Respiratory Disorders

Learning Objectives

By the end of this topic, you should be able to:

• Explain the pathophysiology of asthma, COPD, pneumonia, and pulmonary embolism (PE).
• Differentiate asthma from COPD using clinical features, spirometry, and reversibility.
• List the diagnostic workup and first-line treatment for each condition.
• Recognize red-flag features that indicate a respiratory emergency.
• Apply Wells' criteria and imaging choices to a suspected PE case.
• Identify common misconceptions students carry into exams about these disorders.

Quick Answer

Respiratory disorders cover a spectrum from reversible airway disease (asthma) to irreversible airflow limitation (COPD), infection of lung parenchyma (pneumonia), and vascular obstruction (pulmonary embolism). They matter because they are among the most common causes of acute presentations and hospital admissions worldwide, and each has a distinct mechanism, diagnostic pathway, and treatment that examiners love to test side by side. Asthma is inflammatory and largely reversible; COPD is structural damage from chronic irritant exposure and largely irreversible; pneumonia is infective consolidation; PE is a mechanical/thrombotic blockage of pulmonary circulation. Getting these four mechanisms straight in your head is the fastest way to answer most respiratory questions correctly.

Overview of the Respiratory System

Before diving into specific disorders, briefly review the key components involved:

1. Lungs – the primary organs of gas exchange (O2 in, CO2 out) across the alveolar-capillary membrane.
2. Trachea – the windpipe connecting the larynx to the bronchi.
3. Bronchi and bronchioles – branching airways that carry air to the alveoli; their smooth muscle tone is what asthma attacks.
4. Diaphragm and chest wall muscles – generate the pressure changes that drive ventilation.

Nearly every respiratory disease you study disrupts one of three things: the airway (asthma, COPD), the alveoli/parenchyma (pneumonia), or the vasculature (PE). Keep asking "which of these three is broken?" and the differentials become much easier to sort.

Common Respiratory Disorders

1. Asthma

Asthma is a chronic inflammatory disease of the airways characterized by recurring, largely reversible episodes of wheezing, breathlessness, chest tightness, and cough, usually worse at night or early morning.

Key points:

• Inflammation causes bronchial hyperresponsiveness and reversible airway constriction (mediated by mast cells, eosinophils, IgE).
• Triggers include allergens, cold air, exercise, viral infections, stress, and NSAIDs.
• Spirometry shows an obstructive pattern (FEV1/FVC < 0.7) that improves by ≥12% and 200 mL after a bronchodilator — this reversibility is the diagnostic hallmark.
• Treatment is stepwise: short-acting beta-agonist (SABA) for relief, inhaled corticosteroid (ICS) as the controller, adding long-acting beta-agonist (LABA) or leukotriene antagonists for persistent disease.

Example: A 22-year-old develops wheeze and breathlessness only during football practice. Peak flow rises after a pre-exercise salbutamol puff — classic exercise-induced asthma with demonstrable reversibility.

2. Chronic Obstructive Pulmonary Disease (COPD)

COPD is a progressive, largely irreversible airflow limitation caused by chronic lung damage. It encompasses two overlapping phenotypes: emphysema (alveolar wall destruction, "pink puffer") and chronic bronchitis (mucus hypersecretion, productive cough ≥3 months for 2 consecutive years, "blue bloater").

Key points:

• The dominant cause is long-term exposure to inhaled irritants, above all cigarette smoke; alpha-1 antitrypsin deficiency is the classic cause in a young non-smoker.
• Spirometry shows FEV1/FVC < 0.7 that does not normalize significantly with a bronchodilator — this lack of reversibility separates it from asthma.
• Management follows GOLD staging: bronchodilators (LABA/LAMA) as the backbone, ICS added only for frequent exacerbators, plus smoking cessation, pulmonary rehabilitation, vaccination, and long-term oxygen therapy if chronically hypoxic (PaO2 ≤ 55 mmHg).
• Acute exacerbations are treated with bronchodilators, systemic steroids, and antibiotics if purulent sputum is present.

