COPD, Emphysema & Chronic Bronchitis

It is predicted that Chronic Obstructive Pulmonary Disease (COPD) will become the fourth leading cause of death worldwide within the next few years, accounting for more than 145,000 deaths and afflicting more than 24 million Americans. COPD is preventable and treatable, but is not necessarily reversible. Airflow limitations caused by noxious particles or gases, such as cigarette smoke, progressively worsen, often, despite treatment. COPD diagnoses account for the greatest number of patients receiving oxygen therapy, currently. Though COPD is primarily a degenerative disease of the respiratory system, classified into 4 stages, it causes systemic breakdown throughout the body. Obstructive respiratory issues, in general, are those that cause blockage of the airways that correspond with smooth airway muscle spasms and often affect exhalation. The term, COPD, represents the closely related diseases of Emphysema, Chronic Bronchitis and the long-term consequences of continued Asthma, with many patients having Emphysema and Chronic Bronchitis co-morbid diagnoses. In this degenerative respiratory disease, airflow is chronically obstructed, the alveoli are hyper-inflated and mucus is secreted in large amounts; along with emphysematous destruction of alveolar walls (impairing gas exchange) and a loss of elasticity in the respiratory tract from lung expansion to alveolar function (National Heart, Lung & Blood Institute, 2005; Fragoso, 2015; Ferrand, 2014; Samsam, 2015; Shier Butler, Lewis, 2015; Talaro & Chess, 2012; Steidl et al., 2014).

Patients often experience cough, phlegm, wheezing, diminishing breath sounds and a progressively slow development of dyspnea that occurs in the later stages of COPD that can sometimes require the need for artificial supply of O2 and is frequently associated with a reduction in functional ADL status and QOL. As the disease progresses, and hyperinflation ensues, patients may develop barrel chest. Barrel chest is combined with diaphragm flattening and a dimpling inward of the chest wall at the level of the diaphragm on inspiration, a symptoms known as the Hoover sign. At this point in COPD progression, a patient may use the accessory muscles of inspiration to draw a breath, instead of the primary muscles, and develop edema from an abnormal enlargement of the right side of the heart known as cor pulmonale (Ferrand, 2014; Samsam, 2015; Shier Butler, Lewis, 2015; Talaro & Chess, 2012; Steidl et al., 2014).

COPD patients experience changes in cognitive capacity due to hypoxemia or hypercapnia. The hypoxic drive of the healthy respiratory tract detects a lowered partial pressure of serum CO2 and drives the body to increase ventilation in order to maintain a balanced serum pH. Hypoxemia occurs when the partial pressure of serum O2 is below healthy levels, preventing it from binding to hemoglobin in order to be transported to the body’s tissues. Hypercapnia occurs when a patient has depressed ventilatory response to acute increases in arterial CO2, partly because of the altered acid/base balance and partly because of lung mechanics dysfunction that prevents them from increasing their ventilation appropriately (National Heart, Lung & Blood Institute, 2005; Fragoso, 2015; Ferrand, 2014; Samsam, 2015; Shier Butler, Lewis, 2015; Talaro & Chess, 2012; Steidl et al., 2014; Incalzi et al., 2014).

Approximately half of all COPD patients have Emphysema, where emphysematous destruction of the alveolar walls enlarges the lungs and impairs airway movement in and out of the respiratory tract. This causes a cough that never seems to go away or that gets worse over time, a frequent need to clear one’s throat, dyspnea or trouble with physical activity. Emphysema often affects more men than women, however, the rates of Emphysema are increasing in women. Patients need to forcefully expel air in order to empty the lungs but the forceful expulsion of air can put pressure on the airways from the outside, compressing them and causing those airways to collapse. Excessive coughing may result in airway collapse. As alveoli are destroyed, there is less surface area available for gas exchange, which increases the demand on the heart to circulate blood through the body and reduces the amount of O2 to be available to the tissues of the body (Ferrand, 2014; Samsam, 2015; Shier Butler, Lewis, 2015; Talaro & Chess, 2012).

