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INTRODUCTION
T Allergic asthma is a clinical syndrome characterized by episodic reversible airway obstruction, increased bronchial reactivity and airway inflammation. T Asthma is now recognized to result from complex interactions among inflammatory cells, their mediators, airway epithelium and smooth muscle and the nervous system. T In susceptible individuals, these interactions can lead to symptoms of breathlessness, wheezing, cough, and chest tightness. T Risk factors for allergic asthma include a family history of allergic disease, the presence of allergic specific immunoglobulin E (IgE) aeroallergen exposure, viral respiratory illness, and a lower socioeconomic status. T Of these multiple risk factors, environmental exposure in sensitized individuals is a major contributor to the underlying inflammatory process. T Allergies trigger asthmatic attacks in 60-90% of children and in 50% of adults. T Approximately 75-80 % of patients with asthma has positive (immediate) skin test results. T In children this sensitization is associated with later development of asthma and possibly, atopy.

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T The IgE level is associated with the prevalence and severity of airway hyperactivity (AHR) and asthma. T Symptoms pulmonary functions test findings, and air way hyperreactivity improve with avoidance of environmental allergens. T Mite and cockroach antigens are common, and exposure and sensitization has been shown to increase asthma morbidity. T Removing even one of many allergens can result in clinical improvement. T Although most people with asthma have aeroallergen-induced symptoms, some individuals manifest symptoms with non-allergic triggers. T As many as 10% of people with asthma are sensitive to nonsteroidal anti-inflammatory drugs (NSAIDS). T Approximately 5-10% of people with asthma has occupation or industry induced airway disease. T Many individuals develop symptoms after viral respiratory tract infections. T Although thus triggers act through different pathways the resulting effects on the airway is the same each lead to airway inflammation with increased bronchial reactivity. T Allergen avoidance and other environmental control efforts are feasible and effective. However patients frequently are not complaint with such measures.

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T Asthma is an active area of research, with published literature nearly doubling every decade to a combined 61,072 articles published in 2000. T Studies originally focused on symptoms relief by reversing airway obstruction, but current studies is focused on identifying the causes of asthma and treating the underlying inflammation. T STATISTICS: T Frequency: T In the India: Allergic asthma affects 11.3 million people. T Internationally: Allergic asthma affects more than 100 million people worldwide. T Mortality/Morbidity: T The death rate from asthma is 17.7 deaths per million people. Mortality has increased, especially in children who live in the inner city, despite advances in disease understanding and therapy. T The number of deaths annually decreased from 5067(1960-1962) to a low of 1870(1975-1995) and then increased to 5429(1993-1995). T Annually, allergic asthma is responsible for 1.5 million emergency department visits, 500,000 hospital admissions (third leading preventable cause) and 100 million days of restricted activity.

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T Medical expenses and lost work and productivity cost an estimated $12.7 billion in 1998. T Increased morbidity is multifactorial and may include increased exposure to indoor allergens, less exposure to viral infections early in life, more environmental pollution, over use of beta-2 agonistic, under use of anti-inflammatory medications and limited access to or education about health care. T Race: T Females, ethnic minorities, people with a low annual family income, and those with poor access to or education about health care have worse outcomes than other individual. T Hospitalization and death rates are 3 times greater in African, Americans. T Sex: T In children, boys have been shown to be at greater risk for asthma than girls. In children younger than in years, the prevalence is twice as high in boys compared to girls. T The difference narrows with age, and women aged 40 years have a greater prevalence than men of the same age. T Age: T Disease onset can occur in persons of any age, but children after present when younger than 6 years. T Many children out grow asthma, especially boys who have no personal or family history of atopy. Perinatal exposure to allergens or passive smoke has been postulated to make out growing asthma less likely.
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ANATOMY
The cavity of thorax contains the right and left pleural cavities, which are completely invaginated and occupied by the lungs. A thick medium portion called the mediastinum separates the right and left pleural cavities. The lungs are the respiratory organs situated in the thoracic cavity. Each lung invaginates the corresponding pleural cavity. The right and left lungs are separated by the mediastinum. The lungs are spongy in texture. In the young the lungs are brown or gray in the colour, gradually they become mottled black because of the deposition of the inhaled carbon particles. The right lung weights about 625 ms. it is about 50 gms heavier than the left lung. Two layers of serous membrane collectively called as the pleural membrane enclose and protect the each lung.

The inner layer, the visceral pleura cover the lungs themselves. Between the parietal and visceral pleurae is a small potential space. The pleural cavity, which contains a lubricating fluid, secreted by the membrane. This fluid reduces friction between the membranes and allows them to move easily on the another during the breathing.

THE PLEURA:

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Like the peritoneum, the pleura are a serous membrane, which is lined by the mesothelium. There are 2 pleural sacs one either side of the mediastinum.

In some diseases the pleural cavity may become filled with the air (pneumothorax) fluid (pleural effusion) blood (haemothorax) or pus (emphysema).

PULMONARY PLEURA:
It covers the surfaces and fissures of the lung, except at the hilum and along the attachment of the pulmonary ligament where it is continuous with the parietal pleura. It is firmly adherent to the lung and cannot be separated from it.

PARIETAL PLEURA:
It is thicker than the pulmonary pleura and is subdivided into 4 parts. 1. 2. 3. 4. Costal Diaphragmatic. Mediastinal Cervical.

It is related anteriorly to the subclavian artery and the scalenus anterior, posteriorly to the neck of the first rib and structures
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lying over it laterally to the scalenus medius and medially to the large vessels of the neck.

PULMONARY LIGAMENT: The parietal pleura surrounding the root of the lung extends downwards beyond the root as a fold called the pulmonary ligament. It provides a dead space into which the pulmonary veins can expand during the increased venous return.

RECESS OF PLEURA:
There are two folds (recesses) of the parietal pleura, which acts as the reserve spaces for the lung to expand during the deep inspiration. The costomediastinal recess lies to the anteriorly, behind the sternum and the Costal cartilages, between the Costal and the Mediastinal pleurae, particularly in relation to the cardiac notch of the left lung. This recess is possibly filled up by the anterior margin of the lungs even during quiet breathing. The costodiaphragmatic recess lies inferiorly between the costal and the diaphragmatic pleura. Vertically it is measures about 5 cms, and extends from the 8th to 10th ribs, along the midaxilary line.

SURFACE MARKING OF THE PLEURA:

There are 4 surface markings of the pleura they are
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1. 2. 3. 4.

Cervical pleura.

Anterior margin. Inferior margin. Posterior margin.

NERVE SUPPLY OF PLEURA:

The parietal pleura develop from the somato pleura layer of the lateral plate mesoderm, and are supplied by the somatic nerves. These are the intercostal and the phrenic nerves. The parietal pleura are pain sensitive. The costal and peripheral nerves and the Mediastinal pleura and the central part of the diaphragmatic pleurae by the phrenic nerves. The pulmonary pleura develop from the splanchnopleuric layer of the lateral plate mesoderm, and are supplied by the autonomic (sympathetic) nerves derived from the spinal segments T4 and T5. The nerves accompany the bronchial vessels. This part of the pleura is not sensitive to pain. BLOOD SUPPLY AND LYMPHATIC DRINAGE OF THE PLEURA: The parietal pleura are a part and parcel of the thoracic wall. Its blood supply and lymphatic drainage, therefore, the same as that of the body wall. Intercostal, internal thoracic and musculophrenic arteries supply it. The veins drain mostly into the azygos and the internal thoracic veins.
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The lymphatics drain into the intercostal, internal mammary, posterior Mediastinal and the diaphragmatic nodes.

The pulmonary pleura, like the lung is applied by the bronchial arteries and is drained by the broncho pulmonary lymph nodes.

GROSS ANATOMY:
The lungs extend from the diaphragm to just slightly above clavicles and lie against the ribs anteriroly and posteriorly. The broad inferior portion of the lung, the base is concave and fits over the convex area of the diaphragm. The narrow superior portion of the lung is termed, the apex. The surface of the lung lying against the ribs. The costal surface is rounded to match the curvature of the ribs. The Mediastinal (media) surface of each lung contains a region the hilus, through which bronchi, pulmonary blood vessels, lymphatic vessels and nerves enters and exit. These structures are held together by the pleura and the connective tissue and constitute the root of thelung. Medially the left lung also contains concavity the cardiac notch in which the heart lies. The right lung is thicker and broader than the left. It is also somewhat shorter than the left because the diaphragm is higher on the right side to accommodate the liver that lies below it.

FISSURES AND LOBES OF LUNGS:

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The right lung is divided into 3 lobes : 1. 2. 3. Superior middle and inferior

By two fissures, oblique and horizontal. The left lung is divided into two lobes by the oblique fissure. The oblique fissure cuts into the whole thickness of the lung, except at the hilum. It passes obliquely downwards and forwards crossing the posterior border about 2 inches below the apex and the inferior border about 2 inches from the median plane. Due to the oblique plane of the fissure the lower lobe is more posterior and the upper (and middle) lobe more anterior. In the right lung, the horizontal fissures pass from the anterior border upto the oblique fissure and separate a wedge shaped middle lobe from the upper lobe. The fissure runs horizontally at the level of the 4th costal cartilage and meets the oblique fissure in the mid-axillary line.

The tongue shaped projection of the left lung below the cardiac notch is called the lingual. It corresponds to the middle lobe of the right lung. The number of lobes may vary in either lung. The right lung may have only two lobes (superior and inferior) and the left lung may have three lobes. Accessory lobes may also be present.
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The lungs expand maximally in the inferior direction because the movements of the thoracic wall and the diaphragm are maximal towards the base of the lung. The presence of the oblique fissure of catch lung allows a more uniform expansion of the whole lung.

Each lobe of the lung receives its own secondary (lobar) bronchus. Thus the right primary bronchus gives rise to the secondary (lobar) bronchi called the superior, middle and inferior secondary (lobar) bronchi. The left primary bronchus gives rise to a superior and an inferior secondary (lobar) bronchus with in the substance of thelung, the tertiary (segmental) bronchi, which are constant in both origin and distribution. There are 10 tertiary bronchi in each lung. The segment of lung tissue that each supplies is called as the Bronchopulmonary Segment. Bronchial and pulmonary disorders such as the tumors or abscesses may be localized in a bnronchopulmonary segment and may be surgically removed with out a seriously disrupting surrounding lung tissue.

