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Pulmonary Function Testing

🎧 Pulmonary Function Testing — deep-dive podcast

📋 Key Information Summary

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  • Spirometry is the cornerstone pulmonary function test (PFT); an FEV1/FVC ratio below the lower limit of normal (LLN) defines airflow obstruction; fixed ratio <0.70 alone may overdiagnose in older adults and underdiagnose in younger adults.
  • Quality criteria per ATS/ERS 2019: ≥3 acceptable manoeuvres, reproducibility of FEV1 and FVC within 150 mL (≥200 mL in adults), back-extrapolated volume <5% of FVC or <100 mL.
  • A positive bronchodilator response is an increase in FEV1 or FVC ≥200 mL AND ≥12% from baseline after 400 µg salbutamol MDI via spacer.
  • Lung volumes by body plethysmography are the gold standard; gas dilution (helium dilution or nitrogen washout) underestimates trapped gas. TLC <LLN confirms restriction; elevated RV/TLC ratio suggests air trapping.
  • DLCO measures gas transfer across the alveolar-capillary membrane; correct for haemoglobin (anaemia lowers DLCO), carboxyhaemoglobin (smoking), and altitude. Reduced DLCO is seen in emphysema, pulmonary fibrosis, pulmonary vascular disease, and anaemia.
  • An isolated reduction in DLCO with normal spirometry and lung volumes raises suspicion for pulmonary vascular disease (e.g., pulmonary hypertension, pulmonary embolism).
  • Methacholine challenge (bronchoprovocation) is indicated when spirometry is normal but asthma is clinically suspected; a fall in FEV1 ≥20% at ≤8 mg/mL (PC20) supports airway hyperresponsiveness.
  • Cardiopulmonary exercise testing (CPET) differentiates cardiac, pulmonary, deconditioning, and musculoskeletal causes of exertional dyspnoea using VO2max, anaerobic threshold, and ventilatory equivalents.
  • Respiratory muscle strength is assessed by maximal inspiratory pressure (MIP/SNIP) and maximal expiratory pressure (MEP); reduced values suggest neuromuscular causes of respiratory failure.
  • Spirometry is available in most Australian general practices and respiratory clinics; lung volumes, DLCO, bronchoprovocation, and CPET require specialised respiratory laboratory referral (MBS items available for spirometry and DLCO).
  • In Aboriginal and Torres Strait Islander populations, spirometry access is limited in remote communities; interpreter use, culturally safe technique coaching, and use of appropriate reference equations are essential.
  • Always interpret PFTs in clinical context — pattern recognition (obstructive, restrictive, mixed, isolated gas transfer defect) guides differential diagnosis and further investigation.
🎬 Pulmonary Function Testing — clinical explainer

Introduction & Australian Epidemiology

Pulmonary function testing (PFT) encompasses a range of objective, non-invasive measurements that assess the mechanical and physiological properties of the lungs and respiratory system. PFTs are essential for diagnosing respiratory disease, quantifying severity, monitoring disease progression, evaluating treatment response, assessing pre-operative risk, and determining disability.

In Australia, chronic respiratory diseases affect approximately 7 million people and are the third leading cause of disease burden. Chronic obstructive pulmonary disease (COPD) affects 1 in 13 Australians aged ≥40 years, while asthma affects approximately 11% of the population. Despite this burden, spirometry is underutilised in Australian primary care — studies suggest fewer than 30% of patients with newly diagnosed COPD undergo confirmatory spirometry.

The Australian Commission on Safety and Quality in Health Care (ACSQHC) and the Thoracic Society of Australia and New Zealand (TSANZ) recommend spirometry as the standard for diagnosing and monitoring obstructive airway diseases. Medicare Benefits Schedule (MBS) item numbers support spirometry (MBS 11503, 11505, 11506) and diffusing capacity testing (MBS 11506) when performed in accredited facilities.

This guideline covers the four principal domains of pulmonary function testing: spirometry, lung volume measurement, diffusing capacity, and specialised testing including bronchoprovocation, exercise testing, and respiratory muscle strength assessment.

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Accreditation: Australian respiratory laboratories should be accredited through the TSANZ/NATA spirometry accreditation program to ensure standardised technique and quality. General practices performing spirometry should follow RACGP/TSANZ minimum standards.
Pulmonary Function Testing clinical infographic — pathophysiology, clinical clues, diagnosis, imaging, and management
Tap or click image to enlarge — Pulmonary Function Testing: pathophysiology, clinical clues, diagnosis, imaging, and management.
Pulmonary Function Testing infographic, full size

Spirometry

Technique

Spirometry measures the volume of air an individual can inhale and exhale as a function of time. The forced vital capacity (FVC) manoeuvre is the fundamental measurement, yielding the key parameters: FEV1 (forced expiratory volume in 1 second), FVC, and the FEV1/FVC ratio.

