Approach to respiratory symptoms and the chest examination

After this session, you will be able to take a focused history for common respiratory symptoms and understand the basic pathophysiology behind them. Always check drug doses and local protocols against the Kenya MoH guidelines and your hospital formulary.

Definition

Respiratory symptoms are subjective complaints related to the respiratory system, indicating an underlying abnormality in breathing, gas exchange, or airway function. A chest examination is the objective physical assessment of the thoracic cavity and its contents to identify signs of respiratory disease.

Anatomy and physiology you need

The respiratory system comprises the upper airways (nose, pharynx, larynx), lower airways (trachea, bronchi, bronchioles), and lungs (alveoli, pulmonary vasculature, interstitial tissue). The pleura (visceral and parietal) enclose the lungs. The diaphragm and intercostal muscles facilitate breathing.

• Airways: Conduct air to and from the alveoli. Mucociliary escalator clears debris.
• Alveoli: Site of gas exchange (oxygen into blood, carbon dioxide out).
• Pulmonary vasculature: Transports blood for gas exchange.
• Pleura: Lubricated surfaces allow frictionless lung movement.
• Respiratory muscles: Generate pressure gradients for ventilation.
• Respiratory control centre: In brainstem, regulates breathing rate and depth.

Causes and risk factors

Pathophysiology

Cough: Irritation of airway receptors (mechanical/chemical) → Afferent nerve impulses (vagus, glossopharyngeal, trigeminal, phrenic) → Cough centre (medulla) → Efferent impulses (vagus, phrenic, spinal nerves) → Deep inspiration → Glottis closure, diaphragmatic/intercostal muscle contraction → Increased intrathoracic pressure → Sudden glottis opening → Explosive expulsion of air and irritants.

Dyspnoea: Increased ventilatory drive (e.g., hypoxia, hypercapnia, acidosis) OR Increased work of breathing (e.g., airway obstruction, reduced lung compliance) OR Respiratory muscle weakness OR Psychological factors → Mismatch between ventilatory demand and capacity → Sensation of breathlessness.

Haemoptysis: Damage to bronchial or pulmonary vasculature (e.g., inflammation, infection, tumour, trauma) → Erosion of vessel wall → Leakage of blood into airways → Expectorated with cough.

Wheeze: Narrowing of airways (bronchoconstriction, mucosal oedema, intraluminal secretions/foreign body) → Turbulent airflow through constricted lumen → Vibration of airway walls → High-pitched whistling sound.

Chest Pain (Pleuritic): Inflammation/irritation of parietal pleura (rich nerve supply) → Pain fibres stimulated by movement (breathing, coughing) → Sharp, localized pain, often worse on inspiration.

Clinical features

History: key discriminators

• Cough: Duration (<3 weeks acute vs >8 weeks chronic, e.g., tuberculosis, post-nasal drip, asthma). Sputum character: purulent (bacterial infection), foul-smelling (lung abscess, anaerobic bronchiectasis), large-volume morning expectoration (bronchiectasis), pink frothy (acute pulmonary oedema).
• Dyspnoea: Onset speed: hyperacute/minutes (pulmonary embolism, tension pneumothorax), hours to days (pneumonia, asthma, acute heart failure), months to years (COPD, idiopathic pulmonary fibrosis). Relation to posture: orthopnoea/PND (left ventricular failure, bilateral diaphragmatic weakness), trepopnoea (unilateral pleural effusion). Exertional tolerance (NYHA/mMRC functional staging).
• Haemoptysis: Volume: massive (>100–600 mL/24h; threatens asphyxiation) vs non-massive. Blood mixed with purulence (bronchiectasis, pneumonia), frank blood clots (cavitary TB, bronchogenic carcinoma, pulmonary infarction), blood-streaked (bronchitis).
• Wheeze: Expiratory polyphonic (widespread bronchospasm/mucosal oedema in asthma, COPD); monophonic/stridor (fixed central airway obstruction, foreign body, bronchial tumour).
• Chest pain: Pleuritic (sharp, worsened by inspiration/coughing: pleuritis, PE, pneumonia); non-pleuritic/retrosternal (pericarditis, musculoskeletal, myocardial ischaemia).

Chest examination

General inspection and hands

• Clubbing: Loss of the Lovibond angle due to megakaryocyte/platelet-derived PDGF entrapment in digital capillary beds. Causes: bronchogenic carcinoma, bronchiectasis, lung abscess, idiopathic pulmonary fibrosis, empyema (rare/absent in simple COPD or uncomplicated asthma).
• Cyanosis: Peripheral (vasoconstriction/poor perfusion); central (deoxyhaemoglobin >5 g/dL in arterial blood, inspected under the tongue: severe hypoxaemia).
• Accessory muscle use / Hoover sign: Scalene and sternocleidomastoid use reflects high work of breathing. Paradoxical inward movement of lower ribs during inspiration (Hoover sign) indicates flattened, low-lying diaphragms in severe hyperinflation (COPD).

