Chronic Obstructive Pulmonary Disease: Emphysema COPD is a disease state characterized by airflow limitation that is not fully reversible

. COPD is defined as a disease state characterized by the presence of airflow obstruction that is generally progressive, may be accompanied by airway hyperreactivity, and may be partially reversible. Emphysema is a pathologic term that describes an abnormal distension of the air spaces beyond the terminal bronchioles, with destruction of the walls of the alveoli. (Smeltzer, 2008) Emphysema is the presence of overdistended, non-functional alveoli, which may rupture resulting to loss of aerating surface. (Udan) Emphysema is characterized by abnormal and permanent enlargement of the airspaces distal to the terminal bronchioles which results in destruction of the walls of the alveoli. 2 types Panlobular (panacinar)- there is a destruction of the respiratory bronchioles, alveolar duct and alveolus. All air spaces within the lobule are essentially enlarged but there is little inflammatory disease. Dilatation and destruction involves entire acinus

Centrilobular (centroacinar)- pathologic changes take place mainly in the center of the secondary lobule, preserving the peripheral portions of the acinus. Dilatation and destruction involve central part of acinus


The respiratory system consists of two lungs, conducting airways, and associated blood vessels. The major function of the respiratory system is gas exchange. During ventilation, air is taken into the body on inhalation (inspiration) and travels through respiratory passages to the lungs. Oxygen (O2) in the lungs replaces carbon dioxide (CO2) in the blood during perfusion, and then CO2 is expelled from the body on exhalation (expiration).

Conducting airways The conducting airways allow air into and out of structures within the lung that perform gas exchange. The conducting airways include the upper airway and the lower airway.

Upper airway The upper airway consists of the: • • • • Nose Mouth Pharynx Larynx

The upper airway allows air to flow into and out of the lungs. It warms, humidifies, and filters inspired air and protects the lower airway from foreign matter.

Lower airway The lower airway consists of: • • • • Trachea Right and left mainstem bronchi Five secondary bronchi Bronchioles

The lower airways facilitate gas exchange. Each bronchiole descends from a lobule and contains terminal bronchioles, alveolar ducts, and alveoli. Terminal bronchioles are “anatomic dead spaces” because they don’t participate in gas exchange. The alveoli are the chief units of gas exchange.

In addition to warming, humidifying, and filtering inspired air, the lower airway provides the lungs with defense mechanisms, including: 1. Irritant reflex The irritant reflex is triggered when inhaled particles, cold air, or toxins stimulate irritant receptors. Reflex bronchospasm then occurs to limit the exposure, followed by coughing, which expels the irritant. 2. Mucociliary system The mucociliary system produces mucus, which traps foreign particles. Foreign matter is then swept to the upper airway for expectoration. A breakdown in

the epithelium of the lungs or the mucociliary system can cause the defense mechanisms to malfunction. This allows atmospheric pollutants and irritants to enter and inflame the lungs. 3. Secretory immunity Secretory immunity protects the lungs by releasing an antibody in the respiratory mucosal secretions that initiates an immune response against antigens contacting the mucosal.


The lungs are air-filled, spongelike organs. They’re divided into lobes (three lobes on the right, two lobes on the left). Lobes are further divided into lobules and segments.

The lungs contain about 300 million pulmonary alveoli, which are grapelike clusters of air-filled sacs at the ends of the respiratory passages. Here, gas exchange takes place by diffusion (passage of gas molecules through respiratory membranes). In diffusion, O2 is passed to the blood for circulation through the body. At the same time, CO2 –a cellular waste product that’s gathered by the blood as it circulates–is collected from the blood for disposal out of the body through the lungs.

Alveoli consist of type I and type II epithelial cells: 1. Type I cells form the alveolar walls, through which gas exchange occurs 2. Type II cells produce surfactant, a lipid-type substance that coats the alveoli. During inspiration, the alveolar surfactant allows the alveoli to expand uniformly. During expiration, the surfactant prevents alveolar collapse.

Breathing mechanics

The amount of air that reaches the lungs carrying O2 and then departs carrying CO2 depends on three factors: • Lung volume and capacity o • • Lung volume and capacity is the amount of air that’s moved in and out of the lungs

Compliance (the lungs’ ability to expand) Resistance to airflow o Resistance refers to opposition to airflow. Changes in resistance may occur in the lung tissue, chest wall, or airways.

Neurochemical control The respiratory center of the central nervous system (CNS) is located in the lateral medulla oblongata of the brain stem. Impulses travel down the phrenic nerves to the diaphragm and then down the intercostals nerves to the intercostals muscles between the ribs. There, they change the rate and depth of respiration.

Chemoreceptors respond to the hydrogen ion concentration (pH) of arterial blood, the partial pressure of arterial carbon dioxide (PaCO2), and the partial pressure of arterial oxygen (PaO2). Central chemoreceptors respond indirectly to arterial blood by sensing changes in the pH of cerebrospinal fluid (CSF). PaCO2 also helps regulate ventilation (by impacting the pH of CSF). If PaCO2 is high, the respiratory rate increases. If PaCO2 is low, the respiratory rate decreases. The respiratory center also receives information from peripheral chemoreceptors in the carotid and aortic bodies (small neurovascular structures in the carotid arteries and on either side of the aorta). These chemoreceptors respond to decreased PaO2 and decreased pH. Either change results in increased respiratory drive within minutes.

Etiology Predisposing Genetic Rationale Deficiency of Alpha-antitrypsin, an enzyme inhibitor that protects the lung parenchyma from injury. This deficiency predisposes young people to rapid development of lobular emphysema, even if they do not smoke. Approximately 1 to 2 percent of people with emphysema have an inherited deficiency of a protein called AAt, which protects the elastic structures in the lungs. Without this protein, enzymes can cause progressive lung damage, eventually resulting in emphysema. If you're a smoker with a lack of AAt, emphysema can begin in your 30s and 40s. The progression and severity of the disease are greatly accelerated by smoking. Although the lung damage that occurs in emphysema develops gradually, most people with tobacco-related emphysema begin to experience symptoms of the disease between the ages of 40 and 60.

