INDEX

INTRODUCTION TO RESPIRATORY DISEASES

INTRODUCTION TO OBSTRUCTIVE DISEASES

ANATOMY OF RESIRATORY SYSTEM

PHYSIOLOGY OF RESPIRATION

TYPES & DEFINITIONS

EPIDEMIOLOGY

RISK FACTORS

PATHOLOGY

PATHOGENESIS

SIGNS AND SYMPTOMS

STAGES OF COPD

COMPLICATIONS OF COPD

OTHER TYPES OF OBSTRUCTIVE DISEASE

DIAGNOSIS OF OBSRUCTIVE DISEASES

DIFFERENTIAL DIAGNOSIS

CLINICAL MANAGEMENT

PHYSIOTHERAPY ASSESSMENT

PHYSIOTHERAPY MANAGEMENT

CONCLUSION

BIBILOGRAPHY

INTRODUCTION TO RESPIRATORY DISEASE

Respiratory Diseases can be broadly divided into

OBSTRUCTIVE TYPE

&

RESTRICTIVE TYPE

OBSTRUCTIVE DISEASE

It include conditions in which there is a

resistance to air flow either through reversible factors such

as bronchospasm or inflammation or through irreversible

factors such as airway fibrosis or loss of elastic recoil owing

to damage to the airway and the alveoli.

RESTRICTIVE DISORDERS

These are characterised by reduced

lung compliance leading to the loss of lung volume, which

may be caused by disease affecting the lungs, pleura, chest

wall or neuromuscular mechanisms.

INTRODUCTION TO COPD

Chronic obstructive lung disease

(COLD), also known as chronic obstructive pulmonary disease

(COPD), is characterized by a limitation of the airflow in the

lung, which develops over time and is not totally reversible.

The major diseases in this category are:

EMPHYSEMA

CHRONIC BRONCHITIS

ASTHAMATIC BRONCHITIS

BRONCHIECTASIS

CYSTIC FIBROSIS

NOTE :-

EMPHYSEMA & CHRONIC BRONCHITIS comes under

chronic obstructive pulmonary disease hence they are shown under

a common heading COPD.

PLEASE CONSIDER

DEFINITION

CHRONIC BRONCHITIS :-

It is defined as chronic cough and expectoration

for at least 3 months a year for at least 2 successive years.

EMPHYSEMA :-

It is defined as chronic respiratory disease where there is

over-inflation of the air sacs (alveoli) in the lungs, causing a decrease in

lung function, and often, breathlessness.

ASTHMATIC BRONCHITIS :-

It is defined as acute episode of airway obstruction is

characterized by airway hyperactivity to various stimuli that results in

recurrent wheezing brought about by edema and bronchospasm.

BRONCHIECTASIS:-

It is defined as a condition that is characterised by the

permanent dilatation of the bronchi associated with destruction of elastic

and muscular components of their walls, usually due to acute or chronic

infection.

CYSTIC FIBROSIS :-

It is defined as a hereditary disorder of exocrine glands,

with high sodium chloride content in sweat and pancreatic insufficiency,

resulting in mal-absorption. There is hypertrophy and hyperplasia of

mucus-secreting glands, resulting in excessive mucus production in the

lining of bronchi, which predisposes the patient to chronic

bronchopulmonary infection.

Anatomy & Physiology of the

Respiratory System

Human Respiratory System

The respiratory system consists of

all the organs involved in breathing. These include the nose, pharynx,

larynx, trachea, bronchi and lungs.

The respiratory system does two very important things: it brings oxygen

into our bodies, which we need for our cells to live and function properly;

and it helps us get rid of carbon dioxide, which is a waste product of

cellular function.

The nose, pharynx, larynx, trachea and bronchi all work like a system of

pipes through which the air is funnelled down into our lungs. There, in

very small air sacs called alveoli, oxygen is brought into the bloodstream

and carbon dioxide is pushed from the blood out into the air.

The Upper Airway and Trachea

During breathing, air enters into body through nose or

mouth. From there, it travels down your throat through the larynx

(or voice box) and into the trachea (or windpipe) before entering

into the lungs. All these structures act to funnel fresh air down from

the outside into the body.

The upper airway is important because it must always stay

open to be able to breathe. It also helps to moisten and warm the

air before it reaches the lungs.

The Lungs

Structure

The lungs are paired, cone-shaped organs which take up most of

the space in our thorax, along with the heart.

Their role is to take oxygen into the body, which we need for our

cells to live and function properly, and to help us get rid of carbon

dioxide, which is a waste product.

We have two lungs, a left lung and a right lung. These are divided

up into 'lobes', or big sections of tissue separated by 'fissures' or

dividers. The right lung has three lobes but the left lung has only

two, because the heart takes up some of the space in the left side

of our chest.

The lungs can also be divided up into even smaller portions, called

'bronchopulmonary segments'. These are pyramidal-shaped areas

which are also separated from each other by membranes. There

are about 10 of them in each lung. Each segment receives its own

blood supply and air supply.

Physiology of Breathing

When a person inhales, air travels through the following pathways

into the lungs:

Air is carried from the trachea (the windpipe) into the lung through

flexible airways called bronchi.

Like the branches of a tree, bronchi divide successively into over a

million smaller airways called bronchioles.

The bronchioles lead to grape-like clusters of microscopic sacs

called alveoli.

In each adult lung there are millions of these tiny alveoli. The thin

membrane of the alveoli allows oxygen and carbon dioxide to pass

to and from capillaries.

During deep inhalation, the elastic alveoli unfold and unwind

to allow this passage to occur

Capillaries, the smallest of our blood vessels, carry blood

throughout the body. Red blood cells carry oxygen throughout the

body, and return carbon dioxide to the lungs; white blood cells are

the critical infection fighters in our body.

Mechanics of Breathing

To take a breath in, the external intercostal muscles

contract, moving the ribcage 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.

This is the mechanism behind lung collapse if there is air

in the pleural space (pneumothorax).

The Respiratory System Through the Ages

Breathing for the Premature Baby

When a baby is born, it must convert from getting all of its oxygen

through the placenta to absorbing oxygen through its lungs. This is

a complicated process, involving many changes in both air and

blood pressures in the baby's lungs. For a baby born preterm

(before 37 weeks gestation), the change is even harder. This is

because the baby's lungs may not yet be mature enough to cope

with the transition. The major problem with a preterm baby's lungs

is a lack of something called 'surfactant'. This is a substance

produced by cells in the lungs which helps keep the air sacs, or

alveoli, open. Without surfactant, the pressures in the lungs

change and the smaller alveoli collapse.

This reduces the area across which oxygen and carbon dioxide

can be exchanged, and not enough oxygen will be taken in.

Normally, a foetus will begin producing surfactant from around 28-

32 weeks gestation.

When a baby is born before or around this age, it may not have

enough surfactant to keep its lungs open. The baby may develop

something called 'Neonatal Respiratory Distress Syndrome', or

NRDS.

Signs of NRDS include tachypnoea (very fast breathing), grunting,

and cyanosis (blueness of the lips and tongue). Sometimes NRDS

can be treated by giving the baby artifically made surfactant by a

tube down into the baby's lungs.

The Respiratory System and Ageing

The normal process of ageing is associated with a number of

changes in both the structure and function of the respiratory

system. These include:

Enlargement of the alveoli. The air spaces get bigger and lose

their elasticity, meaning that there is less area for gases to be

exchanged across. This change is sometimes referred to as 'senile

emphysema'.

The compliance (or springiness) of the chest wall decreases, so

that it takes more effort to breathe in and out.

The strength of the respiratory muscles (the diaphragm and

intercostal muscles) decreases. This change is closely connected

to the general health of the person.

