The Mammalian Lung
~7 min read · Tier toggle changes depth (T1 plain · T2 standard · T3 rigour)
You should recall the general principles of diffusion across exchange surfaces and understand how partial pressures drive gas movement in biological systems.
Why this matters
The mammalian lung is a highly specialised organ that maximises gas exchange efficiency to support high metabolic rates.
Unlike the tracheal system of insects, which relies on direct diffusion through air-filled tubes, the mammalian lung utilizes a vast, moist surface area to facilitate the rapid exchange of oxygen and carbon dioxide between the air and the blood. This structural complexity allows mammals to sustain the high energy demands of endothermy and active locomotion. By understanding the anatomical and physiological adaptations of the lung, we can appreciate how evolutionary pressures have shaped an organ that balances the need for efficient gas transfer with the mechanical requirements of breathing.
The Architecture of Air and Blood
Imagine the mammalian lung not as a simple bag, but as a complex, branching tree where the leaves are microscopic sacs. Air enters through the trachea and bronchi, eventually reaching the alveoli, which are the tiny, grape-like clusters where gas exchange actually occurs. The key to the lung's success is the intimate relationship between these air sacs and the surrounding capillaries. The walls of the alveoli and the capillaries are extremely thin, often only one cell thick, creating a minimal barrier for gases to cross. This thinness is crucial because it reduces the distance gases must travel, allowing oxygen to diffuse rapidly into the blood and carbon dioxide to diffuse out. Furthermore, the surface area is immense; if you were to flatten out all the alveoli in a human lung, they would cover an area roughly the floor area of a badminton court. This large area ensures that even though the concentration gradient for oxygen is relatively small, the total amount of gas exchanged is sufficient to meet the body's needs. The entire system is kept moist, which is essential because gases must dissolve in a liquid medium before they can diffuse across cell membranes. This combination of thinness, vast area, and moisture creates an optimal environment for the continuous and efficient exchange of respiratory gases, supporting the high metabolic rates characteristic of mammals.
Diffusion Across the Respiratory Membrane
The movement of gases across the respiratory membrane is governed by Fick's law of diffusion. This principle states that the rate of diffusion is directly proportional to the surface area and the concentration gradient, and inversely proportional to the thickness of the membrane. In the context of the lung, the concentration gradient is determined by the partial pressures of the gases in the alveolar air and the pulmonary capillary blood. Oxygen has a higher partial pressure in the alveoli than in the deoxygenated blood, driving its diffusion into the bloodstream. Conversely, carbon dioxide has a higher partial pressure in the blood than in the alveoli, driving its diffusion out into the air space to be exhaled. The respiratory membrane itself consists of several layers: the alveolar epithelium, the alveolar basement membrane, the capillary basement membrane, and the capillary endothelium. These layers are fused in many areas, creating a very thin barrier that minimises the diffusion distance. Any thickening of this membrane, such as in pulmonary fibrosis, significantly reduces the rate of gas exchange, leading to hypoxemia. The efficiency of this process is also dependent on the solubility of the gas in the liquid medium; oxygen is less soluble than carbon dioxide, but its steeper partial pressure gradient compensates for this difference.
Ventilation and Alveolar Gas Composition
Ventilation is the mechanical process of moving air into and out of the lungs, but it is not simply a matter of filling and emptying the entire lung volume. A significant portion of the air in the respiratory tract, known as the dead space, does not participate in gas exchange. This includes the air in the trachea, bronchi, and bronchioles. Only the air that reaches the alveoli is available for diffusion. The composition of alveolar air differs from that of atmospheric air due to the continuous exchange of gases with the blood. Oxygen is removed from the alveolar air by diffusion into the blood, while carbon dioxide is added from the blood into the alveoli. As a result, the partial pressure of oxygen in the alveoli is lower than in atmospheric air, and the partial pressure of carbon dioxide is higher. Additionally, alveolar air is saturated with water vapour, which further reduces the partial pressures of the dry gases. The balance between ventilation and perfusion (blood flow) is critical for efficient gas exchange. If ventilation is too low relative to blood flow, the alveolar oxygen partial pressure falls, and carbon dioxide rises, leading to poor gas exchange. Conversely, if ventilation is too high, the alveolar oxygen partial pressure rises, but this is less efficient in terms of energy expenditure. The body tightly regulates ventilation to match the metabolic demands of the tissues, ensuring that the alveolar gas composition remains within a narrow range that supports optimal diffusion.
