DISSERTATION ON

“A STUDY ON CHRONIC OBSTRUCTIVE

PULMONARY DISEASES"

Dissertation submitted to

Ananta Institute of Medical Sciences and

Research
In partial fulfilment of the regulationsfor the
Award of the degree of

Doctorate of Pharmacy

B N COLLEGE OF
PHARMACY,UDAIPUR –
313001

Ananta Institute of Medical Sciences and Research

Udaipur - 313001

JANUARY – 2022

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CONTENTS PAGE No

1) Introduction 3

2) Aim and objective 5

3) Material and Methods 6

4) Risk Factors 10

5) Pathophysiology 12

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INTRODUCTION

- Severe Chronic Obstructive Pulmonary Disease (COPD) is a

common problem in patients hospitalized on respiratory
medicine wards. The burden of disease is great both for
those directly affected and for society. The majority of the
patients dependent on home oxygen treatment are former
smokers with COPD. Still, this is just the top of an iceberg,
since predominantly only cases of advanced COPD get
hospital care. Mild and moderate cases seldom find their way
to the hospital, and it is known that many of them are not
recognized at all by medical care providers.

- Several national and international guidelines concerning

diagnosis and care of COPD have been published during recent
years. There has been a focus on COPD also from the World
Health Organization (WHO), according to which COPD is to be
expected to be the third most common cause of death in
year 2020. Both patients and physicians are aware of the
disease COPD to a considerably higher degree today than 15
years ago. Misclassification of advanced COPD as asthma is
more unusual today compared to earlier. There has been a
diagnostic shift over time. There are many consultations
concerning respiratory symptoms and lung function
impairment, and the question at issue today is more often
than previously “is this COPD?” Increased awareness of
COPD in both society and health care facilitates correct
identification of the disease, and provision of proper
information and care to the patients. However, there are still
many questions to ask when encountering these patients.
Which individuals will develop COPD and why? How can we
measure and predict future decline in lung function in these
patients, both early and late in the course of the disease?
These questions lead further to other considerations. Is
earlier identification of COPD possible in our health care
system? What signs should raise suspicion of the disease? These
questions are important, as early diagnosis will create the

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 necessary conditions for preventive actions against further
disease progress, above all smoking cessation. There is still
lack of knowledge in the field of COPD-epidemiology,
especially concerning the development and course of the
disease.
- The Obstructive Lung Disease in Northern Sweden (OLIN)
Studies started in 1985, collecting longitudinal
epidemiological data with a focus on allergy and obstructive
pulmonary diseases. The overall aim was to find possible
preventable risk factors permitting intervention in the course
of these diseases. Work is in progress. This thesis is focused
on COPD epidemiology, and is based on the analyses of both
cross- sectional and longitudinal data from the OLIN studies.
COPD and mainly prevalence, incidence, under diagnosis,
decline in lung function, risk factors and gender differences will
be discussed.

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Aim and objective

- To estimate the prevalence of COPD in the general population of

India based on the Spiro metric criteria for COPD according to
the BTS, ERS, GOLD and ATS guidelines.

- To estimate the distribution by disease severity in prevalent COPD

according to the BTS and GOLD criteria.

- To examine the impact of smoking on COPD.

- To examine other determinants of COPD, including gender.

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MATERIAL AND METHODS

a) COPD should be considered in any patient who has dyspnea, chronic cough
or sputum production, and/or a history of exposure to risk factors for the
disease Spirometry is required to make the diagnosis in this clinical context.
b) The presence of a post-bronchodilator FEV1/FVC < 0.70 confirms the
presence of persistent airflow limitation and thus of COPD in patients with
appropriate symptoms and significant exposures to noxious stimuli.
c) Spirometry is the most reproducible and objective measurement of airflow
limitation. It is a noninvasive and readily available test. Despite its good
sensitivity, peak expiratory flow measurement alone cannot be reliably
used as the only diagnostic test because of its weak specificity. The WHO
has defined a minimum set of interventions for the diagnosis of COPD in
primary care.

A. CHEST X-RAY

The pulmonary artery width≥ 20mm relates directly to the presence of

pulmonary arterial hypertension .The high value for hilar cardiothoracic ratio
has 95% sensitivity and 100% specificity for the presence of pulmonary
hypertension in patients with COPD.

These are used as initial screening test for the presence of pulmonary
hypertension, but they do not predict the level of pulmonary artery pressure in
individual patients.

B. ELECTROCARDIOGRAPHY

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 The voluminous lungs have an insulating effect and thus diminish
transmission of electrical potentials to the electrodes. The heart descends
to a lower position in the thorax due to lowering of diaphragm and alters
the position of heart relative to the conventional electrodes. The
electrocardiography abnormalities in COPD and with right heart
involvement are 10.
 Decreased magnitude of electrocardiograph wave deflections.
 P-waves with right atrial enlargement, p-pulmonale i.e., tall peaked
waves in II, III and aVF (P wave > 2.5mm)
 QRS abnormalities: Right axis deviation and QRS > 90*. At times with
extreme northwest QRS axis there is the S1S2S3 syndrome. In precordial
leads there is a general loss of R wave amplitude in all precordial leads.
With right ventricular hypertrophy R/S amplitude in V6<VTendency for
incomplete right bundle branch block. Electrocardiography appears to be
specific but has a low sensitivity in picking upright ventricular
hypertrophy.

