Background: Pathologic conditions resulting in increased intra-abdominal pressure (IAP) can influence respiratory function by altering diaphragmatic function at end-exhalation and by restricting thoracic expansion during tidal ventilation. Increased IAP can reduce lung volume at end-expiration to generate poorly ventilated or collapsed lung units, as indicated by reduced FRC. At end-inspiration, increased IAP drives up plateau pressure, often prompting a modification of ventilatory strategy so as to reduce plateau pressure and potentially damaging transpulmonary forces. Because the relative impact of IAP on these two key parameters of tidal ventilation is not well defined, we evaluated IAP transmission to the esophagus and monitored FRC in a swine model of increased IAP. Methods: Four deeply anesthetized swine were ventilated at f=15, Vt= 10 ml/kg, I:E = 1:2 and PEEP = 1 cmH2O. A tracheostomy tube was surgically inserted into
the peritoneal cavity and a range of IAP levels (0,5,10,15,20,25 mmHg) were randomly applied via a constant positive pressure system. esophageal pressure manometry and FRC measurements (Carestation, GE Healthcare) were obtained at each IAP. Results: Increasing IAP reduced FRC as displayed in figure 1; the majority of the reduction occurring at IAP of 15 mmHg. The esophageal pressure relationship to increasing IAP (figure 2) displays markedly different effects at end-inspiration, as compared to end-expiration. Mean fractional transmission of abdominal to esophageal pressure at end-inspiration was 0.408 and linear over the IAP range studied. Mean fractional transmission of end-expiratory pressure was minimal at 0.037, despite a marked decline in FRC. Conclusions: 1) Increasing intra-abdominal pressure reduces FRC in a curvilinear fashion, but this reduction is not tracked by changes in end-expiratory trans-alveolar pressure. 2) Rising IAP stiffens the most flexible portion of the chest wall, markedly worsening apparent tidal compliance of the respiratory system.