Breathing depends on pressure gradients created by diaphragm contraction and elastic recoil of lung tissue. Lung compliance—the change in volume per unit pressure change—reflects the elastic properties of lung parenchyma and chest wall. Airway resistance is proportional to airway radius to the 4th power, making small airways disproportionately important. Gas exchange occurs across the alveolar-capillary membrane by simple diffusion driven by partial pressure gradients.
Measure your own lung volumes and capacities using spirometry. Trace air pathways through progressively smaller generations of airways to understand how resistance increases nonlinearly.
You already know the anatomy of the respiratory tract and that ventilation moves air in and out. This topic explains the *mechanics* — the physical forces that make breathing work — and the *chemistry* of how gases actually cross from air into blood. Both depend on gradients: pressure gradients for bulk airflow, and partial pressure gradients for diffusion.
Inspiration begins with diaphragm contraction. When the diaphragm flattens, it increases thoracic volume. Because the pleural space is sealed and the lungs are attached to the chest wall by surface tension across the thin pleural fluid layer, lung volume increases too. By Boyle's Law, increasing volume decreases pressure — alveolar pressure drops below atmospheric, and air flows down the pressure gradient into the lungs. Expiration at rest is passive: the diaphragm relaxes, elastic recoil of the lung tissue compresses alveolar volume, pressure rises above atmospheric, and air flows out. Lung compliance — the volume increase per unit pressure increase — reflects how easily the lungs stretch. Reduced compliance (stiff lungs, as in pulmonary fibrosis) means more muscular effort is needed for each breath. Increased compliance (as in emphysema, where elastic tissue is destroyed) makes inflation easy but expiration hard because passive recoil is lost.
Airway resistance is governed by Poiseuille's Law: resistance is inversely proportional to the *fourth power* of airway radius. Halving an airway's diameter multiplies its resistance 16-fold. This is why bronchospasm — even modest airway narrowing — produces dramatic increases in breathing work. Paradoxically, total cross-sectional area increases enormously as airways branch toward the alveoli, so resistance is actually highest in the large, central airways, not the terminal bronchioles.
Gas exchange occurs across the alveolar-capillary membrane, a barrier less than 0.5 μm thick. Oxygen diffuses from alveolar air (partial pressure ~100 mmHg) into pulmonary capillary blood (arriving at ~40 mmHg), while CO₂ diffuses in the opposite direction (from ~46 mmHg in blood to ~40 mmHg in alveoli). This diffusion is passive — no active transport — and depends on membrane area, membrane thickness, and the partial pressure gradient. Your prerequisite knowledge of hemoglobin's cooperative oxygen binding explains how blood loads oxygen so efficiently even though the driving gradient is modest: the sigmoidal O₂-hemoglobin dissociation curve means small drops in pO₂ trigger large unloading of oxygen at the tissues, while small rises in pO₂ drive nearly complete loading at the alveoli.