Respiratory Revision Guide ✅

🫁 Respiratory medicine is best revised as a pattern-recognition subject: airway disease, infection, pleural disease, vascular disease, interstitial disease, malignancy and respiratory failure. For exams and ward work, always link the symptom to physiology: wheeze = airflow obstruction, pleuritic pain = pleura, crackles = alveoli/interstitium, hypoxia = gas exchange failure, and raised CO₂ = ventilatory failure.

✅ 1. Respiratory Anatomy and Physiology

🧠 Exam pearl: The lungs are not just “bags of air” - they are a gas-exchange surface with very thin alveolar membranes, a huge capillary network and elastic recoil. Disease causes symptoms by affecting airflow, diffusion, perfusion, or ventilation.

🫁 1.1 Airways

• Upper airway: nose, pharynx, larynx - obstruction here causes stridor, not wheeze.
• Conducting airways: trachea, bronchi and bronchioles - move air but do not perform gas exchange.
• Small airways: bronchioles less than 2 mm - important in asthma, COPD and bronchiolitis.
• Alveoli: main site of gas exchange; surrounded by pulmonary capillaries.
• Type I pneumocytes: thin cells allowing diffusion of oxygen and carbon dioxide.
• Type II pneumocytes: produce surfactant, reducing surface tension and preventing alveolar collapse.
• Macrophages: remove inhaled particles and pathogens; overloaded in smokers and occupational lung disease.

🩸 1.2 Ventilation, Perfusion and Diffusion

• Ventilation: movement of air into and out of alveoli.
• Perfusion: blood flow through pulmonary capillaries.
• Diffusion: movement of gas across the alveolar-capillary membrane.
• V/Q mismatch: most common mechanism of hypoxaemia; seen in asthma, COPD, pneumonia and PE.
• Shunt: blood passes through lungs without being oxygenated; severe pneumonia, atelectasis and ARDS.
• Dead space: ventilated but poorly perfused lung; classic in pulmonary embolism.
• Diffusion impairment: thickened interstitium reduces gas transfer; seen in pulmonary fibrosis.

📌 Clinical reasoning: Oxygenation is mainly about V/Q matching and diffusion, whereas CO₂ clearance is mainly about alveolar ventilation. This is why a patient can be hypoxic with normal CO₂ in pneumonia, but hypercapnic in COPD, obesity hypoventilation or neuromuscular weakness.

🩺 2. Respiratory Symptoms

🌬️ 2.1 Breathlessness

• Acute breathlessness: asthma attack, COPD exacerbation, pneumonia, PE, pneumothorax, pulmonary oedema, anaphylaxis.
• Chronic breathlessness: COPD, asthma, ILD, heart failure, anaemia, obesity, deconditioning, anxiety, pulmonary hypertension.
• Orthopnoea/PND: suggests heart failure, but severe COPD and obesity may also worsen lying flat.
• Platypnoea: breathlessness worse upright; can occur in right-to-left shunts or hepatopulmonary syndrome.
• Trepopnoea: breathlessness in one lateral position; may suggest unilateral lung disease or cardiac disease.

🤧 2.2 Cough

• Acute cough: usually viral URTI, acute bronchitis, pneumonia, asthma exacerbation or PE.
• Chronic cough (>8 weeks): asthma, reflux, upper airway cough syndrome, ACE inhibitor, COPD, bronchiectasis, ILD, lung cancer.
• Productive purulent sputum: infection or bronchiectasis.
• Dry cough: asthma, ILD, ACE inhibitor, reflux, viral illness.
• Red flags: haemoptysis, weight loss, persistent hoarseness, smoking history, recurrent pneumonia, abnormal CXR.

🩸 2.3 Haemoptysis

• Common causes: acute bronchitis, pneumonia, bronchiectasis, lung cancer, PE, TB.
• Massive haemoptysis is an airway emergency: the patient can die from asphyxiation before blood loss.
• Stabilise first: ABCDE, oxygen, IV access, group and save/crossmatch, senior respiratory/ENT/ICU input.
• Position bleeding lung down if the side is known to protect the unaffected lung.
• Investigations: CXR, FBC, clotting, U&E, CRP, CT thorax/CT angiography, bronchoscopy depending on severity.

