1. Dep.Anatomi FKUSU

2. Embriologi Tunasparu terbentuk pada usia 4minggu. Dibentuk dari suatu divertikulum pada dinding ventralusus depan,yangmeluas ke arah kaudal (divertikulum respiratorium=tunasparu). Mulamula tunasparu mempunyai hubungan terbuka dengan usus depan,selanjutnya terpisah menjadi bagian dorsalyaitu esofagus dan bagian ventralyaitu trakea dan tunasparu. 3. Thispageshowsventralviewsoftheesophagusanddevelopinglungs,accompaniedbycrosssectionalviews throughtheareabetweentheblackarrows.Notehowthelungstartsasanevagination,fromtheesophogeal endoderm,calledthelarygotracheal groove(1).Asthethe larygotracheal groovegrows,itdevelopstwo outcroppingsatitscaudalend,thelungbuds(2).Asthelungbudsgrow,theybranchrepeatedlyformingthe primarybronchiandstembronchi(3)whichbranchfurthertoformbronchioles,whichwilleventually developterminalairsacs(alveoli)tocompletetheadultlung.Also,notehowthetrachea,onceattachedasa ventralgrooveontheesophagus,hasseparatedtobecomeadistincttube(3). 4. Saat pemisahan dengan usus depan,tunasparu membentuk trakea dan tunasbronkialis. Pada awal minggu ke5masingmasing tunas membesar membentuk bronkus utama kiri dan kanan. Bronkus utama kiri membentuk dua cabang sekunder dan kanan membentuk tiga cabang sekunderkiri dua lobus dan kanan tiga lobus. 5. Tunasparu berkembang terus menembus ke dalam rongga selom (kanalis perikardioperitonealis). Akhirnya kanalis perikardioperitonealis terpisah dengan rongga peritoneumdan perikardium masingmasing oleh lipatan pleuroperitoneal dan lipatan pleuroperikardial Tersisa rongga pleuraprimitif berkembang menjadi pleuravisceralis (mesoderm)dan pleuraparietalis (mesodermsomatik). Perkembangan selanjutnya bronkus sekunder terus bercabang secara dikotomi, membentuk 10bronkus tersier (segmental) di kanan dan 8di kiri. Akhir bulan ke6terbentuk 17generasi anak cabang. Pasca lahir terbentuk 6anak cabang tambahan. Saat lahir bifurcatio trakea akan terletak berhadapan dengan V.thoracalis ke4. 6. Pematangan paru Sampai bulan ke7prenatalbronkioli terus bercabang menjadi saluran yanglebih banyak dan lebih kecil (tahap kanalikular), dan suplai darah terus meningkat. Pernapasan dapat berlangsung jika beberapa sel bronkiolus respiratorius berbentuk kubus berubah menjadi sel gepeng yang tipis. Sel tersebut berhubungan dengan banyak kapiler darah dan getah bening,ruangruang di sekitarnya dikenal sebagai sakus terminalis(alveoliprimitif). Selama bulan ke7telah terdapat banyak kapiler yangmenjamin pertukaran gassehingga janin prematur dapat bertahan hidup. Selama dua bulan prenataldan beberapa tahun pasca lahir jumlah sakus terminalis terus meningkat. 7. Terdapat dua jenis sel epitel :Sel epitel alveolitipe I dan sel epitel alveolitipe II. Sel epitel alveolitipe I,membentuk sawar darahudara dengan endotel. Sel epitel alveolitipe IImenghasilkan surfaktan (berkembang pada akhir bulan ke6),suatu cairan kaya fosfolipid dan mampu menurunkan tegangan permukaan pada antarmuka udaraalveolus. Sebelum lahir paru mengandung kadar klorida tinggi, sedikit protein,sedikit lendir dari bronkus dan surfaktan. 8. Saat lahir,pernapasan dimulai,sebagian besar cairan paru cepat diserap oleh kapiler darah dan getah bening dan sejumlah kecil mungkin dikeluarkan melalui trakea dan bronkus selama proses kelahiran. Ketika cairan diserap di sakus alveolaris,surfaktan mengendap sebagai lapisan fosfolipid tipis pada selaput sel alveoli. Tanpa ada surfaktan,alveoliakan menguncup selama ekspirasi (atelektasis) Alveoliakan terus dibentuk selama 10tahun pertama kehidupan setelah lahir. 9. Korelasi klinik Kelainan pemisahan esofagus dan trakea oleh septum esofagotrakealis mengakibatkan atresia esofagus dengan atau tanpa fistulatrakeoesofagealis. Surfaktan sangat penting untuk mempertahankan hidup pada bayi prematur. Jika jumlah surfaktan tidak cukuptegangan membran permukaan udaraairmenjadi tinggi,resiko alveolikolaps saat ekspirasi sangat besarSindroma Gawat Pernapasan(RDS). Pada keadaan ini alveoliakan kolaps dan mengandung banyak membran hialin dan badanbadan lamelarPenyakit Membran Hialin (20%dari semua kematian bayi baru lahir). 10. Bagaimana membedakan bayi meninggal sebelum lahir dan meninggal sesudah lahir,ditinjau dari parunya? 11. ThankYou.Uahhhhhh 12. ANATOMY OF RESPIRATORY SYSTEM Dr. Mega Sari Sitorus, Mkes. 13. Organization and Functions of the Respiratory System Consists of an upper respiratory tract (nose to larynx) and a lower respiratory tract ( trachea onwards) . Conducting portion transports air. - includes the nose, nasal cavity, pharynx, larynx, trachea, and progressively smaller airways, from the primary bronchi to the terminal bronchioles Respiratory portion carries out gas exchange. - composed of small airways called respiratory bronchioles and alveolar ducts as well as air sacs called alveoli 14. Respiratory System Functions 1. supplies the body with oxygen and disposes of carbon dioxide 2. filters inspired air 3. produces sound 4. contains receptors for smell 5. rids the body of some excess water and heat 6. helps regulate blood pH 15. Breathing Breathing (pulmonary ventilation). consists of two cyclic phases: inhalation, also called inspiration - draws gases into the lungs. exhalation, also called expiration - forces gases out of the lungs. 16. Upper Respiratory Tract Composed of the nose and nasal cavity, paranasal sinuses, pharynx (throat), larynx. All part of the conducting portion of the respiratory system. 17. Respiratory mucosa A layer of pseudostratified ciliated columnar epithelial cells that secrete mucus Found in nose, sinuses, pharynx, larynx and trachea Mucus can trap contaminants Cilia move mucus up towards mouth 18. Nose Internal nares - opening to exterior External nares opening to pharynx Nasal conchae - folds in the mucous membrane that increase air turbulence and ensures that most air contacts the mucous membranes 19. Nose rich supply of capillaries warm the inspired air olfactory mucosa mucous membranes that contain smell receptors respiratory mucosa pseudostratified ciliated columnar epithelium containing goblet cells that secrete mucus which traps inhaled particles, lysozyme kills bacteria and lymphocytes and IgA antibodies that protect against bacteria 20. Upper Respiratory Tract 21. Nose provides and airway for respiration moistens and warms entering air filters and cleans inspired air resonating chamber for speech detects odors in the air stream rhinoplasty: surgery to change shape of external nose 22. Paranasal Sinuses Four bones of the skull contain paired air spaces called the paranasal sinuses - frontal, ethmoidal, sphenoidal, maxillary Decrease skull bone weight Warm, moisten and filter incoming air Add resonance to voice. Communicate with the nasal cavity by ducts. Lined by pseudostratified ciliated columnar epithelium. 23. Paranasal sinuses 24. Pharynx Common space used by both the respiratory and digestive systems. Commonly called the throat. Originates posterior to the nasal and oral cavities and extends inferiorly near the level of the bifurcation of the larynx and esophagus. Common pathway for both air and food. 25. Pharynx Walls are lined by a mucosa and contain skeletal muscles that are primarily used for swallowing. Flexible lateral walls are distensible in order to force swallowed food into the esophagus. Partitioned into three adjoining regions: Nasopharynx Oropharynx laryngopharynx 26. Nasopharynx Superior-most region of the pharynx. Covered with pseudostratified ciliated columnar epithelium. Located directly posterior to the nasal cavity and superior to the soft palate, which separates the oral cavity. Normally, only air passes through. Material from the oral cavity and oropharynx is typically blocked from entering the nasopharynx by the uvula of soft palate, which elevates when we swallow. In the lateral walls of the nasopharynx, paired auditory/eustachian tubes connect the nasopharynx to the middle ear. Posterior nasopharynx wall also houses a single pharyngeal tonsil (commonly called the adenoids). 27. Oropharynx The middle pharyngeal region. Immediately posterior to the oral cavity. Bounded by the edge of the soft palate superiorly and the hyoid bone inferiorly. Common respiratory and digestive pathway through which both air and swallowed food and drink pass. Contains nonkeratinized stratified squamous epithelim. Lymphatic organs here provide the first line of defense against ingested or inhaled foreign materials. Palatine tonsils are on the lateral wall between the arches, and the lingual tonsils are at the base of the tongue. 28. Laryngopharynx Inferior, narrowed region of the pharynx. Extends inferiorly from the hyoid bone to the larynx and esophagus. Terminates at the superior border of the esophagus and the epiglottis of the larynx. Lined with a nonkeratinized stratified squamous epithelium. Permits passage of both food and air. 29. Lower Respiratory Tract Conducting airways (trachea, bronchi, up to terminal bronchioles). Respiratory portion of the respiratory system (respiratory bronchioles, alveolar ducts, and alveoli). 30. Larynx Voice box is a short, somewhat cylindrical airway ends in the trachea. Prevents swallowed materials from entering the lower respiratory tract. Conducts air into the lower respiratory tract. Produces sounds. Supported by a framework of nine pieces of cartilage (three individual pieces and three cartilage pairs) that are held in place by ligaments and muscles. 31. Larynx Nine c-rings of cartilage form the framework of the larynx thyroid cartilage (1) Adams apple, hyaline, anterior attachment of vocal folds, testosterone increases size after puberty cricoid cartilage (1) ring-shaped, hyaline arytenoid cartilages (2) hyaline, posterior attachment of vocal folds, hyaline cuneiform cartilages - (2) hyaline corniculate cartilages - (2) hyaline epiglottis (1) elastic cartilage 32. Larynx Muscular walls aid in voice production and the swallowing reflex Glottis the superior opening of the larynx Epiglottis prevents food and drink from entering airway when swallowing pseudostratified ciliated columnar epithelium 33. Sound Production Inferior ligaments are called the vocal folds. - are true vocal cords because they produce sound when air passes between them Superior ligaments are called the vestibular folds. - are false vocal cords because they have no function in sound production, but protect the vocal folds. The tension, length, and position of the vocal folds determine the quality of the sound. 34. Sound production Intermittent release of exhaled air through the vocal folds Loudness depends on the force with which air is exhaled through the cords Pharynx, oral cavity, nasal cavity, paranasal sinuses act as resonating chambers that add quality to the sound Muscles of the face, tongue, and lips help with enunciation of words 35. Conducting zone of lower respiratory tract 36. Trachea A flexible tube also called windpipe. Extends through the mediastinum and lies anterior to the esophagus and inferior to the larynx. Anterior and lateral walls of the trachea supported by 15 to 20 C-shaped tracheal cartilages. Cartilage rings reinforce and provide rigidity to the tracheal wall to ensure that the trachea remains open at all times Posterior part of tube lined by trachealis muscle Lined by ciliated pseudostratified columnar epithelium. 