CHRONIC

OBSTRUCTIVE
PULMONARY
DISEASE
Submitted To:
Prof. Ma. Nancy T. Martinez

Submitted By:
Ramos, Hiyasmin
Ferrer, Sheena Leigh
Bunagan, Judy-Ann
Manuel, Marc Dave
Adviento Jonathan
Ordinario, Nicole
Ravelo, Larrisa
So, Charmaine
Turo, Emerjay
Castro, Jayson
Japson, Leslie
Urbano, Shyra

BSRT 2B
  Chronic Obstructive Pulmonary Disease (COPD) - is a preventable and treatable (it
means treatments are available that could be used to slow the progression of the COPD
and help people to manage their symptoms) disease with some significant
extrapulmonary effects that may contribute to the severity in individual patients. Its
pulmonary component is characterized by airflow limitation that is not fully reversible.
The airflow limitation is usually progressive and associated with an abnormal
inflammatory response of the lung to noxious particles or gases.
 COPD is the 4th leading cause of death worldwide and is projected to be the 3 rd leading
case in the year 2020. Incidence rate of COPD was 8.9/1000 person-years and is higher
in males and in smokers. Proportion of female COPD participants without a history of
smoking was 27.2% while proportion was 7.3% in males
 Burden of Obstructive Lung Disease (BOLD) –has used standardized methodology
comprising questionnaires and pre and post bronchodilator spirometer to assess the
prevalence and risk factors of COPD in people aged 40 around the world. BOLD
reported worse lung function with prevalence of COPD in GOLD Grade 2.

PATHOGENESIS OF COPD

Cigarette smoking is the real

culprit of the many cases of COPD. When these foreign particles called irritants enter the body,
it irritates the airways. Normally, the body has its inflammatory response to fight these irritants.
The body has the so-called inflammatory cells. These inflammatory cells are neutrophils,
macrophages, T-lymphocytes, B-lymphocytes, eosinophil and epithelial cells. They have normal
amounts found in the body. But once the irritants such as cigarette smoke continuously invade
the airways, then, our body’s normal mechanism is disrupted. The inflammatory cells have
specific patterns found in COPD patients, in which, they are all increased or they are activated.
Once these inflammatory cells increase, it will release inflammatory mediators which are known
to attract more inflammatory cells and amplifies further inflammation. As the number of cells
continues to rise, the body cannot anymore respond to these chronic irritants, thus, this causes
inflammation in the lungs.

In addition with lung inflammation, oxidative stress is also seen as a factor that adds to COPD
pathology. Oxidative stress is evident when there is an excess amount of oxidants and
increased amounts of reactive oxygen species (ROS) that exceeds the capability of antioxidants
to counteract the harmful effects of it. Oxidants present in cigarette smoke are molecules that
cause damage to lungs. In normal individuals, oxidants are being wiped out by the antioxidants
to counter its damaging effect in the body especially to tissues and cells. But, due to constant
smoking of an individual, these oxidants become too much in amount that the antioxidants
cannot anymore fight its damaging effect which results in imbalance between oxidants and
antioxidants that gives rise to the so-called oxidative stress. On the other hand, reactive oxygen
species is generated when a molecule, for example, oxygen, it has eight electrons. When
oxygen gains another electron, then, there will be an imbalance in the number of paired
electrons because there is an unpaired electron that has been added. When this happens, the
free radicals become highly reactive which can cause damage to macromolecules in the body
and thereby contributing to the development and progression of COPD.

Just like oxidative stress, proteinase-antiproteinase imbalance also contributes to the disease
process of COPD. Proteinase breaks down connective tissue components, like elastin, which is
a major component of connective tissue in parenchyma. Proteinases are increased in COPD
patients. Imbalance happens when number of proteinases exceeds the amount of
antiproteinases in the body. If this happens, then, antiproteinases cannot anymore protect the
tissues from being broken down by these proteinases. Thus, if proteinases continue with this
act, this will lead to destruction in connective tissue components of the lungs resulting to an
inflammation.

To sum it up, COPD is caused by inflammation in the lung that is caused by the chronic irritants
(cigarette smoke) taken in consistently by an individual which is further added up by the burden
of oxidative stress and protease-antiprotease imbalance.

PATHOLOGICAL CHANGES
Pathological changes characteristic of COPD are found in the proximal airways, peripheral
airways, lung parenchyma, and pulmonary vasculature. The pathological changes include
chronic inflammation, with increased numbers of specific inflammatory cell types in different
parts of the lung, and structural changes resulting from repeated injury and repair. In general,
the inflammatory and structural changes in the airways increase with disease severity and
persist on smoking cessation.

When inflammatory cells present in proximal airways (trachea, bronchi > 2 mm internal
diameter) are active due to abnormal changes, Macrophages, CD8+ (cytotoxic) T lymphocytes,
few neutrophils or eosinophils cells are actively secreting to normalize the changes. However,
too much secretion of inflammatory cells could lead to structural changes: Goblet cells, enlarged
submucosal glands (both leading to mucus hypersecretion), squamous metaplasia of
epithelium.