🗣️ 2.4 Wheeze versus Stridor

• Wheeze: musical expiratory sound from lower airway narrowing; asthma/COPD.
• Stridor: harsh inspiratory sound from upper airway obstruction; croup, epiglottitis, tumour, foreign body, vocal cord dysfunction.
• Silent chest in asthma is ominous - it may mean airflow is too low to generate wheeze.

🧪 3. Respiratory Investigations

📈 3.1 Spirometry

• Obstructive pattern: FEV1/FVC reduced; seen in asthma, COPD and bronchiectasis.
• Restrictive pattern: FEV1 and FVC reduced proportionally with preserved or high FEV1/FVC; confirmed with lung volumes.
• Bronchodilator reversibility supports asthma, but absence of reversibility does not exclude it.
• COPD requires persistent airflow obstruction after bronchodilator testing in the appropriate clinical context.
• Peak flow variability supports asthma and is useful for monitoring acute attacks.

🩻 3.2 Chest X-ray

• Consolidation: air-space shadowing; suggests pneumonia, pulmonary oedema, haemorrhage or malignancy.
• Hyperinflation: flattened diaphragms, increased AP diameter; suggests COPD/asthma.
• Pneumothorax: visible pleural line with absent peripheral lung markings.
• Pleural effusion: blunted costophrenic angle, meniscus sign.
• Interstitial markings: reticular/nodular shadowing; consider fibrosis, oedema, infection or malignancy.

🧬 3.3 ABG and VBG

• Type 1 respiratory failure: low PaO₂ with normal/low PaCO₂ - gas exchange problem.
• Type 2 respiratory failure: low PaO₂ with high PaCO₂ - ventilatory failure.
• Acute respiratory acidosis: high CO₂ with low pH and little bicarbonate compensation.
• Chronic respiratory acidosis: high CO₂ with renal bicarbonate retention; pH may be near-normal.
• VBG is useful for pH and CO₂ trend, but ABG is needed when precise oxygenation is important.

🚨 Ward pearl: A normal oxygen saturation does not exclude respiratory failure if the patient is receiving high-flow oxygen. Always interpret saturations alongside the oxygen delivery device, work of breathing and blood gas.

💨 4. Asthma

Asthma is a chronic inflammatory airway disease characterised by variable airflow obstruction, bronchial hyperresponsiveness and symptoms that vary over time. The key pathology is airway inflammation with smooth muscle constriction, mucus production and airway oedema.

🔍 4.1 Clinical Features

• Variable wheeze, cough, chest tightness and breathlessness.
• Symptoms often worse at night, early morning, with exercise, cold air, allergens or viral infection.
• Personal or family history of atopy supports the diagnosis.
• Examination may be normal between attacks.
• Consider alternative diagnoses if symptoms are fixed, inspiratory, associated with weight loss, or have poor response to asthma treatment.

🧪 4.2 Diagnosis

• Use objective testing where possible: spirometry, bronchodilator reversibility, FeNO, peak flow variability.
• FeNO supports eosinophilic airway inflammation but is not diagnostic alone.
• Peak flow diary can show diurnal variability, particularly when spirometry is normal.
• Do not diagnose asthma solely from symptoms if objective testing is available.

💊 4.3 Chronic Management

• Check inhaler technique at every review - poor technique is a common cause of “treatment failure”.
• Provide a personalised asthma action plan.
• Identify triggers: smoking, allergens, occupational exposures, NSAIDs, beta-blockers, reflux and rhinitis.
• Inhaled corticosteroids reduce airway inflammation and exacerbation risk.
• MART regimens use ICS/formoterol as both maintenance and reliever in suitable patients.
• Escalate therapy according to control, exacerbations, objective markers and adherence.

🚨 4.4 Acute Asthma Attack

• Life-threatening features: SpO₂ <92%, silent chest, cyanosis, poor respiratory effort, arrhythmia, hypotension, exhaustion, altered consciousness.
• Initial treatment: high-flow oxygen, salbutamol nebulisers, ipratropium in severe/life-threatening attacks, oral prednisolone or IV hydrocortisone.
• Consider IV magnesium sulfate in severe attacks not responding to initial bronchodilators.
• Normal or rising PaCO₂ in an acute severe asthma attack is a pre-arrest sign.
• Early senior, anaesthetic and ICU input if poor response or exhaustion.