37. Trachea At the level of the sternal angle, the trachea bifurcates into two smaller tubes, called the right and left primary bronchi. Each primary bronchus projects laterally toward each lung. The most inferior tracheal cartilage separates the primary bronchi at their origin and forms an internal ridge called the carina. 38. Bronchial tree A highly branched system of air-conducting passages that originate from the left and right primary bronchi. Progressively branch into narrower tubes as they diverge throughout the lungs before terminating in terminal bronchioles. Incomplete rings of hyaline cartilage support the walls of the primary bronchi to ensure that they remain open. Right primary bronchus is shorter, wider, and more vertically oriented than the left primary bronchus. Foreign particles are more likely to lodge in the right primary bronchus. 39. Bronchial tree The primary bronchi enter the hilus of each lung together with the pulmonary vessels, lymphatic vessels, and nerves. Each primary bronchus branches into several secondary bronchi (or lobar bronchi). The left lung has two secondary bronchi.The right lung has three secondary bronchi. They further divide into tertiary bronchi. Each tertiary bronchus is called a segmental bronchus because it supplies a part of the lung called a bronchopulmonary segment. 40. Bronchial Tree Secondary bronchi tertiary bronchi bronchioles terminal bronchioles with successive branching amount of cartilage decreases and amount of smooth muscle increases, this allows for variation in airway diameter during exertion and when sympathetic division active bronchodilation mediators of allergic reactions like histamine bronchoconstriction epithelium gradually changes from ciliated pseudostratified columnar epithelium to simple cuboidal epithelium in terminal bronchioles 41. Respiratory Zone of Lower Respiratory Tract 42. Conduction vs. Respiratory zones Most of the tubing in the lungs makes up conduction zone Consists of nasal cavity to terminal bronchioles The respiratory zone is where gas is exchanged Consists of alveoli, alveolar sacs, alveolar ducts and respiratory bronchioles 43. Respiratory Bronchioles, Alveolar Ducts, and Alveoli Lungs contain small saccular outpocketings called alveoli. They have a thin wall specialized to promote diffusion of gases between the alveolus and the blood in the pulmonary capillaries. Gas exchange can take place in the respiratory bronchioles and alveolar ducts as well as in the alveoli, each lung contains approximately 300 to 400 million alveoli. The spongy nature of the lung is due to the packing of millions of alveoli together. 44. Respiratory Membrane squamous cells of alveoli . basement membrane of alveoli. basement membrane of capillaries simple squamous cells of capillaries about .5 in thickness 45. Cells in Alveolus Type I cells : simple squamous cells forming lining Type II cells : or septal cells secrete surfactant Alveolar macrophages 46. Gross Anatomy of the Lungs Each lung has a conical shape. Its wide, concave base rests upon the muscular diaphragm. Its superior region called the apex projects superiorly to a point that is slightly superior and posterior to the clavicle. Both lungs are bordered by the thoracic wall anteriorly, laterally, and posteriorly, and supported by the rib cage. Toward the midline, the lungs are separated from each other by the mediastinum. The relatively broad, rounded surface in contact with the thoracic wall is called the costal surface of the lung. 47. Lungs Left lung divided into 2 lobes by oblique fissure smaller than the right lung cardiac notch accommodates the heart 48. Right divided into 3 lobes by oblique and horizontal fissure located more superiorly in the body due to liver on right side 49. Pleura and Pleural Cavities The outer surface of each lung and the adjacent internal thoracic wall are lined by a serous membrane called pleura. The outer surface of each lung is tightly covered by the visceral pleura. while the internal thoracic walls, the lateral surfaces of the mediastinum, and the superior surface of the diaphragm are lined by the parietal pleura. The parietal and visceral pleural layers are continuous at the hilus of each lung. 50. Pleural Cavities The potential space between the serous membrane layers is a pleural cavity. The pleural membranes produce a thin, serous pleural fluid that circulates in the pleural cavity and acts as a lubricant, ensuring minimal friction during breathing. Pleural effusion pleuritis with too much fluid 51. Blood supply of Lungs pulmonary circulation - bronchial circulation bronchial arteries supply oxygenated blood to lungs, bronchial veins carry away deoxygenated blood from lung tissue superior vena cava Response of two systems to hypoxia pulmonary vessels undergo vasoconstriction bronchial vessels like all other systemic vessels undergo vasodilation 52. Respiratory events Pulmonary ventilation = exchange of gases between lungs and atmosphere External respiration = exchange of gases between alveoli and pulmonary capillaries Internal respiration = exchange of gases between systemic capillaries and tissue cells 53. Two phases of pulmonary ventilation Inspiration, or inhalation - a very active process that requires input of energy.The diaphragm, contracts, moving downward and flattening, when stimulated by phrenic nerves. Expiration, or exhalation - a passive process that takes advantage of the recoil properties of elastic fiber. The diaphragm relaxes.The elasticity of the lungs and the thoracic cage allows them to return to their normal size and shape. 54. Muscles that ASSIST with respiration The scalenes help increase thoracic cavity dimensions by elevating the first and second ribs during forced inhalation. The ribs elevate upon contraction of the external intercostals, thereby increasing the transverse dimensions of the thoracic cavity during inhalation. Contraction of the internal intercostals depresses the ribs, but this only occurs during forced exhalation. Normal exhalation requires no active muscular effort. 55. Muscles that ASSIST with respiration Other accessory muscles assist with respiratory activities. The pectoralis minor, serratus anterior, and sternocleidomastoid help with forced inhalation, while the abdominal muscles(external and internal obliques, transversus abdominis, and rectus abdominis) assist in active exhalation. 56. Ventilation Control by Respiratory Centers of the Brain The trachea, bronchial tree, and lungs are innervated by the autonomic nervous system. The autonomic nerve fibers that innervate the heart also send branches to the respiratory structures. The involuntary, rhythmic activities that deliver and remove respiratory gases are regulated in the brainstem within the reticular formation through both the medulla oblongata and pons. 57. Respiratory Values A normal adult averages 12 breathes per minute = respiratory rate(RR) Respiratory volumes determined by using a spirometer 58. RESPIRATORY SYSTEM Departement of Physiology Medical faculty of UNIVERSITAS SUMATERA UTARA 59. Introduction Primary function of respiration to obtain O2 for use by cells and to eliminate CO2 the cells produce 60. Introduction Non respiratory function of the respiratory system - provides a route for water loss and heat elimination - enhances venous return - contributes to the maintenance of normal acid-base balance - enables speech,singing, and other vocalization - defends againts inhaled foreign matter 61. Introduction Removes, modifies, activates, or inactivates various materials passing through the pulmonary circulation 62. Respiration - internal respiration; intra cellular metabolic processes carried out within the mitochondria, which use O2 and produce CO2 63. - external respiration; encompresses 4 steps; 1. air is alternately moved in and out of the lungs so that exchange of air can occur between atmosphere and the alveoli ventilation 2. O2 and CO2 are exchanged between air in the alveoli and blood within the pulmonary capillaries diffusion 3. O2 and CO2 are transported by the blood between the lungs and tissues 4. exchange of O2 and CO2 takes place between the tissues and the blood by the process of diffusion across the sistemic capillaries 64. The alveolar walls consist of a single layer of flattened Type I alveolar cells (thin and wall forming) Type II alveolar cells secrete pulmonary surfactant, a phospholipoprotein complex that faciitates lung expansion Defensive alveolar macrophages are present within the lumen of alveoli 65. Minute pores of Kohn exist in the walls between adjacent alveoli permits airflow between adjoining alveoli collateral ventilation 66. Lungs Right lung 3 lobes Left lung 2 lobes No muscle within alveoli walls to cause them to inflate and deflate during brething process The only muscle within the lungs is the smooth muscle in the walls of the arteriols and bronchioles 67. Lungs Changes in the lung volume are brought about through changes in the dimension of the thorax cavity The rib cage provides bony protection for the lungs and the heart Rib cage formed by 12 pairs of curved ribs which join the sternum anteriorly and the thoracic vertebrae (backbone) posteriorly 68. Diaphragm is a large dome-shaped sheet of scletal muscle forms the floor of thoracic cavity 69. Pleural sac pleural sac separates each lung from thoracic wall and other surrounding structures - pleura visceral cover the lungs surface - pleura parietal lines the 1.mediastinum 2.superior face of diaphragm 3.inner thoracic wall 70. Pleural sac The interior of the pleural sac is known as pleural cavity The surfaces of the pleura secrete a thin intra pleural fluid, which lubricates the pleural surfaces as they slide past each other during respiratory movements 71. RESPIRATORY MECHANICS Air flows in and out of the lungs by moving down alternately reversing pressure gradients established between the alveoli and the atmosphere by cyclical respiratory musle activity 72. Three different pressure consideration are important in ventilation 1. atmospheric (barometric) pressure is the pressure exerted by the weight of the air in the atmosphere on objects on earths surface. At sea level = 760 mmhg, and diminishes with increasing altitude above sea level as the column of air above earths surface correspondingly decreases 73. 