Obstructive and Inflammatory Lung Disease DR ISAZAEHFAR Obstructive

Obstructive and Inflammatory Lung Disease DR. ISAZAEHFAR

Obstructive and Inflammatory Lung Disease Emphysema n Chronic Bronchitis n Asthma n

Chronic Obstructive Pulmonary Disease: COPD Disease of airflow obstruction that is not totally reversible n. Chronic Bronchitis n. Emphysema

New Definition n Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily caused by cigarette smoking. Although COPD affects the lungs, it also produces significant systemic consequences.

COPD

COPD n In COPD, less air flows in and out of the airways because of one or more of the following: n The airways and air sacs lose their elastic quality. The walls between many of the air sacs are destroyed. The walls of the airways become thick and inflamed. The airways make more mucus than usual, which tends to clog them. n n n

COPD: Etiology Cigarette smoking n Recurrent respiratory infection n Alpha 1 -antitrypsin deficiency n Aging n

Chronic Bronchitis Recurrent or chronic productive cough for a minimum of 3 months for 2 consecutive years. n Risk factors n Cigarette smoke n Air pollution n

Chronic Bronchitis Pathophysiology n n Chronic inflammation Hypertrophy & hyperplasia of bronchial glands that secrete mucus Increase number of goblet cells Cilia are destroyed

Chronic Bronchitis Pathophysiology n Narrowing of airway Starting w/ bronchi smaller airways airflow resistance work of breathing Hypoventilation & CO 2 retention hypoxemia & hypercapnea n n

Chronic Bronchitis Pathophysiology Bronchospasm often occurs n End result n Hypoxemia n Hypercapnea n Polycythemia (increase RBCs) n Cyanosis n Cor pulmonale (enlargement of right side of heart) n

Chronic Bronchitis: Clinical Manifestations n In early stages n n Clients may not recognize early symptoms Symptoms progress slowly May not be diagnosed until severe episode with a cold or flu Productive cough • Especially in the morning • Typically referred to as “cigarette cough” n n Bronchospasm Frequent respiratory infections

Chronic Bronchitis: Clinical Manifestations n Advanced stages Dyspnea on exertion Dyspnea at rest n Hypoxemia & hypercapnea n Polycythemia n Cyanosis n Bluish-red skin color n Pulmonary hypertension Cor pulmonale n

Chronic Bronchitis: Diagnostic Tests n PFTs n n ABGs n n n FVC: Forced vital capacity FEV 1: Forcible exhale in 1 second FEV 1/FVC = <70% Pa. CO 2 Pa. O 2 CBC n Hct

Emphysema n n n Abnormal distension of air spaces Actual cause is unknown Abnormal permanent enlargement of the airspaces distal to the terminal bronchioles accompanying destruction of the airspaces walls

Emphysema: Pathophysiology n Structural changes n n Hyperinflation of alveoli Destruction of alveolar & alveolar-capillary walls Small airways narrow Lung elasticity decreases

Emphysema: Pathophysiology n Mechanisms of structural change n Obstruction of small bronchioles Proteolytic enzymes destroy alveolar tissue Elastin & collagen are destroyed n n Support structure is destroyed “paper bag” lungs

Emphysema: Pathophysiology n n n The end result: Alveoli lose elastic recoil, then distend, & eventually blow out. Small airways collapse or narrow Air trapping Hyperinflation Decreased surface area for ventilation

Emphysema: Clinical Manifestations n Early stages n n Dyspnea Non productive cough Diaphragm flattens A-P diameter increases • “Barrel chest” n Hypoxemia may occur • Increased respiratory rate • Respiratory alkalosis n Prolonged expiratory phase

Emphysema: Clinical Manifestations n Later stages Hypercapnea n Purse-lip breathing n Use of accessory muscles to breathe n Underweight n • No appetite & increase breathing workload n Lung sounds diminished

Emphysema: Clinical Manifestations

COPD Symptoms n Productive cough n Breathlessness n Chest infection n Other symptoms of COPD can be more vague, weight loss, tiredness and ankle swelling.

