrical impedance tomography (EIT) at the bedside to guide PEEP selection in a patient with ARDS complicated by pneumothorax due to methicillin-resistant Staphylococcus aureus infection. By using minimal PEEP to maintain positive end-expiratory transpulmonary pressure and visualizing lung reopening with EIT, the optimal PEEP level was reaffirmed, even if traditionally considered high. The patient’s condition improved, and successful weaning from the ventilator was achieved, leading to a transfer out of the intensive care unit.Clinical trial registration: https://clinicaltrials.gov/show/NCT04081142, identifier NCT04081142.

Esophageal pressure is the closest estimate of pleural pressure. Changes in esophageal pressure reflect changes in intrathoracic pressure and affect transpulmonary pressure, both of which have multiple effects on right and left ventricular performance. During passive breathing, increasing esophageal pressure is associated with lower venous return and higher right ventricular afterload and lower left ventricular afterload and oxygen consumption. In spontaneously breathing patients, negative pleural pressure swings increase venous return, while right heart afterload increases as in passive conditions; for the left ventricle, end-diastolic pressure is increased potentially favoring lung edema. Esophageal pressure monitoring represents a simple bedside method to estimate changes in pleural pressure and can advance our understanding of the cardiovascular performance of critically ill patients undergoing passive or assisted ventilation and guide physiologically personalized treatments.

Transpulmonary pressure is an essential physiologic concept as it reflects the true pressure across the alveoli, and is a more precise marker for lung stress. To calculate transpulmonary pressure, one needs an estimate of both alveolar pressure and pleural pressure. Airway pressure during conditions of no flow is the most widely accepted surrogate for alveolar pressure, while esophageal pressure remains the most widely measured surrogate marker for pleural pressure. This review will cover important concepts and clinical applications for esophageal manometry, with a particular focus on how to use the information from esophageal manometry to adjust or titrate ventilator support. The most widely used method for measuring esophageal pressure uses an esophageal balloon catheter, although these measurements can be affected by the volume of air in the balloon. Therefore, when using balloon catheters, it is important to calibrate the balloon to ensure the most appropriate volume of air, and we discuss several methods which have been proposed for balloon calibration. In addition, esophageal balloon catheters only estimate the pleural pressure over a certain area within the thoracic cavity, which has resulted in a debate regarding how to interpret these measurements. We discuss both direct and elastance-based methods to estimate transpulmonary pressure, and how they may be applied for clinical practice. Finally, we discuss a number of applications for esophageal manometry and review many of the clinical studies published to date which have used esophageal pressure. These include the use of esophageal pressure to assess lung and chest wall compliance individually which can provide individualized information for patients with acute respiratory failure in terms of setting PEEP, or limiting inspiratory pressure. In addition, esophageal pressure has been used to estimate effort of breathing which has application for ventilator weaning, detection of upper airway obstruction after extubation, and detection of patient and mechanical ventilator asynchrony. [ABSTRACT FROM AUTHOR]

Introduction: Lung protective ventilation (LPV) comprising low tidal volume (VT) and high positive end-expiratory pressure (PEEP) may compromise cerebral perfusion in acute brain injury (ABI). In patients with ABI, we investigated whether LPV is associated with increased intracranial pressure (ICP) and/or deranged cerebral autoregulation (CA), brain compensatory reserve and oxygenation. Methods: In a prospective, crossover study, 30 intubated ABI patients with normal ICP and no lung injury were randomly assigned to receive low VT [6 ml/kg/predicted (pbw)]/at either low (5 cmH2O) or high PEEP (12 cmH2O). Between each intervention, baseline ventilation (VT 9 ml/kg/pbw and PEEP 5 cmH2O) were resumed. The safety limit for interruption of the intervention was ICP above 22 mmHg for more than 5 min. Airway and transpulmonary pressures were continuously monitored to assess respiratory mechanics. We recorded ICP by using external ventricular drainage or a parenchymal probe. CA and brain compensatory reserve were derived from ICP waveform analysis. Results: We included 27 patients (intracerebral haemorrhage, traumatic brain injury, subarachnoid haemorrhage), of whom 6 reached the safety limit, which required interruption of at least one intervention. For those without intervention interruption, the ICP change from baseline to "low VT/low PEEP" and "low VT/high PEEP" were 2.2 mmHg and 2.3 mmHg, respectively, and considered clinically non-relevant. None of the interventions affected CA or oxygenation significantly. Interrupted events were associated with high baseline ICP (p < 0.001), low brain compensatory reserve (p < 0.01) and mechanical power (p < 0.05). The transpulmonary driving pressure was 5 ± 2 cmH2O in both interventions. Partial arterial pressure of carbon dioxide was kept in the range 34–36 mmHg by adjusting the respiratory rate, hence, changes in carbon dioxide were not associated with the increase in ICP. Conclusions: The present study found that most patients did not experience any adverse effects of LPV, neither on ICP nor CA. However, in almost a quarter of patients, the ICP rose above the safety limit for interrupting the interventions. Baseline ICP, brain compensatory reserve, and mechanical power can predict a potentially deleterious effect of LPV and can be used to personalize ventilator settings. Trial registrationNCT03278769. Registered September 12, 2017. [ABSTRACT FROM AUTHOR]