2. intra alveolar pressure (intrapulmonary) pressure within alveoly 3. intrapleural pressure the pressure within the pleural sac = intrathoracic pressure, it is pressure exerted outside the lungs within the thoracic cavity. usually less than atmospheric pressure averaging 756 mmhg at rest 756 mmhg is sometimes referred to as pressure of -4 mmhg (just negative when compared with the normal atmosphere pressure) 74. The negative intra pleural pressure is due to; 1. surface tension of alveolar fluid 2. elasticity of lungs 3. elasticity of thoracic wall 75. Intra pleural pressure does not equilibrate with atmosphere or intra pulmolmonary pressure because there is no direct communication between the pleural and either atmosphere or the lungs 76. Intra pleural fluids cohesiveness and transmural pressure gradient ( the net outward pressure differential ) hold the thoracic wall and lungs in close apposition, streching the lungs to fill the thorax cavity 77. The transmural pressure gradient and intra pleural fluids cohesiveness prevent the thoracic wall and the lungs pulling away from each other except to the slightest degree 78. Normally, air does not enter the pleural cavity, because there is no communication between the cavity and either atmosphere or alveoli If the lungs punctured (by a stab wound or broken rib) air flows down its pressure gradient from higher atmospheric pressure and rushes into the pleural space pneumothorax 79. Intra pleural and intra alveolar are now equilibrated with atmospheric pressure, so transmural pressure gradient no longer exists, with no force present to stretch the lungs collapses The intra pleural fluids cohesiveness can not hold the lungs and thoracic wall in apposition in the absence of the transmural pressure gradient 80. Air flows down a pressure gradient During inspiration intra alveolar pressure< atmospheric pressure During expiration intra alveolar pressure> atmospheric pressure Intra alveolar pressure can be changed by altering the volume of the lungs, in accordance with Boyles law 81. Boyles law states that at any constant temperature, the pressure exerted by a gas varies inversely with the volume of the gas 82. Respiratory muscles Respiratory muscles that accomplish breathing do not act directly on the lungs to change their volume, instead change the volume of the thoracic cavity causing a corresponding change in lung volume because the thoracic wall and lungs are linked together 83. Diaphragm innervated by nervus phrenicus M.intercostalis ext innervated by nervus intercostalis During inspiration diaphragm and m.intercostalis ext contract on stimulation of this nerves 84. When diaphragm contact it descend downward, enlarging the volume of thoracic cavity by increasing its vertical dimension When m. intercostalis ext contract its fibers run downward and forward between adjacent ribs enlarging the thoracic cavity in both lateral and anteroposterior dimensions 85. At the end of inspiration the inspiratory muscles relax Diaphragm assume its original dome shaped position The elevated rib cage falls because of gravity when m. intercostalis ext relax The chest wall and stretch lungs recoil because of their elastic properties 86. Deeper inspiration can be accompished by contracting the diphragm and m.intercostalis ext. more forcefully and by bringing the accessory inspiratory muscles into play to further enlarge thorax cavity 87. During quite breathing, expiration is normally a passive process, because it is accomplished by elastic recoil of the lungs on the relaxation of inspiratory muscles To produce such a forced, active expiration expiratory muscles must contract to further reduce the volume of the thoracic cavity and lungs 88. During forcefull expiration the intrapleural pressure exceed the atmopheric pressure, but the lungs do not collapse because the intra alveolar pressure also increased correspondingly, a transmural pressure gradient still exists 89. Airway resistance influences airflow rates F= P R F = airflow rate P= difference between atmopheric and inra alveolar pressure (pressure gradient) R = resistance of airway, determined by their radii 90. The primary determinant of resistance to airflow is the radius of the conducting airways The airways normally offer such low resistance that only very small pressure gradient of 1-2 mmHg need be created to achieve adequate rates of airflow in and out of the lungs 91. Normally modest adjustment in airway size can be accomplished by autonomic nerv. Syst. Regulation to suit the bodys need Parasympathetic stimulation promotes bronchiolar smooth muscle contraction, which increases airway resistance by producing bronchoconstriction 92. Sympathetic stimulation and to a greater extent its associated hormone epinephrine, bring about bronchodilation Airway resistance is abnormally increased with chronic obstructive pulmonary disease such as; - chronic obstuctive pulmonary disease (COPD) - chronic bronchitis - asthma -emphysema 93. During the respiratory cycle, the lung alternately expand during inspiration and recoil during expiration Two interrelated concepts are involved in pulmonary elasticity; - elastic recoil refers to how readily the lungs rebound after having been stretched 94. - compliance refers to how much effort required to stretch or distend the lungs is a measure of magnitude of change in lung volume accomplished by a given change in the transmural pressure gradient 95. Pulmonary elastic behaviour depends mainly on 2 factors: 1. highly elastic connective tissue 2. alveolar surface tension 96. Alveolar surface tension displayed by the thin liquid film that lines each alveolus At an air-water interface, the water molecules at the surface are more strongly attached to other surrounding water molecules than to the air above the surface. 97. The tremendous surface tension of pure water is normally counteracted by pulmonary surfactan, a complex mixture of lipids and proteins Pulmonary surfactan intersperses between the water molecules in the fluid lining the alveoli and lowers the alveolar surface tension, because the cohesive force between a water molecule and a pulmonary surfactan molecule is very low 98. By lowering the alveolar surface tension, pulmonary surfactan provides two benefits; 1. increases pulmonary compliance 2. reduces the lungs tendency to recoil One of the important factors to maintain the stability of the alveoli 99. According to the law of La Place, the magnitude of the inward directed collapsing pressure is directly proportional to the surface tension and inversely proportional to the radius of the bubble 100. P= 2T r P = inward directed collapsing pressure T = surface tension r = radius of bubble 101. A second factor that contributes to alveolar stability is the interdependence among neighboring alveoli If an alveolus starts to collapse, the surrounding alveoli are stretched as their walls are pulled in the direction of the caving in alveolus, in turn these neighbouring alveoli, by recoiling in resistance to being stretched exert expanding forces on the collapsing alveolus and therby help keep it open 102. Normally only 3% of the total energy is used for quiet breathing The work of breathing may be increased in four different situations; 1. when pulmonary compliance is decreased 2. when airway resistance is increased 3. when elastic recoil is decreased 4. when there is a need for increased ventilation 103. The changes in lung volume can be measured using a spirometer Lung volumes and capacities; - tidal volume (TV) the volume of air entering or leaving the lungs during a single breath= 500 ml - inspiratory reserve volume (IRV) the extra volume of air that can be maximally inspired over and above the typical resting tidal volume= 3000 ml 104. Inspiratory capacity (IC) the max volume of air that can be inspired at the end of a normal quiet expiration (IC= IRV+TV)= 3500 ml Expiratory reserve volume (ERV) the extra volume of air that can be actively expired by Maximal contraction of the expiratory muscles beyond that normally passive expired at the end of a typical resting tidal volume= 1000ml 105. Residual volume(RV) the minimum volume of air remaining in the lungs even after a maximal expiration= 1200 ml Functional residual capacity(FRC) the volume of air in the lungs at he end of a normal passive expiration (FRC= ERV+RV)= 2200 ml 106. Vital capacity (VC) the maximum volume of air that can be moved our during a single breath following a maximal inspiration (VC= IRV+TV+ERV) the VC represents the maximum volume change possible within the lungs= 4500 ml Total lung capacity (TLC) the maximum volume of air that the lungs can hold (TLC= VC+RV)= 5700 ml 107. Forced expiratory volume in one second (FEV1) the volume of air that can be expired during the first second of expiration in a VC determination usually, FEV1 is about 80% of VC 108. Alveolar ventilation is less than pumonary ventilation because of presence of dead space 109. Normal Dead Space Volume. The normal dead space air in a young adult man is about 150 milliliters,This increases slightly with age. The volume of all the space of the respiratory system other than the alveoli and their other closely related gas exchange areas; this space is called the anatomic dead space. 110. Any ventilated alveoli that do not participate in gas exchange with blood are considered alveolar dead space Physiologic Dead Space this is the total dead space in the lung system the anatomic dead space plus alveolar dead space. 111. Pulmonary ventilation= tidal volume x respiratory rate Alveolar ventilation per minute is the total volume of new air entering the alveoli and adjacent gas exchange areas each minute Alveolar ventilation= (tidal volume- dead space volume)x resp rate 112. GAS EXCHANGE Gas exchange at both the pulmonary capillary and the tissue capillary levels involves simple passive diffusion of O2 and CO2 down partial pressure gradients No active transport exist for these gases 113. gas exchange between the alveolar air and the pulmonary blood occurs through the membranes of all the terminal portions of the lungs All these membranes are collectively known as the respiratory membrane= pulmonary membrane 114. the following different layers of the respiratory membrane: 1. A layer of fluid lining the alveolus and containing surfactant that reduces the surface tension of the alveolar fluid 2. The alveolar epithelium composed of thin epithelial cells 3. An epithelial basement membrane 4. A thin interstitial space between the alveolar epithelium and the capillary membrane 5. A capillary basement membrane that in many places fuses with the alveolar epithelial basement membrane 6. The capillary endothelial membrane 115. the overall thickness of the respiratory membrane in some areas is as little as 0.2 micrometer, and it averages about 0.6 micrometer 116. According to Ficks law of diffusion; the diffusion rate of a gas through a sheet of tissue also depends on the surface area and thickness of the membrane through which the gas is diffusing and on the diffusion coeficient of the particular gas Factors are relatively constant under resting situation 117. During exercise ; 1. the surface area available for exchange can be physiologically increased to enhance the rate of gas transport 2. When the pulmonary blood pressure is raised by increased cardiac output, many of previously closed pulmonary capillaries are forced open increases surface area of blood available for exchange 118. 