Asthma and COPD diagnosis and maintenance

Diagnostic Evaluation of Obstructive Airway Diseases

Obstructive lung diseases are characterised by limitation of expiratory airflow resulting from airway inflammation, hyperresponsiveness, smooth muscle contraction, and structural parenchymal remodeling. Differentiating asthma from chronic obstructive pulmonary disease (COPD) is essential for selecting appropriate maintenance pharmacotherapy and preventing acute life-threatening decompensations.

Asthma Diagnostic Confirmation

In Australian clinical practice, a diagnosis of asthma requires two distinct elements: a compatible clinical history of episodic respiratory symptoms (wheeze, shortness of breath, chest tightness, and cough) and objective documentation of variable expiratory airflow limitation.

• Spirometry with Bronchodilator Reversibility: Spirometry is the definitive first-line diagnostic investigation. Airflow limitation is established by a reduced forced expiratory volume in 1 second to forced vital capacity ratio ($\text{FEV}_1/\text{FVC} < 0.70$ or below the lower limit of normal). Significant bronchodilator reversibility is defined as an increase in $\text{FEV}_1$ of greater than 12% and greater than $200\text{ mL}$ from baseline, measured 10 to 15 minutes after inhaling $400\ \mu\text{g}$ of salbutamol via a spacer.
• Peak Expiratory Flow (PEF) Variability: When spirometry is normal or inconclusive, diurnal PEF variability exceeding 20% over 1 to 2 weeks (calculated from twice-daily recordings) provides objective support for asthma.
• Fractional Exhaled Nitric Oxide (FeNO): A FeNO level $\ge 35\text{ ppb}$ in non-smoking adults indicates eosinophilic airway inflammation and predicts positive responsiveness to inhaled corticosteroids (ICS), although a normal FeNO does not exclude asthma.
• Bronchial Provocation Testing: In patients with normal spirometry and normal reversibility, bronchial challenge testing (using direct agents such as methacholine or indirect agents such as inhaled mannitol) demonstrates bronchial hyperresponsiveness through a 20% drop in $\text{FEV}_1$.

COPD Diagnostic Confirmation

COPD is a preventable and treatable disease characterized by persistent respiratory symptoms and non-reversible or partially reversible airflow limitation caused by airway and alveolar abnormalities, predominantly driven by tobacco smoking or occupational exposures in Australia.

• Post-Bronchodilator Spirometry: The cornerstone of diagnosis is a post-bronchodilator $\text{FEV}_1/\text{FVC} < 0.70$. Unlike asthma, significant reversibility to normal values is absent, establishing persistent fixed airflow obstruction.

• Spirometric Grading: Airflow limitation severity is staged using post-bronchodilator $\text{FEV}_1$ percent predicted: Stage 1 (Mild, $\text{FEV}_1 \ge 80\%$), Stage 2 (Moderate, $50\% \le \text{FEV}_1 < 80\%$), Stage 3 (Severe, $30\% \le \text{FEV}_1 < 50\%$), and Stage 4 (Very Severe, $\text{FEV}_1 < 30\%$).

• Typical Onset: Asthma: Childhood or young adulthood, frequently atopic; COPD: Mid-to-late adulthood (>40 years), heavy smoking history

• Symptom Pattern: Asthma: Variable, diurnal, episodic, night/early morning waking; COPD: Progressive, chronic dyspnoea on exertion, chronic cough

• Spirometry: Asthma: Reversible obstruction ($\Delta\text{FEV}_1 > 12\%$ and $> 200\text{ mL}$); COPD: Fixed obstruction (post-bronchodilator $\text{FEV}_1/\text{FVC} < 0.70$)

• Airway Pathology: Asthma: Eosinophilic and CD4+ T-cell mediated (Th2 pattern); COPD: Neutrophilic and CD8+ T-cell mediated, parenchymal destruction

• Primary Treatment: Asthma: Inhaled corticosteroids (ICS) foundational at all stages; COPD: Long-acting bronchodilators (LAMA / LABA) foundational

Maintenance Management Frameworks

National Asthma Council Australia Stepwise Algorithm

The National Asthma Council (NAC) Australia guidelines have departed from short-acting beta-2 agonist (SABA) monotherapy due to clinical evidence demonstrating that regular or frequent SABA use causes beta-receptor downregulation, increases bronchial hyperresponsiveness, and escalates severe exacerbation and mortality risks.

1. Anti-Inflammatory Reliever (AIR) Therapy (Steps 1 & 2): For adults and adolescents with mild asthma, as-needed low-dose budesonide-formoterol ($200/6\ \mu\text{g}$) taken whenever symptoms occur is preferred. Delivering an ICS alongside every bronchodilator dose treats underlying airway inflammation at the earliest sign of symptom worsening.
2. Maintenance and Reliever Therapy (MART) (Steps 3 & 4): For patients experiencing daytime symptoms more than twice weekly or night waking, a fixed daily maintenance regimen of budesonide-formoterol combined with the same inhaler as an as-needed reliever provides optimal asthma control and halves exacerbation rates compared to fixed-dose regimens using separate SABA relievers.
3. Add-on Specialist Therapies (Step 5): Patients uncontrolled on medium-to-high dose ICS-LABA warrant add-on long-acting muscarinic antagonists (LAMA, such as tiotropium) and phenotype-directed biologic agents (e.g., omalizumab for severe allergic asthma; mepolizumab, benralizumab, or dupilumab for severe eosinophilic asthma).

COPD Maintenance Pharmacotherapy

COPD maintenance prioritizes symptom reduction, exercise tolerance improvement, and exacerbation prevention.

• Pulmonary rehabilitation: Offer to appropriate symptomatic patients, especially after exacerbation. Eligibility depends on symptoms and function rather than a single FEV1 threshold.
• Inhaled Bronchodilators: Monotherapy with a LAMA (e.g., tiotropium, glycopyrronium, umeclidinium) or LABA (e.g., indacaterol, formoterol) is initiated for breathlessness. LAMA monotherapy shows slight superiority over LABA monotherapy in reducing exacerbation frequency.
• Dual Bronchodilation (LAMA + LABA): Indicated for patients with persistent dyspnoea or recurrent exacerbations on monotherapy. Fixed-dose single-inhaler LAMA/LABA combinations achieve superior bronchodilation and lung deflation.
• COPD inhaled corticosteroids: Consider exacerbation history, blood eosinophils and coexisting asthma. Benefits and pneumonia risks differ between patients; neither a single eosinophil value nor the COPD label alone supplies a universal indication or prohibition.

Primary references (checked 7 October 2026): Australian Asthma Handbook.