Which of the following statement(s) is/are true concerning the pulmonary response to shock?

c. The initial physiologic changes of ARDS involve the capillary endothelial cells and the type I pneumocyte

d. Mechanisms proposed in the pathogenesis of ARDS include injury from mediators of inflammation elsewhere and from activated cellular elements

e. A decrease in lung compliance may result from the loss of type I pneumocytes

Contributing pathophysiologic processes to the pulmonary manifestations of shock include the pulmonary component of the cardiovascular response, disruption of the normal lung mechanics, and acute lung injury or ARDS due to sepsis. Pulmonary function may be further compromised by pathology intrinsic to the lung itself, including pulmonary contusion, aspiration, airway obstruction, pneumonia, pneumothorax, hemothorax, and atelectasis. The acute pulmonary vascular response to shock largely parallels that of the systemic vasculature. The increase in pulmonary vascular resistance, which may proportionally exceed that of the systemic circulation, transiently accompanies the systemic adrenergic response. ARDS is a syndrome of progressive lung injury that may arise as a direct consequence of shock or other disease processes. The characteristic findings of ARDS are the presence of pulmonary edema, hypoxemia, and significantly decreased lung compliance. The pulmonary edema is noncardiac in origin and occurs in the face of normal left heart pressures. The hypoxemia results from the development of intrapulmonary shunting and perfusion of under and nonventilated alveoli. The decrease in lung compliance results from the loss of surfactant and lung volume in combination with the presence of interstitial fluid and alveolar edema. Progressive histologic changes of ARDS become apparent in pulmonary capillaries, interstitium, and alveoli. Initially, interstitial edema develops with swelling of the capillary endothelial cells and the type I pneumocytes. The type I pneumocytes subsequently slough, and alveolar edema ensues. Functional surfactant is lost with a significant increase in alveoli opening pressure and decrease in alveolar surface tension. Mechanisms proposed in the pathogenesis of ARDS include injury from mediators of inflammation elaborated elsewhere, and from activated cellular blood elements.