3. the alveolar membranes are stretched further than normal because of the larger tidal volumes (deeper breathing) 119. Ventilation-perfussion ratio Two factors determine the PO2 and the PCO2 in the alveoli: (1) the rate of alveolar ventilation and (2) the rate of transfer of oxygen and carbon dioxide through the respiratory membrane. It made the assumption that all the alveoli are ventilated equally, and that blood flow through the alveolar capillaries is the same for each alveolus. 120. However, even normally to some extent, and especially in many lung diseases, some areas of the lungs are well ventilated but have almost no blood flow, whereas other areas may have excellent blood flow but little or no ventilation. a highly quantitative concept has been developed to help us understand respiratory exchange when there is imbalance between alveolar ventilation and alveolar blood flow. This concept is called the ventilation- perfusion ratio. 121. the ventilation-perfusion ratio is expressed as Va/Q Va (alveolar ventilation) Q (blood flow) When Va is normal and Q also normal the ventilation perfusion ratio is also said to be normal resting situation= 0.8 l/mnt When there is both normal alveolar ventilation and normal alveolar capillary blood flow (normal alveolar perfusion), exchange of oxygen and carbon dioxide through the respiratory membrane is nearly optimal, 122. Va/Q normal curve 123. When the ventilation(Va) is zero, yet there is still perfusion (Q) of the alveolus, the Va/Q is zero Or, at the other extreme, when there is adequate ventilation (Va) but zero perfusion(Q), the ratio Va/Q is infinity. At a ratio of either zero or infinity, there is no exchange of gases through the respiratory membrane of the affected alveoli 124. When Va/Q is equal to zero the air in the alveolus comes to equilibrium with the blood oxygen and carbon dioxide because these gases diffuse between the blood and the alveolar air. Because the blood that perfuses the capillaries is venous blood returning to the lungs from the systemic circulation, it is the gases in this blood with which the alveolar gases equilibrate. 125. The effect on the alveolar gas partial pressures when Va/Q equals infinity is entirely different from the effect when Va/Q equals zero because now there is no capillary blood flow to carry oxygen away or to bring carbon dioxide to the alveoli. Therefore, instead of the alveolar gases coming to equilibrium with the venous blood, the alveolar air becomes equal to the humidified inspired air. That is, the air that is inspired loses no oxygen to the blood and gains no carbon dioxide from the blood. 126. Whenever Va/Q is below normal, there is inadequate ventilation to provide the oxygen needed to fully oxygenate the blood flowing through the alveolar capillaries. A certain fraction of the venous blood passing through the pulmonary capillaries does not become oxygenated. This fraction is called shunted blood. 127. The total quantitative amount of shunted blood per minute is called the physiologic shunt. This physiologic shunt is measured in clinical pulmonary function laboratories by analyzing the concentration of oxygen in both mixed venous blood and arterial blood (along with simultaneous measurement of cardiac output) 128. the physiologic shunt can be calculated by the following equation: Qps = CiO2 - CaO2 Qt CiO2 - CvO2 Qps is the physiologic shunt blood flow perminute Qt is cardiac output per minute CiO2 is the concentration of oxygen in the arterial blood if there is an ideal ventilation-perfusion ratio CaO2 is the measured concentration of oxygen in the arterial blood and CvO2 is the measured concentration of oxygen in the mixed venous blood. 129. The greater the physiologic shunt, the greater the amount of blood that fails to be oxygenated as it passes through the lungs. 130. In a normal person at the top of the lung,Va/Q is as much as 2.5 times as great as the ideal value, which causes a moderate degree of physiologic dead space in this area of the lung. in the bottom of the lung, there is slightly too little ventilation in relation to blood flow,with Va/Q as low as 0.6 times the ideal value. In this area, a small fraction of the blood fails to become normally oxygenated, and this represents a physiologic shunt. 131. inequalities of ventilation and perfusion decrease slightly the lungs effectiveness for exchanging oxygen and carbon dioxide. during exercise, blood flow to the upper part of the lung increases markedly, so that far less physiologic dead space occurs, and the effectiveness of gas exchange now approaches optimum. 132. O2 transport Once oxygen has diffused from the alveoli into the pulmonary blood, it is transported to the peripheral tissue capillaries almost entirely in combination with hemoglobin. the transport of oxygen and carbon dioxide by the blood depends on both diffusion and the flow of blood. 133. Normally, about 97 per cent of the oxygen transported from the lungs to the tissues is carried in chemical combination with hemoglobin in the red blood cells. The remaining 3 per cent is transported in the dissolved state in the water of the plasma and blood cells. 134. Maximum Amount of Oxygen That Can Combine with the Hemoglobin of the Blood. On average, the 15 grams of hemoglobin in 100 milliliters of blood can combine with a total of almost exactly 20 milliliters of oxygen if the hemoglobin is 100 per cent saturated. This is usually expressed as 20 volumes percent. 135. the oxygen molecule combines loosely and reversibly with the heme portion of hemoglobin.When PO2 is high, as in the pulmonary capillaries, oxygen binds with the hemoglobin, but when PO2 is low, as in the tissue capillaries, oxygen is released from the hemoglobin. 136. Oxygen-Hemoglobin Dissociation Curve. 137. the oxygen-hemoglobin dissociation curve, which demonstrates a progressive increase in the percentage of hemoglobin bound with oxygen as blood Po2 increases, which is called the per cent saturation of hemoglobin. 138. a number of factors can displace the dissociation curve in one direction or the other; 1. when the blood becomes slightly acidic, with the pH decreasing from the normal value of 7.4 to 7.2, the oxygen-hemoglobin dissociation curve shifts, on average, about 15 per cent to the right. Conversely, an increase in pH from the normal 7.4 to 7.6 shifts the curve a similar amount to the left. 139. 2. changes carbon dioxide concentration 3. changes blood temperature 4. changes 2,3-biphosphoglycerate (BPG),a metabolically important phosphate compound present in the blood in different concentrations under different metabolic conditions.(increased in hypoxic condition O2 released) 140. Carbon monoxide combines with hemoglobin at the same point on the hemoglobin molecule as does oxygen it can therefore displace oxygen from the hemoglobin, thereby decreasing the oxygen carrying capacity of blood. it binds with about 250 times as much tenacity as oxygen 141. CO2 transport the amount of carbon dioxide in the blood has a lot to do with the acid- base balance of the body fluids An average of 4 milliliters of carbon dioxide is transported from the tissues to the lungs in each 100 milliliters of blood. 142. To begin the process of carbon dioxide transport, carbon dioxide diffuses out of the tissue cells in the dissolved molecular carbon dioxide form. The dissolved carbon dioxide in the blood reacts with water to form carbonic acid (70 per cent) catalized by carbonic anhidrase enzyme the reaction occurs so rapidly in the red blood cells 143. In another fraction of a second, the carbonic acid formed in the red cells (H2CO3) dissociates into hydrogen and bicarbonate ions (H+ and HCO3 ) Most of the hydrogen ions then combine with the hemoglobin in the red blood cells, because the hemoglobin protein is a powerful acid-base buffer. 144. In turn, many of the bicarbonate ions diffuse from the red cells into the plasma, while chloride ions diffuse into the red cells to take their place. This is made possible by the presence of a special bicarbonate-chloride carrier protein in the red cell membrane that shuttles these two ions in opposite directions at rapid velocities. Thus, the chloride content of venous red blood cells is greater than that of arterial red cells, a phenomenon called the chloride shift. 145. In addition to reacting with water, carbon dioxide reacts directly with amine radicals of the hemoglobin molecule to form the compound carbaminohemoglobin (CO2Hb) 23% This combination of carbon dioxide and hemoglobin is a reversible reaction that occurs with a loose bond, so that the carbon dioxide is easily released into the alveoli, where the Pco2 is lower than in the pulmonary capillaries 7% 146. A small amount of carbon dioxide also reacts in the same way with the plasma proteins in the tissue capillaries. This is much less significant for the transport of carbon dioxide because the quantity of these proteins in the blood is only one fourth as great as the quantity of hemoglobin. 147. the Bohr effect; increase in carbon dioxide in the blood causes oxygen to be displaced from the hemoglobin an important factor in increasing oxygen transport binding of oxygen with hemoglobin tends to displace carbon dioxide from the blood. the Haldane effect important factor in increasing CO2 transport 148. REGULATION OF RESPIRATION respiratory center is composed of several groups of neurons located bilaterally in the medulla oblongata and pons of the brain stem 149. It is divided into three major collections of neurons: (1) a dorsal respiratory group (inspiratory center), located in the dorsal portion of the medulla, which mainly causes inspiration (2) a ventral respiratory group (expiratory center), located in the ventrolateral part of the medulla, which mainly causes expiration (3) the pneumotaxic center,located dorsally in the superior portion of the pons, which mainly controls rate and depth of breathing. The dorsal respiratory group of neurons plays the most fundamental role in the control of respiration. 150. The dorsal respiratory group of neurons are located within the nucleus of the tractus solitarius The nucleus of the tractus solitarius is the sensory termination of both the vagal and the glossopharyngeal nerves, which transmit sensory signals into the respiratory center from (1) peripheral chemoreceptors (2) baroreceptors, and (3) several types of receptors in the lungs. 151. The basic rhythm of respiration is generated mainly in the dorsal respiratory group of neurons. The nervous signal that is transmitted to the inspiratory muscles, mainly the diaphragm in normal respiration, it begins weakly and increases steadily in a ramp manner for about 2 seconds. Then it ceases abruptly for approximately the next 3 seconds, which turns off the excitation of the diaphragm and allows elastic recoil of the lungs and the chest wall to cause expiration. 