Tujuan dari Respirasi

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Tujuan dari Respirasi
adalah untuk menyediakan oksigen bagi seluruh
jaringan tubuh dan membuang karbon dioksida ke
atmosfer
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Hidung

• Udara masuk disaring, dihangatkan dan
  dilembabkan oleh mukosa respirasi.
• Partikel kasar disaring oleh rambut hidung.
• halus terjerat dalam lapisan mukus.
• Udara masuk faring bebas debu, suhu sebanding
  suhu tubuh, kelembaban hampir 100

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Rongga torax

• Paru adalah organ elastis terletak pada rongga
  dada/torax.
• Paru dilapisi oleh lapisan tipis kontinu yg
  mengandung kolagen jar elastis yg disebut
  PLEURA
• Pleura Parietalis melapisi rongga dada sedang
  Pleura viseralis melapisi paru .
• Rongga pleura ruangan yg memisahkan pleura
  parietalis viseralis
• Cairan pleura lapisan tipis antara pleura
  parietalis dg viseralis berfungsi memudahkan
  kedua permukaan tersebut bergerak selama
  pernapasan untuk mencegah pemisahan torax
  paru.
• Tekanan rongga pleura lt tekanan atmosfer untuk
  mencegah kolaps paru.

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Rongga torax

• 3 faktor yg mempertahankan tekanan negatif
  intrapleura normal
• Jaringan elastis paru memberikan kekuatan kontinu
  yg cenderung menarik paru menjauh dr rangka
  torax.
• Kekuatan osmotik yg terdapat di seluruh membran
  pleura.
• Kekuatan pompa limfatik.
• Diafragma otot berbentuk kubah yg membentuk
  dasar rongga torax memisahkan rongga tersebut
  dari rongga abdomen.

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Anatomi Saluran Pernapasan
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Anatomi Saluran Pernapasan
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Alveoli

• Terdapat 2 tipe sel alveolar
• Pneumosit tipe I lap tipis menyebar menutupi gt
  90 daerah permukaan.
• Pneumosit tipe II tanggung jawab pada sekresi
  surfaktan.
• Alveolus suatu gelembung gas yang dikelilingi
  oleh jaringan kapiler batas antara cairan
  gas membentuk tegangan muka yang cenderung
  mencegah pengembangan saat inspirasi cenderung
  kolaps saat ekspirasi.
• Alveolus dilapisi zat lipoprotein (surfaktan)
  dapat mengurangi tengangan permukaan resistensi
  saat inspirasi mencegah kolaps alveolus
  (expirasi).

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LUNGS 2
Bronchopulmonary segments Lobules Alveolar wall
cell types
respiratory bronchiole
terminal bronchiole
pulmonary artery branch
alveolar sac
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Alveoli

• Pembentukan pengeluaran surfaktan oleh
  pneumosit tipe II disintesis secara cepat dari
  asam lemak yang diekstraksi dari darah, dg
  kecepatan pergantian yg cepat. Bila aliran darah
  ke paru terganggu (emboli) akibatnya jumlah
  surfaktan pada daerah tersebut berkurang.
• Produksi surfaktan dirangsang oleh ventilasi
  aktif, volume tidal yg memadai, hiperventilasi
  periodik (cepat dalam) yg dicegah oleh kons O2
  yang tinggi (inspirasi).
• Pemberian O2 kons tinggi jangka lama (pasien dg
  ventilasi mekanik) menurunkan produksi
  surfaktan menyebabkan kolaps alveolar.

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Pernafasan terdiri dari 4 proses

• Ventilasi Keluar masuknya udara karena adanya
  selisih tekanan yang terdapat antara atmosfer dan
  alveolus
• Distribusi Pembagian udara ke cabang -cabang
  bronkhus
• Transportasi dan Difusi
• - Transport O2 dan CO2 dalam darah dan cairan
  tubuh ke dan dari sel
• - Difusi O2 dan CO2 antara darah dan
  alveoliPertukaran gas-gas antara alveoli dan
  kapiler dipengaruhi oleh tekanan parsial O2 CO2
  dalam atmosfer
• Perfusi Aliran darah yang membawa O2 ke jaringan

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JENIS RESPIRASI

• RESPIRASI EXTERNAL
• O2 DIBAWA DARI UDARA LUAR SAMPAI KE KAPILER
• 2. RESPIRASI INTERNAL
• O2 DARI KAPILER SAMPAI KE SEL PADA JARINGAN.

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RESPIRASI EXTERNAL
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RESPIRASI INTERNAL
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INSPIRATION
Active process Boyles Law
Phrenic nerves (C3-5) Thoracic nerves (T1 T11)
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EXPIRATION
Passive process at rest
elastic recoil surface tension
internal intercostals (11 pairs)
external abdominal oblique
internal abdominal oblique
transversus abdominis
rectus abdominis
760 mmHg
762 mmHg
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Perubahan diafragma saat inspirasi ekspirasi
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Otot Pernapasan
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COMPLIANCE
Compliance is the ease with which the lungs and
thoracic wall can be expanded during inspiration.
Related to two factors
elasticity surface tension
Compliance is decreased with any condition that
destroys lung tissue (emphysema) fills lungs with
fluid (pneumonia) produces surfactant deficiency
(premature birth, near-drowning) interferes with
lung expansion (pneumothorax)
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PULMONARY VOLUMES, CAPACITIES, AND RATES
maximum inspiration
6000 ml
5000 ml
IRV
VC
TLC
4000 ml
3000 ml
TV
2000 ml
ERV
1000 ml
RV
maximum expiration
SPIROGRAM
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Kontrol Pernapasan