Surfactant and Mechanical Stability
One of the major challenges facing the alveoli is the tendency for them to collapse due to surface tension. The inner surface of the alveoli is lined with a fluid layer that contains water molecules, which attract each other, creating a surface tension that pulls the alveolar walls inward. Without a counteracting force, this surface tension would cause the alveoli to collapse at the end of each expiration, making re-inflation extremely difficult and energetically costly. To prevent this, the alveolar type II cells produce a substance called pulmonary surfactant. Surfactant is a mixture of lipids and proteins that reduces the surface tension of the alveolar fluid. By lowering the surface tension, surfactant reduces the inward pull on the alveolar walls, thereby preventing collapse and facilitating easier re-inflation. Surfactant also helps to equalize the pressure between alveoli of different sizes, preventing smaller alveoli from emptying into larger ones. This mechanical stability is crucial for maintaining the large surface area required for gas exchange. Deficiencies in surfactant, as seen in neonatal respiratory distress syndrome, lead to alveolar collapse and severe hypoxemia, highlighting the importance of this substance in lung function. The production and regulation of surfactant are tightly controlled, and production rises sharply only in the last weeks of gestation (from about 34 weeks), which is why premature babies are most at risk.
The concept
Gas exchange surfaces
Why exchange surfaces are thin, moist and large.
A common misconception is that the partial pressure of oxygen in the alveoli is the same as in atmospheric air. In reality, the alveolar oxygen partial pressure is significantly lower due to the addition of water vapour and the continuous diffusion of oxygen into the blood. This difference is crucial for understanding the driving force for oxygen diffusion into the blood. C
Worked example
Problem. Use the alveolar gas equation, \(P_{A\mathrm{O_2}} = F_{I\mathrm{O_2}}(P_{\text{atm}} - P_{\mathrm{H_2O}}) - P_{a\mathrm{CO_2}}/R\), to find the alveolar oxygen partial pressure (a) at sea level (\(P_{\text{atm}} = 760\ \mathrm{mmHg}\)) and (b) at about 3000 m (\(P_{\text{atm}} = 523\ \mathrm{mmHg}\)). Take \(F_{I\mathrm{O_2}} = 0.21\), water vapour pressure at body temperature \(P_{\mathrm{H_2O}} = 47\ \mathrm{mmHg}\), arterial \(P_{\mathrm{CO_2}} = 40\ \mathrm{mmHg}\) and respiratory quotient \(R = 0.8\).
- (a) Inspired oxygen after humidification: \(0.21 \times (760 - 47) = 0.21 \times 713 = 149.7\ \mathrm{mmHg}\).
- Oxygen displaced by carbon dioxide: \(40/0.8 = 50\ \mathrm{mmHg}\), so \(P_{A\mathrm{O_2}} = 149.7 - 50 \approx 100\ \mathrm{mmHg}\), well below the 160 mmHg of dry air.
- (b) At 3000 m: \(0.21 \times (523 - 47) = 0.21 \times 476 = 100.0\ \mathrm{mmHg}\), so \(P_{A\mathrm{O_2}} \approx 100 - 50 = 50\ \mathrm{mmHg}\).
- The driving gradient for oxygen into blood arriving at about 40 mmHg falls from about 60 to about 10 mmHg. Breathing harder lowers \(P_{a\mathrm{CO_2}}\) and wins back some of the loss, which is why ventilation rises at altitude.
Units check. Every term is a partial pressure in mmHg; \(F_{I\mathrm{O_2}}\) and \(R\) are dimensionless.
Three quick tests
- What is the primary function of pulmonary surfactant?
Answer
It reduces surface tension in the alveoli, preventing collapse and facilitating re-inflation. - Why is the partial pressure of oxygen in the alveoli lower than in atmospheric air?
Answer
Due to the addition of water vapour and the continuous diffusion of oxygen into the blood. - How does the thickness of the respiratory membrane affect gas exchange?
Answer
A thicker membrane increases the diffusion distance, reducing the rate of gas exchange.
Back to BU-106 →
Every lecture and every concept in this unit, with prerequisites and threads.
Lecture notes checked line by line by the editor; every number in the worked example was recomputed.
Concepts cited: T-029 · Threads: regulation, systems