Abstract Background The use of pressure-controlled ventilation (PCV) during one lung ventilation (OLV) has been popular to avoid high airway pressure. We experienced a case of a significant reduction of tidal volume (TV) after commencement of chest tube drainage under PCV following lower lobectomy, which required re-thoracotomy to evaluate the degree of air leak. Case presentation A 70-year-old man was scheduled for a lower lobectomy. OLV was managed by PCV. The driving pressure was set at 15–20 cmH2O with 4 cmH2O of positive end-expiratory pressure (PEEP). A chest drainage tube was placed after completion of lobectomy. To switch OLV to two lung ventilation (TLV), PCV settings were changed to the driving pressure at 10 cmH2O with 4 cmH2O of PEEP, which generated 450 ml of TV. Immediately after applying drainage (−10 cmH2O), TV decreased down to 250 ml. To maintain 450 ml of TV, PCV was switched to volume-controlled ventilation with 450 ml of TV, which raised the plateau pressure close to 24 cmH2O. Re-thoracotomy was done; however, significant findings were not detected. Conclusions We experienced a case of a significant reduction of TV immediately after chest tube drainage following lower lobectomy. Probably, negative intrapleural pressure increased the residual volume, which might have significantly affected the limited lung volume after lobectomy, resulting in decreasing TV during PCV.

Abstract Background Prone positioning in combination with the application of low tidal volume and adequate positive end-expiratory pressure (PEEP) improves survival in patients with moderate to severe acute respiratory distress syndrome (ARDS). However, the effects of PEEP on end-expiratory transpulmonary pressure (Ptpexp) during prone positioning require clarification. For this purpose, the effects of three different PEEP titration strategies on Ptpexp, respiratory mechanics, mechanical power, gas exchange, and hemodynamics were evaluated comparing supine and prone positioning. Methods In forty consecutive patients with moderate to severe ARDS protective ventilation with PEEP titrated according to three different titration strategies was evaluated during supine and prone positioning: (A) ARDS Network recommendations (PEEPARDSNetwork), (B) the lowest static elastance of the respiratory system (PEEPEstat,RS), and (C) targeting a positive Ptpexp (PEEPPtpexp). The primary endpoint was to analyze whether Ptpexp differed significantly according to PEEP titration strategy during supine and prone positioning. Results Ptpexp increased progressively with prone positioning compared with supine positioning as well as with PEEPEstat,RS and PEEPPtpexp compared with PEEPARDSNetwork (positioning effect p

