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Active Cycle of Breathing Techniques (ACBT)

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What is a Active Cycle of Breathing Techniques?

The Active cycle of breathing techniques (ACBT) is a simple pattern of breathing to

loosen and clear secretions improve ventilation

This leaflet is intended to remind you what you were taught by your Physiotherapist.

The parts of the ACBT are

Breathing control
This is normal gentle breathing using the lower chest, with relaxation of the upper chest and shoulders. It helps you to relax between the deep breathing and huffing.

Deep breathing
These are slow deep breaths in followed by a three second hold with a relaxed breath out. 3 4 deep breaths are enough.

This is a medium sized breath in, followed by a fast breath out through an open mouth, using the muscles of the chest and stomach to force the breath out. This will move secretions along the airways to a point where you can cough them up. Huffing is a less tiring way of clearing your secretions than coughing.

This should follow 2 3 huffs OR a deep breathe in. Dont cough unless secretions are ready to be cleared.

Active cycle of breathing

This is a flexible technique and can be varied to suit you.

In what position should I practice this breathing technique?

You can use this method of breathing in whatever position you find is most comfortable, or seems to clear most secretions, for example, sitting in a chair, lying on your side, or tipped if this helps.

What other techniques can I use with the Active Cycle of Breathing (ACBT)?
It is often beneficial to hold for three seconds at the end of one or all of the deep breaths. If your physiotherapist advises, you (or a helper) can clap your chest while you breathe out.

How often should I spend doing it?

If you have a chronic respiratory condition but you are very well, 10 minutes will be long enough to ventilate your lungs and clear any secretions. You can do it as long as you are clearing any secretions but 20 minutes is usually long enough for any one treatment. If you have an infection and your cough is more productive than usual, you will need to practice the cycle more often during the day.

These are general guidelines. If your physiotherapist suggests changes to the Active Cycle of Breathing, please follow their advice as this will be tailored to your individual needs.

Further information
If you have any queries or concerns, please contact Physiotherapy Department on 01271 322379.

Pryor J, Prasad S 2008 Physiotherapy for Respiratory and cardiac Problems Adults and Peadiatrics, 4th Edition. Churchill Livingstone, London

Bronchiectasis is an abnormal dilation of the proximal and medium-sized bronchi (>2 mm in diameter) caused by weakening or destruction of the muscular and elastic components of the bronchial walls. Affected areas may show a variety of changes, including transmural inflammation, edema, scarring, and ulceration, among other findings. Distal lung parenchyma may also be damaged secondary to persistent microbial infection and frequent postobstructive pneumonia. Bronchiectasis can be congenital or acquired but is most often the latter.1 Congenital bronchiectasis usually affects infants and children and results from developmental arrest of the bronchial tree. The more commonly acquired forms occur in adults and older children and require an infectious insult, impairment of drainage, airway obstruction, and/or a defect in host defense. The tissue is also damaged in part by the host response of neutrophilic proteases, inflammatory cytokines, nitric oxide, and oxygen radicals. This results in damage to the muscular and elastic components of the bronchial wall. Additionally, peribronchial alveolar tissue may be damaged, resulting in diffuse peribronchial fibrosis.4 The result is abnormal bronchial dilatation with bronchial wall destruction and transmural inflammation. The most important functional finding of altered airway anatomy is severely impaired clearance of secretions from the bronchial tree. Impaired clearance of secretions causes colonization and infection with pathogenic organisms, contributing to the common purulent expectoration observed in patients with bronchiectasis. The result is further bronchial damage and a vicious cycle of bronchial damage, bronchial dilation, impaired clearance of secretions, recurrent infection, and more bronchial damage.5 In 1950, Reid characterized bronchiectasis as cylindrical, cystic, or varicose in nature.6

Cylindrical bronchiectasis involves diffuse mucosal edema, with resultant bronchi that are dilated minimally but have straight, regular outlines that end squarely and abruptly (see Media File 1). Cystic or saccular bronchiectasis has ulceration with bronchial neovascularization and a resultant ballooned appearance that may have air-fluid levels (see Media File 2). Varicose bronchiectasis has a bulbous appearance with a dilated bronchus and interspersed sites of relative constriction and, potentially, obstructive scarring. The latter may subsequently result in postobstructive pneumonitis and additional parenchymal damage (see Media File 3).

