Chronic Obstructive pulmonary Disease

Respiratory Disease Condition

1. CHRONIC OBSTRUCTIVE PULMONARY DISEASE Mrs dipali dumbre Medical surgical nursing scon

2. CHRONIC OBSTRUCTIVE PULMONARY DISEASE COPD is also known as chronic obstructive lung disease (COLD), chronic obstructive airway disease (COAD) Chronic obstructive pulmonary disease (COPD) includes chronic bronchitis and emphysema.

3. Definition “COPD is a chronic disorder of the airway characterized by progressive airflow limitation which is associated with an abnormal inflammatory response of the lungs to noxious particles or gases and is irreversible .” The term chronic obstructive pulmonary disease encompasses two types of obstructive airway diseases, chronic bronchitis and emphysema.

4. Chronic bronchitis “It is the presence of chronic productive cough for 3 months in each of 2 consecutive years in a patient in whom other causes of chronic cough have been excluded .” Emphysema “It is an abnormal permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis .”

5. Etiology 1. Cigarette Smoking The major risk factor for developing COPD is cigarette smoking. When cigarettes are smoked, tar is inhaled, which contains approximately 4000 chemicals. Over 60 carcinogens have been isolated from cigarette smoke, including cyanide, formaldehyde, and ammonia . Nicotine is probably not a carcinogen, but it has other deleterious effects . It acts by stimulating the sympathetic nervous system, resulting in increased heart rate, increased peripheral vasoconstriction, increased BP, and increased cardiac workload.

6. Cigarette smoke has several direct effects on the respiratory tract . The irritating effect of the smoke causes hyperplasia of cells, including which subsequently results in increased production of mucus . Hyperplasia reduces airway diameter and increases the difficulty in clearing secretions. Smoking reduces the ciliary activity and may cause actual loss of ciliated cells. Smoking also produces abnormal dilation of the distal air space with destruction of alveolar walls . Many cells develop large, atypical nuclei, which are considered a precancerous condition.

7. After a short time of smoking, changes in small airway function can develop . In the early stages these changes are mostly inflammatory with mucosal edema and an influx of inflammatory cells . In later stages, however, thickening of the airway wall occurs by a remodeling process related to tissue repair and the inability of cilia to clear mucus, thus resulting in accumulation of inflammatory exudates in the airway lumen.

8. Quitting smoking can prevent or delay the development of airflow limitation or reduce its progression. Carbon monoxide (CO) is a component of tobacco smoke. CO has a high affinity for hemoglobin and combines with it more readily than does O 2 thereby reducing the smoker's O 2 -carrying capacity.

9. 2. Occupational Chemicals and Dusts: If a person has intense or prolonged exposure to various dusts, vapors, irritants, or fumes in the workplace. Exposure to these irritants causes the airways to be hyperresponsive .

10. 3. Air Pollution. High levels of urban air pollution are harmful to persons with existing lung disease. However , the effect of outdoor air pollution as a risk factor for COPD appears to be small compared to the effect of cigarette smoking. Another risk factor for COPD development is fossil fuels that are used for indoor heating and cooking . Many women, particularly worldwide who have never smoked, are developing COPD because of cooking with these fuels in poorly ventilated areas .

11. 4. Infection . Infections are a risk factor for developing COPD. Severe recurring respiratory tract infections in childhood have been associated with reduced lung function and increased respiratory symptoms in adulthood . Recurring infections impair normal defense mechanisms, making the bronchioles and alveoli more susceptible to injury.

12. 5. Heredity Alpha 1-antitrypsin deficiency is a genetic condition that is responsible for about 2% of cases of COPD. In this condition, the body does not make enough of alpha 1-antitrypsin. Alpha 1-antitrypsin protects the lungs from damage caused by protease enzymes, such as elastase and trypsin, that can be released as a result of an inflammatory response to tobacco smoke.