Emphysema: Clinical Manifestations n Pulmonary function • residual volume, lung capacity, DECREASED FEV 1, vital capacity maybe normal n Arterial blood gases n n Normal in moderate disease May develop respiratory alkalosis Later: hypercapnia and respiratory acidosis Chest x-ray n n Flattened diaphragm hyperinflation

COPD Diagnostic tests Symptoms n Physical examination n Sample of sputum n Chest x-ray n High-resolution CT (HRCT scan) n Pulmonary function test (spirometery) n Arterial blood gases test n Pulse oximeter n

Goals of Treatment: Emphysema & Chronic Bronchitis Improved ventilation n Remove secretions n Prevent complications n Slow progression of signs & symptoms n Promote patient comfort and participation in treatment n

Collaborative Care: Emphysema & Chronic Bronchitis Treat respiratory infection n Monitor spirometry and PEFR n Nutritional support n Fluid intake 3 lit/day n O 2 as indicated n

Collaborative Care: Medications n Anti-inflammatory n n Bronchodilators n n n Corticosteroids Beta-adrenergic agonist: Proventil Methylxanthines: Theophylline Anticholinergics: Atrovent Mucolytics: Mucomyst Expectorants: Guaifenisin Antihistamines: non-drying

Collaborative Care: Emphysema & Chronic Bronchitis n Client teaching n n n Support to stop smoking Conservation of energy Breathing exercises • Pursed lip breathing • Diaphragm breathing n Chest physiotherapy • Percussion, vibration • Postural drainage n Self-manage medications • Inhaler & oxygen equipment

COPD Medical management n n n Give antibiotics to treat infection Give bronchodilators to relieve bronchospasm, reduce airway obstruction, mucosal edema and liquefy secretions. Chest physiotherapy and postural drainage to improve pulmonary ventilation. Proper hydration helps to cough up secretions or tracheal suctioning when the patient is unable to cough. Steroid therapy if the patient fails to respond to more conservative treatment.

COPD classification based on spirometry Severity Postbronchodilator FEV 1/FVC Postbronchodilator FEV 1% predicted At risk >0. 7 >80 Mild COPD <0. 7 >80 Moderate COPD <0. 7 50 -80 Severe COPD <0. 7 30 -50 Very severe COPD <0. 7 <30 SPIROMETRY is not to substitute for clinical judgment in the evaluation of the severity of disease in individual patients.

Management based on GOLD Postbronchodilator FEV 1 (% predicted)

COPD Preventive measures n To prevent irritation and infection of the airways, instruct the patient to: n Avoid exposure to cigarette, pipe, and cigar smoke as well as to dusts and powders. n Avoid use of aerosol sprays. n Stay indoors when the pollen count is high. n Stay indoors when temperature and humidity are both high

COPD Preventive measures (cont…) n Use air conditioning to help decrease pollutants and control temperature n Avoid exposure to persons known to have colds or other respiratory tract infection n Avoid enclosed, crowded areas during cold and flu season. n Obtain immunization against influenza and

COPD Preventive measures (cont…) n To ensure prompt, effective treatment of a developing respiratory infection, instruct the patient to do the following: - n Report any change in sputum color character, increased tightness of the chest, increased dyspnea, or fatigue. n Call the physician if ordered antibiotics do not relieve symptoms within 24 hours.

Asthma Reversible inflammation & obstruction n Intermittent attacks n Sudden onset n Varies from person to person n Severity can vary from shortness of breath to death n

Difference between COPD and Asthma n In COPD there is permanent damage to the airways. The narrowed airways are fixed, and so symptoms are chronic (persistent). Treatment to open up the airways, is therefore limited. n In asthma there is inflammation in the airways which makes the muscles in the airways constrict. This causes the airways to narrow. The symptoms tend to come and go, and vary in severity from time to time. Treatment to reduce inflammation and to open up the airways usually works well. n COPD is more likely than asthma to cause a chronic (ongoing) cough with sputum.

Difference between COPD and asthma (cont…) n Night time waking with breathlessness or wheeze is common in asthma and uncommon in COPD. n COPD is rare before the age of 35 whilst asthma is common in under-35.

Asthma n Triggers Allergens n Exercise n Respiratory infections n Drugs and food additives n Nose and sinus problems n GERD n Emotional stress n

Asthma: Pathophysiology n n Swelling of mucus membranes (edema) Spasm of smooth muscle in bronchioles n n Increased airway resistance Increased mucus gland secretion

Asthma: Pathophysiology n Early phase response: 30 – 60 minutes n Allergen or irritant activates mast cells n Inflammatory mediators are released • histamine, bradykinin, leukotrienes, prostaglandins, plateletactivating-factor, chemotactic factors, cytokines n Intense inflammation occurs • Bronchial smooth muscle constricts • Increased vasodilation and permeability • Epithelial damage n Bronchospasm • Increased mucus secretion • Edema

