Transcript COPD in 2009

COPD in 2009
Perspective of
Respiratory Physicians
Ramesh Kaul, MD M. Surgery FCCP
Slide Copyright www.thorax.us Ramesh Kaul MD 2009
Speaker disclosure
• Presently Speaker for Astra Zeneca( Symbicort)
• Previous speaker for GlaxoSmithKline (Advair)
• Previous speaker for Boeringer Inghelheim
(Spiriva , Atrovent)
No funding was received from any Organization for this lecture at
36th Annual Western PSRC Seminar in Respiratory Care and Sleep
Medicine.
Information presented mostly from reading Chest, GOLD and AJRCCM
Slide Copyright www.thorax.us Ramesh Kaul MD 2009
WHY A NEW NAME COPD
• Classical picture is no more seen of Pink
Puffer of Emphysema
• Blue Bloater Of Chronic Bronchitis
• Early awareness by Providers of care
• Early Intervention
• Smoking Cessation
• Avoidance of Precipitating factors
Slide Copyright www.thorax.us Ramesh Kaul MD 2009
Epidemiology of COPD
• COPD is the 4th leading cause of death, and the 2nd
leading cause of disability in the U.S. And yet, COPD is
under-diagnosed and under-treated:
• About 24 million U.S. adults have evidence of impaired
lung function
• 12 million people have been diagnosed with COPD
• 5.8 million COPD patients are untreated
• The COPD death rate among women is increasing
REFERENCES
GOLD 2008 and American Thoracic Society
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Socioeconomic factors in COPD
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Poverty
Congested Living space
Lack of Education
Use of Biomass fuels, wood stoves
Inner City population has more prevalence
Stress of environment
Lack of funds for treatment in exacerbations
Malnourishment
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Pollution in COPD
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Second hand tobacco smoke
Wood, leaves and coal burning
Plastic and paper burning
Welding
Spraying of crops
Unclean air ducts with dust
Farming with exposure to animal excreta
Exposure to moldy hay, and gases in silos.
Spray painting
Fireworks fumes.
Animal fur, cat and dog dander
Gas fumes, diesel fumes and the list goes on and on
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Definition of COPD
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COPD: Definition World Health Organization
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Chronic obstructive pulmonary disease (COPD) is a lung disease characterized by
chronic obstruction of lung airflow that interferes with normal breathing and is not fully
reversible. The more familiar terms 'chronic bronchitis' and 'emphysema' are no
longer used, but are now included within the COPD diagnosis. COPD is not simply a
"smoker's cough" but an under-diagnosed, life-threatening lung disease.
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A COPD diagnosis is confirmed by a simple test called Spirometry, which measures
how deeply a person can breathe and how fast air can move into and out of the
lungs. Such a diagnosis should be considered in any patient who has symptoms of
cough, sputum production, or dyspnea (difficult or labored breathing), and/or a history
of exposure to risk factors for the disease. Where Spirometry is unavailable, the
diagnosis of COPD should be made using all available tools. Clinical symptoms and
signs, such as abnormal shortness of breath and increased forced expiratory time,
can be used to help with the diagnosis. A low peak flow is consistent with COPD, but
may not be specific to COPD because it can be caused by other lung diseases and
by poor performance during testing. Chronic cough and sputum production often
precede the development of airflow limitation by many years, although not all
individuals with cough and sputum production go on to develop COPD.
