This document defines COPD as a disease characterized by airflow obstruction due to chronic bronchitis or emphysema. It affects 4-6% of white males and 1-3% of white females in the US. The two main types are emphysema, which causes permanent enlargement of airspaces, and chronic bronchitis, characterized by a cough with sputum. Smoking is the primary risk factor and causes an inflammatory response that destroys lung tissue over time. Symptoms include dyspnea, cough, and limited lung function is diagnosed through pulmonary testing. Treatment focuses on smoking cessation and bronchodilators while oxygen therapy can improve outcomes for severe cases.

1. COPD
Emphysema
Chronic Bronchitis

2. Definition
 A disease state characterized by the
presence of airflow obstruction due to
chronic bronchitis or emphysema; the
airflow obstruction is generally
progressive, may be accompanied by
airflow hyperactivity, and may be viewed
as partially reversible.
 Includes emphysema and chronic
bronchitis

3. Prevalence
 COPD occurs in 4-6% of white males,
and 1-3% of adult white females
 The 4th most common cause of death in
the United States
 14.2 million people in U.S. have COPD
 Highest mortality rate is in white men,
and the lowest is in hispanic women.

4. Types of COPD
 Emphysema
 Permanent and destructive enlargement of airspaces
distal to the terminal bronchioles without obvious fibrosis
and with loss of normal architecture
 Always involves clinically significant airflow limitation.
 “pink puffer”
 Chronic Bronchitis
 Presence of a cough productive of sputum not attributable
to other causes on most days for at least 3 months over 2
consecutive years
 May be present in the absence of airflow limitation.
 “blue bloater”

5. COPD

6. Pathogenesis of COPD
 Increased number of activated
polymorphonuclear cells and macrophages
produce elastases (such as human leukocyte
elastase), resulting in lung destruction.
 Increased oxidative stress caused by free
radicals in cigarette smoke, the oxidants
released by phagocytes, and
polymorphonuclear leukocytes all may lead to
apoptosis or necrosis of exposed cells

7. Pathogenesis of COPD (cont.)
 Emphysema
 3 morphologic patterns:
 Centricacinar:
 focal destruction limited to the
respiratory bronchioles and the
central portions of acinus
 associated with cigarette
smoking
 most severe in the upper lobes
 Panacinar:
 involves the entire alveolus
distal to the terminal bronchiole
 develops in patients with
homozygous alpha1-antitrypsin
(AAT) deficiency
 most severe in the lower lung
zones
 Distal acinar:
 Also called paraseptal
 least common form
 involves distal airway
structures, alveolar ducts, and
sacs
 localized to fibrous septa or to
the pleura and leads to
formation of bullae (can result
in pneumothorax)
 Chronic Bronchitis
 Mucus gland enlargement
 Airway atrophy, focal
squamous metaplasia, ciliary
abnormalities, variable
amounts of airway smooth
muscle hyperplasia,
inflammation, and bronchial
wall thickening
 Respiratory bronchioles
display a mononuclear
inflammatory process, lumen
occlusion by mucous plugging,
goblet cell metaplasia, smooth
muscle hyperplasia, and
distortion due to fibrosis
 Airway walls to deform and
narrow the airway lumen

10. Risk Factors
 SMOKING!
 48 million smokers in the U.S.
 3000 new people take up smoking daily
 Nearly all patients with symptomatic
COPD are current or former smokers
 10-20% of smokers will develop
symptomatic COPD.
 In men who smoke one pack/day, the
drop in FEV1 per year was 9 mL more
than in non-smokers
 Occupational Exposures
 Dusts, gases, fumes
 Alpha1-antitrypsin deficiency
 Alpha1-antitrypsin is an important
protease inhibitor that usually presents
elastases from causing lung
destruction

11. Symptoms
 Dyspnea
 Cough (usually worse in morning,
sputum production)
 Wheezing
 Cyanosis
 Right heart failure
 Weight loss, anorexia

12. Physical Exam
 RR, HR, O2 saturation
 Gen: Barrel-chest, accessory muscle
use
 CV: Quiet heart sounds
 Resp: Decreased breath sounds,
wheezing, rhonchi, crackles

13. Labs
 CBC:  Hgb/Hct
 ABG: pH, pCO2
 Chemistry: HCO3

14. Emphysema

15. Diagnosis of COPD
 Look for secondary polycythemia:
 Hct >52% in males, Hct>47% in females
 Measure alpha1-antitrypsin levels in all
patients 40 years or younger, or in those
with family history.
 Hyperinflation see on chest x-ray
 Bullae seen on Chest x-ray or CT scan

