Chronic Obstructive pulmonary disease Yuqi Zhou, M.D & Ph.D Pulmonary Medicine 3rd Affiliated Hospital of Sun-Yat Set University
Prevention and prognosis
Chronic Obstructive Pulmonary Disease (COPD) is a disease state characterized by the presence of airflow obstruction due to chronic bronchitis or emphysema ; the airflow obstructive is generally progressive, may be accompanied by airway hyperreactivity, and may be partially reversible.
Chronic Bronchitis (CB) is a clinical diagnosis defined by excessive secretion of bronchial mucus and is manifested by daily productive cough for 3 months or more in at least 2 consecutive years.
Emphysema is a pathologic diagnosis that denotes abnormal permanent enlargement of air spaces distal to the terminal bronchiole, with destruction of their walls and without obvious fibrosis.
Fig 1 . Venn diagram illustrating the overlap between the diagnosis of chronic bronchilitis, emphysema and asthma,and their contribution to COPD.
Unite States, 14 million diagnosed, equal number undiagnosed.
The 4th leading cause of death in the U.S.
120,000 deaths reported annually, the death rate from COPD is increasing rapidly.
Annual cost up to $31.9 billion in U.S.
To 2020, COPD will become the fifth cause of disease economic burden in the world.
Most important one. Dose -and duration-dependent decline of lung function. 15% develop disabling symptoms in their 40s and 50s. 80%, expose to tobacco smoke.
Environmental tobacco smoke, occupational dusts and chemicals, indoor air pollution from biomass fuel.
Outdoor air pollution, airway infection, familial factors, allergy.
Hereditary factors ( deficiency of α1-antiprotease )
Pathogenesis of Emphysema
Lung neutrophils, macrophages, mononuclear cells -> elastase and other proteases -> Excessive lysis of elastin and other structural proteins in the lung matrix.
Nonspecific airway stimuli -> Atopy and the tendency for bronchoconstriction
Chronic Bronchitis Emphysema Bronchiolitis Small airways disease
Symptoms and signs
Present in the fifth or sixth decade of life and usually for 10 years or more
Shortness of breath
Dyspnea on exertion; at rest.
Frequent exacerbations of illness. “Hallmark”
Early course :Absent symptoms; The late stage of COPD: Pneumonia, pulmonary hypertension, cor pulmonale, chronic respiratory failure.
Death : occurs during an exacerbation.
Two symptom patterns Decreased minute ventilation Increased minute ventilation Exercise ventilation Severe oxygen desaturation, without OSA. Mild to moderate oxygen desaturation, with OSA. Nocturnal ventilation Cardiac output normal. PAP ↑ ↑ Cardiac output normal to slightly low. PAP ↑ Hemodynamics Increased perfusion to low V/Q areas Increased ventilation to high V/Q areas Special evaluations V/Q matching Total lung capacity normal or ↑ DLco normal, Static lung compliance normal Total lung capacity ↑ DLco reduced, Static lung compliance ↑ Pulmonary function tests Elevated hemoglobin. PaO 2 ↓PaCO 2 ac↑,X-ray, increased interstitial markings (“dirty lung”) Normal hemoglobin. PaO 2 ↓PaCO 2 ac↓,X-ray, hyperinflation. Laboratory studies Chronic cough, purulent sputum, overweight, peripheral edema. Age 30-40y Dyspnea, mucoid sputum, thin, chest is quiet. Age 50y History and physical examination Blue bloaters Pink puffers
Patient with emphysema
Provide objective information about pulmonary function.
Assess the results of therapy.
Early course: abnormal closing volume, reduced midexpiratory flow rate.
Later: FEV1 and FEV1/FVC reduction.
Severe case: RV ↑TLC↑, RV/TLC ↑ indicate air trapping.
