COPD (Chronic Obstructive Pulmonary Disease): Difference between revisions

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== Clinically Relevant Anatomy<br>  ==


add text here relating to '''''clinically relevant''''' anatomy of the condition<br>  
== Introduction ==
[[File:Copd versus healthy lung.jpeg|right|frameless|310x310px]]
Chronic obstructive pulmonary disease (COPD)<ref name=":1">Hillas G, Perlikos F, Tsiligianni I, Tzanakis N. Managing comorbidities in COPD. International journal of chronic obstructive pulmonary disease. 2015 Jan 7:95-109.</ref> is a common and treatable disease characterised by progressive airflow limitation and tissue destruction. It is associated with structural [[Lung Anatomy|lung]] changes due to chronic [[Inflammation Acute and Chronic|inflammation]] from prolonged exposure to noxious particles or gases, most commonly cigarette smoke. Chronic inflammation causes airway narrowing and decreased lung recoil. The disease often presents with cough symptoms, [[Dyspnoea|dyspnea]], and sputum production. Symptoms can range from being asymptomatic to [[Respiratory Failure|respiratory failure]].<ref name=":0">Agarwal AK, Raja A, Brown BD. Chronic obstructive pulmonary disease (COPD). StatPearls [Internet]. 2020 Jun 7.Available from:https://www.ncbi.nlm.nih.gov/books/NBK559281/ (accessed 24.5.2021)</ref>


== Causes<br> ==
== Epidemiology ==
COPD is primarily present in [[Smoking Cessation and Brief Intervention|smokers]] and those over 40. Prevalence increases with age and is currently the third most common cause of morbidity and mortality worldwide. In 2015, the prevalence of COPD was 174 million, and there were approximately 3.2 million deaths due to COPD worldwide. However, the prevalence is likely to be underestimated due to the under diagnosis of COPD.<ref name=":0" />


*Smoking - The primary risk factor for COPD is chronic tobacco smoking. In the United States, 80 to 90% of cases of COPD are due to smoking.<ref>Young RP, Hopkins RJ, Christmas T, Black PN, Metcalf P, Gamble GD (August 2009). "COPD prevalence is increased in lung cancer, independent of age, sex and smoking history". Eur. Respir. J. 34 (2): 380–6</ref><br>
== Etiology ==
*Occupational exposure - Intense and prolonged exposure to workplace dusts found in coal mining, gold mining, and the cotton textile industry and chemicals such as cadmium, isocyanates, and fumes from welding have been implicated in the development of airflow obstruction, even in nonsmokers.<ref>Devereux, Graham (May 2006). "ABC of chronic obstructive pulmonary disease. Definition, epidemiology, and risk factors". BMJ 332 (7550): 1142–4</ref> Workers who smoke and are exposed to these particles and gases are even more likely to develop COPD. Intense silica dust exposure causes silicosis, a restrictive lung disease distinct from COPD; however, less intense silica dust exposures have been linked to a COPD-like condition.<ref>Hnizdo E, Vallyathan V (April 2003). "Chronic obstructive pulmonary disease due to occupational exposure to silica dust: a review of epidemiological and pathological evidence". Occup Environ Med 60 (4): 237–43</ref> The effect of occupational pollutants on the lungs appears to be substantially less important than the effect of cigarette smoking.<ref>Loscalzo, Joseph; Fauci, Anthony S.; Braunwald, Eugene; Dennis L. Kasper; Hauser, Stephen L; Longo, Dan L. (2008). Harrison's Principles of Internal Medicine (17th ed.). McGraw-Hill Professional</ref><br>
COPD is caused by prolonged exposure to harmful particles or gases.  
*Air pollution - Studies in many countries have found that people who live in large cities have a higher rate of COPD compared to people who live in rural areas.[<ref>Halbert RJ, Natoli JL, Gano A, Badamgarav E, Buist AS, Mannino DM (September 2006). "Global burden of COPD: systematic review and meta-analysis". Eur. Respir. J. 28 (3): 523–32</ref> Urban air pollution may be a contributing factor for COPD as it is thought to slow the normal growth of the lungs although the long-term research needed to confirm the link has not been done. In many developing countries indoor air pollution from cooking fire smoke (often using biomass fuels such as wood and animal dung) is a common cause of COPD, especially in women.<ref>Kennedy SM, Chambers R, Du W, Dimich-Ward H (December 2007). "Environmental and occupational exposures: do they affect chronic obstructive pulmonary disease differently in women and men?". Proceedings of the American Thoracic Society 4 (8): 692–4.</ref><br>
*Genetics - Some factor in addition to heavy smoke exposure is required for a person to develop COPD. This factor is probably a genetic susceptibility. COPD is more common among relatives of COPD patients who smoke than unrelated smokers.<ref>ilverman EK, Chapman HA, Drazen JM, et al. (June 1998). "Genetic epidemiology of severe, early-onset chronic obstructive pulmonary disease. Risk to relatives for airflow obstruction and chronic bronchitis". Am. J. Respir. Crit. Care Med. 157 (6 Pt 1): 1770–8</ref>] The genetic differences that make some peoples' lungs susceptible to the effects of tobacco smoke are mostly unknown<br>
*Autoimmune disease - There is mounting evidence that there may be an autoimmune component to COPD.<ref>Agustí A, MacNee W, Donaldson K, Cosio M. (2003). "Hypothesis: does COPD have an autoimmune component?". Thorax 58 (10): 832–4</ref> Many individuals with COPD who have stopped smoking have active inflammation in the lungs.<ref name="Rutgers">Rutgers, Steven R.; Postma, Dirkje S.; Ten Hacken, Nick H. .T.; Kauffman, Henk F.;van der Mark,Thomas W; Koeter, Gerard H.; Timens, Wim (2000). "Ongoing airway inflammation in patients with COPD who do not currently smoke". Thorax 55 (1): 12–18.</ref>The disease may continue to get worse for many years after stopping smoking due to this ongoing inflammation.<ref name="Rutgers" /> This sustained inflammation is thought to be mediated by autoantibodies and autoreactive T cells.<ref>Feghali-Bostwick CA, Gadgil AS, Otterbein LE, et al. (January 2008). "Autoantibodies in patients with chronic obstructive pulmonary disease". Am. J. Respir. Crit. Care Med. 177 (2): 156–63. doi:10.1164/rccm.200701-014OC</ref><br>