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Classification of Severity of
COPD
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Stage Characteristics
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Stage 0: At Risk • normal Spirometry • chronic symptoms (cough, sputum production)
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Stage I: Mild COPD • FEV1/FVC < 70%• FEV1 ≥ 80% predicted
with or without chronic symptoms (cough, sputum production)
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Stage II: Moderate COPD • FEV1/FVC < 70% • 50% ≤ FEV1 < 80% predicted
with or without chronic symptoms (cough, sputum production)
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Stage III: Severe COPD • FEV1/FVC < 70% • 30% ≤ FEV1 < 50% predicted
with or without chronic symptoms (cough, sputum production)
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Stage IV: Very Severe COPD • FEV1/FVC < 70%• FEV1 ≤ 30% predicted or FEV1 <
50% predicted plus chronic respiratory failure
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Ref GOLD Newletter AUG 8/29/03
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Differential Diagnosis of COPD
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COPD: older patient, smoker, irreversible , Dyspnea and cough. CD8 T Lymphocytes
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Macrophages and Neutrophils in sputum
Asthma: younger patients , allergic, reversible, IGE and RAST positive CD4 T
Lymphocytes
Eosinophils in airways and sputum.
Congestive Heart Failure: Dyspnea, Rales , large heart, ECHO and Chest XRAY
diagnostic
Pneumoconiosis: Occupational diseases, restriction and diffusion defect
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Obliterative Bronchiolitis: young, fumes, Rheumatoid Arthritis, Expiration CT
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shows hypo dense areas.
Bronciectasis: sputum in excess, crackles and clubbing, HRCT
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Diffuse Panbronchiolitis: Chronic sinusitis, non smoker HRCT Chest X ray
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nodular.
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Pulmonary Fibrosis: HRCT diagnostic, Restrictive lungs, Honey combing severe
diffusion defect, Increased FEV1/FEV
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Tuberculosis: Dyspnea, any age, toxic symptoms, wasted, X Ray and Sputum are
positive
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Medical HX in COPD
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Shortness of breath
Cough
Production of sputum, quantity, color, blood in sputum
Fever
Loss of weight
Smoking
Inhalation injury
Occupational exposure
Mood
Appetite
Chest discomfort
Exercise tolerance
Sleep disorder
Palpitations
Pollution
Socioeconomic status
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Exam in COPD
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Skin color, dryness, ecchymosed, increased creases.
Nail beds, clubbing,
Nasal flaring, septum , turbinate, uvula, oral space
Accessory muscle use, AP diameter
Thoracic-abdominal breathing assessment
Auscultation wheeze, rhonchi, Rales, air movement and trapping
palpation and percussion
Tracheal position
Heart sounds with augmented right heart sounds
Jugular veins and distension
Orthopnea
Walk test
Evaluate Tremors , muscle strength
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Occupational Exposure in COPD
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Spray painting
Arc welding
Farming
Miners
Vegetable spraying
Lawn mowing
Furnaces
Barbers/Beauticians
Hospitals
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Genetics in COPD
• Alpha -1 Anti Trypsin deficiency
ZZ type require treatment, testing available without charge by squeezing a drop of blood on a paper
and mailing to lab.
Genetic counseling done
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Our office we test every new patient and at least once in established patient
We follow levels in below normal patients
Once established significantly deficient Home IV therapy is given weekly.
Alpha-1 Antitrypsin Deficiency (A1AD) is a hereditary disorder characterized by low levels of a protein
called alpha-1 antitrypsin (A1AT) which is found in the blood. This deficiency may predispose an
individual to several illnesses but most commonly appears as emphysema, less commonly as liver
disease, or more rarely, as a skin condition called panniculitis.
A deficiency of A1AT allows substances that break down protein (proteolytic enzymes) to attack
various tissues of the body. This results in destructive changes in the lungs (emphysema) and
may also affect the liver and skin. Alpha-1 Antitrypsin is ordinarily released by specialized,
granular white blood cells (neutrophils) in response to infection or inflammation. A deficiency of
Alpha-1 Antitrypsin results in unbalanced (relatively unopposed) rapid breakdown of proteins
(protease activity), especially in the supporting elastic structures of the lungs. This destruction
over many years leads to emphysema and is accelerated by smoking and some occupational
exposures.
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Testing in COPD
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PFT: Pulmonary function tests TLC, FEV1/FVC, Diffusion, MVV.
