Either class of agents has a rapid onset of action, relieves symptoms, and improves lung function. Among these agents, the choices are short-acting β 2-agonists or an anticholinergic. 1 The initial therapy for COPD patients who experience symptoms intermittently are short-acting bronchodilators.
However, the use of bronchodilators may not be associated with significant improvements in pulmonary function measurements such as FEV 1. 1, 24 In patients with COPD, the clinical benefits of bronchodilators include increased exercise capacity, decreased air trapping in the lungs, and relief of symptoms.
1, 24 - 31 Bronchodilators work by reducing the tone of airway smooth muscle (relaxation), thus minimizing airflow limitation. Additionally, the dose-response relationship using FEV 1 is relatively flat for single-agent therapy. Combining different bronchodilator therapies improves efficacy and is preferred over increasing the dose of a single agent, due to increased risk of adverse drug reactions. 1 Clinicians should advise, counsel, and observe patient technique with the devices frequently and consistently. The inhaled route is the preferred route for β 2-agonists and anticholinergics, but attention must be paid to proper inhaler technique. 1 Bronchodilator medications commonly utilized for COPD include β 2-agonists, anticholinergics, and theophylline ( theophylline would be considered a last-line agent because of potential adverse reactions). They reduce symptoms and improve exercise tolerance and quality of life. 12īronchodilators are the mainstay of treatment for symptomatic COPD. 11 Respiratory infections, both viral and bacterial, may contribute to the pathogenesis of COPD and are considered a risk factor. 10 Oxidative stress, or a depletion of antioxidants in the lungs plays a role in the development of COPD and can initiate lung inflammation and injury. A positive association has been found between birth weight and forced expiratory volume in 1 second (FEV 1) in adulthood. 6-9 Another potential risk factor is impaired lung growth during gestation, birth, and childhood. 4 Inhalation exposure risk factors include occupational dusts and chemicals (chemical agents and fumes), indoor air pollution (wood, animal dung, crop residues, and coal burned in open fires), and outdoor air pollution. Patients presenting with COPD at an early age or a strong family history should be screened for this disorder. 5 Patients with AAT deficiency develop COPD at an early age (20-50 years). 4 This hereditary deficiency is a recessive trait most commonly seen in individuals of Northern European descent. 3 A rare genetic disorder called alpha 1 antitrypsin (AAT) deficiency is a risk factor for COPD. The most common risk factor for COPD is cigarette smoking, however, not all smokers develop COPD, which suggests a possible genetic factor or predisposition.
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