The Respiratory System

📋 Key Information Summary

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Cough characterisation is the single most informative respiratory symptom — document onset, duration (acute <3 weeks, subacute 3–8 weeks, chronic >8 weeks), timing, productive vs dry, sputum colour/volume, and haemoptysis.
Haemoptysis always requires investigation — the three most common causes in Australia are bronchiectasis, lung cancer, and pulmonary embolism; CT pulmonary angiography (CTPA) is the first-line imaging study.
Dyspnoea should be graded using the mMRC Dyspnoea Scale (0–4); characterise as exertional vs rest, acute vs progressive, and identify specific patterns (PND, orthopnoea, Kussmaul, Cheyne-Stokes).
Paroxysmal nocturnal dyspnoea (PND) and orthopnoea suggest left ventricular failure; measure BNP/NT-proBNP and arrange transthoracic echocardiography.
Sleep apnoea screening uses the STOP-BANG questionnaire; definitive diagnosis requires overnight polysomnography or home sleep study (MBS item 12203).
Occupational exposure history is mandatory — ask about asbestos, silica, coal dust, isocyanates, and agricultural dusts; consider compensable disease under state WorkCover schemes.
Tracheal deviation — away from the side suggests large pleural effusion or tension pneumothorax; toward the side suggests lobar collapse or fibrosis. This is an emergency if tension pneumothorax is suspected.
Chest expansion — bilateral reduction is seen in COPD/hyperinflation and diffuse fibrosis; unilateral reduction suggests effusion, consolidation, or collapse on that side.
Consolidation signs (dull percussion, increased tactile fremitus, bronchial breathing, crackles) differ from pleural effusion (stony dull, reduced fremitus, absent breath sounds) — the distinction is critical for diagnosis.
Pneumothorax — hyper-resonant percussion, absent breath sounds, reduced tactile fremitus on the affected side; tension pneumothorax is a clinical diagnosis (tracheal deviation, hypotension, JVP distension) requiring immediate needle decompression.
Fibrotic lung disease produces fine late inspiratory (Velcro) crackles bilaterally at the lung bases, often with reduced chest expansion; refer to respiratory medicine and order HRCT thorax.
Aboriginal and Torres Strait Islander Australians have 2.5× the rate of respiratory disease hospitalisation compared to non-Indigenous Australians; rheumatic fever, bronchiectasis, and chronic suppurative lung disease are significantly more prevalent, particularly in remote communities.
Auscultation technique — compare sides systematically using the diaphragm; ask the patient to breathe deeply through the mouth; listen for at least one full respiratory cycle at each site bilaterally.

Introduction & Australian Epidemiology

Respiratory disease is a leading cause of morbidity and mortality in Australia. Chronic obstructive pulmonary disease (COPD) is the fifth leading cause of death nationally, while lung cancer remains the leading cause of cancer death in both men and women. Asthma affects approximately 2.7 million Australians (10.8% of the population), making Australia one of the highest-prevalence countries globally. Community-acquired pneumonia accounts for over 100,000 hospital admissions annually, and the burden of respiratory disease is disproportionately borne by Aboriginal and Torres Strait Islander Australians and rural/remote populations.

A systematic approach to respiratory history and examination is the foundation of clinical assessment. The respiratory history focuses on symptom characterisation — cough, sputum, haemoptysis, dyspnoea, wheeze, chest pain, and relevant exposures — while the examination employs inspection, palpation, percussion, and auscultation to identify physical signs that localise pathology and guide investigation. This article provides a structured framework for Australian clinicians in primary care and hospital settings.

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Safety-critical reminder: Haemoptysis, acute severe dyspnoea at rest, tension pneumothorax signs (tracheal deviation, hypotension, absent breath sounds unilaterally), and stridor are respiratory emergencies. Do not delay investigation or management while completing a full examination — initiate resuscitation and emergency referral simultaneously.

Respiratory History

A thorough respiratory history characterises each symptom in detail, identifies risk factors and exposures, and determines functional impact. The approach below covers the cardinal respiratory symptoms in the order they should be systematically assessed.

Cough

Cough is the most common symptom prompting respiratory consultation. Characterise each of the following:

Duration: Acute (<3 weeks) — typically viral URTI, acute bronchitis, or pneumonia. Subacute (3–8 weeks) — post-infectious cough, Bordetella pertussis, or resolving pneumonia. Chronic (>8 weeks) — consider asthma, COPD, GORD, ACE inhibitor use, post-nasal drip, bronchiectasis, lung cancer, or interstitial lung disease.
Timing and pattern: Nocturnal cough suggests asthma or GORD; early morning productive cough is typical of bronchiectasis and chronic bronchitis; cough with eating suggests aspiration or tracheo-oesophageal fistula.
Character: Whooping (pertussis), brassy/tracheal (tracheal irritation), barking (croup in children).
Productive vs dry: A productive cough warrants sputum characterisation. A change from previously productive to dry should raise suspicion for bronchial obstruction (mucus plugging or endobronchial lesion).
Triggers: Cold air, exercise, allergens (asthma), dust/occupational exposure, meals (aspiration).

