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The mammalian lung is the largest internal surface in any vertebrate body. Folded into the chest cavity of an adult human is approximately 70 m² of alveolar epithelium — roughly the area of half a tennis court — separated from the pulmonary blood by less than 1 μm of tissue. This surface is the terminus of a branching airway tree that begins at the larynx and ends, twenty-three generations of branching later, in some 300 million alveoli. The whole structure is ventilated tidally — air in, air out, through the same passages — by a muscular pump that uses Boyle's law to convert volume changes into pressure differences. This lesson examines the conducting airways, the respiratory zone, the ventilation mechanism, the surfactant system that keeps alveoli open, and the clinical conditions that disrupt each component. The lung is a textbook application of every principle from Lesson 0 — vast internal surface area, minimal diffusion distance, steep gradient maintained by ventilation.
This lesson maps to AQA 7402 Section 3.3.2 — Gas exchange (refer to the official AQA specification document for exact wording). The specification requires that students understand the gross structure of the human gas exchange system, the essential features of the alveolar epithelium as a surface over which gas exchange takes place, and the mechanism of pulmonary ventilation.
Air enters via the nose or mouth, passes through the pharynx and larynx, and descends the trachea — a flexible tube reinforced by C-shaped rings of hyaline cartilage that prevent collapse during inspiration. The trachea bifurcates at the carina into the left and right primary bronchi, which enter the lungs and divide into secondary (lobar) bronchi, tertiary (segmental) bronchi, and progressively finer branches. The transition from bronchus to bronchiole is structural: bronchi contain cartilage, bronchioles do not. The smallest bronchioles (terminal bronchioles, ~0.5 mm diameter) lead into the respiratory bronchioles, which carry occasional alveoli budding from their walls, and then into the alveolar ducts and finally the alveolar sacs — clusters of alveoli sharing a common opening.
flowchart TD
T[Trachea<br/>~12 mm bore<br/>C-shaped cartilage rings] --> PB[Primary bronchi<br/>complete cartilage rings]
PB --> SB[Secondary, tertiary bronchi<br/>cartilage plates]
SB --> BR[Bronchioles<br/>smooth muscle<br/>no cartilage]
BR --> TB[Terminal bronchioles<br/>~0.5 mm]
TB --> RB[Respiratory bronchioles<br/>occasional alveoli on wall]
RB --> AD[Alveolar ducts]
AD --> AS[Alveolar sacs]
AS --> AL[Alveoli<br/>~300 million per lung<br/>~70 m² total surface]
The total airway path comprises a conducting zone (trachea to terminal bronchioles, 16 generations, no gas exchange) and a respiratory zone (respiratory bronchioles to alveoli, 7 further generations, all gas exchange). The conducting zone is the anatomical dead space — roughly 150 mL in a human — through which inspired air passes without exchange.
The conducting airways are lined with pseudostratified ciliated columnar epithelium interspersed with mucus-secreting goblet cells. Each ciliated cell carries ~200 motile cilia, each ~6 μm long, beating at ~12 Hz in a coordinated metachronal wave that drives mucus upward at ~1 cm min⁻¹. The goblet cells secrete a thin layer of mucus that traps inhaled dust, microorganisms and particulates. The cilia sweep this contaminated mucus up to the pharynx, where it is swallowed (the mucociliary escalator). Cilia function is impaired by cigarette smoke, which paralyses ciliary beat and stimulates goblet cell hyperplasia — the underlying mechanism of smoker's cough and chronic bronchitis.
The bronchiolar walls contain a layer of smooth muscle under autonomic control. Parasympathetic (cholinergic) stimulation contracts this muscle, narrowing the airway (bronchoconstriction); sympathetic stimulation via β₂-adrenergic receptors relaxes it (bronchodilation). Asthma medications (β₂-agonists such as salbutamol) exploit this pathway to reverse bronchoconstriction.
The alveolar wall itself is built from two cell types. Type I pneumocytes (squamous alveolar cells) are extremely thin (~0.1 μm), cover ~95 % of the alveolar surface and constitute the diffusion barrier. Type II pneumocytes (granular alveolar cells) are cuboidal, occur sparsely between Type I cells, and secrete pulmonary surfactant — a phospholipid-protein film, principally dipalmitoylphosphatidylcholine, that coats the alveolar surface. Type II cells also serve as the alveolar stem cell, dividing to replace damaged Type I cells.
The barrier between alveolar air and erythrocyte cytoplasm has six layers in series: alveolar fluid film, surfactant, Type I pneumocyte, fused basement membrane, capillary endothelium, plasma. Total thickness is ~0.5–1.0 μm — the thinnest internal exchange barrier in the vertebrate body. Each alveolus is wrapped in a dense capillary mesh so tight that the surface area of pulmonary capillaries (~70 m²) approximately equals that of the alveolar surface. The two surfaces are effectively coextensive, so the diffusing area and the perfused area are matched.
A red blood cell traverses an alveolar capillary in ~0.75 s at rest. Oxygen equilibration with alveolar gas is complete within ~0.25 s, leaving a substantial safety factor — during exercise, when cardiac output rises and transit time falls, oxygenation can still be completed. CO₂ equilibrates even faster because its diffusion coefficient in water is ~20 times that of O₂.
Mammalian ventilation is a textbook application of Boyle's law: at constant temperature, P × V = constant for a given quantity of gas. The thoracic cavity is sealed by the rib cage, the diaphragm and the parietal pleura. Inside is the lung, sheathed in the visceral pleura. A thin layer of pleural fluid lies between the two pleural surfaces, coupling them mechanically without rigid attachment.
