COPD: Understanding Pathophysiology and Collaborative Care

1. COPD, Asthma and Cystic Fibrosis ZoyaMinasyan, RN- MSN-Edu

2. COPD: Pathophysiology • Defining features • Irreversible airflow limitations during forced exhalation due to loss of elastic recoil • Airflow obstruction due to mucous hypersecretion, mucosal edema, and bronchospasm

3. COPD: Pathophysiology • Supporting structures of lungs are destroyed. • Air goes in easily, but remains in the lungs. • Bronchioles tend to collapse. • Causes barrel-chest look • Pulmonary vascular changes • Blood vessels thicken. • Surface area for diffusion of O2decreases. • Common characteristics • Mucous hypersecretion • Dysfunction of cilia • Hyperinflation of lungs • Gas exchange abnormalities

4. COPD: Description • Includes • Chronic bronchitis • Emphysema (in which the air sacs are dilated or enlarged and lack flexibility, so that breathing is impaired) • Risk factors • Cigarette smoking • Occupational chemicals and dust • Air pollution • Infection • Heredity • Aging

5. COPD: Cigarette Smoking • Airway obstruction develops in 15% of smokers. • 80% to 90% of COPD deaths are related to tobacco smoking. • Effects of nicotine • Stimulates sympathetic nervous system • Increases HR • Causes peripheral vasoconstriction • Increases BP and cardiac workload • ↓ Amount of functional hemoglobin • ↑ Platelet aggregation • Problems with CAD • Increased production of mucus • Lost or decreased ciliary activity

6. COPD: Cigarette Smoking • Carbon monoxide • ↓ O2 carrying capacity • ↑ Heart rate • Passive smoking (second-hand smoke) • ↓ Pulmonary function • ↑ Risk of lung cancer

7. COPD • Occupational & Environmental • COPD can develop with intense or prolonged exposure to • Dusts, vapors, irritants, or fumes • High levels of air pollution • Fumes from heating or cooking in poorly ventilated areas • Infection • Recurring infections impair normal defense mechanisms.

8. COPD • Aging • Some degree of emphysema is common because of physiologic changes of aging lung tissue. • Heredity • -Antitrypsin (AAT) deficiency • Genetic risk factor for COPD • Accounts for 3% of COPD

9. COPD: Clinical Manifestations • Develops slowly • Diagnosis is considered with • Cough • Sputum production • Dyspnea • Exposure to risk factors • Dyspnea usually prompts medical attention.

10. COPD: Clinical Manifestations • Causes chest breathing • Use of accessory and intercostal muscles • fatigue • Physical examination findings • Prolonged expiratory phase • Wheezes • Decreased breath sounds • Bluish-red color of skin • cyanosis

11. COPD Complications Cor pulmonale Exacerbations of COPD Acute respiratory failure Peptic ulcer disease Depression/anxiety

12. COPD: CorPulmonale • Hypertrophy of right side of heart • Result of pulmonary hypertension (the pressures on the right side of the heart must increase to push blood into the lungs). • Eventually causes right-sided heart failure • Dyspnea • Distended neck veins • Hepatomegaly with upper quadrant tenderness • Peripheral edema • Weight gain

13. COPD: Exacerbations • to make an already bad or problematic situation worse • Signaled by change in usual • Dyspnea • Cough • Sputum • Primary causes • Infection • Air pollution

14. COPD: Acute Respiratory Failure • Caused by • Exacerbations • Cor pulmonale • Discontinuing bronchodilator or corticosteroid medication • Overuse of sedatives and opioids • Surgery or severe, painful illness involving chest or abdomen

15. COPDDepression/Anxiety Approximately 50% of COPD patients experience depression. If patient become anxious because of dyspnea, teach pursed lip breathing.

16. COPD: Diagnostic Studies • Diagnosis confirmed by pulmonary function tests • Chest x-rays, spirometry, history, and physical examination. • ABG typical findings • Low PaO2 • ↑ PaCO2 • ↓ pH • ↑ Bicarbonate level found in late stages of COPD • 6-Minute walk test to determine O2 desaturation in the blood with exercise • ECG can show signs of right ventricular failure.

17. COPD: Collaborative Care • Primary goals of care • Prevent progression. • Relieve symptoms. • Prevent/treat complications. • Promote patient participation. • Prevent/treat exacerbations. • Improve quality of life and reduce mortality risk. • Irritants should be evaluated and avoided. • Smoking cessation Examples: the nurse should teach the patient to avoid aerosol hair sprays and smoke-filled rooms. • The most common antibiotics given for outpatients are macrolides (e.g., azithromycin [Zithromax]), doxycycline, and cephalosporins (e.g., cefpodoxime [Vantin]).

18. COPD: Collaborative Care • Drug therapy • O2 therapy is used to • Reduce work of breathing • Reduce workload on the heart • Bronchodilators • Relax smooth muscle in the airway • Improve ventilation of the lungs • ↓ Dyspnea • Inhaled route is preferred. • β2-Adrenergic agonists(e.g., fluticasone/salmeterol [Advair])

19. Oxygen-Conserving Cannula Low-Flow DeliveryDevices: Nasal Cannula. Low-Flow Delivery Devices: Simple Face Mask. Low-Flow Delivery Devices: Partial and Non-Rebreathing Masks. Fig. 29-11 A

20. Oxygen-Conserving Cannula High-Flow Delivery Devices: Tracheostomy Collar. High-Flow Delivery Devices: Venturi Mask. Low-Flow Delivery Devices: Oxygen-Conserving Cannula. Fig. 29-11 A

21. COPD: Collaborative Care • O2 delivery systems are high or low flow. • Low flow is most common. • Low flow is mixed with room air, and delivery is less precise than high flow. • Humidification • Used because O2 has a drying effect on the mucosa • Supplied by nebulizers, vapotherm, and bubble-through humidifiers • Complications of oxygen therapy • Combustion • O2 toxicity • Absorption atelectasis • Infection

22. COPD: Collaborative Care • Respiratory and physical therapy • Breathing retraining • Effective coughing • Chest physiotherapy • Percussion • Vibration

23. COPD: Collaborative Care • Breathing retraining • Decreases dyspnea, improves oxygenation, and slows respiratory rate • Pursed lip breathing • Prolongs exhalation and prevents bronchiolar collapse and air trapping • Effective coughing • Main goals • Facilitate removal of secretions.

24. COPD: Collaborative Care • Percussion • Hands in a cuplike position to create an air pocket • Air-cushion impact facilitates movement of thick mucus. A thin towel should be placed over the area to be percussed, or the patient may choose to wear a T-shirt or hospital gown.

25. COPD: Collaborative Care • Nutritional therapy • Weight loss and malnutrition are common. • Pressure on diaphragm from a full stomach causes dyspnea. • Difficulty breathing while eating leads to inadequate consumption. • To decrease dyspnea and conserve energy • Rest at least 30 minutes before eating. • Use bronchodilator. • Eat five to six small meals. • Cold foods may cause less fullness than hot foods. • Avoid • Foods that require a great deal of chewing • Exercises and treatments 1 hour before and after eating • Gas-forming foods High-calorie, high-protein diet is recommended. Fluids (intake of 3 L/day) should be taken between meals.

26. Nursing Management: Nursing Assessment • Obtain complete health history and conduct a complete physical assessment. • See Table 29-24 in textbook for COPD-specific information.

27. Nursing Management: Nursing Diagnoses Ineffective airway clearance Impaired gas exchange Imbalanced nutrition: Less than body requirements Risk for infection Insomnia

28. Nursing Management: Planning • Goals • Prevention of disease progression • Ability to perform ADLs • Relief from symptoms • No complications related to COPD • Knowledge and ability to implement long-term regimen • Overall improved quality of life

29. Nursing ManagementNursing Implementation • Health promotion • Abstain from or stop smoking. • Avoid or control exposure to occupational and environmental pollutants and irritants. • Early detection of small-airway disease • Early diagnosis and treatment of respiratory tract infection • Awareness of family history of COPD and AAT deficiency

30. Nursing Management: Nursing Implementation • Activity considerations • Modify ADLs to conserve energy. • Walk 15 to 20 minutes a day at least 3 times a week with gradual increases. • Adequate rest. • Sleep • Can be difficult because of coughing • Nasal saline sprays, decongestants, or nasal steroid inhalers can help. • Psychosocial considerations • Healthy coping is difficult. • May feel guilt, depression, anxiety, social isolation, denial, and dependence

31. Nursing Management: Evaluation • Expected outcomes • Normal breath sounds • Effective coughing • Return of PaO2 to normal range for patient • Improved mental status • Maintenance of normal body weight • Normal serum protein levels • Feeling of being rested • Improvement in sleep pattern • Awareness of need to seek medical attention • Behaviors minimizing risk of infection • No infection

32. Question When reviewing the arterial blood gases of a patient with COPD, the nurse identifies late stage COPD with which of the following results? 1. pH 7.26, PaCO2 58 mm Hg, PaO2 60 mm Hg, HCO330 mEq/L 2. pH 7.30, PaCO2 45 mm Hg, PaO2 55 mm Hg, HCO318 mEq/L 3. pH 7.40, PaCO2 40 mm Hg, PaO2 70 mm Hg, HCO325 mEq/L 4. pH 7.52, PaCO2 30 mm Hg, PaO2 80 mm Hg, HCO335 mEq/L - - - -

33. Asthma – Definition • Chronic inflammatory disorder of airways • Causes airway hyper-responsiveness leading to wheezing, breathlessness, chest tightness, and cough.

