Pulmonary Function Tests (PFT): Understanding Your Lung Function Series

1. Overview: What this panel reveals and why it is important

Pulmonary function testing is not a single breath nor a solitary number—it is a physiological interrogation of the respiratory system. Unlike a blood test that measures concentration, PFTs measure capacity, flow, and exchange—the mechanical properties of the lung and chest wall, the integrity of the alveolar-capillary interface, and the integrated neural drive to breathe.

The panel answers three distinct questions:

· Is there airflow obstruction? (Spirometry: FEV₁, FVC, FEV₁/FVC)

· Is there restriction of lung volume? (Lung volumes: TLC, RV)

· Is gas exchange impaired? (Diffusing capacity: DLCO)

No single parameter is diagnostic in isolation. A reduced FEV₁ may indicate obstructive lung disease—or poor effort—or restrictive pathology with proportional reduction. A reduced FVC may indicate restriction—or air trapping in severe obstruction—or neuromuscular weakness. The power lies in pattern recognition across the flow–volume loop, lung volume compartments, and diffusing capacity.

The PFT panel also integrates response to therapy. Pre‑ and post‑bronchodilator spirometry distinguishes reversible obstruction (asthma) from fixed obstruction (COPD). Comparison of spirometry with lung volumes separates true restriction from pseudo‑restriction due to hyperinflation. DLCO distinguishes emphysema (low) from asthma (normal) and from interstitial lung disease (low to very low).

Thus, the PFT panel is a conversation between the patient’s effort, the machine’s calibration, and the clinician’s interpretation of the flow–volume contour. Listen to the shape of the curve. Interpret the lung volumes. Treat the physiology—not the isolated number.

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2. What does it measure

A complete pulmonary function test includes spirometry, static lung volumes, and diffusing capacity. Reference equations are population‑specific; values below are approximate for a middle‑aged adult of average height.

A. Spirometry (Forced Vital Capacity manoeuvre)

· Forced vital capacity (FVC): Total volume of air exhaled with maximal effort. Reference >80% predicted. Reduced in restrictive disorders and severe obstruction.

· Forced expiratory volume in 1 second (FEV₁): Volume exhaled in the first second. Reference >80% predicted. Reduced in obstructive and restrictive disorders.

· FEV₁/FVC ratio: The critical discriminant. Normal >0.70–0.75 (age‑dependent; lower limit of normal decreases with age). Ratio <0.70 confirms obstruction.

· Forced expiratory flow 25–75% (FEF₂₅–₇₅): Average flow during middle half of exhalation. More sensitive for early small airways disease, but highly effort‑dependent and variable.

· Flow–volume loop: Visual pattern; concave shape suggests obstruction; reduced peak flow with normal contour suggests poor effort or restriction.

B. Static lung volumes (Body plethysmography or gas dilution)

· Total lung capacity (TLC): Volume of air in lungs at maximal inspiration. Reference >80% predicted. Low TLC confirms restriction. High TLC indicates hyperinflation (emphysema, chronic asthma).

· Residual volume (RV): Volume remaining after maximal exhalation. Elevated in obstruction (air trapping). Reference 80–120% predicted.

· RV/TLC ratio: Normally <0.35–0.40. Elevated in obstruction; markedly elevated in emphysema.

C. Diffusing capacity (DLCO – single‑breath carbon monoxide)

· DLCO corrected for haemoglobin (DLCOc): Measures gas transfer across alveolar‑capillary membrane. Reference >80% predicted.

· Low DLCO: Loss of alveolar surface area (emphysema), interstitial lung disease, pulmonary vascular disease, anaemia.

· High DLCO: Polycythaemia, left‑to‑right shunt, alveolar haemorrhage (Goodpasture, vasculitis), asthma (sometimes).

D. Additional tests (not in all panels)

· Bronchodilator responsiveness: Increase in FEV₁ or FVC ≥12% and ≥200 mL post‑bronchodilator. Supports asthma diagnosis; absence does not exclude asthma.

