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At rest, there is a negative intrapleural pressure. This provides a transpulmonary pressure, causing the lungs to expand. If humans didn't maintain a slightly negative pressure even when exhaling, their lungs would collapse on themselves because all the air would rush towards the area of lower pressure. Intra-pleural pressure is sub-atmospheric.
The alveolar pressure is estimated by measuring the pressure in the airways while holding one's breath. [2] The intrapleural pressure is estimated by measuring the pressure inside a balloon placed in the esophagus. [2] Measurement of transpulmonary pressure assists in spirometry in availing for calculation of static lung compliance.
The diaphragm is the most important muscle of respiration, [3] and separates the thoracic cavity, containing the heart and lungs, from the abdominal cavity: as the diaphragm contracts, the volume of the thoracic cavity increases, creating a negative pressure there, which draws air into the lungs. [4]
This negative pressure leads to expansion of the chest, which causes a decrease in intrapulmonary pressure, and increases flow of ambient air into the lungs. As the vacuum is released, the pressure inside the tank equalizes to that of the ambient pressure, and the elastic recoil of the chest and lungs leads to passive exhalation.
The pleural cavity transmits movements of the ribs muscles to the lungs, particularly during heavy breathing. During inhalation the external intercostals contract, as does the diaphragm. This causes the expansion of the chest wall, that increases the volume of the lungs. A negative pressure is thus created and inhalation occurs.
Pulmonary compliance is calculated using the following equation, where ΔV is the change in volume, and ΔP is the change in pleural pressure: = For example, if a patient inhales 500 mL of air from a spirometer with an intrapleural pressure before inspiration of −5 cm H 2 O and −10 cm H 2 O at the end of inspiration.
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. [28]
NPPE develops as a result of significant negative pressure generated in the chest cavity by inspiration against an upper airway obstruction. These negative pressures in the chest lead to increase venous supply to the right side of the heart while simultaneously creating more resistance for the left side of the heart to supply blood to the rest of the body (). [4]