🧠 Exam pearl: In asthma, the dangerous blood gas is not “low CO₂” - that is expected because patients hyperventilate. A normal CO₂ may mean the patient is tiring and no longer ventilating adequately.

🚬 5. Chronic Obstructive Pulmonary Disease (COPD)

COPD is a chronic, usually progressive disease with persistent airflow obstruction, classically due to smoking-related small airway inflammation and emphysematous destruction. The key physiological problem is expiratory airflow limitation, causing air trapping, hyperinflation and increased work of breathing.

🔍 5.1 Clinical Features

• Progressive exertional breathlessness, chronic cough and sputum production.
• Risk factors: smoking, occupational dust/fumes, biomass exposure, alpha-1 antitrypsin deficiency.
• Signs: prolonged expiratory phase, wheeze, reduced breath sounds, hyperinflated chest, pursed-lip breathing.
• Advanced disease: weight loss, cor pulmonale, peripheral oedema, cyanosis, polycythaemia.

🧪 5.2 Diagnosis and Assessment

• Post-bronchodilator FEV1/FVC below diagnostic threshold supports COPD in a symptomatic patient.
• CXR helps exclude lung cancer, heart failure, fibrosis and bronchiectasis.
• Assess symptom burden with MRC dyspnoea scale and exacerbation history.
• Consider alpha-1 antitrypsin deficiency if young, minimal smoking history, basal emphysema or family history.
• Blood eosinophils can help guide inhaled corticosteroid use in some patients.

💊 5.3 Stable COPD Management

• Smoking cessation is the most important disease-modifying intervention.
• Vaccination: annual influenza, COVID-19 boosters as eligible, and pneumococcal vaccination.
• Pulmonary rehabilitation improves exercise tolerance, breathlessness and quality of life.
• Bronchodilators: SABA/SAMA for symptoms; LABA/LAMA for persistent breathlessness.
• ICS may reduce exacerbations in selected patients but increases pneumonia risk.
• Long-term oxygen therapy may benefit chronically hypoxaemic patients after formal assessment.

🚨 5.4 Acute Exacerbation of COPD

• Features: worsening breathlessness, increased sputum volume or purulence, wheeze, cough, fatigue.
• Controlled oxygen: target 88–92% if at risk of hypercapnic respiratory failure pending blood gas.
• Nebulised bronchodilators: salbutamol plus ipratropium.
• Steroids: prednisolone course unless contraindicated.
• Antibiotics if sputum purulence, pneumonia, severe illness or ventilatory support required; follow local guidance.
• NIV if persistent respiratory acidosis despite optimal medical therapy.

⚠️ Clinical pearl: Oxygen is a drug. In COPD with CO₂ retention risk, excessive oxygen can worsen hypercapnia through V/Q effects, the Haldane effect and reduced hypoxic drive in some patients.

🦠 6. Pneumonia and Lower Respiratory Tract Infection

🔍 6.1 Community-Acquired Pneumonia

• Symptoms: fever, cough, sputum, pleuritic chest pain, dyspnoea, rigors, confusion in older patients.
• Signs: tachypnoea, tachycardia, focal crackles, bronchial breathing, dullness to percussion, hypoxia.
• Common pathogens: Streptococcus pneumoniae, Haemophilus influenzae, atypicals, respiratory viruses.
• CXR confirms consolidation but early CXR can be normal in dehydration or early disease.
• Assess severity using clinical judgement and scores such as CRB-65/CURB-65.

💊 6.2 Management Principles

• Oxygen if hypoxic; target range depends on CO₂ retention risk.
• Antibiotics should match severity, likely organism, allergies and local antimicrobial guidance.
• Do not delay antibiotics in sepsis or severe pneumonia while awaiting investigations.
• Obtain cultures when clinically appropriate, especially before IV antibiotics if this will not delay treatment.
• Reassess at 48–72 hours: stop, narrow, switch IV-to-oral, or continue with documented duration.
• Consider repeat imaging if symptoms persist or malignancy risk is present.

