Lung Volumes & Mechanics
What spirometry can and can't see, and why alveoli don't collapse
Lung volumes and capacities
Volumes vs capacities. Four non-overlapping volumes — tidal (TV), inspiratory reserve (IRV), expiratory reserve (ERV), and residual (RV) — make up the lung. A capacity is the sum of two or more volumes.
| Measure | Definition | Typical adult value |
|---|---|---|
| Tidal volume (TV) | Air moved in a quiet breath | ~500 mL |
| Inspiratory reserve (IRV) | Extra air inhaled after a normal inspiration | ~3000 mL |
| Expiratory reserve (ERV) | Extra air exhaled after a normal expiration | ~1200 mL |
| Residual volume (RV) | Air left after maximal expiration; cannot be exhaled | ~1200 mL |
| Inspiratory capacity (IC) | IRV + TV | ~3500 mL |
| Functional residual capacity (FRC) | ERV + RV; volume after a normal tidal expiration | ~2400 mL |
| Vital capacity (VC) | IRV + TV + ERV | ~4700 mL |
| Total lung capacity (TLC) | All four volumes | ~6000 mL |
Measurement: what spirometry cannot see
The residual-volume blind spot. A spirometer records only air that moves in or out, so it cannot measure RV or any capacity containing it (FRC, TLC). These require body plethysmography, helium dilution, or nitrogen washout. Spirometry does measure TV, IRV, ERV, IC, VC, and timed flows such as FEV1.
Two patterns. Obstructive disease limits expiratory flow and traps air; restrictive disease shrinks the lungs. Full lung volumes separate the two when spirometry alone is ambiguous.
| Feature | Obstructive (e.g., emphysema) | Restrictive (e.g., pulmonary fibrosis) |
|---|---|---|
| FEV1/FVC | ↓ (below about 0.7) | Normal or ↑ |
| TLC | Normal or ↑ | ↓ |
| RV and FRC | ↑ (air trapping) | ↓ |
| Compliance and recoil | ↑ compliance, ↓ recoil in emphysema | ↓ compliance, ↑ recoil |
| Pressure–volume curve | Shifted up and left | Shifted down and right |
| Least costly breathing | Slow, deep breaths | Rapid, shallow breaths |
Recoil, compliance, and FRC
FRC as equilibrium. At FRC the inward elastic recoil of the lung exactly balances the outward recoil of the chest wall. Airway pressure is zero, no air flows, and the system is at rest; intrapleural pressure is negative, holding the lung against the chest wall.
Pneumothorax. Air in the pleural space breaks this coupling: the lung collapses inward and the chest wall springs outward.
Compliance. Compliance = ΔV/ΔP, the distensibility of the lung and the inverse of elastance. It is high in emphysema and aging (lost elastic recoil) and low in pulmonary fibrosis, pulmonary edema, and neonatal RDS.
Emphysema vs fibrosis. Emphysematous lungs are easy to inflate but hard to empty: with little recoil and loss of the radial traction that holds small airways open, airways collapse on expiration, trapping air and raising FRC and RV (barrel chest). Fibrotic lungs are small and stiff, with strong recoil and a low TLC.
Surfactant and surface tension
Law of Laplace. Collapsing pressure P = 2T/r, where T is surface tension and r the alveolar radius. Small alveoli therefore have higher collapsing pressure and would empty into larger ones. Surfactant lowers T more in small alveoli, where its molecules are packed more densely, stabilizing alveoli of different sizes.
Surfactant. Mostly dipalmitoylphosphatidylcholine (DPPC, lecithin), secreted by type II pneumocytes, which also serve as stem cells that regenerate type I cells after injury. By lowering surface tension it raises compliance, prevents end-expiratory collapse, and reduces the work of breathing. Synthesis starts around week 20 of gestation and matures around week 35.
Neonatal respiratory distress syndrome
- Surfactant deficiencyImmature type II pneumocytes.
- High surface tensionSmall alveoli collapse at end-expiration (Laplace).
- Diffuse atelectasisCompliance falls and the work of breathing rises.
- Hypoxemia and hyaline membranesGrunting, retractions, tachypnea; ground-glass (reticulogranular) chest film.
Risk factors. Prematurity, maternal diabetes (fetal hyperinsulinemia suppresses surfactant synthesis), and cesarean delivery (without the glucocorticoid surge of labor).
Prevention and treatment. Antenatal maternal betamethasone accelerates fetal surfactant production; exogenous surfactant treats established NRDS. Supplemental O2 and mechanical ventilation risk bronchopulmonary dysplasia and retinopathy of prematurity.
Persistent hypoxia in NRDS keeps the ductus arteriosus open, so a PDA often complicates the course.
Airway resistance and the work of breathing
Airway resistance. By Poiseuille, resistance is proportional to 1/r⁴, so radius dominates. The medium-sized bronchi are the major site of resistance; small airways contribute little because their huge total cross-sectional area is arranged in parallel. Resistance falls at high lung volumes, as radial traction pulls airways open, and rises with bronchoconstriction.
Work of breathing. Total work = elastic work (stretching lung and chest wall) + resistive work (moving gas through airways). Patients choose the pattern that minimizes their dominant cost: rapid, shallow breaths in restrictive disease to limit elastic work, and slow, deep breaths in obstructive disease to limit resistive work.