All of these changes mean that an older person might have

more difficulty coping with increased stress on their respiratory

system, such as with an infection like pneumonia, than a younger

person would.

EPIDEMIOLOGY

Chronic Obstructive Pulmonary Disease (COPD) is one of the

leading causes of morbidity and mortality in the industrialized and the

developing countries.

COPD has been estimated to be the number FOUR to

cerebrovascular diseases in the World to cause death. In 2020

COPD will probably become the third leading cause of death all

over the world, following the trend of increasing prevalence of lung

cancer.

The impact of this respiratory disease worldwide is expected to

increase with a heavy economic burden on individuals and society.

In most of the world, COPD prevalence and mortality are still

increasing and likely will continue to rise in response to increases

in smoking, particularly by women and adolescents.

Morbidity :- The limited data that are available indicate

that morbidity due to COPD increases with age and is greater in

men than women

Mortality :- COPD is currently the fourth leading cause of

death in the world , and further increases in the prevalence and

mortality of the disease can be predicted in the coming decades

RISK FACTORS of COPD :-

Exposure to tobacco smoke :-

The most significant risk factor for COPD is long-term

cigarette smoking. The more years you smoke and the more packs you

smoke, the greater your risk. Symptoms of COPD usually appear about

10 years after you start smoking. Pipe smokers, cigar smokers and

people exposed to large amounts of second hand smoke also are at risk.

Occupational exposure to dusts and chemicals :-

Long-term exposure to chemical fumes, vapours and dusts can irritate and inflame your lungs.

Gastro oesophageal reflux disease (GERD ) :-

This condition is a severe form of acid reflux the backflow of acid and other stomach contents into your oesophagus. GERD can make COPD worse and may even cause it in some people.

Age:-

COPD develops slowly over years, so most people are at least 40 years old when symptoms begin.

Genetics:-

A rare genetic disorder known as alpha-1-antitrypsin deficiency is the source of a few cases of COPD. Researchers suspect that other genetic factors may also make certain smokers more susceptible to the disease.

Cigarette smoking:-

The primary cause of COPD is exposure to tobacco

smoke Clinically significant COPD develops in 15% of

cigarette smokers.

Age of initiation of smoking, total pack-years, and current

smoking status predict COPD mortality. People who smoke

have a greater annual decline in FEV1. Overall, tobacco

smoking accounts for as much as 90% of the risk.

Second hand smoke, or environmental tobacco smoke,

increases the risk of respiratory infections, augments asthma

symptoms, and causes a measurable reduction in pulmonary

function.

Air pollution:-

Although the role of air pollution in the etiology of COPD is

unclear, the effect is small when compared to cigarette

smoking.

The use of solid fuels for cooking and heating may result in

high levels of indoor air pollution and the development of

COPD.

Airway hyper responsiveness:-

Airway hyper responsiveness (i.e., Dutch hypothesis)

stipulates that patients who have nonspecific airway hyper

reactivity and who smoke are at increased risk of developing

COPD with an accelerated decline in lung function.

Nonspecific airway hyper reactivity is inversely related to

FEV1 and may predict a decline in lung function.

The possible role of airway hyper responsiveness as a risk

factor for the development of COPD in people who smoke is

unclear. Moreover, bronchial hyper reactivity may result from

airway inflammation observed with the development of

smoking-related chronic bronchitis.

Alpha1-antitrypsin deficiency : -

AAT deficiency is the only known genetic risk factor for

developing COPD and accounts for less than 1% of all cases

in the United States. AAT is a protease inhibitor produced by

the liver that acts predominantly by inhibiting neutrophil

elastase in the lungs.

CLASSIFICATION

Emphysema can be classified into primary and secondary.

However, it is more commonly classified by location.

Emphysema can be subdivided into panacinary and centroacinary

(or panacinar and centriacinar, or centrilobular and panlobular).

Panacinary (or panlobular) emphysema is related to the destruction

of alveoli, because of an inflammation or deficiency of alpha 1-

antitrypsin. It is found more in young adults who do not have

chronic bronchitis.

Centroacinary (or centrilobular) emphysema is due to destruction of

terminal bronchiole mucosis, due to chronic bronchitis. This is found

mostly in elderly people with a long history of smoking or extreme

cases of passive smoking.

Other types include distal acinar and irregular.

A special type is congenital lobar emphysema (CLE).

Congenital lobar emphysema

CLE is results in overexpansion of a pulmonary lobe and resultant

compression of the remaining lobes of the ipsilateral lung, and

possibly also the contra lateral lung. There is bronchial narrowing

because of weakened or absent bronchial cartilage.

CLE is potentially reversible, yet possibly life-threatening, causing

respiratory distress in the neonate.

PATHOLOGY

Airway Pathology in COPD Pathway

The pathological hallmarks of COPD are destruction of the lung

parenchyma, which characterizes emphysema, inflammation of the

peripheral airways, which characterizes bronchiolitis, and inflammation

of the central airways which characterizes chronic bronchitis.

Functional consequence of these abnormalities is expiratory airflow

limitation.

As flow is the result of a driving pressure (elastic recoil of the lung) and

of an opposing resistance (airway obstruction), it is best to refer to the

changes in flow seen in smokers as airflow limitation, rather than airflow

obstruction, since both loss of elastic recoil and increase in airway

resistance play an important role in the observed decrease in flow .

Emphysema will contribute to the airflow limitation by reducing the

elastic recoil of the lung through parenchyma destruction, as well as by

reducing the elastic load applied to the airways through destruction of

alveolar attachments.

On the other hand, bronchiolitis will contribute to the airflow limitation by

narrowing and obliterating the lumen and by actively constricting the

airways. The role of symptoms of chronic bronchitis in the development

of chronic airflow limitation is still controversial. In fact, chronic sputum

production has traditionally been considered to be irrelevant to the

development of chronic airflow limitation.

However, a recent study has shown that chronic sputum production was

significantly associated with both an increased decline in FEV1 and an

increased risk of subsequent hospitalization because of COPD,

suggesting a causal role of mucus hyper secretion in the development of

chronic airflow limitation in smokers.

PATHOGENESIS

Chronic obstructive pulmonary disease

(COPD) is characterized and defined by limitation of expiratory

airflow.

This can result from several types of anatomical lesions, including

loss of lung elastic recoil and fibrosis and narrowing of small

airways.

Inflammation, oedema, and secretions also contribute variably to

airflow limitation. Smoking can cause COPD through several

mechanisms.

First, smoke is a powerful inducer of an inflammatory response.

Inflammatory mediators, including oxidants and proteases, are

believed to play a major role in causing lung damage.

Smoke can also alter lung repair responses in several ways.

Inhibition of repair may lead to tissue destruction that

characterizes emphysema, whereas abnormal repair can lead to

the peribronchiolar fibrosis that causes airflow limitation in small

airways.

Genetic factors likely play a major role and probably account for

much of the heterogeneity susceptibility to smoke and other

factors. Many factors may play a role, but to date, only alpha-1

protease inhibitor deficiency has been unambiguously identified.

Exposures other than cigarette smoke can contribute to the

development of COPD. Inflammation of the lower respiratory tract

that results from asthma or other chronic disorders may also

contribute to the development of fixed airway obstruction.

COPD is not only a disease of the lungs but is also a systemic

inflammatory disorder. Muscular weakness, increased risk for

atherosclerotic vascular disease, depression, osteoporosis, and

abnormalities in fluids and electrolyte balance may all be

consequences of COPD.

Advances in understanding the pathogenesis of COPD have the

potential for identifying new therapeutic targets that could alter the

natural history of this devastating disorder.

