Tujuan dari Respirasi

adalah untuk menyediakan oksigen bagi seluruh jaringan tubuh dan membuang karbon dioksida ke atmosfer

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 %

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 < tekanan atmosfer: untuk mencegah kolaps paru.

Rongga torax
3 faktor yg mempertahankan tekanan negatif intrapleura normal:
1. Jaringan elastis paru memberikan kekuatan kontinu yg cenderung menarik paru menjauh dr rangka torax. 2. Kekuatan osmotik yg terdapat di seluruh membran pleura. 3. Kekuatan pompa limfatik.

Diafragma: otot berbentuk kubah yg membentuk dasar rongga torax & memisahkan rongga tersebut dari rongga abdomen.

Anatomi Saluran Pernapasan

Anatomi Saluran Pernapasan

Alveoli
Terdapat 2 tipe sel alveolar: Pneumosit tipe I: lap tipis menyebar & menutupi > 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).

LUNGS 2
Bronchopulmonary segments Lobules Alveolar wall cell types
simple squamous epithelial cell macrophage (dust cell) septal cell (produces surfactant)
terminal bronchiole respiratory bronchiole

pulmonary artery branch

alveolar sac

Type II alveolar cell making surfactant

surfactant

Type I alveolar cell

macrophage blood capillary

respiratory membrane

endothelial cell

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.

Pernafasan terdiri dari 4 proses :

1. Ventilasi : Keluar masuknya udara karena adanya selisih tekanan yang terdapat antara atmosfer dan alveolus 2. Distribusi : Pembagian udara ke cabang -cabang bronkhus 3. Transportasi dan Difusi - Transport O2 dan CO2 dalam darah dan cairan tubuh ke
dan dari sel - Difusi O2 dan CO2 antara darah dan alveoli

Pertukaran gas-gas antara alveoli dan kapiler dipengaruhi oleh tekanan parsial O2 & CO2 dalam atmosfer 4. Perfusi : Aliran darah yang membawa O2 ke jaringan

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

RESPIRASI EXTERNAL

RESPIRASI INTERNAL

INSPIRATION Active process Boyles Law

Process
thoracic volume pleural volume intrapleural pressure lung volume intrapulmonic pressure air flow into the lungs
760 mmHg 760 mmHg

Inspiratory muscles
Phrenic nerves (C3-5) Thoracic nerves (T1 T11)

760 mmHg BEFORE INSPIRATION

758 mmHg DURING INSPIRATION

FORCED INSPIRATION

EXPIRATION
Passive process at rest
elastic recoil surface tension
internal intercostals (11 pairs)

Process
thoracic volume pleural volume intrapleural pressure lung volume intrapulmonic pressure air flow of the lungs

external abdominal oblique internal abdominal oblique transversus abdominis rectus abdominis 760 mmHg

Forced expiration
internal intercostals (11 pairs) rectus abdominis abdominal obliques transversus abdominis

762 mmHg

Perubahan diafragma saat inspirasi & ekspirasi

Otot Pernapasan

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)

PULMONARY VOLUMES, CAPACITIES, AND RATES

Volumes
tidal volume (500 ml)
6000 ml

maximum inspiration

5000 ml

anatomical dead space (150 ml) alveolar ventilation (350 ml) physiological dead space inspiratory reserve volume (3000 ml) expiratory reserve volume (1200 ml) residual volume (1300 ml)

IRV VC
4000 ml

TLC

3000 ml

TV
2000 ml

Capacities
total lung capacity (TV+IRV+ERV+RV) vital capacity (TV+IRV+ERV) (4700 ml) inspiratory capacity (TV+IRV) functional residual capacity (RV+ERV)

ERV

1000 ml

maximum expiration SPIROGRAM

RV

Rates
maximum voluntary ventilation = TV x breaths/minute alveolar ventilation rate = alveolar ventilation x breaths/minute

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

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.

Kontrol Pernapasan

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.

26

Derajat Dyspnea
Tingkat 0 Derajat Normal Kriteria Tidak ada kesulitan bernapss kecuali dengan aktivitas berat. Terdapat kesulitan bernapas, napas pendek-pendek ketika terburu-buru atau ketika berjalan menuju puncak landai.

