Chronic obstructive lung disease (COPD): A collective term used to describe the condition of airway

obstruction
1. Reasons for airway obstruction

A. Obstruction caused by excessive secretion

B. Obstruction caused by increased muscle activity and bronchus
constriction
C. Obstruction caused by destruction of lung tissue, causing loss of
elasticity then loss of radial traction force

A. Considering the pathologies...

a. Type A and B should belong to chronic bronchitis (increased secretion due to inflammation and inflammation causes
fibrosis near bronchi so the bronchi become larger)
b. Type C should belong to emphysema because destruction of lung tissue, especially the elastic tissue elastin can cause
loss of lung recoiling force and then loss of radial traction
2. Pathology 1: Emphysema
A. Pathophysiology
a. We know that both alveoli and capillary walls are made up of elastin, namely some elastic tissue
α 1-antitrypsin will produce anti-protease, which is an enzyme produced by our
body naturally to fight against elastase
Lysosomal elastase is another enzyme produced by our body naturally to break
down elastin in alveoli and capillaries

1. Congenital cause: alpha 1-antitrypsin deficiency

A. Imbalance amount between protease and and anti-protease, leading to
excessive breakdown of elastin in alveoli and capillaries
2. Cigarette cause:
A. Cause more neutrophil release so there is more protease
B. Pathological change
In respiratory zone...we have respiratory bronchi and alveoli
1. Centriacinar
A. Destruction occurs at respiratory bronchi
2. Panacinar
A. Destruction of alveolar wall

a. The situation is that there are less "folds" inside our lung, so the gaseous exchange area decreases and hypoventilation
occurs. Notes: Panacinar type has larger loss of surface area then centriacinar type.
3. Pathology 2: Chronic bronchitis
A. Pathophysiology

As its name suggests, it is about inflammation of bronchi. And the image at the left shows
inflammatory changes: (A is normal, and B is abnormal)
1. Increased secretion, at mucosa
2. Increased cellular infiltration, at submucosa
3. Globet cells hypertrophy
4. Due to inflammation, there may be edema of bronchi and fibrosis around bronchi, causing
thickened smooth muscle around.

The inflammatory changes start at smaller airway first, then progress to larger airway.

B. Causes of chronic bronchitis

a. Smoking
b. Air pollution
4. Comparison between consequences caused by the two pathologies
A. Result of blood gas analysis
a. Emphysema: relatively normal result of blood gas analysis
1. By compensating respiratory pattern (use of accessory muscle, extending expiratory time), patient can keep being
hyperventilated initially.
b. Chronic bronchitis: poor result of blood gas analysis, ↑PCO2, ↓PO2
1. Involving direct obstruction of airway and can't be compensated by any breathing mechanism, causing
hypoventilation.
B. Color of patient
a. Emphysema: pink puffer (looks pink) due to compensatory breathing pattern
b. Chronic bronchitis: blue bloaters due to hypoventilation (cyanosis)
C. Heart condition
a. Emphysema: rarely cause heart problem
1. The capillary walls and alveoli are destroyed at the same time. Although destruction of lung causes hypoventilation,
but destroying these 2 things at the same time will lead to matching of V/Q ratio, imposing no stress to heart.
b. Chronic bronchitis: can cause heart failure/pulmonary edema
1. Obstruction of airway only induce hypoventilation. In order to match the V/Q ratio, there will be vasoconstriction,
leading to high pulmonary blood pressure. This will cause back pressure to heart and peripheral edema.
 D. Sputum
a. Emphysema: less sputum volume
1. No inflammation so no sputum... make sense?
b. Chronic bronchitis: purulent sputum (because many sputum so it causes irritation of airway and chronic cough)
1. Inflammation in nature so...
2. Expectoration of sputum on most days for at least 3 months in 2 successive years.
E. X-ray appearance

Due to... Due to...

1. Heart involvement Increased work of breathing,
2. Inflammation of harder muscle pull
bronchi

F. Gaseous retention
a. Emphysema: barrel chest
1. Cuz the dead zone at emphysema is particularly large, there is many gas trapped
b. COPD: not much
5. Common signs and symptoms of COPD
A. No matter what consequences they cause, the similar thing is that both of them cause obstruction in lung.
B. Problems caused by airway obstruction...
a. Increased SOB
b. Poor ET
c. Hyper-inflated lung
d. Impaired gas exchange
e. Chronic cough
Diagnosis of COPD: General procedure and framework
Measurements involved in diagnosis and classification:
1. Spirometry
2. GOLD scale: airflow limitation
3. modified medical research council dyspnoea scale (mMRC)
4. CAT-COPD assessment test, measuring severity of COPD symptoms
1. Spirometry: no need explain right
2. GOLD scale
A. We only do the test for patients with FEV1/FVC < 0.70 i.e. FEV1 already impaired
B. We apply bronchodilator to patients and do the measurement of FEV1 again
C. Compare the FEV1 value obtained to predicted one