ROOT OF LUNG:

It is a short, broad pedicle, which connects the medial surface of lung to the mediastinum. It is formed by the structures, which either enter or come out of the lung at the hilum. The roots of the lungs lie opposite to the bodies of the 5th, 6th, and 7th thoracic vertebrae.

Contents: the root is made up of the following structures.

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Principal bronchus on theleft side, and eparterial and hyparterial bronchi on the right side. One pulmonary artery. Two pulmonary veins-inferior and superior.

Bronchial arteries, one on the right side and two on left side. Bronchial veins.

Anterior and posterior pulmonary plexus of nerves. Lymphatics of the lung. Broncho pulmonary lymph nodes. Areolar tissue.

ARRANGEMENT OF STRUCTURE OF ROOT:

A. From before backwards (similar on two sides) B. Superior pulmonary vein. Pulmonary artery. Bronchus.

From above down wards (differs on 2 sides)

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a) Right side 1. 2. 3. 4. Eparterial bronchus. Pulmonary artery. Hyparterial bronchus. Inferior pulmonary vein

b) Left side: 1. 2. 3. Pulmonary artery. Bronchus. Inferior pulmonary vein.

RELATION OF THE ROOT:

A. Anterior a) common on two sides 1. 2. 3. b) on the right side 1.Superior venacava 2.Apart of right atrium. B. Posterior :
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Phrenic nerves. Pericardiophrenic vessels. Anterior pulmonary plexus.

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a) Common on two sides. 1. Vagus nerve. 2. Posterior pulmonary plexus. b) on left side 1.descending thoracic aorta. C. Superior. a) On right side-terminal part of azygos vein. b) On left side-arch of aorta. D. Inferior : a) Pulmonary ligament.

SURFACE MARKINGS OF THE LUNG:

The apex of the lung coincides with the cervical pleura, and is represented by a line convex upwards rising one inch above the medial 1/3 of the clavicle. The anterior border of the lung corresponds very closely to the anterior margin of the pleura and is obtained by joining: i. A point at the sternoclavicular joint. ii. Another point at the median plane at the sternal angle.

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iii.A third point in the median plane just above the xiphisternal joint.

The anterior border of the left lung corresponds to the anterior margin of the pleura up to the level of the 4th costal cartilage. In the lower part it presents a cardiac notch of variable size. From the level of the 4th cartilage it passes laterally for 3.5 cms. From the sternal margin and then curves downwards and medially to reach the 6th costal cartilage 4cms from the medial plane.

In the region of the cardiac notch the pericardium is covered only by a double layer of pleura, the area of the cardiac notch is dull in percussion and is called Area of superficial cardiac dullness.

The lower border of the each lung lies two ribs higher than the pleural reflection. It crosses the 6th rib in the mid clavicular line, the 8th rib, in the mid axillary line, the 10th rib at the lateral border of the erector spinae and 2 ends 2cms lateral to the 10th thoracic spine. The posterior border coincides with the posterior margin of the pleural reflection except that its lower end lies at the level of the 10th thoracic spine.

The oblique fissure can be drawn by joining: A point 2cms lateral to 3rd thoracic spine. Another point on the 5th rib in the mid axillary line and.

i.

ii.

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A third point on the 6th Costal cartilage 7.5cms from the median plane.

The horizontal fissure is represented by a line joining : i. A point on the anterior border of the right lung at the level of the 4th costal cartilage. A second point on the 5th rib in the midaxillary line.

ii.

BRONCHIAL TREE:

The trachea divides at the level of the lower border of the 4th thoracic vertebra into two primary (principal) bronchi, one for each lung.

The right principal bronchus is shorter (1 inch), wider and more in line with the trachea than the left principal bronchus. Principal bronchus is longer (2 inches) and narrower and most oblique than the right bronchus. Each principle bronchus enters the lung through the hilum and divides into secondary (lobar) bronchi one of each lobe of the lungs. Each lobar bronchus is divided into tertiary (segmental) bronchi one for each Bronchopulmonary segment (10 on right side and 8 on left side).

The segmental bronchioles. Still smaller branches are called as the respiratory bronchioles.

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Each respiratory bronchiole aerates a small part of the lung known as a pulmonary unit. The respiratory bronchioles ends in microscopic passages which are termed(in that order) 1. 2. 3. Alveolar ducts. Atria. Air saccules. gaseous exchange

4. Pulmonary alveoli takes place in the alveoli.

BRONCHI:
At the sternal angle, the trachea divides into right primary branches, which goes into the left lung. The right primary bronchus is more vertical, shorter and wider than the left. As a result, an aspirated object is more likely to enter and lodge in the right primary bronchus and then the left.

Like the trachea, the primary bronchi contain incomplete rings of the cartilage and are lined by the pseudo-stratified ciliated columnar epithelium. On entering the lungs, the primary bronchi divides to form smaller bronchi-the secondary (labor) bronchi one for each lobe of the lung, the secondary bronchi continues to branch forming still smaller bronchi called tertiary bronchi, that divides into bronchioles. Bronchioles in turn branch respectively into even smaller bronchioles and eventually into tubes called as terminal bronchioles.

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This continues the branching from the trachea resembles a tree trunk with its branches and is commonly referred to as the Bronchial Tree.

ALVEOLAR CAPILLARY (Respiratory) MEMBRANE:

The exchange of the respiratory gases between the lungs and the blood takes place by diffusion across the alveolar and capillary walls. Collectively, the layers through which the respiratory gas diffuses are known as Alveolar-capillary membrane. (1) A layer of types I and II alveolar cells with free alveolar macrophages that constitutes the alveolar wall. (2) An epithelial basement membrane underneath the alveolar wall. (3) A capillary basement membrane that is often used to the epithelial basement membrane. (4) The endothelial cells of the capillary.

ARTERIAL SUPPLY OF LUNGS: The bronchial arteries supply the nutrition to the bronchial tree and the pulmonary tissue. On the right side there is one bronchial artery which arises either from the 3rd posterior intercostal artery or from the upper left bronchial artery.
1.

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2. On the left side there are two bronchial arteries both of which arise from the descending thoracic aorta. 3. The upper opposite vertebra T5 and the lower just below the left bronchus.

Deoxygenated blood is brought to the lungs by the pulmonary arteries and oxygenated blood is returned to the heart by the pulmonary veins. There are precapillary anastomes between the bronchial and pulmonary arteries.

These connections enlarge when anyone of them is obstructed in a disease.

VENOUS DRINAGE OF THE LUNGS:

The venous drainage from the first one or two divisions of the bronchi is carried by bronchial veins usually there are two bronchial veins on each side. The right bronchial veins drain into the left superior intercostal vein or into the hemiazygos vein. The greater part of the venous blood from the lungs is drained by the pulmonary veins. LYMPHATIC DRINAGE OF THE LUNGS: There are 2 sets of lymphatics both of which drains into the Bronchopulmonary nodes. 1. Superficial vessels drain the peripheral lung tissue lying beneath the pulmonary pleura. The vessels pass
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round the borders of the lung and margins of the fissures to reach the hilum. 2. Deep lymphatics drain the bronchial tree the pulmonary vessels and the connective tissue septa. They run towards the hilum where they drain into the broncho pulmonary nodes.

The superficial vessels have a number of valves. The deep vessels donot have valves at all or only a few valves are being present.

BRONCHO PULMONARY SEGMENTS:

Definition: the broncho pulmonary segments are well-defined sectors of the lung, each one of which is aerated by a tertiary or segmental bronchus. With its apex directed towards the root of the lung. There are 10 segments present on the right side and 8 segments present on the left side.

Intersegmental planes-each segment is surrounded by a connective tissue which is continuous on the surface with the pulmonary pleura thus the brochopulmonary segments are independent respiratory unit. Relation of these to pulmonary veins: Near the hilum the veins are ventromedial to the bronchus.

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It should be noted that the broncho pulmonary segment is not a broncho vascular segment because it does not have its own vein. Relation to pulmonary artery: The branches of the pulmonary artery accompany the bronchi thus the each segment has its own pulmonary artery unlike the pulmonary vein.

PHYSIOLOGY OF RESPIRATION
The principal purpose of respiration is to supply the cells of the body with the oxygen and remove the carbondioxide produced by cellular activities. The three basic processes of respiration are Pulmonary ventilation External (pulmonary) respiration Internal (tissue) respiration

Pulmonary ventilation: It is a process by which the gases are exchanged between the atmosphere and the lung alveoli. The bulk of air between the atmosphere and lungs occurs for the same reason that blood flows.

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Through the body a pressure inside the lungs is less than the air pressures I the atmosphere. Air moves out of the lungs is greater then the pressure in the atmosphere.

Inspiration: Breathing in of air is called as the inspiration (inhalation). Just before each inspiration, the air pressure inside the lungs equals the pressure of the atmosphere, which is about 760mm Hg or 1 atmosphere at sea levels. For air to flow in to the lungs, the pressure inside the lungs must become lower the Pressure in the atmosphere.

This condition is achieved by increasing the volume of the lungs. For inspiration to occur, the lung must be expand. This increases lung volume and thus decreases the pressure in the lungs below the atmospheric pressure. The first step in expanding the lungs involves contraction of the principal inspiratory muscles the diaphragm and external intercostals. The diaphragm the most important muscle of inspiration is a dome-shaped skeletal muscle that forms the floor of the thoracic cavity. It is innervated by fibers of the phrenic nerves, which emerges form both sides of the spinal cord at cervical levels 3,4, and 5.

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Contraction of the diaphragm causes it to flatten, lowering its dome. This increases the vertical dimension of the thoracic cavity and also accounts for the movement of about 75% of the air that enters the lungs during the inspiration. The distance the diaphragm moves during inspiration ranges from 1 cm during normal quiet breathing up to about 10 cm during heavy breathing. Advanced pregnancy excessive obesity or continuing abdominal clothing can prevent a complete decent of the diaphragm. At the same time the diaphragm contracts, the external intercostals contracts, their skeletal muscles run obliquely downwards and forward between adjacent ribs and when there muscles contract, the ribs are pulled upward and sternum is pushed forwards. This increases the anterior-posterior dimension of the thoracic cavity. During the normal breathing the pressure between the two-pleural layers called as the intrapleural (intrathorasic) pressure, is always below the atmospheric pressure. (It may become temporarily higher than the atmospheric pressure only during modified respiratory movement such as coughing or straining during defecation). As the diaphragm contracts and the overall size of the thoracic cavity increases the intrapleural pressure falls to about 754mm Hg. Consequently, the walls of the lungs are pulled outwards. The partial and the visceral pleurae normally adhere strongly to each other because of the below atmospheric pressure between them and because of the surface tension created by their moist adjoining surfaces. As the thoracic cavity expands, the visceral pleura and lungs are pulled along with it.

