Handbook of Practical Chest Physiotherapy

Handbook of Practical
Chest Physiotherapy
Handbook of Practical
Chest Physiotherapy
Pushpal Kumar Mitra

BPT, MIAP, SRP (Eng), MCSP (UK)
Lecturer in Physiotherapy
National Institute for the Orthopaedically Handicapped
Kolkata
JAYPEE BROTHERS
MEDICAL PUBLISHERS (P) LTD
New Delhi
Published by
Jitendar P Vij
Jaypee Brothers Medical Publishers (P) Ltd
B-3 EMCA House, 23/23B Ansari Road, Daryaganj
New Delhi 110 002, India
Phones: +91-11-23272143, +91-11-23272703, +91-11-23282021, +91-11-23245672,
Rel: 32558559, Fax: +91-11-23276490, +91-11-23245683
e-mail: jaypee@jaypeebrothers.com Visit our website: www.jaypeebrothers.com
Branches
 2/B, Akruti Society, Jodhpur Gam Road Satellite, Ahmedabad 380 015
Phones: +91-079-26926233, Rel: +91-079-32988717, Fax: +91-079-26927094
e-mail: ahmedabad@jaypeebrothers.com
 202 Batavia Chambers, 8 Kumara Krupa Road, Kumara Park East, Bengaluru 560 001
Phones: +91-80-22285971, +91-80-22382956, Rel: +91-80-32714073,
Fax: +91-80-22281761, e-mail: bangalore@jaypeebrothers.com
 282 IIIrd Floor, Khaleel Shirazi Estate, Fountain Plaza, Pantheon Road,
Chennai 600 008 Phones: +91-44-28193265, +91-44-28194897,
Rel: +91-44-32972089, Fax: +91-44-28193231
e-mail: chennai@jaypeebrothers.com
 4-2-1067/1-3, 1st Floor, Balaji Building, Ramkote Cross Road, Hyderabad 500 095,
Phones: +91-40-66610020, +91-40-24758498, Rel:+91-40-32940929,
Fax:+91-40-24758499, e-mail: hyderabad@jaypeebrothers.com
 No. 41/3098, B & B1, Kuruvi Building, St. Vincent Road, Kochi 682 018,
Kerala, Phones: 0484-4036109, +91-0484 2395739, +91-0484 2395740
e-mail: kochi@jaypeebrothers.com
 1-A Indian Mirror Street, Wellington Square,
Kolkata 700 013, Phones: +91-33-22451926, +91-33-22276404, +91-33-22276415,
Rel: +91-33-32901926 Fax: +91-33-22456075, e-mail: kolkata@jaypeebrothers.com
 106 Amit Industrial Estate, 61 Dr SS Rao Road, Near MGM Hospital,
Parel, Mumbai 400 012
Phones: +91-22-24124863, +91-22-24104532, Rel: +91-22-32926896
Fax: +91-22-24160828, e-mail: mumbai@jaypeebrothers.com
 “KAMALPUSHPA” 38, Reshimbag,
Opp. Mohota Science College, Umred Road, Nagpur 440 009 (MS)
Phones: Rel: 3245220, Fax: 0712-2704275
e-mail: nagpur@jaypeebrothers.com
Handbook of Practical Chest Physiotherapy

© 2007, Pushpal Kumar Mitra
All rights reserved. No part of this publication should be reproduced, stored in a retrieval
system, or transmitted in any form or by any means: electronic, mechanical, photocopying,
recording, or otherwise, without the prior written permission of the author and the publisher.
This book has been published in good faith that the material provided by author is original.
Every effort is made to ensure accuracy of material, but the publisher, printer and author will
not be held responsible for any inadvertent error(s). In case of any dispute, all legal matters
are to be settled under Delhi jurisdiction only.
First Edition: 2007

ISBN 81-8448-095-4
Typeset at JPBMP typesetting unit
Printed at Gopsons Papers Ltd., Noida
Foreword
In the field of respiratory medicine, the development which occurred in

recent times mostly tend to reduce the morbidity and improve the quality of
life of the patient. Though the pharmacological intervention remains mostly
the same, the importance of chest physical therapy was mostly neglected.
But the remarkable improvement which is brought about by meticulous
chest physiotherapy needs no further comments. But, unfortunately in
Indian scenario a book especially devoted to chest physiotherapy was
lacking. The effort by Dr. P.K. Mitra in this regard is really an eye-opener for
all.
This book is not only going to help the undergraduate physiotherapy

students but also will be of help to respiratory nurses and doctors with interest
in respiratory medicine. This book will fulfil the lacunae of proper chest
physiotherapy training in our country.
Dr Saibal Moitra
Preface
In prolonged morbidity of any kind, in which the patient is confined to the

bed, several systemic complications are to be expected. The respiratory and
circulatory complications are the foremost and have far reaching effect on
the long-term functional ability of the patient. This earlier was regarded as
of little consequence to the final outcome of the treatment. The result of
such approach was that the therapist was asked to mobilize the body segments
and treat the movement dysfunctions, in isolation. No or little attention was
paid to subtler issues like exercise intolerance, respiratory incompetence,
lack of functional endurance, etc. After a prolonged bedrest or immobili-
zation, the patients were proclaimed cured by the doctor, but were often
unable to go back to the per-morbid lifestyle due to simple but persistent
problems like shortness of breath or inability to work for long.
With the emphasis of modern healthcare shifting towards reducing
duration of morbidity, minimizing hospital stay and improving the post-
morbid quality of life of the patient, the catchword at present times is a
holistic approach to healthcare.
The holistic approach to healthcare tends to look at the final outcome of
any treatment measure, in terms of loss of man day, cost of hospitalization
and the successful reintegration of the client into a productive post-morbid
life.
Healthcare professionals, including physiotherapists, have now to treat
not only the cause of morbidity, but also identify, prevent and treat the
short as well as long-term adverse effects of such morbidity. This includes an
ever-growing number of people affected by respiratory disorders, helped to
no end by increasingly polluted air in our cities.
With respiratory medicine having resurgence in modern healthcare, the
importance of chest physiotherapy as a complementary measure, is gaining
acceptance and popularity worldwide.
Chest physiotherapy has traditionally been treated as an additional skill,
which the all therapist were supposed to learn about, but few if any, regarded
and practiced it as their principal means of earning a living, because the
profession was dominated by orthopedic and to some extent, neurological
orientation.
viii Handbook of Practical Chest Physiotherapy
This volume, like its predecessor in the series of practical handbooks in
physiotherapy, is designed not only to reorient the practicing physiotherapist
in the art of chest physiotherapy, but also to help the undergraduates to
unravel the complicated issues connected with respiratory medicine, in a
simple, easy to understand format.
No effort has been spared to make the volume as free of factual errors as
possible. Readers are to note that several new concepts that have been
proposed in this volume have been on trial and most have been accepted
by the mainstream of respiratory care.
Pushpal Kumar Mitra

Contents
1. Functional Anatomy of the Respiratory Mechanism ............... 1
2. Applied Physiology of Respiration ....................................... 18
3. Respiratory Pathophysiology ................................................ 29
4. Clinical Evaluation of Patients with Respiratory Disorders .. 39
5. Chest X-ray for the Physiotherapist ..................................... 66
6. Management of Major Respiratory Diseases ........................ 78
7. Techniques of Physical Therapy Treatment in

Respiratory Disorders ........................................................110
8. Management of Respiratory Emergencies ........................... 149
Index ............................................................................................. 183

CHAPTER ONE
Functional Anatomy of the

Respiratory Mechanism
SKELETAL COMPONENTS OF THE RIB CAGE AND

THE UPPER GIRDLE
To begin our quest for chest physiotherapy we must first understand the
meaning of the word “chest” and what it is made of. To understand chest
physiotherapy, it is not only the knowledge of the structure and function of
the lung that is relevant, but also how to use the musculo-skeletal mechanics
of the thorax to ones advantage, to perform the act of breathing with
minimum of energy expenditure.
We all know that the there is a bony vertebral column consists of thirty
three vertebral bones. On the vertebral column is attached the bony rib cage
and that houses the lungs and the heart.
The rib cage is made up of 12 pairs of C shaped ribs, which are attached
at the back to the thoracic vertebra and majority of them also at the front to
the sternum. The secondary components of the rib cage are the clavicle and
the scapula. All of these bony components together make the thorax.
The Role of the Vertebral Column

The vertebral column is the axis of the thorax that has to meet the two
contradictory requirements that of stability and flexibility at the same time,
so that you can hold a heavy bag and turn around at the same time. The
vertebral column can be viewed as the mast of a ship. This mast rests on the
solid base of the pelvis, extending to the head. At the level of shoulder, it
supports the main yard arm, set transversely. This is the scapular girdle. At all
levels along the vertebral column, ligaments and muscles are arranged on
either side to act as secondary fixators—linking the mast to its base, i.e. the
pelvis. This secondary system of fixators is closely related to the scapular
girdle and is diamond shaped with its long axis vertical and short axis horizontal.
In the position of symmetry, the forces on either side are in equilibrium and
the mast is held upright (Fig. 1.1).
2 Handbook of Practical Chest Physiotherapy
FIGURE 1.1: The vertebral column is like a flexible rod or ship’s mast, fixed on the solid base of
the pelvis. It is unique in its function that it can move in different axis at the same time, which
provides the human body with its fluidity and grace of motion. The muscles in the front, back and
sides of the thorax act as the stabilizers for the vertebral column, holding it upright against the
force of gravity, allowing it to meet two contradictory requirements, i.e. stability, as well as,
mobility. The bony rib cage further provides the thorax, as well as the vertebral column with the
required structural rigidity.
Human beings are bi-pedal in nature, the vertical alignment of the

vertebral column, in response to the gravitational force is most essential, to
ensure unobstructed function of the lungs and other organs of the thoraco-
abdominal cavity. The primary consideration of the chest therapist
should, therefore, be to ensure upright vertebral posture and
discourage stooping (Kyphosis) or tilting (Scoliosis) of the vertebral
column.
The Rib Cage

The bony thorax protects the heart and lungs. It provides the site of attachment
for the muscles of inspiration, and also gives attachment to the upper extremity
muscles.
The posterior surface (back) is formed by the 12 thoracic vertebrae and
the posterior part of the 12 ribs. The anterior part (front) is formed by the
sternum and the costal cartilages and the lateral surface is formed by the ribs.
At birth the thorax is almost circular, but during childhood and adolescence,
it becomes more elliptical in shape, until in adulthood when it becomes wider
from side to side then it is from front to back.
Functional Anatomy of the Respiratory Mechanism 3
The ribs articulate posteriorly with the bodies and the transverse
processes of the thoracic vertebrae and anteriorly join the sternum via the
costal cartilages. The first seven ribs are known as the true ribs, as their cartilages
attach directly to the sternum. The eighth to tenth ribs have common
cartilaginous attachment to the ribs above. The eleventh and the twelfth ribs
are floating ribs as they have no attachment with the sternum at all. Anteriorly,
the sternum provides a bony protective plate over the heart, and is composed
of the manubrium, the body and the xiphoid process.
Articulations of the chest wall include the manubriosternal,
xiphisternal, costovertebral, costotransverse, costosternal and
interchondral joints (Figs 1.2 and 1.3).
FIGURE 1.2: Bones and articulations of the rib cage
FIGURE 1.3: Articulations of the ribs with the thoracic vertebra

ARTHROKINEMATICS OF THE THORACIC CAGE:

ANALYSIS OF MOVEMENT OF BREATHING
Each rib is connected to the vertebral column by two synovial joints: the
costotransverse and the costovertebral. At the spinal end, each rib has
two articular surfaces (Fig. 1.3).
The distal one articulates with the transverse process of the dorsal vertebra
forming the costotransverse joint. It has strong ligaments that restrict gross
ranges of motion. Proximally each rib articulates with the superior border of
the lower vertebra and inferior border of the upper vertebra, forming the
costovertebral joint. Anteriorly, each rib (except the eleventh and the twelfth)
continues as the costal cartilage that articulates with the sternum. The first rib
attaches to sternum directly forming a synchondrosis.1
Movement of the Ribs Occurring at these Joints

Ligaments restrain movement at the costovertebral and costotransverse joint.
These two joints form a mechanical axis about which the movement of rib
can take place. The direction of this axis with respect to the sagittal plane
decides the direction of movement of the rib. For upper vertebrae, this axis
is more mediolateral. The upper ribs rotate about this axis causing anterior
elevation also known as the pump handle motion. For the lower vertebrae,
the axis happens to be more anteroposterior, causing the ribs to elevate in a
lateral direction causing what is also known as the bucket handle motion of
inspiration.
Therefore, during inspiration, elevation of the ribs causes
increase in the transverse diameter of the lower thorax and
anteroposterior diameter of the upper thorax (Fig. 1.4).
Movement of Thoracic Vertebral Column

In the skeleton, the thoracic column by itself is more mobile where it is
connected with the thoracic cage. The thoracic column is connected to the
thoracic cage by multiple joints and all the components of the cage play a
role in orienting and limiting the basic movements of the column.
Lateral Flexion
It occurs in frontal plane, range 20-40 degrees. The articular processes of
two vertebra slide relative to each other. It is limited by impact of the articular
process on the side of movement and also by the contralateral ligamentum
flava and intertransverse ligaments. On the contralateral side: the thorax is
FIGURE 1.4: Movement of ribs about the axis formed by the

costotransverse and costovertebral joints
elevated (1), the intercostal spaces widen (3), the thoracic cage is enlarged
(5) and the chondrocostal angle of the tenth rib tends to open out (7). On
the ipsilateral side; the thoracic cage is lowered (2) and shrinks (6), the
intercostal spaces are narrowed (4) and the chondrocostal angle becomes
smaller (8) (Fig. 1.5).
FIGURE 1.5: Lateral flexion of trunk and its effect on lung shape
Axial Rotation
When one vertebra rotates, other articular processes slide relative to each
other. This is followed by the rotation and twisting of the discs in the thoracic
region. A similar movement is generated in the ribs leading to distortion of
the thoracic cage:
1. Accentuation of the concavity of the rib on the side of vertebral rotation
2. Flattening of the concavity of the rib on the opposite side
3. Accentuation of the costo-chondral concavity on the side opposite to
vertebral rotation
4. Flattening of the concavity of the costo-chondral angle on the side of
rotation (Fig. 1.6).
FIGURE 1.6: Axial rotation of trunk and its effect on rib cage
The range of movement decreases with age, as the flexibility of the thoracic
column diminishes. As a result it is not uncommon to find the thorax almost
rigid in the elderly.
Flexion
During flexion the space between two vertebrae opens out posteriorly. The
range of movement (ROM) is 20-45 degrees. It occurs in the sagittal plane in
forward bending. The ligamentum flavum, posterior longitudinal ligament,
the interspinous and the supraspinous ligaments limit flexion. During flexion,
all the angles between the various segments of the thorax and between the
thorax and vertebral column open out. Conversely, during extension, all
these angles become smaller (Fig. 1.7).
FIGURE 1.7: Trunk flexion and its effect on rib cage
Extension
The ROM of extension of the thoracic spine is 20 to 45 degrees. It occurs in
the sagittal plane. It is associated with the movement of backward bending,
elevation of both arms, and during the inspiratory phase. It is limited by the
articular and the spinous processes. The anterior longitudinal ligament
becomes taut while the Ligamentum flavum, posterior longitudinal ligament,
and the interspinous ligament are relaxed Thoracic movement during
inspiration and expiration.2
Mechanics of Breathing
To take a breath in, the external intercostals muscles contract, moving the rib
cage up and out. The diaphragm moves down at the same time, creating
negative pressure within the thorax. The lungs are held to the thoracic wall
by the pleural membranes, and so expand outwards as well. This creates
negative pressure within the lungs, and so air rushes in through the upper
and lower airways.
Expiration is mainly due to the natural elasticity of the lungs, which tend
to collapse if they are not held against the thoracic wall by the negative
pressure (suction force) maintained within the pleural space. This is why
lungs collapse if there is air in the pleural space, which is called the
pneumothorax.
Contracting of the diaphragm and raising the ribs expand the thoracic
cavity, producing a tidal flow of air in the lungs. Contraction of the diaphragm
moves it downwards and expands the volume of the thoracic cavity, creating
a negative pressure within the cavity, drawing atmospheric air, at a higher
pressure into the lungs.
During quiet breathing, contraction of the diaphragm accounts for most
of the force behind inspiration. Diaphragm is supplied by phrenic nerve
which originates from cervical spinal cord (C 3-5). If spinal cord is damaged
at or above this level, respiration is inhibited, sometimes leading to death.
The external intercostals muscles, located between ribs, also aid inspiration,
causing the ribs to move upward and outward, expanding the thoracic cavity
further.
At rest expiration is mostly passive — lungs contract due to elasticity,
expelling most of the air taken in during inspiration. During exertion, internal
intercostals and the abdominal muscles aid expiration by pulling the ribs
downward and inward, reducing thoracic cavity, to generate positive pressure
within the thoracic cavity.
Inspiration Expiration
Diaphragm descends Diaphragm ascends
Rib cage elevates and/or expands Rib cage descends and/or contracts
Increased intrathoracic volume Decreased intrathoracic volume
Decreased intrathoracic pressure Increased intrathoracic pressure
‘High pressure’ atmospheric air flows ‘High pressure’ air in lung flows out toward
into ‘low pressure’ lung. ‘low pressure’ exterior.
MUSCLES OF RESPIRATION AND THEIR FUNCTION IN

DIFFERENT STAGES OF RESPIRATION
During quiet breathing, the predominant muscle of respiration is the
diaphragm (Fig. 1.8). As it contracts, pleural pressure drops, which lowers
the alveolar pressure, and draws air in down the pressure gradient from
mouth to alveoli. Expiration during quiet breathing is predominantly a passive
phenomenon, as the respiratory muscles are relaxed and the elastic lung
and chest wall return passively to their resting volume, the functional residual
capacity.
However, during exercise, many other muscles become important to
respiration. During inspiration, the external intercostals raise the lower ribs
up and out, increasing the lateral and anterior-posterior dimensions of the
thorax. The scalene muscles and sternomastoids also become involved, serving
to raise and push out the upper ribs and the sternum. During active expiration,
the most important muscles are those of the abdominal wall (including the
FIGURE 1.8: The diaphragm
rectus abdominus, internal and external obliques, and transversus

abdominus), which drive intra-abdominal pressure up when they contract,
and thus push up the diaphragm, raising pleural pressure, which raises alveolar
pressure, which in turn drives air out. The internal intercostals assist with
active expiration by pulling the ribs down and in, thus decreasing thoracic
volume.3
Shortening of diaphragmatic fibers pulls inferiorly on central tendon and
superiorly on lower ribs. During inspiration, the diaphragm’s central tendon
descends until it is fixed or stabilized by forces that develop in: elongated
mediastinal structures, which pull upward on the diaphragm and compress
the abdominal contents, which push upward on the descending diaphragm.4
When the central tendon becomes stable, it is still superior to the diaphragm’s
mobile attachments on the lower ribs. Therefore, the diaphragm’s muscular
lines of application elevate the lower ribs (Fig. 1.9).
FIGURE 1.9: Movement of the diaphragm during the breath cycle

Type of Breathing Muscles of Inspiration Muscles of Expiration
Quiet Diaphragm Expiration is passive

(primary muscles) external intercostals Elastic recoil of lung tissue
surface tension
gravity on ribs
internal intercostals
Forced Sternocleidomastoid Abdominal muscles

(secondary or accessory muscles) Scalene External oblique
Pectoralis major Internal oblique
Pectoralis minor Rectus abdominus
Serratus anterior lower iliocostalis
Serratus posterior superior lower longissimus
Upper iliocostalis Serratus posterior inferior
OUTLINE OF RESPIRATORY ANATOMY

This sub-section on Respiratory Anatomy represent a four part study of the
respiratory system, following the path of air from the mouth and nose to the
alveolar level, where oxygen trades places with carbon dioxide. The respiratory
system is situated in the thorax, and is responsible for gaseous exchange
between the circulatory system and the outside world. Air is taken in via the
upper airways (the nasal cavity, pharynx and larynx) through the lower airways
(trachea, primary bronchi and bronchial tree) and into the small bronchioles
and alveoli within the lung tissue. The lungs are divided into lobes; the left
lung is composed of the upper lobe, the lower lobe and the lingula (a small
remnant next to the apex of the heart), the right lung is composed of the
upper, the middle and the lower lobes (Fig. 1.10, Plate 1).
Part 1: Upper Respiratory Tract

The Upper Respiratory Tract or Airways extends from the mouth and the
nasal passage to just above the larynx.
• The epiglottis is a leaf-shaped “flap” of cartilage that protects the rest of
the respiratory system from foreign objects. The epiglottis acts as a valve
or lid, automatically opening for breathing and closing when you swallow
food or liquids. The epiglottis is also important in producing an effective
cough. During a cough the epiglottis is closed and then when sufficient
pressure is built up, suddenly opens for a quick release of air, producing
cough.
• The external nares are the opening to the nasal cavity and are lined with
fine hairs that serve as filters for large particles of dust suspended in the
air that we breathe, and they form the first line of defense against inhaled
dust partcles, bacteria, virus and other inhaled pathogens.
• The frontal sinuses are air pockets, located deep within the facial bones
over and below the eyes, i.e. in the frontal and maxillary bones. Those
pockets or cavities serve to strengthen and lighten these bones. They
become painful and get inflamed when infected by airborne virus or
bacterium. This condition is known as sinusitis.
• The hard palate forms the roof of the mouth and the floor of the nasal
cavity.
• The soft palate extends from the hard palate and forms the back of the
roof of the mouth. The soft palate supports the structure known as the
uvula (that little thing that hangs down in the back of your throat). The
soft palate and uvula play an important part in the development of certain
kinds of obstructive sleep apnea.
• The nasal concha is mucus lined folds that cool, humidify, and filter
the air after entering the nasal passage. The inferior nasal concha is the
largest, located near the floor of the nasal cavity. It also covers the opening
to the nasolacrimal ducts (tear ducts). The middle nasal concha is located
midway up the nasal cavity and just behind the opening to the frontal
sinus. This area is important for the sense of smell. The superior nasal
concha is located near the roof of the nasal cavity and just before the
opening to the sphenoid sinus. This area is also important for the sense of
smell.
• The nasal cavity serves as a filter, air conditioner and humidifier for the
inhaled air before it enters the lungs. It is also rich in nerve ending from
the olfactory bulb that gives us the sense of smell. It is also where most
attacks of cold begin.
• The nasal bone forms the base for the cartilage that forms the nose and
nasal septum.
The pharynx is the common opening of the digestive and respiratory
systems. It receives air from the nasal cavity and air, food and water
from the mouth. Inferiorly, the pharynx leads to separate openings of
the respiratory system namely the larynx and of the digestive system,
i.e. esophagus (Fig. 1.11, Plate 1). Pharynx can be divided into three (3)
regions:
• Nasopharynx
• Oropharynx
• Laryngopharynx
• The naso-pharynx is the upper part of the pharynx and connects the
nasal passages with the rest of the respiratory system. The pharynx is the
area most commonly called the “back of the throat”.
• Oropharynx is the lower part of the pharynx and connects the upper
airways to the larynx via the epiglottis, lined with stratified squamous
epithelium that provides protection against abrasion.
• Laryngopharynx extends from the tip of the epiglottis to the openings of
the larynx and esophagus. It is lined with squamous epithelium
• The eustachian tubes connects the middle ear with the upper airways.
Mucus from colds or other infections can be forced up this tube with
coughing, sneezing, or nose blowing and result in middle ear infections.
• Tonsils located along with the lingual and palatine surfaces are considered
to be part of the lymphatic system, thus important in the immune system.
At one time was common to have infected and inflamed tonsils removed
surgically in the childhood, but with the advent of broad-spectrum
antibiotics, that practice has been discarded.
• The tongue, located in the floor of the mouth is a muscle important for
eating, speak, and the sense of taste.
Part 2: Lower Respiratory Tract

• The lower respiratory tract starts from the larynx (Figs 1.12A and B, Plate
2) and consists of trachea, and main bronchi, extending from the back of
the throat to the first branching of the bronchial tree. The Larynx and its
structures form the opening to the trachea and lower airways.
• The epiglottis is a leaf-shaped “flap” of cartilage that protects the rest of
the respiratory system from foreign objects. The epiglottis acts as a valve
or lid, automatically opening for breathing and closing when you swallow
food or liquids. The epiglottis is also important in producing an effective
cough. During a cough the epiglottis is closed and then when sufficient
pressure is built up, suddenly opens for a quick release of air.
• The hyoid bone is the support structure for the tongue and various muscles
that allows the tongue to function.
• The laryngeal prominence is also known as the “Adam’s Apple”. It is the
upper forward protruding part of the thyroid cartilage.
• The thyroid cartilage is the largest cartilage of the larynx and is attached
by the thyroid membrane to the hyoid bone. The thyroid cartilage houses
the structures of the epiglottis and vocal cords.
• The esophagus is the passageway to the stomach.
• The glottis is the opening between the Vocal Cords (Fig. 1.13, Plate 2). It
differentiates the upper respiratory tract from the lower airways. Due to
the narrowness of this opening, it is susceptible to inflammation and
swelling of the vocal cords and surrounding tissues.
• The vocal cords form the opening called the Glottis. They also make
speech possible by vibrating when air passes through them.
• The wall of laryngopharynx houses the larynx and opening to the
Esophagus.
The Trachea is the beginning of the Tracheo-Bronchial Tree (Fig. 1.14)
and consists of the largest diameter of the lower airway tract. It is made
up of a series of “C” shaped tracheal cartilages and connective tissue (Fig.
1.15). These cartilages form a rigid tube with a soft pliable area at the
back of the trachea extending its full length and into the left and right
main stem Bronchi.
FIGURE 1.14: The tracheo- FIGURE 1.15: Cross-sectional view of trachea

bronchial tree
• The tracheal cartilages or Ttacheal cartilaginous rings are the support

structures of the trachea. These are not complete rings; they are “C”
shaped. This shape allows the trachea to be ridged forward for structure
and protection. It also allows the trachea to be soft and pliable in the back
where it is in close proximity to the esophagus.
• The right and left main stem bronchi are similar in many ways to the
Trachea. Their structure is supported with cartilaginous rings and lead
into the right and left lungs.
• At a microscopic level the trachea and main stem bronchi are lined with
structures referred to as cilia.
• Cilia propel mucus and foreign particles toward the larynx where they
can enter the esophagus and be swallowed.
Viewed at the microscopic level, the cilia appear like vast fields of waving
wheat or grass (Fig. 1.16).
FIGURE 1.16: Microscopic view of cilia
Cilia in the trachea and bronchi move mucus and any trapped particles
up toward the larynx to be expelled from the lungs. There are also cilia in the
naso and oropharynx that move secretions down toward the throat.
Interspersed among the cilia are specialized cells called Goblet cells
that produce mucus. There are two types of mucus, one very thin and liquid.
The other is thick and viscous. The thick layer of mucus sits on top of the
thinner. Cilia are able to grab hold of this thicker layer and propel it in the
intended direction (Fig.1.17).The depths of the thin and thick layers of
mucus are especially important for the cilia to be able to do their job.
As asthmatics, we tend to develop an increase in the thick mucus during
attacks, this overproduction of thick mucus interferers with the cilia’s ability
to move it.
FIGURE 1.17: The workings of the cilia
Other factors that effect cilia are smoking and chronic infections (i.e.
Chronic Bronchitis or Bronchiectasis). Cigarette smoke slows down the action
of cilia; chronic infections decrease the number of ciliated cells and increase
the number of goblet cells. Both of these factors decrease the ability of the
lungs to clear foreign particles and bacteria, and the increased mucus
production give bacteria a perfect place to grow, thus increasing the chances
of infection.
Part 3: The Lungs and the Major Bronchi (Fig. 1.18):
• After the trachea splits into the main stem bronchi at the Carina, these
main bronchi then continue to divide. Right bronchus is shorter and wider
and is more vertical than the left bronchus.
• Main bronchi extend from the mediastinum to the lungs.
• The lining of the bronchi is the same as the trachea and the bronchi are
supported by “C”-shaped cartilage rings
• The right main stem bronchus divides into three lobar branches; upper,
middle, and lower lobe bronchi.
• The left main stem bronchus divides into two lobar branches — the upper
and lower lobar bronchi.
• The lobar bronchi divide into the segmental bronchi; leading into
1. Right upper lobe, anterior, apical, and posterior segments;
2. Right middle lobe, medial and lateral segments;
3. Right lower lobe, anterior, medial, lateral, posterior, and superior
segments;
4. Left upper lobe, apical-posterior, anterior, superior lingular, inferior
lingular segments;
5. Left lower lobe, anterior, medical, lateral, posterior, and superior
segments.
FIGURE 1.18: The lungs, the lobes of the lungs and

the major bronchi supplying the lobes
• The segmental bronchi continue to divide into smaller and smaller airways.
• As they divide, the cartilaginous support, as in the trachea and main
bronchi, slowly begins to disappear and is replaced by bronchial smooth
muscle.
• When the diameter of the bronchi reach 1 mm, all cartilaginous support
has gone, and we call these small bronchi Bronchioles.
• The bronchioles continue to divide until we reach the terminal bronchioles,
which are made up of the respiratory bronchioles and alveolar ducts.
• These structures are at the very surface of the lungs, covered by the
visceral pleura.
• This continuing branching of the airways creates the surface area of the
lung.
• The total surface area of the alveoli is equivalent to the area of a tennis
court.
• The significance of the change from cartilaginous support to smooth muscle
is very important to patients with respiratory disorders, particularly in
COPD.
• Lungs are the principal organs of respiration and on a volume basis; they
are one of the largest organs of the body.
• Each lung is conical in shape with its base resting on the diaphragm and
its apex extending superiorly to a point approximately 1” superior to
each clavicle.
• Right lung is larger than the left lung.
• Right lung has three lobes and left lung two lobes (Fig. 1.19, Plate 3).
Part 4: The Microscopic Features of the Lungs and Bronchial Tree

Most of the working parts of the lungs that participate in the gas exchange
are at the microscopic level. This passage concentrates on those microscopic
features of the lungs.
Role of Alveoli in Respiration

The main function of the lungs is to facilitate gas exchange between carbon
dioxide in the blood stream and oxygen in the air. At the very end of the
bronchial tree are the alveoli. They appear like bunches of grapes at the
ends of the bronchioles (Fig. 1.20). The alveoli first start to appear on the
respiratory bronchioles, these bronchioles lack the smooth muscle of the
terminal bronchioles. The smooth muscles surrounding the terminal
bronchioles are those muscles that respond easily to emergency medications
FIGURE 1.20: The structure of the alveoli
like bronchodilators, to relieve the muscle spasm. Anti-inflammatory agents

like steroid work on the mucous membrane. During an attack these muscles
contract, squeezing the bronchioles and the mucus layer swells up, making
them still smaller. The inner lining of these airways are where steroids and
other anti-inflammatory medications work. By reducing inflammation, the
inner diameter of the airways is enlarged.
REFERENCES
1. Clemente CD. Anatomy (2nd ed). Baltimore: Urban and Schwarzenberg 1981
2. Kapandji IA. Functional components of the vertebral column. In I.A. Kapandji (Ed):
The physiology of the joints: Vol. 3. The trunk and the vertebral column. New York:
Churchill Livingstone 1974.
3. Rasch PJ, Burke RK. Kinesiology and Applied Anatomy (6th ed). Philadelphia: Lea
and Febiger 1978.
4. Poole DC, Sexton WL, Farkas GA, Powers SK, Reid MB. Diaphragm structure and
function in health and disease. Medicine and Science in Sports and Exercise 1997;
29: 738-54.
5. Diagrams and figures adapted from web site http://www.cayuga-cc.edu/people/
facultypages/greer/biol204/resp3/resp1-3.html
CHAPTER TWO
Applied Physiology
of Respiration
As we have studied in the previous chapter, each branch of the bronchial

tree eventually subdivides to form numerous, very narrow terminal
bronchioles, which terminate in the alveoli. The alveoli are the physiologically
functional unit of the lungs, where the exchange of gasses takes place. There
are many millions of alveoli in each lung, presenting a massive surface area
for the gas exchange to occur.
MECHANISM OF GAS EXCHANGE

Points to Ponder
• The respiratory system is specifically designed to bring in oxygen from
the atmospheric air into the body and remove carbon dioxide from the
body.
• This exchange takes place through the alveoli-capillary complex located
at the periphery of the lungs.
• Each alveolus is very closely associated with a network of capillaries carrying
deoxygenated blood from the pulmonary artery.
• The network of capillaries is so dense that a sheet of blood covers the
alveoli.
• The capillary and alveolar walls are very thin, allowing rapid exchange of
gases by passive diffusion along concentration gradients.
• CO2 moves into the alveolus from the blood in the capillaries, as its
concentration is much lower in the alveolus than in the blood.
• O2 moves out of the alveolus into the blood stream, as continuous flow
of blood through the capillaries prevents saturation of the blood with O2
and allows maximal transfer across the membrane (Fig. 2.1).
• The blood thus oxygenated in the lungs is carried by the pulmonary
vein to the heart, from where it is pumped to different organs by the
heart.
Applied Physiology of Respiration 19
FIGURE 2.1: Interface of the gas and the blood at the alveolar level
Blood Gases: Keywords, Clinical Significance and Normal Values

PO2—Partial pressure or tension of oxygen in blood.
PaO2—Partial pressure or tension of oxygen in arterial blood, showing the
volume of oxygen dissolved in plasma: 80-100 mm Hg.
SaO2—Oxygen saturation of peripheral blood in capillary network, showing
the percentage of hemoglobin in blood saturated with oxygen, representing
the ability of the blood to carry oxygen: 95-98%.
PaCO2—Partial pressure or tension of carbon dioxide in arterial blood, which
determines the respiratory acid-base balance and therefore oxygen uptake
capacity of the blood: 35-45 mm Hg.
HCO3—Bicarbonate ions present in blood, indicates the metabolic acid-
base balance in blood: 22-26 mmol/liter.
Blood pH—Hydrogen ion concentration in blood, indicates acid-base
balance, which is a sensitive index to changes in respiratory or metabolic
acid-base balance: 7.35-7.45.
LUNG VOLUMES
Lung functions as the below of a harmonium, expanding and contracting
repeatedly, drawing air in from the atmosphere to extract oxygen and release
carbon dioxide dissolved in blood.
Points to Ponder
• A person with an average ventilation rate of 7.5 L/min will breathe in and
out 10,800 liters of gas each day.
• From this gas, the person will take in about 420 liters of oxygen (19
moles/day) and will give out about 340 liters of carbon dioxide (15 moles/
day).
• The ratio of the CO2 expired, compared to the O2 inspired, is called the
respiratory quotient (RQ)
• RQ = CO2 out/O2 in = 340/420 = 0.81.
• In cellular respiration, for burning of one molecule of glucose,
CO2 released = O2 utilized; RQ = 1.
• The overall RQ is less than 1 in normal circumstances because our
diet is a mixture of carbohydrates, proteins and fat; the RQ for
metabolizing fat is only 0.7.
• The lungs also give off large amounts of heat and water vapor.
• The efficiency of breathing depends upon the volume of air that moves
through the lungs with every breath.
• Efficiency of respiration depends on the extent of uptake of oxygen and
release of carbon dioxide by the blood flowing through the lungs.
Ventilation
• Respiratory rate (RR) and tidal volume (TV) determine the pulmonary
ventilation (PV).
• The total amount of air moved in and out of the lungs each minute is
called pulmonary ventilation (Minute Volume): The PV depends upon 2
factors:
• The size of each breath (tidal volume: TV)
• The number of breaths/minute (respiratory rate: RR)
• PV = RR × TV
• For example: suppose your tidal volume is 500 mL (0.5 liters) and
you breath 15 times/minute; your pulmonary ventilation (minute volume)
= 15 breaths/min × 0.5 L/breath = 7.5 L/min.
• Apart from tidal movement of air, we also have in reserve some inspiratory
and expiratory volumes to meet emergencies facing the respiratory system.
• During exercise we can increase the tidal volume by expanding both

inspiration and expiration volumes of each breath, to cope with increased
demand for oxygen and to release greater than normal volume of carbon
dioxide into the atmosphere.
• The extra capacity for inspiration available for exercise is called the
Inspiratory Reserve Volume (IRV). IRV in a normal individual is about
2.5 liters.
• The extra capacity for expiration available for exercise is called the
Expiratory Reserve Volume (ERV). ERV is about 1.5 liters
• After maximum expiration some air is still present in the lungs- this is
called the residual volume (RV). The RV is about 1.5 liters — this volume
of air is not available for respiration.1
The Maximum Usable Lung Volume is called the Vital Capacity

• The maximum volume available for breathing is the vital capacity (VC); it
is the sum of the TV, ERV and IRV (Fig. 2.2).
• VC = IRV + TV + ERV.
• An average VC is about 3.5 liters, but there is a lot of variation.
• The VC allows pulmonary ventilation to increase by a factor of 5-10.
• The vital capacity cannot be used for sustained exercise- it requires too
much work for maximal inspiration and expiration.
FIGURE 2.2: Lung volumes are measured with a respirometer,

which makes tracing on a graph similar to the one above
• Numerical values are put in for the different respiratory volumes.
• For example, vital capacity is measured by taking a maximal inspiration
(Max In) and then breathing out maximally (Max Out).
• Forced expiratory volume in 1 second (FEV1) is a measure of lung
obstruction. The subject takes a maximum inspiration and then breaths
out as fast as possible. A person with normal lungs will expire about 70-
85% of his VC in one second. A person with lung obstruction (asthma,
emphysema, bronchitis) will force out a much smaller percentage of
inhaled air in 1 second.
Oxygen Uptake in the Lungs

