Chapter 30: Gas Exchange in the Lungs

The fundamental mechanism of breathing depends on pressure differences across the lungs and chest wall, with intrapleural pressure creating a seal that couples lung expansion to thoracic movement. Inspiration occurs when the diaphragm and external intercostal muscles contract, generating negative pressure within the pleural space that pulls the lungs open and allows atmospheric air to flow inward. Expiration typically results from passive elastic recoil of lung tissue and the chest wall returning to their resting state, though forced expiration recruits internal intercostal and abdominal muscles. Two critical properties determine how readily the lungs expand: compliance, which measures the volume change per unit pressure change, and elastance, which represents the tendency of lung tissue to resist deformation. Surfactant plays a vital role by reducing surface tension at the air-liquid interface within alveoli, preventing their collapse during expiration and maintaining uniform inflation. Airway resistance opposes airflow and varies inversely with airway diameter, meaning even modest narrowing dramatically increases resistance and work of breathing. The pleura and interactions between the lung and thoracic cage maintain functional residual capacity, the volume of air remaining after passive expiration. Clinical conditions illustrate these principles: restrictive diseases decrease compliance by stiffening lung tissue, while obstructive diseases increase resistance through airway narrowing or loss of elastic support. Understanding these mechanical relationships is essential for recognizing why conditions like asthma and chronic obstructive pulmonary disease impair ventilation and for designing effective mechanical ventilation strategies in clinical settings.