Sputum

When present, characterise sputum carefully:

Feature	Description	Suggests
Mucoid (clear/white)	Translucent, may be tenacious	Asthma, COPD (stable), viral infection
Mucopurulent (yellow)	Opaque yellow	Bacterial infection, acute exacerbation of COPD/bronchiectasis
Purulent (green)	Thick green, may be foul-smelling	Bronchiectasis, lung abscess, Pseudomonas infection
Rust-coloured	Brown-tinged	Streptococcus pneumoniae pneumonia (classical)
Pink frothy	Blood-tinged, foam-like	Pulmonary oedema
Currant jelly	Red-brown, gelatinous	Klebsiella pneumoniae
Copious (>100 mL/day)	Large volume daily, often worse on waking	Bronchiectasis, pulmonary alveolar proteinosis

In Australian practice, sputum culture and sensitivity should be sent for patients with chronic productive cough, suspected bronchiectasis (including Pseudomonas aeruginosa screening), or treatment failure. Nucleic acid amplification testing (NAAT) for Mycobacterium tuberculosis is indicated if TB is suspected — notify the state/territory public health unit under mandatory notification requirements.

Haemoptysis

Haemoptysis (coughing blood from the respiratory tract) must always be investigated. Differentiate from epistaxis (nosebleed) and haematemesis (vomiting blood).

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Major haemoptysis is defined as >200 mL in 24 hours or any haemoptysis causing haemodynamic instability. This is a medical emergency — secure the airway, establish large-bore IV access, position patient with the bleeding side down (if lateralised), and arrange urgent bronchoscopy and interventional radiology. Transfuse as needed and crossmatch blood.

Common causes in Australia (in approximate order of frequency):

Bronchiectasis (most common cause overall)
Lung cancer / bronchial carcinoma
Pulmonary embolism
Acute lower respiratory tract infection / pneumonia
Tuberculosis (consider in ATSI communities, migrants from high-prevalence countries)
Mitral stenosis (rare but classical)
Coagulopathy / anticoagulant use

Initial investigations: FBC, coagulation studies, sputum cytology, CT thorax with contrast (CTPA if PE suspected), and bronchoscopy for persistent or recurrent haemoptysis.

Dyspnoea

Dyspnoea (breathlessness) should be characterised by onset (acute vs chronic), pattern (constant vs episodic), provocation (exertional vs rest), and severity. The modified Medical Research Council (mMRC) Dyspnoea Scale provides a standardised functional grading:

Grade	Description	Functional Impact
mMRC 0	Breathless only with strenuous exercise	No limitation on daily activities
mMRC 1	Short of breath when hurrying on level ground or walking up a slight hill	Mild limitation
mMRC 2	Walks slower than people of the same age on level ground because of breathlessness, or has to stop for breath when walking at own pace	Moderate limitation
mMRC 3	Stops for breath after walking about 100 metres or after a few minutes on level ground	Severe limitation
mMRC 4	Too breathless to leave the house, or breathless when dressing or undressing	Very severe limitation

Wheeze

Wheeze is a continuous, high-pitched musical sound produced by airflow through narrowed airways. Enquire about:

Timing: Episodic (asthma), persistent (COPD), nocturnal (asthma, GORD), exercise-induced (EIB/asthma).
Triggers: Allergens, cold air, exercise, respiratory infections, occupational exposures, NSAIDs/aspirin (Samter's triad).
Associated features: Atopy (eczema, allergic rhinitis, hayfever), family history of asthma, smoking history.
Silent chest: A patient in severe respiratory distress without audible wheeze is a danger sign — indicates critically reduced airflow. Treat as life-threatening asthma.

Chest Pain (Respiratory)

Respiratory chest pain is typically pleuritic — sharp, worsened by inspiration and coughing, and localised. Differentiate from cardiac chest pain (central, pressure-like, exertional, radiating to jaw/arm).

Pleuritic pain: Pneumonia, pulmonary embolism, pneumothorax, pleurisy, mesothelioma (especially with asbestos exposure history).
Localised chest wall pain: Rib fracture, costochondritis, muscle strain, metastatic bone disease.
Referred shoulder pain: Diaphragmatic irritation (subphrenic abscess, hepatic pathology) via phrenic nerve (C3–C5).

Occupational and Environmental Exposure

A detailed occupational history is mandatory in all respiratory assessments. Australia has significant occupational lung disease burden, particularly in mining, construction, and agriculture.

Exposure	Occupation / Industry	Condition
Asbestos	Construction, shipbuilding, brake mechanics, mining (Wittenoom)	Asbestosis, mesothelioma, pleural plaques
Silica	Mining (sandstone, quarrying), tunnelling, stonemasonry, sandblasting	Silicosis, progressive massive fibrosis, increased TB risk
Coal dust	Coal mining (Hunter Valley, QLD)	Coal workers' pneumoconiosis (black lung)
Isocyanates	Spray painting, foam manufacturing, plastics	Occupational asthma
Grain dust, animal dander	Agriculture, farming	Hypersensitivity pneumonitis, organic dust toxic syndrome
Beryllium	Electronics, aerospace manufacturing	Berylliosis (chronic granulomatous disease)

Document duration and intensity of exposure, use of personal protective equipment (PPE), and whether the condition may be compensable under relevant state/territory workplace health and safety legislation (e.g., Safe Work Australia, WorkCover).