3. mMRC

Assessment of severity of COPD: BOLD index

Treatment of COPD: Acute Exacerbation of COPD (AECOPD)
1. Classification of AECOPD and consequences
Take the pathology shown on the table at the left: (for reference)
AECOPD is caused by a sudden increase in airway inflammation

1. Type 1
A. ↑ dyspnoea, sputum; ↓PEFR
B. Presented as increased inflammatory response
2. Type 2: 2 of the above symptoms
A. Increased in inflammation
3. Type 3
A. 1 of 3 + URTI, fever, wheeze
B. infection in upper respiratory tract and fever means severe infection
C. wheeze means excessive bronchus constriction
D. Type 3 is the most severe form of inflammation
2. Management of AECOPD
A. Detection of AECOPD
B. Prevention of AECOPD
C. Pharmacological management
1. Bronchodilation
A. β-2 agonist: Used for parasympathetic nervous system and relax smooth muscle
B. Anticholinergic: inhibit sympathetic signals, which causes bronchoconstriction
2. Oral corticosteroids
A. Reduce inflammation, easy
3. Antibiotics
A. Maybe it can relieve the cause for acute onset of inflammation?
B. Shorten recovery time and reduce risk of relapse

D. Oxygenation: NIV
a. Indication 1: Respiratory acidosis
1. PaCO2 ≥45 mmHg and Arterial pH ≤7.35
b. Indication 2: Severe dyspnoea with clinical signs
1. Respiratory muscle fatigue, Increased work of breathing, retraction of intercostal spaces
2. Reason behind: NIV system provide positive pressure to push oxygen to patient body, reducing the work of breathing
c. Indication 3: Persistent hypoxemia despite supplementary Oxygen therapy
Treatment of COPD: Stable COPD
1. Pharmacological management
A. General medications use in stable COPD

B. Follow-up Pharmacological management

There are two predominant symptoms for chronic COPD: Dyspnea and Exacerbations
So, the medications used depends on which kind of symptoms the patient has.

Dyspnea: ↓inflammation, ↑ bronchoconstriction

Exacerbations: ↑ inflammation, ↓ bronchoconstriction

Effect of drugs:
1. LAMA & LABA: For both kinds of COPD, bronchoconstriction is the primary
symptom so bronchodilators (LAMA & LABA) are the first line of treatment
2. ICS: Inhibiting inflammatory cell recruitment but have a weaker effect on airflow
improvement
3. Roflumilast: non-steroid long-term inflammation control , can't address immediate
acute inflammation and bronchoconstriction
4. Azithromycin: Chronic smoking can cause bacterial infection. Using a antibiotics can
reduce bacterial inflammation caused by chronic smoking

a. So the general idea is application of LAMA & LABA cuz they reduce the primary symptoms of bronchoconstriction
b. Depends on whether the patient's main cause is inflammation or not, choose to apply ICS
1. Indication for inflammation: presence of eosinophils (by EOS, eosinophils counts), an kind of immune cells
A. EOS ≥300
B. EOS ≥100 + ≥2 moderate exacerbations/1 hospitalization
c. But we know ICS, steroid use can be harmful to patient so we have to stop if...
1. Lack of response of ICS
2. Pneumonia
3. Inflammation reduces i.e. EOS smaller than 100
d. Roflumilast and Azithromycin as supportive treatment
2. Non-pharmacological management
A. Smoking Cessation
B. Pulmonary Rehabilitation
a. Overall aim: ↑ functional capacity & ↑ quality of life via exercise
b. Rehab goals:
1. General mobility
2. Functional capacity
3. Intercostal muscle training (IMT)
4. SpO2 monitoring
5. Breathing control
6. Pulmonary hygiene (secretion removal?)
c. Outcome measures

C. Vaccination (Flu/ Pneumococcal vaccination)

D. Oxygen therapy and hypoxic drive
Hypoxic drive as contraindication of oxygen therapy:
Due to prolonged increase in PCO2, the respiratory center get used to a low O2 level.
Ventilation is then stimulated by a low blood oxygen levels.

So if we suddenly increase the O2 to patient, the respiratory center may stop

functioning.