== Mechanism of Injury / Pathological Process<br> ==
* Cigarette smoking is the most common cause of COPD worldwide.<ref name=":1" />
* Other causes may include second-hand smoke, environmental and occupational exposures,alpha-1 antitrypsin deficiency (AATD)<ref name=":0" /> ageing <ref name=":2">Agustí A, Vogelmeier C, Faner R. COPD 2020: changes and challenges. American Journal of Physiology-Lung Cellular and Molecular Physiology. 2020 Nov 1;319(5):L879-83.</ref>and  gene-environment interactions (GxE)<ref name=":2" /> .
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| {{#ev:youtube|T1G9Rl65M-Q|412}} <ref>Animated COPD Patient. Understanding COPD. Available from: https://www.youtube.com/watch?v=T1G9Rl65M-Q [last accessed 31/5/2022]</ref>
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It is not fully understood how tobacco smoke and other inhaled particles damage the lungs to cause COPD. The most important processes causing lung damage are:
== Mechanism of Injury / Pathological Process  ==
[[File:Healthy alveoli Primal.png|right|frameless|399x399px]]
COPD is an inflammatory condition involving the airways, [[Lung Anatomy|lung]] parenchyma, and pulmonary vasculature.<ref name=":0" /> [[Emphysema]] describes one of the structural changes seen in COPD where there is the destruction of the [[Alveoli|alveolar]] air sacs (gas-exchanging surfaces of the lungs) leading to obstructive physiology.


*Oxidative stress produced by the high concentrations of free radicals in tobacco smoke.
Image 2: Healthy Alveoli.
*Cytokine release due to inflammation as the body responds to irritant particles such as tobacco smoke in the airway.
*Tobacco smoke and free radicals impair the activity of antiprotease enzymes such as alpha 1-antitrypsin, allowing protease enzymes to damage the lung.


== Clinical Presentation  ==
The process is thought to involve [[Free Radicals|oxidative stress]] and protease-antiprotease imbalances. In emphysema, an irritant (e.g., smoking) causes an [[Inflammation Acute and Chronic|inflammatory]] response. Neutrophils and macrophages are recruited and release multiple inflammatory mediators. Oxidants and excess proteases lead to the destruction of the air sacs. The protease-mediated destruction of elastin leads to a loss of elastic recoil and results in airway collapse during exhalation.


==== Chronic bronchitis  ====
* The inflammatory response and obstruction of the airways cause a decrease in the [[Spirometry|forced expiratory volume]] (FEV1), and tissue destruction leads to airflow limitation and impaired gas exchange.
* Hyperinflation of the lungs is often seen in imaging studies and occurs due to air trapping from airway collapse during exhalation.
* The inability to exhale fully also causes elevations in carbon dioxide (CO2) levels.
* With disease progression the reduction in [[Ventilation and Weaning|ventilation]] or increase in '''physiologic dead space''' leads to CO2 retention.
* Acute exacerbations of COPD are common and usually occur due to a trigger (e.g., [[Bacterial Infections|bacterial]] or [[Viral Infections|viral]] [[pneumonia]], environmental irritants). There is an increase in inflammation and air trapping, often requiring [[Corticosteroid Medication|corticosteroid]] and bronchodilator treatment.<ref name=":0" />


Lung damage and inflammation in the large airways results in chronic bronchitis. Chronic bronchitis is defined in clinical terms as a cough with sputum production on most days for 3 months of a year, for 2 consecutive years.<ref name="Longmore">Longmore, J. M.; Murray Longmore; Wilkinson, Ian; Supraj R. Rajagopalan (2004). Oxford handbook of clinical medicine. Oxford [Oxfordshire]: Oxford University Press. pp. 188–9. ISBN 0-19-852558-3</ref> In the airways of the lung, the hallmark of chronic bronchitis is an increased number (hyperplasia) and increased size (hypertrophy) of the goblet cells and mucous glands of the airway. As a result, there is more mucus than usual in the airways, contributing to narrowing of the airways and causing a cough with sputum. Microscopically there is infiltration of the airway walls with inflammatory cells. Inflammation is followed by scarring and remodeling that thickens the walls and also results in narrowing of the airways. As chronic bronchitis progresses, there is squamous metaplasia (an abnormal change in the tissue lining the inside of the airway) and fibrosis (further thickening and scarring of the airway wall). The consequence of these changes is a limitation of airflow.<ref>Kumar P, Clark M (2005). Clinical Medicine (6th ed.). Elsevier Saunders. pp. 900–1. ISBN 0702027634</ref>  
== Clinical Presentation  ==
[[File:Dyspnea 01.png|right|frameless|399x399px]]
COPD will typically present in adulthood and often during the winter months. Patients usually present with complaints of chronic and progressive [[Dyspnoea|dyspnea]], cough, and sputum production. Patients may also have wheezing and chest tightness. While a smoking history is present in most cases, there are many without such a history. They should be questioned on exposure to second-hand smoke, occupational and [[An Introduction to Environmental Physiotherapy|environmental]] exposures, and family history.<ref name=":1" /><ref name=":2" />


Patients with advanced COPD that have primarily chronic bronchitis rather than emphysema were commonly referred to as "blue bloaters" because of the bluish color of the skin and lips (cyanosis) seen in them.<ref>Chung C, Delaney J, Hodgins R (2008). "Respirology". in Somogyi, Ron; Colman, Rebecca. The Toronto notes 2008: a comprehensive medical reference and review for the Medical Council of Canada Qualifying Exam - Part 1 and the United States Medical Licensing Exam - Step 2. Toronto: Toronto Notes for Medical Students. p. R9. ISBN 0-9685928-8-0</ref> The hypoxia and fluid retention leads to them being called "Blue Bloaters."
COPD is a complex interaction between [[asthma]], [[Chronic Bronchitis|chronic bronchitis]], and [[emphysema]].  