· Maximal voluntary ventilation (MVV): Estimate of ventilatory reserve; reduced in neuromuscular disease, poor effort, obstruction.

· Arterial blood gas (ABG): PaO₂, PaCO₂, pH, HCO₃⁻. Assesses gas exchange and ventilatory failure (hypercapnia). Not part of routine outpatient PFT.

· Six‑minute walk test (6MWT): Integrated assessment of exercise capacity, desaturation.

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3. Other factors connected to this panel

Preanalytical and biological variables:

· Patient effort – the single greatest variable: PFTs are volitional. Poor effort reduces FVC, FEV₁, and may mimic restriction or obstruction. Flow–volume loop with premature termination, inconsistent efforts, or submaximal inhalation should be interpreted with caution.

· Instruction and coaching: Standardised coaching improves reproducibility. At least three acceptable manoeuvres required; reproducibility within 150 mL for FVC and FEV₁.

· Time of day: Diurnal variation; asthmatics often have lower values in early morning. Serial tests should be performed at similar times.

· Recent bronchodilator use: Short‑acting beta‑agonists (albuterol) – withhold 4–6 hours; long‑acting beta‑agonists (salmeterol, formoterol) – withhold 12 hours; long‑acting muscarinic antagonists (tiotropium) – withhold 24–48 hours. Failure to withhold may mask obstruction.

· Recent smoking: Carbon monoxide from tobacco smoke elevates exhaled CO, artificially lowers DLCO measurement. Avoid smoking ≥1 hour before testing (preferably abstain).

· Meal timing: Large meal before testing may restrict diaphragmatic excursion; avoid heavy meals 2 hours prior.

· Oxygen supplementation: If patient uses supplemental oxygen, it is typically discontinued during testing (with monitoring) to avoid interfering with gas dilution techniques.

· Medications affecting respiratory drive: Opiates, benzodiazepines, sedatives – may reduce effort, lower MVV, contribute to hypercapnia.

Demographic and physiological factors:

· Age: FEV₁ and FVC peak at 20–25 years, then decline 20–30 mL/year (faster in smokers). The lower limit of normal for FEV₁/FVC ratio decreases with age; a fixed ratio of 0.70 overdiagnoses COPD in the elderly and underdiagnoses in young adults. Use GLI (Global Lung Function Initiative) reference equations, which provide age‑specific lower limits of normal.

· Sex: Males have larger lung volumes even after height adjustment. Reference equations are sex‑specific.

· Height: The strongest predictor of lung volumes; standing height measured without shoes.

· Ethnicity: Differences in proportional trunk‑to‑leg length affect predicted values. GLI equations incorporate ethnic‑specific adjustments (Caucasian, African American, North East Asian, South East Asian). Use of race‑specific correction is evolving; some guidelines now recommend using average reference values to avoid underestimation of lung disease in minority populations.

· Body mass index:

· Obesity (BMI >30): Reduces FVC, FEV₁ (restrictive pattern), but FEV₁/FVC ratio normal or increased; TLC normal or mildly reduced; DLCO normal or increased (increased blood volume). Obesity hypoventilation syndrome → hypercapnia.

· Underweight: Reduced respiratory muscle strength, lower lung volumes.

· Pregnancy: Progressive decrease in FRC and RV (diaphragm elevation); FVC and FEV₁ remain stable; TLC decreases 5–10% near term. DLCO unchanged or slightly increased.

· Muscle strength: Neuromuscular disorders reduce FVC, TLC; upright vs supine drop in FVC suggests diaphragmatic weakness.

· Altitude: Residing at high altitude reduces predicted DLCO (thinner alveolar membrane?); reference equations usually sea‑level based.

Medications affecting PFT components (other than bronchodilators):

· Amiodarone: Pulmonary toxicity → restrictive pattern, low DLCO.

· Methotrexate, nitrofurantoin, bleomycin, busulfan: Drug‑induced interstitial lung disease → restriction, low DLCO.

· Aspirin / NSAIDs: Can provoke asthma (aspirin‑exacerbated respiratory disease).

