COPD is a chronic lung condition with ongoing respiratory symptoms (dyspnea, cough, sputum) caused by airway and/or alveolar abnormalities, producing persistent airflow obstruction that is not fully reversible and often progressive. Two processes overlap in most clients:

"Blue bloater" and "pink puffer" are traditional terms; most clients show features of both.

Key mechanism — air trapping. Narrowed airways and lost elastic recoil make exhalation difficult. Air stays in the lungs, causing hyperinflation, a flattened diaphragm, and increased work of breathing. Ventilation–perfusion (V/Q) mismatch causes hypoxemia; in advanced disease, alveolar hypoventilation also causes hypercapnia (CO₂ retention) and chronic respiratory acidosis with renal compensation (raised HCO₃⁻).

Risk factors

• Tobacco smoking — the leading cause; smoking cessation is the single most effective intervention to slow progression
• Secondhand smoke, occupational dusts and chemicals, indoor air pollution from biomass fuel
• Alpha-1 antitrypsin deficiency — genetic; suspect in early-onset emphysema or in non-smokers
• History of asthma, childhood respiratory infections, aging

COPD vs. asthma: asthma airflow limitation is largely reversible with bronchodilators; COPD limitation is persistent.

Long-term consequence: chronic hypoxemia → pulmonary vasoconstriction → pulmonary hypertension → right-sided heart failure (cor pulmonale). Chronic hypoxemia also stimulates secondary polycythemia.

Subjective

• Progressive dyspnea, first on exertion, later at rest
• Chronic cough, with or without sputum
• Fatigue, reduced activity tolerance, weight loss (emphysema)
• Frequent respiratory infections

Objective

• Use of accessory muscles (sternocleidomastoid, scalene), tripod position
• Pursed-lip breathing, prolonged expiratory phase
• Barrel chest (increased anteroposterior diameter)
• Diminished breath sounds (emphysema); wheezes or coarse crackles may be present with bronchospasm or secretions
• Hyperresonance on percussion
• Cyanosis, clubbing (late)
• Signs of cor pulmonale: jugular venous distension, peripheral edema, hepatomegaly

*GOLD grades describe airflow limitation only. Treatment decisions use symptoms and exacerbation history (GOLD groups):

ABG interpretation (common exam pattern)

pH 7.28, PaCO₂ 65 mmHg, HCO₃⁻ 30 mEq/L → pH is acidotic and PaCO₂ is elevated = respiratory acidosis. HCO₃⁻ is rising but pH has not returned to the normal range = partially compensated. (A normal pH would mean fully compensated; a normal HCO₃⁻ would mean uncompensated.)

Stable COPD

• Smoking cessation — counseling plus pharmacotherapy
• Bronchodilators (mainstay)
  • Short-acting: SABA (albuterol), SAMA (ipratropium) — for symptom relief
  • Long-acting: LABA (e.g., salmeterol, formoterol), LAMA (e.g., tiotropium)
  • Group A: a bronchodilator (short- or long-acting)
  • Groups B and E: LABA + LAMA is the default initial therapy
• Inhaled corticosteroids (ICS) — for exacerbation-prone clients (group E), especially with blood eosinophils ≥ 300 cells/µL, given as LABA + LAMA + ICS (triple therapy). ICS is never used alone in COPD and increases the risk of pneumonia
• Persistent exacerbations despite triple therapy with high eosinophils: a biologic (e.g., dupilumab, mepolizumab) may be added
• Pulmonary rehabilitation — exercise training, education, breathing techniques
• Vaccinations — influenza, pneumococcal, COVID-19, RSV, and others per national schedule
• Long-term oxygen therapy (LTOT) — for severe resting hypoxemia: PaO₂ ≤ 55 mmHg or SaO₂ ≤ 88%, or PaO₂ 55–60 mmHg with pulmonary hypertension, cor pulmonale/edema, or polycythemia (Hct > 55%). Used ≥ 15 hours/day; improves survival. Reassess oxygen need 60–90 days after starting
• Advanced disease: noninvasive ventilation for chronic hypercapnia, lung volume reduction, transplant, palliative care

Acute exacerbation (acute worsening of dyspnea, cough, or sputum)

• Short-acting inhaled bronchodilators first (SABA with or without SAMA)
• Systemic corticosteroids — short course (5 days)
• Antibiotics (usually 5–7 days) when all three cardinal symptoms are present (↑dyspnea, ↑sputum volume, ↑sputum purulence), when two are present and one is purulence, or when ventilatory support is needed
• Controlled oxygen titrated to SpO₂ 88–92%
• Noninvasive positive-pressure ventilation (NIV) for acute hypercapnic respiratory acidosis; intubation if NIV fails

Listed in priority order.

