Pulmonary Consequences of Harnessing the Thoracic Pump

Abstract

Background: Intrathoracic pressure regulation (ITPR) utilizes a device that enhances venous return to the heart and cardiac preload by inducing negative end expiratory pressure in mechanically ventilated patients. Recent findings from a porcine model did not show appreciable effect on mean arterial pressure (MAP), however a potential harmful pulmonary effect of the ITPR device in the setting of lung injury was identified, therefore necessitating further investigation.

Methods: Intubated and mechanically ventilated swine underwent a combination of hemorrhage with or without lung injury. With the animals in group 1 only, repeated bronchoalveolar lavage was performed until a PaO₂:FIO₂ (P:F) ratio of < 250 was reached. All animals underwent pressure-controlled hemorrhage to a MAP of 40 ± 5 mm Hg. The ITPR device was started at a setting of -3 cm H₂O and incrementally decreased by 3 cm H₂O after 30 minutes on each setting with 15 minutes of recovery to a nadir of -12 cm H₂O with group 1. The ITPR device was set to -12 cm H₂O and operated continuously for 2 hours with group 2. Vital signs, lung mechanics, and arterial blood gases were recorded every 30 minutes. Lungs were extracted following euthanasia for gross examination and histology.

Results: Group 1 animals demonstrated a lower partial pressure of oxygen and P/F ratio at the -12 mm Hg device setting compared to baseline. Group 2 animals, demonstrated increased plateau pressures and decreased lung compliance, end expiratory lung volume, and P/F ratio at 30 and 90-minute time points compared to baseline. Lung gross and histologic analysis showed heavily damaged and hemorrhagic lungs without undergoing lung injury compared to control pig lungs from the previously published study in which there were no injury or ITPR use. Lungs from ITPR over 2 hours grossly appeared worse than lungs exposed to lung injury.

Conclusions: In this study, ITPR provided a modest increase in MAP following hemorrhage but was not without untoward pulmonary consequences. With group 1 there was a reduction in oxygenation found when the device was utilized at the -12 mm Hg setting. However, in group 2 worsening in oxygenation and pulmonary mechanics was observed, that changed early in the ITPR device use and remained through the 2-hour ITPR application. Gross pathology showed noticeable lung damage. These results support our previous findings that demonstrate potential pulmonary damage caused by the ITPR device use even with short term use.

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