13. 6. Aging Aging results in changes in the lung structure, the thoracic cage, and the respiratory muscles. As people age there is gradual loss of the elastic recoil of the lung. The lungs become more rounded and smaller. The number of functional alveoli decreases as a result of the loss of the alveolar supporting structures and loss of the intraalveolar septum.

14. pathophysiology COPD is characterized by chronic inflammation found in the airways and pulmonary vasculature . The pathogenesis of COPD is complex and involves many mechanisms. T he primary process is inflammation. The inflammatory process starts with inhalation of noxious particles and gases (e.g., cigarette smoke, air pollution). The predominant inflammatory cells, macrophages and lymphocytes (primarily CD8 cells), increase and release inflammatory mediators, including leukotrienes, interleukins, and tumor necrosis factor .

15. These mediators cause damage to the lung tissue. Later, neutrophils infiltrate into the lungs and release more inflammatory mediators . The airways become inflamed, resulting in increased numbers of enlarged goblet cells . This results in excess mucus production (or chronic bronchitis). Peripheral Airway Remodeling Peripheral airways (small bronchi and bronchioles with internal diameter <2 mm) undergo repeated cycles of injury and repair of the airway walls with resultant structural remodeling. Increased collagen and scar tissue formation in the walls cause fibrosis .

16. Lung Parenchymal Dustruction Destruction of the lung parenchyma in COPD patients results in emphysema . Destruction of the lung parenchyma is thought to be due to an imbalance of proteinases/ antiproteinases . This occurs as a consequence of inflammation, but there can be a genetic basis to the proteinase imbalance . Individuals have elastin, which provides the structural makeup of the connective tissue of the alveolar wall

17. In a healthy person, proteinases (elastase is the main component) in the parenchyma function to break down the alveolar walls (elastin). Normally, proteinase inhibitors (called α 1 -antitrypsin [AAT]) prevent this destructive process . In smokers the numbers of neutrophils, macrophages, and other inflammatory cells are increased and with the inflammatory process overwhelm the body's normal AAT defense. Therefore there is destruction of the basic elastin structure of the parenchyma.

18. Pulmonary vascular changes Pulmonary vascular changes can begin early in the disease. Inflammatory cells infiltrate the smooth muscle of the blood vessels causing thickening as the disease advances. In severe cases, collagen deposition in the vessels along with emphysematous destruction of the capillary bed occurs,

19. COPD Pathology These changes in the lungs result in the following characteristic disease manifestations: M ucus hypersecretion, D ysfunction of the cilia A irflow limitation H yperinflation of the lungs G as exchange abnormalities P ulmonary hypertension C or pulmonale

20. Emphysema “It is an abnormal permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis.”

21. Classification of the emphysema Centrilobular Emphysema: It involves dilation and destruction of the respiratory bronchioles and is the most commonly seen in upper lobes in mild disease. Panlobular Emphysema: It is type of emphysema involves destruction of the alveolar ducts, alveolar sacs, and respiratory bronchioles.

22. Clinical manifestation Dyspnea is often progressive, and usually occurs with exertion. However , patients may dismiss the importance of this symptom as they rationalize, “I'm just getting older.” In late stages of COPD, dyspnea may be present at rest. As more alveoli become over distended, increasing amounts of air are trapped. This causes a flattened diaphragm and an increased anterior-posterior diameter of the chest, forming the typical barrel chest .

23. Cough: initially may be intermittent. Later it is present every day, but is seldom present during the night. There are ranges in the amount of sputum produced. Wheezing and chest tightness Due to the bareel chest patient may sit upright with arms supported on a fixed surface such as an overbed table (tripod position) .

24. The patient may naturally purse lips on expiration (pursed-lip breathing) and use accessory muscles, such as those in the neck, to aid with inspiration. Edema in the ankles may be the only clue to right-sided heart involvement.

