COPD

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

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

COPD

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

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:

Chronic Bronchitis

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)

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

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

Symptoms
Dyspnea
Cough (usually worse in morning, sputum

production)
Wheezing
Cyanosis
Right heart failure
Weight loss, anorexia

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

crackles

Labs
CBC: Hgb/Hct
ABG: pH, pCO2
Chemistry: HCO3

Emphysema

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

Pulmonary Function Tests

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)

Pulmonary Function Tests

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.

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

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.

Treatment of COPD (cont.)

Pulmonary Rehabilitation

Aimed at keeping patient conditioned with exercise, perception of

dyspnea, quality of life and self-efficacy.

Surgery

Bullectomy

Lung volume reduction surgery

Resection of large bullae compressing normal lung

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.

Treatment of COPD

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