SEMINAR ON

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

SUBMITTED TO: SUBMITTED BY:

MRS.BHAGYAMMA MADAM N.SONIYA

ASSI.PROFESSOR MSC (N) 2nd yr

GOVERNMENT COLLEGE OF NURSING

SOMAJIGUDA.HYDERABAD
OBJECTIVES

GENERAL OBJECTIVES:

By the end of the seminar students will be able to know about Chronic obstructive
pulmonary disease (COPD) gain in depth knowledge and how to manage the
patients .

SPECIFIC OBJECTIVES : by the end of the class,the students will be able to

 Define Chronic obstructive pulmonary disease (COPD)

 Enumerate the Incidence of Chronic obstructive pulmonary disease
(COPD)
 Explain briefly about Anatomy and Physiology of respiratory system
 enlist the stages of COPD
 list down the causes and risk factors of Chronic obstructive
pulmonary disease (COPD)
 discuss the pathophysiology
 Discuss about signs and symptoms of COPD
 Explain in detail about the diagnostic investigations of COPD
 Describe about Prevention of disease
 Describe about medical and surgical management of COPD
 Enumerate about nursing management of COPD
 Enumarate the prognosis of COPD
 STUDENT PROFILE

Name of the student : N.soniya

Class : Msc(N) II year

Subject : Medical Surgical Nursing

Topic ; Chronic obstructive pulmonary disease

Group : 07

Place : Government college Of Nursing

Date and Time : 02-6-2021

Method of teaching : Lecture cum Discussion

AV aids : chart on diagnostic evaluation

Flash cards on risk factors of COPD

Chart on clinical manifestation of COPD

Guides : Mrs.Bhagyamma madam

Assistant professor
 Chronic Obstructive Pulmonary Disease (COPD)

INTRODUCTION

Chronic Obstructive Pulmonary Disease (COPD) represents an important public

health challenge and is a major cause of chronic morbidity and mortality
throughout the world. Chronic obstructive pulmonary disease (COPD) refers to a
group of lung diseases that block airflow and make breathing difficult.

Emphysema and chronic bronchitis are the two most common conditions that make
up COPD. Chronic bronchitis is an inflammation of the lining of your bronchial
tubes, which carry air to and from your lungs. Emphysema occurs when the air
sacs (alveoli) at the end of the smallest air passages (bronchioles) in the lungs are
gradually destroyed.

Damage to your lungs from COPD can't be reversed, but treatment can help control
symptoms and minimize further damage.

INCIDENC

GLOBALLY

COPD is currently the fourth leading cause of death in the world1 but is projected
to be the 3 rd leading cause of death by 2020. More than 3 million people died of
COPD in 2012 accounting for 6% of all deaths globally. Globally, the COPD
burden is projected to increase in coming decades because of continued exposure
to COPD risk factors and aging of the population.
INDIA

Crude estimates suggest there are 30 million COPD patients in India. India
contributes the highest COPD mortality in the world COPD Burden in India

TELANGANA

Chronic obstructive pulmonary disease (COPD) is one of India’s biggest killers

and Telangana feels its strain acutely. In 2020, there were 19,000 deaths from
COPD in Telangana out of 8.4 lakh deaths nationwide. 

DEFINITION

COPD, a common preventable and treatable disease, is characterized by persistent

airflow limitation that is usually progressive and associated with an enhanced
chronic inflammatory response in the airways and the lung to noxious particles or
gases

-luwis

Chronic obstructive pulmonary disease (COPD) is characterized by chronic airflow

limitation and a range of pathological changes in the lung, some significant extra-
pulmonary effects, and important comorbidities which may contribute to the
severity of the disease in individual patients

-brunner&suddarth

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung

disease that causes obstructed airflow from the lungs.

-JOICE M BLACK
ANATOMY AND PHYSIOLOGY OF RESPIRATYORY SYSTEM

The Lungs and Respiratory System allow us to breathe.

 They bring oxygen into our bodies (called inspiration, or inhalation)

and send carbon dioxide out (called expiration, or exhalation).
 The respiratory system of animals is crucial for the life as it allows the
exchange of gases between an organism and the environment
 This exchange of oxygen and carbon dioxide is called respiration.
 The average human exhales 0.35 L of water each day. The amount
varies with air temperature, relative humidity, and level of activity, so
the range is probably 0.3 L to 0.45 L per day.
 Dysfunction of the respiratory system ultimately leads to hypoxia.
There are four classifications of hypoxia etiology: hypoventilation,
right-to-left-shunt, V/Q mismatch, and diffusion limitations

PARTS OF THE RESPIRATORY SYSTEM

Nose and Mouth :Air enters the respiratory system through the nose or the
mouth. If it goes in the nostrils, the air is warmed and humidified. Cilia (tiny
hairs) protect the nasal passageways and other parts of the respiratory tract,
filtering out dust and other particles that enter the nose through the breathed
air.

Pharynx (throat): The nasal cavity and the mouth openings meet at the
pharynx at the back of the nose and mouth. The pharynx is part of the
digestive system as well as the respiratory system because it carries both
food and air. At the bottom of the pharynx, this pathway divides in two, the
esophagus, which leads to the stomach and the other for air. The epiglottis, a
small flap of tissue, covers the air-only passage when we swallow, keeping
food and liquid from going into the lungs.

The Larynx (voice box): Top part of Trachea. This short tube contains a
pair of vocal cords, which vibrate to make sounds.
Tracheobronchial tree: Network of alveoli, bronchioles, bronchi and
trachea.