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When the volume of the lungs increases, the pressure inside the lungs called as the alveolar (intra pulmonic) pressure drops from 760-758 mm Hg. A pressure gradient is thus established between the atmospheric pressure and the alveoli. Air rushes from the atmosphere into the lungs due to the lungs due to gas pressure difference and the inspiration takes place. The term for normal quiet breathing is eupnea. Eupenea involves shallow, deep or combined shallow and deep breathing. Shallow breathing is called costal breathing. It consists of upward and outward movement of the external intercostal muscles. The intercortal muscles receive innervation from the intercostal nerves, which emerges from the thoracic segments of the spinal cord.

Deep breathing is called as the diaphragmatic breathing. It consists of the outward movement of the abdomen as a result of the contraction and descent of the diaphragm. During deep, labored inspiration, accessory muscles of inspiration also participate in increasing the size of the sternocleidomastoid, which elevate the superior two ribs, and the pectoralis minor, which elevates the third through fifth ribs. Inspiration is an active process because it is initiated by skeletal muscle contraction.

EXPIRATION:

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Breathing out of is called as the expiration (exhalation) is also achieved by a pressure gradient, but in this case the gradient is reversed. The pressure in the lungs is greater than the pressure of the atmosphere. Normal expiration during quiet breathing, unlike inspiration, is a passive process since no muscular contractions are involved. It depends on two factors: 1. The recoil of elastic fibers that were stretched during the inspiration and 2. The inward pull of the surface tension due to the film of the alveolar fluid.

Expiration starts when the inspiratory muscles relax, the ribs moves downwards and as the diaphragm relaxes, its dome moves upwards owing to its elasticity.

These movements decrease the vertical and anterior-posterior dimensions of the thoracic cavity.

Also surface tension exerts an inward pressure or pull and the elastic basement membranes of the alveoli and the elastic fibers in bronchioles and alveolar ducts recoil. As a result, lung volume decreases to 762 mm Hg. Air them flows from the area of higher pressure in the alveoli to the area of lower pressure in the atmosphere. Expiration becomes active during the laboured breathing and when air movement out of the lungs is impeded. During these

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time muscles of expiration abdominal and the internal intercostals contracts. Contraction of the abdominal muscles moves the inferior ribs downwards and compresses the abdominal viscera, thus forcing the diaphragm upward. Contraction of the internal intercostals, which extend downwards and backward between adjacent ribs, pulls the ribs downwards.

MODIFIED RESPIRATORY MOVEMENTS

Respirations also provides humans with methods for expressing emotions such as laughing, yawning, sighing, and sobbing moreover, respiratory air can be used to expel foreign matter from the lower air passages through actions such as sneezing, coughing. All there movements are the reflexes but some of them also can be initiated voluntarily.

PULMONARY AIR VOLUMES AND CAPACITIES:

In the clinical practice, the word respiration means one inspiration plus one expiration. The healthy adult averages 12 Respirations a minute and moves about 6 liters of air into and out of the lungs while at rest. A lower than normal volume of air exchanges is usually a sign of pulmonary malfunction. The apparatus commonly used to measure the volume of air exchanged during the breathing and the rate of the ventilation is a spirometer or respirometer.

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The record is called as the spirogram. Inspiration is recorded as an upward deflection and expiration is recorded as a down ward deflection.

PULMONARY VOLUMES: The volume of the air inspired is called as the tidal volume> The total air taken in during one minute is called the Minute volume of respiration. It is calculated by multiplying the tidal volume by the normal breathing rate per minute. This additional inhaled air is called as the Inspiratory reserve volume. If air inhaled normally and then exhaled as forcibly as possible then it should be able to push out 1200ml of air in addition to the 500ml of tidal volume. It is called as the expiratory reserve volume even after the expiratory reserve volume is expelled a good deal of air also remains in the non-collapsible air passageways. This air the Residual volume amounts to about 1200ml. Opening the thoracic cavity allows the intrapleural pressure to equal the atmospheric pressure, forcing out some of the residual volume. The remaining air is called as the Minimal volume. The presence of the minimal volume can be demonstrated by placing a piece of lung in water and watching it float. The fetal lungs contain no air and so the lung of a stillborn will not float in water.

PULMONARY CAPACITIES

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Pulmonary capacities are the combinations of specific lung volumes. The Inspiration capacities the total inspiratory ability of the lungs in sum of tidal volume plus inspiratory reserve volumes. The functional residual capacity is the sum of residual volume plus the expiratory reserve volume. Vital capacity is the sum of the inspiratory reserve volume, tidal volume and the expiratory reserve volume. Finally the total lung capacity is the sum of all volumes.

EXCHANGE OF OXYGEN AND CARBONDIOXIDE At birth, as soon as the lungs fill with air, oxygen starts to diffuse down its concentration gradient from the alveoli into the blood through the interstitial fluid, and finally into the cells. Carbondioxide diffuses in the opposite direction from the cells, through the alveoli. To understand how these gasses are exchanged in the body there are 3 gas laws: 1. 2. 3. Charless law. Daltons law and Henrys law.

PHYSIOLOGY OF EXTERNAL (PULMONARY) RESPIRATION:

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***************************************************************** ALLERGIC ASTHMA External (pulmonary) respiration is the exchange of O2 and CO2

between the alveoli of the lungs and pulmonary blood capillaries. It results in the conversion of the deoxygenated blood coming from the heart to oxygenated blood (saturated with O2) returning to the heart. During the inspiration atmospheric air containing O2 enters the alveoli. Deoxygenated blood is pumped from the right ventricle through the pulmonary arteries into the pulmonary capillaries surrounding the alveoli. The PO2 of alveolar air is 105 mm Hg. If you are at rest, the PO2 of the deoxygenated blood entering your pulmonary capillaries is only 40mm Hg. As a result of this difference in P02 there is a net diffusion of oxygen from the alveoli into the deoxygenated blood until equilibrium is reached, and the PO2 of the new oxygenated blood there is a net diffusion of CO2 in the opposite direction. The PO2 of the deoxygenated blood is 45mm Hg.

Where as that of the alveolar air is 0 mm Hg. This is the PCO2 of fully oxygenated blood. Thus the PO2 and PCO2 of oxygenated blood leaning the lungs are the same as in the alveolar air. The CO2 That diffuses into the alveolar and is eliminated from the lungs during expiration. The rate of this expiration depends on various factors like:

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1. 2. 3. 4.

Partial pressure difference. Surface area of gas exchange. Diffusion distance. Breathing rate and depth.

PHYSIOLOGY OF INTERNAL RESPIRATION; No matter how quickly the blood flows through the pulmonary capillaries it picks up a maximal amount of O2 so that blood returning to the heart is fully oxygenated blood into the aorta and through the systemic arteries to capillaries to the tissue cells. The exchange of O2 and CO2 between the tissues and the blood capillaries called as the internal respiration. It results in the conversion of oxygenated blood into the deoxygenated blood oxygenated blood entering tissue capillaries has on a PO2 of 102mm Hg where as tissue cells have an average PO2 of 40mm Hg.

Because of this difference in PO2in the blood decreases to 40mm Hg. This is the average POvof deoxygenated blood entering tissue vennules when at resting condition. At rest, only about 25% of the available oxygen in oxygenated blood actually enter tissue cells. This amount is sufficient to support the needs of respiratory cells. Thus deoxygenated blood still retains considerable oxygen.

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During exercise more oxygen diffuses form blood into active cells.

TRANSPORT OF O2 AND CO2:

The transport of gases between the lungs and body tissue is a function of the blood. When the O2 and CO2 enter the blood, certain physical and chemical changes occurs that helps in gas transport and the exchange.

CONTROL OF RESPIRATION:

During strenuous exercise, the O2 use can increase as much as 30-fold. Thus the mechanisms hurt exist to match the respiratory effort to metabolic demand. Portions of the nervous system in the medulla and pons control the basic rhythm of respiration. There are principal mechanisms involved in the nervous control of the rhythms of respiration.

NERVOUS CONTROL:
The size of the thorax is affected by the action of the respiratory nucleus. This nucleus contracts and relaxes as a result of nerve impulses transmitted to them from centers in the brain.

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MEDULLARY RHYTHMICITY AREA:

The function of the medullary rhythmicity areas is to control the basic rhythm of respiration. The basic rhythm of respiration is being determined by nerve impulses generated in the inspiratory area. At the beginning of the expiration. The inspiratory area is inactive but after three seconds it suddenly and automatically becomes active. The impulses reach the diaphragm by the phrenic nerves and the external intercostal muscles by the intercostal nerves.

PNEUMOTAXIC AREA: Although the medullary rhythmicity area controls the basic rhythm of respiration, other parts of the brainstem helps to co-ordinate the transition between inspiration and expiration. One of there is the pneumotaxic area in the upper pons. It continuously transmits inhibitory impulses to the inspiratory area.

APNEUSTIC AREA: This is another part of the brain stern that co-ordinates the transition between inspiration and expiration is the aponeurotic area in the lower pans. It sends the stimulatory impulse to the inspiratory area that activates it and prolongs inspiration.

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REGULATION OF RESOPIRATORY CENTRE ACTIVITY:

Although the basic rhythm of the respiration is set and co-ordinate by the respiratory center, the rhythm can be modified in response to metabolic demands by the nerve impulses to the center.

AETIOLOGY
The aetiology of asthma is likely multifactorial combination of genetic and environmental factor leads to the development of asthma.

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Atopy is predisposition to allergic disease and is the main risk factor for developing asthma.

A hygienic hypothesis proposes that cleaner environments have led to immunological stresses, preventing development of asthma.

Measles infection, bacille-calmette-guerin vaccine administration, hepatitis-A, seropositivity and other stimuli that increase and may inhibit allergic response.

In selected series, vaccinations, fewer childhood infections, liberal use of antibiotics, more processed food in diets, smaller familiars, and less expensive to day environments have been associated with increased Atopy, and asthma.

Allergic asthma is more common in urban damage epithelium so it is more sensitive to allergens.