1
Patient Preparation
Withhold short-acting bronchodilators (SABA/SAMA) ≥4 hours, long-acting β2-agonists (LABA) ≥12 hours, long-acting muscarinic antagonists (LAMA) ≥24 hours, and theophylline ≥48 hours before testing. Avoid smoking ≥1 hour prior. Measure standing height without shoes. Record age, sex, and ethnicity for reference equations.
2
Equipment Calibration
Spirometer must be calibrated daily with a 3 L calibration syringe (±3.5% accuracy). Volume devices (water-seal, bellows) require weekly linearity checks. Flow-based devices (turbine, pneumotachograph) require daily calibration checks per ATS/ERS 2019 standards.
3
Manoeuvre Instruction
Patient seated upright, nose clip applied. Explain: "Take the deepest breath you can, seal lips around the mouthpiece, blast the air out as hard and fast as possible, keep blowing until your lungs are completely empty (≥6 seconds in adults, ≥3 seconds in children ≥10 years)." Demonstrate the technique.
4
Performance & Reproducibility
Obtain a minimum of 3 acceptable manoeuvres (maximum 8 attempts per session). Best two FEV1 and FVC values must be within 150 mL of each other (or 100 mL if FVC <1 L). Select the highest FEV1 and highest FVC (they need not come from the same curve).

Quality Criteria (ATS/ERS 2019 Standards)

Criterion Requirement
Good start Back-extrapolated volume (BEV) <5% of FVC or <100 mL (whichever is greater); time to peak expiratory flow <120 ms (ideally <75 ms in adults)
Free from artefact No cough (in first 1 second), glottis closure, early termination, leak, or obstructed mouthpiece
Satisfactory end-of-test Plateau in volume-time curve: volume change <25 mL in final 1 second (≥1 second exhalation); exhalation time ≥6 seconds (adults), ≥3 seconds (children ≥10 years)
Reproducibility Largest two FEV1 values within 150 mL; largest two FVC values within 150 mL
Minimum acceptable curves ≥3 acceptable curves; report best FEV1 and best FVC (from any curve)
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Quality grading: Results that do not meet reproducibility criteria should be graded C or D (ATS/ERS 2019). Grade D results (only 1 acceptable curve) can be interpreted with caution. Results from fewer than 2 acceptable curves (Grade E/F) should not be used for clinical decision-making.

Key Parameters

Parameter Definition Clinical Significance
FEV1 Volume exhaled in the first second of a forced manoeuvre Marker of airflow limitation severity; used for COPD staging (GOLD), asthma monitoring, pre-operative assessment
FVC Total volume exhaled during forced manoeuvre Reduced in restriction, air trapping, and submaximal effort
FEV1/FVC ratio Proportion of FVC exhaled in 1 second Ratio <LLN (or <0.70 for COPD diagnosis per GOLD) indicates obstruction; ratio ≥LLN with low TLC confirms restriction
FEF25–75% Forced expiratory flow during middle 50% of FVC Sensitive to small airway disease; highly variable; low specificity in isolation
PEF Peak expiratory flow rate Useful for asthma self-monitoring; effort-dependent; poor for diagnosis

Interpretation Framework

Use the lower limit of normal (LLN) (5th percentile of predicted) rather than fixed ratios for interpretation. The GLI-2012 (Global Lung Function Initiative) reference equations are recommended for Australian populations, incorporating age, sex, height, and ethnicity.

Pattern FEV1/FVC FEV1 FVC Common Causes
Normal ≥LLN ≥LLN ≥LLN No significant ventilatory defect
Obstructive <LLN Reduced Normal or reduced Asthma, COPD, bronchiectasis, cystic fibrosis
Restrictive ≥LLN (or elevated) Reduced Reduced proportionally IPF, ILD, chest wall disease, obesity, neuromuscular
Mixed <LLN Reduced Reduced Combined COPD + fibrosis, advanced disease
Non-specific ≥LLN Reduced ≥LLN Suboptimal effort, early disease; requires lung volumes for confirmation

Severity Classification (FEV1 % Predicted)

Severity grading uses FEV1 as a percentage of predicted (GLI-2012 equations). This applies to both obstructive and restrictive patterns once the pattern is confirmed.

