describe gas exchange between air in the alveoli and blood in the capillaries

Gas‑Exchange System (Cambridge 9700 – Topic 9)

Learning Objective

Describe the gas exchange that occurs between the air in the alveoli and the blood in the surrounding pulmonary capillaries, linking anatomy, histology and functional significance of the respiratory system (AO1, AO2).

1. Anatomy & Histology of the Gas‑Exchange System

1.1 Airway hierarchy (macroscopic view)

• Trachea – main conduit from the larynx to the bronchi.
• Bronchi – primary (right & left) and secondary (lobar) branches that conduct air into each lung lobe.
• Bronchioles – smaller, cartilage‑free tubes that end in the terminal bronchioles.
• Alveolar ducts & sacs (alveoli) – terminal air‑filled structures where gas exchange occurs.
• Pulmonary capillaries – dense network that surrounds every alveolus, providing the blood side of the exchange surface.

1.2 Histological features (microscopic view)

2. The Respiratory Membrane

• Three‑layer structure:

  1. Alveolar epithelium (type I cells)
  2. Fused basement membranes of alveolus and capillary
  3. Capillary endothelium

• Surface area (A): ≈ 70 m² (≈ the floor area of a small bedroom).
• Thickness (T): ≈ 0.5 µm – one‑half of a micrometre, allowing rapid diffusion.
• Both A and T are incorporated into Fick’s law (see Section 3).

3. Gas‑Exchange Mechanism

3.1 Partial‑pressure gradients (sea‑level values)

3.2 Quantitative description – Fick’s law

\[

\text{Rate of diffusion} = \frac{D \, A}{T}\,\Delta P

\]

• D – diffusion coefficient (higher for CO₂ than O₂ because CO₂ is more soluble in plasma).
• A – surface area of the respiratory membrane.
• T – membrane thickness.
• ΔP – difference in partial pressure of the gas between alveolar air and capillary blood.

3.3 Direction of gas movement

1. O₂: moves from alveolar air (≈ 100 mm Hg) into blood (≈ 40 mm Hg) because PO₂ (alveolus) > PO₂ (blood).
2. CO₂: moves from blood (≈ 46 mm Hg) into alveolar air (≈ 40 mm Hg) because PCO₂ (blood) > PCO₂ (alveolus).

3.4 Diffusion coefficients

• CO₂ diffuses roughly 20 times faster than O₂ (larger D) because it is more soluble in the aqueous phase.
• The large surface area and extremely thin membrane compensate for the slower diffusion of O₂, ensuring sufficient uptake.

3.5 Sample calculation (AO2)

Question: If emphysema reduces the effective alveolar surface area by 30 %, how does the rate of O₂ diffusion change, assuming all other variables remain constant?

Solution (using Fick’s law):

1. Original rate: \(R0 = \dfrac{D\,A0}{T}\Delta P\).
2. New surface area: \(A{\text{new}} = 0.70A0\).
3. New rate: \(R{\text{new}} = \dfrac{D\,(0.70A0)}{T}\Delta P = 0.70R_0\).
4. Thus, O₂ diffusion falls to 70 % of the normal value – a 30 % reduction.

3.6 Ventilation–perfusion (V/Q) matching

Efficient gas exchange requires that the volume of air reaching an alveolus (ventilation) is proportionate to the blood flow through its capillaries (perfusion). Typical V/Q ≈ 1.0. Mismatches (e.g., pulmonary embolism – high V/Q; chronic bronchitis – low V/Q) reduce the effective ΔP and impair oxygen uptake.

4. Factors Influencing the Rate of Diffusion (AO2)

• Surface area (A) – ≈ 70 m² in a healthy adult; reduced in emphysema or after surgical removal of lung tissue.
• Membrane thickness (T) – ≈ 0.5 µm; increased in pulmonary fibrosis, pulmonary oedema or interstitial inflammation.
• Partial‑pressure difference (ΔP) – falls at high altitude or in hypoventilation.
• Diffusion coefficient (D) – inherent property of the gas; CO₂ > O₂.
• Ventilation–perfusion matching – any V/Q mismatch lowers the effective ΔP for O₂.

5. Clinical Relevance (optional but useful for AO3)

• Pulmonary oedema – fluid fills alveolar spaces, increasing T and diluting surfactant, impairing diffusion.
• Emphysema – destruction of alveolar walls reduces A, markedly lowering diffusion capacity.
• Pulmonary fibrosis – thickened interstitium raises T, slowing gas transfer.
• High altitude – reduced atmospheric PO₂ lowers alveolar PO₂, decreasing the O₂ gradient.
• Pulmonary embolism – blockage of capillary flow creates a high V/Q region (ventilation without perfusion), reducing overall O₂ uptake.

Practical investigation idea (AO3)

Use a simple model lung (a syringe with a rubber bulb) connected to a gas‑collection apparatus. Compare the volume of O₂ collected when the model lung is:

• Open to the atmosphere (normal ventilation).
• Partially occluded to simulate reduced ventilation.
• Filled with a thin layer of water to mimic increased diffusion distance.

Plot the collected O₂ volume against the experimental manipulation to illustrate how changes in A, T or ventilation affect diffusion rate.

6. Suggested Diagram

7. Summary

Gas exchange in the lungs relies on a vast, ultra‑thin respiratory membrane (≈ 70 m² surface area, ≈ 0.5 µm thickness). Differences in partial pressures of O₂ and CO₂ drive diffusion according to Fick’s law. The efficiency of this process is governed by anatomical structure (large surface area, minimal thickness), histological specialisations (type I & II cells, surfactant, smooth muscle), diffusion coefficients, and proper ventilation–perfusion matching. Pathologies that alter surface area, membrane thickness, or pressure gradients impair oxygen uptake and carbon‑dioxide removal, which can be explored through practical investigations.