C hronic O bstructive P ulmonary D isease

Chronic Obstructive

Pulmonary Disease

Chronic Obstructive

Pulmonary Disease

Chen xin M.D., Pulmonary Medicine

zhujiang hospital, southern medical university

Chen xin M.D., Pulmonary Medicine

zhujiang hospital, southern medical university

IntroductionIntroduction

• Chronic Obstructive Pulmonary Disease (COPD) is a major cause of chronic morbidity and mortality throughout the world. Many people suffer from this disease for years and die prematurely from it or its complications. COPD is the fourth leading cause of death in the world, and further increases in its prevalence and mortality can be predicted in the coming decades.

• Chronic Obstructive Pulmonary Disease (COPD) is a major cause of chronic morbidity and mortality throughout the world. Many people suffer from this disease for years and die prematurely from it or its complications. COPD is the fourth leading cause of death in the world, and further increases in its prevalence and mortality can be predicted in the coming decades.

DefinitionDefinition

• COPD is a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients.

• Its pulmonary component is characterized by airflow limitation that is not fully reversible.

• The airflow limitation is usually progressive and associated with the chronic inflammatory response of the lung to noxious particles or gases.

• acute exacerbations and It's complications influence the severity of the disease

• COPD is a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients.

• Its pulmonary component is characterized by airflow limitation that is not fully reversible.

• The airflow limitation is usually progressive and associated with the chronic inflammatory response of the lung to noxious particles or gases.

• acute exacerbations and It's complications influence the severity of the disease

DefinitionDefinition

• Airflow limitation• Not completely reversible• Progressive• Inflammation• “Bronchitis” & “Emphysema” no longer

in definition• The most common form of COPD is a

combination of chronic bronchitis and emphysema.

• Airflow limitation• Not completely reversible• Progressive• Inflammation• “Bronchitis” & “Emphysema” no longer

in definition• The most common form of COPD is a

combination of chronic bronchitis and emphysema.

Burden of COPDBurden of COPD

• COPD is a leading cause of morbidity and mortality worldwide and results in an economic and social burden that is both substantial and increasing.

• COPD prevalence, morbidity, and mortality vary across countries and across different groups within countries.

• The burden of COPD is projected to increase in the coming decades due to continued exposure to COPD risk factors and the changing age structure of the world’s population.

• COPD is a leading cause of morbidity and mortality worldwide and results in an economic and social burden that is both substantial and increasing.

• COPD prevalence, morbidity, and mortality vary across countries and across different groups within countries.

• The burden of COPD is projected to increase in the coming decades due to continued exposure to COPD risk factors and the changing age structure of the world’s population.

Percent Change in Age-Adjusted Death Rates, U.S.,

1965-1998

Percent Change in Age-Adjusted Death Rates, U.S.,

1965-1998

00

0.50.5

1.01.0

1.51.5

2.02.0

2.52.5

3.03.0

Proportion of 1965 Rate Proportion of 1965 Rate

–59%–59% –64%–64% –35%–35% +163%+163% –7%–7%

CoronaryHeart

Disease

CoronaryHeart

Disease

StrokeStroke Other CVDOther CVD COPDCOPD All OtherCauses

All OtherCauses

Of the six leading causes of death in the United States, only COPD has been increasing steadily since 1970

Source: Jemal A. et al. JAMA 2005

Disease Trajectory of a Patients with COPD

Disease Trajectory of a Patients with COPD

Symptoms

Exacerbations

Exacerbations

ExacerbationsDeterioration

End of Life

Risk FactorsRisk Factors

GenesExposure to particles• Tobacco smoke• Occupational dusts,

organic and inorganic• Indoor air pollution from

heating and cooking with biomass in poorly ventilated dwellings

• Outdoor air pollution

GenesExposure to particles• Tobacco smoke• Occupational dusts,

organic and inorganic• Indoor air pollution from

heating and cooking with biomass in poorly ventilated dwellings

• Outdoor air pollution

Lung growth and development

Oxidative stress

Gender

Age

Respiratory infections

Socioeconomic status

Nutrition

Comorbidities

Lung growth and development

Oxidative stress

Gender

Age

Respiratory infections

Socioeconomic status

Nutrition

Comorbidities

Risk FactorsRisk Factors

NutritionNutrition

InfectionsInfections

Socio-economic Socio-economic statusstatus

Aging PopulationsAging Populations

Pathology Pathology

• Pathological changes characteristic of COPD are found in the proximal airways, peripheral airways, lung parenchyma, and pulmonary vasculature. These changes include chronic inflammation, and structural changes resulting from repeated injury and repair.

