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National Homoeopathic Medical College &

Hospital, Lucknow

DISSERTATION

ON

STUDY OF

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

AND ITS

HOMOEOPATHIC MANAGEMENT

GUIDE

DR. V.N VERMA

PRESENTED BY
2

Gyanendra Kumar Rai (Batch-2004

ACKNOWLEDGEMENT

First of all I am grateful to Almighty who showered his blessings


throughout the writing of this Dissertation.

Gratitude is expressed to respected DR. V. K VIMAL Principal,


National Homoeopathy Medical Collage, Lucknow for his whole hearted
cooperation, valuable guidance, constructive criticism and compiling the
intricate details whenever required in the Dissertation.

I am also deeply indebted to DR. V.N VERMA for his sustained


support for this endeavor from the beginning.

The entire subjects related to my project deserve appreciation for their


unflinching support during gestation period of the Dissertation.

Last but not the least I express thanks to all those persons who are directly
or indirectly related to completion of the Dissertation.
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CERTIFICATE BY PRINCIPAL

I hereby certify that VIJAY VISHWAKARMAhas prepared his


dissertation on the topic allotted to him; Study of Chronic Obstructive
Pulmonary Disease and its Homoeopathic Management under
my guidance and his work is up to my satisfaction.

During the course of preparation he showed keen interest in his work, I


wish him success in life.

Prof. (Dr.) A. N. Mishra

Principal

NATIONAL HOMOEOPATHIC

MEDICAL COLLEGE AND HOSPITAL LUCKNOW


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CERTIFICATE BY GUIDE

I hereby certify that Gyanendra Kumar Rai has prepared his dissertation on
the topic allotted to him; Study of Chronic Obstructive Pulmonary
Disease and its Homoeopathic Management under my guidance
and his work is up to my satisfaction.

During the course of preparation he showed keen interest in his work, I


wish him success in life.

Dr. D. S. Tomar

Lecturer

NATIONAL HOMOEOPATHIC

MEDICAL COLLEGE AND HOSPITAL LUCKNOW


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INDEX

CONTENTS PAGE NUMBER

1. INTRODUCTION

2. AIMS & OBJECTIVES

3. REVIEW OF LITERATURE

A. REVIEW OF GENERAL

MEDICAL LITERATURE

B. REVIEW OF HOMOEOPATHIC

MEDICAL LITERATURE

4. MATERIAL & METHODS


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5. MANAGEMENT & HOMOEOPATHIC

TREATMENT

6. ANNEXURE

A. CASE FORMATION

B. GRAPHS

C. SYNOPSIS OF CASES

7. BIBLIOGRAPHY.
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AIMS AND OBJECTIVES

To see the role of deep acting and short acting medicines in treatment.

To see Homoeopathic dosage directions.

To see miasmatic and constitutional background in the treatment.

To see the auxiliary management in the treatment.


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REVIEW OF LITERATURE

Anatomy of Lungs

The lungs flank the heart and great vessels in the chest cavity.

Air enters and leaves the lungs via a conduit of cartilaginous passageways
the bronchi and bronchioles. In this image, lung tissue has been dissected
away to reveal the bronchioles.

The Lungs (Pulmones)


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The lungs are the essential organs of respiration; they are two in number,
placed one on either side within the thorax, and separated from each other
by the heart and other contents of the mediastinum. The substance of the
lung is of a light, porous, spongy texture; it floats in water, and crepitates
when handled, owing to the presence of air in the alveoli; it is also highly
elastic; hence the retracted state of these organs when they are removed
from the closed cavity of the thorax. The surface is smooth, shining, and
marked out into numerous polyhedral areas, indicating the lobules of the
organ: each of these areas is crossed by numerous lighter lines.

Front view of heart and lungs

At birth the lungs are pinkish white in color; in adult life the color is a dark
slaty gray, mottled in patches; and as age advances, this mottling assumes a
black color. The coloring matter consists of granules of a carbonaceous
substance deposited in the areolar tissue near the surface of the organ. It
increases in quantity as age advances, and is more abundant in males than
in females. As a rule, the posterior border of the lung is darker than the
anterior.

The right lung usually weighs about 625 gm., the left 567 gm., but much
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variation is met with according to the amount of blood or serous fluid they
may contain. The lungs are heavier in the male than in the female, their
proportion to the body being, in the former, as 1 to 37, in the latter as 1 to
43.

Each lung is conical in shape, and presents for examination an apex, a


base, three borders, and two surfaces.

The apex (apex pulmonis) is rounded, and extends into the root of the
neck, reaching from 2.5 to 4 cm. above the level of the sternal end of the
first rib. A sulcus produced by the subclavian artery as it curves in front of
the pleura runs upward and lateralward immediately below the apex.

The base (basis pulmonis) is broad, concave, and rests upon the convex
surface of the diaphragm, which separates the right lung from the right lobe
of the liver, and the left lung from the left lobe of the liver, the stomach, and
the spleen. Since the diaphragm extends higher on the right than on the left
side, the concavity on the base of the right lung is deeper than that on the
left. Laterally and behind, the base is bounded by a thin, sharp margin
which projects for some distance into the phrenicocostal sinus of the
pleura, between the lower ribs and the costal attachment of the diaphragm.
The base of the lung descends during inspiration and ascends during
expiration.
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Pulmonary vessels, seen in dorsal view of the heart and lungs. The lungs have been
pulled away from the median line, and a part of the right lung has been cut away to
display the air-ducts and bloodvessels.

Surfaces The costal surface (facies costalis; external or thoracic


surface) is smooth, convex, of considerable extent, and corresponds to the
form of the cavity of the chest, being deeper behind than in front. It is in
contact with the costal pleura, and presents, in specimens which have been
hardened in situ, slight grooves corresponding with the overlying ribs.

The mediastinal surface (facies mediastinalis; inner surface) is in contact


with the mediastinal pleura. It presents a deep concavity, the cardiac
impression, which accommodates the pericardium; this is larger and
deeper on the left than on the right lung, on account of the heart projecting
farther to the left than to the right side of the median plane. Above and
behind this concavity is a triangular depression named the hilum, where
the structures which form the root of the lung enter and leave the viscus.
These structures are invested by pleura, which, below the hilus and behind
the pericardial impression, form the pulmonary ligament. On the right lung
immediately above the hilus, is an arched furrow which accommodates the
azygos vein; while running upward, and then arching lateralward some
little distance below the apex, is a wide groove for the superior vena cava
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and right innominate vein; behind this, and nearer the apex, is a furrow for
the innominate artery. Behind the hilus and the attachment of the
pulmonary ligament is a vertical groove for the esophagus; this groove
becomes less distinct below, owing to the inclination of the lower part of the
esophagus to the left of the middle line. In front and to the right of the
lower part of the esophageal groove is a deep concavity for the
extrapericardiac portion of the thoracic part of the inferior vena cava. On
the left lung immediately above the hilus, is a well-marked curved furrow
produced by the aortic arch, and running upward from this toward the apex
is a groove accommodating the left subclavian artery; a slight impression in
front of the latter and close to the margin of the lung lodges the left
innominate vein. Behind the hilus and pulmonary ligament is a vertical
furrow produced by the descending aorta, and in front of this, near the base
of the lung, the lower part of the esophagus causes a shallow impression.

Mediastinal surface of right lung.

Borders. The inferior border (margo inferior) is thin and sharp where it
separates the base from the costal surface and extends into the
phrenicocostal sinus; medially where it divides the base from the
mediastinal surface it is blunt and rounded.
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The posterior border (margo posterior) is broad and rounded, and is


received into the deep concavity on either side of the vertebral column. It is
much longer than the anterior border, and projects, below, into the
phrenicocostal sinus.

The anterior border (margo anterior) is thin and sharp, and overlaps the
front of the pericardium. The anterior border of the right lung is almost
vertical, and projects into the costomediastinal sinus; that of the left
presents, below, an angular notch, the cardiac notch, in which the
pericardium is exposed. Opposite this notch the anterior margin of the left
lung is situated some little distance lateral to the line of reflection of the
corresponding part of the pleura.

Mediastinal surface of left lung.

Fissures and Lobes of the Lungs.the left lung is divided into two lobes, an
upper and a lower, by an interlobular fissure, which extends from the costal
to the mediastinal surface of the lung both above and below the hilus. As
seen on the surface, this fissure begins on the mediastinal surface of the
lung at the upper and posterior part of the hilus, and runs backward and
upward to the posterior border, which it crosses at a point about 6 cm.
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below the apex. It then extends downward and forward over the costal
surface, and reaches the lower border a little behind its anterior extremity,
and its further course can be followed upward and backward across the
mediastinal surface as far as the lower part of the hilus. The superior lobe
lies above and in front of this fissure, and includes the apex, the anterior
border, and a considerable part of the costal surface and the greater part of
the mediastinal surface of the lung. The inferior lobe, the larger of the two,
is situated below and behind the fissure, and comprises almost the whole of
the base, a large portion of the costal surface, and the greater part of the
posterior border.

The right lung is divided into three lobes, superior, middle, and
inferior, by two interlobular fissures. One of these separates the inferior
from the middle and superior lobes, and corresponds closely with the
fissure in the left lung. Its direction is, however, more vertical, and it cuts
the lower border about 7.5 cm. behind its anterior extremity. The other
fissure separates the superior from the middle lobe. It begins in the
previous fissure near the posterior border of the lung, and, running
horizontally forward, cuts the anterior border on a level with the sternal
end of the fourth costal cartilage; on the mediastinal surface it may be
traced backward to the hilus. The middle lobe, the smallest lobe of the right
lung, is wedge-shaped, and includes the lower part of the anterior border
and the anterior part of the base of the lung.
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The right lung, although shorter by 2.5 cm. than the left, in consequence of
the diaphragm rising higher on the right side to accommodate the liver, is
broader, owing to the inclination of the heart to the left side; its total
capacity is greater and it weighs more than the left lung.

