Acute Exacerbation of COPD

Causes of Exacerbations

  • Infections: Most common cause, both viral (e.g., influenza) and bacterial (e.g., Haemophilus influenzae, Streptococcus pneumoniae).
  • Environmental factors: Air pollution, cold weather.
  • Other factors: Non-adherence to medications, comorbid conditions such as heart failure.

Signs and Symptoms of Exacerbation

  • Increased breathlessness, cough, and sputum production (often purulent).
  • Wheezing, chest tightness.
  • Increased use of rescue inhalers.
  • Cyanosis, confusion in severe cases due to hypoxia and hypercapnia.

Investigations in AECOPD

  • ABG: To assess oxygenation and carbon dioxide levels.
  • Chest X-ray: To rule out pneumonia or pneumothorax.
  • ECG: To assess for cardiac complications like arrhythmias or heart failure.
  • Blood tests: Full blood count, CRP, and blood cultures if infection is suspected.
  • Sputum culture: If infection is suspected.

Management of AECOPD

  • Bronchodilators: Increased doses of SABAs and SAMAs.
  • Systemic corticosteroids: Oral prednisolone (usually 30-40 mg for 5 days).
  • Antibiotics: If signs of bacterial infection are present.
  • Oxygen therapy: Aim for 88-92% saturation to prevent CO2 retention and worsening hypercapnia.

Oxygen Delivery and Non-invasive Ventilation

  • Controlled oxygen delivery (e.g., via Venturi mask) is essential to prevent over-oxygenation.
  • Non-invasive ventilation (NIV): Used in patients with hypercapnic respiratory failure or acidosis (pH < 7.35) despite controlled oxygen therapy. It helps reduce work of breathing and improves gas exchange.

Oxygen Targets

The traditional hypoxic drive theory suggested that COPD patients rely on low oxygen levels to stimulate breathing, and providing too much oxygen could suppress this drive. However, this theory has been largely disproven, and more accurate explanations for oxygen-induced hypercapnia include:

  1. Haldane Effect: When oxygen is administered, it displaces carbon dioxide (CO2) from haemoglobin. In COPD patients, who already have impaired gas exchange, this leads to an increase in CO2 in the blood, causing hypercapnia.
  2. Ventilation-Perfusion (V/Q) Mismatch: In COPD, there are regions of the lung where ventilation (air flow) and perfusion (blood flow) are not well matched. Supplemental oxygen improves oxygenation in areas with poor ventilation, but may also reduce vasoconstriction in poorly ventilated areas, causing blood to flow to these regions. This results in worsened V/Q mismatch, leading to an accumulation of CO2 in the bloodstream.

These mechanisms explain why oxygen therapy must be carefully titrated in COPD patients. The goal is to maintain oxygen saturations between 88-92%, to optimise oxygenation while avoiding worsening hypercapnia.