9.1 Chronic Obstructive Pulmonary Disease (COPD), Asthma & Pneumonia

Chronic Obstructive Pulmonary Disease (COPD), Asthma & Pneumonia

Clinical Core Insight: In acute respiratory care, matching oxygen delivery to underlying pathophysiology is a critical nursing competency. In patients with Chronic Obstructive Pulmonary Disease (COPD) who are chronic carbon dioxide retainers, uncontrolled high-flow oxygen blunts ventilatory drive, worsens ventilation-perfusion mismatch, and precipitates hypercapnic coma; their prescribed target oxygen saturation is 88–92%. Conversely, in acute severe and life-threatening asthma, oxygen retention is not the initial hazard—severe hypoxaemia kills rapidly, and oxygen must be administered at maximum concentrations targeting 94–98%.

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Chronic Obstructive Pulmonary Disease (COPD)

Chronic Obstructive Pulmonary Disease (COPD) is a common, preventable, and treatable chronic respiratory disorder characterized by persistent, progressive, largely irreversible airflow limitation. In Ireland, COPD represents one of the highest causes of emergency hospital admissions and mortality, with a substantial burden on acute medical assessment units (AMAUs) and respiratory wards.

Pathophysiological Subtypes

COPD encompasses two classic, frequently overlapping pathophysiological entities driven primarily by long-term cigarette smoke exposure, biomass fuel inhalation, or alpha-1 antitrypsin deficiency:

1. Chronic Bronchitis (Airway Disease):
   • Clinical Definition: Presence of a persistent, productive cough for at least 3 consecutive months in 2 consecutive years, in the absence of other cardiopulmonary etiologies.
   • Mechanisms: Chronic airway irritation leads to goblet cell hyperplasia, submucosal gland hypertrophy, excessive mucus hypersecretion, ciliary dysfunction, and chronic inflammatory infiltration (CD8+ T-lymphocytes, neutrophils, macrophages) within the bronchial walls. This produces progressive airway narrowing and bronchial wall thickening.
2. Emphysema (Parenchymal Destruction):
   • Pathological Definition: Abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of alveolar walls and capillary beds without obvious fibrosis.
   • Mechanisms: Imbalance between alveolar proteases (e.g., neutrophil elastase) and antiproteases (alpha-1 antitrypsin), coupled with oxidative stress. Destruction of elastin eliminates alveolar radial traction, causing dynamic small airway collapse during expiration, severe air trapping, pulmonary hyperinflation, and impaired gas exchange surface area.

+-----------------------------------------------------------------------------+
|                     PATHOPHYSIOLOGICAL CASCADE OF COPD                      |
+-----------------------------------------------------------------------------+
| Inhaled Cigarette Smoke / Toxic Biomass Particles                           |
|   --> Recruitment of Alveolar Macrophages & Neutrophils (Elastase Release)   |
|   --> Protease-Antiprotease Imbalance & Alveolar Wall Destruction (Emphysema)|
|   --> Mucus Hypersecretion, Goblet Cell Hyperplasia (Chronic Bronchitis)    |
|   --> Loss of Elastic Recoil + Small Airway Collapse on Expiration          |
|   --> Dynamic Hyperinflation & Air Trapping                                 |
|   --> V/Q Mismatch --> Hypoxaemia & Chronic Hypercapnia (CO2 Retention)     |
+-----------------------------------------------------------------------------+

Diagnostic Spirometric Threshold

Spirometry is the diagnostic gold standard. Airflow obstruction is confirmed when the post-bronchodilator ratio of Forced Expiratory Volume in 1 second to Forced Vital Capacity is reduced: $\text{FEV}_1 / \text{FVC} < 0.70$ Severity is graded against predicted post-bronchodilator $\text{FEV}_1$: GOLD 1 (Mild: $\ge 80%$), GOLD 2 (Moderate: $50% - 79%$), GOLD 3 (Severe: $30% - 49%$), and GOLD 4 (Very Severe: $< 30%$).

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Acute Exacerbation of COPD (AECOPD)

An acute exacerbation is defined as an acute worsening of respiratory symptoms (dyspnoea, cough, sputum) beyond normal day-to-day variations that necessitates a change in regular medication. Exacerbations are most commonly triggered by tracheobronchial viral infections (rhinovirus, influenza) or bacterial pathogens (Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis), as well as environmental pollutants.