Hypersecretion of inflammatory cells to normalize the changes in Peripheral airways

(bronchioles < 2mm i.d.) which include: Macrophages, T lymphocytes (CD8+ > CD4+), B
lymphocytes, lymphoid follicles, fibroblasts, few neutrophils or eosinophils can lead to structural
changes of airway wall thickening, peribronchial fibrosis, luminal inflammatory exudate, airway
narrowing (obstructive bronchiolitis) Increased inflammatory response and exudate correlated
with disease severity.

Pathological changes in Lung parenchyma (respiratory bronchioles and alveoli) leads to

secretion of higher than normal range of inflammatory cells: Macrophages, CD8+ T
lymphocytes. As a result of abnormal secretion there are some structural changes: Alveolar wall
destruction, apoptosis of epithelial and endothelial cells
• Centrilobular emphysema: dilatation and destruction of respiratory bronchioles; most
commonly seen in smokers
• Panacinar emphysema: destruction of alveolar sacs as well as respiratory bronchioles; most
commonly seen in alpha-1 antitrypsin deficiency

When inflammatory cells present in Pulmonary vasculature are active due to abnormal
changes inflammatory cells, Macrophages, T lymphocytes Structural changes are playing role.
Which in return causes structural changes such as thickening of intima, endothelial cell
dysfunction, smooth muscle pulmonary hypertension.

RISK FACTORS

a. Genes- having severe hereditary deficiency of alpha-1- antitrypsin of which an abnormal

protein cannot control nuetrophil elastase that leads to destruction of alveoli. Normally,
elastin imparts elasticity of tissues and its presence allows the lung to function as an
elastic bag. However, the mutation in SERPINA1 gene causes alpha-1-antitrypsin
deficiency. This gene provides instructions for making the alpha-1-antitrypsin, which
protects body from powerful enzyme called neutrophil elastase that is released from
white cells to fight infection but attacks normal tissue. The mutation now in SERPINA1
that leads to deficiency can lead to alveolar destruction due to uncontrolled nuetrophil
elastase. Alpha-1- antitrypsin deficiency may not only cause lung disease but also
cause liver disease.
b. Tobacco Smoke- Cigarette smoking is by far the most commonly encountered risk
factor for COPD. Cigarette smokers have a higher prevalence of respiratory symptoms
and lung function abnormalities, a greater annual rate of decline in FEV1, and a greater
COPD mortality rate than nonsmokers.
c. Occupational Dusts and Chemicals- Occupational exposures are an underappreciated
risk factor for COPD. These exposures include organic and inorganic dusts and
chemical agents and fumes
d. Indoor Air Pollution- Wood, animal dung, crop residues, and coal, typically burned in
open fires or poorly functioning stoves, may lead to very high levels of indoor air
pollution. The evidence that indoor pollution from biomass cooking and heating in poorly
ventilated dwellings is an important risk factor for COPD (especially among women in
developing countries) continues to grow.
e. Lung growth - is related to processes occurring during gestation, birth, and exposures
during childhood. Reduced maximal attained lung function (as measured by spirometry)
may identify individuals who are at increased risk for the development of COPD. Any
factor that affects lung growth during gestation and childhood has the potential for
increasing an individual’s risk of developing COPD
f. Oxidative Stress- lungs are continuously exposed to oxidants generated either
endogenously from phagocytes and other cell types or exogenously from air pollutants
or cigarette smoke. In addition, intracellular oxidants, such as those derived from
 mitochondrial electron transport, are involved in many cellular signaling pathways. Lung
cells are protected against this oxidative challenge by well-developed enzymatic and
nonenzymatic systems. When the balance between oxidants and antioxidants shifts in
favor of the former—i.e., an excess of oxidants and/or a depletion of antioxidants—
oxidative stress occurs. Oxidative stress not only produces direct injurious effects in the
lungs but also activates molecular mechanisms that initiate lung inflammation. Thus, an
imbalance between oxidants and antioxidants is considered to play a role in the
pathogenesis of COPD
g. Infections (viral and bacterial) -may contribute to the pathogenesis and progression of
COPD, and the bacterial colonization associated with airway inflammation, and may also
play a significant role in exacerbations.
h. Nutrition- Malnutrition and weight loss can reduce respiratory muscle strength and
endurance, apparently by reducing both respiratory muscle mass and the strength of the
remaining muscle fibers.
i. Socioeconomic Status-evidence that the risk of developing COPD is inversely related
to socioeconomic status. It is not clear, however, whether this pattern reflects exposures
to indoor and outdoor air pollutants, crowding, poor nutrition, or other factors that are
related to low socioeconomic status.

