Respiratory Diseases and Management

Respiratory diseases are among the most common presentations in UAE emergency departments and outpatient clinics. The desert environment, sandstorms, high rates of smoking including shisha, and occupational dust exposure contribute to a high burden of asthma, COPD, respiratory infections, and in recent years, viral respiratory illnesses including MERS-CoV and COVID-19. For the DOH (UAE) examination, nurses must demonstrate competence in assessing respiratory conditions, administering oxygen appropriately, and managing acute respiratory emergencies.

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🟢 Lite — Quick Review (1h–1d)

Rapid summary for last-minute revision before your exam.

Common Respiratory Presentations:

Condition	Key Features	SpO₂ Target	Key Treatment
Asthma (acute)	Wheezing, dyspnoea, chest tightness; reversible	≥ 94%	Salbutamol neb, ipratropium, steroids
COPD exacerbation	Chronic dyspnoea + increased sputum/purulence	88–92%	Antibiotics if purulent, bronchodilators, steroids
Pneumonia	Fever, cough, consolidation on CXR	≥ 94%	Antibiotics (CAP vs HAP)
Pleural effusion	Dyspnoea, stony dullness, reduced breath sounds	≥ 94%	Drain if symptomatic
Pneumothorax	Sudden onset dyspnoea, absent breath sounds, hyperresonance	≥ 94%	Tension = emergency needle decompression
Pulmonary embolism	Sudden dyspnoea, tachycardia, pleuritic chest pain, hypoxia	≥ 94%	Anticoagulation ± thrombolysis

ABG Patterns — Quick Reference:

Disorder	pH	PaCO₂	HCO₃⁻
Respiratory acidosis	↓	↑	N (acute) / ↑ (compensated)
Respiratory alkalosis	↑	↓	N (acute) / ↓ (compensated)
Metabolic acidosis	↓	N	↓ (compensated) → hyperventilate
Metabolic alkalosis	↑	N	↑ (compensated) → hypoventilate

⚡ Exam Tip: A SpO₂ of 88% in a COPD patient on room air should prompt you to check an ABG. The patient may have a high CO₂ level (hypercapnia) that is not being corrected — they may be dependent on hypoxia to drive their breathing (hypoxic respiratory drive). Use controlled oxygen (Venturi mask) carefully.

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🟡 Standard — Regular Study (2d–2mo)

Standard content for students with a few days to months.

1. Asthma — Pathophysiology and Management

Pathophysiology:

• Type I hypersensitivity reaction (IgE-mediated)
• Mast cell degranulation → histamine, leukotrienes, prostaglandins → bronchoconstriction, oedema, mucus hypersecretion
• Both large airways (wheezing) and small airways (dyspnoea, cough)
• Inflammatory cell infiltrate: Eosinophils (allergic/atopic asthma)

Asthma Severity Classification (GINA):

• Intermittent: Symptoms <2x/week; nighttime symptoms <2x/month; SABA use <2 days/week
• Mild persistent: Symptoms >2x/week but not daily; nighttime >2x/month
• Moderate persistent: Daily symptoms; nighttime >1x/week; SABA daily
• Severe persistent: Symptoms throughout the day; frequent nighttime; limited activity

Acute Asthma Management:

1. O₂ to maintain SpO₂ ≥ 94% (target 94–98%)
2. SABA: Salbutamol 5 mg nebulised with O₂ (can repeat every 20 min × 3 initially)
3. Ipratropium bromide 0.5 mg nebulised (add to first 2–3 doses; not beyond)
4. Systemic steroids: IV methylprednisolone or oral prednisolone (given early, within 1 hour)
5. Magnesium sulphate 2 g IV over 20 min (for severe/refractory cases)
6. If not responding → consider ICU; intubation if exhausted/confused/comatosed

Devices — Inhaler Technique:

• MDI (metered-dose inhaler): Shake, exhale fully, seal lips, press while slow inhalation, hold 10 sec
• Spacer/Volumatic: Reduces need for coordination; essential for children and elderly
• Turbuhaler/Dry powder: Breathe in fast and deep (not slow); no shaking needed
• Nebuliser: For acute severe asthma; 6–8 L/min O₂ source

2. COPD — Chronic Obstructive Pulmonary Disease

Definition: Progressive, partially reversible airflow obstruction — not fully reversible

Pathology:

• Chronic bronchitis: Productive cough for ≥3 months in ≥2 consecutive years; Reid index > 0.5
• Emphysema: Alveolar wall destruction → loss of elastic recoil → air trapping → hyperinflation; “pink puffer”

COPD Exacerbation Triggers:

• Respiratory infection (Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis — most common bacterial causes)
• Cold weather, air pollution, non-compliance with inhalers
• ~30% have no identifiable trigger

Management of COPD Exacerbation:

1. Controlled oxygen therapy: Target SpO₂ 88–92%; use Venturi mask for precision
2. Bronchodilators: Nebulised salbutamol + ipratropium (du-neb) — q20 min initially
3. Systemic corticosteroids: Oral prednisolone 30–40 mg for 5 days
4. Antibiotics if purulent sputum: Amoxicillin-clavulanate, or doxycycline, or azithromycin
5. BiPAP/NIV if PaCO₂ elevated and pH < 7.35 despite above measures
6. Intubation and ventilation if NIV fails or patient is unconscious/exhausted