Oxygen uptake in the lungs is increased about seventy times due the presence
of hemoglobin in the red blood corpuscles.
Points to Ponder
• In the lungs oxygen must enter the alveoli and be in close approximation
to the alveolar membrane adjacent to the capillary network, to be
absorbed by the hemoglobin present in the blood.
• A small amount of oxygen dissolves directly in the blood plasma, but
98.5% of the oxygen is carried by hemoglobin.
• All of the hemoglobin in blood is found within the red blood cells ( RBC
or erythrocytes).
• The hemoglobin content of the blood is about 15 gm/deciliter (deciliter
= 100 mL).
• Red cell count is about 5 million per microliter.
Each molecule of Hemoglobin can bind four Oxygen molecules. This
molecule of hemoglobin is then said to be 100% saturated.
• Hemoglobin is a protein molecule with 4 protein subunits (2 alphas and
2 betas)
• Each of the 4 subunits contains a haeme group which gives the protein
a red color
• Each haeme group has an iron atom in the center which can bind an
oxygen molecule (O2)
• Thus the 4 haeme group in a hemoglobin molecule can carry a
maximum of 4 oxygen molecules.
When hemoglobin is saturated with oxygen it has a bright red color;
as it loses oxygen it becomes bluish (cyanosis)
Hematocrit
In Normal Blood, the percentage of cellular content by volume is just below
50%. The volume percentage of cells in the blood is called the Hematocrit.
• Blood consists of cells suspended in serum
• More than 99% of the cells in the blood are red blood cells designed to
carry oxygen and 25% of all the cells in the body are RBCs
• Normal hematocrit is about 40% for women and 45% for men.
At Sea Level the Partial Pressure of O2 is High Enough to Give Nearly
100% Saturation of Hemoglobin
• As the partial pressure of oxygen in the alveoli increases the hemoglobin
in the red cells passing through the lungs rises until the hemoglobin is
100% saturated with oxygen.
• At 100% saturation each hemoglobin carries 4 O2 molecules.
• This is equal to 1.33 mL O2 per gram of hemoglobin.
• A person with 15 gm Hb /deciliter can carry:
• Max O2 carriage = 1.33 mL O2/gm × 15 gm/deciliter = 20 mL O2/
deciliter
Hemoglobin Dissociation Curve

At 100% saturation; each hemoglobin molecule binds 4 oxygen
molecules. At high altitudes, hemoglobin saturation may be well below 100%
(Fig. 2.3):2
• At the alveolar partial tension of O2 (PaO2) at 105 mm of Hg, at sea level,
the hemoglobin saturation will be about 97% saturated.
• At 12,000 feet altitude the alveolar PaO2 will be about 60 mm Hg and
thus the hemoglobin will be 90% saturated.
• At 29,000 feet, i.e. on the top of Mt. Everest, alveolar PaO2 will be about
24 mm Hg and the hemoglobin will be only 42% saturated
• At very high altitudes most climbers must breath pure oxygen from O2
tanks.
• During acclimatization to high altitude the hematocrit can rise to about
60%- this increases the amount of oxygen that can be carried.
• However, hematocrit above 60%, seen in patients with chronic respiratory
failure, is not useful, because the blood viscosity will increase to the point
where it impairs circulation.
FIGURE 2.3: A plot of % of saturation against partial tension of O2

gives an S-shaped hemoglobin dissociation curve
Blood pH and Respiratory Acidosis

Active tissues produce a lot of acid (carbonic and lactic) and this helps to
unload oxygen from the hemoglobin. Acid conditions of the blood help
release O2 in the tissues.2
• Hemoglobin must bind oxygen tightly to load up efficiently in the lungs,
but this makes it hard to release the oxygen in the tissues.
• Some unloading occurs because the tissue pO2 is low, causing oxygen to
diffuses from the blood.
• At low pH hemoglobin has a lower affinity for oxygen; this will cause
more oxygen to come off in the tissues—important in exercise.
• The increased unloading of O2 at low pH is known as the Bohr effect
(Fig. 2.4).
CLINICAL IMPLICATION OF BLOOD GAS ABNORMALITIES

Hypoxia, Hypoxemia and Hypercapnia
Hypoxia can be defined as oxygen deficiency in the tissue. Brain tissue is the
most sensitive to hypoxia; a complete lack of oxygen can cause
unconsciousness in 15 sec and irreversible damage to the brain within 2 min.
Cardiac muscles are also extremely sensitive to hypoxia and may suffer
irreversible damage if deprived of oxygen for more than 8 minutes.
FIGURE 2.4: Relation of blood pH to oxygen saturation: The left curve is at pH 7.4, the middle
curve is at pH 7.1, and the right curve is at pH 6.8. For any pO2 the hemoglobin is more saturated
at pH 7.4 than at pH 6.8.
Hypoxia can be of several types and have several causes because oxygen
delivery and use can be interrupted at several sites (Table 2.1).
Table 2.1: Causes and types of hypoxia
Type of O2 uptake Hemoglobin Efficiency of O2 utilization

hypoxia in lungs concentration circulation in the tissue
Hypoxic Low Normal Normal Normal

Anemic Normal Low Normal Normal
Ischemic Normal Normal Low Normal
Histotoxic Normal Normal Normal Low
Points to Ponder
• Hypoxic may be caused by hypoxemia, high altitude, pulmonary edema,
hypoventilation, emphysema or collapsed lung.
• Anemic causes of hypoxia may be iron deficiency, hemoglobin mutations,
carbon monoxide poisoning.
• Ischemic causes of hypoxia may be hypovolumic shock, heart failure,

embolism
• Histotoxic causes of hypoxia are due to poisoning.
Hypoxemia: It is the deficiency of oxygen in arterial blood, caused by anemia,
hypoventilation, gas diffusion abnormality between alveoli and capillary
network, wasted perfusion through a collapsed or consolidated lung segment,
wasted ventilation due to increased dead space or high altitude.
Hypercapnia: It is greater than expected retention of carbon dioxide in arterial
blood or tissue, caused mainly due to hypoventilation. Carbon dioxide
poisoning (Hypercapnia) typically causes headache and drowsiness.
Hypocapnia: It is lesser than expected concentration of carbon dioxide in
arterial blood or tissue occurring mainly due to hyperventilation or
uncontrolled oxygen inhalation.
Clinical Signs of Blood Gas Abnormality

Brain has the highest consumption of oxygen. Oxygen starvation (Hypoxia)
has quickest progressive effect on functioning of the brain as indicated in the
Table 2.2.
Table 2.2: Effect of oxygen starvation on the functioning of the brain
PaO2 < 55 mm Hg Memory loss
PaO2 < 40 mm Hg Brain tissue damage
PaO2 < 30 mm Hg Unconsciousness
PaO2 < 20 mm Hg Death
Other common features of hypoxia are rapid shallow breathing,

rapid pulse and confusion. However, people being progressively deprived of
oxygen over long period of time tend to compensate for chronic hypoxia by
increasing number of RBC in blood (Polycythemia) and increasing the
efficiency of perfusion in vital organs like the brain, heart and kidney. Such
people can tolerate oxygen deprivation to an extent that would otherwise
kill a person. Pearl divers, diving without oxygen tanks, develop the ability to
stay underwater for long periods through practice. They develop the ability
to work in a largely anaerobic environment, using very little oxygen to stay
alive under water.
ALTERED STATES OF NORMAL RESPIRATORY PHYSIOLOGY3

Aging reduces respiratory muscle strength along with loss of elastic recoil of
the lungs and chest wall mobility, leading to increased work of breathing and
therefore easy fatigue. These people have lowered tidal volume, PaO2, as
well as, reduced response to inhaled oxygen, bronchodilators and other
reliever drugs.
• Clinically it means that patients over 60 years need extra respiratory
exercises and frequent change of position to maximize air entry to the
lower zone of the lungs. Increased collateral ventilation in an aging lung
means that, holding breath for a few seconds at the peak of inspiration
can improve oxygen uptake. Weaning elderly patients from ventilator
support is very difficult because they develop dependence on assisted
breathing due to respiratory muscle weakness and low tidal volumes.
Obesity leads to reduced lung volumes and lung compliance due to large
visceral mass obstructing the movement of the diaphragm, leading to
poor ventilation of the lung bases. They tend to breath rapid and shallow
and have poor exercise tolerance.
• Clinically it means that in people with body mass index more than 30,
postural drainage is contraindicated, as the head down position will push
the visceral mass against the diaphragm, reducing its excursion even more.
The obese patients need particular attention to their respiratory mechanism
following any abdominal and thoracic surgery.
Posture of an individual affects the lung volumes, ventilation, compliance,
ventilation perfusion matching, gas exchange, muscle work and upward
movement of lung secretions on the mucocilliary escalator. Lung volume
is progressively better utilized as the posture changes from supine to
standing. In standing, the diaphragm can move downwards easily, because
the weight of the viscera is not resting on it, as it happens in supine position.
Ventilation and gas exchange is also better in a lung that is hanging down,
as in upright posture. However, the increased tone of trunk stabilizers,
mainly abdominal muscles, in standing increases intra-abdominal pressure
which restricts the movement of diaphragm.
• Clinically it means that passive measures like alterations in posture of a
patient can actually provide great therapeutic benefit at no extra cost. If a
patient is too ill to stand, the least the therapist can do is use pillows to get
the patient propped up at the head end. Further, since side lying has
been proved to optimise gas exchange than supine (Dean1985), a high
side lying position should help a breathless patient.
Exercise increases ventilation, oxygen demand and uptake, pulmonary
perfusion, dilatation of airways and mucus transport.
• Clinically it means that in a normal lung PaO2 falls at the first few minutes
of exercise, to regain normalcy as the perfusion and ventilation adapts to
increased demands for oxygen. In chronic obstructive disorders this
adaptation of PaO2 is reduced so that exercise tolerance is reduced. In
acute obstructive or restrictive disorders the adaptation does not take
place at all. Such patients can become breathless even with slight exertion.
The therapist must be aware of the exercise limitations of the patient and
plan treatment accordingly. Placing excessive demand on an ailing
respiratory apparatus may trigger a disaster.
Sleep leads to low lung volumes and poor oxygen uptake. It also reduces
the rate and depth of breathing due to low respiratory drive, leading to
carbon dioxide build up and oxygen desaturation in blood.
• Clinically it means that a failing respiratory system is most likely to shut
down during sleep. In such cases respiratory support like Bi-pap or oxygen
supplementation must be maintained during sleep. At the same time, the
therapist must remember that sleep allows the body to heal itself and
should not be interrupted for routine chest PT.
REFERENCES
1. Interactive respiratory physiology: Johns Hopkins School of Medicine, 1994.
2. The hemoglobin dissociation curves by J. W. Severinghaus; Simple, accurate
equations for human blood O2 dissociation computations; Journal of Applied
Physiology vol. 46: 599-602, 1979.
3. Physiotherapy in respiratory care: Alexandra Hough, section 1.10- 1.15, pp13-15,
Chapman & Hall.
Handbook of Practical Chest Physiotherapy 29
CHAPTER THREE
Respiratory
Pathophysiology
AN OVERVIEW
In the previous chapters we have studied the structure and function of the
two major components of the respiratory system; the airways, and the lung
parenchyma, each having a distinct role to play in the act of respiration.
The airways comprises of tubes of progressively narrowing diameters,
responsible for conducting the stream of atmospheric air to the depths of the
lungs (Chapter 1, Fig. 1.18).
The lung parenchyma consists of the alveoli-capillary complex, where
the exchange of gases takes place between atmospheric air, enclosed by thin
walled alveolar sacks and a sheet of blood flowing through a dense network
of capillaries, surrounding the alveolar sacs (Chapter 2, Fig. 2.4).
The natures of disorder that develop in these two distinct components of
the respiratory apparatus are also unique for each;
A. In the airways, the main disorder may be obstruction to the airflow. Such
disorders develop gradually over long period of time and are commonly
known as chronic obstructive pulmonary disorder (COPD).
B. In the lung parenchyma, main disorder may be loss of compliance or
inability of the lung to expand. Such disorders restrict expansion of the
lungs and are commonly known as restrictive lung dysfunction (RLD).
CHRONIC OBSTRUCTIVE PULMONARY DISORDER (COPD)

Synonyms and Keywords: Asthma, Bronchitis, COPD, COLD, Emphysema
Chronic obstructive pulmonary diseases (COPD) are a group of devastating
disorders that causes great human suffering. COPD are currently one of the
leading causes of death worldwide, particularly in industrial belts having high
degree of air pollution.
Historical Background
• In Western Europe, Badham (1808) and Laennec (1827) made the classic
description of chronic bronchitis and emphysema in the early 19th century.
• British medical textbooks of the 1860s described the familiar clinical picture
of chronic bronchitis as an advanced disease with repeated bronchial
infections that ended in right heart failure.
• Overall, this malady caused more than 5% of all deaths in the Middle
Ages and earlier. The conditions were most common among the poor;
therefore, it was attributed to “bad” living.
• Developments towards treatment of COPD in the 20th century include
the recognition of airflow obstruction as a key factor in determining
disability, widespread use of spirometry to assess degree of airway
obstruction, and the improvement of laboratory investigations methods
to assess blood gas saturation etc.
Definition
COPD is defined as a disease characterized by the presence of airflow
obstruction in the lungs. It consists of a group of disorders like Asthma, Chronic
Bronchitis and Emphysema. These disorders are usually chronic, with episodes
of acute exacerbation, triggered by inhaled irritants, common cold or sudden
variation in weather conditions. The airflow obstruction generally is
progressive, may be accompanied by airway hyper-reactivity and may
sometimes be partially reversible.
• Asthma is defined clinically as episodic, variable and reversible airway
obstruction characterized by tightness of chest, wheeze and non-productive
cough.
• Chronic bronchitis is defined clinically as the presence of a chronic
productive cough for 3 months during each of 2 consecutive years, other
causes of the cough being excluded.
• Emphysema is defined as an abnormal, permanent dilatation of the air
spaces distal to the terminal bronchioles, accompanied by destruction of
the alveolar septa, loss of elastic fibrous tissue and without obvious fibrosis.
Asthma and chronic bronchitis are defined in clinical terms and emphysema
in terms of anatomical changes in the lung parenchyma that leads to the
loss of elastic recoil.
Pathophysiology
Chronic obstructive pulmonary disease or COPD is the most common chronic
lung disease.
Respiratory Pathophysiology 31
Chronic: persisting for a long time
Obstruction: the state of being clogged
Pulmonary: pertaining to the lungs or the pulmonary artery.
Disease: a definite morbid process, often with a characteristic train of
symptoms.
In COPD, main pathological changes occur in the large (central) airways
in the early stage, the small (peripheral) bronchioles in the mid stage and the
lung parenchyma in the late stage of the disease. The exact pathogenic
mechanisms for such obstructive changes taking place in the airways are not
clear but are likely to involve diverse mechanisms as detailed below:
• The tissues that actually make up the lining proximal airway contains
connective tissue, mucus producing cells goblet cells and ciliated cells-
these cells have little whip-like hairs that extend into the airway and are
responsible for moving mucus and debris out of the airway. This is where
the irritants like dust mites, pollen, molds, etc. do their damage (Fig. 3.1).
• When under attack by COPD, such irritants triggers and causes the mucous
membrane in the airway to be inflamed and swollen and a large volume
of mucus is secreted.
• The increased number of activated polymorphonuclear leukocytes and
macrophages, which release elastases in a manner that cannot be
counteracted effectively by antiproteases, resulting in lung destruction.
• The primary offender has been human leukocyte elastases, with a possible
synergistic role suggested for proteinase 3 and macrophage-derived matrix
proteinase, cysteine proteinase, and a plasminogen activator.
• Additionally, increased oxidative stress caused by free radicals in cigarette
smoke, the oxidants released by phagocytes, and polymorphonuclear
leukocytes all may lead to apoptosis or necrosis of exposed cells.
• Excess mucus is produced in an attempt to protect the airway.
Unfortunately, in some COPD like asthma this reaction also can get out
of control.
• The swelling starts to close off some air passages causing air trapping. The
excess mucus becomes thick and overwhelms the cilia, which can only move
the thickened mucus slowly and with difficulty, and the patient with COPD
develops severe coughing spells, which also causes further irritation to the
airways. This is a “Vicious Cycle” produced during COPD attacks.
• In most COPD and in asthma, medications concentrate their actions to
this region of the airways. Steroids, inhaled and oral, reduce swelling of
the mucous membrane, aerosols with water vapor help moisten and
FIGURE 3.1: Pathophysiology of COPD
mobilize thick mucus, and other medication help stabilizes certain cells
(like mast cells) within the walls of the airways.
Clinical Features of COPD

The characteristic clinical features of COPD are:
Reduced entry and exit of air in the lung, due to several reversible and
irreversible factors:
• The reversible factors in COPD are:
1. Spasm of bronchial smooth muscles
2. Inflammation of the airway mucous membrane
3. Hypersecretion and retention of mucus in the airways, reducing the
lumen and forming mucus plugs that block the airways.
Reversible factors are easily treated with appropriate medication and chest
PT to help reduce respiratory distress and facilitate recovery.
• Irreversible factors contributing to COPD are:
1. Distortion and fibrous thickening of walls of the airway, as seen in
bronchiectasis
2. Damaged alveolar septum, as seen in emphysema, resulting in loss of
radial traction, which keeps open the unsupported airway, i.e. the
respiratory bronchiole.
3. Other irreversible factors causing airway obstruction are tumors or
foreign objects stuck in the passage.
The typical patient is asymptomatic until middle age, when his ability to
exercise or do strenuous work gradually declines, and he begins to develop
a productive cough.
Points to Ponder
• The presentation of any COPD consists of breathlessness, wheeze, cough,
air entrapment and expectoration of mucus.
• The extent of each component may vary, depending upon the type of
underlying disorder, i.e. Asthma, Chronic Bronchitis or Emphysema (Fig.
3.2).
• The clinical features of these disorders often overlap. A case of asthma
may significant element of emphysema or a case of chronic bronchitis
may have audible wheeze due to significant bronchospasm, commonly
seen in asthma.
• It is essential for the therapist to be able to distinguish between the
dominant components of each disorder, their specific management
protocol, in order to provide necessary inputs to the overall management
plan.
FIGURE 3.2: Changes occurring in the airway in COPD
Compensatory Mechanisms Adopted by the Body in COPD

The surface area presented for gas exchange by the alveoli of an adult is
equivalent to the area of a tennis court. The alveoli have walls that are a
single cell in thickness. Surrounding each alveolus is a network of capillaries,
also a single cell in thickness. Alveoli function like small bellows of the
harmonium, expanding to bring in fresh air containing oxygen and contracting
to expel carbon dioxide. This expansion and contraction also helps to move
blood through the pulmonary capillary system. This thin barrier is easily
crossed by Oxygen and Carbon Dioxide.
Problems presented during acute COPD attack are generally the blockage
of the flow of air in and out of the alveoli. Mucus obstruction and
bronchospasm prevent free exchange of gasses and allow blood to bypass
the alveoli without picking up Oxygen and retaining Carbon Dioxide. The
deoxygenated blood mixes with oxygenated blood that has passed through
working alveoli. Blood oxygen levels drop and carbon dioxide level rise.
Points to Ponder
• The body fights this rise of carbon dioxide in the blood by increasing the
rate of respiration. This is very effective in lowering the amount of carbon
dioxide, but does little to raise the oxygen level of the blood.
• However as the rate of respiration rises, the depth of each breath is
reduced. As a result of such shallow breathing, smaller volume of air
enters the lung with each breath, carrying smaller volume of oxygen.
• Rapid shallow breathing generates greater turbulence of air in the proximal
large diameter airway, increasing the resistance to incoming air. Hardly
any air inhaled during inspiration gets a chance to reach the gas exchange
interface, before it is expelled from the proximal airways by the cycle of
expiration. The lungs remain expanded by the trapped dead gas.
• To increase the uptake of oxygen from this meager supply of fresh air in
the lungs, the body responds by increasing the number of RBC in the
blood – a situation known as Polycythemia. However, more RBC makes
the blood thicker and difficult to flow through the capillary network in the
lungs, causing even less oxygen uptake.
• Shallow rapid breathing costs more energy and the patient become
breathless and easily fatigued with activity. To cope, the body tends to
self-limit activity level and progressive disability sets in.
When it comes to COPD, it’s the bronchial tree where all the action
takes place.
• The bronchial tree is shaped like an inverted tree; the main trunk is called
the trachea, which is a large cartilage ringed tube. The trachea branches
into the left and right main bronchi. The main bronchi branch further
into the segmental and sub-segmental bronchi. All these branches have
cartilage rings that prevent the walls of these airways from collapsing
inward.
• Just before the bronchial tubes end in alveoli, the cartilaginous rings
disappear. This segment of the airway is called respiratory bronchioles.
These airways are likely to narrow severely due to bronchial muscle spasm
and this is where wheezing takes place.
• Emergency medications work primarily by relaxing the bronchial smooth
muscle lining the respiratory bronchioles. Such drugs dilate the lumen of
the airway through broncho-dilatation by muscle relaxation.
• Above this point, where cartilage is supporting the airways, there is minimal
smooth muscle spasm and very little beneficial effect from medications
takes place.
• Anti-inflammatory drugs, like steroids are useful to reduce the swelling of
the mucous membrane lining the larger airways.
• Air entry can be improved further by clearing secretions from the larger
airways with the help of Chest Physiotherapy (CPT), but only when
significant amount of secretions are present
RESTRICTIVE LUNG DYSFUNCTIONS (RLD)

Synonyms and related keywords: pulmonary fibrosis, kypho-scoliosis,
sarcoidosis, interstitial pneumonitis, intrinsic lung diseases, pneumonitis,
diseases of lung parenchyma, interstitial lung disease, pneumonitis, idiopathic
fibrotic diseases, connective-tissue diseases, drug-induced lung disease, primary
lung disease, extrinsic lung disorders, extra-parenchymal diseases, lung
restriction, impaired ventilatory function, respiratory failure, idiopathic
pulmonary fibrosis, IPF, total lung capacity, TLC.
Definition
Restrictive lung diseases are characterized by reduced lung volume, either
because of an alteration in lung parenchyma or because of a disease of the
pleura, chest wall, or neuromuscular apparatus.
Points to Ponder
• In physiological terms, restrictive lung diseases are characterized by reduced
total lung capacity (TLC), vital capacity, or resting lung volume.
• Other clinical features are preserved airflow and normal airway resistance,
which are measured as the functional residual capacity (FRC). If caused
by parenchymal lung disease, restrictive lung disorders are accompanied
by reduced gas transfer, which may be marked clinically by rapid de-
saturation with exercise.
• The many disorders that cause reduction or restriction of lung volumes
may be divided into two major groups based on anatomical structures
involved.
Intrinsic Lung Diseases (ILD)

These diseases of the lung parenchyma are caused by inflammation or
scarring of the lung tissues; as interstitial lung disease, resulting in filling of the
interstitial space with exudates or choking of alveolar air spaces with post
inflammatory debris, as in pneumonitis. These diseases can be characterized
according to etiological factors. They include idiopathic fibrotic diseases,
connective tissue diseases, drug-induced lung disease, and primary diseases
of the lungs, e.g. Sarcoidosis.
Extra-parenchymal Diseases
The chest wall, pleura, and respiratory muscles are the components of the
respiratory pump, and they need to function normally for effective ventilation.
Diseases of these structures result in lung restriction, impaired ventilatory
function, and respiratory failure, e.g. non-muscular diseases of the chest wall
like ankylosing spondylitis or neuromuscular disorders like myopathy, spinal
cord lesions, and polio, etc.
Pathophysiology of Restrictive Lung Dysfunctions1

• Air flows to and from the alveoli as lungs inflate and deflate during each
respiratory cycle. Lung inflation is accomplished by a contraction of
respiratory, diaphragmatic, and external intercostal muscles, whereas lung
deflation is passive.
• FRC is the volume of air in the lungs when the respiratory muscles are
fully relaxed and no airflow is present. The volume of FRC is determined
by the balance of the inward elastic recoil of the lungs and the outward
elastic recoil of the chest wall.
• Restrictive lung diseases are characterized by a reduction in FRC and
other lung volumes because of pathology in lungs, pleura, or the structures
of the thoracic cage.
• The distensibility of the respiratory system is called compliance, the volume
change produced by a change in the distending pressure.
• Lung compliance is independent of the thoracic cage, which is a semi-
rigid container. The compliance of an intact respiratory system is an
algebraic sum of the compliances of both of these structures; therefore, it
is influenced by any disease of the lungs, pleura, or chest wall.
• In cases of intrinsic lung disease, the physiological effects of diffuse
parenchymal disorders reduce all lung volumes by the excessive elastic
recoil of the lungs, in comparison to the outward recoil forces of the chest
wall. Expiratory airflow is reduced in proportion to lung volume.
• Arterial hypoxemia in these disorders is primarily caused by ventilation-
perfusion mismatching, with further contribution from an intrapulmonary
shunt. The diffusion of oxygen is impaired, which contributes a little towards
hypoxemia at rest but is primarily the mechanism of exercise-induced
de-saturation.
• Hyperventilation at rest and on exertion is caused by the reflexes arising
from the lungs and the need to maintain minute ventilation by reducing
tidal volume and increasing respiratory frequency.
• In cases of extrinsic disorders of the pleura and thoracic cage, the total
compliance by the respiratory system is reduced, and, hence, lung volumes
are reduced.
• As a result of atelectasis, gas distribution is not uniform, resulting in
ventilation-perfusion mismatch and hypoxemia. In kypho-scoliosis the
lateral curvature, anteroposterior angulations, Kyphosis, or several of these
conditions are present. The Cobb angle, an angle formed by 2 limbs of a
convex prime curvature of the spine, is an indication of the severity of
disease. An angle greater than 100° is usually associated with respiratory
failure.
• Neuromuscular disorders affect an integral part of the respiratory system,
a vital pump. The respiratory pump can be impaired at the level of the
central nervous system, spinal cord, peripheral nervous system,
neuromuscular junction, or respiratory muscle. The pattern of ventilatory
impairment is highly dependent on the specific neuromuscular disease.
Epidemiology
The incidence of chronic interstitial lung diseases in persons with collagen
vascular diseases is variable. Kypho-scoliosis is the most common extrinsic
disorder causing RLD. It is associated with an incidence of mild deformities
amounting to 1 case per 1000 persons, with severe deformity occurring in 1
case per 10,000 persons. Other non-muscular and neuromuscular disorders
are rare. The worldwide prevalence of fibrotic lung diseases is difficult to
determine because studies have not been performed.
Sex: Lymphangioleiomyomatosis (LAM) and lung involvement in tuberous
sclerosis occur exclusively in pre-menopausal women. Men are more likely
to have pneumoconiosis because of occupational exposure, IPF, and collagen
vascular diseases (e.g., rheumatoid lung). Worldwide, sarcoidosis is slightly
more common in women.
Age: Some intrinsic lung diseases present in patients aged 20-40 years. These
include sarcoidosis, collagen vascular–associated diseases, and histiocytosis
X. Most patients with IPF are older than 50 years.
REFERENCE
1. “Patho-physiology of COPD & RLD’ adapted from web site of WWW. MED-
HELP.COM
CHAPTER FOUR
Clinical Evaluation of
Patients with Respiratory
Disorders
SCREENING TECHNIQUES USED BY

PHYSIOTHERAPISTS
INTRODUCTION
Management of respiratory disorders is a multidisciplinary effort.
The Physiotherapist is an indispensable member of the respiratory care
team, with valuable inputs in all stages of patient care.
It is, therefore, essential for the physiotherapist to have fundamental
knowledge of anatomy, physiology and various pathology of the respiratory
system and be able to apply the same knowledge to clinically to evaluate the
respiratory function, interpret test results and screen a patient for pulmonary
disorders.
In the previous chapters, the pulmonary anatomy, physiology, patho-
physiology and the essentials of respiratory disorders have been covered in
reasonable detail. This knowledge should give the aspiring chest physiotherapist
basic understanding of respiratory disorders.
However, to deliver effective and rational chest physiotherapy in these
conditions, an accurate, problem-oriented assessment is essential.
What is a Problem-oriented Assessment ?

A problem-oriented assessment focuses on analyzing the symptoms of the
patient, trying to detect the underlying physical/physiological causes producing
the symptom.
For example, a patient with asthma may report with inability to tolerate
moderate exertion.
A conventional symptom based approach will dictate the patient to
conserve energy to avoid fatigue.
A problem solving approach, on the other hand, will prompt the therapist
to ask “WHY’ does the patient fatigue so easily?
A series of questions should follow:
• The patient is unable to tolerate exertion because of energy wasted due
to excessive workload of breathing. Why?
• Because enough oxygen is not reaching his blood. Why?
• Because his lungs are hyperinflated with dead gas, which is not allowing
atmospheric oxygen to reach the gas-blood interface.
Thus by asking a few searching questions the therapist determines that if
the lungs are emptied of dead gas, space can be created for fresh atmospheric
oxygen to reach the blood stream at the depth of the lungs, thereby reducing
the workload of breathing. Hence, the lungs must be emptied of dead gas
with expiratory exercises to make space for oxygen rich fresh air.
Justification for this advice is based on the lower than normal peak
expiratory flow rate, due to narrowing of the airway.
Points to Ponder
• Problem-oriented assessment focuses on analysis of the patient problem
• Problem-solving approach to the treatment saves both time and resources
• Neither is wasted on unnecessary investigations, observation and
treatment.
Building the Clinical Database

• Interaction with team members: Physiotherapists are referred cases
by the physician, sometimes on the suggestions from the nursing
personnel. However, the real scope of physiotherapy has to be clarified
by the therapist himself to the other members of the team. Most cases
regarded to be too ill to receive physiotherapy often reflect a poor
understanding of the scope of physiotherapy on the part of the referring
physician.
• Attending ward rounds on a regular basis helps build rapport with the
team and makes other team members aware of the ability of the therapist
to deliver in specific clinical situations.
• Following the clinical notes and charts: Clinical records are divided
into two sections:
1. First section includes personal details of the patient, like name, age,
sex, address, height and body weight, provisional / final diagnosis and
some times the reason for referral.
2. Second section provides the clinical information based on history of
the present illness, previous medical history, drug history, family history,
social history, physical assessment, tests, laboratory investigations,
imaging techniques etc.
Clinical Examination of Patients with Respiratory Disorders 41
The therapist can get valuable information regarding the problem at hand,
its possible causes and what has already been done to solve the problem.
Further course of action can then be pondered.
SUBJECTIVE EVALUATION
Interviewing the Patient
Subjective evaluation should always give maximum importance to the subject
of the evaluation—the problem of the patient.
Patient interview should consist of open ended questions like “What, when,
how?” Such questions allow the patient to discuss the most important problem
from his / her perspective. It usually helps highlight the most troubling
symptoms and some times bring out hidden issues that may need urgent
attention. Interview should be gradually focused on to the core symptoms of
the disorder for confirmation and clarification.
Points to Ponder
The main symptoms of respiratory disorders are:
• Breathlessness
• Cough
• Sputum
• Wheeze
• Chest pain
The duration, severity, pattern of onset and reliving/aggravating factors for
each of the above symptoms must be explored during the interview.
1. Breathlessness or dyspnea is the conscious awareness of the act
of breathing.
Since the body spends approximately 5% of its metabolic energy output for
breathing, under normal circumstances we are not consciously aware of the
act of breathing. However, if more energy is required to draw air into the
lungs, due to various causes like: narrowing of airway, reduced compliance
of the lung tissue, chronic hyperinflation of the lungs, reduced oxygen uptake
in the lungs due to increased ventilation- perfusion mismatch, anemia etc,
the patient becomes aware of the increased workload of breathing. This is
breathlessness.
Points to Ponder
• Breathlessness, from whatever the cause, usually worsens with activity
and gets better with rest.
• The most important yardstick while evaluating breathlessness is to find
out how much exercise or activity makes the patient breathless.
Following grading (Table 4.1) proposed by New York Heart association
(1964) may provide a convenient yardstick to measure breathlessness in
cardiac patients. The same may be used for grading breathlessness in patients
with respiratory disorders as well.
Table 4.1: Grading of breathlessness according to symptoms
Class 1 No symptoms with activities of daily living. Occurs only with violent exertion
like running up staircase, fast cycling, and vigorous work out.
Class 2 Becomes breathless with activities like walking up staircase, making bed,
carrying heavy loads etc.
Class 3 Becomes breathless with ADL like bathing, dressing etc.
Class 4 Breathless even at rest.
2. Cough is a protective reflex that involves explosive expulsion of air through

a closed glottis to expel or bring up mucus secretions from the tracheo-
bronchial tree and gets rid of inhaled irritant or foreign body trapped in the
mucus.
Points to ponder
• Cough reflex is triggered by stimulation of receptors located in the airway
by inhaled irritants.
• Everyone coughs at some time or the other but paroxysmal, persistent,
productive/nonproductive cough, that keeps the patient awake at night
and hinders normal functioning must viewed with suspicion.
• Nature of the cough may indicate the type of underlying pathology:
a. Loud, barking cough indicates laryngeal or tracheal disorder
b. Cough immediately after eating or drinking indicates aspiration
c. Chronic productive cough that has been persistent over months may
indicate chronic bronchitis or bronchiactesis
d. Persistent dry cough indicate presence of interstitial lung disease
e. Nocturnal cough in children or young adults usually indicate asthma
but in the elderly same may indicate cardiac disease
f. Chronic cough producing only scanty mucus may arise from use of
drugs like ACE inhibitors.
• Persistent violent coughing spells may cause secondary problems like
fracture of the ribs, back pain and stress incontinence. The interview should
clarify these issues.
3. Sputum is the excess mucus secreted in the airway that is brought up by

the mucocilliary escalator expelled by coughing and huffing. The mucus
contains trapped foreign particles that has been inhaled, cellular debris,
bacteria, blood etc.
Points to ponder
• Up to 100 ml of sputum is brought up daily in normal adults.
• Any increase in the volume of sputum is abnormal.
• Sputum may be estimated as 1 teaspoon / ½ cup / 1 cup.
Table 4.2: Sputum chart*
Expectorated Description Grading Odour Possible causes

material of the material (Adapted of sputum
from
Miller’63)
Saliva Clear watery fluid S None Normal
Mucoid White M1 None Non-infected

chronic bronchitis
or asthma
Mucopurulent Mucus with trace of pus M2 Faint fishy Pneumonia,

2/3 mucus 1/3 pus P1 smell in most cases Cystic fibrosis,
1/3 mucus 2/3 pus P2 of aerobic infection Bronchiectasis
Frank purulent Thick viscous>2/3rd pus P3 Offensive odour Haemophilus

Yellow in anaerobic Pseudomonas
Dark green / Brown infections Pneumococcus
Rusty Mycoplasm
Red jelly Klebsiela
Frothy Pink or white mucus F None Pulmonary

edema
Hemoptysis Mucus mixed with H None Tuberculosis

blood, ranging Bronchiectasis
from flakes of Lung infarction
blood to fresh Carcinoma
or old blood Vasculitis
Decompression
sickness- Bends
Trauma
*(Adapted from Table 1.1, P7, Assessment & Investigation of patients’ problems; Sally Middleton,
Peter G Middleton; Physiotherapy for Respiratory and cardiac Problems, 3rd Ed; Elsevier)
4. Wheeze is a whistling sound produced by air rushing through airway

narrowed by mucosal edema.
Wheezing is felt by the patient as a tightness of the chest. In advanced
cases it may be audible to the patient at the mouth, as a whistling sound.
Points to ponder
• The interviewer must be careful to distinguish wheeze from stridor. Stridor
is a loud sound caused by obstruction in the proximal airway like
nasopharynx, larynx and trachea.
• Factors worsening and relieving the wheeze must also be clarified.
5. Chest pain may originate from the inflammation of the trachea, pleural
membrane and pericardium or from cardiac muscle ischemia or from
musculoskeletal causes or from esophageal reflux.
Chest Pain is a purely subjective phenomenon; hence its nature, intensity
and variables, i.e. relieving and aggravating factors can be learned solely
from interviewing the patient.
Points to ponder
• Chest pain is frequently misinterpreted by the patient as a sign of heart
problem, because it is felt in an area very close to the heart.
• The therapist must be extra careful to rule out pain of cardiac origin while
trying to identify the cause of chest pain.
The following chart (Table 4.3) short lists different conditions which may
produce chest pain. This chart may be used as quick guide for analysis and
interpretation of different types of chest pain, their presentation and their
possible cause.
6. Other symptoms like fever, headache, edema, sleeplessness, etc. are
clinically significant, if correlated with other symptoms.
Points to ponder
• High fever is common in respiratory tract infections, low grade fever
may indicate presence of malignancy or connective tissue disease and
evening rise of temperature may indicate pulmonary tuberculosis.
• Headache, particularly occurring in the morning, in a patient with
respiratory disorder, may indicate carbon dioxide retention due to
respiratory failure. This must be confirmed or ruled out by blood gas
analysis.
• Edema of the feet, face and hands in a patient with respiratory
dysfunction may indicate Cor pulmonale, i.e. right ventricular heart failure
due to hypoxic pulmonary hypertension and hypertension.
• Loss of sleep may indicate nocturnal hypoxemia, cor pulmonale, right
ventricular strain, etc.
7. Assessment of functional limitations and the quality of life:
In an individual with respiratory dysfunction, assessment of the quality of life
involves the degree of independence the person has to participate in common
Table 4.3: Understanding chest pain: nature and causes
Clinical condition Description of pain
Pleurisy—-Inflammation Sudden onset, sharp, localized stabbing pain, increases in deep

of the parietal pleural, breathing or coughing with no localized tenderness
hemothorax, malignancy
Pulmonary embolism / Pleural pain with / or without central chest pain

