CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) subtitle style Click to edit Master

Presented By: Fretzie Anne G. Gomez, CMT, RN

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Global Initiative for

Chronic bstructive O ung L isease

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Korea United States Australia Yugoslavia Canada Peru Moldova New Zealand Portugal Austria China Italy Syria Thailand Greece Nepal United Kingdom United Arab Emirates Malta Hong Kong ROC Chile

Philippines
Quezon City, PH

Teresita S. deGuia, MD Philippine Heart Center

GOLD National Leaders

Norway India Pakistan Switzerland Georgia Macedonia Iceland France Czech Turkey Belgium Slovakia Denmark Republic Singapore Uruguay Romania Columbia Ukraine 5/27/12 Argentina Sweden Venezuela Egypt Poland
Mexico

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

- COPD is a preventable and treatable

disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. (GOLD)
- COPD is a lung disease characterized

by chronic obstruction of lung airflow 5/27/12 that interferes with normal breathing

 COPD is a progressive disease that

makes it hard to breathe. "Progressive" means the disease gets worse over time.(National Heart Lung and Blood Institute)
The

airflow limitation is usually progressive & is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily caused by cigarette smoking. 5/27/12

Epidemiology of COPD
COPD is the 4th leading cause of death,

and the 2nd cause of disability in the U.S. and yet, COPD is under diagnosed and under-treated:
About 24 million U.S adults have

evidence of impaired lung function.

12 million people have been diagnosed

with COPD.
5.8 million COPD patients are

UNTREATED.
The COPD death rate among women is 5/27/12

COPD includes:
Chronic Bronchitis

is the chronic inflammation of bronchi characterized by productive cough that lasts 3 months a year for 2 consecutive years.
Emphysema

- isa long-term, progressive disease of the lungs that primarily causes shortness of breath due to overinflation of the alveoli (air sacs in the 5/27/12

Stages of COPD:
STAGE I (mild) -Often minimal shortness of breath with or without cough and/or sputum. Usually goes unrecognized that lung function is abnormal -FEV >80% of predicted

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STAGE II (moderate) -Often moderate or severe shortness of breath on exertion, with or without cough, sputum or dyspnea. Often the first stage at which medical attention is sought due to chronic respiratory symptoms or an exacerbation - FEV 50-80% of predicted
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STAGE III (severe) -more severe shortness of breath, with or without cough, sputum or dyspnea - often with repeated exacerbations which usually impact quality of life, reduced exercise capacity, fatigue - FEV 30 50% of predicted

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STAGE IV (very severe) -appreciably impaired quality of life due to shortness of breath - possible exacerbations which may even be life threatening at times -FEV Less than 30% of predicted - or less than 50% with chronic respiratory failure

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Anatomy & Physiology of Respiratory System

Parts of the Resp. System:
1. 2. 3. 4. 5. 6. 7. 8.

Nasal Cavity Larynx Pharynx Trachea Bronchi Bronchioles Alveoli Lungs

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Human Respiratory System

1. Nasal cavity: Air enters

nostrils, is filtered by hairs, warmed, humidified, and sampled for odors as it flows through a maze of spaces.
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2. Pharynx (Throat): Intersection where pathway for air and food cross. Most of the time, the pathway for air is open, except when we swallow. 3. Larynx (Voice Box): Reinforced with cartilage. Contains vocal cords, which allow us to make sounds by voluntarily tensing muscles.

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4. Trachea (Windpipe): Rings of cartilage maintain shape of trachea, to prevent it from closing. Forks into two bronchi. 5. Bronchi (Sing. Bronchus): Each bronchus leads into a lung and branches into smaller and smaller bronchioles, resembling an inverted tree.
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6. Bronchioles: Fine tubes that allow passage of air. Muscle layer constricts bronchioles. Epithelium of bronchioles is covered with cilia and mucus.
Mucus traps dust and other

particles.