• Inhaled cigarette smoke and other noxious particles cause lung inflammation, a normal response which appears to be amplified in patients who develop COPD.

• Pathological changes characteristic of COPD are found in the proximal airways, peripheral airways, lung parenchyma, and pulmonary vasculature. These changes include chronic inflammation, and structural changes resulting from repeated injury and repair.

• Inhaled cigarette smoke and other noxious particles cause lung inflammation, a normal response which appears to be amplified in patients who develop COPD.

• Lung inflammation is further amplified by oxidative stress and an excess of proteases in the lung.

• Lung inflammation is further amplified by oxidative stress and an excess of proteases in the lung.

LUNG INFLAMMATIONLUNG INFLAMMATION

COPD PATHOLOGYCOPD PATHOLOGY

OxidativeOxidativestressstress ProteinasesProteinases

Repair Repair mechanismsmechanisms

Anti-proteinasesAnti-proteinasesAnti-oxidantsAnti-oxidants

Host factorsAmplifying mechanisms

Cigarette smokeCigarette smokeBiomass particlesBiomass particles

ParticulatesParticulates

Source: Peter J. Barnes, MD

Pathogenesis of COPD

Cigarette smoke Cigarette smoke (and other irritants)(and other irritants)

PROTEASES PROTEASES Neutrophil elastaseNeutrophil elastaseCathepsinsCathepsinsMMPsMMPs

Alveolar wall destructionAlveolar wall destruction(Emphysema)(Emphysema)

Mucus hypersecretionMucus hypersecretion

CD8CD8+ +

lymphocytelymphocyte

Alveolar Alveolar macrophagemacrophage

EpithelialEpithelialcellscells

FibrosisFibrosis(Obstructive(Obstructivebronchiolitis)bronchiolitis)

FibroblastFibroblast

MonocyteMonocyteNeutrophilNeutrophil

Chemotactic factorsChemotactic factors

Inflammatory Cells Involved in COPD


Anti-proteases

SLPI 1-AT

Proteolysis

OO22--, H, H220022

OHOH.., ONOO, ONOO--

Mucus secretion

Plasma leak Bronchoconstriction

NF-NF-BB

IL-8IL-8

NeutrophilNeutrophilrecruitmentrecruitment

TNF-TNF-

IsoprostanesIsoprostanes

↓ ↓ HDAC2HDAC2

↑↑InflammationInflammationSteroidSteroid

resistanceresistance

Macrophage NeutrophilOxidative Stress in COPD


Mucus gland hyperplasia

Goblet cellhyperplasia

Mucus hypersecretion Neutrophils in sputum

Squamous metaplasia of epithelium

↑ Macrophages

No basement membrane thickening

Little increase in airway smooth muscle

↑ CD8+ lymphocytes

Changes in Large Airways of COPD Patients

Changes in Large Airways of COPD Patients


Disrupted alveolar attachments

Inflammatory exudate in lumen

Peribronchial fibrosisLymphoid follicle

Thickened wall with inflammatory cells- macrophages, CD8+ cells, fibroblasts

Changes in Small Airways in COPD Patients


Alveolar wall destruction

Loss of elasticity

Destruction of pulmonarycapillary bed

↑ Inflammatory cells macrophages, CD8+ lymphocytes


Changes in Lung Parenchyma in COPD

Endothelial dysfunction

Intimal hyperplasia

Smooth muscle hyperplasia

↑ Inflammatory cells (macrophages, CD8+ lymphocytes)

