Atlas of pathophysiology, 2 Edition
Part II - Disorders
Asthma is a reactive airway disorder characterized by inflammation and episodic airway obstruction. Such obstruction results from bronchospasms, increased mucus secretion, and mucosal edema. It's a type of chronic obstructive pulmonary disease, a group of lung diseases characterized by increased airflow resistance. Although it's a chronic disorder, patients can suffer from acute exacerbations.
Children younger than age 5 are the fastest growing segment of the population with asthma. Incidence of asthma is 5% to 10% of the population.
Asthma may result from sensitivity to extrinsic or intrinsic allergens. Extrinsic, or atopic, asthma begins in childhood; typically, patients are sensitive to specific external allergens. Many patients with asthma, especially children, have both intrinsic and extrinsic asthma.
· Animal dander
· House dust or mold
· Kapok or feather pillows
· Food additives, including sulfites and some dyes
· Noxious fumes
Patients with intrinsic, or nonatopic, asthma react to internal, nonallergenic factors.
· Emotional stress and anxiety
· Endocrine changes
· Temperature or humidity variations
· Coughing or laughing
· Genetic factors
In asthma, bronchial linings overreact to various stimuli, causing inflammation and smooth-muscle spasms that severely constrict the airways. When the hypersensitive patient inhales a triggering substance, abnormal antibodies stimulate mast cells in the lung interstitium to release both histamine and leukotriene. Histamine attaches to receptor sites in the larger bronchi, where it causes swelling in smooth muscles. Leukotriene attaches to receptor sites in the smaller bronchi and causes swelling of smooth muscle there. It also causes fatty acids called prostaglandins to travel by way of the bloodstream to the lungs, where they enhance histamine's effects.
Histamine stimulates the mucous membranes to secrete excessive mucus, further narrowing the bronchial lumen. On inhalation, the narrowed bronchial lumen can still expand slightly, allowing air to reach the alveoli. On exhalation, increased intrathoracic pressure closes the bronchial lumen completely. Mucus fills the lung bases, inhibiting alveolar ventilation. Blood, shunted to alveoli in other lung parts, still can't compensate for diminished ventilation.
When status asthmaticus occurs, hypoxia worsens, expiratory flow slows, and expiratory volumes decrease. If treatment isn't initiated, the patient begins to tire. Acidosis develops as arterial carbon dioxide increases. The situation becomes life-threatening when no air movement is audible on auscultation (a silent chest) and partial pressure of arterial carbon dioxide (PaCO2) rises to over 70 mm Hg.
Signs and symptoms
· Sudden dyspnea, wheezing, and tightness in the chest
· Coughing that produces thick, clear, or yellow sputum
· Tachypnea, along with use of accessory respiratory muscles
· Rapid pulse
· Profuse perspiration
· Hyperresonant lung fields
· Diminished breath sounds
Diagnostic test results
· Pulmonary function tests reveal low-normal or decreased vital capacity, and increased total lung and residual capacities.
· Serum IgE levels may increase from an allergic reaction.
· Sputum analysis indicates the presence of Curschmann's spirals (casts of airways), Charcot-Leyden crystals, and eosinophils.
· Complete blood count with differential reveals an increased eosinophil count.
· Chest X-rays may show hyperinflation with areas of atelectasis.
· With arterial blood gas analysis, partial pressure of arterial oxygen and PaCO2 are usually decreased, except in severe asthma, when PaCO2 may be normal or increased, indicating severe bronchial obstruction.
· Skin testing identifies specific allergens.
· Bronchial challenge testing evaluates the clinical significance of allergens identified by skin testing.
· Electrocardiography shows sinus tachycardia during an asthma attack or right axis deviation and peaked P wave (indicating cor pulmonale during a severe attack that resolves after the attack).
· Identification and avoidance of precipitating factors
· Desensitization to specific antigens
· Low-flow humidified oxygen
· Inhaled steroids such as triamcinolone acetonide
· Leukotriene inhibitors such as montelukast sodium
· Long-acting bronchodilators such as formoterol
· Mast cell stabilizers, such as cromolyn sodium or nedocromil sodium
· Aminophylline or theophylline
· Short-acting bronchodilators, such as albuterol or levalbuterol
· Oral or I.V. corticosteroids
· Mechanical ventilation
· Relaxation exercises