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