==== Emphysema  ====
== Evaluation ==
[[File:Spirometry1.jpg|right|frameless]]
COPD is often evaluated in patients with relevant symptoms and risk factors. The diagnosis is confirmed by [[spirometry]]. Other tests may include a [[Six Minute Walk Test / 6 Minute Walk Test|6-minute walk test]], laboratory testing, and [[Medical Imaging|radiographic imaging.]] 
*Assessment - A diagnosis of COPD should be considered in patients over the age of 35 who have a risk factor (generally smoking) and who present with exertional breathlessness, chronic cough, regular sputum production, frequent winter ‘[[bronchitis]]’ or wheeze.
*X-Ray - An X-ray of the chest may show an over-expanded lung (hyperinflation) and can be useful to help exclude other lung diseases.
*[[Pulmonary Function Test|Pulmonary function tests]] - Essential in the diagnosis, staging, and monitoring of COPD. [[Spirometry]] is performed before and after administering an inhaled bronchodilator. Inhaled bronchodilators may be short-acting beta2-agonist (SABA), short-acting anticholinergic, or a combination of both. A ratio of the forced expiratory volume in one second to forced vital capacity (FEV1/FVC) less than 0.7 confirms the diagnosis of COPD. Patients with significantly reduced FEV1 and signs of dyspnea should be evaluated for oxygenation with pulse [[Oxygen Therapy|oximetry]] or [[Arterial Blood Gases|arterial blood gas]] analysis.
*[[Blood Tests|Blood tests]] - A blood sample taken from an artery can be tested for [[Arterial Blood Gases|blood gas levels]] which may show low oxygen levels ([[Hypoxaemia|hypoxemia]]) and/or high carbon dioxide levels ([[Respiratory Failure|respiratory acidosis]]). A blood sample taken from a vein may show a high [[Blood Physiology|blood]] count (reactive polycythemia), a reaction to long-term hypoxemia.
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| {{#ev:youtube|YwcNbVnHNAo|412}} <ref>Armando Hasudungan. Understanding Spirometry - Normal, Obstructive vs Restrictive. Available from: https://www.youtube.com/watch?v=YwcNbVnHNAo [last accessed 31/5/2022]</ref>
| {{#ev:youtube|s8pXdtp_Duw|412}} <ref>nhswestminster. Spirometry Procedure. Available from: https://www.youtube.com/watch?v=s8pXdtp_Duw [last accessed 31/5/2022]</ref>
|}
== Outcome Measures  ==
[[File:Oximetre.jpg|right|frameless]]
There can be a different number of ways of measuring the impact or change of someone's COPD, examples being lung function, [[Lung Volumes|lung volumes]] and [[Therapeutic Exercise|exercise]] capacity. A cross-sectional study recommends [[Cardiopulmonary Exercise Testing (CPET) In Adults|cardiopulmonary exercise testing]] (CPET) as an efficient tool in assessing functional capacity and prognosis in Heart Failure and COPD patients<ref>da Luz GC, Rossi CF, Tinoco AG, Marinho RS, de Faria CP, da Silva AT, Oliveira CR, Borghi-Silva A, Mendes RG, Goi RM. [https://pubmed.ncbi.nlm.nih.gov/32152432/ The Value of Cardiopulmonary Exercise Testing in Determining Severity in Patients with Systolic Heart Failure and COPD]. Scientific Reports (Nature Publisher Group). 2020 Dec 1;10(1).</ref>. 


Lung damage and inflammation of the alveoli results in emphysema. Emphysema is defined as enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls.<ref name="Longmore" /> &nbsp;The destruction of air space walls reduces the surface area available for the exchange of oxygen and carbon dioxide during breathing. It also reduces the elasticity of the lung itself, which results in a loss of support for the airways that are embedded in the lung. These airways are more likely to collapse causing further limitation to airflow. The effort made by patients suffering from emphysema during exhalation, causes a pink color in their faces, hence the term commonly used to refer to them, "pink puffers".
Other [[Outcome Measures|outcome measures]] include:


== Diagnostic Procedures  ==
Bleep Test; Shuttle Walk Test; Ergometry; [[Borg Rating Of Perceived Exertion|BORG RPE]]; [[Six Minute Walk Test / 6 Minute Walk Test|6-minute walk test]] is commonly performed to assess the submaximal functional capacity of a patient. This test is performed indoors on a flat and straight surface. The length of the hallway is usually 100 feet, and the test measures the distance the patient walks over a period of 6 minutes<ref name=":0" />; [[Grip Strength]]; [[30 Seconds Sit To Stand Test|30 seconds Sit to stand]]


*Assessment - A diagnosis of COPD should be considered in patients over the age of 35 who have a risk factor (generally smoking) and who present with exertional breathlessness, chronic cough, regular sputum production, frequent winter ‘bronchitis’ or wheeze
According to a longitudinal study<ref>Bernabeu-Mora R, Oliveira-Sousa SL, Sánchez-Martínez MP, García-Vidal JA, Gacto-Sánchez M, Medina-Mirapeix F. [https://pubmed.ncbi.nlm.nih.gov/32243447/ Frailty transitions and associated clinical outcomes in patients with stable COPD: A longitudinal study.] Plos one. 2020 Apr 3;15(4):e0230116.</ref>, changes in [[Introduction to Frailty|frailty]] status of COPD patients were associated with significant clinical outcomes related to dyspnea;  mobility; [[Physical Activity|physical activity]]; handgrip and [[Quadriceps Muscle|quadriceps]] strength. It was found that five times sit-to-stand and exacerbations were independent predictors of the improvement in frailty status.
*[[Spirometry|Spirometry]] - The presence of airflow obstruction should be confirmed by performing post-bronchodilator spirometry. All health professionals involved in the care of people with COPD should have access to spirometry and be competent in the interpretation of the results
== Management / Interventions ==
*X-Ray - An x-ray of the chest may show an over-expanded lung (hyperinflation) and can be useful to help exclude other lung diseases.<br>
[[File:Smoking man.jpg|right|frameless]]
*Pulmonary function tests - Complete pulmonary function tests with measurements of lung volumes and gas transfer may also show hyperinflation and can discriminate between COPD with emphysema and COPD without emphysema.<br>
The primary goals of treatment are to control symptoms, improve the [[Quality of Life|quality of life]], and reduce exacerbations and mortality. The non-pharmacological approach includes [[Smoking Cessation and Brief Intervention|smoking cessation]] and [[Pulmonary Rehabilitation| Pulmonary rehabilitation]].  
*[[Blood Tests|Blood tests ]]- A blood sample taken from an artery can be tested for blood gas levels which may show low oxygen levels (hypoxemia) and/or high carbon dioxide levels (respiratory acidosis). A blood sample taken from a vein may show a high blood count (reactive polycythemia), a reaction to long-term hypoxemia.<br>


<br>
Annual [[influenza]] [[Vaccines|vaccination]] is recommended in all patients with COPD.