The Root of the Lung (radix pulmonis).A little above the middle of
the mediastinal surface of each lung, and nearer its posterior than its
anterior border, is its root, by which the lung is connected to the heart and
the trachea. The root is formed by the bronchus, the pulmonary artery, the
pulmonary veins, the bronchial arteries and veins, the pulmonary plexuses
of nerves, lymphatic vessels, bronchial lymph glands, and areolar tissue, all
of which are enclosed by a reflection of the pleura. The root of the right lung
lies behind the superior vena cava and part of the right atrium, and below
the azygos vein. That of the left lung passes beneath the aortic arch and in
front of the descending aorta; the phrenic nerve, the pericardiacophrenic
artery and vein, and the anterior pulmonary plexus, lie in front of each, and
the vagus and posterior pulmonary plexus behind each; below each is the
pulmonary ligament.

The chief structures composing the root of each lung are arranged in a
similar manner from before backward on both sides, viz., the upper of the
two pulmonary veins in front; the pulmonary artery in the middle; and the
bronchus, together with the bronchial vessels, behind. From above
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downward, on the two sides, their arrangement differs, thus:

On the right side their position iseparterial bronchus, pulmonary artery,


hyparterial bronchus, pulmonary veins, but on the left side their position is
pulmonary artery, bronchus, pulmonary veins. The lower of the two
pulmonary veins, is situated below the bronchus, at the apex or lowest part
of the hilus.

Divisions of the Bronchi.Just as the lungs differ from each other in the
number of their lobes, so the bronchi differ in their mode of subdivision.

The right bronchus gives off, about 2.5 cm. from the bifurcation of the
trachea, a branch for the superior lobe. This branch arises above the level of
the pulmonary artery, and is therefore named the eparterial bronchus. All
the other divisions of the main stem come off below the pulmonary artery,
and consequently are termed hyparterial bronchi. The first of these is
distributed to the middle lobe, and the main tube then passes downward
and backward into the inferior lobe, giving off in its course a series of large
ventral and small dorsal branches. The ventral and dorsal branches arise
alternately, and are usually eight in numberfour of each kind. The branch
to the middle lobe is regarded as the first of the ventral series.

The left bronchus passes below the level of the pulmonary artery before it
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divides, and hence all its branches are hyparterial; it may therefore be
looked upon as equivalent to that portion of the right bronchus which lies
on the distal side of its eparterial branch. The first branch of the left
bronchus arises about 5 cm. from the bifurcation of the trachea, and is
distributed to the superior lobe. The main stem then enters the inferior
lobe, where it divides into ventral and dorsal branches similar to those in
the right lung. The branch to the superior lobe of the left lung is regarded as
the first of the ventral series.

The serous coat is the pulmonary pleura it is thin, transparent, and invests
the entire organ as far as the root.

The subserous areolar tissue contains a large proportion of elastic fibers; it


invests the entire surface of the lung, and extends inward between the
lobules.

The parenchyma is composed of secondary lobules which, although closely


connected together by an interlobular areolar tissue, are quite distinct from
one another, and may be teased asunder without much difficulty in the
fetus. The secondary lobules vary in size; those on the surface are large, of
pyramidal form, the base turned toward the surface; those in the interior
smaller, and of various forms. Each secondary lobule is composed of several
primary lobules, the anatomical units of the lung. The primary lobule
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consists of an alveolar duct, the air spaces connected with it and their
bloodvessels, lymphatics and nerves.

The intrapulmonary bronchi divide and subdivide throughout the entire


organ, the smallest subdivisions constituting the lobular bronchioles. The
larger divisions consist of: (1) an outer coat of fibrous tissue in which are
found at intervals irregular plates of hyaline cartilage, most developed at
the points of division; (2) internal to the fibrous coat, a layer of circularly
disposed smooth muscle fibers, the bronchial muscle; and (3) most
internally, the mucous membrane, lined by columnar ciliated epithelium
resting on a basement membrane. The corium of the mucous membrane
contains numerous elastic fibers running longitudinally, and a certain
amount of lymphoid tissue; it also contains the ducts of mucous glands, the
acini of which lie in the fibrous coat. The lobular bronchioles differ from the
larger tubes in containing no cartilage and in the fact that the ciliated
epithelial cells are cubical in shape. The lobular bronchioles are about 0.2
mm. in diameter.

Part of a secondary lobule from the depth of a human lung, showing parts
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of several primary lobules. 1, bronchiole; 2, respiratory bronchiole; 3,


alveolar duct; 4, atria; 5, alveolar sac; 6, alveolus or air cell: m, smooth
muscle; a, branch pulmonary artery; v, branch pulmonary vein; s, septum
between secondary lobules. Camera drawing of one 50 section. X 20
diameters.

Each bronchiole divides into two or more respiratory bronchioles, with


scattered alveoli, and each of these again divides into several alveolar ducts,
with a greater number of alveoli connected with them. Each alveolar duct is
connected with a variable number of irregularly spherical spaces, which
also possess alveoli, the atria. With each atrium a variable number (25) of
alveolar sacs are connected which bear on all parts of their circumference
alveoli or air sacs. (Miller.)

The alveoli are lined by a delicate layer of simple squamous epithelium,


the cells of which are united at their edges by cement substance. Between
the squames are here and there smaller, polygonal, nucleated cells. Outside
the epithelial lining is a little delicate connective tissue containing
numerous elastic fibers and a close net-work of blood capillaries, and
forming a common wall to adjacent alveoli
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Schematic longitudinal section of a primary lobule of the lung (anatomical


unit); r. b., respiratory bronchiole; al. d., alveolar duct; at., atria; a. s.,
alveolar sac; a, alveolus or air cell; p. a.: pulmonary artery: p. v., pulmonary
vein; l., lymphatic; l. n., lymph node

Vessels and Nerves. The pulmonary artery conveys the venous


blood to the lungs; it divides into branches which accompany the bronchial
tubes and end in a dense capillary net-work in the walls of the alveoli. In
the lung the branches of the pulmonary artery are usually above and in
front of a bronchial tube, the vein below.

The pulmonary capillaries form plexuses which lie immediately beneath


the lining epithelium, in the walls and septa of the alveoli and of the
infundibula. In the septa between the alveoli the capillary net-work forms a
single layer. The capillaries form a very minute net-work, the meshes of
which are smaller than the vessels themselves; their walls are also
exceedingly thin. The arteries of neighboring lobules are independent of
each other, but the veins freely anastomose.

The pulmonary veins commence in the pulmonary capillaries, the radicles


coalescing into larger branches which run through the substance of the
lung, independently of the pulmonary arteries and bronchi. After freely
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communicating with other branches they form large vessels, which


ultimately come into relation with the arteries and bronchial tubes, and
accompany them to the hilus of the organ. Finally they open into the left
atrium of the heart, conveying oxygenated blood to be distributed to all
parts of the body by the aorta.

The bronchial arteries supply blood for the nutrition of the lung; they are
derived from the thoracic aorta or from the upper aortic intercostal arteries,
and, accompanying the bronchial tubes, are distributed to the bronchial
glands and upon the walls of the larger bronchial tubes and pulmonary
vessels. Those supplying the bronchial tubes form a capillary plexus in the
muscular coat, from which branches are given off to form a second plexus
in the mucous coat; this plexus communicates with small venous trunks
that empty into the pulmonary veins. Others are distributed in the
interlobular areolar tissue, and end partly in the deep, partly in the
superficial, bronchial veins. Lastly, some ramify upon the surface of the
lung, beneath the pleura, where they form a capillary network.

The bronchial vein is formed at the root of the lung, receiving superficial
and deep veins corresponding to branches of the bronchial artery. It does
not, however, receive all the blood supplied by the artery, as some of it
passes into the pulmonary veins. It ends on the right side in the azygos
vein, and on the left side in the highest intercostal or in the accessory
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hemiazygos vein.

Nerves.the lungs are supplied from the anterior and posterior


pulmonary plexuses, formed chiefly by branches from the sympathetic and
vagus. The filaments from these plexuses accompany the bronchial tubes,
supplying efferent fibers to the bronchial muscle and afferent fibers to the
bronchial mucous membrane and probably to the alveoli of the lung. Small
ganglia are found upon these nerves.

How does the normal lung work?

The lung is the organ for gas exchange; it transfers oxygen from the air into
the blood and carbon dioxide (a waste product of the body) from the blood
into the air. To accomplish gas exchange the lung has two components;
airways and alveoli. The airways are branching, tubular passages that allow
air to move in and out of the lungs. The wider segments of the airways are
the trachea and the two bronchi (going to either the right or left lung). The
smaller segments are called bronchioles. At the ends of the bronchioles are
the alveoli, thin-walled sacs. (The airways and alveoli can be conceptualized
as bunches of grapes with the airways analogous to the stems and the
alveoli analogous to the grapes.) Small blood vessels (capillaries) run in the
walls of the alveoli, and it is across the thin walls of the alveoli where gas
exchange between air and blood takes place.
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Breathing involves inspiration followed by exhalation. During inspiration,


muscles of the diaphragm and the rib cage contract and expand the size of
the chest (as well as the airways and alveoli) causing negative pressure
within the airways and alveoli. As a result, air is sucked through the airways
and into the alveoli. During exhalation, the same muscles relax to their
resting positions, shrinking the chest and creating positive pressure within
the airways and alveoli. As a result, air is expelled from the lungs.

The walls of the bronchioles are weak and have a tendency to collapse,
especially while exhaling. Normally, the bronchioles are kept open by the
elasticity of the lung. Elasticity of the lung is supplied by elastic fibers which
surround the airways and line the walls of the alveoli. When lung tissue is
destroyed, as it is in patients with COPD who have emphysema, there is loss
of elasticity and the bronchioles can collapse and obstruct the flow of air.
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Respiratory Process

Respiratory values

The tidal volume (500ml) multiplied by the respiratory rate (14


breaths/min) is the minute volume (7,000ml/min). Not all of the tidal
volume takes part in respiratory exchange, as this process does not start
until the air or gas reaches the respiratory bronchioles (division 17 of the
respiratory tree). Above this level the airways are solely for conducting,
their volume being known as the anatomical dead-space. The volume of the
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anatomical dead-space is approximately 2ml/kg or 150ml in an adult,


roughly a third of the tidal volume. The part of the tidal volume which does
take part in respiratory exchange multiplied by the respiratory rate is
known as the alveolar ventilation (approximately 5,000ml/min).