Two phases of response occur. It will be illustrated in the bellow diagram: Allergen exposure Other causes

IgE increase and

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Sensitization

Inflammation and hyperactivity

Trigger

Asthma attack

Causes or triggers of asthma can be divided as follows: 1. Allergic: Aeroallergens can include seasonal pollen, mold spores, and dust mites, animal allergens, and food (especially in children). 2. Non-allergic: Thus may include smoke, odors, cold air and weather, chemicals, medications leg, aspirin, other NSAIDS, exercise hormonal changes-ex; pregnancy, menstrual cycle.

PATHOLOGY:
Asthma was used to be considered a brochospastic disease with the treatment directed to airway smooth muscle. Histopathologic study of airways from the patients with asthma who died during serve attack of asthma has shown that an
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inflammatory response is playing a dominant role than the response in airway smooth muscle.

These patients exhibit airway inflammation even when they are symptom free. The cause of inflammation is unknown. The Histopathologic study has shown airway smooth muscle hypertrophy, thickening of the basement membrane, mucus deposits in the terminal bronchioles with glandular hyperplasia and inflammatory cell infiltration in the lamina propria. Many different cells such as eosinophils, neutrophils, lymphocytes and mononuclear cells have been involved in the pathogenesis of asthma and they produce a variety of inflammatory mediators which are released into the airway wall where they interact in a complex manner that activate several target cells in the airway resulting in brochoconstrction, microvascular congestion, plasma leakage leading to submucosal edema, mucus hypersecretion from hypertrophied goblet cells mucous glands, and plugging of airway lumen by viscus mucus and stimulation of neural reflexes. There is presence o marked inflammation in the airways with infiltration of inflammatory cells especially eosinophils, macrophages, macrophages, mast cells, basophils, lymphocytes and neutrophils, epithelial dell sloughing into the lumen and plugging of airway lumen by viscous mucus, plasma, inflammatory cells and debris.

Sloughed clumps of airway epithelium, remains of major basic proteins from activated eosinophilis and concentric layers of mucus, debris and cells are characteristic. There is smooth muscle hyperplasia. Bronchial biopsy specimens from patients with mild asthma have also revealed presence o inflammation, which includes denudation of airway epithelium, collagen deposition beneath the basement membrane and increased inflammatory cell infiltrate.
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Pathologically the response to bronchospasm occurs in 2 forms. They are 1.) Sensitization stage: Exposure to allergens, especially in fetal or early IgE, antibiotics in the serum. IgE become fixed to mast cells, which then react to antigens and release brochocontrctor substances such as histamine. 2.) Hyper reactive stage: Continued exposure lead to chronic low-grade inflammation of airways, causing bronchial reactivity. Once asthma has developed, removal from exposure to the allergens, if delayed does not always prevent continuing asthma. Inflammation and hyper reactivity causes air way obstruction by three ways: 1. 2. 3. Mucosal edema Broncho spasm Gelatenous mucus plugging

PATHOPHYSIOLOGY
The allergic response in the airway is the result of a complex infraction of most cells, eosiuophills, lymphocytes, macrophages, dendritic cells, and neutrophils.

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Inhalation challenge studies with allergens reveal an early allergic response (EAR) which occurs with in minutes and peaks at 20 minutes following inhalation. Clinically the manifestations of the EAR in the airway include bronchial constriction, airway edema, and mucus plugging. These effects are the result of mast cell-derived mediators. 4-10 hours later, one see the late allergic response (LAR) which is characterized by cellular infiltration into the airway and is most likely caused by cytokine mediated recruitment of lymphocytes and eosinophils. Antigen presenting cells (for example macrophages, dendrific cells) In the airway capture, process and present antigen to helper to cells, which inturn become activated and promotes B-cell IgE production and esnophilic recruitment. This leads to degranulation of the mast cells. Performed mast cell medication, such as histamine, and proteases are released leading to the EAR. Newly formed mediators such as leukotriene and prostaglandin D2 and also contribute to the EAR. Pro-inflammatory cytokinens are released form the mast cells and generated after mast cell activation.

These cytokinens contribute to the LAR by attracting neutrophils and eosinophils. The eosinophils release major basic protein eosinophilc cationic protein, eosinophinic derived neurotoxin and eosinophilc peroxide
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in to the air way causing epithelial denudation and exposure of nerve endings.

The ongoing inflammatory process eventually results in hypertrophy of smooth muscle, hyperplasia of mucus glands, thickening of basement membranes and continuing cellular infiltration. These long-term changes of the airway, referred to as airway remodeling, can ultimately lead to fibrosis and irreversible airway obstruction in some, but not most, patients.

CLINICAL TYPES
Allergy induced asthma is an early onset asthma.
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It is an atopic type. It occurs by inspired allergens or by ingested allergens. Significant family history is seen skin test is positive. Allergy induced asthma is off 4 types:1.) 2.) 3.) 4.) Episodic asthma. Exercise induced asthma. Chronic asthma and Severe asthma.

Episodic and Exercise induced asthma: In this from of the disease the patient has no respiratory symptoms between episodes of asthma. Paroxysms of wheeze and dyspnoea may occur at anytime and can be of sudden onset.

Episodes of asthma can be triggered by allergens, exercise, viral infections such as the common cold, or may be apparently spontaneous.
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Attacks may be mild or severe and may last for hours, days or even weeks. Chronic asthma: Symptoms of chest tightness, wheeze, and breathlessness on exertion, together with spontaneous cough and wheeze during the night, may be chronic unless controlled by appropriate therapy. Episodes of severe acute asthma can occur and cough productive of mucoid sputum with recurrent episodes of frank respiratory infection is common in this type of asthma. Severe asthma: The term has replaced status asthmaticus as the description of life-threatening attacks of asthma.

The patient usually adopts an up right position fixing the shoulder girdle to assist the accessory muscles of respiration. There is often an unproductive cough, which aggravates respiratory distress. The respiratory symptoms are accompanied by tachycardia, pulsus paradoxus, sweating, and in severe cases, central cyanosis.

CLINICAL FEATURES
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The most common sign of allergic asthma is wheezing, which involves a tight feeling is the chest and a high-pitched whistling sound heard during exhalation.

The attacks of dyspnoea common at night. An asthmatics expiration will be prolonged due to the increased resistance to airflow through the lungs.

Mild- cough, wheezing, shortens of breath, fever may indicate a pulmonary infection.

Moderate- some one having an asthma attack may sit up stiffly while resting on straight arms, the neck and abdominal muscles assist in inhalation.

Severe- wheezing may decrease due to poor/absent air movement; retractions become (cyanotic). The person may experience respiratory arrest and arrhythmias.

The latter is marked especially if there is co-existent infection and is associated with mucopurrulent or purulent expectoration.

When the attacks are severe there is increased work of breathing with flaming of nostrils, poorly moving low diaphragm, sternomastoids, and intercostal regions breath sounds.

High-pitched expiratory wheeze is common. The patient becomes fatigued with tachypnoea and hyposaemia and often dehydrated.
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There may be pulsus parodoxus from high intrapulmonary pressure.

The extensive mucus plugging and marked narrowing of airway makes the breath sounds to appear more distant. The jugular venous pressure is raised during expiration due to co-existent elevated intra thoracic pressure and returns to normal on inspiration.

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SEVERITY OF ALLERGIC ASTHMA

Allergic asthma may be mild, moderately sever or severe. This gradation is based on symptoms, sign peak expiratory flow, and study of arterial oxygen tension.

Severity of asthma: Mild Moderate Severe

1. SYMPTOMS a.) Breathlessness On walking while walking at rest. b.) Attitude. Can lie down. Prefers sitting Leans forward. c.) Talks in Sentences Phrases Words. d.) Alertness May be agitated. Agitated Usually agitated. d 2.SIGNS. a.) Pulse rate/min. < 100. 100-120. >120. b.) Respiratory Increased Increased often>30/min. Rate. c.)Use of Accessory No Yes Yes. Muscles and Suprasternal Retractions. d.) Wheeze end-expiratory Loud Very loud. d.) Pulsus Parodixus Absent May be present Often present.
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3.) Peak flow predicted. 4.) Oxygen level <60mm Hg.

>80%

60-80%.

<60%

NormalPaO2. >60mm Hg

DANGEROUS SIGNS
These signs indicate unresponsiveness of asthma; Cyanosis. Use of accessory muscles of respiration. PaO2< 600mmHg and PaO2 >45 mm Hg. Hyperinflation on chest radiograph. Tachycardia with pulse rate> 120/min. Pulsus paradoxus. Pneumothorax and Disturbances in consciousness.

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INVESTIGATIONS
The diagnostic procedures must be in a position to give an answer after careful physical examination, lab studies, imaging studies, other tests, radiographic examination, and histological findings.

PHYSICAL EXAMINATION:

Head and neck: Nasal mucosa swelling, discharge, polyps or sinus percussion tenderness may suggest associated allergic rhinitis or sinusitis. Wheezing heard only or mostly over the neek may suggest vocal cord dysfunction (VCD) or other laryngeal abnormality.

Cardiac: Findings are normal. Patinets with status asthmaticus may have a pulsus paradoxus greather than 10mmHg.

Respiratory: During an acute asthma exacerbation, lung examination findings may include wheezing, rhonchi, hyperinflation, or prolonged expiratory time with severe disease, lung auscultation may reveal absent breath sounds or sings of respiratory distress and failure. Focal wheezing may indicate forign body or other airway obstruction such as tumor.

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Skin: Cheek the patient for atopic dermatitis.

Vital signs: (normal values). Parameter Infant Heart rate 120b/min. Blood pressure 75/50mmHg. Respiratory rate 40br/min. PaO2 75-80mmHg. PaCo2 34-54mmHg PH 7.26-7.41 Tidal volume 20ml.
Temparature-98.6
o

Adult 60-100b/min. 120/80mmHg. 12-18br/min. 95-100mmHg. 34-45mmHg. 7.35-7.45 500ml.

F, or 37 o C.

Abnormal values: Temperature- Core temperature increase indicates infection. Heart rate- Tachycardia: HR greater than 100b/min. Bradycardia: HR less than 60b/min. Respiration: Rate: Tachypnea is a rate greater than 18 br/min. Apnea means no respiration. Rhythm: Regular or irregular.
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Amplitude:

Shallow, deep.