Changes in Pulmonary Arteries in COPD Patients


YYYYYY

Mast cellMast cell

CD4+ cellCD4+ cell(Th2)(Th2)

EosinophilEosinophil

AllergensAllergens

Ep cellsEp cells

ASTHMAASTHMA

BronchoconstrictionBronchoconstrictionAHRAHR

Alv macrophageAlv macrophage Ep cellsEp cells

CD8+ cellCD8+ cell(Tc1)(Tc1)

NeutrophilNeutrophil

Cigarette smokeCigarette smoke

Small airway narrowingSmall airway narrowingAlveolar destructionAlveolar destruction

COPDCOPD

Reversible IrreversibleAirflow LimitationAirflow Limitation


Chronic hypoxiaChronic hypoxia

Pulmonary vasoconstrictionPulmonary vasoconstriction

MuscularizationMuscularization

Intimal Intimal hyperplasiahyperplasia

FibrosisFibrosis

ObliterationObliteration

Pulmonary hypertensionPulmonary hypertension

Cor pulmonaleCor pulmonale

Death

EdemaEdema

Pulmonary Hypertension in COPD


NormalNormalInspiration

Expiration

alveolar attachments

Mild/moderateMild/moderateCOPD COPD

loss of elasticity

Severe Severe COPD COPD

loss of alveolar attachments

closure

small small airwayairway

Dyspnea↓ Exercise capacity

Air trappingAir trappingHyperinflationHyperinflation

↓ ↓ HealthHealthstatusstatus

Air Trapping in COPD


Macrophages

TNF- IL-8 IL-6

Bacteria Viruses Non-infective Pollutants

Epithelial cells

Oxidative stressOxidative stress

Neutrophils

Inflammation in COPD Exacerbations


Chronic bronchitisChronic bronchitis

• Chronic bronchitis is an inflammation and eventual scarring of the lining of the bronchial tubes.

• Symptoms of chronic bronchitis include chronic cough, increased mucus, frequent clearing of the throat and shortness of breath.

• Chronic bronchitis is an inflammation and eventual scarring of the lining of the bronchial tubes.

• Symptoms of chronic bronchitis include chronic cough, increased mucus, frequent clearing of the throat and shortness of breath.

EmphysemaEmphysema

Emphysema causes irreversible lung damage. The walls between the air sacs within the lungs lose their ability to stretch and recoil. They become weakened and break. Elasticity of the lung tissue is lost, causing air to be trapped in the air sacs and impairing the exchange of oxygen and carbon dioxide. Also, the support of the airways is lost, allowing for obstruction of airflow.

Emphysema causes irreversible lung damage. The walls between the air sacs within the lungs lose their ability to stretch and recoil. They become weakened and break. Elasticity of the lung tissue is lost, causing air to be trapped in the air sacs and impairing the exchange of oxygen and carbon dioxide. Also, the support of the airways is lost, allowing for obstruction of airflow.

EmphysemaEmphysema

• Symptoms of emphysema include cough, shortness of breath and a limited excercise tolerance. Diagnosis is made by pulmonary function tests, along with the patient’s history, examination and other tests.

• Symptoms of emphysema include cough, shortness of breath and a limited excercise tolerance. Diagnosis is made by pulmonary function tests, along with the patient’s history, examination and other tests.

COPD 病理学特点COPD 病理学特点

气道炎症

粘膜纤毛功能障碍

气道阻塞

气道结构改变

平滑肌收缩增加胆碱能释放支气管高反应性 ?