Pulmonary infarction
Pneumothorax Severe raw central chest pain with/or without pleural pain
Primary / Secondary Depends on site

carcinoma
Rib fracture Sharp, localized stabbing pain, increases in deep breathing or

coughing with marked localized tenderness
Costochondritis- Localized tenderness at costochondral junctions, resulting in

Inflammation of the guarding of inspiration, forceful pulling or pushing
costosternal cartilage
due to viral infections
Fibromyalgia of the Superficial pain that increases on deep inspiration or coughing or

scapulothoracic and sneezing or with some body movements. Usually caused by
pectoral muscles. unaccustomed exercises causing strain of scapulothoracic
muscles or due to violent coughing
Neuralgia- caused by Band-like pain around thorax, occasionally associated with

T4 syndrome, herpes paresthesia along the distribution of the nerve to intercostal
zoster, etc. muscles.
Ischemic heart disease- Dull, retrosternal pain or heaviness, worsening with exertion,
caused by myocardial commonly described as a weight or band-like pressure on the
ischemia or infarction. chest, occasionally radiating to the jaw or either arm. It may be
associated with nausea, vomiting and palpitations.
Pericarditis- inflammation Dull, retrosternal pain, worsening with deep inspiration and
of the pericardium caused relieved by sitting down. May mimic pain of angina or pleurisy.
by bacterial or viral infection,
trauma or tumor
Esophageal reflux Retrosternal burning pain, worsening with lying supine or bending
forward
Mediastinal shift due Severe, poorly localized central discomfort or pain

to pneumothorax
activities of daily living (ADL), earning money, meeting social responsibilities

and enjoy leisure activities.
Points to ponder
• Simple questions, which may answer yes / no, should be asked to find
out how independent the person is in his/ her day to day life.
• The answers to these questions should show the extent of functional
limitation and therefore the quality of life of the affected person.
• This information will help the therapist to plan effective treatment which
the patient can do, with/or without supervision.
• Repeating the questions after few days of treatment will help to assess the
outcome and effectivity of the treatment.
8. Assessment of Disease Awareness
The fear of the unknown leads to anxiety in a patient with respiratory
dysfunction. During the interview it is important to find out how much does
the patient know about the disorder he is suffering from?
Points to ponder
• The therapist should counsel the patient regarding the relevant details of
the disease, without scaring the patient.
• The nature of the disorder, triggering factors, preventive measures,
expected course of the disease, treatment options and their expected
outcome must be explained in simple, non-medical terms.
OBJECTIVE CLINICAL EVALUATION

Where patient interview provides subjective information outlining the patient’s
perception of the disorder, the objective assessment of a patient provides
verifiable clinical data which can be reproduced repeatedly.
Objective clinical evaluation involves:
1. General observation
2. Physical examination
3. Laboratory investigations like blood / body fluid examinations, ECG, Lung
function tests.
4. Imaging techniques like X-ray, CT scan, and MRI.
Points to Ponder
• The objective clinical findings should correlate with the complaint of the
patient and the presenting symptoms.
• If symptoms can be clinically verified, it may help to establish a provisional
diagnosis.
• Any difference between the clinical objective findings and the symptoms
call for a review of the diagnosis or looking for differential diagnosis.
• Both sets of information should be available to the physiotherapist from
the medical records and charts in the patient file.
• However, it is always relevant for the therapist to repeat some key clinical
examinations on the patient before proceeding with planning and
executing treatment measures.
1. General observation of the patient begins the moment the therapist

sets eyes on the patient. Ideally a patient on bed should be viewed from the
foot end or from the front as the patient walks into the therapy section.
Points to ponder
• The general appearance- does the patient appear anxious or relaxed?
• The color—is it healthy or pale or bluish?
• The extent of respiratory distress: Does the patient become restless walking
into the room or undressing for clinical examination? Is he breathless
even at rest: sitting in front of you or lying on bed?
• Pattern of speech—Does he speak with normal fluency or gasps while
speaking or is too breathless to speak?
For evaluating a patient in intensive care, the following additional
points must be observed:
• Presence and extent of ventilatory support needed: whether patient needs
only moist oxygen or continuous positive pressure ventilation or
intermittent positive pressure ventilation?
• Rout of ventilation being used: whether using face mask or nasal cannula
or endotracheal intubations or breathing through tracheostomy?
• Level of oxygen saturation in blood: it can be checked through a pulse
oximeter; (Normal 96-98%).
• Level of cardiovascular support: whether the patient is using temporary /
permanent pacemaker or drugs to stabilize blood pressure, cardiac rhythm
and rate and any other devices like central venous pressure monitors etc?
• Level of consciousness must be checked in patients with chronic carbon
dioxide. Such patients are at high risk of aspiration and unable to cough
effectively to clear secretions from the airway. Glasgow coma scale is the
most appropriate rating tool for the evaluating the level of consciousness.
• Location and number of tubes, drains and catheters, etc. being used.
2. Vital signs: The body temperature, heart rate, blood pressure are called
the vital signs. These signs are called vital signs because they indicate essential
physiological functions of the body and their stability is vital for survival
(Table 4.4).
Points to ponder
• In most health care facilities the vital signs are recorded by the physician’s
assistant or the nurse as soon as the patient reports for treatment.
• In critically ill patients, the vital signs are updated every 2 hours by the
nursing staff. These recordings are noted on the patient’s bedside ticket.
Table 4.4: Vital signs – normal values, causes of fluctuations
Vital sign Normal range Cause of rise Cause of fall
Body temperature- 36.5 – 37.5°C Fever—caused by Hypothermia –

may be recorded lowest in the morning infection or caused by prolonged
from mouth; axilla or highest in the inflammation. exposure to cold air /
rectum. afternoon. For every Increases metabolic water, hypo-volumic
rate, heart rate, shock, poisoning.
Oral temp should not 0.6°C (1°F) rise in
respiratory rate, Lowers metabolic,
be recorded within 15 body temperature the
oxygen consumption oxygen consumption heart, respiratory
minutes of drinking
and carbon dioxide carbon dioxide rate, oxygen
hot / cold liquid or
production increases production consumption and
food or smoking.
by 10% . carbon dioxide
production
Heart rate—can be 60- 100 per min in > 100 per min at rest. < 60 per min at rest
measured by listening adults; Mostly heart Heart rate may rise (normal in athletes)
through a beat and arterial due to anxiety,
Heart rate may fall
stethoscope at the pulses are identical; if exercise, fever,
due to beta blockers
apex of the heart; a heart beat does not anemia, hypoxia,
Pulse rate by produce a pulse it bronchodilators and
palpating the radial/ means poor stroke cardiac drugs.
femoral/carotid volume, due to weak
arteries. heart, low volume of
blood etc.
Blood pressure – 90/ 60 to 140 / 90 mm Hypertension; Blood Hypotension; Blood

recorded as systolic/ of Mercury (Hg) pressure greater than pressure lower than
diastolic pressure 145 / 95 mmHg. 90 / 60 mmHg.
measured by
Caused by increased Caused by heart
sphygmomanometer. failure / blood loss /
tone of arteries/
Systole indicates
aortic valve disease. reduced tone of
peak and diastole arteries.
indicates the minimum
Postural hypotension;
arterial pressure in a
Drop in blood
cardiac cycle.
pressure > 5 mmHg
while sitting up from
lying.
• The therapist attending the patient must review vital signs recorded in the
bedside ticket and if necessary should recheck the same before starting
therapy.
• During review of the vital signs, the therapist should specifically look for
any drastic fluctuation in the vital signs in the previous few hours.
• Unstable vital signs are a major contraindication for any
physiotherapy.
• If the consultant physician has specifically asked for therapy to be given,
but the therapist finds vital signs of the patient to be unstable, the matter
must be clarified from the medical officer on duty before any therapy is
given.
• In a physiotherapy clinic or home care setting, the therapist must check

the vital signs before and after therapy, particularly in patients with known
hypertensive/cardiac ischemic/arrhythmic disorders.
Vital signs may vary widely in individuals depending on age, sex, activity
level and most importantly underlying pathology.
Table 4.4 provides a range of normal values for vital signs and causes of
fluctuation in vital signs, as a ready reckoner in clinical practice.
3. Additional signs:
• Respiratory rate: Normal 12- 16 breaths per minute. Any increase in the
rate of respiration > 20 breaths per minute is called Tachypnea. It is
commonly seen in any form of exertion, lung disease, metabolic acidosis,
high fever or anxiety. Slowing of the rate < 10 breath per minute is
called Bradypnea. It is usually associated with depression of brain activity
due to intoxication due to alcohol or drugs, cerebral stroke, degeneration
or atrophy of brain.
• Body weight: Obesity or under nourishment, both can adversely affect
respiratory function. Though body weight is routinely recorded during
observation, it is highly variable from person to person depending on
build, age or sex.
• Body mass index (BMI) is a far better indicator of the ideal weight of an
individual. BMI is calculated by dividing the weight in Kg by the square of
the height in meters. The normal BMI of an individual should be 20- 25
Kg / m2, those < 20 can be called underweight and those > 25 should
be called overweight.
4. Observation of the hands, feet and eyes:
• Edema—collection of fluid initially seen around ankle and feet, later being
seen in abdominal cavity, sacrum, face etc. The skin appears stretched
and shiny and pits on pressure. Indicates fluid overload in the circulatory
system, due to low albumin level in blood, defective venous or lymphatic
drainage, prolonged steroid use or chronic renal failure. Excess fluid in
blood means sustained cardiac overload and finally cardiac failure.
• Clubbing—bulbous shape, with loss of angle between nail and nail-bed,
seen in tips of fingers and toes. The cause of clubbing is unknown, though
it is a fairly consistent finding in cardiac or pulmonary conditions which
produce chronic hypoxia.
• Cyanosis—bluish color of the skin or oral mucous membrane, caused by
chronic hypoxemia. The degree of blueness is directly proportional to
the percentage of carboxyhemoglobin (hemoglobin not saturated by
oxygen) in blood. An anemic patent therefore has to be significantly
hypoxic to be cyanosed. A polycythimic patient on the other hand will
turn blue even if slightly hypoxic.
• Anemia—A common finding in respiratory disorders, clinically detected
by pallor of the face or the sclera of the eyeball. Results in poor oxygen
transport and chronic hypoxia.
5. Observation of the chest:
• Shape of the chest: The male patient should be undressed to his skin
and the female patient to her undergarments in the presence of a female
attendant or nurse, to visualize the shape of the chest. The chest should
be visually examined to eliminate or confirm presence of following
deformities, which can seriously reduce chest expansion:
Points to ponder
• Kyphosis: Increased forward curvature of the thoracic spine, giving the
person a hunched back appearance. In young persons it is usually caused
by habitual stooping posture, as in jewellers, goldsmith, watchmakers or
bookworms. Elderly persons with osteoporosis can develop such deformity
due to collapse of the thoracic vertebral bodies. Kyphosis causes crowding
of ribs, restricting chest expansion by limiting the bucket handle movement
and the pump handle movement of the sternum, severely compromising
the ability to expand the lungs.
• Kyphoscoliosis: Increased forward curvature of the thoracic spine along
with lateral bending to one side. Causes may be postural or structural.
Restriction on breathing is much worse than only Kyphosis.
• Pectus carinatum (Pigeon chest): Present in severe childhood asthma, the
sternum is prominent and protruding. No significant restriction to breathing
as such but indicates a weak constitution associated with childhood asthma
or chronic respiratory dysfunction.
• Pectus excavatum (Funnel chest): Sternum is sunk inwards causing no
significant problem in breathing except cosmetic problem.
• Hyperinflation (Barrel chest): Aging and Kyphosis, often along with COPD,
can cause the ribs to be held horizontally, leading to a rigid barrel shaped
chest, with very little expansion. This occurs due to loss of elastic recoil of
the lungs, which allows the lungs to remain hyperinflated even on
expiration.
6. Breathing pattern (Table 4.5)
During a breath cycle, the abdominal wall and the bony thorax move in
relation to one another, in a set pattern and rate, the diaphragm acting as
Table 4.5: Types and causes of abnormal breathing patterns
Abnormal breathing Presentation Causes

patterns
Prolonged expiration The I : E ratio increases to COPD — due to reduced airflow

1 : 3 to 1 : 4 during expiration, due to dynamic
closure of floppy terminal airway
Pursed lip breathing Blowing through pursed lips To create backpressure during
with cheek bloated, commonly expiration, to keep the floppy
seen in COPD with air terminal airway open
entrapment
Apnea Stoppage of breathing for Unknown, some times associated

> 15 seconds, usually seen with depression of CNS
during sleep
Hypoapnea Slow breathing with Carbon dioxide narcosis in chronic

diminished ventilation lung diseases
Kussmaul’s breathing Rapid deep breathing Metabolic acidosis
Cheyne-Stoke breathing Irregular breathing with Heart failure, CO2 narcosis, CNS
cycles of few deep breaths depression or drugs
followed by a phase of apnea
Ataxic breathing Irregular deep and shallow Cerebellar disorders

breathing
Apneustic breathing Prolonged inspiration Brain damage
the prime mover and the intercostals as stabilizers. During labored breathing,
the muscles of neck and the upper girdle also participate in these movements.
The breathing pattern in different individuals varies with age, sex, build and
exercise tolerance. In the same individual the breathing pattern may change
depending on level of exertion, emotional stress and most importantly in the
presence of any respiratory pathology. The breathing pattern can be described
by the extent of movement performed and therefore the workload taken by
the muscles of each mechanical component of breathing. The three
components are denoted as follows: D- for diaphragm, C- for chest and N-
for neck and their muscle workload denoted numerically from 0-4, where 0
means no activity or workload and 4 means maximum overload. The therapist
must observe the breathing pattern and the changes therein carefully before,
during and after therapy, as it may provide vital clues to nature of the disorder,
degree of distress to the patient, as well as, to the effectivity of treatment.
Points to ponder
• Normal Breathing should be effortless and regular at 12-16 breaths /
min. Normal breathing pattern in an adult male can be described as 3D-
1C. This means ¾ of the workload of breathing is borne by the muscle of
diaphragm and 1/3 by the muscle of the chest. In a normal female the
resting breathing pattern is usually 2D-2C.
• The normal ratio of inspiration time ( I ) : expiration time ( E ) is 1 : 1.5.
• On physical exertion or mental stress, the oxygen demand increases
in the body, resulting in changes in breathing pattern in an otherwise
healthy individual. The chest heaves, the neck muscles become cord like.
• The resting breathing pattern may change from 3D- 1C to an emergency
breathing pattern- like 2D-2C or 1D- 2C- 1N.
• The respiratory rate also shows proportionate rise along with changes in
breathing pattern.
• Such changes in breathing pattern are not abnormal, but merely indicate
recruitment of less used accessory muscles for breathing, since the prime
mover like the diaphragm alone can’t cope with the workload of breathing,
to meet the oxygen demand in a fight or flight situation.
• Once the emergency is past, the breathing pattern and rate returns to
normal resting state, usually within two minutes.
• The rapidity with which the breathing pattern and rate returns to normal
indicates the level of cardiopulmonary fitness in an individual.
PHYSICAL EXAMINATION OF THE CHEST

Palpation
• Palpation of trachea at the center of the sternal notch should be done by
index and thumb.
Points to ponder:
1. Trachea may shift away from the affected lung due to pressure of fluid
in plural effusion or air in pneumothorax.
2. It may be pulled towards the affected side by a fibrosed or collapsed
lung.
• Palpation and measurement of chest expansion should be done from
behind the patient. Ask the patient to breathe out fully. On the bare back
of the patient place both hands with thumbs touching each other, at the
midline, over the spinous process of T8. The fingers should be spread out
on either sides of the chest wall. Ask the patient to breathe in fully. The
separation between the tips of the thumb should be 3-5 cm and equal on
both sides.
Points to ponder:
1. Though not very accurate, the manual technique gives the therapist a
chance to feel and detect any abnormality in movements of the ribs
during inspiration.
2. The degree of chest expansion should always be confirmed with a
tape measure.
• Palpation for spontaneous / surgical emphysema must be done to detect
air trapped in subcutaneous tissue of the chest wall, neck and face. Trapped
air under the skin crackles under the fingertips during palpation.
Points to ponder:
1. It indicates leakage of air from the lungs to the mediastinum, from
where it seeps under the skin of the chest wall.
2. Any pneumothorax must be treated with caution because vigorous
percussion may worsen the leakage of air into the pleural space and
therefore contraindicated.
• Palpation for vocal fremitus is done to measure vibration produced by
speech transmitted through the chest wall. The examiner places flat palms
on both sides of the upper chest wall. The patient is asked to say 9-9-9
repeatedly. The vibration thus generated is felt by the examiner first over
the upper zone and then in turn, over the middle and the lower lung
zone.
Fewer vibrations are felt over the upper zone because it is damped by
large volume of air in this part of the lung. Vibrations become progressively
stronger in lower lung, where more solid mass of lung tissue transmits the
vibrations better.
Points to ponder:
• Localized and stronger than usual fremitus over any specific lung zone
may indicate consolidation of the lung tissue.
• Reduced fremitus indicates pneumothorax or hydrothorax, i.e.
presence of air or fluid in the pleural space.
Chest Percussion
Hyperextend the middle finger of one hand and place the distal
interphalangeal joint firmly against the patient’s chest. With the end, not the
pad, of the opposite middle finger, use a quick flick of the wrist to strike first
finger (Fig. 4.1). Categorize what you hear as normal, dull, or hyper-resonant.
Practice your technique until you can consistently produce a “normal”
percussion note on your presumably normal) partner before you work with
FIGURE 4.1: Percussion of the chest
patients. Chest wall must be percussed from top to bottom and on both
sides for comparison of resonance.
Points to Ponder
• Resonance on percussion of the chest wall is produced by the vibration
of the chest wall, like the skin of a drum, over the lungs filled with air.
• When the residual volume of air in the lung is normal, the resonance of
the percussion or the percussion note is also normal.
• If there is air entrapment the resonance is increased and the percussion
note is booming.
• If there is consolidation of the lung tissue the percussion note becomes
dull.
• If there is pleural effusion, the percussion note becomes stony dull.
Auscultation of the Chest

Auscultation of the chest is the technique of listening to and interpreting the
sounds produced in the thorax by the movement of air in the proximal
airways and the blood in the chambers of the heart and through the great
vessels. It is used to verify observed and palpated findings, both before and
after the treatment. Auscultation is done by a stethoscope. A stethoscope
consists of a metallic chest piece connected by flexible rubber or plastic Y
tubing to two rubber earpieces. The chest piece consists of a diaphragm on
one surface and a bell on the other. The diaphragm is used to listen to breath
sounds and the bell for heart sounds (Fig. 4.2).
FIGURE 4.2: Typical stethoscope and its components
Points to Ponder
• Listening to the chest should be done in a quiet room, having good light
and no cross ventilation.
• The patient is made to sit on a chair or on the edge of the bed with the
chest exposed and asked to breathe in and out through the mouth. Side
lying position may be used for patients who are unable to sit up.
• The sound of the air moving in and out of the chest may initially be
listened to at the mouth, which is barely audible in normal lungs. However
in asthma or chronic bronchitis, wheeze and crackle from distal airways
can be heard at the mouth. The patient may be asked to cough to clear
the airway before actual auscultation with the stethoscope is done, because
these may mask the breath sounds. The diaphragm of the stethoscope is
placed on the chest wall and as the patent continues to breathe through
open mouth; the diaphragm is moved from top to the bottom of the rib
cage, sequentially from lateral to medial, over the auscultation points,
visualizing the lobes and fissures of the lung (Fig. 4.3).
Breath sounds heard through the stethoscope may vary depending
upon the thickness of the chest wall, extent of ventilatory effort of the
patient and the hearing acuity of the examiner.
• The main use of the breath sounds are in their interpretation and clinical
correlation to other findings.
Interpretation and Clinical Correlation of Breath Sounds

Breath sounds are produced by turbulent air flow. They are categorized by
the size of the airways that transmit them to the chest wall and on to the
FIGURE 4.3: The auscultation points on the back (left side) and the front (right side)
stethoscope. The general rule is, the larger the airway, the louder and higher
pitched the sound. Vesicular breath sounds are low pitched and normally
heard over most lung fields. Tracheal breath sounds are heard over the
trachea. Bronchovesicular and bronchial sounds are heard in between.
Inspiration is normally longer than expiration (I > E).
Breath sounds are decreased when normal lung tissue is displaced by air
as in emphysema or pneumothorax or by fluid as in pleural effusion. Breath
sounds shift from vesicular to bronchial when there is fluid in the lung
parenchyma itself, e.g. pneumonia.
Adventitious (Extra) Lung Sounds

Extra sounds that originate in the lungs and airways are referred to as
“adventitious” and are always abnormal, but not always significant.
Points to Ponder
• Rales or crackles: These are high pitched, discontinuous sounds similar to
the sound produced by rubbing your hair between your fingers.
• Wheezes: These are generally high pitched and “musical” in quality.
Stridor is a harsh inspiratory wheeze associated with upper airway
obstruction.
• Rhonchi: These often have a “snoring” or “gurgling” quality. Any extra
sound that is not a crackle or a wheeze is probably rhonchi.
Peak Flow Rate Monitoring (Fig. 4.5)

Peak flowmeters are inexpensive, hand-held devices used to monitor
pulmonary airflow function, which measures how fast air comes out the
lungs when you exhale forcefully. This measure is called a peak expiratory
flow or “PEF” and is measured in liters per minute (L / min). The peak flow
roughly correlates with the FEV1. How to Use a Peak Flow Meter Readings
from the meter can help recognize early changes that indicate attack of asthma
and by taking medications before symptoms appear, the patient may be
able to stop the episode quickly and avoid a severe asthma episode.
The peak flowmeter also can be used to:
• Learn what triggers asthma
• Decide when to add or stop medications
• Know when to seek emergency care
FIGURE 4.5: Peak flowmeter
How to Use the Peak Flowmeter; Instructing the Patient

• Measure the peak flow rate when you wake up and before you sleep at
night.
• Stand up, if you can. Set the marker to zero (Fig. 4.6). Most peak flow
meters have a little marker that you can slide down toward the mouthpiece
as far as it will go.
FIGURE 4.6: Setting the marker to zero
• Open your mouth and take as deep a breath as you can. Hold the peak
flowmeter in your hand. Keep your fingers away from the numbers
(Fig. 4.7).
FIGURE 4.7: Holding the peak flowmeter
• Close your lips around the mouthpiece. Don’t put your tongue in the
hole. Blow out one time, as FAST and as HARD as you can (Fig. 4.8). Try
not to breathe out through your nose. If that happens, use a nose clip.
FIGURE 4.8: Blow as hard as you can
• The marker will go up and stay there. Don’t touch the marker. Find the
number where the marker stopped. Blow and record the readings three
times (Fg. 4.9).
• Write the best reading in your asthma diary (Fig. 4.10).
FIGURE 4.9: Read the peak flow rate in liters/min FIGURE 4.10: Record flow rate
in the asthma diary
“Personal best” Peak Expiratory Flow Rate

The “personal best” peak expiratory flow is the highest peak flow one can
achieve over a 2- to 3-week period when asthma is under good control. The
personal best PEFR is the benchmark to which all other subsequent peak
flow readings will be compared.
Finding Asthma Zones

Keeping a daily record of PEFR and understanding how PEFR relates to
changes in asthma will help better manage asthma episodes. To help patients
understand this relationship, health care providers use a system of asthma
zones.
There are three asthma zones:
• Green Zone
• Asthma is well-controlled.
• PEF is 80 to 100% of personal best.
• Yellow Zone
• Asthma is flaring up or is poorly controlled.
• PEF is 50 to 80% of personal best.
• Red Zone
• Asthma is severe; requires emergency care.
• PEF is less than 50% of personal best.
To find the ranges for asthma zones, multiply the personal best PEFR by
1 (100%), .8 (80%) and .5 (50%).
Points to Ponder
Assuming a best effort PEFR of 400 L /min, the zones would be as follows:
• Green Zone: 80 to 100% of 400 = 320 (400 × .8) to 400 (400 ×
1)
• Yellow Zone: 50 to 80% of 400 = 200 (400 × .5) to 320 (400 ×
.8)
• Red Zone: < 50% of 400 = less than 200 (400 × .5)
These personalized ranges should be recorded in an asthma diary for
easy reference, to be included in the Asthma Action Plan. If one is in the
Yellow or Red Zone, he will need to adjustment of dosage of medications.
The Daily Asthma Diary (Table 4.6)

The patient can record daily PEFR and symptom scores in a Daily Asthma
Diary. This diary will help to evaluate how well the current Asthma Action
Plan is working. The diary also will help to identify when changes are occurring
in the status of asthma.
Points to ponder:
• Fill in the date each day.
• Take PEF readings each morning before asthma medications are taken.
• Compare PEF reading with personal best.
• If a PEF reading is less than 80% of the personal best, one must follow
the instructions were given in the Asthma Action Plan.
• When performing the evening peak flow, one should also record the
number of puffs of reliever inhaler that was needed.
Table 4.6: The asthma diary

Date PEF # of Puffs of Cough Wheeze Short Breath Tight Chest
Readings rescue inhaler
A.M. P.M.
RESPIRATORY DISTRESS SYNDROME

Persons having difficulty breathing often show signs that they are not getting
enough oxygen. This indicates respiratory distress. It is important for the
therapist to learn the signs of respiratory distress, to respond appropriately.
• Breathing rate: An increase in the number of breaths per minute may
indicate that a person is having trouble breathing or not getting enough
oxygen.
• Color changes: A bluish color seen around the mouth, on the inside of
the lips, or on the fingernails may occur when a person is not getting as
much oxygen as needed. The color of the skin may also appear pale or
gray.
• Grunting: A grunting sound can be heard each time the person exhales.
This grunting is the body’s way of trying to keep some air in the lungs so
that the terminal airway will stay open, preventing air entrapment.
• Nose flaring: The spreading of the external nares while breathing may
indicate harder work to breathe.
• Retractions of the neck: The chest appears to sink in just below the
neck and/or under the breastbone with each breath indicating increased
respiratory effort. One way of trying to bring more air into the lungs.
• Sweating: There may be increased sweat on the head, but the skin may
feel cool or clammy to touch. This may happen when the breathing rate
is very fast.
• Wheezing: A tight, whistling or musical sound heard with each breath
may indicate that the air passages may be smaller in diameter, making it
more difficult to breathe.
In this chapter I have tried to give essential tips to the aspiring chest
physiotherapist for evaluating a patient with respiratory symptom. However
without systematic record of the findings of this evaluation, the entire effort
will be pointless.
Hence to summarize this chapter I present a comprehensive pulmonary
symptoms questionnaire cum evaluation format. This format may be used
as it is by the beginner, to be upgraded and adapted as experience grows
and insights develop.
Pulmonary Symptoms Questionnaire cum evaluation chart
Name __________________________________________________Age ______Sex_______
Address______________________________________________________________________
Date of First Reporting_______________Telephone number________________________
Complaint of ________________________________________________________________
Duration of symptoms_________Pattern of symptoms: Episodic / Progressive / static
Provisional Diagnosis ________________________________________________________
Descriptive analysis of symptoms
Degree of Breathlessness: Feels breathless since _______Years_____ months
Becomes breathless walking up stairs or slight hill Grade I
On level ground, walks slower than person of the same general

condition, age and sex Grade II
Becomes breathless while doing house work, talking or dressing Grade III
Has to rest after walking on level ground for 100 yards Grade IV
Nature of cough: Has cough since ______ Years _______ months
Has cough for three consecutive months or more in a year, for two
consecutive years Grade I
Has bouts of cough for four to six times a day, four or more days I a week Grade II
Morning cough on most of the days of the week throughout the year Grade III
Daily persistent cough Grade IV
Has occasional cough, usually associated with common cold Normal

Sputum production: Bringing up sputum from the chest since ____ years ____ months
Sputum from the chest, 3 consecutive months or more Grade I
Sputum from the chest: Twice a day, for four or more days per week Grade II
Sputum from the chest in the morning only Grade III
Sputum from the chest throughout the day Grade IV
Sputum color is White / Yellow / Gray / Green (strike off inapplicable)
Sputum is blood stained / has clots of blood / has fresh blood (strike off inapplicable)
Sputum smells Neutral / Fowl (strike off inapplicable)
Wheezing or feeling of tightness in the chest
Feels tightness in the chest or has heard wheezing at the mouth since ___ Years____Months.
Wheezing is triggered by common cold/cold air/dust/smoke/mental stress/physical

exertion/mental stress (strike off inapplicable). Frequency of wheezing
attack: ___________________________
Wheezes Only with episodes of common cold Grade I
Wheezes Occasionally, even without any cough and cold, mostly seasonal Grade II
Wheezes Daily wheezing during night time only Grade III
Daily wheezing throughout the day and night Grade IV
History of cigarette smoking: Age started ______ Packs per day______ Age stopped ____
History of occupational pulmonary exposure
Occupation: Office worker / Farmer / Industrial worker / Crafts man / Homemaker / Student
Job description______________________________________________________________
Number of dependants____________ approximate family income per month________________
Description of Home environment: Rural / Urban / Slum (strike off inapplicable)
Risk of Hazardous exposure at work or home elicited through (please circle): Dust
/ Dampness / Paint / Flowering plants / Pets / Chemical fumes / Toxic gases / Flour mill / Stone
crusher / Asbestos factory / Thermal power plant
Years of exposure ___________________ Level of exposure :- Mild / Moderate / Severe
Chest Physical Examination: Please tick if present or cross if absent
Patient having respiratory distress walking in to the clinic
Patient having respiratory distress while sitting in the clinic
Clubbing of the finger tips
Bluish color seen around lips, ear lobes or tongue
Bluish color seen on nail beds of fingers

Lymphadenopathy : swelling of lymph glands in neck, axilla and groin
Chest expansion ( measure in centimeters with a tape at the level of nipples)
Breathing pattern 1C : 3 D 2C:2D 1N:2C:1D 2N:2C
Intensity of breath sounds (please tick) Decreased Increased WNL
Early inspiratory crackles
Late inspiratory crackles
Wheezing can be heard through stethoscope or naked ear
Pedal edema : swelling of the feet
Peak expiratory flow rate (in liters / minute)
Blood pressure ( Measure with patient sitting, from left arm only)
Radial pulse rate
Resting Respiratory Rate ( observe and count the rise and fall of the abdomen
with each breath from one side, with the patient in supine position)
Chest X- ray / MRI /CT scan report (To be recorded by the therapist from observing the film
or from the report of the radiologist. Tick if present cross if absent)
In Airflow Disorders of the lungs the Chest X-ray/Scan may show following findings
Hyperinflation of the lungs
Flat diaphragms- half or full
Elongation of the heart shadow with airspace behind sternum
Presence of emphysematous bullae
In Interstitial Disorders of the lungs the Chest X-ray/Scan may show following findings
Reduced lung volumes
Presence of opacities in the lung fields
Type of Opacities (please tick) Nodular Reticulo-nodular Linear
Severity of opacities Mild Moderate Severe
Location of opacities in lung zones Upper Middle Lower Global
Other features Pleural findings Eggshell Kypho-

calcification scoliosis Kyphosis
Rating of Impairment by pulmonary function tests done on ______/ ______/_____

(please circle appropriate value)
Mild Moderate Severe
FVC1 % 60-79 40-59 40 or less
FEV1, % 60-79 40-59 40 or less
FEV1/FVC% 60-69 40-59 40 or less
Dsb1 % 60-79 40-59 40 or less
EXVO2, mL/kg 20-24 16-19 15 or less
Final Diagnosis _________________________________________________________

Chest Physiotherapy Treatment plan: (Circle appropriate) No. of sittings per week____
1. Breathing Exercises:
Relaxed Diaphragmatic / Segmental / Lateral costal / Pursed lip / End inspiratory
Holds
Incentive spirometer; setting _____l/min; ______ repetitions per sitting ______
sittings/day
2. Nebuliser with_________________________________________ duration_____ rep.