Sleep Apnoea Screening

Obstructive sleep apnoea (OSA) affects an estimated 5–10% of Australian adults and is an independent risk factor for cardiovascular disease, hypertension, and motor vehicle accidents. Screening questions include:

Witnessed apnoeas during sleep (partner or family report)
Excessive daytime sleepiness (Epworth Sleepiness Scale score >10)
Unrefreshing sleep, morning headaches
Nocturnal choking or gasping
Loud snoring

The STOP-BANG questionnaire is the preferred screening tool: Snoring, Tiredness, Observed apnoeas, Pressure (hypertension), BMI >35, Age >50, Neck circumference >40 cm, male Gender. A score ≥3 indicates high risk for OSA. Refer for sleep study (MBS item 12203 for Level 1 polysomnography; MBS item 12250 for Level 2 home-based study).

Dyspnoea Characterisation

Beyond grading severity with the mMRC scale, the pattern of dyspnoea provides critical diagnostic information. The following patterns should be specifically sought during the respiratory history.

Paroxysmal Nocturnal Dyspnoea (PND)

The patient wakes from sleep, typically 1–2 hours after lying flat, with severe breathlessness and a sensation of suffocation. Relief is obtained by sitting upright or standing by an open window. PND results from redistribution of fluid from the lower limbs into the central circulation when recumbent, increasing pulmonary venous pressure and causing interstitial pulmonary oedema.

Most common cause: Left ventricular failure (cardiac asthma).
Differential: Nocturnal asthma (also relieved by upright position but typically with wheeze), COPD (less commonly nocturnal-specific), OSA (different pattern — apnoeas followed by gasping, not sustained dyspnoea).
Key investigations: BNP/NT-proBNP, CXR (pulmonary venous congestion, upper lobe diversion, interstitial oedema, Kerley B lines, bilateral pleural effusions), transthoracic echocardiography.

Orthopnoea

Breathlessness when lying flat that is immediately relieved by sitting up. Patients typically measure the number of pillows they require (e.g., "3-pillow orthopnoea"). Orthopnoea correlates with severity of heart failure — the more pillows required, the more severe the pulmonary congestion.

Left heart failure: Most common cause. Document the number of pillows used and whether the patient has taken to sleeping in a chair.
Bilateral diaphragm paralysis: Severe orthopnoea due to abdominal contents splinting the diaphragm; patients may prefer to sleep sitting or prone.
Obesity / ascites: Increased intra-abdominal pressure restricts diaphragmatic excursion.
Severe COPD with hyperinflation: Less commonly causes true orthopnoea but may worsen when supine.

Obstructive Sleep Apnoea Pattern

Unlike PND, OSA-related dyspnoea manifests as repeated cycles of apnoea and arousal through the night. The patient may not perceive breathlessness per se but reports:

Witnessed apnoeas by the bed partner (cessation of airflow with continued chest/abdominal movement for >10 seconds)
Choking or gasping arousals from sleep
Excessive daytime somnolence (Epworth Sleepiness Scale >10)
Morning headaches, poor concentration, irritability

Untreated OSA is associated with systemic hypertension, atrial fibrillation, heart failure, stroke, and increased perioperative risk. Continuous positive airway pressure (CPAP) is first-line treatment for moderate-to-severe OSA (AHI ≥15 or AHI ≥5 with symptoms).

Kussmaul Breathing

Kussmaul breathing is a deep, rapid, laboured breathing pattern reflecting metabolic acidosis with respiratory compensation. The pattern is regular, with increased tidal volume (hyperpnoea) rather than true hyperventilation.

Most common cause: Diabetic ketoacidosis (DKA).
Other causes: Lactic acidosis (sepsis, metformin toxicity, mesenteric ischaemia), renal failure (uraemic acidosis), toxic ingestions (salicylates, methanol, ethylene glycol).
Assessment: ABG showing low pH, low HCO₃⁻, elevated anion gap, respiratory compensation (expected PaCO₂ = 1.5 × [HCO₃⁻] + 8 ± 2 — Winter's formula).
Management: Treat the underlying cause. In DKA, initiate insulin infusion (Actrapid® 0.1 unit/kg/hr IV), aggressive IV fluid resuscitation (0.9% NaCl), and potassium replacement per local protocol.

Cheyne-Stokes Respiration

Cheyne-Stokes respiration is a cyclical pattern of breathing characterised by alternating periods of progressively increasing then decreasing tidal volume (crescendo–decrescendo), interspersed with periods of apnoea (typically 10–20 seconds). The cycle length is usually 45–90 seconds.

Cardiac causes: Severe congestive heart failure (most common association), with prolonged circulation time delaying the chemoreceptor feedback loop.
Neurological causes: Stroke (particularly bilateral hemispheric), traumatic brain injury, raised intracranial pressure.
High altitude: Periodic breathing at altitude due to the hypoxic ventilatory response.
Significance: In heart failure, Cheyne-Stokes respiration is an independent marker of poor prognosis. Consider cardiac optimisation, CPAP/bi-level PAP, and specialist respiratory/cardiology input.

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Clinical pearl: Observe the patient's breathing pattern for at least 2 minutes before approaching the bedside in an acutely unwell patient. The pattern of breathing (tachypnoea, Kussmaul, Cheyne-Stokes, ataxic/Biot's) can immediately narrow the differential diagnosis and guide emergency management.

Respiratory Examination

The respiratory examination follows the standard approach: inspection, palpation (tracheal position, chest expansion, tactile vocal fremitus), percussion, and auscultation. Always compare sides systematically and expose the chest adequately while maintaining patient dignity.