16. Pulmonary Function Tests

17. Diagnosis of COPD – Pulmonary
Function Tests
  Forced Expiratory Volume for 1 second
(FEV1)
 FEV1/FVC (Forced Vital Capacity) ratio
  Total Lung Capacity (TLC)
  Forced Residual Capacity (FRC)
  Residual Volume (RV)
  Vital Capacity (VC)

18. Pulmonary Function Tests

19. COPD Exacerbation
 Typically manifest as increased sputum production, more purulent
sputum and worsening of dyspnea.
 Although infectious etiologies account for most exacerbations, exposure
to allergens, pollutants or inhaled irritants may also play a role.
 Bacterial infection is a factor in 70 to 75 percent of exacerbations, with
up to 60 percent caused by
 Streptococcus pneumoniae
 Haemophilus influenzae
 Moraxella catarrhalis
 Antibiotic therapy has a small but important effect on clinical recovery and
outcome.
 Respiratory fluoroquinolone (Levofloxacin, Moxifloxacin)
 Ceftriaxone + azithromycin
 Short courses of systemic corticosteroids may provide important benefits
in patients with exacerbations of COPD.
 Oxygen therapy to keep saturation Between 90-93%
 Non-invasive ventilation such as BiPAP can be helpful in avoiding
intubation/mechanical ventilation.

20. Treatment of COPD
 SMOKING CESSATION!
 Short-acting bronchodilators
 albuterol
 Long-acting bronchodilator
 salmeterol
 Combination of anti-cholinergic and -agonist bronchodilator
 Ipratropium + albuterol (combivent)
 Tiotropium (spiriva)
 Methylxanthines (Theophylline)
 Has anti-inflammatory affect, and improves respiratory muscle function, stimulates
the respiratory center, and promotes bronchodilation
 Adverse effects include anxiety, tremors, insomnia, nausea, cardiac arrhythmia, and
seizures
 Inhaled corticosteroids
 Fluticasone (Flovent), budesonide (Pulmicort)
 Combination of Inhaled corticosteroid and long-acting -agonist
 Fluticasone + salmeterol (Advair)
 Oral Corticosteroids

21. Treatment of COPD (cont.)
 Oxygen Therapy
 Continous oxygen has been shown to cut mortality in half or
decrease morbidity when compared with non-continous
oxygen
 Continuous (24 hours/day)
 Resting Pa02 of 55 mm HG, or Resting oxygen saturation < 88%
 Resting Pa02 of 56-59 mmHg or Oxygen Sat. <89% in presence of
dependent edema (suggestive of CHF), P pulmonale on ECG (P
wave more than 3 mm in inferior leads) or cor pulmonale, or
erythrocytosis (Hct > 56)
 Noncontinuous
 During exercise – when PaO2 is < 55 mmHg or Oxygen sat. < 88%
with low level of exercise.
 During sleep if Pa02 is < 55 mmHg or Sa02 less than 88% with
associated complications such as pulmonary hypertension, daytime
somnolence, cardiac arrythmias.

22. Treatment of COPD (cont.)
 Pulmonary Rehabilitation
 Aimed at keeping patient conditioned with exercise,
perception of dyspnea, quality of life and self-efficacy.
 Surgery
 Bullectomy
 Resection of large bullae compressing normal lung
 Lung volume reduction surgery
 Pneumonectomy of nonuniform emphysematous lung
 Double lung transplantation
 Can be life-saving, but is costly, can be lack of donor
availability and requires lifelong immunosuppression.

23. Treatment of COPD

24. Stages of COPD
Stage FEV1/FV
C Ratio
FEV1
%
Clinical Findings
At Risk >0.7 Patients who smoke, patients exposed to
high pollutants, and patients with recurrent
respiratory symptoms/infections. Give
influenza and pneumonia vaccines.
Mild < 0.7 >80 Add short-acting bronchodilator as needed
Moderate <0.7 50-80 Add regular treatment with one or more
long-acting bronchodilator and add
Pulmonary rehabilitation
Severe <0.7 30-50 Add inhaled corticosteroids if repeated
exacerbations
Very
Severe
< 0.7 <30 Add long-term oxygen if chronic respiratory
failure; Consider surgical treatments

25. Take Home Points
 Smoking is the number one cause of
COPD!
 If smoking is stopped once COPD
diagnosed, the progression of disease
can slow down.
 Treat COPD exacerbations with
antibiotics and possibly with steroids.
 Continuous oxygen is shown to decrease
morbidity and mortality in COPD