The Process of Breathing

Core Concepts

Boyle's law: volume changes create pressure gradients

Boyle's law states that, at a constant temperature, the pressure of a gas is inversely proportional to its volume (P = k/V). When the thoracic cavity expands, the gas inside the lungs has more room, so its pressure falls below atmospheric pressure. Air then rushes in until pressures equalize. When the cavity shrinks, lung volume decreases, pressure rises above atmospheric, and air flows out. The pressures involved are tiny — at rest, intra-alveolar pressure dips about 1 mmHg below atmospheric during inspiration and rises about 1 mmHg above it during expiration (commonly taught reference values; atmospheric pressure, about 760 mmHg at sea level, is the zero reference). The key exam idea: air does not move because lungs "suck it in"; it moves because the lungs create a pressure difference that the atmosphere then equalizes.

Inspiration is active; resting expiration is passive

Inspiration begins when the brainstem's respiratory centers signal the diaphragm and external intercostal muscles. The diaphragm contracts and flattens while the intercostals lift the ribs up and outward; both actions enlarge the thoracic cavity, stretch the lungs, and lower intra-alveolar pressure. Relaxed expiration reverses this: the muscles stop contracting, elastic recoil returns the lungs and chest wall to their resting size, volume decreases, and air is pushed out — no muscle work required. Forced expiration (during exercise, coughing, or blowing up a balloon) recruits the abdominal muscles (which push the diaphragm up) and the internal intercostals (which pull the ribs down). This active/passive distinction is one of the most frequently tested facts in respiratory physiology.

The pressure trio: atmospheric, intra-alveolar, and intrapleural

Three pressures matter. Atmospheric pressure (0 mmHg) is the reference. Intra-alveolar (intrapulmonary) pressure, inside the alveoli, oscillates just above and below atmospheric with each breath. Intrapleural pressure, in the space between the visceral and parietal pleurae, stays negative relative to atmospheric (about −4 mmHg at rest, dropping to about −6 to −8 mmHg during strong inspiration — commonly taught reference values). The intrapleural space is negative because the chest wall wants to expand outward while the lungs' elastic recoil wants to collapse inward; the two pull against each other across the thin fluid film of the pleural space, like two springs tugging on opposite ends of a rope. This negative pressure is what keeps the lungs stretched against the chest wall. If air enters the pleural space (pneumothorax), the negative pressure is lost, the lung recoils and collapses, and ventilation of that lung stops.

Compliance, surface tension, and the job of surfactant

Compliance is how easily the lungs and chest wall stretch (change in volume per unit change in pressure, ΔV/ΔP): high compliance means easy to inflate, low compliance means stiff. Two forces resist expansion: the lungs' elastic tissue and the surface tension of the thin fluid film lining the alveoli. Surface tension tries to shrink each air-liquid interface, and small spheres are especially vulnerable: by Laplace's law, the pressure needed to keep a small bubble open is greater than for a large one. Alveoli avoid collapse because type II alveolar cells secrete surfactant, a lipoprotein that lowers surface tension — and lowers it more when the alveolus is small — stabilizing the lung. Reduced surfactant (as in premature infants) makes lungs stiff and prone to collapse — the basis of respiratory distress syndrome in newborns, covered in the development topic later in this chapter.

Airway resistance

Resistance to airflow is normally low and comes mostly from the medium-sized bronchi: the many small airways act as parallel pathways, so their combined resistance is small. By Poiseuille's law, resistance ∝ 1/r⁴, so a small change in airway diameter produces a large change in resistance — which is why bronchoconstriction (as in an asthma attack) sharply increases the work of breathing, while sympathetic bronchodilation, or bronchodilator medication, relieves it. Parasympathetic activity constricts airways; sympathetic activity dilates them.

Lung volumes, capacities, and ventilation rates

Spirometry divides air into measurable volumes (commonly taught approximations for an average adult): tidal volume (TV, ~500 mL per quiet breath), inspiratory reserve volume (IRV, ~3100 mL), expiratory reserve volume (ERV, ~1200 mL), and residual volume (RV, ~1200 mL, air that can never be exhaled). Capacities are combinations: inspiratory capacity = TV + IRV; functional residual capacity = ERV + RV; vital capacity = TV + IRV + ERV; total lung capacity = VC + RV. Spirometry can measure everything except RV, FRC, and TLC, because those include air that never leaves the lungs. Two rate equations are high-yield: minute ventilation = tidal volume × breaths per minute (about 6 L/min at rest: 500 mL × 12), and alveolar ventilation = (tidal volume − dead space) × breaths per minute. Dead space is air that fills the conducting airways and never reaches gas-exchange surfaces (~150 mL); alveolar ventilation is the number that matters for gas exchange — which is why rapid, shallow "panting" wastes air on dead space.

Common Confusions