Esophageal pressure (Pes) monitoring is a minimally invasive advanced respiratory monitoring method with the potential to guide ventilation support management. Pes monitoring enables the separation of lung and chest wall mechanics and estimation of transpulmonary pressure, which is recognized as an important risk factor for lung injury during both spontaneous breathing and mechanical ventilation. Appropriate balloon positioning, calibration, and measurement techniques are important to avoid inaccurate results. Both the approach of using absolute expiratory Pes values and the approach based on tidal Pes difference have shown promising results for ventilation adjustments, with the potential to decrease the risk of ventilator-induced lung injury. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Introduction: Positive end-expiratory pressure (PEEP) and prone positioning can improve gas exchange by promoting uniform lung aeration. However, elevated ventilation pressures may increase intracranial pressure (ICP) and disrupt cerebral autoregulation. This study investigated the effects of PEEP on ICP and cerebral autoregulation in a porcine model with healthy lungs and normal ICP, comparing prone and supine positions. Cerebral autoregulation was assessed through cerebrovascular reactivity using the pressure reactivity index (PRx). We also explored whether other baseline variables influenced potential variances in ICP and PRx., Methodology: Twelve anesthetized pigs were randomized to begin in either supine or prone position, across PEEP of 5, 10, 15, and 20 cmH 2 O. Continuous monitoring included esophageal pressure to calculate end-inspiratory and end-expiratory transpulmonary pressures. The ICM+ ® software (University of Cambridge Enterprise, Cambridge, United Kingdom) was used for high-resolution data collection, signal processing and ICP curve analysis. Linear mixed-effects models and ANOVA were used to analyze changes in ICP and PRx and the influence of position. An exploratory correlation analysis was conducted on baseline variables potentially related to the ICP increase., Results: Mean ICP increase was 1.0 mmHg ± 0.9 at 10 cmH 2 O PEEP, 2.0 mmHg ± 1.7 at 15 cmH 2 O PEEP, and 3.1 mmHg ± 1.6 at 20 cmH 2 O PEEP compared to a baseline PEEP of 5 cmH 2 O ( p  < 0.001). The effect of PEEP increase on ICP was not influenced by body position. PRx remained unaffected by PEEP. PEEP-induced increases in ICP were higher in cases of higher baseline ICP, higher central venous pressure, lower respiratory system elastance and lower end-inspiratory and end-expiratory transpulmonary pressures., Conclusion: Increasing PEEP elevates ICP regardless of body position without adversely affecting cerebral autoregulation in a healthy porcine model. Baseline ICP, central venous pressure, respiratory system elastance and end-inspiratory and end-expiratory transpulmonary pressure may influence the magnitude of ICP changes., Competing Interests: Peter Smielewski receives part of the licensing fees for ICM+ software, licensed by Cambridge Enterprise Ltd., University of Cambridge, Cambridge. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2025 Hammervold, Beqiri, Smielewski, Storm, Nielsen, Guérin and Frisvold.)

Abstract Background In robot-assisted laparoscopic prostatectomy (RALP), concerns include the formation of atelectasis and reduced functional residual capacity. The present study aimed to examine the feasibility of positive end-expiratory pressure (PEEP) setting based on transpulmonary pressure (Ptp) as well as the effects of incremental PEEP on respiratory mechanics, blood gases, cerebral oxygenation (rSO2), and hemodynamics. Methods Fourteen male patients who were scheduled to receive RALP were recruited. Patients received mechanical ventilation (tidal volume of 6 mL kg−1) and were placed in Trendelenburg position with positive-pressure capnoperitoneum. PEEP levels were increased from 0 to 15 cmH2O (5 cmH2O per increase) every 30 min. PEEP levels were assessed where end-expiratory Ptp levels of ≥0 cmH2O were achieved (PtpEEP0). Airway pressure, esophageal pressure, cardiac index, and blood gas and rSO2 values were measured after 30 min at each PEEP step and respiratory mechanics were calculated. Results With increasing PEEP levels from 0 to 15 cmH2O or PtpEEP0, the values of PaO2 and respiratory system compliance increased, and the values of driving pressure decreased. The median PEEP level associated with PtpEEP0 was 15 cmH2O. Respiratory system compliance values were higher at PtpEEP0 than those at PEEP5 (P = 0.02). Driving pressure was significantly lower at PtpEEP0 than at PEEP5 (P = 0.0036). The cardiac index remained unchanged, and the values of rSO2 were higher at PtpEEP0 than at PEEP0 (right; P = 0.0019, left; P = 0.036). Conclusions PEEP setting determined by transpulmonary pressure can help achieve higher respiratory system compliance values and lower driving pressure without disturbing hemodynamic parameters.

Introduction: This retrospective study attempted to assess the recruitability of the lungs that were affected by acute respiratory distress syndrome (ARDS) due to COVID-19. This was done with the combined use of transpulmonary pressure monitoring (to limit the stress), measurement of end-expiratory lung volume (EELV) (to measure the actual volume gain and be within limits of strain), electrical impedance tomography (EIT), and compliance (to diagnose overdistension). Recruitment was judged clinically by an increase in the SpO2 values. Methods: Retrospective data from the charts and progress sheets were collected from 27 patients admitted to the intensive care unit (between February 2021 and June 2021) with a ratio of arterial Partial pressure of oxygen (PaO2 in mmHg) to fractional inspired oxygen (FiO2)