COPD

https://next.amboss.com/us/article/3h0Sdf?q=chronic+obstructive+pulmonary+disease


Definition

COPD is a chronic disease of the lungs in which there is:

  1. Obstruction/narrowing of small airways, which is not fully reversible. This limits the airflow, mainly during expiration
  2. Inflammation in the airways
  3. Gas exchange problem in the alveoli

It is a preventable & treatable disease.


Etiologies

  1. Smoking: Most common cause worldwide
  2. Smoke from burning fossil fuels, e.g., coal, wood, oil, etc.
  3. Climate pollution
  4. Occupational exposure to harmful gases/particles (e.g., coal miners)
  5. Alpha-1 antitrypsin deficiency (COPD at a young age + cirrhosis)

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Classification

Two conditions come under COPD:

  1. Emphysema
  2. Chronic bronchitis

Most COPD patients have a combination of both.


Emphysema

Emphysema is characterized by:

  • Narrowing of the terminal bronchioles plus destruction of the alveolar walls

This leads to:

a) Hyperinflation: During expiration, lungs don’t collapse fully, so air gets trapped inside (so total lung capacity TLC is increased)

b) Gas exchange problems: Alveolar damage → poor gas exchange causing hypoxia and CO₂ retention

Clinical Features:

  • Patients are breathless but not cyanosed
  • CO₂ retention is not so bad like chronic bronchitis
  • These patients are called “pink puffers” (skin is pinkish)

Normal vs. Emphysema

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Alveoli Changes in Lung Diseases

NOTE THE ALVEOLAR WALL DAMAGE

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alamy - CT2782


Chronic Bronchitis

Chronic bronchitis is defined as:

  • Productive cough, for 3 consecutive months, for at least 2 years (in the absence of any other etiology) → 3M 2Y

Features:

a) Hypoxia & CO₂ retention (CO₂ retention is much more than emphysema)

b) Patients cyanosed & edematous (blue bloaters)


Comparison: Emphysema vs. Chronic Bronchitis

FeatureEmphysemaChronic Bronchitis
1) HypoxiaYesYes
2) CO₂ retentionYes, but not too muchToo much
3) CyanosisNoYes
4) Skin colorPink puffersBlue bloaters

COPD Phenotypes

img-3.jpeg Pink Puffer

img-4.jpeg Blue Bloater


Symptoms of COPD

Primary Symptoms:

  • Dyspnea
  • Productive cough
  • Wheezing/chest tightness

Important Notes:

  • Initial stages are asymptomatic. Signs/symptoms appear when it is advanced.
  • Patients frequently have acute exacerbations, mostly due to viral infections and exposure to pollutants.

Physical Findings

Physical signs of COPD are present only in advanced disease.

1) Inspection

  • Cyanotic or pink color
  • May look dyspneic
  • Hyperinflated barrel chest
  • Use of accessory muscles of respiration

2) Palpation

  • Decreased chest expansion

3) Percussion

  • Hyper resonant chest (why?)

4) Auscultation

  • Decreased breath sounds
  • Wheezing & crackles may be present

Barrel Chest


Important Note on Clubbing

CLUBBING IS NOT A FEATURE OF COPD


Complications

  1. Type 2 respiratory failure (low O₂, high CO₂)

    • (high CO₂ can cause ---?)
  2. Pulmonary hypertension

  3. Right heart failure (cor pulmonale) due to (2)

  4. Polycythemia (in emphysema)

  5. Pneumothorax (due to rupture of bullae)

    • (Bullae are small air cavities in the lungs, often seen in COPD & asthma)

Bulla

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Investigations

1) Chest X-Ray (CXR)

  • Hyperinflated dark lung fields
  • Poor vascular markings
  • Flattened diaphragm
  • Wide intercostal spaces
  • Bullae may be seen

COPD on X-Ray

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Normal X-Ray

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2) Spirometry

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Key Spirometry Measurements

FEV₁ (Forced Expiratory Volume in 1 second) → air coming out in the 1st sec. of expiration

FVC (Forced Vital Capacity) → total air coming out forcefully (after a deep inspiration)


Spirometry Findings in COPD

  • Spirometry is definitive for diagnosis (in the context of history & examination)
  • Shows an obstructive pattern
  • FEV₁ is reduced, FVC is reduced & FEV₁/FVC ratio is also reduced (obstructive pattern)
  • FEV₁/FVC ratio is always less than 0.7 (<70%)
  • Residual volume (RV) high due to air trapping
  • Total lung capacity (TLC) increased due to air trapping

3) CT Chest

  • Shows more detailed pathology but not done routinely

4) CBC

  • May show polycythemia

5) Arterial Blood Gas (ABG)

  • Shows Type 2 respiratory failure in late COPD (low O₂, high pCO₂)

Most COPD patients have high PCO₂ in ABG, even at baseline. They are stable with this PCO₂.

6) ECG

May show features of cor pulmonale:

  • Right axis deviation
  • Right ventricle hypertrophy

When to Suspect COPD

Consider COPD in anyone who has:

  • Chronic cough, dyspnea and sputum, PLUS
  • History of exposure to risk factors like smoking or environmental pollution, PLUS
  • FEV₁/FVC ratio less than 0.7, even after bronchodilation

Severity of COPD (GOLD Criteria)

Based on FEV₁, COPD has 4 severity stages:

GOLD StageSeverityFEV₁/FVCFEV₁ % of Predicted
GOLD IMild COPD<0.7>80%
GOLD IIModerate COPD<0.750-80%
GOLD IIISevere COPD<0.730-50%
GOLD IVVery Severe COPD<0.7<30%

GOLD: Global Initiative for Chronic Obstructive Lung Disease

FEV₁: Forced Expiratory Volume in 1 second

FVC: Forced Vital Capacity


Management

COPD is a chronic disease but it is characterized by acute exacerbations, due to various factors. So, there is:

  • Treatment of the chronic stable patient
  • Treatment for acute exacerbations

Aims of Chronic Treatment

  • To improve signs/symptoms
  • To reduce exacerbations
  • To improve survival
  • To slow the disease progression

Treatment of Chronic Stable Patient

  1. Stop smoking & avoid exposure to pollutants
  2. Inhaled bronchodilators
  3. Inhaled corticosteroids (ICS)
  4. Theophylline (not routinely)
  5. Oxygen therapy

Only smoking cessation & O₂ therapy have shown to improve survival.


