Repeated endo-tracheal tube disconnection generates pulmonary edema in a model of volume overload: an experimental study

Abstract

Background An abrupt lung deflation in rodents results in lung injury through vascular mechanisms. Ventilator disconnections during endo-tracheal suctioning in humans often cause cardio-respiratory instability. Whether repeated disconnections or lung deflations cause lung injury or oedema is not known and was tested here in a porcine large animal model. Methods Yorkshire pigs (~ 12 weeks) were studied in three series. First, we compared PEEP abruptly deflated from 26 cmH2O or from PEEP 5 cmH2O to zero. Second, pigs were randomly crossed over to receive rapid versus gradual PEEP removal from 20 cmH2O. Third, pigs with relative volume overload, were ventilated with PEEP 15 cmH2O and randomized to repeated ETT disconnections (15 s every 15 min) or no disconnection for 3 h. Hemodynamics, pulmonary variables were monitored, and lung histology and bronchoalveolar lavage studied. Results As compared to PEEP 5 cmH2O, abrupt deflation from PEEP 26 cmH2O increased PVR, lowered oxygenation, and increased lung wet-to-dry ratio. From PEEP 20 cmH2O, gradual versus abrupt deflation mitigated the changes in oxygenation and vascular resistance. From PEEP 15, repeated disconnections in presence of fluid loading led to reduced compliance, lower oxygenation, higher pulmonary artery pressure, higher lung wet-to-dry ratio, higher lung injury score and increased oedema on morphometry, compared to no disconnects. Conclusion Single abrupt deflation from high PEEP, and repeated short deflations from moderate PEEP cause pulmonary oedema, impaired oxygenation, and increased PVR, in this large animal model, thus replicating our previous finding from rodents. Rapid deflation may thus be a clinically relevant cause of impaired lung function, which may be attenuated by gradual pressure release.

Hiccup-like Contractions in Mechanically Ventilated Patients: Individualized Treatment Guided by Transpulmonary Pressure

“…Additionally, they promote high transpulmonary pressure and large tidal volume, both linked to lung damage. Animal studies have shown that abrupt deflation, following a sustained lung inflation, could induce acute lung injury mediated by acute left ventricular decompensation as a result of increased left ventricular preload and afterload [ 11 , 15 ]. Finally, diaphragmatic contractions may elicit lung injury irrespective of VT changes, secondary to a phenomenon known as ‘Pendelluft’.…”

Spontaneous Breathing and Pendelluft in Patients with Acute Lung Injury: A Narrative Review

“…This phenomenon has been described in patients with vigorous inspiratory effort against airway obstruction and is also called post-obstructive pulmonary edema [23]. In animal studies, abrupt deflation after sustained inflation, which is associated with a dramatic decrease in intrapulmonary pressure, could cause acute lung injury mediated by the significant vascular leakage and acute decompensation of the left ventricle [24,25]. These data imply that lung injury may also be caused by the abrupt and large change in intrathoracic pressure.…”

Role of cardiopulmonary interactions in development of ventilator-induced lung injury—Experimental evidence and clinical Implications

“…A similar experimental plan was performed in a porcine model (Katira et al, 2022), wherein the increase in LVEDP was not…”

“…Modulation of mechanical ventilation to optimize the CP interactions may help reduce forces on both sides of alveolar capillary membrane. Moreover, limiting lung deflations due to ventilator disconnections not only improves lung function but may also reduce lung injury from atelectasis and vascular forces (Maggiore et al, 2003;Maggiore et al, 2013;Katira et al, 2022).…”

“…the airway pressures, Paw; tidal volume, Vt; and airflow) on the development of VILI, as well their respective impact on the pulmonary vasculature. More recently, experimental evidence has illustrated the contribution of the heart and its interaction with the lungs in the generation of lung injury through changes in both microvascular permeability and endothelial injury (Katira et al, 2017a;Katira et al, 2018;Katira et al, 2022).…”