== Outcome Measures  ==
The classes of commonly used medications in COPD include:


add links to outcome measures here (see [[Outcome Measures|Outcome Measures Database]])  
* Bronchodilators (beta2-agonists, antimuscarinics, methylxanthines),
* Inhaled [[Corticosteroid Medication|corticosteroids]] (ICS) and systemic glucocorticoids,
* Phosphodiesterase-4 (PDE4) inhibitors,
* [[Antibiotics|Antibiotics.]]


== Management / Interventions<br> ==
=== Exercise ===


==== Stopping Smoking  ====
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| {{#ev:youtube|VR7QnSnHmBU|412}}
| <ref>Burke Rehabilitation. COPD Treatments &amp; Rehab: Upper Body Exercises. Available from: http://www.youtube.com/watch?v=VR7QnSnHmBU[last accessed 13/02/15]</ref>
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Encouraging patients with COPD to stop smoking is one of the most important components of their management. All COPD patients still smoking, regardless of age, should be encouraged to stop, and offered help to do so, at every opportunity
Exercise prescription is a key component of pulmonary rehabilitation programmes, part of the non-pharmacological approach to managing COPD. There is a high level of evidence for the benefits of pulmonary rehabilitation for people with COPD<ref>Roisin RR, Rabe KF, Anzueto A, et al. Global strategy for diagnosing, managing, and preventing chronic obstructive pulmonary disease. Bethesda, MD: Global Initiative for Chronic Obstructive Lung Disease, 2008; 1–91.</ref> [[Strength Training|Strength]] and endurance exercises are endorsed for people with COPD.<ref>Skinner, Margot. Strength and endurance exercises are endorsed for people with COPD. Physical Therapy Reviews, Volume 14, Number 6, December 2009, pp. 418-418(1)</ref>


==== Exercise ====
Use of [[Exercise and Protein Supplements|protein supplements]], in combination with exercise, could also be beneficial. Refer to the dietician.


Exercise prescription is a key component of pulmonary rehabilitation programmes, which are part of the non-pharmacological approach to managing COPD. There is a high level of evidence for the benefits of pulmonary rehabilitation for people with COPD<ref>Roisin RR, Rabe KF, Anzueto A, et al. Global strategy for the diagnosis management, and prevention of chronic obstructive pulmonaryfckLRdisease. Bethesda, MD: Global Initiative for Chronic Obstructive Lung Disease, 2008; 1–91.</ref> Strength and endurance exercise are endorsed for people with COPD<ref>Skinner, Margot. Strength and endurance exercise endorsed for people with COPD.  Physical Therapy Reviews, Volume 14, Number 6, December 2009 , pp. 418-418(1)</ref><br>
Muscles that are required for arm exercise are also involved in the movement of the chest wall during respiration, and thus, the need to breathe often compromises the individual’s ability to undertake daily activities. Therefore, exercise prescription involving arm exercise needs to be carefully prescribed.<ref>Ennis S, Alison J, McKeough Z. The effects of arm endurance and strength training on arm exercise capacity in people with chronic obstructive pulmonary disease. Phys Ther Rev 2009;14(4):226–39.</ref> The evidence showed that patients with COPD have limb muscle dysfunction, a key systemic consequence.<ref>Spruit MA, Singh SJ, Garvey C, ZuWallack R, Nici L, Rochester C, Hill K, Holland AE, Lareau SC, Man WD, Pitta F. An official American Thoracic Society/European Respiratory Society statement: key concepts and advances in pulmonary rehabilitation. American Journal of Respiratory and critical care medicine. 2013 Oct 15;188(8):e13-64.</ref>


Muscles that are required for arm exercise are also involved in movement of the chest wall during respiration and thus the need to breathe often compromises the individual’s ability to undertake daily activities, therefore exercise prescription&nbsp; involving arm exercise needs to be carefully prescribed<ref>Ennis S, Alison J, McKeough Z. The effects of arm endurance and strength training on arm exercise capacity in people with chronic obstructive pulmonary disease. Phys Ther Rev 2009;14(4):226–39.</ref><br>
=== Promote Effective Inhaled Therapy ===
 
==== Promote effective inhaled therapy ====
 
In people with stable COPD who remain breathless or have exacerbations despite use of short-acting bronchodilators as required, offer the following as maintenance therapy:


In people with stable COPD who remain breathless or have exacerbations despite the use of short-acting bronchodilators as required, offer the following as maintenance therapy:
*if forced expiratory volume in 1 second (FEV1)≥50% predicted: either long-acting beta2 agonist (LABA) or long-acting muscarinic antagonist (LAMA)  
*if forced expiratory volume in 1 second (FEV1)≥50% predicted: either long-acting beta2 agonist (LABA) or long-acting muscarinic antagonist (LAMA)  
*if FEV1&lt;50% predicted: either LABA with an inhaled corticosteroid (ICS) in a combination inhaler, or LAMA
*if FEV1&lt;50% predicted: either LABA with an inhaled corticosteroid (ICS) in a combination inhaler or LAMA
 
Offer LAMA in addition to LABA + ICS to people with COPD who remain breathless or have exacerbations despite taking LABA + ICS, irrespective of their FEV1
 
==== Provide pulmonary rehabilitation  ====
 
Pulmonary rehabilitation should be made available to all appropriate people with COPD including those who have had a recent hospitalisation for an acute exacerbation
 
==== Use non-invasive ventilation  ====
 
Non-invasive ventilation (NIV) should be used as the treatment of choice for persistent hypercapnicventilatory failure during exacerbations not responding to medical therapy. It should be delivered by staff trained in its application, experienced in its use and aware of its limitations. When patients are started on NIV, there should be a clear plan covering what to do in the event of deterioration and ceilings of therapy should be agreed.
 
