Mechanics of breathing
Mechanics of breathing: compliance, surfactant, pleural pressure and airway resistance
Inspiration is active and quiet expiration is passive recoil; compliance, surfactant and airway resistance decide how hard breathing is. Covers Laplace's law, L:S ratio, closing capacity, Poiseuille, heliox and the work of breathing.
The core idea
Air flows from high to low pressure. To breathe in, the chest must expand so that alveolar pressure falls below atmospheric. The lungs follow the chest wall because the visceral and parietal pleura are held together by a thin fluid film at negative intrapleural pressure; this negative pressure is what keeps the lung inflated.
Muscles and chest wall movements
| Phase | Muscles | Notes |
|---|---|---|
| Quiet inspiration | Diaphragm (phrenic, C3–C5), external intercostals | Diaphragm gives most of the tidal volume |
| Quiet expiration | None | Passive elastic recoil of lung and chest wall |
| Forced inspiration | Sternocleidomastoid, scalenes, pectoralis minor, serratus anterior | Lift and fix the upper ribs |
| Forced expiration (cough, sneeze, FVC) | Rectus abdominis, obliques, transversus abdominis, internal intercostals | Push the diaphragm up and pull ribs down |
- Pump-handle movement: the upper ribs (2nd to 6th) rise and the sternum moves forward, increasing the anteroposterior diameter; produced mainly by the external intercostals.
- Bucket-handle movement: the lower ribs swing upward and outward, increasing the transverse diameter.
- Diaphragmatic descent increases the vertical diameter.
Pressures through a breath
| Pressure | At rest (end of expiration) | During quiet inspiration |
|---|---|---|
| Alveolar | 0 (atmospheric) | About −1 cmH₂O, so air flows in |
| Intrapleural | About −5 cmH₂O | Falls to about −7.5 cmH₂O |
| Transpulmonary (alveolar − pleural) | +5 | Rises, keeping the lung expanded |
- If air enters the pleural space (pneumothorax), intrapleural pressure becomes atmospheric, the lung recoils inward and collapses, and the chest wall springs slightly outward.
- In the upright lung, intrapleural pressure is more negative at the apex, so apical alveoli are larger at rest; basal alveoli sit on a steeper part of the compliance curve and are better ventilated per breath.
Compliance
Compliance = change in volume ÷ change in transpulmonary pressure, about 200 mL/cmH₂O for both lungs alone and about 110 mL/cmH₂O for lungs and chest wall together. A compliant lung inflates easily; it is inversely related to elastic recoil (elastance).
| Low compliance (stiff) | High compliance (floppy) |
|---|---|
| Pulmonary fibrosis | Emphysema (destroyed elastic tissue) |
| Pulmonary oedema, ARDS | Old age |
| Surfactant deficiency (neonatal RDS) | Normal lung during deflation (hysteresis) |
| Atelectasis, pneumonia | |
| Chest wall: obesity, kyphoscoliosis, circumferential chest burn eschar |
- Emphysema, most strongly linked to smoking, destroys alveolar walls; the lungs are large, overinflated and recoil poorly, so air is trapped and expiration is slow.
- A full-thickness circumferential chest burn forms a rigid eschar that stops the chest expanding: airway pressures rise and tidal volumes fall. Escharotomy releases it (cutting dead skin needs little anaesthesia).
- ARDS (for example after pancreatitis) produces stiff, low-compliance lungs with PaO₂/FiO₂ below 300 (severe below 100). Low tidal volume ventilation of about 6 mL/kg predicted (height-based) body weight limits overdistension injury and improves survival.
- Hysteresis: the pressure–volume curve differs between inflation and deflation, mainly because of surface tension; a saline-filled lung shows almost none.
Surface tension and surfactant
The fluid lining alveoli has surface tension that pulls them inward. By the law of Laplace, P = 2T/r: the collapsing pressure is directly proportional to surface tension and inversely proportional to radius. Without surfactant, small alveoli would empty into large ones.
Surfactant is mainly phospholipid, especially dipalmitoylphosphatidylcholine (DPPC, lecithin), with surfactant proteins A–D and calcium, secreted by type II pneumocytes from lamellar bodies. Its hydrophilic heads sit in the fluid and its hydrophobic tails face the air, so the molecules spread between surface water molecules and weaken their attraction. It:
- lowers surface tension (to well below that of plain water), increasing compliance and reducing the work of breathing
- lowers it more in small alveoli, where it is more concentrated, stabilising alveoli of different size
- reduces the suction of fluid from capillaries into alveoli, keeping them dry
Surfactant deficiency raises surface tension, lowers compliance and causes widespread alveolar collapse (atelectasis), hypoxaemia and hyaline membranes: neonatal respiratory distress syndrome (hyaline membrane disease), the commonest cause of respiratory failure and death in premature babies.