Inspection

Begin inspection from the end of the bed before touching the patient. Assess the following:

General appearance: Cachexia (malignancy, chronic lung disease, TB), distress level, use of accessory muscles (sternocleidomastoid, scalenes, intercostals), pursed lip breathing (COPD), tripod positioning (severe COPD or asthma).
Respiratory rate: Normal 12–20 breaths/min in adults. Tachypnoea (>20) is an early and sensitive sign of respiratory compromise. Bradypnoea (<10) suggests respiratory depression (opioids, CNS pathology) and impending respiratory arrest.
Pattern: Regular vs irregular, depth (shallow vs deep), see Cheyne-Stokes and Kussmaul above.
Chest shape:
- Barrel chest — increased AP diameter (>1:1 with transverse), seen in COPD/hyperinflation.
- Pectus excavatum (funnel chest) — may be associated with Marfan syndrome and can restrict lung volumes.
- Pectus carinatum (pigeon chest) — may follow childhood chronic respiratory disease (e.g., severe asthma).
- Kyphoscoliosis — restricts lung volumes; causes and exacerbates type 2 respiratory failure.
Scars: Thoracotomy (lobectomy, pneumonectomy, lung transplant), chest drain scars, median sternotomy (cardiac surgery — may indicate valvular heart disease).
Visible masses or asymmetry: Tumour, abscess, pneumothorax (asymmetric chest expansion visible).
Hands and peripheries: Clubbing (bronchiectasis, lung cancer, fibrosing alveolitis, mesothelioma, cyanotic heart disease), nicotine staining (smoking), peripheral cyanosis, CO₂ retention flap (asterixis), tar staining, tarantula sign (hypertrophic pulmonary osteoarthropathy with wrist tenderness).
Face and neck: Central cyanosis (tongue, best seen in natural light), Horner's syndrome (miosis, ptosis, anhidrosis — Pancoast tumour), raised JVP (right heart failure, tension pneumothorax, SVC obstruction), tracheal tug (hyperinflation).

Tracheal Position

Assess tracheal position by placing one finger on either side of the trachea in the suprasternal notch. The trachea should be central. Deviation is assessed by the space between the trachea and the sternocleidomastoid muscle on each side.

Tracheal Deviation	Away From	Toward
Large pleural effusion	✓ (away from effusion)
Tension pneumothorax	✓ (away from pneumothorax)
Lobar collapse (complete)		✓ (toward collapse)
Pulmonary fibrosis		✓ (toward fibrosis)
Pneumonectomy		✓ (toward side of surgery)
Upper lobe collapse / fibrosis		✓ (toward affected side)

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Tension pneumothorax — tracheal deviation AWAY from the affected side, with hypotension, tachycardia, distended neck veins, and absent breath sounds on the affected side — is a clinical diagnosis requiring immediate needle decompression (14G cannula, 2nd intercostal space, midclavicular line) before chest X-ray. Do not delay for imaging.

Chest Expansion

Place both hands on the patient's chest with thumbs meeting in the midline at the level of the 10th rib posteriorly. Ask the patient to take a deep breath in. Observe the symmetry and excursion of the thumbs.

Normal: Symmetrical thumb separation of 3–5 cm (≥5 cm in young adults).
Reduced bilaterally: COPD (hyperinflation reduces diaphragmatic excursion), ankylosing spondylitis (costovertebral joint stiffness), diffuse pulmonary fibrosis, severe obesity.
Reduced unilaterally: Pleural effusion, pneumonia/consolidation, pneumothorax, lobar collapse, rib fractures, unilateral diaphragm paralysis.

Percussion

Percuss both sides systematically, comparing equivalent areas. Place the middle finger of the non-dominant hand firmly on the chest wall (pleximeter finger) and strike its distal interphalangeal joint with the tip of the middle finger of the dominant hand (plexor finger). Use a quick, sharp wrist action.

Percussion Note	Quality	Causes
Resonant	Normal, low-pitched, hollow	Normal lung
Dull	Higher-pitched, shorter, thud-like	Consolidation, lobar collapse, pulmonary mass
Stony dull	Very high-pitched, dead, flat	Pleural effusion (classical finding)
Hyper-resonant	Lower-pitched than normal, booming	Pneumothorax, COPD (bilateral)
Impaired	Slightly duller than normal	Small effusion, mild consolidation, pleural thickening

Percussion landmarks: Percuss anteriorly from apex to base bilaterally, then posteriorly. Identify the level of the diaphragm on each side (normally at the 6th rib anteriorly, right side slightly higher due to the liver). A raised hemidiaphragm suggests collapse below, diaphragm paralysis, or subphrenic pathology.

Tactile Vocal Fremitus

Place the ulnar border or ball of the hand on the chest wall. Ask the patient to say "ninety-nine" or "one-one-one" in a deep voice. Feel for the vibrations transmitted through the chest wall. Compare sides systematically.

Increased fremitus: Consolidation (solid tissue transmits sound better than air-filled lung). Classical finding in lobar pneumonia.
Decreased or absent fremitus: Pleural effusion (fluid between lung and chest wall dampens transmission), pneumothorax (air in pleural space), pleural thickening, bronchial obstruction (complete — no air movement past obstruction).
Normal: Air-filled lung transmits vibrations normally; should be symmetrical.

Auscultation

Use the diaphragm of the stethoscope firmly applied to the chest wall. Ask the patient to breathe deeply through the mouth. Listen for at least one full respiratory cycle at each site. Always compare sides.