==== Manage exacerbations  ====
 
The frequency of exacerbations should be reduced by appropriate use of inhaled corticosteroids and bronchodilators, and vaccinations
 
The impact of exacerbations should be minimised by:
 
*giving self-management advice on responding promptly to the symptoms of an exacerbation
*starting appropriate treatment with oral steroids and/or antibiotics
*use of non-invasive ventilation when indicated
*use of hospital-at-home or assisted-discharge schemes
 
==== Ensure multidisciplinary working  ====
 
COPD care should be delivered by a multidisciplinary team
 
== Managing symptoms and conditions in stable COPD  ==
 
==== Breathlessness and exacerbations  ====
 
*Manage breathlessness and exercise limitation with inhaled therapy
*For exacerbations or persistent breathlessness:
**use long-acting bronchodilators or LABA + ICS
**consider adding theophylline if still symptomatic
*Offer pulmonary rehabilitation to all suitable people
*Refer patients who are breathless, have a single large bulla on a CT scan and an FEV1 less than 50% predicted for consideration of bullectomy
*Refer people with severe COPD for consideration of lung volume reduction surgery if they remain breathless with marked restrictions of their activities of daily living, despite maximal medical therapy (including rehabilitation), and meet all of the following:
**FEV1 greater than 20% predicted
**PaCO2 less than 7.3 kPa
**upper lobe predominant emphysema
**TLCO greater than 20% predicted
*Consider referring people with severe COPD for assessment for lung transplantation if they remain breathless with marked restrictions of their activities of daily living despite maximal medical therapy. Considerations include:
**age
**FEV1
**PaCO2
**homogeneously distributed emphysema on CT scan
**elevated pulmonary artery pressures with progressive deterioration
**comorbidities
**local surgical protocols
 
==== Frequent exacerbations  ====
 
*Optimise inhaled therapy
*ffer vaccinations and prophylaxis
*Give self-management advice
*Consider osteoporosis prophylaxis for people requiring frequent oral corticosteroids
 
==== Cor pulmonale  ====
 
*Consider in people who have peripheral oedema, a raised venous pressure, a systolic parasternal heave, a loud pulmonary second heart sound
*Exclude other causes of peripheral oedema
*Perform pulse oximetry, ECG and echocardiogram if features of cor pulmonale
*Assess need for LTOT
*Treat oedema with diuretic
*Angiotensin-converting enzyme inhibitors, calcium channel blockers, alpha-blockers are not recommended
*Digoxin may be used where there is atrial fibrillation
 
==== Respiratory failure  ====


*Assess for appropriate oxygen
Offer LAMA in addition to LABA + ICS to people with COPD who remain breathless or have exacerbations despite taking LABA + ICS, irrespective of their FEV1.
*Consider referral for assessment for long-term domiciliary NIV therapy


==== Abnormal BMI ====
=== Provide Pulmonary Rehabilitation ===
[[File:Exercise older person.jpg|right|frameless]]
[[Pulmonary Rehabilitation|Pulmonary rehabilitation]] (PR) <ref>Holland AE, Cox NS, Houchen-Wolloff L, Rochester CL, Garvey C, ZuWallack R, Nici L, Limberg T, Lareau SC, Yawn BP, Galwicki M. Defining modern pulmonary rehabilitation. An official American Thoracic Society workshop report. Annals of the American Thoracic Society. 2021 May;18(5):e12-29.</ref>should be available to all appropriate people with COPD, including those with a recent hospitalisation for an acute exacerbation. A randomised study suggests positive outcomes with functional electrostimulation in patients with severe chronic obstructive pulmonary disease hospitalised for acute exacerbation<ref>Lopez-Lopez L, Torres-Sanchez I, Rodriguez-Torres J, Cabrera-Martos I, Cahalin LP, Valenza MC. [https://pubmed.ncbi.nlm.nih.gov/31769337-randomized-feasibility-study-of-twice-a-day-functional-electrostimulation-in-patients-with-severe-chronic-obstructive-pulmonary-disease-hospitalized-for-acute-exacerbation/ Randomized feasibility study of twice a day functional electrostimulation in patients with severe chronic obstructive pulmonary disease hospitalized for acute exacerbation.] Physiotherapy theory and practice. 2019 Nov 23:1-8.</ref>. A study suggests that patients affected with COPD and pulmonary hypertension experience a lower exercise capacity and quality of life<ref>Blanco I, Valeiro B, Torres-Castro R, Barberán-García A, Torralba Y, Moisés J, Sebastián L, Osorio J, Rios J, Gimeno-Santos E, Roca J.[Effects of Pulmonary Hypertension on Exercise Capacity in Patients With Chronic Obstructive Pulmonary Disease. Archivos de bronconeumologia. 2019 Nov 23.</ref>. Another randomised controlled trial examining the effects of virtual training (VR) and exercise training on the rehabilitation of patients with COPD  suggests that pulmonary rehabilitation program supplemented with VR training has positive outcomes in improving physical fitness in patients with COPD<ref>Rutkowski S, Rutkowska A, Kiper P, Jastrzebski D, Racheniuk H, Turolla A, Szczegielniak J, Casaburi R. [https://pubmed.ncbi.nlm.nih.gov/32021150-virtual-reality-rehabilitation-in-patients-with-chronic-obstructive-pulmonary-disease-a-randomized-controlled-trial/ Virtual Reality Rehabilitation in Patients with Chronic Obstructive Pulmonary Disease: A Randomized Controlled Trial.] International Journal of Chronic Obstructive Pulmonary Disease. 2020;15:117.</ref>. Studies suggest PR was useful in patients with moderate to severe COPD<ref>Lee AL, Butler SJ, Varadi RG, Goldstein RS, Brooks D. [https://pubmed.ncbi.nlm.nih.gov/32131643/ The Impact of Pulmonary Rehabilitation on Chronic Pain in People with COPD.] COPD: Journal of Chronic Obstructive Pulmonary Disease. 2020 Mar 3:1-0.</ref>. A prospective, multisite, randomised controlled trial will determine whether an 8-week PR programme (exercise training will comprise: overground or treadmill walking, lower limb stationary cycling, and lower and upper limb strengthening exercises) is equivalent to a 12-week PR programme in people with COPD<ref>Bishop J, Spencer L, Alison J. [https://pubmed.ncbi.nlm.nih.gov/32933927/ Effect of a pulmonary rehabilitation programme of 8 weeks compared to 12 weeks duration on exercise capacity in people with chronic obstructive pulmonary disease (PuRe Duration): protocol for a randomised controlled trial]. BMJ open respiratory research. 2020 Sep 1;7(1):e000687.</ref>.   


*Refer for dietetic advice
=== Utilise a Multidisciplinary Team  ===
*Offer nutritional supplements if the BMI is low
*Pay attention to weight changes in older patients (especially&gt;3 kg)


==== Chronic productive cough  ====
A multidisciplinary team should deliver COPD care.


