Makindo Medical Notes

🌬️ COPD is preventable – 🚭 smoking cessation is the single most effective measure. 🔑 Diagnostic hallmark = irreversible obstruction on spirometry (FEV1/FVC <70% with <10% reversibility). 📉 Prognosis worsens with age, exacerbations, and progressive FEV1 decline.

🚨 Emergency Management of Acute COPD Exacerbation

ABC 🩺 – Check airway, SpO₂, ECG & BP. Watch for fatigue, confusion, or impending arrest. Oxygen 💨 – Controlled O₂ via Venturi (24–28%). Target SpO₂ 88–92% (avoid hyperoxia ⚠️). Bronchodilators 💨💊 – Nebulised Salbutamol 2.5–5 mg q4–6h + Ipratropium 500 µg q4–6h (air-driven if hypercapnia). Steroids 💉 – Prednisolone 30–40 mg PO × 5–7d, or IV Hydrocortisone 100 mg q6h if NBM. Antibiotics 🦠 – If infective trigger (↑ sputum purulence/volume, ↑ breathlessness). Choices: Amoxicillin / Doxycycline / Clarithromycin (per policy). Ventilation 😷 – NIV (BiPAP) if pH <7.35 + PaCO₂ >6.5. Intubate if coma, severe acidosis, or NIV fails. Fluids 💧 – Correct K⁺/Mg²⁺. Avoid overload. Monitor nutrition 🍲 in frail/cachectic patients. Prophylaxis 🩸 – LMWH (unless contraindicated), chest physio, early mobilisation 🚶. Escalation 📜 – Discuss ceilings of care, DNACPR, and document plans. 💡 Exam Tip: Confusion + rising PaCO₂ + acidosis = 🚨 urgent NIV. 🎯 Target sats = 88–92%, never 100%.

📖 About COPD

• 🚬 A progressive lung disease, almost always related to smoking.
• 🫁 Overlaps emphysema (alveolar destruction) + chronic bronchitis (productive cough ≥3 months in 2 consecutive years).
• 🔥 Pathophysiology: heightened inflammatory response → protease–antiprotease imbalance → elastin destruction → air trapping + mucus plugging → hypoxia + hypercapnia.
• ❤️ Chronic hypoxia → pulmonary hypertension → cor pulmonale.

📖 Emphysema

• Pathological diagnosis → abnormal, permanent enlargement of airspaces distal to the terminal bronchioles, with destruction of alveolar walls and no obvious fibrosis.
• Classic types:
  • 🔺 Centrilobular – upper lobes, strongly linked with smoking.
  • 🔻 Panacinar – lower lobes, seen in alpha-1 antitrypsin deficiency.
• Clinical pearl – Patients often thin, tachypnoeic, with “pursed-lip” breathing → the old term “pink puffers.”

📖 Chronic Bronchitis

• Clinical diagnosis → chronic productive cough for ≥3 months per year, for at least 2 consecutive years, where no other cause explains the symptoms.
• Caused by goblet cell hyperplasia and mucus gland hypertrophy → excessive mucus secretion.
• Clinical pearl – Patients often overweight, cyanosed, oedematous from cor pulmonale → the old term “blue bloaters.”

💡 Tip for exams: COPD = umbrella term → most patients have a mix of emphysema and chronic bronchitis features. Spirometry shows the same: irreversible airflow obstruction (FEV1/FVC <70%).

⚠️ Causes / Risk Factors

• 🚬 Smoking (main risk factor; not all smokers develop COPD).
• 🧬 Genetics: alpha-1 antitrypsin deficiency → early panacinar emphysema.
• ⛏️ Occupational exposure: coal dust, cadmium, chemical fumes.
• 🌿 Cannabis smoking also contributes.

🧑‍⚕️ Clinical Features

• Symptoms: exertional dyspnoea, chronic cough, sputum production, winter bronchitis, fatigue.
• Signs: barrel chest, prolonged expiration 😮‍💨, pursed-lip breathing, wheeze, cyanosis 💙, ankle oedema.
• Phenotypes: – “Blue bloater” → chronic bronchitis type, hypoxia + CO₂ retention + cor pulmonale. – “Pink puffer” → emphysema type, thin, tachypnoeic, normocapnic until late.

🔎 Investigations

• 🧪 Spirometry: FEV1/FVC <70%, <10% reversibility = obstructive + irreversible.
• 📸 CXR: hyperinflation, flat diaphragm, bullae.
• 🧪 AAT levels: if <40 yrs or strong FHx.
• 📈 BODE index (BMI, Obstruction, Dyspnoea, Exercise) predicts prognosis.
• BNP/Echo: differentiate from heart failure.

📊 GOLD Severity (by FEV1 % predicted)

Stage	Severity	FEV1 % Predicted	Features
1	Mild	≥80%	Often asymptomatic or mild cough
2	Moderate	50–79%	Exertional breathlessness, cough
3	Severe	30–49%	Frequent exacerbations, activity limitation
4	Very Severe	<30%	Respiratory failure, life-threatening exacerbations

📉 Prognosis – BODE Index

• 0–2 pts → 80% 4-year survival
• 3–4 pts → 67%
• 5–6 pts → 57%
• 7–10 pts → 18%

💊 Chronic Management (NICE)