Normal breath sounds:

Vesicular: Soft, low-pitched, inspiratory sound with a short expiratory phase (ratio approximately 3:1). Heard over most of the lung peripheries.
Bronchial: Louder, higher-pitched, with a longer expiratory phase and a gap between inspiration and expiration. Normally heard only over the trachea. If heard peripherally, it indicates consolidation conducting sound from the bronchial tree to the chest wall.

Added sounds (adventitious sounds):

Sound	Description	Timing	Causes
Fine crackles (velcro-type)	High-pitched, brief, non-sustained, like Velcro separating	Late inspiratory	Pulmonary fibrosis (IPF, asbestosis), pulmonary oedema
Coarse crackles (rales)	Low-pitched, bubbling, louder	Early inspiratory	Secretions (pneumonia, bronchiectasis, COPD), pulmonary oedema
Wheezes	High-pitched, musical, continuous	Mainly expiratory	Asthma, COPD, airway narrowing
Rhonchi	Low-pitched, snoring-like, continuous	Expiratory (may clear with cough)	Secretions in large airways (bronchitis, bronchiectasis)
Pleural rub	Creaking or grating, like leather on leather	Both inspiration and expiration	Pleurisy (inflammation of pleural surfaces), PE
Stridor	High-pitched, harsh, inspiratory	Mainly inspiratory	Upper airway obstruction (foreign body, anaphylaxis, croup, tumour) — emergency

Vocal resonance: Ask the patient to say "ninety-nine" while auscultating. Increased vocal resonance (words clearly transmitted) over consolidation; decreased over effusion or pneumothorax. Whispering pectoriloquy (whispered "one-two-three" clearly heard) is a more sensitive sign of consolidation.

Auscultation Sites

Anterior chest: Apices (above clavicles), upper zones (2nd–4th interspaces), lower zones (5th–6th interspaces) — all compared bilaterally.

Posterior chest: Apices (below spine of scapula), upper zones (above the scapular spine), middle zones (between scapular spines and bases), lower zones (below the scapular angles) — all compared bilaterally. Ask the patient to fold their arms forward to move the scapulae laterally.

Axillae: Often overlooked — the right middle lobe and lingula are best auscultated with the arm raised above the head.

Chest Signs of Common Conditions

The following tables summarise the classical examination findings of common respiratory conditions. In clinical practice, signs are often partial or atypical — the combination of findings with the history guides the working diagnosis and investigation strategy.

Consolidation (Lobar Pneumonia)

Classic Signs

Consolidation

Inspection: Tachypnoea, reduced expansion on affected side
Trachea: Central (unless complicated)
Expansion: Reduced on affected side
Percussion: Dull
Fremitus: Increased
Auscultation: Bronchial breathing, increased vocal resonance, crackles (early), whispering pectoriloquy

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Clinical pearl — consolidation: The key distinguishing feature from effusion is increased tactile fremitus and vocal resonance. Solid lung tissue (alveoli filled with inflammatory exudate) transmits sound from the bronchial tree to the chest wall better than normal air-filled lung. Bronchial breathing heard over the peripheral lung is pathognomonic of consolidation.

Pleural Effusion

Classic Signs

Pleural Effusion

Inspection: Reduced expansion on affected side
Trachea: Deviated away from effusion (if large, >1 L)
Expansion: Reduced on affected side
Percussion: Stony dull (classical), dull-bounded superiorly by Ellis-Damoiseau line
Fremitus: Decreased or absent
Auscultation: Absent or markedly reduced breath sounds, reduced vocal resonance

Additional signs of large effusion: Mediastinal shift to opposite side (confirmed on CXR), reduced chest expansion, stony dull percussion from base to a curved upper margin (Ellis-Damoiseau line). Above this line, there may be a band of referred bronchial breathing (compressed lung). At the upper border of effusion, a pleural friction rub may be heard if the pleurae are inflamed.

Pneumothorax

Urgent Assessment

Pneumothorax

Inspection: May be clinically silent if small; tachypnoea and reduced expansion if larger
Trachea: Central (simple); deviated away (tension)
Expansion: Reduced on affected side
Percussion: Hyper-resonant
Fremitus: Absent
Auscultation: Absent breath sounds on affected side

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Tension pneumothorax: Tracheal deviation away from affected side + hypotension + tachycardia + raised JVP + absent breath sounds + hyper-resonance = clinical diagnosis, do NOT wait for CXR. Immediate needle decompression: 14G cannula, 2nd intercostal space, midclavicular line, ipsilateral side. Followed by intercostal catheter insertion (Seldinger or surgical technique) and underwater seal drainage. In the emergency department, point-of-care ultrasound (POCUS) can rapidly distinguish pneumothorax from other causes of absent breath sounds (lung sliding absent, barcode/stratosphere sign on M-mode).

Chronic Obstructive Pulmonary Disease (COPD)

Typical Signs

COPD

Inspection: Barrel chest, pursed-lip breathing, tripod position, cachexia (in severe disease), use of accessory muscles, quiet speaking voice
Trachea: Central
Expansion: Bilaterally reduced
Percussion: Bilateral hyper-resonance
Fremitus: Bilaterally reduced
Auscultation: Prolonged expiratory phase, widespread expiratory wheeze, reduced breath sounds globally, scattered coarse crackles (if concurrent bronchitis)
Other signs: Raised JVP (if cor pulmonale), peripheral oedema, CO₂ retention flap (asterixis), bounding pulse (CO₂ retention), plethora, cyanosis

Note: In severe COPD with acute exacerbation, the chest may be "silent" (absent wheezes) — this indicates critically reduced air movement and is a danger sign.

