Obstructive Disease Is Characterized by an Increase in Airway Resistance That Is Measured

8

Department of Medical Nursing, Faculty of Nursing, Chiang Mai University

Teaching Material for 561314: Adult Nursing II

For International Program Nursing Students

Semester I Academic Year 2007

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Principle of Holistic of Nursing Care for Adult with Common Problem in Respiratory Diseases (Obstructive Pattern)

Assist. Prof. Dr. Nitaya Pinyokham

Obstructive disease is characterized by an increase in airway resistance that is measured as a decrease in peak expiratory flow rates. In some cases, there is a miss-match between the FEV1/FVC ratio. The normal person exhales most of the inspired air in the 1st second; this ratio on normal subjects is around 0.8, this means that 80% of the expired air is expelled the 1st second.

The group of diseases in obstructive lung include emphysema, bronchitis, asthma, chronic obstructive pulmonary disease (COPD), bronchiectasis, byssinosis, bronchiolitis, Asbestosis. In this article, only COPD is illustrated its pathophysiology, predisposing factors, diagnosis, management, and nursing intervention.

Normal Lung

Figure 2 COPD Lung

COPD

Chronic obstructive pulmonary disease (COPD), also known as chronic obstructive airway disease (COAD), is a group of diseases characterized by limitation of airflow in the airway that is not fully reversible. COPD is the umbrella term for chronic bronchitis, emphysema and a range of other disorders. It is most often due to tobacco smoking[1] but can be due to other airborne irritants such as coal dust, asbestos or solvents, as well as preserved meats containing nitrites. [1] COPD is the fourth leading cause of death in America, claiming the lives of 122,283 Americans in 2003 and the number of women dying from the disease has surpassed the number seen in men.

The main symptoms of COPD include dyspnea (shortness of breath) lasting for months or perhaps years, possibly accompanied by wheezing, and a persistent cough with sputum production.[2] It is possible the sputum may contain blood (hemoptysis), usually due to damage of the blood vessels of the airways. Severe COPD could lead to cyanosis (bluish decolorization usually in the lips and fingers) caused by a lack of oxygen in the blood. In extreme cases it could lead to cor pulmonale due the extra work required by the heart to get blood to flow through the lungs.[3]

COPD is particularly characterized by a ratio of forced expiratory volume over 1 second (FEV1) to forced vital capacity (FVC) being < 0.7 and the FEV1 < 70% of the predicted value [4] Other signs include a rapid breathing rate (tachypnea) and a wheezing sound heard through a stethoscope. Pulmonary emphysema is NOT the same as subcutaneous emphysema, which is a collection of air under the skin that may be detected by the crepitus sounds produced on palpation.[5]

Pathophysiology

Chronic bronchitis

Bronchitis is inflammation of the bronchi (medium-size airways) in the lungs. Acute bronchitis is usually caused by viruses or bacteria and may last several days or weeks.

Bronchitis

Acute bronchitis usually resolves in 7-10 days with no underlying lung disease. Chronic bronchitis however is dependent on early recognition and smoking cessation which improves the outcome significantly.

Chronic bronchitis is defined in clinical terms as a cough with sputum production on most days for 3 months of a year, for 2 consecutive years. Chronic bronchitis is hallmarked by hyperplasia (increased number) and hypertrophy (increased size) of the goblet cells (mucous gland) of the airway, resulting in an increase in secretion of mucus which contributes to the airway obstruction. Microscopically there is infiltration of the airway walls with inflammatory cells, particularly neutrophils. Inflammation is followed by scarring and remodeling that thickens the walls resulting in narrowing of the small airway. Further progression leads to metaplasia (abnormal change in the tissue) and fibrosis (further thickening and scarring) of the lower airway. The consequence of these changes is a limitation of airflow.[10].

Emphysema

Emphysema is a type of chronic obstructive lung disease. It is often caused by exposure to toxic chemicals or long-term exposure to tobacco smoke.

Emphysema is defined histologically as the enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls.[9] The enlarged air sacs (alveoli) of the lungs reduces the surface area available for the movement of gases during respiration. This ultimately leads to dyspnea in severe cases. The exact mechanism for the development of emphysema is not understood, although it is known to be linked with smoking and age.

Emphysema

The outcome is better for patients with less damage to the lung who stop smoking immediately. Still, patients with extensive lung damage may live for many years so predicting prognosis is difficult. Death may occur from respiratory failure, pneumonia, or other complications.

Predisposing Factors

1) Cigarette smoking. A primary factor of COPD is chronic tobacco smoking. In the United States, around 90% of cases of COPD are due to smoking[6] (are smoker or former smokers) Not all smokers will develop COPD, but continuous smokers have at least a 25% risk.[7] If you smoke 30 cigarettes per day you are 20 times more likely to die from COPD than non-smokers (Asthma Foundation, 2007).

2) Pollutions

-Occupational pollutants. Some occupational pollutants, such as cadmium and silica, have shown to be a contributing risk factor for COPD. The people at highest risk for these pollutants include coal workers, construction workers, metal workers and cotton workers, amongst others. However, in most cases these pollutants are combined with cigarette smoking further increasing the chance of developing COPD. These occupations are commonly associated with other respiratory diseases, particularly pneumoconiosis (black lung disease).

-Air pollution. Urban air pollution may be a contributing factor for COPD as it is thought to impair the development of the lung function. In developing countries indoor air pollution, usually due to biomass fuel, has been linked to COPD, especially in women.

4) Genetics or family factors. Very rarely, there may be a deficiency in an enzyme known as alpha 1-antitrypsin which causes a form of COPD and hyper reactive airways (Asthma Foundation, 2007). Alpha 1-antitrypsin (AAT) is a substance found in several places throughout the body and is important in preventing breakdown of cells, particularly those in the lungs and liver. People who are deficient of this substance are at increased risk of emphysema and cirrhosis of liver (Asthma Foundation, 2007).

5) Other risk factors. Increasing age, male gender, allergy, repeated airway infection and general impaired lung function are also related to the development of COPD. In addition, urbanization, social class, and diet may also have some impact in development of COPD but their overall effect is not known(Asthma Foundation, 2007). COPD is a common cause of disability of the older people in Thailand. It is estimated that about half of the acute exacerbation definitely due to bacterial infection (e.g. Chlamydia pneumoniae and others).

Sings and Symptom

The signs and symptoms of chronic obstructive pulmonary disease (COPD) include:

·  Cough

·  Sputum (mucus) production

·  Shortness of breath, especially with exercise

·  Wheezing (a whistling or squeaky sound when you breathe)

·  Chest tightness

The early signs of COPD for which many people seek medical attention before being formally diagnosed include marked shortness of breath with exertion, a cough that won’t go away, or frequent respiratory infections. This is often at a point when the disease is already advanced. Many people might be identified earlier if their doctors routinely screen all patients who are smokers or previous smokers.

Diagnosis

The diagnosis of COPD is usually suggested by symptoms; it is a clinical diagnosis and no single test is definitive. A comprehensive history from the patient is very important with regard to smoking and occupation. Physical examination with a plethysmograph can reveal the true extent of COPD.

The severity of COPD can be classified as follows using spirometry (see above):

Severity / Post-bronchodilator FEV1 /FVC / FEV1% predicted
At risk / >0.7 / ≥80
Mild COPD / ≤0.7 / ≥80
Moderate COPD / ≤0.7 / 50-80
Severe COPD / ≤0.7 / 30-50
Very Severe COPD / ≤0.7 / <30 or 30-50 with Chronic Respiratory Failure symptoms

Management

Although COPD is not curable, it can be controlled in a variety of ways.

1) Smoking cessation

Smoking cessation is one of the most important factors in slowing down the progression of COPD. Even at a late stage of the disease it can reduce the rate of deterioration and prolong the time taken for disability and death.[10]

2) Occupational change

Workers may be able to transfer to a significantly less contaminated area of the company depending on circumstances. Often however, workers may need complete occupational change.

3) Pharmacotherapy

Bronchodilators

There are several types of bronchodilators used clinically with varying efficacy: β2 agonists, M3 antimuscarinics, leukotriene antagonists, cromones and xanthines.[11] These drugs relax the smooth muscles of the airway allowing for improved airflow. The change in FEV1 may not be substantial, but changes in the vital capacity are significant. Many patients feel less breathless after taking bronchodilators.

β2 agonists. There are several highly specific β2 agonists available. Salbutamol (Ventolin) is the most widely used short acting β2 agonist to provide rapid relief and should be prescribed as a front line therapy for all classes of patients. Other β2 agonists are Bambuterol, Clenbuterol, Fenoterol, and Formoterol. Longer acting β2 agonists such as Salmeterol act too slowly to be used as relief for dypsnea so these drugs should be used as a secondary therapy. An increased risk is associated with long acting β2 agonists due to decreased sensitivity to inflammation so generally the use of a concomitant corticosteroid is indicated[2][3][4].

M3 muscarinic antagonists (anticholinergics. Derived from the deadly agaric Amanita muscaria, specific antimuscarinics were found to provide effective relief to COPD. Inhaled antimuscarinics have the advantage of avoiding endocrine and exocrine M3 receptors. The quaternary M3 muscarinic antagonist Ipratropium is widely prescribed with the β2 agonist salbutamol. [5]. Ipratropium is offered combined with salbutamol (Combivent) and with fenoterol (Duovent). Tiotropium provides improved specificity for M3 muscarinic receptors.

Cromones. Cromones are mast cell stabilizers that are thought to act on a chloride channel found on mast cells that help reduce the production of histamine and other inflammatory factors. Chromones are also thought to act on IgE-regulated calcium channels on mast cells. Cromoglicate and Nedocromil, which has a longer half-life, are two chromones available.[12]

Leukotriene antagonists. More recently leukotriene antagonists block the signalling molecules used by the immune system. Montelukast, Pranlukast, Zafirlukast are some of the leukotrienes antagonists.[13]

Xanthines. Theophylline is the prototype of the xanthine[14] class of drug. Teas are natural sources of methylxanthines, xanthines and caffeine while chocolate is a source of theobromine. Caffeine is approximately 16% metabolized into theophylline. Nebulized theophylline is used in the EMR for treatment of dyspnea (Difficulty in breathing). Patients need continual monitoring as theophylline has a narrow therapeutic range. More aggressive EMR interventions include IV H1 antihistamines and IV dexamethasone.

Corticosteroids

Inhaled corticosteriods (specifically glucocorticoids) act in the inflammatory cascade and may improve airway function considerably,[10] however the long term value has not been proven. Corticosteroids are often combined with bronchodilators in a single inhaler. Some of the more common inhaled steroids in use are beclomethasone, mometasone, and fluticasone.

Salmeterol and fluticasone are combined (Advair), however the reduction in death from all causes among patients with COPD in the combination therapy group did not reach the predetermined level of statistical significance.[15][16]

TNF antagonists

Tumor necrosis factor antagonists (TNF) are the most recent class of medications designed to deal with refractory cases. Tumor necrosis factor-alpha is a cachexin or cachectin and is considered a so-called biological drug. They are considerered immunosopressive with attendant risks. These rather expensive drugs include infliximab, adalimumab and etanercept.[17]

Vaccination

Patients with COPD should be routinely vaccinated against influenza, pneumococcus and other diseases to prevent illness and the possibility of death.[11]

Oxygen therapy: Indicators for O2 therapy are following:

·  Severe airflow obstruction with FEV1 of less than 30% of predicted.

·  Cyanosis

·  Polycythaemia

·  Peripheral oedema

·  Elevated jugular venous pressure

·  Oxygen saturation under 92% when breathing air.

·  Consider assessment for moderate airflow obstruction (FEV1 30 to 49% of predicted). Evidence level D

·  All practices should have a pulse oximeter to identify patients needing LTOT. Evidence level D

·  Oxygen concentrators should be used to supply the LTOT at home.

·  Ambulatory oxygen therapy may be of benefit in those who wish to continue therapy outside the home. Evidence level D.

·  Short bursts of oxygen therapy for episodes of breathlessness should only be used if all other methods fail. Evidence level C.

Pulmonary rehabilitation

Pulmonary rehabilitation is a program of disease management, counseling and exercise coordinated to benefit the individual.[18] Pulmonary rehabilitation has been shown to relieve difficulties breathing and fatigue. It has also been shown to improve the sense of control a patient has over their disease as well as their emotions.[19]

Diet

A recent French study conducted over 12 years with almost 43,000 men concluded that eating a Mediterranean diet "halves the risk of serious lung disease like emphysema and bronchitis". [6]

Surgery

For some people with severe COPD, surgery may be recommended. Surgery is usually done for people who have:

·  Severe symptoms

·  Not had improvement from taking medicines

·  A very hard time breathing most of the time

The two types of surgeries considered in the treatment of severe COPD are: bullectomy and lung volume reduction surgery (LVRS).

Prognosis

A good prognosis of COPD relies on an early diagnosis and prompt treatment. Most patients will have improvement in lung function once treatment is started, however eventually signs and symptoms will worsen as COPD progresses. The median survival is about 10 years if two-thirds of expected lung function was lost by diagnosis.

Nursing Intervention

Nursing diagnosis: Impaired gas exchange

Definition of impaired gas exchange: By the process of diffusion the exchange of oxygen and carbon dioxide occurs in the alveolar-capillary membrane area. The relationship between ventilation (airflow) and perfusion (blood flow) affects the efficiency of the gas exchange. Normally there is a balance between ventilation and perfusion; however, certain conditions can offset this balance, resulting in impaired gas exchange. Chronic conditions such as chronic obstructive pulmonary disease (COPD) put these patients at greater risk for hypoxia.