Occurs in patients with COPD
Results in an increase in the work of breathing
Places respiratory muscles at a mechanical disadvantage
Contributes to the sensation of breathlessness (dyspnea)
Images courtesy of Denis O’Donnell, Queen’s University, Kingston, Canada
Spirometry: Normal and COPD
Pulmonary function tests ---Static lung volumes in a normal subject(A) and a patient with COPD
Arterial Blood Gas
Early: No abnormal
It should be measured when:
(1)Hypoxemia or hypercapnia is suspected
(2)FEV1 is <40% of predicted
(3)Right heart failure.
Chronic bronchitis can cause hypoxemia and compensated respiratory acidemia
Examination of the sputum
Smear and culture.
Pathogens including Streptococcus pneumonia, Haemophilus influenzae, Moraxella catarrhalis.
Tachycardia, typical abnormalities of cor pulmonale. Supraventricular arrhythmias and ventricular irritability
Streptococcus pneumoniae Haemophilus Influenza
Chronic bronchitis: Nonspecific peribronchial and perivascular marking.
Emphysema: 50% cases, hyperinflation with flattening of the diaphragm or peripheral arterial efficiency. Parenchymal bullae in the setting.
Pulmonary hypertension: enlargement of central pulmonary arteries. Doppler echocardiography.
Chest X-ray film
Bronchial asthma (see table 1)
Table 1 Points that differentiate asthma from COPD COPD Asthma History Smoker or ex-smoker Nearly all Possibly Symptoms under age 45 Uncommon Often Chronic productive cough Common Uncommon Breathlessness Persistent and progressive Variable Winter bronchitis Common Uncommon Investigations Serial PEF Obstructive picture May be normal Day to day and diurnal variation Reversibility testing Minimal variation Usually<15% or 200ml change Usually>15% or 200ml change
Recurrent pneumonia and hemoptysis, digital clubbing, radiographic abnormalities.
Severe α1-antiprotease deficiency:
Appearance of panacinar, bibasilar emphysema early in life, usually in the third or fourth decade, hepatic cirrhosis and hepatocellular carcinoma may occur.
Occurs in children and younger adults.
Central airway obstruction
Flow-volume loops may help.
Pulmonary hypertension, cor pulmonale, chronic respiratory failure are common.
Spontaneous pneumothorax occurs in a small fraction of patients.
Precipitating factors should be sought.
Left ventricular failure is important.
The empirical therapy with a diuretic is appropriate.
Follow the standards in GOLD.
The most important intervention in patients with COPD.
Simply telling : succeed 5%
Intervention group: Up to 22% at 5 years.
(behavior modification, drugs)
5 “R” strategy
Supplemental oxygen can alter the natural history of COPD with hypoxemia.
Benefits: longer survival,
reduced hospitalization need,
better quality of life.
flow rate 1-3L/min, duration time:15h/d
PaO 2 greater than 55mmHg.
Table 2 Home oxygen therapy Group Ⅱ PaO 2 =56-59mmHg or S aO 2 =89% if there is evidence of any of the following 1.Dependent edema suggesting congestive heart failure 2.Pulmonary on ECG (P wave >3 mm in standard lead Ⅱ,Ⅲ, or aVF) 3.Hematocrit >56% Group Ⅰ(any of following) 1. PaO 2 ≤55mmHg or S aO 2 ≤88% taken at rest breathing room air, while awake. 2.During sleep (prescription for nocturnal oxygen use only) (1) PaO 2 ≤55mmHg or S aO 2 ≤88% for a patient whose awake ,resting, room air PaO 2 is ≥56mmHg or S aO 2 ≥89% or (2)Decrease in PaO 2 >56mmHg or decrease in S aO 2 >5% associated with symptoms or signs reasonably attributed to hypoxemia(e.g.,impaired cognitive processes,nocturnal restlessness, insomnia) 3.During exercise (prescription for oxygen use only during exercise) (1) PaO 2 ≤55mmHg or S aO 2 ≤88% taken during exercise for a patient whose awake ,resting, room air PaO 2 is ≥56mmHg or S aO 2 ≥89% and (2) There is evidence that the use of supplemental oxygen during exercise improves the hypoxemia that was demonstrated during exercise while breathing room air.