1. Airway and breathing
   • Position upright: high-Fowler's or tripod (leaning forward) to lower the diaphragm and use accessory muscles
   • Monitor respiratory rate, work of breathing, SpO₂, mental status
   • Oxygen: titrate to SpO₂ 88–92% using low-flow nasal cannula or a Venturi mask for precise FiO₂. Never withhold oxygen from a hypoxemic client.
   • Watch for CO₂ narcosis: headache, drowsiness, confusion, decreased respiratory rate. Obtain ABG and notify the provider
   • Avoid sedatives, hypnotics, and opioids unless ordered and closely monitored — they depress respiration and worsen CO₂ retention
2. Breathing techniques
   • Pursed-lip breathing: inhale through the nose, exhale slowly through pursed lips (exhalation about twice as long as inhalation). This keeps airways open, reduces air trapping, and slows the breathing rate
   • Diaphragmatic (abdominal) breathing to improve efficiency
3. Secretion clearance
   • Adequate fluid intake (unless restricted, e.g., with cor pulmonale or heart failure)
   • Huff (controlled) coughing, chest physiotherapy as ordered, suction if needed
4. Medication administration
   • Give bronchodilators before corticosteroid inhalers when both are scheduled
   • Beta₂-agonists: tachycardia, palpitations, tremor, hypokalemia
   • Anticholinergics: dry mouth, urinary retention; use caution with narrow-angle glaucoma and prostatic hyperplasia; keep spray out of the eyes
5. Activity and energy conservation
   • Plan rest periods, pace activities, avoid prolonged bed rest
   • Encourage participation in pulmonary rehabilitation
6. Nutrition
   • Small, frequent, high-calorie, high-protein meals
   • Rest before meals; use oxygen during meals if prescribed
   • Drink fluids between meals rather than with meals to avoid early fullness
   • Avoid gas-forming foods; limit excess carbohydrates, which increase CO₂ production
7. Infection prevention and psychosocial support — anxiety worsens dyspnea; teach relaxation and stay with the client during dyspnea episodes

• Stop smoking and avoid secondhand smoke, dust, and air pollution
• Inhaler technique — know which device you have
  • Metered-dose inhaler (MDI): shake, exhale fully, seal lips, start a slow, deep breath and press the canister at the same time; hold the breath for up to 10 seconds; for a quick-relief bronchodilator, NAEPP advises about 15–30 seconds between puffs (no wait for other medicines), while many leaflets (e.g., albuterol HFA) say about 1 minute and shake again, so follow the leaflet or prescriber; use a spacer if prescribed
  • Dry-powder inhaler (DPI): do not shake; exhale away from the device (never into it); seal lips and inhale quickly and forcefully; no spacer
  • Rinse the mouth after inhaled corticosteroids to prevent oral candidiasis
• Practice pursed-lip and diaphragmatic breathing daily
• Oxygen safety: no smoking; keep oxygen at least 10 ft (3 m) from open flames and heat sources; use water-based lubricant, not petroleum-based products, on lips and nostrils; use the prescribed flow rate only
• Stay up to date on vaccinations (influenza, pneumococcal, COVID-19, RSV as recommended in your country) — respiratory infections are a major trigger of exacerbations
• Recognize early exacerbation signs: increased dyspnea, change in sputum color or amount, fever — follow the action plan and contact the provider early
• Maintain nutrition and a healthy weight; stay active within tolerance

Call the provider immediately for decreasing level of consciousness, respiratory rate falling while the client appears exhausted, or SpO₂ that cannot be maintained in the target range.

• COPD = persistent, not fully reversible airflow limitation; smoking is the major preventable cause
• Diagnosis: post-bronchodilator FEV₁/FVC < 0.70
• Typical signs: accessory muscle use, barrel chest, diminished breath sounds, prolonged expiration, pursed-lip breathing
• Oxygen target SpO₂ 88–92%, titrated — but never withhold oxygen from a hypoxemic client
• ABG in chronic COPD: respiratory acidosis with metabolic (renal) compensation
• Exacerbation: short-acting inhaled bronchodilators first, then systemic steroids, antibiotics if indicated
• Pursed-lip breathing prevents airway collapse and reduces air trapping
• Rest before meals; small, frequent, high-calorie, high-protein meals
• GOLD group E = ≥ 1 moderate or severe exacerbation in the past year; LABA + LAMA is the default maintenance therapy; ICS never alone
• MDI: slow deep breath; DPI: fast forceful breath, no shaking
• Rinse mouth after inhaled corticosteroids
• Avoid sedatives and opioids unless ordered — risk of CO₂ retention
• Vaccinations (influenza, pneumococcal, COVID-19, RSV) reduce exacerbations and hospitalization