• Otot pernapasan diatur oleh neuron reseptor
  pada pons medula oblongata.
• Faktor utama pengaturan pernapasan respon dari
  pusat kemoreseptor dalam pusat pernapasan
  terhadap tekanan persial CO2 dan pH darah arteri

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Kontrol Pernapasan

• Persarafan parasimpatis/ kolinergik (mll nervus
  fagus) menyebabkan kontraksi otot polos bronkus
  shg menyebabkan bronkokonstriksi peningkatan
  sekresi kel mukosa sel goblet.
• Rangsangan simpatis ditimbulkan epinefrin mll
  reseptor adrenergik-beta2 menyebabkan relaksasi
  otot polos bronkus, bronkodilatasi,
  berkurangnya sekresi bronkus.
• Sistem saraf nonkolinergik non adrenergik (NANC)
  melibatkan berbagai mediator seperti ATP, oksida
  nitrat, substance P, dan VIP (vasoactive
  intestinal peptide) respon penghambatan, meliputi
  bronkodilatasi, dan diduga berfungsi sebagai
  penyeimbang terhadap fungsi pemicuan oleh sistem
  kolinergik.

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Kontrol Pernapasan
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Signs and Symptoms of Pulmonary Disease

• Dyspnea subjective sensation of uncomfortable
  breathing, feeling short of breath
• Ranges from mild discomfort after exertion to
  extreme difficulty breathing at rest.
• Usually caused by diffuse and extensive rather
  than focal pulmonary disease.

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Derajat Dyspnea
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Dyspnea cont.

• Due to
• Airway obstruction
• Greater force needed to provide adequate
  ventilation
• Wheezing sound due to air being forced through
  airways narrowed due to constriction or fluid
  accumulation
• Decreased compliance of lung tissue

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Signs of dyspnea

• Flaring nostrils
• Use of accessory muscles in breathing
• Retraction (pulling back) of intercostal spaces

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BATUK

• Batuk merupakan gejala tersering penyakit
  pernapasan
• Batuk merupakan reflex pertahanan yang timbul
  akibat iritasi percabangan trakeobronkial
• Batuk yang berlangsung lebih dari 3 minggu harus
  diselidiki untuk memastikan penyebabnya.
• Bronkhitis kronik, asma, tubercolosis dan
  pneomonia merupakan penyakit yang secara tipikal
  memiliki batuk sebagai gejala yang mencolok

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Cough may result from

• Inflammation of lung tissue
• Increased secretion in response to mucosal
  irritation
• Inhalation of irritants
• Intrinsic source of mucosal disruption such as
  tumor invasion of bronchial wall
• Excessive blood hydrostatic pressure in pulmonary
  capillaries
• Pulmonary edema excess fluid passes into airways

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• When cough can raise fluid into pharynx, the
  cough is described as a productive cough, and the
  fluid is sputum.
• Production of bloody sputum is called hemoptysis
• Usually involves only a small amount of blood
  loss
• Not threatening, but can indicate a serious
  pulmonary disease
• Tuberculosis, lung abscess, cancer, pulmonary
  infarction.

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• Cough that does not produce sputum is called a
  dry, nonproductive or hacking cough.
• Acute cough is one that resolves in 2-3 weeks
  from onset of illness or treatment of underlying
  condition.
• Us. caused by URT infections, allergic rhinitis,
  acute bronchitis, pneumonia, congestive heart
  failure, pulmonary embolus, or aspiration.

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• A chronic cough is one that persists for more
  than 3 weeks.
• In nonsmokers, almost always due to postnasal
  drainage syndrome, asthma, or gastroesophageal
  reflux disease
• In smokers, chronic bronchitis is the most common
  cause, although lung cancer should be considered.

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SPUTUM

• Pembentukan sputum
• Orang dewasa normal mukus sekitar 100 ml
  dalam saluran napas tiap hari Mukus diangkut
  menuju faring dengan gerakan pembersihan silia
  yang melapisi saluran pernapasan bila mukus
  berlebihan proses pembersihan tidak efektif
  
• mukus tertimbun membran mukosa akan terangsang
  mukus dibatukkan keluar sebagai sputum.

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SPUTUM

• Sputum yang berwarna kekuning-kuningan
  menunjukkan infeksi.
• Sputum yang berwarna hijau merupakan petunjuk
  penimbunan nanah timbul karena adanya
  verdoperoksidase yang dihasilkan oleh
  polimorfonuklear (PMN).
• Sputum yang berwarna merah muda dan berbusa
  merupakan tanda edema paru akut.
• Sputum yang berlendir lekat dan warna abu-abu
  atau putih merupakan tanda bronkhitis kronik.
  Sedangkan sputum yang berbau busuk merupakan
  tanda abses paru atau bronkiektasis.

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Cyanosis

• When blood contains a large amount of
  unoxygenated hemoglobin, it has a dark red-blue
  color which gives skin a characteristic bluish
  appearance.
• Most cases arise as a result of peripheral
  vasoconstriction result is reduced blood flow,
  which allows hemoglobin to give up more of its
  oxygen to tissues- peripheral cyanosis.
• Best seen in nail beds
• Due to cold environment, anxiety, etc.

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• Central cyanosis can be due to
• Abnormalities of the respiratory membrane
• Mismatch between air flow and blood flow
• Expressed as a ratio of change in ventilation (V)
  to perfusion (Q) V/Q ratio
• Pulmonary thromboembolus - reduced blood flow
• Airway obstruction reduced ventilation
• In persons with dark skin can be seen in the
  whites of the eyes and mucous membranes.

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Jari Tabuh

• Jari tabuh adalah perubahan bentuk normal falang
  distal dan kuku tangan dan kaki serta ditandai
  dengan
• Kehilangan sudut kuku yang normalnya 160 derajat.
  
