---

COPD — Complete MBBS-Level Study Guide (GOLD Framework)

---

1. DEFINITION (Conceptual Core)

---

2. RISK FACTORS

• Cigarette smoking — far and away the #1 risk factor (dose = pack-years)
• Biomass fuel combustion (cooking/heating in poorly ventilated spaces)
• Occupational dust (mines, grain, cotton mills)
• α₁-antitrypsin (A1AT) deficiency — genetic cause; screen ALL COPD patients at least once
• Childhood respiratory infections → impaired lung growth → lower peak FEV₁
• Secondhand smoke, maternal smoking during pregnancy

---

3. PATHOPHYSIOLOGY (Conceptual)

• Normal: Neutrophil elastase balanced by A1AT
• In COPD/smoking: A1AT overwhelmed → unchecked elastase → alveolar wall breakdown

• Loss of elastic recoil → dynamic collapse of small airways during expiration → air trapping
• Mucus gland hypertrophy + goblet cell hyperplasia → chronic bronchitis physiology
• V/Q mismatch → hypoxemia
• Late: hypercapnia, cor pulmonale, polycythemia

---

4. CLINICAL FEATURES

• Dyspnea on exertion (cardinal symptom)
• Chronic cough + sputum production
• Wheezing

• Barrel chest (↑AP diameter), hyperresonance
• Diminished breath sounds, prolonged expiration
• Use of accessory muscles
• Pursed-lip breathing

---

5. DIAGNOSIS

Step 1: Clinical suspicion

Step 2: Spirometry — THE GOLD STANDARD

FEV₁/FVC < 0.70

• ↑ TLC, FRC, RV (hyperinflation, air trapping)
• ↓ DLCO in emphysema (alveolar destruction)

Step 3: GOLD Spirometric Severity Grading

Step 4: GOLD ABCD Classification (combines symptoms + exacerbation risk)

• mMRC Scale (0–4): 0 = only with strenuous exertion → 4 = too breathless to leave house
• CAT Score (0–40): ≥10 = significant impact

Investigations

---

6. STABLE COPD MANAGEMENT

Principle: Goals of treatment

1. Reduce symptoms and improve exercise tolerance
2. Reduce frequency/severity of exacerbations
3. Slow disease progression
4. Prolong survival

A. Smoking Cessation — #1 MOST IMPORTANT INTERVENTION

• Only intervention proven to slow FEV₁ decline
• NRT (nicotine patch/gum), Varenicline, Bupropion
• Counseling + pharmacotherapy = best combo

B. Pharmacotherapy — Inhaled Route is Preferred

• Never monotherapy in COPD
• Indicated if eosinophils >300 cells/μL, or persistent exacerbations on LABA+LAMA
• Withdraw if <2 exacerbations/year AND eosinophils <300 cells/μL

C. Initial Pharmacotherapy by ABCD Group

D. Non-Pharmacological Therapy

LTOT Indications (memorize)

• PaO₂ ≤55 mmHg or SpO₂ ≤88% at rest
• PaO₂ 56–59 mmHg or SpO₂ <89% if cor pulmonale, right heart failure, or polycythemia (Hct >55%)

---

7. ACUTE EXACERBATION OF COPD (AECOPD)

Definition

• Respiratory infection (most common) — viral > bacterial
• Air pollution, non-compliance, cardiac causes

Assessment

• ABG: assess hypoxemia, hypercapnia, pH
• CXR: exclude pneumonia, pneumothorax, pulmonary edema
• ECG: detect arrhythmias

Treatment (Stepwise)

• SABA ± SAMA (ipratropium) via nebuliser — first-line
• Combine albuterol + ipratropium in acute setting

• Prednisolone 30–40 mg orally for 5 days (not longer — no added benefit >2 weeks)
• Reduces treatment failures by ~46%, shortens hospital stay
• ↑ risk of hyperglycemia