*Consider mucolytic therapy
=== Palliative Setting  ===


==== Anxiety and depression  ====
*[[Opioids]] should be used when appropriate for the palliation of breathlessness in people with end-stage COPD unresponsive to other medical therapy
 
*Screen for anxiety and depression using validated tools in people who:
**are hypoxic
**are severely breathless or
**have recently been seen or treated at a hospital for an exacerbation
*Refer to NICE guidelines ‘[http://www.nice.org.uk/CG91 Depression with a chronic physical health problem]’<ref>National Institute for Health and Clinicl Excellence.  Chronic obstructive pulmonary disease: Management of chronic obstructive pulmonary disease in adults in primary and secondary care.  Available from http://guidance.nice.org.uk/CG91 [last accessed 2/8/10]</ref>.
 
==== Alpha-1 antitrypsin deficiency  ====
 
*Offer referral to a specialist centre to discuss the clinical management of this condition
*Alpha-1 antitrypsin replacement therapy is not recommended
 
==== Palliative setting  ====
 
*Opioids should be used when appropriate for the palliation of breathlessness in people with end-stage COPD unresponsive to other medical therapy  
*Use benzodiazepines, tricyclic antidepressants, major tranquillisers and oxygen to treat breathlessness  
*Use benzodiazepines, tricyclic antidepressants, major tranquillisers and oxygen to treat breathlessness  
*Provide access to multidisciplinary palliative care teams and hospices
*Provide access to multidisciplinary palliative care teams and hospices


== Differential Diagnosis<br> ==
== Resources ==
 
add text here relating to the differential diagnosis of this condition<br>


== Key Evidence  ==
*[[Clinical Guidelines: Cardiopumlonary#COPD|Clinical Guidelines for COPD]]
 
*[https://www.mesothelioma.com/ Mesothelioma Resources for Patients]
add text here relating to key evidence with regards to any of the above headings<br>
 
== Resources <br>  ==
 
==== Clinical Guidelines  ====
 
[[Clinical Guidelines: Cardiopumlonary#COPD|Clinical Guidelines for COPD]]  


==== Videos  ====
==== Videos  ====


{| width="100%" cellspacing="1" cellpadding="1"
{| class="FCK__ShowTableBorders" cellspacing="1" cellpadding="1" width="100%"
|-
|-
| {{#ev:youtube|aktIMBQSXMo|300}}  
| {{#ev:youtube|aktIMBQSXMo|412}} <ref>Healthguru. Understanding Chronic Obstructive Pulmonary Disease (COPD#1). Available from: https://www.youtube.com/watch?v=aktIMBQSXMo [last accessed 31/5/2022]</ref>
| {{#ev:youtube|ttdma8PnFJI|300}}
| {{#ev:youtube|ttdma8PnFJI|412}} <ref>Healthguru. Treating Chronic Obstructive Pulmonary Disease (COPD #2). Available from: https://www.youtube.com/watch?v=ttdma8PnFJI [last accessed 31/5/2022]</ref>
|}
|}


== Case Studies  ==
add links to case studies here (case studies should be added on new pages using the [[Template:Case Study|case study template]])<br>
== Recent Related Research (from [http://www.ncbi.nlm.nih.gov/pubmed/ Pubmed])  ==
<div class="researchbox">
<rss>http://eutils.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi?rss_guid=1xIhmOfNk2wL2xFDEJUVIGZpGeS5VmsLVj1FywiqHDPMHsXQ1G|charset=UTF-8|short|max=10</rss>
</div>
== References  ==
== References  ==


References will automatically be added here, see [[Adding References|adding references tutorial]].
<references />


<references />
[[Category:Cardiopulmonary]]
[[Category:Cardiopulmonary - Conditions]]
[[Category:Chronic_Respiratory_Disease]]
[[Category:Chronic Respiratory Disease - Conditions]]
[[Category:Glasgow_Caledonian_University_Project]]
[[Category:Acute Care]]
[[Category:Conditions]]
[[Category:Non Communicable Diseases]]
[[Category:Older People/Geriatrics]]
[[Category:Older People/Geriatrics - Conditions]]

Latest revision as of 15:26, 26 June 2023

Introduction[edit | edit source]

Copd versus healthy lung.jpeg

Chronic obstructive pulmonary disease (COPD)[1] is a common and treatable disease characterised by progressive airflow limitation and tissue destruction. It is associated with structural lung changes due to chronic inflammation from prolonged exposure to noxious particles or gases, most commonly cigarette smoke. Chronic inflammation causes airway narrowing and decreased lung recoil. The disease often presents with cough symptoms, dyspnea, and sputum production. Symptoms can range from being asymptomatic to respiratory failure.[2]

Epidemiology[edit | edit source]

COPD is primarily present in smokers and those over 40. Prevalence increases with age and is currently the third most common cause of morbidity and mortality worldwide. In 2015, the prevalence of COPD was 174 million, and there were approximately 3.2 million deaths due to COPD worldwide. However, the prevalence is likely to be underestimated due to the under diagnosis of COPD.[2]

Etiology[edit | edit source]

COPD is caused by prolonged exposure to harmful particles or gases.

  • Cigarette smoking is the most common cause of COPD worldwide.[1]
  • Other causes may include second-hand smoke, environmental and occupational exposures,alpha-1 antitrypsin deficiency (AATD)[2] ageing [3]and gene-environment interactions (GxE)[3] .
[4]

Mechanism of Injury / Pathological Process[edit | edit source]

Healthy alveoli Primal.png

COPD is an inflammatory condition involving the airways, lung parenchyma, and pulmonary vasculature.[2] Emphysema describes one of the structural changes seen in COPD where there is the destruction of the alveolar air sacs (gas-exchanging surfaces of the lungs) leading to obstructive physiology.

Image 2: Healthy Alveoli.

The process is thought to involve oxidative stress and protease-antiprotease imbalances. In emphysema, an irritant (e.g., smoking) causes an inflammatory response. Neutrophils and macrophages are recruited and release multiple inflammatory mediators. Oxidants and excess proteases lead to the destruction of the air sacs. The protease-mediated destruction of elastin leads to a loss of elastic recoil and results in airway collapse during exhalation.

