CT scan of the chest showing a<unk>  on the person's left side (right side on the image). A chest tube is in place (small black mark on the right side of the image), the air-filled pleural cavity (black) and ribs (white) can be seen. The heart can be seen in the center. The thoracic cavity is the space inside the chest that contains the lungs, heart, and numerous major blood vessels. On each side of the cavity, a pleural membrane covers the surface of lung (visceral pleura) and also lines the inside of the chest wall (parietal pleura). Normally, the two layers are separated by a small amount of lubricating serous fluid. The lungs are fully inflated within the cavity because the pressure inside the airways (intrapulmonary pressure) is higher than the pressure inside the pleural space (intrapleural pressure). Despite the low pressure in the pleural space, air does not enter it because there are no natural connections to an air-containing passage, and the pressure of gases in the bloodstream is too low for them to be forced into the pleural space. Therefore, a<unk>  can only develop if air is allowed to enter, through damage to the chest wall or damage to the lung itself, or occasionally because microorganisms in the pleural space produce gas. Once air enters the pleural cavity, the intrapleural pressure increases resulting in the difference between the intrapulmonary pressure and the intrapleural pressure (defined as the transpulmonary pressure) to equal zero which cause the lungs to deflate in contrast to a normal transpulmonary pressure of ~4 mm Hg. Chest-wall defects are usually evident in cases of injury to the chest wall, such as stab or bullet wounds ("open<unk> "). In secondary spontaneous<unk> es, vulnerabilities in the lung tissue are caused by a variety of disease processes, particularly by rupturing of bullae (large air-containing lesions) in cases of severe emphysema. Areas of necrosis (tissue death) may precipitate episodes of<unk> , although the exact mechanism is unclear. Primary spontaneous<unk>  (PSP) has for many years been thought to be caused by "blebs" (small air-filled lesions just under the pleural surface), which were presumed to be more common in those classically at risk of<unk>  (tall males) due to mechanical factors. In PSP, blebs can be found in 77% of cases, compared to 6% in the general population without a history of PSP. As these healthy subjects do not all develop a<unk>  later, the hypothesis may not be sufficient to explain all episodes; furthermore,<unk>  may recur even after surgical treatment of blebs. It has therefore been suggested that PSP may also be caused by areas of disruption (porosity) in the pleural layer, which are prone to rupture. Smoking may additionally lead to inflammation and obstruction of small airways, which account for the markedly increased risk of PSPs in smokers. Once air has stopped entering the pleural cavity, it is gradually reabsorbed. Tension<unk>  occurs when the opening that allows air to enter the pleural space functions as a one-way valve, allowing more air to enter with every breath but none to escape. The body compensates by increasing the respiratory rate and tidal volume (size of each breath), worsening the problem. Unless corrected, hypoxia (decreased oxygen levels) and respiratory arrest eventually follow.
Pneumothorax
Hemothorax
Pneumatosis
Chylothorax
Costochondritis
Urinothorax
Traumatic cardiac arrest
Hydropneumothorax