Spontaneous breathing with airway pressure release ventilation favors ventilation in dependent lung regions and counters cyclic alveolar collapse in oleic-acid-induced lung injury: a randomized controlled computed tomography trial.
BACKGROUND
Experimental and clinical studies have shown a reduction in intrapulmonary shunt with spontaneous breathing during airway pressure release ventilation (APRV) in acute lung injury. This reduction was related to reduced atelectasis and increased aeration. We hypothesized that spontaneous breathing will result in better ventilation and aeration of dependent lung areas and in less cyclic collapse during the tidal breath.


METHODS
In this randomized controlled experimental trial, 22 pigs with oleic-acid-induced lung injury were randomly assigned to receive APRV with or without spontaneous breathing at comparable airway pressures. Four hours after randomization, dynamic computed tomography scans of the lung were obtained in an apical slice and in a juxtadiaphragmatic transverse slice. Analyses of regional attenuation were performed separately in nondependent and dependent halves of the lungs on end-expiratory scans and end-inspiratory scans. Tidal changes were assessed as differences between inspiration and expiration of the mechanical breaths.


RESULTS
Whereas no differences were observed in the apical slices, spontaneous breathing resulted in improved tidal ventilation of dependent lung regions (P < 0.05) and less cyclic collapse (P < 0.05) in the juxtadiaphragmatic slices. In addition, with spontaneous breathing, the end-expiratory aeration increased and nonaerated tissue decreased in dependent lung regions close to the diaphragm (P < 0.05 for the interaction ventilator mode and lung region).


CONCLUSIONS
Spontaneous breathing during APRV redistributes ventilation and aeration to dependent, usually well-perfused, lung regions close to the diaphragm, and may thereby contribute to improved arterial oxygenation. Spontaneous breathing also counters cyclic collapse, which is a risk factor for ventilation-associated lung injury.
Wrigge
Hermann
H
Department of Anaesthesiology and Intensive Care Medicine, University of Bonn, Sigmund-Freud-Strasse 25, D-53105 Bonn, Germany. Hermann.Wrigge@ukb.uni-bonn.de
Zinserling
Jörg
J
Neumann
Peter
P
Muders
Thomas
T
Magnusson
Anders
A
Putensen
Christian
C
Hedenstierna
Göran
G
D000818:Animals; D045422:Continuous Positive Airway Pressure / Q000379:methods*; D004195:Disease Models, Animal; D007090:Image Interpretation, Computer-Assisted; D019301:Oleic Acid; D010101:Oxygen Consumption; D011650:Pulmonary Alveoli / Q000503:physiopathology; D011859:Radiography; D011897:Random Allocation; D012016:Reference Values; D012119:Respiration; D012128:Respiratory Distress Syndrome / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000628:therapy*; D013552:Swine; D013990:Tidal Volume; D016896:Treatment Outcome
D019301:Oleic Acid