Asthma

Typical Signs

Asthma

completely normal

Inspection: Tachypnoea, accessory muscle use, speaking in words/phrases (moderate) or single words (severe)
Trachea: Central
Expansion: May be bilaterally reduced in severe attack
Percussion: Normal or resonant (hyperinflation in severe attack)
Fremitus: Normal or reduced bilaterally
Auscultation: Widespread bilateral expiratory polyphonic wheeze (high and low pitch). In severe/life-threatening attack, may be "silent chest" (no wheeze — ominous sign)

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Life-threatening asthma signs: SpO₂ <92%, peak flow <33% predicted, silent chest, cyanosis, altered consciousness, bradycardia, hypotension, inability to speak. These patients require ICU admission, continuous salbutamol nebulisation, IV magnesium sulphate (2 g over 20 min), and early consideration of intubation and mechanical ventilation. Refer to the Australian Asthma Handbook (NAC) for current guidelines.

Pulmonary Fibrosis

Classic Signs

Pulmonary Fibrosis

Inspection: Tachypnoea, clubbing (present in ~50% of IPF cases), cyanosis in advanced disease
Trachea: Central (may deviate toward the more affected side in unilateral disease)
Expansion: Bilaterally reduced
Percussion: Impaired or dull (bilateral bases)
Fremitus: May be increased at bases (denser fibrotic tissue)
Auscultation: Bilateral fine late inspiratory crackles (Velcro crackles) — classically at the lung bases, not clearing with cough. End-inspiratory squeaks may suggest hypersensitivity pneumonitis or COP.

Investigation pathway: If fibrotic signs are detected on examination, arrange high-resolution CT thorax (HRCT — MBS item 56300/56303), FVC and DLCO on spirometry, and refer to respiratory medicine. Autoimmune serology (ANA, RF, anti-CCP, anti-Scl-70, anti-Jo-1) should be sent if connective tissue disease-associated ILD is suspected. Multidisciplinary discussion (respiratory physician, radiologist, pathologist) is the gold standard for ILD diagnosis.

Quick Reference: Differentiating Key Chest Signs

Sign	Consolidation	Pleural Effusion	Pneumothorax	Fibrosis
Expansion	↓ Unilateral	↓ Unilateral	↓ Unilateral	↓ Bilateral
Percussion	Dull	Stony dull	Hyper-resonant	Impaired
Tactile fremitus	↑ Increased	↓ Decreased	↓ Absent	Normal / ↑
Breath sounds	Bronchial	Absent / ↓↓	Absent	Vesicular with crackles
Added sounds	Crackles, ↑ vocal resonance	None / pleural rub	None	Fine Velcro crackles
Trachea	Central	Deviated away (large)	Central / deviated away (tension)	Central

COPD vs Asthma: Examination Differentiation

Feature	COPD	Asthma
Chest shape	Barrel chest	Normal (unless severe chronic)
Expansion	Bilaterally reduced	Normal (or ↓ in acute severe)
Breath sounds	Quiet, prolonged expiration	Wheeze (polyphonic, expiratory)
Added sounds	Rhonchi, coarse crackles	Polyphonic wheeze
Reversibility	Limited (<12% and <200 mL improvement post-bronchodilator)	Significant (>12% and >200 mL improvement)
Clubbing	Absent (if present, suspect lung cancer)	Absent
Peripheral oedema	May be present (cor pulmonale)	Absent

Special Populations

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Paediatric Considerations

Respiratory rate: Higher normal ranges — neonates 30–60/min, infants 25–50/min, children 20–30/min, adolescents 12–20/min. Tachypnoea is the earliest sign of respiratory distress in children.

Examination technique: Auscultate with the stethoscope under the child's clothing or warm the diaphragth first to reduce distress. Observe from the end of the bed before approaching. Allow the child to sit on the parent's lap.

Chest signs of bronchiolitis: Wheeze, fine crackles, hyperinflation, subcostal/intercostal recession, nasal flaring, grunting in infants.

Foreign body aspiration: Consider in any child with sudden-onset unilateral wheeze, reduced breath sounds, or recurrent pneumonia in the same lobe. Inspiratory and expiratory CXR (look for air trapping on the affected side on expiration) or CT thorax.

Croup vs epiglottitis: Croup — barking cough, inspiratory stridor, gradual onset. Epiglottitis — drooling, tripod position, muffled voice, rapid onset — medical emergency. Do not examine the throat or distress the child; maintain a calm environment and prepare for emergency intubation.

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Pregnancy

Normal physiological changes: Tidal volume increases by 40%, respiratory rate is unchanged, residual volume and FRC decrease (diaphragm elevation). PaCO₂ falls to ~30 mmHg (compensated respiratory alkalosis). Dyspnoea is common from early pregnancy.

Examination interpretation: Basal crackles may be normal in late pregnancy due to atelectasis. Mild peripheral oedema is physiological. Distinguish from pathological findings (wheeze, unilateral signs, haemoptysis).

VTE risk: Pregnancy is a prothrombotic state — pleuritic chest pain and dyspnoea warrant CTPA (low-dose protocol) or V/Q scan to exclude PE. Wells score applies but thresholds for investigation should be lower.

