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Ventilation is driven by pressure gradients created by diaphragm and intercostal muscle contraction, with airflow resisted by airway resistance and movement opposed by elastic recoil of the lungs and chest wall. Lung compliance (change in lung volume per unit change in pressure) reflects the elastic properties of collagen and elastin fibers and the surface tension at the air-liquid interface in alveoli. Pulmonary surfactant, produced by type II alveolar cells, dramatically reduces surface tension and increases compliance, preventing alveolar collapse at low volumes. The work of breathing (pressure × volume) increases dramatically when compliance decreases (pulmonary fibrosis, acute respiratory distress syndrome) or airway resistance increases (asthma, COPD).
Measure lung compliance using spirometry with simultaneous esophageal pressure measurement to derive the compliance curve. Compare compliance in healthy lungs vs. fibrotic or edematous lungs. Study how surfactant-deficient lungs (respiratory distress syndrome) collapse.
The intrapleural pressure is not a vacuum but slightly negative (-5 cm H2O); pneumothorax (air entry into pleural space) allows atmospheric pressure and lung recoil to collapse the lung.
From your knowledge of the respiratory system and passive transport, you know that the lungs are the site of gas exchange and that substances move down concentration or pressure gradients without energy input. Pulmonary ventilation — the movement of air into and out of the lungs — applies this principle mechanically: air flows because of pressure gradients created by the action of respiratory muscles, not because the lungs actively pull air in. The lungs themselves have no skeletal muscle; they are passive, elastic structures that expand and recoil in response to forces applied to them.
The key to understanding ventilation is intrapleural pressure — the pressure in the thin fluid-filled space between the lung surface (visceral pleura) and the chest wall (parietal pleura). At rest, this pressure is slightly negative (about −5 cm H₂O) because the lungs are constantly trying to collapse inward (elastic recoil) while the chest wall is trying to spring outward, and the sealed pleural space between them transmits this tug-of-war as a sub-atmospheric pressure. During inspiration, the diaphragm contracts and flattens, and the external intercostal muscles lift the ribs outward, expanding the thoracic cavity. This expansion makes the intrapleural pressure even more negative (about −8 cm H₂O), which stretches the lungs and drops the intra-alveolar pressure below atmospheric pressure. Air then flows in down this pressure gradient — from the atmosphere (760 mmHg) into the alveoli (roughly 758 mmHg). Quiet expiration is largely passive: the diaphragm relaxes, the elastic recoil of the lungs pulls the thorax back to its resting position, alveolar pressure rises above atmospheric pressure, and air flows out. Forced expiration recruits the internal intercostals and abdominal muscles to actively compress the thorax.
Lung compliance measures how easily the lungs expand — technically, the change in volume per unit change in pressure (ΔV/ΔP). High compliance means the lungs stretch easily; low compliance means they resist expansion. Two factors determine compliance. The first is the elastic tissue (collagen and elastin fibers) in the lung parenchyma — these provide structural recoil, like a rubber band that stretches and snaps back. The second, and often more important, is surface tension at the air-liquid interface lining the alveoli. Water molecules at this interface attract each other, creating an inward-directed force that tends to collapse alveoli. Without countermeasures, the smallest alveoli would collapse into larger ones (LaPlace's law predicts that smaller spheres with the same surface tension generate higher collapsing pressure). Pulmonary surfactant, a phospholipid mixture produced by type II alveolar cells, dramatically reduces this surface tension, preventing small alveoli from collapsing and making the lungs much more compliant. Premature infants who lack surfactant develop neonatal respiratory distress syndrome — their stiff, surfactant-deficient lungs require enormous muscular effort to inflate.
The clinical significance of compliance and resistance becomes clear in disease. In pulmonary fibrosis, excess scar tissue stiffens the lungs, reducing compliance — patients must generate much greater pressure changes to move the same volume of air, dramatically increasing the work of breathing. In emphysema, destruction of elastic tissue makes the lungs abnormally compliant (they expand easily) but they lose their elastic recoil, making expiration difficult and trapping air. In asthma and COPD, the primary problem is increased airway resistance from bronchospasm, inflammation, and mucus — the airways narrow, requiring greater pressure gradients to drive the same airflow. In each case, the fundamental mechanics are the same: ventilation depends on pressure gradients, and anything that impairs the generation of those gradients (reduced compliance) or the flow of air through them (increased resistance) compromises the ability to move air and exchange gases.