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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. Don’t cough unless secretions are ready to be cleared.

Active cycle of breathing

please contact Physiotherapy Department on 01271 322379. you will need to practice the cycle more often during the day. lying on your side. If your physiotherapist advises. for example. 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. sitting in a chair. 10 minutes will be long enough to ventilate your lungs and clear any secretions. . Further information If you have any queries or concerns. or seems to clear most secretions. you (or a helper) can ‘clap’ your chest while you breathe out. You can do it as long as you are clearing any secretions but 20 minutes is usually long enough for any one treatment.This is a flexible technique and can be varied to suit you. If you have an infection and your cough is more productive than usual. How often should I spend doing it? • • • If you have a chronic respiratory condition but you are very well. 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 ‘tipped’ if this helps. please follow their advice as this will be tailored to your individual needs. These are general guidelines. If your physiotherapist suggests changes to the Active Cycle of Breathing.

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

recurrent infection. potentially. Impaired clearance of secretions causes colonization and infection with pathogenic organisms. inflammatory cytokines.5 In 1950. with or without air-fluid . The more commonly acquired forms occur in adults and older children and require an infectious insult. bronchial dilation. regular outlines that end squarely and abruptly (see Media File 1). Fusiform (cylindrical) bronchiectasis (the most common type) refers to mildly inflamed bronchi that fail to taper distally. peribronchial alveolar tissue may be damaged.1 Congenital bronchiectasis usually affects infants and children and results from developmental arrest of the bronchial tree. because areas of dilation are mixed with areas of constriction. or varicose in nature. scarring. The pooled sputum provides an environment conducive to the growth of infectious pathogens.4 The result is abnormal bronchial dilatation with bronchial wall destruction and transmural inflammation. impairment of drainage. obstructive scarring. impaired clearance of secretions. Bronchiectasis can be congenital or acquired but is most often the latter. The tissue is also damaged in part by the host response of neutrophilic proteases. The latter may subsequently result in postobstructive pneumonitis and additional parenchymal damage (see Media File 3). cystic. among other findings. contributing to the common purulent expectoration observed in patients with bronchiectasis. with resultant bronchi that are dilated minimally but have straight. There are three types of brochiectasis. creating a self-perpetuating cycle of further damage to the lungs. The more infections that the lungs experience.Pathophysiology 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. and these areas of the lungs are thus very vulnerable to infection. resulting in diffuse peribronchial fibrosis. edema. causing sputum to pool inside the dilated areas instead of being pushed upward[4]. In varicose bronchiectasis. the bronchial tubes become more inelastic and dilated. Saccular (cystic) bronchiectasis is characterized by severe and irreversible ballooning of the bronchi peripherally. Reid characterized bronchiectasis as cylindrical. This results in damage to the muscular and elastic components of the bronchial wall. nitric oxide. the more damaged the lung tissue and alveoli become. Varicose bronchiectasis has a bulbous appearance with a dilated bronchus and interspersed sites of relative constriction and. Distal lung parenchyma may also be damaged secondary to persistent microbial infection and frequent postobstructive pneumonia. varying by level of severity. and/or a defect in host defense. Cystic or saccular bronchiectasis has ulceration with bronchial neovascularization and a resultant ballooned appearance that may have air-fluid levels (see Media File 2). Additionally. Affected areas may show a variety of changes. Pathogenesis 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. airway obstruction. The most important functional finding of altered airway anatomy is severely impaired clearance of secretions from the bronchial tree.6 • • • Cylindrical bronchiectasis involves diffuse mucosal edema. and more bronchial damage. including transmural inflammation. and ulceration. the bronchial walls appear beaded. When this happens. The result is further bronchial damage and a vicious cycle of bronchial damage. and oxygen radicals.

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

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