Dilation of the bronchial walls results in airflow obstruction and impaired clearance of secretions because the dilated areas disrupt normal air pressure in the bronchial tubes, causing sputum to pool inside the dilated areas instead of being pushed upward[4]. The pooled sputum provides an environment conducive to the growth of infectious pathogens, and these areas of the lungs are thus very vulnerable to infection. The more infections that the lungs experience, the more damaged the lung tissue and alveoli become. When this happens, the bronchial tubes become more inelastic and dilated, creating a self-perpetuating cycle of further damage to the lungs. There are three types of brochiectasis, varying by level of severity. Fusiform (cylindrical) bronchiectasis (the most common type) refers to mildly inflamed bronchi that fail to taper distally. In varicose bronchiectasis, the bronchial walls appear beaded, because areas of dilation are mixed with areas of constriction. Saccular (cystic) bronchiectasis is characterized by severe and irreversible ballooning of the bronchi peripherally, with or without air-fluid

levels.[5] Chronic productive cough is prominent, occurring in up to 90% of patients with bronchiectasis. Sputum is produced on a daily basis in 76% of patients.[6] Generally, persons suffering from bronchiectasis tend to be infected by Haemophilus influenzae early on in the disease course. Secondary infection is usually due to Staphylococcus aureus; followed by Moraxella catarrhalis and finally Pseudomonas aeruginosa. Bronchiectasis is an abnormal inflammatory response of the lungs resulting in airflow limitations (Downs and Appel 2007). Irreversible dilation of the bronchi occurs (Barker 2002),and is associated with destruction of the muscular and elastic components of the bronchial walls (Emmons 2007). The destruction of the supportive muscular and elastic components of the bronchial walls results in permanent bronchial dilation and inflammation (Pruitt and Jacobs 2005). The distended bronchi have a tendency to retain secretions (Crowley 1997). The retained secretions become infected, triggering an ongoing and persistent host inflammatory response (Pryor and Prasad 2002). The features of such a response include vasodilation, increased capillary permeability resulting in movement of fluid from the intravascular compartment to the tissues, increased macrophage activity and localised oedema. This persistent inflammatory response leads to a loss of respiratory cilia and progressive airway obstruction asa result of the oedema and excess mucus. These changes greatly impair removal of bronchial secretions (Gould 2006). A cycle of inflammation, infection, damage and further inflammation results, leading to further dilation and damage to the respiratory passages. Patients with bronchiectasis may experience repeated episodes of infection, produce copious amounts of sputum and become increasingly breathless (Sharpies ei a/2002). Sputum culture often identifies the presence o Staphylococcus aureus, Haemophilus inuenzae or Pseudomonas aeruginosa (Selby 2002). Dilation of the airways increases the 'dead space', that is, the volume of air contained within the respiratory passages that does not participate in gas exchange. As a consequence,less air reaches the respiratory surfaces and the patient experiences breathlessness. Bronchiectasis is associated with transmuralinfection and inflammation, which is related to there lease of chemical proinflammatory mediators. Pro-inflammatory mediators cause airway inflammation and an increase in airflow limitation (Downs and Appel 2007). Respiratory obstruction occurs in the presence of prolonged inflammatory secretions, and micro-organisms contribute to airway damage and recurrent infection (Barker2002). Neutrophils and T lymphocytes are found in the bronchial mucosa of patients with established bronchiectasis (Gaga eia/1998),which highlights the disease's inflammatory nature. Bronchiectasis usually results from infection and presents in the middle and older age groups(Maa eia/2007). However, inhalation of a foreignbody, and allergic, auto-immune and chemical lungdamage, can also predispose individuals bronchiectasis (Mysliwiec and Pina 1999).Congenital disorders such as cystic fibrosis and primary ciliary dyskinesia can lead to this condition (Payne 2006). Primary ciliary dyskinesia leads to the development of bronchiectasis as the cilia are unable to clear the air passages effectively.This results in the retention of secretions and leads to recurrent infections. Other conditions associated with bronchiectasis include allergic bronchopulmonary aspergillosis,immunodeficiency states (Emmons 2007) body aspiration and benign airway tumours (Pruitt and Jacobs 2005). Typical clinical features of bronchiectasis are shown in Box 1. Emmons (2007) states that a chronic productive cough is present in up to 90% of patients with

bronchiectasis and that 76%ofpatients produce sputum on a daily basis. These disabling features have an adverse effect on individuals' physical and social activities. Ultimately, disease progression in bronchiectasis leads to hypoxaemia and in some instances respiratory failure (Selby 2002).