Palpation

• Tracheal position: Pulled toward pathology in lung collapse (atelectasis) and severe unilateral apical fibrosis due to volume loss. Pushed away from pathology in large pleural effusions and tension pneumothorax due to mass effect. Central in consolidation and uncomplicated pulmonary fibrosis.
• Chest expansion: Asymmetric reduction occurs on the affected side in unilateral disease (pleural effusion, pneumonia, pneumothorax, collapse). Symmetrically reduced in diffuse fibrosis or severe emphysema.
• Tactile vocal fremitus (TVF): Low-frequency vocal resonance transmitted to the chest wall. Increased in consolidation (solid tissue conducts sound waves better than aerated lung). Decreased or absent in pleural effusion, pneumothorax, and collapse (fluid, air, or plugged bronchi attenuate sound transmission).

Percussion

• Stony dull: Pleural effusion (fluid dampens acoustic vibration entirely).
• Dull: Consolidation (alveolar air replaced by exudate), lung collapse, or extensive pleural thickening.
• Resonant: Normal aerated lung.
• Hyper-resonant: Pneumothorax (air within the pleural space) or severe emphysema (loss of alveolar septa with air trapping).

Auscultation

• Breath sounds:
  • Bronchial breathing: Harsh, high-pitched with an inspiratory-expiratory gap; occurs over consolidation when the patent supplying bronchus directly transmits tubular sound to the chest wall without alveolar filtering.
  • Reduced/absent: Pleural effusion (fluid insulates sound), pneumothorax (pleural air insulates sound), severe asthma ("silent chest" due to negligible airflow), or bronchial obstruction/collapse.
• Added sounds:
  • Crackles (crepitations): Discontinuous, explosive sounds. Fine, late-inspiratory, unaltering with cough: idiopathic pulmonary fibrosis (abrupt opening of fibrotic alveoli). Coarse, early/mid-inspiratory, altering with cough: bronchiectasis, bronchitis, pneumonia (air bubbling through fluid in large airways).
  • Wheeze: Continuous, musical sounds caused by airway wall oscillation in narrowed lumina during expiration.
  • Pleural friction rub: Grating, leathery sound from inflamed visceral and parietal pleura sliding against each other (disappears if an effusion develops).
• Vocal resonance: Whispering pectoriloquy and bronchophony are increased over consolidated lung, as solid tissue enhances the transmission of high-frequency speech components.

Differential diagnosis

Investigations

Diagnosis and severity

• Diagnostic synthesis: Integrate chronological history with structural signs:
  • Parenchymal consolidation: Dullness, bronchial breathing, increased vocal resonance, coarse crackles.
  • Pleural collection: Stony dullness, absent breath sounds, reduced vocal resonance.
  • Pneumothorax: Hyper-resonance, absent breath sounds, deviation of mediastinum if tension physiology develops.
  • Chronic airway limitation: Prolonged expiratory phase, hyper-resonance, wheeze, quiet heart sounds.
• Physiological severity stratification:
  • Mild: SpO2 ≥94%, respiratory rate 16–20 breaths/min, normal speech, heart rate <100 bpm.
  • Moderate: SpO2 90–93%, respiratory rate 21–29 breaths/min, phrases interrupted by breathlessness, heart rate 100–120 bpm.
  • Severe: SpO2 <90%, respiratory rate ≥30 breaths/min, accessory muscle retraction, inability to speak full sentences, heart rate >120 bpm, PaO2 <60 mmHg on room air.
  • Life-threatening: Cyanosis, silent chest, feeble respiratory effort, bradycardia, hypotension, confusion, exhaustion, or hypercapnic coma (PaCO2 rising, acidaemia).
• Immediate stabilization:
  • Controlled oxygen therapy: Deliver high-flow oxygen via reservoir mask in acute hypoxaemic failure (target SpO2 94–98%); use titrated low-flow oxygen via Venturi mask (target SpO2 88–92%) in patients at risk of hypercapnic respiratory failure (severe COPD).
  • Bronchodilator therapy: Nebulised short-acting beta-2 agonists (e.g., salbutamol) combined with short-acting muscarinic antagonists (e.g., ipratropium bromide) for reversible bronchospasm.
  • Systemic anti-inflammatory therapy: Systemic corticosteroids (e.g., oral prednisolone or intravenous hydrocortisone) to blunt airway mucosal inflammation in severe asthma or COPD exacerbations.
  • Emergency decompression: Immediate needle decompression followed by intercostal chest tube insertion for tension pneumothorax; therapeutic thoracocentesis for massive pleural effusion causing respiratory compromise.