Functional residual capacity (FRC) is the volume of air in the lungs at the
end of a normal expiration. The point at which this occurs (and hence the
FRC value) is determined by a balance between the inward elastic forces of
the lung and the outward forces of the respiratory cage (mostly due to
muscle tone). FRC falls with lying supine, obesity, pregnancy and
anaesthesia, though not with age. The FRC is of particularly importance to
anaesthetists because:

During apnoea it is the reservoir to supply oxygen to the blood

As it falls the distribution of ventilation within the lungs changes


leading to mismatching with pulmonary blood flow

If it falls below a certain volume (the closing capacity), airway closure


occurs leading to shunt (see later - Ventilation/perfusion/shunt) Resistance
/ compliance

In the absence of respiratory effort, the lung will come to lie at the point of
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the FRC. To move from this position and generate respiratory movement,
two aspects need to be considered which oppose lung expansion and airflow
and therefore need to be overcome by respiratory muscle activity. These are
the airway resistance and the compliance of the lung and chest wall.

Resistance of the airways describes the obstruction to airflow provided by


the conducting airways, resulting largely from the larger airways (down to
division 6-7), plus a contribution from tissue resistance resulting produced
by friction as tissues of the lung slide over each other during respiration. An
increase in resistance resulting from airway narrowing such as
bronchospasm leads to obstructive airways disease.

Work of breathing

Of the two barriers to respiration, airway resistance and lung compliance, it


is only the first of these, which requires actual work to be done to overcome
it. Airway resistance to flow is present during both inspiration and
expiration and the energy required to overcome it, which represents the
actual work of breathing, is dissipated as heat.

Although energy is required to overcome compliance in expanding the lung,


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it does not contribute to the actual work of breathing as it is not dissipated


but converted to potential energy in the distended elastic tissues. Some of
this stored energy is used to do the work of breathing produced by airways
resistance during expiration.

Diffusion

The alveoli provide an enormous surface area for gas exchange with
pulmonary blood (between 50-100m2) with a thin membrane across which
gases must diffuse. The solubility of oxygen is such that its diffusion across
the normal alveolar-capillary membrane is an efficient and rapid process.
Under resting conditions pulmonary capillary blood is in contact with the
alveolus for about 0.75 second in total and is fully equilibrated with alveolar
oxygen after only about a third of the way along this course. If lung disease
is present which impairs diffusion there is therefore still usually sufficient
time for full equilibration of oxygen when at rest. During exercise, however,
the pulmonary blood flow is quicker, shortening the time available for gas
exchange, and so those with lung disease are unable to oxygenate the
pulmonary blood fully and thus have a limited ability to exercise.

For carbon dioxide, which diffuses across the alveolar-capillary membrane


20 times faster than oxygen, the above factors are less liable to compromise
transfer from blood to alveoli.
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Ventilation / perfusion / shunt

In an ideal situation the ventilation delivered to an area of lung would be


just sufficient to provide full exchange of oxygen and carbon dioxide with
the blood perfusing that area. In the normal setting, whilst neither
ventilation (V) nor perfusion (Q) is distributed evenly throughout the lung,
their matching is fairly good, with the bases receiving substantially more of
both than the apices.

For perfusion, the distribution throughout the lung is largely due to the
effects of gravity. Therefore in the upright position this means that the
perfusion pressure at the base of the lung is equal to the mean pulmonary
artery pressure (15mmHg or 20cmH2O) plus the hydrostatic pressure
between the main pulmonary artery and lung base (approximately
15cmH2O). At the apices the hydrostatic pressure difference is subtracted
from the pulmonary artery pressure with the result that the perfusion
pressure is very low, and may at times even fall below the pressure in the
alveoli leading to vessel compression and intermittent cessation of blood
flow.
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The distribution of ventilation across the lung is related to the position of


each area on the compliance curve at the start of a normal tidal inspiration
(the point of the FRC). Because the bases are on a more favourable part of
the compliance curve than the apices, they gain more volume change from
the pressure change applied and thus receive a greater degree of
ventilation. Although the inequality between bases and apices is less
marked for ventilation than for perfusion, overall there is still good V/Q
matching and efficient oxygenation of blood passing through the lungs.

Disturbance of this distribution can lead to V/Q mismatching .For an area


of low V/Q ratio the blood flowing through it will be incompletely
oxygenated, leading to a reduction in the oxygen level in arterial blood
(hypoxaemia). Providing some ventilation is occurring in an area of low
V/Q, the hypoxaemia can normally be corrected by increasing the FiO2,
which restores the alveolar oxygen delivery to a level sufficient to oxygenate
the blood fully.

V/Q mismatch occurs very commonly during anaesthesia because the FRC
falls leading to a change in the position of the lung on the compliance curve.
The apices, therefore, move to the most favourable part of the curve whilst
the bases are located on a less favourable part at the bottom of the curve.

At the extremes of V/Q mismatch, an area of lung receiving no perfusion


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will have a V/Q ratio of (infinity) and is referred to as alveolar dead-space,


which together with the anatomical dead-space makes up the physiological
dead-space. Ventilating the dead space is, in effect, wasted ventilation, but
unavoidable.

In contrast an area of lung receiving no ventilation, owing to airway closure


or blockage, its V/Q ratio will be zero and the area is designated as shunt.
Blood will emerge from an area of shunt with a PO2 unchanged from the
venous level (5.3kPa or 40mmHg) and produce marked arterial
hypoxaemia. This hypoxaemia cannot be corrected by increasing the FiO2,
even to 1.0, as the area of shunt receives no ventilation at all. The well-
ventilated parts of the lung cannot compensate for the area of shunt
because Hb is fully saturated at a normal PO2 . Increasing the PO2 of this
blood will not increase the oxygen content substantially .

In the case of shunt, therefore, adequate oxygenation can only be re-


established by restoring ventilation to these areas using measures such as
physiotherapy, PEEP or CPAP, which clear blocked airways and reinflate
areas of collapsed lung. Because closing capacity (CC) increases
progressively with age, and is also higher in neonates, these patients are at
particular risk during anaesthesia as the FRC may fall below CC and airway
closure result.
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Oxygen Transport

From an atmospheric level of 21kPa (21%), the partial pressure of oxygen


falls in 3 stages before the arterial blood is reached. Firstly the inspired air
is humidified by the upper respiratory tract, the saturated vapour pressure
of water (6.2kPa or 47mmHg) reducing the PO2 to around 19.7kPa
(148mmHg). In the alveoli the continuous exchange of carbon dioxide for
oxygen reduces the PO2 to about 14.4kPa (108mmHg) and finally the small
physiological shunt normally present reduces it to approximately 13.3kPa
(100mmHg).

Oxygen carriage

After transfer of oxygen across the alveolar capillary membrane, an efficient


carriage system is needed to transport it to the tissues for use in cellular
respiration. The oxygen content in the blood is the sum of that bound to
haemoglobin (Hb) and that dissolved in plasma, which is normally a minor
contribution in patients breathing air. Hb is a large protein containing 4
subunits, each containing a ferrous (Fe2+) ion within a haem group. Up to
4 oxygen molecules can bind reversibly to each Hb molecule, one to each of
the Fe2+ sites. The main factor that determines the extent of oxygen
binding to Hb is the PO2, the relationship between which is shown in figure
8.
32

The initial flat part of the curve occurs because the binding of the first
oxygen molecule causes a small structural change to Hb facilitating the
binding of subsequent oxygen molecules. The shape of the curve means that
a fall in PO2 from the normal arterial value will have little effect on the Hb
saturation (and therefore oxygen content) until the steep part of the curve
is reached, normally around 8kPa (60mmHg). Once the PO2 has reached
this level, however, a further decrease in PO2 will result in a dramatic fall in
the Hb saturation.

Causes of hypoxia

Hypoxia indicates the situation where tissues are unable to undergo normal
oxidative processes because of a failure in the supply or utilisation of
oxygen. The causes of hypoxia can be grouped in to 4 categories:

Hypoxic hypoxia

Hypoxic hypoxia is defined as an inadequate PO2 in arterial blood. This can


result from an inadequate PO2 in the inspired air (such as at altitude),
33

major hypoventilation (from central or peripheral causes) or from


inadequate alveolar-capillary transfer (such as shunt or V/Q mismatch).

Anemic hypoxia

The oxygen content of arterial blood is almost all bound to Hb. In the
presence of severe anaemia, the oxygen content will therefore fall in
proportion to the reduction in Hb concentration, even though the PO2 is
normal. The normal compensatory mechanism to restore oxygen delivery is
an increase in cardiac output, but when this can no longer be sustained
tissue hypoxia results. Conditions in which Hb is rendered ineffective in
binding oxygen, such as carbon monoxide poisoning, produce a reduction
in oxygen carriage similar to anaemia.

Circulatory or stagnant hypoxia

If circulatory failure occurs, even though the oxygen content of arterial


blood may be adequate, delivery to the tissues is not. Initially tissue
oxygenation is maintained by increasing the degree of oxygen extraction
34

from the blood, but as tissue perfusion worsens this becomes insufficient
and tissue hypoxia develops.

Histotoxic hypoxia

This describes the situation where cellular metabolic processes are


impaired to prevent oxygen utilisation by the cells, even though oxygen
delivery to the tissues is normal. The best-known cause of histotoxic
hypoxia is cyanide poisoning, which inhibits cytochrome oxidase.

Pathophysiology

Chronic Bronchitis

Chronic bronchitis is defined in clinical terms as a cough with sputum


35

production on most days for 3 months of a year, for 2 consecutive years.

Chronic bronchitis is hallmarked by the increased number


(hyperplasia) and increased size (hypertrophy) of the mucus-secreting
(goblet) cells of the airway. This, along with enlargement of the mucous
gland, results in an increase in production of mucus which contributes to
the airway obstruction. Microscopically there is infiltration of the airway
walls with inflammatory cells, particularly neutrophils. Inflammation is
followed by scarring and remodelling that thickens the walls resulting in
narrowing of the small airway. Further progression leads to an abnormal
change (metaplasia) in the nature of the tissue along with further
thickening and scarring (fibrosis) of the lower airway. The consequence of
these changes is a limitation of airflow.

Emphysema

There is permanent enlargement of the alveoli due to the destruction of the


walls between alveoli in emphysema. The destruction of the alveolar walls
reduces the elasticity of the lung overall. Loss of elasticity leads to the
36

collapse of the bronchioles, obstructing airflow out of the alveoli. Air


becomes "trapped" in the alveoli and reduces the ability of the lung to
shrink during exhalation. The reduced expansion of the lung during the
next breath reduces the amount of air that is inhaled. As a result, less air for
the exchange of gasses gets into the lungs. This trapped air also can
compress adjacent less damaged lung tissue, preventing it from functioning
to its fullest capacity.