SIGNS and SYMPTOMS

Many of the signs of COPD are caused by the body's attempt to

compensate for a damaged respiratory system.

Symptoms develop as a direct result of disease processes

SIGNS

Signs of COPD are consequences of the anatomical changes

caused by the disease processes

Barrel chest

Pursed-lip breathing

Productive cough and

Cyanosis

Barrel-chest :-

One telling sign is the change in the shape of the chest, known as

barrel chest.

When the lungs become enlarged, the diaphragm is displaced

downward and able to contract efficiently.

Then the chest wall is enlarged, making the accessory muscles

(muscles in the neck, upper chest, and between the ribs) less

efficient as well.

These changes contribute to shortness of breath. This becomes

apparent when a person with COPD tries do something with the

arms raised above the head, such as changing a light bulb in a

ceiling fixture, and becomes short of breath.

To compensate, a person with COPD often sits leaning forward

with their arms supported on a surface in front of them or on their

knees. This stabilizes the upper chest and shoulders and allows

them to use accessory respiratory muscles more efficiently.

Pursed-lip breathing :-

Because airflow out of the lungs becomes limited,

exhalation takes longer. Because the alveoli lose their elasticity,

one tries to shorten the time needed for exhalation by forcefully

exhaling.

Unfortunately, forced exhalation increases pressure on the lungs

and causes structurally weakened airways to collapse. To prevent

airways from closing during forced exhalation, pursed-lip breathing

is used.

In this the lips are narrowed together, which slows exhalation at

the mouth. This keeps positive pressure in the airways, thus

preventing their collapse and allowing some forced exhalation.

Productive cough :-

A productive cough is caused by inflammation and

excessive amounts of mucus in the airways. Coughing becomes

less effective because of

obstructed airflow.

Cyanosis :-

People who have a poor supply of oxygen usually have a

bluish tinge to their skin, lips, nail beds. Called cyanosis.

Symptoms

Shortness of Breath (Dyspnea)

Dyspnea, the most common symptom of COPD.

It comes on gradually and is first noticed during physical exertion

or during acute exacerbations. So it usually begins at60s and. 70s

and slowly becomes more prominent .

It is closely associated with lung function decline and it is not

always associated with low oxygen in the blood.

Patients often wonder why Dyspnea occurs so long after beginning

to smoke, say 50 to 60 years later.

Some patients have even quit smoking several years before

symptoms appear.

The main reason is that lung function declines slowly with age,

even in a nonsmoker.

At approximately age 30, people begin to lose lung function at

expiratory volume in 1 second FEV1.

People who smoke lose lung function at a more rapid rate,

approximately 125 mL/year.

Because the lungs have a considerable amount of reserve, a

large portion must become nonfunctional before symptoms occur.

If can take more than 30 years to lose enough Lung function to

experience symptoms.

Chronic Cough:-

Chronic cough typically begins as morning cough

and slowly progresses to an all-day cough.

The cough usually produces small amounts of

sputum (less than 60ml/day) and is clear or whitish but may be

discolored.

Sputum production decreases when one quits smoking.

Wheezing :-

It is a high pitched sound of air passing through narrowed

airways. A person with copd may wheeze during on acute

exacerbation or chronically.

Sometimes the wheezing is heard only at night or with exertion.

Hemoptysis :-

COPD is one of the more common causes of hemoptysis

(coughing up blood).

It usually occurs during an acute exacerbation, when there is a lot

of coughing with purlent sputum (sputum containing pus).

Usually, there are only very small amounts of blood streaking the

sputum. Hemoptysis may be a sign of lung cancer in a patient with

COPD, so any blood appearing in the sputum should be brought to

a doctor's attention.

Weight Loss :-

Patient with COPD work hard and burn a lot of calories just

breathing.

Lower Extremity Edema :-

In severe cases of COPD. Pulmonary artery pressures increase

and the right ventricle of the heart contracts less efficiently.

When the heart is unable to pump enough blood to meet the needs

of the kidneys and liver, edema (swelling) in the feet, ankles, and

lower legs results.

SOME IMPORTANT CLINICAL AND HISTORICAL DIFFERENCES CAN EXIST BETWEEN THE TYPES OF COPD.

In the chronic bronchitis group, classic symptoms include the

following:

o Productive cough, with progression over time to intermittent

dyspnoea

o Frequent and recurrent pulmonary infections

o Progressive cardiac/respiratory failure over time, with

oedema and weight gain

In the emphysema group, the history is somewhat different and

may include the following set of classic symptoms:

o A long history of progressive dyspnoea with late onset of

non-productive cough

o Occasional mucopurulent relapses

o Eventual cachexia and respiratory failure

Physical

Depending on the type of COPD, physical examination may vary.

Chronic bronchitis (blue bloaters)  

Patients may be obese.

Frequent cough and expectoration are typical.

Use of accessory muscles of respiration is common.

Coarse rhonchi and wheezing may be heard on auscultation.

Patients may have signs of right heart failure (i.e., Cor

Pulmonale), such as oedema and cyanosis.

Because they share many of the same physical signs, COPD

may be difficult to distinguish from congestive heart failure

(CHF). One crude bedside test for distinguishing COPD from

CHF is peak expiratory flow. If patients blow 150-200 ml or

less, they are probably having a COPD exacerbation; higher

flows indicate a probable CHF exacerbation.

Emphysema (pink puffers)  

o Patients may be very thin with a barrel chest.

o They typically have little or no cough or expectoration.

o Breathing may be assisted by pursed lips and use of

accessory respiratory muscles; they may adopt the tripod

sitting position.

o The chest may be hyper resonant, and wheezing may be

heard; heart sounds are very distant.

o Overall appearance is more like classic COPD exacerbation.

Stages of COPD

Stage I: mild COPD: Characterized by mild airflow limitation

(FEV1/FVC < 0.70, FEV1 80% predicted). Symptoms of chronic

cough and sputum production may be present, but not always.

At this stage, the individual is usually unaware that his or her lung

function is abnormal.

Stage II: moderate COPD: Characterized by worsening airflow

limitation (FEV1/FVC < 0.70, 50% FEV1 < 80% predicted), with

shortness of breath typically developing on exertion and cough and

sputum production sometimes also present.

This is the stage at which patients typically seek medical attention

because of chronic respiratory symptoms or an exacerbation of

their disease.

Stage III: severe COPD: Characterized by further worsening of

airflow limitation (FEV1/FVC < 0.70, 30% FEV1 < 50% predicted),

greater shortness of breath, reduced exercise capacity, fatigue,

and repeated exacerbations that almost always have an impact on

patients' quality of life.

Stage IV: very severe COPD: Characterized by severe airflow

limitation (FEV1/FVC < 0.70, FEV1 < 30% predicted or FEV1 < 50%

predicted plus the presence of chronic respiratory failure).

Respiratory failure is defined as an arterial partial pressure of O2

(PaO2) less than 8.0 kPa (60 mm Hg), with or without an arterial

partial pressure of CO2 (PaCO2) greater than 6.7 kPa (50 mm Hg)

while breathing air at sea level.

Respiratory failure may also lead to effects on the heart such as

Cor Pulmonale (right heart failure).

Clinical signs of Cor Pulmonale include elevation of the jugular

venous pressure and pitting ankle oedema. Patients may have stage IV COPD even if their FEV1 is greater

than 30% predicted whenever these complications are present. At this stage, quality of life is very appreciably impaired and

exacerbations may be life threatening.

