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PY6.1-13 | Respiratory Physiology — Part 1
CLINICAL SCENARIO
You breathe about 20,000 times a day without thinking about it. But try holding your breath for 60 seconds — your body FORCES you to breathe. Your diaphragm contracts against your will, your chest heaves, and air rushes in. Why can't you override this? Because the brainstem's respiratory centres treat breathing like a heartbeat — non-negotiable. By the end of this module, you'll understand every step: from the muscle contraction that creates negative pressure, to the gas exchange at the alveolar membrane, to the chemoreceptor that detected rising CO₂ and forced you to inhale.
WHY THIS MATTERS
As a doctor, respiratory physiology is your diagnostic toolkit. In the emergency department, you'll use pulse oximetry (PY6.8), arterial blood gases (PY6.9), and peak flow (PY6.13) within the first minutes of seeing a breathless patient. In the ICU, you'll set ventilator parameters based on lung compliance (PY6.3), dead space (PY6.5), and V/Q matching (PY6.10). In general practice, you'll interpret spirometry (PY6.4) to diagnose asthma and COPD. And in anaesthesia, you'll manage airway resistance, surfactant physiology, and the oxyhaemoglobin dissociation curve in every surgical case.
RECALL
From Anatomy (AN21), you know that the thoracic cage changes volume during breathing through pump-handle movement (upper ribs, AP expansion) and bucket-handle movement (lower ribs, transverse expansion), plus diaphragmatic descent (vertical expansion). You know that the intercostal muscles are layered (external = inspiration, internal = expiration). You know the pleura has a visceral layer (on the lung) and a parietal layer (on the chest wall) with a thin pleural space between them. Now we'll see HOW these structures create the pressure changes that drive airflow.
Functional Anatomy for Physiology (PY6.1)
Before diving into mechanics, let's map the respiratory tract as a physiologist sees it — not by anatomy but by function:
Figure: Functional Anatomy for Physiology (PY6.1)
The conducting zone (nose to terminal bronchioles) — moves air but does NO gas exchange. This is "anatomical dead space" (about 150 mL). It includes: nasal cavity → pharynx → larynx → trachea → main bronchi → lobar bronchi → segmental bronchi → terminal bronchioles. Air is warmed, humidified, and filtered here. The walls contain cartilage (for support) and smooth muscle (for bronchoconstriction/dilation).
The respiratory zone (respiratory bronchioles → alveolar ducts → alveoli) — where gas exchange happens. This is the business end of the lung. You have about 300 million alveoli with a combined surface area of ~70 m² — the size of half a tennis court, all packed into your chest.
The respiratory membrane (= alveolar-capillary membrane) — the barrier across which O₂ and CO₂ diffuse. It's only 0.2–0.5 μm thick and has these layers:
1. Alveolar epithelium (Type I pneumocytes — flat, for gas exchange)
2. Epithelial basement membrane
3. Interstitial space (very thin)
4. Capillary basement membrane
5. Capillary endothelium
Type II pneumocytes are cuboidal cells that secrete surfactant — we'll see why this is critical in the next section.
Key number: The pulmonary capillary blood takes about 0.75 seconds to transit the alveolar capillary. Gas exchange is complete in just 0.25 seconds — giving a threefold safety margin. This matters in exercise, when transit time shortens.
Mechanics of Breathing — How Air Moves (PY6.2)
Air flows from high pressure to low pressure. Breathing works by changing thoracic volume to change intra-alveolar pressure:
Figure: Mechanics of Breathing — How Air Moves (PY6.2)
Boyle's Law: P₁V₁ = P₂V₂ — at constant temperature, if volume increases, pressure decreases (and vice versa).