The exchange of carbon dioxide and oxygen between air and the blood in
the capillaries takes place across the thin walls of the alveoli. Destruction of
the alveolar walls decreases the number of capillaries available for gas
exchange. This adds to the decrease in the ability to exchange gases.

Usually, energy is only required for inhalation to inflate the lungs. The
stretch of the lungs and distension of the chest cavity springs back to rest
during exhalation, a passive process that does not require energy. However,
in emphysema, inefficient breathing occurs because extra effort and energy
has to be expended to empty the lungs of air due to the collapse of the
airways. This essentially doubles the work of breathing, since now energy is
required for both inhalation and exhalation. In addition, because of the
reduced capacity to exchange gases with each breath (due to the collapse of
37

the bronchioles and loss of capillaries), it is necessary to breathe more


frequently.

What causes COPD?

Smoking is responsible for 90% of COPD in the United States. Although not
all cigarette smokers will develop COPD, it is estimated that 15% will.
Smokers with COPD have higher death rates than nonsmokers with COPD.
They also have more frequent respiratory symptoms (coughing, shortness
of breath, etc.) and more deterioration in lung function than non-smokers.

Effects of passive smoking or "second-hand smoke" on the lungs are not


well-known; however, evidence suggests that respiratory infections,
asthma, and symptoms are more common in children who live in
households where adults smoke.

Cigarette smoking damages the lungs in many ways. For example, the
irritating effect of cigarette smoke attracts cells to the lungs that promote
38

inflammation. Cigarette smoke also stimulates these inflammatory cells to


release elastase, an enzyme that breaks down the elastic fibers in lung
tissue.

Air pollution can cause problems for persons with lung disease, but it is
unclear whether outdoor air pollution contributes to the development of
COPD. However, in the non-industrialized world, the most common cause
of COPD is indoor air pollution. This is usually due to indoor stoves used
for cooking.

Some occupational pollutants such as cadmium and silica do increase the


risk of COPD. Persons at risk for this type of occupational pollution include
coal miners, construction workers, metal workers, cotton workers, etc.
(Most of this risk is associated with cigarette smoking and these
occupations, an issue not well controlled for. These occupations are more
often associated with interstitial lung diseases, especially the
pneumoconioses) Nevertheless, the adverse effects of smoking cigarettes on
lung function are far greater than occupational exposure.

Another well-established cause of COPD is a deficiency of alpha-1


antitrypsin (AAT). AAT deficiency is a rare genetic (inherited) disorder that
accounts for less than 1% of the COPD in the United States.
39

As discussed previously, normal function of the lung is dependent on elastic


fibers surrounding the airways and in the alveolar walls. Elastic fibers are
composed of a protein called elastin. An enzyme called elastase that is
found even in normal lungs (and is increased in cigarette smokers) can
break down the elastin and damage the airways and alveoli. Another
protein called alpha-1 antitrypsin (AAT) (produced by the liver and released
into the blood) is present in normal lungs and can block the damaging
effects of elastase on elastin.

The manufacture of AAT by the liver is controlled by genes which are


contained in DNA-containing chromosomes that are inherited. Each person
has two AAT genes, one inherited from each parent. Individuals who inherit
two defective AAT genes (one from each parent) have either low amounts of
AAT in the blood or AAT that does not function properly. The reduced
action of AAT in these individuals allows the destruction of tissue in the
lungs by elastase to continue unopposed. This causes emphysema by age 30
or 40. Cigarette smoking accelerates the destruction and results in an even
earlier onset of COPD.

Individuals with one normal and one defective AAT gene have AAT levels
that are lower than normal but higher than individuals with two defective
genes. These individuals MAY have an increased risk of developing COPD if
they do not smoke cigarettes; however, their risk of COPD probably is
40

higher than normal if they smoke. Though their Alpha-1 antitrypsin blood
levels may be in the normal range, the function of this enzyme is impaired
to relative to normals.

Symptoms of COPD

Typically, after smoking 20 or more cigarettes a day for more than twenty
years, patients with COPD develop a chronic cough, shortness of breath
(dyspnea) and frequent respiratory infections.

In patients affected predominantly by emphysema, shortness of breath may


be the major symptom. Dyspnea usually is most noticeable during
increased physical activity, but as emphysema progresses, dyspnea occurs
at rest.

In patients with chronic bronchitis as well as bronchiectasis, chronic cough


and sputum production are the major symptoms. The sputum is usually
clear and thick. Periodic chest infections can cause fever, dyspnea,
coughing, production of purulent (cloudy and discolored) sputum and
wheezing. (Wheezing is a high pitched noise produced in the lungs during
exhalation when mucous, bronchospasm, or loss of lung elasticity obstructs
airways.) Infections occur more frequently as bronchitis and bronchiectasis
progress.
41

In advanced COPD, patients may develop cyanosis (bluish discoloration of


the lips and nail beds) due to a lack of oxygen in blood. They also may
develop morning headaches due to an inability to remove carbon dioxide
from the blood. Weight loss occurs in some patients, primarily (other
possibility is reduced intake of food) because of the additional energy that is
required just to breathe. In advanced COPD, small blood vessels in the
lungs are destroyed, and this blocks the flow of blood through the lungs. As
a result, the heart must pump with increased force and pressure to get
blood to flow through the lungs. (The elevated pressure in the blood vessels
of the lungs is called pulmonary hypertension.) If the heart cannot manage
the additional work, right heart failure also known as Cor pulmonale results
and leads to swelling of the feet and ankles. Patients with COPD may cough
up blood (hemoptysis). Usually hemoptysis is due to damage to the inner
lining of the airways and the airways' blood vessels; however, occasionally,
hemoptysis may signal the development of lung cancer.
42

MATERIAL & METHODS

DIAGNOSIS OF COPD

COPD usually is first diagnosed on the basis of a medical history which


discloses many of the symptoms of COPD and a physical examination
which discloses signs of COPD. Other tests to diagnose COPD include chest
x-ray, computerized tomography (CT or CAT scan) of the chest, tests of
lung function (pulmonary function tests) and the measurement of oxygen
and carbon dioxide levels in the blood.

COPD is suspected in chronic smokers who develop shortness of breath


with or without exertion, have chronic persistent cough with sputum
production, and frequent infections of the lungs such as bronchitis or
pneumonia. Sometimes COPD is first diagnosed after a patient develops a
respiratory illness necessitating hospitalization. Some physical findings of
COPD include enlarged chest cavity and wheezing. Faint and distant breath
sounds are heard when listening to the chest with a stethoscope. Air is
trapped in the lungs from the patients inability to empty their lungs with
exhalation. This extra air dampens the sounds heard and results in the
overinflated chest cavity.
43

In patients affected predominantly with emphysema, the chest x-ray may


show an enlarged chest cavity and decreased lung markings reflecting
destruction of lung tissue and enlargement of air-spaces. In patients with
predominantly chronic bronchitis, the chest x-ray may show increased lung
markings which represent the thickened, inflamed and scarred airways.
Computerized tomography (CT or CAT scan) of the chest is a specialized x-
ray that can accurately demonstrate the abnormal lung tissue and airways
in COPD. Chest x-rays and CT scans of the chest also are useful in excluding
lung infections (pneumonia) and cancers. CT scan of the chest usually is not
necessary for the routine diagnosis and management of COPD.

The most commonly used pulmonary function test is spirometry, a test


which quantitates the amount of airway obstruction. During spirometry,
the patient takes a full breath and then exhales fast and forcefully into a
tube connected to a machine that measures the volume of expired air. The
FEV1 (the volume of air expired in 1 second) is a reliable and useful
measure of airflow obstruction. This is compared to the total amount of air
blown out of the lungs, the forced vital capacity (FVC). The ratio of the
FEV1 to the FVC is usually 70%. When obstruction is present, this ratio is
reduced; the lower the RATIO, the greater the airway obstruction. The
FEV1 can be determined again after treatment with bronchodilators.
44

Improvement in FEV1 after bronchodilator treatment means that airway


obstruction is reversible. Demonstrating improvement in FEV1 also helps
doctors select the proper bronchodilators for patients. Measurements of
FEV1 AND FVC can be repeated over time to determine how rapidly airway
obstruction is progressing.

Oxygen and carbon dioxide levels can be measured in samples of blood


obtained from an artery, but this requires inserting a needle into an artery.
A less invasive method to measure oxygen levels in the blood is called pulse
oximetry. Pulse oximetry works on the principle that the degree of redness
of hemoglobin (the protein in blood that carries oxygen) is proportional to
the amount of oxygen, that is, the more oxygen there is in blood, the redder
the blood. A probe (oximeter) is placed around a fingertip. On one side of
the finger the probe shines a light. Some of the light is transmitted through
the fingertip, and the transmitted light is measured on the opposite side of
the finger by the probe. Depending on the redness of the blood within the
fingertip (that is, the amount of oxygen in the blood) more or less light is
transmitted through the fingertip. Thus, by measuring the amount of light
transmitted, it is possible to determine the amount of oxygen in the blood.
45

Treatment is available for COPD

The goals of COPD treatment are 1) to prevent further deterioration in lung


function, 2) to alleviate symptoms, 3) to improve performance of daily
activities and quality of life. The treatment strategies include 1) quitting
cigarette smoking, 2) taking medications to dilate airways
(bronchodilators) and decrease airway inflammation, 3) vaccinating against
46

flu influenza and pneumonia and 4) regular oxygen supplementation and 5)


pulmonary rehabilitation.

Quitting cigarette smoking

The most important treatment for COPD is quitting cigarette smoking.


Patients who continue to smoke have a more rapid deterioration in lung
function when compared to others who quit. Aging itself can cause a very
slow decline in lung function. In susceptible individuals, cigarette smoking
can result in a much more dramatic loss of lung function. It is important to
note that when one stops smoking the decline in lung function eventually
reverts to that of a non-smoker.

Unfortunately, only about one third of the patients can abstain from
smoking long term. Reasons for difficulty in quitting include nicotine
addiction, stress in the workplace and at home, depression, peer pressure,
and advertising from cigarette companies.