Mild
FEV1 ≥70% predicted
May be asymptomatic or have mild exertional limitation
Monitoring, risk factor modification
Moderate
FEV1 60–69% predicted
Functional impairment on exertion; may require pharmacotherapy
Outpatient specialist review recommended
Severe
FEV1 <60% predicted
GOLD COPD staging uses different cut-offs (mild ≥80%, moderate 50–79%, severe 30–49%, very severe <30%)
Significant functional limitation; specialist management required
Pulmonologist, consider supplemental oxygen assessment

Bronchodilator Response

Bronchodilator reversibility testing assesses the degree of acute improvement in airflow following administration of a short-acting bronchodilator. It is performed after baseline spirometry.

Protocol: Administer salbutamol 400 µg (8 puffs via MDI and spacer) OR ipratropium bromide 160 µg (4 puffs via MDI and spacer). Wait 15 minutes (salbutamol) or 30 minutes (ipratropium). Repeat spirometry. A positive response is defined as an increase in FEV1 or FVC ≥200 mL AND ≥12% from baseline.
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Important: A positive bronchodilator response does not confirm asthma, nor does a negative response exclude it. Up to 50% of stable COPD patients may demonstrate reversibility. Interpret in clinical context. Conversely, some asthma patients may not reverse when well-controlled or during an asymptomatic interval.

Lung Volumes

Measurement Techniques

Lung volume measurement provides essential information beyond spirometry. While spirometry measures dynamic volumes (FEV1, FVC), it cannot measure total lung capacity (TLC), residual volume (RV), or functional residual capacity (FRC) — these require body plethysmography or gas dilution techniques.

Technique Principle Measures Advantages Limitations
Body plethysmography Boyle's law (P1V1=P2V2) applied during panting manoeuvres in a sealed box FRC (thoracic gas volume), then TLC and RV calculated Gold standard; measures all lung volumes including trapped gas; fast (~3 min) Expensive equipment; claustrophobic patients; artefact from glottic closure or shallow panting
Helium dilution Equilibration of known helium concentration in a closed circuit FRC (gas-communicating volume); TLC and RV derived Widely available; less expensive than plethysmography Underestimates FRC when significant air trapping (non-communicating gas); equilibration time 3–7 min
Nitrogen washout Washout of endogenous nitrogen using 100% O2 FRC; also provides distribution of ventilation (closing volume) Additional ventilation distribution information Underestimates FRC with air trapping; requires leak-free system; O2 washout contraindicated in some patients

Lung Volume Compartments

Volume Definition Measurement
TLC (Total Lung Capacity) Volume of air in lungs at maximal inspiration FRC + IC (inspiratory capacity) or RV + VC
RV (Residual Volume) Volume remaining after maximal expiration TLC − VC or FRC − ERV
FRC (Functional Residual Capacity) Volume at end of normal tidal expiration (relaxation equilibrium) Directly measured by plethysmography or gas dilution
RV/TLC ratio Proportion of TLC that is residual volume Calculated; elevated in air trapping and hyperinflation
IC (Inspiratory Capacity) Volume from end-tidal expiration to maximal inspiration TLC − FRC

Restrictive Pattern Confirmation

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Critical rule: A restrictive pattern on spirometry (reduced FEV1 and FVC with normal or elevated FEV1/FVC ratio) must be confirmed by lung volume measurement. TLC <LLN (by plethysmography or gas dilution) confirms true restriction. If TLC is normal, the pattern is termed "non-specific" rather than restrictive. Spirometry alone cannot diagnose restriction.

Common causes of confirmed restriction (TLC <LLN):

  • Pulmonary: Idiopathic pulmonary fibrosis (IPF), hypersensitivity pneumonitis, sarcoidosis, pneumoconiosis, radiation pneumonitis
  • Extrapulmonary — chest wall: Severe kyphoscoliosis, ankylosing spondylitis (advanced), flail chest, pectus excavatum (severe)
  • Extrapulmonary — pleural: Pleural effusion, pleural thickening, mesothelioma
  • Extrapulmonary — neuromuscular: Motor neurone disease, muscular dystrophy, myasthenia gravis, diaphragmatic paralysis
  • Extrapulmonary — abdominal: Obesity (BMI >30), massive ascites, pregnancy (late)

Air Trapping and Hyperinflation

Elevated RV and RV/TLC ratio indicate air trapping, a hallmark of obstructive lung disease. In COPD:

  • RV >120% predicted and/or RV/TLC >40% suggests significant air trapping
  • Static hyperinflation (elevated FRC and IC reduction) correlates with dyspnoea severity and exercise limitation
  • Dynamic hyperinflation during exercise is an important therapeutic target (e.g., with LAMA/LABA therapy, lung volume reduction surgery)
  • A markedly elevated TLC (>120% predicted) with elevated RV suggests emphysema (loss of elastic recoil leading to overdistension)

Diffusing Capacity (DLCO)

Technique — Single-Breath Method

The diffusing capacity for carbon monoxide (DLCO, also known as transfer factor TLCO) is measured using the single-breath technique, which is the standard method in Australian respiratory laboratories.