  • The inflammatory response and obstruction of the airways cause a decrease in the forced expiratory volume (FEV1), and tissue destruction leads to airflow limitation and impaired gas exchange.
  • Hyperinflation of the lungs is often seen in imaging studies and occurs due to air trapping from airway collapse during exhalation.
  • The inability to exhale fully also causes elevations in carbon dioxide (CO2) levels.
  • With disease progression the reduction in ventilation or increase in physiologic dead space leads to CO2 retention.
  • Acute exacerbations of COPD are common and usually occur due to a trigger (e.g., bacterial or viral pneumonia, environmental irritants). There is an increase in inflammation and air trapping, often requiring corticosteroid and bronchodilator treatment.[2]

Clinical Presentation[edit | edit source]

Dyspnea 01.png

COPD will typically present in adulthood and often during the winter months. Patients usually present with complaints of chronic and progressive dyspnea, cough, and sputum production. Patients may also have wheezing and chest tightness. While a smoking history is present in most cases, there are many without such a history. They should be questioned on exposure to second-hand smoke, occupational and environmental exposures, and family history.[1][3]

COPD is a complex interaction between asthma, chronic bronchitis, and emphysema.

Evaluation[edit | edit source]

Spirometry1.jpg

COPD is often evaluated in patients with relevant symptoms and risk factors. The diagnosis is confirmed by spirometry. Other tests may include a 6-minute walk test, laboratory testing, and radiographic imaging.

  • Assessment - A diagnosis of COPD should be considered in patients over the age of 35 who have a risk factor (generally smoking) and who present with exertional breathlessness, chronic cough, regular sputum production, frequent winter ‘bronchitis’ or wheeze.
  • X-Ray - An X-ray of the chest may show an over-expanded lung (hyperinflation) and can be useful to help exclude other lung diseases.
  • Pulmonary function tests - Essential in the diagnosis, staging, and monitoring of COPD. Spirometry is performed before and after administering an inhaled bronchodilator. Inhaled bronchodilators may be short-acting beta2-agonist (SABA), short-acting anticholinergic, or a combination of both. A ratio of the forced expiratory volume in one second to forced vital capacity (FEV1/FVC) less than 0.7 confirms the diagnosis of COPD. Patients with significantly reduced FEV1 and signs of dyspnea should be evaluated for oxygenation with pulse oximetry or arterial blood gas analysis.
  • Blood tests - A blood sample taken from an artery can be tested for blood gas levels which may show low oxygen levels (hypoxemia) and/or high carbon dioxide levels (respiratory acidosis). A blood sample taken from a vein may show a high blood count (reactive polycythemia), a reaction to long-term hypoxemia.
[5]
[6]

Outcome Measures[edit | edit source]

Oximetre.jpg

There can be a different number of ways of measuring the impact or change of someone's COPD, examples being lung function, lung volumes and exercise capacity. A cross-sectional study recommends cardiopulmonary exercise testing (CPET) as an efficient tool in assessing functional capacity and prognosis in Heart Failure and COPD patients[7]

Other outcome measures include:

Bleep Test; Shuttle Walk Test; Ergometry; BORG RPE; 6-minute walk test is commonly performed to assess the submaximal functional capacity of a patient. This test is performed indoors on a flat and straight surface. The length of the hallway is usually 100 feet, and the test measures the distance the patient walks over a period of 6 minutes[2]; Grip Strength; 30 seconds Sit to stand

According to a longitudinal study[8], changes in frailty status of COPD patients were associated with significant clinical outcomes related to dyspnea; mobility; physical activity; handgrip and quadriceps strength. It was found that five times sit-to-stand and exacerbations were independent predictors of the improvement in frailty status.

Management / Interventions[edit | edit source]

Smoking man.jpg

The primary goals of treatment are to control symptoms, improve the quality of life, and reduce exacerbations and mortality. The non-pharmacological approach includes smoking cessation and Pulmonary rehabilitation.

Annual influenza vaccination is recommended in all patients with COPD.

The classes of commonly used medications in COPD include:

  • Bronchodilators (beta2-agonists, antimuscarinics, methylxanthines),
  • Inhaled corticosteroids (ICS) and systemic glucocorticoids,
  • Phosphodiesterase-4 (PDE4) inhibitors,
  • Antibiotics.

Exercise[edit | edit source]

[9]

Exercise prescription is a key component of pulmonary rehabilitation programmes, part of the non-pharmacological approach to managing COPD. There is a high level of evidence for the benefits of pulmonary rehabilitation for people with COPD[10] Strength and endurance exercises are endorsed for people with COPD.[11]

Use of protein supplements, in combination with exercise, could also be beneficial. Refer to the dietician.

Muscles that are required for arm exercise are also involved in the movement of the chest wall during respiration, and thus, the need to breathe often compromises the individual’s ability to undertake daily activities. Therefore, exercise prescription involving arm exercise needs to be carefully prescribed.[12] The evidence showed that patients with COPD have limb muscle dysfunction, a key systemic consequence.[13]

Promote Effective Inhaled Therapy[edit | edit source]

In people with stable COPD who remain breathless or have exacerbations despite the use of short-acting bronchodilators as required, offer the following as maintenance therapy:

  • if forced expiratory volume in 1 second (FEV1)≥50% predicted: either long-acting beta2 agonist (LABA) or long-acting muscarinic antagonist (LAMA)
  • if FEV1<50% predicted: either LABA with an inhaled corticosteroid (ICS) in a combination inhaler or LAMA

Offer LAMA in addition to LABA + ICS to people with COPD who remain breathless or have exacerbations despite taking LABA + ICS, irrespective of their FEV1.

Provide Pulmonary Rehabilitation[edit | edit source]

Exercise older person.jpg

Pulmonary rehabilitation (PR) [14]should be available to all appropriate people with COPD, including those with a recent hospitalisation for an acute exacerbation. A randomised study suggests positive outcomes with functional electrostimulation in patients with severe chronic obstructive pulmonary disease hospitalised for acute exacerbation[15]. A study suggests that patients affected with COPD and pulmonary hypertension experience a lower exercise capacity and quality of life[16]. Another randomised controlled trial examining the effects of virtual training (VR) and exercise training on the rehabilitation of patients with COPD  suggests that pulmonary rehabilitation program supplemented with VR training has positive outcomes in improving physical fitness in patients with COPD[17]. Studies suggest PR was useful in patients with moderate to severe COPD[18]. A prospective, multisite, randomised controlled trial will determine whether an 8-week PR programme (exercise training will comprise: overground or treadmill walking, lower limb stationary cycling, and lower and upper limb strengthening exercises) is equivalent to a 12-week PR programme in people with COPD[19].