PATHOPHYSIOLOGY
1. Airflow Limitation and Air Trapping-The extent of inflammation, fibrosis, and luminal
exudates in small airways is correlated with the reduction in FEV1 and FEV1/FVC ratio,
and probably with the accelerated decline in FEV1 characteristic of COPD . This
peripheral airway obstruction progressively traps air during expiration, resulting in
hyperinflation. Although emphysema is more associated with gas exchange
abnormalities than with reduced FEV1, it does contribute to air trapping during
expiration. This is especially so as alveolar attachments to small airways are destroyed
when the disease becomes more severe. Hyperinflation reduces inspiratory capacity
such that functional residual capacity increases, particularly during exercise (when this
abnormality is known as dynamic hyperinflation), and this results in dyspnea and
limitation of exercise capacity. It is now thought that hyperinflation develops early in the
disease and is the main mechanism for exertional dyspnea. Bronchodilators acting on
peripheral airways reduce air trapping, thereby reducing lung volumes and improving
symptoms and exercise capacity.
2. Gas Exchange Abnormalities- result in hypoxemia and hypercapnia, and have several
mechanisms in COPD. In general, gas transfer worsens as the disease progresses. The
severity of emphysema correlates with arterial PO2 and other markers of ventilation-
perfusion (VA/Q) imbalance. Peripheral airway obstruction also results in VA/Q
imbalance, and combines with ventilatory muscle impaired function in severe disease to
reduce ventilation, leading to carbon dioxide retention. The abnormalities in alveolar
ventilation and a reduced pulmonary vascular bed further worsen the VA/Q
abnormalities.
3. Mucus Hypersecretion- resulting in a chronic productive cough, is a feature of chronic
bronchitis and is not necessarily associated with airflow limitation. Conversely, not all
patients with COPD have symptomatic mucus hypersecretion. When present, it is due
to mucous metaplasia with increased numbers of goblet cells and enlarged submucosal
glands in response to chronic airway irritation by cigarette smoke and other noxious
agents. Several mediators and proteases stimulate mucus hypersecretion and many of
 them exert their effects through the activation of epidermal growth factor receptor
(EGFR).
4. Pulmonary Hypertension- Mild to moderate pulmonary hypertension may develop late
in the course of COPD and is due to hypoxic vasoconstriction of small pulmonary
arteries, eventually resulting in structural changes that include intimal hyperplasia and
later smooth muscle hypertrophy/hyperplasia. There is an inflammatory response in
vessels similar to that seen in the airways and evidence for endothelial cell dysfunction.
The loss of the pulmonary capillary bed in emphysema may also contribute to increased
pressure in the pulmonary circulation. Progressive pulmonary hypertension may lead to
right ventricular hypertrophy and eventually to right-side cardiac failure (cor pulmonale).
5. Systemic features -It is increasingly recognized that COPD involves several systemic
features, particularly in patients with severe disease. Cachexia is commonly seen in
patients with severe COPD. There may be a loss of skeletal muscle mass and
weakness as a result of increased apoptosis and/or muscle disuse. Patients with COPD
also have increased likeliness of having osteoporosis, depression and chronic anemia.
Increased concentrations of inflammatory mediators, including TNF-, IL-6, and oxygen-
derived free radicals, may mediate some of these systemic effects. There is an increase
in the risk of cardiovascular diseases, which is correlated with an increase in C-reactive
protein (CRP).

DIAGNOSIS OF COPD

 Symptoms of COPD always include:

1) Cough, 2) Sputum production and 3) Shortness of Breath.
 Risk factors include: Tobacco smoking, Occupation (e.g Coal Worker) and Pollution.
 The diagnosis should be confirmed by SPIROMETRY, the presence of a post-
bronchodilator FEV1/FVC < 0.70 confirms the presence of persistent airflow limitation
and thus of COPD.
 Spirometry is a measure of air flow and lung volumes during a forced expiratory
maneuver from full inspiration. It is also a method of assessing lung function by
measuring the total volume of air the patient can expel from the lungs after a maximal
inhalation.
 Technique for performing spirometry;
 Before performing the forced expiration, tidal (normal) breaths can be taken first,
then a deep breath taken in while still using the mouthpiece, followed by a further
quick, full inspiration.
 Alternatively, a deep breath can be taken in, then the mouth placed tightly around
the mouthpiece before a full expiration is performed.
 The patient can be asked to completely empty their lungs then take in a quick full
inspiration, followed by a full expiration
 The latter technique can be useful in patients who may have achieve a larger
inspiration following expiration.
 For FVC and FEV1, the patient takes a deep breath in, as large as possible, and blows
steadily for as long as possible until there is no air left.
 The measurements to be really concerned in spirometry are:
 FVC – Forced Vital Capacity – full amount of air that can be exhaled with effort
in a complete breath
 FEV1- Forced Expiratory Volume in One Second- the volume of air that can
be forced out in one second after taking a deep breath
 FEV1/FVC ratio- measurement of the amount of air you can forcibly exhale from
your lungs
 When performing spirometry or pulmonary function tests three values are reported:
 Actual
 Predicted- what the patient should have performed based on:
1. Age 2. Height 5. Ethnicity
3. Sex 4. Weight
Each person has a unique characteristic and body composition that’s why
measurements can be different when performing spirometry.
 %Predicted- a comparison of the actual value to the predicted value