Trachea:  The walls of the trachea are strengthened by stiff rings of

cartilage to keep it open. The trachea is also lined with cilia, which sweep
fluids and foreign particles out of the airway so that they stay out of the
lungs. These 2 procedure occur at the trachea 1. Endotracheal tube
(intubation) 2.Tracheostomy.

Carina: The angle made between the two primary bronchi when they
diverge at the tracheal bifurcation; it is richly innervated with sensory nerve
endings to respond to the arrival of any aspirated material by initiating a
cough reflex; it may be visualised as a ridge within the bronchial tree when
using a bronchoscope

Bronchi: At its bottom end, the trachea divides into left and right air tubes
called bronchi, which connect to the lungs. Within the lungs, the bronchi
branch into smaller bronchi and even smaller tubes called bronchioles.

Lungs: The functional units of respiration and are key to survival (each lung
weighing approximately 1.1 kg). The structure of the lung is well suited for
efficient exchange of respiratory gases.
  Through the airway and vascular trees, fresh gases and venous blood are
delivered to and removed from a large alveolar capillary surface area.
 In an adult, inhaled air enters the trachea and is delivered to the alveoli
with a surface area of ∼140 m2, roughly the size of a tennis court.
 Similarly, the pulmonary vascular tree begins as the main pulmonary
artery and repeatedly bifurcates into arterioles and capillaries that cover
85–95% of the alveolar surface.
 An exceptionally thin membrane of only 1 μm separates the alveolar gas
and blood compartments, allowing gases to diffuse rapidly between them.
 Due to the relatively large blood volume within the alveolar capillaries,
blood flow slows and the transit time for blood increases, normally to
0.25–0.75 s, allowing more time for gas exchange.
 The fantastic design that allows this gas exchange within the thoracic
cavity has been highlighted by comparing this engineering feat to that of
folding a letter so that it fits into a thimble
 Lungs are affected by a wide range of pathology that results in a diverse
range of illnesses

Alveoli: Bronchioles end in tiny air sacs called alveoli, where the exchange
of oxygen and carbon dioxide actually takes place. Each person has hundreds of
millions of alveoli in their lungs.
 The Thorax houses the bronchial tree, lungs, heart, and other structures.

The top and sides of the thorax are formed by the ribs and attached muscles,
and the bottom is formed by the diaphragm.

The chest walls form a protective cage around the lungs and other contents
of the chest cavity
 STAGES OF COPD

Stage I:

Mild COPD - Characterized by mild airflow limitation (FEV1/FVC < 0.70; FEV1
≥ 80% predicted). Symptoms of chronic cough and sputum production may be
present, but not always. At this stage, the individual is usually unaware that his or
her lung function is abnormal.

Stage II:

Moderate COPD - Characterized by worsening airflow limitation (FEV1/FVC <

0.70; 50% ≤ FEV1 < 80% predicted), with shortness of breath typically developing
on exertion and cough and sputum production sometimes also present. This is the
stage at which patients typically seek medical attention because of chronic
respiratory symptoms or an exacerbation of their disease.

Stage III:

Severe COPD - Characterized by further worsening of airflow limitation

(FEV1/FVC < 0.70; 30% ≤ FEV1 < 50% predicted), greater shortness of breath,
reduced exercise capacity, fatigue, and repeated exacerbations that almost always
have an impact on patients’ quality of life.

Stage IV:

Very Severe COPD - Characterized by severe airflow limitation (FEV1/FVC <

0.70; FEV1 < 30% predicted or FEV1 < 50% predicted plus the presence of
chronic respiratory failure). Respiratory failure is defined as an arterial partial
pressure of O2 (PaO2) less than 8.0 kPa (60 mm Hg), with or without arterial
partial pressure of CO2 (PaCO2) greater than 6.7 kPa (50 mm Hg) while breathing
air at sea level. Respiratory failure may also lead to effects on the heart such as cor
pulmonale (right heart failure). Clinical signs of cor pulmonale include elevation of
the jugular venous pressure and pitting ankle edema. Patients may have

ETIOLOGY

Emphysema

Inflammation destroys these fragile walls of the air sacs, causing them to lose their
elasticity. As a result, the bronchioles collapse, and air becomes trapped in the air
sacs, which overstretches them and interferes with ability to exhale
(hyperinflation). In time, this overstretching may cause several air sacs to rupture,
forming one larger air space instead of many small ones. Because the larger, less-
elastic sacs aren't able to force air completely out of lungs when exhale, patient
breathes harder to take in enough oxygen and to eliminate carbon dioxide.

Chronic bronchitis - may increase the frequency of total and severe

exacerbations.factors related to low socioeconomic status.

Asthma and airway hyper-reactivity - asthma may be a risk factor for the
development

Alpha-1-antitrypsin deficiency

In about 1 percent of people with COPD, the disease results from a genetic
disorder that causes low levels of a protein called alpha-1-antitrypsin. Alpha-1-
antitrypsin (AAt) is made in the liver and secreted into the bloodstream to help
protect the lungs. Alpha-1-antitrypsin deficiency can affect the liver as well as the
lungs. Damage to the liver can occur in infants and children, not just adults with
long smoking histories. For adults with COPD related to AAt deficiency, treatment
options are the same as those for people with more common types of COPD. Some
people can be treated by replacing the missing AAt protein, which may prevent
further damage to the lungs.

Risk factors

Non modifiable risk factors

Age.