/day____
3. Forced expiratory Techniques: Huffing ______cycles; Coughing _____cycles

Assisted coughing ____cycles; blowing _______cycles
4. Percussion techniques: Clapping__ Shaking__Vibration__
5. Postural Drainage position _____________________________________Duration____
6. Exercise tolerance regime

Static Cycling ____ Min; Treadmill ____Min; Stepper _____Min; Twister ____ Min
7. Relaxation Exercises: ____________________________________Duration ______Min
8. Yoga Asana ________________________________________________No. of rep____
Signature
Follow up record (to be filled up at monthly intervals)
Date of Symptom status Medicines Fresh problems Fresh advice

review (Better/Same/Worse) taken
(Yes/ No)
CHAPTER FIVE
Chest X-ray for the

Physiotherapist
INTRODUCTION
If a picture is worth a thousand words, the images from a chest X-ray can be
invaluable in detecting problems of the heart or lungs.
DEFINITION
The X-rays are a form of invisible electromagnetic radiation that can penetrate
the body and produce an image on an X-ray film. Photographs taken with
the help of X-ray are called radiographs. Chest X-rays include views of the
lungs, heart, a small portion of the gastrointestinal tract, thyroid gland and
the bones of the chest area.
Points to Ponder
• A chest X-ray (radiograph) can help determine whether a patient has
heart or lung problem; reveal fluid in the lungs, show enlargement of the
heart, identify pneumonia and many other conditions — like detecting a
broken rib or two.
• X-rays that pass through areas of the body where there is air, such as in
the lungs, the X-ray will appear black. Soft tissues, such as fat, skin, muscle,
appear in different shades of gray. Dense structures, such as bone, appear
white. X-rays are two-dimensional images; therefore many images of
different angles may be needed to make an accurate diagnosis.
• Despite the numerous high-tech imaging procedures now available, the
basic chest X-ray remains a core tool in helping diagnose problems of the
cardiovascular and pulmonary systems. Chest X-rays are painless, quick
and relatively inexpensive.
• A chest X-ray should be ordered on complaint of persistent cough, an
injury involving the chest, complains of chest pain or difficulty in breathing.
• Chest X-rays are usually ordered for a single check of an organ’s condition,
and some times serial X-rays are ordered to compare with previous studies.
Chest X-ray for the Physiotherapist 67
SCOPE OF CHEST X-RAY

Routine chest X-ray can be used to see the following:
The condition of lungs: Chest X-rays can reveal structural changes or
abnormalities in the lungs due to primary lung disorders or those that arise
from heart problems, e.g. fluid accumulation in the lungs (pulmonary edema),
as a result of congestive heart failure. X-rays can also help to detect cancer or
infection in the lungs.
The size and outline of the heart: Changes in the size and shape of the heart
may indicate a variety of conditions, such as heart failure, congenital heart
disease, fluid around the heart (pericardial effusion) and problems with heart
valves.
Blood vessels: Because the outlines of the large vessels near the heart — the
aorta and pulmonary arteries and veins are visible on chest X-rays, they may
reveal aortic aneurysms or other blood vessel problems, or congenital heart
disease.
Calcium deposits: Chest X-rays can detect the presence of calcium in the
heart or blood vessels. Its presence may indicate damage to heart valves,
coronary arteries, heart muscle or the protective sac that surrounds the heart
(pericardium). Calcium deposits in the lungs may be from an old, resolved
infection or a more serious disease.
Indications for requesting a chest X-ray

Most common reasons for performing chest X-rays are:
• Pulmonary disorders: Chest radiographs are frequently ordered to
diagnose or rule out pulmonary disorders such as Pneumonia, Tuberculosis,
Emphysema or Pneumothorax (presence of air or gas in the chest cavity
outside the lungs).
• Cancer: A chest X-ray may be ordered by a physician to check for possible
cancer of the lungs, thyroid, lymphoid tissue, or bones of the thorax.
• Cardiac disorders: While less sensitive than echocardiography, chest X-
ray can be used to detect disorders like congestive heart failure or
pulmonary edema.
• Other conditions: Chest X-rays are used to detect trauma to the rib cage
or lungs, see foreign bodies that may have been swallowed or inhaled,
and to evaluate response to treatment for various diseases. Often the
chest X-ray is also used to verify correct placement of chest drainage
tubes or angiocatheters or electrodes of pacemaker.
Precautions to be observed during chest X-ray
• Pregnant women, particularly those in the first or second trimester, should
not have chest X-rays, unless absolutely necessary.
• If the X-ray is ordered, women who are pregnant or suspected to be
pregnant must wear a protective lead apron covering the lower abdomen.
• Though, the amount of radiation from one chest X-ray procedure is
minimal, care should always be taken to avoid overexposure, particularly
for children or very old patients.
Chest X-ray Procedure

• Routine chest X-rays consist of two views, the frontal view (referred to as
posterior anterior or PA) and the lateral (side) view.
• It is preferred that the patient stand for this examination, particularly
when looking for collection of fluid in the lungs.
• During the actual time of exposure, the patient should hold his or her
breath for a few seconds. Any motion at this moment could spoil the
quality and sharpness of the exposure.
• The chest X-ray may be performed in an X-ray clinic or a hospital radiology
department.
• In case of bedridden patients, a portable chest X-ray may be taken.
• Portable films are of poorer quality than those taken with fixed equipment,
but for some patients or in some situations portable X-rays are the only
choice.
• Bedridden patients may be propped up with pillows, as upright a position
as possible, to get a clear picture. Alternatively they may be positioned in
prone lying, the film cassette placed below the chest and exposure taken
from above.
Preparation for Chest X-ray

• There is no need for advance preparation for chest X-rays.
• Before X-ray, a hospital gown should replace all street clothing on the
upper body, long hair must be tied up and all jewellery must be removed.
Risks
• The only risk associated with chest X-ray is minimal exposure to radiation,
particularly for pregnant women and children. Such patients should use
protective lead aprons to cover the rest of the body during the X-ray
procedure.
• Technologists should be careful to check possible dislodging of any tubes
or monitors in the chest area during positioning a patient bedridden.
X- ray Reporting
A radiologist, or physician specially trained in the technique and interpretation
of X-rays, will evaluate the results, whether normal or abnormal, and provide
the findings in the form of a written report. However, the physiotherapists
should have working knowledge of interpreting X-rays for ease of working
and avoiding mistakes. Abnormal findings should always be clinically
correlated with the physical findings, medical history and other diagnostic
tests to reach a final diagnosis.
The Art of Reading the Chest X-ray (Figs 5.1 to 5.16)

• The films to be placed on the view box as though the therapists were
facing the patient with his left on his/ her right side.
• An AP film, taken from the same distance (6') enlarges the shadow of the
heart which is far anterior in the chest and makes the posterior ribs appear
more horizontal.
Anatomical landmarks in PA and lateral view
FIGURE 5.1: PA or posterior anterior view of the chest; taken with the film in front of the patient
as close to the chest as possible, beam behind at a distance of six feet; patient usually upright;
distance of beam determines magnification, clarity and sharpness
FIGURE 5.2: Identifying the different organs: Key to

interpretation of PA view X-ray of the chest
FIGURE 5.3: Lateral view- left side of the chest against film holder (cassette); beam from
right at a distance of six feet. Lesions located behind the left side of the heart or in the
base of the lungs are often invisible on the PA view because the heart or diaphragm
shadow hides it. The heart in left lateral X-ray is less magnified since it is closer to the film
Chest X-ray in Disease Conditions
FIGURE 5.4: Pneumonia: X-rays are most effective when compared to previous studies:
Pneumonia is seen on these radiographs as white patches and irregular areas of density.
Posterior - anterior and lateral chest radiographs at the left demonstrate a 4.5 cm round
opacity in the superior segment of the right lower lobe (indicated by arrows). The lungs are
otherwise clear, and the costophrenic sulci are sharp. Follow-up chest radiographs on the
right were taken two weeks later, following antibiotic treatment, to show nearly complete
resolution of the round mass
FIGURE 5.5: Bronchopneumonia: Since

the bronchi, which are usually not visible,
can be seen in this X-ray, a diagnosis of
broncho pneumonia may be made with
the above X-ray
FIGURE 5.6: Empyema or pulmonary abscess: X- ray showing

empyema or a pulmonary abscess in the middle lobe of right
lung, indicated by the arrow
FIGURE 5.7: Asthma: This chest X-ray shows widening of

the intercostal space and horizontal ribs, suggesting
hyperinflation of the lungs, associated commonly with asthma
FIGURE 5.8: Hilar enlargement: Hilar mass or enlargements

are seen at the right side of midline of the lungs, where vessels
and nerves enter into the lungs, is a common finding in
pulmonary hypertension, lymphadenopathy in TB, sarcoidosis,
lymphoma and cancer
FIGURE 5.9: Interstitial lung disease : This chest X-ray shows

fiber like deposits, mostly in the lower portions of the lungs.
Such image is associated with Interstitial lung diseases
FIGURE 5.10: Hydrothorax: X-ray showing the air- fluid level

in left pleural space due to pneumonic hydrothorax
FIGURE 5.11: Pleural effusion: X-ray shows ground glass

translucency at right lung middle and lower zone, indicating
pleural effusion
FIGURE 5.12: Pulmonary edema: X-ray showing

pulmonary edema, secondary to congestive cardiac failure
FIGURE 5.13: Atelectasis: This X-ray shows homogeneous

opacity due to atelectasis of the left lung in an asthmatic
with the heart and trachea pulled to the left side of the
thoracic cavity indicated by the arrow
FIGURE 5.14: Emphysema: Chest X-ray of a chronic smoker

shows severe emphysema of the lungs, with prominent black
patches indicating emphysematous bullae
FIGURE 5.15: Rib fractures with traumatic pneumothorax:

Anteroposterior (AP) chest radiograph demonstrates a lateral
lower-rib (12th) fracture on the left side (white arrow). An
associated left subcutaneous pneumothorax dissects along
the left chest wall (black arrow)
FIGURE 5.16: Inhaled foreign bodies, like the coin can usually be
located in the X-rays they will look different from any other tissue
or structure in the chest
• In a supine film, the diaphragm will be higher and the lung volumes less
than in a standing patient.
CHAPTER SIX
Management of Major
Respiratory Diseases
We can survive without food for a month, without water for days but we
would live only for a few minutes without air. The most important cause of
human suffering is the inability to breathe freely. There are many of diseases
that affect the respiratory system, creating impediments to ventilation,
mismatched perfusion and ultimately inadequate exchange of gasses in the
lungs. This chapter explores the intricacies of such disorder in reasonable
detail and looks at the most rational way of managing such disorders from
the point of view of a physiotherapist.
CHRONIC OBSTRUCTIVE PULMONARY DISORDER

Definition
Chronic Obstructive Pulmonary Disorder (COPD) is a term that includes a
large group of lung diseases which interferes with normal breathing due to
narrowing of the airway. Such narrowing of the airway may be anatomical
or functional in nature. The most common disease conditions that are included
in the group of COPD are Asthma, Chronic Bronchitis and Emphysema.
However, Asthma is no longer regarded as a true COPD because it has a
different long-term prognosis and management protocol.
Cause
The causes of such diseases are not fully understood. It is generally agreed
that the most important cause of chronic bronchitis and emphysema is cigarette
smoking and that of asthma is an allergy. Causes such as air pollution and
occupational exposures may play a role in development of COPD, especially
when combined with cigarette smoking. Heredity also plays a contributing
role in some types of emphysema due to alpha 1 anti-trypsin deficiency.
Symptoms
Chronic bronchitis and emphysema are the most common long-term lung
conditions under COPD group which cause shortness of breath. Each
Management of Major Respiratory Diseases 79
condition can occur by itself, but most people have a mixture of the two
problems. There may be an added “asthma” component, which simply means
that some people have an improvement in lung function and breathlessness
with the use of bronchodilators and anti-inflammatory medications.
COPD usually occurs in people who have smoked or who continue to
smoke cigarettes. A small proportion of people who develop emphysema do
so as a result of an inherited condition called Alpha 1 anti-trypsin deficiency
which makes them particularly susceptible to the adverse effects of smoking.
In spite of narrowed airways, people with COPD are still able to breathe
in sufficient air. However on breathing out, the terminal airways may collapse
earlier than the alveoli, which cause air to be trapped in the lungs and the
lungs gradually hyperinflate. This causes an uncomfortable sensation of
tightness in the chest and contributes to the feeling of breathlessness. Pursed
lip expiration breathing techniques, medications and even surgery can deflate
the lungs to a degree, reducing the severity of the symptom, making people
feel less uncomfortable.
No matter what is the cause of breathlessness- Asthma; chronic bronchitis,
Emphysema, Bronchiactesis or Heart failure, it often causes anxiety and a
loss of self-confidence as it worsens. As a result people often get out less and
have less social contact. Together with the physical disability this can lead to
depression.
Disease Course
COPD develops very gradually. One needs to have lost about half the lung
function before developing symptoms of breathlessness. Breathlessness may
first become apparent when walking up hills or stairs. In advanced cases,
breathlessness can occur with activities of daily living (ADL) like dressing or
bathing. In such cases only about 20% of lung function remains intact.
It is therefore extremely important in COPD to find out whether everything
has been done to try and alleviate the symptoms and whether appropriate
adjustments to the condition has been made. This in turn allows maintaining
as good a quality of life as possible. Adapting to any limitations and ensuring
that other members of the family and friends understand the condition can
do a lot to relieve anxiety and lift depression.
Risk Factors
Smokers are at greatest risk of developing COPD. This not only means people
who like to puff away at the slightest excuse, but also those passive smokers
who inhale secondhand smoke. Malnourishment, constant exposure to smoke
or dust, unhealthy living conditions and alcohol abuse may increase the risk
of developing COPD. For some conditions like asthma there may be a familial
tendency.
Associated Problems
People with COPD are at greater risk of developing associated disorders such
as coronary artery disease, pneumonia, stroke and even lung cancer.
TYPICAL CLINICAL PRESENTATION OF COPD

COPD present in two typical varieties. The physiology of a patient coping
with constant hypoxia may respond either by making do with whatever
minimum amount of oxygen is available in blood and therefore have chronic
hypoxia and manifest all signs of hypoxemia and carbon dioxide retention.
Such patients usually have a barrel shaped chest, habitual hypoventilation,
drowsiness, central and peripheral cyanosis, fluid retention and often exhibit
signs of cor pulmonale. Such patients become used to very low levels of
oxygen in blood.
These types of cases are called blue bloaters (Fig. 6.1). Unguarded oxygen
supplementation in blue bloaters can upset their respiratory drive and the
patient may drift off to a stupor, coma and death in their sleep.
FIGURE 6.1: A blue bloater; note the corpulent belly

indicating fluid retention, barrel shaped chest and
bluish tinge of the skin
Alternatively, to cope with short supply of oxygen, a patient may increase
his rate or depth of ventilation, trying to wash out as much carbon dioxide as
possible from the blood, at extreme cost of energy. These cases are so busy
breathing that they do not have time to sleep, eat or drink. Their net energy
expenditure for breathing shoots up from just 5% to a stupendous 25% of
total metabolic output. As a result these cases are malnourished, fatigued,
dehydrated, but never cyanosed. They habitually hyperventilate, have flushed
appearance and are dependant on very weak hypercapnic drive to continue
breathing. They are called pink puffers (Fig. 6.2). Again massive oxygen
supplementation in such cases can wash off critical balance of carbon dioxide
in their blood and this may lead to respiratory arrest. Most often such patients
die of respiratory fatigue.
FIGURE 6.2: Pink puffer; note the emaciated

appearance, prominent accessory muscles of
respiration, pink complexion and the typical elevated
protracted shoulder girdle. You can also see the
patient puffing away through pursed lips
DIAGNOSIS: INVESTIGATIONS/TESTS
Lung Function Tests
Peak Flowmeter: This device measures the rate of airflow out of the lungs
during forced expiration. (Please see Chapter 4, page 57-59; Figs 4.5 to
4.10). The air flow rate is measured in liters per minute. The volume of air
expirated in the first one second of the expiratory cycle is known as (Forced
expiratory volume in the first second) FEV1. This is often used to measure
the severity of COPD. Lower the FEV1, greater the degree of airway
obstruction, provided FVC is not severely decreased, patient is not having
any musculoskeletal problems and compliance of the lung is adequate.
Spirometry: A spirometer is a device used to assess lung function. Spirometry
is the evaluation of lung function with a spirometer, one of the most common
pulmonary function tests and may be necessary for any/all of the following
reasons:
• to determine how well the lungs receive, hold, and utilize air
• to monitor a lung disease
• to monitor the effectiveness of treatment
• to determine the severity of a lung disease
• to find out whether the lung disease is restrictive (decreased airflow) or
obstructive (disruption of airflow).
The spirometer is a device into which a person has to breathe in and out.
It measures volumes of air displaced by the lungs during a cycle of inspiration.
From these volumetric readings various components of volume changes that
take place in the lungs during respiration can be measured. Spirometry
provides information regarding Vital Capacity (VC), Tidal Volume (TV),
Expiratory Volume (EV), Expiratory Reserve Volume (ERV), Residual Volume
(RV) etc. In COPD most of the values of these readings are abnormal.
Chest X-ray
Everyone who is diagnosed with/ suspected of COPD should have a chest X-
ray performed. This may support the diagnosis as it may show over inflation
of the lungs and helps to exclude other diagnoses such as lung cancer and
heart failure (Please refer to Chapter 5).
Blood Tests
Patients with confirmed diagnosis of COPD at young age may have their
Alpha 1 antitrypsin level in the blood tested. It is also worthwhile getting
Hemoglobin percentage estimated as anemia can contribute to breathlessness.
A RBC count can be done in people with worsening lung function to detect
polycythemia; fall in oxygen levels in blood may lead to an increase in blood
cells. Arterial blood gas analysis of patients with COPD helps to establish the
need for long-term oxygen therapy.
ECG
People with COPD are at increased risk of coronary artery disease and it is
worthwhile ensuring that they have not had a previous heart attack and
have weakness of the heart muscle contributing to breathlessness. Further,
as the severity of chronic bronchitis and emphysema worsens, it is important
to ensure that the right side of the heart is not under strain and which may
indicate presence of pulmonary hypertension.
CT Scan of the Chest

This may be useful where a diagnosis of emphysema has been made. This
would help exclude other lung conditions like bronchiectasis, cystic fibrosis,
tumors, etc. If abnormalities are disclosed in the chest X-ray further
investigation through CT scan may be done.
Sputum Culture
Some people who continue to have discolored sputum despite being on
antibiotics, or who have frequent infective exacerbations of chronic bronchitis,
need to have sputum cultured. Certain bacteria are frequently found in
people with chronic bronchitis and are not necessarily causing problems, but
merely reflecting the severity of bronchitis. Others may have unusual infections
with for example, fungi (aspergillus) or atypical TB organisms and which
may require specific treatment.
Bronchoscopy
This investigation is usually not warranted, but if one should cough up blood,
a bronchoscopy may be done to exclude lung cancer, to detect the site of
bleeding or to undergo laser coagulation.
PRIMARY TREATMENT STRATEGY FOR COPD

Smoke Cessation
Smoke cessation gives medications a better chance to work and leads to an
improvement in rate of survival, no matter how severe the condition is.
Smoke cessation is gaining increased recognition and hopefully funding in
acknowledgment that it is an extremely important part of therapy.
Bronchodilator Therapy
The most commonly used are called beta agonists which may help open up
the airways a little leading to some deflation of the lungs and reduction in
breathlessness. Their effect tends to last from minutes to hours. They can be
taken 1-2 puffs 4 times a day or as required. Another type of reliever is the
anticholinergic inhaler taken 2 puffs 3-4 times a day. If one benefits from
both beta agonist and anticholinergic therapy, then for ease of administration
it is helpful to try combination of both drugs 2 puffs 4 times a day.
In long-acting inhaled beta agonists, the effect may last for 12-14 hours.
They are available in inhaler form. The major benefit from long-acting inhaled
bronchodilator/reliever medications is that people often feel grateful that
there is less need for them to reach for the short acting beta agonist therapy
and which leads to greater confidence and improvement in quality of life.
Inhaled Steroids
Clinical trials suggest that there is no benefit from inhaled steroids if people
continue to smoke. For those who have given up smoking, improvement in
lung function can be shown for 3-6 months after starting therapy at reasonably
high doses. There is no evidence to suggest any further benefit, apart from a
possible reduction in frequency of episodes of bronchitis in severe COPD.
Oral Steroids
Treatment of episodes of acute exacerbation of COPD often requires oral
steroid therapy. Depending on the severity of the attack, either 20-40 mg a
day should be employed. If the attack is associated with “mucky” sputum,
then an antibiotic should also be used.
Oral steroids as a short course emergency measure will allow adequate
time to try and improve lung function and gain control over symptoms.
Subsequently one should not get trapped into continuing oral steroid therapy.
One needs to gradually withdraw oral steroids through tapering dose.
Continuing on oral steroids, the short-term benefits will be overtaken in a
few months to a year by the adverse effects of oral steroid therapy.
Dopamine Agonists
Initial studies suggest they are useful in reducing mucus and cough and in
improving breathlessness, and seem to work directly on the airways and
possibly the breathing center.
Phospho-diesterase Inhibitors
Another new line of therapy for COPD which shows promise.
Oxygen Therapy
Once oxygen levels get to below a certain level there is strain on the right
side of the heart, indicating need for oxygen therapy. To be useful it must be
taken for at least 16 hours a day.
Chest Physiotherapy
Help of a chest physiotherapist is mostly called for during acute exacerbations
of COPD, to reduce the work load of breathing, prevent respiratory fatigue
and drain excess mucus from the airway, with combination of humidification,
positioning and postural drainage. Deep breathing exercises may be used to
maximize oxygen uptake and release of carbon dioxide in the lung. In
conjunction with appropriate medical treatment, physical therapy can produce
most satisfactory outcome in COPD (please refer to Chapter 7).
Pulmonary Rehabilitation
Role of chest physiotherapist does not end with the remission of acute
exacerbation of COPD. It is also very effective in management of chronic
respiratory conditions, to improve exercise tolerance and the quality of life in
the majority of COPD patients after remission of an acute attack. People with
COPD benefit from graded strengthening of the muscles of diaphragm, chest,
arms and legs. They also benefit from improving cardiovascular fitness. The
pulmonary rehabilitation programs usually show an improvement in quality
of life, exercise tolerance and a reduction in frequency of hospital admissions.
The improvements can be sustained by continuing the program at home
with periodic supervision on outpatient basis.
SECONDARY TREATMENT MEASURES USED IN COPD

Flu Vaccination
Flu vaccination has proven benefit for anyone with COPD, contributing to a
55% reduction in episodes of acute exacerbation.
Pneumococcal Vaccine
There is less evidence to support pneumococcal vaccine. However, with
frequent infections, it should be considered.
Mucolytic Agents
There is some evidence that mucolytic agents, drugs which reduce the tenacity
of sputum which allows it to be cleared more easily, are beneficial in COPD.
Diet
It is important to maintain good nutrition. When the lungs begin to fail, it
costs more energy to breath and one may begin to lose weight. This can be
a protective mechanism, since becoming lighter means that the lungs and
heart need to work less hard. However, if the weight reduces to below a
certain level, the diaphragm and chest wall muscles may not work as well.
Antibiotics
Antibiotics are of proven benefit acute exacerbation of COPD associated
with discolored mucus. Some people who have frequent episodes of bronchitis
may benefit from “prophylactic” antibiotics (i.e. taking antibiotics regularly).
Immunoglobulin Therapy
A very small group of people have low immunoglobulin levels. If recurrent
infections are common in such people, immunoglobulin therapy may need
to be administered 3-6 times weekly. This problem is seen more often in
association with Alpha 1 antitrypsin deficiency.
Inhalation Therapy
There are a number of inhalers available for administering beta agonist
treatments. For COPD, one should use metered dose inhalers, press and
breathe devices, in association with a spacer. This ensures getting the right
dose of medication to the airways. It also means that one can use a large
number of puffs, >10-20 puffs of the drug via the spacer every hour or two
during flare ups COPD. This is a much cheaper and effective way of
administering these drugs than a nebuliser.
Nebulisers have become popular in the management of COPD. However,
there is no extra benefit from using them over say 20 puffs of Ventolin via a
metered dose inhaler delivered through a spacer device. As such, depositing
10 or 15 doses of Ventolin into the appropriate spacing device and
subsequently inhaling it while breathing normally is as effective as a nebuliser
at much less cost.
Summary
COPD is a common disorder and is almost always associated with smoking.

It is the fourth most common cause of death in the world and the fourth
most common cause of hospital admission. It continues to increase in
prevalence and is expected to become the number one cause of death in
near future. The best strategy to manage COPD is to stop smoking before
too much damage to the lungs has occurred. If someone smokes and has
symptoms of cough and sputum production, or have become aware of
breathlessness when climbing stairs or hills, then he/she must obtain a lung
function test (the best screening test is spirometry). If defined as one of the
25% of people worldwide who are disabled in terms of reduced lung function,
then it is essential to stop smoking.
BRONCHIAL ASTHMA
Definition
Asthma is a chronic, inflammatory disease of the airway, presenting with
recurrent, episodic exacerbation of partially reversible breathing problems.
The asthma presents with following characteristics narrowing of the airway
due to (Fig. 6.3, Plate 3):
• Bronchial muscle spasm
• Inflammation and swelling of the mucous membrane lining the airway
• Excessive secretion of mucous.
Symptoms of Asthma
The following are the most common symptoms for asthma, though each
individual may experience symptoms differently.
1. Attack of asthma starts with tightness of chest and shortness of breath,
usually triggered by sudden exertion, exposure to cold breeze, common
cold or emotional stress.
2. In most cases, the only symptom may be tightness of the chest and
shortness of breath, some times accompanied by dry cough, worsening
at night. Mostly people tend to ignore such symptoms as “chestynesss”.
3. As the disease progresses, cough may become productive and audible
wheezing may occur, along with severe shortness of breath.
4. The symptoms may become accelerated in few cases resulting in a medical
emergency. Such presentation is known as Status Asthmaticus and needs
intensive care management.
5. In the chronic stage, asthma may also be associated with symptoms of
other respiratory problems such as emphysema, bronchitis, and lower
respiratory infections.
Causes of Asthma
The cause of the asthma is not yet known, although it has been established
that in 35-55% of the cases it occurs due to allergic inflammation of the
airway due to inhaled airborne allergens like pollen, animal dander or dust
mites. Further, asthma attacks may be triggered by pharmacological stress
due to specific drug use (aspirin/propanolol), pathological factors such as
viral infections (rhinitis/ sinusitis), emotional stress, environmental stress
(exposure to sudden cold) and exercise induced stress, all of which may
affect the immune system and may trigger or aggravate an attack. However,
these reactions are considered to be more of a response than a cause.
What happens during an Asthma Attack?

Persons with asthma have acute episodes of breathlessness when the air
passages in their lungs get narrower, and air entry or exit becomes
progressively more difficult. These problems are caused by an oversensitivity
of the lungs and airways.
• Lungs and airways overreact to certain triggers and become inflamed
and clogged.
• Breathing becomes harder and the patient may feel tightness of chest.
• There may be cough. It is usually dry initially but becomes productive
later.
• Wheezing or whistling sound, which is typical of asthma, occurs due to
spasm of muscles that surround the airways, and the inner lining of the
airways swells and pushes inward. Mucous membranes that line the airways
secrete extra mucus. The mucus can form plugs that further narrow the
air passages. The rush of air through the narrowed airways produces the
wheezing sounds.
Who are at Risk from Asthma?

Although anyone may have an asthma attack, it most commonly occurs in:
• Children, till the age of 5
• Adults in their 30s
• Adults older than 65
• People living in industrial urban communities with high levels of air pollution
or in cold damp climate.
• People having a family history of asthma
• Personal medical history of allergies.
How is Asthma Diagnosed?

To diagnose asthma and distinguish it from other lung disorders, physicians
rely on a combination of medical history, physical examination, and laboratory
tests, which may include:
• Peak flow monitoring (PFM): It is a device used to measure the fastest
speed in which a person can blow air out of the lungs. During asthma or
other respiratory flare up, the large airways in the lungs slowly begin to
narrow. This will slow the speed of air leaving the lungs and can be
measured by a PFM. This measurement is very important in evaluating
how well or how poorly the disease is being controlled (Please see Chapter
4, page 57-59; Figs 4.5 to 4.10)
• Chest X-rays: Detects changes in the size and shape of the lung fields,
shows the position of the diaphragm, mediastinum, heart and vascular
markings. In asthma X-ray commonly shows flattening of the domes of
the diaphragm, indicating hyperinflation of the lungs due to trapped air.
Bronchovascular markings become prominent indicating circulatory
overload (Fig. 5.7, Chapter 5, page 72)
• Blood gas analysis: Arterial blood is drawn to analyze the amount of
carbon dioxide and oxygen saturation in blood, which are typically
abnormal during an acute attack of asthma (Please see Chapter 2)
• Allergy tests: Traces of different protein substances are introduced sub-
dermally to test for allergic skin reactions. Detecting the allergen that triggers
an asthma attack is the first step in its prevention.
TREATMENT FOR ASTHMA

Medical treatment for asthma is determined by the physician based on
following factors:
• Age, general condition and medical history
• Extent of the respiratory disability, mainly shortness of breath and exercise
intolerance.
• Tolerance for specific medications, procedures or therapies
• Present stage and the expected course of the disease
• Opinion or preference of the patient
As yet, there is no cure for asthma. However, it can often be controlled
with prescription medications that may help to modify, prevent or relieve
symptoms, and by learning ways to cope with episodes of exacerbation.
ASTHMA MEDICATIONS
Bronchial Muscle Spasm Relievers or Bronchodilators
These medicines relax the layer of muscle in the wall of the airway, allowing
them to open up the lumen of constricted airway.
• Short-acting beta agonist bronchodilators such as Ventolin are known
work for up to 4-6 hours and are effective in relieving symptoms in mild
asthma.
• Anti-cholinergic drugs are another short-acting bronchodilator, unrelated
to the beta agonist group. It works by blocking the constricting action of
the vagus nerve on bronchial muscle.
• Long-acting beta agonist bronchodilators — their action continues for up
to 12 hours. Long-acting beta agonist inhalers are taken regularly twice
daily.
Caution
• Avoid using high doses of relievers for long periods. The shorter-acting
beta agonist inhalers can be taken when needed, but if the patient needs
8 puffs or more per day on a regular basis, he/she must get medical
attention.
• Long periods on high doses of the beta agonist inhalers are associated
with increased airway irritability and worsening of asthma. The best way
to minimize the dose of reliever inhalers is to take preventive inhalers
regularly.
• Tremor of hands and a rapid heartbeat are sometimes noticed while using
a beta-agonist reliever inhaler, but these are usually mild. They are not
dangerous, and they disappear once the medicine has been used for a
few weeks.
Two types of reliever medications are available in the market
1. Beta-agonist tablets — available in tablet/syrup form as Ventolin
(Salbutamol)
2. Theophylline tablets or capsules or injections — Nausea and headaches
are common side effects, which can be minimized by taking these
medicines after food. These medicines also have anti-inflammatory
actions, thus acting as a preventive medicine, although they act mainly as
relievers.
Preventive Medication or Anti-inflammatory Drugs
This group of medications acts by reducing airway inflammation, which is
the primary problem in asthma and other COPD. They act in the following
manner:
• Preventive medication works by stopping the white blood cells from
releasing the chemicals they would otherwise produce during inflammatory
reaction.
• As the inflammation settles, the asthma gradually calms down and the
muscle irritability reduces.
• Although people feel well within a few weeks of taking regular preventive
treatment, it takes between one and two years at least before the
inflammation in the airways to settle.
• They work only when taken regularly every day — usually twice a day.
After a few weeks the symptom starts settling down and then less reliever
medication is needed.
Preventive/Controller medication fall into three main categories:
a. Corticosteroids: Inhaled steroids are best because of the small doses
involved. Steroid tablets, such as Prednisolone, are needed when
symptoms are severe. While using inhaled steroids, the patient can reduce
the amount of steroid which is absorbed into the body by up to 80% by
gargling with water, rinsing the mouth and spitting the water out. Gargling,
rinsing and spitting also reduce the chances of the inhaled steroid affecting
other systems adversely.
b. Cromolyn: These are not steroids. They are less effective than steroid but
sometimes work well in children. They generally need to be taken three
or four times a day, whereas inhaled steroids are usually only taken twice
a day.
c. Leukotriene inhibitors: These act as anti-inflammatory agents. These
substances are not important in all asthmatics. Experience is still being
gathered to decide which people with asthma actually benefit from
leukotriene antagonist tablet treatment.
COPING WITH ASTHMA: LIFESTYLE MODIFICATIONS

People with asthma can learn to identify and avoid the things that trigger an
episode, and educate themselves about medications and other asthma
management strategies. According to the Guidelines for the Diagnosis and
Management of Asthma, published by the National Heart, Lung, and Blood
Institute of New Zeeland, Asthma is a chronic disease. It has to be monitored
all the time, not just when symptoms are present.
Four Essential Components of Asthma Treatment
1. The use of objective measurement of lung function like the spirometry
and/or peak expiratory flow rate to access the severity of asthma, and to
monitor the course of treatment.
2. The use of medication designed to reverse and prevent the airway mucosal
layer inflammation in asthma, to delay the narrowing of airways.
3. The use of measures to avoid or eliminate trigger factors that induce
asthma flare-ups, including the consideration of immunotherapy.
4. Patient education that includes a partnership among the patient, family
members, therapist and the physician.
ASTHMA IN CHILDHOOD
(Ref: Asthma in Childhood - a patient’s guide, Dr Jan Sinclair –Pediatrician;
the Medic8® Family Health Guide web page)
Juvenile Asthma is one of the commonest chronic medical conditions to
affect children and research from around the world shows that there is a lot
more asthma among children today than there was 20 years ago. The reasons
for the increase are not entirely clear though some factors have been
suggested:
Genetic factor: Having a parent with allergy, particularly with asthma, is an
important factor that increases the chance of a child having asthma. Genetics
do not explain the worldwide increase in asthma, since this does not change
quickly over the short term.
Allergy: Being allergic to airborne allergens found inside the home is the
most important risk factor for a child having asthma. In general house dust
mite is the most significant indoor allergen. Changes in home structure and
lifestyle (e.g. energy efficient houses with more carpeting and a more indoor
lifestyle) may be increasing the impact of allergy on children’s lungs.
Cigarette smoke: Passive smoking is associated with childhood wheezing,
particularly in children less than 6 years.
Other factors: Numerous other factors have been studied to see if they may
have contributed to the increase in asthma. It has been suggested that smaller
families may be one factor, as children with several older siblings appear less
likely to develop asthma. Dietary changes are also suggested to play a role,
with changing fat intake from saturated animal fat to polyunsaturated vegetable
oils and margarine.
Allergen Avoidance for Prevention or Treatment of Asthma
Most children and many adults who have asthma are allergic to the airborne
allergens inside the home. For families where there is a strong allergic tendency,
avoiding having pets and attempting to reduce dust mite as much as possible
may be worthwhile.
Allergen avoidance may also be regarded as a treatment for allergic
asthma. Knowing which allergens to avoid is an important first step, and this
can be determined by allergy skin tests.
The biggest exposure to dust mite takes place in the bed, hence this is the
best place to start.
• Have dust mite impermeable covers on the mattress, pillow, and blankets.
If there is more than one bed in the room, have such covers on each
bed.
• All the bedding on top of the special mite covers should be either hot
washed (>55°C) or dried in sunshine, on a regular basis.
• Exclude soft toys from the bed, or if that is not possible then either hot
wash the toys, or freeze them (in a plastic bag) for 24 hours every couple
of weeks.
• Carpet and floor rugs have a lot of dust mite in them. Regular vacuuming
may reduce this, but hard floors are the best option if possible. Other
surfaces should be mopped regularly.
• Allergens other than dust mite may also be important in asthma. The
bedrooms must be absolutely pet free zone, and if possible wash the pet
regularly.
• Although not an allergen, cigarette smoke is an irritant trigger for
asthmatics, and avoidance of both active and passive smoking is important.
RECENT ADVANCES IN ASTHMA THERAPIES

(Ref: NEW ASTHMA THERAPIES - a patient’s guide Dr Shaun Holt -
Clinical Research Fellow; the Medic8® Family Health Guide web page)
The present trend is to phase out the production of asthma inhalers containing
CFC’s due to potential damage to the environment. Only a small proportion
of medicine from current devices gets down as far as the lungs, the rest being
deposited in the mouth and throat. Better devices which deliver more drugs
to the target site will hopefully increase the effectiveness of current drugs.
Preventive drugs, such as inhaled steroids, are usually taken twice a day.
However, new research has shown that it may well be possible to get the
same effect from taking a higher dose only once a day. Salbutamol is one of
the commonest symptom relieving drugs. Recent work has shown that the
drug actually consists of two very similar drugs, or isomers, in equal amounts.
Tests show that only one of these isomers relieves symptoms of asthma and
the other may actually be bad for asthma. Research is underway to develop
a product containing only the “good” part of salbutamol.
New Drugs
The most promising new drug in development is called “Anti-Ig E antibody”.
Many asthmatics react to allergens such as house dust mites and pollens; by
producing high levels of a blood protein called Ig E. This protein can start a
chain of events leading to an asthma attack. Without Ig E, the asthma attacks
become much less severe, if at all. The new drug removes excess Ig E from
the blood and therefore greatly improves the symptoms of asthma. During
an asthma attack, many chemicals are released and these chemicals are being
targeted by new drugs which may help asthma. Targets include IL4, IL5,
Tryptase, PAF and Neurokinin.
An Asthma Vaccine
Research is underway on a potential vaccine which could possibly prevent
asthma from occurring in the first place. The vaccine is based on BCG, which
is used to prevent TB infection.
CHRONIC BRONCHITIS
Definition
Chronic bronchitis is a long-term inflammation of the bronchi characterized
by chronic cough, increased production, retention and expectoration of
mucus.
To be classified as chronic bronchitis the patient must have:
• Cough with expectoration on most days for at least three months per
year, for two years in a row.
• Other causes of symptoms, such as tuberculosis or other lung diseases,
must be excluded.
Symptoms of Chronic Bronchitis

Primary symptoms of chronic bronchitis are:
• cough
• expectoration (spitting out) of mucus
Chronic bronchitis may also present with:
• Respiratory exacerbation — frequent and severe respiratory infections
• Airway obstruction – narrowing and plugging of the bronchi
• Dyspnoea – difficulty in breathing
• Disability – due to limited exercise tolerance.
Further symptoms may include:
• Cyanosis – lips and skin may appear blue
• Crepitations and crackle – abnormal breath sounds
• Peripheral edema – swelling of the feet
• Cor pulmonale – right sided heart failure
The symptoms of chronic bronchitis may resemble other lung conditions
and must be confirmed by a trained specialist.
CAUSES OF CHRONIC BRONCHITIS

Cigarette smoking is cited as the most common contributor to chronic
bronchitis, followed by bacterial or viral infections of the upper respiratory
tract and air-borne environmental pollution. Chronic bronchitis is often
associated with other pulmonary diseases such as:
• pulmonary emphysema
• pulmonary fibrosis
• asthma
• tuberculosis
• sinusitis
• upper respiratory infections.
How is Chronic Bronchitis Diagnosed?

In addition to a complete medical history and physical examination, the
following tests may be needed to confirm the diagnosis of chronic bronchitis:
Pulmonary Function Tests

Spirometry – Spirometry in chronic bronchitis determines how well the lungs
receive, hold, and utilize air as well as, monitor the effectiveness of treatment,
determine the severity of the disease.
Peak flow monitoring (PFM) – During bronchitis flare up, the large airways in
the lungs slowly begin to narrow. This will slow the speed of air leaving the
lungs and can be measured by a PFM. This measurement is very important
in evaluating how well or how poorly the disease is being controlled (Please
see Chapter 4, page 57-59; Figs 4.5 to 4.10).
Arterial blood gas (ABG) – Laboratory blood test that evaluates the lungs’
ability to provide blood with oxygen and remove carbon dioxide, and to
measure the pH (acidity) of the blood.
Pulse oximetry – Bedside monitoring that helps to monitor oxygen saturation
continuously and indicate the need for oxygen supplementation in acute
exacerbation of chronic bronchitis.
Chest X-ray – PA view shows deviations in the normal configuration of the
lung and mediastinal shadow. Common findings in chronic bronchitis may
be prominent broncho-vascular markings, enlarged heart shadow, hyper-
inflation of the lungs, emphysematous bullae etc.
TREATMENT FOR CHRONIC BRONCHITIS

Treatment for chronic bronchitis is determined based on age, general
condition, past history, extent of disease progression and tolerance for specific
medications, procedures, or therapies.
Treatment may include:
• Oral medications – Anti-inflammatory agents, mucolytics agents,
expectorants
• Inhaled bronchodilators
• Oxygen supplementation
• Segmental or sleeve resection to remove damaged area of lung
• Chest physiotherapy.
PULMONARY EMPHYSEMA
Definition
Emphysema is a chronic lung disease in which alveoli may be destroyed,
narrowed, collapsed, stretched, and permanently over-inflated.
Over-inflation of the air-sacs is a result of a breakdown of the walls of the
alveoli, and causes a decrease in respiratory function and breathlessness.
Damage to the air sacs is irreversible and results in permanent cavities in the
tissues of the lungs, called emphysematous bullae.
How does Emphysema Develop?