Nicotine in cigarettes is addictive, and, therefore, cessation of smoking can


cause symptoms of nicotine withdrawal including anxiety, irritability,
anger, depression, fatigue, difficulty concentrating or sleeping, and intense
craving for cigarettes. Patients likely to develop withdrawal symptoms
typically smoke more than 20 cigarettes a day, need to smoke shortly after
47

waking up in the morning, and have difficulty refraining from smoking in


non-smoking areas. However, some 25% of smokers can stop smoking
without developing these symptoms. Even in those smokers who develop
symptoms of withdrawal, the symptoms will decrease after several weeks of
abstinence.

To help those patients with symptoms of withdrawal during the early weeks
of smoking cessation, nicotine chewing gum (Nicorette Gum) and nicotine
skin patches (Transderm Nicotine) are available in the United States. Both
the gum and skin patches can deliver enough nicotine into the blood to
reduce but not totally eliminate withdrawal symptoms. Nicotine
replacement methods in conjunction with intense patient education and
behavioral modification programs have improved the rates at which
individuals quit smoking. Nicotine skin patches are easy to use. They
generally are used for four to six weeks, sometimes with a tapering period
of several additional weeks. The addiction potential of nicotine skin patches
is low.

Bupropion (Zyban, Wellbutrin) is an antidepressant that has been found to


decrease cravings for cigarettes. It has been shown to be of benefit to
patients who want to quit smoking. Recently, varencline (Chantix), a new
medication is available to aid in smoking cessation, has been approved for
use in the US. Varenicline works in two ways; by cutting the pleasure of
48

smoking and reducing the withdrawal symptoms that lead smokers to light
up again and again. This medicine is taken over a 12 week course and can
work in ways that bupropion does not.

In addition to nicotine withdrawal symptoms, quitting cigarette smoking


also may lead to weight gain of about 8-10 pounds on average though more
in some patients. Quitting smoking also can lead to depression and
worsening of symptoms of chronic ulcerative colitis. Therefore quitting
smoking should be undertaken with a doctor's supervision. Nevertheless,
the benefits of quitting smoking (decreasing the rate of lung deterioration,
decreasing risks of heart attack, lung cancer and other cancers, decreasing
the chance of developing stomach ulcers, etc.) far outweigh these potential
negative effects.

For more information on quitting cigarette smoking, please read the


Smoking and Quitting Smoking article.

Bronchodilators

Treating airway obstruction in COPD with bronchodilators is similar but


not identical to treating bronchospasm in asthma. Bronchodilators are
medications that relax the muscles surrounding the small airways thereby
opening the airways. Bronchodilators can be inhaled, taken orally or
49

administered intravenously. Inhaled bronchodilators are popular because


they go directly to the airways where they work. As compared with
bronchodilators given orally, less medication reaches the rest of the body,
and, therefore, there are fewer side effects.

Metered dose inhalers (MDIs) are used to deliver bronchodilators. An MDI


is a pressurized canister containing a medication that is released when the
canister is compressed. A standard amount of medication is released with
each compression of the MDI. To maximize the delivery of the medications
to the airways, the patient has to learn to coordinate inhalation with each
compression. Incorrect use of the MDI can lead to deposition of much of
the medication on the tongue and the back of the throat instead of on the
airways.

To decrease the deposition of medications on the throat and increase the


amount reaching the airways, spacers can be helpful. Spacers are tube-like
chambers attached to the outlet of the MDI canister. Spacer devices can
hold the released medications long enough for patients to inhale them
slowly and deeply into the lungs. Proper use of spacer devices can greatly
increase the proportion of medication reaching the airways.
50

The role of oxygen as therapy in COPD

Sufficient oxygen is a requirement for the proper function of tissues in the


body. Among all individuals, including those with COPD, there is a
protective mechanism in the lung that causes constriction of blood vessels
in areas of the lung that have a low concentration of oxygen because they
are not being ventilated well. Constriction of the blood vessels in these
areas prevents blood from traveling through these poorly-ventilated parts
of the lung where there can be little exchange of oxygen (and carbon
dioxide). Instead, blood is diverted to other well-ventilated parts of the lung
where exchange can take place. Unfortunately, although this mechanism
improves the efficiency of oxygen and carbon dioxide exchange, the
constriction of the blood vessels also causes the blood pressure in the lungs
to rise, a condition called pulmonary hypertension. The increased pressure
requires the heart to work extra hard to pump blood to the lungs, and the
right side of the heart (which is the side of the heart that pumps blood to
the lungs) may fail from the extra work. This often can be detected first in a
patient by the presence of ankle swelling.

Oxygen from tanks or concentrators (devices that concentrate oxygen in the


air) that is inhaled by patients with COPD through masks or cannulas can
relax the blood vessels and decrease blood pressure in the lung. This
decreases the work that the right side of the heart must perform and can
51

improve heart failure. Newer technology allows for very light weight tanks
that supply many hours of oxygen therapy. These devices increase the
mobility and hence the quality of life in these COPD patients.

Oxygen requirements can vary in patients with COPD. Some require oxygen
continuously while others only need oxygen with exercise or sleep. These
needs are determined by measurements of oxygen levels either with an
arterial blood gas (ABG) measurement or by oximetry. It is important to
note that not all patients perceive their oxygen requirements correctly.
Thus, some patients with COPD can have severely reduced levels of oxygen
and be unaware of it. These patients may resist using oxygen; however,
many scientific studies have demonstrated that using oxygen appropriately
prolongs the lives of these patients.

What else is available for treating COPD?

Pulmonary rehabilitation has become a cornerstone in the management of


moderate to severe COPD. Pulmonary rehabilitation is a program of
education regarding lung function and dysfunction, proper breathing
techniques (diaphragmatic breathing, pursed lip breathing), and proper use
of respiratory equipment and medications. An essential ingredient in this
52

program is the use of increasing physical exercise to overcome the reduced


physical capacity that usually has developed over time. In addition,
occupational and physical therapies are used to teach optimal and efficient
body mechanics.

Lung volume reduction surgery (LVRS) has received much fanfare in the
lay press. LVRS is a surgical procedure used to treat some patients with
COPD. The premise behind this surgery is that the over-inflated, poorly-
functioning upper parts of the lung compress and impair function of the
better-functioning lung elsewhere. Thus, if the over-inflated portions of
lung are removed surgically, the compressed lung may expand and function
better. In addition, the diaphragm and the chest cavity achieve more
optimal positioning following the surgery, and this improves breathing
further. The best criteria for choosing patients for LVRS are still uncertain.
A national study was completed in 2003. Patients primarily with
emphysema at the top of their lungs, whose exercise tolerance was low even
after pulmonary rehabilitation, seemed to do the best with this procedure.
On average, lung function and exercise capacity among surviving surgical
patients improved significantly following LVRS, but after two years
returned to about the same levels as before the procedure. Patients with
forced expiratory volume in FEVI of less than 20% of predicted and either
diffuse disease on the CAT scan or lower than 20% diffusing capacity or
elevated carbon dioxide levels had higher mortality. The role of LVRS is at
53

present is very limited.

Future Directions in COPD

As opposed to bronchial asthma, which has been well researched in the last
20 years, COPD has not been fully investigated. There is significant
evidence that COPD is an inflammatory process just as is bronchial asthma,
however, it seems that there are different patterns of lung inflammation in
these patients. The mechanisms of baseline inflammation in COPD and
inflammation during exacerbation of the disease need to be investigated
and better understood. There is minimal or no information on the
molecular mechanisms of inflammation in stable COPD patients. This latter
issue becomes important particularly in the area of treatments. Currently,
there are numerous clinical trials looking to intervene at the various
inflammatory pathways.

A newer class of medications that work to reduce this inflammation is being


developed. They are referred to as PDE4 inhibitors. Drugs under
investigation include rolipram, piclamilast, cilomilast, and Roflumilast.
These inhibitors reduce the number and the activity of the different types of
inflammatory cells and inflammatory substances seen in COPD.

The concept of attempting to reduce hyperinflation is intriguing. Less


54

invasive procedures than LVRS are being developed to reduce this air
trapping. Investigational devices are being studied that are valve-like and
are placed directly in the airways by bronchoscope. The effectiveness of
these devices is unknown.

Another area of interest is the genetic mechanisms of why only a fraction of


smokers develop emphysema. A third area of research interest is the role of
nerve receptors in the lungs, which is currently the focus of final clinical
trials. Finally, methods for early detection of COPD need to be refined.
55

HOW SERIOUS IS CHRONIC OBSTRUCTIVE LUNG


DISEASE?

Impaired lung function reduces survival, even in nonsmokers. Chronic


obstructive lung disease is responsible for more than 100,000 deaths in the
US each year, making it the fourth leading cause of death. It is the only
major cause of death that is rising in both prevalence and mortality.

General Outlook

Chronic obstructive lung disease is progressive, although when patients


stop smoking the disease often levels off. Patients with frequent acute
exacerbations of COLD are at higher risk for disease deterioration,
including reduced quality of life and increasing rates of hospitalizations.
Acute exacerbations can be defined as the following:

Worsened shortness of breath

Increased in thickness and color change in sputum


56

Increased sputum volume

can be triggered by respiratory infections, environmental conditions,


or medical disorders (eg, heart failure, infections outside the lungs,
pulmonary embolisms.)

Outlook for Patients with Emphysema. If emphysema is detected before it


causes symptoms, there may be some chance of reversing it, although
permanent changes in the alveoli usually occur even in young smokers.
Patients with the inherited form of early-onset emphysema are at risk for
early death unless the disease is treated and its progression halted or
slowed. Emphysema patients who experience severe involuntary weight
loss (which indicates muscle wasting) have a poorer outlook, regardless of
lung function.

Outlook for Patients with Chronic Bronchitis. Chronic bronchitis does not
cause as much lung damage as emphysema, although the airways become
blocked from mucous plugs and narrowing due to inflammation. This poor
ventilation causes reduced levels of oxygen and high carbon dioxide levels.

Limitations in Daily Life

Nearly half of those with COLD report that daily activities are limited. They
57

have trouble walking upstairs or carrying even small packages. Breathing


becomes hard work.