弹性收缩降低

增加炎症细胞数量 / 活性- 中性粒细胞 ,- 巨噬细胞 ,- CD8+ 淋巴细胞提高 IL-8, TNF, LTB4

蛋白酶 / 抗蛋白酶失衡粘膜水肿

肺泡破坏上皮增生腺体过度增大杯状细胞变形气道纤维化

粘液过度分泌粘液粘性增加减少纤毛转运粘膜损伤

PathophysiologyPathophysiology

• Increased mucus production and reduced mucociliary clearance - cough and sputum production

• Loss of elastic recoil - airway collapse

• Increase smooth muscle tone• Pulmonary hyperinflation• Gas exchange abnormalities -

hypoxemia and/or hypercapnia

• Increased mucus production and reduced mucociliary clearance - cough and sputum production

• Loss of elastic recoil - airway collapse

• Increase smooth muscle tone• Pulmonary hyperinflation• Gas exchange abnormalities -

hypoxemia and/or hypercapnia

Chronic bronchitis Emphysema

asthma

COPDCOPD

GOALS of COPD MANAGEMENTUPDATED 2011

GOALS of COPD MANAGEMENTUPDATED 2011

• Relieve symptoms • Prevent disease progression• Improve exercise tolerance• Improve health status• Prevent and treat complications• Prevent and treat exacerbations• Reduce mortality

• Relieve symptoms • Prevent disease progression• Improve exercise tolerance• Improve health status• Prevent and treat complications• Prevent and treat exacerbations• Reduce mortality

Four Components of COPD Management

Four Components of COPD Management

1. Assess and monitor disease 2. Reduce risk factors3. Manage stable COPD

I. EducationII. Pharmacologic/Non-

pharmacologic

4. Manage exacerbationsI. Diagnosis and Assessment of

SeverityII. Home/Hospital Management

1. Assess and monitor disease 2. Reduce risk factors3. Manage stable COPD

I. EducationII. Pharmacologic/Non-

pharmacologic

4. Manage exacerbationsI. Diagnosis and Assessment of

SeverityII. Home/Hospital Management

Assess and Monitor COPD: Key Points

Assess and Monitor COPD: Key Points

•A clinical diagnosis of COPD should be considered in any patient who has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease.•The diagnosis should be confirmed by spirometry. A post-bronchodilator FEV1/FVC < 0.70 confirms the presence of airflow limitation that is not fully reversible.•Comorbidities are common in COPD and should be actively identified.

•A clinical diagnosis of COPD should be considered in any patient who has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease.•The diagnosis should be confirmed by spirometry. A post-bronchodilator FEV1/FVC < 0.70 confirms the presence of airflow limitation that is not fully reversible.•Comorbidities are common in COPD and should be actively identified.

Diagnosis of COPDDiagnosis of COPD

SYMPTOMScoughcoughsputumsputum

shortness of breathshortness of breath

EXPOSURE TO RISKFACTORS tobaccotobacco

occupationoccupationindoor/outdoor pollutionindoor/outdoor pollution

clinical diagnosisclinical diagnosis

è

SPIROMETRY

diagnosis

Key Indicators for COPD Diagnosis

Key Indicators for COPD Diagnosis

Chronic cough Present intermittently or every day often present throughout the day; seldom only nocturnal

Chronic sputum production Present for many years, worst in winters. Initially mucoid – becomes purulent with exacerbation

Dyspnoea that is Progressive (worsens over time)Persistent (present every day)Worse on exerciseWorse during respiratory infections

Acute bronchitis Repeated episodes

History of exposure to risk factors Tobacco smoke (including beedi) occupational dusts and chemical smoke from home cooking and heating fuel

Physical signsPhysical signs

• Large barrel shaped chest (hyperinflation)

• Prominent accessory respiratory muscles in neck and use of accessory muscle in respiration

• Low, flat diaphragm• Diminished breath

sound

• Large barrel shaped chest (hyperinflation)

• Prominent accessory respiratory muscles in neck and use of accessory muscle in respiration

• Low, flat diaphragm• Diminished breath

sound

SpirometrySpirometry

• Diagnosis

• Assessing severity

• Assessing

prognosis

• Monitoring

progression

• Diagnosis

• Assessing severity

• Assessing

prognosis

• Monitoring

progression

SpirometrySpirometry

• FEV1 – Forced expired volume in the first second

• FVC – Total volume of air that can be exhaled from maximal inhalation to maximal exhalation

• FEV1/FVC% - The ratio of FEV1 to FVC, expressed as a percentage.

