Copd

chronic pulmonary disease

1. Copd By- Dr. Akshita (PT) MPT-Cardiopulmonary D.C.PT Certified BLS & ACLS

2. INTRODUCTION OBSTRUCTIVE LUNG DISEASE Several abbreviations can be found in the literature for a pulmonary disorder characterized by increased airway resistance, particularly noticeable by a prolonged forced expiration. Some of these are chronic obstructive pulmonary disease (COPD), chronic obstructive airway disease (COAD), chronic airway obstruction (CAO), and chronic obstructive lung disease (COLD).

3. Chronic obstructive pulmonary disease (COPD) is a generic term that refers to lung diseases that result in air trapping in the lungs, causing hyperinflation of the lungs, and a barrel-chest deformity . There are two entities in COPD namely- Chronic Bronchitis (ii) Emphysema .

4. Respiratory system

5. → Nose—warms the air breathed in and filters out bacteria and debris. Nasal breathing is important for best lung function. ↓ Pharynx—is an oval fibro-muscular sac located behind the nasal cavity, mouth, and larynx, it is passageway that conducts air from the nose to the voice box. The pharynx also conducts food from the mouth to the esophagus, the tube that leads to the stomach. It is approx. 12to 14 cm long. It opens into the nasal cavity ( nasopharynx ), mouth (oral pharynx) and larynx ( laryngopharynx ).

6. -The nasopharynx is a continuation of the nasal cavities . It lies behind the nose and above the soft palate. -The oral pharynx extends from the soft palate to the epiglotis It opens into the mouth anteriorly through the oropharyngeal isthmus. -The laryngopharynx lies behind the larynx and extends from the epiglotis above to the inlet of the esophagus.

7. ↓ Larynx—The larynx is a complex structure composed of cartilages and cords moved by sensitive muscles. It acts as a sphincteric valve with its rapid closure, preventing food, liquids, and foreign objects from entering the airway. It controls airflow, and at times closes so that thoracic pressure may be raised and the upper airways cleared by a propulsive cough when the larynx opens. Expiratory airflow vibrates as it passes over the contracting vocal chords, producing the sounds used for speech.

8. Lower Respiratory Tract

9. ↓ Trachea—windpipe. The trachea is a semi-rigid, cartilaginous tube approximately 10 to II cm long and 2.5 cm wide. It lies infront of the esophagus, descending with a slight inclination to the right from the level of the cricoid cartilage.It travels behind the sternum into the thorax to the sternal angle (opposite the fifth thoracic vertebra), where it divides to form the right and left main-stem bronchi.

10. Tracheobronchial Tree

11. ↓ Bronchi—two tubes that lead from the trachea to the lungs. The bronchi divide into many smaller airways, called bronchioles. The bronchi of the airways continue to divide until there are approximately 23 generations . - The main, lobar, and segmental bronchi are made up of the first four generations. -The sub segmental bronchi extend from the fifth to the seventh generation.

12. -The terminal bronchioles extend from the twelfth to the sixteenth generation. -The respiratory bronchioles extend from the seventeenth to the nineteenth generation. -They are considered a transitional zone between bronchioles and alveoli. Alveolar ducts extend from the twentieth to the twenty-second generation. -The twenty-third generation of air passages is called alveolar sacs. They are essentially the same as alveolar ducts, except that they end as blind pouches.

13. ↓ Lungs —Two lungs, each covered with its otherwise free in the thoracic cavity. -The lungs are light, soft spongy organs, pleurae-the visceral pleura and the parietal pleura-lie within the thoracic cavity. -Each lung is attached to the heart and the trachea by its root and the pulmonary ligament. It is whose color darkens with age as they become impregnated with inhaled dust

14. -They are covered with the visceral pleura, a thin, glistening serous membrane that covers all surfaces of the lung. - Each lung has an apex, base, arid three surfaces (costal, medial, and diaphragmatic). -There are also three borders (anterior, inferior, and posterior). Each lung is divided by fissures into separate lobes

15. In the right lung the oblique fissure separates the lower lobe from the middle, whereas the horizontal fissure separates the upper lobe from the middle. The right lung is heavier and wider than the left lung. It is also shorter because of the location of the right lobe of the liver. The left lung is divided into upper and lower lobes by the oblique fissure. It is longer and thinner than the right lung, because the hem1 and pericardium are located in the left thorax. The lungs are connected to the upper airways by the trachea and main-stem bronchi.

16. ↓ Alveoli —millions of tiny air sacs in the lungs, surrounded by tiny blood vessels called capillaries. This is where the exchange of oxygen and carbon dioxide takes place. These sacs look like bunches of grapes. → Pleura —a membrane that covers the lungs and helps them move freely.

17. MOVEMENTS OF THE THORAX The frequency of movement of the bony thorax joints is greater than that of almost any other combination of joints in the body. Two types of movements have been described-the pump-handle movement and the bucket-handle movement . The upper ribs are limited in their ability to move. Each pair swings like a pump handle, with elevation thrusting the sternum forward. This forward movement increases the anteroposterior diameter and the depth of the thorax and is called the pump-handle movement.

18. In the lower ribs, there is little antero -posterior movement. During inspiration, the ribs swing outward and upward, each pushing against the rib above during elevation. This bucket handle movement increases the transverse diameter of the thoracic cage. Thus during inspiration, the thorax increases its volume by increasing its anteroposterior and transverse diameters .

19. MUSCLES OF RESPIRATION

20. Inspiration Inspiration - is an active movement involving the contraction of the diaphragm and intercostals. Additional muscles may come into play during exertion in health. The accessory muscles include the sternocleidomastoids , scalenes , serratus anterior, pectoralis major and minor, trapezius , and erector spinae

21. Expiration Expiration is a passive process, occurring when the intercostals and diaphragm relax. Their relaxation allows the ribs to drop to their pre- inspiratory position and the diaphragm to rise. These activities compress the lungs, raising intra thoracic pressure above atmospheric pressure, and thereby contributing to air flow out of the lungs.

