10.3 Pulmonary Ventilation Mechanics & Respiratory Control
Key Takeaways
- Quiet inspiration is active, driven by diaphragm and external intercostal contraction that lowers intrapleural pressure below atmospheric; quiet expiration is passive elastic recoil.
- Intrapleural pressure is negative throughout the normal cycle, roughly -5 cm H2O at rest, and a breach of that seal causes pneumothorax and lung collapse.
- Pulmonary surfactant from type II pneumocytes lowers surface tension and, by Laplace's law, keeps small alveoli from emptying into large ones.
- Residual volume cannot be exhaled and therefore cannot be measured by spirometry, so total lung capacity and functional residual capacity also require indirect methods.
- Central medullary chemoreceptors respond to CSF hydrogen ion generated from carbon dioxide and are the dominant drive to breathe; peripheral carotid and aortic bodies respond strongly to oxygen only when arterial PO2 falls below about 60 mmHg.
Why Ventilation Is a Pressure Problem
Air is not pulled into the lung; it flows down a pressure gradient created by changing thoracic volume. Boyle's law ($P_1V_1 = P_2V_2$ at constant temperature) is the governing relationship: increase the volume of a sealed container and its pressure falls.
The Respiratory Cycle
Inspiration (always active):
- The diaphragm contracts and flattens, and the external intercostals elevate the ribs in a bucket-handle motion.
- Thoracic volume increases, so intrapleural pressure falls further below atmospheric.
- The lungs, coupled to the chest wall by the fluid seal of the pleural cavity, expand with it.
- Intrapulmonary (alveolar) pressure falls about $1\text{ mmHg}$ below atmospheric and air flows in until the two equalize.
Quiet expiration (passive): the muscles relax and elastic recoil of stretched lung tissue plus the inward pull of surface tension shrink thoracic volume, raising alveolar pressure above atmospheric so air flows out. Forced expiration is active, recruiting the internal intercostals and abdominal muscles.
The negative intrapleural pressure is the whole trick. At functional residual capacity it sits near $-5\text{ cm H}_2\text{O}$ and drops to about $-8$ during inspiration, because the lung's elastic recoil pulls inward while the chest wall recoils outward. Puncture the pleural space and the pressure equalizes with atmosphere: the lung collapses and the chest wall springs out — a pneumothorax.
Compliance, Elastic Recoil and Surface Tension
Compliance is the change in volume per unit change in pressure, $C = \Delta V / \Delta P$ — how easily the lung inflates. It falls in fibrosis (stiff lung, hard to inflate) and rises in emphysema (destroyed elastin, easy to inflate but poor recoil, so air trapping occurs).
Roughly two-thirds of elastic recoil comes not from tissue but from surface tension at the air–liquid interface of the alveolus. Laplace's law for a sphere gives collapsing pressure
so at equal surface tension a small alveolus generates a larger collapsing pressure than a large one and would empty into its neighbor. Pulmonary surfactant, a phospholipid-rich secretion (chiefly dipalmitoylphosphatidylcholine) from type II pneumocytes, lowers $T$ and does so more effectively at smaller radii, equalizing pressures and stabilizing small alveoli. Surfactant appears late in gestation, which is why premature infants develop neonatal respiratory distress syndrome.
Lung Volumes and Capacities
| Volume | Definition | Typical adult value |
|---|---|---|
| Tidal volume (TV) | Air moved in one quiet breath | ~500 mL |
| Inspiratory reserve (IRV) | Additional air inhaled beyond TV | ~3000 mL |
| Expiratory reserve (ERV) | Additional air exhaled beyond TV | ~1100 mL |
| Residual volume (RV) | Air remaining after maximal exhalation | ~1200 mL |
Capacities are sums of volumes:
- Vital capacity $= \text{IRV} + \text{TV} + \text{ERV}$ (~4600 mL) — the maximum voluntarily moved.
- Total lung capacity $= \text{VC} + \text{RV}$ (~5800 mL).
- Functional residual capacity $= \text{ERV} + \text{RV}$ — the volume left after a quiet exhalation.
- Inspiratory capacity $= \text{TV} + \text{IRV}$.