Although the lung damage that occurs in emphysema develops gradually, most
people with tobacco-related emphysema begin to experience symptoms of the
disease between the ages of 50 and 60

gender - aging and female gender increase COPD risk.

hereditary

At deficiency is a hereditary condition that occurs when patient inherits two

defective genes, one from each parent. Although severe AAt deficiency is rare,
millions of people carry a single defective AAt gene
Modifiable risk factors

smoking

Cigarette smoke is by far the most common cause of emphysema. The damage
begins when tobacco smoke temporarily paralyzes the microscopic hairs (cilia) that
line bronchial tubes. Normally, these hairs sweep irritants and germs out of
airways. But when smoke interferes with this sweeping movement, irritants remain
in bronchial tubes and infiltrate the alveoli, inflaming the tissue and eventually
breaking down elastic fibers
protein deficiency

plays a role In a small percentage of people, emphysema results from low levels of
a protein called alpha-1-antitrypsin (AAt), which protects the elastic structures in
lungs from the destructive effects of certain enzymes. A lack of AAt can lead to
progressive lung damage that eventually results in emphysema.

Occupational exposure

to chemical fumes . From certain chemicals or dust from grain, cotton, wood or
mining products may lead to emphysema. The risk is even greater if patient
smokes. Exposure to indoor and outdoor pollution . Breathing indoor pollutants
such as fumes from heating fuel as well as outdoor pollutants – car exhaust, for
instance – increases the risk of emphysema.

Tobacco smoke - including cigarette, pipe, cigar, water-pipe and other types of
tobacco smoking popular in many countries, as well as environmental tobacco
smoke(ETS)

Indoor air pollution - from biomass fuel used for cooking and heating in poorly
vented dwellings, a risk factor that particularly affects women in developing
countries

Occupational exposures - including organic and inorganic dusts, chemical agents

and fumes, are under-appreciated risk factors for COPD.

Outdoor air pollution - also contributes to the lungs’ total burden of inhaled
particles,although it appears to have a relatively small effect in causing COPD.
Lung growth and development - any factor that affects lung growth during
gestation and childhood (low birth weight, respiratory infections, etc.) has the
potential to increase an individual’s risk of developing COPD.

Socioeconomic status - there is strong evidence that the risk of developing COPD
is inversely related to socioeconomic status.10 It is not clear, however, whether
this pattern reflects exposures to indoor and outdoor air pollutants, crowding, poor
nutrition, infections, or other

of airflow limitation and COPD.

Infections

Infections (viral and bacterial) may contribute to the pathogenesis and progression
of COPD49, and the bacterial colonization associated with airway inflammation50,
and may also play a significant role in exacerbations51. A history of severe
childhood respiratory infection has been associated with reduced lung function and
increased respiratory symptoms in adulthood38,41,52. There are several possible
explanations for this association (which are not mutually exclusive). There may be
an increased diagnosis of severe infections in children who have underlying airway
hyperresponsiveness, itself considered a risk factor for COPD. Susceptibility to
viral infections may be related to another factor, such as birth weight, that is
related to COPD. HIV infection has been shown to accelerate the onset of
smoking-related emphysema; HIV-induced pulmonary inflammation may play a
role in this process5

Oxidative Stress The lungs are continuously exposed to oxidants generated either
endogenously from phagocytes and other cell types or exogenously from air
pollutants or cigarette smoke
 PATHOPHYSIOLOGY

Abnormal inflammatory response of the lungs due to toxic gases

Responseoccurs in the airways ,parenchyma & pulmonary vasculature

Narrowing of the airway takes place

Destruction of parenchyma leads to emphysema.

Destruction of lung parenchyma leads to an imbalance of

proteinases/antiproteinases.(this proteinases inhibitors prevents the destructive

process)

Pulmonary vascularchanges Thickening of vessels Collagen deposit Destruction of

capillary beds.

Mucus hypersecretion(cilia dysfunction, airflowlimitation ,corpulmonale(RVF)

CLINICAL MANIFESTATIONS
Chronic cough

A chronic cough is often the first symptom to develop. Early on it may just occur
occasionally or may not result in sputum. When a cough persists for more than
three months each year for at least two years, in combination
with sputum production and without another explanation, it is by definition chronic
bronchitis. Chronic bronchitis can occur before the restricted airflow and thus
COPD fully develops. The amount of sputum produced can change over hours to
days. In some cases, the cough may not be present or may only occur occasionally
and may not be productive

Shortness of breath

Shortness of breath is a common symptom and is often the most

distressing.  Typically, the shortness of breath is worse on exertion of a prolonged
duration and worsens over time. In the advanced stages, or end stage pulmonary
disease, it occurs during rest and may be always present.

Wheezing and chest tightness

Wheezing and chest tightness are nonspecific symptoms that may vary between
days, and over the course of a single day. These symptoms may be present in Stage
I: Mild COPD, but are more characteristic of asthma or Stage III: Severe COPD
and Stage IV: Very Severe COPD. Audible wheeze may arise at a laryngeal level
and need not be accompanied by auscultatory abnormalities. Alternatively,
widespread inspiratory or expiratory wheezes can be present on listening to the
chest. Chest tightness often follows exertion, is poorly

Physical activity limitation

COPD often leads to reduction in physical activity, in part due to shortness of
breath.In later stages of COPD muscle wasting (cachexia) may occur.  Low levels
of physical activity are associated with worse outcomes.

Sputum production. There is a hyperstimulation of the goblet cells and the

mucus-secreting gland leading to overproduction of sputum.

Weight loss. Dyspnea interferes with eating and the work of breathing is energy
depleting.