| Lung maturity factor | Effect |
|---|---|
| Gestation | Production starts about 24 weeks, adequate by about 34–35 weeks |
| Fetal cortisol | Main physiological stimulus to surfactant synthesis and lung maturation |
| Antenatal betamethasone or dexamethasone | Accelerates maturity; given for threatened preterm delivery |
| Thyroid hormone | Helps |
| Maternal diabetes (fetal hyperinsulinaemia) | Delays maturity |
| Lecithin:sphingomyelin ratio | Above 2 in amniotic fluid predicts mature lungs |
Closing capacity and postoperative atelectasis
Small airways have no cartilage and are held open by radial traction. Closing capacity is the lung volume at which dependent small airways begin to close. It rises with age, smoking and obesity. Normally FRC is above it. After upper abdominal surgery, pain, splinting, supine posture and diaphragm dysfunction lower FRC below closing capacity, so basal airways close during tidal breathing and the alveoli beyond them collapse. This causes reduced breath sounds at the bases and mild fever on day 1–2; deep breathing, early mobilisation and good analgesia prevent it.
Airway resistance
- Poiseuille's law: for laminar flow, resistance = 8ηl/πr⁴, so halving the radius raises resistance 16-fold.
- Yet the medium-sized bronchi (around the 4th to 8th generations) give the greatest resistance. The smallest bronchioles are individually narrow but so numerous in parallel that their total resistance is low.
- Flow is turbulent in the large airways and at high flow rates. Turbulent resistance depends on gas density, not viscosity. Heliox (helium–oxygen) has a low density, so it reduces turbulent resistance and the work of breathing in upper airway obstruction such as severe croup while steroids act; it carries only about 21–30% oxygen, so it is unsuitable in severe hypoxia.
- Bronchodilation: beta-2 stimulation (adrenaline, salbutamol), high lung volume.
- Bronchoconstriction: vagal M3 stimulation, histamine, leukotrienes, cold air, irritants, low lung volume.
- Lung volume: resistance falls at high volumes as radial traction pulls airways open. In emphysema loss of traction lets airways collapse on forced expiration (dynamic compression); pursed-lip breathing keeps them open.
- Increased airway resistance lowers FEV₁ and peak flow and increases the work of breathing.
Work of breathing
| Component | Share in quiet breathing |
|---|---|
| Elastic (compliance) work | About 65% |
| Airway resistance work | About 28% |
| Tissue viscous resistance | About 7% |
Quiet breathing uses only about 3–5% of total body oxygen consumption, rising greatly in disease. Restrictive patients minimise elastic work with rapid shallow breaths; obstructive patients minimise resistive work with slow deep breaths.
Remember Surfactant from type II cells beats Laplace; airway resistance peaks in medium bronchi; quiet expiration is free recoil.
Exam trap Greatest airway resistance is in the medium-sized bronchi, not the terminal bronchioles.
Exam trap Emphysema increases compliance; fibrosis, oedema and surfactant deficiency decrease it.
How FCPS asks about this
- Laplace's law: P = 2T/r; small alveoli collapse unless surfactant lowers T.
- Surfactant source and function: type II pneumocytes, DPPC; lowers surface tension, raises compliance, prevents collapse and oedema; absence causes neonatal RDS.
- Main fetal stimulus for surfactant: cortisol; maternal diabetes delays it; L:S above 2 means mature.
- Compliance increased in: emphysema and old age; decreased in fibrosis, oedema, RDS, chest wall burns.
- Basal atelectasis after upper abdominal surgery: FRC falls below closing capacity.
- Most of the work of breathing: elastic work, about 65%.
- Heliox in croup: low density reduces turbulent airway resistance.
Test yourself on this topic
5 of the 30 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
Why are patients after upper abdominal surgery especially prone to basal atelectasis?
Answer: FRC falls below closing capacity
After upper abdominal incisions, pain causes shallow breathing, poor cough and diaphragmatic splinting, while lying supine and anaesthesia also reduce functional residual capacity. When FRC falls below closing capacity, small basal airways close during normal breathing and the alveoli behind them collapse. Good analgesia (often epidural), early mobilisation, sitting up, deep breathing exercises and incentive spirometry help prevent it.
Postoperative atelectasis
- ↓ FRC (pain, supine, anaesthesia)
- FRC < closing capacity
- Basal airway closure
- Prevent: analgesia, mobilise, breathe deep
Remember Low FRC closes small airways.
Exam trap Early postoperative fever (day 1–2) is often attributed to atelectasis, but other causes must be excluded.
Why the other options are wrong
- Surfactant production stops completely It is reduced only locally, not stopped.
- Airway resistance falls too low Not the mechanism.
- The diaphragm becomes hypertrophied Not the mechanism.
- Lung compliance rises sharply Compliance falls with atelectasis.