Emphysema develops gradually, in all people independent of whether they
smoke or not. With aging, it is likely one would be breathless on exertion as
a result of a loss of alveoli. People who smoke destroy their alveoli at a much
more rapid rate than is expected with aging. Those who are most susceptible
to the bad effects of smoking will develop breathlessness in their 40s or 50s,
whilst others may not develop the problem until their 70s. When sufficient
air sacs have been destroyed, the airways which feed them become floppy
and narrow, making it harder and harder to breath.
Symptoms of Pulmonary Emphysema

The following are the most common symptoms for pulmonary emphysema.
However, each individual may experience symptoms differently.
Early symptoms of pulmonary emphysema may include:
• Shortness of breath
• Dry ineffective cough
Late symptoms may include:
• Extreme fatigability
• Anxiety and depression
• Sleep problems
• Heart problems
• Weight loss
The symptoms of pulmonary emphysema may resemble other lung
conditions; hence a confirmation of the diagnosis must be done by a trained
specialist.
Causes of Pulmonary Emphysema

Emphysema does not develop suddenly, but occurs very gradually. The lung
has a system of elastic fibers that provides the lung tissue with elastic recoil
and allows the lungs to expand and contract. Pulmonary emphysema occurs
when a breakdown in the chemical balance that protects the lungs against
the destruction of the elastic fibers occurs.
There are a number of reasons for the breakdown in chemical balance:
smoking, exposure to air pollution, exposure to irritating fumes and dusts on
the job or a rare, inherited form of the disease called alpha 1-antitrypsin
(AAT) deficiency, which causes early onset pulmonary emphysema
How is Pulmonary Emphysema Diagnosed?

physician may request Chest X-ray to detect hyperinflation of the lungs and
emphysematous bullae (Please see Chapter 5, Page 76, Fig. 5.14). Sputum
culture is often performed to determine if an infection is present.
Treatment for Pulmonary Emphysema
The goal of treatment for people with pulmonary emphysema is to live more
comfortably with the disease by providing relief of symptoms and preventing
progression of the disease with minimal side effects.
Treatment methods may include:
• quitting smoking – the single most important factor for maintaining healthy
lungs
• antibiotics for bacterial infections
• oral bronchodilators and other inhaled medications
• exercise – including breathing exercises to strengthen the muscles
• oxygen supplementation
• wedge and sleeve resection surgery to remove damaged area of the
lung.
BRONCHIECTASIS
What is Bronchiectasis?
It is a disease of the airway characterized by permanent dilatation and
distortion of the airways caused by chronic inflammation due to recurrent
infections of the lining of the airway. In bronchiectasis the airways have been
irreversibly damaged and as a result are abnormally dilated, often irregular
and do not taper normally. The flow of air in and out of the lungs is thus
impeded, leading to breathlessness.
Normally the air passages produce small amounts of clear mucus. This is
swept along by small hair-like structures (cilia) which line the airways. This
mucus is then swallowed – generally without us being aware. This mucus
traps any particles or neutralizes any harmful substances which have been
inhaled. Excess amounts of mucus, such as may occur in an infection, are
cleared by coughing.
In bronchiectasis these clearance mechanisms of the lung are impaired.
The cilia are damaged and do not clear the mucus effectively. The cough is
less effective at clearing dilated and damaged airways. Hence, physiotherapy
is needed to help clear these secretions.
Normally the airways in the lung are sterile. In bronchiectasis, because of
the inability to clear secretions effectively, these secretions become infected.
As a result of this infection the airways produce more secretions which in
turn become infected. Thus, most people with bronchiectasis even have a
chronic cough and produce sputum.
What Causes Bronchiectasis?
In many cases of bronchiectasis a clear-cut cause cannot be identified.
Some respiratory infections in childhood can damage the airways and
lead to bronchiectasis. These may be viral infections, such as cause some
types of bronchiolitic diseases or measles or bacterial infections, such as
whooping cough. In most cases it is thought that the damage to the airways
occurs in early childhood although the symptoms may only become apparent
in early adulthood.
There are specific conditions that may cause bronchiectasis. These include
cystic fibrosis and defects of the immune system - such as a deficiency of
immunoglobulin which protect against infection.
Occasionally bronchiectasis can occur following inhalation of a foreign
body – such as peanut or other objects. If detected early these foreign objects
can be removed and any damage may be avoided.
What are the Symptoms of Bronchiectasis?

Most people with bronchiectasis have a chronic cough. In most cases, sputum
is produced and this is often infected with yellow/green color rather than
white/clear. The volume of sputum is variable but tends to increase when
there is an acute infection. The sputum is usually foul smelling. This can be
embarrassing and is a reason to seek medical attention.
Occasionally, small amounts of blood may be coughed up, called
hemoptysis. This is due to the breaking of small blood vessels in the lining of
the airways, and generally indicates an infection and the need for antibiotics.
Very occasionally larger amounts of blood may be coughed up. This can
be frightening and is a reason to go to the nearest Emergency Department.
However, virtually all episodes stop spontaneously.
Many persons with bronchiectasis feel generally tired. This usually
improves as the chronic infection in the airways is brought under better
control.
Sometimes appetite is reduced and may even lead to loss of weight.
The chronic infection in bronchiectasis may cause damage to the lungs
and impair the function of the lungs. As a result the person may feel short of
breath or have reduced exercise tolerance.
Persons with bronchiectasis sometimes have wheeze, as in asthma.
Often there is also chronic infection in the nose and sinuses.
What Tests are Likely to be Done?

Chest X-ray: Sometimes the chest X-ray will confirm the presence of
bronchiectasis. However, the routine chest X-ray may be normal or non-
specific. In such cases special X-ray tests like bronchogram are then required.
A small amount of radio-opaque dye is injected in the airway. The patient is
then positioned in various positions to distribute the dye throughout the
lung fields. A series of X-rays are taken with the patient in various positions.
Pooling of the radio-opaque dye at specific dilated and distorted spots in the
bronchial tree helps detect the focus of the bronchiectasis. Such accurate
localization helps the therapist to plan most appropriate postural drainage
position. However with wide spread use of CT scan and MRI scan
bronchogram has become redundant.
CT/ MRI scan of chest: This is now the best test for the diagnosis of
bronchiectasis. It also provides information on the type and extent of
bronchiectasis as well as other valuable information for the specialist.
Sputum culture and sensitivity: Chronic pockets of infection in the airway
are the main problem in bronchiectasis. Specimens of sputum is collected in
sterile container and cultured in the laboratory to see what sort of organisms
it contains. The colony of organisms thus cultured is tested for sensitivity to
different antibiotics. The most effective antibiotic is then used to treat the
infection with maximum specificity.
What can be Done to Manage Bronchiectasis?

The most important component of treatment is regular physiotherapy to
clear secretions from the lungs. There are a number of different methods to
do this and an individual program will have to be developed by the respiratory
physiotherapist. These clearance techniques should be undertaken regularly
at home and more frequently when there is an acute infection. All persons
with bronchiectasis should also maintain a regular exercise program.
All patients with bronchiectasis are at greater risk of respiratory infections.
These are indicated by increased volume and purulence of sputum, coughing
up of blood, fever and chill, pain in the chest and general malaise. Under
these circumstances, antibiotics are generally needed. Patients who have
wheeze (or narrowing of airways) may be given inhaled bronchodilators.
Sometimes asthma preventive inhalers are also used in bronchiectasis. It
is thought that these medicines may reduce the inflammation within the
airways and prevent further damage.
Attention will also be paid to treatment of any nose or sinus problems,
reflux or indigestion symptoms.
Occasionally the segment of the lung along with bronchial segment
affected by bronchiectasis can be removed surgically by sleeve resection.
Can Bronchiectasis be Prevented?
Because the damage to the airways is thought to occur as a result of childhood
infections, any prevention needs to take place in childhood. Children should
be vaccinated against measles and whooping cough to prevent this damage
to airways early in childhood. A cough (particularly a moist cough) that persists
in a child is a reason to seek medical attention.
What is the outlook for persons with Bronchiectasis?

Although bronchiectasis cannot be cured, almost all persons with bronchiectasis
live long and productive lives.
Regular treatment with chest physiotherapy, exercise program and other
therapies, mean that symptoms can be reduced, and many infective
exacerbations prevented.
With such treatment, the majority of persons remain stable for many
years. This is particularly the case for persons in whom correct treatment was
started before substantial lung damage occurred.
Prompt antibiotic treatment of any infections also reduces the risk of further
lung or airway damage.
All persons with bronchiectasis should be reviewed by a respiratory
specialist; preferably in the context of a multidisciplinary team with a specific
interest in this condition. For the majority of patients long-term follow-up by
a respiratory specialist is not required but under these circumstances regular
review by the family doctor is most important.
PNEUMONIA
What is Pneumonia?
Pneumonia is an inflammation of the lungs caused by bacteria, viruses, or
chemical irritants. It is a serious infection or inflammation in which the alveoli
are filled with pus and exudates. Pneumonia may present as:
• Lobar pneumonia affects one or more lobes of the lungs.
• Bronchial pneumonia or bronchopneumonia affects diffuse patches of
lung tissue, involving primarily the terminal airway and then spreading to
the alveolar sacks.
Types of Pneumonia
A. Bacterial pneumonia is caused by various bacteria. The Streptococcus
pneumoniae is the most common bacterium that causes bacterial
pneumonia. It usually occurs when the body is weakened in some way,
such as illness, malnutrition, old age, or impaired immunity, and the

bacteria are able to work their way into the lungs. Bacterial pneumonia
can affect all ages, but those at greater risk are: persons who abuse alcohol,
who are debilitated, postoperative patients, persons with preexisting
respiratory diseases or viral infections or who have weakened immune
system.
The symptoms of bacterial pneumonia include:
• chills and rigor
• severe chest pain
• high temperature
• profuse perspiration
• rapid pulse
• rapid breathing
• bluish color to lips and nail beds
• confused mental state or delirium
• cough that produces rust-colored or greenish mucus
B. Viral pneumonia is caused by various viruses, and is the cause of half of
all cases of pneumonia. Early symptoms of viral pneumonia are similar to
bacterial pneumonia. Later on there may be increasing breathlessness
and a worsening of the cough. Viral pneumonias may make a person
susceptible to secondary bacterial pneumonia.
C. Mycoplasm pneumonia has somewhat different symptoms and physical
signs. It is caused by Mycoplasm or fungi, the smallest free-living agents
of disease in humankind, which have the characteristics of both bacteria
and viruses, but which are not classified as either. They generally cause a
mild, widespread pneumonia that affects all age groups. Symptoms include
a severe cough that may produce some mucus.
D. Aspiration pneumonias may be caused by accidentally inhaling of food,
liquid, gases or dust, or by fungi into the airway. These inhaled objects set
up inflammatory reaction within the airway. This inflammation spreads to
the lung parenchyma, setting up pneumonitis.
How is Pneumonia Diagnosed?

Diagnosis is usually made based on the season and the extent of the illness,
but may include the following tests to confirm the diagnosis:
Chest X-ray – a ground glass appearance of the affected lung field indicating
consolidation as in case of lobar pneumonia (See Fig. 5.4), diffuse scattered
shadow in bronchopneumonia (See Fig. 5.5)
Blood tests – ABG to analyze the increase in the amount of carbon dioxide
and reduction of oxygen in the blood and blood culture to identify infective
organism.
Sputum culture – performed on the expectorated material that is coughed
up from the lungs to determine nature of infection present and the antibiotic
that it is sensitive to. Physical examination of sputum may also provide vital
clues to the nature and severity of infection (See Table 4.2).
Treatment for Pneumonia

Treatment of bacterial pneumonia involves administration of organism
specific antibiotics. Broad spectrum antibiotics are more suitable in Viral
and Mycoplasm pneumonias, to prevent secondary opportunistic infections
and speed recovery. Supportive treatments include appropriate diet, oxygen
therapy, pain medication, management of cough and chest physiotherapy.
Chest physiotherapy should be given very carefully in acute stage of any
pneumonitis, mostly to avoid pain from inflamed pleural membrane and to
prevent hemoptysis from ruptured arterioles. Deep breathing exercises within
pain tolerance limit may be given, along with breath holding at the end of
inspiration, to maintain the elasticity of the lungs and to promote collateral
ventilation.
As the infection is controlled and the inflammation in the lung tissue settles,
the focus of chest physiotherapy should shift to drainage of secretions
containing pus from the lungs. This is achieved by humidification followed
by postural drainage. The most appropriate position for postural drainage
may be decided based on the latest chest X-ray. The therapist should avoid
using vigorous percussion on the chest wall, if any pain is present on deep
breathing, as this indicates lingering inflammation of the pleural membrane.
Vibrations are a better option in such cases and if applied properly can be as
effective as percussion. Deep breathing and breath holding must continue to
gain better ventilatory efficiency.
As the output of secretions from the lung reduces, the physiotherapist
should further shift focus of therapy to increase the exercise tolerance of the
patient through graded exercise programme. The emphasis of such
programme should be to increase the pulmonary fitness of the patient to
such an extent so that he/ she can return to the life style and work environment
he/ she enjoyed before the illness.
INTERSTITIAL LUNG DISEASES (PULMONARY FIBROSIS)
What are Interstitial Lung Diseases?
Interstitial lung disease, or ILD, is a common term that includes more than
180 chronic lung disorders, which are usually chronic, nonmalignant (non-
cancerous) and noninfectious in nature.
Interstitial lung diseases cause fibrosis (scarring) of interstitium, the tissue
that exist between the air sacs of the lungs. The symptoms and course of
these diseases may vary from person to person, and from disease to disease,
but the common link between the many forms of ILD is that they all begin
with an inflammation. Changes associated with ILD are:
• Bronchiolitis—inflammation that involves the bronchioles (small airways)
• Alveolitis—inflammation that involves the alveoli (air sacs)
• Vasculitis—inflammation that involves the small blood vessels (capillaries)
Though the exact cause is debated, most of interstitial lung diseases are
believed to be caused by inhaled pollutant or drug-induced, commonly
diagnosed as pneumoconiosis or hypersensitivity pneumonitis.
The other causes of ILD may be:
• Pulmonary tuberculosis and sarcoidosis
• Idiopathic pulmonary fibrosis
• Bronchiolitis obliterans
• Histiocytosis X
• Chronic eosinophilic pneumonia
• Collagen vascular disease
• Granulomatous vasculitis
• Goodpasture’s syndrome
• Pulmonary alveolar proteinosis
How does Interstitial Lung Disease occur?

In interstitial lung disease, the lung is affected in three ways:
1. Lung tissue is damaged in some known or unknown way.
2. The walls of the air sacs in the lungs become inflamed.
3. Scarring (fibrosis) begins in the interstitium.
Fibrosis results in permanent loss of lung tissue’s ability to absorb oxygen
from the atmospheric air. Alveolar membrane, the lung tissue surrounding
the alvioli, and the lung capillaries, all are destroyed by the formation of scar
tissue.
The diseases may run a gradual course or a rapid course. People with ILD
may notice variation in symptoms - from very mild, to moderate, to very
severe. The condition may remain the static for long periods of time or it
may change quickly. The course of ILDs is unpredictable. As the disease
progress, the lung tissue thickens and becomes stiff. The work of breathing
then becomes more difficult, demanding more energy. Sometimes the diseases
improve with medication, if treated as soon as the inflammation occurs.
What are the Symptoms of Interstitial Lung Diseases?

The following are the most common symptoms for interstitial lung diseases.
However, each individual may experience symptoms differently.
General symptoms of ILD may include:
• Shortness of breath, especially on exertion
• Early onset of fatigue and feeling of weakness
• Loss of appetite
• Weight loss
• Dry cough that does not produce expectoration of sputum
• Tightness of chest
• Labored breathing
• Coughing out of blood
The symptoms of interstitial lung diseases may resemble other lung
conditions like pulmonary tuberculosis or cancer, to be ruled out by the
specialist physician
How are Interstitial Lung Diseases Diagnosed?

physician may also request the following tests:
Pulmonary function tests – diagnostic tests that help to measure the lungs’
ability to exchange oxygen and carbon dioxide appropriately. The tests are
usually performed with special machines that the person must breathe into.
Spirometry – a spirometer is a device used to assess lung function. Spirometry,
the evaluation of lung function with a spirometer, is one of the simplest, most
common pulmonary function tests and may be necessary to determine how
well the lungs receive, hold, and utilize atmospheric oxygen. It is also used to
monitor a lung disease, to monitor the effectiveness of treatment, to determine
the severity of a lung disease and to determine whether the lung disease is
restrictive (decreased compliance) or obstructive (disruption of airflow) in
nature. Routine tests also include Chest X-rays, Blood gas analysis, broncho-
alveolar lavage - to remove cells from lower respiratory tract to help identify
cause of inflammation and lung biopsy — to remove tissue from the lung for
examination in the pathology laboratory.
Treatment for Interstitial Lung Diseases

Specific treatment will be determined based on age, general condition and
the past history of the disease, its extent and rate of progression. The patient/
family members must be explained the course of the disease and its long
term implication, including progressive disability that usually accompanies
the disease.
Treatments may include:
• Oral medications, including corticosteroids
• Influenza vaccine
• Pneumococcal pneumonia vaccine
• Oxygen supplementation from portable containers
• Lung transplantation
Physiotherapy is of limited value, though deep breathing and breath-
holding exercises tends to stretch the lung parenchyma and help retain some
degree of compliance in the lung parenchyma.
PULMONARY TUBERCULOSIS
What is Tuberculosis?
Tuberculosis (TB) is a chronic bacterial infection that usually affects the lungs,
resulting in pockets of caseous necrosis of the lung parenchyma followed by
healing through fibrosis. TB spreads primarily as an airborne droplet infection.
There is a difference between being infected with the TB bacterium and
having active tuberculosis disease. Many patients carry tuberculosis bacterium
without showing any clinical symptoms.
There are 3 important ways to describe the stages of TB. They are as
follows:
1. Exposure: This occurs when a person has been in contact, or exposed to,
another person who is thought to have or does have TB. The exposed
person will have a negative skin test, and normal chest X-ray, and no
signs or symptoms of the disease.
2. TB infection: This occurs when a person has the TB bacteria in his/her
body, but does not have symptoms of the disease. This person would
have a positive skin test, but a normal chest X-ray.
3. TB disease: This describes the person that has signs and symptoms of an
active infection. The person would have a positive skin test and a positive
chest X-ray.
The predominant TB bacterium is Mycobacterium tuberculosis (M.
tuberculosis). Most people infected with M. tuberculosis never develop active
TB. However, in people with weakened immune systems, especially those
with HIV (human immunodeficiency virus), TB organisms can overcome the
body’s defenses, multiply, and cause an active disease.
Who is at Risk for Developing TB?

TB affects all ages, races, income levels, and both genders. Those at higher
risk include the following:
• People who live or work with others who have TB
• Medically unmonitored populations, living in unhygienic environment
• People in group settings, such as nursing homes
• People who abuse alcohol, intravenous drugs
• People with impaired immune systems like AIDS or the elderly or the
children.
What are the Symptoms of TB?

The following are the most common symptoms for pulmonary TB. However,
each individual may experience symptoms differently.
• Persistent cough and low grade fever in the evenings.
• Easily fatigued
• Loss of appetite and body weight
• Night perspiring
• In the late stages coughing up blood stained sputum
The symptoms of TB may resemble other lung conditions or medical
problems. Suspected cases must consult a physician for a diagnosis.
What Causes TB?

The TB bacterium is spread through the air; however, repeated exposure is
necessary before a person will become infected. It is not likely to be transmitted
through personal items, such as clothing, bedding, or other items that a
person with TB has touched. Adequate ventilation is the most important
measure to prevent the transmission of TB.
How is TB Diagnosed?
TB is diagnosed with a TB skin test (Mantoux test). In this test, a small amount
of tuberculin antigen serum is injected into the top layer of the skin. If a
certain size bump develops within two or three days, the test may be positive
for tuberculosis infection. Additional tests to determine if a person has TB
disease include Elisa test, X-rays and sputum tests for acid fast bacilli (AFB).
Routine TB skin tests are suggested for those in high-risk categories or
those who live or work in close contact with people who are at high-risk or
those who have never had a TB skin test.
Recommendations for skin testing in children, from the American Academy
of Pediatrics are as follows:
Immediate testing is recommended if the child is thought to have been
exposed in the last 5 years or has an X-ray that looks like TB or has any
symptoms of the disease.
Yearly skin testing is recommended for Children with HIV, children that are
in jail or orphanage or living in the street.
Testing every 2 to 3 years is recommended for children that are exposed to
high-risk people.
Treatment for Tuberculosis

Treatment includes medications – in various combinations of Isoniazid,
Rifampin, Pyrazinamide, Ethambutol, or Streptomycin, which may be
prescribed for a period of time up to six months or more. Patients usually
begin to improve within a few weeks of the start of treatment. The patient is
not usually contagious once treatment begins, provided that treatment is
carried through to the end, as prescribed by a physician.
Physiotherapy is contraindicated in active pulmonary TB, though in the
stage of remission deep breathing and breath holding exercises tends to
stretch the fibrosis in the lung parenchyma and help retain some degree of
compliance.
PULMONARY SARCOIDOSIS
What is Sarcoidosis?
Sarcoidosis is a rare form of chronic inflammation found in the lungs. It
causes small lumps, or granulomas, which generally heal and disappear on
their own. However, for those granulomas that do not heal, the tissue can
remain inflamed and become scarred, or fibrotic.
Pulmonary sarcoidosis can develop into pulmonary fibrosis, which
distorts the structure of the lungs and can interfere with breathing.
Bronchiectasis, in which pockets form in the airway of the lung and become
sites for infection, usually follow.
What are the Symptoms of Sarcoidosis?

Most sarcoidosis patients do not exhibit symptoms and probably are unaware
they have the disease. Pulmonary sarcoidosis can cause loss of lung volume
(the amount of air the lungs can hold) and loss of lung compliance.
The following are the most common symptoms for sarcoidosis. However,
each individual may experience symptoms differently. Symptoms may include:
• Shortness of breath
• Cough that will not go away
• Skin rashes on face, arms, or shins
• Inflammation of the eyes
• Weight loss
• Fatigue
• Night sweats
• Fever
Who is at Risk for Sarcoidosis?

Sarcoidosis occurs in all races and both genders, but the most susceptible
populations seem to be of African-American, Scandinavian, German, Irish,
or Puerto Rican origin.
Sarcoidosis is usually diagnosed by elimination. That is, other lung disorders
that have similar symptoms are progressively eliminated, leading to a diagnosis
of sarcoidosis.
Treatment for Sarcoidosis

Treatment may include the use of corticosteroids for controlling chronic
inflammation of the lung tissue. Chest physiotherapy is purely symptomatic.
CHAPTER SEVEN
Techniques of Physical
Therapy Treatment in
Respiratory Disorders
Part 1: Overview of Chest Physical Therapy
DEFINITION
Chest physical therapy is the term for a group of physiotherapy treatments,
designed to improve respiratory efficiency by promoting expansion of the
lungs, strengthening respiratory muscles, and eliminating secretions from the
lungs.
Purpose
The purpose of chest physical therapy, also called chest physiotherapy, is to
help patients breathe more freely. This is achieved by increasing the lung
volumes; decreasing the work of breathing and clearing secretions from the
airway. Techniques of chest physical therapy include relaxed positioning,
turning in bed, deep breathing exercises, effective coughing chest percussion
and vibration and postural drainage.
Chest physiotherapy is usually done in the stage of acute exacerbations
of most respiratory diseases, in conjunction with suctioning of secretions from
the airway and administration of inhaled drugs like bronchodilators to relieve
spasm of bronchial smooth muscles, anti-inflammatory agents to reduce the
inflammation of mucous membrane and expectorant through nebuliser or
aerosol spray to get rid of excess mucus secretions.
In the chronic stage of a respiratory disease, when the acute respiratory
distress is relatively less, chest physiotherapy aims at improving exercise tolerance
and improving the quality of life. This is called pulmonary rehabilitation.
Points to Ponder
• Chest physical therapy can be used with newborns, infants, children, and
adults.
Techniques of Physical Therapy Treatment 111
• Patients who are breathless, have problems in clearing secretions from

their lungs and ventilate properly benefit from chest physical therapy.
• Specifically, patients with lung diseases such as bronchitis, pneumonia,
asthma or any other chronic obstructive pulmonary disease (COPD) or
restrictive lung disorder benefit from chest physical therapy.
• Some patients with cystic fibrosis or neuromuscular diseases like Guillain-
Barré syndrome or progressive muscle weakness (myasthenia gravis or
myopathy or tetanus) may receive chest physical therapy as a supportive
measure.
• Patients who are likely to aspirate their mucous secretions due to weak
swallowing and coughing reflexes, because of diseases such as cerebral
palsy or muscular dystrophy, also need regular chest physical therapy.
• Patients, who are bedridden or confined to a wheelchair, or who cannot
breathe deeply because of postoperative pain need chest physical therapy
to maintain proper ventilation.
Precautions
Chest physical therapy should not be performed on people with
• Bleeding from the lungs
• Fractured ribs
• Damaged chest walls
• Active pulmonary tuberculosis
• Acute asthma
• Recent heart attack
• Pulmonary embolism
• Active hemorrhage
• Some spinal injuries.
SCOPE OF CHEST PHYSIOTHERAPY

Chest physical therapy can be performed in a variety of settings, including
critical care units, hospitals, nursing homes, outpatient clinics, and at the
patient’s home. Depending on the circumstances, chest physical therapy may
be performed by anyone from a respiratory care therapist to a trained
member of the patient’s family. Different patient conditions require different
levels of training.
Chest physical therapy consists of a variety of procedures that are applied
depending on the patient’s health and condition. Hospitalized patients should
be reevaluated frequently to establish which procedures are most effective
and best tolerated. Patients receiving long-term chest physical therapy at
home should be reevaluated about every three months.
OVERVIEW OF TECHNIQUES USED IN CHEST PHYSIOTHERAPY
Positioning
Positioning the patient appropriately induces relaxation. It is the single most
important passive intervention that can be used by the physiotherapists to
reduce workload of breathing in a breathless patient (also see Chapter 2).
Though this technique is least dramatic, it is an essential component of chest
PT, because most lung volumes are responsive to positioning.
Turning
Turning in bed from side to side promotes lung expansion and better
matching of ventilation with perfusion. Patients unable to get up from bed
due to extreme breathlessness or weakness or immobilization may turn
themselves or be turned by a care giver. The head end of the bed should be
elevated to facilitate better air entry in the lungs. The head end of the bed
may sometimes be lowered to promote drainage of secretions from the lungs,
if the patient can tolerate this position. Critically ill patients and those
dependent on mechanical ventilation should be turned once every one or
two hours round the clock.
Deep Breathing and Breath Holding Exercises

Deep breathing helps to expand the lung bases and breath holding encourages
better distribution of the air into all sections of the lung through channels of
collateral ventilation. The patient either sits propped up in bed or in a straight
back chair and inhales smoothly and deep, pushing the abdomen out to
draw maximum amounts of air into the lung. At the end of inspiration, the
patient is asked to hold the breath for a few seconds.
Forced Expiratory Technique

After holding the breath for a few seconds at the peak of inspiration, the
abdominal muscles are contracted to exhale forcefully to empty the lungs of
all dead gas to the maximum possible extent. In COPD such forced exhalation
should be done through pursed lips, to maintain some backpressure of air in
the airway that prevents the collapse of terminal airways at the beginning of
forced expiration. This ensures that no air remains trapped in the alveoli.
Deep breathing exercises followed by forced expirations in cyclic order should
be practiced several times a day.
Coughing
Cough is an involuntary protective reflex that is usually triggered when a
foreign particle enters the airway. It is accompanied by active contraction of
muscles of expiration. Coughing helps loosen secretions sticking the walls of
the airways in the lungs, so that the mucus can be expectorated or suctioned
out in patients unable to expectorate. Patients sit upright and inhale deeply
through the mouth and then exhale in short puffs or coughs. Coughing is
repeated several times a day.
Postural Drainage
Postural drainage uses the force of gravity to assist in effectively draining
secretions from the lungs and into the central airway, from where they can
either be coughed up or be suctioned out. The patient is placed in a head or
chest down position and is kept in this position for up to 15 minutes. Critical
care patients and those depending on mechanical ventilation receive postural
drainage therapy four to six times daily. Percussion and vibration may be
performed in conjunction with postural drainage.
Percussion
Percussion is rhythmically striking the chest wall with cupped hands. It is also
called cupping, clapping, or tapotement. The purpose of percussion is to
generate shock waves in the lungs to break up thick secretions in the lungs so
that they can be more easily removed. Percussion is performed on each lung
segment for one to two minutes at a time.
Vibration
As with percussion, the purpose of vibration is to help break up lung secretions.
Vibration can be either mechanical through a vibrator or manual. It is
performed as the patient breathes deeply. When done manually, the person
performing the vibration places his or her hands against the patient’s chest
and creates vibrations by quickly contracting and relaxing arm and shoulder
muscles while the patient exhales. The procedure is repeated several times
each day for about five exhalations.
Preparation for Chest PT

The only preparation needed for chest physical therapy is an evaluation of
the patient’s condition and determining which chest physical therapy
techniques would be most beneficial (See Chapter 4).
Aftercare of Chest PT
Patient should gargle and rinse the mouth to lessen the bad taste or odor of
the secretions they spit out and to wash off excess inhaled drugs trapped in
the mouth and gullet.
Risks and Complications of Chest PT

Risks and complications associated with chest physical therapy depend on
the health of the patient. Although chest physical therapy generally gives no
problems, in some patients it may cause.
• Oxygen desaturation, particularly if the head is kept lowered for drainage
• Raised intracranial pressure
• Fall in blood pressure
• Bleeding in the lungs
• Pain or injury to the ribs, muscles, or spine
• Vomiting
• Cardiac arrhythmia
Expected Response
The patient is considered to be responding positively to chest physical therapy
if some, but not necessarily all, of these changes occur:
• Increased volume of sputum secretions
• Changes in breath sounds
• Improved vital signs
• Improved chest X-ray
• Increased oxygen saturation in the blood, as measured by oximeter or
arterial blood gas (ABG) values
• Patient reports of ease in breathing
Part 2: Techniques of Chest Physiotherapy:

Application and Uses
Physiological effect of chest physical therapy can occur on three fundamental
parameters of respiration:
• Airflow characteristics of the airway
• Elastic compliance of the lung parenchyma
• Matching of the ventilation with the perfusion
While managing any respiratory disorder, the physical therapy techniques
should be adapted to the symptoms of the disease. The therapist should be
able to detect clinical signs of respiratory distress in a patient and take

appropriate steps to reduce the distress.
SIGNS OF RESPIRATORY DISTRESS

Oxygen starvation leads to respiratory distress. Below is a list of some of the
signs that may indicate that a person is having respiratory distress.
Increased Breathing Rate

Increase in the number of breaths per minute may indicate that a person is
having trouble breathing or not getting enough oxygen.
Color Changes
Bluish color (Cyanosis) seen around the mouth, on the inside of the lips,
under side of tongue or the nail beds may indicate oxygen starvation.
Grunting
Grunting sound can be heard each time the person exhales. This grunting is
the body’s way of trying to maintain backpressure of air in the lungs so that
the terminal airways will stay open.
Nose Flaring
The nose spreading open while breathing hard indicating increased work of
breathing.
Elevation of Shoulders
The shoulder girdle is pulled upwards with each breath, with the help of
accessory muscles of respiration, to bring more air into the lungs.
Sweating
Patient may break into cold sweat, mostly while breathing fast and shallow.
Wheezing
Patient feels tightness of chest, often associated with shortness of breath and
whistling sound heard with inspiration, indicating constriction of the airways.
Signs and symptoms of most respiratory disorders usually overlap one
another. The physiotherapy management plan should therefore takes into
account the severity of individual symptoms, their overlapping pattern, and
use individual techniques of chest physical therapy in a logical sequence, to
provide holistic management of troublesome symptoms.
TECHNIQUE OF MANAGING BREATHLESSNESS

The most troubling symptom in any respiratory disorder is breathlessness. In
a breathless patient, symptoms like anxiety, severe shortness of breath and
respiratory fatigue will have to be managed by the therapist. The therapist
will also have to realize that, in the acute stage of such disorders, the patient
will not be able to tolerate vigorous maneuvers, because of easy respiratory
fatigue. The most acceptable form of treatment will be that which reassures
the patient, does not increase the workload of breathing and induces
relaxation.
SOS FOR SHORTNESS OF BREATH

Following instructions can be given to the breathless patient to manage acute
exacerbations of severe breathlessness.
Steps to Follow
Tell your patients, When on the Brink … Always Think
STEP 1: Stop whatever you are doing and take rest in a comfortable position,
leaning forward or backward on a support, in lying, sitting or standing.
STEP 2: Put your head down, the chin coming closer to the chest.
STEP 3: Slump your shoulders.
STEP 4: Breathe in through open mouth.
STEP 5: Blow out through open mouth.
STEP 6: Breathe in and blow out as fast as necessary.
STEP 7: Gradually begin to blow out for longer periods, but never forcibly.
Use pursed lip breathing during expiration, if you find it effective to empty
the lungs.
STEP 8: Slow down the breathing rate very gradually.
STEP 9: Begin to use your nose for breathing only when you feel the
breathlessness has reduced.
STEP 10: Begin diaphragmatic breathing. Practice for ten repetitions.
STEP 11: Stay in relaxed position for 5 minutes more.
Remember:
Breathlessness on exertion is expected in any individual and is more likely in
a patient with respiratory dysfunction. It is definitely uncomfortable, but not
harmful or dangerous.
RELAXED POSITIONING
Positioning the patient appropriately to induce relaxation has a very important
role in reducing breathlessness in respiratory distress.
The therapist has to choose and teach the patient to relax an optimum
position from supine, slumped sitting, half lying, high side lying, side lying ¼
turned towards prone, high sitting or standing, depending upon patient
tolerance, preference, before starting chest PT.
Fully supported, propped up positioning on the bed, using a number of
pillows under the head and back and one underneath the knee helps to
relax the abdominal muscles. This position usually gives best result in relaxing
the patient who is breathless at rest and sharply reduces the work of breathing.
Exchange of gasses in the lungs can be manipulated by appropriate
positioning. In unilateral pneumonia with consolidation of one lung or
following thoracotomy or fracture of ribs on one side chest wall, side lying
with the affected lungs uppermost give dramatic improvement in oxygen
uptake. In this position the better ventilated lower lung also gets maximum
perfusion, reducing the Va /Q mismatch.
A pulse oximeter may be used to verify the effectivity of specific position
in improving oxygen uptake and the same may be demonstrated to the
patient, nurse or care giver. Specific instructions should be given to all
concerned to maintain the correct position of the patient for stipulated period
and change the position at specific intervals.
Points to Ponder
• Relaxed positioning should support the body segments adequately, so
that minimum energy is spent to maintain postural stability. With a stable
supported posture there is minimum postural muscle activity. This energy
saving strategy is invaluable in breathlessness because it reduces fatigue.
• Bedridden patients should adopt side lying ¼ turned towards prone so
that the diaphragm is relieved of the weight of viscera and can move
freely during breathing.
• What seems to be technically the most appropriate position, like crook
lying or half lying, may not always be tolerated by the patient, because
maintaining the lung volume is difficult in these positions.
• Many patients prefer sitting on bed, leaning forward on a support, during
severe respiratory distress. In such case, several pillows or a bed side
breakfast trolley placed in the front of a sitting patient on bed may be
used as support.
• The therapist should be careful not to interfere with the position adopted
naturally by the patient during acute respiratory distress, as this may trigger
even more breathlessness.
• The approach of the therapist should be to coax the patient, rather than
command, into adopting a technically more acceptable position during
acute breathlessness.
However, it may not be possible for the suddenly breathless patient to
find a bed to lie down at all times. This is particularly true for those cases that
show episodic exacerbations of breathlessness on exertion. Instructions as
follows are meant for these patients.
• SIT with your back against the back of the chair. The head and shoulders
leaning forward in a relaxed manner, hands and forearms resting on
thighs. Try not to lean forward on your forearms as this will restrict the
movement of the diaphragm.
• SIT leaning back into chair in a slumped position, your head rolled
forwards, shoulders sagging down, hands resting on stomach, feet on
floor, knees stretched outward.
• STANDING, lean back on a wall or lean forward on a railing. Keep the
feet slightly apart and a comfortable distance from the wall. The head
should be slumped forward and shoulders should be relaxed.
In all these position the patient should do the steps detailed in “SOS
FOR SOB” until the breathing becomes normal.
TECHNIQUE OF MAXIMIZING LUNG VOLUMES

In a breathless patient, maximum ventilation with minimum effort
helps gain optimum oxygen saturation and gets rid of excess carbon
dioxide from the blood.
• In COPD, the patient is unable to exhale fully due to floppy terminal
airways collapsing before the lung can empty itself of dead gas and
therefore be unable to inhale adequate volumes of fresh air.
• In RLD, the patient is unable to breath in sufficient air due to inability to
expand the lungs because of any number of causes ranging from pain
inhibition to loss of elastic recoil of lungs to weakness of muscles of
inspiration.
• COPD and RLD lead to progressive hypoxia, breathlessness, fatigue and

ultimately respiratory failure. However, mild breathlessness provokes the
patient to breathe deeply. The therapist may induce mild breathlessness
in a sedentary patient by graded exercises like turning in bed, sitting up,
getting out of bed to a chair, walking or cycling.
• A breathless patient will automatically try to breathe deep and hard. This
impulse can be used to increase the lung volume and exercising the
muscles of inspiration.
• The patients should be instructed to watch out for feeling slight shortness
of breath. As soon as breathlessness appears, the exercise should be
stopped; patient positioned in appropriate relaxed stance and asked to
breathe slow and deep through open mouth till breathlessness disappears.
• With training, most patients learn to increase the exercise threshold
gradually, improving the oxygen uptake capacity of their lungs, even
without constant supervision of the therapist.
• In severely breathless patients however, there is a risk of respiratory failure
due to fatigue arising from increased respiratory effort. In such cases
oxygen supplementation is needed during breathing exercise and
sometimes mechanical assistance to ventilation is necessary to maintain
adequate lung volume.
BREATHING EXERCISES
Teaching patients to breathe effectively is another very important aspect of
chest physiotherapy for asthmatic bronchitis, chronic bronchitis, or
emphysema. In most lung disorders, the patient has to usually work very
hard to breathe, because the breathing is ineffective in optimizing ventilation
with perfusion. The workload of breathing further increases during exertion
or acute exacerbation of symptoms. However, because he is not breathing
properly, this hard work for breathing does not make the patient feel better
and he becomes tired easily.
There are several things the therapist can do to improve breathing in a
tired and breathless patient by making him/ her as comfortable as possible.
The process of chest PT should preferably begin with supported side lying
position ¼ turned towards prone, frequent sips of water, any reliever drugs
that may be indicated, counseling to reduce anxiety and discourage talking.
Most patients automatically adopt compensatory breathing techniques to
cope with breathlessness and other respiratory dysfunctions. The wise thing
to do is not to tinker with the natural pattern and technique of breathing in
a tired patient. The natural breathing pattern of the patient should be gradually
integrated into a more effective pattern through breathing exercises.
The breathing exercises should start only when the patient is relaxed
enough to cooperate. To begin with, the patient must relax the head, neck
and shoulders when doing breathing exercises. The patient must lean forward
in sitting or standing when exhausted and short of breath while doing
breathing exercises.
While the patient is doing the breathing exercise the therapist should
place both hands on either anterior lower chest wall, covering dome of the
diaphragm with the fingertips as a means of feedback and for detecting
unnecessary strain on the part of the patient.
DIFFERENT BREATHING TECHNIQUES

