Abstract

In acute lung injury, atelectasis is common and frequently develops in the dependent and diaphragmatic regions. Attempts to recruit lung with positive pressure constitute a major aim in the management of acute respiratory distress syndrome but are associated with overdistension and injury in nonatelectatic regions. To test the hypothesis that continuous negative abdominal pressure using an iron lung would augment positive end-expiratory pressure in recruiting atelectatic lung. An in vivo rabbit model of ventilator-induced lung injury was used in which a recruitment maneuver followed by positive end-expiratory pressure (110 cm H2O) had no effect on oxygenation. Addition of sustained continuous negative abdominal pressure (-5 cm H2O) to the positive end-expiratory pressure significantly increased the end-expired lung volume and PaO2 but impaired ventricular preload and cardiac output (suggested by echocardiography). Addition of transient (15 mins) continuous negative abdominal pressure resulted in comparable and lasting (60 mins) increases in PaO2. Sustained, but not transient, continuous negative abdominal pressure was associated with hemodynamic depression and lactic acidosis, which appeared (illustrative echocardiography, n = 2) to be caused by decreased cardiac preload. Computerized tomography (n = 2) suggested that continuous negative abdominal pressure was an effective adjunct to positive end-expiratory pressure for recruiting atelectasis in dependent and diaphragmatic regions. In surfactant-depleted but noninjured lungs, sustained continuous negative abdominal pressure augmented lung recruitment and oxygenation in the setting of higher (but not lower) levels of positive end-expiratory pressure and reduced central venous oxygenation. Continuous negative abdominal pressure may be a potential adjunct to positive end-expiratory pressure in the recruitment of diaphragmatic atelectasis. The approach ultimately might be useful when ceilings exist on the level of desired positive end-expiratory pressure.

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