• Rasa halus berongga pada dasar kuku.
• Ujung jari menjadi besar.
• jari tabuh berhubungan dengan peyakit paru (TB,
  abses paru, atau kanker paru). Penyakit
  kardiovaskuler (tetralogi fallot atau
  endokarditis infektif) atau penyakit hati kronik

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Next

• 2. Hipoksia (O2 yang tidak adekuat dalam tingkat
  jaringan) dan Hipoksemia (PaO2 dibawah normal
  normal 80-100 mmhg).
• Tanda dan gejala hipoksemia dan hipoksia tidak
  spesifik dan mencakup takipnea, dispnea, sakit
  kepala, pikiran yang bingung, takikardi, dan
  sianosis.
• 3. Hipokapnia dan hiperkapnia
• Hipokapnia didefinisikan sebagai menurunnya
  PaCO2 lt35 mmhg. Penyebab langsung selalu
  hiperventilasi alveolar (eliminasi CO2 lebih
  cepat daripada produksinya).
• Hiperkapnia / asidosis respiratorius merupakan
  meningkatnya PaCO2 gt45 mmhg. Penyebab langsung
  adalah selalu hipoventilasi alveolar (kegagalan
  dalam mengeliminasi CO2 secepat produksinya).

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Pain

• Originates in pleurae, airways or chest wall
• Inflammation of the parietal pleura causes sharp
  or stabbing pain when pleura stretches during
  inspiration
• Usually localized to an area of the chest wall,
  where a pleural friction rub can be heard
• Laughing or coughing makes pain worse
• Common with pulmonary infarction due to embolism

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• Inflammation of trachea or bronchi produce a
  central chest pain that is pronounced after
  coughing
• Must be differentiated from cardiac pain
• High blood pressure in the pulmonary circulation
  can cause pain during exercise that often
  mistaken for cardiac pain (angina pectoris)

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Respiratory Disorders

• Respiratory disorder can be classified into
  different group
• Respiratory tract infection
• Common cold,Influenza,Pneumonias,T.B
• Disorder of lung inflation
• Pleural pain and pleural effusion
• Obstructive air way disorders
• Bronchial asthma, COPD, Emphysema, Bronchitis
• Pulmonary vascular disorder
• Lung cancer

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INFLUENZA

• Penyakit yang disebabkan oleh virus influenza.
  Gejala yang ditimbulkan antara lain pilek,
• hidung tersumbat, bersin- bersin, dan tenggorokan
  terasa gatal. Perlu diketahui virus iniselalu
  hanya bisa menembus saluran pernafasan atas saja
  , sehingga bisa disimpulkansaluran respirasi
  yang lebih dalam sangat resisten immun terhadap
  virus ini.

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Asthma

• is a chronic inflammatory disorder of the airways
  in which many cells and cellular elements play a
  role
• In susceptible individuals, this inflammation
  causes recurrent episodes of wheezing,
  breathlessness, chest tightness and coughing,
  particularly at night or in the early morning..

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• Causes and Triggers
• Allergies such as to pollens, mold spores, pet
  dander, and dust mites
• Infections (colds, viruses, flu, sinus infection)
  
• Exercise
• Aspirin or nonsteroidal anti-inflammatory drug
  (NSAID) hypersensitivity, sulfite sensitivity
• Use of beta-adrenergic receptor blockers
  (including ophthalmic preparations)

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Cont

• Irritants such as strong odors from perfumes or
  cleaning solutions, air pollution, and tobacco
  smoke
• Weather (changes in temperature and/or humidity,
  cold air)
• Strong emotions such as anxiety, laughter,
  crying, and stress
• Industrial triggers (wood, grain dust, cotton
  dust, isocyanate containing paints, aluminum,
  hair spray, penicillins)
• Beta blockers even in form of eye drops

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Comorbid condition

• Gastroesophageal reflux disease
• Chronic sinusitis or rhinitis
• OSA (obstructive sleep apnoe)
• Obesity
• Alergy bronchopulmonary aspergilosis

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ASMA

• Asma ekstrinsik (alergik)
• (alergen, spt debu,blu halus, serbuk)
• intrinsik (idiopatik)
• (fak nonspesifik spt flu, latihan fisik,
  emosi dapat memicu serangan asma)
• campuran
• (Komponen asma instrinsikEkstrinsik)

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Two main pathophysiologic types of asthma
Extrinsic asthma common in children, associated
with a genetic predisposition and is precipitated
by a known allergens. It is related to the
formation of antibody IgE in the body
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Immunological Mechanisms in Respiratory Diseases
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Patofisiologi Asma
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• Intrinsic asthma tend to develop in adulthood,
  and symptoms are triggered by non-allergic
  factors such as
• Viral infection, irritants which cause epithelial
  damage and mucosal inflammation
• Emotional upset which mediates excess
  parasympathetic input
• Exercise which causes water ad heat loss from the
  airways

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• Pathophysiology
• Release of inflammatory mediator produce
  bronchial smooth muscle spasm
• Vascular congestion
• Increase vascular permeability
• Edema formation
• Production of thick tenacious mucus
• Impair mucociliary function
• Thickening of air way wall
• Increase response of bronchial smooth muscle
• Damage epithelium produce hyper responsiveness
  and obstruction

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Faktor2 yang mengakibatkan obstruksi ekspirasi
pada asma bronkial. A. Potongan melintang dari
bronkiolus yang mengalami oklusi akibat spasme
otot, mukosa yang membengkak, dan mukus dalam
lumen, B . Potongan memanjang dari bronkiolus
gambar
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The mechanism of inflammation in asthma can
be Acute early recruitment of cells to the
airways Subacute resident and recruited cells
are activated to cause a more persistent pattern
of inflammation Chronic cells damage is
persistent and subject to ongoing repair,
permanent change in the airway may occur with
airway remodelling
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Gambaran klinik

• Batuk yang memburuk pada malam hari
• Sesak nafas
• Mengi atau Wheezing (a high-pitched whistling
  sound that occurs when exhaling) due to turbulent
  airflow through a narrowed airway
• nafas pendek tersengal-sengal.
• Produksi sputum meningkat, sulit tidur
• Hambatan pernafasanan reversibel
• Adanya peningkatan gejala pada saat olahraga,
  infeksi virus, eksposur terhadap alergen dan
  perubahan musim.
• Terbangun di malam hari krn gejala seperti di
  atas .

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Investigations

• Pulmonary function testing (spirometry) Forced
  expiratory volume (FEV)
• Methacholine or histamine challenge testing
• Exercise testing
• Peak expiratory flow rate monitoring

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Forced expiratory volume (FEV)
Normal subject
Volume (litres)
Asthma patient
FVC
FEV1
1
2
3
4
Time (second)
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Impairment
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Drug categories
Bronchodilators Provide symptomatic relief of
bronchospasm due to acute asthma exacerbation
(short-acting agents) or long-term control of
symptoms (long-acting agents)
Leukotriene receptor antagonists Direct
antagonist of mediators responsible for airway
inflammation in asthma
Corticosteroids Highly potent agents that are
the primary choice for treatment of chronic
asthma and prevention of acute asthma
exacerbations. Numerous inhaled corticosteroids
are used for asthma and include beclomethasone
(Beclovent, Vanceril), budesonide (Pulmicort
Turbuhaler), flunisolide (AeroBid), fluticasone
(Flovent), and triamcinolone (Azmacort).
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Mast cell stabilizers Prevent the release of
mediators from mast cells, which results in
airway inflammation and bronchospasm. Indicated
for maintenance therapy of mild-to-moderate
asthma or prophylaxis for EIA
5-Lipoxygenase inhibitors Inhibit the
formation of leukotrienes. Leukotrienes activate
receptors that may be responsible for events
leading to the pathophysiology of asthma,
including airway edema, smooth muscle
constriction, and altered cellular activity
associated with inflammatory reactions
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Three Steps of Asthma Treatment Step 1 -
Control bronchospasm with short- acting b2
agonists or long-acting salmeterol Step 2 -
Control inflammation with inhaled corticosteroids
or leukotriene antagonist Step 3 - Control
severe exacerbation with oral corticosteroids
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Step 1 Is to control bronchospasm with inhaled
b2 agonists. Short-acting b2agonists are
appropriate for patients with mild, intermittent
asthma who do not require daily maintenance
therapy. Inhaled b2 agonists are effective, work
quickly within 2 to 3 minutes and provide acute
relief for up to 4 to 6 hours Remember that
short-acting b2 agonists are indicated for use as
rescue bronchodilators during acute attacks of
bronchospasm.
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When daily maintenance therapy is needed for more
persistent symptoms, the long-acting b2 agonist
salmeterol is an excellent and effective choice
in treatment Salmeterol can be taken once or
twice a day as an inhaled bronchodilator The
bronchodilating action of salmeterol is delayed
in onset (20-30 minutes) but frequently lasts 8
to 12 hours when taken properly.
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Step 2 Is to control inflammation when there is
evidence of persistent or frequently recurring
symptoms with inhaled corticosteroids or
leukotriene antagonists, or the non-steroidal
anti-inflammatory agents cromolyn sodium or
nedocromil sodium This is maintenance
anti-inflammatory therapy without any direct
bronchodilator effect.
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Inhaled corticosteroids and oral corticosteroids
are used to control inflammation in asthma
Corticosteroids prevent the migration of
inflammatory cells and increase the
responsiveness of airway b2 receptors Corticostero
ids have been shown to reduce acute bronchial
hyperresponsiveness to irritants and may
chronically blunt the early airway response to
irritants with continued use The new inhaled
corticosteroid, fluticasone propionate, appears
to possess a higher potency than other inhaled
corticosteroids. Like other inhaled
corticosteroids, fluticasone is indicated for the
maintenance treatment of asthma as prophylactic
therapy Recent studies have shown that it can
reduce oral prednisone use while improving asthma
control.
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Inhaled nonsteroidal anti-inflammatory drugs like
cromolyn or nedocromil may reduce symptoms in
patients with mild to moderate asthma They are
frequently prescribed in children and in adults
with allergic asthma They inhibit the activation
of mast cells and eosinophils, block inhaled
neurogenic stimuli, and may reduce airway
temperature changes that can trigger an asthma
attack Nedocromil may allow the reduction of
corticosteroid use in selected patients
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Step 3 Is to control severe exacerbations with
systemic oral corticosteroids, i.e. prednisone 1
mg/kg or 40 to 60 mg daily for 1 to 2 weeks Many
patients are steroid-dependent and frequently
develop cushingnoid features such as
hyperglycemia, fluid retention, weight gain with
moon facies, and easy bruisability
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Anticholingeric drugs like ipratropium may have
an adjunctive role in asthma therapy They block
vagal pathways and produce bronchodilation by
decreasing airway vagal tone They are less potent
than b2 agonists and have a slow onset of
action While they may reduce mucus secretion,
there is no evidence that they modulate the
inflammatory response
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Oral theophylline and intravenous aminophylline
were once the mainstay of asthma treatment,
especially nocturnal asthma Originally thought to
act as a phosphodiesterase inhibitor to increase
cAMP, these methylxanthines are now though to
antagonize adenosine, a mediator of acute
inflammation Theophyllines reverse bronchospasm,
enhance mucociliary clearance, and increase
diaphragmatic contraction
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However, theophylline is probably useful as an
adjunct to b2 agonists and anti-inflammatory
drugs Any benefit may be diminished somewhat by a
narrow therapeutic range (5 to 15 µg/ml) which
can lead to serious and toxic consequences, e. g.
seizures, tachyarrhythmias when exceeded Its use
in the emergency treatment of asthma is not
recommended but recent evidence suggest it may
modulate chronic asthma symptoms more effectively
than is generally perceived.
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The use of cytotoxic agents, e. g. methotrexate,
cyclosporine can not be recommended unless
standard therapy with b2 agonists and
anti-inflammatory drugs have failed
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leukotriene receptor antagonists, Specifically,
LTD4 receptor antagonist and 5-lipoxygenase
inhibitors can completely block the acute phase
response and block part of the delayed phase
response Blocking the generation of leukotrienes
or blocking their actions on cells may be helpful
in control of asthma and treatment of asthma
attacks
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DEFINISI PPOM/COPD