Anthonisen Criteria for Severity & Antibiotic Prescription

The Anthonisen criteria guide clinical severity assessment and the requirement for antimicrobial therapy:

• Type 1 (Severe Exacerbation): Presence of all three cardinal symptoms:
  1. Worsening dyspnoea (breathlessness)
  2. Increased sputum volume
  3. Increased sputum purulence (yellow/green discoloration)
• Type 2 (Moderate Exacerbation): Presence of any two cardinal symptoms.
• Type 3 (Mild Exacerbation): Presence of any one cardinal symptom plus at least one secondary feature (upper respiratory tract infection within 5 days, fever without other cause, increased wheeze, or increased cough frequency by 20%).

[!IMPORTANT] Antimicrobial Prescribing Rule: Sputum purulence is the single most reliable clinical indicator of bacterial infection in AECOPD. Antibiotics are strictly indicated for Type 1 exacerbations and for Type 2 exacerbations only if sputum purulence is one of the two cardinal symptoms.

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Controlled Oxygen Therapy in Hypercapnic Respiratory Failure

In healthy individuals, the primary chemical driver of ventilation is arterial carbon dioxide tension ($\text{PaCO}_2$), detected by central medullary chemoreceptors. In chronic hypercapnic COPD patients, prolonged hypercapnia causes renal bicarbonate retention that buffers cerebral spinal fluid pH, desensitizing central chemoreceptors. Consequently, peripheral chemoreceptors in the carotid and aortic bodies (sensitive to arterial $\text{PaO}_2$) assume a dominant regulatory role—the so-called "hypoxic drive".

The Triple Mechanism of Oxygen-Induced Hypercapnia

Administering uncontrolled high-concentration oxygen to a hypercapnic COPD patient precipitates acute respiratory acidosis through three distinct mechanisms:

1. Reversal of Hypoxic Pulmonary Vasoconstriction (V/Q Mismatch): Hypoxic alveoli naturally undergo vasoconstriction to divert capillary blood flow toward well-ventilated lung units. High supplemental oxygen floods poorly ventilated alveoli, abolishing vasoconstriction. Blood flows through poorly ventilated zones, drastically increasing physiological dead space and preventing $\text{CO}_2$ clearance.
2. The Haldane Effect: Oxygenation of deoxygenated haemoglobin reduces its affinity for carbon dioxide. As haemoglobin becomes saturated with oxygen in capillary beds, bound $\text{CO}_2$ is rapidly unloaded into plasma, sharply elevating arterial $\text{PaCO}_2$.
3. Blunting of Hypoxic Ventilatory Drive: Suppressing the peripheral hypoxic drive reduces minute ventilation and respiratory rate, further diminishing alveolar $\text{CO}_2$ excretion.

Target Saturation & Controlled Delivery Devices

• Target $\text{SpO}_2$ Range: 88% to 92% for all patients at risk of hypercapnic respiratory failure.
• Delivery Equipment:
  • Venturi Masks (High-flow fixed performance): Start with a 24% (blue) or 28% (white) Venturi valve operating at manufacturer-specified flow rates (typically 2–4 L/min for 24%, 4 L/min for 28%). Venturi masks provide a constant, reliable fraction of inspired oxygen ($\text{FiO}_2$) regardless of the patient's respiratory rate or tidal volume.
  • Nasal Cannulae: 1 to 2 L/min, titrated carefully based on serial arterial blood gases (ABGs).
• Safety Mandate: Never withhold oxygen from a severely hypoxaemic patient ($\text{SpO}_2 < 85%$) out of fear of hypercapnia. Administer titrated oxygen immediately to achieve $\text{SpO}_2 \ge 88%$ and check an ABG within 30–60 minutes.

The COPD Patient on the INEWS Chart

This is a point overseas nurses regularly get wrong, because the UK and Irish charts differ.

INEWS Version 2 has a single SpO2 row. There is no Scale 1 / Scale 2 system on the Irish chart - that belongs to the UK NEWS2 chart. On INEWS V2, SpO2 is scored as: 96% or above = 0; 94-95% = 1; 92-93% = 2; 91% or below = 3. Any supplemental oxygen separately scores 2 on the inspired oxygen row.