C. ECHOCARDIOGRAPHY
Because of the deficiencies of clinical examination in detecting pulmonary
artery hypertension in patients who have COPD and because pulmonary
artery pressure (Ppa) is a good predictor of prognosis in these individuals, a
number of attempts have been made to develop non-invasive methods to
estimate it. Echocardiographic measurements of systolic, diastolic and
pulmonary pressures have been shown to correlate with PPA measured by
the cardiac catheterization studies. 11 The most useful and accurate
method of estimating pulmonary artery pressure in patients with chronic

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 obstructive pulmonary disease is systolic trans tricuspid gradient calculated
from tricuspid regurgitation detected by continuous wave Doppler
echocardiography. Continuous wave Doppler determination of tricuspid
regurgitation jet velocity and application of modified Bernoulli’s equation
(TG = 4V2, in which V is the velocity of tricuspid regurgitation jet and TG is
the systolic right ventricular to right atrial pressure gradient across the
tricuspid valve) permits reliable estimation of pulmonary artery pressure.
Two dimensional echocardiography can be used to assess right ventricular
Dimensions and wall thickenings and hence to detect right ventricular
volume and pressure over load in patients with COPD. Echocardiography
can again be used to assess progression of disease or response to treatment
by serial measurements of pulmonary artery pressure and right heart
parameters.

METHOD OF ASSESSING CARDIAC FUNCTION IN

PATIENTS

a) WITH COPD
The pulmonary haemodynamic and right ventricular function an be
assessed by measuring pressure and flow which involves the use of invasive
techniques like cardiac catheterization. The non-invasive techniques which
include radiograph, electrocardiography, Echocardiography, radionuclide,
ventriculography and magnetic resonance imaging have proved to be useful
in assessing COPD patients.

b) SPIROMETRY

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Because of imprecisions in the clinical findings, objective evaluation for
detecting the presence, assessing severity and reversibility of airflow
obstruction is essential for the diagnostic evaluation of COPD. Spirometry is
the most robust test of airflow limitation in patients with COPD.
Forced expiratory volume in one second (FEV1) is recommended as the
measurement of choice as
 FEV1 is a reliable objective measurement.
 It is simple and relatively quick to measure in all stages of the disease.
 The forced expiratory manoeuvre records FEV1and also FVC . FEV1 / FVC
ratio less than 70% is diagnostic of airway obstruction.

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Risk factors

 Risk factors for COPD include:

i. Exposure to tobacco smoke - The most significant risk factor for COPD is
long-term cigarette smoking. The more years you smoke and the more
packs you smoke, the greater your risk. Pipe smokers, cigar smokers and
marijuana smokers also may be at risk, as well as people exposed to
large amounts of second hand smoke. People with asthma. Asthma, a
chronic inflammatory airway disease, may be a risk factor for developing
COPD. The combination of asthma and smoking increases the risk of
COPD even more.
ii. Occupational exposure to dusts and chemicals - Long-term exposure to
chemical fumes, vapours and dusts in the workplace can irritate and
inflame your lungs.
iii. Exposure to fumes from burning fuel - In the developing world, people
exposed to fumes from burning fuel for cooking and heating in poorly
ventilated homes are at higher risk of developing COPD.
iv. Genetics - The uncommon genetic disorder alpha-1-antitrypsin
deficiency is the cause of some cases of COPD. Other genetic factors
likely make certain smokers more susceptible to the disease.

Complications

 COPD can cause many complications, including:

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 i. Respiratory infections - People with COPD are more likely to catch colds,
the flu and pneumonia. Any respiratory infection can make it much more
difficult to breathe and could cause further damage to lung tissue.
ii. Heart problems - For reasons that aren't fully understood, COPD can
increase your risk of heart disease, including heart attack
iii. Lung cancer - People with COPD have a higher risk of developing lung
cancer.
iv. High blood pressure in lung arteries - COPD may cause high blood
pressure in the arteries that bring blood to your lungs (pulmonary
hypertension).
v. Depression - Difficulty breathing can keep you from doing activities that
you enjoy. And dealing with serious illness can contribute to the
development of depression.

Prevention

Unlike some diseases, COPD typically has a clear cause and a clear path of
prevention, and there are ways to slow the progression of the disease. The
majority of cases are directly related to cigarette smoking, and the best way to
prevent COPD is to never smoke — or to stop smoking now. If you're a long
time smoker, these simple statements may not seem so simple, especially if
you've tried quitting — once, twice or many times before. But keep trying to
quit. It's critical to find a tobacco cessation program that can help you quit for
good. It's your best chance for reducing damage to your lungs.

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Pathophysiology

The aorta has different functions. It does not just serve as a channel for the last
phase of the heartbeat (systole) but it also functions as a storage space for
blood. The aorta stores half of the ejected blood volume of the heart for every
beat. During diastole, the aorta recoils and forces the reserved blood volume
towards the peripheral circulation. This phenomenon is referred to as the
Windkessel function, which is the earliest model used to explain the arterial
system (118). In healthy people, the normal left ventricular ejection fraction
results in a pulse pressure with a moderately slow pulse wave velocity at 5 to 7
m/s (115), during diastole, the pulse wave is reflected at different points in
distal arteries which branch at the origin of arterioles. This reflected wave acts
together with the slow pulse wave to produce the dichotic notch. The end
result of these two pressure waves determines the final aortic blood pressure
shape and waveform (119). In younger, compliant blood vessels, pulse
pressure amplification takes place when the reflected pulse wave returns
during diastole which results in a higher pulse pressure in the peripheral
arteries when compared to the central arteries. In contrast, as we age, the
reflected wave achieves the central pulse during systole due to the increased
pulse wave velocity, in turn increasing the systolic blood pressure. When the
increased systolic blood pressure is divided by the pulse pressure, this process

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is referred to as the augmentation index, which is considered an aortic stiffness
marker. When mechanical stress disturbs the elastin or the arterial wall elastic
fibres, the augmentation index increases Occupational exposure to chemical
fumes and dusts is another risk factor for COPD. If you work with these types
of lung irritants, talk to your supervisor about the best ways to protect
yourself, such as using respiratory protective equipment.

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