Criteria for Normal Post- Bronchodilator Spirometry

 For normal post- Bronchodilator Spirometry, the FEV1 and FVC should be greater or
equal to 80% than %predicted and the FEV1/ FVC ratio is greater than 0.7- 0.8L,
depending on age.
 Values for FEV1 and and FVC are measured in liters and are also expressed as a
percentage of the predicted values for that individual.
 The ratio of FEV1/FVC is normally between 0.7 and 0.8. Values below 0.7 are a marker
of airway obstruction, except in older adults where values 0.65 – 0.7 may be normal.
 It is important to know this values because this will serve as your guide in determining
what your patient underlying issues are.
Normal Spirogram Pattern

 In a patient with normal lung function, the volume- time curve should rise rapidly and
smoothly and plateau within 3-4 seconds. With increasing degrees of airway obstruction
it takes longer to blow out the air- up to 15 seconds- and the upward slope of the
spirogram is much less steep.

Obstructive Pattern
 FEV1:<80% predicted
 FVC: can be normal or reduced, usually to a lesser degree than FEV1
 FEV1/FVC:<70% predicted

 In patient with obstructive lung function, we can see that the volume –time curve
decreases as to with normal and this is due to the weakness of respiratory muscles to
function properly, thus the patient having a hard time to blow air due to obstruction
present in his/her lungs.
 ASSESSMENT OF COPD

 Assess degree of airflow limitation, its impact on the patient’s health status and the risk
of future events (such as exacerbations, hospital admission or death)
 To achieve these goals, COPD assessment must consider the following aspects:
 The presence and severity of the spirometric abnormality
 Current nature and magnitude of the patient’s symptoms
 Exacerbation history and future risk
 Presence of comorbidities

Diagnosis of Airway Obstruction

The spirometric criterion required for a diagnosis of COPD is an FEV1/FVC ratio

below 0.7 after bronchodilator.

GOLD SPIROMETRIC CRITERIA FOR COPD SEVERITY

I: Mild COPD  FEV1/FVC < 0.7 At this stage, the patient
 FEV1 ≥ 80% may not be aware that
their lung function is
predicted
abnormal.
II: Moderate COPD  FEV1/FVC <0.7 Symptoms usually
 50% ≤ FEV1 < progress at this stage, with
shortness of breath
80% predicted
typically developing on
exertion.
III: Severe COPD  FEV1/FVC < 0.7 Shortness of breath
 30% ≤FEV1 < typically worsens at this
stage and often limits
50% predicted
patients’ daily activities.
Exacerbations are
especially seen beginning
at this stage.
IV: Very Severe COPD  FEV1/FVC < 0.7 At this stage, quality of life
 FEV1 < 30% is very appreciably
impaired and
predicted or
exacerbations may be life-
 FEV1 < 50% threatening.
predicted plus
chronic
respiratory failure

 Assessment of symptoms
In the past, COPD was viewed as a disease largely characterize by breathlessness. A
simple measure of breathlessness such as the Modified British Medical Research
Council (mMRC) Questionnaire was consideres adequate for assessment of symptoms,
as the mMRC relates well to other measures of health status and predicts future
mortality risk. However, it is now recognized that COPD impacts patients beyond
 dyspnea. For this reason, a comprehensive assessment of symptoms is recommended
using measures such as the COPD Assessment Test and the COPD Control
Questionnaire.
Combined Assessment

 Modified MRC Dyspnea Scale

 CAT Assessment
 Refined ABCD Assessment tool

The refined ABCD Assessment tool is used to understand the impact of COPD on an
individual patient’s symptomatic assessment with the patients spirometric classification
and/or risk of exacerbation. The patient should undergo spirometry to determine the
severity of airflow limitation. They should also undergo assessment of either dyspnea
using mMRC or symptoms using CAT. Finally, their history of moderate and severe
exacerbation should be recorded.

The combined assessment for COPD is used in all of the patients to categorized
the level or severity for his/her condition also there is a different approach of
medication in each category.
PHARMACOLOGICAL TREATMENT
1. Initial treatment

 Rescue short-acting bronchodilators should be prescribed to all patients for immediate

symptom relief

GOLD recommendations for initial pharmacological therapy based on GOLD group

Group A:

Group A patients should be offered bronchodilator treatment based on its effect on

breathlessness. This can be either a short- or a long-acting bronchodilator and this should be
continued if benefit is documented .