ABG: Arterial Blood Gas PO2 PCO2 PH
Exercise Test: Good test for overall pulmonary efficiency
ECHO: EKG, Right heart Catheterization
CT CHEST: lung and bronchial anatomy
• Ventilation perfusion Scan: bulla, mismatch, vascular deficit
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Hb and HCO3 in blood: Tests for severity and chronic state
Sputum: Tests for colonization in Bronchitis
MIP MEP: Muscular and Breathing power efficiency
Sleep study: Explains COPD exacerbations in sleep
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Systemic Effects in COPD
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Pulmonary hypertension
Cor Pulmonale
Osteoporosis
Depression
Normochromic normocytic anemia
Skeletal muscle wasting
Increased risk of Coronary artery Disease
correlates with increasing CRP
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PFT in COPD
• Spirometry reduced FEV1, FEV1/FVC ratio, Reduced
FEF25-75 Helps in classification of severity and disability
• Pre and Post B2-Agonist therapy shows reversibility
• Lung Volumes hyperinflation, increased air trapping,
Reduced Vital capacity, Increased RV
• MVV is reduced due to flow obstruction and muscle
weakness
• DLCO is reduced more frequently in loss of alveolar unit,
atelectasis, mucus plugs, air trapping. Less reduction of
DLCO in bronchitis
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Radiology in COPD
• HRCT High resolution chest CT shows anatomy
of airway, lung parenchyma, bulla, atelectasis.
• Chest X Rays Pneumothorax, radiological
changes of emphysema, hyperinflation,
rarification of parenchyma, cardiac silhouette
• Ventilation and perfusion scans
• Fluoroscopy for procedures, developing
countries use as a diagnostic tool in
occupational surveillance
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Smoking in COPD
• Smoking is the main culprit in COPD it has
noxious gases, heat, CO, SO2 , tar.
• Cascade of inflammation CD8, Interleukins,
Neutrophils and Macrophages Destructive
enzymes released by inflammatory cells
• Cessation the first line in COPD management.
• Welbutrin works better with women
• Nicotine patch, gum, inhaler
• Chantix
• Hypnosis
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Counseling in COPD
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Quit smoking
Vaccination influenza
Pneumococcal vaccine not as important
Use of inhalers
Mouth rinsing after inhaler use
Over use of certain inhalers
While with Pets and children
Washing hands
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Medications in COPD
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Short acting Anticholinergics
Long acting Anticholinergic
Short acting B2-agonists
Long acting B2-agonists
Inhaled glucocorticosteroids
Systemic glucocorticosteroids
Combined long acting B2-agonists plus glucocorticosteroids in
one inhaler
• Combined short acting B2-agonists plus Anticholinergic in one
inhaler
• Methylxanthines
• Systemic glucocorticosteroids
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Beta Agonists in COPD
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• Short acting B2-Agonists: Salbutamol ( albuterol )(4-6hrs) , fenoterol
(4-6hrs), levalbuterol (6-8hrs), terbutaline94-6hrs)
• Excellent bronchodilator and quick effect. Therapy for All stages,
mostly rescue and as needed dosing every 4 to 6 hours for shortness
of breath.
• Relax airway smooth muscles by stimulation of B2- adrenergic
receptors which increases cyclic AMP and produce antagonist effect
to bronchoconstriction.
• Excess doses cause tremors, anxiety, tachycardia, arrhythmias,
hypokalemia
• Long acting B2-Agonists (LABA ) salmetrol(12+ hrs),
formoterol(12+hrs) ,Arformoterol(12+hrs) Therapy for Stage 2 ,3 and
stages 4 of COPD.
Slide Copyright www.thorax.us Ramesh Kaul MD 2009
Anticholinergics in COPD
• Short acting Anticholinergics started with historical Atropine
atomizers and smoking atropa plant
• Research brought quaternary compound of atropine called
iprotropium bromide(6-8 hrs) now nebulised and inhaler. and
oxitropium bromide (7-9hrs) in solution and inhaler.