25. Over time, hypoxemia (PaO 2 <60 mm Hg or O 2 saturation <88%) may develop with hypercapnia (PaCO 2 >45 mm Hg ) later in the disease . The bluish-red color of the skin results from polycythemia and cyanosis. Polycythemia develops as a result of increased production of red blood cells as the body attempts to compensate for chronic hypoxemia. Hemoglobin concentrations may reach 20 g/dl (200 g/L) or more. Cyanosis develops when there is at least 5 g/dl (50 g/L) or more of circulating unoxygenated hemoglobin.

26. Classification of COPD Classification Level of Severity FEV1 Results STAGE 0 Mild FEV 1 > 80% predicted STAGE 1 Moderate FEV 1 50 - 80% predicted STAGE 2 Severe 30 - 50% predicted STAGE 4 Very Severe FEV 1 <30% predicted

27. Diagnostic evaluation History and physical examination Pulmonary function tests Chest x-ray Serum α 1 -antitrypsin levels Sputum specimen for Gram stain and culture ABGs ECG Exercise testing with oximetry Echocardiogram or cardiac nuclear scans

28. Collaborative Therapy 1. Cessation of cigarette smoking 2. Bronchodilator therapy : “Bronchodilator drug therapy relaxes smooth muscles in the airway and improves the ventilation of the lungs, thus reducing the degree of breathlessness”. β 2 -Adrenergic agonists: Salmeterol ( Serevent ) is a widely used long-acting β 2 -adrenergic agonist, Formoterol ( Foradil ) is another long-acting β 2 agonist . Anticholinergic agents: Methylxanthine

29. Corticosteroids (oral for exacerbations, inhaled corticosteroids ) Inhaled corticosteroid therapy may be beneficial for patients with moderate-to-severe COPD . Inhaled corticosteroid combined with long-acting β 2 -adrenergic agonists (e.g., fluticasone/ salmeterol [Advair]) are more effective than the single-drug therapy. 3. O 2 Therapy O 2 therapy is frequently used in the treatment of COPD and other problems associated with hypoxemia. Long-term O 2 therapy (LTOT) improves survival, exercise capacity, cognitive performance, and sleep in hypoxemic patients.

30. Methods of Administration A, Simple face mask. B, Plastic face mask with reservoir bag. C, Venturi mask. D, Tracheostomy mask. E, Face tent. F, Standard nasal cannulas.

31. Complications of Oxygen therapy Combustion: O 2 supports combustion and increases the rate of burning . This is why it is important that smoking be prohibited in the area in which O 2 is being used.

32. CO 2 Narcosis: The two chemoreceptors in the respiratory center that control the drive to breathe respond to CO 2 and O 2 . Normally, CO 2 accumulation is the major stimulant of the respiratory center. Over time some COPD patients develop a tolerance for high CO 2 levels (the respiratory center loses its sensitivity to the elevated CO 2 levels). Although O 2 administration should be titrated to the lowest effective dose.

33. O 2 Toxicity: Pulmonary O2 toxicity may result from prolonged exposure to a high level of O 2 (PaO 2 ). The development of O 2 toxicity is relatively rare, but is determined by patient tolerance, exposure time, and effective dose. High concentrations of O 2 damage alveolar-capillary membranes, inactivate pulmonary surfactant, cause interstitial and alveolar edema, and decrease compliance . The amount of O 2 administered should be just enough to maintain the PaO 2 within a normal or acceptable range for the patient.

34. Absorption Atelectasis: Normally, nitrogen, which constitutes 79% of the air that is breathed, is not absorbed into the bloodstream . This prevents alveolar collapse . When high concentrations of O 2 are given, nitrogen is washed out of the alveoli and replaced with O 2 . If airway obstruction occurs, the O 2 is absorbed into the bloodstream and the alveoli collapse . This process is called absorption atelectasis.

35. Infection. Infection can be a major hazard of O 2 administration . Heated nebulizers present the highest risk . The constant use of humidity supports bacterial growth, with the most common infecting organism being Pseudomonas aeruginosa . Disposable equipment that operates as a closed system should be used.