Example: A 40-pack-year smoker develops progressive exertional dyspnea and a chronic productive cough. Spirometry confirms fixed obstruction; the mainstay of care is smoking cessation plus a LAMA/LABA inhaler, not steroids alone.

3. Pneumonia

Pneumonia is an infection that inflames and fills the alveoli with exudate, causing consolidation on imaging. It may be caused by bacteria (most commonly Streptococcus pneumoniae), viruses, fungi, or aspiration of gastric/oral contents.

Key points:

• Presents with fever, productive cough, pleuritic chest pain, tachypnea, and crackles or bronchial breathing over the consolidated area.
• Severity and disposition (home vs. hospital vs. ICU) are commonly assessed using the CURB-65 score (Confusion, Urea > 7 mmol/L, Respiratory rate ≥ 30, Blood pressure < 90/60, Age ≥ 65).
• Chest X-ray shows lobar consolidation (typical bacterial) or diffuse bilateral infiltrates (atypical/viral).
• Empirical antibiotics are chosen by setting: amoxicillin for mild community-acquired pneumonia, a macrolide added for atypical cover, and broader IV cover for hospital-acquired or severe disease.

Example: An elderly patient develops fever and a productive cough after an influenza-like illness. CURB-65 score of 3 prompts hospital admission and IV antibiotics rather than outpatient treatment.

4. Pulmonary Embolism (PE)

Pulmonary embolism occurs when a thrombus, usually from a deep vein thrombosis (DVT) in the leg, travels to and lodges in the pulmonary arteries, obstructing blood flow and causing V/Q mismatch.

Key points:

• Risk factors follow Virchow's triad: venous stasis (immobility, long flights, surgery), hypercoagulability (malignancy, pregnancy, oral contraceptives), and endothelial injury (trauma, prior DVT).
• Presents with sudden-onset pleuritic chest pain, dyspnea, tachycardia, and occasionally hemoptysis or syncope in massive PE.
• Clinical probability is scored with the Wells' criteria; low-probability patients are screened with a D-dimer (high sensitivity, low specificity — a negative result rules PE out), while high-probability or D-dimer-positive patients go straight to CT pulmonary angiography (CTPA), the imaging gold standard.
• Treatment is anticoagulation (LMWH, DOACs, or unfractionated heparin in renal failure or hemodynamic instability); massive PE with hypotension warrants thrombolysis.

Example: A patient develops sudden pleuritic chest pain and breathlessness two weeks after hip replacement surgery. A high Wells' score sends them directly to CTPA rather than a D-dimer, confirming a segmental PE treated with anticoagulation.

Diagnosis and Treatment

Respiratory disorders share a common diagnostic toolkit, applied differently depending on whether the airway, parenchyma, or vasculature is involved:

• Chest X-ray – hyperinflation in COPD, consolidation in pneumonia, usually normal or subtle (Hampton's hump/Westermark sign) in PE.
• Spirometry – the key test to separate asthma (reversible) from COPD (fixed obstruction).
• Blood tests – D-dimer for PE, inflammatory markers and blood cultures for pneumonia.
• CTPA/V-Q scan – definitive imaging for PE.
• Medications – inhalers (SABA/ICS/LABA/LAMA), antibiotics, anticoagulants, and oxygen therapy, chosen according to the specific disease.

Prevention and Management

• Avoiding known triggers (allergens, irritants, smoke) — central to asthma control.
• Smoking cessation — the single most effective intervention in COPD.
• Vaccination (influenza, pneumococcal) to reduce pneumonia risk, especially in the elderly and COPD patients.
• Early mobilization and DVT prophylaxis (compression stockings, LMWH) in hospitalized or post-surgical patients to prevent PE.
• Following medication regimens and completing antibiotic courses.