· ACE inhibitors: Cough; does not alter spirometry.

· Beta‑blockers: May provoke bronchospasm in reactive airways; non‑selective agents contraindicated in asthma/COPD.

· Glucocorticoids: No direct effect on lung mechanics; inhaled steroids improve asthma control.

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4. Disorders related to abnormal values: Pattern recognition

PFT interpretation follows a stepwise algorithm anchored to FEV₁/FVC ratio and TLC.

a. Obstructive pattern (Airflow limitation)

Laboratory profile:

· FEV₁/FVC < lower limit of normal (or <0.70 fixed)

· FEV₁ reduced (<80% predicted) – severity graded by FEV₁ % predicted

· FVC normal or reduced (air trapping may lower FVC)

· TLC normal or increased; RV and RV/TLC increased (hyperinflation, air trapping)

· DLCO: normal in asthma; reduced in emphysema (key discriminator)

· Bronchodilator response: present in asthma, minimal/absent in COPD

Differential diagnosis:

· Asthma: Variable obstruction, reversibility, normal DLCO, atopy, eosinophilia.

· COPD (emphysema / chronic bronchitis): Fixed obstruction, low DLCO (emphysema), chronic symptoms, smoking history.

· Bronchiectasis: High-resolution CT diagnostic; may have obstructive or mixed pattern.

· Bronchiolitis obliterans: Fixed obstruction, normal DLCO, air trapping on expiratory CT; post‑lung transplant, rheumatoid arthritis, inhalational injury.

· Central airway obstruction (tracheal stenosis, tumour): Flow‑volume loop shows fixed or variable intrathoracic/extrathoracic pattern; FEV₁/FVC may be falsely normal or low.

Outlier scenarios:

· FEV₁/FVC <0.70 but FEV₁ >100% predicted: Often seen in tall, young athletes; still obstructive if ratio below LLN; correlates with increased lung elasticity.

· Preserved ratio impaired spirometry (PRISm): FEV₁/FVC normal but FEV₁ and FVC both <80% predicted. Heterogeneous group: obesity, early interstitial lung disease, asthma with airway remodeling, or poor effort.

· Severe obstruction with very low FEV₁ (<30%) but preserved DLCO: Consider severe asthma, cystic fibrosis, bronchiolitis; not emphysema.

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b. Restrictive pattern (Reduced lung volume)

Laboratory profile:

· TLC <80% predicted (mandatory for confirmation)

· FEV₁ and FVC proportionally reduced → FEV₁/FVC ratio normal or increased (>0.70–0.75)

· RV normal or reduced

· DLCO: variable – helps localise restriction

Differential diagnosis by DLCO:

Low DLCO → Intrinsic parenchymal / interstitial lung disease:

· Idiopathic pulmonary fibrosis (IPF), nonspecific interstitial pneumonia (NSIP), hypersensitivity pneumonitis, connective tissue disease‑associated ILD, asbestosis, sarcoidosis (stage II‑IV).

· DLCO often disproportionately reduced relative to lung volumes (impaired gas exchange).

Normal DLCO → Extrapulmonary / chest wall / pleural / neuromuscular:

· Chest wall deformity: Kyphoscoliosis, ankylosing spondylitis, pectus excavatum.

· Pleural disease: Pleural thickening, effusion, fibrothorax.

· Neuromuscular weakness: ALS, myasthenia gravis, muscular dystrophy, diaphragm paralysis. FVC often falls >20% when supine.

· Obesity: Restrictive pattern with normal DLCO, normal or elevated FEV₁/FVC.

· Post‑surgical: Lobectomy, pneumonectomy.

High DLCO → Rare:

· Alveolar haemorrhage, polycythaemia, left‑to‑right shunt.

Outlier scenarios:

· Reduced TLC, reduced FVC, normal FEV₁/FVC, reduced DLCO: Interstitial lung disease until proven otherwise; proceed to HRCT.