Barrel chest. In patients with emphysema, barrel chest thorax

configuration results from a more fixed position of the ribs in the inspiratory
position and from loss of elasticity.

Other symptoms

In COPD, breathing out may take longer than breathing in.  Chest tightness may
occur, but is not common and may be caused by another problem. Those with
obstructed airflow may have wheezing or decreased sounds with air entry
on examination of the chest with a stethoscope.

DIAGNOSTIC FINDINGS
History collection
A detailed medical history of a new patient known or thought to have COPD
should assess:
• Patient’s exposure to risk factors, such as smoking and occupational or
environmental exposures
• Past medical history, including asthma, allergy, sinusitis, or nasal polyps;
respiratory infections in childhood; other respiratory diseases
• Family history of COPD or other chronic respiratory disease
• Pattern of symptom development: COPD typically develops in adult life and most
patients are conscious of increased breathlessness, more frequent “winter colds,”
and some social restriction for a number of years before seeking medical help.
• History of exacerbations or previous hospitalizations for respiratory disorder:
Patients may be aware of periodic worsening of symptoms even if these episodes
have not been identified as exacerbations of COPD.
• Presence of comorbidities, such as heart disease, malignancies, osteoporosis, and
muscloskeletal disorders, which may also contribute to restriction of activity15.
• Appropriateness of current medical treatments: For example, beta-blockers
commonly prescribed for heart disease are usually contraindicated in COPD.
• Impact of disease on patient’s life, including limitation of activity, missed work
and economic impact, effect on family routines, feelings of depression or anxiety
• Social and family support available to the patient
• Possibilities for reducing risk factors, especially smoking cessation
Physical Examination
Though an important part of patient care, a physical examination is rarely
diagnostic in COPD. Physical signs of airflow limitation are usually not present
until significant impairment of lung function has occurred and their detection has a
relatively low sensitivity and specificity. A number of physical signs may be
present in COPD, but their absence does not exclude the diagnosis.
Inspection
. • Central cyanosis, or bluish discoloration of the mucosal membranes, may be
present but is difficult to detect in artificial light and in many racial groups.
• Common chest wall abnormalities, which reflect the pulmonary hyperinflation
seen in COPD, include relatively horizontal ribs, “barrel-shaped” chest, and
protruding abdomen.
• Flattening of the hemi-diaphragms may be associated with paradoxical in-
drawing of the lower rib cage on inspiration, and widening of the xiphosternal
angle.
• Resting respiratory rate is often increased to more than 20 breaths per minute and
breathing can be relatively shallow
. • Patients commonly show pursed-lip breathing, which may serve to slow
expiratory flow and permit more efficient lung emptying18.
• COPD patients often have resting muscle activation while lying supine. Use of
the scalene and sternocleidomastoid muscles is a further indicator of respiratory
distress.
• Ankle or lower leg edema can be a sign of right heart failure.

Palpation and percussion.

• Detection of the heart apex beat may be difficult due to pulmonary
hyperinflation.
• Hyperinflation also leads to downward displacement of the liver and an increase
in the ability to palpate this organ without it being enlarged.
Auscultation.
• Patients with COPD often have reduced breath sounds, but this finding is not
sufficiently characteristic to make the diagnosis19. 36 MANAGEMENT OF
COPD
• The presence of wheezing during quiet breathing is a useful pointer to airflow
limitation. However, wheezing heard only after forced expiration has not been
validated as a diagnostic test for COPD.
• Inspiratory crackles occur in some COPD patients but are of little help
diagnostically.
• Heart sounds are best heard over the xiphoid area
Arterial blood gas measurement
. The development of respiratory failure is indicated by a PaO2 < 8.0 kPa (60 mm
Hg) with or without PaCO2 > 6.7 kPa (50 mm Hg) in arterial blood gas
measurements made while breathing air at sea level. Screening patients by pulse
oximetry and assessing arterial blood gases in those with an oxygen saturation
(SaO2) < 92% is a useful way of selecting patients for arterial blood gas
measurement42. However, pulse oximetry gives no information about CO2
tensions. Clinical signs of respiratory failure or right heart failure include central
cyanosis, ankle swelling, and an increase in the jugular venous pressure. Clinical
signs of hypercapnia are extremely nonspecific outside of exacerbations

Spirometry

Spirometry measures the amount of airflow obstruction present and is generally

carried out after the use of a bronchodilator, a medication to open up the airways.
Two main components are measured to make the diagnosis, the forced expiratory
volume in one second (FEV1), which is the greatest volume of air that can be
breathed out in the first second of a breath, and the forced vital capacity (FVC),
which is the greatest volume of air that can be breathed out in a single large breath.
Normally, 75–80% of the FVC comes out in the first second [77] and a FEV1/FVC
ratio less than 70% in someone with symptoms of COPD defines a person as
having the disease.  Based on these measurements, spirometry would lead to over-
diagnosis of COPD in the elderly. The National Institute for Health and Care
Excellence criteria additionally require a FEV1 less than 80% of predicted. People
with COPD also exhibit a decrease in diffusing capacity of the lung for carbon
monoxide (DLCO) due to decreased surface area in the alveoli, as well as damage to
the capillary bed. Evidence for using spirometry among those without symptoms in
an effort to diagnose the condition earlier is of uncertain effect, so currently is not
recommende

Blood tests

A blood test can show other conditions that can cause similar symptoms to COPD,
such as a low iron level (anaemia) and a high concentration of red blood cells in
your blood (polycythaemia).