Ciliary Escalator: Cilia beat

upwards and remove trapped particles from lower respiratory 5/27/12 airways. Rate about 1 to 3 cm per

Mechanics of Breathing

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Pathogenesis
Environmental & Occupational Exposure CD8+ Lymphocy te
Protease Inhibitor

SMOKIN G

Genetic susceptibilit y Neutroph il

Childhood Respiratory infections

Alveolar Macropha ge
Airway Inflammation and Remodeling

Proteas e Airflow Limitation

Tissue Destruction

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Changes in Lung Parenchyma in COPD

Alveolar wall destruction

Loss of elasticity Destruction of pulmonary capillary bed Inflammatory cells macrophages, CD8+ lymphocytes 5/27/12

Risk Factors for COPD

-Socioeconomic factors Poverty -Exposure to particles Congested Living space Tobacco smoking Lack of Education Occupational dust Use of Biomass fuels, wood stoves Indoor air pollution Inner City population Outdoor air pollution has more prevalence - Gender Stress of environment Lack of funds for - Age treatment in - Respiratory infections exacerbations 5/27/12 Malnourishment

-Genes

Socioeconomic status Aging Population Genes

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CHRONIC BRONCHITIS

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PATHOPHYSIOLOGY OF CHRONIC BRONCHITIS Nicotine

Edema of the bronchial wall
Hypersecretion of the bronchial mucus gland

Airway obstruction Increase airway resistance Impairment of ventilation Impairment of gas exchange

Contraction of the smooth muscle of the bronchioles

Hypoxia

Cyanosis

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Blue

Manifestations:
Long-term Cough

-accompanied by increased mucus production

Shortness of breath Wheezing Fever Cyanosis
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EMPHYSEMA

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Types of Emphysema:
Panlobular (panacinar)

-destruction of respiratory bronchiole, alveolar duct and alveolus.

Centrilobular (centroacinar)

-pathologic changes take place mainly in the center of the secondary lobule.

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PATHOPHYSIOLOGY OF EMPHYSEMA
Smoking
Stimulates alveolar macrophages Release of protease and elastase
Loss of the lung elastic recoil Overdistention of ALVEOLI

Retention of CO2
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Impaired ventilation
Hypoxemia, Hypercarbia DOB

Increase in RR Redness of skin PINK PUFFER

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Manifestations:
Cough Dyspnea Chest pain Wheezing Barrel chest Cold clammy skin Decreased metabolism

- weakness -anorexia -weight loss

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Diagnostic Exams:
Pulmonary function tests

(PFTs)
They measure how much air lungs can hold
and the flow of air in and out of lungs.

They can also measure the amount of gases

exchanged across the membrane between alveolar wall and capillary membrane.

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Chest X-ray
is performed to evaluate the lungs, heart

and chest wall.

is rarely useful for diagnosing chronic

bronchitis, although they sometimes show mild scarring and thickened airway walls.
Shows increased in AP diameter,

overinflation and presence of bullae.

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Clear signs of COPD include the following:

Abnormally large amounts of air spaces in

the lung.

A flattened diaphragm. A smaller heart; if heart failure is present,

however, the heart becomes enlarged and there may not be signs of overinflated lungs.

Exaggerated lung inflation in upper areas.

5/27/12 Larger amounts of air in the lower lungs in

Arterial blood gases (ABG) analysis

These blood tests measure how the lungs

transfer oxygen to bloodstream and how effectively they remove carbon dioxide.

Low

oxygen (hypoxia) and high carbon dioxide (hypercapnia) levels often indicate chronic bronchitis, but not always emphysema. A blood gas analysis that shows very low oxygen levels is useful for determining which patients would benefit fromoxygen therapy.

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Pulse Oximetry
This test involves use of a small device
that attaches to the fingertip.

The oximeter measures the amount of To help determine whether patient needs

oxygen in the blood differently from the way it's measured in blood gas analysis. supplemental oxygen, the test may be performed at rest, during exercise and overnight.

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Sputum examination
Analysis of cells in sputum can help

determine the cause of some lung Computerized tomography problems.

(CT)

scan

A CT scan can detect emphysema sooner

than an X-ray can, but it can't assess the severity of emphysema as accurately as can a pulmonary function test.

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Test for alpha-1 antitrypsin deficiency

Physicians

Carbon Monoxide Diffusing Capacity carbon monoxide diffusing The lung

capacity (DLCO) test determines how effectively gases are exchanged between the blood and airways in the lungs. Patients should not eat or exercise before the test, and they should not have smoked for 24 hours.
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will typically test for the protective enzyme alpha-1 antitrypsin in COPD patients who are nonsmokers and who develop emphysema in their 30s.

