Lung volumes and pressures

Epithelial function in health

Mucociliary clearance by ciliated columnar epithelial cells
Mucus as a contributor to pathogen clearance (eg by use of antitrypsins)
Clinical implications of increased or decreased mucous viscosity in the airways
Roles of type I and type II alveolar pneumocytes
You should cross-reference the principles of lung volumes and pressures to the anatomy


The upper respiratory tract includes the nose, pharynx and larynx; the lower respiratory tract starts at the trachea. The airways, blood vessels and lymphatics enter each lung at the lung root or hilum, where the pulmonary nerve plexus receives autonomic nerves from the vagus and sympathetic trunk.

The vagus contains sensory afferents from lung receptors and bronchoconstrictor parasympathetic efferents leading to the airways; sympathetic nerves are bronchodilatory. Each lung lobe is made up of several wedge-shaped bronchopulmonary segments supplied by their own segmental bronchus, artery and vein.
The bronchial circulation supplies airways down to the terminal bronchioles. Respiratory bronchioles and below obtain nutrients from the pulmonary circulation.

Epithelium and airway clearance

Trachea to the respiratory bronchioles are lined with ciliated columnar epithelial cells. Goblet cells and submucosal glands secrete thick, gel-like mucus. Synchronous beating of the cilia moves the mucus /debris to the mouth (muco-ciliary clearance). Increase in the thickness / viscosity of the mucus (e.g. asthma, cystic fibrosis) or reduced activity of cilia (e.g. smoking) impairs muco-ciliary clearance leading to recurrent infections. Mucus has substances that protect the airways from pathogens (e.g. antitrypsins, lysozyme, immunoglobulin A).

Alveoli and alveolar ducts are lined by unciliated cells, and largely very thin type I alveolar pneumocytes (alveolar cells; squamous epithelium). These form the gas exchange surface with the capillary endothelium (alveolar–capillary membrane). A few type II pneumocytes secrete surfactant which reduces the surface tension and prevents alveolar collapse. Macrophages (mobile phagocytes) in the airways ingest foreign materials and destroy bacteria; in the alveoli, they take the place of cilia by clearing debris.

Knowledge and definitions of typical lung volumes for adults
Tidal volume
Vital capacity
Residual volume
Functional residual capacity
Anatomical and alveolar dead space .


Respiratory muscles
Diaphragm; contraction pulls down the dome, reducing thoracic pressure (negative), and drawing air into the lungs. The external intercostal muscles assist by elevating the ribs and increasing the dimensions of the thoracic cavity.
Quiet breathing is normally diaphragmatic; accessory inspiratory muscles (e.g. scalene, sternomastoids) aid inspiration if airway resistance or ventilation is high.
Expiration is by passive recoil of the lungs and chest wall, but assisted by the contraction of abdominal muscles which speed recoil of the diaphragm by raising abdominal pressure during high rates(e.g. exercise).

Lung volumes and pressures
The tidal volume (TV) – volume of air drawn into and out of the lungs during normal breathing (∼500 mL).
The vital capacity (VC) – maximum tidal volume, when an individual breathes in and out as far as possible.
The difference in volume between a resting and maximum expiration is the expiratory reserve volume (ERV); the equivalent for inspiration is the inspiratory reserve volume (IRV).
The volume in the lungs after a maximum inspiration is the total lung capacity (TLC), and that after a maximum expiration is the residual volume (RV).
The functional residual capacity (FRC) is the volume of the lungs at the end of a normal breath.

The small pleural space, has a negative pressure (intrapleural pressure: –0.2 to –0.5 kPa). Perforation of the chest therefore allows air to be sucked into the pleural space, and the chest wall expands while the lung collapses (pneumothorax).
Fibrosis increases recoil and therefore reduces FRC, whereas in emphysema, recoil is reduced and FRC increases.

During inspiration, the expansion of the thoracic cavity makes the intrapleural pressure more negative, causing the lungs and alveoli to expand, and drawing air into the lungs. During expiration, intrapleural and alveolar pressures rise (Less negative. Positive pressures only during forced expiration like Cough).

The dead space refers to the volume of the airways that does not take part in gas exchange. The anatomical dead space includes the respiratory tract down to the terminal bronchioles; it is normally ∼150 mL.
The alveolar dead space refers to alveoli incapable of gas exchange; in health, it is negligible (can increase in pathologic conditions).
The physiological dead space is the sum of the anatomical and alveolar dead spaces.

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