COMPLICATIONS OF COPD

COPD complications can be serious and even life-

threatening. Proper recognition of signs and symptoms as well as

adherence to a medical plan of care is paramount to successful

treatment. The following provides a detailed list of the complications of

COPD:

1. Cor Pulmonale

Cor Pulmonale is caused by an increase in blood pressure in the

pulmonary artery, the vessel that carries blood from the heart to the

lungs. This leads to enlargement and subsequent failure of the right side

of the heart.

2. Acute Exacerbation of COPD

In its simplest terms, an exacerbation can be

defined as a worsening of COPD symptoms. Many people with COPD

suffer several episodes of acute exacerbation a year, often leading to

increased hospitalizations, respiratory failure and even death.

3. Pulmonary Hypertension

Pulmonary hypertension occurs when there is abnormally high pressure

within the blood vessels of the lungs.

Normally, the blood flows from the heart to pass through the lungs,

where blood cells pick up oxygen and deliver it to the body.

In pulmonary hypertension, the pulmonary artery is thickened. This

means less blood is able to flow through the blood vessels

4. Pneumothorax

Pneumothorax is defined as the accumulation of air or gas in the space

between the lung and the chest wall.

Pneumothorax occurs because of a hole that develops in the lung, which

allows air to escape in the space around the lung, causing the lung to

partially or completely collapse.

People who have COPD are at greater risk for pneumothorax because

the structure of their lungs is weak and vulnerable to the spontaneous

development of these types of holes

5. Secondary Polycythemia

Secondary polycythemia is acquired from a rare

disorder that is characterized by an overproduction of red blood cells in

the blood.

When too many red blood cells are produced, the blood becomes thick,

hindering its passage through the smaller blood vessels.

In patients with COPD, secondary polycythemia can occur as the body

tries to compensate for decreased amounts of oxygen in the blood.

6. Respiratory Failure

Respiratory failure occurs when the lungs are

unable to successfully extract sufficient oxygen and/or remove the

carbon dioxide from the body.

DIAGNOSIS

Pulmonary Function Tests (PFTs)

Pulmonary function tests are the primary diagnostic tools for COPD.

Lung biopsy is rarely used to diagnose emphysema.

There are four components to pulmonary function testing:

Spirometry,

Post bronchodilator spirometry

Lung volumes and

Diffusion capacity.

Spirometry: -

The most reliable way to determine reversible airway

obstruction is with spirometry.

It is a simple test procedure that measures the amount of air

entering and leaving the lungs.

With the patient sitting comfortably in front of the spirometry

machine. The machine measures airflow that passes through the

inhalation port attached to the machine. The inhalation device is

usually a disposable cardboard tube or a reusable tube that can be

sterilized after use.

Those most commonly used for interpretation are

(1) forced expiratory volume after 1 second [FEV1]

(2) forced vital capacity [FVC]and

(3) forced expiratory flow at 25%-75% of maximal lung

volume [FEF25-75].

For COPD the results may be:-

The amount of air exhaled (forced vital capacity, or FVC) is

reduced, compared to a person with normal lung function.

The amount of air exhaled during the initial 1 second (FEV1) is

reduced and is reduced to a greater degree than the entire FVC.

Therefore, the ratio of air exhaled after 1 second is low compared

to the total amount of air exhaled. In healthy lungs, 70%-75% of all

the air exhaled after maximum inhalation (FVC) is exhaled within

the first second (FEV1), known as the FEV1/FVC ratio. In lungs

with COPD, the FEV1/FVC ratio falls below 70%-75

PREVENTION

Lifestyle modifications that can help prevent COPD, or improve function

in COPD patients, include:

Quitting smoking

Avoiding respiratory irritants and infections

Avoiding allergens

Maintaining good nutrition

Drinking lots of fluids

Avoiding excessively low or high temperatures

Very high altitudes

Maintaining proper weight,

Exercising to increase muscle tone.

Avoid smoking tobacco or exposure to second hand tobacco smoke.

Smoking is the leading cause of COPD. Although you cannot undo the

damage that smoking has already caused, you can prevent further lung

damage by quitting. Avoiding conditions that may irritate the lungs can

reduce breathing problems in people with COPD. These conditions

include indoor and outdoor air pollution; smog; cold, dry air; hot, humid

air; or high altitudes. Avoiding respiratory illnesses, such as the flu

(influenza) and pneumonia, can decrease the risk of your COPD

worsening. Talk with your doctor about getting vaccinations

against them. Use appropriate protective gear (e.g. face mask) in the

workplace to avoid inhaling hazardous substance. Get plenty of physical

activity for good lung health. If you already have COPD, avoid colds and

flu’s, which can worsen the disease. Get annual flu and pneumococcal

vaccinations to avoid such infections. Quitting smoking is the most

important thing you can do to prevent or slow damage to your lungs.

 

CLINICAL MANAGEMENT

Non-drug treatment

Advice on how to respond promptly to symptoms of an

exacerbation, including starting oral corticosteroid therapy,

starting antibiotic therapy if their sputum is purulent and adjusting

their bronchodilator therapy to control their symptoms.

Advice on when and how to contact a health care professional if

symptoms do not improve.

Smoking cessation: an up to date smoking history, including pack

years smoked (number of cigarettes smoked per day, divided by

20, multiplied by the number of years smoked), should be

documented for everyone with COPD. An assessment of their

"readiness to change" should also be made.2

Nutrition: BMI should be calculated. If the BMI is abnormal (high or

low), or changing over time, the patient should be referred for

dietetic advice. If the BMI is low, patients should also be given

nutritional supplements to increase their total calorific intake, and

be encouraged to take exercise to augment the effects of

nutritional supplementation.

Drug therapy

Bronchodilator therapy:

Long-acting bronchodilators are not suitable for the relief

of acute bronchospasm but may have additional benefits

over combinations of short-acting drugs. However they

may also have additional side effects:

Long acting beta2 agonists:

o The use of long term beta2 agonists in the absence of

inhaled steroids appears to carry an increased

incidence of death or near death complications in

some groups.3

o Recent research has also suggested that patients

taking long acting beta2 agents also appear to have

more difficulties during an exacerbation due to down

regulation of the receptors.

o Therefore the role of long acting beta2 agonists in the

management of COPD is currently being re-

evaluated.

Tiotropium (a long-acting anticholinergic bronchodilator):4

o Is effective in controlling symptoms and improve

exercise capacity in patients who continue to

experience problems despite the use of short-acting

drugs.

o Tiotropium reduces COPD exacerbations and hospital

admissions and improves health-related quality-of-life

in patients with moderate and severe disease.

o Tiotropium possibly slows the decline in FEV1.

o Additional long-term studies are required to evaluate

its effect on mortality and change in FEV1, to confirm

its role compared to, or in combination with, long-

acting beta2-agonists, and to assess its effectiveness

in mild and very severe COPD.

Mucolytic drug therapy: should be considered in patients

with a chronic cough productive of sputum and continued

if there is symptomatic improvement (e.g. reduction in

frequency of cough and sputum production).

Theophylline: should only be used after a trial of short-

acting bronchodilators and long-acting bronchodilators, or

in patients who are unable to use inhaled therapy.

Phosphodiesterase type 4 inhibitors: there is insufficient

long-term data on which to base any evidence statements

or recommendations.

Inhaled corticosteroids:

o None of the inhaled corticosteroids currently

available are licensed for use alone in the treatment

of COPD.

o Oral corticosteroid reversibility tests do not predict

response to inhaled corticosteroid therapy.

o Inhaled corticosteroids should be prescribed for

patients with an FEV1 50% or less of predicted, who

are having 2 or more exacerbations requiring

treatment with antibiotics or oral corticosteroids in a

12 month period.

o The aim of treatment is to reduce exacerbation rates

and slow the decline in health status and not

necessarily to improve lung function.