• FEV1 – Forced expired volume in the first second

• FVC – Total volume of air that can be exhaled from maximal inhalation to maximal exhalation

• FEV1/FVC% - The ratio of FEV1 to FVC, expressed as a percentage.

Flow Normal obstruction

restrictions Mixed

RVTLCVolum

Flow-volume curveFlow-volume curve

Chest X-raysChest X-rays

Emphysema Hyperinflation Flattened

diaphragms Decreased

vascular markings

Chronic Bronchitis Usually normal

Emphysema Hyperinflation Flattened

diaphragms Decreased

vascular markings

Chronic Bronchitis Usually normal

Flatdiaphragm

IncreasedRetrosternal

air

Hyper-inflated

Chest X-raysChest X-rays

Assess and Monitor COPD:

Spirometry GOLD 2006


Spirometry GOLD 2006

• Spirometry should be performed after the administration of an adequate dose of a short-acting inhaled bronchodilator to minimize variability.

• A post-bronchodilator FEV1/FVC < 0.70 confirms the presence of airflow limitation that is not fully reversible.

• Where possible, values should be compared to age-related normal values to avoid overdiagnosis of COPD in the elderly.

• Spirometry should be performed after the administration of an adequate dose of a short-acting inhaled bronchodilator to minimize variability.

• A post-bronchodilator FEV1/FVC < 0.70 confirms the presence of airflow limitation that is not fully reversible.

• Where possible, values should be compared to age-related normal values to avoid overdiagnosis of COPD in the elderly.

COPD classification based on spirometry GOLD 2006

COPD classification based on spirometry GOLD 2006

Severity Postbronchodilator FEV1/FVC

Postbronchodilator FEV1% predicted

Mild COPD <0.7 >80

Moderate COPD

<0.7 50-80

Severe COPD <0.7 30-50

Very severe COPD

<0.7 <30

SPIROMETRY is not to substitute for clinical judgment in the evaluation of the severity of

disease in individual patients.


GOLD 2011


GOLD 2011

• Clinical symptoms • Spirometry• risk of acute exacerbations • complications

Global strategy for the diagnosis, management, and prevention of chronic

obstructive pulmonary disease Revised 2011

• Clinical symptoms • Spirometry• risk of acute exacerbations • complications

Global strategy for the diagnosis, management, and prevention of chronic

obstructive pulmonary disease Revised 2011

Assess and Monitor COPD: Clinical symptoms

Assess and Monitor COPD: Clinical symptoms

• COPD assessment test (CAT) including eight common clinical problem, to

evaluate the health damage of patients with COPD

• modified british medical research council (mMRC)

Having a good correlation with health condition and can predict the future risk of death

• COPD assessment test (CAT) including eight common clinical problem, to

evaluate the health damage of patients with COPD

• modified british medical research council (mMRC)

Having a good correlation with health condition and can predict the future risk of death

mMRC

CAT

mMRC

CAT

Assess and Monitor COPD: risk of acute exacerbations

Assess and Monitor COPD: risk of acute exacerbations

History of acute exacerbations : the number of acute exacerbations is more than 2

times in the last year

Spirometry: FEV1 < 50 % Pred as a high risk index

History of acute exacerbations : the number of acute exacerbations is more than 2

times in the last year

Spirometry: FEV1 < 50 % Pred as a high risk index

Comprehensive Assessment

Comprehensive Assessment

Risk 4 Risk(GOLD) 3 ≥ 2 (AE) 2 1 1 0 mMRC 0-1 mMRC 2+ CAT< 10 CAT> 10+

symptoms （ mMRC or CAT ）

Risk 4 Risk(GOLD) 3 ≥ 2 (AE) 2 1 1 0 mMRC 0-1 mMRC 2+ CAT< 10 CAT> 10+

symptoms （ mMRC or CAT ）

C D

A BA:Fewer symptoms, lower risk B: more symptoms, lower riskC: Fewer symptoms,higher riskD: more symptoms, higher risk

Arterial Blood Gas (ABGs)Arterial Blood Gas (ABGs)

• An ABG is done from a sample drawn from one of your arteries. The blood is then analyzed by a special machine, which records the amount of carbon dioxide (waste gas) and oxygen in your blood. One of the uses of this test is to determine whether or not you need any extra oxygen.

