IntroductionWhen alveoli collapse the traction forces exerted on their walls by adjacent expanded units may increase and concentrate. These forces may promote its re-expansion at the expense of potentially injurious stresses at the interface between the collapsed and the expanded units. We developed an experimental model to test the hypothesis that a local non-lobar atelectasis can act as a stress concentrator, contributing to inflammation and structural alveolar injury in the surrounding healthy lung tissue during mechanical ventilation.MethodsA total of 35 rats were anesthetized, paralyzed and mechanically ventilated. Atelectasis was induced by bronchial blocking: after five minutes of stabilization and pre-oxygenation with FIO2 = 1.0, a silicon cylinder blocker was wedged in the terminal bronchial tree. Afterwards, the animals were randomized between two groups: 1) Tidal volume (VT) = 10 ml/kg and positive end-expiratory pressure (PEEP) = 3 cmH2O (VT10/PEEP3); and 2) VT = 20 ml/kg and PEEP = 0 cmH2O (VT20/zero end-expiratory pressure (ZEEP)). The animals were then ventilated during 180 minutes. Three series of experiments were performed: histological (n = 12); tissue cytokines (n = 12); and micro-computed tomography (microCT; n = 2). An additional six, non-ventilated, healthy animals were used as controls.ResultsAtelectasis was successfully induced in the basal region of the lung of 26 out of 29 animals. The microCT of two animals revealed that the volume of the atelectasis was 0.12 and 0.21 cm3. There were more alveolar disruption and neutrophilic infiltration in the peri-atelectasis region than the corresponding contralateral lung (control) in both groups. Edema was higher in the peri-atelectasis region than the corresponding contralateral lung (control) in the VT20/ZEEP than VT10/PEEP3 group. The volume-to-surface ratio was higher in the peri-atelectasis region than the corresponding contralateral lung (control) in both groups. We did not find statistical difference in tissue interleukin-1β and cytokine-induced neutrophil chemoattractant-1 between regions.ConclusionsThe present findings suggest that a local non-lobar atelectasis acts as a stress concentrator, generating structural alveolar injury and inflammation in the surrounding lung tissue.

The distension index %E(2), derived from the VDSCM considering flow-dependencies, seems able to identify tidal recruitment/overdistension induced by Vt and PEEP independent of flow waveform in healthy lung-anesthetized patients.

PEEPminE1 better identifies the open-lung PEEP independently of the adjusted Vt, and may be a practical, more individualized approach for PEEP titration.

BACKGROUND: Early exercise has been recommended in critically ill patients, but its impact on subject-ventilator interaction is still unclear. Therefore, the aim of this study was to evaluate the occurrence of subject-ventilator asynchrony during passive exercise in mechanically ventilated subjects. METHODS: This study included deeply sedated subjects who were under mechanical ventilation for < 72 h. Subjects were coupled to a cycle ergometer and maintained at rest for 5 min (baseline period). After this period, they started 20 min of passive exercise, followed by 10 min of rest (recovery period). The occurrence of asynchrony was monitored by the analysis of flow and airway pressure waveforms, registered throughout the protocol during the baseline, exercise, and recovery periods. Hemodynamic and respiratory parameters were registered at the end of each period. Finally, arterial blood gas analysis was performed twice, at the end of the baseline period and at the end of the recovery period. RESULTS: 8 subjects were enrolled (63.3 6 16.7 y old, 50% male). The asynchrony index increased during exercise (median 32.1% [interquartile range (IQR) 18.6-47.6%]), compared to baseline (median 6.6% [IQR 3.9-10.4%]), returning to initial levels during the recovery period (median 2.7% [IQR 0-12.2%]). The most frequent types of asynchrony were ineffective triggering (index of 11.8% [IQR 1.2-22.5%] during exercise, compared to 2.0% [IQR 1.4-4.4%] at baseline), and insufficient flow (index of 11.7% [IQR 4.7-19.3%] during exercise, compared to 2.0% [IQR 1.1 to 3.3%] at baseline). There were no significant changes in the hemodynamic and respiratory variables. CONCLUSIONS: Early cycle ergometer passive exercise in deeply sedated subjects can worsen subject-ventilator interaction, due to ineffective triggering and insufficient flow. Adjustments in the ventilatory parameters may be necessary to avoid asynchrony during exercise.