22. Respiratory muscles ( anteriorly )

23. Respiratory muscles( posteriorly )

24. MUSCLES OF RESPIRATION Diaphragm The diaphragm is the principal muscle of respiration. During quiet breathing, the diaphragm contributes approximately two thirds of the tidal volume in the sitting or standing positions, and approximately three fourths of the tidal volume in the supine position. It is also estimated that two thirds of the vital capacity in all positions is contributed by the diaphragm. The diaphragm is a large, dome-shaped muscle that separates the thoracic and abdominal cavities .

25. Diaphragm

26. This large muscle can be divided into right and left halves. Each half is made up of three parts- sternal , lumbar, and costal. These three parts are inserted into the central tendon, which lies just below the heart. The sternal part arises from the back of the xiphoid process and descends to the central tendon. The position of the diaphragm and its range of movement vary with posture, the degree of distention of the stomach, size of the intestines, size of the liver, and obesity. The average movement of the diaphragm in quiet respiration is 12.5 mm on the right and 12 mm on the left. This can increase to a maximum of 30 mm on the right and 28 mm on the left during increased ventilation.

27. Each half of the diaphragm is innervated by a separate nerve-the phrenic nerve on that side. Contraction of the diaphragm increases the thoracic volume vertically and transversely. The central tendon is drawn down by the diaphragm as it contracts. As the dome descends, abdominal organs are pushed forward, as far as the abdominal walls will allow. When the dome can descend no farther, the costal fibers of the diaphragm contract to increase the thoracic diameter of the thorax.

28. Intercostals The external intercostals extend from the tubercles of the ribs, above, down, and forward to the costochondral junction of the ribs below, where they become continuous with the anterior intercostal membrane. There are 11 external intercostal muscles on each side of the sternum. They are thicker posteriorly than anteriorly , and thicker than the internal intercostal muscles. They are innervated by the intercostal nerves, and contraction draws the lower rib up and out toward the upper rib. This action increases the volume of the thoracic cavity.

29. Intercostals

30. There are also 11 internal intercostals per side. These are considered primarily expiratory in function. Studies have shown that the intercartilaginous or parasternal portion of the internal intercostals contracts with the external intercostals during inspiration to help elevate the ribs. Besides their respiratory functions, the intercostal muscles contract to prevent the intercostal spaces from being drawn in or bulged out during respiratory activity.

31. Contraction of the interosseous portions of the intercostals depresses the ribs and may aid in forceful exhalation. This muscle is innervated by the adjacent intercostals nerves.

32. Sternocleidomastoid The sternocleidomastoids (SCMs) are strong neck muscles arising from two heads, one from the manubrium and one from the medial part of the clavicle. These two heads fuse into one muscle mass that is inserted behind the ear into the mastoid process. It is innervated by the accessory nerve and the second cervical nerve. There are two of these muscles, one on each side of the neck.

33. When one SCM contracts, it tilts the head toward the shoulder of the same side and rotates the face toward the opposite shoulder. If the two SCM muscles contract together, they pull the head forward into flexion. When the head is fixed, they assist in elevating the sternum, increasing the anteroposterior (AP) diameter of the thorax. The SCMs are the most important accessory muscles of inspiration. Their contractions can be observed in all patients during forced inspiration and in all patients who are dyspneic . These muscles become visually predominant in patients who are chronically dyspneic .

34. Sternocleidomastoid

35. Scalenes The anterior, medial, and posterior scalenes are three separate muscles that are considered as a functional unit. They are attached superiorly to the transverse processes of the lower five cervical vertebrae and inferiorly to the upper surface of the first two ribs. They are innervated by related cervical spinal nerves. These muscles are primarily supportive neck muscles, but they can assist in respiration through reverse action. When their superior attachment is fixed, the scalenes act as accessory respiratory muscles and elevate the first two ribs during inspiration.

36. Scalenes

37. Serratus Anterior The serratus anterior arises from the outer surfaces of the first eight or nine ribs. It curves backward, forming a sheet of muscle that inserts into the medial border of the scapula. It is innervated by the long thoracic nerve (cervical nerves CS, C6, and C7). There are two of these muscles, one on each side of the body. Normally, they assist in forward pushing of the arm (as in boxing or punching). When the scapulae are fixed, they act as accessory respiratory muscles and elevate the ribs to which they are attached.

38. Pectoralis Major The pectoralis major is a large muscle arising from the clavicle, the sternum, and the cartilages of all the true ribs. This muscle sweeps across the anterior chest to insert into the intertubercular sulcus of the humerus . It is innervated by the lateral and medial pectoral nerves and cervical nerves CS, C6, C7, C8, and T1. There are two of these muscles, one on each side of the body.

39. This muscle acts to rotate the humerus medially and to draw the arm across the chest. In climbing and pull-ups, it draws the trunk toward the arms. In forced inspiration when the arms are fixed, it draws the ribs toward the arms, thereby increasing thoracic diameter.

40. Pectoralis Minor The pectoralis minor is a thin muscle originating from the outer surfaces of the third, fourth, and fifth ribs near their cartilages. It inserts into the coracoid process of the scapula. It is innervated by the pectoral nerves (cervical nerves C6, C7, and C8).

41. There are two of these muscles, one on each side of the body. They contract with the serratus anterior to draw the scapulae toward the chest. During deep inspiration, they contract to elevate the ribs to which they are attached.