Ringan

Sedang

Berjalan lebih lambat daripada kebanyakan orang berusia sama karena sulit bernapas atau harus berhenti berjalan untuk bernapas. Berhenti berjalan setelah 90 meter untuk bernapas atau setelah berjalan beberapa menit. Terlalu sulit bernapas bila meninggalkan rumah atau sulit bernapas ketika memakai baju atau membuka baju.

3 4

Berat Sangat berat

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

28

Signs of dyspnea:
Flaring nostrils Use of accessory muscles in breathing Retraction (pulling back) of intercostal spaces

29

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

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
31

 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.

32

 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.

33

 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.

34

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.

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.

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.
37

 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.
38

Jari Tabuh
Jari tabuh adalah perubahan bentuk normal falang distal dan kuku tangan dan kaki serta ditandai dengan 1. Kehilangan sudut kuku yang normalnya 160 derajat. 2. Rasa halus berongga pada dasar kuku. 3. 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

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 <35 mmhg. Penyebab langsung selalu hiperventilasi alveolar (eliminasi CO2 lebih cepat daripada produksinya). Hiperkapnia / asidosis respiratorius merupakan meningkatnya PaCO2 >45 mmhg. Penyebab langsung adalah selalu hipoventilasi alveolar (kegagalan dalam mengeliminasi CO2 secepat produksinya).

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
41

 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)

42

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

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

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..

mast cells

eosinophils

T lymphocytes

Cells
epithelial cells Macrophages

neutrophils

Causes and Triggers

oAllergies such as to pollens, mold spores, pet dander, and dust mites oInfections (colds, viruses, flu, sinus infection) oExercise oAspirin or nonsteroidal anti-inflammatory drug (NSAID) hypersensitivity, sulfite sensitivity oUse of beta-adrenergic receptor blockers (including ophthalmic preparations)

Cont

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

oGastroesophageal reflux disease oChronic sinusitis or rhinitis oOSA (obstructive sleep apnoe) oObesity oAlergy bronchopulmonary

aspergilosis

COMORBID CONDITION

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 instrinsik+Ekstrinsik)

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

Immunological Mechanisms in Respiratory Diseases

Patofisiologi Asma

Intrinsic asthma; tend to develop in

adulthood, and symptoms are triggered by nonallergic factors such as; 1. Viral infection, irritants which cause epithelial damage and mucosal inflammation 2. Emotional upset which mediates excess parasympathetic input 3. Exercise which causes water ad heat loss from the airways

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

gambar

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

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

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 .

Investigations
Pulmonary function testing (spirometry) Forced expiratory volume (FEV)
Methacholine or histamine challenge testing

Exercise testing
Peak expiratory flow rate monitoring

Forced expiratory volume (FEV)

Normal subject
Volume (litres)

Asthma patient
FVC

FEV1

Time (second)

Component of Severity
Symptoms Nighttime awakening

Classification of Asthma Severity (>12 yrs)

Intermittent

Persistent
Mild
>2 d/wk but not daily 3-4x/mo >2 d/wk but not daily & not >1x on any day Minor limitation
FEV1 : >80% predicted FEV1/FVC: normal

Moderate
Daily >1x/wk but not nightly

Severe
Throughout the day Often 7x/wk Several times per day Extremely limited
FEV1: <60% FEV1/FVC: reduced 5%

<2 d/wk <2 d/mo

Impairment

SABA use

<2 d/wk

Daily

Interference with activity

NONE
Normal FEV1 between exacerbations FEV1: >80% predicted FEV1/FVC: normal

Some limitation
FEV1: >60% but <80% predicted FEV1/FVC: reduced 5%

Lung function

RISK

Exacerbations requiring oral steroids

0-1/yr

2/yr

Consider severity and interval since last exacerbation as they may fluctuate over time in any severity category

Recommended Treatment Step

Step 1

Step 2

Step 3

Step 4 or 5

& consider short OS burst

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).

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

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

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.

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.

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 antiinflammatory agents cromolyn sodium or nedocromil sodium This is maintenance anti-inflammatory therapy without any direct bronchodilator effect.

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 Corticosteroids 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.