The practical consequence: a COPD patient whose stable baseline saturation is 89% on 1 L/min will score 3 for SpO2 plus 2 for oxygen every single time observations are taken, and there is no alternative scale to move them onto.

The correct route is a modified escalation and response protocol, not a second scale. Under NCEC National Clinical Guideline No. 1:

• the escalation and response protocol must not be modified within the first 24 hours following admission;
• after 24 hours, only a Registrar or Consultant may document a modified INEWS Escalation and Response Protocol on the observation chart, recording the rationale, the altered response and a review timeframe;
• the modified protocol must be reviewed at least every 24 hours;
• the nurse continues to record true observed values and the true calculated score - what changes is the documented response, never the numbers.

The 88-92% target itself remains entirely valid: it is an oxygen prescription for a patient at risk of hypercapnic respiratory failure, written in the medication record, and it is what you titrate to. It is simply not an INEWS scale.

[!CAUTION] Over-oxygenation still needs to be caught, and on the Irish chart it is caught by the nurse, not by the scoring grid. If a patient prescribed a target of 88-92% is sitting at 98% on 4 L/min, the INEWS score may look reassuring while the patient drifts into hypercapnia. Reduce the oxygen to the prescribed target, check an arterial blood gas, and document.

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Pharmacotherapy for AECOPD

1. Nebulised Bronchodilators:
   • Short-Acting Beta-2 Agonist (SABA): Salbutamol 2.5 mg to 5 mg.
   • Short-Acting Muscarinic Antagonist (SAMA): Ipratropium bromide 500 mcg.
   • Administered combined every 4–6 hours, or more frequently in severe distress.
2. CRITICAL NURSING RULE: Air-Driven Nebulisers:
   • In COPD patients at risk of hypercapnia, nebuliser chambers MUST BE DRIVEN BY COMPRESSED MEDICAL AIR (at 6–8 L/min), never by high-flow oxygen.
   • Driving a nebuliser with 8–10 L/min oxygen delivers an uncontrolled $\text{FiO}_2$ of $60% - 80%$ for 15 minutes, which can precipitate acute hypercapnic coma.
   • If the patient is hypoxaemic, administer concurrent oxygen via nasal prongs at 1–2 L/min underneath the air-driven nebuliser mask to maintain $\text{SpO}_2$ at 88–92%.
   • If medical air is unavailable, limit oxygen-driven nebulisation to a maximum flow of 6 L/min for a maximum of 10 to 15 minutes, then revert immediately to controlled Venturi oxygen.
3. Systemic Corticosteroids:
   • Oral Prednisolone 30 mg daily for 5 days (per HSE and GOLD guidelines). Short courses improve $\text{FEV}_1$, accelerate symptomatic recovery, reduce hospital length of stay, and prevent early relapse without requiring a prolonged tapering schedule.
   • If the patient cannot tolerate oral intake, administer IV Hydrocortisone 100 mg 6-hourly.
4. Antimicrobial Therapy:
   • Indicated if sputum is purulent (Anthonisen Type 1 or Type 2 with purulence) or if the patient requires mechanical ventilation.
   • First-line oral empiric agents per Irish HSE community/hospital guidelines: Amoxicillin 500 mg TDS, or Doxycycline 200 mg stat then 100 mg OD, or Co-amoxiclav 625 mg TDS for 5 days.

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Non-Invasive Ventilation (NIV / BiPAP)

Non-Invasive Ventilation delivered as Bilevel Positive Airway Pressure (BiPAP) is the evidence-based standard of care for acute hypercapnic respiratory failure in COPD.

Clinical Indications

NIV is indicated when acute Type 2 respiratory failure persists despite at least 1 hour of optimal medical management (controlled oxygen, nebulised bronchodilators, systemic steroids): $\text{Arterial pH} < 7.35 \quad \text{AND} \quad \text{PaCO}_2 > 6.0\text{ kPa (45 mmHg)}$

Operational Parameters & Settings

• Inspiratory Positive Airway Pressure (IPAP): Initiated at 10–12 $\text{cmH}_2\text{O}$ and rapidly titrated in increments of 2–3 $\text{cmH}_2\text{O}$ up to 16–20 $\text{cmH}_2\text{O}$. IPAP unloads fatigued inspiratory muscles, increases tidal volume, and washes out retained carbon dioxide.
• Expiratory Positive Airway Pressure (EPAP): Set at 4–5 $\text{cmH}_2\text{O}$. EPAP maintains alveolar patency at end-expiration, recruits collapsed lung units, and counters intrinsic positive end-expiratory pressure (intrinsic PEEP / auto-PEEP).
• Repeat ABG Schedule: An arterial blood gas must be taken 1 hour after initiating NIV, and 1 hour after any major pressure change, to ensure correction of acidaemia and reduction of $\text{PaCO}_2$.