Complications from Oxygen Deprivation

Over time, both varieties of COLD cause low oxygen levels ( hypoxia) and
high levels of carbon dioxide ( hypercapnia). In order to boost oxygen
delivery, the body compensates in a number of ways:

The rate of breathing is increased.

More red blood cells are produced to increase the blood's oxygen-
carrying capacity.

The heart rate increases to pump more blood.

Vessels in the lung constrict to force blood and oxygen through the
circulatory system.

Eventually these activities can lead to very serious and even life-threatening
conditions:

Patients with prolonged and severe hypoxia and hypercapnia are at


58

risk for acute respiratory failure, which can cause heart rhythm
abnormalities or other life threatening conditions if not treated
immediately.

Abnormally high pressure in the lungs ( pulmonary hypertension )


can cause a complication called cor pulmonale , in which the right ventricle
of the heart enlarges, eventually leading to heart failure.

Low oxygen levels can also impair mental functioning and short-term
memory.

Infections

Any disease that affects the lungs is dangerous for COLD patients.
Pneumonia can cause acute attacks of chronic bronchitis, which in turn
may precipitate acute respiratory failure, which is life threatening for COLD
patients. Viral or bacterial infections in the lungs, seasonal changes, certain
medications, and exposure to irritants in the air may also trigger serious
lung events.
59

HOMOEOPATHIC APPROACH

Homoeopathy revolves around vital force, for it believes in natures law of


cure.

Aphorism 26 A weaker dynamic affection is permanently extinguished in


the living organism by a stronger one, if latter (whilst differing in kind) is
similar in manifestation.

We the Hahnemannian followers believe vital force gets deranged by a


dynamic power (Explain in foot note of Aphorism 12) and this deranged
60

vital force begins to gives it manifestation in form of sign and symptoms


which we call as disease. This deranged vital force can only be corrected by
Homoeopathic medicines which have dynamic power embedded in them.
They cure on the lines of Similia Similibus Curantur. For this a proper case
taking as indicated in aphorism 83-104 has to be taken and only those
medicine are to be prescribed which are similimum to the case following to
the norms of drug proving as indicated in aphorism 105-145.

The heart of the prescription is the analysis of the case which involves,

1. We must perceive what is to be cured and ask what is the most


important in this case?

2. Analysis of the symptom i.e. they have to be graded according to


the grade they need to sort in the end.

3. Etiology i.e. exciting or maintain cause not from materialistic


point of view.

Every case needs to be individualized. According to homoeopathy a single


individual may have different layers of predisposition; each gives way to the
61

other that is to say during the process of cure if symptoms which were
according to similimum medicine have been removed, the left over will
form different layer and will at times required different medicine. All these
layers need to be eradicated to come to the cure.

COPD is not a single layer disease; it has large number of layers of pre
disposition with miasmatic block.

Constitutional Prescribing in Homoeopathy

According to Dr. Von Grauvogyl, there are three constitution..

1. Hydrogenoid

2. Oxygenoid

3. Carbonitrogenoid

COPD lies in oxygenoid constitution which corresponds to Hahnemanns


62

syphilis.

Grauvogyl says constitution whether is of grave character. The blood is a


product of organism and its elaboration is hundred down from parents to
children for generations. Immunity may also be inherited. A weekend
power resistance destructive energy of oxygen may be acquired by attacks
of acute disease, which is leading cause in COPD. Organism causing attack
induces the most instance process of reduction. So changing the
constitution of the body as to render it unable to resist an immediate influx
of oxygen. Oxygenoids or worst when dryness is changing to humidity,
before storms, before and during tempestuous winds and better when it
begins to rain and electrical equilibrium is restored. They are worse in foggy
weather and when with a temperate air, mist rise cold sea air and low
altitudes.

MIASMATIC APPROACH

The word miasm has originated from Greek word which literally means
obnoxious agent but Dr. Hahnemann has used this in much more precise
form and is used in sense of chronic syndrome. His repeated failures of
complete cure in chronic diseases led him to bring forth miasmatic
63

approach.

In Aphorism 5 he says, Useful to the physician in assisting him to cure in


the whole history of the chronic disease, to enable him to discover its
fundamental cause which is generally due to chronic miasm.

According to Hahnemann there are three miasm; psora, syphilis, and


sycosis, COPD lies largely in domain of Syphillitic maism, which is
characterized by distruction and there is obvious destruction in alveoli in
case of COPD. Patient feels worse at night and during morning hours. There
is barking cough which may be paroxysmal and cough is an accompanied by
tasteless yellowish, greenish or clear sticky thread like discharge. Dyspnoea
before going to bed or lying down is indicative of syphilitic miasm. For
reference purposes miasmatic approach in respiratory system a chart
covering all miasm. (ANNEXTURE I)
64

MEDICINES FOR COPD ALONG WITH INDICATION


IN HOMOEOPATHY

ACONITE NAP

Physical and mental restlessness.Acute, sudden and violent attack of


asthma. Complaints caused by exposure to dry cold weather, draught of cold
air. Oppresed breathing on least motion. Hoarse dry cough, child grasps at
throat every time he coughs. Very sensitive to inspired air. Cough dry, short,
65

hacking worse at night and after midnight.

ANT TART

Hoarseness. Great rattling of mucus but very little is expectorated.


Burning sensation in chesst, which extends to throat? Raoid, short difficult
breathing; seems as if he would suffocate, must sit up. Dizziness with cough.
Dyspnea relieved by eructation. Cough and dyspnea better on lying on right
side. Asthma after vaccination.

ARS -ALB

Unable to lie down. Fears suffocation, air passages constricted. Asthma


< midnight. Burning in chest. Suffocative cattarh, cough worse after midnight
,lying on back. Expectoration scanty, frothy, wgeezing resoiration.
Unquenchable thist and restlessness.
66

ARS IOD

Slight hacking cough with dry and stopped up nostrils. Pneumonia that
fails to clear up. Cough dry, with little difficult expectoration. Hay fever also
present.

AMBRA GRISEA

Asthmatic breathing with eructation of gas. Nervous, spasmodic cough,


with hoarseness and eructation on waking in morning, worse in presence in
other people. Choking when hawking up phlegm.

BAR CARB

Dry, suffocative cough, especially in old people full of mucus, but


lacking strength to expectorate worse every change of weather. Larynx feels as
if smoke were inhaled. Stitches in chest, worse inspiration. Lungs feel full of
smoke.
67

CARB VEG

Wheezing and rattling of mucus in chest. Occasional spells of long


coughing attacks. Cough with burning in chest worse in evening, open air, after
eating and talking. Breath cold must be fanned. Asthma in aged with blue skin.

CHAMOMILLA

Sensitive, irritable, thirsty, hot and numb. Hoarseness, hawking,


rawness of larynx. Irritable, dry, tickling cough, suffocative tightness of chest
with bitter expectoration in daytime. Rattling of mucus in childs chest.

CONIUM

Dry cough, almost continuous, hacking worse evening and at night,


caused by dry spot in larynx with itching in chest and throat when lying down,
talking or laughing and during pregnancy. Expectoration only after long
68

coughing.

IPECAC

Dyspnea. Constant constriction in chest, wheezing cough. Cough incessant


and violent with every breath. Chest seems full of phlegm but does not yield to
coughing, suffocative cough. Child becomes stiff and blue in the face. Cough
with nausea.

KALI CARB

Cutting pain in chest; worse lying on right side. Hoarseness and loss of
voice. Dry hard cough about 3 am with stitching pains and dryness of pharynx.
Whole chest is very sensitive. Expectoration scanty and tenacious, but
increasing in morning and after eating; aggravated right lower chest and lying
on painful side.
69

KALI SULPH

Coarse rales. Rattling of mucus in chest. Post grippal cough, especially


in children. Bronchial asthma, with yellow expectoration. Cough worse in
evening and in hot atmosphere.

SAMBUCUS

Chest oppressed with pressure in stomach and nausea. Hoarseness


with tenacious mucus in larynx .Paroxysmal, suffocative cough, coming on
about midnight with crying and dyspnea. Child awakes suddenly, nearly
suffocating, sits up, can not expire.

SENEGA

Cough often ends in a sneeze. Rattling in chest oppressed on


ascending. Bronchial catarrh, with sore chest walls; much mucus; difficult
raising of tough, profuse mucus, in the aged. Astenic bronchitis of old people
with chronic nephritis or chronic emphysema. Old asthmatics with congestive
70

attacks. Exudations in pleura.

ARS ALB

The patient is leaning thin and debilitated with waxy look of the skin.
Very fastidious wants everything neat, clean and in order. Chilly patient. He
has great fear of death. Thinks he is incurable. Mentally restless but physically
too weak to move about. Burning pain relieved by heat except in head. Great
prostration. Complaints return periodically. Desires for acids, coffee, alcohol,
cold drinks. Thirst for small quantities of water at small intervals in acute
states but in chronic state there is no thirst. Asthma comes on or aggravated by
suppressed eruptions, cold things and cold food. All symptoms are aggravated
by midday and midnight and ameliorated by heat.

CALC CARB

Leucophlegmatic constitutions. Fair, fatty and flabby patients who


becomes easily fatigued on walking with much sweating, cold extremities and
sour smell of the body. Tendency to obesity in youth. Great apprehension. Fear
71

of animals in evening, of infections, of insanity. The least mental excitement


causes profuse return of menstrual flow. Chilly patient. Sweats profusely, while
sleeping wetting pillow far around. Desire of eggs, undigestible things.
Aversion to meat, fat, milk and coffee. Sleep position on back, on side. All
symptoms < cold air, wet weather, cold water, morning. > lying on painful side.

IODUM

Profound debility and general emaciation with a low cachectic condition.


Very hot patient. Ravenous hunger; feels relieved while eating and after eating.
Losing flesh while eating well. All glands of the body are hypertrophied and
enlarged except the mammary gland. Intense restlessness and apprehension.
Discharges are acrid and corrosive. Pulsation all over the body. Sensation of
constriction and ssqueezing, especially in heart. All symptoms are worse from
warmth in general and better from cold in general.

KALI CARB
72

The patient is very much oversensitive to touch. Pains are stitching,


darting, worse during rest and lying on affected side. Bag like swelling between
the upper eyelids and eyebrows. Backache accompanies all complaints. Sweat,
backache and weakness as a combination found in this medicine. Great
debility, so much so that drops into a chair or throws him on the bed
completely exhausted. Early morning aggravation is very characteristic
particularly between 2 to 4 am. All symptoms < after coition, at rest, in
morning, in cold weather, from coffees and soup, lying on painful side and left
side. > by warm weather, by rocking, during day when moving about.