Breathing through pursed lips, like when sucking or blowing reduce
breathlessness, slows down the respiratory rate, increases tidal volume,
increase effectivity of expiration by pneumatically splinting the floppy terminal
airway, as well as, optimizing ventilation and perfusion. Pursed lip
breathing works best in COPD, when the patient is severely breathless either
at rest or with minimal exertion.
Technique
a. The patient should be explained the scope and importance of the
technique.
b. The patient should adopt most comfortable position of his choice, usually
forward lean supported sitting.
c. Asked to slowly inhale through nose or mouth.
d. And passively blow out through pursed lips (as if blowing out a candle).
e. For training, a lighted candle may be placed at distance of 50 cm to 1
meter at face level, in front of the patient. The patient is asked to try and
bend the flame away from him for as long as he can, without blowing it
out all together. This ensures prolonged expiration so that the lungs are
emptied of dead gas, as well as, teach breath control to the patient.
f. Additional hand pressure from the therapist may be applied to the lower
third of the rib cage and upper abdomen, to gently prolong the expiration.
g. Care must be taken not to prolong the expiration for too long; otherwise
the patient may end up becoming more breathless.
h. Intrathoracic pressure should not be allowed to increase too much during
expiration through pursed lip; otherwise the terminal airways may collapse.
DIAPHRAGMATIC OR BELLY BREATHING

Diaphragmatic or “Belly breathing” is done by allowing the belly to stick out
while breathing in and then pulling the belly in while breathing out against
pursed lips. Diaphragmatic breathing is used to increase ventilation, improve
gas exchange, reduce work of breathing, maintain or improve mobility of
chest wall, prevent hypostatic collapse of alveoli in lung bases and facilitate
relaxation. It is used in postoperative or post-traumatic respiratory
complications, COPD and RLD.
Technique
technique.
b. Position the patient in semi-reclining position, preferably in half lying on
bed or slumped sitting on a low sofa.
c. Therapist’s hands should be placed over sub-costal angle, at the base of
the rib cage of the patient, tips of the fingers approximating just over the
dome of the diaphragm.
d. Gentle pressure should be applied to the rib cage and diaphragm by the
therapist throughout the expiration cycle.
e. At the end of expiration the pressure applied should be firm to expel
maximum possible stale air from the lungs.
f. The patient to be asked to inhale deeply and smoothly, against slight
resistance applied through the hands of the therapist.
g. Near the end of inspiration cycle the pressure on the chest wall should be
released suddenly, so that maximum possible inspiration takes place.
h. As the patient becomes used to the technique, he should be allowed to
practice independently, while sitting in a chair, standing, walking, stair
climbing etc.
SEGMENTAL BREATHING
Segmental breathing is used to improve ventilation in lung segments, alter
regional distribution of gas and maintain or restore functional residual volume,
chest mobility and lung compliance. It is used in patients with pleuritic, surgical
or traumatic pain inhibition that is restricting movement of a portion of the
chest wall and is at risk of developing atelectasis of the underlying lung segment.
Segmental breathing is contraindicated in case of chronic hypoventilation
due to massive pneumothorax, bronchogenic tumor or presence of intercostal
drainage tubes.
Technique
technique.
b. Modified postural drainage position may be given to the patient, depending
upon the location, so that maximum air entry will be possible to the
affected segment.
c. The therapist should apply light pressure over the affected segment during
expiration, which should be increased slightly at the commencement of
inspiration. The purpose of this pressure is to give feedback to the patient
as to where to focus maximum effort.
d. The pressure is released suddenly in the middle of inspiration cycle. This
allows the ribs to spring out, drawing even more air into the affected
segment.
END INSPIRATORY HOLD (SUSTAINED MAXIMAL INSPIRATION)

Collateral channels of ventilation exist between adjacent lung segments, which
can be opened on holding the breath for 3 to 5 seconds at the peak of
inspiration, resulting in better distribution of the inspired air, optimizing
ventilation and perfusion through out the entire lung. This type of breath
holding is most suitable for patients with chronic pulmonary diseases like
asthma, chronic bronchitis, resolving pneumonia etc. However, in a severely
breathless patient, end inspiratory breath holding should not be used, as it
may interfere with the rapid rate of breathing, making the patient more
breathless.
Procedure
a. Patient should be asked to inhale slowly through the mouth to maximal
inspiration.
b. At the peak of inspiration, the patient may be asked to sniff in a little bit
more air into the lungs. This end inspiratory sniff helps open the channels
of collateral ventilation even more.
c. Hold maximal inspiration for a slow count of five (approx. 3-5 seconds)
d. Passively exhale the full inspired volume.
e. Breath holding at the end of inspiration can be practiced with each breath,
on alternate breath or after every five breaths, depending upon comfort,
effectiveness and tolerance of the patient.
f. Incentive spirometer may be used while doing end inspiratory holds
because this device can measure and encourage deep inspiration.
g. At all times the therapist must keep vigil for any signs of increasing
breathlessness, fatigue, shoulder girdle tension and anxiety.
OTHER METHODS OF MAXIMIZING LUNG VOLUMES

Single Percussion Technique
A single percussion, given with one cupped hand between the scapulae,
during end inspiratory hold, generates a shockwave, which spreads through
out the lungs, opening up the collapsed alveoli. This further improves alveolar
ventilation, resulting in better exchange of gases.
Graded Physical Exercises

Often patients make the mistake of avoiding physical exertion to prevent
shortness of breath, believing it will protect their lungs and heart. Nothing
could be less true. Exercises are the most effective tool for increasing lung
volume in any patient, even if unable to get out of bed. Any patient can
learn how to exercise more even if they have a lung condition that makes
them breathless. As we all know, any muscle will become weak if disused.
This is true for the muscles of respiration. Exercise help strengthen these
muscles, which in turn help stop respiratory inadequacy and thus shortness
of breath.
• A bedridden patient may be asked to turn a fixed number of times within
a fixed period, say 5 turns every hour. If there is no increase in severity of
breathlessness with this regime, the number of turns per hour can be
increased.
• A patient who is able to get out of bed, but is unable to walk, can be
advised to transfer to a chair several times during the day. This may
progress to walking around the bed a few times and then to walking
normally in the ward.
• During graded exercise training, some degree of breathlessness is
desirable, as it promotes better ventilation. But the therapist must be alert
for any signs of respiratory distress to stop the exercises immediately.
Points to Ponder
Before starting any type of exercise training program the patient must be
evaluated and declared fit by the pulmonologist.
1. The exercise prescribed should be designed to improve endurance, having
low resistance and high repetition rate. The intensity of the exercises should
induce slight breathlessness in the patient, which however should not
cause any distress and disappear with few minutes of rest.
2. Before starting, allow the patient to relax for 5 minutes. Record the pulse,
respiration rate and PEFR before starting.
3. Start with light, free hand, warm-up exercises. As the exercise tolerance
improves induct cycling, rowing, walking, etc. into the exercise program.
4. Allow adequate rest periods in between exercise sessions, preferably two
minute break after five minutes of each exercise.
5. Insist on appropriate breathing techniques during and in between exercise.
6. Commit the patient to a regular exercise program.
7. Never allow exercise on a full stomach.
8. Avoid sudden bursts of activity like lifting heavy objects.
9. Exercise training must be done in a controlled environment and in
moderation. Watch for warning signs and take appropriate steps in case
sudden increase in breathlessness, sweating, nausea, dryness of throat,
dizziness etc.
TECHNIQUE OF REMOVING EXCESS

SECRETIONS FROM THE LUNGS
Effective Coughing
Coughing is the natural way of removing foreign substances from the lungs.
In COPD there is an excess production of mucus. This mucus irritates nerve
endings in the tracheo-bronchial tree and causes frequent involuntary
coughing.
To conserve energy and oxygen, the patient must practice and master
the method of controlled coughing.
Coughing has an important “cleaning action” and the patient should be
trained to cough effectively every morning and evening, in such a way that
can clear the lungs of mucus with two or three coughs.
Points to Ponder
• Cough is an involuntary protective reflex that is usually triggered when a
foreign particle enters the airway. It is accompanied by active contraction
of muscles of expiration.
• It can be defined as an “ Explosive expiration through a closed glottis”
• To generate this explosive air pressure, enough expansion of the chest
and normal lumen of the airway must be maintained. The elastic recoil of
the lung should keep the terminal airway open till the end of expiration.
• In respiratory disorders, cough is utilized by the body to get rid of excess
mucus secretions from the airway.
• Narrowing of the airways, air entrapment due to floppy terminal airway

and weakness of muscles of expiration prevent the patient from coughing
effectively.
To Teach the Patient to Cough Effectively

• Position the patient in upright position, with adequate support to the
head neck and back, preferably in high sitting or propped up on bed.
• Ask the patient to take few deep breaths. Place your hands, with fingers
outstretched over the chest wall of the patient, to feel the chest expanding
with inspiration.
• Ask the patient to hold breath for a few seconds at the peak of inspiration.
This will open up channels for collateral ventilation in the lungs.
• Ask the patient to “Huff” a couple of times. Each huff is a short oscillatory
explosive expiration (Ha! Ha!).
• Huffing is more effective in patients with collapsible terminal airway, e.g.
COPD, because it prevents too high intrathoracic pressure which may
cause premature closure of the airway.
• Huffing helps mobilize secretions progressively upwards in through the
bronchial tree, keeping the terminal airway open for complete evacuation
of dead gas and secretions from the alveolar space.
• After three to five huffs, ask the patient to huff very hard at the end of
inspiration. This usually triggers an effective cough.
• Breathing moist or humid air, and drinking plenty of fluids every day
helps this cleaning action of cough. A drink of water taken prior to
coughing can be helpful.
• Coughing is easier in a sitting position with the head slightly forward.
Controlled, effective coughing should make a hollow sound.
• The moisture helps to thin out the mucus so that it can be coughed up
more easily.
• The patient might also be recommended to have inhaled bronchodilator
or anti-inflammatory drugs that open the airways and help increase the
normal flow of mucus out of the lungs.
ASSISTED COUGHING
Assisted cough should be used when the abdominal muscles of the patient
fails to generate sufficient intra-abdominal pressure to produce an effective
cough. The hands of the therapist provide the force behind the air exhaled
by the patient to generate an effective cough. It is indicated in high spinal
cord lesion, GB syndrome, bulbar palsies, advanced primary muscle disease,
near drowning, etc.
Procedure
1. Supine (Horizontal/Trendelenburg) position or sitting upright, with the
head resting against a firm surface are the positions of choice for assisted
coughing.
2. The hands of the therapist, usually balled in to a fist, are placed below the
sub-costal angle (solar plexus) of the patient (As in Heimlich maneuver
used in treatment of choking).
3. The patient is asked inhale deeply and then attempt to cough.
4. As the patient begins to cough, a therapist presses inwards and upwards
with the balled fist, forcing the diaphragm upwards and expels the air
effectively.
5. This process brings up secretions from the airways, which can be either
expectorated or suctioned out.
6. The therapist has to be extremely careful not to press hard against the
floating ribs or the xiphoid process, as this may cause a very painful injury
to the patient.
7. Assisted cough may be used as a follow-up measure after postural drainage,
chest percussion and vibrations. Not more than 2 to 3 assisted cough
should be given in one sitting.
Postural Drainage
Postural drainage is a low-tech procedure which often supersedes many
hi-tech devices in effective removal of secretions from the lungs. This procedure
takes into account the force of gravity, position of lung segments in relation
to gravity and the alignments of the representative bronchus where they
meet the main bronchus. Like a can of condensed milk is emptied by turning
it up side down, in PD the patient’s lung can be emptied of thick, tenacious
secretions by simply positioning the patient in such a way that the force of
gravity can drain the secretions from inner recess of the lungs, through smaller
airways into the main bronchus. Once the secretions drain into the main
bronchus, it is carried upward by the muco-ciliary escalator, to be coughed
out easily (Fig. 7.1).
Indications for Postural Drainage

Postural drainage should be done in the presence of increased pulmonary
secretions, aspiration or atelectasis.
FIGURE 7.1: The head down position of the patient is indicative of primary principle
of postural drainage. In this position the force of gravity draws the secretions out
from the smaller diameter airways into larger diameter main bronchus, indicated
by black arrow
Contraindications for Postural Drainage

Main objection to the use of postural drainage is the use of Trendelenburg
(Head Down) position in the following conditions/complications/situation:
1. Circulatory disorders like pulmonary edema, congestive cardiac failure
or hypertension
2. Abdominal problems like obesity, ascites (Excess fluid in abdominal cavity),
pregnancy, hiatus hernia, full stomach or gastroenteritis.
3. Neurological disorders like recent CVA, head injury, raised intracranial
pressure or confirmed aneurysm.
4. Respiratory symptoms like severe breathlessness.
In all of the above cases, head down position must not be used for postural
drainage. In such cases modified postural drainage positions like side lying ¾
turned towards supine or prone may be used as an alternative measure.
Preparation for Postural Drainage

• A quite, well lit room, with no cross draught of cold breeze is suitable for
PD. The room should allow adequate privacy to undress and position the
patient for extended periods. For bed ridden patient PD can be done at
bed side, using pillows for support.
• A postural drainage plinth is very essential for positioning the patient
accurately in appropriate drainage posture (Fig. 7.2). Such plinths may
also be portable, so that it can also be used in the ward for bedside PD.
Alternatively, for very sick patients, who can’t be taken out of bed, several
pillows may be used position the patient appropriately on the bed itself.
FIGURE 7.2: A three section postural drainage plinth, with adjustable head
board to position the patient from horizontal to full up-right sitting. The lower
third folds upwards, allowing flexion of the hip and knee in crook lying
position
Procedure for Postural Drainage

• Explain the procedure to the patient, telling why it is important for the
treatment.
• Place the patient in appropriate postural drainage position and ask the
patient to maintain the position for at least 20-30 minutes.
• Cover the chest wall with a sheet before doing percussion. This will prevent
reddening of the skin over the chest wall due to percussion.
Sequence of Drainage Positions (Fig. 7.3)

1. Upper lobes, anterior segments
2. Upper lobe, posterior segment, right posterior bronchus
3. Upper lobe, posterior segment, right posterior bronchus
4. Right middle lobe
5. Left lingula
6. Lower lobes, apical segment
7. Lower lobes, anterior basal segment
8. Lower lobe, lateral basal segment
9. Lower lobes, posterior basal bronchus
FIGURE 7.3: Positions for complete postural drainage
CHEST PERCUSSION
Chest percussion is performed by rhythmic clapping, applied with the cupped
hands of the therapist over a specific area of the chest wall that corresponds
to the involved segment of the lungs. The shock waves generated by the
percussion is believed to pop open half collapsed alveoli and terminal airways,
in addition to shaking loose secretions sticking to the walls of the airway.
Experience has shown that percussion of the chest is effective in clearing
secretions from the tracheobronchial tree, particularly when used in
conjunction with postural drainage.
Indication for using Chest Percussion

• Excessive secretions in the lungs.
• Aspiration of saliva or vomitus or food particles or liquids into the airway
due to faulty swallowing mechanism (Bulbar palsy), unconsciousness etc.
• Atelectasis (Collapse of alveolar sacks) due to mucus plugs obstructing
the airway.
Contraindications for Using Postural Drainage

• General contraindication: Pain of the chest wall in postoperative,
pleurisy, acute lobar pneumonia, fractured ribs may be worsened by
percussion.
• Circulatory contraindication: Risk of hemoptysis may increase with
percussion in presence of aneurysm, increased bleeding and clotting time,
Hemorrhagic pneumonia and terminal stages of TB or CA etc.
• Musculoskeletal contraindication: Flail chest, bone metastasis, severe
osteoporosis, spontaneous pneumothorax etc.
FIGURE 7.4: Position hand when

performing chest percussions
Procedure for Chest Percussion

1. The procedure must be explained to the patient.
2. The patient must be placed in an appropriate position, taking care to
support the head, neck, thorax, pelvis and lower limbs adequately to
avoid any inadvertent movement in unstable segments and making sure
that the position does not make the patient breathless. Percussion may
be done in different postural drainage positions as per sequential order
to get desired resullts.
3. The area of the chest wall, corresponding to the involved lung segment
must be exposed and inspected closely for any tender points, bony lesion,
rigidity of the rib cage, hyper-resonant percussion note indicating
pneumothorax, suture line and drainage tubes if any in case of post-
operative conditions and chest X-ray for any peripheral emphysematous
bullae. In the presence of any of the above, the percussion technique
should be suitably modified or avoided all together.
4. The chest wall is then covered with a light sheet, to avoid reddening of
the skin due to percussion.
5. Percussion is given over the chest wall corresponding to the underlying
involved lung segment. The force applied through clapping should be
light, rapid and rhythmical, being adequate to cause quivering of the
patient’s voice. The duration of percussion may be 5 minutes per postural
drainage position. However, the comfort level of the patient and clinical
improvement should be used as a final guide to application of percussion.
CHEST VIBRATION
Chest vibration or shaking the chest wall is applied using both hands of the
therapist placed on anterior-posterior or later aspects of the rib cage. It is
applied usually throughout the cycle of expiration, following maximum
inspiration. Chest shaking sets up coarse vibrations in the airway, helping to
loosen secretions sticking to the walls of the airway. Shockwaves thus generated
helps open up the terminal airway and the alveoli. It may be used following
chest percussion or in isolation, done in appropriate drainage position.
Indications and contraindications of chest vibrations are similar to those of
chest percussion. However it is deemed by many clinicians to be safer and
more effective option than chest percussion, particularly in the very young
and very old patients. In addition, most patients find the procedure more
comfortable than percussion, helping them relax better and therefore be
able to focus on breathing maneuvers and maintain drainage position for
longer periods.
Procedure for Chest Percussion

1. The patient should be explained the procedure.
2. As the patient inhales deeply, therapist’s hands are placed on either side
of the chest wall (AP or LAT) with the fingers parallel to ribs (Fig. 7.5).
3. As the patient exhales, the therapist provides a jarring motion to the rib
cage, with enough force to make the patients voice to quiver.
4. The duration of the shaking depends on the need, tolerance and clinical
response to the procedure. However, up to 10 cycles of maximum
inspiration followed by complete expiration, with concurrent shaking, is
deemed adequate in most cases. If more than 10 cycles of deep breathing
tried in one sitting, it may lead to a sudden drop in PaCO2, making the
patient feel dizzy due to hyperventilation. If less than 5 cycles are used, it
may prove to be ineffective.
5. During applying chest vibrations it is
customary to squeeze the chest slightly
till the end of expiration. This empties
the lung of dead gases. This squeezing
is released suddenly at the end of
expiration so that the rib cage can
spring back during inspiration, drawing
maximum possible air into the lungs.
FIGURE 7.5: Position hands when
performing chest vibrations
Part 3: Devices used in Chest Physiotherapy

PEAK FLOWMETER
A peak flowmeter (Fig. 7.7) is a simple device with a mouthpiece and a
measuring system with a pointer. Blowing through the mouthpiece as hard
and fast as you can enables the speed of the air which has been blown out to
be recorded.
To use a peak flowmeter correctly
1. Take as deep a breath in as possible,
2. Secure the mouthpiece to between your lips.
3. Blow out as hard and fast as possible, emptying your chest of air in the
first second.
FIGURE 7.7: Peak flowmeter
In asthma, as in all COPD, narrowed airways slow down the speed of

airflow, resulting in a lower reading on the peak flowmeter. After taking an
inhaled reliever, waiting 10 or 15 minutes and then repeating the peak flow
measurement, a higher reading will usually be seen (also See Chapter 4).
INCENTIVE SPIROMETER
Incentive spirometer is an inexpensive, easy to use, mechanical device, used
to increase airflow and inspiratory volumes, through controlled and sustained
deep inspiration, giving the patient visual feedback on their performance
throughout the cycle of inspiration (Fig. 7.8, Plate 4). Incentive spirometry is
designed to mimic natural sighing or yawning by encouraging the patient to

take slow, deep breaths. When the patients lie in bed for a long time, after
surgery, or if are having a lot of pain, they tend to take shallow breaths and
not cough as often as needed. Inhaling deeply helps mobilize secretions and
open up areas of the lungs that may have become collapsed. Non-operative
and postoperative patients increase lung volume by keeping the instrument’s
inhalation-sensitive ball suspended with inhalation. Flow passages vary in
diameter, affecting the energy required to raise the ball, which stays suspended
as long as the patient maintains this effort. Flow indicator dial can be adjusted
to indicate flow rates in ml/second.
Technique of using Incentive Spirometer

• Position the patient in upright sitting or propped up in bed
• Demonstrate the working of the incentive spirometer on a demonstration
unit.
• Record the PEFR of the patient by a peak flowmeter.
• Set the inhalation rate of the incentive spirometer in proportion to the
PEFR.
• Stress the need to keep the flow sensitive ball floating at the middle level
of the chamber for as long as possible. This will ensure smooth, steady,
inspiration, generating a laminar airflow, ensuring maximum ventilation.
• The exercise should be repeated for 5-10 times every hour.
Inhaled Medications and Delivery Devices

In most respiratory disorders, the greatest bronchodilatation is achieved fastest
and with fewest side effects by using the inhaled aerosol route of delivery.
This allows a higher concentration of active drug to reach the target airway
with a lower total dose than is possible by oral or injected routes of delivery
(Fig. 7.9). The common methods of aerosol delivery currently available are
nebulization and metered dose-inhalation (MDI). If equivalent doses and
correct inhalation techniques are used, these methods are equally effective
for treating children and adults with acute or chronic respiratory distress.
Nebulizers
A nebulizer consists of an electrical air pump which pumps air through plastic
connecting tubing which is attached at its other end to a nebuliser bowl, and
either a face mask or mouthpiece. High pressure oxygen, instead of
compressed air, may also be used to nebulize appropriate medication (Fig.
FIGURE 7.9: Comparison of drug dosage and effectivity of delivery to the lungs
using oral and inhaled route of drug administration
7.10). A mist of medication spray issues from the face mask or mouthpiece
and this is inhaled.
FIGURE 7.10: Working of a compressed air/oxygen driven nebulizer chamber
Bronchodilator, mucolytics and anti-inflammatory agents can be adminis-

tered effectively by nebulization, using either an electric air compressor
(Fig. 7.11) or continuous flow oxygen at six to eight liters per minute.
Procedure
• The 1 ml of bronchodilator/ mucolytics/anti-inflammatory drug and 4 ml
of normal saline or sterile water are placed in the plastic nebulizer
compartment.
FIGURE 7.11: Electric nebuliser
• One end of the oxygen tubing should be attached to a nebulizer and the
other to the electric air compressor or oxygen regulator.
• A t-piece or mask is attached to the top of the nebulizer compartment.
Infants and young children require the aerosol mask.
• The mask is securely fastened to the face of the patient and the patient
asked to take relaxed deep breath (Fig. 7.12).
FIGURE 7.12: Technique of giving nebulizer through a

face mask. Note the nebulizer chamber attached
below the mask
• The patient should be treated until the liquid in the nebulizer has been
almost used up, which usually occurs in five to ten minutes. It is unnecessary
to nebulize until all the liquid has been used - in practice about 0.25 to
0.5 ml will be left in the nebulizer bowl when a spluttering sound occurs
and little of the residual fluid is being nebulized.
• If normal saline or sterile water is not available for diluting the drug,
drinking water should be strained with a cloth and boiled for 20 minutes,
then allowed to cool.
• The tubing and nebulizer should be washed with non-residue soap
(dishwashing detergent) and dried prior to reuse (but not sterilized with
ethylene oxide because of the risk of formation of toxic by-products).
Boiling or autoclaving will destroy the tubing.
Points to Ponder
Small children and people with respiratory disabilities, who are unable to use
other inhaled drug delivery devices, need a nebulizer. Nebulizers are generally
used in an emergency-type situation, to give the high dose of medication
needed to treat an asthma attack. Sometimes people with very troublesome
asthma require a nebulizer lifelong.
• Drug delivery through these systems requires careful attention to the design
of the nebulizer.
• The respirable output is defined as the volume of respirable droplets
produced per minute and is critical for the effectivity of the treatment. In
simple terms, the respirable output means density of the mist generated
by the nebulizer. If the respirable output of a nebulizer system is low, the
mist is thin. Such mist is ineffective for delivering sufficient dose of
bronchodilator or other inhaled drugs to the lungs.
• The diameter of individual droplets should be less than 5 microns to be
effectively inhaled to the deeper reaches of the lung.
• In case when electric compressors, and oxygen cylinders and regulators
are unavailable, the best alternative is the administration of bronchodilators
through pressurized metered-dose inhalers with spacer device (MDI).
• A second, but less recommended alternative is the use of a foot-pump to
drive a mechanical nebulizer. The foot-pump suitable for this purpose
must be robust, durable and easy to operate and maintain. It must also
be grease-free, because grease particles must not be inadvertently mixed
with the bronchodilator and delivered to the airways.
• Only well-designed and efficient mechanical nebulizers should be used.
They must produce a high respirable output when driven by the foot-
pump at a stroke rate that can be maintained by the health worker for
the time needed to nebulize about 5 ml of solution.
• The instructions for administration are the same as described above for
electric air compressor or oxygen-driven nebulizers.
METERED DOSE INHALER (MDI) DEVICES

The original asthma inhalers came in the form of a glass bowl with a hand-
held rubber pump which was squeezed, creating a jet of medication aerosol.
Modern inhaler devices deliver inhaled medications in a measured dose, for
treatment of wide range of respiratory disorders. The size of the inhaled
particles is very small so that it can travel right down into the lungs, and does
not just impact in the throat.
Types of Inhalers
1. Multiple dose inhalers are the preferred modern option for treating
asthma in children, teenagers and COPD in adults, both for managing
acute attacks and for regular preventive therapy (Fig. 7.13).
FIGURE 7.13: A metered dose inhaler
2. Dry powder devices: This includes Disk halers, Spin halers, and
Turbuhalers, all of which need a good breath in to activate them. Children
from age 5 or 6 years onwards may be able to manage these devices.
3. Breath activated aerosols: These require a good inspiration power in
order to get the drug into the lungs, but need less co-ordination. The
breath-activated aerosol may be an effective device for children aged 8
and older patients.
All inhaled medications should ideally be given through spacers.
What is a Spacer?
A spacer is a large chamber which is fitted to an inhaler medication used for
asthma, emphysema or bronchitis. Instead of inhaling directly from the
inhaler, a dose from the inhaler is sprayed into the spacer then the spacer is
inhaled from, either through a mouthpiece or a mask (Fig. 7.14).
FIGURE 7.14: A volumetric spacer
Advantages of a Spacer
• Patients do not need to coordinate with an inhaler. They can breathe in
and out several times with the chamber.
• The spacer reduces the amount of medicine from the inhaler which hits
the mouth and throat rather than going to the lungs. The benefit of this is
that there is less side effects in the mouth and throat, e.g. hoarseness or
oral thrush from steroid inhalers. Additionally, less medicine will be
swallowed and then absorbed from the intestine into the rest of the body,
which is also good.
• With a spacer, the patient will get more of the inhaled medicine at the
right spot in the lungs where it does the most good.
• As many adults and most children cannot coordinate very well with their
inhaler, using a spacer is a good idea for nearly everyone who is using an
inhaler. For a child it is far easier to use an inhaler with a spacer than the
inhaler alone.
• A spacer may not be as effective as a nebulizer for getting the medicine to
the lungs, but is faster to use than a nebulizer, and less expensive.
• Each brand of spacer has been devised to work with particular MDI. It is
important to make sure that the MDI and spacer are compatible to get
the best use from them.
• New spacers should be washed in detergent before use, as otherwise the
static of the plastic may interfere with the initial few doses. Spacers should
then be washed every week or so to keep them working properly (wash
in liquid detergent and shake dry).
How to Use an Inhaler?

1. Shake the inhaler well.
2. Fit the inhaler to the inhaler hole of the spacer opposite to the mouthpiece
and spray one puff into the spacer.
3. Put patient’s mouth around the mouthpiece ensuring there are no gaps.
Ask to breathe slowly and deeply from the mouthpiece of the spacer and
hold the breath for 10 seconds if possible. Repeat two or three times with
the mouthpiece still in the mouth (Fig. 7.15).
FIGURE 7.15: Method of using a metered dose inhaler
4. If the doctor has prescribed two different medications, wait for one minute
then follow steps 1 to 3 with the new medicine. Never spray the two puffs
into the spacer together as it is not nearly as effective as doing them
separately.
5. If a mask is being used make sure the mask is placed firmly on the face,
and after use with steroid inhalers wipe the face clean with warm water.
6. For children, instead of holding the breath for 10 seconds they could
take five deep slow breaths instead.
Cleaning the Spacer

The spacer should be cleaned before first usage and thereafter once a week.
Wash in warm water and allow drip-drying.
Before the very first use it is recommended to spray 10 puffs of the
bronchodilator inhaler, e.g. Ventolin, sprayed into it. This reduces the possibility
of the medicine sticking to the walls of the spacer instead of going into the air
to be inhaled.
Check regularly for cracks or other problems. If used regularly the spacer
may need to be replaced every 6 to 12 months.
Part 4: Chest Physiotherapy Techniques in

Surgical Conditions
INTRODUCTION
The thoracic cavity is a rigid structure, with some movements possible
between each rib due to its articulation with the sternum in the front and the
thoracic vertebra at the back. These individual movements do not take place
independent of each other. The rib cage moves as an unit in response to
contraction of muscles of respiration, resulting in expansion on inspiration
and contraction on expiration (Please read Chapter 1). The abdominal
cavity on the other hand has non-rigid walls, made up of layers of muscles,
all of which participate in the act of breathing.
Both are closed cavities, separated by the diaphragm and operate on the
principle of closely balanced hydro-pneumatic pressure system that regulates
the air entry and exit to the lungs. Surgical incision that opens the abdominal
or the chest wall upsets this delicate balance of pressure between the two
cavities, thereby upsetting the rhythm of respiration. Respiratory complications
following abdominal and thoracic surgery are therefore the most important
complication to be tackled by the chest physiotherapist.
Why does surgery of chest and abdomen create respiratory

complications?
The reasons why any surgery on the chest or the abdomen wall may
compromise respiratory efficiency are listed below:
1. Pain inhibition: Any wound will cause pain, more so when it is stretched.
A surgical wound on the chest or abdominal wall is liable to stretch
repeatedly during breathing or coughing. This creates severe pain every
time the patient tries to breathe deeply or cough. Due to the fear of pain,
the patient consciously avoids deep breathing and coughing. This leads
to hypoventilation, hypoxemia and retention of pulmonary secretions
due to ineffective cough effort. Chronic hypoventilation leads to collapse
of lung segments and pooling of secretion leads to chest infections.
2. Hypersecretion of mucus: Irritation of the proximal airway due to
introduction of endotracheal tube and use of anesthetic gases lead to
hypersecretion of mucus.
3. Inhibition of muco-cilliary transport: Most thoracic and abdominal surgeries
are done under general anesthesia. The anesthetic gasses used in general
anesthesia suppress the upward sweeping action of cillia, so essential to
transport excess mucus secretions to be propelled upwards for eventual
expectoration. This leads to pooling of mucus in the airways leading to
atelectasis and alveolar spaces leading to consolidation. Prolonged
collection of mucus also invites chest infection.
4. Venous stasis: Inhibition of deep breathing due to postoperative pain
reduces the excursion of diaphragm. The up and down movement of the
diaphragm like a piston, creates a suctioning effect within the thoracic-
abdominal cavity. This suctioning effect is vital to draw venous blood
away from the lower limbs and return it to the lungs for re-oxygenation.
Weak suctioning by the diaphragm results in pooling of blood in the
major veins of lower limbs. This is called venous stasis. Pooled blood
tends to become sticky and form clots within the vein due to aggregation
of platelets and increased clotting factors following surgery. This is called
deep vein thrombosis. A small piece of this clot, called an embolus, may
break off and be carried by the blood stream to vulnerable areas like
pulmonary, cardiac or cerebral circulation. If the clot gets stuck in a blood
vessels of these areas and blocks blood circulation it can have disastrous
consequences; pulmonary embolism, cardiac or cerebral embolic stroke.
Intervention by the chest physiotherapists should therefore focus on
minimizing the effect of the above mentioned complications and promote
early recovery. Such intervention should begin well before the surgery and
must continue till the patient resumes normal life.
PREOPERATIVE CHEST PHYSIOTHERAPY TECHNIQUES
It involves patient evaluation, education, training and treatments aimed at
minimizing the frequency and severity of postoperative respiratory
complications.
Principal objectives of preoperative chest PT are to:
• Determine baseline cardiorespiratory function
• Treat any pre-existing disorder of the lungs, circulatory and musculoskeletal
system, which may complicate postoperative outcome.
• Maintain and enhance ventilatory capacity and lung compliance
• Educate the patient and the care givers about the expected postoperative
complications, how to detect them and the role of appropriate
physiotherapy measures in minimizing complications, discomfort and
hasten recovery.
Specific preoperative preparation needed for patients with COPD
and needing a general anesthesia.
History-taking and subjective assessment should focus on:
• Duration and severity of the pre-existing COPD
• Nature of drug / oxygen dependence.
• Whether the patient has had any difficulties involving anesthesia and
surgery on earlier occasions?
• The degree of alertness, orientation, knowledge and understanding of
the proposed operation, in the patient are important observations to
make. Hypoxia, if present, can impede mental performance. It will also
indicate whether the person will be able to co-operate with the
physiotherapy treatment after the surgery.
• A long interview can be tiring for someone who is breathless. Therapist
should keep the questions brief and to the point and ask only closed
questions to minimize talking.
Objective Assessment
This includes:
• Recording the patient’s baseline clinical recordings like body weight,
height, temperature, pulse, blood pressure, respiratory rate and pattern,
peak flow recordings (pre- and post-nebulizer/inhaler/s) oxygen saturation
levels etc.
• Routine laboratory testing of sputum, urine and blood will be advised by
the physician but the reports should be reviewed by the therapist from
the case file.
• Assessing the person’s skin condition, particularly if the person is bedridden,

and also if the person’s skin condition is poor as a result of taking steroids
for prolonged periods.
Planning the Care

A care plan will need to be developed which addresses needs uncovered
during the assessment process and also on whether the surgical procedure is
to be performed under general or spinal or epidural anesthesia. The operative
strategy of the surgical team will also need to be made clear to the
physiotherapist, the respiratory nurse specialist, and the theatre nurse who is
to be responsible for the person’s care. These members of the care team will
need to visit the person, introduce themselves and discuss the part they will
each play during the preoperative, intraoperative and postoperative periods.
Implementing
Preoperative information and education of the patient regarding procedures
that will be performed during the preoperative and postoperative period
contributes greatly to the reduction of stress and anxiety that can accompany
hospital admission for surgery. Pre-existing respiratory disorders leads to
further insecurity and anxiety in the patient.
Chest physiotherapy coupled with exercises to be carried out
postoperatively, will have to be taught and their importance in early recovery
reinforced. Physical therapy approach should demonstrate techniques of
minimizing postoperative pain, e.g. TENS over suture line, relaxed positioning
using rolls and pillows, maximizing lung volumes through deep breathing
and breath holding exercises, secretion removal through postural drainage,
incentive spirometry, use of supportive straps and contracture/DVT prophylaxis
by foot ankle movements.
Additional Points to Consider

People with asthma, chronic bronchitis and emphysema tend to have
irritable airways, and intubations may provoke coughing attacks.
Inhaled anesthetic gases can act as irritants to the bronchial mucosa. Specific
physical needs relating to the person’s respiratory disorder - prescribed drugs
will be administered and the person’s response to these monitored, for
example by conducting peak flow recordings and measuring oxygen
saturation levels at agreed intervals. Such monitoring will enable important
decisions to be made:
1. Whether humidified oxygen needs to be administered and if so at what
percentage, and if administration is to be by mask or via nasal cannula?
2. The point at which any bronchodilators are to be withheld prior to the
induction of the anesthetic will need to be ascertained.
POSTOPERATIVE PHYSIOTHERAPY TECHNIQUES

Postoperative physiotherapy mainly focuses on treating the adverse effects
of chest infections, apart from managing chronic hypoventilation, circulatory
complications and exercise intolerance following any major surgery. It should
be geared towards decreasing the frequency and severity of postoperative
complications.
Objectives of Postoperative Chest Physiotherapy