42. Pectorals

43. Trapezius The trapezius consists of two muscles that form a diamond-shaped sheet extending from the head down the back and out to both shoulders . Its upper belly originates from the external occipital protuberance and curves around the side of the neck to insert into the posterior border of the clavicle. The middle part of the muscle arises from a thin diamond-shaped tendinous sheet, the supraspinous ligaments and the spines o f the upper thoracic region, and runs horizontally to insert into the spine of the scapula. Its lower belly arises from the supraspinous ligaments and the spines of the lower thoracic region, and runs upward to be inserted into the lower border of the spine of the scapula.

44. This large muscle is innervated by the external or spinal part of the accessory nerve and cervical nerves C3 and C4. Its main function is to rotate the scapulae in elevating the arms and to control their gravitational descent. It also braces the scapulae and raises them, as in shrugging the shoulders. Its ability to stabilize the scapulae makes it an important accessory muscle in respiration. This stabilization enables the serratus anterior and pectoralis minor to elevate the ribs.

45. Trapezius

46. Erector Spinae The erector spinae is a large muscle extending from the sacrum to the skull. It originates from the sacrum, iliac crest, and the spines of the lower thoracic and lumbar vertebrae. It separates into a lateral iliocostalis , an intermediate longissimus , and a medial spinalis column. This muscle mass inserts into various ribs and vertebral processes all the way up to the skull.

47. It is innervated by the related spinal nerves. These muscles extend, laterally flex, and rotate the vertebral column. They are considered accessory respiratory muscles through their extension of the vertebral column. In deep inspiration, these muscles extend the vertebral column, allowing further elevation of the ribs

48. Errector spinae

49. Rectus Abdominis The rectus abdominis rises from the pubic crest and extends upward to insert into the xiphoid process and the costal margin of the fifth, sixth, and seventh costal cartilages . It is innervated by related spinal nerves, and its action is considered within the context of the other abdominal muscles.

50. Rectus Abdominis

51. Obliqus Extenus Abdominis This muscle arises in an oblique line from the fifth costal cartilage to the twelfth ribs. Its posterior fibers attach in an almost vertical line with the iliac crest. The other fibers extend down and forward to attach to the front of the xiphoid process, the linea alba, and below with the pubic symphysis . It is innervated by the lower six thoracic spinal nerves.

52. Obliquus Intemus Abdominis This muscle originates from the lumbar fascia, the anterior two thirds of the iliac crest, and the lateral two thirds of the inguinal ligament. Its posterior fibers run almost vertically upward to inselt into the lower borders of the last three ribs. The other fibers join an aponeurosis attached to the costal margin above, the linea alba in the midline and the pubic crest below. It is innervated by the lower six thoracic nerves and the first lumbar spinal nerves.

53. Obliqus Abdominis

54. Transversus Abdominis The transversus abdominis arises from the inner surface of the lower six costal cartilages, the lumbar fascia, the anterior two thirds of the iliac crest, and the lateral one third of the inguinal ligament . It runs across the abdomen horizontally to insert into the aponeurosis extending to the linea alba. It is innervated by the lower six thoracic nerves and the first lumbar spinal nerves.

55. Transversus Abdominis

56. Pulmonary Volumes and Capacities The tidal volume is the volume of air inspired or expired with each normal breath; it amounts to about 500 milliliters in the adult male. 2. The inspiratory reserve volume is the extra volume of air that can be inspired over and above the normal tidal volume when the person inspires with full force; it is usually equal to about 3000 milliliters.

57. 3. The expiratory reserve volume is the maximum extra volume of air that can be expired by forceful expiration after the end of a normal tidal expiration; this normally amounts to about 1100 milliliters. 4.The residual volume is the volume of air remaining in the lungs after the most forceful expiration; this volume averages about 1200 milliliters. 5.The inspiratory capacity equals the tidal volume plus the inspiratory reserve volume. This is the amount of air (about 3500 milliliters) a person can breathe in, beginning at the normal expiratory level and distending the lungs to the maximum amount.

58. 6. The functional residual capacity equals the expiratory reserve volume plus the residual volume. This is the amount of air that remains in the lungs at the end of normal expiration (about 2300 milliliters). 7.The vital capacity equals the inspiratory reserve volume plus the tidal volume plus the expiratory reserve volume. This is the maximum amount of air a person can expel from the lungs after first filling the lungs to their maximum extent and then expiring to the maximum extent (about4600 milliliters).

59. 8. The total lung capacity is the maximum volume to which the lungs can be expanded with the greatest possible effort (about 5800 milliliters); it is equal to the vital capacity plus the residual volume. All pulmonary volumes and capacities are about 20 to 25 per cent less in women than in men, and they are greater in large and athletic people than in small and asthenic people.

60. Chronic Bronchitis

61. Chronic Bronchitis Chronic bronchitis is a disease of the airways. It is characterized by excess mucus secretion and productive cough. The cough is called a smokers' cough in the early stages but once mucus production has been excessive for 3 months a year for over 2 years, this becomes the inadequate but traditional definition of chronic bronchitis.

62. Cigarette smoking is the most important risk factor in the development of chronic bronchitis. The cause of chronic bronchitis is believed to be related to long-term irritation of the tracheobronchial tree. The most common cause of irritation is cigarette smoking. Repeated inhalation of tobacco smoke irritates the sensitive lining of the airways, leading to inflammation, mucus hyper secretion and sometimes bronchospasm . Inflammation is the key process. It causes narrowing first in the distal small airways and then in the proximal large airways.

63. Inhaled cigarette smoke stimulates the goblet cells and mucous glands to secrete more mucus. This smoke also inhibits cilliary action. The hyper secretion of mucus and impaired cilia lead to a chronic productive cough. Pathologically, there is an increase in the size of the tracheo -bronchial mucous glands (increased Reid index) and goblet cell hyperplasia (Mitchell, 1968; Reid, 1960; Stoller and Wiedemann, 1990). Mucous cell metaplasia of bronchial epithelium results in a decreased number of cilia. Cilliary dysfunction and disruption of the continuity of the mucous blanket are common. In the peripheral airways, bronchiolitis , bronchiolar narrowing, and increased amounts of mucus are observed ( Cosio , 1978; Wright, 1992).