• Indicated if: ≥2 cardinal symptoms (especially purulent sputum), signs of pneumonia, need for mechanical ventilation
• Agents: amoxicillin-clavulanate, azithromycin, doxycycline, or fluoroquinolone

• Target SpO₂ 88–92% (avoid over-oxygenation → suppresses hypoxic drive in CO₂ retainers)
• Recheck ABG 30 minutes after starting O₂

• Indication: pH <7.35 with PaCO₂ >45 mmHg + RR >25 — reduces need for intubation

• When NIV fails or is contraindicated
• Indications: pH <7.25, PaO₂ <40 mmHg, mental status change (confusion/lethargy)

Indications for Hospitalization

• Severe dyspnea not responding to initial treatment
• New cyanosis or change in mental status
• Failure of outpatient therapy
• Significant comorbidities (CHF, arrhythmia)
• Underlying pneumonia

Indications for ICU

• pH <7.25 or PaCO₂ >60 mmHg or PaO₂ <40 mmHg
• Hemodynamic instability
• Altered consciousness

---

8. QUICK DIFFERENTIATORS — COPD vs. ASTHMA

---

9. HIGH-YIELD MNEMONICS / EXAM FACTS

• COPD diagnosis = Spirometry: post-BD FEV₁/FVC <0.70
• GOLD 1–4 = Mild/Moderate/Severe/Very Severe (FEV₁ cutoffs: 80, 50, 30%)
• GOLD A–D = Symptom + exacerbation risk matrix → guides initial inhaler choice
• Only proven survival benefits: Smoking cessation + LTOT (in hypoxemic patients)
• LAMA > LABA for exacerbation prevention (Group C)
• ICS not monotherapy; adds pneumonia risk; use when eos >300 or persistent exacerbations
• AECOPD O₂ target = 88–92% (not 100%)
• Systemic steroids for exacerbations = 5 days (not >2 weeks)
• A1AT screen — every COPD patient at least once
• Roflumilast (PDE-4 inhibitor) = for severe COPD with chronic bronchitis phenotype + frequent exacerbations
• β-blockers are NOT contraindicated in COPD (for CV indications)

---

10. COMPLICATIONS OF COPD

• Cor pulmonale — RV hypertrophy from pulmonary hypertension (chronic hypoxia → vasoconstriction)
• Polycythemia — compensatory response to chronic hypoxemia
• Spontaneous pneumothorax — bullae rupture
• Respiratory failure — Type 2 (hypercapnic) in advanced disease
• Lung cancer — strong association; screen with low-dose CT if ≥20 pack-years, age 50–80, quit ≤15 years ago
• OSA-COPD overlap — higher risk of hypercapnia and pulmonary hypertension

---

---

COPD Management — Complete MBBS-Level Guide (GOLD Framework)

---

THE BIG PICTURE — Goals of Management

1. Reduce symptoms (dyspnea, cough)
2. Improve exercise tolerance and quality of life
3. Reduce frequency and severity of exacerbations
4. Slow disease progression
5. Prolong survival

---

PART 1: STABLE COPD MANAGEMENT

Step 0: GOLD ABE Classification (guides initial therapy)

Key concept: GOLD 1-4 grades = spirometric severity (FEV₁ %) → tells you prognosis. GOLD A/B/E groups = symptoms + exacerbation risk → tells you what drug to start.

---

A. SMOKING CESSATION — Single Most Important Intervention

• Only intervention that slows the rate of FEV₁ decline
• Improves survival; reduces exacerbation risk
• Options:
  • Nicotine replacement therapy (NRT) - patch, gum, lozenge, inhaler, nasal spray
  • Varenicline (nicotinic receptor partial agonist) - most effective
  • Bupropion (dopamine/noradrenaline reuptake inhibitor)
  • Combine pharmacotherapy + counseling for best results

---

B. PHARMACOTHERAPY

1. Bronchodilators (Foundation of Treatment)

Memory hook: LAMA > LABA for exacerbation prevention (tiotropium is the prototype)