Under this group are patients with low risk and low symptom burden and the severity of airflow
limitation is mild to moderate. Wherein the use of bronchodilators may produce smooth muscle
relaxation resulting in improved airflow obstruction, improved symptoms and decreasein the
frequnecy and severity of exacerbations, but they do not enhance survival. (e.g CAT <10)

Group B:

Initial therapy should consist of a long-acting bronchodilator for patients with severe
breathlessness initial therapy with two bronchodilators may be considered.

Under this group are patients with low risk and higher symptom burden and the severity of
airflow limitation is mild to moderate.wherein the use of LABA or LAMA (long acting
brochodilator) significantly improve lung function, dyspnea, health status and reduce
exacerbation rates (e.g. CAT ≥10)

Group C:

Initial therapy should consist of a LAMA.

Under this group are patients with high risk and low symptom burden and the severity of airflow
limitation is severe to very severe.Wherein LAMA have greater effect on exacerbation
reduction.(e.g CAT <10).

Group D:

Under this group are patients with high risk and higher symptom burden and the severity of
airflow limitation is severe to very severe. (e.g CAT >20)

Wherein general, therapy can be started with a LAMA as it has effects on both breathlessness
and exacerbations for patients with more severe symptoms, especially driven by greater
dyspnea and/or exercise limitation, LAMA/LABA may be chosen as initial treatment in some
patients, initial therapy with LABA/ICS may be the first choice; this treatment has the greatest
likelihood of reducing exacerbations ICS may cause side-effects such as pneumonia, so should
be used as initial therapy only after the possible clinical benefits versus risks have been
considered
2. Management cycle

GOLD recommendations for the ongoing management of COPD: review, assess, adjust

Figure 3: GOLD COPD management cycle

This is needed to know whether the treatment goals (e.g. reduction of symptoms and future risk
of exacerbations) have been achieved and if not and also to know whether there are any
correctable barriers to successful treatment such as poor inhaler technique or poor adherence.

*escalation and de-escalation of pharmacotherapy pertains if the response to initial therapy is

suffficient, treatment should be continued. However, if the patient is continuing to have
problems, GOLD has introduced a new algorithm providing recommendtions on how to modify
the therapy to deal with persistent dyspnea, continuing exacerbations or both.
3. Follow-up pharmacological management

An algorithm depicting the GOLD recommendations for adjusting or escalating treatment based
on dyspnoea and exacerbations

Figure 4: Follow-up pharmacological treatment

Dyspnoea

If a patient continues to experience dyspnoea while on LABA+ICS therapy, GOLD recommends

escalating their treatment to LABA+LAMA+ICS. If a patient is taking LAMA monotherapy and
still experiences breathlessness, their treatment should be escalated to dual bronchodilator
therapy with LABA+LAMA. If a patient is currently on LABA+LAMA and is still breathless, GOLD
recommends considering changing to a different inhaler device or different molecules, as well
as undertaking investigations to look for other causes of breathlessness such as heart failure or
atrial fibrillation.1

Exacerbation

For patients with persistent exacerbations on LABA or LAMA monotherapy, GOLD recommends
escalating to either LABA+LAMA or LABA+ICS depending on the patient’s blood eosinophil
count. Escalation to LABA+ICS therapy is recommended if the patient’s blood eosinophil count
is:

≥300 cells/µl or

≥100 cells/µl and the patient has had at least two moderate exacerbations (i.e. requiring
treatment with antibiotics and/or prednisolone) or one severe exacerbation (i.e. hospitalised).
 For patients who do not fit into the above criteria, escalation to LABA+LAMA is recommended
because there is very little likelihood of benefit from treatment with ICS in this group, and there
is evidence that they may be at greater risk of developing pneumonia. If the patient is already
on LABA+ICS and is continuing to have exacerbations then the recommended escalation is to
triple therapy with LABA+LAMA+ICS.

De-escalation of treatment

De-escalation strategies are currently limited to patients who are taking ICS. De-escalation of
ICS can be considered if:

 The patient experiences pneumonia there was an inappropriate indication for the ICS
when they were first prescribedthere was a lack of response (i.e. no change in the
frequency of exacerbations following the introduction of ICS therapy).

 De-escalation may also be considered in patients with COPD receiving treatment who
return with resolution of some symptoms that subsequently may require less therapy.
For patients who have had their treatment de-escalated, it is important to monitor them
under close medical supervision to ensure they do not deteriorate as a result of the
changes
MANAGEMENT OF STABLE COPD
We are managing the COPD to retain from further exacerbations.