152. the inspiratory signal is a ramp signal it causes a steady increase in the volume of the lungs during inspiration 153. There are two qualities of the inspiratory ramp that are controlled, as follows: 1. Control of the rate of increase of the ramp signal, so that during heavy respiration, the ramp increases rapidly and therefore fills the lungs rapidly. 2. Control of the limiting point at which the ramp suddenly ceases. This is the usual method for controlling the rate of respiration; that is, the earlier the ramp ceases, the shorter the duration of inspiration. This also shortens the duration of expiration. Thus, the frequency of respiration is increased. 154. A pneumotaxic center, located dorsally in the nucleus parabrachialis of the upper pons, transmits signals to the inspiratory area. effect of this center is to control the switch-off point of the inspiratory ramp, thus controlling the duration of the filling phase of the lung cycle. 155. When the pneumotaxic signal is strong, inspiration might last for as little as 0.5 second, thus filling the lungs only slightly; when the pneumotaxic signal is weak, inspiration might continue for 5 or more seconds, thus filling the lungs with a great excess of air. 156. The function of the pneumotaxic center is primarily to limit inspiration. This has a secondary effect of increasing the rate of breathing, because limitation of inspiration also shortens expiration and the entire period of each respiration. 157. ventral respiratory group of neurons, found in the nucleus ambiguus rostrally and the nucleus retroambiguus caudally. 158. The function of this neuronal group; 1. The neurons of the ventral respiratory group remain almost totally inactive during normal quiet respiration. 2. There is no evidence that the ventral respiratory neurons participate in the basic rhythmical oscillation that controls respiration. 3. the ventral respiratory area contributes extra respiratory drive 4. especially important in providing the powerful expiratory signals to the abdominal muscles during very heavy expiration. 159. Hearing Breur Reflex Most important, located in the muscular portions of the walls of the bronchi and bronchioles throughout the lungs are stretch receptors that transmit signals through the vagi into the dorsal respiratory group of neurons when the lungs become overstretched. 160. when the lungs become overly inflated, the stretch receptors activate an appropriate feedback response that switches off the inspiratory ramp and thus stops further inspiration Hering-Breuer inflation reflex. is not activated until the tidal volume increases to more than three times normal (greater than about 1.5 liters per breath). 161. The ultimate goal of respiration is to maintain proper concentrations of oxygen, carbon dioxide, and hydrogen ions in the tissues. Excess carbon dioxide or excess hydrogen ions in the blood mainly act directly on the respiratory center 162. Oxygen, in contrast, does not have a significant direct effect on the respiratory center of the brain in controlling respiration. Instead, it acts almost entirely on peripheral chemoreceptors located in the carotid and aortic bodies, and these in turn transmit appropriate nervous signals to the respiratory center for control of respiration. 163. Arterial PO2 is monitored by peripheral chemoreceptors The arterial PO2 must fall below 60 mmhg before the peripheral chem. Respond by sending afferent impulses to inspiratory centers increasing ventilation 164. Central chemoreceptors sensitive to changes in CO2 induced H+ concentration in the brain extracellular fluid (ECF) 165. Changes in arterial H+ concentration cannot influence the central chemoreceptors, because H+ cannot cross the blood brain barrier the peripheral chem. Are highly responsive to the fluctuation in contrast to their unsensitiveness to arterial PCO2 and PO2 until it falls below 60 mmhg 166. Bronkiektasis kelainan anatomik dilatasi bronkus yang kronik dan menetap. Bronkus yang terkena biasanya berukuran sedang (generasi 4-9). Karakteristik bronkiektasis yaitu kerusakan dari dinding bronkus, pembuluh darah, jaringan elastis dan komponen otot-otot polos 167. Penyebab bronkiektasis yang pasti belum diketahui, namun banyak faktor yang dapat mengakibatkan terjadinya bronkiektasis : 1. Acquired Bronchiectasis 2. Congenital Bronchiectasis 168. ACQUIRED BRONCHIECTASIS 1. FAKTOR OBSTRUKSI Sebagian besar cabang bronkus yang kecil Akibat aspirasi mukus masuk ke dalam lumen bronkus yang menyebabkan kolaps bagian distal. Keadaan ini menyebabkan tekanan intraluminer proksimal dilatasi bronkus. Bila terjadi infeksi pada bronkus yang mengalami dilatasi ini serta terjadi destruksi dinding bronkus, maka akan terjadi dilatasi bronkus yang permanen. 169. Obstruksi dapat disebabkan : Aspirasi benda asing Mucous plaque Bronchogenic carcinoma Pembesaran KGB di hilus yang menyebabkan bronkiektasis pada distal bronkus. Kondisi yang telah disebutkan diatas menyebabkan gangguan mekanisme mucociliary cleareance dan gangguan ini akan menyebabkan berkembangnya infeksi bakteri 170. 2. INFEKSI PARU BERULANG (Recurrent Pulmonary Infection) Infeksi saluran nafas akut misalnya bronkopneumonie destruksi jaringan peribronkhial penarikan dinding bronkhus dilatasi bronkhus 171. Bronkiektasis pada umumnya dijumpai pada individu yang mempunyai recurrent dan infeksi saluran pernapasan bawah dalam jangka waktu lama Seperti anak-anak ; penderita bronkopneumonia akibat komplikasi sekunder seperti cacar, measle, influenza yang akan menderita bronkiektasis pada usia dewasa 172. 3. Inhalasi dan Aspirasi Bronkiektasis pada umumnya dijumpai akibat inhalasi oleh gas ammoniak atau teraspirasi cairan lambung. 173. Sindroma kartagener. 20% penderita dengan dextrocardia menderita bronkiektasis. Gejala jelas bila kena infeksi : pertusis, influensa dan morbili . Fibrosis kistik paru ( Cystic Fibrosis ) Kelainan Sistemik Gangguan rheumatologik Inflammatory Bowel Disease AIDS FAKTOR KONGENITAL 174. MANIFESTASI KLINIS Batuk kronis yang produktif terutama pagi hari, sputum banyak, sepanjang hari (wet bronchiectasis). Batuk kering kadang disertai hemoptisis dry bronchiectasis Sputum putih dan kadang-kadang warna kuning infeksi berat 400 - 500 cc/hari . Batuk darah 50 -70% kasus masif. Demam berulang Nyeri dada Sesak napas Akut eksaserbasi 175. PEMERIKSAAN FISIS Suara pernapasan : - bronkial - ekspirasi memanjang Suara tambahan ronki basah / ronki kering Clubbing finger Kasus berat gagal napas 176. 1. Sumbatan bronkus (Bronchial obstruction) o Tumor endobronkial o Bronkolitiasis dan gangguan inflamasi seperti tuberkulosis dan aspirasi benda asing. 2. Infeksi o Infeksi paru nekrotik yang tidak diobati o Disebabkan oleh Klebsiella, Staphylococcus, M. tuberculosis, M.non tuberkulosis, Mycoplasma pneumoniae, dll. KONDISI-KONDISI YANG BERHUBUNGAN DENGAN BRONKIEKTASIS 177. 3. Inflamasi Ulserasi asam lambung aspirasi bronkiektasis 4. Aspergilosis Bronkopulmoner Alergi o Ditandai dengan bronkospasme, bronkiektasis dan sekret yang mengandung aspergillosis o Reaksi hypersensitif thd antigen yang terhirup di trakeobronkhial. o Bronkiektasis terjadi akibat sumbatan sekret yang mengandung hipa dan aspergilus. KONDISI-KONDISI YANG BERHUBUNGAN DENGAN BRONKIEKTASIS 178. 5. Defisiensi Imun o Terjadi pada penderita defisiensi imun kongenital maupun didapat. o Limfosit B yang abnormal. o Hipogammaglobulinemia kongenital atau didapat penurunan hilangnya IgG. 6. Defisiensi Alfa-1 Antitripsin KONDISI-KONDISI YANG BERHUBUNGAN DENGAN BRONKIEKTASIS 179. 7. Diskinesia Silia Primer Sindroma kartagener ( dextrocardia, bronkiektasis , sinusitis syndrome) 8. Fibrosis Kistik Gangguan transportasi klorida penumpukan klorida dlm sel sel kering sekret kental membatu iritasi kronik infeksi berulang KONDISI-KONDISI YANG BERHUBUNGAN DENGAN BRONKIEKTASIS 180. Klasifikasi Reid tahun 1950 membagi bronkiektasis atas 3 tipe : 1. SILINDRIK 2. VARIKOSA 3. KISTIK ATAU SAKULAR KLASIFIKASI GAMBARAN RADIOLOGIS 181. Gambaran foto toraks bisa normal Corakan bronkovaskuler bertambah Atelektasis Struktur cincin (ringlike structure) Dilatasi dan penebalan saluran napas (tram lines) Mucus plugging finger in glove Diagnosa pasti : bronkografi masukkan zat kontras ke saluran nafas ( Daonosil, Lipiodol ) GAMBARAN RADIOLOGIS 182. FOTO TORAKS BRONKIEKTASIS 183. 1. SILINDRIK Seringkali dihubungkan dengan kerusakan parenkim paru, terdapat penambahan diameter bronkus bersifat reguler, lumen distal bronkus tidak begitu melebar 2. VARIKOSA Pelebaran bronkus lebih lebar dari bentuk silindrik dan bersifat irregular. Gambaran garis irregular dan distal bronkus yang mengembang adalah gambaran khas pada bentuk varikosa. 184. 3. SAKULER / KISTIK Dilatasi bronkus sangat progresif ke perifer, bronkus. Pelebaran bronkus ini terlihat sebagai balon, kelainan ini biasanya terjadi bronkus yang besar, pada bronkus generasi ke 4. 185. CYLINDRICAL BRONCHIECTASIS 186. CYLINDRICAL BRONCHIECTASIS 187. VARICOSE BRONCHIECTASIS 188. VARICOSE BRONCHIECTASIS 189. CYSTIC BRONCHIECTASIS 190. CYSTIC BRONCHIECTASIS 191. Sputum 3 lapisan : lapisan atas jernih ,lapisan tengah serous dan lapis bawah keruh ( pus dan cellular debris). Sebaiknya sputum diambil dari aspirasi transtrakeal pulasan gram, biakan serta uji resistensi. Umumnya dijumpai H. influenza P. aeruginosa 192. Penatalaksanaan penderita bronkiektasis pada dasarnya terdiri dari 4 hal : 1. Pemberian obat-obatan 2. Fisioterapi 3. Pembedahan 4. Usaha pencegahan. PENATALAKSANAAN 193. 1. Antibiotika Diberi bila terjadi perubahan sifat sputum dari mukoid purulen Sesuai dengan hasil uji resistensi 2. Bronkodilator Beta agonist, antikolinergik atau teofilin Diberi pada pasien dengan gambaran bronkitis kronis dan obstruksi jalan nafas. 1. PEMBERIAN OBAT-OBATAN 194. 3. Mukolitik dan Ekspektoran Mengencerkan sekret Merangsang sekresi dahak dari saluran napas 4.Steroid Inhalasi Terbukti dalam mengurangi produksi sputum Menurunkan angka eksaserbasi. PEMBERIAN OBAT-OBATAN.. 195. Mengeluarkan sekret dalam saluran napas memperbaiki fungsi paru Cara : latihan napas dan drainase postural Posisi drainase postural tergantung dari lokasi segmen yang terkena 2. FISIOTERAPI 196. Pengobatan konservatif yang adekuat tetap ada keluhan. Infeksi berulang Batuk darah berulang masif Operasi : segmentektomi, lobektomi atau pneumonektomi. Transplantasi paru 3. PEMBEDAHAN 197. Imunisasi Menghindari paparan rokok Pengobatan adekuat pada pneumonie, pertusis , morbili. 4. UPAYA PENCEGAHAN 198. SINDROMA KARTAGENER 199. SINUSITIS MAKSILARIS 200. DEXTROCARDIA 201. CT SCAN TORAKS BRONKIEKTASIS 202. SOAL UKDI Laki-laki berusia 67 tahun datang ke RS dengan keluhan utama batuk berdahak. Hal ini dialami Os sejak 4 hari yang lalu. T 37,5 C. Pada foto thoraks, didapati gambaran Honey Bee dan air fluid level pada segmen inferior paru. Diagnosanya adalah? A. Pneumonia B. Bronkiektasis C. Bronkitis D. Bronkitis kronik E. TB milier 203. Chronic Recurrent Cough and Childhood Asthma Helmi Lubis Ridwan M. Daulay Wisman Dalimunthe Rini S. Daulay 1 204. Definition of cough a sudden explosive expiratory maneuver that tends to clear materials from the airways and prevent aspiration of food or fluid 2 205. Physiologic or pathologic? 