36. 4 . Surgical Therapy for COPD Three different surgical procedures have been used in severe COPD . A. LUNG VOLUME REDUCTION SURGERY (LVRS). The goal of therapy is to reduce the size of the lungs by removing about 30% of the most diseased lung tissue so the remaining healthy lung tissue can perform better. The rationale for this type of surgery is that by reducing the size of the hyperinflated emphysematous lungs, there is decreased airway obstruction and increased room for the remaining normal alveoli to expand and function. The procedure reduces lung volume and improves lung and chest wall mechanics.

37. B . BULLECTOMY This procedure is used for patients with emphysematous COPD who have large bullae (>1 cm). The bullae are usually resected via thoracoscope . In certain patients this procedure has resulted in improved lung function and reduction in dyspnea.

38. C . LUNG TRANSPLANTATION COPD patients are the largest group of patients on waiting lists for lung transplantation. Although single-lung transplant is the most commonly used technique because of a shortage of donors. In some cases LVRS is a bridge until transplantation. In appropriately selected patients with very advanced COPD, lung transplantation improves functional capacity and enhances quality of life. However , rejection and effects of immunosuppressive therapy remain an obstacle.

39. 5. Respiratory and Physical Therapy Respiratory therapy (RT) and physical therapy (PT) rehabilitation activities are performed by respiratory therapists or physical therapists depending on the institution. RT and/or PT activities include B reathing retraining, E ffective cough techniques C hest physiotherapy.

40. 6. Breathing Retraining The patient with COPD develops an increased respiratory rate with a prolonged expiration to compensate for the obstruction to airflow resulting in dyspnea . In addition, the accessory muscles of breathing in the neck and upper part of the chest are used excessively to promote chest wall movement. These muscles are not designed for long-term use, and as a result the patient experiences increased fatigue. Breathing exercises may assist the patient during rest and activity (e.g., lifting, walking, stair climbing) by decreasing dyspnea, improving oxygenation, and slowing the respiratory rate.

41. PURSED-LIP BREATHING: The rationale for using pursed-lip breathing (PLB) is to prolong exhalation and thereby prevent bronchiolar collapse and air trapping. The patient should be taught PLB before, during, and after any activity causing dyspnea or tachypnea. The patient is taught to inhale slowly through the nose and then to exhale slowly through pursed lips, almost as if whistling. Exhalation should be at least three times as long as inhalation.

42. 7. Effective Coughing Many patients with COPD have developed ineffective coughing patterns that do not adequately clear their airways of sputum. The main goals of effective coughing are to conserve energy, reduce fatigue, and facilitate removal of secretions. Huff coughing is an effective technique that the patient can be easily taught. Huff Coughing :  Huff coughing , or huffing, is an alternative to deep  coughing  if you have trouble clearing your mucus. Take a breath that is slightly deeper than normal. Use your stomach muscles to make a series of three rapid exhalations with the airway open, making a "ha, ha, ha" sound.

43. 8. Chest Physiotherapy Chest physiotherapy (CPT) is indicated in the patient with ( 1) Excessive bronchial secretions who has difficulty clearing secretions with expectorated sputum production greater than 25 ml per day, ( 2) R etained secretions in the presence of an artificial airway (3) lobar atelectasis caused by or suspected of being caused by mucous plugging . Chest physiotherapy consists of P ercussion V ibration p ostural drainage Percussion, vibration, and postural drainage may assist in bringing secretions into larger, more central airways.

44. Percussion: Percussion is performed in the appropriate postural drainage position with the hands in a cuplike position. The hands are cupped, and the fingers and thumbs are closed.

45. Vibration: It is accomplished by tensing the hand and arm muscles repeatedly and pressing mildly with the flat of the hand on the affected area while the patient slowly exhales a deep breath. The vibrations facilitate movement of secretions to larger airways .