1. PULMONARY REHABILITATION

 Most effective therapeutic strategy to improve shortness of breath, health status

and exercise tolerance.
 Benefits: reduce symptoms; reduces hospitalizations among patients who have
had a recent exacerbations; improve quality of life; and increase physical and
emotional participation in everyday activities.
Components:

a. Exercise Training
 Type and amount of exercise will depend and should be further determined by
the patient’s abilities and preferences. Always take into consideration that
exercises should start at a level that patient can handle. Amount of time the
patient exercise will be increased in time and the level of difficulty will change
based on the patient ability.
 Exercise sessions begin with stretching exercises or warm-ups, followed by
exercise for arms and legs.
 Usually patients will do both exercises to build their strength and exercises to
build their endurance.
 Activities: Treadmill, Level Walking, Walking Test, Rowing, Cycle Ergometer,
Stair Climbing, Arm Ergometer, Light Weights, Pulleys, Elastic Bands
 To build strength, patients may use weights and lifting devices.
 And to build endurance, activities might include walking on a treadmill or in a
corridor and/or using a stationary cycle.
 A variety of continuous cycle ergometer protocols are imposed every 30 seconds
to 4 minutes.
 The 12- minute walking test requires that the patient cover as much distance as
possible in a measured level corridor, resting only if necessary. The 2- or 6-
minute variation of the 12- minute walking test is useful for those patients unable
to complete the latter.
 Using treadmill will achieve the symptom - limiting end point in 10 to 15 minutes.
 Benefits: increased endurance and strength; increased maximum oxygen
consumption; increased perception of quality of life/sense of well-being; and build
energy levels so that patient can perform more activities without getting tired and
reduced intensity of breathlessness.
b. Nutrition Counseling
 Patients with advanced COPD are often noticed to have decreased body
weight. Decreased BMI is associated with increased mortality because it is
associated with poor exercise capacity and pulmonary status. 30% of severe
COPD patients have protein-calorie malnutrition, so nutritional
supplementations should be considered.
  COPD patients are usually advised to take small frequent meals because this
can reduced breathlessness.
 Food that are beneficial for COPD patients: High-fiber foods, high-protein foods,
fresh fruits and vegetables and food high in vitamins and minerals.
 Benefits: Maintaining a healthy body weight; increasing energy levels; improving
muscle strength; reducing breathlessness; and lowering the risk of respiratory
infections.

c. Education
 Respiratory therapists will identify and explain to the patient about the physical
and psychosocial changes related to chronic pulmonary disease to set realistic
individual goals.
 RT will educate and help the patients in developing skills in self-care techniques
for optimal symptom management and overall health maintenance.
 Content of Pulmonary Rehabilitation education: Breathing retraining, stress and
relaxation, medications, smoking cessation, and oxygen therapy.
 Patients will learn new ways to breathe during stressful times and while being
active and they will practice breathing techniques during exercise sessions.
 Patients will also learn about their medications; what the medications do and how
to properly use their inhalers.
 Part of the program also educates the patients about oxygen therapy; they will be
tested at rest and with exercise to see if oxygen may help them.
 And, if the patients’ smoke, the program will provide support for them to stop or
guide them to a program that can help you to stop smoking- smoking cessation.

2. OXYGEN THERAPY

 One of the non-pharmacologic treatments for patients suffering COPD; mainly

with patients with Stage IV: Very Severe COPD.
 Oxygen therapy can benefit COPD patients with severe resting hypoxemia which
defines as PaO2 that is < or equal to 55 mmHg with signs of right-side strain or
polycythemia.
 Goal to increase the PaO2 from 55 mmHg to 80 mmHg and SaO2 from <88% to
90%.
 According to GOLD Standard, the long-term administration of oxygen therapy to
patients with chronic respiratory failure has been shown to increase the survival
rate of patients with severe resting hypoxemia.
 Long-term oxygen therapy should be used at least 15 hours a day with periods of
interruptions, as possible. But if you want to get the maximal benefit of this
therapy, patient can use it 24 hours a day.
 Breathlessness in COPD patients may be relieved with oxygen therapy.
 When a patient is placed to a long-term oxygen therapy, he/she should be
monitored and re-evaluated after 60-90 days.
 When a COPD patient is exposed to too much oxygen over a long period of time,
there will be damage inside the lungs, and the patient can also feel headache,
sleepiness or confusion, increased coughing, and shortness of breath as the
airways are irritated.
  One more benefit of oxygen therapy to patients with COPD is, it slows down or
even prevents right-side heart failure which then can lead to more complications.
 Oxygen is usually given to hypercapnic patients via venturi facemask (4L/min)
with no more than 28% during exacerbation. If the patient is not hypercapnic,
keep the oxygen saturation >90%.
 But nasal cannulas/nasal prongs are more preferred by the patients because it
allows them to eat, drink, and speak and is more comfortable to wear when
receiving oxygen for a long time.
 Nasal prongs are used with 2L/min that aims for are 88-92% are used for
patients with history of COPD and used after checking the arterial blood gas of
the patients.
 Healthcare professionals, especially respiratory therapists should be aware that
inappropriate oxygen therapy in patients with COPD may lead to respiratory
depression.

