COPD Pathophysiology | Nursing School Notes

Chronic Obstructive Pulmonary Disorder (COPD) is a preventable chronic inflammatory pulmonary illness that obstructs the airflow in the lungs.

In simple terms, COPD is a condition that develops slowly over a very long period. As it starts to become worse, COPD begins to irritate the inner linings of the lungs causing inflammation. Over time, this inflammation will start to reduce the airflow that goes into the lungs, and hence create several problems such as difficulty breathing, coughing and sputum production.

Most of these problems can be treated and made less problematic, but unfortunately, the damage done to the lungs can not be fully reversed. This means that if the individual does not manage the condition well in the beginning, it will slowly develop into a very serious and life-threatening illness.

In these notes, we’ll be going over the:

1. Pathophysiology of COPD

2. Types of COPD

3. Risk Factors of COPD

4. Symptoms of COPD

But before diving into this topic, you must first understand the basics. So start off by reading the Anatomy and Physiology of the Respiratory System, and then come back to understand COPD and its manifestations.

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The Pathophysiology of COPD

In most cases, individuals who develop COPD would first report mild symptoms around the age of 40years. From there on it’s a downhill battle, because unless they take drastic measures to improve their lifestyle and take in the correct treatment, their symptoms are expected to become increasingly worse. – And this idea of an illness worsening over time is what we call a Progressive Illness.

Typically, the airflow limitation in COPD is triggered by an environmental irritant such as tobacco smoking or air pollution. The body senses that these irritants should not enter the lungs, and as a defence mechanism it sets off several things to block the irritant. But in doing so, it triggers a severe inflammation in the airways.

In fact, this abnormal inflammatory reaction is so severe that it affects every single structure of the respiratory system. It affects the:

1. Proximal Airways (Trachea & Bronchi): By multiplying the amount of Goblet Cells and enlarging the Submucosal Glands, which causes hypersecretion of mucus.

2. Peripheral Airways (Bronchioles): By thickening the airway wall, causing peribronchial fibrosis and secreting exudate in the airways. This process is known as Obstructive Bronchiolitis, and over time the repetitive damage-and-repair process creates scar tissue which continues to make the airway lumen even more narrow.

3. Parenchyma (Bronchioles and Alveoli): By decreasing the elastic recoil of alveoli and losing their attachments, it damages the alveolar wall. In addition, the abnormal inflammation could also trigger the release of Proteinases and Anti-Proteinases. Both of which would damage the lung parenchyma if they’re imbalanced.

4. Pulmonary Vasculature: By increasing g the thickness of the vessel lining, and causing hypertrophy to the smooth muscle. In turn, leading to pulmonary hypertension.

Looking at that list, you can see how COPD affects every single structure in the respiratory system. But in most cases, individuals with COPD would not have all the problems at once, at least not at the start of the illness. For this reason,  COPD is divided into two types, depending on which part of the respiratory system it affects.

The Two Types of COPD

1. Chronic Bronchitis (Affects the bronchial tubes)

2. Emphysema (Affects the Alveoli)

The Pathophysiology of Chronic Bronchitis

Earlier we mentioned that COPD occurs when the body triggers an abnormal inflammatory reaction in the respiratory system. In some individuals, that inflammation specifically affects the bronchial tube, hence why one of the types of COPD is called Chronic Bronchitis.

The condition triggers the increase of mucus-secreting glands and goblet cells and ultimately the hypersecretion of mucus. In fact, for someone to be diagnosed with Chronic Bronchitis, they must have had a cough and constant sputum production for a minimum of 3 months in 2 consecutive years.

Unfortunately, the process doesn’t stop there. The hypersecretion of mucus can be seen as the first domino that tips over, and then it continues to tip the rest. Because from there on, one bad thing will trigger the next:

1. The excess mucus starts to add up and eventually blocks the airways. This process is called Mucus Plugging and it hinders the Ciliary Function.

