COPD
Michele Ritter, M.D.Argy Teaching Resident, Feb. 2007
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
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 COPDHighest mortality rate is in white men,
and the lowest is in hispanic women.
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:
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
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
DyspneaCough (usually worse in morning,
sputum production)WheezingCyanosisRight heart failureWeight loss, anorexia
Physical Exam
RR, HR, O2 saturationGen: Barrel-chest, accessory muscle
useCV: Quiet heart soundsResp: Decreased breath sounds,
wheezing, rhonchi, crackles
Labs
CBC: Hgb/HctABG: 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-rayBullae 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
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.
Treatment of COPD
Stages of COPDStage FEV1/
FVC 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
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