• Long acting Tiotropium inhaled(24+hrs) aerolised powder.
• ipratropium bromide/salbutamol (Combivent)
• fenoterol/ipratropium bromide (Berodual)
• Mechanism: Blockage of acetycholine on M3 receptors.
• It is believed COPD the cholinergic tone is very high and mediates
in bronchoconstriction
Side Effects
Relatively safe
Dryness of mouth, Blurring of vision, Prostatic symptoms reported,
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Methylxanthines and steroids in COPD
• Theophyllin PO or IV and Aminophyllin IV
non specific inhibitors of all subsets of phospho-diesterase enzyme. Cytochrome
P450 metabolism drug interactions are many.
• Theophyllin side effects are large, as drugs of this class have low
therapeutic index.
• Methylxanthines may trigger atrial fibrillation, ventricular
arrhythmias, Insomnia, anxiety, seizures
• Methyl prednisone IV or PO Prednisone or Methyl prednisolone for
short term benefit in exacerbation
• Steroid Side effects are steroid psychosis, thrush, hyperglycemia,
elevated blood pressures, gastritis
• Chronic treatment with systemic corticosteroids should be avoided
as benefit-risk ratio is poor
• Steroid side effects are osteoporosis, fractures, steroid myopathy,
weight gain, hirsutism , steroid acne, cushingoid moon facies
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Inhaled Steroids in COPD
• Front line therapy for COPD stages 3 and 4
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Budenoside Nebulizer
Inhaled fluticasone
Inhaled triamcinolone
Inhaled beclomethasone
Inhaled budenoside
LABA and budenoside mixed in inhaler
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Other Treatments in COPD
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Oxygen Therapy Benefit For all stage 4 COPD
Mucolytics Benefit some with thick mucus
Antioxidants No proven benefit N-Acetyl Cystiene
Anabolic steroids no benefit
Immunoregulators : still in research these may help
Antitussives no benefit for regular use
Narcotics no benefit except palliative care and symptoms
of dyspnea relief in some.
Nedocromil not tested adequately
Leukotriene modifiers not tested adequately
Herbal treatments no benefit
Acupuncture or hypnosis no benefit on disease may help
in smoking cessation in rare subjects.
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Surgery in COPD
• Bullectomy makes space for normal collapsed
segments of lung, increases breathing space
• Lung Volume reduction surgery improves
compliance and diaphragm function.
• Lung transplant for end stage COPD.
• Enroll patients with End stage COPD in
transplant programs ahead of time.
• Pulmonary rehab prior to surgery
• Chest tubes if spontaneous Pneumothorax
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Bronchoscopy in COPD
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Bronchial toilet
Removal of mucus plugs
Resistant Pneumonia may need cultures
Different approaches of bronchoscopic lung
volume reduction have been described
radiofrequency fenestration of the bronchial wall
with stent placement
umbrella blockers
injection of fibrin glue.
Endo-bronchial valve (EBV)
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Mechanical Ventilation
• BIPAP in COPD
• Non-Invasive Mechanical Ventilation for
Acute COPD
• Transtracheal Augmented Ventilation (TTAV) is
the only technology that augments ventilation
during SBT in weaning trials in tracheotomised
COPD.
• Mechanical Ventilation in AECOPD
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Pulmonary Rehab in COPD
• Effective tool in improving ADLs (activities of daily living )
• Builds Self esteem and decreases social stigma in group therapy.
• Cost can be from thousands of dollars to $50 per month at
subsidized institutions.
• No improvement in lung function, helps only in performance and
quality of life.
• Improves adherence to use of Inhalers and lesser exacerbations
due to compliance.
• Pulmonary rehab RT and RN help in early evaluation and prevention
of exacerbations
• Better use of various gadgets like spacers, Flutter valve, BIPAP,
CPAP oxygen in judicious fashion
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Acapella and Flutter valve
• Flutter valve mucus
Acapella (Oscillating PEP) available
clearing device
in market and help clear mucus.
