Tujuan dari Respirasiadalah untuk menyediakan oksigen bagi seluruh jaringan tubuh dan membuang karbon dioksida ke atmosfer

HidungUdara 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).

Bronchopulmonary segmentsLobulesAlveolar wall cell types

LUNGS 2

terminal bronchiole

respiratory bronchiole

pulmonary artery branch

alveolar sac

simple squamous epithelial cellmacrophage (dust cell)septal cell (produces surfactant)

Type I alveolar cell

Type II alveolar cell making surfactant

blood capillary

endothelial cell

macrophage

surfactant

respiratory membrane

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 bronkhus3. 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 KAPILER2. RESPIRASI INTERNAL

O2 DARI KAPILER SAMPAI KE SEL PADA JARINGAN.

RESPIRASI EXTERNAL

RESPIRASI INTERNAL

Active processBoyle’s Law

INSPIRATION

FORCED INSPIRATION

Inspiratory muscles

Phrenic nerves (C3-5)Thoracic nerves (T1 – T11)

thoracic volume pleural volume intrapleural pressure lung volume intrapulmonic pressureair flow into the lungs

760 mmHg

760 mmHg

760 mmHg

758 mmHg

BEFORE INSPIRATION DURING INSPIRATION

Process

Passive process at rest

EXPIRATION

internal intercostals(11 pairs)

internal intercostals (11 pairs)rectus abdominisabdominal obliquestransversus abdominis

Forced expiration

thoracic volume pleural volume intrapleural pressure lung volume intrapulmonic pressureair flow of the lungs

Process

external abdominal oblique

internal abdominal obliquetransversus abdominisrectus abdominis

760 mmHg

762 mmHg

elastic recoilsurface tension

Perubahan diafragma saat inspirasi & ekspirasi

Otot Pernapasan

Compliance is the ease with which the lungs and thoracic wall can be expanded during inspiration.

COMPLIANCE

elasticitysurface tension

Related to two factors:

destroys lung tissue (emphysema)fills lungs with fluid (pneumonia)produces surfactant deficiency (premature birth, near-drowning)interferes with lung expansion (pneumothorax)

Compliance is decreased with any condition that:

PULMONARY VOLUMES, CAPACITIES, AND RATES

SPIROGRAM

Volumes

tidal volume (500 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)

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

Ratesmaximum voluntary ventilation = TV x breaths/minutealveolar ventilation rate = alveolar ventilation x breaths/minute

IRV

ERV

TV

RVmaximum expiration

VC TLC

6000 ml

5000 ml

4000 ml

3000 ml

2000 ml

1000 ml

maximum inspiration

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 Derajat Kriteria

0 Normal Tidak ada kesulitan bernapss kecuali dengan aktivitas berat.

1 Ringan Terdapat kesulitan bernapas, napas pendek-pendek ketika terburu-buru atau ketika berjalan menuju puncak landai.

2 Sedang Berjalan lebih lambat daripada kebanyakan orang berusia sama karena sulit bernapas atau harus berhenti berjalan untuk bernapas.

3 Berat Berhenti berjalan setelah 90 meter untuk bernapas atau setelah berjalan beberapa menit.

4 Sangat berat Terlalu sulit bernapas bila meninggalkan rumah atau sulit bernapas ketika memakai baju atau membuka baju.

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 hiperkapniaHipokapnia 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 roleIn susceptible individuals, this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness and coughing, particularly at night or in the early morning..

eosinophils

epithelial cells

neutrophils

Macropha-ges

T lympho-cytes

mast cells

Cells

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)

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

stressoIndustrial triggers (wood, grain dust, cotton dust,

isocyanate containing paints, aluminum, hair spray,

penicillins)oBeta blockers even in form of eye drops

Cont……

oGastroesophageal reflux disease

oChronic sinusitis or rhinitis

oOSA (obstructive sleep apnoe)

oObesity

oAlergy bronchopulmonary

aspergilosis

COMORBID CONDITION

ASMAAsma 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 non-allergic 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

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

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)V

olum

e (l

itre

s)

Time (second)