Oral corticosteroids:

o Maintenance use of oral corticosteroid therapy in

COPD is not normally recommended. If oral

corticosteroids cannot be withdrawn following an

exacerbation, the dose of oral corticosteroids should

be kept as low as possible.

o Patients treated with long term oral corticosteroid

therapy should be monitored for the development of

osteoporosis.

Combination therapy:

o If patients remain symptomatic on monotherapy,

effective combinations include:

Beta 2-agonist and anticholinergic

Beta 2-agonist and theophylline

Anticholinergic and theophylline

Long-acting beta 2-agonist and inhaled

corticosteroid

Combination treatment should be discontinued if there is

no benefit after 4 weeks.

Delivery systems:

o In most cases bronchodilator therapy is best

administered using a hand held inhaler device

(including a spacer device if appropriate).

o There is no evidence to suggest superiority of

nebulised therapy over the use of an MDI with a

spacer device.

Non-invasive ventilation:

o Adequately treated patients with chronic hypercapnia

ventilator failure who have required assisted

ventilation (whether invasive or non-invasive) during

an exacerbation or who are hypercapnia or acidosis

on oxygen therapy should be referred to a specialist

centre for consideration of long-term NIV.

Treatments not recommended include anti-oxidant

therapy with alpha-tocopherol and beta-carotene

supplements, anti-tussive therapy and prophylactic

antibiotic therapy.

Vaccination and anti-viral therapy

Pneumococcal vaccination and an annual influenza vaccination

should be offered to all patients with COPD.

Antiviral for influenza: zanamivir and oseltamivir are recommended

for the treatment of at-risk adults who present with influenza-like

illness and who can start therapy within 48 hours of the onset of

symptoms.

Zanamivir should be used with caution in people with COPD

because of a risk of bronchospasm and patients prescribed

zanamivir should have a fast-acting bronchodilator available.

Lung surgery

Patients who are breathless, and have a single large bulla on a CT

scan and an FEV1 less than 50% predicted should be referred for

consideration of bullectomy.

Patients with severe COPD who remain breathless with marked

restrictions of their activities of daily living despite maximal medical

therapy should be referred for consideration of lung volume

reduction surgery if they meet all of the following criteria:

1. FEV1 more than 20% predicted 2. PaCO2 less than 7.3kPa 3. Upper lobe predominant emphysema 4. TLCO more than 20% predicted

Patients with severe COPD who remain breathless with marked

restrictions of their activities of daily living despite maximal medical

therapy should be considered for referral for assessment for lung

transplantation bearing in mind comorbidities and local surgical

protocols.

Considerations include: age, FEV1, PaCO2, homogeneously

distributed emphysema on CT scan, elevated pulmonary artery

pressures with progressive deterioration.

Palliative care

Opioids should be used when appropriate to palliate

breathlessness in patients with end-stage COPD which is

unresponsive to other medical therapy.

Benzodiazepines, tricycle antidepressants, major tranquillisers and

oxygen should also be used when appropriate for breathlessness

in patients with end stage COPD unresponsive to other medical

therapy.

Patients with end stage COPD and their family and carers should

have access to the full range of services offered by

multidisciplinary palliative care teams, including admission to

hospices.

ASTHMA

Asthma is an obstructive lung disease where the bronchial tubes

(airways) are extra sensitive (hyper responsive).

The airways become inflamed and produce excess mucus and the

muscles around the airways tighten making the airways narrower.

It is characterised functionally by the presence of airflow

obstruction which is variable over short periods of time, or is

reversible with treatment.

Asthma is usually triggered by breathing in things in the air such as

dust or pollen that produce an allergic reaction.

It may be triggered by other things such as an upper respiratory

tract infection, cold air, exercise or smoke.

Asthma is a common condition and affects over 300 million people

around the world.

Asthma causes recurring episodes of wheezing, breathlessness,

chest tightness, and coughing, particularly at night or in the early

morning.

AETIOLOGY

The aetiology of asthma is complex, and multiple environmental

and genetic determinants are implicated.

Living in farms, large families, childhood infections, including

parasites, exposure to pets in early life.

Obesity may also increase the risk of asthma.

Smokers may be at high risk.

PATHOPHYSIOLOGY

The inhalation of an allergens rapidly interacts with mucosal mast

cells via an IgE dependent mechanism,

Resulting in release of mediators such as histamine and the

cysteinyl leukotrienes with resulting in bronchi constriction.

Airway hyper reactivity is integral to diagnosis of asthma.

Others factors are the behaviour of airway smooth muscles,

degree of airway narrowing and influence of neurogenic

mechanism.

TYPES OF ASTHMA

It is divided into two types:

Extrinsic asthma

Intrinsic asthma

Extrinsic asthma

Extrinsic asthma is also called atopic asthma.

It occurs in younger age group. Patients are sensitive to different

factors like pollen, dust, mites, and have family history.

These subjects show immediate skin reaction.

Intrinsic asthma

It is called non-atopic asthma which tends to occur in older

patients.

It is precipitated by chronic bronchitis, strenuous exercise, stress

or anxiety.

Respiratory infections are also common cause.

CLINICAL FEATURES

Recurrent episodes of wheezing, chest tightness, breathlessness

and cough.

The patient will prefer to sit upright with shoulder girdle fixed to

assist accessory muscles of respiration

Nocturnal asthma is common with cough and wheeze during

sleep.

Mild intermittent asthma are usually asymptomatic

Breath sounds are vesicular.

Crackles may also be heard if sputum is present.

On percussion hyper-resonant.

In persistent asthma the pattern is one chronic wheeze and

breathlessness.

Cough variant asthma may be present with cough as dominant

symptom.

INSVESTIGATIONS

Asthma is diagnosed by the characteristic pattern of symptoms.

A peak flow meter can record variations in the severity of asthma

over time.

Spirometry, a measurement of lung function, can provide an

assessment of the severity, reversibility, and variability of airflow

limitation, and help confirm the diagnosis of asthma.

An elevated sputum or peripheral blood eosinopil count may be

observed.

In radiological examination of acute asthma hyperinflation and

lobar collapse may be seen.

Induced sputum and exhaled breath allow the non invasive

assessment of airway inflammation.

In emergency department doctors use capnography which

measures the amount of exhaled carbon dioxide along with pulse

oxymetry.

More recently, exhaled nitric oxide has been studied as breath test

indicative of airway inflammation in asthma.

MEDICAL TREATMENT

The most effective treatment for asthma is identifying triggers,

such as pets or aspirin and limiting or eliminating exposure to

them.

Desensitization is currently the only known cure to the disease.

Other form of treatment includes relief medication, prevention

medication, long-acting beta agonists and emergency treatment.

Bronchodilators are recommended for short term relief in all

patients

For those with persistent disease low dose inhaled glucocorticoids

or leukotriene modifier’s mast cell stabilizer or theophylline may be

administered

For sever patients a higher dose of glucocortcoids with long acting

inhaled beta2 agonist

Beta2 agonist like salbutamol, levabuterol, terbutaline and

bitolterol are used.

Nebulised salbutamol or terbutaline often combined with

ipratropium is given.

System steroids, oral or intravenous like prednisolne,methyl

prednisone, dexamethasone or hydrocortisone are used

Methylxanthines like theophylline, aminophylline may be used

Intubation and mechanical ventilation for patients with respiratory

arrest

Heliox is used in hospital setting as it has more laminar flow than

ambient air and moves easily through constricted airways.

BRONCHIECTASIS

Bronchiectasis is a disease that causes localized, irreversible

dilation of part of the bronchial tree.

It is classified as an obstructive lung disease, along with bronchitis

and cystic fibrosis.