COMPLICATIONS:
Pulmonary Hypertension

COR Pulmonale

Malnutrition

Skeletal Muscle Dysfunction

Atelectasis

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Medical Management
Pharmacotherapy

-Expectorants (guaiafenesin) / Mucolytic (mucosolvan) -Bronchodilators (Salbutamol, Theophylline, Terbutaline) These drugs can help relieve coughing, shortness of breath and trouble breathing by opening constricted airways, but they're not as effective in treating emphysema as they 5/27/12 are in treating asthma.

-Steroids

Administered for anti-inflammatory effects. (Solu-medrol, Beclomethasone). Although inhaled steroids have fewer side effects than oral steroids do, prolonged use can weaken bones and increase the risk of high blood pressure, cataracts and diabetes. -Antibiotics Only to treat infectious exacerbations of COPD
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Non-Pharmacologic Treatment

Rehabilitation: All COPD patients benefit from exercise training programs, improving with respect to both exercise tolerance and symptoms of dyspnea and fatigue. Oxygen Therapy: The long-term administration of oxygen (> 15 hours per day) to patients with chronic respiratory failure has been shown to increase survival.

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Diet - High calorie, High Protein and low

Carbohydrate
Bronchial Hygiene Measures

-Steam Inhalation -Aerosol Inhalation -Medimist inhalation

Chest Physiotherapy

-Percussion

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Surgery in COPD
Lung transplant

-Replaces a sick lung with a healthy lung from a person who has just died.
Lung Volume Reduction Surgery

-Removes part of one or both lungs, making room for the rest of the lung to work better. It is used only for severe emphysema.
Bullectomy

-Removes the part of the lung that has been 5/27/12 damaged by the formation of large, air-filled

Nursing Management
Ineffective airway clearance r/t

excessive, thickened mucus production.

Ineffective breathing pattern r/t

shortness of breath, mucus, bronchoconstriction, and airway irritants.

Impaired gas exchange r/t alveolar

and capillary changes and ventilation-perfusion imbalance.

Activity intolerance r/t hypoxemia. 5/27/12

Ineffective airway clearance r/t excessive, thickened mucus production. Plan: Patient will maintain airway patency.
Interventions: 1. Adequately hydrate the patient. 2. Monitor respirations and breath

sounds.
3. Teach and encourage the use of

diaphragmatic breathing and coughing exercise.

4. Elevate head of the bed/ position
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breath, mucus, and bronchoconstriction.

Plan: Patient will establish effective

respiratory pattern AEB absence of cyanosis and other signs of hypoxia.

Intervention: 1. Teach patient diaphragmatic and pursed-lip

breathing. periods.

2. Encourage alternating activity with rest 3. Elevate head of the bed or have the client

sit up in the chair, as appropriate.

4. Assist the client in the use of5/27/12 relaxation

Plan: Patient will demonstrate improved

Impaired gas exchange r/t alveolar and capillary changes and ventilationperfusion imbalance.
ventilation and adequate oxygenation of tissues AEB ABG within normal limits.

Interventions: 1. Position client in the semi-Fowlers position. 2. Monitor clients oxygen saturation

continuously by pulse oximetry.

3. Maintain adequate intake and output for

mobilization of secretions.
4. Encourage adequate rest and limit activity. 5. Keep environment allergen-free or pollutant5/27/12

Activity intolerance r/t imbalance between oxygen supply and report measurable increase in demand. Plan: Patient will
activity tolerance.
Interventions: 1. 2. 3. 4. 5.

Plan care to carefully balance rest periods with activities. Promote comfort measures and provide relief of pain. Assist patient in learning appropriate safety measures. Evaluate clients actual and perceived limitations in light of usual status.
5/27/12 Encourage use of relaxation techniques.

Knowledge deficit regarding disease process and prognosis related to less information.
Plan: Patient will participate in the learning

process.

Interventions: 1. Ascertain level of knowledge including

anticipatory needs.
2. Provide positive reinforcement. 3. Determine clients ability/ readiness to learning. 4. Help patient identify or develop short and long

term goals.
5. Provide information relevant only to the

situation.

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Health Education
Breathing Exercises

-Diaphragmatic breathing -Pursed-lip breathing -Deep breathing exercise

Smoking cessation

Nutritional counselling
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