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COPD (Chronic Obstructive Pulmonary Disease)

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Contents
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1 Clinically Relevant Anatomy

2 Causes
3 Mechanism of Injury / Pathological Process
4 Clinical Presentation
4.1 Asthma
4.2 Chronic bronchitis
4.3 Emphysema
5 Diagnostic Procedures
6 Outcome Measures
6.1 Lung function - Forces Expiratory Volume in 1 second (FEV1)
6.2 Lung Volumes
6.3 Exercise Capacity
7 Management / Interventions
7.1 Stopping Smoking
7.2 Exercise
7.3 Promote effective inhaled therapy
7.4 Provide pulmonary rehabilitation
7.5 Use non-invasive ventilation
7.6 Manage exacerbations
7.7 Ensure multidisciplinary working
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 8 Managing symptoms and conditions in stable COPD
8.1 Breathlessness and exacerbations
8.2 Frequent exacerbations
8.3 Cor pulmonale
8.4 Respiratory failure
8.5 Abnormal BMI
8.6 Chronic productive cough
8.7 Anxiety and depression
8.8 Alpha-1 antitrypsin deficiency
8.9 Palliative setting
9 Resources
9.1 Videos
10 Case Studies
11 Recent Related Research (from Pubmed)
12 References

Clinically Relevant Anatomy

See this page for information on the anatomy
of the lungs

The Lungs

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Causes
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.[1]
Occupational exposure - Intense and
prolonged exposure to workplace dusts
found in coal mining, gold mining, and the
cotton textile industry and chemicals such [2]
as cadmium, isocyanates, and fumes from
welding have been implicated in the
development of airflow obstruction, even in
nonsmokers.[3] 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.[4] The effect of occupational
pollutants on the lungs appears to be substantially less important than the
effect of cigarette smoking.[5]
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.[[6] 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.[7]
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.[8]] The genetic differences that make
some peoples' lungs susceptible to the effects of tobacco smoke are
mostly unknown
Autoimmune disease - There is mounting evidence that there may be an
autoimmune component to COPD.[9] Many individuals with COPD who have
stopped smoking have active inflammation in the lungs.[10]The disease
may continue to get worse for many years after stopping smoking due to
this ongoing inflammation.[10] This sustained inflammation is thought to
be mediated by autoantibodies and autoreactive T cells.[11]
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Mechanism of Injury / Pathological Process
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:
Oxidative stress produced by the high concentrations of free radicals in
tobacco smoke.
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
COPD is a complex interaction between Chronic Bronchitis, Emphysema and
Asthma

Asthma
Asthma is a chronic lung disease which is a very common respiratory
condition. It is also known as a reactive airway disease which is inconvenient
most of the time but manageable. Asthma is caused by inflammation and
constriction of bronchial walls which leads to a series of spasmodic attacks of
wheezing and shortness of breath as a result of the hyper-reactivity of
smooth muscle in the bronchial walls and in the absence of any other
apparent cause. There are various factors such as exposure to cigarette
smoke, climate change, physical exertion or emotional stress that causes
asthma. It begins during childhood and the disease is commonly triggered by
viral infection[12].
Asthma can be diagnosed by the presence of the signs and symptoms. The
diagnosis is normally confirmed by presenting a response to a inhaled
bronchodialator. Often pulmonary function tests, chest x-rays and blood tests
can also be done in order to confirm the diagnosis.

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Chronic bronchitis
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.[13] 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 Bronchitis
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.[14]
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.[15] The hypoxia
and fluid retention leads to them being called "Blue Bloaters."

Emphysema

A lateral chest x-ray of a person with emphysema. Note the barrow chest and
flap diaphragm.

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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.[13] 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".

Diagnostic Procedures
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.
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
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 - 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.
[16]
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.

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Outcome Measures
Follow the link here for a list of outcome measures within Physio-pedia .

There can be a different number of ways of measuring the impact or change

of someone's COPD, examples being from lung function, lung volumes and
exercise capacity.