34. Pathophysiology • Primary response is chronic inflammation from exposure to allergens or irritants. • Leading to airway hyperresponsiveness and acute airflow limitations • Inflammatory mediators cause early-phase response. • Vascular congestion • Edema formation • Production of thick, tenacious mucus • Thickening of airway walls

35. Pathophysiology • Late-phase response • Occurs within 4 to 10 hours after initial attack • Can be more severe than early phase and can last for 24 hours or longer • If airway inflammation is not treated or does not resolve, it may lead to irreversible lung damage.

36. Early Phase Response of Asthma Triggered by Allergen Allergic asthma is triggered when an allergen cross-links IgE receptors on mast cells, which are then activated to release histamine and other inflammatory mediators (early-phase response). A late-phase response may occur due to further inflammation.

37. Triggers of Asthma Allergens • May be seasonal or year round depending on exposure to allergen • House dust mites • Cockroaches • Furry animals • Fungi • Molds

38. Triggers of Asthma • Air Pollutants:Can trigger asthma attacks • Cigarette or wood smoke • Vehicle exhaust • Elevated ozone levels • Sulfur dioxide • Exercise: Induced or exacerbated after exercise • Pronounced with exposure to cold air • Breathing through a scarf or mask may ↓ likelihood of symptoms

39. Triggers of Asthma • Respiratory Infection: • ↑ inflammation hyper-responsiveness of the tracheo-bronchial system • Nose and Sinus Problems: Allergic rhinitis and nasal polyps • Large polyps are removed • Sinus problems are usually related to inflammation of the mucous membranes • Emotional Stress: • Attacks can trigger panic and anxiety. • Extent of effect is unknown. • Occupational Factors: • Exposure to diverse agents • Arrive at work well, but experience a gradual decline

40. Triggers of Asthma: Drugs and Food Additives Sensitivity to aspirin and NSAIDs • Wheezing develops in about 2 hours. • β-Adrenergic blockers (e.g., metoprolol [Toprol]) or topical eyedrops (e.g., timolol [Timoptic]) may trigger asthma as the result of bronchospasm. • Food allergies may cause asthma symptoms. • Avoidance diets

41. Clinical Manifestations • Unpredictable and variable • Recurrent episodes of wheezing, breathlessness, cough, and tight chest • May be abrupt or gradual • Lasts minutes to hours • Expiration may be prolonged. • Inspiration-expiration ratio of 1:2 to 1:3 or 1:4 • Bronchospasm, edema, and mucus in bronchioles narrow the airways. • Air takes longer to move out. • Cough variant asthma • Cough is only symptom. • Bronchospasm is not severe enough to cause airflow obstruction.

42. Clinical Manifestations • Difficulty with air movement can create a feeling of suffocation. • Patient may feel increasingly anxious. • An acute attack usually reveals signs of hypoxemia. • Restlessness • ↑ anxiety • Inappropriate behavior • ↑ pulse and blood pressure • Pulsus paradoxus (drop in systolic BP during inspiratory cycle >10 mm Hg)

43. Complications • Severe acute attack • Respiratory rate >30/min • Pulse >120/min • Life-threatening asthma • Too dyspneic to speak • Perspiring profusely • Drowsy/confused • Require hospital care and often admitted to ICU

44. Diagnostic Studies Detailed history and physical exam Pulmonary function tests Chest x-ray ABGs Oximetry Allergy testing Blood levels of eosinophils Sputum culture and sensitivity

45. Collaborative Care • Severe exacerbations • IV corticosteroids are administered every 4 to 6 hours, then are given orally. • The length of oral prednisone treatment for both severe and life-threatening asthma after discharge is usually about 10 days. • Continuous monitoring of patient is critical. • IV magnesium sulfate is given as a bronchodilator. • Supplemental O2 is given by mask or nasal cannula for 90% O2 saturation. • Arterial catheter may be used to facilitate frequent ABG monitoring. • IV fluids are given because of insensible loss of fluids.

46. Drug Therapy • Three types of antiinflammatory drugs • Corticosteroids • Leukotriene modifiers • Monoclonal antibody to IgE

47. Drug Therapy • Corticosteroids (e.g., beclomethasone, budesonide(Pulmicort)) • Suppress inflammatory response • Inhaled form is used in long-term control. • Systemic form to control exacerbations and manage persistent asthma • Oropharyngeal candidiasis, hoarseness, and a dry cough are local side effects of inhaled drug. • Can be reduced using a spacer or by gargling after each use

48. Spacer Example of an Aero Chamber spacer used with a metered-dose inhaler.

49. Drug Therapy • Leukotriene modifiers or inhibitors (e.g., zafirlukast, montelukast, zileuton) • Block action of leukotrienes—potent bronchoconstrictors • Have both bronchodilator and antiinflammatory effects • Not indicated for acute attacks • Used for prophylactic and maintenance therapy

50. Drug Therapy • Anti-IgE (e.g., Xolair) • ↓ circulating free IgE levels • Prevents IgE from attaching to mast cells, preventing release of chemical mediators • Subcutaneous administration every 2 to 4 weeks