Gaseous Exchange

Gaseous Exchange

🟢 Lite — Quick Review (1h–1d)

Rapid summary for last-minute revision before your exam.

Gaseous exchange is the passive, diffusion-driven movement of O₂ and CO₂ between an organism’s respiratory surface and the environment, governed by Fick’s Law: Rate ∝ (A × D × ΔP) / T, where A = surface area, D = diffusion coefficient, ΔP = partial pressure gradient, and T = membrane thickness. In humans, O₂ enters alveoli (PO₂ ≈ 104 mmHg) and diffuses into pulmonary capillary blood (PO₂ ≈ 40 mmHg), while CO₂ moves the opposite way (alveolar PCO₂ ≈ 40 mmHg, blood PCO₂ ≈ 45 mmHg). O₂ is carried ~98.5% bound to haemoglobin (forming oxyhaemoglobin, 4 O₂ per Hb) and only ~1.5% dissolved in plasma. MDCAT pointers: (1) Know all four lung volumes and capacities (TV, IRV, ERV, RV) and their sums; (2) Vital Capacity (VC) = TV + IRV + ERV is a frequent one-step calculation; (3) Memorise the Bohr effect — ↑CO₂ or ↓pH shifts the O₂–Hb curve right, unloading more O₂ at tissues.

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🟡 Standard — Regular Study (2d–2mo)

Standard content for students with a few days to months.

The Diffusion Gradient and Respiratory Surface

Gas exchange is purely physical — no ATP is used. The driving force is the partial pressure gradient between alveolar air and capillary blood. Atmospheric air has PO₂ ≈ 160 mmHg, but after humidification and mixing with residual air, alveolar PO₂ settles at ~104 mmHg. Deoxygenated pulmonary arterial blood arrives with PO₂ ≈ 40 mmHg and PCO₂ ≈ 45 mmHg, creating steep gradients that drive O₂ inward and CO₂ outward. The human respiratory surface is the alveolar wall: a single layer of squamous (Type I) pneumocytes fused to capillary endothelium, giving a total barrier thickness of <0.5 µm and a combined surface area of ~70 m².

Ventilation vs. Perfusion

Ventilation is bulk flow of air in the alveoli; perfusion is blood flow through pulmonary capillaries. A healthy V/Q ratio is ~0.8. Mismatch (e.g. V/Q = 0 in pneumonia, V/Q = ∞ in pulmonary embolism) drastically reduces gas exchange and is a common MCQ stem.

Mechanics of Breathing

Inspiration is active: the diaphragm contracts and flattens, external intercostals lift the ribs, thoracic volume rises, intrapleural pressure becomes more negative, and intrapulmonary pressure falls below atmospheric (~−1 mmHg), drawing air in. Expiration during quiet breathing is passive — elastic recoil of lungs and chest wall raises intrapulmonary pressure to ~+1 mmHg.

Lung Volumes and Capacities

Volume/Capacity	Symbol	Typical Adult Value
Tidal volume	TV	500 mL
Inspiratory reserve volume	IRV	3000 mL
Expiratory reserve volume	ERV	1100 mL
Residual volume	RV	1200 mL
Inspiratory capacity	IC = TV + IRV	3500 mL
Functional residual capacity	FRC = ERV + RV	2300 mL
Vital capacity	VC = TV + IRV + ERV	4600 mL
Total lung capacity	TLC = TV + IRV + ERV + RV	5800 mL

Gas Transport in Blood

O₂ binds Fe²⁺ in haemoglobin’s haem groups; each Hb tetramer carries up to 4 O₂. CO₂ is carried as HCO₃⁻ (~70%, via carbonic anhydrase in RBCs: CO₂ + H2O ⇌ H2CO₃ ⇌ H⁺ + HCO₃⁻), as carbamino-haemoglobin (~23%), and dissolved in plasma (~7%). The chloride shift moves Cl⁻ into RBCs to balance exported HCO₃⁻.

Common MDCAT Question Patterns

• Numerical: “Vital capacity of a patient is 4.6 L, RV = 1.2 L, find TLC.”
• Conceptual: identify the cell type secreting surfactant (Type II pneumocytes).
• Curve interpretation: a right-shifted O₂–Hb dissociation curve indicates ↑temperature, ↑PCO₂, ↑2,3-BPG, or ↓pH.

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🔴 Extended — Deep Study (3mo+)

Comprehensive coverage for students on a longer study timeline.

Edge Cases and Regulatory Nuances

Surfactant (a phospholipid–protein complex, mainly dipalmitoylphosphatidylcholine) lowers alveolar surface tension according to Laplace’s law (P = 2T/r). Without it, small alveoli would collapse into large ones. Premature infants lacking surfactant develop neonatal respiratory distress syndrome (NRDS). The Bohr effect is mathematically described by a rightward shift in the O₂–Hb dissociation curve: at any given PO₂, Hb saturation falls, so respiring tissues (high CO₂, low pH, high temperature) unload O₂ more readily, while oxygenated lungs (low CO₂, high pH) load O₂ efficiently — a beautiful example of allosteric regulation. The Haldane effect is its mirror: oxygenation of blood in the lungs displaces CO₂ from Hb, aiding CO₂ removal.

Neural Control

The medullary rhythmicity centre (dorsal + ventral respiratory groups) generates the basic rhythm. The pneumotaxic centre in the upper pons shortens inspiration, while the apneustic centre in the lower pons prolongs it. Chemoreceptors — central (medulla, sensitive to ↑CO₂ / ↓pH of CSF) and peripheral (carotid and aortic bodies, sensitive to ↓PO₂, ↑PCO₂, ↓pH) — modulate the rhythm. Notably, CO₂ is the dominant drive in healthy humans, not O₂.

Worked Example

Q: A spirometer trace shows TV = 0.5 L, IRV = 3.0 L, ERV = 1.1 L, RV = 1.2 L. Calculate the inspiratory capacity and total lung capacity.

• IC = TV + IRV = 0.5 + 3.0 = 3.5 L
• TLC = TV + IRV + ERV + RV = 0.5 + 3.0 + 1.1 + 1.2 = 5.8 L

Adjacent Topics to Link

Connect this topic to: respiratory pigments in different animals (haemocyanin, haemerythrin), high-altitude acclimatisation (increased 2,3-BPG, hyperventilation, polycythaemia), and acid–base balance via the bicarbonate buffer system.

Practice Prompts

1. A patient has a V/Q ratio of 0 in one lung lobe. Predict the effect on arterial PO₂ and PCO₂, and explain why.
2. Explain how the chloride shift maintains electrochemical neutrality in erythrocytes during systemic CO₂ uptake.

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