LYCOPODIUM

The patients are intellectually keen but physically weak. Upper part of
the body is emaciated, lower part semi dropsical. Complaints start on right side
and go to left. Sourness of the discharges. Intolerance of cold drinks; craves
everything warm. Desire for sweet things, warm food and drink. Aversion to
tobacco, bread, coffee. Canine hunger, but few mouthfuls fill up to the throat.
Acidity, wind and bloating of abdomen especially the lower abdomen. Half
open condition of the eyes during sleep. Right foot hot and left cold. All
symptoms < from 4 8 pm, right side, from heat, warm air. > From warm food
and drink (only stomach and throat symptoms); from uncovering the head and
73

loosening the garments, in open air.

MEDORRHINUM

In all cases of constitutional effects of maltreated or suppressed gonorrhea


when best selected remedy fail to relieve or permanently improve. Soreness all
over the body especially glands with burning in hands and feet. Trembling all
over the body. State of collapse, wants to be fanned all the time. Coldness all
over still does not like covering. Intense restlessness and fidgety feeling in legs
and feet. Inordinate craving for liquor, salt, sweet and acid. Backache relieved
by profuse urination. Dyspnea relieved by lying on face and protruding tongue.
All symptoms < when thinking of them, from sunrise to sunset, heat,
thunderstorm, covering and sweat. > at seashore, lying on stomach and damp
weather.
74

NATRUM SULPH

Hydrogenoid constitution. Left sided affections. Worse by dampness of


weather, in damp house and cellers. Discharges are thick, yellowish and
greenish. Ailments from abuse of quinine, neglected cases of gonorrhoea and
mental trauma. Music makes her sad. Constant desire to take deep breath in
wet weather. Burning thirst for cold drinks, especially in evening. All symptoms
< damp basement, damp weather, rest, lying down and music. >dry weather,
pressure, changing position.

PHOSPHORUS

Tall slender persons with narrow chest. Tubercular diathesis. Burning


anywhere and everywhere all over the body. A weak, empty all gone sensation
in head, chest and abdomen. Craving cold things, ice-cream, acids, wine, sour
things, salts and fatty food. Aversion to tobacco, sweets tea pudding, coffee.
Oversensitiveness of all senses. Restlessness, constant fidgety feeling all over
the body. Vicarious menstruation. All symptoms < evening and before
midnight, lying on left side, during a thunderstorm, any change of weather and
extremes of temperature. > lying on right side, from being rubbed or
magnetized, from cold water, cold food and in darkness.
75

SILICEA

Highly chilly patient. Wraps himself with warm clothing even in hot
summer weather. Bad effects of vaccination. Every little injury suppurates.
Want of grit either moral or physical. Very sensitive to all impressions.
Obstinate constipation, when partly expelled recedes back. Constipation before
during and after menses. Desire for cold drinks, cold food, ice cream. Seats of
hands, toes feet axillae very offensive. All symptoms < in new moon and full
moon, cold, during menses, from washing and uncovering. > By warmth,
wrapping up head and in summer.

SULPHUR

Complaints that are continually relapsing. Standing is the most


uncomfortable position. Burning anywhere and everywhere on the body. A
weak empty all gone sensation in the stomach. Congestion in single parts.
Intense craving for sweets, acid, alcohol, beer. Aversion to milk, meat and
business. Discharges are offensive and acrid. All symptoms < standing, at rest,
warmth of bed, washing, bathing, from alcoholic stimulants and changeable
weather. > dry warm weather and lying on right side.
76

THUJA

Fig warts, condylomata and wart like excrescences upon the mucous
membrane and cutaneous surface of the body. It is a left sided drug. Bad effects
of vaccination. Sweat only on the covered parts or all over body excepting the
head especially at night. Vertigo when closing the eyes. Desire for salt, cold
food and drinks. Rheumatism, prostatitis, impotency linked with suppressed
gonorrhoea. All symptoms < at night, at 3 pm and 3 am, from cold,damp air,
cold water, after taking breakfast, fat , coffee, tea, tobacco, touch. > in open air,
warmth, by movement, pressure, rubbing.

PREVENTIVE CARE
77

Don't smoke

If you already smoke, quit before there has been permanent damage
to your lungs

If you have COPD, avoiding respiratory infections is very important.


Your doctor will recommend that you receive an influenza vaccine each year
and that you receive a pneumococcal vaccine once in your lifetime to
protect you from pneumonia. Caused by this particular organism.

Eating foods rich in antioxidants, magnesium and other minerals,


and omega-3 fatty acids (including fruits, vegetables, and fish) may help
prevent the development of COPD in the first place avoid worsening of your
symptoms if you already have this lung condition.

Diet

Some evidence suggests that poor nutrition, particularly deficiencies in


antioxidants and certain minerals including vitamins A, C, and E,
potassium, magnesium, selenium, and zinc is associated with having COPD
and, possibly, with worsened lung function. Such nutrients can be obtained
from an adequate daily intake of fresh fruits and vegetables, nuts, and
whole grains.
78

Exercise

Exercise helps some people with COPD. By strengthening your legs and
arms and improving endurance, you may reduce breathlessness somewhat.
Walking, for example, is a good exercise to build endurance. Talk to your
doctor and/or respiratory therapist about how to build up slowly and safely.
Attending a comprehensive pulmonary rehabilitation is the best way to
learn exercise and safe breathing techniques (see below).

Breathing

There are breathing exercises (for example, a pursed lip technique,


breathing from the diaphragm, or using a spirometer [breathing device]
twice a day) that may help improve lung function. Talk to your doctor about
working with a respiratory therapist in order to learn such exercises. It is
important, when learning breathing techniques, to work with an
appropriately trained professional because the techniques are not good for
everyone with COPD. Attending pulmonary rehabilitation is the best way to
learn exercise and breathing techniques.

Nutrition and Dietary Supplements

Because supplements may have side effects or interact with


79

medications, they should be taken only under the supervision of a


knowledgeable healthcare provider. Be sure to talk to your physician about
any supplements you are taking or considering taking.

Bromelain

Although not studied in people with COPD specifically, bromelain (a


mixture of protein-digesting enzymes found in pineapples [Ananas
comosus]) can help reduce cough and diminish mucus production from a
respiratory infection. In theory, therefore, it may be able to do the same if
you have chronic bronchitis.

Magnesium

Magnesium deficiency may be associated with an increased risk of


developing emphysema and other lung diseases. Sometimes, intravenous
magnesium (that is, magnesium delivered through a vein) is part of the
treatment for a COPD flare-up in the hospital. The doctor will determine if
this is necessary or appropriate.
80

It is not known whether eating foods rich in magnesium or taking


magnesium supplements will reduce your chances of developing
emphysema. Such foods, however, including legumes, whole grains, and
green leafy vegetables, should be a regular part of a healthy diet anyway.

Some clinicians recommend checking your magnesium level (a simple


blood test) if you have COPD and taking magnesium supplements if your
levels are low.

N-acetylecysteine (NAC)

A review of scientific studies found that NAC may help dissolve mucus
and improve symptoms associated with chronic bronchitis and
emphysema. Smokers may also benefit from NAC supplementation. Studies
on large groups of people have found that NAC appears to have cancer
prevention properties in people who are at risk for lung cancer (like chronic
smokers who are also at risk for COPD).

Omega-3 Fatty Acids

Some experts believe that dietary and supplemental forms of omega-3


fatty acids, including alpha-linolenic acid (ALA) found in walnuts and
flaxseeds, may prove helpful as part of your treatment for COPD. Scientific
81

research is needed.

Vitamin C

According to some clinicians, taking vitamin C supplements is "safe and


reasonable" if you have COPD, especially if you continue to smoke.
Research to date is limited, however, and more studies are needed to know
if this is truly helpful if you have COPD. In the interim, it is worthwhile to
obtain adequate amounts of vitamin C by eating plenty of fresh fruit. In
fact, just increasing the amount of fruit you eat by one or two servings per
week may help improve lung function.

Other

Other supplements that have gained popularity for COPD, but need
further study before comment can be made regarding their value include:

Coenzyme Q10

L-carnitine
82

MASTER CHART

S. Name Ag Presenting Prescription Prescrip- Result


N e/ Complaints Basis tion
o Se
x

Anurag 36/ Dyspnoea so much Medicine was Kali nit. Relieved


1. Rai. m that breath cant be prescribed on the 30/tds for 3 .
held long enough to therapeutic basis. days.
drink, though thirsty
with oppression of
chest.
83

Bhavya 35/ Dyspnoea and Medicine was Lobelia Relieved


2. Bhatnag m constriction of chest prescribed on the 30/tds for 3 .
ar. worse by any exertion. therapeutic basis. days.
Attacks are preceded
by prickling all over
the body.

Jaya 40 Shortness of breath Medicine was Ipecauch Slight


3. Verma. /f with incessant and prescribed on the 30/ tds for 3 improve
violent cough which therapeutic basis. days. ment.
aggravates with every
breath with constant
nausea.
84

4 Meenaks 52/ Asthama, hot patient, Medicine was Pulsatilla 1 Slight


. hi. m aggravated in closed prescribed on the m /3 doses improve
and warm room, amel constitutional and sl/ tds ment.
in open air. Mild and basis. for 7 days.
yielding nature.
Weeps easily even
while narrating her
complaints.

Om 40 Dyspnoea agg on Medicine was Psorinum Relieved


5. Prakash /m sitting up and relieved prescribed on the 30/ tds for 3 .
by lying down and therapeutic basis. days.
keeping arms wide
apart. Patient is chilly.
85

Akash 42/ Asthmatic attacks Medicine was Nux Vomica Slight


6. m with gastric prescribed on the 30/ tds for 4 improve
disturbances relieved therapeutic basis. days. ment.
by belching with
feeling of constriction
in lower part of chest.