Asthma: Pathophysiology n Late phase response: 5 – 6 hours n Characterized by inflammation n Eosinophils and neutrophils infiltrate Mediators are released mast cells release histamine and additional mediators Self-perpetuating cycle Lymphocytes and monocytes invade as well Future attacks may be worse because of increased airway reactivity that results from late phase response n n • Individual becomes hyperresponsive to specific allergens and non-specific irritants such as cold air and dust • Specific triggers can be difficult to identify and less stimulation is required to produce a reaction

Asthma: Early Clinical Manifestations n n n n Expiratory & inspiratory wheezing Dry or moist non-productive cough Chest tightness Dyspnea Anxious &Agitated Prolonged expiratory phase Increased respiratory & heart rate Decreased PEFR

Asthma: Early Clinical Manifestations n Wheezing n Chest tightness Dyspnea n Cough n Prolonged expiratory phase [1: 3 or 1: 4] n

Asthma: Severe Clinical Manifestations n n n n Hypoxia Confusion Increased heart rate & blood pressure Respiratory rate up to 40/minute & pursed lip breathing Use of accessory muscles Diaphoresis & pallor Cyanotic nail beds Flaring nostrils

Endotracheal Intubation

Classifications of Asthma n Mild intermittent Mild persistent n Moderate persistent n Severe persistent n

Asthma: Diagnostic Tests n Pulmonary Function Tests n FEV 1 decreased • Increase of 12% - 15% after bronchodilator indicative of asthma n n n PEFR decreased Symptomatic patient n eosinophils > 5% of total WBC n Increased serum Ig. E n Chest x-ray shows hyperinflation ABGs n Early: respiratory alkalosis, Pa. O 2 normal or near-normal n severe: respiratory acidosis, increased Pa. CO 2,

Asthma: Collaborative Care n Mild intermittent n Avoid triggers Premedicate before exercising n May not need daily medication n n Mild persistent asthma n Avoid triggers Premedicate before exercising n Low-dose inhaled corticosteroids n

Asthma: Collaborative Care n Moderate persistent asthma n Low-medium dose inhaled corticosteroids n Long-acting beta 2 -agonists Can increase doses or use theophylline or leukotriene-modifier [singulair, accolate, zyflo] n n Severe persistent asthma n High-dose inhaled corticosteroids n Long-acting inhaled beta 2 -agonists Corticosteroids if needed n

Asthma: Collaborative Care n Acute episode n FEV 1, PEFR, pulse oximetry compared to baseline n O 2 therapy Beta 2 -adrenergic agonist n • via MDI w/spacer or nebulizer • Q 20 minutes – 4 hours prn n Corticosteroids if initial response insufficient • Severity of attack determines po or IV • If poor response, consider IV aminophylline

Asthma Medications: Antiinflammatory n Corticosteroids n n n Not useful for acute attack Beclomethasone: vanceril, beclovent, qvar n Leukotriene modifiers n Interfere with synthesis or block action of leukotrienes n Have both bronchodilation and anti-inflammatory properties Not recommended for acute asthma attacks Should not be used as only therapy for persistent asthma Accolate, Singulair, Zyflo Cromolyn & nedocromil n Inhibits immediate response from exercise and allergens n Prevents late-phase response Useful for premedication for exercise, seasonal asthma Intal, Tilade n n n

Asthma Medications: Bronchodilators n 2 -adrenergic agonists n Rapid onset: quick relief of bronchoconstriction n Treatment of choice for acute attacks If used too much causes tremors, anxiety, tachycardia, palpitations, nausea Too-frequent use indicates poor control of asthma Short-acting n n n • Albuterol[proventil]; metaproterenol [alupent]; bitolterol [tornalate]; pirbuterol [maxair] n Long-acting • Useful for nocturnal asthma • Not useful for quick relief during an acute attack • Salmeterol [serevent]

Asthma Medications: Bronchodilators con’t n Methylxanthines n Anticholinergics n Less effective than betaadrenergics n Inhibit parasympathetic effects on respiratory system n Useful to alleviate bronchoconstriction of early and late phase, nocturnal asthma Does not relieve hyperresponsiveness Side effects: nausea, headache, insomnia, tachycardia, arrhythmias, seizures Theophylline, aminophylline n Increased mucus n Smooth muscle contraction Useful for pts w/adverse reactions to beta-adrenergics or in combination w/betaadrenergics n n n Ipratropium [atrovent] n Ipratropium + albuterol [Combivent]

Asthma: Client Teaching n n Correct use of medications Signs & symptoms of an attack n n n Dyspnea, anxiety, tight chest, wheezing, cough Relaxation techniques When to call for help, seek treatment Environmental control Cough & postural drainage techniques