1 2 3 4

Asthma patient

Normal subject

FEV1FVC

Componentof

Severity

Classification of Asthma Severity (>12 yrs)

Intermittent

Persistent

Mild Moderate Severe

Symptoms <2 d/wk>2 d/wk

but not dailyDaily

Throughout the day

Nighttime awakening <2 d/mo 3-4x/mo

>1x/wk but not nightly

Often 7x/wk

SABA use <2 d/wk>2 d/wk

but not daily &not >1x on any day

DailySeveral times

per day

Interference with activity NONE Minor limitation Some limitation

Extremely limited

Lung function

• Normal FEV1 between exacerbations• FEV1: >80% predicted• FEV1/FVC: normal

• FEV1 : >80%

predicted

• FEV1/FVC: normal

• FEV1: >60% but

<80% predicted

• FEV1/FVC:

reduced 5%

• FEV1: <60%

• FEV1/FVC:

reduced 5%

RISK Exacerbations requiring oral steroids

0-1/yr ≥2/yrConsider 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

Impa

irmen

t

Leukotriene receptor antagonists Direct antagonist of mediators responsible for airway inflammation in asthma

Bronchodilators Provide symptomatic relief of bronchospasm due to acute asthma exacerbation (short-acting agents) or long-term control of symptoms (long-acting agents)

Drug categories

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).

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

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

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 anti-inflammatory 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 drugsAny 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.

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,

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

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 (menghambat aksi dari enzym protease) 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.

The theory of interplayThe 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.

NeutrophilsNeutrophils

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 .

KLINISKLINIS

Keluhan utama: sesak napas, batuk, dahak Sesak timbul progresif sp mengganggu aktivitas,men-dadak memberat bila tjd eksaserbasiBatuk kronis, memberat pagi hari, dahak mukoid purulen bila eksaserbasiSuara mengi (wheezing) Batuk darah blood-streaked purulen sputum (eksa-

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

Noxious particles

and gases

Lung inflammation

Host factors

COPD pathology

ProteinasesOxidative stress

Anti-proteinasesAnti-oxidants

Repair mechanisms

PATOLOGI

• Saluran napas besar Hipertrofi kelenjar & pe jumlah sel Goblet hipersekresi mukus

• Saluran napas kecilRecycled injury & repair dinding sal. napas remodeling (pe kolagen & jar. ikat) penyempitan lumen & obstruksi sal. napas

• Parenkim paruDestruksi 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 COPDPathophysiology 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 yangsudah 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 bronchitisPathophysiology of chronic bronchitis IrritantsIrritants

↓ ↓Hyperplasia and hypertrophy of Hyperplasia and hypertrophy of mucous secreting cellmucous secreting cell ↓ ↓ Thick mucousThick mucous ↓ ↓ Air trappingAir trapping Sticky coating ↑Sticky coating ↑ ↓ ↓ Air way obstructionAir way obstruction Impaired ciliary function ↑Impaired ciliary function ↑ ↓ ↓ EdemaEdema Decrease mucous clearance ↑Decrease mucous clearance ↑ ↓ ↓ Bronchial wall thickness and Bronchial wall thickness and Lung defense system compromise inflammationLung defense system compromise inflammation ↓ ↑ ↓ ↑Vulnerable for infection → More infection more mucusVulnerable 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.

VENTILATIONVENTILATION

WORK OF WORK OF BREATHINGBREATHING

NORMAL COPDNORMAL COPD

SEVERE COPDSEVERE COPD

MODERATE COPDMODERATE COPDThe cost of work at a The cost of work at a given ventilation for given ventilation for ‘normal’ and COPD ‘normal’ and COPD patients (ACSM, patients (ACSM, 1998)1998)

• 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

DefinitionDefinition Abnormal permanent Abnormal permanent

enlargement of air spaces enlargement of air spaces distal to the terminal distal to the terminal bronchioles, accompanied bronchioles, accompanied by the destruction of the by the destruction of the walls and without obvious walls and without obvious fibrosisfibrosis

Emphysema is characterized Emphysema is characterized by loss of elasticity of the by loss of elasticity of the lung and abnormal lung and abnormal permanent enlargement of permanent enlargement of air spaces with destruction air spaces with destruction of the alveolar walls and of the alveolar walls and capillary beds. capillary beds.