1
Inspiration
After maximal exhalation, patient rapidly inhales to TLC a test gas mixture containing 0.3% CO, trace helium (or neon), 21% O2, balance N2.
2
Breath Hold
Hold breath at TLC for 10 seconds (±2 seconds). Avoid Valsalva or Müller manoeuvres. A glottic closure pressure <20 cmH2O is acceptable.
3
Exhalation
Rapid exhalation; discard first 750–1000 mL (dead space) and analyse the next 500–1000 mL (alveolar sample) for CO and helium concentrations.
4
Calculation
DLCO = rate of CO uptake ÷ alveolar CO driving pressure. Expressed as mL/min/mmHg (or mmol/min/kPa in SI units). Repeat after ≥4 minutes; average two measurements within 10% or 3 mL/min/mmHg.

Quality Requirements

  • Inspired volume ≥85% of largest FVC (to ensure adequate alveolar sampling)
  • Breath-hold time 8–12 seconds
  • Inspiratory time <2.5 seconds (rapid inhalation to TLC)
  • No evidence of Valsalva or Müller manoeuvre during breath hold
  • Alveolar sample collected within 3 seconds of exhalation onset
  • Two measurements within 10% of each other or 3 mL/min/mmHg

Interpretation

DLCO is expressed as a percentage of predicted (using GLI-2017 reference equations). Interpretation requires correction for confounding variables:

DLCO Level Interpretation
≥LLN (usually ≥80% predicted) Normal gas transfer
60–79% predicted Mildly reduced
40–59% predicted Moderately reduced
<40% predicted Severely reduced
>140% predicted Elevated (consider obesity correction, polycythaemia, left-to-right shunt, early pulmonary haemorrhage)

Causes of Altered DLCO

Reduced DLCO
  • Emphysema — loss of alveolar-capillary surface area (hallmark of COPD with emphysema phenotype)
  • Interstitial lung disease — IPF, NSIP, hypersensitivity pneumonitis, sarcoidosis, drug-induced ILD
  • Pulmonary vascular disease — pulmonary hypertension, chronic pulmonary embolism
  • Pneumonectomy/lobectomy — reduced lung volume
  • Anaemia — reduced haemoglobin for CO binding (must correct)
  • Restrictive chest wall/pleural disease — severe obesity, kyphoscoliosis, pleural effusion
  • Early interstitial disease — DLCO may fall before spirometry or volumes change
Elevated DLCO
  • Polycythaemia — increased haemoglobin mass
  • Left-to-right intracardiac shunt — increased pulmonary blood flow
  • Pulmonary haemorrhage — CO uptake by intra-alveolar blood (Goodpasture, vasculitis)
  • Obesity — increased pulmonary blood volume (corrected by indexing to alveolar volume: DLCO/VA or KCO)
  • Asthma — mildly elevated DLCO may occur during acute exacerbation (increased pulmonary blood volume)
  • Exercise — increased cardiac output and pulmonary blood flow

Corrections

  • Haemoglobin correction (mandatory): DLCOcorrected = DLCOmeasured × factor. For males: factor = 10.22/(Hb + 1.72); for females: factor = 9.38/(Hb + 1.72). Using standard ATS/ERS equations. Significant in anaemia (Hb <100 g/L) where uncorrected DLCO may falsely suggest parenchymal disease.
  • Carboxyhaemoglobin (COHb) correction: Smokers may have COHb 5–15%, which reduces the CO driving force and lowers measured DLCO. Correct using: DLCOcorrected = DLCOmeasured × (1.0 + 0.0136 × COHb%).
  • Altitude correction: Not typically required for Australian sites (most facilities at sea level or moderate altitude). At altitude, inspired PO2 is lower; DLCO may be elevated due to compensatory mechanisms.
  • KCO (DLCO/VA): The transfer coefficient (KCO) is DLCO indexed to alveolar volume (VA). A normal or elevated KCO with reduced DLCO and reduced VA suggests restriction (extrapulmonary). A low KCO with low DLCO suggests intrinsic alveolar-capillary disease (emphysema, fibrosis).

Specialized Testing

Bronchoprovocation Testing (Methacholine Challenge)

Bronchoprovocation testing assesses airway hyperresponsiveness (AHR) and is indicated when clinical suspicion for asthma is high but spirometry is normal (FEV1 ≥70% predicted) and bronchodilator reversibility is negative.

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Contraindications: FEV1 <70% predicted (or <1.5 L), recent myocardial infarction or stroke (<3 months), uncontrolled hypertension (systolic >200 mmHg or diastolic >100 mmHg), known aortic/cerebral aneurysm, current use of cholinesterase inhibitors, inability to perform reliable spirometry. Relative contraindications: pregnancy, breastfeeding, current β-blocker use.
Protocol Details
Agent Methacholine (Provocholine®) — cholinergic agonist causing bronchoconstriction; or mannitol (Aridol®) — osmotic stimulus (TGA-approved in Australia)
Method (5-breath dosimeter) Doubling concentrations from 0.03 mg/mL to 16 mg/mL (or 32 mg/mL); 5 breaths per concentration via dosimeter; spirometry 60–90 seconds after each dose
Endpoint 20% fall in FEV1 from post-diluent baseline (PC20) or cumulative dose (PD20)
Positive result PC20 ≤16 mg/mL (or PD20 ≤200 µg cumulative dose)
Interpretation PC20 <1 mg/mL = highly suggestive of active asthma; 1–4 mg/mL = moderate AHR; 4–16 mg/mL = mild AHR (may be seen in allergic rhinitis, post-viral, COPD); >16 mg/mL = negative
Mannitol (Aridol®) Capsule-based dry powder inhalation; dose escalation from 0 mg to 160 mg; PD15 ≤635 mg = positive; available on PBS (authority required) in some settings; simpler to administer than methacholine in non-specialist labs

Exercise Testing

Exercise testing evaluates the physiological response to exertion and is indicated for unexplained dyspnoea, exercise-induced bronchoconstriction (EIB), pre-operative assessment, and disability evaluation.

Exercise-Induced Bronchoconstriction (EIB) Testing

  • Protocol: 6–8 minutes of high-intensity exercise (≥85% predicted maximum heart rate) on a treadmill or cycle ergometer in dry air (relative humidity <50%)
  • Spirometry performed at baseline, then 5, 10, 15, 20, and 30 minutes post-exercise
  • Positive: ≥10% fall in FEV1 from baseline (some guidelines use ≥15%)
  • Eucapnic voluntary hyperpnoea (EVH) is an alternative provocation — breathing dry air containing 5% CO2 at 85% maximal voluntary ventilation for 6 minutes; sensitive for elite athlete assessment
  • EIB is a major concern in Australian elite athletes; sports-specific screening using EVH is recommended by the Australian Institute of Sport (AIS) and World Anti-Doping Agency (WADA)

Cardiopulmonary Exercise Testing (CPET)

CPET is the gold standard for evaluating exertional dyspnoea and exercise capacity. It integrates cardiovascular, pulmonary, and musculoskeletal responses during incremental exercise.

Parameter Definition Clinical Interpretation
VO2max (peak VO2) Maximum oxygen consumption at peak exercise Overall exercise capacity marker; <80% predicted = reduced; used for transplant listing, disability assessment
Anaerobic threshold (AT) O2 consumption at which anaerobic metabolism supplements aerobic (V-slope method) <40% predicted = severe deconditioning or cardiac limitation; critical for pre-operative risk assessment (pneumonectomy candidacy: AT >15 mL/kg/min)
VE/VCO2 slope Ventilatory equivalent for CO2 (efficiency of ventilation) Elevated (>34) suggests pulmonary vascular disease, heart failure, or respiratory muscle weakness
O2 pulse VO2 ÷ heart rate (stroke volume × arteriovenous O2 difference) Low or flat O2 pulse = cardiac limitation (reduced stroke volume)
Respiratory exchange ratio (RER) VCO2 ÷ VO2 at peak exercise RER ≥1.10 confirms maximal effort; <1.0 may indicate submaximal test
SpO2 at peak exercise Oxygen saturation during maximal exertion Desaturation >4% from baseline or SpO2 <88% = exercise-induced hypoxaemia
Breathing reserve 1 − (peak VE / MVV); MVV = FEV1 × 35–40 <20% suggests ventilatory limitation (pulmonary cause of dyspnoea)

CPET Differential Patterns

Pattern VO2max AT Breathing Reserve Heart Rate Reserve Cause
Normal Normal Normal Normal Normal Deconditioning or non-cardiopulmonary cause of dyspnoea
Cardiac Preserved Exhausted early Heart failure, valvular disease, CAD, pulmonary hypertension
Pulmonary (ventilatory) ↓ or normal Exhausted Preserved COPD, ILD, bronchiectasis
Pulmonary vascular Preserved or mild↓ Exhausted early Pulmonary hypertension; ↑ VE/VCO2, flat O2 pulse, exercise desaturation
Deconditioning Preserved Preserved Physical inactivity; responds to training

Respiratory Muscle Strength

Respiratory muscle testing evaluates the strength of inspiratory and expiratory muscles and is indicated when neuromuscular disease, unexplained dyspnoea, or hypercapnic respiratory failure is suspected.

Test Method Normal Values Abnormal Suggests
MIP (PImax) Maximal inspiratory pressure from RV against occluded airway; sustained for ≥1 second Males: −120 to −80 cmH2O; Females: −90 to −60 cmH2O (age-dependent) MIP <−80 cmH2O (males) or <−60 cmH2O (females) = inspiratory muscle weakness; MIP <−30 cmH2O = severe weakness, may predict weaning failure
SNIP Sniff nasal inspiratory pressure from FRC through occluded nostril; more reproducible and comfortable than MIP Males: ≥80 cmH2O; Females: ≥70 cmH2O Preferred over MIP in many centres; SNIP <70 cmH2O (males) or <60 cmH2O (females) = inspiratory weakness; particularly useful in neuromuscular disease monitoring
MEP (PEmax) Maximal expiratory pressure from TLC against occluded airway Males: 200–150 cmH2O; Females: 150–100 cmH2O MEP <60 cmH2O = expiratory muscle weakness (impaired cough); critical for secretion management risk

Clinical applications:

  • Diagnosis and monitoring of neuromuscular diseases (MND/ALS, myasthenia gravis, muscular dystrophy, post-polio syndrome)
  • Predicting weaning failure in mechanically ventilated patients (MIP more negative than −20 to −30 cmH2O suggests ability to wean)
  • Assessing eligibility for non-invasive ventilation (NIV) in neuromuscular disease (typically when FVC <50% or MIP <−60 cmH2O)
  • Pre-operative assessment for major thoracic or upper abdominal surgery
  • Monitoring disease progression in MND (serial SNIP and FVC measurements every 2–3 months)
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Medicare items: CPET and methacholine challenge are available at specialised respiratory laboratories in major Australian centres. MBS items for spirometry (MBS 11503), lung volumes (MBS 11505), and DLCO (MBS 11506) are available when ordered by a medical practitioner. CPET may be billed under exercise physiology or respiratory medicine specialist consultation items.

Monitoring & Follow-Up

Serial pulmonary function testing is essential for monitoring disease progression and treatment response. The following guidelines apply:

Every 3–6 months
Severe COPD (GOLD 3–4), rapidly progressive ILD, cystic fibrosis, neuromuscular disease with respiratory involvement (SNIP/FVC), post-lung transplant surveillance
Every 6–12 months
Moderate COPD (GOLD 1–2), stable ILD on treatment, asthma with moderate-severe persistent or frequent exacerbations, bronchiectasis, occupational lung disease monitoring
Annually
Mild/controlled asthma, post-occupational exposure surveillance, pre-employment baseline (if hazardous exposure), stable COPD on established therapy
As clinically indicated
Post-bronchodilator optimisation (6–8 weeks after therapy change), pre-operative assessment, new symptom evaluation, medication toxicity monitoring (e.g., amiodarone, methotrexate)
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Excessive FEV1 decline: Normal age-related FEV1 decline is approximately 20–30 mL/year. A decline >40 mL/year in COPD or >60 mL/year in smokers/occupational lung disease warrants urgent reassessment. Declines greater than 150 mL in a single year should trigger investigation for superimposed pathology (pneumonia, PE, disease exacerbation, equipment error).

Special Populations

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Pregnancy

FRC decreases by 20–30% in the third trimester due to diaphragmatic elevation by the gravid uterus; TLC may decrease by 5–10%.
FEV1, FVC, and FEV1/FVC remain unchanged in healthy pregnancy.
DLCO may increase by 15–20% due to increased pulmonary blood volume; correct for haemoglobin (pregnancy increases Hb mass but may dilutionally lower Hb concentration).
Spirometry and DLCO are safe throughout pregnancy. Methacholine challenge is relatively contraindicated. CPET can be performed with careful monitoring.
Use GLI-2012 reference equations; pregnancy-specific adjustments are not required for spirometry parameters.
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Paediatrics

Children aged ≥6 years can generally perform acceptable spirometry with appropriate coaching and incentives.
ATS/ERS 2019 paediatric criteria: accept exhalation time ≥3 seconds (instead of 6 seconds) for children aged 10–17 years if volume-time curve shows a plateau.
GLI-2012 reference equations incorporate ethnicity — use the "Other/Mixed" group for Australian children of mixed ethnicity where no specific GLI equation exists.
Lung volumes and DLCO: generally feasible from age 8–10 years; body plethysmography may be challenging in younger children due to cooperation requirements.
Methacholine challenge is safe in children ≥5 years when performed by experienced paediatric respiratory scientists; PC20 thresholds differ from adults.
Consider interrupter technique (Rint) or impulse oscillometry (IOS) in children unable to perform forced manoeuvres — these measure respiratory resistance without requiring maximal effort.
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Elderly (≥65 years)

Age-related decline in FEV1, FVC, and DLCO is physiological; use age-adjusted GLI-2012 reference equations (LLN) rather than fixed ratios.
Fixed ratio (FEV1/FVC <0.70) overestimates obstruction in the elderly (up to 50% false positive in those >70 years) — always use LLN.
Respiratory muscle strength declines with age; MIP may decrease 10–25% from age 40 to 80.
CPET: maximal heart rate decreases; use age-predicted maximum (220 − age) for target heart rate calculation. VO2max declines approximately 10% per decade after age 30.
Coordination and cognitive impairment may affect spirometry quality; consider simple spirometry with extended exhalation time and repeat attempts with rest periods.
Frailty, kyphosis, and dental prostheses may affect spirometry technique — ensure comfortable seating, remove dentures if seal is inadequate, and allow adequate rest between manoeuvres.
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Renal Impairment

Chronic kidney disease (CKD) may affect lung volumes due to fluid overload, pulmonary oedema, and uraemic pleuritis — TLC may be reduced, mimicking restriction.
Anaemia of CKD reduces DLCO; haemoglobin correction is mandatory. Post-transplant erythrocytosis may elevate DLCO.
Dialysis patients: perform PFTs mid-cycle (at least 4 hours post-dialysis) to minimise fluid shift effects.
Renal impairment does not affect spirometry interpretation per se but should be considered in the overall clinical context when lung volumes are reduced or DLCO is abnormal.
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Hepatic Impairment

Hepatopulmonary syndrome (HPS) may cause a markedly reduced DLCO with normal spirometry and lung volumes; orthodeoxia and platypnoea are characteristic.
Hepatic hydrothorax (right-sided pleural effusion) may reduce lung volumes ipsilaterally.
Pre-liver transplant PFTs include DLCO and pulse oximetry (resting and standing SpO2) as screening for HPS. Contrast-enhanced echocardiography (bubble study) is the confirmatory test.
Smoking status must be documented, as cigarette smoking and alcohol-related lung disease may independently affect PFTs in patients with hepatic disease.
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Immunocompromised

HIV-associated COPD: FEV1 decline is accelerated; spirometry should be performed at diagnosis and annually in smokers with HIV.
Post-transplant monitoring: lung transplant recipients require serial spirometry (FEV1 is the primary graft surveillance parameter; a ≥10% sustained decline may indicate chronic lung allograft dysfunction — CLAD). Haematopoietic stem cell transplant recipients may develop restrictive defects from bronchiolitis obliterans syndrome (BOS) or chronic GVHD.
Immunosuppressive drug-related ILD (methotrexate, bleomycin, checkpoint inhibitors): DLCO is the most sensitive early indicator, often falling before radiographic changes.
Pre-biologic therapy baseline PFTs are recommended for agents with pulmonary toxicity risk (e.g., TNF-α inhibitors, rituximab).
In immunocompromised patients, PFTs should be interpreted with concurrent HRCT and clinical assessment — isolated DLCO reduction may indicate early opportunistic infection or drug toxicity.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Australians experience a disproportionate burden of chronic respiratory disease. COPD mortality is 2.5 times higher in Indigenous Australians compared with non-Indigenous Australians. Asthma prevalence is higher, and bronchiectasis remains a significant cause of morbidity, particularly in remote Northern Territory and Far North Queensland communities. Despite this, access to pulmonary function testing remains inequitable.

Access to spirometry
Most remote Aboriginal Community Controlled Health Services (ACCHOs) lack spirometry equipment and trained respiratory scientists. Point-of-care spirometry programs (e.g., Lung Health Check initiatives) are expanding but coverage remains limited. Portable turbine-based spirometers with quality feedback (e.g., EasyOne Air, ndd) are recommended for remote use with appropriate training.
Reference equations
GLI-2012 equations include a category for "Other/Mixed" but do not have a specific equation for Aboriginal and Torres Strait Islander peoples. Some evidence suggests that healthy Indigenous Australians may have lower predicted FEV1 and FVC (5–10% lower) than non-Indigenous Australians of the same height, age, and sex. Clinical interpretation should consider this; using GLI "Other/Mixed" ethnicity category is the current recommended approach until population-specific equations are validated.
Cultural safety
Spirometry requires patient trust and cooperation. Aboriginal and Torres Strait Islander health workers should be trained in spirometry coaching to facilitate culturally safe testing. Language barriers are significant — use interpreters and culturally appropriate explanations. Same-sex operators may be preferred. Explain the purpose and process of testing clearly and allow adequate time.
Environmental factors
Household biomass fuel exposure, recurrent childhood respiratory infections, and tobacco smoking (approximately 40% of Aboriginal and Torres Strait Islander adults smoke daily) contribute to accelerated lung function decline. Early-life disadvantage, prematurity, and low birth weight are more prevalent and adversely affect maximal attained lung function.
Childhood lung function
Australian Indigenous children may have reduced lung function from infancy, associated with maternal smoking in pregnancy, prematurity, overcrowded housing, and recurrent lower respiratory tract infections. The WATCH study (WA Aboriginal Child Health) demonstrated lower FEV1 from early childhood. Early spirometry screening in at-risk children is advocated.
Workforce and training
The RACGP and TSANZ spirometry training courses should be made available free of charge to remote health service staff. Telehealth spirometry supervision (remote interpretation by respiratory scientists) is a viable model to improve quality and access. The Lung Foundation Australia provides resources for spirometry in primary care, including culturally tailored materials.
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Recommendations: All Aboriginal and Torres Strait Islander adults with respiratory symptoms should have access to quality-assured spirometry. Advocate for spirometry equipment and trained personnel in all ACCHOs. Annual spirometry should be considered for smokers aged ≥40 years and those with recurrent respiratory infections. Ensure use of appropriate reference equations and interpret results in clinical context, acknowledging potential population-level differences in predicted values.

📚 References

  1. 1. Graham BL, Steenbruggen I, Miller MR, et al. Standardization of spirometry 2019 update: an official American Thoracic Society and European Respiratory Society technical statement. Am J Respir Crit Care Med. 2019;200(8):e70–e88.
  2. 2. Graham BL, Brusasco V, Burgos F, et al. 2017 ERS/ATS standards for single-breath carbon monoxide uptake in the lung. Eur Respir J. 2017;49(1):1600016.
  3. 3. Wanger J, Clausen JL, Coates A, et al. Standardisation of the measurement of lung volumes. Eur Respir J. 2005;26(3):511–522.
  4. 4. Quanjer PH, Stanojevic S, Cole TJ, et al. Multi-ethnic reference values for spirometry for the 3–95 year age range: the Global Lung Function 2012 equations. Eur Respir J. 2012;40(6):1324–1343.
  5. 5. Stanojevic S, Graham BL, Cooper BG, et al. Official ERS technical standards: Global Lung Function Initiative reference values for the carbon monoxide transfer factor for adults. Eur Respir J. 2017;50(1):1700010.
  6. 6. Coates AL, Wanger J, Cockcroft DW, et al. ERS technical standard on bronchial challenge testing: general considerations and performance of methacholine challenge tests. Eur Respir J. 2017;49(5):1601526.
  7. 7. American Thoracic Society; American College of Chest Physicians. ATS/ACCP statement on cardiopulmonary exercise testing. Am J Respir Crit Care Med. 2003;167(2):211–277.
  8. 8. Laveneziana P, Albuquerque A, Aliverti A, et al. ERS statement on respiratory muscle testing at rest and during exercise. Eur Respir J. 2019;53(6):1801214.
  9. 9. Toelle BG, Xuan W, Peat JK, Marks GB. Childhood factors that predict asthma in young adulthood. Eur Respir J. 2004;23(1):66–70.
  10. 10. Chang AB, Brown N, Toombs M, et al. Lung disease in Indigenous children. Paediatr Respir Rev. 2014;15(4):325–332.
  11. 11. Australian Institute of Health and Welfare (AIHW). Chronic respiratory conditions in Aboriginal and Torres Strait Islander people. Canberra: AIHW; 2023.
  12. 12. Abramson MJ, Crockett AJ, Dabscheck E, et al. The COPD-X Plan: Australian and New Zealand Guidelines for the management of Chronic Obstructive Pulmonary Disease 2024. Lung Foundation Australia and Thoracic Society of Australia and New Zealand; 2024.
  13. 13. Gibson PG, McDonald VM, Marks GB. Asthma in older adults. Lancet. 2010;376(9743):803–813.
  14. 14. Borg BM, Thompson BR. The use of lung function in Indigenous Australians: a review of the current knowledge. Respirology. 2019;24(8):737–746.