• To minimize postoperative pain
• To maximize ventilation
• To remove excess pulmonary mucus secretion
• To ensure adequate venous return
• To activate the patient at the earliest and minimize hospital stay.
Why or how does chest infection happen?
Anesthesia and surgery interfere with the normal ways in which the lungs
keep themselves clear of secretions and infection. Pain from the surgical
wounds, especially after chest or abdominal operations, inhibit deep breathing
and make effective coughing more difficult. This leads to retention of secretions
in the lungs, which act as a culture medium for inhaled pathogen leading to
chest infection.
How likely is a patient to get postoperative chest infection?
In one survey, 1 in 5 patients who had thoracic or abdominal surgery under
general anesthesia had some degree of chest infection although most of
these were not severe.1 Chest infection is less common with most other types
of surgery and anesthesia.
Who are at high risk of developing postoperative chest infection?
How likely a patient to get a chest infection depends on:2
• State of health before the operation, in particular whether there is pre-
existing chest disease or history of smoking.
• The type of operation; chest and abdominal operations are more likely
to cause chest infection.
• How long the patient is likely to be lying in bed and be unable to sit in a
chair or walk about.
• How urgent the operation is; there is more time to get the patient into the
best possible condition if the operation is pre-planned.
• The type of anesthesia being used; risk of chest infection is highest with
general anesthesia.
• Patient’s age; very young or very old people are more likely to get a chest
infection, but the risk is not much higher in fairly healthy elderly persons.
What are the symptoms of postoperative chest infection?
While developing a chest infection the patients may feel feverish and breathless.
They are also likely to have a productive cough and may bring up green or
yellow colored sputum. The coughing may be painful and not powerful
enough to clear the sputum. Some people get a dry but persistent cough
after an anesthesia due to irritation of the airway by the endotracheal
intubation and due to anesthetic gases. This is common and does not mean
getting a chest infection. It normally lasts only a day or two.
What treatment can be given?
Chest infections are usually treated with antibiotics. These may be given
orally or intra-venuously. Chest physiotherapy is also an integral part of this
treatment. The chest physiotherapy includes pain management,
appropriate positioning, deep breathing exercises, assisted coughing,
postural drainage and early activation.
A. Postoperative pain management may be done effectively by the
physiotherapist through application of TENS and using Binder Straps over
the suture line.
• A two pole, portable, battery operated TENS unit with four electrodes
may be used.
• The dressing is removed exposing the suture. The suture line and the
surrounding area are cleaned with surgical alcohol. This removes any
grease and exudates crust from the wound.
• Sterile, single use adhesive electrodes are used for this kind of application.
The electrodes are positioned on either ends of the suture line, one pole
on each side. Self-adhesive electrodes can be left in position for 3 weeks
at a stretch and used repeatedly.
• TENS with high frequency (150-300 Hz) and low intensity may be given
in case of mild to moderate pain. In severe pain, low frequency (10-50
Hz) TENS at high intensity close to pain threshold is recommended. TENS
may be applied for 8- 12 hours per day, for as many days as the pain
remains.
• TENS is most effective in patients who have not received narcotic analgesics
in the postoperative phase. TENS can, however, be given in conjunction
with NSAIDs.
• Elastic binder straps are recommended for supporting the suture in
thoracic and abdominal surgery. These straps minimize movement
between the flaps of the suture and thus reduce pain. Binder straps also
give a sense of security to the patient and reduce their apprehension that
the suture may open if they take a deep breath or cough hard, hence
ensure better compliance to breathing exercises, forced expiration, etc.
B. Positioning the patient accurately after surgery supports the suture
thus reducing pain, ensures free drainage, prevents alveolar hypostasis and
relaxes the patient thus ensuring better exercise tolerance. Positioning on
bed may be done using pillows and rolls.
• In thoracotomy the patient is usually positioned in side lying, with the
operated side uppermost. This prevents kinking of the drainage tubes
and allows the remaining portion of the operated lung to expand fully.
• In pneumonectomy the patient is positioned either in half lying with the
head end propped up to 45° or in side lying with the sound side uppermost.
This position ensures that the bronchial stump of the removed lung is not
soaked in postoperative exudates allowed to collect in the empty space
left by the excised lung. The postoperative exudates are rich in proteolytic
enzymes and any soakage of the bronchial stump may result in dissolving
of the cat gut sutures at the end of the bronchial stump. Opening of the
bronchial stump will result in siphoning of the surgical exudates to the
sound lung, creating serious respiratory complications. This is known as
Bronchopulmonary fistula.
• In abdominal surgery the preferred position is crook lying, with the head
elevated to 30° and the hip-knee flexed at 15° respectively. This ensures
that the abdominal wall remains relaxed and the patient is able to practice
deep breathing and coughing without severe pain.
C. Deep breathing exercises must be taught to the patient thoroughly
before the operation, so that the patient is able to do these exercises even in
spite of postoperative pain and drowsiness after anesthesia.
• Diaphragmatic breathing must be done with the suture line being supported
by the binder strap. In addition the therapist may stand facing the patient,
slightly away on one side, supporting the suture, placing hands on either
side of the suture line in a firm, gentle hold, approximating the ends of
the suture towards each other. This kind of hand hold reduces the pain
further and instills confidence in the patient.
• Costal and segmental breathing may also be practiced in similar manner

or using pillow support over the painful segment of the chest wall.
• End inspiratory breath holding should be encouraged in all postoperative
cases except in where pneumothorax is suspected.
D. Assisted coughing may be given, with the patient in upright position,
in severe cough inhibition. It is a common complication following any general
anesthesia and due to pain following thoracic and abdominal surgery. Care
must be taken not to press hard on the suture line during the maneuver.
E. Postural drainage is frequently used following Thoracic and abdominal
surgeries to remove excess secretion from the lungs. However, if the vital
signs are unstable following surgery, it should be withheld till the patient
stabilizes. Percussion should not be done over the suture line, and the drainage
tubes must be clamped before changing the position of the patient. Unclamped
drainage may lead to siphoning of the contents of the drainage bottle into
the lungs / abdomen if the bottles ever reach a position higher than the
patient.
Inhaled oxygen will often need to be given through a light plastic facemask
or nasal cannula, particularly to prevent desaturation during chest PT. In
severe respiratory compromise, non-invasive positive pressure ventilation
(Bi-PAP) may be recommended. This device forces oxygen into the lungs
under pressure through a sealed mask covering the mouth and/or nose. This
helps to expand the lungs better.
F. Early activation is the buzzword in present day technology intensive
and high cost health care system. The physiotherapist from the outset should
try to improve the exercise tolerance of the patient at the earliest, so that the
hospital stay can be minimized. To achieve this, from the day one after the
surgery, the patient should be encouraged to turn in bed independently and
be propped up to a sitting position on the bed. The patient may be allowed
to sit with legs out of bed on day two, be allowed to stand on day three, walk
few steps around the bed on day four, and walk along the hospital corridor
on day five and so on. Sutures are usually removed on the seventh day and
the patient allowed to go home. This plan may be followed in most of the
abdominal and thoracic surgery cases, except where forbidden by the surgeon
due to so due to presence of complications.
What is the prognosis of postoperative chest complications?
It may take a couple of months before the patient feels back to normal again
but most people have no long-term after effects. Occasionally, the chest
infection may turn very serious and respiratory failure may appear. This is
most likely in patients with pre-existing lung disease or in heavy smokers or
with severe debility. In such cases it may be necessary to perform endotracheal
intubation and use a positive pressure ventilator. This is done in the intensive
care unit (ICU), with the patient under general anesthesia. This is a life-
threatening situation and fatalities are common from this kind of serious
chest infection.
What precautions should be taken to prevent a chest infection?
Good pain relief after surgery is important to make sure that the patient can
breathe and cough easily.
Preoperative evaluation of the patient’s respiratory ability and training to
achieve the best possible conditioning before surgery always help.3 In a smoker,
the most useful thing to do is to stop smoking at least six weeks before operation
to get the full benefit of stopping.4
REFERENCES
1. Hall JC, et al. A multivariate analysis of the risk of pulmonary complications after
laparotomy. Chest 1991;99:923–27.
2. Arozullah AM, et al. Development and validation of multifactorial risk index for
predicting postoperative pneumonia after major noncardiac surgery. Ann Intern
Med 2001;135:847–57.
3. Smith AF. Postoperative pulmonary infection. In: Clinical Evidence, Issue 13. BMJ
Books, London 2004.
4. Bluman LG, et al. Preoperative smoking habits and postoperative pulmonary
complications. Chest 1998;113:148–52.
CHAPTER EIGHT
Management of
Respiratory Emergencies
Respiratory failure is an emergency situation characterized by impairment of

gas exchange between atmospheric air and circulating blood, resulting in a
failure in the movement of gases in and out of the lungs.
In intrapulmonary gas exchange, oxygen is transferred to arterial blood
(oxygenation) and carbon dioxide eliminated from it. Impaired gas exchange
in the lungs usually results in primary hypoxemia, because the carbon dioxide
can diffuse out much faster than that of Oxygen can be absorbed into the
blood.
Further, reduced respiratory effort due to fatigue, postoperative/pleural
pain, COPD or RLD, may cause inadequate alveolar ventilation, leading to
carbon dioxide retention, producing primary hypercapnia, although
hypoxemia occurs as well.
In many disorders simultaneous hypoxia and hypercapnia may occur,
but selective or disproportionate impairment of one or the other is more
common.
HYPOXEMIA
The following mechanisms may act alone or together to cause arterial
hypoxemia:
• A decrease in the partial pressure of inspired O2
• Hypoventilation
• Impaired diffusion
• Regional ventilation/perfusion (V/Q) mismatching
• Shunt (the direct bypass of systemic venous blood to the arterial
circulation)
• The admixture of abnormally de-saturated venous with arterial blood.
HYPERCAPNIA
Hypoventilation is the most common cause of hypercapnia. Major
mechanisms that can cause or contribute to hypercapnia are:
• Insufficient respiratory drive,
• Defective ventilatory pump,
• Increased workload of breathing leading to respiratory muscle fatigue
• Intrinsic lung disease with severe V/Q mismatching. The last two
mechanisms often coexist.
Hypoventilation is inadequate ventilation. The lungs just can’t draw in
enough air to effect sufficient exchange of gases.
Hypoventilation can be due to:
• Decrease in total minute ventilation; often called global hypoventilation
• Increase in dead space ventilation
• Drug overdose suppressing the brainstem respiratory centers
• Wasted ventilation, occurs when lung regions are well ventilated but under
perfused with blood
• Wasted perfusion, when well-perfused alveoli are ventilated with gas that
contains a high fraction of CO2
• Shunt, when well perfused alveoli do not receive any air at all. Such
regions eliminate less than their normal share of CO2.
Etiology
Respiratory failure, resulting in hypoxemia and/or hypercapnia may be caused
by airway obstruction; dysfunction of lung parenchyma; and ventilatory pump
failure.
Airway obstruction caused by COPD and dysfunction of lung parenchyma
resulting from RLD have been dealt with in great detail in Chapters 3 and 6
of this volume. Ventilatory pump failure may be caused by
1. primary dysfunction of the CNS respiratory centers
2. dysfunction of the ventilatory neuromuscular apparatus, or
3. Structural abnormalities of the chest wall that prevent effective transmission
of respiratory muscle forces, e.g. disorders like flail chest, kyphoscoliosis.
Hypoventilation can also occur when the inspiratory muscles of the
diaphragm and rib cage contract asynchronously as in diaphragmatic paralysis,
quadriplegia, or acute CVA.
Acute hyperinflation of the lungs severely reduces the efficiency of the
ventilatory pump even when the strength of individual muscle fibers remains
normal. Not only are the inspiratory muscle fibers fore-shortened, producing
less force, but also the muscle work is increased due to reduced compliance
of the lung.
Management of Respiratory Emergencies 151
Signs and Symptoms

The clinical signs and symptoms of respiratory failure are nonspecific and
may be minimal even when hypoxemia, hypercapnia, and respiratory acidosis
are severe. The fatigue of ventilatory muscles is the most easily detected sign
of impending or ongoing respiratory failure.
The primary physical signs of ventilatory fatigue are:
1. Vigorous use of accessory ventilatory muscles
2. Persistent tachypnea and tachycardia
3. Declining tidal volume
4. Irregular or gasping breathing patterns
5. Paradoxical abdominal motion.
In addition, acute hypoxemia may cause cardiac arrhythmia, altered
consciousness, confusion and coma.
Chronic hypoxemia is generally well tolerated by patients with adequate
cardiovascular reserve and does not have any dramatic presentation.
However, if the hypoxemia has been building up over long period of time
and the patient has PaO2 < 60 mm Hg over prolonged period, pulmonary
arteriolar vasoconstriction and increase pulmonary vascular resistance will
lead to pulmonary hypertension, right ventricular hypertrophy (Cor
pulmonale), and eventual right ventricular failure.
The effects of acute hypercapnia are much less well tolerated than those
of chronic hypercapnia. Acute hypercapnia may cause changes in sensorium,
ranging from personality changes, headache, confusion and drowsiness.
Diagnosis
• Blood gas measurement (PaO2, PaCO2, and pH value of arterial blood) is
the main tool for diagnosing and judging the severity of respiratory failure.
In many cases, it must be repeated frequently to assess deterioration or
improvement.
• Neuromuscular function is evaluated by observing the breathing pattern
and measuring vital capacity, tidal volume, breathing frequency, and
maximal inspiratory pressure. The ratio of breathing frequency to tidal
volume is particularly helpful; > 100 breaths/min/L indicates severe
weakness or fatigue.
• The intensity respiratory distress is assessed by looking at the respiratory
rate (+ if > 30/min), vigorous use of accessory ventilatory muscles,
paradoxical abdominal motion.
PRIMARY TREATMENT OF RESPIRATORY FAILURE
The primary aims of management in respiratory failure are:
• To maintain adequate O2 supply to lungs
• To reduce workload of breathing
• To maintain electrolyte and pH balance
• To prevent further damage to the lungs from O2 toxicity, baro-trauma,
infection, or other iatrogenic complications.
Complications of respiratory failure are atelectasis, fluid overload,
bronchospasm, increased secretions, and chest infection respond to specific
treatment like breath holding and single clap technique, diuretics,
bronchodilators, mucolytics, humidification, postural drainage and antibiotics.
O2 THERAPY
Respiratory distress and failure is best managed by increasing the amount of
inspired oxygen, if wasted ventilation / perfusion is not the cause of hypoxemia.
The goal of supplemental oxygen therapy is to increase oxygen saturation of
hemoglobin to at least 85 to 90%.
Many patients with chronic hypoxemia tolerate a PaO2 < 55 mm Hg;
even though PaO2 between 60 and 80 mm Hg is usually desirable for adequate
O2 delivery to tissues and for reducing pulmonary hypertension induced by
hypoxemia. The minimum flow rate of oxygen that provides an acceptable
PaO2 should be selected.
In COPD, maximum flow rate of oxygen(FlO2) at 40% of the inspired air
usually suffices. Any more oxygen content in the inspired air will lead to
oxygen toxicity. Oxygen toxicity can occur with higher concentration or due
to prolonged duration of exposure to supplemental oxygen. Sustained
elevations in oxygen flow result in inflammatory changes, alveolar infiltration,
and, eventually, pulmonary fibrosis. Oxygen can be given via nasal cannula
or a face mask. With a face mask, the flow of oxygen at 2 to 4 L/min ordinarily
can raise PaO2 to therapeutic levels.
Excessive oxygen administration is a common cause of respiratory
depression in the management of COPD with CO2 retention. In such patients
with chronic hypercapnia, the respiratory center may become insensitive to
changes in PaCO2 and respond primarily to hypoxic stimuli. If concentration
of oxygen in blood rises excessively, the hypoxic ventilatory drive is obliterated,
and as a result more CO2 retention may take place with worsening respiratory
acidosis.
MECHANICAL VENTILATION
Indications for Commencing Mechanical Ventilation
There are three reasons for commencing mechanical ventilation:
• Airway protection—e.g. in unconscious patients following a head injury
• Ventilation failure—stroke, myasthenia gravis, Guillain-Barre syndrome,
etc.
• Oxygenation failure—which is caused by either increased dead space
ventilation (pulmonary embolism/hypovolemia) or increased shunt
(pneumonia, ARDS, pulmonary edema).
A number of criteria are conventionally given to help decide on whether
or not to ventilate patients:
1. Respiratory rate >35 breaths/minute.
2. PaCO2 >55 mmHg (acute retention, respiratory acidosis).
3. PaO 2 <70mmHg on 100% oxygen or an AO 2 -aO 2 gradient of
>400mmHg.
4. Severe head injury - control of CO2
5. Airway protection / bronchopulmonary toilet.
The patient in case 2 requires ventilation on the basis of deteriorating
blood gases (respiratory failure). The third patient requires intubation for
airway protection, and for controlled ventilation with 100% O2 to reduce the
carboxyhemoglobin load.
Positive Pressure Mechanical Ventilation

Positive pressure ventilation consists of specialized techniques for
increasing mean alveolar air pressure to reopen closed alveolar units, thereby
reducing right-to-left shunt, promote better oxygenation, get rid of trapped
carbon dioxide and reduce the need for supplemental oxygen.
Air is forced into the lungs using different types of positive pressure
ventilation, which are Continuous positive airway pressure (CPAP), Bi-
level positive airway pressure (Bi PAP), Positive end-expiratory
pressure (PEEP).
Continuous Positive Airway Pressure (CPAP)

It is a non-invasive technique that uses a sealed face mask (Fig. 8.1), recruits
lung volume and often improves the PaO2/FIO2 ratio. Air is forced into the
lungs at a preset pressure, which is slightly above the inspiratory suction
force generated by the patient. Such ventilatory support reduces work-load
on muscles of respiration and pneumatically splints the floppy terminal airway
so that they can be kept open till full expiration can occur. It is most often
used in patients needing mild to moderate ventilatory support, e.g. acute
atelectasis or pulmonary edema. The disadvantage of CPAP is that it can
interfere with relaxed passive expiration till the end of the cycle. This
continuous positive pressure at times leads to pressure damage to delicate
lung tissue (Baro-trauma).
Bi-level Positive Airway Pressure (Bi-PAP)

Bi-PAP, applied in the same way as CPAP, varies airway pressure about two
different levels of ventilatory cycle, a higher pressure during inspiration to fill
the lungs with air and a lower positive pressure during expiration to keep the
terminal airways splinted open so that all the dead gas from the alveolar
space can be expelled, accomplishing both ventilatory assistance and higher
end-expiratory lung volumes. Bi-PAP is most commonly used as a partial
ventilatory support device, to reduce the workload of breathing in acute
exacerbations of COPD. It can also be used as a step down measure leading
up to weaning of mechanical ventilatory support. To use Bi-PAP successfully,
the patient must have some ventilatory effort remaining. The ventilatory
capacity of the patient can be further built up by breathing exercises, done
while under Bi-PAP support. Respiratory failure usually gets worse at night
during sleeping. This occurs because many patients who can breathe on
their own and keep good oxygen saturation when awake, tends to de-saturate
FIGURE 8.1: The sealed face mask for of CPAP or Bi-PAP ventilation
when they fall asleep. In such cases Bi-PAP support is prescribed during sleep,
mostly from 9 p.m. to 6 a.m. to ensure that critical desaturation does not
take place during sleep and the patient has restful slumber without fighting
for breath.
Positive End-Expiratory Pressure (PEEP)

Positive end-expiratory pressure (PEEP) is recommended for all patients
of respiratory failure who are unable to sustain voluntary ventilation. PEEP
at low levels (3 to 5 cm H2O) can benefit virtually all intubated, mechanically
ventilated patients with respiratory failure. Positive end-expiratory pressure
(PEEP) helps compensate for the volume loss that accompanies the supine
posture and endotracheal intubation. The patients under PEEP are usually
sedated to the levels of deep sleep so that they do not fight the forces generated
by the ventilator. Volume-recruiting effects and ability of the PEEP to improve
the PaO2 can be nullified if vigorous expiratory muscle contraction forces
lung volume to lower than the relaxed end-expiratory (equilibrium) position.
When this breathing pattern is evident, sedation or paralysis can help.
The optimal level of PEEP to be used produces function of tidal volume.
Higher levels of PEEP are usually required with small tidal volumes (< 7 mL/
kg). PEEP may need to be more than 15 cm H2O to effect acceptable arterial
oxygenation at a well-tolerated flow rate of oxygen. When pulmonary
infiltration is predominantly unilateral, delivering the same level of PEEP to
both lungs may be ineffective, because it diverts blood from the healthy lung
to the diseased one. With independent lung ventilation, the pattern of lung
inflation, flow rate of oxygen, and PEEP may be tailored to each lung.
OTHER SUPPORTIVE MEASURES FOR MANAGEMENT OF

RESPIRATORY FAILURE
Some supportive measures that do not directly interfere with ventilation can
help compensate for impaired gas exchange.
Optimizing hemoglobin (Hb) concentration in blood can improve
its oxygen carrying capacity, although if the hematocrit becomes too high
(Polycythemia), oxygen delivery to the tissue can be impaired due to increased
blood viscosity. Although controversial, the optimal Hb for most acutely ill
patients with severe hypoxemia may be in the range of 10 to 12 g/dl. Blood
transfusion is a valuable component to correct anemia in patient on ventilatory
support.
Reducing tissue oxygen requirement can be equally effective in
improving oxygen delivery to the tissue. Since fever, agitation, overfeeding,
vigorous respiratory activity, shivering, sepsis, burns, tissue injury, seizures,
and other common clinical conditions increase oxygen consumption,
aggressive steps should be taken to control these symptoms. Sedation and
pharmacologic paralysis reduce oxygen consumption in patients who remain
agitated or those who fight the ventilator. However, prolonged paralysis must
be avoided because it silences the cough mechanism, creates a monotonous
breathing pattern that encourages secretion to collect in the dependent regions
of the lungs and may produce muscle weakness and atrophy due to disuse.
Maintaining cardiac output by the appropriate use of intravenous
fluids and ionotropic drugs is crucial in the treatment of hypoxemia. In many
lung conditions extra-vascular water tends to accumulate readily in the lungs.
Fluids should therefore be used judiciously. A delicate balance must be
maintained because severe fluid restriction, although often reducing lung
water and improving oxygen exchange, may compromise perfusion of the
gut, kidneys, and other vital organs leading to irreversible damage.
Assisting failing circulation, whether from cardiac or non-cardiac
causes, using measures that include fluid manipulation, ionotropic drugs,
and reduction of O2 consumption, may help correct a low PaO2. In patients
with pulmonary edema, diuretics and other measures may help mobilize
extra-vascular lung water, thereby increasing lung compliance, reducing
cardiac asthma, and lessening the workload of the respiratory muscles.
Relieving cardiac ischemia, lessening left ventricular afterload, or using a
calcium channel blocker may decrease pulmonary vascular congestion and
hypoxemia in patients with diastolic cardiac dysfunction.
Corticosteroids benefit patients with acute asthma or an exacerbation
of COPD. However it is not used routinely for diffuse parenchymal pulmonary
diseases, pulmonary edema, or ARDS. The increased catabolism, protein
wastage, and risk of infection arising from corticosteroids far outweigh the
potential therapeutic benefit in the first phase of respiratory failure.
Nonetheless, certain patients like those with vasculitis, fat embolism, acute
eosinophilic pneumonia, or allergic reactions contributing to hypoxemia may
benefit from corticosteroids.
Position changes may be beneficial. The change from the supine to
upright position produces an increase in lung volume equivalent to about
5 to 12 cm H2O PEEP, depending on thoracic compliance. Whenever
possible, recumbent bedridden patients should be turned often every two
hours, especially during coma or induced paralysis. Alternating side lying
positions maximally stretches different regions of the lung and improves
drainage of secretion. When one lung is affected disproportionately,
oxygenation may improve dramatically when the good lung is in the lowermost
position in side lying. However, care should be taken to ensure that secretions
from the infiltrated lung are not aspirated into the airways of the sound lung.
Furthermore, certain patients with ARDS undergo marked oxygen
desaturation when repositioned for reasons that are poorly understood. The
prone position is often dramatically effective in the early stages of ARDS.
Although the reason for this response is not completely understood,
redistribution of resting lung volume with expansion of the dorsal areas is
likely to be the primary benefit.
Clearing secretions from upper and lower airways is crucial for proper
air entry and gas exchange. Oral or intravenous hydration may help keep
secretions adequately liquefied. Occasionally, mucolytic drugs like potassium
iodide preparations, acetylcysteine are used if secretions remain tenacious
despite adequate hydration and humidification of inspired air. Antibiotics
and corticosteroids may help reduce the volume of secretions in most patients.
Establishing Artificial Airway

If the patient’s own coughing efforts are ineffective, chest physiotherapy
techniques like positioning, chest percussion and assisted coughing may be
helpful to mobilize the secretions. However, secretions retained in the upper
airway must be removed by suctioning through an oral-pharyngeal airway
tube (Fig. 8.2).
FIGURE 8.2: Oral pharyngeal airway tube: Utilizes a dual channel design that
permits access of a suction catheter even if the airway shifts or is partially
occluded, making resuscitation less cumbersome. Rigid bite block helps keep the
victims airway from collapsing, insuring unobstructed ventilation
An oral-pharyngeal or a nasal pharyngeal tube (Fig. 8.3) is introduced

through the mouth or the nose respectively to provide an unobstructed
FIGURE 8.3: Soft plastic nasal airways

made of soft material that provides
greater patient comfort
pathway to the lower reaches of the pharynx. Secretions in the lower airways
can be sucked out through a catheter introduced through the oral / nasal
pharyngeal tube, past the vocal cords via the nose or mouth (Fig. 8.4)
FIGURE 8.4: Technique of introducing an oral-pharyngeal airway
If this method is unsuccessful or the lower airway secretions are too

copious, an artificial airway through an endotracheal tube or tracheostomy
is usually required. Criteria for intubation and mechanical ventilation include
progressive respiratory acidosis, hypoxemia, and circulatory dysfunction. For
short periods, an oral or nasal endotracheal tube can be used; if suctioning is
required for prolonged periods, a tracheostomy may be necessary.
Moistening all inspired gas mixtures delivered to the trachea helps
ensure the reduced viscosity of secretions. Oxygen has severe drying effect
on the airway mucosal membrane. Supplemental oxygen should always be
moistened by bubbling it through water using a Wolfe’s bottle. A heated
humidifier attached to a ventilator moisturizes the inspiratory air stream most
effectively; alternatively, hygroscopic disposable humidifiers (artificial noses)
can be placed in the common channel of the ventilator circuit to recover
exhaled moisture and return it to inhaled air.
Bronchodilators are indicated when bronchospasm and bronchial

mucosal edema are factors contributing to hypoxia. Airway resistance can be
decreased and gas exchange improved by beta-adrenergic or anti-cholinergic
drugs given as aerosols and by Theophylline derivatives or Corticosteroids
given orally or through intravenous route. Nebulizers driven by pressurized
gas is used to deliver inhaled medication, which may be attached to a
mechanical ventilator through a T piece. Metered-dose inhalers can be used
with or without a ventilator.
Antibiotics with broad spectrum coverage are routinely given to control
infection in patients under ventilatory support. This is done to forestall any
opportunistic secondary infection since such patients are particularly vulnerable
due to lowered immunity and invasive treatment measures to the respiratory
tract.
Precautions to be Taken While Managing Respiratory Failure

• In patients with acute lung injury/disease, positive airway pressure,
supplemental oxygen, vasopressor and vasodilator drugs are potentially
dangerous. Hence, the need for and the level of ventilator support, and
the flow rate of oxygen should be frequently reassessed.
• Mean intra-thoracic pressure can often be reduced by allowing the patient
as much ventilatory support as is comfortable, using intermittent positive
pressure ventilation.
• Semiconscious, agitated, confused, or disoriented patients under
mechanical ventilation must be restrained and sedated, because abrupt
ventilator disconnection and accidental extubation can rapidly produce
lethal bradycardia, arrhythmia, hypoxemia, asphyxia, or aspiration of
gastric contents.
• In patients with pulmonary edema, the interruption of PEEP for even
brief periods during suctioning or physiotherapy may cause profound
desaturation that is difficult to reverse because the lung volume falls and
the airways flood with edematous fluid. Bagging the patient continuously
with 100% oxygen during suctioning and physiotherapy is therefore
essential.
• Paralyzed patients must be carefully monitored because ventilation is totally
machine-dependent. Because air swallowing and paralytic ileus are
common, the stomach should be periodically decompressed with a flatus
tube in most recently intubated patients. The clinician must be ready to
decompress a lung tension cyst or a spontaneous pneumothorax as soon
as they appear.
TYPES OF MECHANICAL VENTILATION
In modern clinical practice, Positive Pressure Ventilation (PPV) is the only
form of support for acute respiratory failure. Ventilators that apply negative
pressure to the chest, e.g. iron lungs, poncho-wrap, etc. are not used these
days because they require a rigid structural support to create a vacuum
compartment enclosing the thorax and abdomen, that greatly impedes
intensive care nursing.
Before instituting mechanical ventilation, the clinician must select the mode
of ventilation, i.e.:
1. The type and frequency of machine-supported ventilatory cycles
2. The flow rate of oxygen to be delivered
3. The sensitivity of the machine to patient efforts, and
4. The level of PEEP to be applied.
The essential components of mechanical ventilations are specific volume
of air being pushed in to the lungs at specific pressure within a specific time
period completing the cycle of inspiration and expiration. Hence, Ventilator
cycles can regulate either by pressure generated or flow rate and may be
cycled based on air pressure / volume / flow time.
Pressure-cycled ventilators are simple in design and low in cost.
However, because the tidal volume delivered during each respiratory cycle
depends on the duration of the inspiratory phase and the impedance to the
airflow due to airway resistance or loss of lung compliance, these ventilators
do not reliably provide a specified tidal volume or minute ventilation. Their
use is confined to non-intubated patients requiring air splinting of terminal
airway or large tidal volumes to reverse atelectasis.
Volume-cycled ventilators have been since long, the standard type of
ventilatory support for all forms of severe respiratory failure. All modern
ventilators can provide volume cycled ventilation, as well as, several other
modes ventilatory support that vary in waveform, cycles, percentage of
support provided, and method of terminating the machine-aided cycle. For
most patients with moderate respiratory dysfunction, who can tolerate a
pressure sealed nasal or face mask, ventilation can be accomplished without
endotracheal intubation.
Full ventilatory support is designed to perform the complete work of
breathing and attempts to provide an adequate tidal volume at a specified
frequency. Flow-regulated volume-cycled breaths are the standard. The
clinician selects the desired tidal volume, inspiratory flow waveform, e.g.
constant or decelerating, and peak flow rate. Once these are selected, peak
airway cycling pressure varies depending on the impedance to inflation and
end-expiratory alveolar pressure. When the pressure-regulated, time-cycled

variant pressure-controlled ventilation is used, the pressure and inspiratory
duration are selected and tidal volume is allowed to vary with inflation
impedance. Either type of cycle can be set to occur at a fixed rate for
controlled ventilation or allowed to vary in response to patient effort for
assisted ventilation. A backup frequency rate is specified to trigger the machine
into full ventilatory if the patient fails to generate required rate or pressure
through the mask or mouthpiece to trigger the machine cycle.
Partial ventilatory support is indicated during the process of withdrawal
or weaning from mechanical ventilation, when the patient can comfortably
perform a portion of the breathing workload without distress. Assistance can
be provided for every spontaneous breath with pressure support, a flow-
cycled technique that rapidly builds airway pressure to a fixed level with
every breath. High or low levels of assistance can be provided, depending
on the minimum inspiratory pressure selected. On latest equipments, the
shape of the pressure waveform and the flow off-switch criterion can be
adjusted. Pressure support helps to overcome endotracheal tube resistance,
which can be surprisingly high during respiratory failure. When the appropriate
level of pressure is given, pressure support tends to be comfortable in that
the patient has some control over the flow profile and cycle duration.
Synchronized intermittent mandatory ventilation uses either flow-regulated,
volume-cycled or pressure-regulated, time-cycled breaths to provide the
machine support at a frequency determined by the clinician. The level of
support is varied not by adjusting the cycle characteristics but by adjusting
the number of machine-aided cycles. This type of ventilation is often combined
with pressure support to achieve optimum patient comfort during weaning.
Other forms of less commonly used mechanical ventilation like high-
frequency ventilators (jet or oscillators) cycle small pulses of gas rapidly,
achieving gas exchange with very small excursions of tidal volume. Their
usefulness has been limited in adult patients with respiratory failure, in part
because establishing adequate gas exchange is largely an empiric process
requiring considerable operator skill. Inverse ratio ventilation prolongs the
inspiratory phase to occupy 50% or less of the inspiratory cycle, thereby
raising mean alveolar pressure and slowing end-inspiratory flow. This type of
ventilation is usually used with sedation and paralysis as supportive therapy
for failure of oxygenation. Some of the newest modes regulate the degree of
partial ventilatory support to satisfy tidal volume and/or minute ventilation
criteria with the least required pressure. PEEP can be added to the systems
that provide high-frequency or inverse ratio ventilation as well as to all
conventional modes of ventilation.
COMPLICATIONS OF MECHANICAL VENTILATION
• Any mechanical ventilator may decrease venous return to the thorax,
cardiac output, and systemic BP, especially if the driving pressure into the
lung is high. These problems are likely to occur with high inspiratory
pressure, hypo-volumic lungs, and inadequate vasomotor control due to
drugs, peripheral neuropathy, or muscle weakness.
• Baro-trauma or damage to the lung induced by high cycling pressures,
may take the form of tissue rupture creating pneumo-mediastinum,
pneumothorax, subcutaneous emphysema, systemic gas embolism,
parenchymal lung injury (broncho-pulmonary dysplasia), or pulmonary
edema.
CHEST PHYSIOTHERAPY IN INTENSIVE CARE UNIT

Intensive care units (ICUs) are sections in hospitals that contain specialized
equipment and highly trained staff to treat patients who have a serious illness
or injury. Patients may be admitted to the ICU from an emergency department
or other hospital section, after surgery, or after transfer from another health
care facility.
• Monitors measure body functions such as breathing and heart rate. They
often have alarms that sound to alert the ICU staff when such functions
are outside of a normal range.
• Intravenous catheters (tubes) are inserted in patients’ veins to dispense
medicine, fluids and nutrition as needed. A nasogastric tube may be inserted
through the nose into the stomach. Urinary catheters are used to drain
urine from the bladder.
• Mechanical ventilators (also called respirators) are machines that help
patients breathe through a tube that is inserted through the mouth or
nose into the trachea (windpipe) and is connected to the ventilator (Fig.
8.5).
DISORDERS THAT MAY BE TREATED IN THE ICU

• Acute respiratory distress syndrome (ARDS) is sudden lung failure that
often requires use of a ventilator. It is caused by other illnesses such as
infections or serious injuries.
• Asthma involves obstruction of the airways that causes difficulty breathing,
wheezing, chest tightness and coughing.
• Chronic obstructive pulmonary disease (COPD) makes exhaling difficult.
It is usually caused by smoking-related lung disorders such as emphysema
and chronic bronchitis.
FIGURE 8.5: Equipment commonly used in the ICU
• Pneumonia is an infection of the lungs that may interfere with breathing.