Utilise a Multidisciplinary Team[edit | edit source]

A multidisciplinary team should deliver COPD care.

Palliative Setting[edit | edit source]

  • Opioids should be used when appropriate for the palliation of breathlessness in people with end-stage COPD unresponsive to other medical therapy
  • Use benzodiazepines, tricyclic antidepressants, major tranquillisers and oxygen to treat breathlessness
  • Provide access to multidisciplinary palliative care teams and hospices

Resources[edit | edit source]

Videos[edit | edit source]

[20]
[21]

References[edit | edit source]

  1. 1.0 1.1 1.2 Hillas G, Perlikos F, Tsiligianni I, Tzanakis N. Managing comorbidities in COPD. International journal of chronic obstructive pulmonary disease. 2015 Jan 7:95-109.
  2. 2.0 2.1 2.2 2.3 2.4 2.5 Agarwal AK, Raja A, Brown BD. Chronic obstructive pulmonary disease (COPD). StatPearls [Internet]. 2020 Jun 7.Available from:https://www.ncbi.nlm.nih.gov/books/NBK559281/ (accessed 24.5.2021)
  3. 3.0 3.1 3.2 Agustí A, Vogelmeier C, Faner R. COPD 2020: changes and challenges. American Journal of Physiology-Lung Cellular and Molecular Physiology. 2020 Nov 1;319(5):L879-83.
  4. Animated COPD Patient. Understanding COPD. Available from: https://www.youtube.com/watch?v=T1G9Rl65M-Q [last accessed 31/5/2022]
  5. Armando Hasudungan. Understanding Spirometry - Normal, Obstructive vs Restrictive. Available from: https://www.youtube.com/watch?v=YwcNbVnHNAo [last accessed 31/5/2022]
  6. nhswestminster. Spirometry Procedure. Available from: https://www.youtube.com/watch?v=s8pXdtp_Duw [last accessed 31/5/2022]
  7. da Luz GC, Rossi CF, Tinoco AG, Marinho RS, de Faria CP, da Silva AT, Oliveira CR, Borghi-Silva A, Mendes RG, Goi RM. The Value of Cardiopulmonary Exercise Testing in Determining Severity in Patients with Systolic Heart Failure and COPD. Scientific Reports (Nature Publisher Group). 2020 Dec 1;10(1).
  8. Bernabeu-Mora R, Oliveira-Sousa SL, Sánchez-Martínez MP, García-Vidal JA, Gacto-Sánchez M, Medina-Mirapeix F. Frailty transitions and associated clinical outcomes in patients with stable COPD: A longitudinal study. Plos one. 2020 Apr 3;15(4):e0230116.
  9. Burke Rehabilitation. COPD Treatments & Rehab: Upper Body Exercises. Available from: http://www.youtube.com/watch?v=VR7QnSnHmBU[last accessed 13/02/15]
  10. Roisin RR, Rabe KF, Anzueto A, et al. Global strategy for diagnosing, managing, and preventing chronic obstructive pulmonary disease. Bethesda, MD: Global Initiative for Chronic Obstructive Lung Disease, 2008; 1–91.
  11. Skinner, Margot. Strength and endurance exercises are endorsed for people with COPD. Physical Therapy Reviews, Volume 14, Number 6, December 2009, pp. 418-418(1)
  12. Ennis S, Alison J, McKeough Z. The effects of arm endurance and strength training on arm exercise capacity in people with chronic obstructive pulmonary disease. Phys Ther Rev 2009;14(4):226–39.
  13. Spruit MA, Singh SJ, Garvey C, ZuWallack R, Nici L, Rochester C, Hill K, Holland AE, Lareau SC, Man WD, Pitta F. An official American Thoracic Society/European Respiratory Society statement: key concepts and advances in pulmonary rehabilitation. American Journal of Respiratory and critical care medicine. 2013 Oct 15;188(8):e13-64.
  14. Holland AE, Cox NS, Houchen-Wolloff L, Rochester CL, Garvey C, ZuWallack R, Nici L, Limberg T, Lareau SC, Yawn BP, Galwicki M. Defining modern pulmonary rehabilitation. An official American Thoracic Society workshop report. Annals of the American Thoracic Society. 2021 May;18(5):e12-29.
  15. Lopez-Lopez L, Torres-Sanchez I, Rodriguez-Torres J, Cabrera-Martos I, Cahalin LP, Valenza MC. Randomized feasibility study of twice a day functional electrostimulation in patients with severe chronic obstructive pulmonary disease hospitalized for acute exacerbation. Physiotherapy theory and practice. 2019 Nov 23:1-8.
  16. Blanco I, Valeiro B, Torres-Castro R, Barberán-García A, Torralba Y, Moisés J, Sebastián L, Osorio J, Rios J, Gimeno-Santos E, Roca J.[Effects of Pulmonary Hypertension on Exercise Capacity in Patients With Chronic Obstructive Pulmonary Disease. Archivos de bronconeumologia. 2019 Nov 23.
  17. Rutkowski S, Rutkowska A, Kiper P, Jastrzebski D, Racheniuk H, Turolla A, Szczegielniak J, Casaburi R. Virtual Reality Rehabilitation in Patients with Chronic Obstructive Pulmonary Disease: A Randomized Controlled Trial. International Journal of Chronic Obstructive Pulmonary Disease. 2020;15:117.
  18. Lee AL, Butler SJ, Varadi RG, Goldstein RS, Brooks D. The Impact of Pulmonary Rehabilitation on Chronic Pain in People with COPD. COPD: Journal of Chronic Obstructive Pulmonary Disease. 2020 Mar 3:1-0.
  19. Bishop J, Spencer L, Alison J. Effect of a pulmonary rehabilitation programme of 8 weeks compared to 12 weeks duration on exercise capacity in people with chronic obstructive pulmonary disease (PuRe Duration): protocol for a randomised controlled trial. BMJ open respiratory research. 2020 Sep 1;7(1):e000687.
  20. Healthguru. Understanding Chronic Obstructive Pulmonary Disease (COPD#1). Available from: https://www.youtube.com/watch?v=aktIMBQSXMo [last accessed 31/5/2022]
  21. Healthguru. Treating Chronic Obstructive Pulmonary Disease (COPD #2). Available from: https://www.youtube.com/watch?v=ttdma8PnFJI [last accessed 31/5/2022]