· Reduced TLC, reduced FVC, normal FEV₁/FVC, normal DLCO: Extrapulmonary restriction; evaluate chest wall, pleura, neuromuscular function.

· Reduced TLC with disproportionately preserved FEV₁/FVC >0.80: Severe restriction; may be mislabelled as “supernormal” ratio.

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c. Mixed obstructive–restrictive pattern

Laboratory profile:

· FEV₁/FVC reduced (obstruction)

· TLC reduced (restriction)

· FEV₁ and FVC both reduced, often severely

Differential diagnosis:

· COPD + concomitant ILD: Smoking‑related combined pulmonary fibrosis and emphysema (CPFE) – upper lobe emphysema, lower lobe fibrosis; DLCO severely reduced; often preserved lung volumes despite fibrosis due to hyperinflation.

· Cystic fibrosis with advanced lung disease: Obstruction plus volume loss from fibrosis/atelectasis.

· Sarcoidosis: May have both obstructive (endobronchial granulomas) and restrictive (parenchymal) components.

· Asbestosis with COPD: Occupational exposure.

Outlier scenario:

· Severe obstruction with pseudo‑restriction: Hyperinflation elevates RV, but TLC may be normal or increased. True restriction requires TLC <80%. Severe obstruction can make full inspiration difficult, underestimating TLC; plethysmography preferred.

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d. Isolated low DLCO (Normal spirometry and lung volumes)

Laboratory profile:

· DLCO <80% predicted

· FEV₁/FVC normal, FVC normal, TLC normal

· No obstruction or restriction

Differential diagnosis:

· Pulmonary vascular disease: Chronic thromboembolic pulmonary hypertension, idiopathic pulmonary arterial hypertension, pulmonary vasculitis.

· Early ILD: May present with isolated low DLCO before volumes decline.

· Emphysema: Mild emphysema can cause low DLCO with preserved spirometry.

· Anaemia: Correct DLCO for haemoglobin; low Hb lowers DLCO.

· Alveolar haemorrhage (subacute): DLCO may be elevated acutely (CO binding to intra‑alveolar haemoglobin), then low.

· Smoking: Tobacco reduces DLCO via CO back‑pressure and alveolar damage; DLCO can be low despite normal spirometry.

Outlier scenario:

· Isolated low DLCO, normal spirometry, non‑smoker, normal echocardiogram: Consider pulmonary vascular disease; proceed to CT pulmonary angiography or right heart catheterisation.

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e. Respiratory muscle weakness / Neuromuscular pattern

Laboratory profile:

· FVC reduced (restrictive), but FEV₁/FVC normal or increased

· TLC reduced (restriction)

· RV normal or increased (inability to exhale fully)

· Maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP) reduced

· Supine FVC drop >10–20% indicates diaphragmatic weakness

· DLCO normal (unless aspiration or atelectasis)

Differential diagnosis:

· Amyotrophic lateral sclerosis, myasthenia gravis, Guillain‑Barré, muscular dystrophy, phrenic nerve injury, critical illness neuropathy.

Outlier scenario:

· Normal spirometry but low MIP/MEP: Early respiratory muscle weakness; serial FVC monitoring essential.

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5. Best way to address aberrant levels: A holistic approach

Critical principle: PFTs are a measure of physiology, not a diagnosis. Do not treat a low FEV₁; treat the airway inflammation, the loss of elastic recoil, the respiratory muscle weakness, or the interstitial process that causes it. Empiric inhaled corticosteroids for a restrictive pattern are ineffective and delay diagnosis.

a. Diagnostic algorithm, not therapeutic trial

Step 1: Confirm the abnormality

· Ensure acceptable and repeatable manoeuvres; repeat if effort was suboptimal.

· If FEV₁/FVC reduced but borderline, repeat after bronchodilator; if normalises, confirms reversible obstruction.

· If TLC low by helium dilution but clinical suspicion for restriction, consider body plethysmography (gas trapping may underestimate TLC in obstruction).