1) Smoking Cessation

  • Most important step
  • Survival is improved & lung function also improves
  • Formal smoking cessation programs are very helpful
  • Can also use anti-smoking meds (Nicotine patches, varenicline)
  • Avoid exposure to pollutants e.g., wood fire

2) Inhaled Bronchodilators

Foundation of COPD treatment. Produce bronchodilation.

a) Beta-Agonists:

  • Short-acting (e.g., salbutamol, Ventolin)
  • Long-acting (LABA) (e.g., salmeterol, formoterol)

b) Anticholinergics:

  • Short-acting (ipratropium)
  • Long-acting (tiotropium)

(Short-acting meds are used “AS NEEDED” for acute attack while long-acting are used daily as a baseline therapy)


Bronchodilators

BETA AGONIST

LONG ACTING
(used daily for chronic control)

  • a. Salmeterol
  • b. Formoterol

SHORT ACTING
(used as needed for acute exacerbation)

  • a. Salbutamol (Ventolin)
  • b. Albuterol

ANTICHOLINERGICS

LONG ACTING
(used daily for chr control)

  • a. Tiotropium

SHORT ACTING
(used for acute attack)

  • a. Ipratropium

3) Inhaled Corticosteroids (ICS)

  • They reduce inflammation in the airways
  • Examples: Fluticasone, Budesonide

“Inhaled” steroids are used long-term while I.V. steroids are used for acute attack.

Combinations of a LABA & ICS are available & widely used as chronic baseline therapy.


Important Notes on Bronchodilator Use
  • Short-acting bronchodilators are used for acute exacerbations (they have a quick onset of action), while long-acting agents are used daily for chronic treatment.
  • Short-acting agents can be used as “inhalers” or nebulizer solutions
  • Short-acting agents are not available in combination with steroids

LABA & ICS Combination

ICS + Beta Agonist

DEVICE USED TO INHALE:

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ANOTHER LABA + ICS: ICS + Salmeterol

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Very Important

Poor inhaler technique is a very common cause of not responding to medicines.


4) Theophylline (Aminophylline)

  • Not used too much now, due to toxicities
  • Sometimes added if inhaled bronchodilator therapy is not helping
  • If patient already taking it, don’t stop (COPD will worsen)

5) Oxygen (Long-Term Oxygen Therapy - LTOT) Z

  • Do ABG → start O₂ if pO₂ is low
  • Some patients need it 24 hrs, while others need it for few hours daily
  • Best is at least 15 hrs/day

Indications of LTOT Z
  1. pO₂ of less than 55 mmHg on ABG (even after maximum therapy). Should be done twice, & not during acute exacerbation
  2. pO₂ between 55 to 60, if complications are present (pulmonary HTN, cor pulmonale)

(Normal pO₂ is 60 and above)


Portable Oxygen

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Benefits of LTOT
  1. Improves survival (what else improves survival?)
  2. Improves pulmonary HTN & cor pulmonale
  3. Symptomatic improvement & sense of well-being

Important Warning

Be careful when giving O₂ to COPD patients. It can worsen the CO₂ (why?)


Other Modalities in Management

  1. Pulmonary Rehabilitation: Includes exercise training, nutritional counselling, social support. Should be done for all patients with moderate to severe COPD.

  2. Vaccinations:

    • Yearly flu vaccine
    • Pneumovac every 5 years

Monitoring the Patient’s Progress

How to monitor:

  1. By spirometry
  2. By history

Acute COPD Exacerbation

Characteristics:

  1. Caused by viral/bacterial chest infection or exposure to pollutants (commonest is viral)
  2. Worsening of signs/symptoms acutely
  3. ABG shows severe hypoxia & worsening CO₂

Treatment of Acute Exacerbation

  1. Nebulization with high doses of short-acting bronchodilators (Ventolin +/- ipratropium)
  2. Oral, I.V. or inhaled steroids
  3. “Controlled” oxygen (if needed)
  4. If still no improvement → ventilation

Indications for Ventilation During Acute Attack

  • CO₂ very high
  • Mental status changes (due to high CO₂)
  • No improvement with maximum therapy (oxygen in blood still very low even after giving O₂)

2 ways of ventilation:

a) Intubation and ventilation (if patient drowsy)

b) Non-invasive ventilation (BiPAP) - If patient is awake


Example of Non-Invasive Ventilation: BiPAP

BiPAP = Bilevel Positive Airway Pressure Ventilation

BiPAP is never used in a drowsy patient.

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Clinical Case

Patient Presentation:

  • Chronic smoker
  • Looks bluish & bloated
  • Complains of moderate dyspnea since few months & also productive cough for 2 years
  • AP diameter of the chest is high
  • FEV₁: FVC ratio is less than 0.7, gets only slight improvement after Ventolin

What’s the Diagnosis?

  1. Asthma
  2. Chronic bronchitis ✓
  3. Emphysema

Summary: Very Important Points

LAST SLIDE IS VERY IMPORTANT

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