LAB STUDIES:
The most important test is pulmonary function testing. The serum IgE level is elevated only approximately half the time in-patients with allergic disease. A finding of greater than 15% serum eosinophilia may be observed in-patients with allergic asthma.

IMAGING STUDIES:
Chest radiograph, modified or limited sinus CT scan and echocardiogram are taken to know the onset and condition of the patient.

OTHER TESTS:
1.) Pulmonary function tests:

The pulmonary function studies help in the assessment of severity and documentation of reversibility of the airway obstruction. The measurement of forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) are essential in the assessments of the severity of airway obstruction.

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There is a fall in FEV1/FVC ratio and it and it is less than 70%, FVC reduced due to closure of airways at larger than normal lung volumes.

The severity of asthma is classified into 3 categories based on FEV1 as mild (50% more predicted FEV1) moderate (25-50% predicted FEV1) and severe (less than 25% predicted FEV1). The reversibility of airway obstruction is assessed before and after inhalation of brochodilator. The ratio FEV1/FVC must show an improvement of atleast 25% after bronchodilator aerosol. The measurement of velocity of expelled air through the peak flow meter gives an indication of airway obstruction. Though peak expiratory flow rate (PEFR) is effort dependent it is quite reproducible. It can be measured with a forced complete expiration. Peak flowmeter is inexpensive and portable, allowing the patient to gauge the severity of obstruction and regulate therapy. 2.) Arterial blood gases:

Measurement of arterial blood gases is not useful in Diagnosis of asthma, but the measurement reflects the severity and ventilatory status. A marked ventilation-perfusion in equality is encountered during a severe attack of asthma and it results in hypoxaemia. There appears to be a linear relationship between the severity of hypoxaemia and the airway obstruction.
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In the initial stages of attack, there is hyperventilation and a fall in the level of arterial carbondioxide tension (PaCo2).

There is hypoxaemia if airway obstruction persists the patient may not be able to maintain the required alveolar ventilation.

There is respiratory muscle fatigue resulting in elevation of PaCo2 and fall in arterial oxygen tension (PaO2). There is fall in pH.

Anion gap metabolic acidosis can result from the accumulation of lactic acid in severe asthma. 3.) Examination of sputum:

The expectoration is not marked, however mucus Plugs are characteristically coughed out the sputum appear mucopurrulent or purulent due to the presence of excess of number of eosinophills. Microscopy of sputum reveals clumps of eosinophills clusters of columnar epithelial cells, mucus proteinacewous matter (Creola bodies). Casts of small airways (curshmannis spirals) and breakdown products of eosinophils (charcot-leyden crystals) may also be seen. 4.) Roentgeno graphic study:

The roentgenogram of the chest isonormal in all uncomplicated case of asthma. During severe attack and in longstanding cases, there may be evidence of overinflation.
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Radiograms are useful to recognize the complications like Pneumothorax, labour or segmental collapse from impacted mucus plus, pneumonic shadows, co-existing tuberculosis and changing shadows, from aspergillosis

Chest X-ray:

A two dimensional radiographic film to detect the presence of abnormal material(exudate, blood) or a change in pulmonary parenchyma(fibrosis, collapse). Computerized axial tomography (CAT scan): A computer generated picture of a cross sectional place of the body. Ventilation perfusion (V/Q) scan: Matches the ventilation pattern of the lung to the perfusion pattern to identify the presence of pulmonary emboli. Fluoroscopy: Continuos excursion 5.) X-ray been allows observation of diaphragmatic

Electrocardiogram:

The electrocardiogram during an acute severe asthma may show Tachycardia, ST-wave changes in inferior wall leads, clockwise rotation, and right axis deviation. These abnormalities disappear with subsidance of severity of asthma.
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6.)

Skin tests:

The skin tests are designed to elicit immediate wheal and flare reaction following a prick test.

These tests are helpful in identifying the atopic subjects and the substances to which they are sensitive. The significance of a positive it has to be evaluated in conjunction with the history. Though a positive skin test does not indicate that all allergens are responsible for the symptoms of the patient, it helps to distinguish atopic from non-atopic individuals. A battery of common allergens to which the individuals are exposed in every day life is selected. These allergens include pollen of grass, weed, trees, moulds, fungi, cotton, leather, feather, hairs of animals, cats, dogs, horses, and house dust.

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DIAGNOSIS
The national asthma education and prevention program, expert panel report 2 from the national heart, lung and blood institute (NHLBI) of the national institutes health (NIH) suggests the following stepwise approach to the diagnosis and treatment. Step-1- Mild intermittent: Daytime symptoms 2 or fewer times per week. Nocturnal symptoms 2 or fewer times per month. PEFR or FEV1 equal to 80% of normal or better. PEFR variation less than 20%. Treatment with short-acting brochodilators as needed. Step-2- Mild persistent. Daytime symptoms 3-6 times per week. Nocturnal symptoms 3-4 times per month.
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PEFR or FEV1 equal to 80% of normal or better. PEFR variation 20-30%.

Treatment with daily low dose inhaled glucocorticiods or inhaled cromolyn and short acting bronchodilators as needed. Alternate/notes-sustained release theophylline, oral leukotriene modifier. Step-3-moderate persistent. Daytime symptoms daily. Nocturnal symptoms 5 or more times per month. PEFR or FEV1 equal to 60-80 % of normal. PEFR variation more than 30%. Treatment with daily medium dose inhaled, glucocorticoides and inhaled short-acting bronchodialtors as needed or daily low dose inhaled glucocorticoids and daily long acting inhaled beta-2 agonist and short-acting bronchodilators as needed. Treatment with leukotriene pathway modifier considered.

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Alternate/notes- additionally, if needed for nighttime symptoms, long acting oral beta-2 agonist or theophylline. Step-4-Severe persistent: Day time symptoms always. Nocturnal symptoms frequently. PEFR or FEV1 less than or equal to 60% of normal. PEFR variation more than 30%. Treatment with daily high dose inhaled glucocortidiods, daily long-acting inhaled beta-2 agonist, and short-acting brochodilators as needed. Possible addition of leukotriene pathway modifier. Alternate/notes- additionally, if needed oral glucocorticoids at lowest dose and for the shortest duration required for relief, alternative conditions possible and should be considered.

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DIFFERENTIAL DIAGNOSIS
We can distinguish allergic asthma from the following diseases. Bronchitis. Chronic bronchitis. Emphysema. Foreign body aspiration. Immunoglobulin-G deficiency. Pulmonary embolism. Sarcoidosis. Sinusitis, chronic. Vascular rings. Cystic fibrosis. Congenital cardiac anomalies. Pulmonary anomalies.
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Vocal cord dysfunction. Endo bronchial lesion. Churg-strauss syndrome granulomatosis). (allergic angiitis and

Allergic broncho pulmonary aspergillosis. Reactive airway dysfunction syndrome (RADS): This is a distinct entity caused by exposure to a single, large, inhaled agent, leading to asthma symptoms with in 24 hours and lasting 3 months or longer.

PROGNOSIS AND CLINICAL COURSE

Death from asthma is uncommon. Available mortality statistics indicate a death rate of 17.7deaths per million. The available information on the clinical course of asthma suggests that some where between 50-80% of all patients can expect to have a reasonably good prognosis. The number of children still having asthma 7-10 years after the initial diagnosis varies from 26-78% with an average of 46%; however the percentage who continue to have severe disease is relatively low (6-19%). The natural course of asthma in adult life has been little investigated. Some studies suggests the spontaneous remissions occur in approximately 20% of those who develop the disease as adults and
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40% or so can be expected to improve with less frequent and severe attacks as they grow older.

The prognosis and clinical course depends upon the patient follow up of medical and physiotherapy treatment.

MEDICAL MANAGEMENT
It is given by 2 ways. 1. Step up and 2. Step down.

1.STEP UP MANAGEMENT:
Step-1:

Occasional use of inhaled short acting adrenoceptor agonist brochodilators.

B2-

Short acting brochodilators, such as salbutamol or terbutaline, by inhalation used as required for relief of minor symptoms.

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If more than occasional use is necessary, treatment with inhaled drugs, which have a beneficial effect on the underlying asthmatic inflammatory disease process, should be prescribed. B2-Adrenoceptor agonist therapy alone is only recommended the patient to lead an active normal life free from nocturnal and exercise induced asthmatic symptoms. Step-2:

Regular inhaled anti-inflammatory agents:

Inhaled short actingB2-adrenoceptor agonists as required plus an inhaled steroid in dose up to 800mcg daily. Alternatively sodium cromoglycate or nedocromil sodium can be used instead of an inhaled steroid, but these drugs are rarely effective and they are mainly used in the testament of childhood asthma. Step-3:

High dose inhaled steroids:

Inhaled short acting B2-adrenoceptor agonists as required plus an inhaled steroid in the dose range 800-2000 mcg daily. When steroids in high dose are inhaled via a conventional pressurized metered dose inhaler (MDI) the routine use of a large volume spacer (holding chamber) is recommended. When dry powder inhalers are used, mouth rinsing with spitting out of the rinsing liquid after each treatment should be encouraged.

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Spacers and rinsing are recommended to decrease gastrointestinal absorption of swallowed drug, and to lower the rise of developing the local side effect of oropharyngeal candidiasis. Step-4:

High dose brochodilators

inhaled

steroids

and

regular

Inhaled short acting B2-adrenoceptor agonists as required with an inhaled steroid plus a sequential therapeutic trial of one or more of Inhaled long actingB2-adrnecepotr (salmeterol or formoterol). agonist

Sustained release theophylline. Inhaled ipratropium bromide or oxitropium bromide. Long acting oral B2-adrenoceptor agonist. High dose inhaled bronchodilators. Sodium cromoglycate or nedocromil sodium. Step-5:

Addition of regular oral steroid therapy

Inhaled short actingB2-adrenoceptor agonists as required with an inhaled steroid in high dose and one or more of the long acting
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bronchodilators plus regular prednisolone tablets in the lowest dose necessary to control symptoms in a single daily dose.

If there has been good symptomatic control for 3-6 months a step down of treatment should be made.

3. STEPDOWN MANAGEMENT:
Step-5-Usage of regular oral steroid therapy. Step-4- Long acting bronchodilator therapy is gives regularly and corticosteroids occasionally. Step-3- Long acting bronchodilator therapy is given regularly.