Aging process

Precipitating Tobacco smoking

Smoking depresses the activity of scavenger cells and affects the respiratory tract’s ciliary cleansing mechanism, which keeps breathing passages free if inhaled irritants, bacteria, and other foreign matter. When smoking damages this cleansing mechanism, airflow is obstructed and air becomes trapped behind the obstruction. The alveoli greatly distends, diminishing lung capacity. Smoking also irritates the goblet cells and mucus glands, causing an increased accumulation of mucus, which in turn produces more irritant, infection, and damage to the lungs. In addition, carbon monoxide combines with haemoglobin to form carboxyhemoglobin. Haemoglobin that is bound in carboxyhemoglobin cannot carry oxygen efficiently. Exposure to occupational dusts and This exposure adds to the total burden of chemicals, indoor air pollution, and inhaled particles. outdoor air pollution. Symptoms Symptom Chronic cough and wheezing Dyspnea exertion; Use of accessory muscles; Barrel chest appearance Rationale

People who have chronic obstructive pulmonary disease (COPD) — such as emphysema — often develop a slight barrel chest in the later stages of the disease. Because the lungs are chronically overinflated with air, the rib cage stays partially expanded. This makes breathing less efficient and aggravates any existing shortness of breath.

Weight loss

Dyspnea interferes with eating and the work of breathing is energy-depleting.

Pathophysiology Cigarette smoking; heredity; aging process; environment

Disequilibrium between elastase and antielastase

Destruction of elastic recoil

Overdistention of alveoli

Retention of CO2 hypoxia Respiratory acidosis

Diagnostics: • Spirometry o Used to evaluate airflow obstruction, which is determined by the ration of FEV1 to FVC o Results are expressed as an absolute volume and as a percentage of the predicted value using appropriate normal values for gender, age and height. With obstruction, the patient either has difficulty exhaling or cannot forcibly exhale air from the lungs, reducing the FEV1. Obstructive lung dse is defined as a FEV1/FVC ratio of less than 70% Chest radiograph: o the diaphragm appears flattened and the lung fields translucent o marked and persistend overdistention of the lungs is suggestive of emphysema Pulmonary function measurements o helpful in determining a prognosis o indicate obstruction to gas flow during expiration o airway collapse and air trapping in distal portions of the lung lead to a decrease in FVC and FEV1 and an increase in FRC, RV, and TLC o total lung capacity can increase to twice normal o diffusing capacity is decreased because of destruction of the alveolocapillary membrane o arterial blood gases are usually Normal until late in the disease

Medical Treatment: o o o o o emphysema is not reversible, although its progression can be slowed if the individual stops smoking treatment focuses on minimizing air trapping and relieving dyspnea dyspnea is relieved by relaxation exercises, reconditioning exercises and breathing retaining the individual is taught to maximize ventilation, avoid respiratory irritants and stay away from people with upper respiratory infxns oxygen therapy o as long-term continuous therapy, during exercise or to prevent acute dyspnea surgery: o bullectomy: a surgical option for select pts with emphysema. Bullae are enlarged airspaces that do not contribute to ventialation but occupy space in the thorax; these areas may be excised. Many times, these bullae compress areas of the lung that do have adequate gas



exchange. Bullectomy may help reduce dyspnea and improve lung function o lung volume reduction surgery: remoal of a portion of the diseased lung parenchyma. This reduces hyperinflation and allows the functional tissue to expand, resulting inimproved elastic recoil of the lung and improved chest wall and diaphragmatic mechanics. It does not cure nor improve life expectancy but it may decrease dyspnea, improve lung fxn and improve the pt’s overall quality of life pharmacologic therapy: o BRONCHODILATORS:  Relieve bronchospasm and reduce airway obstruction by allowing increased oxygen distribution throughout the lungs and improving alveolar ventilation

NURSING DIAGNOSIS 1. impaired gas exchange related to destruction of alveolar membranes and capillaries 2. ineffective airway clearance related to destruction of lung tissues and smaller airways. 3. Ineffective tissue perfusion related to impaired transport of 02 across alveolar and capillary membrane. 4. Activity intolerance related to imbalance between o2 suppy and demand 5. fatigue realted to increase physical exertion and poor physical condition 6. risk for infection related to chronic disease process

Nursing management

1) 2) 3) 4)

Rest. To reduce oxygen demands of tissues. Increase oral fluid intake in order to liquefy mucus secretions. Good oral care. To remove sputum and prevent infection. Diet: high calorie-provide adequate source of energy; high protein- helps maintain integrity of alveolar walls; Low carbohydrates- limits carbon dioxide production, the client with COPD has difficulty in exhaling carbon dioxide. 5) Oxygen therapy 1-3 lpm. Don’t give high concentration of O2 to clients with COPD. The drive for breathing may be depressed. 6) Avoid cigarette smoking, alcohol, environmental pollutants. 7) Chest physiotherapy-percussion, vibration and postural drainage

8) Bronchial Hygiene: steam inhalation, aerosol inhalation, medimist inhalation

PROGNOSIS Emphysema is an irreversible degenerative condition. The only known cure for emphysema is lung transplant. However, only a few patients are strong enough to survive it physically. The most important measure to slow the progression of emphysema is for the patient to stop smoking and avoid all exposure to cigarette smoke and other lung irritants. Pulmonary rehabilitation can be very helpful to optimize the patient's quality of life and teach the patient how to actively manage his or her care.

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