VENTILATION IN THE TRAUMA AND SURGICAL PATIENT

Posttraumatic pulmonary failure was recognized as early as World War I, 49 but the syndrome was not referred to as the acute respiratory distress syndrome (ARDS) until 1967. 7 Prior to that time, ARDS was known by many synonyms, including acute massive collapse of the lung, 49 traumatic wet lung, 13 shock lung, congestive atelectasis, 37 Da Nang lung, 21 respirator lung, 47 and pulmonary microembolism syndrome. 11 Impaired oxygenation, decreased pulmonary compliance, and normal or supranormal cardiac function are the clinical manifestations of ARDS. Histologically, pulmonary inflammatory infiltrates, interstitial and alveolar edema, intra-alveolar hemorrhage, microthrombi, loss of type II pneumocytes, surfactant depletion, hyaline membrane deposition, and fibrosis characterize the syndrome. 29 Recent changes in the management of ARDS have led to improved survival rates; however, the mortality rate for patients who develop ARDS remains high (35%). 45,53,57 Two observations were central to the development of treatment strategies that have resulted in improved survival rates for patients with ARDS. One was the documentation that mechanical ventilation with high airway pressures results in alveolar damage. 20,30,55,56 Pneumothorax, pneumomediastinum, and subcutaneous emphysema have long been recognized as manifestations of pulmonary injury owing to high-pressure ventilation (barotrauma). In addition to these macroscopic findings, decreased surfactant production, hyaline membrane deposition, and neutrophil infiltration in the lung parenchyma can be identified after high-pressure ventilation of normal lungs (alveolar stress injury). 17 The histologic features of the pulmonary injury induced by high-pressure ventilation are similar to the features found in ARDS. Lung injury produced by high-pressure ventilation is caused by alveolar overdistention that not only impedes recovery from ARDS, but may contribute to the progression of the disease. The second critical observation was the discovery that patients with ARDS have areas of diseased and nonfunctional lung intermixed with relatively normal lung areas. These normal or functional areas of lung receive a disproportionately large percentage of the tidal volume because they are more compliant. 23 Thus, overdistention of functional areas of lung occurs even when a normal tidal volume is used because the volume is unevenly distributed owing to regional differences in pulmonary compliance found in patients with ARDS. Alveolar overdistention contributes to the disease process and impedes recovery from ARDS. Although there is no reliable and convenient way to directly measure alveolar volume, airway pressure can be used as an indirect measurement of lung volume (analogous to the use of the Swan-Ganz catheter to estimate the left ventricular volume by measuring the pulmonary artery occlusion pressure). The realization that ventilation with high airway pressures was damaging to the lungs resulted in ARDS treatment strategies that keep peak inspiratory pressures below 35 to 40 cm H 2 O. The primary goal of these strategies is to prevent the pulmonary injury produced by alveolar overdistention.