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

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

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

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

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 g/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.

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

leukotriene receptor antagonists,

pecifically, LTD4 receptor antagonist and 5lipoxygenase inhibitors can completely block the acute phase response and block part of the delayed phase response
S

Blocking the generation of leukotrienes or blocking their actions on cells may be helpful in control of asthma and treatment of asthma attacks

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.

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

FAKTOR RISIKO

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

Lingkungan: 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

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.

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.

The theory of interplay

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 .

Neutrophils

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 (eksaserbasi) Nyeri dada (pleuritis, pneumotoraks, emboli paru) Anoreksi & BB menurun progresif jelek

KLINIS

Noxious particles and gases

Host factors

Lung inflammation
Anti-oxidants

Anti-proteinases

Oxidative stress

Proteinases
Repair mechanisms

COPD pathology

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

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.

Pathophysiology of COPD

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).

COPD/PPOM

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. .

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

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.

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

CHANGES IN LUNG VOLUMES

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

SEVERE COPD

WORK OF BREATHING

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

 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.

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.

Etiologi Emphysema

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 >>emphysema Genetics Bronchitis Asthma

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

Dilatation & destruction

+ mucus secretion

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.

Pathophysiology
Affects alveolar membrane
Destruction of alveolar wall Loss of elastic recoil Over distended alveoli

Impaired gas exchange

impaired expiration
h CO2 Hypercapnia Respiratory acidosis

Over distended alveoli

Damage to adjacent pulmonary capillaries h dead space Impaired passive expiration

Damaged pulmonary capillary bed

h pulmonary pressure h work load for right ventricle Right side heart failure (due to respiratory pressure) Cor Pulmonale

Impaired gas exchange

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

 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."

Diagnosis of COPD
SYMPTOMS cough sputum dyspnea
EXPOSURE TO RISK FACTORS tobacco

occupation indoor/outdoor pollution

SPIROMETRY

GAS DARAH ARTERI LABORATORY TEST CHEST X-RAY

109

Spirometry: Normal and COPD

0 1 2 FEV1 FVC
5.200 3.900

FEV1/ FVC
80 % 60 %

Normal COPD
FEV1

4.150 2.350

Liter

COPD
4 5 1 2 FEV1 FVC

Normal
3 4

FVC 5 6 Seconds

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.

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

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

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

 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 < 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) 1-proteinase inhibitor utk pasien yang defisiensi 1antitripsin digunakan per minggu, masih mahal contoh: Prolastin

Tahap terapi pada PPOK yang stabil

Tahap 1 : Ipratropium bromida (MDI) atau nebulizer, 26 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 < 20% step 2 Tahap 2 : Tambahkan -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 -agonis, jika ada perbaikan tapi kecil step 3

 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 g/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 (< 10 g sehari), pertimbangkan penggunaan kortikosteroid inhalasi jika pasien tidak berespon baik kembali ke steroid oral

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)

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

Difference between bronchitis and emphysema

bronchitis Productive cough Dyspnea Wheezing H/O smoking Classic sign Late in course Intermittent Common emphysema Late in common with infection Common Mild Common

Barrel chest
Prolonged expiration Cyanosis Ploycythemia

Occasionally
Always present Common Common

classic
Always present Uncommon Late in course Late in course

Chronic hypoventilation Common

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

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

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

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

BERDASARKAN DERAJAT KOLAPS

Pneumotoraks Totalis Pneumotoraks Partialis

% Kolaps = ( A X B ) ( a X b ) X 100 % (AXB)

Pneumotoraks parsial

Pneumotoraks total

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

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 )

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

Efusi Pleura

Efusi Pleura

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

Fisiologi cavum Pleura

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

Penyebab akumulasi cairan Pleura

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

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

Sitologi cairan Pleura

- Lekosit > 25.000 / mm3 Empyema - Netrophil > Pneumonia, TBC, Pancreatitis - Limphosit > TBC, limphoma, keganasan - Eosinophil > 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

Gambaran Radiologi Efusi Pleura

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

Foto Thorax

Foto Thoraks: Perselubungan Pada hemitoraks Dextra dengan sinus frenicus costalis kanan tumpul

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

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