Chronic Obstructive Pulmonary Disease (COPD)

COPD
Description
Characterized by presence of airflow obstruction Caused by emphysema or chronic bronchitis Generally progressive May be accompanied by airway hyperreactivity May be partially reversible

Emphysema
Description

Abnormal permanent enlargement of the air space distal to the terminal bronchioles
Accompanied by destruction of bronchioles

Chronic Bronchitis
Description

Presence of chronic productive cough for 3 or more months in each of 2 successive years in a patient whom other causes of chronic cough have been excluded

COPD
Causes

Cigarette smoking Primary cause of COPD*** Clinically significant airway obstruction develops in 15% of smokers 80% to 90% of COPD deaths are related to tobacco smoking > 1 in 5 deaths is result of cigarette smoking

COPD
Causes

Cigarette smoking Nicotine stimulates sympathetic nervous system resulting in:

HR Peripheral vasoconstriction BP and cardiac workload

COPD
Causes

Cigarette smoking Compounds problems in a person with CAD Ciliary activity Possible loss of ciliated cells Abnormal dilation of the distal air space Alveolar wall destruction Carbon monoxide

O2 carrying capacity Impairs psychomotor performance and judgment Production of mucus Reduction in airway diameter Increased difficulty in clearing secretions

Cellular hyperplasia

COPD
Causes

Secondhand smoke exposure associated with: Pulmonary function Risk of lung cancer Mortality rates from ischemic heart disease

COPD
Causes

Infection Major contributing factor to the aggravation and progression of COPD Heredity -Antitrypsin (AAT) deficiency (produced by liver and found in lungs); accounts for < 1% of COPD cases

Emphysema results from lysis of lung tissues by proteolytic enzymes from neutrophils and macrophages

Pathophysiology of Chronic Bronchitis and Emphysema

Fig. 28-7

Emphysema
Pathophysiology
Hyperinflation

of alveoli Destruction of alveolar walls Destruction of alveolar capillary walls Narrowed airways Loss of lung elasticity

Emphysema
Pathophysiology
Two

types: Centrilobular (central part of lobule)

Panlobular (destruction of whole lobule)

Emphysema
Pathophysiology

Structural changes are: Hyperinflation of alveoli Destruction of alveolar capillary walls Narrowed, tortuous small airways Loss of lung elasticity

Emphysema
Pathophysiology

Small bronchioles become obstructed as a result of

Mucus Smooth muscle spasm Inflammatory process Collapse of bronchiolar walls

Recurrent infections production/stimulation of neutrophils and macrophages release proteolytic enzymes alveolar destruction inflammation, exudate, and edema

Emphysema
Pathophysiology
Elastin

and collagen are destroyed Air goes into the lungs but is unable to come out on its own and remains in the lung Causes bronchioles to collapse

Emphysema
Pathophysiology
Trapped air hyperinflation and overdistention As more alveoli coalesce, blebs and bullae may develop Destruction of alveolar walls and capillaries reduced surface area for O2 diffusion Compensation is done by increasing respiratory rate to increase alveolar ventilation Hypoxemia usually develops late in disease

Emphysema
Clinical Manifestations
Dyspnea

Progresses in severity Patient will first complain of dyspnea on exertion and progress to interfering with ADLs and rest

Emphysema
Clinical Manifestations
Minimal

coughing with no to small amounts of sputum of alveoli causes diaphragm to flatten and AP diameter to increase

Overdistention

Emphysema
Clinical Manifestations
Patient

becomes chest breather, relying on accessory muscles Ribs become fixed in inspiratory position

Emphysema
Clinical Manifestations
Patient

is underweight (despite adequate calorie intake)

Chronic Bronchitis
Pathophysiology
Pathologic lung changes are: Hyperplasia of mucus-secreting glands in trachea and bronchi Increase in goblet cells Disappearance of cilia Chronic inflammatory changes and narrrowing of small airways Altered fxn of alveolar macrophages infections

Chronic Bronchitis
Pathophysiology
Chronic inflammation Primary pathologic mechanism causing changes Narrow airway lumen and reduced airflow d/t
hyperplasia of mucus glands Inflammatory swelling Excess, thick mucus

Chronic Bronchitis
Pathophysiology
Greater

resistance to airflow increases work of breathing

Hypoxemia

Chronic Bronchitis
Pathophysiology
Bronchioles are clogged with mucus and pose a physical barrier to ventilation Hypoxemia and hypercapnia d/t lack of ventilation and O2 diffusion Tendency to hypoventilate and retain CO2 Frequently patients require O2 both at rest and during exercise

Chronic Bronchitis
Pathophysiology
Cough

is often ineffective to remove secretions because the person cannot breathe deeply enough to cause air flow distal to the secretions Bronchospasm frequently develops More common with history of smoking or asthma

Chronic Bronchitis
Clinical Manifestations
Earliest

symptoms: Frequent, productive cough during winter Frequent respiratory infections

Chronic Bronchitis
Clinical Manifestations
Bronchospasm at end of paroxysms of coughing Cough Dyspnea on exertion History of smoking Normal weight or heavyset Ruddy (bluish-red) appearance d/t

polycythemia (increased Hgb d/t chronic hypoxemia)) cyanosis

Chronic Bronchitis
Clinical Manifestations
Hypoxemia

and hypercapnia Results from hypoventilation and airway resistance + problems with alveolar gas exchange

COPD
Complications
Pulmonary hypertension (pulmonary vessel constriction d/t alveolar hypoxia & acidosis) Cor pulmonale (Rt heart hypertrophy + RV failure) Pneumonia Acute Respiratory Failure

COPD
Diagnostic Studies
Chest x-rays early in the disease may not show abnormalities History and physical exam Pulmonary function studies reduced FEV1/FVC and residual volume and total lung capacity

COPD
Diagnostic Studies

ABGs PaO2 PaCO2 (especially in chronic bronchitis) pH (especially in chronic bronchitis) Bicarbonate level found in late stages COPD

COPD
Collaborative Care

Smoking cessation Most significant factor in slowing the progression of the disease

COPD
Collaborative Care: Drug Therapy

Bronchodilators as maintenance therapy -adrenergic agonists (e.g. Ventolin)

MDI or nebulizer preferred

Anticholinergics

(e.g. Atrovent)

COPD
Collaborative Care: Oxygen Therapy

O2 therapy Raises PO2 in inspired air Treats hypoxemia Titrate to lowest effective dose

COPD
Collaborative Care: Oxygen Therapy
Chronic

O2 therapy at home

Improved prognosis Improved neuropsychologic function Increased exercise tolerance Decreased hematocrit Reduced pulmonary hypertension

COPD
Collaborative Care: Respiratory Therapy
Breathing

retraining
breathing breathing

Pursed-lip

Prolongs exhalation and prevents bronchiolar collapse and air trapping

Diaphragmatic

muscles to achieve maximum inhalation and slow respiratory rate

See text re how to teach

COPD
Collaborative Care: Respiratory Therapy
Huff coughing (Table 28-21) Chest physiotherapy to bring secretions into larger, more central airways Postural drainage Percussion Vibration

Positions for Postural Positions for Postural Drainage

Fig. 28-16

COPD
Collaborative Care
Encourage

patient to remain as active

as possible

COPD
Collaborative Care

Surgical Therapy Lung volume reduction surgery Lung transplant

COPD
Collaborative Care

Nutritional therapy
Full stomachs press on diaphragm causing dyspnea and discomfort Difficulty eating and breathing at the same time leads to inadequate amounts being eaten

COPD
Collaborative Care

Nutritional therapy

To decrease dyspnea and conserve energy Rest at least 30 minutes prior to eating Use bronchodilator before meals Select foods that can be prepared in advance 5-6 small meals to avoid bloating Avoid foods that require a great deal of chewing Avoid exercises and treatments 1 hour before and after eating

COPD
Collaborative Care
Nutritional

therapy

Avoid gas-forming foods High-calorie, high-protein diet is recommended Supplements Avoid high carbohydrate diet to prevent increase in CO2 load

Nursing Management
Nursing Diagnoses
Ineffective airway clearance Impaired gas exchange Imbalanced nutrition: less than body requirements Disturbed sleep pattern Risk for infection

Nursing Management
Nursing Implementation
Health Promotion STOP SMOKING!!! Avoid or control exposure to occupational and environmental pollutants and irritants Early detection of small-airway disease Early diagnosis of respiratory tract infections

Nursing Management
Nursing Implementation
Acute Intervention Required for complications like pneumonia, cor pulmonale, and acute respiratory failure

Nursing Management
Nursing Implementation
Ambulatory and Home Care Pulmonary rehabilitation Control and alleviate symptoms of pathophysiologic complications of respiratory impairment

Nursing Management
Nursing Implementation
Ambulatory and Home Care Teach patient how to achieve optimal capability in carrying out ADLs

Physical therapy Nutrition Education Exercise training of upper extremities to help improve function and relieve dyspnea

Activity considerations

Nursing Management
Nursing Implementation
n n

Ambulatory and Home Care Explore alternative methods of ADLs

Nursing Management
Nursing Implementation
Ambulatory and Home Care Slow, pursed-lip breathing After exercise, wait 5 minutes before using -adrenergic agonist MDI

Nursing Management
Nursing Implementation
Ambulatory and Home Care Sexual activity
Plan during part of day when breathing is best Slow, pursed-lip breathing

Refrain

after eating or other strenuous

activity Do not assume dominant position Do not prolong foreplay

Nursing Management
Nursing Implementation
Ambulatory and Home Care Sleep
Nasal saline sprays Decongestants Nasal steroid inhalers Long-acting theophylline

Decreases bronchospasm and airway obstruction

Nursing Management
Nursing Implementation
Ambulatory and Home Care Psychosocial considerations Guilt Depression Anxiety Social isolation Denial Dependence Use relaxation techniques and support groups

Nursing Management
Nursing Implementation
Ambulatory and Home Care Discourage moving to places above 4000 ft.