Mechanical ventilation consistent with clinical practice did not generate excessive regional strain in heterogeneously aerated supine lungs. However, it allowed worsening of spatial strain distribution in these lungs, associated with increased inflammation. Our results support the implementation of early aeration homogenization in normal lungs.

Parenchymal strain is a key determinant of lung injury produced by mechanical ventilation. However, imaging estimates of volumetric tidal strain (ε = regional tidal volume/reference volume) present substantial conceptual differences in reference volume computation and consideration of tidally recruited lung. We compared current and new methods to estimate tidal volumetric strains with computed tomography, and quantified the effect of tidal volume (V) and positive end-expiratory pressure (PEEP) on strain estimates. Eight supine pigs were ventilated with V = 6 and 12 ml/kg and PEEP = 0, 6, and 12 cmHO. End-expiratory and end-inspiratory scans were analyzed in eight regions of interest along the ventral-dorsal axis. Regional reference volumes were computed at end-expiration (with/without correction of regional V for intratidal recruitment) and at resting lung volume (PEEP = 0) corrected for intratidal and PEEP-derived recruitment. All strain estimates demonstrated vertical heterogeneity with the largest tidal strains in middependent regions (P < 0.01). Maximal strains for distinct estimates occurred at different lung regions and were differently affected by V-PEEP conditions. Values consistent with lung injury and inflammation were reached regionally, even when global measurements were below critical levels. Strains increased with V and were larger in middependent than in nondependent lung regions. PEEP reduced tidal-strain estimates referenced to end-expiratory lung volumes, although it did not affect strains referenced to resting lung volume. These estimates of tidal strains in normal lungs point to middependent lung regions as those at risk for ventilator-induced lung injury. The different conditions and topography at which maximal strain estimates occur allow for testing the importance of each estimate for lung injury.

BACKGROUND: Pneumoperitoneum and nonphysiological positioning required for robotic surgery increase cardiopulmonary risk because of the use of larger airway pressures (Paws) to maintain tidal volume (Vt). However, the quantitative partitioning of respiratory mechanics and transpulmonary pressure (Pl) during robotic surgery is not well described. We tested the following hypothesis: (1) the components of driving pressure (transpulmonary and chest wall components) increase in a parallel fashion at robotic surgical stages (Trendelenburg and robot docking); and (2) deep, when compared to routine (moderate), neuromuscular blockade modifies those changes in Pls as well as in regional respiratory mechanics. METHODS: We studied 35 American Society of Anesthesiologists (ASA) I-II patients undergoing elective robotic surgery. Airway and esophageal balloon pressures and respiratory flows were measured to calculate respiratory mechanics. Regional lung aeration and ventilation was assessed with electrical impedance tomography and level of neuromuscular blockade with acceleromyography. During robotic surgical stages, 2 crossover randomized groups (conditions) of neuromuscular relaxation were studied: Moderate (1 twitch in the train-of-four stimulation) and Deep (1–2 twitches in the posttetanic count). RESULTS: Pneumoperitoneum was associated with increases in driving pressure, tidal changes in Pl, and esophageal pressure (Pes). Steep Trendelenburg position during robot docking was associated with further worsening of the respiratory mechanics. The fraction of driving pressures that partitioned to the lungs decreased from baseline (63% ± 15%) to Trendelenburg position (49% ± 14%, P < .001), due to a larger increase in chest wall elastance (Ecw; 12.7 ± 7.6 cm H2O·L−1) than in lung elastance (El; 4.3 ± 5.0 cm H2O·L−1, P < .001). Consequently, from baseline to Trendelenburg, the component of Paw affecting the chest wall increased by 6.6 ± 3.1 cm H2O, while Pls increased by only 3.4 ± 3.1 cm H2O (P < .001). Pl and driving pressures were larger at surgery end than at baseline and were accompanied by dorsal aeration loss. Deep neuromuscular blockade did not change respiratory mechanics, regional aeration and ventilation, and hemodynamics. CONCLUSIONS: In robotic surgery with pneumoperitoneum, changes in ventilatory driving pressures during Trendelenburg and robot docking are distributed less to the lungs than to the chest wall as compared to routine mechanical ventilation for supine patients. This effect of robotic surgery derives from substantially larger increases in Ecw than Els and reduces the risk of excessive Pls. Deep neuromuscular blockade does not meaningfully change global or regional lung mechanics.