64. The fact that smokers secrete an abnormal amount of mucus makes them susceptible to respiratory infections, and it takes them longer to recover from these infections. In addition, the irritation of smoke in the tracheo -bronchial tree causes broncho -constriction. Although smoking is the most common cause of chronic bronchitis, other agents that have been implicated are air pollution, bronchial infections, and certain occupations.

65. Characterstics 1)Excess mucus secretion and productive cough, excessive for 3 months a year for over 2 years. 2)Stocky in build and dusky in color. 3)The patient exhibits significant use of accessory muscles of respiration. 4)Wheezing may be audible or noted by auscultation. 5) Intercostal or sternal retraction of the chest wall may be noted.

66. 6)Edema in the extremities, particularly around the ankles, and neck vein distention reflect decompensated right heart failure. 7)The patient may report that breathing difficulty began with increased amounts of secretions (with a change in their normal color), which is often difficult to expectorate, and increased cough productivity. 8)Pao2 is reduced, Paco2 increased, and pH reduced. 9) Pulmonary function tests may indicate reduced vital capacity, FEV1, maximum voluntary ventilation, and diffusing capacity and increased FRC and residual volume.

67. These patients are referred to as "blue bloaters,“ because they usually have stocky body build and are "blue" as a result of hypoxemia ( Dornhorst , 1955; Filley et ai, 1968; Fishman , 1988; Nash, Briscoe, and COUl·nand , 1965). Although many of these patients have a high arterial partial pressure of carbon dioxide (Pac02), the pH is normalized by renal retention of bicarbonate (HC03). In the patient with chronic bronchitis, bone marrow tries to compensate for chronic hypoxemia by increased production of red blood cells, leading to polycythemia

68. Polycythemia, in turn, makes the blood more viscous, forcing the heart to work even harder to pump it. Long-term hypoxemia leads to increased pulmonary artery pressure and right ventricular hypertrophy. Individuals with bronchitis often expectorate mucoid brownish-colored sputum. In an exacerbation, usually from infection, they have an even greater amount of purulent sputum. Ventilation-perfusion abnormalities are common, which increase hypoxemia and Paco2 retention (Rochester and Brown, 1976).

69. The respiratory rate increases, as does the use of accessory muscles. The resultant increased work of breathing requires greater oxygen consumption by these muscles, with a greater production of carbon dioxide (C02) than the respiratory system can adequately meet. This contributes to a further drop in the arterial partial pressure of ox ygen (Pao2) and a rise in Paco2. The hypoxemia and acidemia increase pulmonary vessel constriction, which raises pulmonary artery pressure and ultimately leads to right heart failure ( cor pulmonale ).

70. Emphysema

71. Emphysema Emphysema is the second most prevalent disease within the category of COPD. It is primarily a disease of alveoli and smallest airways, with secondary effects on other airways. It is usually caused by damage to the alveoli from smoking. There are following types of emphysema :- 1) Centrilobular Emphysema 2) Paraseptal emphysema 3) Panlobular Emphysema

72. Normal Alveoli VS Alveoli with Emphysema

73. Centrilobular emphysema Centrilobular emphysema is characterized by - Destruction of the respiratory bronchiole. -Edema -Inflammation -Thickened bronchiolar walls. These changes are more common and more marked in the upper lobes and superior segments of the lower lobes.

74. Centriacinar or centrilobular emphysema involves the enlargement and destruction of the first- and second-order respiratory bronchioles, and the alveoli remain intact (mainly the respiratory Bronchioles). This form of emphysema is found more often in men than in women, is rare among nonsmokers, and is common among patients with chronic bronchitis. Male > Females

75. Paraseptal emphysema Paraseptal emphysema involves the periphery of the secondary lobule along the septum. Paraseptal emphysema is not typically associated with the progression of end-stage COPD but can be associated with an increased risk of pneumothorax (PTX)

76. Pan lobular emphysema Pan lobular emphysema, on the other hand, is characterized by destructive enlargement of the alveoli, distal to the terminal bronchiole. It most often involves the lower lobes. This type of emphysema is also found in subjects that have ALPHAj -ANTITRIPSIN deficiency. Airway obstruction in these individuals is caused by loss of lung elastic recoil or radial traction on the bronchioles.

77. When individuals with normal lungs inhale, the airways are stretched open by the enlarging elastic lung, and during exhalation the airways are narrowed as a result of the decreasing stretch of the lung. However, the lungs of patients with panlobular emphysema have decreased elasticity because of disruption and destruction of surrounding alveolar walls. This in turn leaves the bronchiole unsupported and vulnerable to collapse during exhalation.

78. Bullae , emphysematous spaces larger than 1 cm in diameter, may be found in patients with emphysema. It is thought that bullae develop from a coalescence of adjacent areas of emphysema or an obstruction of the conducting airways that permits the flow of air into the alveoli during inspiration but does not allow air to flow out again during expiration.

79. This causes the alveoli to become hyperinflated and eventually leads to destruction of the alveolar walls with a resultant enlarged air space in the lung parenchyma. These bullae can be more than 10 cm in diameter, and by compression, can compromise the function of the remaining lung tissue . If this happens, surgical intervention to remove the bulla is often necessary. Pneumothorax , a serious complication, can result from the rupture of one of these bullae .