3. Pneumonia

Community-Acquired Pneumonia (CAP):

• Streptococcus pneumoniae (most common bacterial cause)
• Atypical organisms: Mycoplasma pneumoniae, Chlamydophila pneumoniae, Legionella
• Viral: Influenza, RSV, COVID-19

Hospital-Acquired Pneumonia (HAP) / Ventilator-Associated Pneumonia (VAP):

• Gram-negative organisms predominate: Pseudomonas aeruginosa, Klebsiella pneumoniae, Acinetobacter
• Often multi-drug resistant (MDR)
• Treatment: Broad-spectrum antibiotics; de-escalate once cultures available

** CURB-65 Score for CAP Severity:**

• Confusion
• Urea > 7 mmol/L
• Respiratory rate ≥ 30/min
• BP < 90/60
• Age ≥ 65
• Score 0–1: Home treatment; 2: Hospital; 3–4: Consider ICU

VAP Prevention Bundle (UAE Standards):

• Elevate head of bed 30–45°
• Daily sedation interruption and spontaneous breathing trial
• Oral chlorhexidine decontamination
• Peptic ulcer prophylaxis (controversial)
• Hand hygiene; PPE; catheter care

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🔴 Extended — Deep Study (3m+)

Comprehensive coverage for students on a longer study timeline.

4. Pulmonary Embolism

Risk Factors (Virchow’s Triad):

1. Stasis: Immobility, prolonged travel (economy class syndrome), CHF
2. Endothelial injury: Surgery, trauma, central lines
3. Hypercoagulability: Pregnancy, OCP use, malignancy, Factor V Leiden, antiphospholipid syndrome

Presentation:

• Sudden dyspnoea (most common)
• Pleuritic chest pain (sharp, worse with inspiration)
• Tachycardia, tachypnoea
• Hypoxaemia (A-a gradient widened)
• haemoptysis (less common)
• Signs of DVT (unilateral leg swelling, tenderness)

Diagnosis:

• Wells Score: >4 = PE likely → proceed directly to CTPA (CT pulmonary angiography)
• D-dimer: Sensitive but not specific; negative result can rule out PE in low-risk patients
• CTPA: Gold standard; shows filling defects in pulmonary arteries

Treatment:

• Anticoagulation immediately (if haemodynamically stable): LMWH or fondaparinux; warfarin or DOAC for long-term
• Thrombolysis (alteplase) if massive PE with haemodynamic instability (systolic BP < 90 or drop > 40; massive PE confirmed)
• Surgical embolectomy or catheter-directed thrombolysis if thrombolysis contraindicated
• IVC filter if anticoagulation contraindicated

5. Pleural Effusion and Pneumothorax

Pleural Effusion:

• Transudate (low protein, low LDH): Heart failure, cirrhosis, nephrotic syndrome
• Exudate (high protein, high LDH): Infection, malignancy, PE, pancreatitis
• Light’s criteria: Pleural protein/serum protein > 0.5; pleural LDH/serum LDH > 0.6; pleural LDH > 2/3 upper limit of normal serum LDH
• Management: Therapeutic thoracentesis if symptomatic; treat underlying cause

Pneumothorax:

• Primary spontaneous: Tall, thin young males; no underlying lung disease
• Secondary spontaneous: COPD, asthma — more dangerous at smaller sizes
• Tension pneumothorax: Medical emergency; mediastinal shift to contralateral side; trachea deviation away from affected side; JVD; hypotension; absent breath sounds
• Tension pneumothorax management: Emergency needle decompression (2nd intercostal space, midclavicular line; OR 5th intercostal space, anterior axillary line) → chest drain

6. Respiratory Failure and ARDS

Type I (Hypoxaemic) Respiratory Failure:

• PaO₂ < 60 mmHg with normal or low PaCO₂
• Causes: V/Q mismatch (pneumonia, pulmonary oedema), shunt, diffusion impairment
• Requires O₂ supplementation; treat underlying cause

Type II (Hypercapnic) Respiratory Failure:

• PaCO₂ > 50 mmHg
• Causes: COPD exacerbation, asthma, sedation/opiates, neuromuscular disease
• Requires ventilation support; COPD patients may develop CO₂ retention on excessive O₂

ARDS (Acute Respiratory Distress Syndrome):

• Severe hypoxaemia (PaO₂/FiO₂ < 300); bilateral pulmonary infiltrates on CXR; non-cardiogenic pulmonary oedema
• Causes: Sepsis (most common), aspiration, trauma, pancreatitis, COVID-19
• Berlin criteria for ARDS classification
• Management: Low tidal volume ventilation (6 mL/kg ideal body weight); prone positioning (significant mortality benefit); neuromuscular blockade; ECMO for refractory cases

Exam Watch: A patient with COPD on controlled O₂ (Venturi mask 28%) who develops confusion and a bounding pulse might be CO₂-retrieved (CO₂ narcosis). The elevated CO₂ suppresses respiratory drive. The priority action is to assess using ABG, consider non-invasive ventilation (BiPAP), and avoid high-flow O₂ which removes the hypoxic drive.

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