Lung function - Forces Expiratory Volume in 1 second (FEV1)

It is known that COPD lungs lose function quicker and more rapidly than non-
COPD lungs. In recognition of this FEV1 is the most important marker to
determine severity and treatment in COPD algorithms, with decline of FEV1
over-time as the marker for disease progression[17]. The ratio of FEV1/FVC
(Forced vital capacity) as well as the percentage predicted FEV1 is a fixed
ratio used in current guidelines to assess the function of lungs.
The strengths of using this measure is that:
FEV1 and FVC measurements are highly reproducible
Poor lung function if a risk factor for all cause of cardiovascular mortality
and poorer health[18]
Limitations being:
FEV1 measurements are based on an artificial manoeuvre and do not
always correlate with clinically relevant outcomes such as dyspnoea,
health status, exercise capacity, or exacerbations[19][20]
Patients with similar FEV1 may represent different underlying phenotypes.
Reference equations for lung function by European Community for Coal
and Steel are disputed and limited in predicting lung function in the
general population [21]
No minimal important difference (MID) has been established yet. It was
suggested that an appropriate range of values for the MID for FEV1 might
be 100-140 mL but the MID for FEV1 remains poorly defined for COPD

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 [22]

Lung Volumes
Changes in absolute lung volumes can occur in COPD patients even in the
absence of FEV1 changes. Progressive hyperinflation due to airflow limitation
and loss of lung elastic recoil not only increases the work required during
inspiration but also profoundly decreases the ventilatory reserve and
increases the sense of effort and dyspnoea[23]
In terms of measurement static lung hyperinflation and its increase during
exercise (dynamic hyperinflation) are measured as elevations of total lung
capacity (TLC), functional residual capacity (FRC), residual volume (RV) and
as a decrease in inspiratory capacity (IC)[17].
Strengths of lung volumes include:
Indices of dynamic hyperinflation correlate better than FEV1 with activity
limitation and exertional dyspnoea and pharmacological and surgical lung
volume reduction have been associated with improvements in exercise
performance and dyspnoea[24][25]
A severely reduced IC/TLC ratio with a threshold value of 25% has been
shown to predict mortality in COPD patients[26]
Weaknesses include:
Body plethysmography remains the gold standard for the measurement of
lung volumes such as TLC, FRC and RV. Spirometrically derived
assessments of lung hyperinflation are more difficult to interpret in the
absence of simultaneous bodyplethysmographic volume measurements to
rule out a concomitant restrictive ventilatory disorder[27]
The reproducibility of FRC, IC and RV in absolute values has yet to be
demonstrated. Measurement of IC alone is not a reliable marker of lung
hyperinflation and does not consistently reflect changes in FRC or TLC[27]
The natural course of dynamic hyperinflation in COPD is unknown and
seems likely to be highly variable among COPD patients [27]

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Exercise Capacity
Includes the 6 Minute Walk test , the Bleep Test, Shuttle Walk Test and
Ergometry.

Management / Interventions
Stopping Smoking
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
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 [28]
evidence for the benefits of pulmonary
rehabilitation for people with COPD[29]
Strength and endurance exercise are endorsed
for people with COPD.[30]
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 involving arm exercise needs to be carefully
prescribed.[31]

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:
if forced expiratory volume in 1 second (FEV1)≥50% predicted: either
long-acting beta2 agonist (LABA) or long-acting muscarinic antagonist
(LAMA)
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 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

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 [32]
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

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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

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 Offer 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
Cor Pulmonale
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
Consider referral for assessment for long-term domiciliary NIV therapy

Abnormal BMI
Refer for dietetic advice
Offer nutritional supplements if the BMI is low
Pay attention to weight changes in older patients (especially>3 kg)

Chronic productive cough

Consider mucolytic therapy

Anxiety and depression

Screen for anxiety and depression using validated tools in people who:
are hypoxic
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 are severely breathless or
have recently been seen or treated at a hospital for an exacerbation
Refer to NICE guidelines ‘Depression with a chronic physical health
problem .’[33]

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
Provide access to multidisciplinary palliative care teams and hospices

Resources
Clinical Guidelines
Clinical Guidelines for COPD
KNGF guidelines for physical therapy in patients withchronic obstructive
pulmonary disease
www.fysionet-
evidencebased.nl/images/pdfs/guidelines_in_english/copd_flowchart%20.pdf

Videos

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Case Studies
Will be added when available.

Recent Related Research (from Pubmed )

References
1. ↑ 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
2. ↑ Animated COPD Patient. Understanding COPD. Available from:
http://www.youtube.com/watch?v=T1G9Rl65M-Q [last accessed
13/02/15]
3. ↑ Devereux, Graham (May 2006). "ABC of chronic obstructive pulmonary
disease. Definition, epidemiology, and risk factors". BMJ 332 (7550):
1142–4
4. ↑ 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
5. ↑ 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
6. ↑ 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
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 7. ↑ 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.
8. ↑ 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
9. ↑ Agustí A, MacNee W, Donaldson K, Cosio M. (2003). "Hypothesis: does
COPD have an autoimmune component?". Thorax 58 (10): 832–4
10. ↑ 10.0 10.1 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.
11. ↑ 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
12. ↑ http://www.atsjournals.org/doi/abs/10.1164/rccm.200809-1512OC
13. ↑ 13.0 13.1 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
14. ↑ Kumar P, Clark M (2005). Clinical Medicine (6th ed.). Elsevier Saunders.
pp. 900–1. ISBN 0702027634
15. ↑ 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
16. ↑ NHS Westminster. Spirometry Procedure. Available from:
http://www.youtube.com/watch?v=s8pXdtp_Duw [last accessed
09/02/13]
17. ↑ 17.0 17.1 Glaab T. Vogelmeier C and Buhl R. Outcome measures in chronic
obstructive pulmonary disease (COPD): strengths and limitations.
Respiratory Research. 2010:11:79
18. ↑ Sin DD, Wu L, Man SF: The relationship between reduced lung function
and cardiovascular mortality: a population-based study and a systematic