80. The principal pathophysiological deficits include irreversible alveolar damage resulting from loss of elastic recoil and the normal tethering of the alveoli, which renders the lung parenchyma excessively compliant and floppy. Excessive distension and dilatation of the terminal bronchioles and destruction of alveoli reduces the surface area for gas exchange. Hence diffusing capacity is correspondingly reduced. The dead space in the lungs and total lung capacity increase significantly. Breathing at normal tidal volume, the patient's airways close beyond that which normally

81. In its non acute, chronic stages the primary problems include inadequate and inefficient gas exchange resulting from the structural damage to the lungs and altered respiratory mechanics of the lungs, chest wall, and their interaction. The lungs are - hyperinflated , the chest wall becomes rigidly fixed in a hyperinflated position, the normal bucket handle and pump handle motions of the chest wall are impaired, the hemi diaphragms are flattened, the mediastinal structures are shifted, and the heart is displaced and rotated, making its function inefficient

82. The normal mucocilliary transport system is ineffective because years of smoking destroy the cilia, reduce their number, and alter their configuration and orientation; thus their function is correspondingly obliterated or impaired. In addition, these patients are unable to generate high transpulmonary pressures and forced expiratory flow rates because of altered respiratory mechanics. Consequently, coughing maneuvers are weak and ineffective.

83. The emphysema patient's most common complaint is dyspnea . Physically, these patients appear thin and have an increased anteroposterior chest diameter. Typically, they breathe using the accessory muscles of inspiration. These patients are often seen leaning forward, resting their forearms on their knees or sitting with their arms extended at their sides and pushing down against the bed or chair to elevate their shoulders and improve the effectiveness of the accessory muscles of inspiration.

84. They may breathe through pursed lips during the expiratory phase of breathing. These patients have been referred to as "pink puffers" because of the increased respiratory work they must do to maintain relatively normal blood gases. On auscultation, decreased breath sounds can be noted throughout most or all of the lung fields. Radiologically , the emphysema patient has overinflated lungs, a flattened diaphragm, and a small, elongated heart (Fig.

85. Pulmonary function tests show a decreased vital capacity, FEY" maximum voluntary ventilation and a greatly reduced diffusing capacity. The total lung capacity is increased, while the residual volume and functional residual capacity are even more increased. Arterial blood gases reflect a mildly or moderately lowered Pao2, a normal or slightly raised Paco2 and a normal pH. These patients, unlike patients with chronic bronchitis, normally will develop heart failure in the end stage of the disease

86. CARDIO-RESPIRATORY ASSESSMENT DEMOGRAPHIC DATA Name: Gender : Address : Marital status: Religion: Occupation: Date of assessment:

87. Occupation: Note the patient’s present job and, if he is retired, whether this was premature due to ill-health. Note should be made if there has been any exposure to asbestos or coal dust (as these can cause fibrosing lung disease later in life), or if the patient has worked in a bakery or on a farm (as yeasts and spores can produce allergic responses).

88. CHIEF COMPLAINTS: - always in patients language

89. The six key symptoms/complaints of respiratory disease are: ● chest pain (that may be extended to chest sensations) ● dyspnoea / breathlessness ● cough ● wheeze ● sputum production ● haemoptysis .

90. Present medical history Breathlessness –  Description of onset o Date o Time o Type : sudden/gradual  Setting o Cause o Circumstances o Activities surrounding onset

91.  Severity o How bad it is o How it affects activities of daily living  Frequency o How often  Duration o How long o Constant/intermittent  Course o Better/worse/same

92.  Associated symptoms o Sweating o Cough o Chest discomfort  Aggravating factors o Position/weather/temperature/anxiety/exercise  Reliving factors o Position/hot/cold/rest

93.  During the status of episode o Can you continue to do what you were doing o Do you have to sit down or lie down o Can you continue to speak  Do the attack cause your lips or nail bed to turn blue

94. Social history: Note the type of living accommodation and whether there are stairs to encounter: whether there is dampness; and how far he lives from shops and social amenities. The patient should be asked Whether he has pets - as there may be an allergy problem; and about his hobbies, as the physiotherapist may be able to advise on suitable breathing patterns for gardening or swimming, etc., each depending on the patient’s disability.

95. Family history: If there is a history of allergy, such as hay fever or s kin problems, the patient should be asked whether there is any relevant family history. If the patient is married, note the health of the spouse. Smoking habits: The patient must be questioned carefully as to how many cigarettes are smoked, whether they are home-made and, if he has given up, when he did so.

96. Past medical history : Note any operations, accidents or illnesses such as rheumatic fever which can cause heart problems; pulmonary tuberculosis which leaves scarring and possible cavities (apparent on the chest radiograph); whooping cough and measles which can cause bronchiectasis through plugging of the small airways.

97. Past medical history Surgeries & hospitilisation o Injuries & accidents o Immunization o Allergies o Medications

98. Personal history : History of smoking - Yes/no Types of tobacco How old when the patient begin smoking How many years the patient smoked How many cigarettes smoked each day Any variation in smoking habits Any attempt to stop smoking Date when the patient last smoked Pack year:

99. History of alcohol intake - yes/no How old when the patient started alcohol How many years the patient consumed How many pegs each day Any variation in alcoholic habits Any attempt to quit alcohol Date when the patient last taken

100. Subjective evaluation of cardinal symptoms

101. Chest pain Ask about the onset, character, severity, duration, radiation, and any previous history of chest pain. A history of chronic pleuritic chest pain going back several months or years could indicate an inflammatory disorder resulting in pleurisy. This can occur in a variety of collagen vascular disorders but is a relatively rare cause of pleuritic chest pain. Chest pain that is dull and persistent in one area, and especially if it is keeping the patient awake at night, could indicate a malignant process within the chest that is affecting the chest wall. Such pains have usually been going on for weeks or more and get progressively worse, and may or may not be augmented by palpation of the chest.