Involved bronchi are dilated, inflamed, and easily collapsible,

resulting in airflow obstruction and impaired clearance of

secretions.

Bronchiectasis is associated with a wide range of disorders, but it

usually results from necrotizing bacterial infections, such as

infections caused by the Staphylococcus or Klebsiella species or

Bordetella pertussis.

PATHOGENSIS

Dilation of the bronchial walls results in airflow obstruction and

impaired clearance of secretions because the dilated areas disrupt

normal air pressure in the bronchial tubes, causing sputum to pool

inside the dilated areas instead of being pushed upward.

The pooled sputum provides an environment conducive to the

growth of infectious pathogens, and these areas of the lungs are

thus very vulnerable to infection.

The more infections that the lungs experience, the more damaged

the lung tissue and alveoli become.

When this happens, the bronchial tubes become more inelastic

and compressed, creating a self-perpetuating cycle of further

damage to the lungs.

TYPES OF BROCHIECTASIS

There are three types of bronchiectasis, varying by level of severity.

Fusiform (cylindrical) bronchiectasis (the most common type)

refers to mildly inflamed bronchi that fail to taper distally.

In varicose bronchiectasis, the bronchial walls appear beaded,

because areas of dilation are mixed with areas of constriction.

Saccular (cystic) bronchiectasis is characterized by severe and

irreversible ballooning of the bronchi peripherally, with or

without air-fluid levels.

Chronic productive cough is prominent, occurring in up to 90% of

patients with bronchiectasis.

Generally, persons suffering from bronchiectasis tend to be

infected by Haemophilus influenza early on in the disease course.

Secondary infection is usually due to Staphylococcus aureus;

followed by Moraxella catarrhalis and finally Pseudomonas

aeruginosa.

CAUSES

There are both congenital and acquired causes of bronchiectasis.

Kartagener syndrome, which affects the mobility of cilia in the

lungs, aids in the development of the disease.

Young's syndrome, which is clinically similar to cystic fibrosis, is

thought to significantly contribute to the development of

bronchiectasis. This is due to the occurrence of chronic, sin

pulmonary infections.

Patients with alpha 1-antitrypsin deficiency have been found to be

particularly susceptible to bronchiectasis. Acquired bronchiectasis

occurs more frequently, with one of the biggest causes being

tuberculosis.

Endobronchial tuberculosis commonly leads to bronchiectasis,

either from bronchial stenosis or secondary traction from fibrosis.

An especially common cause of the disease in children is acquired

immune deficiency syndrome, stemming from the human insulin

immunodeficiency virus.

Other acquired causes of bronchiectasis involving environmental

exposures include respiratory infections, obstructions, inhalation

and aspiration of ammonia and other toxic gases.

SIGNS AND SYMPTOMS

Persistent Cough and purulent sputum is present

The sputum is green, foul smelling and in large volume

Pyrexia, night sweats, anorexia, malaise, weight loss, lassitude

and joint pains are present

Shortness of breath is seen in severe conditions

Haemoptysis is common usually associated with acute infection

Recurrent pneumonia is present

Chronic sinusitis is present in most of patients

In 50% patients clubbing is present

Thoracic mobility decreases

DIAGNOSIS

The diagnosis of bronchiectasis is based on the review of clinical

history and characteristic patterns in high-resolution CT scan

findings.

Such patterns include "tree-in-bud" abnormalities and cysts with

definable borders. In one small study, CT findings of

bronchiectasis and multiple small nodules were reported to have a

sensitivity of 80%, specificity of 87%, and accuracy of 80% for the

detection of bronchiectasis.

Bronchiectasis may also be diagnosed without CT scan

confirmation if clinical history clearly demonstrates frequent,

respiratory infections, as well confirmation of an underlying

problem via blood work and sputum culture samples.

COMPLICATIONS

Recurrent haemoptysis

Pneumonia

Pleurisy and empyema

Respiratory failure

Right ventricular failure

Emphysema and systemic amyloidosis are rare

TREATMENT

Treatment of bronchiectasis is aimed at controlling infections and

bronchial secretions, relieving airway obstruction, and preventing

complications.

This includes the prolonged usage of antibiotics to prevent

detrimental infections, as well as eliminating accumulated fluid with

postural drainage and chest physiotherapy.

Surgery may also be used to treat localized bronchiectasis,

removing obstructions that could cause progression of the disease.

Inhaled steroid therapy that is consistently adhered to can reduce

sputum production and decrease airway constriction over a period

of time, and help prevent progression of bronchiectasis.

One commonly used therapy is beclometasone dipropionate,

which is also used in asthma treatment.

Use of inhalers such as albuterol (salbutamol), fluticasone

(Flovent/Flixotide) and ipratropium (Atrovent) may help reduce

likelihood of infection by clearing the airways and decreasing

inflammation.

PREVENTION

In order to prevent future development of bronchiectasis, an x-ray

of the chest should be taken after any severe attack of measles,

whooping cough or other acute respiratory infection in childhood.

CYSTIC FIBROSIS

Cystic fibrosis (also known as CF, mucovoidosis, or

mucoviscidosis) is a genetic disorder known to be an inherited

disease of the secretory glands, including the glands that make

mucus and sweat.

The hallmarks of cystic fibrosis are salty tasting skin, normal

appetite but poor growth and poor weight gain, excess mucus

production, and coughing/shortness of breath. Males can be

infertile due to the condition Congenital absence of the vas

deferens. Often, symptoms of CF appear in infancy and childhood.

Meconium ileus is a typical finding in newborn babies with CF.

Although technically a rare disease, cystic fibrosis is ranked as one

of the most widespread life-shortening genetic diseases.

CAUSES

Cystic Fibrosis has an autosomal recessive pattern of inheritance.

CF is caused by a mutation in the gene cystic fibrosis

transmembrane conductance regulator (CFTR). The product of this

gene is a chloride ion channel important in creating sweat,

digestive juices and mucus.

Although most people without CF have two working copies

(alleles) of the CFTR gene, only one is needed to prevent cystic

fibrosis. CF develops when neither allele can produce a functional

CFTR protein.

Therefore, CF is considered an autosomal recessive disease.

PATHOPHYSIOLOGY

The protein created by this gene is anchored to the outer

membrane of cells in the sweat glands, lungs, pancreas, and other

affected organs.

The protein spans this membrane and acts as a channel

connecting the inner part of the cell (cytoplasm) to the surrounding

fluid.

This channel is primarily responsible for controlling the movement

of chloride from inside to outside of the cell; however, in the sweat

ducts it facilitates the movement of chloride from the sweat into the

cytoplasm.

When the CFTR protein does not work, chloride is trapped inside

the cells in the airway and outside in the skin.

Because chloride is negatively charged, positively charged ions

cross into the cell because they are affected by the electrical

attraction of the chloride ions.

Sodium is the most common ion in the extracellular space and the

combination of sodium and chloride creates the salt, which is lost

in high amounts in the sweat of individuals with CF. This lost salt

forms the basis for the sweat test.

One theory suggests that the lack of chloride exodus through the

CFTR protein leads to the accumulation of more viscous, nutrient-

rich mucus in the lungs that allows bacteria to hide from the body's

immune system.

Another theory proposes that the CFTR protein failure leads to a

paradoxical increase in sodium and chloride uptake, which, by

leading to increased water reabsorption, creates dehydrated and

thick mucus.

Yet another theory focuses on abnormal chloride movement out of

the cell, which also leads to dehydration of mucus, pancreatic

secretions, biliary secretions, etc.

These theories all support the observation that the majority of the

damage in CF is due to blockage of the narrow passages of

affected organs with thickened secretions.