Step 2: Identify the dominant pattern (see Section 4)

· Obstructive (FEV₁/FVC ↓)

· Restrictive (TLC ↓, FEV₁/FVC normal/↑)

· Mixed (both)

· Isolated low DLCO

· Neuromuscular weakness

Step 3: Determine aetiology

· Obstruction: Asthma (reversibility, triggers, atopy, FeNO), COPD (smoking, alpha‑1 antitrypsin deficiency), bronchiectasis (CT), airway stenosis (flow‑volume loop, bronchoscopy).

· Restriction – low DLCO: High-resolution CT (interstitial pattern, emphysema); autoimmune serologies; hypersensitivity pneumonitis precipitants; occupational history.

· Restriction – normal DLCO: Imaging for pleural disease, chest wall deformity; neuromuscular evaluation (MIP/MEP, supine FVC, neurology referral).

· Isolated low DLCO: Echocardiogram (pulmonary hypertension); CT angiogram (chronic thromboembolism); consider connective tissue disease (scleroderma, lupus).

Step 4: Treat the underlying cause

Obstructive disorders:

· Asthma:

· Inhaled corticosteroids (ICS) – first‑line controller for persistent asthma.

· Long‑acting beta‑agonists (LABA) – add‑on to ICS; never monotherapy.

· Long‑acting muscarinic antagonists (LAMA) – add‑on for severe asthma.

· Biologics (anti‑IgE, anti‑IL5/5R, anti‑IL4R) for severe eosinophilic/allergic asthma.

· Allergen avoidance, smoking cessation, weight management.

· COPD:

· Smoking cessation – single most effective intervention.

· Bronchodilators (LAMA, LABA) – improve symptoms, reduce exacerbations.

· ICS – add for eosinophilic phenotype or frequent exacerbations.

· Pulmonary rehabilitation – improves exercise capacity, quality of life.

· Long‑term oxygen therapy if PaO₂ ≤55 mmHg or ≤59 mmHg with cor pulmonale.

· Non‑invasive ventilation in chronic hypercapnic stable COPD (selected).

· Alpha‑1 antitrypsin augmentation therapy if deficiency and emphysema.

· Bronchiectasis:

· Airway clearance techniques, pulmonary rehab.

· Treatment of underlying cause (IgG deficiency, allergic bronchopulmonary aspergillosis).

· Inhaled antibiotics for frequent Pseudomonas exacerbations.

Restrictive disorders (Interstitial lung disease):

· Idiopathic pulmonary fibrosis:

· Antifibrotic agents (pirfenidone, nintedanib) – slow FVC decline.

· Oxygen therapy, pulmonary rehabilitation, cough management.

· Lung transplantation evaluation.

· Hypersensitivity pneumonitis:

· Antigen avoidance (birds, moulds, humidifiers).

· Corticosteroids for acute/subacute; antifibrotics for chronic fibrotic.

· Connective tissue disease‑associated ILD:

· Immunosuppression (mycophenolate, rituximab, cyclophosphamide) – based on underlying disease.

· Nintedanib approved for systemic sclerosis‑ILD and progressive fibrotic ILD.

· Sarcoidosis:

· Asymptomatic: observation.

· Symptomatic or progressive: corticosteroids, steroid‑sparing agents (methotrexate, azathioprine).

Neuromuscular weakness:

· Treat underlying disease (immune therapy for myasthenia, ALS multidisciplinary care).

· Non‑invasive ventilation for symptomatic hypercapnia or nocturnal hypoventilation.

· Mechanical insufflation‑exsufflation (cough assist) for secretion clearance.

· Diaphragm pacing in selected patients.

Pulmonary vascular disease:

· Pulmonary arterial hypertension – targeted therapy (endothelin antagonists, PDE5 inhibitors, prostacyclin analogues).

· Chronic thromboembolic pulmonary hypertension – pulmonary endarterectomy or balloon angioplasty.

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b. Role of supplements and holistic medicine – supportive only

Airway health and anti‑inflammation:

· Vitamin D3: Deficiency associated with asthma severity, COPD exacerbations, and worse lung function. Supplement to maintain optimal levels (lichen‑derived cholecalciferol).