Management

Immediate Stabilisation

• Airway: Ensure patency. Clear secretions or blood if haemoptysis is present.
• Breathing: Provide supplemental oxygen via nasal prongs, venturi mask, or non-rebreather mask to maintain target saturation (typically 94–98%, or 88–92% in chronic hypercapnic respiratory failure). If tension pneumothorax is suspected clinically, perform immediate emergency needle decompression before requesting a chest radiograph.
• Circulation: Secure intravenous access. Initiate fluid resuscitation if haemodynamically unstable, while monitoring closely to prevent precipitating pulmonary oedema.

Definitive Treatment by Syndrome

• Infection (Pneumonia/Bronchitis): Initiate empiric antibiotics directed against likely community-acquired or hospital-acquired pathogens. Send sputum for microscopy, GeneXpert, and bacterial culture prior to the first dose if possible without delaying care.
• Airflow Limitation (Asthma/COPD exacerbation): Administer inhaled short-acting beta-2 agonists (e.g., salbutamol) combined with anticholinergics (e.g., ipratropium) via nebuliser or metered-dose inhaler with a spacer. Add systemic corticosteroids (e.g., oral prednisolone or IV hydrocortisone) to blunt underlying airway inflammation.
• Pleural Collections: Perform therapeutic thoracocentesis for large, symptomatic pleural effusions. Insert an intercostal chest drain attached to an underwater seal for empyema, haemothorax, or large pneumothoraces.
• Pulmonary Embolism: Initiate therapeutic anticoagulation (e.g., low-molecular-weight heparin or direct oral anticoagulants) immediately if clinical suspicion is high and bleeding risk is acceptable.

Monitoring and Safety

• Serial Assessment: Continually reassess respiratory rate, work of breathing, pulse oximetry, and repeat peak expiratory flow rate (PEFR) post-bronchodilator.
• Red Flags: Watch for signs of respiratory exhaustion (bradypnoea, silent chest, inability to speak, paradoxic abdominal movement), which necessitate prompt ventilatory support (non-invasive ventilation or endotracheal intubation).
• Safety/Contraindications: Avoid high-flow unchecked oxygen in patients with known chronic obstructive pulmonary disease at risk of carbon dioxide retention. Never perform pleural aspiration without confirming percussion dullness and, ideally, bedside ultrasound localisation.

Complications and Prognosis

• Complications: Type 1 (hypoxaemic) or Type 2 (hypercapnic) respiratory failure, empyema, lung abscess, secondary spontaneous pneumothorax, pulmonary hypertension leading to cor pulmonale, and haemodynamic collapse from tension physiology.
• Prognosis: Favourable if identified and treated early (e.g., uncomplicated community-acquired pneumonia, mild asthma). Poor outcomes associate with diagnostic delays, extensive bilateral pathology, underlying structural lung disease, late-presenting tuberculosis, or immunocompromise.

High-Yield Exam Points

• Tracheal Deviation:
  • Pushed away from the lesion: Large pleural effusion, tension pneumothorax.
  • Pulled toward the lesion: Upper lobe collapse, pneumonectomy, severe unilateral fibrosis.
  • Central: Consolidation, pulmonary oedema, asthma.
• Tactile Vocal Fremitus (TVF) & Vocal Resonance (VR):
  • Increased: Consolidation (solid tissue transmits sound and vibration better than aerated lung).
  • Decreased/Absent: Pleural effusion, pneumothorax (fluid or air insulates and decouples the lung from the chest wall).
• Percussion Notes:
  • Stony dull: Pleural effusion.
  • Dull: Consolidation, collapse, pleural thickening.
  • Hyper-resonant: Pneumothorax, severe emphysema.
• Auscultation Distinctions:
  • Bronchial breathing: Harsh, hollow breath sounds with an audible expiratory phase and a distinct pause between inspiration and expiration; indicates patent airways running through dense, consolidated tissue.
  • Reduced/absent air entry: Found in effusion, pneumothorax, or complete bronchial obstruction leading to collapse.
  • Silent chest: In severe asthma, airway obstruction is so tight that airflow is insufficient to produce wheezing; this is an imminent sign of respiratory arrest.

Clinical Case

A 28-year-old male presents to the outpatient clinic with a 3-week history of worsening dry cough, low-grade evening fevers, drenching night sweats, and progressive exertional breathlessness. On examination, he is thin and tachypnoeic. Trachea is deviated to the right. The right hemithorax shows diminished chest expansion, a stony dull percussion note across the right lower and mid-zones, and absent breath sounds and tactile vocal fremitus over the same region. The left lung is clear.