2. ICS Rules (Critical for Exams)

• Never use ICS as monotherapy in COPD (unlike asthma)
• When to ADD ICS:
  • Eosinophils ≥300 cells/μL (strong predictor of ICS response)
  • Persistent exacerbations despite dual bronchodilator (LAMA+LABA)
  • Asthma-COPD overlap
  • History of ≥1 hospitalization or ≥2 moderate exacerbations/year
• When to WITHDRAW ICS: <2 exacerbations/year AND eosinophils <300 cells/μL AND no hospitalizations
• Risk of pneumonia is real - don't use without indication

3. Initial Inhaled Therapy by GOLD Group

Group A: Short-acting BD as needed
     ↓ (if symptomatic)
Group B: LABA or LAMA → LABA + LAMA
     ↓ (if exacerbations)
Group E: LAMA → LABA + LAMA → LABA + LAMA + ICS (if eos ≥100-300)
     ↓ (still exacerbating)
Add Roflumilast or Azithromycin

4. Triple Therapy (LABA + LAMA + ICS)

• Shown to reduce mortality in selected patients (eosinophils ≥300, exacerbations despite dual BD)
• Single inhaler combinations available (e.g., Fluticasone/Umeclidinium/Vilanterol)

5. Other Pharmacological Agents

Roflumilast: not a bronchodilator, not for acute bronchospasm - purely for reducing exacerbation frequency

---

C. NON-PHARMACOLOGICAL THERAPY

1. Pulmonary Rehabilitation

• When to refer: All patients, especially post-exacerbation discharge, at diagnosis, and pre-surgery
• Consists of: aerobic exercise (60-80% of max capacity) + upper limb strength training + education
• Improves exercise capacity, dyspnea, quality of life
• Does NOT improve FEV₁ or survival directly but reduces hospitalization

2. Long-Term Oxygen Therapy (LTOT) - Improves Survival

• Must be used ≥15 hours/day to improve survival
• Target SpO₂ = 88-92% (avoid over-oxygenation → CO₂ retention)
• Nocturnal-only O₂ does NOT improve survival in isolated nocturnal desaturators

3. Noninvasive Positive Pressure Ventilation (NIV/BiPAP)

• Indication: Stable hypercapnic COPD with resting PaCO₂ ≥52 mmHg
• Improves dyspnea, exercise capacity, time to rehospitalization, possibly survival

4. Surgical Options

5. Vaccines (Mandatory)

• Influenza - annually
• Pneumococcal (PCV13/PPSV23)
• COVID-19
• Tdap (pertussis)

6. Nutritional Support

• Low BMI = independent predictor of mortality in COPD
• Small frequent meals; rest before eating (reduces meal-induced dyspnea)
• Nutritional supplementation improves BMI, exercise tolerance, and quality of life in advanced disease

---

PART 2: ACUTE EXACERBATION OF COPD (AECOPD)

Definition

1. ↑ Dyspnea
2. ↑ Sputum volume
3. ↑ Sputum purulence (change in color)

Pathophysiology of AECOPD (conceptual)

• Trigger (infection/pollution) → bronchospasm + mucosal edema + ↑ secretions
• ↑ Airway resistance + intrinsic PEEP (air trapping) + flattened diaphragm
• Patient can't take adequate tidal volumes → alveolar hypoventilation → ↑ PaCO₂
• Respiratory muscle fatigue → vicious cycle → respiratory acidosis
• NIV breaks this cycle by augmenting tidal volume with less effort

Triggers

• Respiratory tract infection (most common) - viral (rhinovirus, influenza) > bacterial (H. influenzae, S. pneumoniae, M. catarrhalis)
• Air pollution
• Non-compliance with medications
• Pulmonary embolism (always consider if sudden onset)
• Cardiac causes (heart failure, arrhythmia)