2. The Bronchial walls thicken making the Bronchial Lumen narrower.

3. Damage and fibrosis occur on the alveoli closest to the bronchioles. In turn, they impact the function of the Alveolar Macrophages which would typically break down any bacteria or foreign particles in the lungs.

4. Lastly, since the Alveolar Macrophages aren’t functioning well, the patient becomes more prone to getting a Respiratory Infection leading to a COPD Exacerbation!

Pathophysiology of Emphysema  

The second type of COPD is Emphysema, unlike Chronic Bronchitis the inflammation affects the alveoli and not the bronchioles. This creates a problem in the gas exchange, which means that oxygen and carbon dioxide are not exchanged effectively. In Emphysema, the airspaces normally found after the terminal bronchioles become distended. This will damage the walls of the alveoli reducing the alveolar surface area that is in direct contact with the pulmonary capillaries.

Now if you’ve understood the Anatomy & Physiology of the Respiratory System, you should know that oxygen and carbon dioxide are exchanged between the surface area of the alveoli and the pulmonary capillaries. So naturally, if the surface area of the alveoli is damaged, then the gases can not be exchanged. This area where no gas exchange can take place is called the Dead Space.

As Emphysema continues to progress, more and more dead spaces are created which limit the oxygen diffusion into the blood, resulting in Hypoxemia (low oxygen levels in the blood). Since oxygen is not entering the blood, the carbon dioxide in the blood has no motivation to leave and so it starts to build up causing Hypercapnia (high CO2 in the blood).

Another issue that develops in Emphysema is Pulmonary Hypertension. This occurs because as the disease manifestations continue to worsen, the alveolar walls will continue to break down shrinking the size of the pulmonary capillary bed. The pulmonary blood flow however remains the same, the only difference now is that there are fewer areas where it can flow through. Because of this, the pressure of the pulmonary blood flow is increased, forcing the right ventricle to maintain a higher blood pressure in the pulmonary artery.

Eventually, the right ventricle will become tired of having to maintain such high pressures and it develops a right-sided heart failure also known as Cor Pulmonale. In addition, the high pressure in the pulmonary arteries and right ventricle stops creating a ‘pool’ of blood in the venous system that takes longer to go through. This backup of blood then causes distended neck veins, dependent oedema and pain in the region of the liver.

Having emphysema doesn’t necessarily mean that the individual would have all the complications mentioned above. In fact, the condition is further subdivided into two types depending on the changes that occur.

The Two Types of Emphysema

1. Pan-Lobular Type/ Panacinar

Pan-lobular Emphysema damages the respiratory bronchioles, the alveolar ducts and the alveolus. When this occurs, the airspaces in each lobule increase in size and making it more difficult to fully empty the lungs. This means that muscular effort would be required to exhale, and the process becomes an active movement.

Most patients who have Pan-Lobular Emphysema would have a hyperinflated chest, nicknamed ‘Barrel Chest’. This symptom develops because the lungs would have stayed overinflated for a long period, forcing the rib cage to remain expanded. Moreover, most patients would also experience weight loss, muscle wasting and dyspnoea during exercise.

2. Centri-Lobular Form

Centri-Lobular Emphysema damages the centre of the secondary lobule, preserving the peripheral portions of the acinus (ie. The terminal airway unit where gas exchange occurs). The condition is characterised by an imbalance in the Ventilation-Perfusion Ratio, making the patients more susceptible to developing Central Cyanosis, Respiratory Failure and Peripheral Oedema.

Risk Factors for COPD

Tobacco Smoking

Roughly 80-90% of the patients suffering from COPD would have been or still are tobacco smokers. Countless studies have shown a direct relationship between the number of cigarettes smoked per year and a decrease in the individual’s lung function. This is because tobacco smoking:

1. Destroys the Scavenger Cells and the Respiratory Tract’s Ciliary Mechanism. This allows irritants, bacteria and foreign matter to pile up and clog the airways, resulting in airflow obstruction and air trapping behind the blockage.