Case Questions and Model Answers

1. What is the clinical syndrome present on the right side of the chest?
Right-sided pleural effusion with associated volume loss or underlying collapse causing the trachea to shift toward the pathology (or a massive effusion where mediastinal shift is atypically fixed by fibrotic pleural changes).

2. Why is tactile vocal fremitus decreased despite the presence of underlying dullness to percussion?
Pleural fluid physically separates the lung parenchyma from the chest wall, reflecting and dampening vibrational acoustic energy rather than conducting it to the examining hand.

3. What is the most appropriate next imaging investigation and bedside procedure?
Obtain an erect posteroanterior (PA) chest radiograph to evaluate the opacification and mediastinal position, followed by a diagnostic pleural tap (thoracocentesis) sent for biochemistry (protein, LDH), microscopy, and GeneXpert MTB/RIF.

Practice Questions

Question 1

A 45-year-old female presents with acute dyspnoea and right pleuritic chest pain. On examination, the trachea is central, the right lower zone is dull to percussion, vocal resonance is markedly increased, and auscultation reveals harsh breath sounds with equal inspiratory and expiratory components and a distinct pause. What is the primary diagnosis?

A. Right-sided pleural effusion B. Right lower lobe lobar consolidation C. Right simple pneumothorax D. Right lower lobe atelectasis from an endobronchial plug

Answer: B. Right lower lobe lobar consolidation
Explanation: Consolidation preserves a patent bronchus surrounded by dense alveolar exudate, which conducts sound exceptionally well, producing dullness, increased vocal resonance, and bronchial breathing.

Question 2

A 22-year-old male with a history of atopy presents to the emergency unit severely short of breath and cyanosed. On auscultation, the chest is remarkably quiet with no audible breath sounds or wheeze bilaterally. What is the immediate physiological explanation for the lack of wheeze?

A. The airway hyper-responsiveness has spontaneously resolved B. Airflow is too low to generate the turbulence necessary to cause airway vibrations C. A large bilateral pneumothorax has occurred D. Mucus plugging has completely shifted to the upper airway

Answer: B. Airflow is too low to generate the turbulence necessary to cause airway vibrations
Explanation: A "silent chest" indicates critical, life-threatening airway narrowing where the minute ventilation and velocity of air are insufficient to create the vibrations perceived as wheeze.

Question 3

A 60-year-old man who is a chronic heavy smoker presents with left-sided pleuritic chest pain. Examination shows decreased expansion on the left, hyper-resonance to percussion across the entire left lung field, and absent breath sounds on the left. His trachea is shifted to the right, and his blood pressure is 80/50 mmHg. What is the immediate next step?

A. Urgent CT pulmonary angiogram B. Immediate needle decompression of the left pleural space C. Send for a portable erect chest radiograph D. Perform formal thoracocentesis with a 50 mL syringe

Answer: B. Immediate needle decompression of the left pleural space
Explanation: Tracheal shift away from a hyper-resonant lung combined with hypotension confirms a tension pneumothorax, which is an immediate clinical emergency requiring decompression before obtaining radiographs.

Question 4

Which of the following physical examination findings correctly differentiates a right middle-lobe collapse caused by a completely obstructing foreign body from a right-sided lobar consolidation?

A. Dullness to percussion is found in consolidation, whereas resonance is found in complete collapse B. Vocal resonance is decreased in complete collapse but increased in consolidation C. The trachea is pushed to the left in complete collapse D. Bronchial breathing is prominent in complete collapse

Answer: B. Vocal resonance is decreased in complete collapse but increased in consolidation
Explanation: In complete collapse due to proximal obstruction, air and sound cannot pass down the bronchus, reducing vocal resonance; in consolidation with an open airway, sound transmission is amplified.

Question 5

A 68-year-old male with long-standing severe dyspnoea has fine, bilateral, end-inspiratory crackles at both lung bases that do not alter with coughing. His finger nails show pronounced clubbing. Which underlying physical alteration causes these crackles?

A. Movement of thin liquid secretions inside large, central airways B. Sudden explosive opening of small, fibrotic peripheral airways during late inspiration C. Friction generated between inflamed, dry parietal and visceral pleural surfaces D. Rapid collapse of dynamic large airways during forced expiration

Answer: B. Sudden explosive opening of small, fibrotic peripheral airways during late inspiration
Explanation: Fine, "velcro-like" end-inspiratory crackles typical of pulmonary fibrosis occur when abnormally stiffened, collapsed distal airspaces are forced open abruptly at the end of deep inspiration.

Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.