Gas Exchange Between Internal and External Environments

Q1, Sample Band 6 response (6 marks), annotated

Feature 1, Large surface area. The human lung contains approximately 500 million alveoli, providing a total gas exchange surface area of approximately 250 m², roughly the area of a tennis court. According to Fick’s law, rate of diffusion is proportional to surface area, so this enormous surface allows a vast number of O₂ and CO₂ molecules to cross simultaneously, providing a rate of exchange sufficient to meet the body’s metabolic demands. [1 mark, SA with mechanism and Fick link]

Feature 2, Thin membrane. The gas exchange barrier consists of a single layer of squamous type I alveolar epithelial cells (~0.2 μm) fused to a single layer of capillary endothelial cells, giving a combined diffusion distance of approximately 0.5 μm. Fick’s law states that rate is inversely proportional to membrane thickness, so this minimal distance allows O₂ and CO₂ molecules to cross in milliseconds, maximising exchange rate. [1 mark, thickness with mechanism and Fick link]

Feature 3, Moist surface. The inner surface of each alveolus is coated with a thin film of fluid containing surfactant. This moisture is essential because O₂ and CO₂ must dissolve in this layer before they can diffuse through the lipid bilayer of the cell membrane. Without a moist surface, molecular gas exchange cannot occur regardless of surface area or membrane thickness. [1 mark, moist surface with mechanism]

Feature 4, Maintained concentration gradient. By Fick’s law, rate is proportional to the concentration gradient. On the air side, continuous ventilation (breathing) constantly refreshes alveolar air with fresh O₂-rich / low-CO₂ air, preventing alveolar pO₂ from falling. On the blood side, continuous blood flow continuously removes O₂-loaded blood and delivers deoxygenated blood with low pO₂, keeping the gradient steep. Without either mechanism the gradients would equilibrate and diffusion would cease entirely. [1 mark, gradient maintenance: ventilation + blood flow]

Marking criteria.

• 1 markLarge surface area: structural description (500 million alveoli, ~250 m²) + Fick link (rate ∝ SA) + functional consequence.
• 1 markThin membrane: combined thickness ~0.5 μm + Fick link (rate inversely proportional to thickness) + functional consequence.
• 1 markMoist surface: fluid/surfactant layer + explanation that gases must dissolve before diffusing.
• 1 markMaintained concentration gradient: ventilation refreshes alveolar air + blood flow removes loaded O₂.
• 1 markAll three structural features explicitly linked to the correct Fick variable (not just named).
• 1 markCoherent, logically structured response that shows the four features work together to maximise gas exchange rate.

Q2, Sample Band 6 response (7 marks), annotated

Fick’s law states that rate of diffusion is proportional to surface area and concentration gradient, and inversely proportional to membrane thickness: Rate ∝ (SA × concentration gradient) / membrane thickness. [1, full law stated]

In emphysema, all three Fick variables are simultaneously impaired in the wrong direction. Surface area decreases dramatically (from ~250 m² to as low as 30 m²) as alveolar walls break down and smaller alveoli merge into fewer, larger air sacs, an approximately 88% reduction in SA, causing a proportional reduction in diffusion rate. [1, SA decrease with mechanism and magnitude] Membrane thickness increases because chronic inflammation thickens remaining alveolar walls and may add mucus layers, increasing the diffusion distance and further reducing rate. [1, thickness increase with mechanism] Concentration gradient is also reduced because impaired ventilation in damaged lung regions means alveolar pO₂ falls and CO₂ rises, shrinking the partial pressure gradient driving exchange. [1, gradient reduction with mechanism]

The combined effect is a collapse in gas exchange rate: even though the patient is breathing room air at normal atmospheric pO₂, so little O₂ crosses per unit time that blood pO₂ is chronically low (hypoxaemia), explaining the need for supplemental O₂. Supplemental O₂ raises the concentration gradient term in Fick’s law (increasing alveolar pO₂ by supplying higher than atmospheric O₂), partially compensating for the reduced SA and increased thickness. [1, combined effect on rate + why supplemental O₂ is needed]

However, supplemental O₂ does not address the underlying structural problem: it does not restore lost alveolar surface area, it does not thin the inflamed membrane, and it does not improve ventilation in damaged regions. It compensates by overdriving the concentration gradient variable to partially offset the other two impaired variables. [2, evaluation: addresses gradient only; does not fix SA or thickness; correct biologically]

Marking criteria.

• 1 markStates Fick’s law correctly (all three variables).
• 1 markSA: identifies decrease (~250 → ~30 m²), explains why (alveolar wall breakdown / merger), states effect on rate.
• 1 markMembrane thickness: identifies increase (inflammation/thickening), states effect on rate (inversely proportional).
• 1 markConcentration gradient: identifies decrease (impaired ventilation, lower alveolar pO₂), states effect on rate.
• 1 markPredicts combined collapse of rate; explains why hypoxaemia occurs and supplemental O₂ is needed.
• 1 markIdentifies that supplemental O₂ compensates by increasing the concentration gradient variable.
• 1 markEvaluates that supplemental O₂ does not restore SA or thin the membrane, it compensates rather than cures.

Q3, Sample Band 6 response (6 marks)

The claim is largely incorrect and contains four identifiable errors. [1, overall evaluative judgement]

Error 1: “oxygen physically pushes its way.” O₂ does not push, it diffuses passively from high to low partial pressure. No active force is involved; the driving force is the partial pressure gradient. [1, refutes pushing; correct: passive diffusion down partial pressure gradient]

Error 2: “larger and thicker alveolar walls = more oxygen.” This is the opposite of the truth. By Fick’s law, rate is inversely proportional to membrane thickness. Larger walls in the sense of more surface area does increase rate, but thicker walls decrease it. Emphysema, where alveoli merge into larger but fewer spaces, dramatically reduces SA and impairs gas exchange. [1, refutes thickness claim; correct Fick relationship]

Error 3: “breathing fast physically forces more oxygen.” Increased breathing rate (hyperventilation) helps by refreshing alveolar air and maintaining the concentration gradient at a higher level (Fick: rate ∝ concentration gradient), not by physically forcing gas. The gas exchange itself is always passive diffusion. [1, refutes “physical force”; correct: gradient maintenance]

Error 4: “heart stops but breathing continues → gas exchange continues.” This is wrong. Without blood flow, blood in pulmonary capillaries would rapidly equilibrate with alveolar air (pO₂ would rise to ~100 mmHg in blood, pCO₂ would equalise). The concentration gradient would collapse to zero and diffusion would stop. Breathing without circulation cannot sustain gas exchange. [1, refutes cardiac arrest claim; correct: gradient collapse without blood flow]

Accurate reformulation: “Gas exchange in the lungs occurs by passive diffusion driven by partial pressure gradients. O₂ diffuses from alveolar air (high pO₂) into blood (low pO₂) and CO₂ in the reverse direction. Efficient exchange requires a large surface area, a thin membrane, a moist surface, and a maintained concentration gradient. Ventilation maintains the gradient on the alveolar side; blood flow maintains it on the blood side. If either ventilation or blood flow stops, the gradient collapses and gas exchange ceases.” [1, scientifically accurate reformulation covering all key points]