Respiration depends on a negative pressure system within the pleural cavity. During inspiration, the diaphragm and external intercostal muscles contract, expanding the thoracic cage and dropping intrapleural pressure below atmospheric pressure. This draws air into the lungs. Expiration is normally a passive process driven by elastic recoil of the lung tissue.
Gas exchange occurs across the alveolar-capillary membrane via simple diffusion. Oxygen moves from the alveoli into the pulmonary capillaries, binding to hemoglobin, while carbon dioxide moves in the reverse direction driven by partial pressure gradients.
Pulmonary disorders broadly divide into two functional categories based on how they alter airflow.
Efficient gas exchange requires matching alveolar ventilation ($V$) with capillary blood perfusion ($Q$). In a healthy lung, the ideal $V/Q$ ratio is approximately 0.8.
Asthma and chronic obstructive pulmonary disease represent the most common obstructive pathologies.
Asthma involves chronic airway inflammation leading to hyper-responsiveness. Trigger exposure causes acute bronchoconstriction, edema of the airway wall, and thick mucus secretion, which narrows the lumen and causes wheezing and dyspnea.
Chronic bronchitis involves long-term irritant exposure, such as tobacco smoke, causing hypertrophy of mucous glands and loss of ciliary function. Emphysema involves the permanent destruction of alveolar walls and loss of elastic recoil, leading to air trapping and hyperinflation of the chest.
Restrictive disorders limit lung expansion through intrinsic parenchymal changes or extrinsic chest wall abnormalities.
Intrinsic diseases, like idiopathic pulmonary fibrosis, begin with alveolar epithelial injury. This triggers an inflammatory response followed by fibroblast proliferation and excessive collagen deposition. The lung tissue becomes stiff, non-compliant, and scarred, severely impairing gas diffusion.
Extrinsic causes include severe scoliosis, obesity-hypoventilation syndrome, and neuromuscular disorders like myasthenia gravis, where the lungs themselves are healthy, but the bellows mechanism fails.
Pulmonary hypertension occurs when mean pulmonary arterial pressure rises above normal thresholds. This condition frequently stems from chronic hypoxia, which causes sustained vasoconstriction of the small pulmonary arterioles.
Over time, this increased vascular resistance forces the right ventricle to work harder against a high-pressure gradient. The resulting right ventricular hypertrophy and eventual failure is known as cor pulmonale. Chronic thromboembolic disease can also obstruct the pulmonary vascular bed, contributing to progressive right-sided heart strain.
When respiratory function falters, the body activates rapid compensatory pathways to maintain tissue oxygenation.
Dyspnea is the subjective sensation of difficult breathing, driven by increased respiratory effort and chemoreceptor stimulation from hypercapnia or hypoxia. Tachypnea and accessory muscle use develop to decrease work of breathing during acute distress.
Cyanosis appears late as deoxygenated hemoglobin rises in the peripheral blood vessels. Chronic hypoxemia triggers erythropoietin release from the kidneys, leading to secondary polycythemia to increase oxygen-carrying capacity.