Tension Pneumothorax: Etiology, Diagnosis, Pathophysiology, and Management

Abstract

The normally air-free pleural cavity exists at subatmospheric pressure to promote pleural apposition and proper lung excursion. Owing to its unique bilayer structure, air introduced into this space either from within the thoracic cavity or from an extrathoracic source causes pleural separation and simple pneumothorax (PTX). Most simple pneumothoracies of a small or static volume in healthy patients do not appreciably impair cardiopulmonary function despite variable collapse of the lung. If increasing pressure develops within this pleural air collection, however, a cascade of pathophysiological changes can result from altered anatomical positions of heart, lung, and great vessels. The development of increasing pressure within the pleural space, with resultant ipsilateral lung collapse and hemithoracic expansion into the mediastinum and the contralateral lung, is termed tension pneumothorax (TPTX). The exact incidence of TPTX is unknown, but it is reported in up to 2 to 3% of all pneumothoracies. Certain medical and surgical disease states—many found within the critical care environment—place patients at higher risk for development of TPTX and also limit physiological tolerance to TPTX once it occurs. Although physical examination and chest radiography generally confirm the occurrence of TPTX, physiological monitoring may herald the development of increasing intrapleural pressure. Expeditious recognition and pleural decompression are necessary to prevent the untoward hemodynamic and respiratory consequences of TPTX. Significant morbidity and mortality may arise from TPTX if treatment is unduly delayed, particularly in mechanically ventilated patients.