EtiologiEmphysemaSmoking the primary risk factorLong-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 & fumesDusts from grains, minerals & other materials

Alpha 1-antitrypsin deficiency >>emphysemaGeneticsBronchitisAsthma

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 growthfactors 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

• Over distended alveoli– Damage to adjacent

pulmonary capillaries– dead space– Impaired passive expiration

Impaired gas exchange

• Impaired gas exchange– impaired expiration

• CO2 • Hypercapnia• Respiratory acidosis

• Damaged pulmonary capillary bed– pulmonary pressure – work load for right ventricle

– Right side heart failure (due

to respiratory pressure) – Cor Pulmonale

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."

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SYMPTOMS

coughcoughsputumsputumdyspneadyspnea

EXPOSURE TO RISKFACTORS

tobaccotobacco

occupationoccupationindoor/outdoor pollutionindoor/outdoor pollution

SPIROMETRYSPIROMETRY

Diagnosis of COPDDiagnosis of COPD

GAS DARAH ARTERILABORATORY TESTCHEST X-RAY

Spirometry: Normal and COPDSpirometry: Normal and COPDSpirometry: Normal and COPDSpirometry: Normal and COPD

0

5

1

4

2

3

Lit

er

1 65432

FVC

FVC

FEV1

FEV1

Normal

COPD

3.900

5.200

2.350

4.150 80 %

60 %NormalCOPD

FVCFEV1 FVCFEV1/

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 toproperly 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)

• α1-proteinase inhibitor utk pasien yang defisiensi α1- antitripsin digunakan per minggu, masih mahal contoh: Prolastin

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 < 20% step 2

• Tahap 2 : Tambahkan β-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 β-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 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 (< 10 μg 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 Difference between bronchitis and emphysemaemphysema

Productive cough

bronchitis

Classic sign

emphysema

Late in common with infection

Dyspnea Late in course Common

Wheezing Intermittent Mild

H/O smoking Common Common

Barrel chest Occasionally classic

Prolonged expiration Always present Always present

Cyanosis Common Uncommon

Chronic hypoventilation

Common Late in course

Ploycythemia Common Late in course

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 pneumotoraksAkibat 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 ARTIFISIALBedakan Tu-pleura dan Tu-paru ( dx )Proteksi Radioterapi Ca mamae ( tx )Haemoptisis Profuse ( tx ). PNEUMOTORAKS TRAUMATIKAkibat trauma pada dada. PNEUMOTORAKS SPONTANIatrogenik causa ??Penyakit kronis TB, COPD, Asma

Berdasarkan jenis fistelPNEUMOTORAKS TERBUKA

P. Intrapleura = P. dunia luar ( two way )Tekanan ekspirasi + 2 = + 2Tekanan inspirasi – 2 = - 2

• PNEUMOTORAKS TERTUTUPP. Intrapleura ≠ P. dunia luar (no way )

P awal + resorbsi paru P jadi – paru belum ngembang sempurna.

Tekanan ekspirasi – 4 =- 4Tekanan inspirasi – 12 = - 1

BERDASARKAN DERAJAT KOLAPS

• Pneumotoraks Totalis• Pneumotoraks Partialis

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

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 akibatkanpeningkatan tekanan intra pleura ( teriak, bersinkeras, mengejan dan batuk keras )

Komplikasi Pneumotoraks* Terjadi Infeksi Efusi Pleura ( Fluidopneumotoraks )Empyema ( Pyopneumotoraks )• Terjadi Trauma Hematotoraks• Udara dari cav. Pleura meluasPneumomediastium Emfisema Cutis* Udara menekan ke organ sekitar Tamponade JantungGagal napas

Efusi Pleura

Efusi Pleura

Adanya Cairan Pleura yang Volume nyalebih 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 hemitoraksDextra dengan sinus frenicus costalis kanan tumpul

Penatalaksanaan Efusi Pleura

- Evakuasi cairan pleura / torakosentesisvolume pengambilan maksimal 1000 ccsetiap 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