• An ABG is done from a sample drawn from one of your arteries. The blood is then analyzed by a special machine, which records the amount of carbon dioxide (waste gas) and oxygen in your blood. One of the uses of this test is to determine whether or not you need any extra oxygen.

Parameters and Predictions

Parameters and Predictions

Parameter Normal Values

Predictions

Arterial PO2 95 mmHg decrease

Arterial PCO2 40 mmHg increases

Aterial pH approx. 7.4 decreases

Arterial HCO3-content

22-26 mEq/L increases

Total Arterial O2 content

20 ml/dL decrease

Differential Diagnosis: Differential Diagnosis: COPD and AsthmaCOPD and Asthma

Differential Diagnosis: Differential Diagnosis: COPD and AsthmaCOPD and Asthma

COPD ASTHMA

Onset in mid-life

Symptoms slowly progressive

Long smoking history

Dyspnea during exercise

Largely irreversible airflow limitation

Onset early in life (often childhood)

Symptoms vary from day to day

Symptoms at night/early morning

Allergy, rhinitis, and/or eczema also present

Family history of asthma

Largely reversible airflow limitation

COPD and Co-Morbidities


COPD patients are at increased risk for: • Myocardial infarction, angina

• Osteoporosis

• Respiratory infection

• Depression

• Diabetes

• Lung cancer

COPD patients are at increased risk for: • Myocardial infarction, angina

• Osteoporosis

• Respiratory infection

• Depression

• Diabetes

• Lung cancer



COPD has significant extrapulmonary

(systemic) effects including:

• Weight loss

• Nutritional abnormalities

• Skeletal muscle dysfunction

COPD has significant extrapulmonary

(systemic) effects including:

• Weight loss

• Nutritional abnormalities

• Skeletal muscle dysfunction

Management of Stable COPD

Reduce Risk Factors: Key Points


Reduce Risk Factors: Key Points

• Reduction of total personal exposure to tobacco smoke, occupational dusts and chemicals, and indoor and outdoor air pollutants are important goals to prevent the onset and progression of COPD.

• Smoking cessation is the single most effective — and cost effective — intervention in most people to reduce the risk of developing COPD and stop its progression.

• Reduction of total personal exposure to tobacco smoke, occupational dusts and chemicals, and indoor and outdoor air pollutants are important goals to prevent the onset and progression of COPD.

• Smoking cessation is the single most effective — and cost effective — intervention in most people to reduce the risk of developing COPD and stop its progression.

• Reducing the risk from indoor and outdoor air pollution is feasible and requires a combination of public policy and protective steps taken by individual patients.

• Reduction of exposure to smoke from biomass fuel, particularly among women and children, is a crucial goal to reduce the prevalence of COPD worldwide.

• Reducing the risk from indoor and outdoor air pollution is feasible and requires a combination of public policy and protective steps taken by individual patients.

• Reduction of exposure to smoke from biomass fuel, particularly among women and children, is a crucial goal to reduce the prevalence of COPD worldwide.


Manage Stable COPD: Key Points


Manage Stable COPD: Key Points

• Bronchodilator medications are central to the symptomatic management of COPD. They are given on an as-needed basis or on a regular basis to prevent or reduce symptoms and exacerbations.

• The principal bronchodilator treatments are ß2-agonists, anticholinergics, and methylxanthines used singly or in combination.

• Regular treatment with long-acting bronchodilators is more effective and convenient than treatment with short-acting bronchodilators.

• Bronchodilator medications are central to the symptomatic management of COPD. They are given on an as-needed basis or on a regular basis to prevent or reduce symptoms and exacerbations.



Management of Stable COPDPharmacotherapy: Bronchodilators

Management of Stable COPDPharmacotherapy: Bronchodilators

• Bronchodilator medications are central to the symptomatic management of COPD .They are given on an as-needed basis or on a regular basis to prevent or reduce symptoms and exacerbations.



