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Learning Objectives
The student will be able to define atelectasis and distinguish its various forms.
The student will be able to describe the pathophysiology and morphology of pulmonary edema, thromboembolism, hypertension, Goodpasture's syndrome, and Wegener's granulomatosis.
The student will be able to distinguish acute from chronic radiation pneumonitis and acute from chronic rejection of pulmonary allografts.
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Atelectasis describes a reduction in lung volume due to incomplete expansion of airspaces or, more commonly, the collapse of previously inflated pulmonary parenchyma. In atelectasis, perfusion of such nonventilated lung creates a physiological shunt that mixes inadequately oxygenated blood from pulmonary arteries with better oxygenated blood in the pulmonary veins (Chap. 9). If the ventilation-perfusion mismatch is sufficiently severe, systemic hypoxemia results. Additionally, atelectatic lung is more likely to become infected. Atelectasis can be subdivided by its pathogenesis.
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In resorption atelectasis (also known as obstruction atelectasis), air is prevented from reaching distal airspaces because of airway obstruction. Then, as more distal air is absorbed, the previously expanded lung collapses. The extent of involvement is determined by the level of obstruction: Obstruction of a major airway can result in collapse of an entire lobe. Most commonly, a mucous or mucopurulent plug is responsible for the obstruction, although any physical obstruction will suffice. In resorption atelectasis, the mediastinum shifts toward the affected side.
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In compression atelectasis (also known as passive atelectasis and as relaxation atelectasis), accumulation of space-occupying material within the pleural space mechanically compresses the lung parenchyma (Fig. 26.1). Compression atelectasis complicates pleural effusion and pneumothorax (see below), as well as pleural tumors (Chap. 31). Additionally, compression atelectasis of basal lung zones complicates peritoneal effusion (ascites) and frequently occurs in bedridden patients due to diaphragmatic elevation. In compression atelectasis, the mediastinum shifts away from the affected side.
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Microatelectasis complicates adult and neonatal respiratory distress syndromes (Chaps. 23 and 39) as well as interstitial inflammatory lung diseases (Chap. 23). Its pathogenesis involves a complex set of events, the most important being deactivation of surfactant in the mature lung or its inadequate synthesis in neonatal lung.
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In the setting of localized or generalized pulmonary fibrosis, the foci of fibrosis contract largely due to the action of myofibroblasts, collapsing adjacent lung tissue and resulting in contraction atelectasis or cicatrization atelectasis.
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Generally, resorption atelectasis, compression atelectasis, and microatelectasis are reversible, while contraction atelectasis is not.