Lung volumes and spirometry
Lung volumes, capacities, dead space and pulmonary function tests (spirometry)
Four lung volumes add up to four capacities; spirometry cannot measure residual volume, FRC or TLC. Learn dead space, FEV₁/FVC patterns, reversibility and transfer factor for obstructive versus restrictive disease.
The core idea
The lung never empties completely. Each breath moves air in and out on top of a volume that always stays behind. Learn the four basic volumes; every capacity is a sum of two or more of them, and a question that describes a manoeuvre ("breathed out normally, then in maximally") is asking you to name the matching capacity.
Volumes and capacities (typical adult male)
| Name | Definition | Approximate value |
|---|---|---|
| Tidal volume (TV) | Air moved in a quiet breath | 500 mL |
| Inspiratory reserve volume (IRV) | Extra air that can be breathed in after a normal inspiration | 3,000 mL |
| Expiratory reserve volume (ERV) | Extra air that can be forced out after a normal expiration | 1,100 mL |
| Residual volume (RV) | Air left after maximal expiration | 1,200 mL |
| Inspiratory capacity (IC) | TV + IRV: maximum breath in starting from the end of a normal expiration | 3,500 mL |
| Functional residual capacity (FRC) | ERV + RV: volume left after a normal tidal expiration | 2,300 mL |
| Vital capacity (VC) | IRV + TV + ERV: maximum breathed out after maximum breath in | 4,600 mL |
| Total lung capacity (TLC) | VC + RV | 5,800 mL |
- Rearranging: IRV = IC − TV, or IRV = VC − (TV + ERV). ERV = FRC − RV.
- Volumes are about 20–25% lower in women.
- FRC is the resting point of the respiratory system: the inward elastic recoil of the lungs exactly balances the outward recoil of the chest wall, with no muscle acting. It is the oxygen store between breaths, which is why preoxygenation fills the FRC with oxygen before intubation.
- Residual volume keeps alveoli open after maximal expiration and prevents complete lung collapse; it exists because small airways close (and the chest wall cannot be compressed further) before the lung empties.
Muscles that move these volumes
- Quiet inspiration is active: the diaphragm produces about two-thirds to three-quarters of tidal volume, helped by the external intercostals.
- Quiet expiration is passive elastic recoil.
- Forced expiration (FVC, peak flow, coughing) uses the abdominal wall muscles (rectus abdominis, external and internal obliques, transversus abdominis) and the internal intercostals.
- Forced inspiration adds sternocleidomastoid, scalenes and other accessory muscles.
What spirometry can and cannot measure
A spirometer records only air that moves, so it measures TV, IRV, ERV, IC, VC, FEV₁, FVC and peak flow. It cannot measure residual volume, and therefore cannot measure FRC or TLC. These need:
- Helium dilution: measures gas in airways that communicate with the mouth; it underestimates volume in severe COPD with trapped air.
- Body plethysmography: measures all gas in the thorax, including trapped gas (based on Boyle's law).
- Nitrogen washout.
Dead space
- Anatomical dead space: the conducting airways from nose to terminal bronchioles, about 150 mL (roughly 2 mL/kg). Measured by Fowler's method (single-breath nitrogen washout).
- Alveolar dead space: alveoli that are ventilated but not perfused. Negligible in health.
- Physiological (total) dead space = anatomical + alveolar. In health the two are nearly equal (about 30% of tidal volume). It rises in pulmonary embolism, emphysema, low cardiac output and positive-pressure ventilation. It is measured with the Bohr equation: VD/VT = (PaCO₂ − PECO₂)/PaCO₂.
| Factor | Effect on anatomical dead space |
|---|---|
| Neck extension, jaw protrusion | Increases (airways stretched longer and wider) |
| Neck flexion | Decreases |
| Deep inspiration (large lung volume) | Increases (airways pulled open) |
| Bronchodilators, atropine | Increase |
| Bronchoconstriction | Decreases |
| Tracheostomy or endotracheal tube | Decreases (bypasses nose, mouth and pharynx; helps weaning) |
| Anaesthetic face mask and circuit | Adds apparatus dead space |
| Body size and age | Increase with size and age |
- Alveolar ventilation = (tidal volume − dead space) × respiratory rate. At the same minute volume, rapid shallow breathing wastes a larger fraction on dead space and ventilates alveoli less than slow deep breathing. Alveolar ventilation, not minute ventilation, sets PaCO₂.
Spirometry patterns
| Measure | Obstructive (asthma, COPD) | Restrictive (fibrosis, chest wall, neuromuscular) |
|---|---|---|
| FEV₁ | ↓↓ | ↓ |
| FVC | ↓ or normal | ↓↓ |
| FEV₁/FVC | < 0.7 | Normal or high (stiff lungs empty fast) |
| TLC | Normal or ↑ (hyperinflation) | ↓ (defines restriction) |
| RV and FRC | ↑ (air trapping) | ↓ |
| Peak flow | ↓ | Normal or slightly ↓ |
| Transfer factor (TLCO) | ↓ in emphysema; normal or ↑ in asthma | ↓ in fibrosis; normal in chest wall and neuromuscular disease |
- In obstruction, airways close early in expiration and trap air, so RV, FRC and TLC increase; vital capacity falls because RV takes up more of TLC.