• Bronchodilator medications are central to the symptomatic management of COPD .They are given on an as-needed basis or on a regular basis to prevent or reduce symptoms and exacerbations.



Algorithm for the management of COPD

Algorithm for the management of COPD

Short acting bronchodilator – as required

Tiotropium

Tiotropium+LABA

Long acting beta agonist

LABA + tiotropium

Add-Inhaled steroids-Theophylline

Mild

Severe

ass

ess

wit

h s

ym

pto

ms

and

spir

om

etr

y


Pharmacotherapy: Glucocorticosteroids

The addition of regular treatment with inhaled

glucocorticosteroids to bronchodilator treatment is appropriate for symptomatic COPD patients with an FEV1 < 50% predicted (Stage III: Severe COPD and Stage IV: Very Severe COPD) and repeated exacerbations.

An inhaled glucocorticosteroid combined with a long-acting ß2-agonist is more effective than the individual components .

Pharmacotherapy for Stable COPD

Pharmacotherapy for Stable COPD

Bronchodilators• Short-acting 2-

agonist – Salbutamol

• Long-acting 2-agonist - Salmeterol and Formoterol

• Anticholinergics – Ipratropium, Tiiotropium

• Methylxanthines - Theophylline

Bronchodilators• Short-acting 2-

agonist – Salbutamol

• Long-acting 2-agonist - Salmeterol and Formoterol

• Anticholinergics – Ipratropium, Tiiotropium

• Methylxanthines - Theophylline

Steroids

• Oral – Prednisolone

• Inhaled - Fluticasone, Budesonide

Steroids

• Oral – Prednisolone

• Inhaled - Fluticasone, Budesonide


Pharmacotherapy: Vaccines

In COPD patients influenza vaccines can reduce serious illness.

Pneumococcal polysaccharide vaccine is recommended for COPD patients 65 years and older and for COPD patients younger than age 65 with an FEV1 < 40% predicted.

Management of Stable COPD All Stages of Disease SeverityAll Stages of Disease SeverityManagement of Stable COPD All Stages of Disease SeverityAll Stages of Disease Severity

• Avoidance of risk factorsAvoidance of risk factors• - smoking cessation- smoking cessation• - reduction of indoor pollution- reduction of indoor pollution• - reduction of occupational - reduction of occupational

exposureexposure• Influenza vaccinationInfluenza vaccination

• Avoidance of risk factorsAvoidance of risk factors• - smoking cessation- smoking cessation• - reduction of indoor pollution- reduction of indoor pollution• - reduction of occupational - reduction of occupational

exposureexposure• Influenza vaccinationInfluenza vaccination

IV: Very Severe III: Severe II: Moderate I: Mild

Therapy at Each Stage of COPD (GOLD2006)

FEV1/FVC < 70%

FEV1 > 80% predicted

FEV1/FVC < 70%

50% < FEV1 < 80% predicted

FEV1/FVC < 70%

30% < FEV1 < 50% predicted

FEV1/FVC < 70%

FEV1 < 30% predicted

or FEV1 < 50% predicted plus chronic respiratory failure

Add regular treatment with one or more long-acting bronchodilators (when needed); Add rehabilitation

Add inhaled glucocorticosteroids if repeated exacerbations

Active reduction of risk factor(s); influenza vaccinationAdd short-acting bronchodilator (when needed)

Add long term oxygen if chronic respiratory failure. Consider surgical treatments

Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease

Revised 2011 Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease

Revised 2011

P First chonice

Second chonice Alternative chonice

A SABA /SAMA prn

LAMA/LABA orSAMA ＆ SABA

Theophylline

B LABA / LAMA LAMA ＆ LABA SABA ＆ /orSAMA ； Theophylline

C ICS/LABA or LAMA

LAMA ＆ LABA PDE-4 inhibitors ； SABA ＆ /orSAMA ； Theophylline

D ICS/LABA or LAMA

ICS ＆ LAMA ICS/LABA ＆ LAMA ； ICS/LABA ＆ PDE-4 inhibitors LAMA ＆ LABA ； LAMA ＆ PDE-4 inhibitors