3 Cough Physiologic Pathologic Pathologic: intensity, frequency, cough characteristic, sputum characteristic Cough without receptor stimulation: psychogenic, habitual cough 206. Cough Model Reflex Voluntary control of cough Placebo effect Exogenous opioids Endogenous opioids Cough control centre Respiratory area of brainstem +ve -ve Cerebral cortex Vagus nerve Sensation of irritation Airway irritation Respiratory muscles COUGH 4 Widdicombe J. Cough. Blackwell publishing 2003; 20 207. Cough Reflex Arc Vagal nerve Trigeminal, Facial Hippoglosus nerve, etc Diaphragm; Intercostal, Abdominal & lumbal muscles Respiratory tract muscles Muscles involve in respiration Cough center Efferent Efector Muscle, Larynx, trachea, and bronchus Afferent Vagal nerve branch Distributed evenly in medulla near by the respiratory center: Under the higher control center Receptor Larynx Trachea Bronchus Ear Gastric Nose Sinus paranasal Trigeminal nerve Nerve Phrenicus, Intercostal & lumbaris Pharynx Glossopharyngeal nerve Pericardium diaphragm Nerve phrenicus 5 Chang AB. Cough 2003;7:1-15. 208. How do we cough ? Inspiratory ExpiratoryCompressive Deep inspiration (150-200% tidal volume) Maximal dilation of tracheo-bronchial tree Glottic closure 0.2 Contraction of thoracic & abdminal muscles vs fixed diaphragm Intrathoracic pressure Expiratory muscles contraction Sudden glottic opening Explosive release of intrathoracic air Cloutier MM: Cough, in : Loughlin GM ed Resp dis in children, 1994 Inspiratory muscles contraction 209. 7 Figure 1. Diagrammatic representation of the changes of the following variables during a representative cough: flow rate, volume, subglottic pressure and sound level. McCool FD. Chest 2006;129:48S-53S. 1 2 3 0 10 20 30 40 50 cmH2O L/s 0.0 Air volume Subglottic pressure Flow rates 1.0 2.0 3.0 4.0 5.0 6.0 positive Flow phase Min flow phase Negative Flow phase Inspiratory phase glottis closure Expiratory phase (explosive) Sound Mechanism of Cough 210. 8 IPS(IDAI): Chronic Recurrent Cough or (Batuk Kronik Berulang / BKB) Chronic: > 2 weeks AND/OR Recurrent: > 3 episodes in 3 months BKB is not a final diagnosis, but lead to a group of diseases with the same manifestation 211. Diagnosis of Asthma Cough and/or wheezing that: Hyperreactivity Nocturnal (variability) Reversibility Episodic Atopic family 9 212. Inflammatory processes Desquamation of epithelium Mucus plug Basement Membrane thickening Neutrophil and eosinophil infiltrationSmooth muscle Hypertrophy and contraction Oedema Hyperplasia of Mucos glands Barnes PJ 10 213. AsthmaNormal Getting to asthmatic inflammation what does it take ??? 11 214. Inflammation in asthma Barnes PJ Chronic inflammation Structural changes Acute inflammation Steroid response Time 12 215. Environment Genetic susceptibility Chronic allergic inflammation (Mast cells, T-Cells, Eosinophils) AIRWAY WALL THICKENING Pathogenesis 13 216. Classification of asthma Severity of attacks (Acute) Mild Moderate Severe Respiratory arrest imminent Class of disease (Chronic) Infrequent episodic asthma Frequent episodic asthma Persistent asthma 14 217. Asthma : chronic respiratory disease, that can have acute exacerbation Asthma Acute Asthma Chronic Asthma 2 aspect of asthma 218. Asthma management Chronic asthma Long term management Algorithm diagnosis & treatment Acute asthma Attack management Algorithm attack management 219. Asthma medication, function category Reliever To relieve / reduce symptoms and/ attack As needed use Bronchodilators 2-agonist, xanthenes, systemic steroid Oral, inhalation, injection Controller To control / prevent symptoms and/ attack Long term use Anti-inflammations Inhaled steroid, ALTR Oral, inhalation, For FEA & PA, not for IEA 220. Acute asthma management Asthma attack / symptoms present: First line therapy 2 agonist Ipratropium bromide Chronic asthma (long term management): First line therapy Inhaled steroid Long-acting 2 agonist (LABA) 221. Asthma Attack 19 222. Why happened ?? 223. Asthma Triggers Attack House dust mite (HDM) Smoke (polution) Food Infection Longterm management failure 224. Pathophysiology Trigger Airway obstruction Nonuniform Hyperinflation ventilation Atelectasis Mismatching of Decreased ventilation and perfution compliance Decreased surfaktant Alveolar hypoventilation Increased work Acidosis of breathing Pulmonary vasoconstriction Bronchocontriction, Mucosal edema, Excessive secretion PaCO2 PaO2 225. 84.4% 3.9% 11.7% Mild Moderate Severe Severity of asthma attack 226. Estimation of severity of asthma attack Sign/ Symptom Mild Moderate Severe Imminent respiratory arrest Activities (infant) Walking (loudly cried) Talking (weak cried) Rest (stop eating) Talking Complete sentences Phrasesor or partial sentences Single words or short phrases Position Can lie down Prefer to seat Tripod-like sitting positions Alertness Maybe agitated Usually agitated Usually agitated Confused Cyanotic Absent Absent Present Wheezing Moderate, end of eksp. Loud, eksp. + insp. Audible Difficult/ cant be heard Breathing difficulties Minimal Moderate Severe 227. Acessory Muscle of respiration Usually not Usually yes Yes Paradoxical movement Retraction No intercostal to mild retraction Moderate +, tracheosterna l retraction Deep +, +, nassal flaring Decrease/ none Respiratory rate Tachypnea Tachypnea Tachypnea Decreasing Pulse rate Normal Tachycardia Tachycardia Bradicardia Pulsus paradoxus Absent (20 mmHg absent (Fatique resp. muscle) PEF / FEV1 - pre-b.dilat. - post-b.dilat (% predictive- >60% >80% value/ % good 40-60% 60-80% -value) 80% PEF/FEV1 15% > 50%> 30% 42 244. Evolving treatment options 1975 1980 1985 1990 1995 2000 Large use of short-acting 2-agonists Fear of short-acting 2-agonists Single inhaler therapy (Symbicort) ICS treatment introduced 1972 Adding LAA to ICS therapy Kips et al, AJRCCM 2000 Pauwels et al, NEJM 1997 Greening et al, Lancet 1992 Bronchospasm Inflammation Remodelling 43 245. Goal of asthma management Minimal (ideally no) chronic symptoms Minimal (infrequent) exacerbations No emergency visits Minimal (ideally no) use of as needed 2- agonist No limitations on activities (exercise) (Near) Normal lung function Minimal (or no) adverse effects from medicine44 246. Allergen avoidance Immuno- therapy Pharmaco- therapy Education Asthma management COSTS GINA, 2002 45 247. Cost ? Availability ? 46 248. Avoidance Avoidance of triggers : House dust mite Pre and during pharmacotherapy GINA, 200247 249. Family Education Aim to: Increase understanding Increse skill Increse satisfaction Increse confidence Increse compliance and self management Patient-family-doctor relationships GINA,2002 48 250. Immunotherapy Desensitisation Controversial Multifactorial triggers Not populair 49 251. Pharmacotherapy Reliever: 2 agonist : inhaler, nebulized, oral Epinephrine : subcutan Theophylline : oral, I.V. Anticholinergic (ipratropium br) : inhaler Steroid : oral, I.M. Controller: Steroid : inhaler LABA : inhaler, oral Leukotrien : oral PNAA, 200250 252. When?? Classifications Controller Reliever Infrequent episodic asthma No Yes Frequent episodic asthma Yes Yes Persistent asthma Yes Yes 51 253. Medications Bronchodilators Antiinflammations Anti-remodelling Anti IgE Immunizations: ?? 52 254. TREATING ASTHMA with Bronchodilators alone is like Painting over rust !!! 53 255. Infrequent episodic asthma No daily medication Treatment of exacerbations depend on severity of attacks -2 agonist as needed 54 256. Frequent episodic and persistent asthma Controller medications: every day Corticosteroid with or without any drugs Combination with LABA, TSR, ALT Gradual reduction if stable in 6-8 weeks 55 257. Anti-inflammations Antihistamine Disodium Cromoglycate (DSCG) Corticosteroids 56 258. Long-term placebo-controlled trial of ketotifen in the management of preschool children with asthma Loftus BG, Price JF J Allergy Clin Immunol 1987; 79:350-5 The results suggest that: Ketotifen has no place in the management of young children with frequent asthma 57 259. Inhaled disodium cromoglycate (DSCG) as maintenance therapy in children with asthma: a systematic review. Tasche MJA, Uijen JHJ, Bernsen RMD, de Jongste JC, van der Wouden JC. Thorax 2000; 55:913-20 Insufficient evidence that DSCG has a beneficial effect as maintenance treatment in children with asthma 58 260. Low dose steroid Medium dose steroid Low dose steroid + LABA Low dose steroid + ALTR Low dose steroid +TSR High dose steroid Medium dose steroid + LABA Medium dose steroid + ALTR Medium dose steroid + TSR ORAL STEROID Longterm management 59 261. Corticosteroids The most effective anti-inflammatory medications Improving lung function Airway hiperresponsiveness: Reducing symptoms Frequency and severity of exacerbations: Improving quality of life 60 262. Epithelial Repair Following Steroid Treatment Before After P Howarth, 1999P Howarth, 199961 263. Steroid efficacy in asthma Benefit Steroid dose Side-effects 62 264. Type of inhalation therapy Metered dose inhaler (MDI) With spacer Without spacer Dry powder inhaler (DPI) Turbuhaler, cyclohaler Nebulizer Jet Ultrasonic 63 265. Benefit of steroid inhalation Low dose Directly to respiratory tract Fast onset Minimal systemic side effects 64 266. LABAs and ICS - complementary modes of action Smooth muscle dysfunction Airway inflammation Bronchoconstriction Bronchial hyperreactivity Hyperplasia Inflammatory mediator release Inflammatory cell infiltration / activation Mucosa oedem Cellular proliferation Epithelial damage Basement membrane thickening Symptoms / exacerbations LABA CS 65 267. CS + LABA Vs CS double dose Increases in PEF and FEV1 Similar improvements in asthma symptoms Similar in use of rescue medications Similar adverse event Similar in sputum markers of airway inflammation Am J Respir Crit Care Med 2000; 161:996-1001 Eur Respir J 2001; 18:262-8 Pediatr Pulmonol 2002; 34:342-50 66 268. Adding LABA to steroid improves FEV1 Pauwels et al, NEJM 1997 Pulmicort 100 g bid Pulmicort 400 g bid Pulmicort 100 g bid + Oxis 9 g bid Pulmicort 400 g bid + Oxis 9 g bid %predicted 70 75 80 85 90 -1 0 1 2 3 6 9 12 Months 67 269. Corticosteroids and LABA improves quality of life of school-age children with asthma *p10mg/L); anti-inflammatory effect is due to an unknown mechanism and may occur at lower concentrations (5-10mg/L). This latter mechanism may involve the inhibition of cell surface receptors for adenosine, which modulate adenylyl cyclase activity (contraction of isolated smooth muscle and to provoke histamine release from mast cells. Most studies show little or no effect on airway hyperresponsiveness Role in therapy Sustained release theophylline is effective in controlling asthma symptoms and improving lung function (i.e., nocturnal symptoms; may be used as an add-on therapy to low or high doses of glucocorticoids) 311. Methylxanthines Side effects (serum concentrations > 15g/mL)* Gastrointestinal symptoms nausea, vomiting CNS Seizures Cardiovascular tachycardia, arrhythmias Pulmonary stimulation of the respiratory center *Monitoring theophylline levels is advised when high-dose therapy (>10mg/kg body weight is used or when a patient develops an adverse effect on the usual dosage 312. Mast Cell Stabilizing Agents Mechanism of Action: inhibit the activation of mast cells within the airway, thereby preventing release of mediators that provoke asthma symptoms. alter the function of delayed chloride channels in the cell membrane considered by some as a type of NSAID. Used for preventing asthma attack Advantages: As the prophylaxis of asthma attack caused by allergen, exercise, aspirin, and working. Used for long term medication Disadvantages: Using dosage four times a day Expensive Less effectivity than inhaled corticosteroid side effects: throat iritation, cough, dry mouth, and bad taste of tongue. 