Classic exam point: residual volume can never be exhaled, so spirometry cannot measure RV, FRC or TLC; these require helium dilution, nitrogen washout or body plethysmography.
Dead space. About $150\text{ mL}$ of each tidal breath fills conducting airways where no gas exchange occurs (anatomic dead space). Alveolar ventilation therefore equals $(\text{TV} - \text{dead space}) \times$ respiratory rate. Shallow rapid breathing moves the same minute volume but ventilates the alveoli far less efficiently than slow deep breathing — a favorite quantitative twist.
Neural Control of Breathing
Breathing is generated by brainstem networks and modulated by chemical feedback.
- Medullary rhythmicity center: the dorsal respiratory group (DRG) sets the basic inspiratory rhythm via the phrenic and intercostal nerves; the ventral respiratory group (VRG) is recruited for forced breathing.
- Pontine respiratory group smooths the transition between inspiration and expiration.
- Voluntary cortical override exists but is limited — rising $\text{CO}_2$ eventually forces a breath, which is why breath-holding cannot be sustained to unconsciousness under normal conditions.
Chemoreceptors
| Receptor | Location | Primary stimulus | Notes |
|---|---|---|---|
| Central | Ventral medulla | $\text{H}^+$ in cerebrospinal fluid, generated from diffused $\text{CO}_2$ | Dominant minute-to-minute drive; $\text{H}^+$ itself cannot cross the blood-brain barrier, but $\text{CO}_2$ can |
| Peripheral | Carotid bodies (glossopharyngeal, CN IX) and aortic bodies (vagus, CN X) | $\downarrow$ arterial $\text{PO}_2$, plus $\uparrow \text{PCO}_2$ and $\downarrow$ pH | Oxygen response is weak until $\text{PaO}_2 < 60\text{ mmHg}$ |
Carbon dioxide, not oxygen, is the normal drive to breathe. This is the single most tested fact in respiratory control. It follows directly from the equilibrium of Section 10.1:
Respiratory Control of Blood pH
The lung is the fast arm of acid-base regulation (the kidney, covered in 10.6, is the slow arm).
- Hyperventilation blows off $\text{CO}_2$, shifting the equilibrium left, lowering $[\text{H}^+]$ and raising pH: respiratory alkalosis.
- Hypoventilation retains $\text{CO}_2$, shifting the equilibrium right and lowering pH: respiratory acidosis.
- A metabolic acidosis is compensated by hyperventilation (Kussmaul breathing in diabetic ketoacidosis), which is a direct application of Le Châtelier's principle to physiology.
The bicarbonate buffer relationship is
Non-Respiratory Airway Functions
The AAMC outline explicitly lists two additional roles for the respiratory tract.
Particulate filtration. Coarse nasal hairs (vibrissae) trap large particles; beyond that the mucociliary escalator — pseudostratified ciliated columnar epithelium with goblet cells (see 8.3) — traps particles in mucus and sweeps them upward toward the pharynx to be swallowed. Alveolar macrophages clear whatever reaches the alveolus. Smoking paralyzes the cilia, which is why the escalator fails and a chronic cough develops.
Thermoregulation and humidification. Extensive nasal and tracheal capillary beds warm inspired air to body temperature and saturate it with water vapor before it reaches the alveoli, protecting the delicate exchange surface. In many mammals the same beds are used in reverse for evaporative cooling by panting: rapid shallow breathing moves air across the moist nasal and oral surfaces, dumping heat as latent heat of vaporization while keeping alveolar ventilation nearly unchanged, so respiratory alkalosis is avoided. Humans rely on sweating instead (see 11.5).
A patient sustains a penetrating chest wound that opens the pleural cavity to the atmosphere. The affected lung collapses immediately. Which mechanism best explains this outcome?
A healthy volunteer voluntarily hyperventilates for two minutes. Which set of changes is expected in arterial blood?
Two subjects have identical minute ventilation of 6000 mL per minute and identical anatomic dead space of 150 mL. Subject A breathes 500 mL twelve times per minute; Subject B breathes 250 mL twenty-four times per minute. What is Subject B's alveolar ventilation relative to Subject A's?