Survival

• COPD


  Common, preventable, and treatable disease characterized by persistent respiratory symptoms and airflow limitations due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases
• COPD definition (practical)


  • Age >40 years
  • Significant exposure (10 pack-year smoking history, biomass exposure, certain occupations)
  • No prior diagnosis of asthma
  • Post bronchodilator FEV1/FVC ratio of <70
• COPD pathophysiology


  1. Increased # of mucus secreting goblet cells à more mucus secretion

  2. Lymphocytic infiltrate (CD8+)

  3. Ulceration of epithelial layer à squamous cell metaplasia with time

  4. Inflammation à scarring and thickening of walls à fibrosis à airflow limitation
• COPD risk factors


  • Smoking
  • Second-hand smoke
  • Alpha1 antitrypsin deficiency
  • Chronic asthma
  • Infections (often the precipitating cause of acute exacerbations)
• COPD diagnosis

  1. Pulmonary function tests (decreased FEV1 and FEV1/FVC ratio, post bronchodilator FEV1/FVC ratio of <70, decreased vital capacity, increased TLC, residual volume & FRC)

  • Significant reversibility after bronchodilator (200ml AND 12%) does NOT exclude COPD; some people may have variable reversibility)

  2. Chest x-ray (useful in severe advanced emphysema and acute exacerbations)

  3. ABG (hypercapnia, hypoxemia)

  4. Alpha 1 antitrypsin level (in patients with family history of premature emphysema)
• COPD types


  • Chronic bronchitis
  • Emphysema
• Chronic bronchitis


  Chronic productive (sputum) cough of at least 3 months per year for at least 2 consecutive years (clinical diagnosis)
• Emphysema


  Permanent enlargement of air spaces distal to terminal bronchioles due to destruction of alveolar walls (pathologic diagnosis)
• Chronic bronchitis pathogenesis


  1. Excess mucus production narrows the airways

  2. Inflammation & scarring in airways + enlarged mucus glands + SM hyperplasia à obstruction
• Emphysema pathogenesis


  1. Elastase enzyme released by PMNs and macrophages digests the human lung and is usually inhibited by alpha 1 antitrypsin

  2. Decrease in alpha 1 antitrypsin à alveolar wall destruction
• Chronic bronchitis and emphysema symptoms

  • Chronic cough
  • Sputum production (white or clear unless infected)
  • Dyspnea, wheeze
  • More prone to infections
• Chronic bronchitis signs

  • End-expiratory wheezing on auscultation, decreased breath sounds
  • Hyperresonance on percussion
  • Prolonged expiratory time
• Blue Bloaters


  • Usually overweight
  • Cyanosis
  • RR normal
  • Tachycardia
  • Signs of high CO2 (bounding pulse, peripheral vasodilation, course flapping tremor, confusion/drowsiness)
• Pink Puffers


  • Thin due to increased BMR
  • Barrel chest
  • Tachypnea
  • Breathing through pursed lips (to prevent alveolar and airway collapse)
  • Patient in distress with accessory muscle use
• COPD treatments


  • Smoking cessation (most important)
  • Home oxygen therapy (if pO2 ≤55 or saturation ≤88%)
  • Influenza and pneumococcal vaccinations
  • Inhaled bronchodilators (anticholinergics or B-agonists or combination)
  • Pulmonary rehabilitation
  • Surgery for selected patients (lung resection/transplantation)
• Inhaled corticosteroids + LAMA or LABA


  Treatment for frequent exacerbations, highly symptomatic, or eosinophils > 300
• LAMA


  Treatment if low exacerbation risk
• complications of COPD


  Complications:

  • Acute exacerbations (due to infections, non-compliance and cardiac problems)

  • Secondary polycythemia (as compensation for chronic hypoxemia)

  o RequiresvenesectionifHct>55%

  • Pulmonary HTN and cor pulmonale.

  • Respiratory failure