Oxygen Modalities:
These are some of the examples of the oxygen modalities for effective therapy.

1. Oxygen Concentrators – used to concentrate the air from the ambient air by removing
the nitrogen to have a product that is oxygen-enriched in the gas stream and will be
inhaled by the patient. These oxygen concentrators are safe but certain precautions are
still needed to be monitored to ensure the safety of the patient. Usually, these oxygen
concentrators are used in the home care and is effective in providing continuing oxygen
on the patient, thus, cost-efficient.

2. Portable Oxygen Concentrators – are generated by a 10-pound battery that will allow
the patient to move whenever he want to go; the patient can also use these when
exercising and sleeping.

3. Oxygen Conserving Devices – it became the standard portable oxygen device

because it’s lightweight and has a long-lasting ambulatory oxygen. The main thing that
this device can do is to eliminate the wastes from the oxygen when the patient is not
breathing.

VENTILATORY SUPPORT

a. Non-Invasive
 NIV may be used as an adjunctive therapy to Pulmonary Rehabilitation that
unloads the respiratory muscles with the aim to increase the intensity of exercise
training in selected patients with stable chronic respiratory disease who have a
suboptimal response to exercise. The benefits appear to be more marked in
patients with stable COPD, and higher tolerated positive pressure may lead to
greater improvements, with improved exercise performance and reduced
dyspnea.
Other modalities for non-invasive ventilatory support:

- Continuous Positive Airway Pressure (CPAP) - Add positive pressure to both

inspiration and expiration
 - Positive End Expiratory Pressure (PEEP) - Add positive pressure to expiration only.
- Intermittent Positive Pressure Breathing (IPPB) - Add positive pressure to
inspiration only. -The above modalities uses positive pressure to minimizes respiratory
efforts (let the patient rest for a while), enhancing the lung expansion leading to less
mechanical ventilation disadvantage. -Positive pressure reduces air trapping in
obstructive lung disease by improving the distribution of ventilation, decreasing the FRC.
-Positive pressure allow same degree of physiologic ventilation.
NOTE: - Applying positive pressure result in stress patient accepting and being
comfortable with ventilatory pattern they could not tolerate during sportaneous breathing.
-In treating COPD, CPAP reduces the load of inspiratory muscle,improves their
efficiency and decreases the energy cost of breathing (emphysema) -PEP was originally
developed to mobolized secretions (bronchitis)

b. Combination of Non-Invasive Ventilation and Oxygen Therapy

 Long-term oxygen therapy (LTOT) and non-invasive ventilation (NIV) are
potentially valuable therapeutic options, especially in COPD patients with severe
lung hyperinflation and exercise-induced desaturation noticed during exercise
training as part of a comprehensive PR programme. The addition of nasal
positive pressure ventilation to LTOT in hypercapnic patients has been shown to
improve arterial blood gases, dyspnea, quality of life and survival. Oxygen sup-
plementation in moderate to severe COPD patients can acutely increase
exercise capacity, the amount of training they can undertake, and thus the
benefits of PR. Alleviation at a certain extend of ventilatory limitation will allow
greater cardiac and muscular stress, with further beneficial effects on stroke
volume and oxygen extraction. SpO2 should be > 88% during exercise; if SpO2
is ≤ 88% while breathing room air, supplemental oxygen should be used to
maintain SpO2 at > 88%.

