![]() ![]() In evaluating the relationship between increasing airway pressures and ventilation volumes, no relationship to air leak was demonstrated. ![]() Serum albumin nadir was slightly lower in the air-leak group (2.2 vs 2.4 g/dL). There were also no differences between the groups with respect to degree of illness as measured by APACHE III scores, highest FiO 2, or oxygenation as measured by PaO 2/FiO 2 ratio. ![]() There was no difference in highest peak airway pressure (47 vs 46 cm H 2O), mean airway pressure (24 cm H 2O in both groups), PEEP level (12.6 vs 11.5 cm H 2O), tidal volume in relation to body weight (11.4 vs 11.7 mL/kg), or 30-day mortality (45.5% vs 39%). Patients with air leaks were younger (45 vs 52 years), smaller (72 vs 76 kg), and more likely to be female. There were 77 patients (10.6%) who developed any kind of air leak, including 50 with pneumothorax (6.9%). All patients in the original surfactant study were included. Respiratory variables had been collected every eight hours throughout the period of mechanical ventilation, and the worst values were identified in the control patients (no air leak) and compared to the values immediately preceding the detection of air leak in the barotrauma patients. This has led to nonconventional modes of ventilation in an attempt to prevent this form of iatrogenic "ventilator-induced lung injury." The data analyzed in this paper came from a prospective, randomized, controlled study demonstrating no effect on outcome of aerosolized synthetic surfactant in sepsis-induced adult ARDS (Anzueto A, N Engl J Med 1996 334:1417-1421).ĭata from the 725 patients enrolled in the surfactant study were re-examined for the development of air leak using conventional chest radiography. Nonuniform distribution of involved areas in ARDS has led to a belief that small tidal volume ventilation with low peak airway pressures might protect the lung from further damage. High airway pressures have been blamed for the development of air leaks and worsening of outcome in acute respiratory distress syndrome (ARDS). However, further studies into ventilation methods that minimize barotrauma are needed.Is Barotrauma Related to Airway Pressures? The importance of preventing overdistention by limiting tidal volume, and preventing small airway closure by the use of positive end-expiratory pressure (PEEP) over the lower inflection point is now known. Possible mechanisms behind barotrauma include the overdistention of the lungs by high peak airway pressures or large tidal volumes, shear stress caused by the repeated opening and closing of small airways or alveolar ducts, and the inflammatory process. The significance of these mechanisms in the clinical setting has been recognized in recent years, and the publication of studies on acute respiratory distress syndrome (ARDS) patients has focused attention on the importance of using methods of ventilation that do not cause barotrauma. Animal research has revealed the main pathophysiological mechanisms by which positive pressure ventilation can cause pulmonary barotrauma accompanying the distention of the lungs, and ultimately lead to permeability pulmonary edema. ![]()
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