Bronchial Asthma

The etymological sense of the word asthma comes from the Greek word meaning panting, i.e. difficulty in breathing.

This disease has an incidence of 3% to 8% among the population. Some 100 to 150 million people worldwide suffer from asthma, with more than 180,000 deaths per year. Most asthma deaths occur in people over 45 years old, and 40% of patients are aged over 75. Worldwide, the economic costs associated with asthma exceed those of tuberculosis and HIV / AIDS combined.

Asthma is an obstruction of the airways characterized by inflammation and hyperirritability thereof. Inhalation does not cause substances which effect on normal individuals may cause bronchoconstriction in asthmatic patients. So asthma does not cause emphysema or other chronic diseases, but alone can be a major cause of disability. An important characteristic of asthma is the extreme variability of both patient to patient and in the same patient at different stages.



To this day no one knows for sure how (or why) a person acquires asthma. It is known that, once acquired, the lungs can react to stimuli that can trigger attacks, or exacerbations, or attacks of Bronchial Asthma.

In general, these attacks of asthma begin or are "triggered" by something that attacks the lungs. These agents are called asthma triggers.

The attacks of asthma may be caused by several factors such as allergens (particularly inhaled or aeroallergens: house dust mites, pollens, animal epithelia, fungi), bacterial or viral infections, occupational agents (dust textiles, timber, grain, volatile paints and adhesives), and tobacco smoke. All these stimuli are inducers of exacerbations, and in addition to causing asthma attacks, frequent exposure to such stimuli may aggravate the chronic inflammation of the airways and increase disease severity. Chemical irritants, emotional factors, physical activity and exaggerated reaction to certain medications (such as beta-blockers, aspirin or indomethacin) are stimuli that trigger exacerbations, but do not aggravate the underlying inflammation.

Because of this wide variety of causes, it can be very difficult to deduce what exactly has caused the attacks of bronchial asthma. However, once discovered the triggering factor of asthma, something must be done to prevent future attacks, which allows some control over the crisis.

Asthma is not a hereditary disease, although there is a genetic predisposition to the disease. The risk of childhood asthma is related to the presence of disease in the parent. If one parent has asthma, the risk of children developing asthma is 25% if both parents are asthmatic this probability increases to about 50%. However, the fact that parents do not have the disease does not mean that the child can not develop it (there is a probability of about 10%).


The etiological classification or pathology of the disease is difficult; however, asthma is traditionally divided into two main categories, based on the presence or absence of an immune disorder:

• Extrinsic asthma (Allergic shape): the asthmatic episode is initiated by a hypersensitivity reaction type I (immediate) induced by exposure to an extrinsic antigen inhalation. There are three recognized types of extrinsic asthma, occupational asthma, allergic bronchopulmonary aspergillosis (bronchial colonization by Aspergillus organisms followed by development of antibody immunoglobulin E [IgE]), and atopic asthma (most common type, usually begins in the first two decades of life, and is commonly associated with other allergic manifestations in the patient and other family members).
• Intrinsic Asthma: mechanisms triggering are non-immune. Various stimuli can initiate a bronchospasm, including aspirin, lung infections (mainly caused by viruses), cold, psychological stress, exercise and inhaled irritants such as sulfur dioxide. However, it should be emphasized that due to the inherent bronchial hyperreactivity, with an individual extrinsic asthma the patient is also susceptible to the development of an asthma attack when exposed to one of the agents mentioned. Thus, in many cases it is not possible to distinguish between pure intrinsic and extrinsic asthma.

Hypersensitivity

It is the occurrence of an immune response in an exaggerated or inappropriate form. It can be caused by various types of antigens and its cause varies from individual to individual. Hypersensitivity does not manifest in the first contact with the antigen, for this to happen there must be the first sensitization.

Type I hypersensitivity

It occurs when an IgE-mediated immune response is directed against environmental antigens, such as mites, house dust, animal dander and pollen. Mast cells bind IgE. The subsequent connection to an allergen induces mast cell degranulation and mediator release which produce allergic reactions.

