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As the pulmonary venous pressure rises, these pressures overwhelm the barriers and fluid enters the alveoli when the pressure is above 25 mmHg. [14] Depending on whether the cause is acute or chronic determines how fast pulmonary edema develops and the severity of symptoms. [12] Some of the common causes of cardiogenic pulmonary edema include:
The alveolar oxygen partial pressure is lower than the atmospheric O 2 partial pressure for two reasons. Firstly, as the air enters the lungs, it is humidified by the upper airway and thus the partial pressure of water vapour (47 mmHg) reduces the oxygen partial pressure to about 150 mmHg.
The increased lung pressure pushes the air out of the lungs. [2] The primary function of ventilation is the replacement of the stale gases in the lungs with oxygen-rich air through the removal of carbon dioxide for oxygenation of the blood. [5] The oxygen is then supplied to the entire body through the circulatory system.
From the punctured lungs or airways, the air travels up the perivascular sheaths and into the mediastinum, from which it can enter the subcutaneous tissues. [17] Spontaneous subcutaneous emphysema is thought to result from increased pressures in the lung that cause alveoli to rupture. [5]
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]
The alveolar air pressure is therefore always close to atmospheric air pressure (about 100 kPa at sea level) at rest, with the pressure gradients that cause air to move in and out of the lungs during breathing rarely exceeding 2–3 kPa. [8] [9] Other muscles that can be involved in inhalation include: [10] External intercostal muscles; Scalene ...