46. Postural Drainage: The purpose of various positions in postural drainage is to drain each segment toward the larger airways . The lungs are divided into five lobes, with three on the right side and two on the left side. There are 18 segments in the lungs, which can be drained by 18 positions. The modified postural drainage positions most often used in clinical practice.

47. Flutter Mucus Clearance Device The Flutter mucus clearance device is a handheld device that is shaped like a small, fat pipe . It provides positive expiratory pressure (PEP) treatment for patients with mucus-producing conditions . The Flutter has a mouthpiece, a high-density stainless steel ball, and a cone that holds the ball. When the patient exhales through the Flutter, the steel ball moves, which causes vibrations in the lungs and loosens mucus. It helps move mucus up through the airways to the mouth where the mucus can be expectorated . Although the Flutter valve is mostly used in patients with cystic fibrosis, it has been effectively used in patients with excessive secretions with COPD and bronchiectasis.

48. High-Frequency Chest Compression ( ThAIRaphy Vest). High-frequency chest compression uses an inflatable vest ( ThAIRaphy vest) with hoses connected to a high-frequency pulse generator. The pulse generator delivers air to the vest, which vibrates the chest . The high-frequency air waves clear all lobes of the lungs. The vest has been found to be more effective than conventional CPT in clearing mucus, and it can be done without the aid of another person. The unit weighs only 30 lb and is quiet. It comes in its own suitcase and is portable.

49. Acapella Acapella is a small handheld device that combines the benefits of both PEP therapy and airway vibrations of the Flutter valve to mobilize pulmonary secretions. It works by using oscillating vibrations that travel to the lung, shaking free mucous plugs that the patient can then cough up. It can be used in virtually any setting as the patients are free to sit, stand, or recline. It improves clearance of secretions, is easier to tolerate than CPT, takes less than half the time of conventional CPT sessions, and facilitates opening of airways.

50. Aerosol Nebulization Therapy Medications for COPD patients are most often delivered via metered-dose or dry powder inhalers . This is the preferred delivery route, although devices that deliver a suspension of fine particles of liquid in a gas, called nebulizers, may also be used to deliver medications to the COPD patient. Nebulizers are usually powered by a compressed air or O 2 generator . At home the patient may have an air-powered compressor; in the hospital, wall O 2 or compressed air is used to power the nebulizer.

51. Aerosolized medication orders must include the medication, dose, diluent, and whether it is to be nebulized with O 2 or compressed air. Medication is nebulized or reduced to a fine spray, and depending on several factors, including droplet size, it can be inhaled into the patient's tracheobronchial tree. The advantage to aerosol-nebulization therapy is that it is easy to use. Medications that are routinely nebulized include albuterol and ipratropium.

52. Nutritional Therapy Weight loss and malnutrition are commonly seen in the patient with severe emphysematous COPD. The cause of this weight loss is not entirely known but is likely multifactorial . Eating becomes an effort because of dyspnea and O 2 desaturation, especially in the later stages of COPD. Patients may require more caloric expenditure than calories ingested. A full stomach presses up on the flattened diaphragm, causing increased dyspnea and discomfort. It is difficult for some patients to eat and breathe at the same time; therefore inadequate amounts of food are eaten. Also large amounts of energy are expended to breathe and maintain even normal activities.

53. Complications Cor Pulmonale . Cor pulmonale is hypertrophy of the right side of the heart, with or without heart failure, resulting from pulmonary hypertension . It is caused by diseases affecting the lungs or pulmonary blood vessels. Cor pulmonale is a late manifestation of chronic pulmonary heart disease. The patient benefits most when a diagnosis of pulmonary heart disease can be made early so therapy can be instituted. In patients with severe COPD, 40% demonstrate cor pulmonale , and the prognosis is poor. In COPD, pulmonary hypertension is caused primarily by constriction of the pulmonary vessels in response to alveolar hypoxia, with acidosis further potentiating the vasoconstriction. Chronic alveolar hypoxia causes vascular remodeling . Chronic hypoxia also stimulates erythropoiesis, which causes polycythemia.