- In restriction, all volumes fall together; FEV₁ and FVC fall in proportion, so the ratio is preserved or high.
Reversibility and gas transfer
- Reversibility: a rise in FEV₁ of at least 12% and 200 mL after a bronchodilator shows reversible airflow obstruction and supports asthma. An FEV₁ rising from 2.0 to 2.5 L (25%, 500 mL) is clearly reversible. A large response with a still-low ratio (for example FEV₁/FVC 40% improving by 18%) is reversible obstruction. A negative test does not exclude asthma, especially when the patient is well or already treated.
- COPD is largely irreversible. An infective exacerbation is treated with bronchodilators, antibiotics if sputum is purulent, and oral prednisolone 30 mg daily for 5 days (check glucose in diabetics).
- Transfer factor (TLCO, DLCO) measures carbon monoxide uptake across the alveolar membrane. It falls when the membrane thickens (pulmonary fibrosis), when surface area is lost (emphysema), when the pulmonary capillary bed is lost (pulmonary embolism, pulmonary hypertension) and in anaemia (correct for haemoglobin). It rises with polycythaemia, alveolar haemorrhage, and sometimes asthma. KCO is transfer factor corrected for alveolar volume.
Flow–volume loops
- Obstruction: a scooped-out (concave) expiratory limb.
- Restriction: a small, tall, narrow loop (small volumes, flows preserved for volume).
- Fixed upper airway obstruction (tracheal stenosis, goitre): both limbs flattened into a box.
- Variable extrathoracic obstruction (vocal cord palsy): flattened inspiratory limb. Variable intrathoracic obstruction: flattened expiratory limb.
Changes worth knowing
- Posture: FRC falls on lying down because abdominal contents push the diaphragm up. It falls further under anaesthesia, in obesity and in late pregnancy, so these patients desaturate quickly.
- Age: loss of elastic recoil raises RV and FRC and lowers VC; TLC stays roughly constant.
- Pregnancy: FRC, ERV and RV fall; tidal volume and minute ventilation rise (progesterone); VC is unchanged.
Remember Capacities are sums of volumes; anything that contains RV (FRC, TLC) cannot be measured by a spirometer.
Exam trap In restrictive disease the FEV₁/FVC ratio is normal or raised, not reduced; the defining finding is a low TLC.
Exam trap Extending the neck increases anatomical dead space; a tracheostomy reduces it.
How FCPS asks about this
- Volume left after a normal expiration: FRC (ERV + RV); after maximal expiration: residual volume.
- Normal expiration then maximal inspiration: inspiratory capacity (TV + IRV); IRV is IC minus TV.
- Cannot be measured by spirometry: RV, FRC, TLC; use helium dilution or body plethysmography.
- Capacity that increases in obstructive disease: TLC, FRC and RV rise from air trapping.
- Restrictive disease: low TLC, low FVC, normal or high FEV₁/FVC; fibrosis also lowers TLCO.
- Physiological dead space: anatomical plus alveolar; measured by the Bohr equation; rises in PE and emphysema.
- Muscles of forced expiration: abdominal wall muscles and internal intercostals.
Test yourself on this topic
5 of the 32 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A 66-year-old woman with a large retrosternal goitre has stridor on exertion. Her flow–volume loop shows flattening of both the inspiratory and the expiratory limbs, giving a box shape. What does this pattern indicate?
Answer: Fixed upper airway obstruction
A flow–volume loop plots flow against lung volume during a forced expiration and a forced inspiration. A rigid narrowing of the central airway (goitre compressing the trachea, tracheal stenosis after intubation) limits peak flow equally in both directions, flattening both limbs into a box. Variable lesions change with breathing: an extrathoracic lesion (vocal cord palsy) narrows further on inspiration, when the airway pressure falls below atmospheric, so the inspiratory limb flattens; an intrathoracic lesion (tracheomalacia, tumour in the lower trachea) narrows on forced expiration, when pleural pressure squeezes the airway, so the expiratory limb flattens. COPD gives a concave, scooped expiratory limb; restriction gives a tall narrow loop with small volumes.
Flow–volume loops
- Fixed upper airway: both limbs flat
- Variable extrathoracic: inspiratory flat
- Variable intrathoracic: expiratory flat
- COPD: scooped expiration
- Restriction: tall, narrow
Remember Rigid narrowing limits flow both ways.
Exam trap Extrathoracic lesions are worse on inspiration; intrathoracic lesions are worse on expiration.
Why the other options are wrong
- Variable extrathoracic obstruction A variable extrathoracic lesion flattens only the inspiratory limb.
- Variable intrathoracic obstruction A variable intrathoracic lesion flattens only the expiratory limb.
- Small airway obstruction from COPD COPD gives a scooped expiratory limb, not a flat one.
- Restrictive lung disease Restriction narrows the loop; flow is near normal for the volume.