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 review of the literature. Chest 2005, 127:1952-1959
19. ↑ Cazzola M, MacNee W, Martinez FJ, Rabe KF, Franciosi LG, Barnes PJ,
Brusasco V, Burge PS, Calverley PMA, Celli BR, Jones PW, Mahler DA,
Make B, Miravitlles M, Page CP, Palange P, Parr D, Pistolesi M, Rennard
SI, Rutten-van Mölken MP, Stockley R, Sullivan SD, Wedzicha JA, Wouters
EF, American Thoracic Society/European Respiratory Society Task Force
on outcomes of COPD: Outcomes for COPD pharmacological trials: from
lung function to biomarkers. Eur Respir J 2008, 31:416-469
20. ↑ 11.Wise RA: The value of forced expiratory volume in 1 second decline
in the assessment of chronic obstructive pulmonary disease progression.
Am J Med 2006, 119:4-11
21. ↑ 12.Pellegrino R, Viegi G, Brusasco V, Crapo RO, Burgos F, Casaburi R,
Coates A, van der Grinten CPM, Gustafsson P, Hankinson J, Jensen R,
Johnson DC, MacIntyre N, McKay R, Miller MR, Navajas D, Pedersen OF,
Wanger J: Interpretative strategies for lung function tests. Eur Respir J
2005, 26:948-968
22. ↑ 4.Cazzola M, MacNee W, Martinez FJ, Rabe KF, Franciosi LG, Barnes PJ,
Brusasco V, Burge PS, Calverley PMA, Celli BR, Jones PW, Mahler DA,
Make B, Miravitlles M, Page CP, Palange P, Parr D, Pistolesi M, Rennard
SI, Rutten-van Mölken MP, Stockley R, Sullivan SD, Wedzicha JA, Wouters
EF, American Thoracic Society/European Respiratory Society Task Force
on outcomes of COPD: Outcomes for COPD pharmacological trials: from
lung function to biomarkers. Eur Respir J 2008, 31:416-469
23. ↑ O'Donnell DE, Laveneziana P: Physiology and consequences of lung
hyperinflation in COPD. Eur Respir Rev 2006, 15:61-67
24. ↑ 17.O'Donnell DE: Is sustained pharmacologic lung volume reduction now
possible in COPD? Chest 2006, 129:501-503
25. ↑ 18.Criner GJ, Belt P, Sternberg AL, Mosenifar Z, Make BJ, Utz JP,
Sciurba F: National Emphysema Treatment Trial Research Group. Effects
of lung volume reduction surgery on gas exchange and breathing pattern
during maximum exercise. Chest 2009, 135:1268-79
26. ↑ 19.Casanova C, Cote C, de Torres JP, Aguirre-Jaime A, Marin JM, Pinto-
Plata V, Celli BR: Inspiratory-to-total lung capacity predicts mortality in
patients with chronic obstructive pulmonary disease. Am J Respir Crit Care
Med 2005, 171:591-597
27. ↑ 27.0 27.1 27.2 O'Donnell DE, Laveneziana P: Physiology and consequences
of lung hyperinflation in COPD. Eur Respir Rev 2006, 15:61-67
28. ↑ Burke Rehabilitation. COPD Treatments &amp;amp;amp;amp; Rehab:
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 Upper Body Exercises. Available from: http://www.youtube.com/watch?
v=VR7QnSnHmBU [last accessed 13/02/15]
29. ↑ 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.
30. ↑ Skinner, Margot. Strength and endurance exercise endorsed for people
with COPD. Physical Therapy Reviews, Volume 14, Number 6, December
2009 , pp. 418-418(1)
31. ↑ 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.
32. ↑ SMACC. Non-Invasive Ventilation. Available from:
http://www.youtube.com/watch?v=QQZvhkBWBgQ [last accessed
13/02/15]
33. ↑ 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]

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