• Penyakit obstruksi saluran nafas kronis dan
  progresif yg ditandai oleh hambatan aliran udara
  yg bersifat non reversibel atau reversibel
  sebagian bersifat progresif berhubungan dg
  respons inflamasi abnormal paru thd partikel atau
  gas beracun.

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Bronkitis kronik emfisema

• Meskipun bronkitis kronik dan emfisema merupakan
  2 proses yg berbeda, tp penyakit ini sering
  ditemukan bersama2 pada penderita COPD.
• Merupakan penyebab kematian terbanyak
• COPD mnyerang pria 2x lebih banyak dari wanita
  karena faktor perokok
• Faktor etiologi utama adalah merokok dan polusi
  udara

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FAKTOR RISIKO

• Host

• Lingkungan

• - Genetik Defisiensi alpha 1 anti tripsin atau
  antiprotease (menghambat aksi dari enzym
  protease)
• - Hipereaktivitas bronkus

• Asap rokok (faktor risiko utama - sigaret)
• Partikel debu bahan kimia perindustrian
• Polusi udara
• Indoor air pollution from heating and cooking
  with biomass in poorly ventilated dwellings
• Infeksi
• Status sosial

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PATOGENESA

• Inflamasi /Keradangan kronis pd sal. napas,
  parenkim paru, sistem vaskuler paru ? pe?
  makrofag, limfosit T (CD8), netrofil ? release
  mediator LB4, IL8, TNF
• Imbalance proteinase anti proteinase
• Stres oksidatif
• Ketiga faktor diatas akan merusak struktur paru.

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The theory of interplay

• is that this inflammatory process which includes
  alveolar macrophages in some way releases
  neutrophil chemotactic factors known as (IL-8 )
  causing neutrophils to emigrate from the blood
  space into the airspace to release elastase .
• In normal circumstances alpha-1-antitrypsin
  binds to the elastase and prevents it from
  binding to elastin thus destroying the structure
  of the lungs.

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Neutrophils

• in the blood and air space release more active
  oxygen species in smokers, than in non smokers,
  these together with the 1017 oxidants in inhaled
  cigarette smoke inactivate the alpha-1-antitrypsin
  at its active site.
• This reduces the ability of alpha-1-antitrypsin
  to bind to elastase by a factor of approximately
  2000 allowing active ealstase to bind to elastin
  and cause the enlargement of the airspace that is
  seen in emphysema P-Selectin , L-seletin
  adhesions are important for the transport of
  inflammatory cells in the systemic circulation .

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KLINIS

• Keluhan utama sesak napas, batuk, dahak
• Sesak timbul progresif sp mengganggu aktivitas,
• men-dadak memberat bila tjd eksaserbasi
• Batuk kronis, memberat pagi hari, dahak mukoid ?
• purulen bila eksaserbasi
• Suara mengi (wheezing)
• Batuk darah ? blood-streaked purulen sputum
  (eksa-serbasi)
• Nyeri dada (pleuritis, pneumotoraks, emboli
  paru)
• Anoreksi BB menurun progresif jelek

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PATOLOGI

• Saluran napas besar
• Hipertrofi kelenjar pe ? jumlah sel Goblet ?
  hipersekresi mukus
• Saluran napas kecil
• Recycled injury repair dinding sal. napas ?
  remodeling (pe ? kolagen jar. ikat) ?
  penyempitan lumen obstruksi sal. napas
• Parenkim paru
• Destruksi parenkim ? emfisema sentrilobuler
  Vaskuler pulmonal, Penebalan dd pembuluh darah

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Pathophysiology

• The different pathogenic mechanisms produce the
  pathological changes which, in turn, give rise to
  the physiological abnormalities in COPD
• mucous hypersecretion and ciliary dysfunction,
• airflow limitation and hyperinflation,
• gas exchange abnormalities,
• pulmonary hypertension,
• systemic effects.

90
Pathophysiology of COPD
91
According to GINA

• What is the difference between asthma and COPD
  (chronic obstructive lung disease)? COPD is a
  collective name for chronic bronchitis and
  emphysema, two diseases that are almost always
  caused by smoking. Many of the symptoms of COPD
  are similar to those of asthma (e.g.
  breathlessness, wheezing, production of too much
  mucus, coughing).

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COPD/PPOM
94
BRONCHITIS KRONIS atau COPD type B

• Bronkitis kronik adalah inflamasi kronis
  saluran nafas yg ditandai dg udema dan
  hiperplasi kelenjar sub mucosal shg terjadi
  produksi mukus berlebihan ke batang bronchial
  akibatnya terjadi peningkatan resistensi sal
  pernafasaan
• secara kronik atau berulang dengan disertai
  batuk, yang terjadi hampir setiap hari selama
  sekurangnya tiga bulan dalam 1 tahun selama 2
  tahun berturut turut. .

95
Etiologi

• Faktor lingkungan
• - Merokok
• - Pekerjaan
• - Polusi udara
• Infeksi berulang
• Faktor host
• - usia
• - jenis kelamin
• - penyakit paru yang
• sudah ada

96
CHRONIC BRONCHITIS

• Chronic bronchitis is defined as "persistent
  cough with sputum production for at least 3
  months in at least two consecutive years".
• The most important cause of chronic bronchitis is
  recurrent irritation of the bronchial mucosa by
  inhaled substances, as occurs in cigarette
  smokers.
• The pathological hallmarks of chronic bronchitis
  are congestion of the bronchial mucosa and a
  prominent increase in the number and size of the
  bronchial mucus glands. Copious mucus may be seen
  within airway lumens. The terminal airways are
  most susceptible to obstruction by mucus.

97
Pathophysiology of chronic bronchitis
Irritants ? Hyperplasia and
hypertrophy of mucous secreting cell
? Thick mucous
?
Air trapping
Sticky coating
? ?

Air way obstruction Impaired ciliary function
?
?
Edema Decrease
mucous clearance
? ?
Bronchial wall
thickness and Lung defense system compromise
inflammation
?
? Vulnerable for infection
? More infection more mucus
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CHANGES IN LUNG VOLUMES
100
VENTILATION COST

• In COPD work of breathing is greater for any
  given level of ventilation than normal.

SEVERE COPD
The cost of work at a given ventilation for
normal and COPD patients (ACSM, 1998)
WORK OF BREATHING
MODERATE COPD
NORMAL COPD
VENTILATION
101

• Damage to the epithelium impairs the mucociliary
  response that clears bacteria and mucus.
  Inflammation and secretions provide the
  obstructive component of chronic bronchitis.
• In contrast to emphysema, chronic bronchitis is
  associated with a relatively undamaged pulmonary
  capillary bed.

102
Emphysema or type A COPD

• Definition
• Abnormal permanent enlargement of air spaces
  distal to the terminal bronchioles, accompanied
  by the destruction of the walls and without
  obvious fibrosis
• Emphysema is characterized by loss of elasticity
  of the lung and abnormal permanent enlargement of
  air spaces with destruction of the alveolar walls
  and capillary beds.

103
EtiologiEmphysema

• Smoking
• the primary risk factor
• Long-term smoking is responsible for 80-90 of
  cases.
• Prolonged exposures to harmful particles and
  gases from
• passive smoke,
• Industrial smoke,
• Chemical gases, vapors, mists fumes
• Dusts from grains, minerals other materials
• Alpha 1-antitrypsin deficiency gtgtemphysema
• Genetics
• Bronchitis
• Asthma

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Pathophysiology

• Exposure to inhaled noxious particles gases
  inflammation imbalance of
  proteinases and anti-proteinases

Dilatation destruction mucus secretion
105
FIG. 1. Inflammatory mechanisms in COPD.
Cigarette smoke (and other irritants) activate
macrophages in the respiratory tract that release
neutrophil chemotactic factors, including IL-8
and LTB4. These cells then release proteases that
break down connective tissue in the lung
parenchyma, resulting in emphysema, and also
stimulate mucus hypersecretion. These enzymes are
normally counteracted by protease inhibitors,
including 1-antitrypsin, SLPI, and TIMP.
Cytotoxic T cells (CD8) may also be recruited and
may be involved in alveolar wall destruction.
Fibroblasts may be activated by growth factors
releases from macrophages and epithelial cells.
CTG, connective tissue growth factor COB,
chronic obstructive bronchiolitis.
106
Pathophysiology

• Affects alveolar membrane
• Destruction of alveolar wall
• Loss of elastic recoil
• Over distended alveoli
• Over distended alveoli?
• Damage to adjacent pulmonary capillaries
• h dead space
• Impaired passive expiration
• ? Impaired gas exchange

• Impaired gas exchange
• impaired expiration
• h CO2 ?
• Hypercapnia
• Respiratory acidosis
• Damaged pulmonary capillary bed
• h pulmonary pressure ?
• h work load for right ventricle ?
• Right side heart failure (due to respiratory
  pressure) ?
• Cor Pulmonale

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Gas Exchange is poor because

• Loss of alveolar structure base thereby causing
  decreased gas exchange surface area
• Mechanically, elastance is lost due to the
  constant stretching of distal airways
• Consequently, these patients are very compliant,
  because the natural tendency for the lung to
  collapse is inadvertently lost

108

• This V/Q mismatch results in relatively limited
  blood flow through a fairly well oxygenated lung
  with normal blood gases and pressures in the
  lung, in contrast to the situation in blue
  bloaters. Because of low cardiac output, however,
  the rest of the body suffers from tissue hypoxia
  and pulmonary cachexia. Eventually, these
  patients develop muscle wasting and weight loss
  and are identified as "pink puffers."

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Diagnosis of COPD
EXPOSURE TO RISK FACTORS
SYMPTOMS
cough
tobacco
sputum
occupation
dyspnea
indoor/outdoor pollution
è
GAS DARAH ARTERI LABORATORY TEST CHEST X-RAY
SPIROMETRY
110
Spirometry Normal and COPD
111

• Normally, the left side of the heart produces a
  higher level of blood pressure in order to pump
  blood to the body the right side pumps blood
  through the lungs under much lower pressure. Any
  condition that leads to prolonged high blood
  pressure in the arteries or veins of the lungs
  (called pulmonary hypertension) will be poorly
  tolerated by the right ventricle of the heart.
  When this right ventricle fails or is unable to
• properly pump against these abnormally high
  pressures, this is called cor pulmonale.