54. This results in increased viscosity of the blood. In COPD there may be an anatomic reduction of the pulmonary vascular bed as seen in emphysema with bullae. These patients would have increased pulmonary vascular resistance.

55. clinical manifestations of chronic pulmonary heart disease and cor pulmonale are related to dilation and failure of the right ventricle with subsequent intravascular volume expansion and systemic venous congestion . Dyspnea is a usual symptom, and is associated with hypoxemia and hypercarbia . Lung sounds are normal or crackles may be heard in the bases of the lungs bilaterally. Heart sound changes include accentuation of the pulmonic component of the second heart sound, right-sided ventricular diastolic S 3 gallop, and a loud pulmonic component of S 2 along the left sternal border. ECG changes include increased P wave amplitude (P pulmonale ), a tendency for right axis deviation, and incomplete right bundle branch block.

56. Overt manifestations of right-sided heart failure may develop, which include Distended neck veins (jugular venous distention), H epatomegaly with right upper quadrant tenderness , Ascites Epigastric distress P eripheral edema W eight gain

57. Management of cor pulmonale includes C ontinuous low-flow O 2 . Long-term O 2 therapy improves survival of hypoxemic patients, especially when used >15 hours per day. Vasodilator therapy has not demonstrated sustained benefit and is not recommended on a routine basis. Although the use of digitalis is not indicated for right-sided heart failure, it may be used when left-sided heart failure is present . Diuretics are generally used, but serum creatinine and blood urea nitrogen (BUN) are needed to monitor renal function as diuretics can cause volume depletion. Electrolytes must be monitored to assess for hypokalemia, which can predispose to dysrhythmias.

58. Exacerbations of COPD. Exacerbations of COPD are signaled by a change in the patient's usual dyspnea, cough, and/or sputum that is different from the usual daily patterns. These flares require changes in management . Patients have an increase in dyspnea, sputum volume, and/or sputum purulence. They may also have nonspecific complaints of malaise, insomnia, fatigue, depression, confusion, decrease in exercise tolerance, increased wheezing, increased cough, or fever without other causes.

59. Acute Respiratory Failure Patients with severe COPD who have exacerbations are at risk for the development of respiratory failure. Frequently, COPD patients wait too long to contact their health care provider when they develop fever, increased cough and dyspnea, or other symptoms suggestive of exacerbations of COPD. An exacerbation of cor pulmonale may also lead to acute respiratory failure . Discontinuing bronchodilator or corticosteroid medication may also precipitate respiratory failure. The use of β-adrenergic blockers (e.g., propranolol [Inderal]) may also exacerbate acute respiratory failure in the patient with a reversible component to the COPD. However , cardioselective β-adrenergic blockers (e.g., atenolol, metoprolol) should not be withheld from patients with mild to moderate diseases because they do not produce clinically significant problems with respiration.

60. Peptic Ulcer and Gastroesophageal Reflux Disease The incidence of peptic ulcer disease is increased in persons with COPD. The reason for this occurrence is partly explained by hypersecretion of gastric acid resulting from increased arterial CO 2 and decreased arterial O 2 tension. This occurs only in patients who chronically retain CO 2 . The ulcers are more commonly in the duodenum rather than stomach and do not cause pain. It is important to test gastric aspirates and feces for occult blood.

61. Depression/Anxiety Patients with COPD experience many losses as the disease progresses over time . They can feel helpless with low self-esteem and unable to vent their emotions for fear of compromising their breathing. The reported prevalence of depression in COPD varies, but may be four times more frequent in COPD than in the general population. Anxiety can complicate respiratory compromise and may precipitate dyspnea and hyperventilation. When a person is exceptionally dyspneic, particularly if it occurs suddenly, the person becomes anxious and tries to breathe faster, thus affecting his or her oxygenation status. Proper screening for anxiety and depression by health care providers is needed for a proper diagnosis.