Initial Assessment

• ABG - quantify hypoxemia, hypercapnia, pH (pH <7.35 = acute respiratory failure)
• CXR - exclude pneumonia, pneumothorax, pulmonary edema
• ECG - detect arrhythmia, cor pulmonale (P pulmonale, right axis deviation)
• Sputum culture if purulent
• FBC - polycythemia, eosinophilia
• Serum electrolytes - hypokalemia (from SABA use)

Treatment of AECOPD - Stepwise

Step 1: Bronchodilators (Immediate)

• SABA (salbutamol/albuterol) + SAMA (ipratropium) via nebuliser
• Combine both - different mechanisms, additive effect
• Frequency: every 20 min initially in severe cases, then q4-6h
• Some patients respond better to anticholinergics, some to β₂-agonists → give both

Step 2: Controlled Oxygen

• Target: SpO₂ 88-92% (NOT 100%)
• Why? Chronic CO₂ retainers rely partially on hypoxic drive; over-oxygenation → abolishes drive → ↑ CO₂ → CO₂ narcosis
• Recheck ABG 30 minutes after starting O₂ to ensure no CO₂ rise
• Start with 28% Venturi mask (2L/min nasal cannula) and titrate

Step 3: Systemic Corticosteroids

• Prednisolone 30-40 mg orally for 5 days (not longer - no benefit beyond 2 weeks)
• IV methylprednisolone if unable to take oral
• Benefits: reduces treatment failure by ~46%, shortens hospital stay by ~1.4 days, improves FEV₁ and dyspnea faster
• Side effect: hyperglycemia (monitor blood sugar)

Step 4: Antibiotics

• ≥2 of: ↑ dyspnea, ↑ sputum volume, purulent sputum - especially if purulence is one of them
• Signs of pneumonia on CXR
• Requiring mechanical ventilation (invasive or non-invasive)

Step 5: NIV (BiPAP) — Key Decision

• pH <7.35 with PaCO₂ >45 mmHg AND respiratory rate >25/min
• Mild-moderate respiratory acidosis (pH 7.25-7.35)
• Patient is conscious and cooperative

• Reduces need for intubation
• Reduces ICU mortality
• Shorter hospital stay
• Avoids complications of intubation (ventilator-associated pneumonia)

• Hemodynamic instability / cardiac arrest
• Loss of consciousness / uncooperative
• Unable to protect airway (↑ aspiration risk)
• Undrained pneumothorax
• Facial trauma / anatomic contraindication

Step 6: Invasive Mechanical Ventilation

• NIV failed or contraindicated
• pH <7.25
• PaO₂ <40 mmHg despite O₂
• Severe hypercapnia (PaCO₂ >60 mmHg)
• Hemodynamic instability
• Altered consciousness (confusion, obtundation)
• Respiratory arrest

Mortality with invasive MV for AECOPD = 17-49% for that hospitalization

Indications for Hospitalization

Indications for ICU Admission

• pH <7.25, severe acidosis
• PaO₂ <40 mmHg, PaCO₂ >60 mmHg
• NIV failure / contraindication
• Hemodynamic instability
• Respiratory arrest

---

PART 3: SURVIVAL-IMPROVING INTERVENTIONS (High-Yield)

Key exam fact: LABAs and LAMAs improve symptoms and reduce exacerbations but do NOT slow FEV₁ decline or improve survival on their own.