112
Prognosis ?

• Indikator umur dan keparahan
• Jika ada hipoksia dan cor pulmonale prognosis
  jelek
• Dyspnea, obstruksi berat saluran nafas, FEV1 lt
• 0.75 L (20) ?? angka kematian meningkat, 50
  pasien berisiko meninggal dalam waktu 5 tahun

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Tujuan Terapi

• Memperbaiki keadaan obstruksi saluran nafas
• Mencegah dan mengatasi eksaserbasi akut
• Menurunkan progresivitas penyakit
• Meningkatkan keadaan fisik dan psikis
• Menurunkan jumlah hari tidak masuk kerja
• Menurunkan lama tinggal di RS
• Menurunkan angka kematian

114
NON FARMAKOLOGI

• Menghentikan kebiasaan merokok
• Rehabilitasi paru-paru secara komprehensif dengan
  OR dan latihan pernafasan
• Perbaikan nutrisi
• Tidak ada obat yang dapat menunda memburuknya
  fungsi paru jika pasien tetap merokok

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• Kortikosteroid ?? benefit is very limited,
  laporan tentang efektivitasnya masih bervariasi,
  kecuali jika pasien juga memiliki riwayat asma
• ?? Oksigen ?? untuk pasien hipoksemia, cor
  pulmonale. Digunakan jika baseline PaO2 turun
  sampai lt 55 mmHg
• ?? Antibiotik ?? digunakan bila ada tanda
  infeksi, bukan untuk maintenance therapy
• ?? Vaksinasi ?? direkomendasikan untuk high-risk
  patients vaksin pneumococcus (tiap 5-10 th) dan
  vaksin influenza (tiap tahun)
• ?? a1-proteinase inhibitor ?? utk pasien yang
  defisiensi a1- antitripsin ?? digunakan per
  minggu, masih mahal ?? contoh Prolastin

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Tahap terapi pada PPOK yang stabil

• Tahap 1 Ipratropium bromida (MDI) atau
  nebulizer, 2-6 puff 4 x sehari, tunjukkan cara
  penggunaan yang tepat, advis pasien ttg
  pentingnya penggunaan teratur dan efek samping yg
  mungkin timbul (mulut kering rasa pahit), jika
  hasil trial perbaikan FEV1 lt 20 ?? step 2
• Tahap 2 Tambahkan ß-agonis MDI atau nebulizer,
  tunjukkan cara penggunaan yang tepat, advis
  pasien ttg pentingnya penggunaan teratur dan efek
  samping yg mungkin timbul (takikardi, tremor) ??
  jika tidak ada perkembangan hentikan ß-agonis,
  jika ada perbaikan tapi kecil ?? step 3

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• Tahap 3 Tambah teofilin,mulai dari 400 mg/hari
  dlm bentuk sustained released, sesuaikan dosis
  setiap interval 3 hari untuk menjaga serum level
  antara 10-15 µg/ml, pantau ESO takikardi, tremor,
  nervous, efek GI jika tidak ada perbaikan ??
  hentikan teofilin dan ??go to step 4
• Tahap 4 Coba dengan kortikosteroid prednison
  30-40 mg/hari selama 2-4 minggu, cek dengan
  spirometer (perbaikan 20), titrasi dosis ke
  dosis efektif terkecil (lt 10 µg sehari),
  pertimbangkan penggunaan kortikosteroid inhalasi
  ?? jika pasien tidak berespon baik ?? kembali ke
  steroid oral

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Terapi antibiotika

• ?? Berdasarkan evidence terbaru yang tersedia,
  antibiotika harus diberikan pada pasien-pasien
  PPOK yang
• ?? Pasien dengan eksaserbasi akut dengan 3 tanda
  utama yaitu increased dyspnea, increased sputum
  volume, increased sputum purulence (Evidence B),
  atau
• ?? Pasien dengan eksaserbasi akut dengan 2 tanda
  utama, jika peningkatan purulensi sputum
  merupakan salah satunya (Evidence C)
• ?? Pasien dengan eksaserbasi parah yang
  membutuhkan ventilasi mekanik, baik invasif
  maupun non-infvasif (Evidence B)

120
Key points

• ??PPOK adalah penyakit yang sebenarnya secara
  potensial dapat dicegah ?? stop smoking
• ??Sekali PPOK terjadi ?? penderita akan
  memerlukan terapi yang kompleks ?? yang
  efikasinya masih diperdebatkan para ahli
• ??Penyakit ini bersifat progresif dan
  ireversibel?? berbiaya besar baik baik personal
  maupun masyarakat

121
Difference between bronchitis and emphysema
122
Bronchitis v. Emphysema

• Easy to decompensate
• Usually relatively easy to treat
• Can cause emphysema
• Rarely are these patients ever having normal
  blood gases

• Usually more difficult to decompensate
• Difficult to treat
• Can be caused by bronchitis
• Early, blood gases are normal

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Patofisiologi pneumotoraks

• Akibat peningkatan tekanan
• Intrabronkial ( batuk/ bersin )
• ?
• Tekanan diteruskan s/d alveoli
• ( locus minoris / Bullae - fibrotik pada alveoli
  )
• ?
• Alveoli robek sehingga
• merobek pleura di sekitarnya
• ?
• Udara masuk intrapleura
• ?
• Pneumotoraks

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Berdasarkan penyebab terjadinya