102. Chest pain Location Onset Date Time Type Sudden/gradual Pattern Frequency : How Severity Recurrence Duration How long it lasts Constant or intermittent Course :better/worse/staying the same

103.  Provoked symptoms(aggravating factors) o Breathing o Positions :Lying flat/side lying o Movement with arms o Rest/exercise o Sleeping/stress/after eating o Stress/anxiety

104.  Quality Dull/ aching/pin prickling/throbbing/knife like/sharp/constricting/sticking/burning/shooting  Radiating  Referred  Relieving factors Rest Positions Analgesics Antacids Hot cold

105.  Severity How it affects ADL VAS scale  Associated symptoms Coughing/breathlessness/palpitations/ hemoptysis /vomiting/ leg pain/weakness/muscle fatigue  Time frame Acute/chronic

106. Dyspnoea Dyspnea , breathlessness or shortness of breath, can be defined as the sensation of difficulty in breathing If there has been an increase in breathlessness, does it vary with position or change of position and has it affected the patient’s lifestyle? Analysis of dyspnoea should be approached in a similar way to that of chest pain, so ask about severity, duration, onset, precipitating factors, and previous history. It is absolutely crucial to ask about the onset. Ask the patient what they were doing at the time when the breathlessness started in order to get some idea as to how sudden the onset was.

107. Types of dyspnea Restrictive dyspnea Obstructive dyspnea Cardiac dyspnea Psychogenic dyspnea Acute dyspnea Chronic dyspnea Recurrent dyspnea Progressive dyspnea Paroxysmal dyspnea Episodic dyspnea Inspiratory dyspnea Expiratory dyspnea Orthopnea one P / Two P/ Three P Treopnea Platypnea PND

108. Orthopnoea : How many pillows does the patient require in order to sleep or he comfortably? (This may influence the choice of starting position for the treatment session.) If the patient suffers from paroxysmal nocturnal dyspnoea which may be caused by slipping down the bed, the physiotherapist can suggest types of back rest or, perhaps, seek advice from the occupational therapist.

109. Paroxysmal Nocturnal Dyspnea Paroxysmal nocturnal dyspnea (PND) is an important type of shortness of breath. This symptom has strong predictive value as a sign of CHF (Hurst, etai , 1990). The patient usually falls asleep in the recumbent position, and 1 or 2 hours later, awakens from sleep with acute shortness of breath. The patient sits upright on the side of the bed or goes to an open window to breathe "fresh air" to get relief from shortness of breath.

110. The mechanism of PND is the transfer of fluid from extravascular tissues into the bloodstream (or intravascularly ) during sleep (Constant, 1993). The intravascular volume of fluid gradually increases until the compromised left ventricle can no longer manage it. The left atrial pressure rises when the rate of lymphatic drainage from the lungs is unable to keep up with the increased volume of tluid . The increased atrial pressure leads to a sufficiently elevated pulmonary capillary pressure to produce interstitial edema. Patients who are light sleepers awaken early with dyspnea .

111. Platypnea Platypnea is the onset of dyspnea when assuming the sitting position from the supine position ( Sharf , 1989). This unusual phenomenon is often found in patients with basilar pulmonary fibrosis or basilar arteriovenous malformation. It can be related to the redistribution of blood flow to the lung bases in the sitting position with resultant ventilation-perfusion mismatching and hypoxemia.

112. Trepopnea Trepopnea refers to dyspnea in one lateral position but not the other (Snider, 1994). It is often produced by unilateral respiratory system pathology such as lung disease, pleural effusion, or airway obstruction. It also is commonly seen in patients with mitral stenosis (Constant, 1993). Occasionally it may be the result of a fall in blood pressure in the left lateral decubitus position. If the patient has ischemic heart disease, the reduction in coronary perfusion can cause either angina or dyspnea .

113. Breathlesnes  Description of onset o Date o Time o Type : sudden/gradual  Setting o Cause o Circumstances o Activities surrounding onset

114.  Severity o How bad it is o How it affects activities of daily living  Frequency o How often  Duration o How long o Constant/intermittent  Course Better/worse/same

115. American Thoracic Society Dyspnea Scale GRADE DEGREE NONE Not troubled with breathlessness except with strenuous exercise 1 SLIGHT Troubled by shortness of breath when hurrying on the level or walking up a slight hill 2 MODERATE Walks slower than people of the same age on the level because of breathlessness or has to stop for breath when walking at own pace on the level

116. GRADE DEGREE 3 SEVERE Stops for breath after walking about 100 yards or after a few minutes on the level 4 VERY SEVERE Too breathless to leave the house or breathless when dressing or undressing

117. visual analogue scale No breathlessness Greatest Breathlesness The visual analogue scale is a vertical line of 100 mm in length. The patient is asked to make a mark along this line that represents his level of breathlessness. The distance of the patient's mark above zero represents the measurement of dyspnea

118.  Associated symptoms o Sweating o Cough o Chest discomfort  Aggravating factors o Position/weather/temperature/anxiety/exercise  Reliving factors o Position/hot/cold/rest

119.  During the status of episode Can you continue to do what you were doing Do you have to sit down or lie down Can you continue to speak Do the attack cause your lips or nail bed to turn blue

120.  Tick the activities disturbed by breathlessness o Climbing stairs ( ) if yes how many steps o Walking ( ) if yes how much distance o Bathing ( ) o Toileting ( ) o Dressing ( ) o Combing ( ) o Shopping ( ) o Grooming ( ) o Speaking ( ) o Any other activities  Exposure to the patients with tuberculosis  Exposure to asbestos/sand blasting/pigeon feeding

121. Wheeze: Ask whether this has increased recently. Is it so bad as to be audible from the foot of the bed? a wheeze is a musical note generated from the lungs that may be a single note (monophonic wheeze) or multiple different notes (polyphonic wheeze). Ask about the onset, duration and periodicity of wheeze. Wheeze that occurs more at night and first thing in the morning, and that may be exacerbated by exercise, is suggestive of asthma and COPD. A pronounced variation in the severity of wheeze (worse at night and in the morning compared to daytime) is more suggestive of asthma, but by no means excludes COPD.

