The pleurae are serous membranes that surround each lung: the parietal pleura lines the thoracic wall continuous with visceral pleura closely applied to the lung surface. At the hilum of each lung, the parietal and visceral pleurae are contiguous. The intrapleural space has sub-atmospheric pressure due to the inherent tendency of the chest wall to expand and the lung to collapse from elastic recoil.

Primary spontaneous pneumothorax seems to result from rupture of a subpleural bleb, usually in an upper lobe.7 These blebs are multiple and have increased wall tension allowing distention and eventual rupture. The mechanism of bleb formation remains unknown, but higher upper lobe transpulmonary pressure, local ischemia from decreased upper lobe blood flow, and subclinical emphysema-like changes have been postulated.37

Chronic obstructive pulmonary disease (COPD) accounts for most cases of secondary spontaneous pneumothorax.4 Other causes include cystic fibrosis, pulmonary infections, interstitial lung disease, AIDS, neoplasms, and drug use. Pneumothorax occurs in 5 percent of AIDS patients, is associated with subpleural necrosis from Pneumocystis infection, and carries a high mortality.8 Because of necrosis of lung tissue and continued air leak, simple aspiration and nondrainage techniques fail in this group of patients.8

Once there is a break in the pleura, air travels down a pressure gradient into the intrapleural space until pressure equilibrium occurs with partial or total lung collapse.9 Altered ventilation perfusion relationships and decreased vital capacity then contribute to dyspnea and hypoxemia.

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