· Magnesium: Intravenous magnesium used in acute severe asthma; oral supplementation not proven to improve chronic asthma control.

· Omega‑3 fatty acids (algae‑derived EPA/DHA): Anti‑inflammatory; some observational studies link higher intake with lower COPD risk and slower lung function decline. Adjunctive; not disease‑modifying.

· N‑acetylcysteine (NAC): 600 mg twice daily; mucolytic and antioxidant. Modest reduction in COPD exacerbations; weak evidence. Not for asthma or ILD.

· Curcumin (bioavailable): Anti‑inflammatory; limited respiratory data; adjunctive only.

· Honey: Symptomatic relief for cough; no effect on lung mechanics.

Pulmonary rehabilitation and breathing retraining:

· Pulmonary rehabilitation: Multidisciplinary intervention including exercise training, education, psychosocial support. Improves dyspnoea, exercise capacity, quality of life in COPD, ILD, pulmonary hypertension. Highest evidence level.

· Pranayama / yogic breathing (slow, deep breathing): May improve respiratory muscle strength, reduce dyspnoea, and enhance quality of life in COPD and asthma. Adjunctive; not a substitute for pharmacotherapy.

· Inspiratory muscle training: Beneficial in respiratory muscle weakness, selected COPD patients with inspiratory muscle weakness.

Herbs and Phytochemicals from Indian subcontinent (adjunctive, not primary):

· Tulsi (Ocimum sanctum): Traditional use for cough, cold; in vitro anti‑inflammatory, bronchodilatory effects. Limited clinical trials in asthma; weak evidence.

· Licorice root (Glycyrrhiza glabra): Demulcent; may soothe throat. Long‑term use causes hypokalaemia, hypertension. Not recommended.

· Vasaka (Adhatoda vasica): Ayurvedic remedy for cough and asthma; some bronchodilator activity in animal studies; insufficient human evidence.

· Never use as substitute for inhaled corticosteroids, bronchodilators, or antifibrotics.

· Avoid all products containing undisclosed corticosteroids, beta‑agonists, or sibutramine (adulterated "herbal" asthma remedies).

Critical warnings:

· Do not use antioxidant supplements (vitamin E, beta‑carotene) in smokers – increased risk of lung cancer and mortality.

· Do not use high‑dose NAC in patients with haemorrhagic conditions (inhibits platelet aggregation).

· Do not use essential oils (eucalyptus, peppermint) near infants or in asthmatics without caution – may trigger bronchospasm.

· Do not delay evidence‑based therapy while trialling herbal remedies in progressive diseases (IPF, PAH, severe asthma).

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c. Dietary and lifestyle approach (plant‑forward, ecologically sustainable)

Core principles for pulmonary health:

· Whole‑food, plant‑forward diet: High in vegetables, fruits, legumes, whole grains, nuts, seeds. Associated with lower COPD prevalence, slower lung function decline, reduced asthma symptoms. Anti‑inflammatory, antioxidant.

· Adequate protein intake: Essential for respiratory muscle strength, especially in underweight COPD, neuromuscular disease. Plant sources: legumes, tofu, tempeh, quinoa, hemp seeds, mycoprotein.

· Maintain healthy body weight:

· Obesity: Restricts lung volumes, worsens OSA, increases dyspnoea. Weight loss improves FVC, FEV₁.

· Underweight: Common in advanced COPD, IPF, TB; increases mortality. Nutritional supplementation (high‑calorie, high‑protein plant‑based) improves weight, respiratory muscle strength.

· Hydration: Adequate fluid intake maintains mucus rheology; avoid excessive hydration (no proven benefit).

· Eliminate tobacco and nicotine products – complete cessation mandatory.

· Alcohol: complete abstinence. Alcohol impairs respiratory muscle function, increases risk of aspiration, worsens OSA, and interacts with respiratory medications (benzodiazepines, opiates). No safe threshold.

