What is a bronchodilator and how does it work in COPD?


As the name suggests, a bronchodilator is a drug that dilates restrictive airways. This reduces total lung volume and makes the work of breathing easier. By performing this role in COPD, it alleviates the issues associated with hyperinflation and reduced lung elasticity. In reducing total lung volume it allows the respiratory muscles to function with less resistance, and in doing so reduces the workload on the muscles making breathing easier (ZuWallack, 2008: 1191).



Anwar (2008:215) states that smooth muscle cells that are involved with the airways are innervated by the parasympathetic nervous system. When an irritant is present, the parasympathetic nervous system causes bronchoconstriction. Bronchodilators work by stimulating the sympathetic nervous system to release noradrenalin which has the effect of relaxing smooth muscle cells and opening the airway. Bronchodilators are generally administered in an atomised or powdered form, but may also be given in other ways such as orally, intravenously and in emergency cases via endotracheal tube.


Classes of Bronchodilators

There are three classes of bronchodilator – beta2 (β2) agonists, muscarinic or anticholinergic agents, and theophylline.



β2 agonists are generally short acting. β2 agonists are respiratory selective and attach to beta receptor sites in the lung and smooth muscle of the airways to cause stimulation of the sympathetic nervous system which in turn causes relaxation and dilation of bronchioles and airways. This allows better flow of gases both from the external atmosphere to the alveoli (to refresh air in bronchi) and out to the external atmosphere which improves gas exchange at alveoli level. Dead space is reduced in the airways by reducing resistance (Kauffman, 2010: 63-64). Evidence shows that regular use of a bronchodilator can reduce symptoms, prevent exacerbations improve exercise tolerance in patients with COPD (Hanania & Donohue, 2007: 527; Bauldoff & Diaz, 2006: 38).

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Figure 17. Action of beta2 agonists. Source http://www.uky.edu



Rescue dose of Short acting bronchodilators

Short acting bronchodilators begin their action within 1-3 minutes. It is for this reason that it is most often charted to quickly relax smooth muscle and immediately improve ventilation. It is effective in relieving the effects of dyspnoea. According to the COPDX management plan (McKenzie, Abramson, Crockett, Glasgow, Jenkins, McDonald, Wood-Baker & Frith, 2010) a short acting bronchodilator should be used in higher doses and titrated based on the effects achieved. They can be used hourly through to sixth hourly. In any case, short acting bronchodilators should be prescribed based on an exacerbation management plan when the patient is at home, and according to the severity of exacerbation when in hospital. Patients in hospital who are admitted with an acute exacerbation of COPD should always have rescue or prn doses of a short acting bronchodilator along with their regular management. In addition to this, a good management plan should also be documented in a patient’s notes to ensure effective management of the exacerbation. There are several short acting β2 agonists and these include salbutamol and terbutaline, and these may be used in combination with an anticholinergic or muscarinic agent such as ipratropium (Anwar, 2008: 216). Side effects of β2 bronchodilators include tachycardia, tremor, hyperactivity, anxiety, insomnia, and in some cases stomach upset. Care should be taken in patients who are prescribed a beta-blocker drug, as these drugs can reduce the effects of a beta 2 agonist.



Muscarinic or Anticholinergic bronchodilators

Muscarinic or anticholinergic agents are often prescribed in conjunction with β2 agonists. They begin their effects within 30-60 minutes of administration and their effects can last up to 24 hours in cases such as tiotropium. When the parasympathetic nervous system is activated, it releases noradrenalin and acetylcholine causing constriction of the airways. Muscarinic agents complement the β2 agonists by preventing acetylcholine from binding with muscarinic receptors in the smooth muscle and sub mucosal glands. This prevents the development of cholinergic effects such as increased mucous secretion, and it also relaxes smooth muscle cells causing a widening of the airways. Side effects are anticholinergic and can include dry mouth, headaches and constipation. Care should also be taken in patients who have glaucoma to avoid contact with the eye mucosa.



Theophylline

Theophylline is an oral or intravenous medication which is less commonly used today, however you may encounter a patient who is prescribed theophylline. It is generally used as a third line bronchodilation agent and prescribed in addition to the above agents. It has a very fine blood plasma therapeutic range, and patients should be closely monitored to ensure that they remain in this range. A plasma concentration above the therapeutic range is equally as ineffective as a sub therapeutic level. In addition, many drugs may react with theophylline such as various antibiotics and antifungal preparations, so prescription is generally undertaken by an experienced medical practitioner. Theophylline is considered to be a respiratory stimulant. It works by improving contractility of the diaphragm and assists corticosteroids through its anti-inflammatory properties (Hanania & Donohue, 2007: 530). Side effects of theophylline include palpitations, tachycardia, arrhythmias, insomnia and gastrointestinal disturbances.



For methods of delivery for a bronchodilator see the page ‘how to I deliver a bronchodilator’. Bronchodilators may be given in combination with a corticosteroid which assists in reducing the inflammatory response in the airways. In an infective exacerbation of COPD a patient may also be prescribed an antibiotic. There is a large body of knowledge involved in these two therapies and it is outside the scope of this site. However, it would be advisable to read further in this area to improve your overall level of knowledge.