🏥 6.3 Hospital-Acquired Pneumonia

• Occurs 48 hours or more after hospital admission or shortly after discharge.
• Risk of Gram-negative organisms and resistant pathogens is higher than in community pneumonia.
• Consider aspiration, immobility, dysphagia, poor oral hygiene and recent antibiotics.
• Management depends on severity, local microbiology and resistance risk.

🧫 7. Tuberculosis

• TB is caused by Mycobacterium tuberculosis and usually affects the lungs, but can involve lymph nodes, bones, CNS, pericardium, abdomen and genitourinary tract.
• Symptoms: chronic cough, haemoptysis, fever, night sweats, weight loss, fatigue.
• CXR: upper zone consolidation, cavitation, miliary pattern, hilar lymphadenopathy.
• Diagnosis: sputum AFB smear/culture, NAAT/PCR, imaging; biopsy/culture for extrapulmonary disease.
• Treatment is prolonged combination therapy to prevent resistance.
• Public health notification and contact tracing are essential.

📌 Exam pearl: Think TB in chronic cough with systemic symptoms, especially with exposure risk, immunosuppression, homelessness, prison exposure or origin/travel from high-incidence regions.

🧱 8. Bronchiectasis

• Definition: permanent abnormal dilatation of bronchi due to chronic airway inflammation and infection.
• Symptoms: chronic productive cough, large sputum volumes, recurrent infections, haemoptysis, fatigue.
• Causes: post-infective, cystic fibrosis, primary ciliary dyskinesia, immunodeficiency, ABPA, aspiration, rheumatoid arthritis.
• CT chest: signet ring sign, tram-track opacities, bronchial wall thickening.
• Sputum culture guides antibiotics; Pseudomonas colonisation suggests more severe disease.
• Management: airway clearance, physiotherapy, vaccination, prompt treatment of exacerbations, macrolide prophylaxis in selected cases.

🫧 9. Pleural Disease

💧 9.1 Pleural Effusion

• Transudate: systemic pressure/protein problem - heart failure, cirrhosis, nephrotic syndrome.
• Exudate: local pleural inflammation/malignancy/infection - pneumonia, cancer, TB, PE, autoimmune disease.
• Symptoms: dyspnoea, pleuritic pain, dry cough.
• Signs: stony dull percussion, reduced breath sounds, reduced vocal resonance.
• Investigations: CXR, ultrasound, diagnostic aspiration unless clear bilateral heart failure pattern.
• Pleural fluid: protein, LDH, pH, glucose, cytology, microbiology, differential cell count.

🫁 9.2 Pneumothorax

• Primary spontaneous: no known lung disease; often tall thin young men.
• Secondary spontaneous: underlying lung disease, especially COPD; more dangerous due to poor reserve.
• Tension pneumothorax: clinical diagnosis - hypotension, severe respiratory distress, tracheal deviation, raised JVP; decompress immediately.
• CXR: pleural line with absent peripheral lung markings.
• Management depends on symptoms, size, primary versus secondary, and physiological compromise.

🦠 9.3 Empyema

• Infected pleural fluid, often after pneumonia.
• Features: persistent fever, pleuritic pain, raised inflammatory markers despite antibiotics.
• Pleural fluid pH <7.2, low glucose or frank pus suggests need for drainage.
• Management: antibiotics plus chest drain; consider intrapleural therapy or surgery if loculated or failing.

🩸 10. Pulmonary Embolism

Pulmonary embolism occurs when thrombus, usually from a leg or pelvic DVT, embolises to the pulmonary arterial circulation. It increases dead space, worsens V/Q mismatch and may cause acute right ventricular strain.

• Symptoms: sudden dyspnoea, pleuritic chest pain, haemoptysis, syncope, palpitations.
• Signs: tachycardia, tachypnoea, hypoxia, low-grade fever, signs of DVT, raised JVP/hypotension in massive PE.
• Risk factors: surgery, immobility, cancer, pregnancy/postpartum, oestrogen therapy, previous VTE, thrombophilia.
• Investigations: ECG, CXR, D-dimer if low/intermediate probability, CTPA, V/Q scan if CTPA unsuitable.
• Risk stratification: haemodynamic instability and RV dysfunction indicate higher risk.
• Treatment: anticoagulation; thrombolysis/embolectomy for massive PE with shock if appropriate.