Carbocisteine ； SABA ＆ /orSAMA ； Theophylline



The Future of COPD ：Phenotypes

The Future of COPD ：Phenotypes

• Clinical Manifestations Age, smoking history, sex,

ethnicity

• Physiological Manifestations• Radiologic Characterization• frequent COPD Exacerbations• Systemic Inflammation

• Clinical Manifestations Age, smoking history, sex,

ethnicity

• Physiological Manifestations• Radiologic Characterization• frequent COPD Exacerbations• Systemic Inflammation

68


Other Pharmacologic Treatments

Antibiotics: Only used to treat infectious exacerbations of COPD

Antioxidant agents: No effect of n-acetylcysteine on frequency of exacerbations, except in patients not treated with inhaled glucocorticosteroids

Mucolytic agents, Antitussives, Vasodilators: Not recommended in stable COPD

69


Non-Pharmacologic Treatments

Rehabilitation: All COPD patients benefit from exercise training programs, improving with respect to both exercise tolerance and symptoms of dyspnea and fatigue.

Oxygen Therapy: The long-term administration of oxygen (> 15 hours per day) to patients with chronic respiratory failure has been shown to increase survival.

70

Management COPD Exacerbations

Key Points

An exacerbation of COPD is defined as:

“An acute event in the course of the disease characterized by a change in the patient’s baseline dyspnea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication in a patient with underlying COPD.”

71


Key Points

The most common causes of an exacerbation are infection of the tracheobronchial tree

and air pollution, but the cause of about one-third of severe exacerbations cannot be identified .

Patients experiencing COPD exacerbations with clinical signs of airway infection (e.g., increased sputum purulence) may benefit from antibiotic treatment .

72

Manage COPD Exacerbations

Key Points

Inhaled bronchodilators

(particularly inhaled ß2-agonists

with or without anticholinergics)

and oral glucocorticosteroids

are effective treatments for

exacerbations of COPD.

Manage COPD Exacerbation

cause and mechanism Manage COPD Exacerbation

cause and mechanism

Wedzicha JA. Lancet 2007 ； 370 ： 786-796 Antonio Anzueto. Proc Am Thorac Soc 2007 ； 4 ： 554–564 Wedzicha JA. Lancet 2007 ； 370 ： 786-796 Antonio Anzueto. Proc Am Thorac Soc 2007 ； 4 ： 554–564

VirusesBacteria

Aerial pollution

COPD airway inflammation is, the more serious, pathological physiology change is, the more evident. leading to a symptom aggravating, so patients much to seek for medical help, usually diagnosed of acute exacerbation

Cardiovascular Co-Morbidities Dynamic hyperinflation

The deterioration of airway inflammation

Symptoms of AECOPD

Expiratory Airflow limitation

Bronchial inflammationHydroncus, mucous

Systemic inflammation

COPD airway inflammation COPD airway inflammation


Key Points

Noninvasive mechanical ventilation in exacerbations improves respiratory acidosis, increases pH, decreases the need for endotracheal intubation, and reduces PaCO2, respiratory rate, severity of breathlessness, the length of hospital stay, and mortality.

Medications and education to help prevent future exacerbations should be considered as part of follow-up, as exacerbations affect the quality of life and prognosis of patients with COPD.

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Global Strategy for Diagnosis, Management and Prevention of COPD: Summary

COPD is increasing in prevalence in many countries of the world.

COPD is treatable and preventable.

The GOLD program offers a strategy to identify patients and to treat them according to the best medications available.

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COPD can be prevented by avoidance of risk factors, the most notable being tobacco smoke.

Patients with COPD have multiple other conditions (comorbidities) that must be taken into consideration.

GOLD has developed a global network to raise awareness of COPD and disseminate information on diagnosis and treatment.

Global Strategy for Diagnosis, Management and Prevention of COPD:

Summary

Documents

C hronic O bstructive P ulmonary D isease