2. Causes the alveoli to become distended minimising their capacity.

3. Damages the Goblet Cells and triggers the hypersecretion of mucus.

4. Produces Carbon Monoxide; a gas that attaches to haemoglobin creating Carboxyhaemoglobin and decreasing the efficiency of its oxygen-carrying capacities.

Genetic Abnormalities: Alpha1AntiTrypsin

Alpha1 AntiTrypsin is a naturally occurring enzyme inhibitor that protects the lung parenchyma from injury. However, there’s a small percentage of individuals who are born with a deficiency in the enzyme inhibitor and it puts them at a higher risk of rapidly developing Pan-Lobular Emphysema even if they do not smoke.

Such individuals can receive Alpha Protease Inhibitor Replacement Therapy to slow the progression of the disease or treat its severity. However, infusion therapy is very expensive and it’s required on an ongoing basis.

Apart from tobacco smoking and genetic deficiencies, other risk factors of COPD include:

1. Air Pollution

2. Occupational Dust

3. Inhalation of Certain Chemicals

The Symptoms of COPD

COPD is characterized by three main symptoms:

1. Chronic Cough

2. Sputum Production

3. Dyspnoea

Every patient presents the symptoms slightly different, some might have a chesty cough while others could have a dry repetitive cough. Some individuals might feel dyspnoea only when exercising, while others can have it so severe that it would limit their daily activities and decrease their quality of life. But one thing that is certain for all COPD patients is that all symptoms start mildly, and then get progressively worse over time. In some cases, dyspnoea is present when eating, and so patients often lose weight because eating becomes an exhausting task as well.

As we’ve already mentioned when explaining Pan- Lobular Emphysema, patients with this type of COPD will have a hyperinflated chest, their supraclavicular fossae retract during inspiration (shoulders go up) and their abdominal muscles contract during inspiration. All because exhalation becomes an active process, and inhalation requires more effort.

Additionally, patients with advanced COPD usually develop secondary conditions including depression because of their new limitations in life, Musculoskeletal wasting from an imbalanced diet, diabetes, and metabolic syndrome.

So all in all here’s the full list of symptoms that COPD presents with:

1. Chronic Cough

2. Sputum Production

3. Dyspnoea

4. Hyperinflated Chest

5. Retraction of the Supraclavicular Fossae on Inspiration

6. Contraction of the Abdominal Muscles on Inspiration

7. Weight Loss

8. Musculoskeletal Wasting

And that is pretty much it for The Pathophysiology of COPD for Nursing Students, next up let’s look at  the Nursing Assessment & Care for Patients with COPD.

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References

1. Hinkle, Janice. Brunner & Suddarth’s Textbook of Medical-Surgical Nursing . Wolters Kluwer Health. Kindle Edition.

2. O’Reilly S. (2016). Chronic Obstructive Pulmonary Disease. American journal of lifestyle medicine, 11(4), 296–302. https://doi.org/10.1177/1559827616656593

3. Hikichi, M., Mizumura, K., Maruoka, S., & Gon, Y. (2019). Pathogenesis of chronic obstructive pulmonary disease (COPD) induced by cigarette smoke. Journal of thoracic disease, 11(Suppl 17), S2129–S2140. https://doi.org/10.21037/jtd.2019.10.43

4. Dotan, Y., So, J. Y., & Kim, V. (2019). Chronic Bronchitis: Where Are We Now?. Chronic obstructive pulmonary diseases (Miami, Fla.), 6(2), 178–192. https://doi.org/10.15326/jcopdf.6.2.2018.0151

5. Goldklang, M., & Stockley, R. (2016). Pathophysiology of Emphysema and Implications. Chronic obstructive pulmonary diseases (Miami, Fla.), 3(1), 454–458. https://doi.org/10.15326/jcopdf.3.1.2015.0175

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