Emphysema patients are also characterized with a large barrel-shaped chest, a poor air pumping system and in the advanced stages, every single breath is difficult.

Diaphragmatic hyperinflation is noted in this population, as well as in patients with COPD. Since emphysema is an obstructive airway disease, more O2 consumption is needed in order to worked the respiratory muscles during inhalation and exhalation, and this comes at a high O2 cost. The increased O2 cost contributes to patients’ limited physical activity and may contribute to the difficulty in weaning patients from mechanical ventilation (Ferrand, 2014; Samsam, 2015; Shier Butler, Lewis, 2015; Talaro & Chess, 2012).

In Chronic Bronchitis, defined as the presence of chronic or recurrent cough that has lasted for 3 consecutive months of the year over the course of 2 consecutive years (Steidl et al., 2014), the bronchial tree is under attack and airflow is obstructed due to inflammation that causes an excess production of mucus and edema. In a healthy individual, approximately 0.1L of mucous is secreted per day, but this increases significantly in the case of Chronic Bronchitis. Additionally, the mucosa becomes thicker and sticky, further impairing ciliary function, blocking or impeding airways that cause air to become stagnant and a breeding ground for bacteria, viruses and pollutants (Ferrand, 2014; Samsam, 2015; Shier Butler, Lewis, 2015; Talaro & Chess, 2012).

When edema is produced due to Chronic Bronchitis, it is considered a form of non-cardiac pulmonary edema, because fluid may leak from the capillaries due to increased respiratory membrane permeability, and increase fluid in the alveoli. Factors that can cause non-cardiac pulmonary edema, or exacerbate edema in Chronic Bronchitis, include bacterial infections, severe allergic reactions called anaphylaxis, smoke inhalation and acute respiratory distress syndrome (ARDS) (Ferrand, 2014; Samsam, 2015; Shier Butler, Lewis, 2015; Talaro & Chess, 201).

In general, patients suffering from Chronic Bronchitis have difficulty with clearing the mucus and the extra effort needed to expel the mucus can scar bronchial tube epithelium. If the mucus is not cleared, there exists a breeding ground for bacteria in the lower airways and an increased the risk of further infection. In contrast to COPD, in Chronic Bronchitis, women are diagnosed more frequently than men. Similar to COPD and Emphysema, the chronic inhalation of cigarette smoke causes Chronic Bronchitis. The degree of dyspnea in Chronic Bronchitis depends on the degree of congestion, the degree of bronchial inflammation, the amount of bronchial mucus secretion and the degree to which airway is obstructed (Ferrand, 2014; Samsam, 2015; Shier Butler, Lewis, 2015; Talaro & Chess, 2012).

If bacterial pneumonia develops in the lower respiratory airways, lung inflammation can increase interstitial lung and pleural fluid production, resulting in pneumonia-related pleural effusions. In many cases, when the pneumonia is treated, the pleural effusions are also resolved. If that fluid contains a high amount of protein, clots can develop and parapneumonic pleural effusions may form; a common cause of fever in ICU patients (Ferrand, 2014; Samsam, 2015; Shier Butler, Lewis, 2015; Talaro & Chess, 2012).

Patients suffering from pneumonia may experience stridor, which is an audible sound that occurs during inspiration and/or expiration that may be high or low pitched and resulted from turbulent airflow as the air passes through a narrowed or obstructed segment in the airway. Stridor is often caused by inspiratory stridor resulting from an obstruction at the laryngeal, nasal, or pharyngeal locations due to a collapse of soft tissues and negative pressures generated in the airway during inspiration. An obstruction within the trachea and bronchi commonly cause expiratory stridor and is not typically related to changing pressures within the airway (Ferrand, 2014; Samsam, 2015; Shier Butler, Lewis, 2015; Talaro & Chess, 2012).

Altering the position of a patient with pneumonia, particularly as a secondary infection in Chronic Bronchitis, can improve respiratory efficiency because altering the gravity-dependent ventilation distribution and perfusion of the respiratory tract can make it easier for the patient to breath (Ferrand, 2014; Samsam, 2015; Shier Butler, Lewis, 2015; Talaro & Chess, 2012).