CHRONIC PULMONARY EMPHYSEMA

Long-term inhalation of tobacco smoke or other irritants causes chronic infection of the bronchi and bronchioles.
This infection damages the normal protective mechanisms of the airways.
The cilia of the respiratory epithelium become partially paralyzed and eventually destroyed.
This damage is caused by toxic substances present in tobacco smoke and air pollution.
Because the cilia cannot function properly, mucus cannot be cleared effectively from the airways.
At the same time, mucus secretion increases, causing further blockage of the airways.
Alveolar macrophages are also inhibited, making them less effective at fighting infection.

Chronic infection, excess mucus, and inflammatory swelling (edema) of the bronchiolar lining together produce chronic obstruction of many small airways.

Because the airways are narrowed, expiration becomes especially difficult.
Air becomes trapped inside the alveoli.
The trapped air overstretches the alveoli.
Overstretching, together with chronic infection, destroys about 50–80% of the alveolar walls.
The emphysematous lung therefore contains:
- Large, overdistended air spaces.
- Marked loss of normal alveolar walls. (Figs. 43.4 and 43.5)

Physiological Effects of Chronic Emphysema

Bronchiolar obstruction increases airway resistance.
As a result, the work of breathing increases greatly.
Expiration is especially difficult.
During expiration:
- Pressure outside the lungs compresses both the alveoli and bronchioles.
- This further narrows the bronchioles.
- Airflow resistance increases even more.

Destruction of alveolar walls greatly reduces the lung’s diffusing capacity.
Consequently:
- Less oxygen diffuses into the blood.
- Less carbon dioxide diffuses out of the blood.

Airway obstruction is more severe in some lung regions than in others.
Therefore:
- Some lung regions are well ventilated.
- Other regions are poorly ventilated.
This produces markedly abnormal ventilation–perfusion (V̇A/Q̇) ratios.
In poorly ventilated regions:
- V̇A/Q̇ is very low.
- This creates a physiological shunt.
- Blood remains poorly oxygenated.
In well-ventilated but poorly perfused regions:
- V̇A/Q̇ is very high.
- This creates a physiological dead space.
- Ventilation is wasted because little blood is available for gas exchange.
Both physiological shunt and physiological dead space can occur simultaneously in the same lungs.

Chronic emphysema usually progresses slowly over many years.
As the disease worsens:
- Hypoxia develops because many alveoli are poorly ventilated and many alveolar walls are destroyed.
- Hypercapnia develops because carbon dioxide cannot be removed efficiently.
The combination of hypoxia and hypercapnia produces severe, prolonged shortness of breath (dyspnea).
This air hunger may continue for years.
Eventually, severe hypoxia and hypercapnia can lead to death.

Chronic pulmonary emphysema is a chronic obstructive and destructive lung disease, most commonly caused by long-term smoking.
Chronic infection damages cilia, increases mucus secretion, and weakens alveolar macrophage function.
Inflammation and mucus obstruct small airways, making expiration difficult and causing air trapping.
Air trapping and infection destroy 50–80% of the alveolar walls, producing enlarged air spaces.
Airway obstruction increases the work of breathing, especially during expiration.
Loss of alveolar walls decreases the lung’s diffusing capacity, reducing oxygen uptake and carbon dioxide removal.
Uneven airway obstruction produces severe ventilation–perfusion mismatch, causing both physiological shunt (low V̇A/Q̇) and physiological dead space (high V̇A/Q̇).
Loss of pulmonary capillaries increases pulmonary vascular resistance, leading to pulmonary hypertension and right-sided heart failure.
The disease progresses slowly, causing chronic hypoxia, hypercapnia, severe dyspnea, and eventually death if advanced.

PREPARE AND MADE BY SELF LEARNING DR SHEEN.