![(A–C; left) Airway pressure-volume curves during low-flow inflation before pneumoperitoneum in the supine position (starting from zero end-expiratory pressure [B] and positive end-expiratory pressure [PEEP] = 5 cm H2O [A]) and after pneumoperitoneum in the Trendelenburg position (starting from PEEP = 5 cm H2O [C]). In the box, we report the pressure (ΔPAW) and volume changes along with the corresponding compliance (C) between start of inflation and airway opening pressure (AOP). Note that this compliance suggests gas compression in an occluded circuit and, hence, complete airway closure.1 Note that, as described in the main text, pneumoperitoneum increases the AOP (and hence the inflation volume needed to overcome it). (A–C; right) Transpulmonary pressure-volume curves during low-flow inflation before pneumoperitoneum in the supine position (starting from zero end-expiratory pressure [B] and PEEP = 5 cm H2O [A]) and after pneumoperitoneum in the Trendelenburg position (starting from PEEP = 5 cm H2O [C]). Transpulmonary pressure (PL) at which AOP is overcome (reported in the box) remains constant after pneumoperitoneum induction, as AOP increases consistently with the rise in esophageal pressures (PES). In other words, the pneumoperitoneum inflation pressure is transmitted to the pleural space, thus increasing PES and AOP in a consistent manner. (D) Multiple pressure-volume curves of the transalveolar pressure (i.e., transpulmonary pressure with patent airways, left) and PES (right) recorded during low-flow inflation and plotted starting from measured end-expiratory lung volume, before pneumoperitoneum in the supine position and after pneumoperitoneum in the Trendelenburg position, respectively. The absence of change in the transalveolar pressure-volume curve indicates that lung recruitment is unmodified, while the esophageal pressure-volume curves show a shift that describes the change in the conditions of the chest wall after pneumoperitoneum: end-expiratory PES is raised by 18 cm H2O, and chest wall compliance is reduced.](https://asa2.silverchair-cdn.com/asa2/content_public/journal/anesthesiology/131/1/10.1097_aln.0000000000002662/3/19ff02.png?Expires=1716474058&Signature=Q3se8f3R37Fa6EBN5ESiy7sHsKae5~vRFsKYOW6Pv4NwoAgCQkIW9iJ~4kBp2tolvY~sdKGuQTXbbcvMa9~jFVDG-rbkg5IrgXjvMx8ezktn5gQ7~hxh1G8~apimOIIudr1LOB5Kst54l7kOmPg~88zXW~gzWYjjU2GZ-1HrMLtPxzWZKzgdWyP8Qhx9i9rYw0DXRcBvmtPbThNx7286dUXzxNCYE9mMO3rrn4Ml1T3Q7v4XrFSqDeSLffIHDynpgpzzJ0tKYPOLZn4F0U9GYkFDMZXVqBvG~hr2dThzGT-ywe6HfYoqBKwjUHZ3iRw5tEe1jP0eKZYXuBuNjKEiSA__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)
(A–C; left) Airway pressure-volume curves during low-flow inflation before pneumoperitoneum in the supine position (starting from zero end-expiratory pressure [B] and positive end-expiratory pressure [PEEP] = 5 cm H2O [A]) and after pneumoperitoneum in the Trendelenburg position (starting from PEEP = 5 cm H2O [C]). In the box, we report the pressure (ΔPAW) and volume changes along with the corresponding compliance (C) between start of inflation and airway opening pressure (AOP). Note that this compliance suggests gas compression in an occluded circuit and, hence, complete airway closure.1 Note that, as described in the main text, pneumoperitoneum increases the AOP (and hence the inflation volume needed to overcome it). (A–C; right) Transpulmonary pressure-volume curves during low-flow inflation before pneumoperitoneum in the supine position (starting from zero end-expiratory pressure [B] and PEEP = 5 cm H2O [A]) and after pneumoperitoneum in the Trendelenburg position (starting from PEEP = 5 cm H2O [C]). Transpulmonary pressure (PL) at which AOP is overcome (reported in the box) remains constant after pneumoperitoneum induction, as AOP increases consistently with the rise in esophageal pressures (PES). In other words, the pneumoperitoneum inflation pressure is transmitted to the pleural space, thus increasing PES and AOP in a consistent manner. (D) Multiple pressure-volume curves of the transalveolar pressure (i.e., transpulmonary pressure with patent airways, left) and PES (right) recorded during low-flow inflation and plotted starting from measured end-expiratory lung volume, before pneumoperitoneum in the supine position and after pneumoperitoneum in the Trendelenburg position, respectively. The absence of change in the transalveolar pressure-volume curve indicates that lung recruitment is unmodified, while the esophageal pressure-volume curves show a shift that describes the change in the conditions of the chest wall after pneumoperitoneum: end-expiratory PES is raised by 18 cm H2O, and chest wall compliance is reduced.
