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Bronchiectasis is a disease in which there is permanent enlargement of parts of the airways of the lung. [5] Symptoms typically include a chronic cough with mucus production. [ 3 ] Other symptoms include shortness of breath , coughing up blood , and chest pain. [ 2 ]
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 nose warms and humidifies air more efficiently than the mouth. A slow drink of warm water may help relieve pain associated with the burning sensation in the lungs.
The residual volume, the volume of air left in the lungs following full expiration, is often increased in COPD, as is the total lung capacity, while the vital capacity remains relatively normal. The increased total lung capacity (hyperinflation) can result in the clinical feature of a barrel chest – a chest with a large front-to-back diameter ...
Areas of emphysema are abnormal, air-filled spaces that usually do not have visible walls, [5] and bullae are very thin walled (<1 mm). [2] Cystic bronchiectasis is irreversible bronchial dilation, which is permanent widening of the bronchioles (small airways) in the lung. [2]
Respiratory diseases, or lung diseases, [1] are pathological conditions affecting the organs and tissues that make gas exchange difficult in air-breathing animals. They include conditions of the respiratory tract including the trachea, bronchi, bronchioles, alveoli, pleurae, pleural cavity, the nerves and muscles of respiration.
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.
In 1976, the first report of the occurrence of familial bronchiectasis in siblings was published, and it supported the theory that WCS was congenital, based on the uniformity of the cartilaginous defect. [13] [9] [10] It may have been the result of an autosomal recessive mutation, but the specific gene has not yet been identified. [3]