Sometimes a blood test may also be done to see if you have alpha-1-antitrypsin
deficiency. This is a rare genetic problem that increases your risk of COPD

Chest X-ray

A chest X-ray can be used to look for problems in the lungs that can cause similar
symptoms to COPD.

Problems that can be shown by an X-ray include chest infections and lung

cancer, although these do not always show.

Exercise testing.

Several types of tests are available to measure exercise capacity, e.g., treadmill and
cycle ergometry in the laboratory – or six-minute and shuttle walking tests , but
these are primarily used in conjunction with pulmonary rehabilitation programs.
Sleep studies

. Sleep studies may be indicated when hypoxemia or right heart failure develops in
the presence of relatively mild airflow limitation or when the patient has symptoms
suggesting the presence of sleep apnea.

CT and ventilation-perfusion scanning.

Despite the benefits of being able to delineate pathological anatomy, routine CT

and ventilation-perfusion scanning are currently confined to the assessment of
COPD patients for surgery. HRCT is currently under investigation as a way of
visualizing airway and parenchymal pathology more precisely

MANAGEMENT

NON PHARMACOLOGICAL MANAGEMENT

Components of pulmonary rehabilitation programs.

The components of pulmonary rehabilitation vary widely from program to program

but a comprehensive pulmonary rehabilitation program includes exercise training,
nutrition counseling, and education.

Exercise training

. Exercise tolerance can be assessed by either bicycle ergometry or treadmill

exercise with the measurement of a number of physiological variables, including
maximum oxygen consumption, maximum heart rate, and maximum work
performed. A less complex approach is to use a self-paced, timed walking test
(e.g., 6-minute walking distance). These tests require at least one practice session
before data can be interpreted. Shuttle walking tests offer a compromise: they
provide more complete information than an entirely self-paced test, but are simpler
to perform than a treadmill test228. Exercise training ranges in frequency from
daily to weekly, in duration from 10 minutes to 45 minutes per session, and in
intensity from 50% peak oxygen consumption (VO2 max) to maximum
tolerated229. The optimum length for an exercise program has not been
investigated in randomized controlled trials but most studies involving fewer than
28 exercise sessions show inferior results compared to those with longer treatment
periods221. In practice, the length depends on the resources available and usually
ranges from 4 to 10 weeks, with longer programs resulting in larger effects than
shorter programs

NUTRITION

Nutrition:  Weight loss & depletion of fat-free mass (FFM) may be observed
inWeight loss & depletion of fat-free mass (FFM) may be observed in stable
COPD patients.stable COPD patients.  Being underweight is associated with an
increased mortality risk.Being underweight is associated with an increased
mortality risk.

Oxygen Therapy

one of the principal nonpharmacologic treatments for patients with Stage IV: Very
Severe COPD190,260, can be administered in three ways: longterm continuous
therapy, during exercise, and to relieve acute dyspnea. The primary goal of oxygen
therapy is to increase the baseline PaO2 to at least 8.0 kPa (60 mm Hg) at sea level
and rest, and/or produce an SaO2 at least 90%, which will preserve vital organ
function by ensuring adequate delivery of oxygen.
PHARMACOLOGIC THERAPY FOR COPD

is used to reduce symptoms, reduce the frequency and severity of exacerbations,

and improve exercise tolerance and health status. To date, there is no conclusive
clinical trial evidence that any existing medications for COPD modify the long-
term decline in lung function.

Bronchodilators

Bronchodilators are medications that increase FEV1 and/or change other

spirometric variables.

 Bronchodilator medications in COPD are most often given on a regular basis to

prevent or reduce symptoms.

 Use of short acting bronchodilators on a regular basis is not generally

recommended. Beta2-agonists

 The principal action of beta2-agonists is to relax airway smooth muscle by

stimulating beta2- adrenergic receptors, which increases cyclic AMP and produces
functional antagonism to bronchoconstriction.

 There are short-acting (SABA) and long-acting (LABA) beta2-agonists.

 Formoterol and salmeterol are twice-daily LABAs that significantly improve

FEV1 and lung volumes, dyspnea, health status, exacerbation rate and number of
hospitalizations, 43 but have no effect on mortality or rate of decline of lung
function.

 Indacaterol is a once daily LABA that improves breathlessness, 44,45 health

status45 and exacerbation rate. 45
 Oladaterol and vilanterol are additional once daily LABAs that improve lung
function and symptoms.46,47

Adverse effects. Stimulation of beta2-adrenergic receptors can produce resting

sinus tachycardia and has the potential to precipitate cardiac rhythm disturbances
in susceptible patients. Exaggerated somatic tremor is troublesome in some older
patients treated with higher doses of beta2-agonists, regardless of route of
administration.

Antimuscarinic drugs

 Antimuscarinic drugs block the bronchoconstrictor effects of acetylcholine on

M3 muscarinic receptors expressed in airway smooth muscle.

 Short-acting antimuscarinics (SAMAs), namely ipratropium and oxitropium and

long-acting antimuscarinic antagonists (LAMAs), such as tiotropium, aclidinium,
glycopyrronium bromide and umeclidinium act on the receptors in different ways.
 A systematic review of RCTs found that ipratropium alone provided small
benefits over short-acting beta2-agonist in terms of lung function, health status and
requirement for oral steroids.

 Clinical trials have shown a greater effect on exacerbation rates for LAMA
treatment (tiotropium) versus LABA treatment.

Adverse effects

. Inhaled anticholinergic drugs are poorly absorbed which limits the troublesome
systemic effects observed with atropine.