• PNEUMOTORAKS ARTIFISIAL
• Bedakan Tu-pleura dan Tu-paru ( dx )
• Proteksi Radioterapi Ca mamae ( tx )
• Haemoptisis Profuse ( tx )
• . PNEUMOTORAKS TRAUMATIK
• Akibat trauma pada dada
• . PNEUMOTORAKS SPONTAN
• Iatrogenik causa ??
• Penyakit kronis? TB, COPD, Asma

126
Berdasarkan jenis fistel

• PNEUMOTORAKS TERBUKA
• P. Intrapleura P. dunia luar ( two way )
• Tekanan ekspirasi 2 2
• Tekanan inspirasi 2 - 2
• PNEUMOTORAKS TERTUTUP
• P. Intrapleura ? P. dunia luar (no way )
• P awal ? resorbsi paru ? P jadi
• ? paru belum ngembang sempurna.
• Tekanan ekspirasi 4 - 4
• Tekanan inspirasi 12 - 1

127
BERDASARKAN DERAJAT KOLAPS

• Pneumotoraks Totalis
• Pneumotoraks Partialis
• Kolaps ( A X B ) ( a X b ) X 100
• ( A X B )

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Pneumotoraks parsial
129
Pneumotoraks total
130
Gejala Klinik

• Sesak mendadak memberat
• - Sesak tak di pengaruhi Posisi
• - Batuk
• - Dada terasa nyeri / kram / kemeng
• - Nampak sakit berat, keluar keringat dingin s/d
  syok
• - Napas tersengal sengal s/d sianosis

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Penatalaksanaan Pneumotoraks

• Antibiotika penyebab
• Anti Tuberkulosa ( OAT )
• Anti Tusif ( codein )
• Bronkhodilator
• Pencahar / Laxan
• Bed Rest / hindari kegiatan yang akibatkan
• peningkatan tekanan intra pleura ( teriak, bersin
• keras, mengejan dan batuk keras )

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Komplikasi Pneumotoraks

• Terjadi Infeksi
• Efusi Pleura ( Fluidopneumotoraks )
• Empyema ( Pyopneumotoraks )
• Terjadi Trauma Hematotoraks
• Udara dari cav. Pleura meluas
• Pneumomediastium Emfisema Cutis
• Udara menekan ke organ sekitar
• Tamponade Jantung
• Gagal napas

133
Efusi Pleura
134
Efusi Pleura

• Adanya Cairan Pleura yang Volume nya
• lebih dari Normal ( Vol. normal 1 20 cc )

135
Fisiologi cavum Pleura
136
Fisiologi Efusi Pleura

• Volume cairan pleura selalu konstan,
• akibat dari
• P. hidrostatik 9 mmHg produksi oleh
  pleura parietalis
• P. koloid osmotik 10 mmHg absorbsi oleh
  pleura viseralis

137
Penyebab akumulasi cairan Pleura

• ? Tekanan koloid osmotik ( Hypolbuminemia )
• ? Permeabilitas kapiler ( Radang, Neoplasma )
• ? Tekanan hirostatik ( Gagal jantung )
• ? Tekanan negatip intrapleura ( Atelektasis )

138
Pemeriksaan Fisik Efisi Pleura

• - Inspeksi nampak sakit, gerak dada sisi sakit
  tertinggal,nampak lebih cembung
• - Palpasi gerak dada sisi sakit tertinggal,
  Fremitus raba sisi sakit turun
• - Perkusi suara ketok sisi sakit redup
  pd.bag.bawah garis Ellis Damoiseau
• - Auskultasi suara napas sisi sakit turun
  /hilang

139
Sitologi cairan Pleura

• - Lekosit gt 25.000 / mm3 ? Empyema
• - Netrophil gt ? Pneumonia, TBC, Pancreatitis
• - Limphosit gt ? TBC, limphoma, keganasan
• - Eosinophil gt ? Emboli , Parasit, Jamur
• - Eritrosit 5 10 ribu/mm3 ? Pneumoni,
• Keganasan
• - Eritrosit 100 ribu / mm3 ? Keganasan, Trauma,
• Infark Paru
• - Sel ganas ? ditemukan pada 50 60
• Keganasan

140
Gambaran Radiologi Efusi Pleura

• lt 300 CC Secara fisik tak ada perubahan.
• Foto PA sinus masih nampak lancip.
• Foto Lat sinus nampak mulai tumpul
• gt 500 cc Gerak dada/ fremitus suara/fremitus
  raba menurun,suara ketok redup
• gt 1000 cc dada cembung, egofoni positip
• gt 2000 cc mediastinum terdorong

141
Foto Thorax
Foto Thoraks Perselubungan Pada
hemitoraks Dextra dengan sinus frenicus costalis
kanan tumpul
142
Penatalaksanaan Efusi Pleura

• - Evakuasi cairan pleura / torakosentesis
• volume pengambilan maksimal 1000 cc
• setiap kali pengambilan
• - Pemasangan WSD
• Efusi Pleura massive
• Efusi Pleura haemorhagic
• Hematotoraks, Empyema
• Chylotoraks, Chiliform

143
FARMAKOLOGI

• Antikolinergik inhalasi first line therapy,
  dosis harus cukup tinggi 2 puff 4 6x/day
  jika sulit, gunakan nebulizer 0.5 mg setiap 4-6
  jam prn, exp ipratropium or oxytropium bromide
• Simpatomimetik second line therapy
  terbutalin, salbutamol
• Kombinasi antikolinergik dan simpatomimetik
  untuk meningkatkan efektifitas
• Metil ksantin ?? banyak ADR, dipakai jika yang
  lain tidak mempan
• Mukolitik ?? membantu pengenceran dahak, namun
  tidak
• memperbaiki aliran udara ?? masih kontroversi,
  apakah bermanfaat secara klinis atau tidak