313. Cromolyn & Nedocromil Dosing QID Dosage Forms MDI or Nebulized solution (Cromolyn) Advantages - alternative to steroids/-agonists Side Effects/Problems Daily dosing required (works prophylactically) Cromolyn (throat irritation or dryness, wheezing, nausea, coughing, and a bad taste in the mouth). Nedocromil (bad taste, nausea, abdominal pain, and vomiting). 314. Leukotriene modifiers Zafirlukast, Montelukast, and Zileuton A relatively new class of anti-asthma drugs that include cysteinyl leukotriene 1 (CysL T1) receptor antagonists (montelukast, zafirlukast) and 5-lipoxeygenase inhibitor (zileuton) 315. Leukotriene modifiers Mode of administration Oral Using dosage four times a day (Zileuton) Mechanism of action Receptor antagonists block the CysLT1 receptors on airway smooth muscle and thus inhibit the effects of cysteinyl leukotrienes that are release from mast cells and eosinophils 5-lipoxygenase inhibitors block synthesis of leukotrienes. 316. Leukotriene modifiers Role in therapy These agents have a small and variable bronchodilator effect, reduce symptoms, improve lung function, and reduce asthma exacerbations. Effect of these drugs is less than that of low- doses of inhaled glucocorticoids. There is evidence that the use of these drugs as an add-on may reduce the dose of inhaled glucocorticoid required by patients with moderate to severe asthma. Note that leukotriene modifiers are less effective than long- acting inhaled beta-2 agonists as an add-on therapy. 317. Leukotriene modifiers Side effects These drugs are usually well tolerated, and few if any class-related effects have been recognized. Zileuton has been associated with liver toxicity and monitoring liver test is recommended There are several reports of Churg-Strauss syndrome associated with the leukotriene modifier therapy (typically associated with a reduction of systemic glucocorticoids) Contraindication: patients with coronary heart disease, and cardiac arrhythmias. 318. IgE Antibody Omalizumab Used as intravenous or intramuscular anti-asthma. diminishing the production of IgE through effects on interleukin 4 or on IgE itself have been evaluated Soluble recombinant IL-4 receptor that can be delivered by aerosol Recombinant human monoclonal antibody that forms complexes with free IgE (rhuMAb or omalizumab blocks the interaction of IgE with mast cells and basophils. Attenuates the early-phase and late phase airway obstruction response to allergen and suppressed the accumulation of eosinophils in the airways Advantages: - Decreasing the degrees of asthma - Reducing the used of corticosteroid - Repaired nasal symptoms for patients with allergic rhinitis. Disadvantage: very expensive 319. Routes of Administration Inhaled Metered dose inhalers (MDI) Spacers Dry powder inhalers (DPI) Nebulized (wet) aerosols Oral Parenteral Subcutaneous Intramuscular Intravenous 320. Pharmacokinetics of anti-asthma Inhaler Sub-cutane Vena portae Blood flow Urine Membrane mucous Oral Excretion 321. Is there an advantage to using a nebulizer, as opposed to an MDI, for delivery of medications for the treatment of asthma? 322. Studies comparing Nebulizers to MDIs with Spacers Chou KJ, et al. Metered-Dose Inhalers with Spacers vs Nebulizers for Pediatric Asthma. Arch Ped Adol Med 149:201-5,1995. Nebulized beta-agonist therapy had been the standard of care for patients with acute asthma exacerbations. Several studies in adults, however, have found metered dose inhaler (MDI) administration to be as effective. Use of the MDI instead of nebulizer administration would be economically beneficial and easier for both patients and clinicians. 323. (MDI+ spacer) vs Nebulizer 324. Are antihistamines useful in the prophylaxis and/or treatment of asthma? 325. Clin Exp Allergy. 29 Suppl 3:98-104,1999. Effectiveness of H1 antagonists in adults with seasonal asthma 326. Conclusions of Analyses severe persistent asthma no significant clinical effect moderate persistent asthma clinical benefits of H1 antagonists are apparent but require higher-than-usual doses and are not worth the risk to patient mild seasonal asthma and allergic rhinitis coexistant significant improvement in asthma symptoms at usual dosing Clin Exp Allergy. 29 Suppl 3:98-104,1999. 327. Key Points Short-acting beta2-agonists: Therapy of choice for relief of acute symptoms and prevention of EIB. Anticholinergics: May provide some additive benefit to inhaled beta2-agonists in severe exacerbations. May be an alternative for patients who do not tolerate inhaled beta2- agonists. Systemic corticosteroids: Used for moderate- to-severe exacerbations to speed and prevent recurrence of exacerbations. 328. Key Points Corticosteroids: Most potent and effective anti- inflammatory medication currently available Cromolyn sodium and nedrocromil: Mild-to- moderate anti-inflammatory medication. Leukotriene inhibitors: May be considered an alternative therapy to low dose inhaled corticosteroids or cromolyn sodium or nedrocromil for patients >12 years of age with mild persistent asthma. 329. Key Points Long-acting beta2-agonists: These drugs are typically used concurrently with anti- inflammatory medications for long-term control of symptoms, especially nocturnal symptoms. Methylxanthines: Sustained release theophylline is a mild-to-moderate bronchodilator used principally as an adjuvant to inhaled corticosteroids for prevention of nocturnal asthma symptoms. 330. Treatment Protocols 331. Etiology Genetic factors Atopy Environmental factors Viruses Allergens Occupational exposure 332. Factors that Influence Asthma Development and Expression Host Factors Genetic Atopy Airway hyperresponsiveness Gender Obesity Environmental Factors Indoor allergens Outdoor allergens Occupational sensitizers Tobacco smoke Air Pollution Respiratory Infections Diet 333. Factors that Exacerbate Asthma Allergens Respiratory infections Exercise and hyperventilation Weather changes Sulfur dioxide Food, additives, drugs 334. Major Cells Implicated in Inflammatory Response Mast cells an important cell type in the asthmatic lung. These cells produce numerous mediators that contribute to the development of asthma, including: histamine, cysteinyl leukotrienes, tryptase, tumor necrosis factor-alpha, prostaglandin D2, and cytokines including IL4, IL-5 and IL-13 Lymphocytes Eosinophils Neutrophils 335. Inflammatory processes Desquamation of epithelium Mucus plug Basement Membrane thickening Neutrophil and eosinophil infiltrationSmooth muscle Hypertrophy and contraction Oedema Hyperplasia of Mucos glands Barnes PJ 336. Severity Days with Symptoms Nights with Symptoms PEF or FEV1.0 Severe Persistent Continual Frequent 60% Moderate Persistent Daily 5/month > 60% < 80% Mild Persistent 3-6/ week 3-4/month 80% Mild Intermittent 2/week 2/month 80% Classification of Asthma Severity: Clinical Features Before Treatment 337. IgE Antibodies 338. Busse, WW, Lemanske, RF: NEJM 344:350-362, 2001 339. DIAGNOSTIK KELAINAN PARUDIAGNOSTIK KELAINAN PARU DepartemenDepartemen PulmonologiPulmonologi dandan IlmuIlmu KedokteranKedokteran RespirasiRespirasi FakultasFakultas KedokteranKedokteran UniversitasUniversitas Sumatera UtaraSumatera Utara MedanMedan--20112011 Prof.Dr.Tamsil Syafiuddin, SpP(K) Dr.Fajrinur Syarani, SpP(K) 340. Anamnesis Sistem Respiratori: Auto anamnesis Allo anamnesis 341. Tujuan Anamnesis: 1. Kemapuan komunikasi (Satu dari 7 area kompetensi dokter) 2. Penalaran klinis terhadap keterlibatan sistem/organ (Menetapkan sistem/organ/anatomi yang terlibat berdasarkan masalah yang ada) 3. Penalaran klinis terhadap diagnosis banding (Melakukan analisis masalah) 4. Penalaran klinis terhadap pemeriksaan lanjutan (Menetapkan pemeriksaan fisik/pemeriksaan penunjang tertentu yang lebih terarah) 342. Problem Analysis Planning Problem Based Learning 343. Sesak napas 1.Air way sistem: Kelainan obstruktif 2 Problem Based Learning Wheezing ? 344. Sesak napas 1.Air way sistem: Kelainan obstruktif / Asma? 2 Problem Based Learning 1.Wheezing ? 2.Riwayat keluarga? 3.Riwayat obat terdahulu? 345. Sesak napas 1.Air way sistem: Kelainan obstruktif / Asma 2 Problem Based Learning 1. Wheezing ? 2. Riwayat keluarga? 3. Riwayat obat terdahulu? 1 .Pemeriksaan fisik Wheezing ? 2. Spirometri/PFR? 3. Radiologi? 346. Problem/masalah/ keluhan/symptom Analysis problem / Differensial Diagnosis Planning: Pemeriksaan fisik Pemeriksaan penunjang Problem Based Learning 347. Batuk Batuk darah Nyeri dada Sesak napas Problem/masalah/ keluhan/symptom Blok Respiratori Planning: Pemeriksaan fisik Pemeriksaan penunjang Inspeksi Palpasi Perkusi Auskultasi Pemeriksaan radiologik : Foto toraks, CT scan toraks Pemeriksaan sputum Pemeriksaan darah Pulse oxymetry AGDA ( analisis gas darah arteri ) Pemeriksaan faal paru : Spirometri dan APE Tindakan invasif : Bronkoskopi dan Torakoskopi 348. BATUK Batuk suatu ekspirasi paksa yang terkoordinasi, diselingi dengan penutupan glotis secara berulang-ulang. Otot-otot ekspirasi berkontraksi melawan glotis yang tertutup sebagian, sehingga menimbulkan tekanan tinggi di dalam paru-paru. Kalau glotis tiba-tiba membuka, arus udara eksplosif yang membersihkan saluran pernapasan. 349. Klasifikasi batuk berdasarkan : Etiologi Waktu Sputum (dahak) 350. AKUT < 2 3 MINGGU KRONIK > 8 MINGGU FOTO TORAKS FOTO TORAKS NORMAL FOTO TORAKS ABNORMAL ETIOLOGI BATUK Viral respiratory tract infection Bacterial infection Inhaled foreign body Inhalation of irritant dusts/fumes Pneumonia Inhaled foreign body Acute extrinsic allergic alveolitis FOTO TORAKS FOTO TORAKS NORMAL FOTO TORAKS ABNORMAL GORD : gastrointestinal reflux disease Asthma Postviral bronchial hiperactivity Sinusitis Smoking ACE inhibitor Irritant dusts/fumes Lung tumour TB paru ILD Bronkiektasis 351. WAKTU (TIMING) Batuk pada waktu pagi : Bronkitis kronis / PPOK Batuk pada waktu malam : Asma Batuk pada siang hari : Post nasal drip (Sinusitis kronik) dan GORD Batuk kering : pada penggunaan ACE inhibitor Batuk pada ketika setelah meminum air mengarah ke kelainan neuromuskular di orofaring. 