122. Cough Cough is the commonest symptom that is associated with pure respiratory disease. The function of cough is to expel unwanted elements from the respiratory tract; that includes both foreign elements and substances generated by the host. Thus cough is a prominent feature of upper respiratory infections, inhalation of irritants such as dusts and chemicals, as a result of lower respiratory infections, and the result of accumulation of products within lung (e.g. in pulmonary oedema ). In addition to this, cough receptors within the lung can be stimulated as happens in interstitial lung disease or in endobronchial sarcoidosis .

123. A quick guide to the causes of chronic cough (more than 6 months) Asthma Worse at night/early morning History of chest heaviiness as a child Family history of atopy Relief by salbutamol (not always) Copd Longstanding smoking Chronic bronchitis Rhinosinusitis Tickly, irritating cough Post-nasal drip sensation History of sinusitis – frontal headache, nasal discharge History of recurrent rhinitis – nasal discharge and blockage Gastro- oesophageal reflux Tickly, irritating cough Acid reflux symptoms Response to proton pump inhibitor

124. Laryngeal hypersensitivity Tickly, irritating cough Voice disturbance Cough precipitated by talking No nocturnal symptoms Vigorous cough Unresponsive to medication other Includes lung cancer, bronchiectasis , interstitial lung disease, eosinophilic bronchitis Requires specialist investigation

125. Characteristics of sputum production in relation to diagnosis Characteristic Likely Diagnosis Acute onset, purulent sputum, clearing after 1–3 weeks Acute bronchitis Pneumonia Regular sputum production, more than a half egg-cupful, varying in purulence Bronchiectasis Occasionally chronic bronchitis ‘Chronic productive cough for more than 3 months in each of 2 consecutive years...’ Medical Research Council criteria for definition of chronic bronchitis

126. Clear or slightly opaque sticky sputum, white yellow or green Asthma Colour of purulent sputum and organism Lime green – Haemophilus influenzae ‘Rusty’ – Streptococcus pneumoniae Dark green – Pseudomonas aeruginosa Foul smell and taste Chronic pulmonary sepsis with cavities in the lung Infection from rotting teeth and associated gum disease

127.  Description Mucoid / mucopurulent /purulent/blood tinged GRADES  Color Clear/colorless like egg white/black/brownish/frothy white/pink/sand Greenish/red jelly/rusty/  Consistency Thin/thick/viscous/tenacious/frothy

128.  Quantity Scanty/ teaspoon / cup /copious /pint or more  Time of the day Morning/evening  Odor

129. Associated symptoms  Hemoptysis  Hoarseness  Voice changes  Dizziness/ fainty syncope  Head ache  Altered sensorium  Ankle swelling  Cyanosis

130. Hemoptysis  Amount : clot/massive  Odor  Color  Appearance  Acute/chronic

131.  Frequency  Streaky/Non streaky/FROTHY BLOOD TINGED  Associated symptoms o Warmth o Bubbling sensation o With chest pain/ dyspnea o WITHOUT COUGHING o Nausea/vomit/cough

132. Constitutional symptoms  Fever  Excessive sweating  Loss of appetite  Nausea  Vomiting  Weight loss  Fatigue  Weakness  Exercise intolerance  Altered sleep pattern

133. Objective assessment Height: Weight: BMI: Clinical presentation: o General appearance: cardiopulmonary distress/anxiety/pain o Awake /alert(conscious)/attentive/comprehensive

134. Body type: - Ectomorphic /endomorphic/ mesomorphic Vital signs: o Temperature o Pulse rate o Respiratory rate o Blood pressure Pulse Rhythm: o regular, o regularly irregular, bigeminy or trigeminy o irregularly irregular if yes  check heart rate ___

135. Inspection & observation HENT (head, eyes, nose, and throat) Head Facial expression Forehead Eyes-PERRLA Eyes-Sclera clear/ muddy,palor,ictrus Eyelid - ptosis Nose –nasal flaring Lips- Cyanosis Lips-Pursed lip breathing

136. Neck Position of trachea: midline/right/left Jugular venous pressure: normal/increased/markedly increased Use of accessory muscles- SCM/ PMi / Tr Prominence of accessory muscles Trail sign Tracheal tug or oliver sign

137. Thorax COPD Posture: rounded shoulders, protruded neck, kyphosis , outstretched hands AP:T Ratio: 5:5/5:6/5:7 barrel chest : present /absent Chest wall deformities: Pectus carinatum / Pectus excavatum / kyphosis / scoliosis/ kyphoscoliosis Type of breathing: rapid/shallow/deep Effort of breathing: minimal on inhalation and passive on exhalation Pattern of breathing: Thoraco abdominal/ abdomino thoracic Abnormal breathing pattern: Apnea/ Biot’s // Cheyne -stokes/ Kussmauls / paradoxical/ asthmatic/flail chest

138. Labored Breathing signs:  Intercostals indrawing /retractions  Supra clavicular indrawing  Sub costal indrawing  Hoovers sign  Harrisons sulcus

139. Abdomen: abdominal paradox Extremities  Upper limb Clubbing: schamroth window test___, grade___,clubbing index__ Cyanosis: Nicotine stain: Capillary filling time: Tremor  Lower limb oedema

140. Palpation o Tracheal position – o Subcutaneous emphysema – o Tenderness on accessory muscles – o Palpation of lymph nodes: axillary /cervical/ supraclavicular - o Symmetry: symmetrical/asymmetrical -  Upper zone  Middle zone  Lower zone

141. o Tactile Vocal fremitus  Upper zone  Middle zone  Lower zone o Tactile rhonchial fremitus – o Percussion - Type of note: resonant/hyper resonant/ stony dullness/woody dullness Level of right border Level of left border Level of heart border Level of diaphragmatic excursion