• Respiratory distress syndrome can occur in infants whose lungs are
underdeveloped, causing difficulty breathing.
• Sepsis is a very serious infection in the blood or tissues.
• Trauma involves injuries, such as from motor vehicle crashes often require
surgery.
Staff in the ICU

• Physicians: Critical care doctors are trained in all aspects of the care of
critically ill patients.
• Nurses: ICU nurses have specialized training in caring for critically ill patients
and provide around-the-clock bedside care and monitoring.
• Respiratory therapists: Monitor patients’ respiration (breathing) and use
equipment, such as respirators, required to improve breathing.
• Physical therapists: Help patients maintain flexibility and muscle strength
to prevent disability and speed recovery.
• Nutritionists: Assess the food and fluid needs of patients.
• Social workers: Help patients and families deal with various aspects of
critical illness, including psychological and financial issues, and help with
recovery after discharge from the hospital.
• Pastoral care staff: Provide spiritual and emotional support for patients
and family members.
INTUBATION FOR MECHANICAL VENTILATION
What is an ET Tube?
An endotracheal tube or an ET tube is a flexible, with an inflatable cuff at the
middle and bevel shaped distal end that goes between the vocal cords and
into the trachea. “Intubated” is the word that means “placing a tube down to
the lungs.” Patients are unable to talk or eat or drink with this tube in.
The “cuff” or balloon at the end of the tube does not allow air to pass
through the “voice box” (vocal cords), mouth, or nose, so the patient cannot
talk. The tube also blocks the epiglottis which is a flap-like tissue that prevents
fluids or food from going into the lungs (Fig. 8.6). For this reason, the patient
is not allowed to drink or eat. Children 2 years old and younger do not have
a cuff or balloon on the end of the endotracheal tube.
After approximately 2-3 weeks of intubation, if the patient still needs
breathing assistance from the ventilator, or if the doctor does not think that
the person will be able to breathe or cough well enough without help, a
“tracheostomy” may be ordered.
FIGURE 8.6: The correct position of an ET tube in the airway;

showing the location of cuff at the middle of trachea
ENDOTRACHEAL TUBES
• There are a number of different types of endotracheal tubes.
• The commonest type is a plastic curved tube with a cuff which is fixed to
the outer surface of the distal end (Fig. 8.7). The cuff is inflated with air to
provide a seal between the tube and the inner lining of the trachea.
There is a small indicator balloon which is attached by a small tube to the
endotracheal tube. This serves to indicate whether the cuff is inflated or
deflated.
FIGURE 8.7: A cuffed endotracheal tube; note the nozzle for air pressure
inflatable bulb at the top, connected to the inflatable cuff at the lower end
• This is the size of the tube in the internal diameter indicated on the side:
e.g. 8.0 = 8 mm internal diameter. Smaller tubes produce increased
resistance to gas flow. Larger tubes may damage the trachea. Hence,
selecting an optimum size is essential for adequate air delivery, as well as,
patient safety. For most women a size 7.5 ET will suffice, and a size 8.0 –
8.5 for most men. The 7.5 ET will actually work well for most patients.
• These tubes are usually measured and cut at their distal ends so that they
don’t slip too far down and enter one of the main bronchi, thus ventilating
only one lung.
• For most women the length tube is sited at 19 – 20 cm from lip level. For
most men this is 21 – 23 cm.
• Longer tubes may sometimes be introduced under X-ray guidance for
preferential ventilation of one lung only.
Other Types of Endotracheal Tubes

• Uncuffed tubes: used in children under the age of 12. This is because
in children the airway is narrowest just below the glottis, and it is essential
that the fit is not too tight leading to ischemic necrosis of the mucosal
lining (Fig. 8.8). When intubating a child there must always be an audible
leak of air.
FIGURE 8.8: An uncuffed ET tube
• Reinforced tubes: These are used under certain circumstances in operation

theatre where there is concern that the ET tube may be damaged or
kinked. The tube contains an internal metal ring that looks like a spring.
The problem with these tubes is that they cannot be cut.
• Double lumen tubes: These are used in thoracic anesthesia, in order to
preferentially ventilate one lung and allow the other lung to collapse.
They are rarely used in ICU, the exception being in lung contusions,
where it may be impossible to ventilate the sick lung without damaging
the healthy one.
• South-facing tubes: These are used in ENT and dental surgery. They
have no role in ICU as suction can only be performed through them with
difficulty.
• North-facing tubes: These are used for nasal intubations in maxillo-facial
surgery. Again they have no role in ICU. Nasal intubations in ICU are
usually performed with standard ET tubes with smaller diameter.
Laryngoscopes
• Laryngoscopes are the instruments used for performing endotracheal
intubations. A laryngoscope consists of a blade, of varying sizes (1 to 4),
which includes a fiber-optic light source, and a handle, which contains
the battery power source for the light (Fig. 8.9).
• For most laryngoscopes the blade is curved. For small babies, one uses a
straight blade. This is because the technique for intubating infants is
different.
FIGURE 8.9: A laryngoscope
THE PROCESS OF INTUBATION

1. Head positioning: This is the single most important aspect from a nursing
point of view. The correct position for the head is “sniffing the morning
air”, with the neck slightly flexed and the head extended. One places a
pillow under the head and neck but NOT under the shoulders. This allows
a straight line of vision from the mouth to the vocal cords (Fig. 8.10).
FIGURE 8.10: The correct position of the head while

attempting intubation using a laryngoscope
2. The laryngoscope is introduced into the right hand side of the mouth,
held open by the left hand. The tongue is swept to the left and the tip of
the blade is advanced until a fold of skin/cartilage is visualized at twelve o’
clock position (Fig. 8.11). This is the epiglottis, and this sits over the glottis
or the opening to the larynx.
FIGURE 8.11: Position of the laryngoscope

while attempting ET intubation
3. The tip of the blade is advanced to the base of the epiglottis and the
entire laryngoscope is lifted upwards and outwards. This flips the epiglottis
upwards and exposes the glottis below. An opening is seen with two white
vocal cords forming a triangle on each side (Fig. 8.12).
FIGURE 8.12: View of the larynx seen using a laryngoscope
4. The tip of the endotracheal tube is advanced through the vocal cords
and once the cuff has passed through, one stops advancing. The tube is
secured at this level and the cuff inflated.
5. There are two types of cuff: high pressure-low volume (which takes 2-3
ml of air) and high volume-low pressure (30 – 50 ml of air). The principle
with both is the same: the cuff is inflated until the leak is abolished. Too
high a cuff pressure will cause ischemic necroses the tracheal mucosa by
cutting off its blood circulation and cause a tracheal stricture.
6. The tube may be secured in a variety of ways, all that is important is that
it is held tightly, and cannot slide up and down the trachea. It is preferable
to secure the tube to the upper jaw (the maxilla) than to the lower one
(the mandible) as this moves up and down.
7. It is usual to insert a naso-gastric tube for feeding at the same time as
intubation takes place.
8. It is worthwhile to suction out the lungs below the level of the tube
following intubation, and collect specimen of mucus for pathology testing.
The ET tube is then connected to the ventilator via a catheter mount.
Anesthesia for Intubation

• When anaesthetizing patients for intubation, anesthetists use “rapid
sequence induction”. The objective is to secure the airway rapidly and
prevent soiling of the lungs with gastric contents.
• The patient goes to sleep with the aid of an intravenous induction agent:
thiopentone or propofol. These cause hypnosis and amnesia. They cause
peripheral vasodilatation and a drop in the blood pressure.
Tracheostomy
Tracheostomy is an artificial surgical opening created in the trachea, just below
the larynx. The purpose of tracheostomy is to provide an alternative airway,
bypassing the upper respiratory tract. A tracheostomy is most commonly
done when the patient needs intubation for more than one week, because
endotracheal intubation through nose or mouth for more than one week
may cause irreversible damage to the walls of the pharynx and larynx. The
tracheostomy tube is much shorter than the ET tube (Fig. 8.13). It is secured
inside the trachea with an inflatable cuff and secured from the outside with
strips of adhesive Elastoplasts attached to the flanges at the top and the
margins of the tracheostomy incision. The tracheostomy may be connected
directly to an oxygen source or a mechanical ventilator. The tracheostomy
incision is kept open for the duration of the artificial airway being used. It is
closed by simple sutures after the tracheostomy tube has been removed.
The respiratory hygiene in a tracheotomy involves covering the tracheostomy
opening with sterile gauze soaked in sterile normal saline, when not connected
to the oxygen source or ventilator. The margins of the tube protruding out
of the trachea must be cleaned twice a day with normal saline and the gauze
pieces packed on the edges of the incision changed daily (Fig. 8.14).
FIGURE 8.13: A tracheostomy tube
FIGURE 8.14: Maintenance of tracheostomy
TECHNIQUE OF ENDOTRACHEAL SUCTION

The upper airway warms, cleans and moistens the air we breathe. The
endotracheal tube bypasses all these safety mechanisms, so that the air
available via the tube is cooler, dryer and not as clean. In response to these
changes, the body produces more mucus. The endotracheal tube is suctioned
frequently to remove mucus from the tube and trachea to allow for easier
breathing. Generally, the patient should be suctioned every 4 to 6 hours and
as needed. There may be large amounts of mucus with a new ET tubes or
tracheostomy. This is a normal reaction to irritation caused by the tube in the
airway. The heavy secretions should decrease in a few weeks. In the hospital,
suctioning is done using sterile technique; however a clean technique is usually
sufficient for most patients even at home. Frequency of suctioning will vary
from patient to patient and will increase with respiratory tract infections. Try
to avoid suctioning too frequently. The more you suction, the more secretions
can be produced.
SUCTION CARE TECHNIQUES

Sterile technique: Must be done using sterile catheters and sterile gloves
under complete aseptic conditions and barrier nursing. This is the most
appropriate technique for removing airway secretions to be used in an ICU,
when the patient is at high risk of cross infections and has poor immunological
defense.
Modified sterile technique: This technique is suitable for patients in high
dependence area, using sterile catheters and clean gloves.
Clean technique: Clean catheter and clean hands are sufficient for home
suctioning is patients with chronic retention of secretions.
Selecting the Appropriate Size of the Suction Catheter

The size of the suction catheter depends on the size of the ET / Tracheostomy
tube. Size 6, 8 or 10 French Units (1 French unit = 0.5 mm) are typical
sizes for neonatal and pediatric endotracheal suction tubes. The larger the
number, the larger the diameter of the suction catheter. It is wise to use a
catheter with an outer diameter that is about half the inner diameter of the
artificial airway (OP tube/ ET tube / Tracheostomy tube) as this will allow air
to enter around it during suctioning. One can also compute the catheter size
by multiplying the artificial airway’s diameter in millimeters by two. For
example, for an ET tube with 8 mm inner diameter; 8 × 2 = 16, a 16
French catheter should be used.
Suction Depths
Shallow suctioning: Suction secretions at the opening of the ET tube that the
patient has coughed up.
Pre-measured suctioning: Suction the length of the ET tube. Suction depth
varies depending on the size of the ET tube.
Deep suctioning: Insert the catheter until resistance is felt. Deep suctioning is
usually not necessary.
One should be careful to avoid vigorous and repeated suctioning, as this
may injure the lining of the airway and cause the patient to de-saturate
dangerously low. It is desirable to give the patient high flow 100% oxygen
few minutes before commencing suctioning and maintain the oxygen flow
rate during suctioning.
Signs that indicate the Patent needs Suctioning

• Rattling mucus sounds audible at the mouth
• Fast shallow breathing
• Bubbles of mucus in endotracheal airway opening
• Dry raspy breathing or a whistling noise from endotracheal airway
• Older children/adults may vocalize or signal a need to be suctioned.
• Signs of respiratory distress.
Equipments needed for Suctioning

• Suction machine: electrical or foot paddle operated
• Suction catheter connecting tubing
• Suction catheters
• Normal saline
• Sterile or clean sputum cup
• 3cc saline ampoules (“bullets”)
• Ambu bag
• Sterile tissues / Gauze
• Sterile disposable gloves (hand-care)
Steps to Perform Endotracheal Suction: A Pictorial Guide
FIGURE 8.15: Connect the sterile, flexible suction tube to the

connector attached to the end of the suction pipe
FIGURE 8.16: Dip the end of th suction catheter in sterile normal

saline to moisten it prior to commencing suction.
FIGURE 8.17: Semi-flexible suction catheters with bulbous ends

can be very handy to use, blunt end prevents trauma
FIGURE 8.18: Pathway of the suction catheter. A. Nasopharyngeal: through the nose up to
pharynx. B. Oropharyngeal: through the mouth up to the pharynx . C. Endotracheal : through
the nose upto the trachea
FIGURE 8.19: Disposing off used suction catheter; note how

the gloves are stripped off in inverted manner enclosing the
used catheter, ready for disposal with minimum contamination
Procedure for Suctioning (Figs 8.15 to 8.19)

• Explain procedure in a way appropriate for patient’s age and
understanding.
• Wash hands before commencing suctioning.
• Set up equipment and connect suction catheter to machine tubing.
• Pour normal saline into cup.
• Put on gloves (optional).
• Turn on suction machine (suction machine pressure for small children
50-100 mm Hg, for older children/adults 100-120 mm Hg).
• Place tip of catheter into saline cup to moisten and test to see that suction
is working.
• Instill sterile normal saline with plastic squeeze ampoule or syringe or eye
dropper into the ET / Tracheostomy tube if needed to moisten thick or
dry secretions. Use saline only if the mucus is very thick, hard to cough
up or difficult to suction. Recommended amount per instillation is
approximately 1-3 cc. Excessive use of saline is not recommended.
• Gently insert catheter into the ET / Tracheostomy tube without applying
suction. Suction only when the pre-measured suctioning length of ET
tube has been reached. Deeper insertion may be needed if the child has
an ineffective cough).
• Put a thumb over opening in catheter to create suction and twirl catheter
between thumb and index finger while withdrawing the catheter so that
the mucus is removed from the walls of the airway. If the catheter has
holes on all sides, twirling is not necessary.
• Avoid suctioning longer than 10 seconds because of oxygen de-saturation.
• Draw saline from cup through catheter to clear catheter.
• For ET tubes with cuffs, it may be necessary to deflate the cuff periodically
for suctioning to prevent pooling of secretions above ET cuff.
• Let the patient rest and breathe freely and then repeat suction if needed
at least after 30 seconds between suctioning.
• Oxygenate as appropriate. Extra oxygen may be given before and after
suction to prevent hypoxia.
• Some patients need extra breaths with an Ambu bag (approximately 3 -
5 breaths). Purposes of bagging are to induce hyper-oxygenation,
hyperinflation, and hyperventilation of the lungs. However, this is usually
not needed for stable patients with no additional respiratory problems.
• The patient’s mouth or nose may also be suctioned after suctioning the
ET / Tracheostomy tube.
• Dispose of the used catheter as shown. Do not put same catheter back
into the ET/ Tracheostomy tubes again.
• Dispose of saline and gloves, turn off machine.
• In home care, catheters may sometimes be used more than once before
disposal or cleaning if the patient needs frequent suctioning. In such cases
keep tip of catheter sterile, and store into original package.
• Note the color, odor, amount and consistency of the secretions and notify
doctor of changes in secretions.
Other Suctioning Devices

1. Small, portable, battery-operated suction machines are available for travel.
The batteries are rechargeable or the machine can be plugged into a car
cigarette lighter (Fig. 8.20).
2. The De Lee suction trap is a small plastic suction device. The caregiver
sucks on a tube to create a negative suction pressure. The secretions are
collected in a sputum trap and do not come in contact with the caregiver
(Fig. 8.21).
3. The In / Exsufflator or the Cough Machine is a new, vacuum-like, non-
invasive technique used as an alternative to traditional suctioning that is
especially helpful for those with an ineffective cough, assisting patients in
the removal of bronchial secretions from the respiratory tract.
FIGURE 8.20: Portable suction unit
FIGURE 8.21: A De Lee suction trap
Keypoints to Ponder
1. Intubation involves the placement of a flexible plastic tube into the trachea.
2. Cuffed curved tubes are used in the ICU.
3. The tube is inserted using a laryngoscope.
4. Anesthesia for intubation may be general, local or sedation.
5. Severe hypotension may follow intubation.
6. Although rapid sequence induction is essential for intubating patients in
ICU, the execution is different as the anesthetic agents are varied as
appropriate.
7. Hypotension following intubation is treated with fluids, vasoconstrictors

and inotropes.
8. Intubation and ventilation are life saving process in the ICU management
of patients; they facilitate airway protection and ventilation.
CHEST PHYSIOTHERAPY IN INTENSIVE CARE UNIT

Giving chest physiotherapy to a critically ill patient in an intensive care unit
can be a daunting experience, not only for the trainee or newly qualified
physiotherapist, but also for the experienced physiotherapists who have never
been exposed earlier to the environment of an ICU.
The ICU is a high dependence area, filled with array of sophisticated
equipments, leads, tubes, different kinds of audible alarms, blinking monitors,
hissing of gas. In the middle of all the hardware is the patient, connected by
many leads, tubes, IV lines and catheters to the equipments surrounding the
bed. The first challenge for the physiotherapist is to get close enough to the
patient to do the job, without getting tangled in the leads and tubes or
accidentally unplugging a life saving device.
The patients commonly admitted to an ICU present with complex multi-
system disorders, with volatile clinical status, that needs to be monitored
closely and continuously. The complexity of it all can deter many inexperienced
professionals, whether nurse, doctor or therapist, to seek out a posting in the
ICU.
However, ICU is an arena where a physiotherapist has a vital role to play,
provided he can adapt and use skills learned from different specialist areas,
to assess the actual status of the patient, how far the patient will tolerate
therapeutic interventions and select appropriate protocol to apply.
It should be remembered that even conscious patient in the ICU will be
disoriented, unable to tell time of the day, unable speak through an ET /
tracheostomy and fatigued from lack of sleep in an alien environment. To
gain the rapport of the patient will ensure cooperation.
Routine physiotherapy is useless in an ICU. Although chest PT. should
primarily focus on the respiratory complications of the patient, an overview
of status of other related systems is essential to decide on the stability of the
patient, suitability for physiotherapy and best course of action that may be
needed.
The following groups of patients need admission to the Intensive Care
Unit for the care of respiratory complications, among other multisystem
dysfunction:
• Neurological disorders: Traumatic brain injury, cerebro-vascular accidents
(Brain stroke), planned surgery of the CNS, Guillain-Barre syndrome
etc.
• Cardiovascular disorders: Acute myocardial ischemia and infarction (Heart
Attack), heart failure, open heart surgery (CABG) etc.
• Respiratory disorders: Acute exacerbations of COPD, status asthmaticus
etc.
The following section attempts to guide the physiotherapist through the
process of interpreting relevant signs and symptoms, planning and
implementing appropriate therapy in each patient group that need intensive
care.
Neurological Disorders (CVA, Head Injury, Craniotomy, GB

syndrome)
Points to Ponder
• Critical clinical signs for the therapist in head injury, CVA and Brain surgery
patients are the level of consciousness, cerebral perfusion pressure (CPP)
and intracranial pressure (ICP).
• Stable ICP below the critical level of <25 mmHg means that the patient
is stable enough to tolerate physiotherapy.
• If the ICP fluctuates or shoots up with handling, physiotherapy should be
withheld, as it may lead to lowered cerebral perfusion (CPP)and worsening
of the neurological status.
• A rise in PaCo2 and Co2 retention due to hypoventilation, atelectasis can
cause raised ICP and reduce CPP. These respiratory complications should
be treated with care by the therapist, so as not to raise the ICP to a
dangerous level.
• Level of consciousness and degree sedation is inversely proportional to
ventilatory drive. Simply keeping the patient awake can ensure better
oxygenation. Therapist and the nurse should be aware of this and interact
with the patient as often as possible, making him breath deeply or change
position in bed to keep him awake. In unconscious patients, frequent
passive turnings, passive movements and cyclic propping up and lowering
of the head end of the bed can lead to better ventilation.
Cardiovascular Disorders (IHD, MI, CCF)

Points to Ponder
• Heart rate and rhythm are key indicators of cardiac health and wellbeing.
• Cardiac arrhythmias are common symptoms in critically ill patients due
to electrolyte imbalance, drug toxicity etc. Physiotherapy in cases of
unstable cardiac arrhythmia may worsen the cardiac symptoms.
• Arterial blood pressure (BP) is a key indicator of rate of blood flow multiplied
by the resistance offered by the blood vessels.
• Hypotension or lowered BP may indicate hypovolemia (Reduced volume
of blood), deep sedation, vasodilatory drugs or primary cardiac
dysfunction. Hypertension or raised BP may indicate inadequate sedation,
analgesia or raised ICP. If uncontrolled, both are contraindications to PT.
• Pulmonary artery pressure (PAP) normally is 1/6 of BP. It provides
information regarding cardiac output, stroke volume and ventricular
workload.
• High PAP indicates high pulmonary vessels resistance or low cardiac output.
These may be worsened during manual hyperinflation (Using Ambu bag).
Respiratory Disorders (Acute exacerbations of COPD, Lower

respiratory tract infections, Interstitial lung diseases, Drowning
etc.)
Points to Ponder
• Level of ventilatory support (full/ assisted/spontaneous) required by the
patient is the primary indicator of the severity of the respiratory
dysfunction.
• Presence of artificial airway or types oxygen delivery devices (Tracheotomy/
Endotracheal tubes/ Oropharyngeal tubes/ Sealed face masks/ Ventury
oxygen mask/Nasal cannula) is the further indication for the extent of
oxygen required.
• Oxygen concentration (ranging from 21 -100%) and O2 flow rate required
(2 liters/min-10 liters/min) to maintain adequate blood gas levels reflect
the degree of primary respiratory failure or impaired gas exchange in
multiple organ failure.
• Respiratory rate in a mechanically ventilated patient can be selectively
increased (as in neurological disorders to lower the PaCO2 and reduce
the ICP) or reduced (as in COPD to maintain high normal PaCO2, to
maintain hypercapnic drive). In assisted ventilation rate of respiration is
progressively reduced as the patient is weaned from the ventilator.
• During spontaneous ventilation, respiratory rate may be raised due to
pain, anxiety, exhaustion, respiratory acidosis and weakness of respiratory
muscles. This eventually leads to respiratory fatigue. Any vigorous chest
PT in such situations will be counter productive. The focus of physiotherapy
should be on inducing relaxation and quite breathing with minimal effort.
• Airway pressure (Peak inspiratory pressure) may be raised due to reduced
lung compliance, fibrosis, ARDS, pulmonary edema, sputum plugging,
retention of secretions or bronchospasm. In some cases, as in sputum
plugging and retention of secretions, chest PT may be a valuable tool,
whereas in acute bronchospasm chest PT is contraindicated.
Chest Physiotherapy in Mechanically Ventilated Patients

Points to Ponder
• In mechanically ventilated patients cardiovascular and respiratory stability
must be ensured before commencing chest PT.
• Manual hyperinflation (Ambu bag) should be used with a PEEP valve to
avoid Baro-trauma in patients with reduced lung compliance and high
peak expiratory end pressure.
• The inspiratory: expiratory (I: E) ratio in mechanical ventilation is altered
to suite requirement of individual patients. Prolonged expiration is used
to reduce CO 2 retention and prolonged inspiration to improve
oxygenation. In such cases vigorous percussion or chest squeezing
may upset the ventilator setting and complicate ventilation.
• Mechanical positive pressure ventilation selectively hyper-ventilates the
uppermost areas of the lung, which are not heavily perfused and vice
versa. To correct this mismatch frequent change of position is essential.
Prone lying has been shown to be maximum benefit in patients with
severe lung disease.
• During weaning a patient, chest physiotherapy should not interfere with
the existing respiratory drive. Manual hyperinflation should not be used
indiscriminately.
• Good positioning and removal of secretions from the airway is essential
during weaning. Use pillows and rolls to support the patient in ¾ turned
towards prone.
• Maintenance physiotherapy for all patients in ICU should include regular
passive movements, muscle and soft tissue stretching, maintaining
anatomical alignment, and inhibiting reflex activity/contractures by
positioning. Light plaster casts or thermoplastic splints may be used for
contracture prophylaxis and reduction of adverse muscle tone. All drains
must be clamped and infusion lines shut off and disconnected before
changing position of the patient and any vigorous shaking / movements
during chest PT.
• Manual hyperventilation using an Ambu bag is essential in sedated or

unconscious patients before chest shaking and during percussion is done.
Short oscillatory inflations do not damage the lungs or interfere with cardiac
output.
Rehabilitation to progress to sitting and standing if the patient achieves
neurological and cardiovascular stability. This will help regain trunk control
and pelvic stability.
Index 183
Index
A corticosteroids 91
Altered states of normal respiratory cromolyn 91
physiology 27 leukotriene inhibitors 91
Alveoli-capillary complex 29
B
Arthrokinematics of the thoracic cage:
Bony vertebral column 1
analysis of movement of
Breathing exercises 119
breathing 4
Bronchial asthma 87
movement of the ribs occurring at these
causes 88
joints 4
characteristics 87
movement of thoracic vertebral column
bronchial muscle spasm 87
4
excessive secretion of mucous 87
axial rotation 6
inflammation and swelling of the
extension 7
mucous membrane lining the
flexion 6
airway 87
lateral flexion 4
diagnosis 89
mechanics of breathing 7
symptoms 87
Articulations of the chest wall 3
treatment 89
costosternal 3
Bronchiectasis 98
costotransverse 3
causes 99
costovertebral 3
management 100
interchondral joints 3
prevention 101
manubriosternal 3
symptoms 99
xiphisternal 3
tests 99
Assisted coughing 125
chest X-ray 99
postural drainage 126
CT/MRI scan of chest 100
contraindications 127
sputum culture and sensitivity 100
indications 126
preparation 127 C
procedure 128 Chest percussion 129
sequence 128 contraindications 129
procedure 126 circulatory contraindication 130
Asthma in childhood 92 general contraindication 129
allergy 92 musculoskeletal contraindication
cigarette smoke 92 130
genetic factor 92 indication 129
other factors 92 procedure 130
Asthma medications 90 Chest physiotherapy 1
bronchial muscle spasm relievers or Chest physiotherapy in intensive care unit
bronchodilators 90 162
anti-cholinergic drugs 90 intravenous catheters 162
long-acting beta agonist mechanical ventilators 162
bronchodilators 90 monitors 162
short-acting beta agonist Chest physiotherapy in intensive care unit
bronchodilators 90 177
caution 90 cardiovascular disorders 178
preventive medication or anti- chest physiotherapy in mechanically
inflammatory drugs 91 ventilated patients 180
neurological disorders 178 hypoxia, hypoxemia and hypercapnia
respiratory disorders 179 24
Chest physiotherapy techniques in surgical Collapsed lung 25
conditions 140
complications 141 D
hypersecretion of mucus 141 Devices used in chest physiotherapy 132
inhibition of muco-cilliary transport incentive spirometer 132
141 inhaled medications and delivery
pain inhibition 141 devices 133
venous stasis 141 nebulizers 133
Chest vibration 131 technique 133
procedure 131 peak flowmeter 132
Chronic bronchitis 94 procedure 134
causes 95 Diaphragmatic or belly breathing 121
asthma 95 techniques 121
pulmonary emphysema 95 Different breathing techniques 120
pulmonary fibrosis 95 Disorders in the ICU 162
sinusitis 95 acute respiratory distress syndrome
tuberculosis 95 (ARDS) 162
upper respiratory infections 95 asthma 162
diagnosis 95 chronic obstructive pulmonary disease
pulmonary function tests 95 (COPD) 162
arterial blood gas (ABG) 96 pneumonia 163
chest X-ray 96 respiratory distress syndrome 163
peak flow monitoring (PFM) 95 sepsis 163
pulse oximetry 96 trauma 163
spirometry 95
E
symptoms 94
Effect of oxygen starvation 26
treatment 96
End inspiratory hold 122
chest physiotherapy 96
procedure 122
inhaled bronchodilators 96
Endotracheal tubes 164
oral medications 96
laryngoscopes 166
oxygen supplementation 96
types 165
Chronic obstructive pulmonary disorder
double lumen tubes 166
(COPD) 29
north-facing tubes 166
associated problems 80
reinforced tubes 166
causes 78
south-facing tubes 166
clinical features 32
uncuffed tubes 165
compensatory mechanisms 33
disease course 79 F
historical background 30 Functional anatomy of the respiratory
pathophysiology 30 mechanism 1
risk factors 79
symptoms 78 G
Cilia 14 Gas exchange at the alveolar level 19
Clinical evaluation of patients with Grading of breathlessness 42
respiratory disorders 39 Gravitational force 2
Clinical implication of blood gas
abnormalities 24 H
clinical signs of blood gas abnormality Hypercapnia 26, 149
26 Hypocapnia 26
Index 185
Hypovolumic shock 26 M
Hypoxemia 26, 149 Mechanical ventilation 153
Bi-level positive airway pressure 154
I continuous positive airway pressure
Incentive spirometer 133 153
Inhaled aerosol route of delivery 133 indications 153
Interstitial lung diseases 104 positive end-expiratory pressure 155
causes 104 positive pressure ventilation 153
bronchiolitis obliterans 104 Mechanism of gas exchange 18
chronic eosinophilic pneumonia Metered dose inhaler (MDI) devices 137
104 cleaning the spacer 140
collagen vascular disease 104 spacer 138
Goodpasture’s syndrome 104 advantages 138
granulomatous vasculitis 104 types 137
histiocytosis X 104 breath activated aerosols 138
idiopathic pulmonary fibrosis 104 dry powder devices 137
pulmonary alveolar proteinosis 104 multiple dose inhalers 137
pulmonary tuberculosis and use an inhaler 139
sarcoidosis 104 Muscles of respiration and their function
diagnosis 105 in different stages of respiration
pulmonary function tests 105 8
spirometry 105
symptoms 105 N
treatment 106 Nasopharynx 11
influenza vaccine 106
lung transplantation 106 O
oral medications, including Objective clinical evaluation of respiratory
corticosteroids 106 disorders 46
oxygen supplementation from additional signs 49
portable containers 106 body mass index 49
pneumococcal pneumonia vaccine body weight 49
106 respiratory rate 49
Intubation 165 breathing pattern 50
anesthesia 169 general observation 47
process 167 observation of the chest 50
head positioning 167 shape of the chest 50
laryngoscope 167 observation of the hands, fee and eyes
tracheostomy 169 49
clubbing 49
K cyanosis 49
Kyphosis 2 edema 49
vital signs 47
L Oropharynx 11
Laryngopharynx 11 Other methods of maximizing lung
Lung parenchyma 29 volumes 123
Lung volumes 20 graded physical exercises 123
blood pH and respiratory acidosis 24 single percussion technique 123
hematocrit 23 Other supportive measures for
hemoglobin dissociation curve 23 management of respiratory
oxygen uptake in the lungs 22 failure 155
ventilation 20 assisting failing circulation 156
clearing secretions 157 oropharynx 12
complications 162 Physical examination of the chest 52
corticosteroids 156 auscultation of the chest 54
establishing artificial airway 157 chest percussion 53
maintaining cardiac output 156 daily asthma diary 60
optimizing hemoglobin (Hb) finding asthma zones 60
concentration in blood 155 green zone 60
position changes 156 red zone 60
precautions 159 yellow zone 60
reducing tissue oxygen requirement interpretation and clinical correlation of
155 breath sounds 55
types 160 adventitious (extra) lung sounds 56
full ventilatory support 160 palpation 52
other forms 161 palpation and measurement of chest
partial ventilatory support 161 expansion 52
pressure-cycled ventilators 160 palpation for spontaneous/surgical
volume-cycled ventilators 160 emphysema 53
Outline of respiratory anatomy 10 palpation for vocal fremitus 53
lower respiratory tract 12 peak flow rate monitoring 57
epiglottis 12 personal best peak expiratory flow
esophagus 12 rate 59
glottis 12 Pneumonia 101
hyoid bone 12 diagnosis 102
laryngeal prominence 12 treatment 103
thyroid cartilage 12 types 101
vocal cords 13 aspiration pneumonias 102
wall of laryngopharynx 13 bacterial pneumonia 101
lungs and the major bronchi 15 mycoplasm pneumonia 102
microscopic features of the lungs and viral pneumonia 102
bronchial tree 16 Polycythemia 26
role of alveoli in respiration 16 Postoperative physiotherapy techniques
upper respiratory tract 10 144
epiglottis 10 chest infection 144
external nares 10 high risk 144
frontal sinuses 11 objectives 144
hard palate 11 prognosis 147
nasal bone 11 symptoms 145
nasal cavity 11 treatment 145
nasal concha 11 Preoperative chest physiotherapy
soft palate 11 techniques 142
Overview of chest physical therapy 110 implementing 143
precautions 111 objective assessment 142
purpose 110 planning the care 143
scope 111 principal objectives 142
Primary treatment strategy for COPD 83
P bronchodilator therapy 84
Passive diffusion 18 chest physiotherapy 85
Peak flowmeter 57 pulmonary rehabilitation 85
Pharynx 11 dopamine agonists 84
laryngopharynx 12 inhaled steroids 84
naso-pharynx 11 oral steroids 84
Index 187
oxygen therapy 85 pathophysiology of restrictive lung
phospho-diesterase inhibitors 85 dysfunctions 36
smoke cessation 83 Rib cage 1
Pulmonary emphysema 96
causes 97 S
diagnosis 97 Scoliosis 2
symptoms 97 Scope of chest X-ray 67
early symptoms 97 art of reading the chest X-ray 69
late symptoms 97 chest X-ray procedure 68
treatment 98 indications for requesting a chest X-ray
antibiotics for bacterial infections 98 67
exercise 98 cancer 67
oral bronchodilators and other cardiac disorders 67
inhaled medications 98 other conditions 67
oxygen supplementation 98 pulmonary disorders 67
quitting smoking 98 precautions to be observed during chest
Pulmonary sarcoidosis 108 X-ray 68
risk factors 109 preparation for chest X-ray 68
symptoms 109 routine chest X-ray 67
treatment 109 blood vessels 67
Pulmonary tuberculosis 106 calcium deposits 67
causes 107 condition of lungs 67
diagnosis 108 size and outline of the heart 67
risk factors 107 X-ray reporting 69
symptoms 107 Screening techniques used by
treatment 108 physiotherapists 39
building the clinical database 40
R interaction with team members 40
Respiratory distress syndrome 61 Segmental breathing 121
breathing rate 61 technique 122
color changes 61 Skeletal components of the rib cage and
grunting 61 the upper girdle 1
nose flaring 61 rib cage 2
retractions of the neck 61 role of the vertebral column 1
sweating 61 Structure of the alveoli 17
wheezing 62 Subjective evaluation of respiratory
Respiratory failure 149 disorders 41
diagnosis 151 interviewing the patient 41
blood gas measurement 151 Symptoms of respiratory disorders 41
intensity respiratory distress 151 assessment of disease awareness 46
neuromuscular function 151 assessment of functional limitations and
etiology 150 the quality of life 44
O2 therapy 152 breathlessness 41
primary treatment 152 chest pain 44
signs and symptoms 151 cough 42
Restrictive lung diseases 35 other symptoms 44
Restrictive lung dysfunctions (RLD) 35 edema 44
epidemiology 37 headache 44
extra-parenchymal diseases 36 high fever 44
intrinsic lung diseases (ILD) 36 loss of sleep 44
sputum 43 coughing 113
wheeze 43 deep breathing and breath holding
Synchondrosis 4 exercises 112
expected response 114
T forced expiratory technique 112
Technique of endotracheal suction 170 percussion 113
equipments 172 positioning 112
other suctioning devices 175 postural drainage 113
procedure 174 preparation for chest PT 113
selecting the appropriate size of the risk and complications 114
suction catheter 171 turning 112
signs 172 vibration 113
steps 172 Thoracic vertebra 3
suction care techniques 171 Thorax 1
clean technique 171 Tracheal cartilages 13
modified sterile 171 Tracheo-bronchial tree 13
sterile technique 171 Transversus abdominus 9
suction depths 171 Trunk flexion 7
deep suctioning 171 Types and causes of abnormal breathing
pre-measured suctioning 171 patterns 51
shallow suctioning 171 apnea 51
Technique of managing breathlessness apneustic breathing 51
116 ataxic breathing 51
Technique of maximizing lung volumes Cheyne-stoke breathing 51
118 hypoapnea 51
Technique of removing excess secretions Kussmaul’s breathing 51
from the lungs 124 prolonged expiration 51
effective coughing 124 pursed lip breathing 51
Techniques of chest physiotherapy: Typical clinical presentation of COPD 80
application and uses 114 diagnosis: investigations/tests 81
signs of respiratory distress 115 blood tests 82
color changes 115 bronchoscopy 83
elevation of shoulders 115 chest X-ray 82
grunting 115 CT scan of the chest 83
increased breathing rate 115 ECG 83
nose flaring 115 lung function tests 81
sweating 115 sputum culture 83
wheezing 115
Techniques used in chest physiotherapy V
112 Vertebral column 2
aftercare of chest PT 114

Handbook of Practical Chest Physiotherapy

Загружено:

Сведения о документе

Авторское право

Доступные форматы

Поделиться этим документом

Поделиться или встроить документ

Параметры публикации

Этот документ был вам полезен?

Это неприемлемый материал?

Авторское право:

Доступные форматы

Handbook of Practical Chest Physiotherapy

Загружено:

Авторское право:

Доступные форматы

Handbook of Practical

Pushpal Kumar Mitra

Handbook of Practical Chest Physiotherapy

First Edition: 2007

In the field of respiratory medicine, the development which occurred in

This book is not only going to help the undergraduate physiotherapy

In prolonged morbidity of any kind, in which the patient is confined to the

Pushpal Kumar Mitra

1. Functional Anatomy of the Respiratory Mechanism ............... 1

2. Applied Physiology of Respiration ....................................... 18

3. Respiratory Pathophysiology ................................................ 29

4. Clinical Evaluation of Patients with Respiratory Disorders .. 39

5. Chest X-ray for the Physiotherapist ..................................... 66

6. Management of Major Respiratory Diseases ........................ 78

7. Techniques of Physical Therapy Treatment in

8. Management of Respiratory Emergencies ........................... 149

Index ............................................................................................. 183

Functional Anatomy of the

SKELETAL COMPONENTS OF THE RIB CAGE AND

The Role of the Vertebral Column

Human beings are bi-pedal in nature, the vertical alignment of the

The Rib Cage

FIGURE 1.2: Bones and articulations of the rib cage

FIGURE 1.3: Articulations of the ribs with the thoracic vertebra

ARTHROKINEMATICS OF THE THORACIC CAGE:

Movement of the Ribs Occurring at these Joints

Movement of Thoracic Vertebral Column

FIGURE 1.4: Movement of ribs about the axis formed by the

FIGURE 1.7: Trunk flexion and its effect on rib cage

Diaphragm descends Diaphragm ascends

Increased intrathoracic volume Decreased intrathoracic volume

Decreased intrathoracic pressure Increased intrathoracic pressure

MUSCLES OF RESPIRATION AND THEIR FUNCTION IN

FIGURE 1.8: The diaphragm

rectus abdominus, internal and external obliques, and transversus

FIGURE 1.9: Movement of the diaphragm during the breath cycle

Type of Breathing Muscles of Inspiration Muscles of Expiration

Quiet Diaphragm Expiration is passive

Forced Sternocleidomastoid Abdominal muscles

OUTLINE OF RESPIRATORY ANATOMY

Part 1: Upper Respiratory Tract

Part 2: Lower Respiratory Tract

FIGURE 1.14: The tracheo- FIGURE 1.15: Cross-sectional view of trachea

• The tracheal cartilages or Ttacheal cartilaginous rings are the support

FIGURE 1.16: Microscopic view of cilia

FIGURE 1.17: The workings of the cilia

FIGURE 1.18: The lungs, the lobes of the lungs and

Part 4: The Microscopic Features of the Lungs and Bronchial Tree

Role of Alveoli in Respiration

FIGURE 1.20: The structure of the alveoli

like bronchodilators, to relieve the muscle spasm. Anti-inflammatory agents

As we have studied in the previous chapter, each branch of the bronchial

MECHANISM OF GAS EXCHANGE

Blood Gases: Keywords, Clinical Significance and Normal Values

• During exercise we can increase the tidal volume by expanding both

The Maximum Usable Lung Volume is called the Vital Capacity

FIGURE 2.2: Lung volumes are measured with a respirometer,

Oxygen Uptake in the Lungs

Hemoglobin Dissociation Curve

FIGURE 2.3: A plot of % of saturation against partial tension of O2

Blood pH and Respiratory Acidosis

CLINICAL IMPLICATION OF BLOOD GAS ABNORMALITIES

Table 2.1: Causes and types of hypoxia

Type of O2 uptake Hemoglobin Efficiency of O2 utilization