4. SURGICAL TREATMENT

a. Bullectomy
 Bullae= enlarged, damaged air sacs.
 These bullae can press down on the surrounding parts of the lungs and can keep
blood from flowing to the healthier sections of the lungs, which reduces the lungs’
ability to absorb oxygen. This can worsen COPD symptoms, such as
breathlessness.
 When they are removed, it alleviate or reduced local symptoms that is usual
indication and it can help the healthier parts of the lungs to start working better.
b. Lung Volume Reduction Surgery (LVRS)
 LVRS is a procedure that is designed to help the patients breathe easier when
the lungs have been damaged by severe COPD.
 LVRS is not recommended treatment to all patients with COPD. It is usually and
successfully done in patients who have severe lung damage (emphysema),
particularly part of upper lung and are younger than 75 years old.
 Common complications: air leaks (air continually escapes the lung into the chest
cavity), pneumonia, blood clots, and the need to have for a breathing machine.
Less common complications: wound infection, heart attack, irregular heart
rhythm, and death.
 c. Lung Transplantation
 Remains the ultimate treatment option for some well selected patients with end
stage pulmonary diseases such as COPD (emphysema).
 A patient can be a valuable candidate for lung transplantation if his end-stage
disease can no longer be treated, resulting in a low 2-y survival, provided the
patient is within a certain defined age window, and there are no current contra-
indications for a lung transplantation.
 After initial contact with the transplant center, the patients will undergo a
pretransplant screening to identify him/her as a good candidate, and to identify
possible risk factors that need to be solved before putting the patient on the
waiting list. These risk factors include diabetes, arterial hypertension, body
weight, coronary artery disease, renal insufficiency.
 Guideline for lung transplant: COPD patients are considered potentially to be in
the transplant window if they meet the following criteria (16, 17): FEV1 < 25% of
predicted (without reversibility) and/or PaCO2 ⩾ 55 mm Hg (7.3 kPa) and/or
elevated pulmonary artery pressures with progressive deterioration, e.g., cor
pulmonale.
 Aims of lung transplantation are on the one hand to improve survival and also to
improve Quality of Life (QOL). Therefore, patients should be well selected and at
present it is very well known that older patients (>65 y) have a worse prognosis,
which has clearly been demonstrated in general but also for some indications
such as IPF. Indeed according to the latest Registry report of the International
Society for Heart and lung Transplantation.
 Transplantation not only improves the survival and the QOL, it also leads to
several negative effects, such as the occurrence of arterial hypertension,
hyperlipidemia, diabetes (calcineurin-induced), renal insufficiency (abnormal
creatinine level in up to 36% of patients within 5 y)
 The current mortality causes are chronic lung allograft dysfunction (with chronic
rejection being the most important one), infections and an increasing prevalence
of cancer.
 The emergence of bronchial carcinoma, which affects up to 10% of the native
lung of patients who underwent a single lung transplantation, led to
systematically diverge from single to double lung transplantation. This may avoid
the occurrence of a native lung cancer, but also infectious problems of the native
lung (especially fungal infections), which have a high mortality rate.
 Despite the occurrence of a whole lot of metabolic negative effects, mainly due to
the current drug treatment.
 NOTE: In case of acute exacerbations, surgery should be postponed.

MANAGEMENT OF EXACERBATIONS
Goal: To reduce the severity of the disease; to prevent the reoccurrence of the future
exacerbation/s.

Most Common Cause:

Respiratory Tract Infection

 Exacerbations are usually caused by a viral or bacterial lung infection, but they
may also be triggered by the things or situations that make it difficult to breathe,
such as smoking or being exposed to smoke or air pollution.
 COPD patients have difficulty clearing their lungs of bacteria, dusts and other
pollutants. This makes them at risk for lung infections that may cause further
damage to the lungs.

1. VENTILATORY SUPPORT
Patients with COPD suffer from chronic inflammation of small airways and lung parenchyma,
resulting in obstructive bronchiolitis, parenchymal destruction, and emphysema. Increased
airway resistance and decreased elastic recoil lead to limited airflow and an impaired ability of
the airways to remain open at the end of expiration. In turn, the collapse of airways at the end of
expiration results in incomplete expiration, higher residual end-expiratory volume, hyperinflation,
and auto–positive end-expiratory pressure (auto-PEEP). Progression of chronic inflammation
and parenchymal destruction result in impaired gas exchange with hypoxemia and hypercapnia.
In case of the need for ventilatory support for acute exacerbations, the use of noninvasive
mechanical ventilation reduces mortality in patients with COPD.

Goal: To improve pulmonary gas exchange and to rest compromised respiratory muscles.

a. Non Invasive
Noninvasive mechanical ventilation provides a significant reduction in endotracheal
intubation and thereby its complications (eg, ventilator-associated pneumonia, tracheal and
laryngeal complications) if considered early in the course of the disease.
Expiratory positive airway pressure applied offsets intrinsic PEEP resulting from expiratory
airflow obstruction. Inspiratory positive airway pressure augments tidal volume for any given
respiratory effort leading to less mechanical disadvantage.

b. Invasive
Although non-invasive ventilatory support is now considered the first choice for the
treatment of selected patients experiencing COPD exacerbations, there are some patients for
whom non-invasive may not be suitable owing to the severity of their conditions.

Major criteria (any one of the following):

 Respiratory arrest
 Loss of consciousness
 Psychomotor agitation requiring sedation
  Hemodynamic instability with a systolic blood pressure less than 70 or greater than 180
mmHg
 Heart rate less than 50 beats/min with loss of alertness
 Gasping for airMinor criteria (any two of the following)

Respiratory rate >35 breath/min

 Worsening acidemia or pH <7.25

 PaO2 less than 40 mm Hg or PaO2/FiO2 less than 200 mm Hg despite oxygen
 Decreasing level of consciousness

Conclusion: Accomplishing gas exchange and alleviating respiratory muscle fatigue may be
accomplished using any mode available on the ventilator, but the choice may vary with the
status of the patient with COPD. For the obtunded or postoperative patient, pressure-support
ventilation may not be the first choice until the patient respiratory drive returns. Therefore, either
assist-control or synchronized intermittent mandatory ventilation, with either volume or pressure
targets, should be used. High inspiratory flow rates are preferred to reduce the inspiratory–
expiratory ratio, thus allowing more time for expiration.