Chronic Obstructive

Pulmonary Disease
Presenter: Dr Moise Mathe
Department : Internal
Medicine/KIU

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 1. Definitions
•Chronic obstructive pulmonary disease:
A lung condition characterized by persistent respiratory symptoms (cough, dyspnea) and airflow limitation
(postbronchodilator FEV1:FVC ratio < 0.70), which is caused by a combination of small airway obstruction
and parenchymal destruction

•Chronic bronchitis:
Productive cough for at least 3 months per year for 2 consecutive years that cannot be explained by an alternative diagnosis

•Emphysema:
Permanent dilatation of pulmonary air spaces distal to the terminal bronchioles that is caused by the destruction of the
alveolar walls and pulmonary capillaries required for gas exchange

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2. Quick look at the respiratory system anatomy

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2. Quick look at the respiratory system anatomy

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 2. Etiology
Exogenous factors
• Tobacco use
• Smoking is the major risk factor for COPD, but those who have quit ≥ 10 years ago are not at increased risk.
• Passive smoking
• Exposure to air pollution or fine dusts
• Nonorganic dust: such as industrial bronchitis in coal miners
• Organic dust: ↑ incidence of COPD in areas where biomass fuel (e.g., wood, animal dung) is regularly burned
indoors

Endogenous factors
• Lung growth and development abnormalities
• Recurrent pulmonary infections and tuberculosis
• Premature birth
• α1-antitrypsin deficiency
• Airway hyperresponsiveness
• Antibody deficiency syndrome (e.g., IgA deficiency)
• Primary ciliary dyskinesia (e.g., Kartagener syndrome)

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 4. Classification
GOLD classification

GOLD spirometric grades inform the prognosis of a patient; GOLD groups guide pharmacological management.
GOLD grades

GOLD spirometric grades

Postbronchodilator FEV1% of the

Grade
predicted value

GOLD 1: mild ≥ 80%

GOLD 2: moderate 50–79%

GOLD 3: severe 30–49%

GOLD 4: very severe < 30%

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 4. Classification
GOLD group assessment
Severity of symptoms
Group Exacerbations in the past year
mMRC dyspnea scale CAT score

GOLD group A •0–1 •0–9

•0
•Or 1 not leading to hospital admission
GOLD group B •≥ 2 •≥ 10

GOLD group E •≥ 2 •Any severity

•Or ≥ 1 leading to hospital admission

mMRC: An assessement tool used to evaluate the extent of a patient’s functional CAT Score: Questionnaire used to quantify impairment in COPD.
disability caused by dyspea.
• 0=Dyspnea only on exeretion.
• 4=Too dyspeic to leave the house or breathless when dressing

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 5. Pathophysiology

Chronic inflammation

It results from significant exposure to noxious stimuli, increased oxidative stress (most commonly due to cigarette smoke) as well
as by increased release of reactive oxygen species by inflammatory cells.
• Promotion of goblet cell proliferation and hypertrophy, mucus hypersecretion, and impaired ciliary function
→ chronic productive cough
• Smooth muscle hyperplasia of the small airways and pulmonary vasculature (mainly due to hypoxic vasoconstriction)
→ pulmonary hypertension → cor pulmonale

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 6. Clinical features

Symptoms are minimal or nonspecific until the disease reaches an advanced stage.

Presenting findings
• Chronic cough with expectoration (expectoration typically occurs in the morning)
• Dyspnea and tachypnea
• Initial stages: only on exertion
• Advanced stages: continuously
• Pursed lip breathing
• The patient breathes in through the nose and breathes out slowly through pursed lips.
• This style of breathing increases airway pressure and prevents bronchial collapse during the last phase of
expiration.
• More commonly seen in patients with emphysema
• Prolonged expiratory phase, end-expiratory wheezing, crackles, muffled breath sounds, and/or
coarse rhonchi on auscultation
• Cyanosis due to hypoxemia
• Tachycardia

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 6. Clinical features

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 6. Clinical features
Pink puffer and blue bloater
According to their clinical appearance, patients with COPD are often categorized as either “Pink Puffer” or “Blue Bloater”.