Extensive use of this class of agents in a wide range of doses and clinical settings
has shown them to be very safe. The main side effect is dryness of mouth.
Methylxanthines

Controversy remains about the exact effects of xanthine derivatives.

 Theophylline, the most commonly used methylxanthine, is metabolized by

cytochrome P450 mixed function oxidases. Clearance of the drug declines with
age.

 There is evidence for a modest bronchodilator effect compared with placebo in

stable COPD.

 Addition of theophylline to salmeterol produces a greater improvement in FEV1

and breathlessness than salmeterol alone.

 There is limited and contradictory evidence regarding the effect of low-dose

theophylline on exacerbation rates.

Adverse effects.

Toxicity is dose-related, which is a particular problem with xanthine derivatives

because their therapeutic ratio is small and most of the benefit occurs only when
near-toxic doses are given.

Combination bronchodilator therapy

 Combining bronchodilators with different mechanisms and durations of action

may increase the degree of bronchodilation with a lower risk of side-effects
compared to increasing the dose of a single bronchodilator.

 Combinations of SABAs and SAMAs are superior compared to either

medication alone in improving FEV1 and symptoms.
 Treatment with formoterol and tiotropium in separate inhalers has a bigger
impact on FEV1 than either component alone

 There are numerous combinations of a LABA and LAMA in a single inhaler

available

 A lower dose, twice daily regimen for a LABA/LAMA has also been shown to
improve symptoms and health status in COPD patients

Respiratory Support Oxygen therapy

 This is a key component of hospital treatment of an exacerbation. Supplemental

oxygen should be titrated to improve the patient’s hypoxemia with a target
saturation of 88- 92%.106

Surgical management

 For those with very severe disease, surgery is sometimes helpful and may
include

 lung transplantation or lung volume-reduction surgery

 which involves removing the parts of the lung most damaged by

emphysema, allowing the remaining, relatively good lung to expand and
work better. It seems to be particularly effective if emphysema
predominantly involves the upper lobe, but the procedure increases the risks
of adverse events and early death for people who have diffuse
emphysema. The procedure also increases the risk of adverse effects for
people with moderate to severe COPD. Lung transplantation is sometimes
performed for very severe COPD, particularly in younger individuals[
 Bullectomy. Removes bullae, large air spaces that form when air sacs collapse

NURSING MANAGEMENT

Nursing Management

Management of patients with COPD should be incorporated with teaching and

improving the respiratory status of the patient.

Nursing Assessment

Assessment of the respiratory systemshould be done rapidly yet accurately.

 Assess patient’s exposure to risk factors.

 Assess the patient’s past and present medical history.

 Assess the signs and symptoms of COPD and their severity.

 Assess the patient’s knowledge of the disease.

 Assess the patient’s vital signs.

 Assess breath sounds and pattern.

Diagnosis

Diagnosis of COPD would mainly depend on the assessment data gathered by the
healthcare team members.

Impaired gas exchange related to chronic inhalation of toxins as evidenced by

shortness of breath Planning & Goals
Goals to achieve in patients with COPD include:

 Improvement in gas exchange.

 Achievement of airway clearance.

 Improvement in breathing pattern.

 Independence in self-care activities.

 Improvement in activity intolerance.

 Ventilation/oxygenation adequate to meet self-care needs.

 Nutritional intake meeting caloric needs.

 Infection treated/prevented.

 Disease process/prognosis and therapeutic regimen understood.

 Plan in place to meet needs after discharge.

Ineffective airway clearance related to bronchoconstriction, as evidenced by

increased mucus production, ineffective cough, and other complications

 The nurse must appropriately administer bronchodilators and

corticosteroids and become alert for potential side effects.

 Direct or controlled coughing. The nurse instructs the patient in direct

or controlled coughing, which is more effective and reduces fatigue
associated with undirected forceful coughing.
  Inspiratory muscle training. This may help improve the breathing
pattern.

 Diaphragmatic breathing. Diaphragmatic breathing reduces respiratory

rate, increases alveolar ventilation, and sometimes helps expel as much
air as possible during expiration.

 Pursed lip breathing. Pursed lip breathing helps slow expiration,

prevents collapse of small airways, and control the rate and depth of
respiration.

Ineffective breathing pattern related to shortness of breathas evidenced by

mucus, bronchoconstriction, and airway irritants.

Activity Intolerance Related to Generalized weakness, Sedentary lifestyle,

Imbalance between oxygen supply and demand evidenced by Verbal report
of fatigue or weakness.

Interventions To improve activity intolerance:

 Manage daily activities. Daily activities must be paced throughout the

day and support devices can be also used to decrease energy expenditure.

 Exercise training. Exercise training can help strengthen muscles of the

upper and lower extremities and improve exercise tolerance and
endurance.

 Walking aids. Use of walking aids may be recommended to improve

activity levels and ambulation.
To monitor and manage potential complications:
  Monitor cognitive changes. The nurse should monitor for cognitive
changes such as personality and behavior changes and memory
impairment.

 Monitor pulse oximetry values. Pulse oximetry values are used to assess
the patient’s need for oxygen and administer supplemental oxygen as
prescribed.

 Prevent infection. The nurse should encourage the patient to be

immunized against influenza and S. pneumonia because the patient is
prone to respiratory infection.

