Chronic obstructive pulmonary disease (COPD) has been identified as the fourth most common cause of death worldwide.1 This disease is treatable and can be prevented if the appropriate measures are taken. Its functional limitation is characterized by restricted airflow that cannot be fully reversed.2 The restricted airflow is commonly progressive and is associated with an abnormal inflammatory response of the lungs.3 Therefore, COPD can also produce significant systemic consequences. The primary cause for COPD is smoking tobacco that can occur in current and former smokers.
COPD is a disease of the airways that produce obstruction to expiratory airflow.1 Obstruction of the airway can be caused by a variety of contributing factors including airways and alveoli that lose their elasticity leading to bronchoconstriction, destruction of the airway walls between the alveoli, thickening and inflammation of airway walls, and secretion of mucus made by the airways. These problems associated with COPD lead to a decreased size of the bronchiole tube and an increased resistance to airflow. Despite the
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The diaphragm and accessory breathing muscles are challenged with increased demands on inspiration, and elevated lung resistance and compliance. Concurrently, the efforts of the muscles of inspiration to produce pressure is decreased due to disadvantageous mechanical nature inflicted by hyperinflation.4 Abnormal gas exchange will also occur and oxygen levels will decrease progressively throughout the disease, which can be identified when examining arterial blood gas (ABG) values. COPD is divided into two types which includes emphysema and chronic bronchitis. The two conditions can be differentiated by assessing ABG values. ABG values indicating emphysema demonstrate a decrease in PaO2 and CO2, whereas chronic bronchitis is noted to have an increase PaO2 and