Asthma can also be classified according to their severity, as shown in the following table:

Degrees	Symptoms	Symptoms Nocturnes	DEMI
1 - Intermittent	<1 time / week or asymptomatic; DEMI; normal between attacks.	≤ 2 per month	≥ 80% predicted Variability<20%
2 - Mild persistent	≥ 1 per week	> 2 per month	≥ 80% predicted Variability 20-30%
3 - Moderate persistent	Daily; Uses Bronchodilators short daily action; Crises affect activity.	> 1 per week	≥ 60% - <80% predicted Variability> 30%
4 - Record	Constants; Activity limitedphysical	Frequent (almost daily)	≤ 60% predicted Variability> 30%

The patient with asthma can measure the degree of airway obstruction, and thus measure the degree of symptoms, helping the doctor to treat. A far easier way to measure airway obstruction is through a device called PEF (peak expiratory flow). Related to this unit, there is a table with the values considered normal for age and height of the patient, but the ideal is to discover what the normal value of each. Thus it is recommended to calculate a resultant average of values obtained by EPF for 20 days (with measurements taken in the morning and evening).

In addition there is a classification for the disease at different levels, there is also a simple and practical way of classifying asthma attacks. Thus, classification is made on: mild, moderate and severe attacks.

Mild crisis:

• Slight fatigue;
• Wheezing or cough when you laugh or make small efforts;
• Tightness in the chest;
• Slight change in PEF (> 80% expected).

Moderate crisis:

• Increased respiratory rate;
• Fatigue with moderate exertion;
• Noticeable discomfort in breathing;
• Dyspnea;
• Wheezing;
• PEF 50-80% of normal patients.

Severe crisis:

• Tachypnea;
• Increased perspiration;
• High respiratory rate;
• Dyspnea;
• Severe discomfort in breathing;
• Use of accessory muscles of inspiration;
• Skin is cold;
• Very intense and frequent cough;
• Nose opens up well and there is the beating of the nasal "wings";
• Fatigue while performing daily activities (talking, walking, eating);
• Cyanosis (noted on the lips and nails);
• Less than normal PEF.

Chronic inflammation of the airways makes them hypersensitive, responding to various stimuli through:

• Increased mucus secretion, hypersecretion;
• Peribronchial muscle contraction: Bronchoconstriction;
• Mucosal edema, with increased inflammation.

The responses to these stimuli cause airway obstruction by decreasing its size and accumulation of mucus.

The National Asthma Education and Prevention Program (NAEPP) of The National Institute of Health (NIH) in association with the World Health Organisation (WHO) recently redefined asthma as a function of its three main characteristics:

• The airways tend to become inflamed, just as the skin becomes inflamed when there is a wound, causing swelling and thus blocking them;
• Cells airway mucus secreting occurs more than usual. This mucus is very thick and tends to obstruct the airway;
• The airway muscles contract, particularly the sphincter of the bronchi.

The correct definition of bronchial asthma may be given by the British Thoracic Society, which states:

Asthma is a chronic inflammatory condition of the airways, causes of which are not completely understood. As a result of inflammation airway becomes narrow-reactive and easily responsive to various stimuli. This can result in coughing, wheezing, chest tightness and breathlessness, which are most common symptoms at night. The narrowing of the airways is usually reversible, but in patients with chronic asthma, the inflammation can determine irreversible airflow obstruction. The pathological features include the presence of inflammatory cells in the airways, plasma exudation, edema, muscle hypertrophy, mucus plugs and epithelial desquamation.

Physical examination: typically reveal tachycardia, tachypnea with prolonged expiration, excessive inflation of the chest with little movement of the diaphragm, and diffuse and acute expiratory wheezing.

Analysis of sputum, purulent sputum may appear due to the higher concentration of eosinophils or an inflammatory response to viral tracheobronchitis. The sputum smear may reveal Cushmann spiral (i.e., mucus which forms a mold in the small airways) or Charcot-Leyden crystals (i.e., degradation products of eosinophils).

