What is COPD?

COPD is an abbreviation for Chronic Obstructive Pulmonary Disease. It is a chronic inflammatory process characterised by constriction of the airways as the result of an irritant, such as dust or pollutants. One of the most common causes is smoking. Exposure to these irritants causes damage to the lung that is irreversible. While smoking cessation or removal of the environmental irritant may result in an improvement in symptoms, it will not reverse the disease process.

COPD is an umbrella term made up of chronic diseases such as bronchitis and emphysema. Bronchitis is a chronic secretion of mucous in the bronchi over a three month or longer period, whereas emphysema is dilation and remodelling of the alveoli resulting in larger less efficient alveoli.

According to the COPDX program (McKenzie, Frith, Burdon & Town, 2003: s10), COPD involves degeneration of lung tissue from chronic mucous production or dilatation and damage to alveoli resulting in a remodelling of the small bronchioles and alveoli. Such remodelling leads to inefficient lung function due to constrictive airways, and causes impaired ability to perform efficient gaseous exchange.


Figure 2 shows a normal healthy bronchi and alveoli compared with a COPD affected bronchi and alveoli. Source http://www.airliquidehealthcare.com.au

Diagnosis of COPD

COPD is generally diagnosed by formal pulmonary function tests. These include spirometry, medical imaging in the form of x-ray and high resolution CT scans, and other tests such as a six minute walk test. It also involves a comprehensive respiratory assessment and history to determine background and exposure to likely triggers for COPD.


Figure 3. A typical COPD chest xray showing hyperinflation of the lungs and a flattening of the diagram. Source http://www.oup.com

The major problem with COPD is that it causes a constriction of the bronchi, via remodelling of the alveoli or through excess mucous production. This causes hyperinflation of the lungs, because the patient simply cannot empty the lungs fully. This is verified when completing spirometry in that the forced expiratory volume in 1 second (FEV1) will be reduced in a patient with COPD (Yawn, 2011: 122-123). Since the patient has difficulty in moving air from the inside to out, it stands to reason, that there will be a large volume of dead space (Space where air sits but does not participate in gaseous exchange) and there will be a reduction in the amount of refreshed air being inhaled. Of the air that is inhaled, much of it will remain in dead space and will have difficulty in reaching viable alveoli. As the lungs are hyper inflated, the respiratory muscles remain stretched and are limited in the amount of elastic recoil that would normally increase the volume of air being exhaled. This effectively traps the air in the lungs causing the additional dead space (Lyne, 2010: 50). Since the respiratory muscles are working so hard, there will be an element of fatigue and lactic acid production caused by anaerobic respiration, leading to a decrease in blood pH. The amount of CO2 in that remains in the blood due to poor gaseous exchange will further decrease pH, and in an attempt to compensate for the reduced pH, will cause the patient’s respiratory rate to increase. In addition, remodelling of the alveoli causes an alteration to shape and size of the alveoli leading to a surface area or collapse of the alveoli (atelectosis) due to an alteration in surface tension and surfactant to maintain the correct shape, elasticity and surface area of the alveoli. In late stages of the disease, there may also be a thickening of the alveolar walls known as pulmonary fibrosis (West, 2008: 85) .


Figure 4. Atelectosis in COPD (specifically emphysema). Source http://www.empowher.com

Atelectosis will contribute further to poor gas exchange and the cycle simply becomes worse. Alveoli that undergo atelectosis cannot participate in gas exchange. As more atelectosis takes place, the ability to exchange gases will worsen. In your patient you will see chronic dyspnoea (shortness of breath) and decreasing oxygen saturations (see what does a decrease in oxygen saturations mean?) (Lyne, 2010: 49). Dyspnoea is discussed in more detail in the page 'what can my patient do to conserve energy and improve oxygenation'.

As CO2 levels continue to chronically rise, the patient will begin to rely on their hypoxic drive to breathe and rely less on their hypercapnic drive which is known as CO2 retention (See What if my patient is a CO2 retainer).There is evidence that regular exercise can stabilise or reduce the effects of COPD, however in a patient with significant symptoms, there is a decrease in exercise tolerance due to dyspnoea and anaerobic respiration at the cellular level due to poor oxygenation and gas exchange. As this process continues, the patient will fatigue and if not managed correctly will have an overall deterioration in condition leading to respiratory failure, multiple organ failure and death (Hanania & Donohue, 2007: 526).