These blockages lead to remodelling and infection in the lung,

damage by accumulated digestive enzymes in the pancreas,

blockage of the intestines by thick faeces, etc

SYMPTOMS

Thick, viscous mucus secretions in the lungs

Repeated infections: The accumulation of sticky, thick mucus in

the lungs creates a favourable environment for infectious

microorganisms to inhabit and flourish.

Stools, pale or clay colour, foul smelling, or stools that float

Recurrent pneumonia

Chronic cough, possibly with blood streaking

Wheezing

Bronchitis

Chronic sinusitis

Asthma

Weight loss, failure to thrive in infants, abdominal swelling

Excessive salt in sweat, dehydration

Failure of newborn to pass stool

Abdominal pain, flatulence

Fatigue

Enlarged fingertips (clubbing)

Changes in colour and amount of sputum (material coughed

up from the lungs)

DIAGNOSIS

CF can be diagnosed at birth, but most often is diagnosed during

the early childhood years in young children (by the age of 3 years)

who have had a history of respiratory infections, excessive fat in

their stools, and who have poor weight gain.

Nearly 8 percent of people with CF are diagnosed at 18 years of

age or older because they have experienced only mild symptoms

of CF.

CF's major symptoms is respiratory infection, a CF diagnosis

sometimes may be confused with other respiratory conditions such

as asthma, pneumonia, or chronic bronchitis.

Genetic Testing

Couples planning a family may decide to have themselves

tested if one or both have a family history of CF

Sweat Test

The sweat test is an accurate, safe, and painless way to

diagnose CF. In the sweat test, a small electric current is used to

carry the chemical pilocarpine into the skin of the forearm. This

stimulates sweat glands in the area to produce sweat. Over a

period of 30 to 60 minutes, sweat is collected on filter paper (or

gauze) and tested for chloride. A chloride reading of more than 60

mEq/L points to CF.

Pulmonary Function Tests :-

PFTs; Spirometry; Spirogram; Lung function tests

Pulmonary function tests (PFTs) are breathing tests that help

measure lung reserve and degree of airflow obstruction. Infant

PFTs are currently being studied.

COMPLICATIONS

Haemoptysis

Spontaneous pneumothorax

Osteoporosis

Liver diseases

Diabetes mellitus

Deformities like kyphosis and lordosis

Cor Pulmonale

MANAGEMENT

The cornerstones of management are proactive treatment of

airway infection, and encouragement of good nutrition and an

active lifestyle.

Targets for therapy are the lungs, gastrointestinal tract (including

insulin treatment and pancreatic enzyme supplements), the

reproductive organs (including Assisted Reproductive Technology

(ART)) and psychological support.

In addition, therapies such as transplantation and gene therapy

aim to cure some of the effects of cystic fibrosis.

Gene therapy aims to introduce normal CFTR to airway.

Theoretically this process should be simple as the airway is easily

accessible and there is only a single gene defect to correct.

However there are some problems associated with these methods

involving efficiency (liposome’s insufficient protein) and delivery

(virus provokes an immune response).

The most consistent aspect of therapy in cystic fibrosis is limiting

and treating the lung damage caused by thick mucus and infection

with the goal of maintaining quality of life.

Intravenous, inhaled, and oral antibiotics are used to treat chronic

and acute infections.

Mechanical devices and inhalation medications are used to alter

and clear the thickened mucus

Antibiotics to treat lung disease

Many CF patients are on one or more antibiotics at all times,

even when they are considered healthy, to suppress the

infection as much as possible.

Many bacteria common in cystic fibrosis are resistant to

multiple antibiotics and require weeks of treatment with

intravenous antibiotics such as vancomycin, tobramycin,

meropenem, ciprofloxacin, and piperacillin.

Inhaled therapy with antibiotics such as tobramycin and

colistin is often given for months at a time in order to improve

lung function by impeding the growth of colonized bacteria.

Inhaled therapy with the antibiotic aztreonam is also being

developed and clinical trials have shown great promise.

Oral antibiotics such as ciprofloxacin or azithromycin are

given to help prevent infection or to control ongoing infection.

Some individuals spend years between hospitalizations for

antibiotics, whereas others require several antibiotic

treatments each year.

Transplantation and gene therapy

Lung transplantation often becomes necessary for individuals

with cystic fibrosis as lung function and exercise tolerance

declines.

Although single lung transplantation is possible in other

diseases, individuals with CF must have both lungs replaced

because the remaining lung would contain bacteria that could

infect the transplanted lung.

A pancreatic or liver transplant may be performed at the same

time in order to alleviate liver disease and/or diabetes.

Gene therapy holds promise as a potential avenue to cure

cystic fibrosis.

Gene therapy attempts to place a normal copy of the CFTR

gene into affected cells. Studies have shown that to prevent the

lung manifestations of cystic fibrosis, only 5–10% the normal

amount of CFTR gene expression is needed.

Ideally, transferring the normal CFTR gene into the affected

epithelium cells would result in the production of functional

CFTR in all target cells, without adverse reactions or an

inflammation response.

PT ASSESSMENT

PATIENT PROFILE:

NAME:

AGE/SEX:

ADDRESS:

SUBJECTIVE ASSESSMENT:

OCCUPATION:

CHIEF COMPLIANT:

PRESENT HISTORY:

PAST HISTORY:

PAST MEDICAL HISTORY:

PRESENT MEDICAL HISTORY:

FAMILYHISTORY:

PRESONAL HISTORY:

OCCUPATIONAL HISTORY:

SOCIO-ECONOMICAL HISTORY:

OBJECTIVE ASSESSMENT:

ON OBSERVATION:

BUILT

POSITION OF PATIENT

POSTURE

BREATHING PATTERN

CLUBBING

CYANOSIS

CHEST WALL DEFORMITIES

OEDEMA

TROPICAL CHANGES

RESPIRATORY MUSCLES

DYSPNOEA

SPUTUM

HAEMOPTYSIS

CHEST PAIN

SKELETAL MOBILITY

ON EXAMINATION

VITAL SIGNS

TEMPERATURE

RESPIRATORY RATE

PULSE RATE BLOOD PRESSURE

ON PALPATION

PRESENCE OF NODULES

TENDERNESS

WARMTH

SWELLING

CHECK THE INSPIRATORY EFFORT

COUGH REFLEX

FREMITUS

ON AUSCULTATION

COARSE CREPITATIONS

WHEEZES

CHEST MEASUREMENTS

LEVEL OF FOURTH COSTAL CARTILAGE

XIPHISTERNUM

NINTH COSTAL CARTILAGE

PHYSIOTHERAPY MANAGEMENT :-

Chronic obstructive pulmonary disease (COPD) is characterised by

intractable dyspnoea, reduced functional capacity and episodes of acute

exacerbation.

Physiotherapy plays a key role in multidisciplinary interventions. The

evidence in relation to airway clearance, pulmonary rehabilitation,

Inspiratory muscle training and non-invasive ventilation is now robust

whilst further evidence is required for other interventions in order to

clarify where application, skills and training should be focused.

The challenge is to translate sound clinical evidence-based practice into

novel models of service with resultant improvements in care for patients

with COPD.

POSITIONING :-

THE PURPOSE OF POSITIONING

1. To improve oxygen transport in acute pulmonary

dysfunction of COPD

2. To improve oxygen transport in the post acute

and chronic stages of COPD

3. To prevent the negative effects of restricted

mobility, particularly those that adversely

affect oxygen transport.

cystic fibrosisA) Relaxed sitting posture (posterior view). Note: Forward head position,tight sub occipital and mid-cervical extensors, tight upper and middle fibres of trapezius, asymmetry and abducted and protracted position of the scapulae, increased thoracic kyphosis, reduced upper lumbar lordosis, posterior rotation of pelvis.

