Chronic Obstructive Pulmonary Disease

Clinical Orientation

A 68-year-old man with a 60-pack-year smoking history is admitted with worsening dyspnea, increased sputum production, and a change in sputum color to yellow-green. His baseline SpO2 is 88% on 2L. Today it is 82%. He is using pursed-lip breathing and has a barrel chest. This is a COPD exacerbation. This chapter answers: What mechanism links COPD to bedside findings, tests, red flags, and nursing priorities?

What Goes Wrong?

COPD = persistent airflow limitation that is not fully reversible. Two main pathologic processes:

Emphysema: Destruction of alveolar walls → loss of elastic recoil → airways collapse during expiration (dynamic airway collapse) → air trapping → hyperinflation. Also: loss of alveolar surface area for gas exchange. "Pink puffer" phenotype — thin, tachypneic, pursed-lip breathing, relatively preserved oxygenation, dyspnea-predominant.

Chronic bronchitis: Chronic inflammation of airways → mucosal thickening, increased mucus production, airway narrowing. Defined clinically: productive cough for ≥3 months/year for ≥2 consecutive years. "Blue bloater" phenotype — stockier, cyanotic, edema (from cor pulmonale), cough-predominant.

Most patients have a mix of both. The key pathophysiology: airflow obstruction → air trapping → hyperinflation → flattened diaphragm (mechanical disadvantage) → increased work of breathing → chronic CO2 retention → chronic compensatory metabolic alkalosis (elevated HCO3).

What the Nurse May See

• Inspection: Barrel chest (increased AP diameter from hyperinflation). Pursed-lip breathing (creates back-pressure to stent airways open during exhalation). Tripod position. Use of accessory muscles. Clubbing (chronic hypoxia).
• Auscultation: Decreased breath sounds (hyperinflation moves airways away from chest wall). Prolonged expiration. Wheezes, rhonchi.
• Percussion: Hyperresonance (air trapping).
• Signs of cor pulmonale: JVD, peripheral edema, hepatomegaly — right heart failure from chronic pulmonary hypertension.
• Exacerbation signs: Increased dyspnea, increased sputum volume/purulence, increased cough. May have fever, tachypnea, tachycardia.

ABG Interpretation in COPD

• Baseline (compensated): pH 7.35-7.38, PaCO2 elevated (50-65), HCO3 elevated (30-36). This is their "normal."
• Acute-on-chronic exacerbation: pH drops below 7.35, PaCO2 rises above baseline, HCO3 may not have risen further yet.
• Never try to "normalize" a COPD patient's PaCO2. It will cause severe metabolic alkalosis (from high HCO3) and respiratory depression.

Nursing Priorities

1. Controlled oxygen therapy: Target SpO2 88-92% (many COPD patients rely partly on hypoxic drive). High-flow O2 can suppress respiratory drive → worsening hypoventilation → rising PaCO2 → CO2 narcosis. Titrate O2 carefully. Monitor for somnolence and rising PaCO2.

1. Bronchodilators: Short-acting beta-agonists + anticholinergics (ipratropium) for exacerbations.

1. Corticosteroids: Systemic steroids for exacerbations — reduce inflammation and shorten recovery.

1. Antibiotics if indicated: Increased sputum purulence + increased dyspnea or sputum volume.

1. Noninvasive ventilation (BiPAP): First-line for acute hypercapnic respiratory failure in COPD. Reduces work of breathing, improves gas exchange, reduces need for intubation. Settings: IPAP (inspiratory support) and EPAP (expiratory — counteracts auto-PEEP).

1. Secretion management: Hydration, humidified O2, chest physiotherapy, effective coughing techniques (huff cough), suctioning if needed.

1. Monitor for CO2 narcosis: Rising PaCO2 + decreasing mental status → may need BiPAP escalation or intubation.

Oxygen Safety in COPD

Red Flags