---

PART 4: MANAGEMENT ALGORITHM (Quick Reference)

CONFIRMED COPD (FEV₁/FVC <0.70 post-BD)
          |
   Assess: GOLD 1-4 (FEV₁ %) + GOLD A/B/E (symptoms + exacerbations)
          |
 ┌────────┴─────────────────────────┐
 |                                  |
STABLE COPD                   AECOPD
 |                                  |
Smoking cessation (always)          SABA + SAMA nebulised
Vaccinations                        Controlled O₂ (SpO₂ 88-92%)
 |                                  Systemic steroids 5 days
Group A → SABA/SAMA PRN             Antibiotics (if criteria met)
Group B → LABA or LAMA               NIV if pH <7.35 + hypercapnia
Group E → LAMA → LABA+LAMA          IMV if NIV fails or pH <7.25
 |
If eos ≥300: add ICS
If persistent exac despite LABA+LAMA+ICS: add Roflumilast
If hypoxemic (PaO₂ ≤55): LTOT
If PaCO₂ ≥52 stable: nocturnal NIV
If upper-lobe emphysema: consider LVRS

---

EXAM HIGH-YIELD FACTS

• O₂ target in AECOPD = 88-92% (not 100%)
• Steroids in AECOPD = 5 days only (not >2 weeks)
• ICS never as monotherapy in COPD
• ICS adds pneumonia risk - justify before prescribing
• Eosinophil count guides ICS: eos ≥300 → add ICS; eos <100 → no ICS benefit
• LAMA preferred over LABA for exacerbation prevention (Group C/E)
• Only survival benefits: smoking cessation + LTOT + LVRS (selected) + triple therapy (selected)
• Roflumilast = oral anti-inflammatory for severe chronic bronchitis phenotype, NOT a bronchodilator
• Azithromycin daily = exacerbation prevention in nonsmokers; watch for QTc and resistance
• β-blockers are NOT contraindicated in COPD (use for cardiac indications)
• After AECOPD hospitalization: 20% readmitted within 30 days; 45% within 1 year; ~20% mortality in the following year

---

---

COPD Classifications — Memory Master Guide

---

CLASSIFICATION 1: GOLD Spirometric Grades (1-4)

What it is

The Numbers

Memory Trick — "The Ladder Going Down"

GRADE 1 → Still on TOP of the ladder     → ≥80% (mostly fine)
GRADE 2 → Halfway down                   → 50-79% (half-ish)
GRADE 3 → Almost at the bottom           → 30-49% (thirty-something)
GRADE 4 → Hit the floor                  → <30% (below 30, critical)

The "50-30" Rule (easiest anchor)

Just remember two numbers: 50 and 30

• FEV₁ 50% divides Grade 2 from Grade 3
• FEV₁ 30% divides Grade 3 from Grade 4
• Grade 1 starts at 80% (easy — it's the "normal-ish" zone)

Visual Anchor

• GOLD 1 = Full tank (≥80%)
• GOLD 2 = Half tank (50-79%)
• GOLD 3 = Low fuel warning (30-49%)
• GOLD 4 = Empty, car stops (<30%)

---

CLASSIFICATION 2: GOLD ABE Groups (Symptom + Exacerbation Risk)

What it is

The Grid

Mnemonic — "ABE = Ants, Bees, Elephants"

Say it once: "Ant, Bee, Elephant — Small, Medium, Dangerous"

---

Alternate Mnemonic for ABE — "Airport Boarding"

• A = Economy class (mild, few symptoms, sit anywhere)
• B = Business class (more symptomatic, needs better seat = long-acting BD)
• E = Emergency exit row (high risk of exacerbation, needs most attention)

---

CLASSIFICATION 3: mMRC Dyspnea Scale (0-4)

The Scale

Mnemonic — "0 to 4 = Gym to Bed"

0 = GYM (only strenuous exercise affects you)
1 = HILL (hurrying or inclines)
2 = FLAT ROAD (can't keep up on flat ground)
3 = 100 YARDS (barely a cricket pitch length)
4 = BED/HOUSE (can't even dress yourself)

The "CAT ≥10 = mMRC ≥2" Bridge

• CAT <10 = mMRC 0-1 = Group A (few symptoms)
• CAT ≥10 = mMRC ≥2 = Group B or E (more symptoms)

---

CLASSIFICATION 4: Exacerbation Severity

Mnemonic — "MBA-I"

• More inhaler → Mild
• Budesonide/antibiotics → Moderate
• Admit to hospital → Severe
• ICU → Very Severe

---

THE MASTER MEMORY FRAMEWORK

Link all 4 systems together in ONE sentence:

"GOLD 1-4 tells you HOW BAD the lungs are. ABE tells you WHAT TO PRESCRIBE. mMRC/CAT tells you HOW BREATHLESS they are. Exacerbation count tells you HOW RISKY they are."

The "Report Card" Analogy

---

QUICK RECALL TABLE — 30-Second Review

GOLD GRADES (FEV₁%):    ≥80 → 50 → 30 → <30
                        G1    G2   G3    G4
                        Mild  Mod  Sev  V.Sev

GOLD GROUPS:   Symptoms low + low exac = A → any BD
               Symptoms HIGH + low exac = B → LABA/LAMA
               HIGH exacerbations (any symptoms) = E → LAMA

mMRC:   0=Gym  1=Hill  2=Flat  3=100yards  4=Housebound

CAT:    <10 = fewer symptoms (= mMRC 0-1 = Group A)
        ≥10 = more symptoms (= mMRC ≥2 = Group B/E)

---

ONE FINAL TRICK — The "1-2-3" Rule

Memorize these 9 numbers and you can answer almost any COPD management MCQ.

---

SPACED REPETITION TIP

1. Day 1: Draw the ABE grid from memory (groups + what triggers each)
2. Day 2: Recite GOLD 1-4 cutoffs without looking
3. Day 3: Write the mMRC scale descriptions 0-4 from memory
4. Day 7: Draw the full management ladder (A→B→E with drugs at each step)
5. Day 14: Do a practice MCQ on a AECOPD case using pH + PaCO₂ values

---

Management of Asthma — Complete MBBS-Level Guide

---

CORE CONCEPT FIRST

Managing only the "present" domain while ignoring "future" risk is incomplete care. A patient comfortable on frequent SABA use may still be at high risk of a fatal attack.

---

CLASSIFICATION OF ASTHMA SEVERITY

Two numbers to anchor this: FEV₁ 60% separates moderate from severe. "Daily symptoms" = at minimum moderate.

---

CLASSIFICATION OF ASTHMA CONTROL

---

PART 1: STABLE ASTHMA — GINA/NAEPP STEPWISE THERAPY

Principle: Step Up / Step Down

• Step Up if not well controlled
• Step Down after ≥3 months of good control (to find minimum effective dose)
• Reassess every 2-6 weeks when stepping up, 3 months when stepping down

---

THE 5-STEP LADDER

STEP 1 — Intermittent Asthma (mildest)

• Reliever only: SABA (salbutamol/albuterol) as-needed
• No daily controller needed
• GINA update: Low-dose ICS-formoterol as-needed preferred over SABA alone (reduces exacerbation risk even in mild asthma)
• Educate on action plan for severe attacks: up to 4 puffs albuterol every 20 min x1 hour

STEP 2 — Mild Persistent

• Add daily controller: Low-dose ICS (e.g., budesonide 200-400 mcg/day, fluticasone 100-250 mcg/day)
• Alternative to ICS: Leukotriene receptor antagonist (LTRA) - montelukast, zafirlukast (less effective than ICS but useful in patients with nasal polyps, aspirin sensitivity, or exercise-induced asthma)
• Continue SABA as-needed reliever

STEP 3 — Moderate Persistent

1. Low-dose ICS + LABA (preferred - most effective) - e.g., fluticasone + salmeterol (Seretide/Advair), budesonide + formoterol (Symbicort)
2. Medium-dose ICS alone

• LABA should NEVER be used as monotherapy in asthma (black-box warning - increased asthma deaths with LABA alone; warning removed for ICS-LABA combinations)
• Alternative additions: LTRA, theophylline, tiotropium (LAMA)

STEP 4 — Severe Persistent (not controlled on Step 3)

• Medium-to-high dose ICS + LABA (core)
• Add-on options:
  • LAMA (tiotropium) - improves lung function and reduces exacerbations in patients with persistent obstruction, high symptom burden, exacerbation history
  • LTRA (montelukast)
  • Sustained-release theophylline
• Refer to specialist

STEP 5 — Severe Refractory Asthma

• High-dose ICS + LABA +/- LAMA
• Biologics (targeted therapy) based on phenotype:

• Oral corticosteroids (low-dose) as last resort — significant toxicity with long-term use

---

SMART Strategy (Single Maintenance And Reliever Therapy)

Budesonide-formoterol used as BOTH the daily controller AND the rescue inhaler

• Works because formoterol has rapid onset (like SABA) + long duration
• Patient uses the same inhaler for scheduled doses AND PRN relief
• Evidence: as effective as higher-dose ICS + separate SABA
• Now in both US (NAEPP 2020) and GINA guidelines
• Available devices: Symbicort (budesonide/formoterol), Breztri, Airsupra (budesonide/albuterol)

---

KEY DRUGS IN DETAIL

---

PART 2: ACUTE SEVERE ASTHMA (ASTHMA ATTACK / STATUS ASTHMATICUS)

Definition of Severity

Silent chest + cyanosis + bradycardia + PaCO₂ rising = near-fatal asthma - act immediately

Treatment of Acute Severe Asthma — Stepwise

1. Oxygen

• Target SpO₂ ≥94-95% (unlike COPD, aim higher in asthma)
• Humidified oxygen via face mask
• Unlike COPD, there is no concern about suppressing hypoxic drive

2. Inhaled SABA (First-Line, Immediate)

• Salbutamol (albuterol) 2.5-5 mg via nebuliser every 20 minutes × 3 doses in the first hour, then as needed
• MDI with spacer is equally effective as nebuliser (2-4 puffs every 20 min)
• In severe/life-threatening: continuous nebulisation
• Can use IV salbutamol if inhaled route is inadequate (rarely)

3. Inhaled SAMA (Add to SABA)

• Ipratropium 0.5 mg nebulised combined with salbutamol
• Additive effect - reduces hospitalisation rates in severe acute asthma
• Most beneficial in first 24-48 hours of presentation

4. Systemic Corticosteroids (Give Early - Within 1 Hour)

• Prednisolone 40-50 mg orally OR Hydrocortisone 200 mg IV if unable to swallow
• Duration: 5 days (no benefit to longer courses in most patients)
• Reduces: inflammation, relapse, need for hospitalisation
• Effect takes 4-6 hours to manifest - give EARLY

5. IV Magnesium Sulphate

• 2g IV over 20 minutes (single dose)
• Mechanism: Mg²⁺ blocks calcium entry into smooth muscle → bronchodilation
• Indications:
  • Severe asthma not responding to bronchodilators after 1 hour
  • SpO₂ <92% / life-threatening features
• Dose in children: 50 mg/kg (max 2g)
• Monitor: BP and cardiac rhythm during infusion

6. Controlled Oxygen + Monitoring

• Pulse oximetry continuous
• Peak flow before and after each treatment
• ABG if SpO₂ <92% or severe attack

7. IV Aminophylline / Theophylline (Controversial, Rarely Used)

• Used if inadequate response to all above
• Load: 5-6 mg/kg IV over 20-30 min (do not give loading dose if already on theophylline)
• Maintenance: 0.5 mg/kg/hr infusion
• Monitor ECG (arrhythmias), serum levels
• Largely fallen out of favour given poor benefit-risk ratio

8. Heliox

• Helium-oxygen mixture (70:30)
• Lower density reduces turbulent flow in narrowed airways
• Used as bridge therapy in refractory severe asthma
• Limited evidence, not widely available

9. Intubation and Mechanical Ventilation (Last Resort)

• Respiratory arrest or near-arrest
• Altered consciousness
• Exhaustion, rising PaCO₂ despite treatment
• SpO₂ <92% not improving
• Silent chest

Intubation in asthma is high-risk: risk of barotrauma, tension pneumothorax, haemodynamic instability. Use lowest tidal volumes, long expiratory time, and permissive hypercapnia strategy.

