Intra-abdominal pressure transmission to the thorax is predominantly at end-inspiration. Experimental intra-abdominal pressure symmetrically influences bladder pressure and airway plateau pressure
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Background: Pathologic conditions that increase intra-abdominal pressure (IAP) can influence respiratory function by altering diaphragmatic function at end-exhalation and by restricting thoracic expansion. 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, prompting a modification of ventilatory strategy to reduce plateau pressure and damaging transpulmonary forces. Because the 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 CPAP system. Esophageal pressure and FRC were obtained at each IAP. Results: Increasing IAP reduced FRC; the majority of the reduction occurring at IAP of 15 mmHg. The esophageal pressure relationship to increasing IAP had different effects at end-inspiration compared to end-expiration. Transmission of abdominal to esophageal pressure at end-inspiration was 0.408. Transmission of end-expiratory pressure was minimal at 0.037, despite a decline in FRC. Conclusions: 1) Increasing intra-abdominal pressure reduces FRC 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 tidal compliance of the respiratory system.