On the first day after a laparotomy, a patient has a temperature of 37.9 °C, is comfortable and has reduced breath sounds at both bases. What is the most likely cause?
Answer: Inflammatory response, atelectasis
A low-grade fever in the first 24–48 hours after surgery is usually the normal inflammatory response to tissue injury, often with basal atelectasis; treatment is early mobilisation, breathing exercises and analgesia. Later causes follow a rough timeline: chest infection (days 2–3), urinary infection (days 3–5), wound infection and anastomotic leak (days 5–7), DVT (days 7–10). A very sick patient on day 1 still needs full assessment.
Postoperative fever
- Day 1–2: inflammation, atelectasis
- Day 2–3: chest infection
- Day 3–5: urinary infection
- Day 5–7: wound, leak
- Day 7–10: DVT
Remember Timing of fever points to its cause.
Exam trap Day 1 fever with a very sick patient may be a missed injury or early necrotising infection.
Why the other options are wrong
- Anastomotic leak Usually days 5–7.
- Deep wound infection Usually days 5–7.
- Deep vein thrombosis Usually later.
- Catheter-related urinary infection Usually days 3–5.
A ventilated patient with severe pancreatitis has bilateral infiltrates, PaO₂/FiO₂ ratio 120 and normal heart function. Lungs need very high pressures to inflate. Which ventilation strategy improves survival?
Answer: Low tidal volume, about 6 mL/kg
In ARDS, inflammation floods and collapses alveoli, reducing compliance and causing shunt. Only part of the lung is ventilated (the 'baby lung'), so normal tidal volumes overstretch it and worsen injury. Lung-protective ventilation with tidal volume about 6 mL/kg predicted body weight, plateau pressure under 30 cmH₂O and adequate PEEP reduces mortality. Prone positioning helps in severe cases.
ARDS ventilation
- Low compliance, shunt
- 6 mL/kg tidal volume
- Plateau < 30 cmH₂O
- Adequate PEEP, prone if severe
Remember Small breaths for a small lung.
Exam trap Use predicted (height-based) body weight, not actual weight.
Why the other options are wrong
- High tidal volume, about 12 mL/kg Overstretches and injures the lung.
- Zero PEEP PEEP is needed to keep alveoli open.
- 100% oxygen with low PEEP Hyperoxia and collapse both harm.
- Hyperventilation to low CO₂ No benefit; reduces cerebral blood flow.
During inspiration the upper ribs rise and the sternum moves forward, increasing the anteroposterior diameter of the chest. What is this movement called, and which muscles mainly produce it?
Answer: Pump-handle movement; external intercostals
Upper ribs (2–6) move upwards and forwards with the sternum (pump-handle), increasing the anteroposterior diameter. Lower ribs swing outwards (bucket-handle), increasing the transverse diameter. External intercostals (with scalenes stabilising the first ribs) raise the ribs; the diaphragm, the main muscle of quiet breathing, increases the vertical diameter.
Rib movements
- Upper ribs: pump-handle, AP diameter
- Lower ribs: bucket-handle, transverse
- Diaphragm: vertical diameter
- Raise ribs: external intercostals
Remember Pump-handle pushes the sternum forward.
Exam trap Quiet expiration is passive elastic recoil.
Why the other options are wrong
- Bucket-handle movement; diaphragm Bucket-handle is lower ribs and transverse diameter; diaphragm is vertical.
- Pump-handle movement; internal intercostals Internal intercostals mainly help forced expiration.
- Caliper movement; abdominal muscles Not this movement.
- Bucket-handle movement; scalenes Bucket-handle is lower ribs.
Cartilage disappears from the airway wall at which level, leaving smooth muscle to control diameter?
Answer: Bronchioles
The trachea has C-shaped cartilage rings, and bronchi have irregular cartilage plates. Bronchioles (under about 1 mm) have no cartilage and no glands, so their calibre depends on smooth muscle and on radial traction from surrounding lung. That is why bronchospasm in asthma and airway collapse in emphysema mainly affect small airways.
Airway wall
- Trachea: C-rings
- Bronchi: cartilage plates
- Bronchioles: no cartilage, no glands
- Held open by radial traction
Remember No cartilage below 1 mm: the bronchiole.
Exam trap Bronchioles also lack submucosal glands.
Why the other options are wrong
- Trachea Has C-shaped rings.
- Main bronchi Have cartilage plates.
- Lobar bronchi Have cartilage plates.
- Segmental bronchi Have cartilage plates.
Where this sits in the CPSP syllabus
- Paper 1: Respiratory system, Mechanics of breathing: compliance, surfactant, airway resistance
- Surgery & Allied, Paper 2: Respiratory system, Mechanics of breathing: compliance, surfactant, airway resistance
- Medicine & Allied, Paper 2: Respiratory system, Mechanics of breathing: compliance, surfactant, airway resistance
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