Step-2- Short acting bronchodilator therapy along with rest are given regularly or long acting bronchodialtor therapy are given occasionally. Step-1- Short acting brochodilator therapy is given along with rest is given occasionally. Allergic asthma is a condition, in which usually requires continuos medical care. Anti-inflammatory medications (especially inhaled glucocorticosteroids) are now the mainstay of therapy. Anti-inflammatory medications are process to improve lung function (FEV1, AHR) and to decrease symptoms, exacerbation frequency, and the need for rescue inhales.

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Short-acting inhaled beta-2, against as needed, are most effective for rapid relief of asthma symptoms. No benefit and some risk of developing tolerance occur with regular long-term use. These agents should still be available to the patient, even if using a long acting beta2-agonist (salmetcrol, Salmeterol added to an inhaled glucocorticoid regimen might be as effective as doubling the dose of glucocorticoid. Of note, the list of medications that combine 2 drugs in a single delivary device in an effort to increase patient convenience and compliance is expanding. Thus include combivent (albuterol and atrovent) and advair (flutocasone and saleterol). Leukotriene pathway modifiers may be useful as first line therapy for mild persistent asthma or as an add on or glucocortocoidsparing medication in others. These agents are less effective than glucocorticoid inhalers but tend to improve compliance because of once-a-day oral dosing. Mast cell stabilizers are also used cromolyn sodium (intal) indirectly block calcium influx into mast cells, preventing inflammatory mediator release. Adults can use it as in a nebulized form, 1 ampule tid/bid. Nedocromil (tilade) has similar effects, although it is structurally distimet. The pediatric dose is 1 ampule nebulizer bid/qid. Using a spacer or holding the inhaler 2 inches from the mouth may improve delivary.
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The recent change from chloro-fluoro carbon to hydro-fluroalkane propellants with smaller particle size may help deliver more medication. The only reliable way to determine if the inhaler is empty is to count the number of doses. Rinse the mouth with water and spit after glucocorticoid inhalers use to prevent oral thrush and dysphonia. An alcohol containing mouthwash may be more effective thus water.

SELF-MANAGEMENT:
Asthma diary: Times when the patient felt extra breath less (or) wheezy should note in his asthma diary and it is as follows. Date Time of day what made the what did he how much or Night. Patient breathless does to help did it help. or Wheezy himself

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PHYSIOTHERAPY ASSESMENT
It is the procedure of knowing patient problems. Assessment have 1. History taking. 2. Observation. 3. Examination. 4. Problem list. 5. Aims. 6. Means and methods.

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1.) History:

The classic history consists of wheeze, cough, and dyspnoea. Chest discomfort is also common. Some patients may have cough without other symptoms. Recurrent chest colds may also suggest the diagnosis. While taking the history, record the following: Age of onset. Frequency and severity of daytime and nocturnal symptoms. Symptoms triggers, such as exercise, animals, irritants (smoke) and occupation (worse on workdays). Seasonal and geographic variation.

Limits on activity, lost work or school days, and quality of life. Number of urgent clinic visits, hospital admissions, intensive care unit (ICU) stays, and need for mechanical ventilation. Past treatments, including oral and inhaled steroid frequency of rescue inhaler use, immunotherapy, and environmental avoidance. Family history of asthma. Personal or family history of atopy, allergy rhinitis or sinusitis. Food allergy. Growth. Atopic dermatitis.
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All patients should be asked about or should complete a questionnaire regarding exacerbation of symptoms, as follows: Allergic: Perennial symptoms: Pet in the home, school, daycare, or work environment, moisture, dampness and humidifier use, mold and musty odors in any part of the home, cockroaches in the home, worsening of symptoms after vacuuming rugs. Seasonal symptoms: Early spring, late spring and summer (grasses), summer and fall (molds); late summary and fall (weeds). Environmental: Personal or secondary tobacco smokes exposure in or out the home. Stoves, fireplaces, or heaters used in home. Sprays or chemical agents at work, home or with hobbies. Symptoms only at one place (i.e. at work during neck with no symptoms on weekends). School or business associated with similar problems. Symptoms after eating (seafood or dried, canned or processed food). Medications such as Beta-blockers, aspirin, or other NSAIDS. On observation: (during attack): 1. Forward bending posture. 2. Built. 3. Altered pattern of breathing.
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4. Accessory muscles are used. 5. Shortness of breath. 6. Wheezy is audible. 7. Chest deformities (barrel chest deformity). 8. Sputum. - May appear mucopurulent or purulent due to the presence of excess number of eosinophils. 9. Cough- normal reflex/productive or non-productive. On examination: Consists of on palpation, on percussion, and on auscultation. f On palpationDecreased chest wall expansion. It can be evaluated by assessing the patient in half lying. Physiotherapist stands beside him and place both hands over the chest wall parellelly then ask the patient to expire. At this time, the thumb tips of both hands are closed to one another then ask the patient to inspire as much as. Then we can observe that both thumbs are separated from each other. In normal individual that denotes symmetrical chest wall expansion. If only one thumb is moving then there is unilateral expansion in one side and denotes abnormality in other side. Vocal resonance:
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Sound of ordinary speech hears through the chest wall. So ask the patient to say R or 99 repeatedly. Sound is attenuated to the lungs. If there is any abnormality or accumulation of secretions in the lungs, there will be dullness or hyper resonant. On percussionHyper resonant. It is elicited by placing one finger firmly on an intercostal space and struck sharply by the middle finger of the opposite hand. Each side of the chest should be percussed alternatively. A percussion note is resonant over normal lung tissue. A booming sound suggests hyper resonance.

f On auscultation Decreased breath sounds.

Silent chest that is insufficient to produce breath sound. Wheezing. Decreased ventilation.

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Using inch tape at three different levels does chest wall expansion is measured. 1. 2. 3. PROBLEM LIST: Breathlessness. Bronchospasm. Decreased ventilation to the lung. Use of accessory muscles. Decreased exercise tolerance. Axilla level Nipple level Xiphoid process level

AIMS OF TREATMENT: 1.) To educate the patient on various allergens and condition. 2.) To have a controlled pattern of breathing. 3.) To reduce use of accessory muscles. 4.) To maximize the ventilation.

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5.) To relieve bronchospasm.

6.) To improve exercise tolerance.

MEANS AND METHODS OF TREATMENT:

HEALTH EDUCATION: The main causes of allergic asthma are aeroallergens, which include seasonal pollen, mold spores, dustmites, animal allergens, and food (especially in children). So asthmatic patient should take care of this and has less exposure to all of this. Educate the asthmatic patients, in selected series, vaccinations, fewer childhood infections, liberal use of antibiotics, and proper bronchodialator therapy, more processed food in diets, small families and less exposure to day care environments have been associated with increased atopy and asthma. Educate the patient about the course of disease and prognosis, that is what made the patient breathless or wheezy, for that what he has to do, and educate how he has to overcome from this. Educate the breathing exercise to overcome the problem. Educate about the diet, aside from avoiding known food allergens or additives, diet is not restricted. Advice in maintaining physical activity and exercise and essential to avoid deconditioning susceptible individuals should decrease outdoor activity during middy and afternoon when pollen counts are highest. DIAPHRAGMATIC BREATHING EXERCISES:
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In asthma diaphragmatic breathing exercises are used To induce relax pattern of breathing To have a control pattern of breathing.

Diaphragmatic breathing exercises carried out in any of relaxed position. Diaphragmatic breathing exercises given by 2 methods. 1.) Concentrates on forward movement of whole abdominal wall. 2.) Concentrates on upper abdominal wall and lower lateral ribs. 1ST METHOD: Position- Relaxed half-lying position or sitting position.

There are 2 schools of thought on diaphragmatic exercises. School-1- concentrates on movement of epigastrium upper abdominal wall lower lateral ribs. School-2- Concentrates on allowing the whole abdominal wall as the diaphragm descends downwards relaxely. In first method, the patient places hands on anterior costal margin or upper abdominal wall and ask the patient to breath out gently as he does, the lower ribs are sinking down and in towards the midline. Points considered in applying the techniques: 1.) During the technique, the patient should relax shoulder and upper chest. 2.) Patient is asked to breathe on his own rate and rhythm. If the patient takes too deep breath he expands, the apical area and chest.
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3.) Expiration is a passive process compared to that of inspiration.

2nd method: Position- half-lying. Therapist places both hands on anterior abdominal wall then ask the patient to breathe out gently. He felt abdomen is sinking down and in and ask him to breath in Through his nose. The air enters the nose is concentrated and directed to abdomen and bulges where the therapist places hands. COSTAL EXPANSIONS EXERCISES: In asthma costal expansion exercises are given To improve ventilation to the lungs after relieving bronchospasm. To mobilize the secretions To improve the thoracic cage movement.

It includes1. Localized basal expansion exercise. 2. Apical expansion exercises. 3. Posterior basal expansion exercises. 1.) Localized basal expansion exercises: Position- Relaxed half-lying or sitting position.
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Technique: The therapist places the palms of the hand over Mid axillary line of 7th and 8th ribs. Ask the patient to breathout gently and therapist applies a firm pressure against chest wall and ask the patient to breath air through nose, the pressure maintained during expiration is maintained upto end of inspiration and pressure is relieved, at the end of inspiration the therapist hand moves along with chest wall and passive expiration occurs. 2.) Apical expansion exercises: Position- Relaxed half-lying or sitting position. Technique: Pressure is applied below the clavicle using the tips of the fingers. The patient is instructed to breathe in and expand the chest upward against the pressure of the fingers. Full inspiration may be held for a moment but the shoulders must remain relaxed. 3.) Posterior basal expansion exercises: Position- Half-lying. Technique: Pressure is given unilaterally over the posterior aspect of the lower ribs and patient can be taught to apply this pressure himself.