• Mechanism of action
probably by counteracting
auto PEEP reducing
hyperinflation and
vibrations causing
mobilization of mucus
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Diet in COPD
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Good nourishment is the key in management of disease state
Anorexic and bulimic individuals may develop emphysema without
smoking and without inhalation injury.
Postmortem studies of patients who died in the Warsaw Ghetto during
World War II suggested that death from starvation was associated with
pulmonary emphysema
The CT measurements of lung density, emphysema, and surface area-tovolume ratio were obtained using the X ray attenuation values found
changes of early emphysema.( 21 subjects vs. 16 controls)
Harvey O. Coxson et al American Journal of Respiratory and Critical Care Medicine Vol 170. pp.
748-752, (2004)
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Nutritional Support for Individuals With COPD A Meta-analysis
Conclusion: Nutritional support had no effect on improving
anthropometric measures, lung function, or functional exercise capacity
among patients with stable COPD
Ivone M. Ferreira, MD, PhD Et al10.1378/chest.117.3.672 CHEST March 2000 vol. 117 no. 3 672-678
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Infections in COPD
• Viral Influenza, Coxsackie, RSV, Rhino, Picorna, Adenovirus
• Bacterial Stenotrophomonas maltophilia. Burkholderia
cepacia. Streptococcus pneumoniae, Haemophilus influenzae.
Haemophilus parainfluenzae,Methicillin-Resistant Staphylococcus
aureus (MRSA), E. coli and Klebsiella pneumoniae,Citrobacter,
Serratia, and Pseudomonas.
• Fungal Candida oropharynx trachea, Aspergillum colonized
and Aspergilomas in cavities
• Mycobacterium
M. avium and rarely M. szulgai
• Atypical Infections Chlamydia pneumoniae, Mycoplasma
pneumoniae and Legionella pneumophila
• Mixed Infections of all above possible.
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Long term Antibiotics in COPD
• Long Term Erythromycin Therapy is Associated with Decreased
COPD Exacerbations
Terence AR Seemungal et al Am. J. Respir. Crit. Care Med., Volume 178, Number 11, December 2008, 11391147
• Investigational
A lot of claims that macrolides like drugs may
decrease exacerbations government trials are enrolling patients.
• Serum levels of procalcitonin increase rapidly in the presence of
infection
Antibiotic Treatment of Exacerbations of COPD*
A Randomized, Controlled Trial Comparing Procalcitonin-Guidance With Standard Therapy
Daiana Stolz, MD et al 10.1378/chest.06-1500 CHEST January 2007 vol. 131 no. 1 9-19
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Risk Assessment in COPD
• Preoperative risk assessment is always done for surgery
• Thoracic, abdominal, surgery effects the diaphragm
thoracic cage effects abdominal breathing
• Neurosurgery CNS drive is suppressed and more central
apneas, less rate and volume, decreases sensing of
CO2 and oxygen
• Orthopedic effect and clearance of anesthetics, pain
medications suppress respiration drive and depth.
• Pre and postoperative CXR,ABG, PFT, Exercise
oximetry, Stair stepper, use of Incentives, life style
modification
Slide Copyright www.thorax.us Ramesh Kaul MD 2009
Take home messages
COPD In 2009
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Smoking and inhalant injury needs to be eliminated from our environment.
Early intervention, counseling , good diet, should be frontline.
Vaccinations, inhalers and Rehab are main management.
Anticholinergics and Long acting are beneficial in Stage one to Four.
Inhaled steroids are beneficial for stages three and Four
LAB2A are beneficial for stages two onwards.
Long term oxygen therapy and sleep studies help in maintenance of
advanced disease
Surgical options for End Stage COPD with LVRS and transplant are
available.
Genetic research to find the sensitive population and prevention of COPD
THANK YOU
These slides are available at www.thorax.us at specials
Slide Copyright www.thorax.us Ramesh Kaul MD 2009