· Caffeine: Not recommended. Caffeine is a weak bronchodilator, but the effect is negligible and inconsistent; carries addiction potential, increases anxiety, impairs sleep, and may interact with bronchodilators (tachycardia). Safe, non‑addictive lifestyle measures are preferred.

Environmental interventions (critical and often overlooked):

· Indoor air quality: Use high‑efficiency particulate air (HEPA) filters; reduce indoor allergens (dust mites, mould, pet dander); avoid biomass fuel combustion (wood, cow dung) for cooking – leading cause of COPD in non‑smoking women in low‑resource settings.

· Occupational exposures: Identify and mitigate exposure to silica, asbestos, coal dust, cotton dust, isocyanates, grain dust.

· Air pollution: Avoid outdoor exertion during high pollution days; use N95 masks when necessary.

Specific considerations:

· Asthma: Identify and avoid triggers (pollens, moulds, animal dander, cockroach, house dust mite). Allergen immunotherapy for selected sensitised patients.

· COPD: Pulmonary rehabilitation; self‑management education; action plan for exacerbations; vaccination (influenza, pneumococcal, COVID‑19, RSV).

· ILD / pulmonary fibrosis: Gastroesophageal reflux is common and may exacerbate fibrosis; anti‑reflux measures (elevate head of bed, avoid late meals, proton pump inhibitors).

· OSA (often coexists with obesity, COPD – overlap syndrome): Weight loss, positional therapy, CPAP.

Note on addictive substances:

This guide does not recommend tea, coffee, alcohol, or tobacco in any form. Alcohol directly impairs mucociliary clearance, depresses ventilatory drive, and worsens sleep‑disordered breathing. Caffeine has trivial and inconsistent bronchodilator effects that do not outweigh its addiction potential, arrhythmogenic risk, and sleep disruption. No addictive substance is necessary for the optimisation of pulmonary function. Safe, non‑addictive lifestyle measures—particularly a whole‑food, plant‑based diet, maintenance of healthy body weight, regular physical activity, pulmonary rehabilitation, and avoidance of environmental pollutants—are both safer and more foundational for long‑term respiratory health.

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6. How soon can one expect improvement and the ideal time frame to retest

Improvement timelines are disease‑ and intervention‑specific.

Asthma:

· Post‑bronchodilator: Immediate (15–30 minutes). Reversibility assessed during same visit.

· Inhaled corticosteroids: Symptom improvement 1–2 weeks; FEV₁ improvement plateaus at 4–8 weeks.

· Biologics: 4–16 weeks for exacerbation reduction; lung function improvement variable.

· Retest: 4–12 weeks after initiating controller therapy; then annually if stable. More frequent if poorly controlled or adjusting therapy.

COPD:

· Smoking cessation: Rate of FEV₁ decline slows to that of never‑smokers (30 mL/year vs 60 mL/year). No acute improvement.

· Bronchodilators: Symptom improvement days; FEV₁ improvement 100–200 mL within 1 hour (reversible component). Fixed obstruction does not normalise.

· Pulmonary rehabilitation: 6–12 weeks for improved exercise capacity, dyspnoea.

· Retest: Not routinely repeated for stable COPD; perform if unexplained symptom change or before major surgery. Annual spirometry in alpha‑1 antitrypsin deficiency.

Interstitial lung disease (IPF, fibrotic ILD):

· Antifibrotics: Slow rate of FVC decline; no improvement. Benefit measured as preservation, not gain.

· Corticosteroids / immunosuppression (NSIP, HP, CTD‑ILD): Improvement may occur over 3–6 months; some respond slowly.

· Retest: Every 3–6 months for progressive disease; every 6–12 months for stable disease.

Neuromuscular weakness:

· Treatment of underlying disease (e.g., myasthenia): FVC improvement days to weeks.

· Non‑invasive ventilation: Symptom improvement (morning headache, fatigue) within days; physiological benefits over weeks.

· Retest: FVC at each clinic visit (3–6 months); more frequent if rapid decline.

