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Among mechanically ventilated patients, asymmetrical lung injury is probably extremely frequent in the intensive care unit but the lack of standardized measurements does not allow to describe any prevalence among mechanically ventilated patients. Many past studies have focused only on unilateral injury and have mostly described the effect of lateral positioning. The good lung put downward might receive more perfusion while the sick lung placed upward receive more ventilation than supine. This usually results in better oxygenation but can also promote atelectasis in the healthy lung and no consensus has emerged on the clinical indication of this posture. Recently, electrical impedance tomography (EIT) has allowed for the first time to precisely describe the distribution of ventilation in each lung and to better study asymmetrical lung injury. At low positive-end-expiratory pressure (PEEP), a very heterogeneous ventilation exists between the two lungs and the initial increase in PEEP first helps to recruit the sick lung and protect the healthier lung. However, further increasing PEEP distends the less injured lung and must be avoided. The right level can be found using EIT and transpulmonary pressure. In addition, EIT can show that in the two lungs, airway closure is present but with very different airway opening pressures (AOPs) which cannot be identified on a global assessment. This may suggest a very different PEEP level than on a global assessment. Lastly, epidemiological studies suggest that in hypoxemic patients, the number of quadrants involved has a strong prognostic value. The number of quadrants is more important than the location of the unilateral or bilateral nature of the involvement for the prognosis, and hypoxemic patients with unilateral lung injury should probably be considered as requiring lung protective ventilation as classical acute respiratory distress syndrome., Competing Interests: LB's laboratory received research grant from Medtronic and Drager, equipment from Sentec, Fisher Paykel, Philps, and fees for lectures from Fisher Paykel., (Thieme. All rights reserved.)

Rationale: Reverse triggering dyssynchrony (RT) is a patient-ventilator interaction where a respiratory muscle contraction is triggered by a passive mechanical insufflation. Its impact on diaphragm structure and function is unknown. Objectives: To establish an animal model of RT with lung injury receiving lung-protective ventilation and to assess its impact on the structure and function of the diaphragm. Methods: Lung injury was induced by surfactant depletion and high-stress ventilation in 32 ventilated pigs. Animals were allocated to receive passive mechanical ventilation (Vt: 10 ml/kg; respiratory rate [RR]: 30-35 breaths/min; n  = 8) or a more lung-protective strategy (Vt: 6-8 ml/kg; n  = 24) with adjustments in RR to facilitate the occurrence of RT for 3 hours. Diaphragm function (transdiaphragmatic pressure [Pdi] during phrenic nerve stimulation [force/frequency curve]) and structure (biopsies) were assessed. The impact of RT on diaphragm function was analyzed according to the breathing effort assessed by the pressure-time product. Measurements and Main Results: Compared with passive ventilation, the protective ventilation group with RT received significantly lower Vt (7 vs. 10 ml/kg) and higher RR (45 vs. 31 breaths/min). An entrainment pattern of 1:1 was the most frequently occurring in 83% of the animals. Breathing effort induced by RT was highly variable across animals. RT with the lowest tercile of breathing effort was associated with 23% higher twitch Pdi compared with passive ventilation, whereas RT with high breathing effort was associated with a 10% lower twitch Pdi and a higher proportion of abnormal muscle fibers. Conclusions: In a reproducible animal model of RT with variable levels of breathing effort and entrainment patterns, RT with high effort is associated with impaired diaphragm function, whereas RT with low effort is associated with preserved diaphragm force.

Background: An abrupt lung deflation in rodents results in lung injury through vascular mechanisms. Ventilator disconnections during endo-tracheal suctioning in humans often cause cardio-respiratory instability. Whether repeated disconnections or lung deflations cause lung injury or oedema is not known and was tested here in a porcine large animal model., Methods: Yorkshire pigs (~ 12 weeks) were studied in three series. First, we compared PEEP abruptly deflated from 26 cmH 2 O or from PEEP 5 cmH 2 O to zero. Second, pigs were randomly crossed over to receive rapid versus gradual PEEP removal from 20 cmH 2 O. Third, pigs with relative volume overload, were ventilated with PEEP 15 cmH 2 O and randomized to repeated ETT disconnections (15 s every 15 min) or no disconnection for 3 h. Hemodynamics, pulmonary variables were monitored, and lung histology and bronchoalveolar lavage studied., Results: As compared to PEEP 5 cmH 2 O, abrupt deflation from PEEP 26 cmH 2 O increased PVR, lowered oxygenation, and increased lung wet-to-dry ratio. From PEEP 20 cmH 2 O, gradual versus abrupt deflation mitigated the changes in oxygenation and vascular resistance. From PEEP 15, repeated disconnections in presence of fluid loading led to reduced compliance, lower oxygenation, higher pulmonary artery pressure, higher lung wet-to-dry ratio, higher lung injury score and increased oedema on morphometry, compared to no disconnects., Conclusion: Single abrupt deflation from high PEEP, and repeated short deflations from moderate PEEP cause pulmonary oedema, impaired oxygenation, and increased PVR, in this large animal model, thus replicating our previous finding from rodents. Rapid deflation may thus be a clinically relevant cause of impaired lung function, which may be attenuated by gradual pressure release., (© 2022. The Author(s).)

Rationale: Asymmetrical lung injury is a frequent clinical presentation. Regional distribution of Vt and positive end-expiratory pressure (PEEP) could result in hyperinflation of the less-injured lung. The validity of esophageal pressure (Pes) is unknown. Objectives: To compare, in asymmetrical lung injury, Pes with directly measured pleural pressures (Ppl) of both sides and investigate how PEEP impacts ventilation distribution and the regional driving transpulmonary pressure (inspiratory - expiratory). Methods: Fourteen mechanically ventilated pigs with lung injury were studied. One lung was blocked while the contralateral one underwent surfactant lavage and injurious ventilation. Airway pressure and Pes were measured, as was Ppl in the dorsal and ventral pleural space adjacent to each lung. Distribution of ventilation was assessed by electrical impedance tomography. PEEP was studied through decremental steps. Measurements and Results: Ventral and dorsal Ppl were similar between the injured and the noninjured lung across all PEEP levels. Dorsal Ppl and Pes were similar. The driving transpulmonary pressure was similar in the two lungs. Vt distribution between lungs was different at zero end-expiratory pressure (≈70% of Vt going in noninjured lung) owing to different respiratory system compliance (8.3 ml/cm H 2 O noninjured lung vs. 3.7 ml/cm H 2 O injured lung). PEEP at 10 cm H 2 O with transpulmonary pressure around zero homogenized Vt distribution opening the lungs. PEEP ≥16 cm H 2 O equalized distribution of Vt but with overdistension for both lungs. Conclusions: Despite asymmetrical lung injury, Ppl between injured and noninjured lungs is equalized and esophageal pressure is a reliable estimate of dorsal Ppl. Driving transpulmonary pressure is similar for both lungs. Vt distribution results from regional respiratory system compliance. Moderate PEEP homogenizes Vt distribution between lungs without generating hyperinflation.