Key Terms

Term	Definition
Reversibility	An improvement in FEV1 of ≥12% and 200 mL after bronchodilator use; present in asthma, typically absent in COPD.
FEV1/FVC ratio	Spirometric ratio used to detect obstructive lung disease; <0.7 defines airflow obstruction in both asthma and COPD.
CURB-65	A five-point pneumonia severity score (Confusion, Urea, Respiratory rate, Blood pressure, Age ≥65) guiding admission decisions.
Virchow's triad	The three mechanisms of thrombus formation: venous stasis, hypercoagulability, and endothelial injury; underlies DVT/PE risk.
Wells' criteria	A clinical scoring system estimating the pretest probability of PE, guiding whether to order a D-dimer or go straight to CTPA.
CTPA	CT pulmonary angiography; the imaging gold standard for confirming or excluding pulmonary embolism.
GOLD staging	A severity classification for COPD based on spirometry and exacerbation history, used to guide inhaler therapy.

Common Mistakes

Misconception 1: "Asthma and COPD are basically the same disease with different names."

• Why it's wrong: Both cause airway obstruction and wheeze, but the underlying mechanism and reversibility are opposite.
• Correct explanation: Asthma is inflammatory and reversible with bronchodilators; COPD is structural lung damage that does not significantly reverse. Spirometry with a bronchodilator challenge is what distinguishes them.

Misconception 2: "A negative chest X-ray rules out pulmonary embolism."

• Why it's wrong: PE is a vascular problem, not a parenchymal one, so the chest X-ray is frequently normal or shows only subtle signs.
• Correct explanation: The X-ray is mainly used to exclude other causes of chest pain/dyspnea (pneumothorax, pneumonia). Confirming or excluding PE requires D-dimer plus CTPA (or V/Q scan), not a plain film.

Misconception 3: "All pneumonia patients need IV antibiotics in hospital."

• Why it's wrong: This ignores severity stratification, which determines site of care.
• Correct explanation: CURB-65 scoring guides disposition — a score of 0-1 can usually be managed at home with oral amoxicillin, while a score of 3+ warrants hospital admission and IV therapy.

Comparison and Connections

Feature	Asthma	COPD	Pneumonia	Pulmonary Embolism
Primary mechanism	Reversible airway inflammation	Irreversible airway/alveolar damage	Infective alveolar consolidation	Thrombotic vascular obstruction
Typical cause	Allergens, exercise, viral triggers	Smoking, chronic irritant exposure	Bacteria, viruses, aspiration	DVT embolizing from leg veins
Spirometry	Obstructive, reversible	Obstructive, fixed	Usually normal (restrictive if severe)	Usually normal
Key investigation	Bronchodilator reversibility test	Post-bronchodilator spirometry	Chest X-ray, CURB-65	Wells' score, D-dimer, CTPA
First-line treatment	SABA + ICS	LAMA/LABA + smoking cessation	Antibiotics per severity	Anticoagulation

Practice Questions

Recall

1. What ratio and cut-off define an obstructive spirometry pattern? Answer guidance: FEV1/FVC < 0.7.
2. Name the five components of the CURB-65 score. Answer guidance: Confusion, Urea >7 mmol/L, Respiratory rate ≥30, Blood pressure <90/60, Age ≥65.

Understanding 3. Why does asthma respond to a bronchodilator challenge on spirometry while COPD typically does not? Answer guidance: Asthma's obstruction is driven by reversible smooth-muscle constriction and inflammation; COPD's obstruction stems from fixed structural damage (alveolar destruction, airway remodeling) that a bronchodilator cannot reverse. 4. Explain why Virchow's triad is relevant to a post-operative patient's risk of pulmonary embolism. Answer guidance: Surgery causes immobility (stasis), tissue trauma (endothelial injury), and often a transient hypercoagulable state — all three arms of the triad are activated simultaneously, which is why post-op patients receive DVT prophylaxis.

Application 5. A 65-year-old smoker with chronic cough and exertional dyspnea has FEV1/FVC of 0.55 that does not improve after salbutamol. What is the diagnosis and next management step? Answer guidance: COPD; manage with smoking cessation counselling plus a LAMA/LABA inhaler, and assess GOLD stage/exacerbation history to decide on ICS. 6. A patient with pleuritic chest pain two weeks post-flight has a low Wells' score. What is the next investigation? Answer guidance: D-dimer test — if negative, PE is effectively excluded; if positive, proceed to CTPA.

Analysis 7. Compare and contrast how you would distinguish pneumonia from pulmonary embolism in a patient presenting with pleuritic chest pain and dyspnea. Answer guidance: Look for fever, productive cough, and consolidation on X-ray (favors pneumonia) versus recent immobility/surgery, clear X-ray, and elevated Wells' score (favors PE); confirm with sputum/blood cultures and CXR for pneumonia, or D-dimer/CTPA for PE. 8. Why might a "pink puffer" (emphysema-predominant COPD) and a "blue bloater" (chronic bronchitis-predominant COPD) present so differently despite sharing the same underlying diagnosis? Answer guidance: Emphysema destroys alveolar surface area, so patients hyperventilate to maintain oxygenation (thin, breathless, pink); chronic bronchitis causes mucus plugging and V/Q mismatch with relative hypoventilation, leading to hypoxia, cyanosis, and fluid retention (bloated, blue) despite similar spirometric obstruction.

FAQ

1. Can a patient have both asthma and COPD? Yes — this is called Asthma-COPD Overlap (ACO), typically seen in older smokers with a history of childhood asthma; they show partial reversibility on spirometry and often need both ICS and bronchodilator therapy.

2. Why is a D-dimer test not used to confirm PE? D-dimer is highly sensitive but poorly specific — it rises with infection, pregnancy, malignancy, and recent surgery. A negative result is useful for ruling PE out in low-probability patients, but a positive result requires CTPA confirmation.

3. Why do COPD patients sometimes need controlled oxygen rather than high-flow oxygen? Chronic CO2 retainers can lose their hypoxic drive to breathe if given uncontrolled high-flow oxygen, potentially worsening hypercapnia and respiratory failure; titrated oxygen (target SpO2 88-92%) is preferred.

4. Is pneumonia always bacterial? No — viruses (including influenza and SARS-CoV-2) and, less commonly, fungi can also cause pneumonia. The distinction matters because antibiotics are ineffective against viral pneumonia.

5. What makes a PE "massive" versus "submassive"? A massive PE causes hemodynamic instability (hypotension or shock) and requires thrombolysis or embolectomy; a submassive PE shows right ventricular strain without hypotension and is usually managed with anticoagulation alone.

Quick Revision

• Asthma = reversible airway obstruction; COPD = fixed airway obstruction. Spirometry with bronchodilator challenge tells them apart.
• COPD's two phenotypes: emphysema ("pink puffer") and chronic bronchitis ("blue bloater").
• Smoking cessation is the single most effective COPD intervention; alpha-1 antitrypsin deficiency causes COPD in young non-smokers.
• Asthma treatment ladder: SABA for relief → ICS as controller → add LABA/leukotriene antagonist for persistent disease.
• Pneumonia severity and disposition are decided using CURB-65.
• Typical bacterial pneumonia shows lobar consolidation; atypical/viral pneumonia shows diffuse bilateral infiltrates.
• PE arises from DVT via Virchow's triad: stasis, hypercoagulability, endothelial injury.
• Wells' score determines whether to order a D-dimer (low probability) or go straight to CTPA (high probability).
• A negative D-dimer effectively excludes PE; a positive one needs CTPA confirmation.
• Anticoagulation is first-line PE treatment; thrombolysis is reserved for massive PE with hemodynamic instability.
• Controlled oxygen (target 88-92%) is used in COPD to avoid suppressing hypoxic respiratory drive.

Related Topics

Prerequisites

• Basic respiratory anatomy and physiology (lungs, airways, gas exchange)
• Spirometry interpretation basics (obstructive vs. restrictive patterns)

Related Topics

• Cardiovascular disorders (right heart strain in massive PE, cor pulmonale in COPD)
• Infectious disease principles (antibiotic selection, sepsis recognition)

Next Topics

• Respiratory failure and mechanical ventilation
• Critical care management of acute respiratory emergencies

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