Once the patient has learned the technique, he is taught to give pressure him self. He has to apply pressure with the back of the fingers or the palm of the opposite hand. When using any of these methods, the patient should not elevate his shoulder girdle or achieve costal expansion by side flexion of the spine. The use of wide belt made of webbing or some other non-extensible material may be helpful. BRONCHODILATOR THERAPY:
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Bronchodialaotor therapy is used to relieve the bronchospasm, which is given through nebilizers or through inhalers. To dilate the bronchus, in general wherever possible, this should be given by aerosol as the doses used are very much smaller than when tablets of the same drug are prescribed and there are many effective selective Beta-2- adrenoceptor antagonists such as sulbutamol, terbutaline, fenoterol and rimiterol. In episodic asthma where mild infrequent symptoms occur the bronchodilator aerosol should be used when symptom occur with some resistant asthma regular use of aerosol is indicated. For exercise induced asthma prior use of the aerosol before exercise will often control symptoms adequately. In chronic asthma it may sometimes be helpful to add an oral bronchodilator as tablets to the aerosol with chronic asthma not responding to bronchodilator therapy alone addition of a corticosteriod aerosol such as beclomethasone diproponate, betamethasone valenrate or budesonide may be very helpful in controlling symptoms, the introduction of steroid aerosols has allowed considerable reduction and often withdrawn of systemic steroids in patients who previously were dependent upon these drugs. EXERCISE TOLERANCE: Breathing control should teach during sitting, standing, and walking climbing stairs and in functional activities to increase exercise tolerance.

ASSESMENT (after an attack): On observation: Accessory muscles are used. Shortness of breath. Cough.
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On examination: Consists of on palpation, percussion, and auscultation.

On palpation- there will be decreased chest wall expansion. On percussion- there will be hyper resonant. On auscultation There will be decreased breath sounds. Wheezing. Silent chest. Decreased ventilation.

Problem list: 1. Accumulation of secretions. 2. Decreased ventilation. 3. Decreased gaseous exchange. 4. Bronchospasm.

Aims of treatment: To educate the patient on various allergens and conditions. To clear the secretion. To increase the ventillaton. To optimize the gaseous exchange.
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To have a controlled pattern of breathing. To relieve bronchiospasm. To improve the inspiration. To improve exercise tolerance. Means and methods of treatment: 1. Health education on various allergens and condition. 2. Postural drainage: Postural drainage is used to loose and drain the secretions and to expectorate secretions. Postural drainage positions:
1.

Upper lobe: It consists of bronchopulmonary segments.

apical,

anterior

and

posterior

a.)

Apical bronchopulmonary segment of right and left upper lobe: Make the patient in half-Lying or sit upright by leaning forwards or backwards or sideward.

b.)

Anterior brochopulmonary segment of right and left upper lobe: Make the patient to lie on his back with arms kept relaxely side of the body. c.) Posterior bronchopulmonary segment of right side of upper lobe: Makes the patient to lie on leftside lying and turn 45o towards his face and place a pillow under the trunk, shoulder, and the knee.

d.)Post brochopulmonary segment of lift side of upper lobe:

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his face (prone) and place 3 pillows in order to elevate the trunk approximately 35 o.
2.)

Middle lobe: a.)Medial and lateral bronchopulmonary segment: (right side). the patient to lie on his back and turn 45 o towards his face and turn 45 o towards his face and position is maintained by placing a pillow from shoulder to hip.
Make The

foot end is elevated upto 35cms(14inches) from the ground or the chest is made to from an angle of 15 o. b.)Lingular segments(left): the patient to lie on his back and turn 45 o towards his face or towards right side and the position is maintained by placing a pillow from shoulder to hip and foot end is elevated upto 35cms(14inch) or chest is made to form an angle of 15 o.
Make

3.)

Lower lobes:

It consists of In right side apical, anterior, posterior, medial and lateral bronchopulmonary segments. In left side- apical, bronchopulmonary segments. anterior, posterior, lateral

a.)Apical broncho pulmonary segment of right and left lower lobes: Make the patient to lie on his face (prone) and place a pillow under the hip, arms relaxely, around the head. There is no elevation in apical bronchopulmonary segment. b.)Anterior basal bronchopulmonary segment of right and left lower lobes: Make the patient to lie on his back and place a pillow under the buttocks knees are bend arm kept relaxely by the side of the body, and the foot end is elevated upto 46 cm (18inches) or chest is made to form an angle of 20 o.
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c.) Posterior basal bronchopulmonary segment of right and left lower lobs:

Make the patient to lie on his face (prone) place pillow under the hip and arms kept relaxely by the side of the body and foot end is elevated upto 46cm(18inches) or make an angle of 20 o.

d.)Medial basal of right and lateral basal of left bronchopulmonary segment of lower lobs: Make the patient to lie on the right side lying and place a pillow under hip and foot end is elevated upto 46cm(18inches) or chest is formed at an angle of 20 o.

e.)Lateral basal of right bronchopulmonary segment of lower lobe: Make the patient in left side lying and place a pillow under the hip and foot end is elevated upto 46cm,or chest is made to form angle of 20o.

Postural drainage with forced expiratory techniques for expectoration is carried out with diaphragmatic breathing exercises. HUFFING: Open expectoration against open glottis. Types: 1. High lung volume huffing- dislodges secretions from proximal airways. 2. Mid lung volume huffing- dislodges secretions from mid airways of zone-II. 3. Low lung volume huffing- Dislodges secretions from tertiary air ways. Technique:
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Ask the patient to take 3-4 deep breaths. Then diaphragmatic breathing exercises are carried out and then 34huffs from mid lung volume to low lung volume. out. Then again diaphragmatic breathing exercises are carried

If the secretions reach the proximal airways then the patient is made to cough or huff with high lung volume inorder to clear the secretions in proximal airways.

COUGHING:
Closed expectoration against closed glottis. For a cough to be effective, there should be 1. High-pressure during expiration. 2. High expiratory flow rate 3. Expiration has to be at higher volumes. Technique of cough: It includes 5 points. 1. An inspiratory gulp of about 90% of total lung capacity is taken.

2. Closure of glottis and trapping of air inside at a powerful positive pressure of about 300mm of Hg.

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3. Ask the patient to mimic swallowing in order to increase the intra-thoracic pressure. 4. For abdominal contraction and internal intercostal muscle contraction ask the patient to pronounce the alphabet K to increase the intra-abdominal pressure. 5. Forcibly expire against the open glottis.

Costal expansion exercises are carried out, to improve ventilation and optimize gaseous exchange. Bronchodilotor therapy is given through nebilizers or through inhalers to relieve the bronchospasm. RAISING THE RESTING RESPIRATORY LEVEL: Raising the resting respiratory level is carried out. The resting respiratory level is the point at which the tidal volume (TV) rests with in the vital capacity (VC). The natural expiratory level is that point at which natural expiration ends and is usually constant. It is the point at which the elasticity or recoil of the rib cage is in balance with the elasticity of the lung tissue. As a result of obstructive airway disease, portions of the lung shut down sooner than other. In there instances of gross expiratory obstruction, there is a sharp decrease in air flow early in the expiatory phase, continuing with expiration only increases muscle work and takes up time, while an ever decreasing amount of air is being moved.

If the breathing cycle is lifted between 200-300ml from the obstructed point, the ventilation will be more efficient greater
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airflow for this work. Therefore, improved function and exercise tolerance can be achieved without attending the course of the disease.

The technique is taught as part of diaphragmatic breathing. The relaxed expiratory phase is watched by the physiotherapist, who directs the patient to begin inspiration a little sooner in the respiratory cycle, thus avoiding prolonged expiration. The tidal volume is maintained, thus in is not just the expiratory level, which is raised, but the whole respiratory level is lifted from the obstructed point. EXERCISE TOLERANCE: Breathing control should taught during sitting, standing, walking, and climbing stairs and in functional activities to increase exercise tolerance.

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PHYSIOTHERAPY MANAGEMENT
Physiotherapy management includes pulmonary rehabilitation, which is defined as a multidimensional continum of services directed to persons with pulmonary diseases and their families, usually by an inter disciplinary team of physiotherapists with the goal of achieving and maintaining the individuals maximum level of independence and functioning in the community. The goal of treatment is to improve function in daily living and quality of life by preventing symptoms and recurrence of exacerbation by preserving optimal lung function. Encourage the patient to participate actively in therapy. Oral and inhaled medications are used for patients with stable disease to reduce dyspnea and improve exercise tolerance. Asthma commonly associated with hypoxemia oxygen therapy is given for these patients. Oxygen reduces mortality rates. Oxygen therapy is generally safe to reduce despnea and improve exercise tolerance. Postural techniques are advised to the patients leaning forwards postures frquently relieve dyspnea in asthmatic patients by reducing respiratory effort. Educate the diaphragmatic breathing exercises to the patient, to induce relaxed pattern of breathing and to have controlled pattern of breathing. Bronchodilator therapy is used to relieve the bronchospasm is given through neubilisers or through inhalers.

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Postural drainage is educated to the patient, in various dependents that is positioning the patient in appropriate broncho pulmonary segments. Postural drainage is used to drain the secretions and to expectorate secretions. Diaphragmatic breathing exercises are educated inorder to induce relax pattern of breathing and to have a control pattern of breathing. Costal expansion exercises are taught to the patient inorder to improve the ventilation to the lungs and optimize gases exchange. Breathing control during sitting, standing, walking, climbing stairs, and in functional activities are taught to the patient in order to increase the exercise tolerance. Raising the resting respiratory level should teach to maintain the normal pattern of breathing (concentrating on oxygen input). Postural drainage by forced expiratory techniques for expectoration by huffing techniques is carried out along with diaphragmatic breathing exercises. Educating the patient on various allergens and condition.

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CASE STUDY-1
Name Age Sex Occupation Address Duration During an attack: On observation: i.) Forward chest). ii.) bending posture(head and upper : Jacob Fernandase.G. : 35 Years. : Male. : Business. : Durgapuram, Vijayawada. : Since 10 Years.

Built- Moderate.

iii.) Altered pattern of breathing with prolonged expiration. iv.) v.) vi.) vii.) Use of accessory muscle. Shortness of breath. Wheezy is audible. Barrel chest deformity (very mild).

viii.) Purulent sputum due to presence of excess number of eosinophils. ix.) x.) xi.) Intermittent coughing. Restlessness. Frequent change of position in sitting.

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On auscultation: i.) Expiratory ronchi is present, at wheezing during both phases of respiration. times

ii.) Decreased breath sound during early stages patient has silent chest that is insufficient to produce breath sound. iii.) No evidence of accumulation of secretion but crackles was heard at times. iv.) On percussion: It was hyper resonant, very high pitched sound, there is evidence of air trapping in the alveoli, and barrel chest deformity suggested that. On examination: Axilla: Nipple: Xiphoid processes: On palpation; Normal symmetry (decreased chest wall movement). Tenderness in costochondral junction. Vocal fremitus increased. Expiration- 75 cms Inspiration-78 cms Expiration- 81cms Inspiration-79 cms Expiration- 72 cms Inspiration- 75 cms Ventilation to the lungs is decreased.