Asthma management: Uncontrolled asthma poses greater risk to the fetus than controller medications. Budesonide (Pulmicort®) is the preferred ICS in pregnancy. Salbutamol is safe. Continue management per the Australian Asthma Handbook.

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Elderly

Reduced respiratory reserve: Decreased chest wall compliance, reduced FEV₁ and FVC, weakened respiratory muscles, blunted cough reflex. Pneumonia may present atypically — confusion, falls, functional decline rather than classic cough/fever.

Examination pitfalls: Kyphoscoliosis is common and alters chest shape and percussion notes. Basal crackles may be due to atelectasis or heart failure rather than pneumonia. Differentiating heart failure from COPD can be clinically challenging — use BNP (≥100 pg/mL suggestive of heart failure) and CXR.

Aspiration: Common in elderly, especially with neurological disease (stroke, dementia, Parkinson's). Aspiration pneumonia classically affects the right lower lobe. Dysphagia screening (bedside swallow assessment) should be part of the respiratory assessment.

Drug interactions: Opioids and benzodiazepines cause respiratory depression. ACE inhibitors cause chronic cough in ~15% of patients — consider switching to ARB if cough develops.

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Renal Impairment

Fluid overload: Patients with CKD or ESKD on dialysis may develop pulmonary oedema rapidly. Signs include bilateral basal crackles, raised JVP, peripheral oedema, and orthopnoea. Urgent fluid removal (dialysis/ultrafiltration) may be required.

Metabolic acidosis: CKD-related metabolic acidosis triggers Kussmaul breathing. ABG will show low pH, low HCO₃⁻ with non-elevated anion gap (if early) or elevated anion gap (if uraemic).

Uraemic pleuritis: Pleuritic chest pain with pleural rub in the context of severe uraemia. Pleural effusion may be exudative with high LDH and low glucose.

Drug clearance: Adjust antibiotic doses in renal impairment when treating pneumonia. Avoid codeine (active metabolites accumulate). Use morphine with extreme caution. Gabapentin and pregabalin require dose reduction.

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Hepatic Impairment

Hepatopulmonary syndrome: In chronic liver disease, intrapulmonary vascular dilatation cause hypoxaemia (platypnoea-orthodeoxia — dyspnoea and desaturation that worsens when upright). Classic finding: clubbing, cyanosis, spider naevi, and orthodeoxia (SpO₂ drop >4% or PaO₂ drop >3 mmHg from supine to upright).

Hepatic hydrothorax: Right-sided pleural effusion (typically 1–3 L) in portal hypertension without cardiac or pulmonary cause. Transudative. May cause significant dyspnoea. Management: sodium restriction, diuretics, TIPS for refractory cases, pleurodesis for recurrent effusions.

Ascites impact: Large-volume ascites elevates the diaphragm and restricts lung expansion. Therapeutic paracentesis may improve respiratory function.

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Immunocompromised

Broad differential: In immunocompromised patients (HIV, chemotherapy, biologics, transplant), respiratory signs may be minimal despite significant pathology. A normal examination does not exclude pneumonia in the immunocompromised — low threshold for CT thorax.

Pneumocystis jirovecii pneumonia (PJP): In HIV with CD4 <200 — exertional dyspnoea, non-productive cough, bilateral fine crackles. SpO₂ may be disproportionately low. LDH elevated. CXR: bilateral perihilar ground-glass opacities. Diagnosis: induced sputum or BAL for PCR. Treatment: TMP-SMX (Bactrim®). Prophylaxis: TMP-SMX when CD4 <200.

Invasive aspergillosis: Consider in neutropenic patients with fever, pleuritic chest pain, and haemoptysis. CT halo sign (nodule with surrounding ground-glass). Galactomannan and β-D-glucan assays. Treatment: voriconazole (Vfend®) 6 mg/kg IV BD day 1 then 4 mg/kg BD.

CMV pneumonitis: Transplant recipients — bilateral interstitial opacities. Diagnosis by CMV PCR on BAL. Treatment: ganciclovir (Cymevene®) 5 mg/kg IV BD, then valganciclovir (Valcyte®) PO for consolidation.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Respiratory disease is one of the leading contributors to the health gap between Aboriginal and Torres Strait Islander Australians and non-Indigenous Australians. The AIHW reports that Indigenous Australians are hospitalised for respiratory disease at 2.5 times the rate of non-Indigenous Australians, with chronic respiratory conditions contributing significantly to the burden of disease. Culturally safe assessment, awareness of unique disease patterns, and addressing barriers to care are essential.

Unique disease burden

Chronic suppurative lung disease / bronchiectasis: Prevalence in remote NT communities is 5–10× higher than non-Indigenous populations. Often develops from childhood lower respiratory tract infections and recurrent pneumonia. Bilateral basal coarse crackles, clubbing, copious purulent sputum are common examination findings.
Rheumatic fever / rheumatic heart disease (RHD): ARF/RHD remains endemic in remote NT, WA, and QLD communities. Mitral stenosis from RHD can cause haemoptysis and pulmonary hypertension. Auscultation may reveal a mid-diastolic rumbling murmur (opening snap + low-pitched diastolic murmur at the apex).
Tuberculosis: TB notification rates in Indigenous Australians are 6–8× higher than non-Indigenous Australians. Consider TB in any ATSI patient with chronic cough (>2 weeks), weight loss, night sweats, or haemoptysis, particularly in remote NT communities. Mandatory notification to public health.
Non-tuberculous mycobacteria (NTM): M. abscessus complex is increasingly identified in remote NT communities, causing chronic suppurative lung disease that is difficult to treat.
Community-acquired pneumonia: Higher rates of hospitalisation, more severe presentations, higher rates of empyema, particularly in children. Staphylococcus aureus (including CA-MRSA) is a more common pathogen than in non-Indigenous populations.
Smoking: Approximately 37% of Indigenous Australians smoke (compared to ~10% non-Indigenous), the single largest modifiable risk factor for respiratory disease.