Pink puffer vs. blue bloater

Pink Puffer Blue Bloater
Main pathomechanism •Emphysema •Chronic bronchitis

•Noncyanotic
•Productive cough
Clinical features •Cachectic
•Overweight
•Pursed-lip breathing
•Peripheral edema
•Mild cough
PaO2 •Slightly reduced •Markedly reduced

PaCO2 •Normal (possibly in •Increased

late hypercapnia) (early hypercapnia)

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 6. Clinical features

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 7. Diagnostics
• Initial tests
• Spirometry
• FEV1:FVC < 70% after bronchodilator inhalation confirms the diagnosis.
• ↓ FEV1 (FEV1 % of the predicted value determines the GOLD spirometric grade.)
• Normal or ↓ FVC
• Serum AAT level: Screen all patients with confirmed COPD for AATD (α1-antitrypsin Deficiency) upon
initial diagnosis.

FEV1 (Forced Expiratory Volume in 1 second)

FVC: Forced Vital Capacity. It is the maximum volume of air that
can be forcefully expired after maximal inspiration

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7. Diagnostics

Initial tests
• Spirometry
• FEV1:FVC < 70% after bronchodilator inhalation confirms the diagnosis.
• ↓ FEV1 (FEV1 % of the predicted value determines the GOLD spirometric grade.)
• Normal or ↓ FVC
• Serum AAT level: Screen all patients with confirmed COPD for AATD (α1-antitrypsin Deficiency) upon initial diagnosis.

Assessment for respiratory failure

• ABG
• Findings
• May show hypoxemic respiratory failure (↓ PO2) with or without hypercapnic respiratory failure (↑ PCO2)
• Chronic hypercapnia due to CO2 trapping is common in patients with severe COPD.

CBC
• Secondary polycythemia, ↑ hematocrit

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7. Diagnostics

• Chest x-ray findings in COPD

• Signs of pulmonary hyperinflation
• Increased anteroposterior diameter; barrel chest
• Pushed down and flattened diaphragm
• Horizontal ribs and widened intercostal spaces
• Hyperlucency of lung tissue (decreased lung markings)
• Signs of bullous emphysema: parenchymal bullae or pulmonary blebs

• CT chest findings
• Similar to CXR findings; may additionally reveal characteristic patterns of emphysema
• Panacinar emphysema: common in patients with AATD
• Centriacinar emphysema: common in patients with COPD and a history of tobacco use

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7. Diagnostics

Lungs are hyperinflated, diaphragm is flattened,

vascular markings are increased

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7. Diagnostics

Air trapping in pulmonary emphysema

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7. Diagnostics

Air trapping in pulmonary emphysema. Barrel chest

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7. Diagnostics

• Chest x-ray findings in COPD

• Signs of pulmonary hyperinflation
• Increased anteroposterior diameter; barrel chest
• Pushed down and flattened diaphragm
• Horizontal ribs and widened intercostal spaces
• Hyperlucency of lung tissue (decreased lung markings)
• Signs of bullous emphysema: parenchymal bullae or pulmonary blebs

• CT chest findings
• Similar to CXR findings; may additionally reveal characteristic patterns of emphysema
• Panacinar emphysema: common in patients with AATD
• Centriacinar emphysema: common in patients with COPD and a history of tobacco use

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 8. Differential diagnoses

Comparison of asthma and COPD

Asthma COPD

Age at diagnosis •Often childhood or adolescence

•Typically > 40 years old
•Nonallergic asthma can manifest after the age of 40

Etiology •Allergic and nonallergic •Cigarette consumption (90% of cases)

Clinical presentation •Episodic (i.e., acute asthma exacerbations with •Insidious onset
asymptomatic phases in-between) •Chronic progression over years

Bronchial obstruction •Reversible •Persistent

Medication •Good response to muscarinic

•Good response to long-term inhaled corticosteroids antagonists (e.g., ipratropium bromide)

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9. Management

• Nonpharmacological management of COPD

• Lifestyle modifications
• Counsel on smoking cessation
• Encourage physical activity to reduce the risk of acute exacerbations.