352. SPUTUM Warna dan bau: Mucoid sputum ( putih, abu-abu ): Bronkitis kronis / PPOK Kuning : Acute lower respiratory tract infection Hijau : Infeksi kronis pada PPOK atau bronkiektasis Dahak berbau : Mengarah ke infeksi bakteri anaerob: seperti bronkiektasis, abses paru dan empiema. 353. Jumlah dahak Volume banyak : Bronkiektasis Tiba-tiba satu waktu memproduksi sputum purulen dgn volume banyak pada ruptur abses paru atau empiema Penderita dengan tiba-tiba sesak dan batuk dengan volume yang banyak berwarna merah jambu pada edema paru, jika terjadi dalam beberapa minggu (bronchorrhoea) pada alveolar cell cancer. 354. BATUK DARAH ( Hemoptisis ) Hemoptisis Ekspektorasi darah atau dahak yang berdarah, berasal dari saluran napas di bawah pita suara. Etiologi : o Infeksi (bakteri, mikobakteria, jamur, dll) o Neoplasma o Trauma dan benda asing o Kelainan kardiovaskuler 355. ETIOLOGI HEMOPTISIS 1. Tumor : Maligna : Kanker paru Benigna : Tumor karsinoid 2. Infeksi : Bronkiektasis TB paru Abses paru Mycetoma Kistik fibrosis 3. Vaskular : Infark paru , Good pasteurs syndrome 4. Trauma : Aspirasi benda asing, trauma toraks, iatrogenik 5. Cardiac : Penyakit katup mitral, Acute left ventricular failure 6. Hematologi : Antikoagulasi dll. 356. DURASI DAN FREKUENSI HEMOPTISIS Hemoptisis intermittent yang berhubungan dengan infeksi saluran napas yang kronik: pada Bronkiektasis. Hemoptisis dialami setiap hari pada : Kanker paru TB paru Abses paru Hemoptisis akut, jumlah yang banyak disertai nyeri dada dan sesak napas pada: Tromboemboli paru dan Infark paru 357. SESAK NAPAS (PENYEBAB) FISIOLOGIS Olahraga Ketinggian PATOLOGI Paru Jantung Anemia Obesitas PSIKOLOGIS Cemas (hiperventilasi) FARMAKOLOGI Efek obat jantung dan paru menginduksi sesak napas SESAK NAPAS (ONSET) MENIT Tromboemboli paru Pneumotoraks Asma Aspirasi benda asing Acute left ventricular failure JAM - HARI Pneumonia Asma PPOK eksaserbasi MINGGU - BULAN Anemia Efusi pleura Penyakit neuromuskular BULAN - TAHUN PPOK Fibrosis paru TB paru 358. Sakit dada/ chest pain: Struktur: Penyebab : Pleura Pneumothorax Pulmonary infarction Muscle Strain (e.g from coughing) Bone Rib fracture or tumour Nerves Herpes zooster, Pancoasts syndrome Heart and great vessels Cardiac ischemia/infarction, aortic dissection/aneurysm Oesophagus Spasm, reflux 359. PEMERIKSAAN FISIK PARU 360. INSPEKSI SISTEM RESPIRASI SECARA KESELURUHAN Frekuensi pernapasan Pola bernapas Penggunaan otot-otot bantu pernapasan (sternokeidomastoideus, pektoralis) TVJ 361. Inspeksi Palpasi Perkusi Auskultasi Pemeriksaan Fisik Sistem Respiratori 362. VENA CAVA SUPERIOR SYNDROME ( TUMOR PARU ) Terlihat venectasi pada dinding dada 363. 1. R Atrium 2. R Ventricle 3. Apex of L Ventricle 4. Superior Vena Cava 5. Inferior Vena Cava 6. Tricuspid Valve 7. Pulmonary Valve 8. Pulmonary Trunk 9. R PA 10. L PA 364. PALPASI (Kelenjar Leher) Infeksi, metastasis kanker paru 365. PERKUSI DINDING DADA Pneumotoraks, Efusi pleura 366. AUSKULTASI SUARA PERNAPASAN SUARA TAMBAHAN 367. PEMERIKSAAN PENUNJANG Pemeriksaan radiologik : Foto toraks, CT scan toraks Pemeriksaan sputum Pemeriksaan darah Pulse oxymetry AGDA ( analisa gas darah arteri ) Pemeriksaan faal paru : Spirometri dan APE Tindakan invasif : Bronkoskopi dan Torakoskopi 368. Foto toraks Pemeriksaan toraks dengan sinar rontgen Tujuan Mengetahui kelainan di paru Dokumentasi pemeriksaan berkala untuk evaluasi penyakit (perbaikan atau perburukan) Indikasi Semua pasien dengan kelainan di paru Pemeriksaan kesehatan (check up) Akan menjalani tindakan bedah Kontraindikasi : tidak ada 369. CT- Scan toraks Pemeriksaan tomografi dada menggunakan komputer Tujuan : Mengetahui kelainan di rongga dada/mediastinum Indikasi: Massa/dicurigai massa di rongga dada/mediastinum Bronkiektasis Pembedahan toraks Penyakit paru interstitial (ILD) Kontraindikasi: Alergi kontras Pasien tidak bisa tidur terlentang 370. PEMERIKSAAN LABORATORIUM Darah Leukosit Leukositosis : Infeksi Bakteri Leukopeni : Infeksi Virus LED meningkat : Infeksi kronis AGDA Menilai fungsi respirasi Faal Hati Bilirubin,SGOT,SGPT meningkat : Hepatitis Imbas Obat OAT Sputum Infeksi Keganasan 371. Uji Mantoux Uji tuberkulin, menyuntikkan tuberkuloprotein intradermal pada daerah volar lengan bawah Tujuan Mengetahui apakah seseorang pernah terinfeksi oleh kuman TB 372. UJI FAAL PARU SPIROMETRI Spirometri alat untuk mengukur fungsi paru Indikasi Menetapkan kelaianan faal paru obstruktif, restriktif atau mixed Evaluasi respon pengobatan: bronkodilator ataupun steroid Evaluasi dan menilai keparahan faal paru Evaluasi pre operasi Menentukan prognosis penyakit 373. BRONKOSKOPI Tindakan invasive dengan memasukkan alat bronkoskop kedalam percabangan bronkus Indikasi diagnostik bronkoskopi : Batuk darah Batuk yang tidak jelas penyebabnya. Mengi setempat yang dicurigai kemungkinan sumbatan oleh benda asing, gumpalan mukus atau tumor. Kelainan gambaran radiologis, gambaran massa, atelektasis dan corakan difus pada parenkim paru. BRONKOSKOPI RIGIDBRONKOSKOPI FLEKSIBEL 374. Tampakan Bronkoskopi 375. Selamat Belajar 376. Obstructive Sleep Apnea Syndrome (OSAS) Prof.Dr.Tamsil Syafiuddin,SpP(K) Dr.Parluhutan Siagian, SpP Department Pulmonology and Respiratory Medicine, Faculty of Medicine, Universitas Sumatera Utara, Medan-Indonesia 2011 377. Definitions Obstructive Sleep Apnea: Reduction or cessation of airflow due to airway collapse during sleep Causes of OSA include: Excessive tissue in oropharynx (tonsils) Decrease in airway muscle tone Base of tongue impinging on soft palate Not always related to obesity 378. OSA was first described not by a clinical doctor, but by Charles Dickens in 1836. Entitled The Posthumous Papers of the Pickwick Club, Dickens depicted an excessively sleepy, overweight boy named Joe who snored and may have had right-sided heart failure. OSA was thereafter called the Pickwickian syndrome History of OSAS However, OSA was not recognized as a clinical disorder until nearly 100 years later 379. Sleep Disorders Medicine Burwell CS in 1956 brought recognition to Obstructive Sleep Apnea Syndrome, which he termed "Pickwickian syndrome In 1965, Gastaut H documented polysomnographic features of apnea in a group of Pickwickian patients. a great deal of research on how the brain functions and controls vital functions such as respiration during sleep 380. A Brief History Of Sleep Medicine 381. 2. In 1996, the American Medical Association recognized sleep medicine as a specialty Overview - The Pursuit of Sleep 1.There are few, if any, medical specialties that do not intersect with the past, present, and future understanding and study of sleep 3. The advances in medicine over time have contributed significantly to the understanding of sleep and sleep research 382. 4. Neurology, psychology, psychiatry, physiology, cardiology, pulmonology, otolaryngology, dentistry, and the list goes on - they are all integral areas of study in the pursuit of sleep 5. Sleep medicine is truly a multidisciplinary science Overview - The Pursuit of Sleep 383. The Last Half of the 20th Century and Beyond Sleep research grew by leaps and bounds in the latter half of the 20th century. Data in chrono-biology, neurochemistry, electrophysiology, neurophysiology, as well as in sleep disorders medicine and pharmacology, all contributed to the understanding of sleep and sleep-related problems Kleitman N- Aserinsky E in 1953, reported periods of eye movements and twitching during sleep, which they called Rapid Eye Movement (REM) sleep 384. Kleitman N - Dement expanded these findings in 1957- 58 using the EEG to record the cyclic pattern of REM and non-REM sleep in humans Tracheostomy, although in use since the first century, was applied to sleep apnea by Wolfgang Kuhlo and Erich Doll in 1972 Uvulopalatopharyngoplasty (UPPP) was an accepted treatment for snoring by 1964, by Tanenosuke Ikematsu and to OSA by Shiro Fujita in 1981 Nasal Continuous Positive Airway Pressure (CPAP) use by 1981, Colin Sullivan described it as a non- surgical option for the treatment of OSA 385. The First Half of the 20th Century Sleep research in the early 1900s was greatly influenced by new diagnostic instruments, surgical options, and clinical procedures The vascular theories were quickly losing popularity for the explanation of sleep Theories that lacked a solid fondation were challenged and rejected The scientific method, reproducible experiments, and defining studies were becoming the standard 386. Electrophysiology Electroencephalogram (EEG), it was determined that the brain is not inhibited during sleep, but is, in fact, very active, particularly in REM sleep In 1929, Berger J, demonstrated differences in brain activity between wakefulness and sleep by recording electrical impulses Loomis A, Harvey AN and Hobart G in 1937, classified sleep into five different stages, A through E 387. Neurophysiology In the 1920s, Nathaniel Kleitman, Father of American Sleep Research Began his research on the regulation of sleep and wakefulness His later research focused on how sleep and wakefulness relate to circadian rhythms and the effects of sleep deprivation 388. Why OSAS is Important ? 389. Obstructive sleep apnea syndrome (OSAS) Has been increasingly recognized as a cause of associated disease 390. OSAS is described as a potentially lethal disease because it leads to hypoxia and hypoxemia. Altered quality of life Daytime sleepiness Neuropsychological dysfunction and cognitive deficits have been associated with OSAS As well as cardiovascular disease, including systemic and pulmonary hypertension Arrhythmias and ischemic heart disease 391. The brain is very sensitive to hypoxia, recurrent decrease of the arterial oxygen saturation (SaO2) in sleep apnea leads to brain injury. Cerebrovascular accidents, ranging from transient ischemic attacks to fatal strokes, are closely associated with sleep apnea 392. Consequences of OSA At risk for Hypertension Cardiac arrhythmias Ischemic heart disease Stroke Daytime somnolence; fatigue Lost productivity Disruptions to family and social activities Automobile accidents 393. Diagnosis of OSA 394. Symptoms of OSA Chronic, load snoring Gasping or choking episodes during sleep Excessive daytime sleepiness Fatigue-related Accidents Cognitive difficulties Personality changes 395. Signs of OSA Obesity, particularly upper body 120 % ideal body weight Large neck girth 17 inches in males; 16 inches in females Systemic hypertension Nasopharyngeal narrowing Unexplained cor-pulmonale or pulmonary hypertension 396. Saluran pernafasan yang normal. Ukuran soft palate dan uvula normal. Saluran nafas atas dari nasofaring, orofaring dan hypofaring ukurannya normal Saluran pernafasan yang tidak normal selama tidur . Banyak tempat terjadi obstruksi pada penderita OSA. Pembesaran soft palate menempati posterior di nasofaring dan oral faring. 397. Pembesaran uvula pada lidah (panah besar) dengan hipertrofi tonsil (panah kecil). Eritema pada faring terjadi trauma dari mendengkur Soft palate memanjang (panah) 398. Diagnosing OSA Polysomnogram (sleep study) At least 6 hours duration Staging of sleep (EEG) Airflow and ventilatory ef