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The respiratory system consists of conducting airways (nasal cavity → pharynx → larynx → trachea → bronchi → bronchioles) and the respiratory zone (respiratory bronchioles → alveolar ducts → alveoli). The ~300 million alveoli provide ~70 m² of surface area for gas exchange. Ventilation is driven by pressure gradients created by volume changes: the diaphragm and external intercostals contract during inhalation, expanding thoracic volume and lowering intrapulmonary pressure below atmospheric. Lung compliance (stretchability) and surfactant (which reduces surface tension and prevents alveolar collapse) are key determinants of respiratory work.
Use a bell-jar lung model to visualize the pressure-volume relationship during breathing. Practice interpreting spirometry traces to identify tidal volume, vital capacity, residual volume, and FEV1.
From your study of gas exchange and diffusion, you know that gases move down concentration gradients across thin membranes. The respiratory system's job is to continuously replenish the air on one side of that membrane — the alveolar side — so the gradient never collapses. To do that, the lungs must move air in and out through a branching network of passages, each level serving a different function. The conducting zone (nose to terminal bronchioles) warms, humidifies, and filters incoming air but performs no gas exchange — it is the delivery system. The respiratory zone begins where the bronchioles become alveolated, and here the actual diffusion you studied occurs across a membrane thinner than a cell.
Breathing is a pressure game. Boyle's law — which you encountered in your study of body organization and gas behavior — states that at constant temperature, pressure and volume are inversely related. The respiratory system exploits this: when the diaphragm contracts and flattens, the thoracic cavity expands; when the external intercostals contract, the rib cage lifts outward. Both movements increase lung volume. Because air in the lungs is now spread over a larger space, its pressure falls below atmospheric (~760 mmHg). Air flows in along this pressure gradient — the lung does not suck; it creates a low-pressure zone that the atmosphere fills. Exhalation is normally passive: the diaphragm relaxes, the chest recoils, volume decreases, pressure rises above atmospheric, and air flows out.
Lung compliance is the stretchability of the lung tissue — how much volume change you get per unit of pressure change. Stiff lungs (low compliance, as in pulmonary fibrosis) require more muscular effort to inflate. But compliance alone would make breathing impossible without one critical ingredient: surfactant. The alveoli are tiny air sacs, and surface tension at the air-liquid interface (La Place's law: pressure = 2T/r) would collapse small alveoli into large ones and require enormous pressure to re-inflate them. Surfactant — a mixture of phospholipids secreted by type II pneumocytes — coats the alveolar surface and reduces surface tension dramatically. Without it, alveoli collapse at the end of each breath (atelectasis). In premature infants whose type II cells are not yet mature, this is life-threatening — the basis for administering synthetic surfactant at birth.
Lung volumes measured by spirometry reflect the functional capacity of the respiratory system. Tidal volume (~500 mL) is the volume of a normal quiet breath. Vital capacity is the maximum volume exhaled after a maximum inhalation. Residual volume (~1.2 L) is the air that stays in the lungs after maximal exhalation — this cannot be measured by spirometry because you cannot exhale it. FEV₁ (forced expiratory volume in 1 second) measures how quickly air moves out and is the key diagnostic for obstructive diseases like asthma (low FEV₁/FVC ratio, because narrowed airways slow expiration) versus restrictive diseases like fibrosis (normal FEV₁/FVC ratio, but small total volumes because stiff lungs cannot expand fully). These traces are your primary clinical window into respiratory mechanics.