142. o Pedal oedema - Pitting/non pitting Grade Level or extent of oedema o Peripheral skin temperature

143. Auscultation Quantity of breath sound- Quality of breath sound – Added sound- o Inspiration : early/mid /late, fine/coarse o Expiration : wheeze/ rhonchi Vocal resonance: whispering pectoriloquy,aegophony

144. Chest expansion-  Upper zone  Middle zone  Lower zone

145. Medical Management

146. EMPHYSEMA Treatment of progressive emphysema that requires hospitalization often includes IV fluids, antibiotics, and low-flow oxygen (Snider, Faling , and Rennard , 1994). Some of these patients also receive bronchodilators, corticosteroids, diuretics, and digitalis. Pursed-lip breathing can relieve dyspnea and improve arterial blood gasses (Muller, Petty, and Filley , 1970;Petty and Guthrie, 1974).

147. Emphysema is associated with a prolonged history of smoking and chronic bronchitis and indicates significant irreversible lung damage. A less common type of emphysema not associated with smoking is alpha-antitrypsin deficiency. Antitrypsin is essential in balancing elastin production and degradation and in preserving optimal lung parenchymal compliance. A deficiency of antitrypsin reduces lung elasticity and contributes to the characteristic increase in lung compliance that is the hallmark of emphysema.

148. Oxygen therapy can reduce hypoxaemia and some of its effects, such as oedema ( Howes et ai ., 1 995). Long-term oxygen reduces mortality for patients with persistent hypoxaemia at Pa02 < 8 kPa (60 mmHg; Leach and Treacher , 1 998). Bronchodilators reduce airflow obstruction in two-thirds of patients with chronic disease, thereby reducing hyperinflation and possibly breathlessness ( Tantucci et ai ., 1 99 8) , but should be used according to need because continuous use can worsen lung function ( Huib , 1 999). Combination therapy with different classes of bronchodilator may be the most beneficial approach (Manning, 2000). A quarter of patients respond to theophylline (Mahon, 1 999).

149. Steroids have been advised for exacerbations but in the chronic state they reduce airways obstruction in only 10% of patients, and continued use is associated with myopathy (Davies et ai ., 1 9 99). However, individuals vary and should be individually assessed ( Yildiz , 2000). Drug assessment should include quality of life scores, peak flow monitoring and sequential testing of different bronchodilators, steroids, combinations and various delivery systems . Short-term reversibility studies should not be substituted for long-term assessments.

150. Inhalers are indicated for acute and chronic disease unless nebulizers are objectively found to be more effective (BTS, 1 997). Some patients respond to· drugs for breathlessness . Many COPD patients have disturbed sleep, for which the hypnotic drug zolpidem has been found to be beneficial without affecting oxygenation, ventilation or physical performance ( Girault et at., 1 996). Severe exacerbations may indicate the need for non-invasive ( Poponick , 1 999) or invasive ventilation. Severe chronic emphysema may indicate the need for surgery, varying from laser ablation of giant bullae to lung volume reduction

151. Physical Therapy Management

152. Principles of physical therapy management The goals of long-term management for the patient with chronic bronchitis include the following:- • Maximize the patient's quality of life, general health, and well-being and hence physiological reserve capacity. • Educate about chronic bronchitis, self-management, effects of smoking, nutrition, weight control, smoking reduction or cessation, other lifestyle factors, medications, infection control, and role of a rehabilitation program.

153. • Facilitate mucociliary transport. • Optimize secretion clearance. • Optimize alveolar ventilation. • Optimize lung volumes and capacities and flow rates. • Optimize ventilation and perfusion matching and gas exchange. • Reduce the work of breathing.

154. Reduce the work of the heart Maximize aerobic capacity and efficiency of oxygen transport. Optimize physical endurance and exercise capacity. Optimize general muscle strength and thereby. peripheral oxygen extraction.

155. The primary interventions for maximizing cardiopulmonary function and oxygen transport in patients with chronic bronchitis include some combination of education, aerobic exercise, strengthening exercises, chest wall mobility exercises, range of motion, body positioning, breathing control and coughing maneuvers , airway clearance techniques, relaxation, activity pacing, and energy conservation. An ergonomic assessment of the patient's work and home environments may be indicated to minimize oxygen demand and energy expenditure in these settings.

156. The use of supplemental oxygen depends on the severity of the disease. Some patients have no need for supplemental oxygen, some need it only during exercise, and some patients require continuous oxygen with proportionately more delivered during activity and exercise compared with rest. Supplemental oxygen is not usually required until lung damage becomes extreme (i.e., the morphological changes are consistent with the irreversible changes associated with emphysema).

157. Education is a principal focus of the long-term management of the patient with chronic bronchitis. Education includes the reinforcement of preventative health practices (e.g., smoking reduction and cessation, cold and flu prevention, flu shots, aerobic exercise, strengthening exercises, nutrition, weight control, hydration, pacing of activities, energy conservation, relaxation, and stress management). Chronic bronchitis and emphysema are often associated with sleep disturbances. Obstructive sleep apnea is increasingly prevalent with disease severity. Thus activity and sleep patterns need to be assessed to ensure sleep is maximally restorative and is not contributing to the patient's symptoms.

158. Aerobic exercise is an essential component of the long-term management of the patient with chronic bronchitis to optimize the efficiency of oxygen transport overall and mobilize and remove secretions (Oldenburg, Dolovich , Montgomery, and Newhouse, 1979).

159. Physical therapy is one component of a comprehensive rehabilitation program in the long-term management of emphysema . Such a program also needs to include information on health promotion and maintenance, ongoing review and log of medications, respiratory support (e.g., oxygen aerosol therapy, and mechanical ventilatory support),

160. THANK YOU