Asthma is caused by inflammation of the airways. These are the small tubes, called bronchi, which carry air in and out of the lungs. In asthma, the bronchi will be inflamed and more sensitive than normal. The airways of the lungs consist of the cartilaginous bronchi, membranous bronchi and gas‐exchanging bronchi, termed the respiratory bronchioles and alveolar ducts. While the first two types function mostly as anatomic dead space, they also contribute to airway resistance. The smallest non‐gas‐exchanging airways, the terminal bronchioles, are approximately 0.5â•›mm in diameter; airways are considered small if they are less than 2â•›mm in diameter. Cellular elements include mast cells, which are involved in the complex control of releasing histamine and other mediators. Basophils, eosinophils, neutrophils and macrophages also are responsible for extensive mediator release in the early and late stages of bronchial asthma. Stretch and irritant receptors reside in the airways, as do cholinergic motor nerves, which innervate the smooth muscle and glandular units. In bronchial asthma, smooth muscle contraction in an airway is greater than that expected for its size if it were functioning normally, and this contraction varies in its distribution.
Pathophysiology
Some of the principal cells identified in airway inflammation include mast cells, eosinophils, epithelial cells, macrophages and activated T lymphocytes. T lymphocytes play an important role in the regulation of airway inflammation through the release of numerous cytokines. Other constituent airway cells, such as fibroblasts, endothelial cells and epithelial cells, contribute to the chronicity of the disease. Other factors, such as adhesion molecules (e.g. selectins, integrins), are critical in directing the inflammatory changes in the airway. Finally, cell‐derived mediators influence smooth muscle tone and produce structural changes and remodelling of the airway. The presence of airway hyper‐responsiveness or bronchial hyperreactivity in asthma is an exaggerated response to numerous exogenous and endogenous stimuli. The mechanisms involved include direct stimulation of airway smooth muscle and indirect stimulation by pharmacologically active substances from mediator‐secreting cells such as mast cells or non‐myelinated sensory neurons. The degree of airway hyper‐responsiveness generally correlates with the clinical severity of asthma. Airway obstruction causes increased resistance to airflow and decreased expiratory flow rates. These changes lead to a decreased ability to expel air and may result in hyperinflation. The resulting over‐distention helps maintain airway patency, thereby improving expiratory flow; however, it also alters pulmonary
mechanics and increases the work of breathing. Bronchial hyper‐responsiveness. Hyperinflation compensates for the airflow obstruction, but this compensation is limited when the tidal volume approaches the volume of the pulmonary dead space; the result is alveolarhypoventilation. Uneven changes in airflow resistance, the resulting uneven distribution of air, and alterations in circulation from increased intra‐alveolar pressure due to hyperinflation all lead to ventilation‐perfusion mismatch. Vasoconstriction due to alveolar hypoxia also contributes to this mismatch. Vasoconstriction is also considered an adaptive response to ventilation/perfusion mismatch.
Signs and symptoms
The symptoms of asthma can range from mild to severe. When asthma symptoms get significantly worse, it is known as an asthma attack. The symptoms include feeling breathless, a tight chest, like a band tightening around it, wheezing, which makes a whistling sound when the patient breathes, coughing, particularly at night, and early morning attacks triggered by exercise, exposure to allergens and other triggers. A severe asthma attack usually develops slowly, taking 6–48 hours to become serious. However, for some people, asthma symptoms can get worse quickly.
What causes asthma symptoms to occur?
Many things can trigger or worsen asthma symptoms. A doctor will help a patient find out which things (called triggers) may cause asthma to flare up if there is contact with them. Triggers can include: allergens from dust, animal fur, cockroaches, mould, and pollens from trees, grasses and flowers, irritants such as cigarette smoke, air pollution, chemicals or dust in the workplace, compounds in home decor products, sprays (such as hairspray), medicines (such as aspirin or other non‐steroidal anti‐inflammatory drugs and non‐selective beta blockers), viral upper respiratory infections (such as colds) and chemicals in food and drinks.
Management
The aim of treatment is to get asthma under control and keep it that way. Everyone with asthma should be able to lead a full and unrestricted life. The treatments available for asthma are effective in most people and should enable them to be free from symptoms. These should include: continuous monitoring of vital signs until the patient is stabilized, and safe administration of prescribed oxygen and medications. Regular PEFR measurement – singular or infrequent peak flows will not accurately reflect the patient’s status. PEFR should be measured every 15–30 minutes after commencement of treatment until conditions stabilize. PEFR can also be used to measure the effectiveness of bronchodilator therapy; therefore, PEFR should be measured pre‐ and post‐inhaled or nebulized beta 2 agonists at least four times a day throughout their stay in hospital. Health promotion – avoidance of triggers, compliance with prescribed pharmacological therapies, smoking cessation and
weight reduction in obese patients may reduce the frequency of asthma attacks.
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