Contraindications to NIV

• Facial trauma, severe burns, or anatomical deformity preventing an airtight mask seal
• Fixed upper airway obstruction
• Active vomiting, severe haematemesis, or high aspiration risk
• Undrained tension pneumothorax
• Severe hemodynamic instability (uncontrolled shock, life-threatening arrhythmias)
• Inability to clear copious respiratory secretions
• Impaired consciousness with a Glasgow Coma Scale (GCS) score $< 8$ (unless hypercapnic coma where a closely supervised trial in an HDU/ICU setting is initiated).

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Acute Severe Asthma

Asthma is a chronic inflammatory disorder of the conducting airways characterized by bronchial hyperresponsiveness, reversible bronchospasm, mucosal edema, and tenacious mucus hypersecretion. Unlike COPD, airflow obstruction in asthma is predominantly reversible, either spontaneously or following bronchodilator therapy.

Severity Stratification in Acute Asthma

The British Thoracic Society (BTS) and Scottish Intercollegiate Guidelines Network (SIGN) guidelines, adopted throughout Irish clinical practice, stratify acute asthma exacerbations into distinct clinical categories:

[!CAUTION] The "Normal" PaCO2 Alarm: In acute asthma, intense tachypnoea initially blows off carbon dioxide, producing a respiratory alkalosis ($\text{PaCO}_2 < 4.7\text{ kPa}$). If an ABG shows a "normal" $\text{PaCO}_2$ (4.7–6.0 kPa) in a severely breathless asthmatic, this is NOT a sign of stability—it signifies that the patient's respiratory muscles are exhausted and ventilatory failure is imminent. This is a medical emergency requiring immediate ICU notification.

Emergency Management of Acute Severe & Life-Threatening Asthma

1. High-Flow Oxygen: Administer high concentrations of oxygen via a non-rebreather reservoir mask at 10–15 L/min, targeting an oxygen saturation of 94% to 98%. Asthmatic patients do not have chronic hypercapnia and are not at risk of oxygen-induced hypoventilation.
2. Nebulised Bronchodilators:
   • Salbutamol 5 mg nebulised back-to-back (every 15–20 minutes, or continuously in life-threatening collapse).
   • Combine with Ipratropium bromide 500 mcg every 4–6 hours.
   • CRITICAL DIFFERENCE FROM COPD: Asthma nebulisers MUST BE DRIVEN BY HIGH-FLOW OXYGEN (6–8 L/min).
3. Systemic Corticosteroids:
   • Oral Prednisolone 40 mg to 50 mg daily for at least 5 days, or IV Hydrocortisone 100 mg to 200 mg 6-hourly.
   • Early systemic corticosteroid administration reduces hospital admissions, halts inflammatory edema, and upregulates beta-2 receptor responsiveness.
4. Intravenous Magnesium Sulphate:
   • Indicated for acute severe asthma with poor initial bronchodilator response or any life-threatening features.
   • Dose: 1.2 g to 2.0 g IV infusion in 100 mL 0.9% Sodium Chloride over 20 minutes.
   • Mechanism: Competes with calcium at voltage-gated channels, producing potent bronchial smooth muscle relaxation.
5. Emergency Escalation (Medical Emergency Team / Dial 2222):
   • If the patient displays a silent chest, bradycardia, confusion, exhaustion, or rising $\text{PaCO}_2$, immediately dial 2222 for the resuscitation team, summon the intensive care team, and prepare for rapid sequence intubation (RSI).

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Pneumonia: Community-Acquired vs Hospital-Acquired

Pneumonia is an acute infection of the pulmonary parenchyma resulting in alveolar exudative consolidation. In hospital practice, distinguishing between community and hospital acquisition dictates empiric antimicrobial coverage:

• Community-Acquired Pneumonia (CAP): Acquired outside of a healthcare facility, or diagnosed within $< 48$ hours of hospital admission. Most common organisms: Streptococcus pneumoniae (classic pneumococcus), Mycoplasma pneumoniae, Chlamydia pneumoniae, Haemophilus influenzae, and respiratory viruses.
• Hospital-Acquired Pneumonia (HAP): Develops $\ge 48$ hours after hospital admission, not incubating at the time of admission. Pathogens are frequently multidrug-resistant and hospital-associated: Pseudomonas aeruginosa, Klebsiella pneumoniae, Escherichia coli, Enterobacter, and Methicillin-Resistant Staphylococcus aureus (MRSA).

CURB-65 Severity Scoring Matrix

The CURB-65 score is a validated clinical prediction rule endorsed by the British Thoracic Society and Irish National Clinical Programmes to evaluate 30-day mortality risk in CAP:

Clinical Stratification & Management Pathway

+-----------------------------------------------------------------------------+
|                        CURB-65 MANAGEMENT PATHWAY                           |
+-------------------+--------------------+------------------------------------+
| Total Score       | 30-Day Mortality   | Recommended Care Disposition       |
+-------------------+--------------------+------------------------------------+
| Score 0 or 1      | Low (< 3%)         | Suitable for outpatient treatment   |
|                   |                    | with oral antibiotics (e.g. amox)  |
+-------------------+--------------------+------------------------------------+
| Score 2           | Intermediate (~9%) | Inpatient hospital admission       |
|                   |                    | Short-stay ward or medical ward    |
+-------------------+--------------------+------------------------------------+
| Score 3 to 5      | High (15% - 40%)   | Urgent inpatient hospital admission|
|                   |                    | Senior medical review; assess for  |
|                   |                    | HDU or ICU level monitoring        |
+-------------------+--------------------+------------------------------------+

Key Nursing Interventions in Pneumonia

1. Diagnostic Microbiology Before Antimicrobial Administration:
   • Obtain a deep-cough sputum specimen for Gram stain and culture.
   • Collect two sets of blood cultures from distinct venepuncture sites using strict aseptic non-touch technique (ANTT) before giving antibiotics.
   • Obtain urine for Pneumococcal and Legionella urinary antigen testing in moderate-to-severe disease.
2. Timely Antimicrobial Administration:
   • Administer empiric intravenous antimicrobials within 4 hours of diagnosis in general admissions.
   • If the patient exhibits clinical signs of severe sepsis or septic shock (INEWS red trigger), administer the first dose of IV antibiotics within the "Golden Hour" (within 60 minutes).
3. Respiratory Support & Hydration:
   • Oxygen therapy titrated to target saturation ($\ge 94%$ in general patients; 88–92% in patients with known COPD).
   • Administer IV crystalloid fluids (e.g., Hartmann's solution or 0.9% NaCl) to replace insensible fluid losses and maintain hydration, which thins viscous bronchial secretions.
4. Chest Physiotherapy & Early Mobilization:
   • Position in high-Fowler's to optimize diaphragmatic excursion. Encourage active cycle of breathing techniques (ACBT) and early ambulation.
   • Administer prescribed analgesia (e.g., paracetamol) to relieve pleuritic chest pain, allowing effective deep breathing and productive coughing without splinting.

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Clinical Traps & Safety Pearls

• Trap 1: Driving COPD Nebulisers with Oxygen. Never connect a COPD patient's nebuliser to an oxygen flowmeter unless medical air is completely absent. Uncontrolled oxygen exposure during nebulisation remains a leading cause of ward-based hypercapnic respiratory arrest.
• Trap 2: Relying on Wheezing in Severe Asthma. The disappearance of wheezing in an asthmatic patient who remains severely breathless is an ominous warning of a "silent chest", representing severe airflow obstruction and impending respiratory arrest.
• Trap 3: Withholding Oxygen in Severe Hypoxaemia. If a COPD patient presents with profound cyanosis and $\text{SpO}_2 < 80%$, do not withhold oxygen while searching for a Venturi mask. Administer oxygen immediately, titrate to 88–92% as soon as equipment is assembled, and obtain an emergency ABG.
• Trap 4: Delaying Antibiotics for Sputum Production. While obtaining sputum cultures prior to antibiotics is best practice, antibiotic administration must never be delayed if the patient is unable to expectorate immediately.