SWATANTRA INSTITUTE OF PHYSIOTHERAPY AND REHABILITATION RAJAHMUNDRY 533105

CERTIFICATE

This is to certify that this project is bonafied record work done by N.V.R.RAO ALAPATI final year B.P.T. and submitted Examination.
October 2009. Regd No: 0436021

to N.T.R. University

of health sciences

Vijayawada, for the

Bachelor of Physiotherapy Degree

INTERNAL EXAMINER

EXTERNAL EXAMINAR

PROJECT GUIDE

PRINCIPAL

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A PROJECT WORK ON OBSTRUCTIVE RESPIRATORY DISORDERS

Submitted to the N.T.R University of health Sciences for Bachelor of Physiotherapy Degree Examinations October 2009

Submitted by N.V.R RAO ALAPATI B.P.T.FINAL YEAR SWATANTRA INSTITUTE OF PHYSIOTHERAPY AND REHABILITATION

RAJAHMUNDRY 533105

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ACKNOWLEDGEMENT
I am glad to submit this project with pleasure. With the blessings of almighty and my parents I am very happy to submit this project. I express my sincere thanks to the Managing Director of Swatantra Institute of Physiotherapy And Rehabilitation, Dr. Ganni Bhaskara Rao M.S, F.I.C.S, for providing the necessary facilities for my project work. I am fortunate enough to have Dr. P. Appa Rao M.P.T (Orthopaedics) our Principal for his valuable guidance and support and I extend my heartful thanks and gratitude to my guide who helped me and rendered his valuable knowledge and time regarding the collection of this information to complete my project successfully. I also express my special and sincere thanks to all our faculty members Dr.B.Syamala M.P.T.(Neurology), Dr. Manivannan M.P.T.(Neurology) Dr. Chaturvedi M.P.T.(Sports) ,Dr. K .Madhu Babu B.P.T. I also glad seniors and friends for their valuable guidance and suggestions throughout the period of my studies. Last but not the least I would like to thank all my seniors, classmates, juniors, and Mr. Kishore (Librarian) who has been very co-operative and supportive during my study period in this campus.

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INDEX INTRODUCTION TO RESPIRATORY DISEASES . 5 ANATOMY OF RESIRATORY SYSTEM....6 PHYSIOLOGY OF RESPIRATION..9 TYPES & DEFINITIONS OF COPD.12 EPIDEMIOLOGY....13 RISK FACTORS.14 PATHOLOGY&PATHOGENESIS....18 SIGNS AND SYMPTOMS22 STAGES OF COPD..29 COMPLICATIONS OF COPD...30 DIAGNOSIS...35 CLINICAL MANAGEMENT37 OTHER TYPES OF OBSRUCTIVE DISEASES............44 PULMONARY REHABILITATION..69 BIBILOGRAPHY...85

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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.

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Anatomy 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.

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 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.

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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.

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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.
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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).

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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

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.

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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, cancer. following the trend of increasing prevalence of lung

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 :women.

The limited data that are available indicate that

morbidity due to COPD increases with age and is greater in men than

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

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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.

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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.

Air pollution
Although the role of air pollution in the etiology of COPD is unclear, the effect is small when compared to cigarette smoking.
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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 or the development of COPD in people who smoke is unclear.

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.

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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 pan lobular). 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.

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.

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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.

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 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.

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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
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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.

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SIGNS & 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

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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.

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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.
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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.

Haemoptysis
COPD is one of the more common causes of hemoptysis (coughing up blood).

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 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.

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SOME IMPORTANT CLINICAL AND HISTORICAL DIFFERENCES CAN EXIST BETWEEN THE TYPES OF COPD.
In the chronic bronchitis group, classic symptoms include the following: Productive cough, with progression over time to intermittent dyspnoea Frequent and recurrent pulmonary infections 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:

A long history of progressive dyspnoea with late onset of non- productive cough

Occasional mucopurulent relapses

Eventual cachexia and respiratory failure

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 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 ronchi 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)

Patients may be very thin with a barrel chest. They typically have little or no cough or expectoration. Breathing may be assisted by pursed lips and use of accessory respiratory muscles; they may adopt the tripod sitting position. The chest may be hyper resonant, and wheezing may be heard; heart sounds are very distant. Overall appearance is more like classic COPD exacerbation.

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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.

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COMPLICATIONS OF COPD
COPD complications can be serious and even lifethreatening. 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.

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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.

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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

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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

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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.

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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.

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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

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CLINICAL MANAGEMENT

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.

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 Avoiding respiratory illnesses, such as the flu (influenza)& pneumonia, can decrease the risk of your COPD worsening.