10. Discharge Criteria and Follow-up

• PEFR ≥75% predicted on discharge
• SpO₂ ≥95% on room air
• Prescribe ICS at discharge (for all except mild intermittent asthma)
• Oral prednisolone course to complete
• Written asthma action plan
• Review inhaler technique
• Follow-up within 48 hours

---

PART 3: TRIGGERING FACTORS — ALWAYS ADDRESS

Always ask about aspirin and β-blocker use. β-blockers (including topical eye drops for glaucoma) can precipitate fatal bronchospasm in asthmatics.

---

PART 4: SPECIAL SITUATIONS

Exercise-Induced Asthma

• Pre-treatment: SABA 15-20 min before exercise
• Alternatives: LTRA (montelukast), cromolyn, warm-up exercises
• ICS reduces airway hyperresponsiveness over time

Aspirin-Exacerbated Respiratory Disease (AERD)

• Triad: Asthma + nasal polyps + aspirin/NSAID sensitivity (Samter's Triad)
• Avoid all NSAIDs, aspirin
• LTRA (montelukast) particularly useful
• Aspirin desensitization possible in specialized centers

Asthma in Pregnancy

• Poorly controlled asthma is more dangerous than well-treated asthma for the fetus
• ICS are safe in pregnancy (all categories) - do not stop
• SABA is safe
• Systemic steroids: use when needed (risk of uncontrolled asthma > risk of steroid)
• Monitor PEFR regularly throughout pregnancy

---

PART 5: MANAGEMENT ALGORITHM — Quick Reference

ASTHMA CONFIRMED (reversible airflow obstruction)
          |
   Assess SEVERITY (if not on treatment)
   or CONTROL (if already on treatment)
          |
 ┌────────────────────────────────────────────┐
 STABLE                              ACUTE ATTACK
    |                                      |
Step 1: Intermittent → SABA PRN      O₂ → target SpO₂ ≥94%
Step 2: Mild persist → + low ICS     Nebulised SABA q20min x3
Step 3: Mod persist → ICS + LABA     Add ipratropium (severe)
Step 4: Severe → medium-high ICS     Systemic steroids EARLY
        + LABA + LAMA/LTRA           IV Mg²⁺ if not improving
Step 5: Refractory → biologics       Aminophylline (rarely)
        Omalizumab/Mepolizumab/       Intubate if life-threatening
        Dupilumab/Tezepelumab
    |
SMART strategy: Budesonide-formoterol
as both controller AND reliever

---

HIGH-YIELD EXAM FACTS

• Drug of choice for acute bronchospasm: Inhaled SABA (salbutamol)
• First-line controller: Low-dose ICS
• LABA NEVER monotherapy in asthma (risk of asthma death)
• Most effective add-on to ICS: LABA (better than doubling ICS dose)
• ICS side effect: Rinse mouth to prevent oral candidiasis
• SMART regimen: Budesonide-formoterol as both controller + reliever
• IV Mg²⁺ dose: 2g over 20 min for acute severe asthma
• O₂ target in acute asthma: ≥94-95% (NOT 88-92% as in COPD)
• Rising PaCO₂ in acute asthma = danger sign (patient is tiring out)
• β-blockers contraindicated in asthma (even topical)
• Aspirin + asthma + nasal polyps = Samter's Triad → use LTRA
• Montelukast black-box warning: Neuropsychiatric events (depression, suicidal ideation)
• Omalizumab: Anti-IgE biologic → for allergic asthma
• Tezepelumab: Broadest biologic → anti-TSLP → works in both T2-high and T2-low asthma
• Theophylline target serum level: 5-15 mcg/mL

---