Inspiration (active process):
1. The diaphragm contracts (flattens), increasing vertical diameter
2. The external intercostals contract, elevating the ribs (pump-handle + bucket-handle movements from AN21)
3. Thoracic volume increases → intrapleural pressure drops (from –5 cmH₂O to –8 cmH₂O)
4. Alveoli expand → intra-alveolar pressure drops below atmospheric (about –1 cmH₂O)
5. Air flows IN along the pressure gradient
Expiration (passive in quiet breathing):
1. The diaphragm and intercostals relax
2. The elastic recoil of the lungs and chest wall compresses the alveoli
3. Intra-alveolar pressure rises above atmospheric (about +1 cmH₂O)
4. Air flows OUT
Forced expiration recruits the internal intercostals (depress the ribs) and abdominal muscles (push the diaphragm up).
Critical concept — intrapleural pressure: The pleural space normally has a negative pressure (subatmospheric) because the lung's elastic recoil pulls inward while the chest wall springs outward. This negative pressure keeps the lungs inflated. If air enters the pleural space (pneumothorax), the negative pressure is lost, and the lung collapses.
Pressure summary during one breath cycle:
| Phase | Intra-alveolar | Intrapleural | Airflow |
|---|---|---|---|
| Before inspiration | 0 (= atmospheric) | –5 cmH₂O | None |
| During inspiration | –1 cmH₂O | –8 cmH₂O | IN |
| End inspiration | 0 | –5 cmH₂O | None |
| During expiration | +1 cmH₂O | –5 cmH₂O | OUT |
Compliance, Elastance & Surfactant (PY6.3)
Compliance = how easily the lung stretches. Defined as the change in volume per unit change in pressure:
C = ΔV / ΔP (mL/cmH₂O)
Normal lung compliance: ~200 mL/cmH₂O. A high compliance means the lung stretches easily (emphysema — destroyed elastic fibres). A low compliance means the lung is stiff (fibrosis — excess collagen).
Elastance (elastic recoil) = the opposite of compliance. It's the tendency of the lung to return to its resting volume. Elastance is high in fibrosis and low in emphysema.
Two forces contribute to elastic recoil:
1. Elastic fibres (elastin and collagen) — structural recoil
2. Surface tension at the air-liquid interface in the alveoli — accounts for 2/3 of the total elastic recoil
The problem with surface tension: Alveoli are lined with a thin film of water. Surface tension at this air-water interface tends to collapse the alveolus — like a wet balloon trying to shrink. By LaPlace's Law (P = 2T/r), smaller alveoli would have higher collapsing pressure and would empty into larger alveoli. All your small alveoli would collapse.
Surfactant — the solution: Secreted by Type II pneumocytes, surfactant is a mixture of phospholipids (mainly dipalmitoylphosphatidylcholine = DPPC) and surfactant proteins (SP-A, SP-B, SP-C, SP-D). It reduces surface tension in proportion to the alveolar size — smaller alveoli get a greater reduction, equalising pressure across alveoli of different sizes.
Surfactant:
• Reduces surface tension → increases compliance → easier to inflate
• Prevents alveolar collapse (atelectasis)
• Reduces the work of breathing
• Keeps alveoli dry (prevents transudation of fluid)
Premature babies lack surfactant (produced from ~24 weeks, mature by ~35 weeks) — they develop Respiratory Distress Syndrome (RDS) with stiff, collapsing lungs. Treatment: exogenous surfactant replacement + CPAP.
SELF-CHECK
A premature neonate at 28 weeks gestation develops respiratory distress with stiff, poorly compliant lungs and bilateral ground-glass opacities on chest X-ray. The fundamental physiological problem is:
A. Excess surfactant production causing alveolar flooding
B. Deficiency of surfactant leading to increased surface tension and alveolar collapse
C. Paralysis of the diaphragm causing inadequate ventilation
D. Obstruction of the conducting airways by meconium
Reveal Answer
Answer: B. Deficiency of surfactant leading to increased surface tension and alveolar collapse
Premature infants lack mature Type II pneumocytes and therefore have deficient surfactant. Without surfactant, surface tension is unopposed → alveoli collapse (atelectasis) → low compliance → increased work of breathing → respiratory distress syndrome (RDS). Treatment is exogenous surfactant replacement. Surfactant production begins at ~24 weeks but matures by ~35 weeks.