A 55-year-old woman with severe kyphoscoliosis is breathless. FEV₁ and FVC are both reduced with a ratio of 0.85, and TLC is low. TLCO is low, but the transfer coefficient (KCO) is raised. Which of the following best explains this pattern?
Answer: Small but normal lungs inside a stiff chest wall
In chest wall or neuromuscular restriction the lungs themselves are normal but cannot expand fully. Total gas transfer (TLCO) falls because alveolar volume is small, but per litre of lung the uptake of CO is normal or high, because the pulmonary capillary blood volume is spread through less expanded lung, so KCO rises. In fibrosis both TLCO and KCO are usually low because the alveolar–capillary membrane itself is damaged. Emphysema, emboli and anaemia all lower KCO.
Extrapulmonary restriction
- Low TLC, ratio normal or high
- TLCO low from small alveolar volume
- KCO normal or raised
- Fibrosis: KCO low
Remember Low TLCO with a high KCO: look at the chest wall.
Exam trap Always look at KCO as well as TLCO; a low TLCO alone cannot separate lung disease from chest wall disease.
Why the other options are wrong
- Thickened alveolar walls from fibrosis Fibrosis lowers KCO as well as TLCO.
- Loss of alveolar capillary bed in emphysema Emphysema lowers KCO.
- Pulmonary emboli blocking capillaries Emboli reduce capillary blood volume and lower KCO.
- Anaemia lowering uptake of carbon monoxide Anaemia lowers KCO.
A man with idiopathic pulmonary fibrosis has reduced FVC and TLC with a normal FEV₁/FVC ratio. Which gas transfer finding is expected?
Answer: Reduced TLCO
Pulmonary fibrosis thickens the alveolar-capillary membrane and destroys capillaries, reducing gas transfer (TLCO, DLCO). Lung volumes are reduced (restrictive pattern) and the FEV₁/FVC ratio is normal or high. TLCO is also reduced in emphysema and pulmonary vascular disease, but raised in alveolar haemorrhage and polycythaemia.
Gas transfer
- Fibrosis: TLCO reduced
- Emphysema: TLCO reduced
- Haemorrhage: TLCO raised
- Restriction with low TLCO: lung disease
Remember Thick membrane, poor transfer.
Exam trap Anaemia lowers TLCO; correct for haemoglobin.
Why the other options are wrong
- Raised TLCO Seen in alveolar haemorrhage, polycythaemia.
- Normal TLCO Abnormal in fibrosis.
- Raised KCO only Not typical.
- TLCO cannot be measured It is routinely measured.
A man with an infective COPD exacerbation is treated with nebulisers and antibiotics. What course of oral prednisolone is usually recommended?
Answer: 30–40 mg daily for 5 days
Oral prednisolone 30–40 mg daily for 5 days in a COPD exacerbation shortens recovery, improves lung function and reduces treatment failure. Five days is as effective as longer courses with fewer side effects, so no taper is needed. Long-term oral steroids are avoided in COPD because of harm.
COPD exacerbation
- Prednisolone 30–40 mg for 5 days
- Bronchodilators
- Antibiotics if purulent sputum
- Controlled oxygen
Remember Five days of steroids for a COPD flare.
Exam trap Check glucose in diabetics on steroids.
Why the other options are wrong
- Single dose only Too short.
- 60 mg daily for 6 weeks Too long; more harm.
- Lifelong low dose Harmful.
- No steroids in COPD Short courses help.
A woman with painful pleurisy takes rapid shallow breaths with a normal minute volume, yet her PaCO₂ is rising. What explains this?
Answer: More of each breath is dead space
Each breath must first fill the conducting airways, about 150 mL of anatomical dead space, before fresh gas reaches the alveoli. Alveolar ventilation = (tidal volume − dead space) × rate, so at 200 mL × 30 a minute it is only 1.5 L/min, against 4.2 L/min at 500 mL × 12, although both minute volumes are about 6 L/min. With less alveolar ventilation, PaCO₂ rises. CO₂ diffuses very easily, so diffusion is not the problem.
Alveolar ventilation
- Alveolar ventilation = (VT − VD) × rate
- Dead space about 150 mL (2 mL/kg)
- Shallow breaths are mostly dead space
- Low alveolar ventilation raises PaCO₂
Remember Small breaths waste most of the air.
Exam trap A normal minute ventilation does not guarantee normal alveolar ventilation; look at the tidal volume.
Why the other options are wrong
- Her CO₂ production has doubled Nothing suggests a large rise in CO₂ production.
- Pleural pain lowers CO₂ diffusion CO₂ diffuses about 20 times more readily than O₂.
- Her central chemoreceptors are depressed She is breathing fast, so her drive is not depressed.
- Shallow breaths increase lung compliance Shallow breathing does not increase compliance.
Where this sits in the CPSP syllabus
- Paper 1: Respiratory system, Lung volumes, capacities and pulmonary function tests
- Surgery & Allied, Paper 2: Respiratory system, Lung volumes, capacities and pulmonary function tests
- Medicine & Allied, Paper 2: Respiratory system, Lung volumes, capacities and pulmonary function tests
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