Sumit 55/ Dyspnoea and Medicine was Arsenic Relieved


7. Singh m oppression of chest prescribed on the album 30/ .
after midnight therapeutic basis. tds for 3
specially at 2 am. days.
With excessive
restlessness and
anxiety, cant even lie
down for the fear of
suffocation. Thirst for
small quantities of
water at small
intervals. Attacks are
amel by blending
forward.
86

Navneet 12/ Asthmatic attacks are Medicine was Natrum Relieved


8. m agg on change of prescribed on the Sulph 1m/ 3 .
weather esp in damp constitutional doses and
weather with rattling basis. sl/ tds for 76
in chest. After each days.
attack he has
diarrhea. An attack
generally comes on
about 4 am. Burning
thirst for cold drinks
and amel in dry
weather.
87

9. Archana 26/ Asthmatic attacks Medicine was Sulphur 1m/ Relieved


f with great burning in prescribed on the 3 doses and .
chest. Dyspnoea constitutional sl/ tds for 7
occurs in the middle basis. days.
of night, relieved by
sitting up. Hot
patient, symptoms agg
during summers,
desire sweets,
excessive
perspiration.
88

1 Alok 40 Dyspnoea and Medicine was Medorrhinu Relieved


0. Shukla /m oppression of chest, prescribed on the m 1m/ 3 .
relieved by lying on constitutional doses and
stomach, agg by basis. sl/ tds for 7
thinking of his days.
complaints and from
sunrise to sunset.
Craving for liquor,
salt, sweet and acid.
Burning in hands and
feet. Collapsed state
during the
attacks,wants to be
fanned all the time.
>damp weather.
89

SYNOPSIS OF CASES

1. Mr. Anurag Rai 36/m/h suffers from dyspnoea so much that breath
cant be held long enough to drink, though thirsty, since last night. He
is also complaining of oppression of chest. On the basis of local
symptoms kali nit. 30 were prescribed.

2. Mr. Bahvya Bhatnagar 45/m/h suffers from dyspnoea and


constriction of chest worse by any exertion. Asthmatic attacks are
preceded by prickling sensation all over the body. The symptoms seen
to arise from stomach. On the basis of local symptom Lobelia 30 was
prescribed.

3. Mrs. Jaya Verma 40/f/h suffers from asthma for last 15 years. During
the attack there is difficult shortness of breathing. She has incessant
and violent cough which increases with every breath. Symptoms are
attended with constant nausea. On the basis of local symptom Ipecac
30 was prescribed.

4. Mrs Meenakshi 52/f/h suffers from asthma since 20 years. She is a


hot patient. Her complaints aggravate in closed and warm room and
90

are relieved in warm room. She is very mild and yielding in


deposition. She weeps very easily even while narrating her
complaints. On the constitutional basis Pulsatilla 1m was prescribed.

5. Mr. Om Prakash 40/m/h suffers from dyspnoea and oppression of


chest since last night. Symptoms are aggravated by sitting up and
better by lying down and keeping arms wide apart. He is very chilly.
On the basis of local symptom Psorinum 30 was prescribed.

6. Mr. Akash 42/m/m suffers from asthmatic attacks with constriction


in lower part of chest. These attacks are brought on by gastric
disturbances. There is some relief by belching and loosening the
clothes. On the basis of local symptom Nux vomica 30 was
prescribed.

7. Mr. Sumit Singh 55/m/h suffers from dyspnoea for last 2 days. The
attacks come after midnight specially at 2 am. During the attack he
becomes excessively restless and anxious, canto the writ petition.
Even lie down for the fear of suffocation. Attacks are ameliorated by
bending forward. He is thirsty during the attack but can drink only a
small quantity of water. On the therapeutic basis Arsenic album 30
was prescribed.
91

8. Mr. Navneet 12/m/h suffers from asthma for last 2 years. The
symptoms aggravated on change of whether especially in damp
weather. There is great rattling in chest. After each attack he suffers
from diarrhea. The attacks generally come on about 4 am with
greenish and copious expectoration. He has burning thirst for cold
waters. Symptoms are ameiliorated in dry weather. On the
constitutional basis Natrum Sulp 1m was prescribed.

9. Mrs. Archana 26/f/h has asthma for the last 10 years. The attacks are
attended with great burning in chest. Dyspnoea occurs in the middle
of night which is relieved by sitting up. She is a hot patient and the
symptoms sggravate in summers. She has strong desire for sweets
and is very thirsty. She has excessive offensive perspiration. On the
constitutional basis Sulphur 1m was prescribed.

10. Mr. Alok Shukla 40/m/h suffers from dyspnoea and oppression of
chest. Asthmatic attacks are relieved by lying on stomach and are
aggravated while thinking of his complaints and from sunrise to
sunset. He has inordinate craving for liquor, salt, sweet and acid.
There is great burning in hands and feet. During the attacks there is a
collapsed state and he wants to be fanned all the time. On the
constitutional basis Medorrhinum 1m was prescribed.
92

AUXILIARY TREATMENT

Herbs

The use of herbs is a time-honored approach to strengthening the body


and treating disease. Herbs, however, contain active substances that can
trigger side effects and interact with other herbs, supplements, or
medications. For these reasons, herbs should be taken with care and only
under the supervision of a practitioner knowledgeable in the field of herbal
medicine. Also, be sure to talk to your physician about any herbs that you
are taking or considering taking.

Herbs that an herbal specialist might recommend based on clinical


experience, particularly during a flare-up of your chronic bronchitis
include:
93

Eucalyptus (Eucalyptus globulus) acts as an expectorant, which


means that it loosens phlegm in the respiratory passages, making it easier
to cough up mucus from your airways.

Garlic (Allium sativum) may help fight infection and has antioxidant
properties (see earlier discussion under Diet in section entitled Lifestyle as
well as the section on Nutrition and Dietary Supplements).

Licorice (Glycyrrhiza glabra) -- used by professional herbalists to


relieve respiratory ailments such as bronchitis; considered a demulcent
(soothing, coating agent); you should not use this herb if you have high
blood pressure.

Lobelia (Lobelia inflata) -- also called Indian tobacco, lobelia has a


long history of use by Native Americans as an herbal remedy for respiratory
ailments including bronchitis. It is considered an effective expectorant,
meaning that it helps clear mucus from the respiratory tract. It is important
to note, however, that lobelia is a potentially toxic herb. It is considered
relatively safe when used in very small doses (particularly homeopathic
doses) or in combination with other herbs that affect the respiratory
system. Lobelia use should only be considered with the guidance of a
qualified healthcare practitioner.
94

Marshmallow (Althea officinalis) long history of use in traditional


healing systems for bronchitis.

Red Clover (Trifolium pretense) used traditionally for spasmodic


cough and bronchitis.

Saw Palmetto (Serenoa repens/Sabal serrulata) -- early in the 20th


century, saw palmetto was listed in the US Pharmacopoeia as an effective
remedy for bronchitis.

Acupuncture

Preliminary studies suggest that acupuncture may help relieve shortness


of breath in those with COPD. More research is needed to know for certain
if this is an effective use of acupuncture.

Similarly, acupressure (a technique much like acupuncture but pressure


from the practitioners thumb or fingers is used instead of needles) may be a
worthwhile addition to attending a pulmonary rehabilitation program
where one learns breathing techniques and exercises to feel less short of
breath. Again, more research in this area would be helpful.
95

If you are trying to quit smoking, acupuncture is an excellent treatment


approach for this purpose.

Mind/Body Medicine

The stress of having COPD is often helped by joining a support group


where members share common experiences and problems.

Yoga and tai chi are practices that use deep breathing techniques and
meditation; these practices may be helpful if you have COPD. Talk to your
doctor about safety for you.

Biofeedback is another method for helping to learn a more relaxed


and, therefore, more comfortable breathing pattern.

Music therapy can help relieve anxiety associated with COPD and,
possibly, shortness of breath.

Listening to relaxation tapes on a regular basis (for example, one or


96

two times per day) may help reduce anxiety and shortness of breath
associatedwithCOPD
97

CASE FORMATION

CASE NO. NAME OF PHYSICIAN.

REG NO INTERN INCHARGE..

PATIENT NAME

AGE/SEX..

OCCUPATION.

RELIGION.

MARITAL STATUS..

ADDRESS

.
98

DIAGNOSIS

CLINICAL HISTORY

CHIEF COMPLAINTS

HISTORY OF PRESENT ILLNESS

PAST ILLNESS

PERSONAL HISTORY

FAMILY HISTORY

FATHER
99

MOTHER

BROTHER

SISTER

W\H

OTHERS

SOCIAL STATUS

DITETIC HABITS

PHYSICAL EXAMINATION

GENERAL EXAMINATION

APPEARANCE BUILD
100

NUTRITIONAL STATUS HYDRATION

ANAEMIA OBVIOUS FOCAL SEPSIS

PULSE TEETH/GUMS

B.P. TONSIL

RESPIRATION EAR

TEMPERATURE SKIN

LOCAL EXAMINATION

SYSTEMIC EXAMINATION

RESPIRATORY SYSTEM

C.V.S.

C.N.S.
101

GENERAL SYMPTOMS

PHYSICAL GENERAL SYMPTOMS

APP- (D/A)

THIRST- SLEEP

REACTION TO H/C DREAMS

STOOL URINE

MENSTRUATION

MENTAL GENERAL SYMPTOMS

WILL

LOVE

HATE
102

FEAR

ANGER

TEMPER.

UNDERSTANDING

INTELLECT

THOUGHT

ILLUSION

HALLUCINATION

DELUSIONS

MEMORY
103

INVESTIGATION

ROUTINE INVESTIGATION

SPECIAL INVESTIGATION

EVALUTION OF SYMPTOMS & RUBRIC FORMATION

CONSULTATION OF REPERTORY

FINAL PRESCRIPTION
104

PROGRESS REPORT

DATE PROGRESS TREATMENT


105

GRAPH

Mortality ration in different age groups


106

BIBLIOGRAPHY

1. Principles of internal medicine by Harrison


107

2. Current medical diagnosis and treatment

3. Robbins pathology

4. Snells anatomy of human body

5. B. D. Chaurasias human anatomy

6. Guytons physiology

7. Tortoras anatomy and physiology

8. Davidsons practice of medicine

9. Clarkes materia medica

10. Boerickes materia medica

11. Kents materia medica

12. Kents philosophy

13. Dubeys text book of materia medica


108

14. Stuart closes philosophy

15. Kents repertory

16. Murphys repertory