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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.
Bronchitis Emphysema
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
Chronic inflammation Hypertrophy & hyperplasia of bronchial glands that secrete mucus Increase number of goblet cells Cilia are destroyed
Narrowing of airway
Starting w/ bronchi smaller airways airflow resistance work of breathing Hypoventilation & CO2 retention hypoxemia & hypercapnea
Hypoxemia Hypercapnea Polycythemia (increase RBCs) Cyanosis Cor pulmonale (enlargement of right side of heart)
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
Advanced stages
Dyspnea on exertion Dyspnea at rest Hypoxemia & hypercapnea Polycythemia Cyanosis Bluish-red skin color Pulmonary hypertension Cor pulmonale
PFTs
FVC: Forced vital capacity FEV1: Forcible exhale in 1 second FEV1/FVC = <70% PaCO2 PaO2 Hct
ABGs
CBC
Emphysema
Emphysema: Pathophysiology
Structural changes
Hyperinflation of alveoli Destruction of alveolar & alveolar-capillary walls Small airways narrow Lung elasticity decreases
Emphysema: Pathophysiology
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
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Early stages
Later stages
Hypercapnea Purse-lip breathing Use of accessory muscles to breathe Underweight
Pulmonary function
residual volume, lung capacity, DECREASED FEV1, vital capacity maybe normal
Normal in moderate disease May develop respiratory alkalosis Later: hypercapnia and respiratory acidosis
Flattened diaphragm hyperinflation
Chest x-ray
Anti-inflammatory
Bronchodilators
Client teaching
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
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Asthma: Pathophysiology
Bronchospasm
Increased mucus secretion Edema
Asthma: Pathophysiology
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
Expiratory & inspiratory wheezing Dry or moist non-productive cough Chest tightness Dyspnea Anxious &Agitated Prolonged expiratory phase Increased respiratory & heart rate Decreased PEFR
Wheezing
Chest tightness
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
FEV1 decreased
Increase of 12% - 15% after bronchodilator indicative of asthma
PEFR decreased
Symptomatic patient
ABGs
Mild intermittent
Avoid triggers
Avoid triggers
Low-medium dose inhaled corticosteroids Long-acting beta2-agonists Can increase doses or use theophylline or leukotriene-modifier [singulair, accolate, zyflo] High-dose inhaled corticosteroids Long-acting inhaled beta2-agonists Corticosteroids if needed
Acute episode
Corticosteroids
Leukotriene modifiers
Not useful for acute attack Beclomethasone: vanceril, beclovent, qvar Inhibits immediate response from exercise and allergens Prevents late-phase response Useful for premedication for exercise, seasonal asthma Intal, Tilade
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
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]
Methylxanthines
Anticholinergics
Less effective than betaadrenergics 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
Inhibit parasympathetic effects on respiratory system Increased mucus Smooth muscle contraction Useful for pts w/adverse reactions to beta-adrenergics or in combination w/betaadrenergics Ipratropium [atrovent] Ipratropium + albuterol [Combivent]
Relaxation techniques When to call for help, seek treatment Environmental control Cough & postural drainage techniques