Hematological studies show the presence of leukocytes and eosinophils as well as the intrinsic shape of allergic disease.

Pulmonary Function Tests: all tests can be changed. The functional residual capacity (FRC) is increased, a second forced expiratory volume (FEV) is decreased, the ratio FEV / FVC is reduced but may improve after inhalation of a bronchodilator. The residual volume (RV), total lung capacity (TLC) and lung compliance are usually increased and often there is an increase of the diffusion of carbon monoxide. After symptomatic recovery TLC and lung compliance return to normal, but the maximum expiratory flow rate can stay low at low lung volumes, and abnormal distribution of ventilation may persist, reflecting strong obstruction of small airways.

Chest radiograph: in general only reveals excessive inflation. Occasional findings include localized density due to a large mucus plug and the dark signal of pneumothorax or pneumomediastinum, reflecting the alveolar tissue disruption caused by high intra-alveolar pressure.

Arterial blood gas, the partial pressure of carbon dioxide is generally low (less than 36 mmHg). The partial pressure of carbon dioxide increases or stays normal (40 mmHg) indicating severe obstruction. The arterial hypoxia is common despite the increased ventilation and results from the sub ventilation of pulmonary segments supplied by narrowed airways.


To make a proper diagnosis of asthma, the possibility of clinical case must be excluded due to one of the following conditions:

• Obstruction of the upper airways;
• Inhalation of foreign body;
• Pulmonary embolism;
• Acute lung edema;
• COPD exacerbation;
• Cystic fibrosis;
• Pneumothorax.

For the physical therapy there are two phases of treatment: asthmatic crisis and inter-crisis period.

Asthmatic crisis

The patient appears very tense and anxious, thorax blocked in inspiratory position, rapid uncontrolled breathing, predominantly upper costal at the expense of accessory muscles of inspiration, complaining of "breathlessness" and "squeak" in the chest, feeling of "chest tightness".

Main objectives:

• Decrease inflammation;
• Relief of bronchospasm;
• Control of breathing.

Treatment:

• Administration of bronchodilators and anti-inflammatory drugs (placing the patient in a relaxed position of greatest comfort);
• Attempting to combat anxiety, seeking a progressive relaxation of the upper chest, shoulder girdle, encouraging an abdominal-diaphragmatic breathing.

During the crisis you should not try to modify the respiratory rhythm or apply techniques to expectorate, as there is danger of serious bronchospasm.

Immediately after the crisis, when there is improvement of bronchospasm and coughing begins to be productive:

• Insist on breath control, reducing the frequency and prolonging expiratory time;
• Facilitate the removal of secretions;
• Relaxation massage (neck and shoulder girdle).

Inter-crisis period

Acquisition of control of breathing and preparation of the patient for a possible crisis.

• Teaching rest positions adopted during the crisis;
• Functional respiratory rehabilitation;
• Exercises costal and abdominal-selective diaphragm;
• Breathing exercises.

Correction assinergias and ventilatory defects.

• RFR;
• Exercises costal, abdominal-selective and global diaphragm;
• Drainage of secretions (if necessary);
• Prevent stiffness and thoracic deformities;
• Relaxation of the shoulder girdle;
• Muscle stretching;
• Easing backpack (with a higher incidence in the sense expiratory).

Teach the patient to inhale through the nose and breathe abdomino-diaphragmaticly directed to apply during the crisis.

Rehabilitation effort

• Try to gradually increase the exercise tolerance;
• Avoid over-protective parents of children with asthma;
• Advice to the patient in case of crisis.

Acute attacks of asthma can start as if it is a simple cold. The most common manifestations of the disease are coughing, wheezing and breathlessness, dyspnea, and tightness of the chest. The symptoms of asthma are related more to the expiration process for their obstructive nature.

The manifestations vary from case to case and depend on the intensity of the disease. In a severe attack of asthma, breathing becomes increasingly difficult and accompanied by sweating, tachycardia, distress and anxiety. The patient can not lie and may not be able to speak and breathing becomes rapid and panting.

