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N24: Class #8 Obstructive and Inflammatory Lung Disease

Emphysema Chronic Bronchitis Asthma

Christine Hooper, Ed.D., RN Spring 2006

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.

Chronic Obstructive Pulmonary Disease: COPD

Disease of airflow obstruction that is not totally reversible

Bronchitis Emphysema

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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


FVC: Forced vital capacity FEV1: Forcible exhale in 1 second FEV1/FVC = <70% PaCO2 PaO2 Hct




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

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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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

Emphysema: Clinical Manifestations

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

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
Flattened diaphragm hyperinflation

Chest x-ray

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


Corticosteroids 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

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


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

Asthma: Pathophysiology

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Swelling of mucus membranes (edema) Spasm of smooth muscle in bronchioles

Increased airway resistance

Increased mucus gland secretion

Asthma: Pathophysiology

Early phase response: 30 60 minutes

Allergen or irritant activates mast cells

Inflammatory mediators are released

histamine, bradykinin, leukotrienes, prostaglandins, plateletactivating-factor, chemotactic factors, cytokines

Intense inflammation occurs

Bronchial smooth muscle constricts Increased vasodilation and permeability Epithelial damage

Increased mucus secretion Edema

Asthma: Pathophysiology

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: 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

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


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] High-dose inhaled corticosteroids Long-acting inhaled beta2-agonists Corticosteroids if needed

Severe persistent asthma

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: Antiinflammatory


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

Cromolyn & nedocromil

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]

Useful for nocturnal asthma
Not useful for quick relief during an acute attack Salmeterol [serevent]

Asthma Medications: Bronchodilators cont



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]

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