Tension pneumothorax is variously defined but is generally thought of as a pneumothorax in which the pressure of intrapleural gas exceeds atmospheric pressure, producing adverse effects, including mediastinal shift associated with cardiovascular collapse, often attributed to reduced venous return and kinking of the great vessels. The mechanism of tension pneumothorax is said to be a valvular defect in the visceral pleura such that air enters the pleural space in inspiration but cannot exit in expiration, leading to a progressive increase in pressure. However, as the driving pressure forcing air into the pleura in inspiration is atmospheric pressure, the pleural pressure can never exceed 1 atm during inspiration in a spontaneously breathing subject. Furthermore, all pneumothoraces must have pressures greater than atmospheric during expiration, or conventional treatment with intercostal tube drainage would not work. Pilot experiments have failed to show any re-entry of pleural gas into the lung in patients with persistent air leaks but no evidence of tension, suggesting these behave as valvular pneumothoraces. Case reports of tension pneumothorax in spontaneously breathing patients are rare, and most patients have other explanations for clinical deterioration. Although a large and rapidly expanding pneumothorax may require urgent intervention, it is unlikely that the effects are mediated by high intrapleural pressures. The term tension pneumothorax in spontaneously breathing patients should be reconsidered.