Step	Therapy	Examples	Notes
🚭 1	Lifestyle	Smoking cessation, flu & pneumococcal vaccines, pulmonary rehab	Most effective intervention
💨 2	SABA or SAMA PRN	Salbutamol / Ipratropium	Rescue therapy
🔄 3	LABA + LAMA	Salmeterol + Tiotropium	Maintenance, ↓ exacerbations
🧯 4	+ ICS	Triple therapy (LABA/LAMA/ICS)	If ≥2 exacerbations/yr or eosinophilia
💊 5	Oral therapy	Theophylline, Roflumilast	Selected cases only
💉 6	LTOT	O₂ >15h/day if PaO₂ ≤7.3 kPa	Improves survival in hypoxaemia
🔪 7	Surgery	Bullectomy, LVRS, transplant	Rare, specialist-selected patients

🚨 Emergency Management of Acute COPD Exacerbation 🫁

Step	🛠️ Intervention	📋 Notes
1️⃣	🩺 ABC	Check airway, SpO₂, ECG, BP. Look for fatigue, confusion, impending arrest.
2️⃣	💨 Oxygen	Controlled O₂ via 24–28% Venturi mask. 🎯 Target sats 88–92% (avoid worsening hypercapnia).
3️⃣	💊 Bronchodilators	Nebulised salbutamol 2.5–5 mg + ipratropium 500 µg q4–6h. Use air-driven nebs if hypercapnic (O₂ can be entrained separately).
4️⃣	💉 Steroids	PO prednisolone 30–40 mg × 5–7 days OR IV hydrocortisone if unable to swallow. Do not taper if short course.
5️⃣	💊 Antibiotics	Indicated if ↑ sputum purulence/volume or ↑ breathlessness. Choices: doxycycline, amoxicillin, or clarithromycin (per local guidelines).
6️⃣	💧 Fluids & Electrolytes	Check U&E; hypokalaemia from β₂-agonists is common. Careful fluid balance in cor pulmonale.
7️⃣	🩸 Blood gases	Repeat ABG after 1 hr: watch for rising PaCO₂ and falling pH (type 2 resp failure). Escalate if pH <7.35.
8️⃣	🧯 NIV (BiPAP)	Indicated if pH 7.25–7.35 with persistent hypercapnia despite optimal therapy. Reduces intubation risk.
9️⃣	💉 Intubation & ICU	For life-threatening exacerbation (pH <7.25, exhaustion, GCS ↓, haemodynamic instability). Call ICU early.
🔟	📦 Other	VTE prophylaxis (LMWH), chest physio, consider theophylline if poor nebuliser response, involve respiratory team for discharge planning.

Teaching Commentary 🧠

Acute COPD exacerbations are medical emergencies. Priorities: - Ventilation: oxygen but avoid overcorrection (target 88–92%). - Relief: bronchodilators + steroids. - Triggers: antibiotics if infective. - Escalation: NIV early if acidosis persists. Always think of the “four Fs”: Fluids, FEV₁ (bronchodilators), Fire (steroids), Flu bugs (antibiotics). Careful monitoring, repeat ABGs, and senior input are crucial.

Cases — Chronic Obstructive Pulmonary Disease (COPD)

• Case 1 — Stable COPD with Exertional Dyspnoea 🚶: A 68-year-old ex-smoker (40 pack-years) presents with progressive breathlessness on exertion and chronic productive cough. Exam: hyperinflated chest, reduced breath sounds. Spirometry: FEV₁/FVC ratio 0.55, FEV₁ 65% predicted. Diagnosis: Moderate stable COPD. Management: Smoking cessation, pulmonary rehabilitation, inhaled LABA + LAMA; annual influenza and pneumococcal vaccines.
• Case 2 — Acute Exacerbation in Hospital 🏥: A 72-year-old man with severe COPD presents with worsening dyspnoea, purulent sputum, and confusion. O₂ sats 83% RA, RR 32, ABG: type 2 respiratory failure (pH 7.28, PaCO₂ 9.2). Diagnosis: Acute exacerbation of COPD with type 2 respiratory failure. Management: Controlled O₂ (target 88–92%), nebulised bronchodilators, oral prednisolone, antibiotics (if purulent sputum), NIV if persistent acidosis, ICU referral if deteriorating.
• Case 3 — Cor Pulmonale 💔: A 74-year-old woman with long-standing COPD presents with ankle swelling, raised JVP, and exertional breathlessness. Exam: peripheral oedema, loud P₂, hepatomegaly. Diagnosis: Cor pulmonale (right heart failure secondary to chronic lung disease). Management: Optimise COPD care, long-term O₂ therapy (if hypoxic), diuretics for oedema, assess for pulmonary hypertension therapy.
• Case 4 — Alpha-1 Antitrypsin Deficiency (Genetic COPD) 🧬: A 45-year-old non-smoker develops progressive dyspnoea, cough, and weight loss. Exam: basal crackles, wheeze, hyperresonant chest. CXR: basal panacinar emphysema. Diagnosis: COPD due to alpha-1 antitrypsin deficiency. Management: Augmentation therapy (where available), inhaled bronchodilators, pulmonary rehab, early consideration of transplant; genetic counselling for family.

Teaching Commentary 🧠

COPD = progressive, largely irreversible airflow limitation (FEV₁/FVC <0.7). - Common causes: smoking, biomass fuel, α₁-antitrypsin deficiency. - Phenotypes: emphysema (pink puffers) vs chronic bronchitis (blue bloaters) — though in practice patients overlap. - Complications: acute exacerbations, type 2 respiratory failure, cor pulmonale, lung cancer. - Management: Always start with smoking cessation + vaccination; then escalate inhalers (SABA → LABA/LAMA → triple therapy); long-term O₂ if PaO₂ persistently <7.3 kPa.