Quiet expiration is therefore passive — driven by elastic recoil, requiring no muscle contraction. Forced expiration (during exercise, coughing or speaking) recruits the internal intercostal muscles (which pull the ribs down and in) and the abdominal muscles (which push the diaphragm upward against the chest cavity), expelling additional air.
flowchart LR
INS[Inspiration] -->|diaphragm contracts<br/>external intercostals contract| V1[Volume ↑]
V1 -->|Boyle's law| P1[Pressure ↓]
P1 --> A1[Air flows IN]
EXP[Expiration] -->|elastic recoil<br/>muscles relax| V2[Volume ↓]
V2 -->|Boyle's law| P2[Pressure ↑]
P2 --> A2[Air flows OUT]
A spirometer trace gives several standard volume and capacity measurements:
| Quantity | Typical adult value | Definition |
|---|---|---|
| Tidal volume (TV) | 500 mL | Volume moved per breath at rest |
| Inspiratory reserve volume (IRV) | 3000 mL | Extra volume inspirable above TV |
| Expiratory reserve volume (ERV) | 1100 mL | Extra volume expirable below TV |
| Residual volume (RV) | 1200 mL | Volume remaining after maximal expiration |
| Vital capacity (VC) | TV + IRV + ERV ≈ 4600 mL | Maximal expirable volume |
| Total lung capacity (TLC) | VC + RV ≈ 5800 mL | Total volume at maximum inspiration |
| FEV₁ | ~80 % of VC | Volume expirable in the first 1 s of a forced expiration |
| FEV₁/VC ratio | >0.7 normal | Index of airway obstruction |
The FEV₁/VC ratio is the standard clinical metric for distinguishing obstructive lung disease (asthma, COPD — ratio falls below 0.7 because forced expiration is slowed by narrowed airways) from restrictive lung disease (pulmonary fibrosis — both FEV₁ and VC fall in proportion, ratio preserved).
Each alveolus is lined with a thin aqueous film. The air–water interface generates a surface tension that tends to collapse the alveolus inward (like a soap bubble). For a sphere, the Laplace relation P = 2γ/r predicts that surface tension γ acting at the air–water interface generates an inward pressure inversely proportional to the radius r. Smaller alveoli would therefore tend to collapse into larger ones — a disastrous outcome that would obliterate the gas-exchange surface.
Surfactant — secreted by Type II pneumocytes from ~24 weeks of foetal life — disrupts hydrogen bonding among water molecules at the interface, reducing surface tension. Critically, surfactant is non-linearly compressible: as an alveolus shrinks, surfactant molecules pack more densely at the interface, lowering γ further, and reducing the collapse pressure exactly when collapse would otherwise be most severe. This stabilises alveoli of different sizes against the Laplace instability.
Premature infants (born before ~28 weeks) often lack sufficient surfactant and develop infant respiratory distress syndrome, treated by exogenous surfactant instillation and positive-pressure ventilation. The adult version, adult respiratory distress syndrome (ARDS), follows septic, traumatic or aspiration injury to Type II pneumocytes and carries 30–40 % mortality.
Patrolling the alveolar surface is the alveolar macrophage, a phagocytic immune cell derived from circulating monocytes. Each alveolus contains one or two macrophages, free in the alveolar lumen and constantly sampling the airspace. They ingest inhaled particulates, microorganisms and dead epithelial debris that escape the mucociliary escalator. Engulfed material is digested by lysosomal enzymes; particles that cannot be digested (carbon, silica, asbestos fibres) are retained within the macrophage indefinitely. Long-term carbon accumulation is visible as the dark colour of smokers' lungs. Silica and asbestos fibres trigger macrophage death, release of inflammatory mediators, and chronic fibrosis — the basis of silicosis and asbestosis. The alveolar macrophage is therefore the innate-immunity arm of the gas-exchange surface, synoptic with course 4 (immunity).
Atmospheric air at sea level has a total pressure of ~101 kPa, of which oxygen accounts for ~21 % — a partial pressure of ~21 kPa. By the time inspired air reaches the alveolus, it has been warmed to 37 °C, fully humidified, and mixed with residual alveolar gas; alveolar pO₂ falls to ~13.3 kPa. Pulmonary capillary blood arriving at the alveolus has pO₂ ~5.3 kPa (returning from systemic tissues). The pO₂ gradient driving diffusion is therefore ~8 kPa.
Carbon dioxide has the reverse gradient. Mixed venous blood arriving at the alveolus has pCO₂ ~6.1 kPa; alveolar air has pCO₂ ~5.3 kPa. The gradient is only ~0.8 kPa — an order of magnitude smaller than the oxygen gradient — but CO₂ diffuses ~20× faster in water than O₂, so the smaller gradient produces an equivalent flux. This is why hyperventilation primarily depletes CO₂ rather than supplements O₂: the CO₂ flux is more easily perturbed because its gradient is small.
The principle that AQA mark schemes reward is partial pressure, not concentration, as the correct driver of gas diffusion. A candidate who refers to "concentration of oxygen in air" loses a mark in higher-band questions; the correct term is partial pressure.
The lung is not glued to the chest wall; it is held against it by negative intrapleural pressure. The pleural fluid (~10 mL in a healthy adult) creates a surface-tension coupling — like two wet glass slides — that allows the lung to slide during ventilation but resists separation. If the parietal pleura is breached (penetrating chest trauma, ruptured alveolar bleb, surgical procedure), air enters the pleural space and equalises pressure with the atmosphere. The lung, no longer held outward, collapses inward under its own elastic recoil. This is a pneumothorax. A tension pneumothorax — in which the breach acts as a one-way valve, admitting air at each inspiration but not releasing it — is a medical emergency, treated by needle decompression and chest drain.
This phenomenon illustrates why ventilation depends on the integrity of the closed thoracic system. Boyle's law works only if the cavity is sealed.
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