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9. Management

• Supportive care
• Recommended immunizations in COPD
• Pneumococcal vaccination
• Influenza vaccination (annual)

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9. Management

• General principles
• Bronchodilators are the mainstay of pharmacological treatment.
• Inhaled corticosteroids (ICS), e.g., budesonide, fluticasone, or beclomethasone, should only be used in
combination with long-acting bronchodilators.

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 9. Management
Overview of commonly used COPD medications
Class Examples

Short-acting beta-2 agonists (SABA) •Inhaled: albuterol (salbutamol)

•Oral: terbutaline

Long-acting beta-2 agonists (LABA) •Salmeterol

•Formoterol
•Budesonide
Inhaled corticosteroids (ICS) •Fluticasone
•Mometasone
•Others: beclomethasone, ciclesonide, triamcinolone
Long-acting muscarinic antagonists (LAMA) •Tiotropium bromide

Short-acting muscarinic antagonists (SAMA) •Ipratropium bromide

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 9. Management

Inhaler with spacer

Inhaler without spacer.

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9. Management

Initial Pharmacological treatment of stable COPD

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 9. Management
Follow-up treatment in COPD
Predominant trait Current treatment Follow-up treatment
•LABA or LAMA monotherapy
•LAMA/LABA combination therapy, e.g., umeclidinium/vilanterol
•OR LABA/ICS combination therapy
Persistent dyspnea
•Consider changing the inhaler or medication within the same class.
•LABA/LAMA combination therapy
•Evaluate for other causes of dyspnea.

•Escalate based on blood eosinophil count.

•LABA or LAMA monotherapy • If < 300 cells/mcL: LAMA/LABA combination therapy
•OR LABA/ICS combination therapy • If ≥ 300 cells/mcL: LAMA/LABA/ICS triple therapy,
e.g., fluticasone furoate/umeclidinium/vilanterol

•Based on blood eosinophil count

• If < 100 cells/mcL, consider adding either:
Persistent exacerbations • Macrolide antibiotic, e.g., azithromycin
•LABA/LAMA combination therapy • PDE4 inhibitor, e.g., roflumilast
• If ≥ 100 cells/mcL: Add ICS to the regimen, e.g., budesonide OR change
to LAMA/LABA/ICS triple therapy,
e.g., fluticasone furoate/umeclidinium/vilanterol

•Consider adding either:

• Macrolide antibiotic
•LABA/LAMA/ICS triple therapy • PDE4 inhibitor
• Consider stopping or reducing the ICS dose if there are adverse effects,
e.g., pneumonia.

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 10. Complications

•Acute exacerbation of COPD

•Cor pulmonale (right heart failure)
We list the most important complications. The selection is not exhaustive.

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 11. Summary
• Chronic obstructive pulmonary disease (COPD) is characterized by chronic respiratory symptoms resulting from airflow obstruction
and alveolar gas exchange abnormalities. It is predominantly caused by inhaled toxins (e.g., tobacco smoke or air pollution).

• Some individuals are genetically predisposed to COPD, particularly those with α1-antitrypsin deficiency (AATD).

• COPD begins with chronic airway inflammation, which usually progresses to emphysema, a condition that is characterized by
irreversible bronchial narrowing and alveolar hyperinflation.

• Clinical features include dyspnea and productive cough and, in later stages, tachypnea, tachycardia, and cyanosis. Diagnosis is primarily
based on clinical presentation and pulmonary function tests (PFTs), which typically show a decreased ratio of forced expiratory
volume (FEV) to forced vital capacity (FVC). Imaging studies are helpful in assessing disease severity and the extent of possible
complications.

• Treatment options mainly consist of short-acting and long-acting bronchodilators and inhaled corticosteroids. Individuals with advanced
disease may benefit from oxygen supplementation and/or noninvasive ventilation.

• COPD can cause complications such as pulmonary hypertension or respiratory failure. The most significant complication is acute
exacerbation of COPD.

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 Thank you

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References

1. The Merck Manuals

2. Medscape
3. Amboss

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