Barriers to respiratory assessment

Geographic remoteness: Limited access to respiratory specialists, spirometry services, bronchoscopy, sleep studies, and thoracic surgery. CT scanners not available in many remote communities — requires aeromedical retrieval or transfer.
Workforce shortages: Remote clinics may be staffed by Aboriginal health practitioners and remote area nurses without advanced respiratory assessment training. Telehealth respiratory consultations are increasingly used.
Language and health literacy: Respiratory symptoms may be described differently or minimised in some cultural contexts. Auscultation and percussion findings should be clearly explained using accessible language and, where possible, interpreters for patients whose first language is not English.
Intermittent care: Patients in remote communities may present to different health services, making longitudinal respiratory follow-up (e.g., serial spirometry for COPD or asthma) challenging. The use of shared electronic health records (e.g., Communicare, Primary Care Information System) is critical.
Overcrowded housing: Contributes to transmission of respiratory infections (pneumococcal disease, influenza, TB) and exposure to environmental tobacco smoke.

Clinical practice recommendations

Perform opportunistic respiratory assessments during any healthcare encounter — many chronic respiratory conditions are underdiagnosed in ATSI communities.
Ensure spirometry is available and performed according to ATS/ERS standards in Aboriginal Community Controlled Health Organisations (ACCHOs) where possible. Spirometry with bronchodilator reversibility is essential for differentiating asthma from COPD.
Screen for bronchiectasis in any ATSI child or young adult with chronic wet cough (>4 weeks) — refer for HRCT thorax and sputum culture.
Support smoking cessation using culturally appropriate resources (e.g., Tackling Indigenous Smoking programme, Quitline 13 7848, Deadly Choices campaign).
Ensure pneumococcal and influenza vaccination is up to date per ATAGI recommendations — free funded vaccines for Indigenous Australians include enhanced pneumococcal (PCV13 and PPSV23) and annual influenza vaccine.
Consider NTM in patients with chronic productive cough not responding to standard antibiotics — obtain sputum for AFB culture (×3 early morning samples).
Use telehealth for specialist respiratory consultation when face-to-face access is limited — the Australian Government telehealth items (MBS items 99200, 99201, etc.) fund video consultations with respiratory physicians.

📚 References

1. Australian Institute of Health and Welfare (AIHW). Respiratory disease in Australia. Cat. no. PHE 290. Canberra: AIHW; 2024.
2. National Asthma Council Australia. Australian Asthma Handbook, Version 2.2. Melbourne: National Asthma Council Australia; 2024. Available from: https://www.asthmahandbook.org.au
3. Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management, and Prevention of COPD: 2024 Report. Available from: https://goldcopd.org
4. Simpson G, Low T, Kette F, et al. Guidelines for the investigation of chronic cough in adults. Thoracic Society of Australia and New Zealand (TSANZ) Position Statement. Respirology. 2023;28(2):115–127.
5. Chang AB, Upham JW, Masters IB, et al. Protracted bacterial bronchitis: The last decade and the road ahead. Pediatr Pulmonol. 2016;51(3):225–242.
6. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Respiratory disease. Canberra: AIHW; 2023.
7. Rheumatic Heart Disease Australia (RHDAustralia). National guidelines for acute rheumatic fever and rheumatic heart disease in Australia. 3rd ed. Darwin: Menzies School of Health Research; 2024.
8. Tsim S, Stobo DB, Alexander L, Kelly C, Blyth KG. The diagnostic performance of routinely acquired and reported computed tomography pulmonary angiography. Clin Radiol. 2017;72(8):694.e1–694.e6.
9. BTS Pleural Disease Guideline Group. British Thoracic Society pleural disease guidelines — 2023 update. Thorax. 2023;78(Suppl 2):s1–s42.
10. Raghu G, Remy-Jardin M, Richeldi L, et al. Idiopathic pulmonary fibrosis (an update) and progressive pulmonary fibrosis in adults: An official ATS/ERS/JRS/ALAT clinical practice guideline. Am J Respir Crit Care Med. 2022;205(9):e18–e47.
11. Chang AB, Bell SC, Byrnes CA, et al. Chronic suppurative lung disease and bronchiectasis in children and adults in Australia and New Zealand: Thoracic Society of Australia and New Zealand and Lung Foundation Australia position statement. Med J Aust. 2010;193(6):356–365.
12. Safe Work Australia. Guide to the Work Health and Safety (WHS) Regulations — Workplace exposure standards for airborne contaminants. Canberra: Safe Work Australia; 2024.
13. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health and Aged Care. Canberra; 2024. Available from: https://immunisationhandbook.health.gov.au
14. Chung KF, Pavord ID. Prevalence, pathogenesis, and causes of chronic cough. Lancet. 2008;371(9621):1364–1374.