 Evaluate client’s actual and perceived limitations or degree of deficit in light

of usual status.
 Assess emotional and psychological factors affecting the current situation.
 Instruct patient in energy-conserving techniques (using chair when
showering, sitting to brush teeth or comb hair, carrying out activities at a
slower pace).
 Note presence of factors contributing fatigue
 Assess the patients response to activity

Outcomes

 Patient will participate in necessary/desired activities.

 Patient will use identified techniques to enhance activity tolerance.

 Patient will report a measurable increase in activity tolerance.

Patient will demonstrate a decrease in physiological signs of intolerance.

Ineffective Coping Related Inadequate relaxation, little or no exercise, work
overload evidenced by in your diagnostic statement evidenced by
Verbalization of inability to cope or ask for help

Interventions

 Evaluate ability to understand events, provide realistic appraisal of situation.

 Note reports of sleep disturbances, increasing fatigue, impaired

concentration, irritability, decreased tolerance of headache, inability to cope
or problem-solve.

 Assist patient to identify specific stressors and possible strategies for coping
with them.

 Encourage patient to evaluate life priorities and goals. Ask questions such as
“Is what you are doing getting you what you want?”

Outcomes

 Patient will identify ineffective coping behavior and consequences.

 Patient will verbalize awareness of own coping abilities/strengths.

Patient will identify potential stressful situations and steps to avoid/modify

them.
Deficient Knowledge Related to Lack of knowledge Information
misinterpretation evidenced by Verbalization of the problem.

Interventions

 Assist the patient in identifying risk factors

 Problem-solve with patient to identify ways in which appropriate lifestyle
changes can be made to reduce modifiable risk factors. Discuss the
importance of eliminating smoking, and assist patient in formulating a plan
to quit smoking.
 Reinforce the importance of adhering to treatment regimen and keeping
follow-up appointments.
 Help patient develop a simple, convenient schedule for taking medications.
 Explain prescribed medications along with their rationale dosage, side
effects.
 Avoid or limit alcohol intake. Notify the physician if unable to tolerate food
or fluid.
 Instruct patient to consult healthcare provider before taking other
prescription or over-the-counter (OTC) medications.
 Review signs and symptoms requiring notification of healthcare provider
 Provide information regarding community resources, and support patient in
making lifestyle changes.
Outcomes

Patient will verbalize understanding of disease process and treatment

regimen.
 Patient will identify drug side effects and possible complications that
necessitate medical attention.

 Patient will describe reasons for therapeutic actions/treatment regimen.

Nursing actions include patient and family teaching, detection and reporting of
adverse treatment effects, compliance assessment and enhancement,
and evaluation of therapeutic effectiveness.

Imbalanced Nutrition More Than Body Requirements Related Excessive

intake in relation to metabolic need, Sedentary activity level.

Interventions.

 Discuss the necessity for decrease calorie intake and limited intake of fats
salts, and sugar as indicated.
 Assess risk of condition associate with obesity
 Determine patient’s desire to lose weight.
 Review usual daily caloric intake and dietary choices
 Establish realistic weight reduction plan with the patient such as 1lb weight
loss per week
 Refer to dietitian as indicated.
Outcome

 Patient will demonstrate change in eating patterns (e.g., food choices,

quantity) to attain desirable body weight with optimal maintenance of health.

Nursing Priorities

1. Maintain airway patency.

 2. Assist with measures to facilitate gas exchange.

3. Enhance nutritional intake.

4. Prevent complications, slow progression of condition.

5. Provide information about disease process/prognosis and treatment

regimen.

Nursing Interventions

Patient and family teaching is an important nursing intervention to enhance self-

management in patients with any chronic pulmonary disorder.

Evaluation

During evaluation, the effectiveness of the care plan would be measured if goals
were achieved in the end and the patient:

 Identifies the hazards of cigarette smoking.

 Identifies resources for smoking cessation.

 Enrolls in smoking cessation program.

 Minimizes or eliminates exposures.

 Verbalizes the need for fluids.

 Is free of infection.

 Practices breathing techniques.

 Performs activities with less shortness of breath.

Complications of COPD

COPD can cause many other health problems, like:

 Respiratory infections. COPD can raise your chances of getting colds, the flu,

and pneumonia. They make it harder for to breathe and could cause more lung
damage. A yearly flu shot and vaccinations against pneumonia can help.
 Heart problems.  COPD can raise your risk of heart disease, including heart
attack. Quitting smoking may lower the odds.
 Lung cancer. People with COPD are more likely to get lung cancer. Quitting
smoking can help.
 High blood pressure in lung arteries. COPD may raise blood pressure in the
arteries that bring blood to lungs. pulmonary hypertension.

 Depression. Trouble breathing can stop you from doing things you like. And
living with a chronic illness can lead to depression. Your doctor can help if you
feel sad, helpless, or think that you may be depressed.

PREVENTION

Prevention of COPD is never impossible. Discipline and consistency are the keys
to achieving freedom from chronic pulmonary diseases.

 Smoking cessation. This is the single most cost-effective intervention to

reduce the risk of developing COPD and to stop its progression.

 Healthcare providers should promote cessation by explaining the risks of

smoking and personalizing the “at-risk” message to the patient.
PROGNOSIS

COPD usually gets gradually worse over time and can ultimately result in death. It
is estimated that 3% of all disability is related to COPD. The proportion of
disability from COPD globally has decreased from 1990 to 2010 due to improved
indoor air quality primarily in Asia. The overall number of years lived with
disability from COPD, however, has increased.