Isolated low DLCO (pulmonary vascular disease):

· PAH therapy: 3–6 months for functional improvement; DLCO rarely normalises.

· Retest: DLCO not routinely repeated; follow 6MWT, echocardiogram, BNP.

Preoperative evaluation:

· Lung resection: Postoperative predicted FEV₁ and DLCO guide operability; retest 3–6 months post‑surgery to establish new baseline.

Retesting intervals (stable, chronic disease):

· Asthma, well‑controlled: Spirometry every 1–2 years.

· COPD, stable: Spirometry not routinely repeated; annual review of symptoms, exacerbations, smoking status.

· ILD, stable: PFTs every 3–6 months; more frequent if progressive.

· Neuromuscular disease: FVC every 3–12 months depending on rate of progression.

· Pre‑employment / surveillance (occupational): As per occupational health schedule.

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Conclusion

Pulmonary function tests are the most direct window into the mechanics of breathing and the integrity of gas exchange. Yet their power is not in isolated numbers—a low FEV₁, a reduced DLCO, a normal TLC—but in pattern recognition across spirometry, lung volumes, and diffusion.

An obstructive defect is not a diagnosis; it is a physiological signature that must be matched to clinical history (asthma vs COPD vs bronchiolitis). A restrictive defect is not a disease; it is a volumetric finding that must be localised to the lung parenchyma (low DLCO) or to the chest wall, pleura, or neuromuscular apparatus (normal DLCO). An isolated low DLCO is not idiopathic; it demands investigation for pulmonary vascular disease or early interstitial involvement.

The holistic management of an abnormal PFT is therefore diagnostic precision first, aetiology‑specific therapy second, and supportive, ecologically sustainable lifestyle interventions always. Inhaled corticosteroids, bronchodilators, antifibrotics, and pulmonary rehabilitation are evidence‑based, life‑altering interventions. Smoking cessation is the single most important intervention in tobacco‑related lung disease.

No addictive substance—whether caffeine, alcohol, or nicotine—is required for the optimisation of pulmonary function. Safe, non‑addictive, ecologically responsible dietary and lifestyle interventions—plant‑forward nutrition, maintenance of healthy body weight, pulmonary rehabilitation, and avoidance of environmental pollutants—are always preferred.

As with all physiological testing, the PFT is a conversation between the patient’s effort, the equipment’s precision, and the clinician’s interpretation. Inspect the flow‑volume loop. Integrate the lung volumes. Treat the patient—not the number.

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Note on dietary recommendations on this site:

For the sake of our environment we adhere to the following dietary preference hierarchy:

1. Plant‑based

2. Fungi / algae / fermented

3. Biotechnology / lab‑grown / cultures

4. Dairy / eggs

5. Meat / fish / poultry (only if no effective alternative exists)

This approach reflects ecological responsibility, antibiotic stewardship, and the urgent need to reduce the environmental footprint of dietary recommendations.

Special note on protein in pulmonary disease:

Plant‑based protein sources are nutritionally adequate for all individuals with respiratory disorders, including those with COPD, ILD, and neuromuscular weakness who require increased protein intake to preserve respiratory muscle strength. Soy, legumes, mycoprotein, and algae provide complete or complementary amino acid profiles. Meat and fish are neither necessary nor preferred.

Special note on addictive substances:

This guide does not recommend tea, coffee, alcohol, or tobacco in any form. Caffeine has trivial bronchodilator properties that do not outweigh its addiction potential, cardiovascular stimulation, and sleep disruption. Alcohol depresses ventilatory drive, impairs mucociliary clearance, and increases aspiration risk. Tobacco is the leading cause of preventable lung disease. Safe, non‑addictive lifestyle interventions—particularly a whole‑food, plant‑based diet, pulmonary rehabilitation, maintenance of healthy body weight, and avoidance of indoor/outdoor air pollution—are both safer and more foundational for long‑term respiratory health. No addictive substance is necessary for the prevention or management of pulmonary disease.

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