B) Relaxed sitting posture (side view). Note: Forward head position, increasedsternocleidomastoid activity, increased low cervical lordosis and thoracic kyphosis, abducted and protracted scapulae, anterior position of humerus in glenoid fossa, internal rotation of humerus, lax abdominal muscles.

POSTURAL DRINAGE:-

BREATHING EXERCISES

These exercises are fundamental interventions for prevention

or comprehensive management of COPD. These exercises are

diaphragmatic.

Breathing exercises are designed to restrain the muscles of

respiration and improve or redistribute ventilation, lessen the work of

breathing, and improve the gas exchange and oxygenation.

Active range of motion exercises, to the shoulders and trunk also

help expand the chest, facilitate deep breathing, and often stimulate the

cough reflex.

Goals of Breathing Exercises

Improve ventilation.

Increase the effectiveness of the cough mechanism.

Prevent pulmonary impairments.

Improve the strength, endurance, and coordination of

respiratory muscles.

Maintain or improve chest and thoracic spine mobility.

Correct inefficient or abnormal breathing patterns.

Promote relaxation.

Teach the patient how to deal with shortness of breath

attacks.

Improve a patient’s overall functional capacity.

TYPE OF BREATHING EXERCISE

Three basic breath-training methods are

diaphragmatic breathing, pursed-lip breathing, and breathing while

bending forward. They can be used to help you get through periods

when you feel more short of breath.

Diaphragmatic Breathing

Pursed-lip Breathing

Breathing while bending forward

Diaphragmatic breathing helps your lungs expand so that they take in

more air. (Your diaphragm is a muscle that helps draw air into your

lungs as you breathe.) Many, but not all, people with COPD find this

breathing method helpful.

Lie on your back, or prop yourself up on several pillows.

With one hand on your belly and the other on your chest, breathe in,

pushing your belly out as far as you can. You should be able to feel

the hand on your belly moving out, while the hand on your chest

should not move.

When you breathe out, you should be able to feel the hand on your

belly moving in.

After you can do this kind of breathing well lying down, you can learn

to do it sitting or standing.

Practice this breathing for 20 minutes, 2 or 3 times a day.

Pursed-lip breathing may help you breathe more air out so that your

next breath can be deeper. Pursed-lip breathing reduces shortness of

breath and improves your ability to exercise.

Breathe in through your nose and out through your mouth while

almost closing your lips.

Breathe in for about 4 seconds, and breathe out for 6 to 8 seconds.

Breathing while bending forward at the waist may make it easier for

you to breathe. Bending forward while breathing may reduce shortness

of breath in those with severe COPD, both at rest and during exercise.

This may be because bending forward allows the diaphragm to move

more easily.

Precautions

Never allow a patient to force expiration. Expiration should be

relaxed and passive. Forced expiration only increases turbulence

in the airways, which can lead to bronchospasm and increased

airway restriction.

Do not allow a patient to take a very prolonged expiration. This

causes the patient to gasp with the next inspiration. The patient’s

breathing pattern then becomes irregular and inefficient.

Do not allow the patient to initiate inspiration with the accessory

muscles and the upper chest. Advise the patient that the upper

chest should be relatively quiet during breathing.

Allow the patient to practice deep breathing for only three or four

inspirations and expirations at a time to avoid hyperventilation.

OTHERS TECHNIQUES USED:

HUMIDIFICATIONS :-

Respiratory gas humidification is a method

of artificial warming and humidifying of respiratory gas for the patient

during mechanical ventilation.

THE ACTIVE CYCLES OF BRETHING TECHNIQUE

It involves three phases repeated in cycles

Breathing Control

The patient is instructed to breath in a relaxed manner using

normal tidal volume.

The upper chest and shoulder remain relax, lower chest and

abdomen should be active.

Preparation for next phase in 5-10 seconds

Thoracic Expansion

The emphasis during this phase is on inspiration.

The patient is instructed to take in a breath to Inspiratory reserve

expiration is passive and relaxed.

Chest percussion shaking or vibration may be performed in

combination within thoracic expansion as the patient exhales.

Forced Expiratory Techniques

It consists of huffing interpersed within breathing control. A huff is

a rapid, forced exhalation but not within maximal effort.

INCREASING/MAINTAINING EXERCISE TOLERANCE

Before Exercise training, the Exercise tolerance and dyspnoea is

done by BORG’S scale for Exertion(R.P.E –RATING PERCEIVED

EXERTION)

15 Point Scale

6 - 20% effort

7 - 30% effort - Very, very light (Rest)

8 - 40% effort

9 - 50% effort - Very light - gentle walking

10 - 55% effort

11 - 60% effort - Fairly light

12 - 65% effort

13 - 70% effort - Somewhat hard - steady pace

14 - 75% effort

15 - 80% effort – Hard

16 - 85% effort

17 - 90% effort - Very hard

18 - 95% effort

19 - 100% effort - Very, very hard

20 - Exhaustion

Training Intensity

Aerobic training is usually target at 60-90% of predicted maximal

heart rate or 50-80% of maximal oxygen intake or 60-90%mhr of

pulse oxymetry.

This level is sustained for 20-45% and repeated 3-4 times a week

Training at this intensity, within is well above the anaerobic

threshold, increase maximal exercise performance, causes

physiologic adaptations in peripheral muscle and improves cardiac

function in healthy subjects.

Most exercise tolerance programs emphasis endurance training,

utilizing periods of sustained exercise for about 20-30 minutes, 2-5

times a week.

Training specificity

Refers to the observation that benefit is gained only in those

activities involving the muscle groups that are specifically trained.

INSPIRATORY MUSCLE TRAINING

Inspiratory muscles may be compromised in majority of lung

diseases and contribute to dyspnoea – exercise limitation and

hypercapnia.

Generally initiated at low intensity then gradually increased to

achieve 60-70% of maximum.

NON-INVASIVE POSITIVE PRESSURE VENTILATION

In selected patients with hypercapnia respiratory failure due to

an acute exacerbation of chronic obstructive pulmonary disease

(COPD), non-invasive positive pressure ventilation (NIPPV) is an

effective adjunct to usual medical therapy.

In controlled trials, it reduced the need for endotra-

cheal intubation, the length of hospital stay, and the

risk of death.

Patients with decompensate respiratory

failure lack sufficient alveolar ventilation, owing to

abnormal respiratory mechanics and Inspiratory

muscle fatigue. For these patients, breathing faster does not fully

compensate.

Non-invasive positive pressure ventilation partially counteracts these

factors by providing a larger tidal volume with the same Inspiratory effort.

Additionally, this treatment can decrease the work of breathing by

partially overcoming auto-PEEP (positive end-expiratory pressure) in

certain situations. Auto-PEEP is pressure greater than the atmospheric

pressure remaining in the alveoli at the end of exhalation. This condition

is related to limited expiratory flow and is common in those with severe

COPD. Non-invasive positive pressure ventilation decreases the

pressure difference between the atmosphere and the alveoli, thereby

reducing the Inspiratory force needed for initiation of Inspiratory effort,

which may reduce the work of breathing.

BIBILOGRAPHY

DAVIDSON-GENERAL MEDICINE

HARRISON’S-INTERNAL MEDICINE

HARSHA MOHAN-PATHOLOGY

JULLIAN-

JENNIFER PRIOR-

TIDY’S PHYSIOTHERAPY

CASH TEXTBOOK OF CARDIOVASCULAR

DISEASE FOR PHYSIOTHERAPY

INTERNET