🧠 Exam pearl: A normal CXR with severe pleuritic breathlessness and tachycardia should make PE more likely, not less likely.

🧬 11. Interstitial Lung Disease and Pulmonary Fibrosis

• ILD affects the interstitium and causes reduced lung compliance, restrictive physiology and impaired gas transfer.
• Symptoms: progressive exertional dyspnoea, dry cough, fatigue.
• Signs: fine end-inspiratory “Velcro” crackles, clubbing, desaturation on exertion.
• Causes: idiopathic pulmonary fibrosis, connective tissue disease, drugs, occupational exposure, hypersensitivity pneumonitis, sarcoidosis.
• Spirometry: restrictive pattern; gas transfer (DLCO) reduced.
• HRCT is key: honeycombing, reticulation, ground-glass change, traction bronchiectasis.
• Management depends on cause: antifibrotics for IPF, immunosuppression for selected inflammatory ILDs, oxygen, pulmonary rehab, transplant referral in severe cases.

🌱 11.1 Sarcoidosis

• Multisystem granulomatous disease with non-caseating granulomas.
• Respiratory: cough, dyspnoea, bilateral hilar lymphadenopathy, pulmonary infiltrates.
• Extra-pulmonary: erythema nodosum, uveitis, arthritis, facial nerve palsy, hypercalcaemia, cardiac involvement.
• Many cases resolve spontaneously; steroids are used for significant organ involvement.

🏭 12. Occupational Lung Disease

• Asbestos: pleural plaques, asbestosis, lung cancer, mesothelioma.
• Silica: upper lobe fibrosis, increased TB risk.
• Coal dust: coal workers’ pneumoconiosis and progressive massive fibrosis.
• Beryllium: granulomatous disease similar to sarcoidosis.
• Occupational asthma: symptoms improve away from work; early recognition prevents permanent disease.
• Always ask about jobs, hobbies, pets, mould, birds, dusts, metals, farms and building work.

🎗️ 13. Lung Cancer

• Major risk factor: smoking; also asbestos, radon, occupational exposures and family history.
• Symptoms: persistent cough, haemoptysis, weight loss, dyspnoea, chest pain, recurrent pneumonia, hoarseness.
• Signs: clubbing, cachexia, lymphadenopathy, pleural effusion, SVCO, Horner syndrome.
• Types: non-small cell lung cancer (adenocarcinoma, squamous, large cell) and small cell lung cancer.
• Paraneoplastic syndromes: SIADH and ectopic ACTH with small cell; hypercalcaemia with squamous cell.
• Investigations: CXR, urgent CT chest/abdomen, PET-CT, bronchoscopy/EBUS/biopsy, staging and performance status.
• Treatment: surgery, radiotherapy, chemotherapy, immunotherapy or targeted therapy depending on stage and histology.

🚩 Red flags needing urgent consideration: haemoptysis, unexplained weight loss, persistent cough, recurrent unilateral pneumonia, persistent hoarseness, clubbing, supraclavicular nodes or abnormal CXR.

😴 14. Obstructive Sleep Apnoea and Obesity Hypoventilation

😴 14.1 OSA

• OSA involves recurrent upper airway collapse during sleep, causing intermittent hypoxia and sleep fragmentation.
• Symptoms: loud snoring, witnessed apnoeas, choking episodes, morning headache, daytime sleepiness, poor concentration.
• Risk factors: obesity, male sex, large neck circumference, alcohol/sedatives, craniofacial anatomy, hypothyroidism.
• Complications: hypertension, AF, road traffic accidents, pulmonary hypertension, insulin resistance.
• Diagnosis: sleep study; assess sleepiness with Epworth Sleepiness Scale.
• Management: weight loss, avoid alcohol/sedatives, CPAP, mandibular advancement device in selected cases.

⚖️ 14.2 Obesity Hypoventilation Syndrome

• Defined by obesity with daytime hypercapnia not explained by another cause.
• Often overlaps with OSA but is more severe physiologically.
• Can cause pulmonary hypertension, right heart failure and recurrent type 2 respiratory failure.
• Management: weight loss, NIV/CPAP depending on sleep study and gas exchange, treat comorbidities.

🚨 15. Respiratory Failure and Oxygen Therapy

🩸 15.1 Type 1 versus Type 2 Respiratory Failure

🎯 15.2 Oxygen Targets

• Most acutely unwell adults: target SpO₂ 94–98%.
• Risk of hypercapnic respiratory failure: target SpO₂ 88–92% pending blood gas.
• Document oxygen target, device and flow rate.
• Repeat blood gases if increasing oxygen requirement, drowsiness, acidosis or CO₂ retention risk.
• Escalate early if increasing work of breathing, exhaustion, confusion or persistent hypoxia.

🌬️ 15.3 NIV and CPAP

• NIV supports ventilation by giving inspiratory and expiratory pressure support.
• Common uses: COPD exacerbation with respiratory acidosis, obesity hypoventilation, neuromuscular ventilatory failure.
• CPAP improves oxygenation and recruits alveoli; useful in cardiogenic pulmonary oedema and some hypoxaemic states.
• Contraindications/concerns: vomiting, inability to protect airway, facial trauma, severe agitation, untreated pneumothorax, peri-arrest.

🆘 16. Respiratory Emergencies

🚨 16.1 Anaphylaxis

• Airway swelling, wheeze, hypotension and urticaria after allergen exposure.
• Immediate IM adrenaline is the key treatment; do not delay for antihistamines or steroids.
• Give high-flow oxygen, lie flat with legs raised if tolerated, IV fluids, repeat adrenaline if needed.

🚨 16.2 Tension Pneumothorax

• Severe respiratory distress, hypotension, unilateral reduced breath sounds, hyper-resonance, tracheal deviation may be late.
• Immediate decompression is required - do not wait for CXR if clinically suspected.
• Follow with definitive chest drain.

🚨 16.3 Acute Upper Airway Obstruction

• Features: stridor, drooling, voice change, agitation, cyanosis, exhaustion.
• Keep patient calm and upright; avoid repeated throat examination if epiglottitis or severe obstruction suspected.
• Call anaesthetics/ENT/ICU early.

🚨 16.4 ARDS

• Acute inflammatory lung injury causing diffuse alveolar damage, severe hypoxaemia and bilateral infiltrates.
• Causes: sepsis, pneumonia, aspiration, pancreatitis, trauma, transfusion, COVID-19 and other severe viral infections.
• Management: treat cause, lung-protective ventilation, prone positioning in severe cases, conservative fluids once shocked state resolved.

📚 17. OSCE / Exam Pearls

• Wheeze is lower airway obstruction; stridor is upper airway obstruction.
• Silent chest in asthma is life-threatening.
• Normal CO₂ in severe asthma can be bad - it may mean fatigue.
• Controlled oxygen matters in COPD and other CO₂ retainers.
• Pleuritic pain plus tachycardia plus normal CXR should prompt PE consideration.
• Stony dull percussion suggests pleural effusion.
• Hyper-resonance with absent breath sounds suggests pneumothorax.
• Fine end-inspiratory crackles and clubbing suggest pulmonary fibrosis.
• Bronchiectasis causes chronic productive cough and recurrent infections.
• Haemoptysis is a red flag until proven otherwise.

📌 18. Quick Differentials Table

📚 References

• NICE/BTS/SIGN. Asthma: diagnosis, monitoring and chronic asthma management. NICE NG245, 2024.
• NICE. Chronic obstructive pulmonary disease in over 16s: diagnosis and management. NICE NG115.
• NICE. Pneumonia: diagnosis and management. NICE NG250, 2025.
• British Thoracic Society. Guideline for oxygen use in adults in healthcare and emergency settings.
• British Thoracic Society. Emergency oxygen target saturation guidance.

⚠️ Disclaimer

This article is for medical education and exam revision. Clinical care should follow current local guidelines, antimicrobial policies, oxygen prescribing protocols, formularies, senior advice and national guidance. Always reassess the patient, because respiratory disease can deteriorate rapidly.