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Vital signs: Respiratory rate > 25/min, then decreasing as the patient tires. Increased PaCo2 as the patient tries. Heart rate>110, then bradycardia if the patient deteriorates. Temperature- normal.

PROBLEM LIST:
i.) ii.) iii.) iv.) v.) vi.) vii.) Breathlessness. Bronchospasm. Decreased ventilation. Use of accessory muscles. Decreased gaseous exchange. Decreased general mobility. Decreased exercise tolerance.

viii.) Decreased chest wall mobility.

AIMS:
To educate the patient on various allergens and conditions. To have a controlled pattern of breathing. To relieve bronchospasm. To maximize the ventilation. To improve exercise. To reduce use of accessory muscles.

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MEANS AND METHODS:

A brief explanation about the condition is given to the patient and explains the preventive measures. Relaxed positions are taught to the patient with appropriate placement of pillows. Diaphragmatic breathing exercises taught to have a control pattern of breathing with own rhythm of respiration and also taught to induce relaxed pattern of breathing, if the patient feels the attack is going to come. Costal expansion exercises are taught preferably in half lying position, sitting upright, leaning slightly forwards. Proper use of inhalers is taught effectively and encouraged to use during an attack. Raising the resting respiratory level is given to shorten the prolonged expiration. General mobility exercises are taught to the patient especially to shoulder trunk and the spine. Exercise tolerance is improved by control breathing initially by walking slowly and as day progressed, made patient to walk briskly with frequent rest periods.

AFTER AN ATTACK
On observation: 1. Forward bending posture (Head and upper chest). 2. Built-moderate. 3. Altered pattern of breathing with prolonged expiration. 4. Use of accessory muscle.
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5. Shortness of breath.

6. Wheezy is audible. 7. Barrel chest deformity (very mild). 8. Purulent sputum due to presence of excess number of eosinophils. 9. Intermittent coughing and frequent change of position in sitting. 10. Restlessness. On auscultation: 1.) Expiratory ronchi is present, at times wheezing during both phases of respiration. 2.) Decreased breath sound during early stages patient has silent chest that insufficient to produce breath sound. 3.) No evidence of accumulation of secretion but crackles was heard at times. 4.) Ventilation to the lungs is decreased. On Percussion: It was hyper resonant, very high pitched sound, there is evidence of air trapping in the alveoli, and barrel chest deformity suggested that.

On examination:
Chest wall expansionAxilla: Expiration- 75 cms Inspiration- 78 cms Expiration- 81 cms Inspiration- 79 cms Expiration- 75 cms

Nipple:
Xiphoid processes:

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Inspiration- 78 cms

On palpation: Normal symmetry (decreased chest wall movement). Tenderness in costochondral junction. Vocal fremitus increased. Vital signs: Respiratory rate>25/min then decreasing as the patient tires. Increased PaCo2 as the patient tries. Heart rate>110, then bradycarida if the patient deteriorates. Temperature- normal.

PROBLEM LIST:
1.) Accumulation of secretions. 2.) Decreased ventilation. 3.) Decreased gaseous exchange. 4.) Prolonged expiration. 5.) Bronchospasm.

AIMS OF TREATMENT:
1.) To clear the secretions. 2.) To increase the ventilation. 3.) To optimize the gaseous exchange.
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4.) To relieve Bronchospasm.

5.) To shorten prolonged expiration.

MEANS AND METHODS:

1. Forced expiratory techniques for expectoration that is huffing techniques is carried out with diaphragmatic breathing exercises. 2. Costal expansion exercises to improve ventilation and optimize gaseous exchange. 3. Raising the resting respiratory level to shorten the prolonged expiration.

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CASE STUDY-2
Name Age Sex Occupation Address Duration DURING AN ATTACK On observation: 1. 2. Forward bending posture(head and upper chest). Built-thin. pattern of breathing with prolonged : Venkaiah.D : 52 years : Male : Coolie : Gandhinagar, vijayawads : since 25 years.

3. Altered expiration. 4. 5. 6. 7.

Use of accessory muscle. Shortness of breath. Wheezy is audible. Barrel chest deformity.

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8. Coughing in series and frequent change of position in sitting. 9. Restlessness. of supra sternal notch and

10. Evacuation supraclavicular fossa.

On auscultation: 1. Expiratory rouchi is present, wheezing occur during both phases of respiration (audible). 2. Decreased breath sound and the patient have silent chest that is insufficient to produce breath sound. 3. Evidence of accumulation secretion and crackles were heard at times. On percussion: It was hyper resonant, very high pitched sound, there is evidence of air trapping in the alveoli, and barrel chest deformity suggested that. On examination: Axilla: Nipple: Xiphoid processes: On palpation: Decreased chest decreased chest wall movement (anterior and posterior). Expiration- 69 cms Inspiration- 72 cms Expiration- 74 cms Inspiration- 77 cms Expiration- 68 cms Inspiration- 71 cms

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Tenderness in costochondral junction. Vocal resonance is increased.

Vital signs: Respiratory rate>25/mm, these decreasing as the patient tires.

Increased PaC02 as the patient tries. Heart rate>110, then bradycardia if the patient detoriates. Temperature- normal.

PROBLEM LIST:
1. Breathlessness. 2. Brouchospasm. 3. Decreased ventilation. 4. Use of accessory muscle. 5. Decreased gaseous exchange. 6. Decreased general mobility. 7. Decreased exercise tolerance. 8. Decreased chest wall mobility.

AIMS:
To educate the patient on various allergens and condition. To have a controlled pattern of breathing. To relieve bronchospasm. To maximize the ventilation.

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To improve exercise tolerance. To reduce use of accessory muscles.

MEANS AND METHODS:

A Brief explanation about the condition is given to the patient and explains the preventive measures.

Relaxed positions are taught to the patient with appropriate placement of pillows. Diaphragmatic breathing exercises taught to have a control pattern of breathing with own rhythm of respiration and also taught to induce relaxed pattern of breathing,if the patient feels the attack is going to come. Costal expansion exercises are taught preferably in half lying position, sitting upright, leaning slightly towards. Proper use inhalers are taught effectively and encouraged to use during an attack. Raising the resting respiratory level is given to shorten the prolonged expiration. General mobility exercises are taught to the patient especially to shoulder trunk and the spine. Exercise tolerance is improved by control breathing initially by walking slowly and as day progressed, made patient to walk briskly with frequent rest periods, also during functional activities.

AFTER AN ATTACK
On observation: 1. Forward bending posture(head and upper chest). 2. Built-thin.
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3. Altered pattern of breathing with prolonged expiration. 4. Use of accessory muscle. 5. Shortness of breath. 6. Wheezy is audible. 7. Barrel chest deformity.

8. Coughing in series and frequent change of position in sitting.

9. Restlessness. 10. Evacuation of supra sternal notch and supraclavicular fossa.

On auscultation: 4. Expiratory rouchi is present, wheezing occur during both phases of respiration (audible). 5. Decreased breath sound and the patient have silent chest that is insufficient to produce breath sound. 6. Evidence of accumulation secretion and crackles were heard at times. On percussion: It was hyper resonant, very high pitched sound, there is evidence of air trapping in the alveoli, and barrel chest deformity suggested that. On examination: Axilla: Nipple: Expiration- 69 cms Inspiration- 72 cms Expiration- 74 cms Inspiration- 77 cms Expiration- 68 cms

Xiphoid processes:

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Inspiration- 71 cms

On palpation: Decreased chest decreased chest wall movement (anterior and posterior). Tenderness in costochondral junction. Vocal resonance is increased.

Vital sings: Respiratory rate>25/mm, these decreasing as the patient tires. Increased PaC02 as the patient tries. Heart rate>110, then bradycardia if the patient deteriates. Temperature- normal.

PROBLEM LIST:
1. Repeated coughing with production of sputum and retained secretions. 2. Hypoxia. 3. Hypoxemia. 4. Decreased ventilation. 5. Bronchospasm.

AIMS AND MEANS:

1. To educate the patient on asthma regarding causes, clinical features, physiotherapy, clinical aspects, factors like allergy. 2. To teach affective cough and bring about the secretions.
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3. Bronchodilator therapy for Bronchospasm. 4. Costal expansion exercise with frequent rest periods (with 2 hours gap) since it is a chronic condition. 5. If patient is hypoxic or hyperemia oxygen therapy is give. 6. To teach the relaxed pattern of breathing in different relaxed positions. 7. To teach effective use of bronchodialotr therapy. 8. To increase exercise tolerance, teach breathing control during walking, functional activity and stair climbing is done.

CONCLUSION
f It has been interpreted and concluded based on the follow up assessment and rehabilitation of asthmatic patientphysiotherapy procedures plays a vital role in remodeling the individual life style. Though bronchospasm and the allergens are considered to be the major culprits. f Education, precaution, and awareness about these to the patient precisely paves way for functionally independent pulmonary system. f In asthmatic individual concise explanation, rational demonstration on breathing exercises and practice of other techniques has brought down the frequency in the attacks of breathlessness. f Despite the availability of modern drugs and inhalers in regard to this cumulative project work in asthma has clearly proved, physiotherapy and its various techniques mentioned is more effective in rehabilitation of patient physically and mentally.
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f The mentioned techniques in this guide is effectively executed, still the physiotherapy procedures are continued. f I conclude with mental contentment by analyzing the patients improvement as a final year student of physiotherapy.

BIBLIOGRAPHY
1.) Ann Thomson, Alison skinner, Joan Piercy. 2.) Alexandra Hough 3.) Braunwald and willson 4.) B.D. Chaursia 5.) Francis J.Bonannon Tidys physiotherapy, 12th edition (1995). Physiotherapy in respiratory care. Principles of internal medicine 11th edition. Human anatomy volume-1 3rd edition(1999). Cardio pulmonary rehabilitation, Basic theory and application 3rd edition(1997). Principles of physiology. 8th edition. anatomy and

6.) Gegrad.J.Tortora

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7.) john macleoid

Davidsons principles and practice of medicine.

8.) K. Sembulingam 9.) Patria A. Downie

nd

Essentials of medical physiology edition(2000). Cashs text book of chest, heart and vascular disorders for physiotherapists. Text book of Human anatomy

10.) T.S. Ranganathan 5th edition(1999).

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