The rate at which COPD worsens varies with the presence of factors that predict a
poor outcome, including severe airflow obstruction, little ability to exercise,
shortness of breath, significant underweight or overweight, congestive heart
failure, continued smoking, and frequent exacerbations. Long-term outcomes in
COPD can be estimated using the BODE index which gives a score of zero to ten
depending on FEV1, body-mass index, the distance walked in six minutes, and
the modified MRC dyspnea scale.[176] Significant weight loss is a bad sign.
[23]
 Results of spirometry are also a good predictor of the future progress of the
disease but are not as good as the BODE index
Rehabilitation
rehabilitation for the lungs to get more air for the lungs to get more air pursed-lip
breathingpursed-lip breathing (like breathing out slowly into a straw)(like
breathing out slowly into a straw) inhaleinhale exhaleexhale
50 rehabilitation rehabilitation sit comfortably sit comfortably && relax your
shoulders relax your shoulders put one hand on your put one hand on your
abdomen. now inhale abdomen. now inhale slowly through yours lowly through
your nose. (push your nose. (push your abdomen out while you abdomen out while
you breathe in)breathe in) then push in your then push in your abdominal muscles
abdominal muscles and breathe out using and breathe out using the pursed-lip the
pursed-lip technique technique for the lungs to get more air for the lungs to get
more air diaphragmatic breathing diaphragmatic breathing

Follow-up

Baseline and outcome assessments of each participant in a pulmonary

rehabilitation program should be made to quantify individual gains and target areas
for improvement. Assessments should include.Detailed history and physical
examination Measurement of spirometry before and after a bronchodilator drug .
Assessment of exercise capacity

Measurement of health status and impact of breathlessness ,Assessment of

inspiratory and expiratory muscle strength and lower limb strength (e.g.,
quadriceps) in patients who suffer from muscle wasting The first two assessments
are important for establishing entry suitability and baseline status but are not used
in outcome assessment. The last three assessments are baseline and outcome
measures. Several detailed questionnaires for assessing health status are available,
including some that are specifically designed for patients with respiratory disease

THEORY APPLICATION

Virginia Henderson
Henderson defined nursing in functional terms. She stated, “The
unique function of the nurse is to assist the individual, sick or well, in the
performance of those activities contributing to health or its recovery that he would
perform unaided if he had the necessary strength, will or knowledge
Henderson identified 14 basic needs of the patient, which comprise the
components of nursing care. These include the following needs:
1. Breathe normally
2. Eat and drink adequately
3. Eliminate body wastes
4. Move and maintain desirable postures
Sleep and rest
6. Select suitable clothes—dress and undress
7. Maintain body temperature within normal range by adjusting clothing and
modifying the environment
8. Keep the body clean and well groomed and protect the integument
9. Avoid dangers in the environment and avoid injuring others

CONCLUSION

As cardiac nursing we should be able to know about respiratory conditions in detail

and how to manage it and various diagnostic investigations and how to control
it.To know the complete management of the copd

RESEAERCH STUDY
1
Comprehensive Health Insights Inc.
2
Humana Inc.
3
Boehringer Ingelheim Pharmaceuticals Inc.

Background:

2017GOLD guidelines recommend the use of ICS containing therapies only in

highly symptomatic patients with COPD at high risk of exacerbations. ICS use in
patients with COPD is associated with an increased risk for pneumonia, diabetes,
and reduced bone density.
Objective:

Assess the proportion of patients with COPD and comorbid pneumonia, diabetes,
osteoporosis, and/or heart failure that receive ICS containing therapies, stratified
by COPD-hospitalization history.

Methods:

A retrospective study using data from a large US health plan was conducted
including patients aged 55-89 years who were continuously enrolled for 12 months
pre- and post-COPD diagnosis (index date) from 1/1/2010 to 12/31/2013. Four
groups were formed for all patients and newly diagnosed patients: no comorbidities
(pneumonia, diabetes, osteoporosis, or heart failure), ≥ 1comorbidities, and with or
without pneumonia in the 12-month pre-index period. Patients were also stratified
by presence of pre-index COPD-hospitalizations. Proportion of patients on ICS
therapy was compared (chi-square) in the 12-months post-index period, among
patients receiving at least one COPD maintenance medication.

Results:

21,503 patients with COPD were identified, of whom 11,188 (52.0%) had ≥ 1
comorbidities, with 2,142 (10.0%) having pneumonia. Proportions of patients with
and without comorbidities receiving ICS was similar (72.6% and to patients
without comorbidities (72.2%, p=0.5203). 77.0% of patients with pneumonia
received ICS, significantly higher than patients without pneumonia (71.9%,
p<0.0001). Similar ICS use was observed for diabetes, osteoporosis and HF. 71.3%
of patients without pre-index COPD-related hospitalizations received ICS. Among
patients without pre-index COPD-related hospitalizations, proportions of patients
with or without comorbidities receiving ICS were similar (71.2% and 71.4%,
p=0.7459) while a significantly higher proportion of patients with pneumonia
compared to without received ICS (74.7% and 71.0%, p=0.0109). Among patients
newly diagnosed with COPD, a similar proportion of patients with and without
comorbidities (70.6% and 69.8%, p=0.3452), and patients with and without
pneumonia (72.2% and 70.0%, p=0.1643) received ICS.

Conclusions:

A large proportion of patients with COPD and comorbidities including pneumonia

received ICS. A majority of these patients did not have a history of COPD-related
hospitalizations. These findings highlight the potential overuse of ICS in patients
with COPD and specific comorbidities, and may not align with GOLD treatment
recommendations.

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3.Luwis’s text book of medical and surgical nursing ;assessment and management
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