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. 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:

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 The use of long term beta agonists in the absence of inhaled steroids appears to carry an increased incidence of death or near death complications in some groups. Recent research has also suggested that patients taking long acting beta agents also appear to have more difficulties during an exacerbation due to down regulation of the receptors. Therefore the role of long acting beta2 agonists in the management of COPD is currently being re-evaluated. Tiotropium (a long-acting anticholinergic bronchodilator):
o

Is effective in controlling symptoms and improve exercise capacity in patients who continue to experience problems despite the use of short-acting drugs. Tiotropium reduces COPD exacerbations and hospital admissions and improves health-related quality-of-life in patients with moderate and severe disease. Tiotropium possibly slows the decline in FEV. Additional long-term studies are required to evaluate its effect on mortality and change in FEV, to confirm its role compared to, or in combination with, long-acting beta2agonists, and to assess its effectiveness in mild and very severe COPD.

o o

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).
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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 longterm 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. Oral corticosteroid reversibility tests do not predict response to inhaled corticosteroid therapy. 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. 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. Patients treated with long term oral corticosteroid therapy should be monitored for the development of osteoporosis.

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 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). 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.

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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.

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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.

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ASTHMA

INTRODUCTION
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.

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DEFINITION
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.

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.

[45]

[46]

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.

[47]

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
[48]

 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.
[49]

 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 modifiers 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

[50]

 Heliox is used in hospital setting as it has more laminar flow than ambient air and moves easily through constricted airways.

[51]

BRONCHIECTASIS
INTRODUCTION
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.

[52]

DEFINITION
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.

PATHOGENESIS
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.

[53]

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.

[54]

 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

[55]

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.
[56]

 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

[57]

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.

[58]

CYSTIC FIBROSIS

INTRODUCTION
Cystic fibrosis (also known as Cystic Fibrosis, 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 cystic fibrosis appear in infancy and childhood.

[59]

 Meconium ileus is a typical finding in newborn babies with cystic fibrosis. Although technically a rare disease, cystic fibrosis is ranked as one of the most widespread life-shortening genetic diseases.

DEFINITION

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.

[60]

CAUSES
Cystic Fibrosis has an autosomal recessive pattern of inheritance. Cystic Fibrosis 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 Cystic Fibrosis have two working copies (alleles) of the CFTR gene, only one is needed to prevent cystic fibrosis. Cystic Fibrosis develops when neither allele can produce a functional CFTR protein.
[61]

 Therefore, Cystic Fibrosis 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 Cystic Fibrosis. 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, nutrientrich mucus in the lungs that allows bacteria to hide from the body's immune system.
[62]

 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 Cystic Fibrosis 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
[63]

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)

[64]

DIAGNOSIS
Cystic Fibrosis can be diagnosed at birth, but most often is diagnosed during the early childhood years in young children
[65]

(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 Cystic Fibrosis are diagnosed at 18 years of age or older because they have experienced only mild symptoms of Cystic Fibrosis. Cystic Fibrosis major symptoms is respiratory infection, a Cystic Fibrosis 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 Cystic Fibrosis. Sweat Test The sweat test is an accurate, safe, and painless way to diagnose Cystic Fibrosis. 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 Cystic Fibrosis.

[66]

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.

[67]

 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 (liposomes 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.

[68]

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 510% 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.

[69]

PULMONARY REHABILITATION
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
[70]

 POSITION OF PATIENT POSTURE BREATHING PATTERN CLUBBING CYANOSIS CHEST WALL DEFORMITIES OEDEMA TROPICAL CHANGES RESPIRATORY MUSCLES DYSPNOEA SPUTUM HAEMOPTYSIS SKELETAL MOBILITY

ON EXAMINATION VITAL SIGNS

TEMPERATURE RESPIRATORY RATE PULSE RATE BLOOD PRESSURE

ON PALPATION
[71]

 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

[72]

PHYSIOTHERAPY INTERVENTION
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

GOALS
Reduce symptoms Decrease disability Increase participation in physical and social activities Improve the overall quality of life of individual Decrease morbidity Increase functional activity Increase neuropsychological condition Decrease rate of respiratory complication and hospitalization Increase ability to work

[73]

AIMS
Reduce dyspnoea Increase muscle endurance Increase muscle strength Ensure long term commitment to exercises Help alley fear and anxiety Increase knowledge of lung conditions To promote self management

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.

[74]

cystic fibrosis
A) 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, increased sternocleidomastoid 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.

[75]

POSTURAL DRAINAGE:-

[76]

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 patients overall functional capacity.

[77]

TYPES 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.

[78]

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.

[79]

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 patients 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.

[80]

THE ACTIVE CYCLES OF BREATHING TECHNIQUE

It involves three phases repeated in cycles BREATHING CONTROL THORACIC EXPANSION FORCED EXPIRATORY TECHNIQUES

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.

[81]

INCREASING/MAINTAINING EXERCISE TOLERANCE

Before Exercise training, the Exercise tolerance and dyspnoea is done by BORGS 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.

[82]

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.

[83]

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 endo-tracheal 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.

[84]

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.

[85]

BIBILOGRAPHY
HUMAN ANATOMY B.D CHAURASIA

TEXT BOOK OF PHYSIOLOGY GUYTON HALL

PRINCIPLES OF INTERNAL MEDICINE HARRISON

CASH TEXT BOOK OF CHEST, HEART AND VASCULAR DISORDER PATRICIA A DOWNIE

PRINCIPLES AND PRACTICE OF MEDCINE DAVIDSON

PHYSIOTHERAPY PROBLEMS

FOR

RESPIRATORY

AND

CARDIAC

JENNIFER A PRYOR TIDYS PHYSIOTHERAPY

[86]