In a fit of extreme gravity the low oxygen content in the circulating blood can cause cyanosis (bluish color) on the face and especially lips. The skin becomes pale and sweaty. These symptoms can be fatal. During crises the following drugs are contraindicated: sedatives, tranquilizers, mucolytics, especturantes.

The term "status asthmaticus" is generally reserved for a severe and prolonged asthma attack unresponsive to treatment and involving bronchospasm so severe that the patient is at risk of developing respiratory failure.


Although there is no cure for asthma, most exacerbations can be prevented. Extrinsic asthma sufferers may take tests aimed at detecting whether the attacks are triggered by any of the most common allergens agents. If a specific cause is discovered several measures can be taken to prevent it. For example, if the asthma attacks are triggered by pollen, the patient should avoid gardens and trips to the field during the spring. You can appeal to the desensitization (a series of injections of the allergen agent), although the results are not always satisfactory. The prophylactic drugs (preventive) proved much more effective in preventing attacks, among them the anti-allergic substances (antihistamines, cromolyn sodium) and inhaled corticosteroids. However, to be effective, they must be administered several times daily, typically with an inhaler.

When the patient recognizes and avoids the triggers of their asthma symptoms, exacerbations and drug therapy are reduced. For that certain measures could be taken, called avoidance measures, such as:

• Do not use cleaning utensils containing fur, as well as carpets and curtains in the room;
• Avoid mold and moisture;
• Use dryers periodically enabling the control of humidity;
• Avoid animals in the private area of the house because of the epithelium of dog's or cat's hair, house dust (mites) and flower pollen can trigger crises;
• Do not use pillows or feather pillows and foam flakes, mainly in the fourth;
• Provide washing clothes in hot water at levels adequate to remove the bedding dust mites and reduce the overuse of cleaning products that hold the smell in the tissue.

Never take medications that are not prescribed by doctors.


The effective treatment of asthma is based on four basic components: objective measures of pulmonary function, drug therapy, measures to control environmental allergens and irritants, and patient education.

Asthma is a disease which, without curing, can be controlled. There are basically two types of drugs that are used in the treatment of asthma: the preventive, or anti-inflammatory, and bronchodilator, or relievers. The preventive or anti-inflammatory drugs are those, which treat the cause of asthma, inflammation of the bronchi. The relievers, or bronchodilators, are those, which are the consequence of asthma: the narrowing of the bronchi, acting on the muscles of the bronchi and causing relaxation of them.

Thus, in acute cases, drugs that open the bronchial tubes are rapidly employed - bronchodilators. These can be conveyed through "firecrackers" or pressurized sprays. These drugs must be used only as drugs for redemption, i.e., when acute attacks of breathlessness.

Asthma is considered an inflammatory disease. It must therefore be treated with anti-inflammatory. We use the anti-inflammatory from mild asthma to persistent, even when the patient is out of crisis (without dyspnea), as yet is known that there is inflammation.

There are at least three groups of anti-inflammatory drugs used in asthma:

• Steroids: is the group with the best results, always used by inhalation (such as "crackers"), have low bioavailability, i.e., without significant systemic effects (do not alter the growth of children, cause less osteoporosis, cataracts, etc.) as opposed to what happens when corticosteroids are administered orally or by injection;
• Chromones: cromolyn and nedocromil, widely used for children, also by inhalation, used primarily in mild asthma;
• Leukotriene modifiers: As for children over 6 months, when orally and may be administered in combination with inhaled glucocorticosteroids, when these alone do not control the disease.

In addition to bronchodilators, "short duration" drugs, used in acute asthma, we have a group composed of two substances of "long duration of action." These are prescribed every twelve hours, sometimes only at night (nocturnal asthma), but always associated with inhaled corticosteroids. They are indicated for chronic asthma in moderate persistent and severe stages. They are never used for merely symptomatic treatment. For inhalation of bronchodilators and anti-inflammatory there are several devices: