Download - Obstructive And Inflammatory Lung Disease
N24: Class #8Obstructive and Inflammatory Lung Disease
Christine Hooper, Ed.D., RN
Spring 2006
Emphysema Chronic Bronchitis Asthma
Class Objectives Differentiate among the etiology,
pathophysiology, clinical manifestations, collaborative care, and appropriate nursing diagnoses of the client with emphysema and chronic bronchitis.
Describe the etiology, pathophysiology, clinical manifestations, collaborative care, and appropriate nursing diagnoses of the client with asthma.
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Chronic Obstructive Pulmonary Disease: COPD
Disease of airflow obstruction that is not totally reversibleChronic BronchitisEmphysema
COPD: Etiology
Cigarette smoking #1 Recurrent respiratory infection Alpha 1-antitrypsin deficiency Aging
Chronic Bronchitis
Recurrent or chronic productive cough for a minimum of 3 months for 2 consecutive years.
Risk factors Cigarette smoke Air pollution
Chronic Bronchitis Pathophysiology Chronic inflammation Hypertrophy &
hyperplasia of bronchial glands that secrete mucus
Increase number of goblet cells
Cilia are destroyed
Chronic Bronchitis Pathophysiology Narrowing of airway
Starting w/ bronchi smaller airways
airflow resistance work of breathing Hypoventilation & CO2
retention hypoxemia & hypercapnea
Chronic Bronchitis Pathophysiology
Bronchospasm often occurs End result
Hypoxemia Hypercapnea Polycythemia (increase RBCs)
Cyanosis Cor pulmonale (enlargement of right side of heart)
Chronic Bronchitis: Clinical Manifestations In early stages
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”
Bronchospasm Frequent respiratory infections
Chronic Bronchitis: Clinical Manifestations
Advanced stages Dyspnea on exertion Dyspnea at rest Hypoxemia & hypercapnea Polycythemia Cyanosis Bluish-red skin color Pulmonary hypertension Cor pulmonale
Chronic Bronchitis: Diagnostic Tests PFTs
FVC: Forced vital capacity FEV1: Forcible exhale in 1 second FEV1/FVC = <70%
ABGs PaCO2 PaO2
CBC Hct
Emphysema Abnormal distension
of air spaces Actual cause is
unknown
Emphysema: Pathophysiology Structural changes
Hyperinflation of alveoli Destruction of alveolar &
alveolar-capillary walls Small airways narrow Lung elasticity decreases
Emphysema: Pathophysiology Mechanisms of
structural change Obstruction of small
bronchioles Proteolytic enzymes destroy
alveolar tissue Elastin & collagen are
destroyed Support structure is destroyed “paper bag” lungs
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Emphysema: Pathophysiology 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 Early stages
Dyspnea Non productive cough Diaphragm flattens A-P diameter increases
• “Barrel chest” Hypoxemia may occur
• Increased respiratory rate• Respiratory alkalosis
Prolonged expiratory phase
Later stages Hypercapnea Purse-lip breathing Use of accessory muscles to breathe Underweight
• No appetite & increase breathing workload Lung sounds diminished
Emphysema: Clinical Manifestations
Emphysema: Clinical Manifestations
Emphysema: Clinical Manifestations
Pulmonary function residual volume, lung capacity, DECREASED FEV1,
vital capacity maybe normal
Arterial blood gases Normal in moderate disease May develop respiratory alkalosis Later: hypercapnia and respiratory acidosis
Chest x-ray Flattened diaphragm hyperinflation
Goals of Treatment: Emphysema & Chronic Bronchitis
Improved ventilation Remove secretions Prevent complications Slow progression of signs & symptoms Promote patient comfort and participation
in treatment
Collaborative Care: Emphysema & Chronic Bronchitis
Treat respiratory infection Monitor spirometry and PEFR Nutritional support Fluid intake 3 lit/day O2 as indicated
Collaborative Care: Medications
Anti-inflammatory Corticosteroids
Bronchodilators Beta-adrenergic agonist: Proventil Methylxanthines: Theophylline Anticholinergics: Atrovent
Mucolytics: Mucomyst Expectorants: Guaifenisin Antihistamines: non-drying
Collaborative Care: Emphysema & Chronic Bronchitis
Client teaching Support to stop smoking Conservation of energy Breathing exercises
• Pursed lip breathing• Diaphragm breathing
Chest physiotherapy• Percussion, vibration• Postural drainage
Self-manage medications• Inhaler & oxygen equipment
Asthma Reversible inflammation & obstruction Intermittent attacks Sudden onset Varies from person to person Severity can vary from shortness of
breath to death
Asthma Triggers
Allergens Exercise Respiratory infections Drugs and food additives Nose and sinus problems GERD Emotional stress
Asthma: Pathophysiology Swelling of mucus
membranes (edema) Spasm of smooth
muscle in bronchioles Increased airway
resistance
Increased mucus gland secretion
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Asthma: Pathophysiology Early phase response: 30 – 60 minutes
Allergen or irritant activates mast cells Inflammatory mediators are released
• histamine, bradykinin, leukotrienes, prostaglandins, platelet-activating-factor, chemotactic factors, cytokines
Intense inflammation occurs • Bronchial smooth muscle constricts
• Increased vasodilation and permeability • Epithelial damage
Bronchospasm • Increased mucus secretion • Edema
Late phase response: 5 – 6 hours Characterized by inflammation 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 • 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: Pathophysiology
Asthma: Early Clinical Manifestations
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
Wheezing
Chest tightness
Dyspnea Cough Prolonged expiratory phase [1:3 or 1:4]
Asthma: Severe Clinical Manifestations
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
Mild intermittent
Mild persistent Moderate persistent Severe persistent
Asthma: Diagnostic Tests Pulmonary Function Tests
FEV1 decreased • Increase of 12% - 15% after bronchodilator indicative of asthma
PEFR decreased
Symptomatic patient eosinophils > 5% of total WBC
Increased serum IgE Chest x-ray shows hyperinflation
ABGs Early: respiratory alkalosis, PaO2 normal or near-normal
severe: respiratory acidosis, increased PaCO2,
Asthma: Collaborative Care Mild intermittent
Avoid triggers Premedicate before exercising May not need daily medication
Mild persistent asthma Avoid triggers Premedicate before exercising Low-dose inhaled corticosteroids
Asthma: Collaborative Care Moderate persistent asthma
Low-medium dose inhaled corticosteroids Long-acting beta2-agonists Can increase doses or use theophylline or
leukotriene-modifier [singulair, accolate, zyflo] Severe persistent asthma
High-dose inhaled corticosteroids Long-acting inhaled beta2-agonists Corticosteroids if needed
Asthma: Collaborative Care Acute episode
FEV1, PEFR, pulse oximetry compared to baseline O2 therapy Beta2-adrenergic agonist
• via MDI w/spacer or nebulizer • Q20 minutes – 4 hours prn
Corticosteroids if initial response insufficient • Severity of attack determines po or IV
• If poor response, consider IV aminophylline
Asthma Medications: Anti-inflammatory
Corticosteroids Not useful for acute attack Beclomethasone: vanceril,
beclovent, qvar Cromolyn & nedocromil
Inhibits immediate response from exercise and allergens
Prevents late-phase response Useful for premedication for
exercise, seasonal asthma Intal, Tilade
Leukotriene modifiers Interfere with synthesis or
block action of leukotrienes
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
Asthma Medications: Bronchodilators 2-adrenergic agonists
Rapid onset: quick relief of bronchoconstriction
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
• Albuterol[proventil]; metaproterenol [alupent]; bitolterol [tornalate]; pirbuterol [maxair]
Long-acting
• Useful for nocturnal asthma
• Not useful for quick relief during an acute attack • Salmeterol [serevent]
Asthma Medications: Bronchodilators con’t Methylxanthines
Less effective than beta-adrenergics
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
Anticholinergics Inhibit parasympathetic
effects on respiratory system
Increased mucus
Smooth muscle contraction Useful for pts w/adverse
reactions to beta-adrenergics or in combination w/beta-adrenergics
Ipratropium [atrovent]
Ipratropium + albuterol [Combivent]
Asthma: Client Teaching Correct use of medications Signs & symptoms of an attack
Dyspnea, anxiety, tight chest, wheezing, cough
Relaxation techniques When to call for help, seek treatment Environmental control Cough & postural drainage techniques
Asthma: Nursing Diagnoses Ineffective airway clearance r/t bronchospasm,
ineffective cough, excessive mucus
Anxiety r/t difficulty breathing, fear of suffocation Ineffective therapeutic regimen management r/t
lack of information about asthma