The most important agents.
Offer improvement in symptoms, exercise tolerance, and overall health status.
Two Anticholinergic ipratropium bromide
2-4 puffs (36-72ug) every 6 hours, longer duration and less side effects.
Short-acting β 2 -agonists (albuterol)
less expensive and more rapid onset of action, more side effects.
Delivered : MDI or nebulizer. As needed.
Combination use is recommended.
Long-acting β 2 -agonists (formoterol, salmeteral) and anticholinergics (tiotropium) appear to achieve superior bronchodilation.
Oral theophylline is a third-line agent in COPD.
Sustained-release theophylline improves arterial oxygen hemoglobin saturation during sleep.
Empirical use : Oral: 0.5mg/kg/d prednisone for 14-21 days
Inhaled: 6-12 weeks therapy
Principles: the baseline FEV1 should be stable and documented on maximal bronchodilator therapy.
If there is no a 20% or greater increase in FEV1, stop the therapy.
Reduction of frequency of AECOPD and increase in self-reported functional status are small and occur with long-term, high-dose inhaled therapy.
(1)To treat an acute exacerbation;
(2)To treat acute bronchitis;
(3) To prevent acute exacerbations of chronic bronchitis (prophylactic antibiotics).
Patients with dyspnea and a change in the quantity or character of sputum benefit the most.
Common agents: Trimethoprim-sulfamethoxazole ,amoxicillin or amoxicillin-clavulanate or doxycycline given for 7-10 days .
Broader spectrum therapy ----severe cases.
(1) Adequate systemic hydration
(2) Effective cough training methods
(3) Use of a handheld flutter device and postural drainage, sometimes with chest percussion or vibration.
(4)Expectorant –mucolytic therapy unhelpful
(5) Cough suppressants and sedatives avoided
(6) Human α1-antitrypsin replacement therapy 60mg/kg once weekly.
Grade aerobic physical exercise program
Help to prevent deterioration of physical condition
Improve the patients ability to carry out daily activities.
Methods: walking 20 minutes three times weekly
Training of inspiratory muscles.
Pursed-lip breathing to slow the rate of breathing
Abdominal breathing exercises to relieve fatigue of accessory muscles of respiratory.
Sed-active-hypnotic drugs ( For example diazepam, 5 mg three times daily) may help very anxious patients.
Intermittent negative-pressure ventilation , transnasal positive-pressure ventilation at home : to rest the respiratory muscles, improve their function, reduce dyspnea.
Bilevel transnasal ventilation system : reduce dyspnea.
Acute worsening of COPD who fails to respond to measures for ambulatory patients.
Patients with acute respiratory failure or complications.( cor pulmonale, pneumothorax)
Inhaled ipratropium bromide and inhaled β2-agonists
Chest physiotherapy (in selected cases)
Cor pulmonle : supplemental oxygen, correction of acidemia, bed rest, salt restriction, diuretics.
Cardiac arrhythmias: depend on treatments of COPD itself.
Respiratory failure: tracheal intubation and mechanical ventilation.
Hypercapnic acute respiratory failure: noninvasive positive-pressure ventilation (NPPV) may reduce the need of intubation and shortened ICU length of stay. Lower risk of infection and less antibiotic use.
Lung injury and ARDS
Surgery for COPD
Lung volume reduction surgery (LVRS or reduction pneumoplasty)
Surgery for COPD
Requirements for lung transplantation:
Severe lung disease;
Limited activities of daily living;
Exhaustion of medical therapy;
Potential for pulmonary rehabilitation,
Limited life expectancy without transplantation
Adequate function of other organ systems,
A good social support system.
2 –year survival rate : 75%; Lung function improved.