top of page

Chronic Obstructive Pulmonary Disease (COPD)

Study Guide ​

​

Definition: 

​

a chronic disease characterised by progressive airflow limitation and not fully reversible with the presence of inflammatory response against toxic gases or particles.

  • Airflow obstruction along with pulmonary parenchymal destruction.

​

Epidemiology:

​

Smoking is the most common cause found in 90% of COPD cases in developed countries. 

  • Only 10-20% of all heavy smokers will develop COPD.

  • By 2020, it is predicted that COPD is going to be third most common cause of death & fifth most common cause of disability worldwide.

  • Mortality is higher in females.

​

Causes:

​

Smoking: the most common cause of COPD. 

  • Alpha 1 antitrypsin deficiency: only 2% of emphysema cases. 

 

 

Pathophysiology:

​

Microscopically:

  • Squamous cells will replace the normal columnar cells.

  • Bronchi & bronchioles infiltration with acute & chronic inflammatory cells with lymphoid follicles in severe cases.

  • Persistent inflammation will result in scaring & fibrosis of bronchi & bronchioles causing narrowing and airflow limitation. 

    • If airflow limitation is combined with loss of lung elastic recoil and small airway collapse during expiration (emphysema).

      • Emphysema is a secondary result of persistent inflammation and destruction. 

      • The resulting V/Q mismatch will decrease the PaO2 and increase the respiratory effort.

Later, if the patient fail to maintain the respiratory efforts the PaCO2 will increase, which will stimulate the respiratory center on the long-term (those patients depend on hypoxemia to drive their ventilation and they become insensitive to CO2).

Most common consistent pathological finding seen in COPD is increased numbers of goblet mucus secreting cells.

Emphysema: abnormal permanent enlargement of alveoli beyond the terminal bronchioles without obvious fibrosis

Clinical correlation:

Take full caution when giving supplemental O2

to COPD patient as that may

suppress their respiratory centre and lead to death in-patient with chronic hypercapnia!

In summary, 3 mechanisms responsible for COPD:

  1. Loss of elasticity of emphysema.

  2. Airway inflammation and scarring. 

  3. Mucus plug

​

Signs & Symptoms

​

Chronic Bronchitis (Blue Bloaters):

  1. Productive cough (white or clear sputum) >3months per year for 2 consecutive years.

  2. Cyanosis and mild dyspnea.

  3. Weight gain and obesity.

  • Emphysema (Pink Puffers): 

  1. Minimal cough.

  2. Dyspnea and pursed lips.

  3. Weight loss.

Diagnosis:

  • Chest X-ray:

    1. Hyperinflation.

    2. Subpleural blebs and parenchymal bullae in emphysema.

  • Pulmonary function test (PFT):

    1. Decreased FEV1/FVC ration <80%.

    2. Normal or increased TLC.

    3. Decreased DLCO2 in emphysema.

  • Arterial blood gases (ABGs):

  1. Increased PCO2 in acute or chronic respiratory acidosis with hypoxemia.

  • Others: 

  • CBC:

    1. Leukocytosis in the context of acute exacerbation.

    2. Secondary polycythemia due to hypoxia.

  • Echocardiogram: to asses the cardiac function.

  • Alpha 1 antitrypsin deficiency: if premature onset of the disease <40 Y/O, or lifelong non-smoker. 

Management:

Non-pharmacological treatment:

  • Smoking & supplemental O2 are the most effective interventions to improve the survival in COPD patients.

    • Criteria for oxygen use if:

      • PO2 < 55 mmHg or O2 saturation < 88%.

      • If the patient has right sided heart failure or elevated hematocrit:

        • PO2 < 66 mmHg or O2 saturation < 90%.

      • The main aim is to raise the O2 saturation > 90%.

  •  BiPAP in cases of nocturnal hypoxia and acute exacerbations.

  • Surgical treatment for bullae or blebs, lung volume reduction, or single lung transplantation.  

    • Pharmacological treatment:

      • Bronchodilators (short acting beta 2 agonist and anti-muscarinic):

        • Inhaled anti-muscarinic agents are the most effective pharmacological treatment in COPD patients.

      • Theophyllines.

      • Corticosteroids.

      • Antibiotics. 

In the setting of fever and CXR infiltrates consider sputum  culture and gram staining. 

S.pneumoniae & H.influenzae are the most common organisms to cause COPD exacerbations.

Management of acute exacerbation: ​

  1. supplemental O2.

  2. Bronchodilator (albuterol).

  3. Antimuscarenic (ipratropium).

  4. IV+ - inhaled steroids.

  5. Antibiotics.

  6. In severe cases: Bip AP or intubation.

Complications:

  • Respiratory failure.

  • Pulmonary hypertension & cor pulmonale.

  • Nocturnal hypoxia:

    1. Most deaths in COPD patients occur at night due to hypoxemia & cardiac arrhythmias. 

​

Prophylaxis:

  • Pneumococcal vaccine every 5 years.

  • Influenza vaccine annually.

​

Prognosis:

Prophylaxis:

  • Pneumococcal vaccine every 5 years.

  • Influenza vaccine annually.

Prognosis:
The level of dyspnea is the best predictor of COPD prognosis.

  • 4 year mortality is measured by the BODE index:

    • 0-2 has 10% rate of mortality.

    • 7-10 has 80% rate of mortality.

  • Progressively decreasing FEV1 is indicator of poor prognosis.

​

General management of COPD:

C: corticosteroids

O: oxygen supplement.

P: prevention of smoking and prophylaxis

D: dilators (beta agonist, & antimuscarenic). 

If pharmacological treatment is insufficient referral to transplantation is needed.

Written by:       Roaa Amer                                                                       
Reviewed by:   Haifa Al Issa
                                 Bayan Alzomaili
                                 Areej Madani

Format editor: Salman Alahmed

bottom of page